Davidović, Radoslav S.

Link to this page

Authority KeyName Variants
orcid::0000-0002-6097-6203
  • Davidović, Radoslav S. (18)
Projects
Molecular determinants for tumor marker design Application of the EIIP/ISM bioinformatics platform in discovery of novel therapeutic targets and potential therapeutic molecules
Functional, Functionalized and Advanced Nanomaterials Light microscopy, electron microscopy, immunomorphologic, molecular biology and genetic investigations of malignant and nonmalignant renal diseases.
Agencia Nacional de Promocion Cientifica y Tecnologica (ANPCyT) of Argentina [PICT-2015/3367] Agencia Nacional de Promocion Cientifica y Tecnologica (ANPCyT) of Argentina [PICT2017/1924]
Carlsberg Distinguished Fellowship [CF18-0314] Consejo Nacional de Ciencia y Tecnologia (CONACyT) [215503]
COST Action BM1405 NGP-net, ELIXIR-IIB, Hungarian Academy of Sciences [LP2014-16], Hungarian Scientific Research Fund [OTKA K 108798], AIRC Research Fellowship, Spanish Ministerio de Educacion Cultura i Deporte PhD Fellowship, Mexican National Council for Science and Technology (CONACYT) [215503], Grant PortoNeuroDRIve'i3S - Norte Portugal Regional Operational Programme (NORTE), under the PORTUGAL Partnership Agreement, through the European Regional Development Fund (ERDF), Direction Generale des Armees, Aix-Marseille University PhD Fellowship, OTKA Grant [PD-OTKA 108772], French Ministry of National Education, Research and Technology PhD Fellowship, ICREAAcademia Award, Odysseus Grant from Research Foundation Flanders (FWO) [G.0029.12], AIRC IG Grant [17753], Italian Ministry of Health [GR-2011-02347754, GR-2011-02346845], Swedish Research Council Grant [VR-NT 2012-5046] Danmarks Grundforskningsfond [DNRF125]
Elixir-GR, Action 'Reinforcement of the Research and Innovation Infrastructure', Operational Programme 'Competitiveness, Entrepreneurship and Innovation' [NSRF] European Regional Development Fund [POCI01-0145-FEDER-029221]
European Regional Development Fund [POCI-01-0145-FEDER-031173] European Union's Horizon 2020 research and innovation programme [778247]. Funding for open access charge: European Union's Horizon 2020 research and innovation programme [778247]
Hungarian Academy of Sciences [LP2014-18] Hungarian Academy of Sciences [PREMIUM-2017-48]
Hungarian National Research, Development, and Innovation Office (NKFIH) [FK-128133] ICREA
Hormonal regulation of expression and activity of the nitric oxide synthase and sodium-potassium pump in experimental models of insulin resistance, diabetes and cardiovascular disorders Cell Cycle Aberrations and the Impact of Oxidative Stress in Neurodegenerative Processes and Malignant Transformation of the Cell
Pain Control and Molecular Mechanisms as Factors for Tissue Regeneration in Dentistry in Healthy and Diabetic Patients Cellular and molecular basis of malignant and cardiovascular diseases-clinical implications
Identification of predictive molecular markers for cancer progression, response to therapy and disease outcome Italian Ministry of Health Young Investigator Grant [GR-2011-02347754]
Ministerio de Economia y Competitividad (MINECO) [BIO2016-78310-R] National Research, Development and Innovation Office [K-125340]
Orszagos Tudomanyos Kutatasi Alapprogramok (OTKA) [K108798] Orszagos Tudomanyos Kutatasi Alapprogramok (OTKA) [K124670]
Portuguese Foundation for Science and Technology Research Foundation Flanders (FWO) [G.0328.16N]

Author's Bibliography

Alignment-free method for functional annotation of amino acid substitutions: Application on epigenetic factors involved in hematologic malignancies

Gemović, Branislava S.; Perović, Vladimir R.; Davidović, Radoslav S.; Drljača, Tamara; Veljković, Nevena V.

(2021)

TY  - JOUR
AU  - Gemović, Branislava S.
AU  - Perović, Vladimir R.
AU  - Davidović, Radoslav S.
AU  - Drljača, Tamara
AU  - Veljković, Nevena V.
PY  - 2021
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8894
AB  - For the last couple of decades, there has been a significant growth in sequencing data, leading to an extraordinary increase in the number of gene variants. This places a challenge on the bioinformatics research community to develop and improve computational tools for functional annotation of new variants. Genes coding for epigenetic regulators have important roles in cancer pathogenesis and mutations in these genes show great potential as clinical biomarkers, especially in hematologic malignancies. Therefore, we developed a model that specifically focuses on these genes, with an assumption that it would outperform general models in predicting the functional effects of amino acid substitutions. EpiMut is a standalone software that implements a sequence based alignment-free method. We applied a two-step approach for generating sequence based features, relying on the biophysical and biochemical indices of amino acids and the Fourier Transform as a sequence transformation method. For each gene in the dataset, the machine learning algorithm–Naïve Bayes was used for building a model for prediction of the neutral or disease-related status of variants. EpiMut outperformed state-of-the-art tools used for comparison, PolyPhen-2, SIFT and SNAP2. Additionally, EpiMut showed the highest performance on the subset of variants positioned outside conserved functional domains of analysed proteins, which represents an important group of cancer-related variants. These results imply that EpiMut can be applied as a first choice tool in research of the impact of gene variants in epigenetic regulators, especially in the light of the biomarker role in hematologic malignancies. EpiMut is freely available at https://www.vin.bg.ac.rs/180/tools/epimut.php.
T2  - PLOS One
T1  - Alignment-free method for functional annotation of amino acid substitutions: Application on epigenetic factors involved in hematologic malignancies
VL  - 16
IS  - 1
SP  - e0244948
DO  - 10.1371/journal.pone.0244948
ER  - 
@article{
author = "Gemović, Branislava S. and Perović, Vladimir R. and Davidović, Radoslav S. and Drljača, Tamara and Veljković, Nevena V.",
year = "2021",
url = "https://vinar.vin.bg.ac.rs/handle/123456789/8894",
abstract = "For the last couple of decades, there has been a significant growth in sequencing data, leading to an extraordinary increase in the number of gene variants. This places a challenge on the bioinformatics research community to develop and improve computational tools for functional annotation of new variants. Genes coding for epigenetic regulators have important roles in cancer pathogenesis and mutations in these genes show great potential as clinical biomarkers, especially in hematologic malignancies. Therefore, we developed a model that specifically focuses on these genes, with an assumption that it would outperform general models in predicting the functional effects of amino acid substitutions. EpiMut is a standalone software that implements a sequence based alignment-free method. We applied a two-step approach for generating sequence based features, relying on the biophysical and biochemical indices of amino acids and the Fourier Transform as a sequence transformation method. For each gene in the dataset, the machine learning algorithm–Naïve Bayes was used for building a model for prediction of the neutral or disease-related status of variants. EpiMut outperformed state-of-the-art tools used for comparison, PolyPhen-2, SIFT and SNAP2. Additionally, EpiMut showed the highest performance on the subset of variants positioned outside conserved functional domains of analysed proteins, which represents an important group of cancer-related variants. These results imply that EpiMut can be applied as a first choice tool in research of the impact of gene variants in epigenetic regulators, especially in the light of the biomarker role in hematologic malignancies. EpiMut is freely available at https://www.vin.bg.ac.rs/180/tools/epimut.php.",
journal = "PLOS One",
title = "Alignment-free method for functional annotation of amino acid substitutions: Application on epigenetic factors involved in hematologic malignancies",
volume = "16",
number = "1",
pages = "e0244948",
doi = "10.1371/journal.pone.0244948"
}
Gemović, B. S., Perović, V. R., Davidović, R. S., Drljača, T.,& Veljković, N. V. (2021). Alignment-free method for functional annotation of amino acid substitutions: Application on epigenetic factors involved in hematologic malignancies.
PLOS One, 16(1), e0244948.
https://doi.org/10.1371/journal.pone.0244948
Gemović BS, Perović VR, Davidović RS, Drljača T, Veljković NV. Alignment-free method for functional annotation of amino acid substitutions: Application on epigenetic factors involved in hematologic malignancies. PLOS One. 2021;16(1):e0244948
Gemović Branislava S., Perović Vladimir R., Davidović Radoslav S., Drljača Tamara, Veljković Nevena V., "Alignment-free method for functional annotation of amino acid substitutions: Application on epigenetic factors involved in hematologic malignancies" PLOS One, 16, no. 1 (2021):e0244948,
https://doi.org/10.1371/journal.pone.0244948 .
1

The CAFA challenge reports improved protein function prediction and new functional annotations for hundreds of genes through experimental screens

Zhou, Naihui; Jiang, Yuxiang; Bergquist, Timothy R; Lee, Alexandra J; Kacsoh, Balint Z; Crocker, Alex W; Lewis, Kimberley A; Georghiou, George; Nguyen, Huy N; Hamid, Md Nafiz; Davis, Larry; Dogan, Tunca; Atalay, Volkan; Rifaioglu, Ahmet S; Dalkıran, Alperen; Cetin Atalay, Rengul; Zhang, Chengxin; Hurto, Rebecca L; Freddolino, Peter L; Zhang, Yang; Bhat, Prajwal; Supek, Fran; Fernández, José M; Gemović, Branislava S.; Perović, Vladimir R.; Davidović, Radoslav S.; Šumonja, Neven; Veljković, Nevena V.; Asgari, Ehsaneddin; Mofrad, Mohammad R.K.; Profiti, Giuseppe; Savojardo, Castrense; Martelli, Pier Luigi; Casadio, Rita; Boecker, Florian; Schoof, Heiko; Kahanda, Indika; Thurlby, Natalie; McHardy, Alice C; Renaux, Alexandre; Saidi, Rabie; Gough, Julian; Freitas, Alex A; Antczak, Magdalena; Fabris, Fabio; Wass, Mark N; Hou, Jie; Cheng, Jianlin; Wang, Zheng; Romero, Alfonso E; Paccanaro, Alberto; Yang, Haixuan; Goldberg, Tatyana; Zhao, Chenguang; Holm, Liisa; Törönen, Petri; Medlar, Alan J; Zosa, Elaine; Borukhov, Itamar; Novikov, Ilya; Wilkins, Angela; Lichtarge, Olivier; Chi, Po-Han; Tseng, Wei-Cheng; Linial, Michal; Rose, Peter W; Dessimoz, Christophe; Vidulin, Vedrana; Dzeroski, Saso; Sillitoe, Ian; Das, Sayoni; Lees, Jonathan Gill; Jones, David T; Wan, Cen; Cozzetto, Domenico; Fa, Rui; Torres, Mateo; Warwick Vesztrocy, Alex; Rodriguez, Jose Manuel; Tress, Michael L; Frasca, Marco; Notaro, Marco; Grossi, Giuliano; Petrini, Alessandro; Re, Matteo; Valentini, Giorgio; Mesiti, Marco; Roche, Daniel B; Reeb, Jonas; Ritchie, David W; Aridhi, Sabeur; Alborzi, Seyed Ziaeddin; Devignes, Marie-Dominique; Koo, Da Chen Emily; Bonneau, Richard; Gligorijević, Vladimir; Barot, Meet; Fang, Hai; Toppo, Stefano; Lavezzo, Enrico; Falda, Marco; Berselli, Michele; Tosatto, Silvio C.E.; Carraro, Marco; Piovesan, Damiano; Ur Rehman, Hafeez; Mao, Qizhong; Zhang, Shanshan; Vucetic, Slobodan; Black, Gage S; Jo, Dane; Suh, Erica; Dayton, Jonathan B; Larsen, Dallas J; Omdahl, Ashton R; McGuffin, Liam J; Brackenridge, Danielle A; Babbitt, Patricia C; Yunes, Jeffrey M; Fontana, Paolo; Zhang, Feng; Zhu, Shanfeng; You, Ronghui; Zhang, Zihan; Dai, Suyang; Yao, Shuwei; Tian, Weidong; Cao, Renzhi; Chandler, Caleb; Amezola, Miguel; Johnson, Devon; Chang, Jia-Ming; Liao, Wen-Hung; Liu, Yi-Wei; Pascarelli, Stefano; Frank, Yotam; Hoehndorf, Robert; Kulmanov, Maxat; Boudellioua, Imane; Politano, Gianfranco; Di Carlo, Stefano; Benso, Alfredo; Hakala, Kai; Ginter, Filip; Mehryary, Farrokh; Kaewphan, Suwisa; Björne, Jari; Moen, Hans; Tolvanen, Martti E.E.; Salakoski, Tapio; Kihara, Daisuke; Jain, Aashish; Šmuc, Tomislav; Altenhoff, Adrian; Ben-Hur, Asa; Rost, Burkhard; Brenner, Steven E; Orengo, Christine A; Jeffery, Constance J; Bosco, Giovanni; Hogan, Deborah A; Martin, Maria J; O’Donovan, Claire; Mooney, Sean D; Greene, Casey S; Radivojac, Predrag; Friedberg, Iddo

(2019)

TY  - JOUR
AU  - Zhou, Naihui
AU  - Jiang, Yuxiang
AU  - Bergquist, Timothy R
AU  - Lee, Alexandra J
AU  - Kacsoh, Balint Z
AU  - Crocker, Alex W
AU  - Lewis, Kimberley A
AU  - Georghiou, George
AU  - Nguyen, Huy N
AU  - Hamid, Md Nafiz
AU  - Davis, Larry
AU  - Dogan, Tunca
AU  - Atalay, Volkan
AU  - Rifaioglu, Ahmet S
AU  - Dalkıran, Alperen
AU  - Cetin Atalay, Rengul
AU  - Zhang, Chengxin
AU  - Hurto, Rebecca L
AU  - Freddolino, Peter L
AU  - Zhang, Yang
AU  - Bhat, Prajwal
AU  - Supek, Fran
AU  - Fernández, José M
AU  - Gemović, Branislava S.
AU  - Perović, Vladimir R.
AU  - Davidović, Radoslav S.
AU  - Šumonja, Neven
AU  - Veljković, Nevena V.
AU  - Asgari, Ehsaneddin
AU  - Mofrad, Mohammad R.K.
AU  - Profiti, Giuseppe
AU  - Savojardo, Castrense
AU  - Martelli, Pier Luigi
AU  - Casadio, Rita
AU  - Boecker, Florian
AU  - Schoof, Heiko
AU  - Kahanda, Indika
AU  - Thurlby, Natalie
AU  - McHardy, Alice C
AU  - Renaux, Alexandre
AU  - Saidi, Rabie
AU  - Gough, Julian
AU  - Freitas, Alex A
AU  - Antczak, Magdalena
AU  - Fabris, Fabio
AU  - Wass, Mark N
AU  - Hou, Jie
AU  - Cheng, Jianlin
AU  - Wang, Zheng
AU  - Romero, Alfonso E
AU  - Paccanaro, Alberto
AU  - Yang, Haixuan
AU  - Goldberg, Tatyana
AU  - Zhao, Chenguang
AU  - Holm, Liisa
AU  - Törönen, Petri
AU  - Medlar, Alan J
AU  - Zosa, Elaine
AU  - Borukhov, Itamar
AU  - Novikov, Ilya
AU  - Wilkins, Angela
AU  - Lichtarge, Olivier
AU  - Chi, Po-Han
AU  - Tseng, Wei-Cheng
AU  - Linial, Michal
AU  - Rose, Peter W
AU  - Dessimoz, Christophe
AU  - Vidulin, Vedrana
AU  - Dzeroski, Saso
AU  - Sillitoe, Ian
AU  - Das, Sayoni
AU  - Lees, Jonathan Gill
AU  - Jones, David T
AU  - Wan, Cen
AU  - Cozzetto, Domenico
AU  - Fa, Rui
AU  - Torres, Mateo
AU  - Warwick Vesztrocy, Alex
AU  - Rodriguez, Jose Manuel
AU  - Tress, Michael L
AU  - Frasca, Marco
AU  - Notaro, Marco
AU  - Grossi, Giuliano
AU  - Petrini, Alessandro
AU  - Re, Matteo
AU  - Valentini, Giorgio
AU  - Mesiti, Marco
AU  - Roche, Daniel B
AU  - Reeb, Jonas
AU  - Ritchie, David W
AU  - Aridhi, Sabeur
AU  - Alborzi, Seyed Ziaeddin
AU  - Devignes, Marie-Dominique
AU  - Koo, Da Chen Emily
AU  - Bonneau, Richard
AU  - Gligorijević, Vladimir
AU  - Barot, Meet
AU  - Fang, Hai
AU  - Toppo, Stefano
AU  - Lavezzo, Enrico
AU  - Falda, Marco
AU  - Berselli, Michele
AU  - Tosatto, Silvio C.E.
AU  - Carraro, Marco
AU  - Piovesan, Damiano
AU  - Ur Rehman, Hafeez
AU  - Mao, Qizhong
AU  - Zhang, Shanshan
AU  - Vucetic, Slobodan
AU  - Black, Gage S
AU  - Jo, Dane
AU  - Suh, Erica
AU  - Dayton, Jonathan B
AU  - Larsen, Dallas J
AU  - Omdahl, Ashton R
AU  - McGuffin, Liam J
AU  - Brackenridge, Danielle A
AU  - Babbitt, Patricia C
AU  - Yunes, Jeffrey M
AU  - Fontana, Paolo
AU  - Zhang, Feng
AU  - Zhu, Shanfeng
AU  - You, Ronghui
AU  - Zhang, Zihan
AU  - Dai, Suyang
AU  - Yao, Shuwei
AU  - Tian, Weidong
AU  - Cao, Renzhi
AU  - Chandler, Caleb
AU  - Amezola, Miguel
AU  - Johnson, Devon
AU  - Chang, Jia-Ming
AU  - Liao, Wen-Hung
AU  - Liu, Yi-Wei
AU  - Pascarelli, Stefano
AU  - Frank, Yotam
AU  - Hoehndorf, Robert
AU  - Kulmanov, Maxat
AU  - Boudellioua, Imane
AU  - Politano, Gianfranco
AU  - Di Carlo, Stefano
AU  - Benso, Alfredo
AU  - Hakala, Kai
AU  - Ginter, Filip
AU  - Mehryary, Farrokh
AU  - Kaewphan, Suwisa
AU  - Björne, Jari
AU  - Moen, Hans
AU  - Tolvanen, Martti E.E.
AU  - Salakoski, Tapio
AU  - Kihara, Daisuke
AU  - Jain, Aashish
AU  - Šmuc, Tomislav
AU  - Altenhoff, Adrian
AU  - Ben-Hur, Asa
AU  - Rost, Burkhard
AU  - Brenner, Steven E
AU  - Orengo, Christine A
AU  - Jeffery, Constance J
AU  - Bosco, Giovanni
AU  - Hogan, Deborah A
AU  - Martin, Maria J
AU  - O’Donovan, Claire
AU  - Mooney, Sean D
AU  - Greene, Casey S
AU  - Radivojac, Predrag
AU  - Friedberg, Iddo
PY  - 2019
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8655
AB  - Background: The Critical Assessment of Functional Annotation (CAFA) is an ongoing, global, community-driven effort to evaluate and improve the computational annotation of protein function. Results: Here, we report on the results of the third CAFA challenge, CAFA3, that featured an expanded analysis over the previous CAFA rounds, both in terms of volume of data analyzed and the types of analysis performed. In a novel and major new development, computational predictions and assessment goals drove some of the experimental assays, resulting in new functional annotations for more than 1000 genes. Specifically, we performed experimental whole-genome mutation screening in Candida albicans and Pseudomonas aureginosa genomes, which provided us with genome-wide experimental data for genes associated with biofilm formation and motility. We further performed targeted assays on selected genes in Drosophila melanogaster, which we suspected of being involved in long-Term memory. Conclusion: We conclude that while predictions of the molecular function and biological process annotations have slightly improved over time, those of the cellular component have not. Term-centric prediction of experimental annotations remains equally challenging; although the performance of the top methods is significantly better than the expectations set by baseline methods in C. albicans and D. melanogaster, it leaves considerable room and need for improvement. Finally, we report that the CAFA community now involves a broad range of participants with expertise in bioinformatics, biological experimentation, biocuration, and bio-ontologies, working together to improve functional annotation, computational function prediction, and our ability to manage big data in the era of large experimental screens. © 2019 The Author(s).
T2  - Genome Biology
T1  - The CAFA challenge reports improved protein function prediction and new functional annotations for hundreds of genes through experimental screens
VL  - 20
IS  - 1
SP  - 244
DO  - 10.1186/s13059-019-1835-8
ER  - 
@article{
author = "Zhou, Naihui and Jiang, Yuxiang and Bergquist, Timothy R and Lee, Alexandra J and Kacsoh, Balint Z and Crocker, Alex W and Lewis, Kimberley A and Georghiou, George and Nguyen, Huy N and Hamid, Md Nafiz and Davis, Larry and Dogan, Tunca and Atalay, Volkan and Rifaioglu, Ahmet S and Dalkıran, Alperen and Cetin Atalay, Rengul and Zhang, Chengxin and Hurto, Rebecca L and Freddolino, Peter L and Zhang, Yang and Bhat, Prajwal and Supek, Fran and Fernández, José M and Gemović, Branislava S. and Perović, Vladimir R. and Davidović, Radoslav S. and Šumonja, Neven and Veljković, Nevena V. and Asgari, Ehsaneddin and Mofrad, Mohammad R.K. and Profiti, Giuseppe and Savojardo, Castrense and Martelli, Pier Luigi and Casadio, Rita and Boecker, Florian and Schoof, Heiko and Kahanda, Indika and Thurlby, Natalie and McHardy, Alice C and Renaux, Alexandre and Saidi, Rabie and Gough, Julian and Freitas, Alex A and Antczak, Magdalena and Fabris, Fabio and Wass, Mark N and Hou, Jie and Cheng, Jianlin and Wang, Zheng and Romero, Alfonso E and Paccanaro, Alberto and Yang, Haixuan and Goldberg, Tatyana and Zhao, Chenguang and Holm, Liisa and Törönen, Petri and Medlar, Alan J and Zosa, Elaine and Borukhov, Itamar and Novikov, Ilya and Wilkins, Angela and Lichtarge, Olivier and Chi, Po-Han and Tseng, Wei-Cheng and Linial, Michal and Rose, Peter W and Dessimoz, Christophe and Vidulin, Vedrana and Dzeroski, Saso and Sillitoe, Ian and Das, Sayoni and Lees, Jonathan Gill and Jones, David T and Wan, Cen and Cozzetto, Domenico and Fa, Rui and Torres, Mateo and Warwick Vesztrocy, Alex and Rodriguez, Jose Manuel and Tress, Michael L and Frasca, Marco and Notaro, Marco and Grossi, Giuliano and Petrini, Alessandro and Re, Matteo and Valentini, Giorgio and Mesiti, Marco and Roche, Daniel B and Reeb, Jonas and Ritchie, David W and Aridhi, Sabeur and Alborzi, Seyed Ziaeddin and Devignes, Marie-Dominique and Koo, Da Chen Emily and Bonneau, Richard and Gligorijević, Vladimir and Barot, Meet and Fang, Hai and Toppo, Stefano and Lavezzo, Enrico and Falda, Marco and Berselli, Michele and Tosatto, Silvio C.E. and Carraro, Marco and Piovesan, Damiano and Ur Rehman, Hafeez and Mao, Qizhong and Zhang, Shanshan and Vucetic, Slobodan and Black, Gage S and Jo, Dane and Suh, Erica and Dayton, Jonathan B and Larsen, Dallas J and Omdahl, Ashton R and McGuffin, Liam J and Brackenridge, Danielle A and Babbitt, Patricia C and Yunes, Jeffrey M and Fontana, Paolo and Zhang, Feng and Zhu, Shanfeng and You, Ronghui and Zhang, Zihan and Dai, Suyang and Yao, Shuwei and Tian, Weidong and Cao, Renzhi and Chandler, Caleb and Amezola, Miguel and Johnson, Devon and Chang, Jia-Ming and Liao, Wen-Hung and Liu, Yi-Wei and Pascarelli, Stefano and Frank, Yotam and Hoehndorf, Robert and Kulmanov, Maxat and Boudellioua, Imane and Politano, Gianfranco and Di Carlo, Stefano and Benso, Alfredo and Hakala, Kai and Ginter, Filip and Mehryary, Farrokh and Kaewphan, Suwisa and Björne, Jari and Moen, Hans and Tolvanen, Martti E.E. and Salakoski, Tapio and Kihara, Daisuke and Jain, Aashish and Šmuc, Tomislav and Altenhoff, Adrian and Ben-Hur, Asa and Rost, Burkhard and Brenner, Steven E and Orengo, Christine A and Jeffery, Constance J and Bosco, Giovanni and Hogan, Deborah A and Martin, Maria J and O’Donovan, Claire and Mooney, Sean D and Greene, Casey S and Radivojac, Predrag and Friedberg, Iddo",
year = "2019",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/8655",
abstract = "Background: The Critical Assessment of Functional Annotation (CAFA) is an ongoing, global, community-driven effort to evaluate and improve the computational annotation of protein function. Results: Here, we report on the results of the third CAFA challenge, CAFA3, that featured an expanded analysis over the previous CAFA rounds, both in terms of volume of data analyzed and the types of analysis performed. In a novel and major new development, computational predictions and assessment goals drove some of the experimental assays, resulting in new functional annotations for more than 1000 genes. Specifically, we performed experimental whole-genome mutation screening in Candida albicans and Pseudomonas aureginosa genomes, which provided us with genome-wide experimental data for genes associated with biofilm formation and motility. We further performed targeted assays on selected genes in Drosophila melanogaster, which we suspected of being involved in long-Term memory. Conclusion: We conclude that while predictions of the molecular function and biological process annotations have slightly improved over time, those of the cellular component have not. Term-centric prediction of experimental annotations remains equally challenging; although the performance of the top methods is significantly better than the expectations set by baseline methods in C. albicans and D. melanogaster, it leaves considerable room and need for improvement. Finally, we report that the CAFA community now involves a broad range of participants with expertise in bioinformatics, biological experimentation, biocuration, and bio-ontologies, working together to improve functional annotation, computational function prediction, and our ability to manage big data in the era of large experimental screens. © 2019 The Author(s).",
journal = "Genome Biology",
title = "The CAFA challenge reports improved protein function prediction and new functional annotations for hundreds of genes through experimental screens",
volume = "20",
number = "1",
pages = "244",
doi = "10.1186/s13059-019-1835-8"
}
Zhou, N., Jiang, Y., Bergquist, T. R., Lee, A. J., Kacsoh, B. Z., Crocker, A. W., Lewis, K. A., Georghiou, G., Nguyen, H. N., Hamid, M. N., Davis, L., Dogan, T., Atalay, V., Rifaioglu, A. S., Dalkıran, A., Cetin Atalay, R., Zhang, C., Hurto, R. L., Freddolino, P. L., Zhang, Y., Bhat, P., Supek, F., Fernández, J. M., Gemović, B. S., Perović, V. R., Davidović, R. S., Šumonja, N., Veljković, N. V., Asgari, E., Mofrad, M. R.K., Profiti, G., Savojardo, C., Martelli, P. L., Casadio, R., Boecker, F., Schoof, H., Kahanda, I., Thurlby, N., McHardy, A. C., Renaux, A., Saidi, R., Gough, J., Freitas, A. A., Antczak, M., Fabris, F., Wass, M. N., Hou, J., Cheng, J., Wang, Z., Romero, A. E., Paccanaro, A., Yang, H., Goldberg, T., Zhao, C., Holm, L., Törönen, P., Medlar, A. J., Zosa, E., Borukhov, I., Novikov, I., Wilkins, A., Lichtarge, O., Chi, P., Tseng, W., Linial, M., Rose, P. W., Dessimoz, C., Vidulin, V., Dzeroski, S., Sillitoe, I., Das, S., Lees, J. G., Jones, D. T., Wan, C., Cozzetto, D., Fa, R., Torres, M., Warwick Vesztrocy, A., Rodriguez, J. M., Tress, M. L., Frasca, M., Notaro, M., Grossi, G., Petrini, A., Re, M., Valentini, G., Mesiti, M., Roche, D. B., Reeb, J., Ritchie, D. W., Aridhi, S., Alborzi, S. Z., Devignes, M., Koo, D. C. E., Bonneau, R., Gligorijević, V., Barot, M., Fang, H., Toppo, S., Lavezzo, E., Falda, M., Berselli, M., Tosatto, S. C.E., Carraro, M., Piovesan, D., Ur Rehman, H., Mao, Q., Zhang, S., Vucetic, S., Black, G. S., Jo, D., Suh, E., Dayton, J. B., Larsen, D. J., Omdahl, A. R., McGuffin, L. J., Brackenridge, D. A., Babbitt, P. C., Yunes, J. M., Fontana, P., Zhang, F., Zhu, S., You, R., Zhang, Z., Dai, S., Yao, S., Tian, W., Cao, R., Chandler, C., Amezola, M., Johnson, D., Chang, J., Liao, W., Liu, Y., Pascarelli, S., Frank, Y., Hoehndorf, R., Kulmanov, M., Boudellioua, I., Politano, G., Di Carlo, S., Benso, A., Hakala, K., Ginter, F., Mehryary, F., Kaewphan, S., Björne, J., Moen, H., Tolvanen, M. E.E., Salakoski, T., Kihara, D., Jain, A., Šmuc, T., Altenhoff, A., Ben-Hur, A., Rost, B., Brenner, S. E., Orengo, C. A., Jeffery, C. J., Bosco, G., Hogan, D. A., Martin, M. J., O’Donovan, C., Mooney, S. D., Greene, C. S., Radivojac, P.,& Friedberg, I. (2019). The CAFA challenge reports improved protein function prediction and new functional annotations for hundreds of genes through experimental screens.
Genome Biology, 20(1), 244.
https://doi.org/10.1186/s13059-019-1835-8
Zhou N, Jiang Y, Bergquist TR, Lee AJ, Kacsoh BZ, Crocker AW, Lewis KA, Georghiou G, Nguyen HN, Hamid MN, Davis L, Dogan T, Atalay V, Rifaioglu AS, Dalkıran A, Cetin Atalay R, Zhang C, Hurto RL, Freddolino PL, Zhang Y, Bhat P, Supek F, Fernández JM, Gemović BS, Perović VR, Davidović RS, Šumonja N, Veljković NV, Asgari E, Mofrad MR, Profiti G, Savojardo C, Martelli PL, Casadio R, Boecker F, Schoof H, Kahanda I, Thurlby N, McHardy AC, Renaux A, Saidi R, Gough J, Freitas AA, Antczak M, Fabris F, Wass MN, Hou J, Cheng J, Wang Z, Romero AE, Paccanaro A, Yang H, Goldberg T, Zhao C, Holm L, Törönen P, Medlar AJ, Zosa E, Borukhov I, Novikov I, Wilkins A, Lichtarge O, Chi P, Tseng W, Linial M, Rose PW, Dessimoz C, Vidulin V, Dzeroski S, Sillitoe I, Das S, Lees JG, Jones DT, Wan C, Cozzetto D, Fa R, Torres M, Warwick Vesztrocy A, Rodriguez JM, Tress ML, Frasca M, Notaro M, Grossi G, Petrini A, Re M, Valentini G, Mesiti M, Roche DB, Reeb J, Ritchie DW, Aridhi S, Alborzi SZ, Devignes M, Koo DCE, Bonneau R, Gligorijević V, Barot M, Fang H, Toppo S, Lavezzo E, Falda M, Berselli M, Tosatto SC, Carraro M, Piovesan D, Ur Rehman H, Mao Q, Zhang S, Vucetic S, Black GS, Jo D, Suh E, Dayton JB, Larsen DJ, Omdahl AR, McGuffin LJ, Brackenridge DA, Babbitt PC, Yunes JM, Fontana P, Zhang F, Zhu S, You R, Zhang Z, Dai S, Yao S, Tian W, Cao R, Chandler C, Amezola M, Johnson D, Chang J, Liao W, Liu Y, Pascarelli S, Frank Y, Hoehndorf R, Kulmanov M, Boudellioua I, Politano G, Di Carlo S, Benso A, Hakala K, Ginter F, Mehryary F, Kaewphan S, Björne J, Moen H, Tolvanen ME, Salakoski T, Kihara D, Jain A, Šmuc T, Altenhoff A, Ben-Hur A, Rost B, Brenner SE, Orengo CA, Jeffery CJ, Bosco G, Hogan DA, Martin MJ, O’Donovan C, Mooney SD, Greene CS, Radivojac P, Friedberg I. The CAFA challenge reports improved protein function prediction and new functional annotations for hundreds of genes through experimental screens. Genome Biology. 2019;20(1):244
Zhou Naihui, Jiang Yuxiang, Bergquist Timothy R, Lee Alexandra J, Kacsoh Balint Z, Crocker Alex W, Lewis Kimberley A, Georghiou George, Nguyen Huy N, Hamid Md Nafiz, Davis Larry, Dogan Tunca, Atalay Volkan, Rifaioglu Ahmet S, Dalkıran Alperen, Cetin Atalay Rengul, Zhang Chengxin, Hurto Rebecca L, Freddolino Peter L, Zhang Yang, Bhat Prajwal, Supek Fran, Fernández José M, Gemović Branislava S., Perović Vladimir R., Davidović Radoslav S., Šumonja Neven, Veljković Nevena V., Asgari Ehsaneddin, Mofrad Mohammad R.K., Profiti Giuseppe, Savojardo Castrense, Martelli Pier Luigi, Casadio Rita, Boecker Florian, Schoof Heiko, Kahanda Indika, Thurlby Natalie, McHardy Alice C, Renaux Alexandre, Saidi Rabie, Gough Julian, Freitas Alex A, Antczak Magdalena, Fabris Fabio, Wass Mark N, Hou Jie, Cheng Jianlin, Wang Zheng, Romero Alfonso E, Paccanaro Alberto, Yang Haixuan, Goldberg Tatyana, Zhao Chenguang, Holm Liisa, Törönen Petri, Medlar Alan J, Zosa Elaine, Borukhov Itamar, Novikov Ilya, Wilkins Angela, Lichtarge Olivier, Chi Po-Han, Tseng Wei-Cheng, Linial Michal, Rose Peter W, Dessimoz Christophe, Vidulin Vedrana, Dzeroski Saso, Sillitoe Ian, Das Sayoni, Lees Jonathan Gill, Jones David T, Wan Cen, Cozzetto Domenico, Fa Rui, Torres Mateo, Warwick Vesztrocy Alex, Rodriguez Jose Manuel, Tress Michael L, Frasca Marco, Notaro Marco, Grossi Giuliano, Petrini Alessandro, Re Matteo, Valentini Giorgio, Mesiti Marco, Roche Daniel B, Reeb Jonas, Ritchie David W, Aridhi Sabeur, Alborzi Seyed Ziaeddin, Devignes Marie-Dominique, Koo Da Chen Emily, Bonneau Richard, Gligorijević Vladimir, Barot Meet, Fang Hai, Toppo Stefano, Lavezzo Enrico, Falda Marco, Berselli Michele, Tosatto Silvio C.E., Carraro Marco, Piovesan Damiano, Ur Rehman Hafeez, Mao Qizhong, Zhang Shanshan, Vucetic Slobodan, Black Gage S, Jo Dane, Suh Erica, Dayton Jonathan B, Larsen Dallas J, Omdahl Ashton R, McGuffin Liam J, Brackenridge Danielle A, Babbitt Patricia C, Yunes Jeffrey M, Fontana Paolo, Zhang Feng, Zhu Shanfeng, You Ronghui, Zhang Zihan, Dai Suyang, Yao Shuwei, Tian Weidong, Cao Renzhi, Chandler Caleb, Amezola Miguel, Johnson Devon, Chang Jia-Ming, Liao Wen-Hung, Liu Yi-Wei, Pascarelli Stefano, Frank Yotam, Hoehndorf Robert, Kulmanov Maxat, Boudellioua Imane, Politano Gianfranco, Di Carlo Stefano, Benso Alfredo, Hakala Kai, Ginter Filip, Mehryary Farrokh, Kaewphan Suwisa, Björne Jari, Moen Hans, Tolvanen Martti E.E., Salakoski Tapio, Kihara Daisuke, Jain Aashish, Šmuc Tomislav, Altenhoff Adrian, Ben-Hur Asa, Rost Burkhard, Brenner Steven E, Orengo Christine A, Jeffery Constance J, Bosco Giovanni, Hogan Deborah A, Martin Maria J, O’Donovan Claire, Mooney Sean D, Greene Casey S, Radivojac Predrag, Friedberg Iddo, "The CAFA challenge reports improved protein function prediction and new functional annotations for hundreds of genes through experimental screens" Genome Biology, 20, no. 1 (2019):244,
https://doi.org/10.1186/s13059-019-1835-8 .
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DisProt: intrinsic protein disorder annotation in 2020

Hatos, András; Hajdu-Soltész, Borbála; Monzon, Alexander M; Palopoli, Nicolas; Álvarez, Lucía; Aykac-Fas, Burcu; Bassot, Claudio; Benítez, Guillermo I; Bevilacqua, Martina; Chasapi, Anastasia; Chemes, Lucia; Davey, Norman E; Davidović, Radoslav S.; Dunker, A Keith; Elofsson, Arne; Gobeill, Julien; Foutel, Nicolás S González; Sudha, Govindarajan; Guharoy, Mainak; Horvath, Tamas; Iglesias, Valentin; Kajava, Andrey V.; Kovacs, Orsolya P; Lamb, John; Lambrughi, Matteo; Lazar, Tamas; Leclercq, Jeremy Y; Leonardi, Emanuela; Macedo-Ribeiro, Sandra; Macossay-Castillo, Mauricio; Maiani, Emiliano; Manso, José A; Marino-Buslje, Cristina; Martínez-Pérez, Elizabeth; Mészáros, Bálint; Mičetić, Ivan; Minervini, Giovanni; Murvai, Nikoletta; Necci, Marco; Ouzounis, Christos A; Pajkos, Mátyás; Paladin, Lisanna; Pancsa, Rita; Papaleo, Elena; Parisi, Gustavo; Pasche, Emilie; Barbosa Pereira, Pedro J; Promponas, Vasilis J; Pujols, Jordi; Quaglia, Federica; Ruch, Patrick; Salvatore, Marco; Schad, Eva; Szabo, Beata; Szaniszló, Tamás; Tamana, Stella; Tantos, Agnes; Veljković, Nevena V.; Ventura, Salvador; Vranken, Wim; Dosztányi, Zsuzsanna; Tompa, Peter; Tosatto, Silvio C E; Piovesan, Damiano

(2019)

TY  - JOUR
AU  - Hatos, András
AU  - Hajdu-Soltész, Borbála
AU  - Monzon, Alexander M
AU  - Palopoli, Nicolas
AU  - Álvarez, Lucía
AU  - Aykac-Fas, Burcu
AU  - Bassot, Claudio
AU  - Benítez, Guillermo I
AU  - Bevilacqua, Martina
AU  - Chasapi, Anastasia
AU  - Chemes, Lucia
AU  - Davey, Norman E
AU  - Davidović, Radoslav S.
AU  - Dunker, A Keith
AU  - Elofsson, Arne
AU  - Gobeill, Julien
AU  - Foutel, Nicolás S González
AU  - Sudha, Govindarajan
AU  - Guharoy, Mainak
AU  - Horvath, Tamas
AU  - Iglesias, Valentin
AU  - Kajava, Andrey V.
AU  - Kovacs, Orsolya P
AU  - Lamb, John
AU  - Lambrughi, Matteo
AU  - Lazar, Tamas
AU  - Leclercq, Jeremy Y
AU  - Leonardi, Emanuela
AU  - Macedo-Ribeiro, Sandra
AU  - Macossay-Castillo, Mauricio
AU  - Maiani, Emiliano
AU  - Manso, José A
AU  - Marino-Buslje, Cristina
AU  - Martínez-Pérez, Elizabeth
AU  - Mészáros, Bálint
AU  - Mičetić, Ivan
AU  - Minervini, Giovanni
AU  - Murvai, Nikoletta
AU  - Necci, Marco
AU  - Ouzounis, Christos A
AU  - Pajkos, Mátyás
AU  - Paladin, Lisanna
AU  - Pancsa, Rita
AU  - Papaleo, Elena
AU  - Parisi, Gustavo
AU  - Pasche, Emilie
AU  - Barbosa Pereira, Pedro J
AU  - Promponas, Vasilis J
AU  - Pujols, Jordi
AU  - Quaglia, Federica
AU  - Ruch, Patrick
AU  - Salvatore, Marco
AU  - Schad, Eva
AU  - Szabo, Beata
AU  - Szaniszló, Tamás
AU  - Tamana, Stella
AU  - Tantos, Agnes
AU  - Veljković, Nevena V.
AU  - Ventura, Salvador
AU  - Vranken, Wim
AU  - Dosztányi, Zsuzsanna
AU  - Tompa, Peter
AU  - Tosatto, Silvio C E
AU  - Piovesan, Damiano
PY  - 2019
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8799
AB  - The Database of Protein Disorder (DisProt, URL: https://disprot.org) provides manually curated annotations of intrinsically disordered proteins from the literature. Here we report recent developments with DisProt (version 8), including the doubling of protein entries, a new disorder ontology, improvements of the annotation format and a completely new website. The website includes a redesigned graphical interface, a better search engine, a clearer API for programmatic access and a new annotation interface that integrates text mining technologies. The new entry format provides a greater flexibility, simplifies maintenance and allows the capture of more information from the literature. The new disorder ontology has been formalized and made interoperable by adopting the OWL format, as well as its structure and term definitions have been improved. The new annotation interface has made the curation process faster and more effective. We recently showed that new DisProt annotations can be effectively used to train and validate disorder predictors. We believe the growth of DisProt will accelerate, contributing to the improvement of function and disorder predictors and therefore to illuminate the ‘dark’ proteome.
T2  - Nucleic Acids Research
T1  - DisProt: intrinsic protein disorder annotation in 2020
VL  - 48
IS  - D1
SP  - D269
EP  - D276
DO  - 10.1093/nar/gkz975
ER  - 
@article{
author = "Hatos, András and Hajdu-Soltész, Borbála and Monzon, Alexander M and Palopoli, Nicolas and Álvarez, Lucía and Aykac-Fas, Burcu and Bassot, Claudio and Benítez, Guillermo I and Bevilacqua, Martina and Chasapi, Anastasia and Chemes, Lucia and Davey, Norman E and Davidović, Radoslav S. and Dunker, A Keith and Elofsson, Arne and Gobeill, Julien and Foutel, Nicolás S González and Sudha, Govindarajan and Guharoy, Mainak and Horvath, Tamas and Iglesias, Valentin and Kajava, Andrey V. and Kovacs, Orsolya P and Lamb, John and Lambrughi, Matteo and Lazar, Tamas and Leclercq, Jeremy Y and Leonardi, Emanuela and Macedo-Ribeiro, Sandra and Macossay-Castillo, Mauricio and Maiani, Emiliano and Manso, José A and Marino-Buslje, Cristina and Martínez-Pérez, Elizabeth and Mészáros, Bálint and Mičetić, Ivan and Minervini, Giovanni and Murvai, Nikoletta and Necci, Marco and Ouzounis, Christos A and Pajkos, Mátyás and Paladin, Lisanna and Pancsa, Rita and Papaleo, Elena and Parisi, Gustavo and Pasche, Emilie and Barbosa Pereira, Pedro J and Promponas, Vasilis J and Pujols, Jordi and Quaglia, Federica and Ruch, Patrick and Salvatore, Marco and Schad, Eva and Szabo, Beata and Szaniszló, Tamás and Tamana, Stella and Tantos, Agnes and Veljković, Nevena V. and Ventura, Salvador and Vranken, Wim and Dosztányi, Zsuzsanna and Tompa, Peter and Tosatto, Silvio C E and Piovesan, Damiano",
year = "2019",
url = "https://vinar.vin.bg.ac.rs/handle/123456789/8799",
abstract = "The Database of Protein Disorder (DisProt, URL: https://disprot.org) provides manually curated annotations of intrinsically disordered proteins from the literature. Here we report recent developments with DisProt (version 8), including the doubling of protein entries, a new disorder ontology, improvements of the annotation format and a completely new website. The website includes a redesigned graphical interface, a better search engine, a clearer API for programmatic access and a new annotation interface that integrates text mining technologies. The new entry format provides a greater flexibility, simplifies maintenance and allows the capture of more information from the literature. The new disorder ontology has been formalized and made interoperable by adopting the OWL format, as well as its structure and term definitions have been improved. The new annotation interface has made the curation process faster and more effective. We recently showed that new DisProt annotations can be effectively used to train and validate disorder predictors. We believe the growth of DisProt will accelerate, contributing to the improvement of function and disorder predictors and therefore to illuminate the ‘dark’ proteome.",
journal = "Nucleic Acids Research",
title = "DisProt: intrinsic protein disorder annotation in 2020",
volume = "48",
number = "D1",
pages = "D269-D276",
doi = "10.1093/nar/gkz975"
}
Hatos, A., Hajdu-Soltész, B., Monzon, A. M., Palopoli, N., Álvarez, L., Aykac-Fas, B., Bassot, C., Benítez, G. I., Bevilacqua, M., Chasapi, A., Chemes, L., Davey, N. E., Davidović, R. S., Dunker, A. K., Elofsson, A., Gobeill, J., Foutel, N. S. G., Sudha, G., Guharoy, M., Horvath, T., Iglesias, V., Kajava, A. V., Kovacs, O. P., Lamb, J., Lambrughi, M., Lazar, T., Leclercq, J. Y., Leonardi, E., Macedo-Ribeiro, S., Macossay-Castillo, M., Maiani, E., Manso, J. A., Marino-Buslje, C., Martínez-Pérez, E., Mészáros, B., Mičetić, I., Minervini, G., Murvai, N., Necci, M., Ouzounis, C. A., Pajkos, M., Paladin, L., Pancsa, R., Papaleo, E., Parisi, G., Pasche, E., Barbosa Pereira, P. J., Promponas, V. J., Pujols, J., Quaglia, F., Ruch, P., Salvatore, M., Schad, E., Szabo, B., Szaniszló, T., Tamana, S., Tantos, A., Veljković, N. V., Ventura, S., Vranken, W., Dosztányi, Z., Tompa, P., Tosatto, S. C. E.,& Piovesan, D. (2019). DisProt: intrinsic protein disorder annotation in 2020.
Nucleic Acids Research, 48(D1), D269-D276.
https://doi.org/10.1093/nar/gkz975
Hatos A, Hajdu-Soltész B, Monzon AM, Palopoli N, Álvarez L, Aykac-Fas B, Bassot C, Benítez GI, Bevilacqua M, Chasapi A, Chemes L, Davey NE, Davidović RS, Dunker AK, Elofsson A, Gobeill J, Foutel NSG, Sudha G, Guharoy M, Horvath T, Iglesias V, Kajava AV, Kovacs OP, Lamb J, Lambrughi M, Lazar T, Leclercq JY, Leonardi E, Macedo-Ribeiro S, Macossay-Castillo M, Maiani E, Manso JA, Marino-Buslje C, Martínez-Pérez E, Mészáros B, Mičetić I, Minervini G, Murvai N, Necci M, Ouzounis CA, Pajkos M, Paladin L, Pancsa R, Papaleo E, Parisi G, Pasche E, Barbosa Pereira PJ, Promponas VJ, Pujols J, Quaglia F, Ruch P, Salvatore M, Schad E, Szabo B, Szaniszló T, Tamana S, Tantos A, Veljković NV, Ventura S, Vranken W, Dosztányi Z, Tompa P, Tosatto SCE, Piovesan D. DisProt: intrinsic protein disorder annotation in 2020. Nucleic Acids Research. 2019;48(D1):D269-D276
Hatos András, Hajdu-Soltész Borbála, Monzon Alexander M, Palopoli Nicolas, Álvarez Lucía, Aykac-Fas Burcu, Bassot Claudio, Benítez Guillermo I, Bevilacqua Martina, Chasapi Anastasia, Chemes Lucia, Davey Norman E, Davidović Radoslav S., Dunker A Keith, Elofsson Arne, Gobeill Julien, Foutel Nicolás S González, Sudha Govindarajan, Guharoy Mainak, Horvath Tamas, Iglesias Valentin, Kajava Andrey V., Kovacs Orsolya P, Lamb John, Lambrughi Matteo, Lazar Tamas, Leclercq Jeremy Y, Leonardi Emanuela, Macedo-Ribeiro Sandra, Macossay-Castillo Mauricio, Maiani Emiliano, Manso José A, Marino-Buslje Cristina, Martínez-Pérez Elizabeth, Mészáros Bálint, Mičetić Ivan, Minervini Giovanni, Murvai Nikoletta, Necci Marco, Ouzounis Christos A, Pajkos Mátyás, Paladin Lisanna, Pancsa Rita, Papaleo Elena, Parisi Gustavo, Pasche Emilie, Barbosa Pereira Pedro J, Promponas Vasilis J, Pujols Jordi, Quaglia Federica, Ruch Patrick, Salvatore Marco, Schad Eva, Szabo Beata, Szaniszló Tamás, Tamana Stella, Tantos Agnes, Veljković Nevena V., Ventura Salvador, Vranken Wim, Dosztányi Zsuzsanna, Tompa Peter, Tosatto Silvio C E, Piovesan Damiano, "DisProt: intrinsic protein disorder annotation in 2020" Nucleic Acids Research, 48, no. D1 (2019):D269-D276,
https://doi.org/10.1093/nar/gkz975 .
25
65
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35

Methylation status of p16 and p14 genes in locally advanced rectal cancer: Potential clinical implication

Kožik, Bojana; Kokanov, Nikola; Knežević-Ušaj, Slavica; Nikolić, Ivan; Davidović, Radoslav S.; Jovanović-Ćupić, Snežana P.; Krajnović, Milena M.

(2018)

TY  - JOUR
AU  - Kožik, Bojana
AU  - Kokanov, Nikola
AU  - Knežević-Ušaj, Slavica
AU  - Nikolić, Ivan
AU  - Davidović, Radoslav S.
AU  - Jovanović-Ćupić, Snežana P.
AU  - Krajnović, Milena M.
PY  - 2018
UR  - http://www.doiserbia.nb.rs/Article.aspx?ID=0354-46641800030K
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8002
AB  - Methylation of p16 and p14 genes is a common event in colorectal cancers; however, their exact role in the prediction of patients' outcome is unclear. We conducted this retrospective study to evaluate their potential predictive and/or prognostic roles. Methylation-specific PCR was used to examine the methylation status of p16 and p14 in pretherapeutic and preoperative biopsy specimens of 60 patients with locally advanced rectal cancer. The methylation status of the examined genes did not affect the response to preoperative chemoradiotherapy (CRT), recurrence rate and overall survival. However, patients with a simultaneous presence of either p16 or p14 methylation and high vascular endothelial growth factor (VEGF) expression showed a significantly worse response to CRT (p=0.005 and p=0.038, respectively). Moreover, patients with both p16 methylation and high VEGF expression had significantly shorter overall survival (p=0.010), while no such association was found in patients with p14 methylation and high VEGF expression. On the other hand, a subgroup of patients with p16 methylation and low VEGF and high epidermal growth factor receptor (EGFR) expression showed a significantly better response to CRT (p=0.024). The obtained results point to the importance of p16 and p14 methylation analyses in combination with VEGF and EGFR expression, aimed at better predicting treatment response and patient outcome. © 2018 by the Serbian Biological Society.
T2  - Archives of Biological Sciences
T1  - Methylation status of p16 and p14 genes in locally advanced rectal cancer: Potential clinical implication
VL  - 70
IS  - 4
SP  - 681
EP  - 690
DO  - 10.2298/ABS180316030K
ER  - 
@article{
author = "Kožik, Bojana and Kokanov, Nikola and Knežević-Ušaj, Slavica and Nikolić, Ivan and Davidović, Radoslav S. and Jovanović-Ćupić, Snežana P. and Krajnović, Milena M.",
year = "2018",
url = "http://www.doiserbia.nb.rs/Article.aspx?ID=0354-46641800030K, http://vinar.vin.bg.ac.rs/handle/123456789/8002",
abstract = "Methylation of p16 and p14 genes is a common event in colorectal cancers; however, their exact role in the prediction of patients' outcome is unclear. We conducted this retrospective study to evaluate their potential predictive and/or prognostic roles. Methylation-specific PCR was used to examine the methylation status of p16 and p14 in pretherapeutic and preoperative biopsy specimens of 60 patients with locally advanced rectal cancer. The methylation status of the examined genes did not affect the response to preoperative chemoradiotherapy (CRT), recurrence rate and overall survival. However, patients with a simultaneous presence of either p16 or p14 methylation and high vascular endothelial growth factor (VEGF) expression showed a significantly worse response to CRT (p=0.005 and p=0.038, respectively). Moreover, patients with both p16 methylation and high VEGF expression had significantly shorter overall survival (p=0.010), while no such association was found in patients with p14 methylation and high VEGF expression. On the other hand, a subgroup of patients with p16 methylation and low VEGF and high epidermal growth factor receptor (EGFR) expression showed a significantly better response to CRT (p=0.024). The obtained results point to the importance of p16 and p14 methylation analyses in combination with VEGF and EGFR expression, aimed at better predicting treatment response and patient outcome. © 2018 by the Serbian Biological Society.",
journal = "Archives of Biological Sciences",
title = "Methylation status of p16 and p14 genes in locally advanced rectal cancer: Potential clinical implication",
volume = "70",
number = "4",
pages = "681-690",
doi = "10.2298/ABS180316030K"
}
Kožik, B., Kokanov, N., Knežević-Ušaj, S., Nikolić, I., Davidović, R. S., Jovanović-Ćupić, S. P.,& Krajnović, M. M. (2018). Methylation status of p16 and p14 genes in locally advanced rectal cancer: Potential clinical implication.
Archives of Biological Sciences, 70(4), 681-690.
https://doi.org/10.2298/ABS180316030K
Kožik B, Kokanov N, Knežević-Ušaj S, Nikolić I, Davidović RS, Jovanović-Ćupić SP, Krajnović MM. Methylation status of p16 and p14 genes in locally advanced rectal cancer: Potential clinical implication. Archives of Biological Sciences. 2018;70(4):681-690
Kožik Bojana, Kokanov Nikola, Knežević-Ušaj Slavica, Nikolić Ivan, Davidović Radoslav S., Jovanović-Ćupić Snežana P., Krajnović Milena M., "Methylation status of p16 and p14 genes in locally advanced rectal cancer: Potential clinical implication" Archives of Biological Sciences, 70, no. 4 (2018):681-690,
https://doi.org/10.2298/ABS180316030K .

DisProt 7.0: a major update of the database of disordered proteins

Piovesan, Damiano; Tabaro, Francesco; Micetic, Ivan; Necci, Marco; Quaglia, Federica; Oldfield, Christopher J.; Aspromonte, Maria Cristina; Davey, Norman E.; Davidović, Radoslav S.; Dosztanyi, Zsuzsanna; Elofsson, Arne; Gasparini, Alessandra; Hatos, Andras; Kajava, Andrey V.; Kalmar, Lajos; Leonardi, Emanuela; Lazar, Tamas; Macedo-Ribeiro, Sandra; Macossay-Castillo, Mauricio; Meszaros, Attila; Minervini, Giovanni; Murvai, Nikoletta; Pujols, Jordi; Roche, Daniel B.; Salladini, Edoardo; Schad, Eva; Schramm, Antoine; Szabo, Beata; Tantos, Agnes; Tonello, Fiorella; Tsirigos, Konstantinos D.; Veljković, Nevena V.; Ventura, Salvador; Vranken, Wim; Warholm, Per; Uversky, Vladimir N.; Dunker, A. Keith; Longhi, Sonia; Tompa, Peter; Tosatto, Silvio C. E.

(2017)

TY  - JOUR
AU  - Piovesan, Damiano
AU  - Tabaro, Francesco
AU  - Micetic, Ivan
AU  - Necci, Marco
AU  - Quaglia, Federica
AU  - Oldfield, Christopher J.
AU  - Aspromonte, Maria Cristina
AU  - Davey, Norman E.
AU  - Davidović, Radoslav S.
AU  - Dosztanyi, Zsuzsanna
AU  - Elofsson, Arne
AU  - Gasparini, Alessandra
AU  - Hatos, Andras
AU  - Kajava, Andrey V.
AU  - Kalmar, Lajos
AU  - Leonardi, Emanuela
AU  - Lazar, Tamas
AU  - Macedo-Ribeiro, Sandra
AU  - Macossay-Castillo, Mauricio
AU  - Meszaros, Attila
AU  - Minervini, Giovanni
AU  - Murvai, Nikoletta
AU  - Pujols, Jordi
AU  - Roche, Daniel B.
AU  - Salladini, Edoardo
AU  - Schad, Eva
AU  - Schramm, Antoine
AU  - Szabo, Beata
AU  - Tantos, Agnes
AU  - Tonello, Fiorella
AU  - Tsirigos, Konstantinos D.
AU  - Veljković, Nevena V.
AU  - Ventura, Salvador
AU  - Vranken, Wim
AU  - Warholm, Per
AU  - Uversky, Vladimir N.
AU  - Dunker, A. Keith
AU  - Longhi, Sonia
AU  - Tompa, Peter
AU  - Tosatto, Silvio C. E.
PY  - 2017
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1464
AB  - The Database of Protein Disorder (DisProt, URL: www.disprot.org) has been significantly updated and upgraded since its last major renewal in 2007. The current release holds information on more than 800 entries of IDPs/IDRs, i.e. intrinsically disordered proteins or regions that exist and function without a well-defined three-dimensional structure. We have re-curated previous entries to purge DisProt from conflicting cases, and also upgraded the functional classification scheme to reflect continuous advance in the field in the past 10 years or so. We define IDPs as proteins that are disordered along their entire sequence, i.e. entirely lack structural elements, and IDRs as regions that are at least five consecutive residues without well-defined structure. We base our assessment of disorder strictly on experimental evidence, such as X-ray crystallography and nuclear magnetic resonance ( primary techniques) and a broad range of other experimental approaches (secondary techniques). Confident and ambiguous annotations are highlighted separately. DisProt 7.0 presents classified knowledge regarding the experimental characterization and functional annotations of IDPs/IDRs, and is intended to provide an invaluable resource for the research community for a better understanding structural disorder and for developing better computational tools for studying disordered proteins.
T2  - Nucleic Acids Research
T1  - DisProt 7.0: a major update of the database of disordered proteins
VL  - 45
IS  - D1
SP  - D219
EP  - D227
DO  - 10.1093/nar/gkw1056
ER  - 
@article{
author = "Piovesan, Damiano and Tabaro, Francesco and Micetic, Ivan and Necci, Marco and Quaglia, Federica and Oldfield, Christopher J. and Aspromonte, Maria Cristina and Davey, Norman E. and Davidović, Radoslav S. and Dosztanyi, Zsuzsanna and Elofsson, Arne and Gasparini, Alessandra and Hatos, Andras and Kajava, Andrey V. and Kalmar, Lajos and Leonardi, Emanuela and Lazar, Tamas and Macedo-Ribeiro, Sandra and Macossay-Castillo, Mauricio and Meszaros, Attila and Minervini, Giovanni and Murvai, Nikoletta and Pujols, Jordi and Roche, Daniel B. and Salladini, Edoardo and Schad, Eva and Schramm, Antoine and Szabo, Beata and Tantos, Agnes and Tonello, Fiorella and Tsirigos, Konstantinos D. and Veljković, Nevena V. and Ventura, Salvador and Vranken, Wim and Warholm, Per and Uversky, Vladimir N. and Dunker, A. Keith and Longhi, Sonia and Tompa, Peter and Tosatto, Silvio C. E.",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1464",
abstract = "The Database of Protein Disorder (DisProt, URL: www.disprot.org) has been significantly updated and upgraded since its last major renewal in 2007. The current release holds information on more than 800 entries of IDPs/IDRs, i.e. intrinsically disordered proteins or regions that exist and function without a well-defined three-dimensional structure. We have re-curated previous entries to purge DisProt from conflicting cases, and also upgraded the functional classification scheme to reflect continuous advance in the field in the past 10 years or so. We define IDPs as proteins that are disordered along their entire sequence, i.e. entirely lack structural elements, and IDRs as regions that are at least five consecutive residues without well-defined structure. We base our assessment of disorder strictly on experimental evidence, such as X-ray crystallography and nuclear magnetic resonance ( primary techniques) and a broad range of other experimental approaches (secondary techniques). Confident and ambiguous annotations are highlighted separately. DisProt 7.0 presents classified knowledge regarding the experimental characterization and functional annotations of IDPs/IDRs, and is intended to provide an invaluable resource for the research community for a better understanding structural disorder and for developing better computational tools for studying disordered proteins.",
journal = "Nucleic Acids Research",
title = "DisProt 7.0: a major update of the database of disordered proteins",
volume = "45",
number = "D1",
pages = "D219-D227",
doi = "10.1093/nar/gkw1056"
}
Piovesan, D., Tabaro, F., Micetic, I., Necci, M., Quaglia, F., Oldfield, C. J., Aspromonte, M. C., Davey, N. E., Davidović, R. S., Dosztanyi, Z., Elofsson, A., Gasparini, A., Hatos, A., Kajava, A. V., Kalmar, L., Leonardi, E., Lazar, T., Macedo-Ribeiro, S., Macossay-Castillo, M., Meszaros, A., Minervini, G., Murvai, N., Pujols, J., Roche, D. B., Salladini, E., Schad, E., Schramm, A., Szabo, B., Tantos, A., Tonello, F., Tsirigos, K. D., Veljković, N. V., Ventura, S., Vranken, W., Warholm, P., Uversky, V. N., Dunker, A. K., Longhi, S., Tompa, P.,& Tosatto, S. C. E. (2017). DisProt 7.0: a major update of the database of disordered proteins.
Nucleic Acids Research, 45(D1), D219-D227.
https://doi.org/10.1093/nar/gkw1056
Piovesan D, Tabaro F, Micetic I, Necci M, Quaglia F, Oldfield CJ, Aspromonte MC, Davey NE, Davidović RS, Dosztanyi Z, Elofsson A, Gasparini A, Hatos A, Kajava AV, Kalmar L, Leonardi E, Lazar T, Macedo-Ribeiro S, Macossay-Castillo M, Meszaros A, Minervini G, Murvai N, Pujols J, Roche DB, Salladini E, Schad E, Schramm A, Szabo B, Tantos A, Tonello F, Tsirigos KD, Veljković NV, Ventura S, Vranken W, Warholm P, Uversky VN, Dunker AK, Longhi S, Tompa P, Tosatto SCE. DisProt 7.0: a major update of the database of disordered proteins. Nucleic Acids Research. 2017;45(D1):D219-D227
Piovesan Damiano, Tabaro Francesco, Micetic Ivan, Necci Marco, Quaglia Federica, Oldfield Christopher J., Aspromonte Maria Cristina, Davey Norman E., Davidović Radoslav S., Dosztanyi Zsuzsanna, Elofsson Arne, Gasparini Alessandra, Hatos Andras, Kajava Andrey V., Kalmar Lajos, Leonardi Emanuela, Lazar Tamas, Macedo-Ribeiro Sandra, Macossay-Castillo Mauricio, Meszaros Attila, Minervini Giovanni, Murvai Nikoletta, Pujols Jordi, Roche Daniel B., Salladini Edoardo, Schad Eva, Schramm Antoine, Szabo Beata, Tantos Agnes, Tonello Fiorella, Tsirigos Konstantinos D., Veljković Nevena V., Ventura Salvador, Vranken Wim, Warholm Per, Uversky Vladimir N., Dunker A. Keith, Longhi Sonia, Tompa Peter, Tosatto Silvio C. E., "DisProt 7.0: a major update of the database of disordered proteins" Nucleic Acids Research, 45, no. D1 (2017):D219-D227,
https://doi.org/10.1093/nar/gkw1056 .
7
170
106
125

DisProt 7.0: a major update of the database of disordered proteins (vol 45, pg D219, 2017)

Piovesan, Damiano; Tabaro, Francesco; Micetic, Ivan; Necci, Marco; Quaglia, Federica; Oldfield, Christopher J.; Aspromonte, Maria Cristina; Davey, Norman E.; Davidović, Radoslav S.; Dosztanyi, Zsuzsanna; Elofsson, Arne; Gasparini, Alessandra; Hatos, Andras; Kajava, Andrey V.; Kalmar, Lajos; Leonardi, Emanuela; Lazar, Tamas; Macedo-Ribeiro, Sandra; Macossay-Castillo, Mauricio; Meszaros, Attila; Minervini, Giovanni; Murvai, Nikoletta; Pujols, Jordi; Roche, Daniel B.; Salladini, Edoardo; Schad, Eva; Schramm, Antoine; Szabo, Beata; Tantos, Agnes; Tonello, Fiorella; Tsirigos, Konstantinos D.; Veljković, Nevena V.; Ventura, Salvador; Vranken, Wim; Warholm, Per; Uversky, Vladimir N.; Dunker, A. Keith; Longhi, Sonia; Tompa, Peter; Tosatto, Silvio C. E.

(2017)

TY  - BOOK
AU  - Piovesan, Damiano
AU  - Tabaro, Francesco
AU  - Micetic, Ivan
AU  - Necci, Marco
AU  - Quaglia, Federica
AU  - Oldfield, Christopher J.
AU  - Aspromonte, Maria Cristina
AU  - Davey, Norman E.
AU  - Davidović, Radoslav S.
AU  - Dosztanyi, Zsuzsanna
AU  - Elofsson, Arne
AU  - Gasparini, Alessandra
AU  - Hatos, Andras
AU  - Kajava, Andrey V.
AU  - Kalmar, Lajos
AU  - Leonardi, Emanuela
AU  - Lazar, Tamas
AU  - Macedo-Ribeiro, Sandra
AU  - Macossay-Castillo, Mauricio
AU  - Meszaros, Attila
AU  - Minervini, Giovanni
AU  - Murvai, Nikoletta
AU  - Pujols, Jordi
AU  - Roche, Daniel B.
AU  - Salladini, Edoardo
AU  - Schad, Eva
AU  - Schramm, Antoine
AU  - Szabo, Beata
AU  - Tantos, Agnes
AU  - Tonello, Fiorella
AU  - Tsirigos, Konstantinos D.
AU  - Veljković, Nevena V.
AU  - Ventura, Salvador
AU  - Vranken, Wim
AU  - Warholm, Per
AU  - Uversky, Vladimir N.
AU  - Dunker, A. Keith
AU  - Longhi, Sonia
AU  - Tompa, Peter
AU  - Tosatto, Silvio C. E.
PY  - 2017
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1465
T2  - Nucleic Acids Research
T1  - DisProt 7.0: a major update of the database of disordered proteins (vol 45, pg D219, 2017)
VL  - 45
IS  - D1
SP  - D1123
EP  - D1124
DO  - 10.1093/nar/gkw1279
ER  - 
@book{
author = "Piovesan, Damiano and Tabaro, Francesco and Micetic, Ivan and Necci, Marco and Quaglia, Federica and Oldfield, Christopher J. and Aspromonte, Maria Cristina and Davey, Norman E. and Davidović, Radoslav S. and Dosztanyi, Zsuzsanna and Elofsson, Arne and Gasparini, Alessandra and Hatos, Andras and Kajava, Andrey V. and Kalmar, Lajos and Leonardi, Emanuela and Lazar, Tamas and Macedo-Ribeiro, Sandra and Macossay-Castillo, Mauricio and Meszaros, Attila and Minervini, Giovanni and Murvai, Nikoletta and Pujols, Jordi and Roche, Daniel B. and Salladini, Edoardo and Schad, Eva and Schramm, Antoine and Szabo, Beata and Tantos, Agnes and Tonello, Fiorella and Tsirigos, Konstantinos D. and Veljković, Nevena V. and Ventura, Salvador and Vranken, Wim and Warholm, Per and Uversky, Vladimir N. and Dunker, A. Keith and Longhi, Sonia and Tompa, Peter and Tosatto, Silvio C. E.",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1465",
journal = "Nucleic Acids Research",
title = "DisProt 7.0: a major update of the database of disordered proteins (vol 45, pg D219, 2017)",
volume = "45",
number = "D1",
pages = "D1123-D1124",
doi = "10.1093/nar/gkw1279"
}
Piovesan, D., Tabaro, F., Micetic, I., Necci, M., Quaglia, F., Oldfield, C. J., Aspromonte, M. C., Davey, N. E., Davidović, R. S., Dosztanyi, Z., Elofsson, A., Gasparini, A., Hatos, A., Kajava, A. V., Kalmar, L., Leonardi, E., Lazar, T., Macedo-Ribeiro, S., Macossay-Castillo, M., Meszaros, A., Minervini, G., Murvai, N., Pujols, J., Roche, D. B., Salladini, E., Schad, E., Schramm, A., Szabo, B., Tantos, A., Tonello, F., Tsirigos, K. D., Veljković, N. V., Ventura, S., Vranken, W., Warholm, P., Uversky, V. N., Dunker, A. K., Longhi, S., Tompa, P.,& Tosatto, S. C. E. (2017). DisProt 7.0: a major update of the database of disordered proteins (vol 45, pg D219, 2017).
Nucleic Acids Research, 45(D1), D1123-D1124.
https://doi.org/10.1093/nar/gkw1279
Piovesan D, Tabaro F, Micetic I, Necci M, Quaglia F, Oldfield CJ, Aspromonte MC, Davey NE, Davidović RS, Dosztanyi Z, Elofsson A, Gasparini A, Hatos A, Kajava AV, Kalmar L, Leonardi E, Lazar T, Macedo-Ribeiro S, Macossay-Castillo M, Meszaros A, Minervini G, Murvai N, Pujols J, Roche DB, Salladini E, Schad E, Schramm A, Szabo B, Tantos A, Tonello F, Tsirigos KD, Veljković NV, Ventura S, Vranken W, Warholm P, Uversky VN, Dunker AK, Longhi S, Tompa P, Tosatto SCE. DisProt 7.0: a major update of the database of disordered proteins (vol 45, pg D219, 2017). Nucleic Acids Research. 2017;45(D1):D1123-D1124
Piovesan Damiano, Tabaro Francesco, Micetic Ivan, Necci Marco, Quaglia Federica, Oldfield Christopher J., Aspromonte Maria Cristina, Davey Norman E., Davidović Radoslav S., Dosztanyi Zsuzsanna, Elofsson Arne, Gasparini Alessandra, Hatos Andras, Kajava Andrey V., Kalmar Lajos, Leonardi Emanuela, Lazar Tamas, Macedo-Ribeiro Sandra, Macossay-Castillo Mauricio, Meszaros Attila, Minervini Giovanni, Murvai Nikoletta, Pujols Jordi, Roche Daniel B., Salladini Edoardo, Schad Eva, Schramm Antoine, Szabo Beata, Tantos Agnes, Tonello Fiorella, Tsirigos Konstantinos D., Veljković Nevena V., Ventura Salvador, Vranken Wim, Warholm Per, Uversky Vladimir N., Dunker A. Keith, Longhi Sonia, Tompa Peter, Tosatto Silvio C. E., "DisProt 7.0: a major update of the database of disordered proteins (vol 45, pg D219, 2017)" Nucleic Acids Research, 45, no. D1 (2017):D1123-D1124,
https://doi.org/10.1093/nar/gkw1279 .
3
39
39
14

MicroRNA in breast cancer: The association with BRCA1/2

Petrović, Nina; Davidović, Radoslav S.; Bajić, Vladan P.; Obradović, Milan M.; Isenović, Esma R.

(2017)

TY  - JOUR
AU  - Petrović, Nina
AU  - Davidović, Radoslav S.
AU  - Bajić, Vladan P.
AU  - Obradović, Milan M.
AU  - Isenović, Esma R.
PY  - 2017
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1614
AB  - Breast cancer (BC) is a heterogeneous disease in an urgent need for developing novel research, classification, and therapy approaches. Breast cancer 1 (BRCA1) and breast cancer 2 (BRCA2) proteins are well described tumor suppressors with great potential to be the subjects of different therapies. MicroRNAs (miRNAs) are genetic elements that might be used to solve the complex BC puzzle. BRCA1 was described to be the target of up to 100 miRNAs. BRCA1 may directly repress miR-155 activity. In addition, miR-15/107/182-mediated downregulation of BRCA1 interrupt DNA repair and may change the course of BC therapy. miR-146a and miR-146-5p silencing BRCA1 may trigger formation of triple-negative and basal-like sporadic BC cases. miR-182 might effect the therapy outcome. miR-21 targeted therapy might be useful for the treatment of BRCA2 mutation carriers. miR-342 overexpression and the absence of functional BRCA1 gene might cause synthetic lethality, which might be used as a base for future therapies. The present review discusses the latest data from studies that focus on the complex network of miRNAs and BRCA1/2 related BCs, which might be important for improving the therapy within the patients with triple-negative BC (TNBC) and basal-like BC, and for understanding the formation of TNBC.
T2  - Cancer Biomarkers
T1  - MicroRNA in breast cancer: The association with BRCA1/2
VL  - 19
IS  - 2
SP  - 119
EP  - 128
DO  - 10.3233/CBM-60319
ER  - 
@article{
author = "Petrović, Nina and Davidović, Radoslav S. and Bajić, Vladan P. and Obradović, Milan M. and Isenović, Esma R.",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1614",
abstract = "Breast cancer (BC) is a heterogeneous disease in an urgent need for developing novel research, classification, and therapy approaches. Breast cancer 1 (BRCA1) and breast cancer 2 (BRCA2) proteins are well described tumor suppressors with great potential to be the subjects of different therapies. MicroRNAs (miRNAs) are genetic elements that might be used to solve the complex BC puzzle. BRCA1 was described to be the target of up to 100 miRNAs. BRCA1 may directly repress miR-155 activity. In addition, miR-15/107/182-mediated downregulation of BRCA1 interrupt DNA repair and may change the course of BC therapy. miR-146a and miR-146-5p silencing BRCA1 may trigger formation of triple-negative and basal-like sporadic BC cases. miR-182 might effect the therapy outcome. miR-21 targeted therapy might be useful for the treatment of BRCA2 mutation carriers. miR-342 overexpression and the absence of functional BRCA1 gene might cause synthetic lethality, which might be used as a base for future therapies. The present review discusses the latest data from studies that focus on the complex network of miRNAs and BRCA1/2 related BCs, which might be important for improving the therapy within the patients with triple-negative BC (TNBC) and basal-like BC, and for understanding the formation of TNBC.",
journal = "Cancer Biomarkers",
title = "MicroRNA in breast cancer: The association with BRCA1/2",
volume = "19",
number = "2",
pages = "119-128",
doi = "10.3233/CBM-60319"
}
Petrović, N., Davidović, R. S., Bajić, V. P., Obradović, M. M.,& Isenović, E. R. (2017). MicroRNA in breast cancer: The association with BRCA1/2.
Cancer Biomarkers, 19(2), 119-128.
https://doi.org/10.3233/CBM-60319
Petrović N, Davidović RS, Bajić VP, Obradović MM, Isenović ER. MicroRNA in breast cancer: The association with BRCA1/2. Cancer Biomarkers. 2017;19(2):119-128
Petrović Nina, Davidović Radoslav S., Bajić Vladan P., Obradović Milan M., Isenović Esma R., "MicroRNA in breast cancer: The association with BRCA1/2" Cancer Biomarkers, 19, no. 2 (2017):119-128,
https://doi.org/10.3233/CBM-60319 .
27

Changes in miR-221/222 Levels in Invasive and In Situ Carcinomas of the Breast: Differences in Association with Estrogen Receptor and TIMP3 Expression Levels

Petrović, Nina; Davidović, Radoslav S.; Jovanović-Ćupić, Snežana P.; Krajnović, Milena M.; Lukic, Silvana; Petrovic, Milan; Roganović, Jelena

(2016)

TY  - JOUR
AU  - Petrović, Nina
AU  - Davidović, Radoslav S.
AU  - Jovanović-Ćupić, Snežana P.
AU  - Krajnović, Milena M.
AU  - Lukic, Silvana
AU  - Petrovic, Milan
AU  - Roganović, Jelena
PY  - 2016
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1308
AB  - Breast cancer (BC) is a heterogeneous group of diseases that still represents a major cause of death in the female population. MicroRNAs (miRNAs, miRs), such as miR-221 and miR-222, have been shown to be involved in BC pathology by acting via its target genes such as tissue inhibitor of metalloproteinase 3 (TIMP3). The main goals of this study were to find differences in miR-221/222 levels of expression in BC groups based on invasiveness, and to investigate the association with estrogen receptor (ER), TIMP3 messenger RNA (mRNA) levels, and clinicopathological characteristics of patients and tumors. In this study, we measured levels of miR-221/222 in 63 breast tissue samples by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) using TaqMan(A (R)) technology and immunohistochemistry. miR-221/222 levels varied significantly across groups based on invasiveness (P LT 0.001). In in situ tumors, miR-221 and miR-222 were negatively associated with ER (P = 0.001, r = -0.714, and P = 0.013, r = -0.585, respectively). In invasive breast carcinomas associated with non-invasive tumors, miR-222 was inversely associated with ER (P = 0.039, r = -0.620). Pure invasive BCs showed a positive correlation of miR-221 and miR-222 with TIMP3 mRNA levels (P = 0.008, r = 0.508, and P = 0.010, r = 0.497, respectively). An increase in miR-221/222 might be an important event for in situ carcinoma formation, and miR-221/222 may be important molecules that highlight potential differences between invasive breast carcinomas associated with non-invasive and pure invasive BCs.
T2  - Molecular Diagnosis and Therapy
T1  - Changes in miR-221/222 Levels in Invasive and In Situ Carcinomas of the Breast: Differences in Association with Estrogen Receptor and TIMP3 Expression Levels
VL  - 20
IS  - 6
SP  - 603
EP  - 615
DO  - 10.1007/s40291-016-0230-3
ER  - 
@article{
author = "Petrović, Nina and Davidović, Radoslav S. and Jovanović-Ćupić, Snežana P. and Krajnović, Milena M. and Lukic, Silvana and Petrovic, Milan and Roganović, Jelena",
year = "2016",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1308",
abstract = "Breast cancer (BC) is a heterogeneous group of diseases that still represents a major cause of death in the female population. MicroRNAs (miRNAs, miRs), such as miR-221 and miR-222, have been shown to be involved in BC pathology by acting via its target genes such as tissue inhibitor of metalloproteinase 3 (TIMP3). The main goals of this study were to find differences in miR-221/222 levels of expression in BC groups based on invasiveness, and to investigate the association with estrogen receptor (ER), TIMP3 messenger RNA (mRNA) levels, and clinicopathological characteristics of patients and tumors. In this study, we measured levels of miR-221/222 in 63 breast tissue samples by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) using TaqMan(A (R)) technology and immunohistochemistry. miR-221/222 levels varied significantly across groups based on invasiveness (P LT 0.001). In in situ tumors, miR-221 and miR-222 were negatively associated with ER (P = 0.001, r = -0.714, and P = 0.013, r = -0.585, respectively). In invasive breast carcinomas associated with non-invasive tumors, miR-222 was inversely associated with ER (P = 0.039, r = -0.620). Pure invasive BCs showed a positive correlation of miR-221 and miR-222 with TIMP3 mRNA levels (P = 0.008, r = 0.508, and P = 0.010, r = 0.497, respectively). An increase in miR-221/222 might be an important event for in situ carcinoma formation, and miR-221/222 may be important molecules that highlight potential differences between invasive breast carcinomas associated with non-invasive and pure invasive BCs.",
journal = "Molecular Diagnosis and Therapy",
title = "Changes in miR-221/222 Levels in Invasive and In Situ Carcinomas of the Breast: Differences in Association with Estrogen Receptor and TIMP3 Expression Levels",
volume = "20",
number = "6",
pages = "603-615",
doi = "10.1007/s40291-016-0230-3"
}
Petrović, N., Davidović, R. S., Jovanović-Ćupić, S. P., Krajnović, M. M., Lukic, S., Petrovic, M.,& Roganović, J. (2016). Changes in miR-221/222 Levels in Invasive and In Situ Carcinomas of the Breast: Differences in Association with Estrogen Receptor and TIMP3 Expression Levels.
Molecular Diagnosis and Therapy, 20(6), 603-615.
https://doi.org/10.1007/s40291-016-0230-3
Petrović N, Davidović RS, Jovanović-Ćupić SP, Krajnović MM, Lukic S, Petrovic M, Roganović J. Changes in miR-221/222 Levels in Invasive and In Situ Carcinomas of the Breast: Differences in Association with Estrogen Receptor and TIMP3 Expression Levels. Molecular Diagnosis and Therapy. 2016;20(6):603-615
Petrović Nina, Davidović Radoslav S., Jovanović-Ćupić Snežana P., Krajnović Milena M., Lukic Silvana, Petrovic Milan, Roganović Jelena, "Changes in miR-221/222 Levels in Invasive and In Situ Carcinomas of the Breast: Differences in Association with Estrogen Receptor and TIMP3 Expression Levels" Molecular Diagnosis and Therapy, 20, no. 6 (2016):603-615,
https://doi.org/10.1007/s40291-016-0230-3 .
1
12
10
11

Significance of Beta-Catenin Expression for the Incidence of Pathological Fractures in Giant Cell Tumors of Bone

Sopta, Jelena; Lujic, Nenad; Kovacevic, Relja; Davidović, Radoslav S.

(2016)

TY  - JOUR
AU  - Sopta, Jelena
AU  - Lujic, Nenad
AU  - Kovacevic, Relja
AU  - Davidović, Radoslav S.
PY  - 2016
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1429
AB  - Aim of the study is to determine the possible roles of p53, cyclin D1, B-catenin and Ki-67 in the increase in risk of fractures in patients with giant cell tumor of bone. The study included a total of 164 patients with giant cell tumor of bone (GCTB), 21 (12.8%) with and 143 (87.2%) without fracture. The samples were analyzed immunohistochemically for expression of Ki-67, p53, cyclin D1 and beta-catenin. According to the immunohistochemical expression of p53 and Ki-67 in mononuclear stromal cells, as well as of cyclin D1 in multinuclear giant cells, there was no significant association with immunopositivity and risk of fractures. However, our research revealed that patients with cytoplasmic expression of beta-catenin in stromal cells had three times more frequent occurrence of pathological fractures, which was highly statistically significant (chi(2) = 7.065; p = 0.008). Moreover, a highly statistically significant correlation between the nuclear expression of beta-catenin in giant cells and the incidence of pathological fractures was also found (chi(2) = 8.824; p = 0.003). The study showed that beta-catenin expression highly correlates with the incidence of pathological fractures in patients with GCTB. Taking into account that beta-catenin is closely linked to activation of the Wnt signaling pathway in GCTB pathogenesis, one could postulate that activation of the Wnt pathway is one of the contributing factors to locally destructive behavior of this tumor, as well as to the incidence of pathological fractures.
T2  - Polish Journal of Pathology
T1  - Significance of Beta-Catenin Expression for the Incidence of Pathological Fractures in Giant Cell Tumors of Bone
VL  - 67
IS  - 4
SP  - 345
EP  - 350
DO  - 10.5114/PJP.2016.65866
ER  - 
@article{
author = "Sopta, Jelena and Lujic, Nenad and Kovacevic, Relja and Davidović, Radoslav S.",
year = "2016",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1429",
abstract = "Aim of the study is to determine the possible roles of p53, cyclin D1, B-catenin and Ki-67 in the increase in risk of fractures in patients with giant cell tumor of bone. The study included a total of 164 patients with giant cell tumor of bone (GCTB), 21 (12.8%) with and 143 (87.2%) without fracture. The samples were analyzed immunohistochemically for expression of Ki-67, p53, cyclin D1 and beta-catenin. According to the immunohistochemical expression of p53 and Ki-67 in mononuclear stromal cells, as well as of cyclin D1 in multinuclear giant cells, there was no significant association with immunopositivity and risk of fractures. However, our research revealed that patients with cytoplasmic expression of beta-catenin in stromal cells had three times more frequent occurrence of pathological fractures, which was highly statistically significant (chi(2) = 7.065; p = 0.008). Moreover, a highly statistically significant correlation between the nuclear expression of beta-catenin in giant cells and the incidence of pathological fractures was also found (chi(2) = 8.824; p = 0.003). The study showed that beta-catenin expression highly correlates with the incidence of pathological fractures in patients with GCTB. Taking into account that beta-catenin is closely linked to activation of the Wnt signaling pathway in GCTB pathogenesis, one could postulate that activation of the Wnt pathway is one of the contributing factors to locally destructive behavior of this tumor, as well as to the incidence of pathological fractures.",
journal = "Polish Journal of Pathology",
title = "Significance of Beta-Catenin Expression for the Incidence of Pathological Fractures in Giant Cell Tumors of Bone",
volume = "67",
number = "4",
pages = "345-350",
doi = "10.5114/PJP.2016.65866"
}
Sopta, J., Lujic, N., Kovacevic, R.,& Davidović, R. S. (2016). Significance of Beta-Catenin Expression for the Incidence of Pathological Fractures in Giant Cell Tumors of Bone.
Polish Journal of Pathology, 67(4), 345-350.
https://doi.org/10.5114/PJP.2016.65866
Sopta J, Lujic N, Kovacevic R, Davidović RS. Significance of Beta-Catenin Expression for the Incidence of Pathological Fractures in Giant Cell Tumors of Bone. Polish Journal of Pathology. 2016;67(4):345-350
Sopta Jelena, Lujic Nenad, Kovacevic Relja, Davidović Radoslav S., "Significance of Beta-Catenin Expression for the Incidence of Pathological Fractures in Giant Cell Tumors of Bone" Polish Journal of Pathology, 67, no. 4 (2016):345-350,
https://doi.org/10.5114/PJP.2016.65866 .

Recurrence of giant cell tumour of bone: role of p53, cyclin D1, beta-catenin and Ki67

Lujic, Nenad; Sopta, Jelena; Kovacevic, Relja; Stevanovic, Vladan; Davidović, Radoslav S.

(2016)

TY  - JOUR
AU  - Lujic, Nenad
AU  - Sopta, Jelena
AU  - Kovacevic, Relja
AU  - Stevanovic, Vladan
AU  - Davidović, Radoslav S.
PY  - 2016
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1298
AB  - To determine various clinical, radiographic, and pathological parameters which may indicate an increased risk of Giant cell tumour of bone (GCTB) recurrence after surgical therapy. The study included a total of 164 GCTB samples; 118 (72 %) primary tumours, and 46 (28 %) recurrences; which were analyzed on immunohistochemistry for expression of Ki67, p53, cyclin D1, and beta-catenin. Among 13 analyzed clinical, radiological, and histological variables, which presented possible predictive factors for the incidence of GCTB relapse, univariate logistic regression (ULR) extract three highly statistically significant parameters: 1) lesion localization, 2) nuclear p53 expression in mononuclear cells, and 3) nuclear cyclin D1 expression in giant multinuclear cells. The multivariate logistic regression (MLR), revealing that p53 expression in mononuclear cells was the most significant predictive factor (HR = 6,181 p LT 0,001), the positivity of which indicated six times higher probability for recurrence in GCTB. The expression of cyclin D1 in giant cells, containing less than 15 nuclei, was also statistically significant (HR = 8,398, p = 0,038) for predicting the recurrence, and demonstrated eight times more frequent recurrence in positive tumours. This study confirmed independent predicting factors for GCTB reccurence: p53 expression in mononuclear tumour cells and cyclin D1 expression in giant multinuclear cells. Results are new addition to generally known parameters, such as: localization of lesion, number of surgical interventions, clear destruction of cortex with the presence of extracompartmental lesion, and histological criteria for malignancy and can help in further research and treatment of GCTB.
T2  - International Orthopaedics
T1  - Recurrence of giant cell tumour of bone: role of p53, cyclin D1, beta-catenin and Ki67
VL  - 40
IS  - 11
SP  - 2393
EP  - 2399
DO  - 10.1007/s00264-016-3292-2
ER  - 
@article{
author = "Lujic, Nenad and Sopta, Jelena and Kovacevic, Relja and Stevanovic, Vladan and Davidović, Radoslav S.",
year = "2016",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1298",
abstract = "To determine various clinical, radiographic, and pathological parameters which may indicate an increased risk of Giant cell tumour of bone (GCTB) recurrence after surgical therapy. The study included a total of 164 GCTB samples; 118 (72 %) primary tumours, and 46 (28 %) recurrences; which were analyzed on immunohistochemistry for expression of Ki67, p53, cyclin D1, and beta-catenin. Among 13 analyzed clinical, radiological, and histological variables, which presented possible predictive factors for the incidence of GCTB relapse, univariate logistic regression (ULR) extract three highly statistically significant parameters: 1) lesion localization, 2) nuclear p53 expression in mononuclear cells, and 3) nuclear cyclin D1 expression in giant multinuclear cells. The multivariate logistic regression (MLR), revealing that p53 expression in mononuclear cells was the most significant predictive factor (HR = 6,181 p LT 0,001), the positivity of which indicated six times higher probability for recurrence in GCTB. The expression of cyclin D1 in giant cells, containing less than 15 nuclei, was also statistically significant (HR = 8,398, p = 0,038) for predicting the recurrence, and demonstrated eight times more frequent recurrence in positive tumours. This study confirmed independent predicting factors for GCTB reccurence: p53 expression in mononuclear tumour cells and cyclin D1 expression in giant multinuclear cells. Results are new addition to generally known parameters, such as: localization of lesion, number of surgical interventions, clear destruction of cortex with the presence of extracompartmental lesion, and histological criteria for malignancy and can help in further research and treatment of GCTB.",
journal = "International Orthopaedics",
title = "Recurrence of giant cell tumour of bone: role of p53, cyclin D1, beta-catenin and Ki67",
volume = "40",
number = "11",
pages = "2393-2399",
doi = "10.1007/s00264-016-3292-2"
}
Lujic, N., Sopta, J., Kovacevic, R., Stevanovic, V.,& Davidović, R. S. (2016). Recurrence of giant cell tumour of bone: role of p53, cyclin D1, beta-catenin and Ki67.
International Orthopaedics, 40(11), 2393-2399.
https://doi.org/10.1007/s00264-016-3292-2
Lujic N, Sopta J, Kovacevic R, Stevanovic V, Davidović RS. Recurrence of giant cell tumour of bone: role of p53, cyclin D1, beta-catenin and Ki67. International Orthopaedics. 2016;40(11):2393-2399
Lujic Nenad, Sopta Jelena, Kovacevic Relja, Stevanovic Vladan, Davidović Radoslav S., "Recurrence of giant cell tumour of bone: role of p53, cyclin D1, beta-catenin and Ki67" International Orthopaedics, 40, no. 11 (2016):2393-2399,
https://doi.org/10.1007/s00264-016-3292-2 .
7
6
6

Skewed X-Chromosome Inactivation in Women Affected by Alzheimers Disease

Bajić, Vladan P.; Mandušić, Vesna; Stefanova, Elka; Božović, Ana M.; Davidović, Radoslav S.; Živković, Lada; Cabarkapa, Andrea; Spremo-Potparević, Biljana

(2015)

TY  - JOUR
AU  - Bajić, Vladan P.
AU  - Mandušić, Vesna
AU  - Stefanova, Elka
AU  - Božović, Ana M.
AU  - Davidović, Radoslav S.
AU  - Živković, Lada
AU  - Cabarkapa, Andrea
AU  - Spremo-Potparević, Biljana
PY  - 2015
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/314
AB  - X-chromosome instability has been a long established feature in Alzheimers disease ( AD). Premature centromere division and aneuploidy of the X-chromosome has been found in peripheral blood lymphocytes and neuronal tissue in female AD patients. Interestingly, only one chromosome of the X pair has been affected. These results raised a question, Is the X-chromosome inactivation pattern altered in peripheral blood lymphocytes ofwomen affected by AD? To address this question, we analyzed the methylation status of androgen receptor promoter which may show us any deviation from the 50 : 50% X inactivation status in peripheral blood lymphocytes ofwomen with AD. Our results showed skewed inactivation patterns ( GT 90%). These findings suggest that an epigenetic alteration on the inactivation centers of the X-chromosome (or skewing) relates not only to aging, by might be a novel property that could account for the higher incidence of AD in women.
T2  - Journal of Alzheimers Disease
T1  - Skewed X-Chromosome Inactivation in Women Affected by Alzheimers Disease
VL  - 43
IS  - 4
SP  - 1251
EP  - 1259
DO  - 10.3233/JAD-141674
ER  - 
@article{
author = "Bajić, Vladan P. and Mandušić, Vesna and Stefanova, Elka and Božović, Ana M. and Davidović, Radoslav S. and Živković, Lada and Cabarkapa, Andrea and Spremo-Potparević, Biljana",
year = "2015",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/314",
abstract = "X-chromosome instability has been a long established feature in Alzheimers disease ( AD). Premature centromere division and aneuploidy of the X-chromosome has been found in peripheral blood lymphocytes and neuronal tissue in female AD patients. Interestingly, only one chromosome of the X pair has been affected. These results raised a question, Is the X-chromosome inactivation pattern altered in peripheral blood lymphocytes ofwomen affected by AD? To address this question, we analyzed the methylation status of androgen receptor promoter which may show us any deviation from the 50 : 50% X inactivation status in peripheral blood lymphocytes ofwomen with AD. Our results showed skewed inactivation patterns ( GT 90%). These findings suggest that an epigenetic alteration on the inactivation centers of the X-chromosome (or skewing) relates not only to aging, by might be a novel property that could account for the higher incidence of AD in women.",
journal = "Journal of Alzheimers Disease",
title = "Skewed X-Chromosome Inactivation in Women Affected by Alzheimers Disease",
volume = "43",
number = "4",
pages = "1251-1259",
doi = "10.3233/JAD-141674"
}
Bajić, V. P., Mandušić, V., Stefanova, E., Božović, A. M., Davidović, R. S., Živković, L., Cabarkapa, A.,& Spremo-Potparević, B. (2015). Skewed X-Chromosome Inactivation in Women Affected by Alzheimers Disease.
Journal of Alzheimers Disease, 43(4), 1251-1259.
https://doi.org/10.3233/JAD-141674
Bajić VP, Mandušić V, Stefanova E, Božović AM, Davidović RS, Živković L, Cabarkapa A, Spremo-Potparević B. Skewed X-Chromosome Inactivation in Women Affected by Alzheimers Disease. Journal of Alzheimers Disease. 2015;43(4):1251-1259
Bajić Vladan P., Mandušić Vesna, Stefanova Elka, Božović Ana M., Davidović Radoslav S., Živković Lada, Cabarkapa Andrea, Spremo-Potparević Biljana, "Skewed X-Chromosome Inactivation in Women Affected by Alzheimers Disease" Journal of Alzheimers Disease, 43, no. 4 (2015):1251-1259,
https://doi.org/10.3233/JAD-141674 .
1
11
11
11

Immunohistochemical expression of nestin in rhabdomyosarcoma: implications for clinicopathology and patient outcome

Glumac, Sofija; Pejić, Snežana; Kovacevic, R.; Dundjerovic, D.; Davidović, Radoslav S.; Ristic, D.; Sopta, J.

(2015)

TY  - JOUR
AU  - Glumac, Sofija
AU  - Pejić, Snežana
AU  - Kovacevic, R.
AU  - Dundjerovic, D.
AU  - Davidović, Radoslav S.
AU  - Ristic, D.
AU  - Sopta, J.
PY  - 2015
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/835
AB  - Rhabdomyosarcoma (RMS) is a highly malignant cancer. Over the last two decades, prognosis for RMS patients has significantly improved, with the exception of those in the high-risk group. In order to identify new prognostic factors, we investigated the expression of nestin in RMS cells and its correlation with clinicopathological features and patient outcome. The analysis of overall survival for all patients (N = 30) revealed 1-, 2-, 3-, 4-, and 5-year survival rates of 93.3, 83.3, 66.7, 63.3, and 63.3%, respectively. Nestin overexpression significantly correlated with survival (P = 0.044). Survival of patients with = 50% nestin-positive cells was 90, 70, and 40% after 1, 2, and 3 years, respectively, and remained unchanged until the end of the investigation period. The study group composed of patients exhibiting nestin expression in GT 50% of cells showed 1-, 2-, 3-, and 4-year survival rates of 95, 90, 80, and 75%, respectively, remaining stable at 75% for the fifth year of observation. A nestin-positive expression rate lower than 50% was observed more frequently in older patients (43.60 +/- 27.58 years; P = 0.028). In addition, higher rates of nestin expression were observed in most embryonal RMS specimens and low-grade tumors, in early stages of the disease, and among younger patients. Our results lead us to propose nestin as possible positive prognostic factor in RMS.
T2  - Genetics and Molecular Research
T1  - Immunohistochemical expression of nestin in rhabdomyosarcoma: implications for clinicopathology and patient outcome
VL  - 14
IS  - 4
SP  - 14649
EP  - 14659
DO  - 10.4238/2015.November.18.29
ER  - 
@article{
author = "Glumac, Sofija and Pejić, Snežana and Kovacevic, R. and Dundjerovic, D. and Davidović, Radoslav S. and Ristic, D. and Sopta, J.",
year = "2015",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/835",
abstract = "Rhabdomyosarcoma (RMS) is a highly malignant cancer. Over the last two decades, prognosis for RMS patients has significantly improved, with the exception of those in the high-risk group. In order to identify new prognostic factors, we investigated the expression of nestin in RMS cells and its correlation with clinicopathological features and patient outcome. The analysis of overall survival for all patients (N = 30) revealed 1-, 2-, 3-, 4-, and 5-year survival rates of 93.3, 83.3, 66.7, 63.3, and 63.3%, respectively. Nestin overexpression significantly correlated with survival (P = 0.044). Survival of patients with = 50% nestin-positive cells was 90, 70, and 40% after 1, 2, and 3 years, respectively, and remained unchanged until the end of the investigation period. The study group composed of patients exhibiting nestin expression in GT 50% of cells showed 1-, 2-, 3-, and 4-year survival rates of 95, 90, 80, and 75%, respectively, remaining stable at 75% for the fifth year of observation. A nestin-positive expression rate lower than 50% was observed more frequently in older patients (43.60 +/- 27.58 years; P = 0.028). In addition, higher rates of nestin expression were observed in most embryonal RMS specimens and low-grade tumors, in early stages of the disease, and among younger patients. Our results lead us to propose nestin as possible positive prognostic factor in RMS.",
journal = "Genetics and Molecular Research",
title = "Immunohistochemical expression of nestin in rhabdomyosarcoma: implications for clinicopathology and patient outcome",
volume = "14",
number = "4",
pages = "14649-14659",
doi = "10.4238/2015.November.18.29"
}
Glumac, S., Pejić, S., Kovacevic, R., Dundjerovic, D., Davidović, R. S., Ristic, D.,& Sopta, J. (2015). Immunohistochemical expression of nestin in rhabdomyosarcoma: implications for clinicopathology and patient outcome.
Genetics and Molecular Research, 14(4), 14649-14659.
https://doi.org/10.4238/2015.November.18.29
Glumac S, Pejić S, Kovacevic R, Dundjerovic D, Davidović RS, Ristic D, Sopta J. Immunohistochemical expression of nestin in rhabdomyosarcoma: implications for clinicopathology and patient outcome. Genetics and Molecular Research. 2015;14(4):14649-14659
Glumac Sofija, Pejić Snežana, Kovacevic R., Dundjerovic D., Davidović Radoslav S., Ristic D., Sopta J., "Immunohistochemical expression of nestin in rhabdomyosarcoma: implications for clinicopathology and patient outcome" Genetics and Molecular Research, 14, no. 4 (2015):14649-14659,
https://doi.org/10.4238/2015.November.18.29 .
2
1
1

Анализа мутационог статуса гена p53 и метилационог статуса промотора гена p14 и p16 у липосаркомима

Davidović, Radoslav S.

(Универзитет у Београду, Биолошки факултет, 2014)

TY  - BOOK
AU  - Davidović, Radoslav S.
PY  - 2014
UR  - http://eteze.bg.ac.rs/application/showtheses?thesesId=3057
UR  - https://fedorabg.bg.ac.rs/fedora/get/o:11308/bdef:Content/download
UR  - http://vbs.rs/scripts/cobiss?command=DISPLAY&base=70036&RID=1024816562
UR  - http://nardus.mpn.gov.rs/123456789/5671
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7280
AB  - Липосаркоми, тумори мезенхималног порекла, представљају најучесталијихистолошки тип саркома меких ткива. Групу карактерише велика разноликосткако у погледу патохистолошке организације тумора тако и биологије понашања.Уобичајена подела липосаркома обухвата следећа три подтипа: а.) добродиферентовани / дедиферентовани, б.) миксоидни / округлоћелијски и в.)плеоморфни. С обзиром на значајне клиничко-патолошке разлике између триподтипа липосаркома, вероватно је да су различити механизми укључени у њиховнастанак и развој. На основу студија које су се фокусирале на истраживањегенетике саркома меких ткива и костију, може се закључити да сигнални путевиp53-p14 и Rb-p16 играју одређену улогу у свим типовима саркома. Разјашњавањеулоге ових сигналних путева у патогенези липосаркома, може да буде доприноскако дијагностици и прогностици липосаркома, тако и дефинисању потенцијалнихтерапеутских циљева. Студија је обухватила испитивање мутационог статуса генар53 и метилационог статуса гена р14 и р16, на 33 узорка липосаркома, сва триподтипа. У циљу свеобухватније анализе испитивана је и експресија протеина р16,циклина D1 и фактора пролиферације Ki-67, применом имунохистохемијскогбојења. Резултати експеримента су показали да промене у сигналним путевимар53-р14 и р16-Rb могу имати значаја у патогенези сва три подтипа липосаркома.Разлике се огледају у квалитету и квантитету промена.
AB  - Liposarcoma, tumors of mesenchymal origin, represent the most frequent type ofsoft tissue sarcomas. The group is characterized by a great diversity regardingpathohistology and biological behavior. The group can be divided into three differentsubtypes: a.) well differentiated / dedifferentiated, b.) myxoid / round cell and c.)pleomorphic. Given the significant clinical and pathological differences between thethree subtypes of liposarcoma, it is likely that different mechanisms are involved in theirformation and development. Based on the studies that have been focused on geneticresearch of sarcoma of soft tissues and bones, conclusion can be drawn that the p53-p14and Rb-p16 signaling pathways play a certain role in sarcomagenesis. Clarification ofthe role of these signaling pathways in the pathogenesis of liposarcoma, could be acontribution towards better diagnostic and prognostic criteria and the identification ofpotential therapeutic targets. The study included examination of the p53 gene mutationstatus and assessment of the p14/p16 gene methylation status in 33 liposarcoma samplesof all three subtypes. For the purpose of more comprehensive analysis, proteinexpression of the p16, cyclin D1 and Ki-67 has been evaluated byimmunohistochemical staining. The results of the study have showed that the alterationsof the targeted signal pathways are important in the pathogenesis of all three subtypes ofliposarcoma. The differences are reflected in the quality and quantity of the detected alterations.
PB  - Универзитет у Београду, Биолошки факултет
T2  - Универзитет у Београду
T1  - Анализа мутационог статуса гена p53 и метилационог статуса промотора гена p14 и p16 у липосаркомима
T1  - Analysis of the p53 gene mutation status and methylation status of the promoters of p14 and p16 genes in liposarcoma
ER  - 
@phdthesis{
author = "Davidović, Radoslav S.",
year = "2014",
url = "http://eteze.bg.ac.rs/application/showtheses?thesesId=3057, https://fedorabg.bg.ac.rs/fedora/get/o:11308/bdef:Content/download, http://vbs.rs/scripts/cobiss?command=DISPLAY&base=70036&RID=1024816562, http://nardus.mpn.gov.rs/123456789/5671, http://vinar.vin.bg.ac.rs/handle/123456789/7280",
abstract = "Липосаркоми, тумори мезенхималног порекла, представљају најучесталијихистолошки тип саркома меких ткива. Групу карактерише велика разноликосткако у погледу патохистолошке организације тумора тако и биологије понашања.Уобичајена подела липосаркома обухвата следећа три подтипа: а.) добродиферентовани / дедиферентовани, б.) миксоидни / округлоћелијски и в.)плеоморфни. С обзиром на значајне клиничко-патолошке разлике између триподтипа липосаркома, вероватно је да су различити механизми укључени у њиховнастанак и развој. На основу студија које су се фокусирале на истраживањегенетике саркома меких ткива и костију, може се закључити да сигнални путевиp53-p14 и Rb-p16 играју одређену улогу у свим типовима саркома. Разјашњавањеулоге ових сигналних путева у патогенези липосаркома, може да буде доприноскако дијагностици и прогностици липосаркома, тако и дефинисању потенцијалнихтерапеутских циљева. Студија је обухватила испитивање мутационог статуса генар53 и метилационог статуса гена р14 и р16, на 33 узорка липосаркома, сва триподтипа. У циљу свеобухватније анализе испитивана је и експресија протеина р16,циклина D1 и фактора пролиферације Ki-67, применом имунохистохемијскогбојења. Резултати експеримента су показали да промене у сигналним путевимар53-р14 и р16-Rb могу имати значаја у патогенези сва три подтипа липосаркома.Разлике се огледају у квалитету и квантитету промена., Liposarcoma, tumors of mesenchymal origin, represent the most frequent type ofsoft tissue sarcomas. The group is characterized by a great diversity regardingpathohistology and biological behavior. The group can be divided into three differentsubtypes: a.) well differentiated / dedifferentiated, b.) myxoid / round cell and c.)pleomorphic. Given the significant clinical and pathological differences between thethree subtypes of liposarcoma, it is likely that different mechanisms are involved in theirformation and development. Based on the studies that have been focused on geneticresearch of sarcoma of soft tissues and bones, conclusion can be drawn that the p53-p14and Rb-p16 signaling pathways play a certain role in sarcomagenesis. Clarification ofthe role of these signaling pathways in the pathogenesis of liposarcoma, could be acontribution towards better diagnostic and prognostic criteria and the identification ofpotential therapeutic targets. The study included examination of the p53 gene mutationstatus and assessment of the p14/p16 gene methylation status in 33 liposarcoma samplesof all three subtypes. For the purpose of more comprehensive analysis, proteinexpression of the p16, cyclin D1 and Ki-67 has been evaluated byimmunohistochemical staining. The results of the study have showed that the alterationsof the targeted signal pathways are important in the pathogenesis of all three subtypes ofliposarcoma. The differences are reflected in the quality and quantity of the detected alterations.",
publisher = "Универзитет у Београду, Биолошки факултет",
journal = "Универзитет у Београду",
title = "Анализа мутационог статуса гена p53 и метилационог статуса промотора гена p14 и p16 у липосаркомима, Analysis of the p53 gene mutation status and methylation status of the promoters of p14 and p16 genes in liposarcoma"
}
Davidović, R. S. (2014). Analysis of the p53 gene mutation status and methylation status of the promoters of p14 and p16 genes in liposarcoma.
Универзитет у Београду
Универзитет у Београду, Биолошки факултет..
Davidović RS. Analysis of the p53 gene mutation status and methylation status of the promoters of p14 and p16 genes in liposarcoma. Универзитет у Београду. 2014;
Davidović Radoslav S., "Analysis of the p53 gene mutation status and methylation status of the promoters of p14 and p16 genes in liposarcoma" Универзитет у Београду (2014)

Methylation-specific PCR: four steps in primer design

Davidović, Radoslav S.; Božović, Ana M.; Mandušić, Vesna; Krajnović, Milena M.

(2014)

TY  - JOUR
AU  - Davidović, Radoslav S.
AU  - Božović, Ana M.
AU  - Mandušić, Vesna
AU  - Krajnović, Milena M.
PY  - 2014
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/74
AB  - Methylation-specific PCR (MSP) is still the method of choice for a single gene methylation study. The proper design of the primer pairs is a prerequisite for obtaining reliable PCR results. Despite numerous protocols describing the rules for MSP primer design, none of them provide a comprehensive approach to the problem. Our aim was to depict a workflow for the primer design that is concise and easy to follow. In order to achieve this goal, adequate tools for promoter sequence retrieval, MSP primer design and subsequent in silico analysis are presented and discussed. Furthermore, a few instructive examples regarding a good versus a poor primer design are provided. Finally, primer design is demonstrated according to the proposed workflow. This article aims to provide researchers, interested in a single gene methylation studies, with useful information regarding successful primer design.
T2  - Central European Journal of Biology
T1  - Methylation-specific PCR: four steps in primer design
VL  - 9
IS  - 12
SP  - 1127
EP  - 1139
DO  - 10.2478/s11535-014-0324-z
ER  - 
@article{
author = "Davidović, Radoslav S. and Božović, Ana M. and Mandušić, Vesna and Krajnović, Milena M.",
year = "2014",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/74",
abstract = "Methylation-specific PCR (MSP) is still the method of choice for a single gene methylation study. The proper design of the primer pairs is a prerequisite for obtaining reliable PCR results. Despite numerous protocols describing the rules for MSP primer design, none of them provide a comprehensive approach to the problem. Our aim was to depict a workflow for the primer design that is concise and easy to follow. In order to achieve this goal, adequate tools for promoter sequence retrieval, MSP primer design and subsequent in silico analysis are presented and discussed. Furthermore, a few instructive examples regarding a good versus a poor primer design are provided. Finally, primer design is demonstrated according to the proposed workflow. This article aims to provide researchers, interested in a single gene methylation studies, with useful information regarding successful primer design.",
journal = "Central European Journal of Biology",
title = "Methylation-specific PCR: four steps in primer design",
volume = "9",
number = "12",
pages = "1127-1139",
doi = "10.2478/s11535-014-0324-z"
}
Davidović, R. S., Božović, A. M., Mandušić, V.,& Krajnović, M. M. (2014). Methylation-specific PCR: four steps in primer design.
Central European Journal of Biology, 9(12), 1127-1139.
https://doi.org/10.2478/s11535-014-0324-z
Davidović RS, Božović AM, Mandušić V, Krajnović MM. Methylation-specific PCR: four steps in primer design. Central European Journal of Biology. 2014;9(12):1127-1139
Davidović Radoslav S., Božović Ana M., Mandušić Vesna, Krajnović Milena M., "Methylation-specific PCR: four steps in primer design" Central European Journal of Biology, 9, no. 12 (2014):1127-1139,
https://doi.org/10.2478/s11535-014-0324-z .
3
10
8
8

Prognostic significance of epigenetic inactivation of p16, p15, MGMT and DAPK genes in follicular lymphoma

Krajnović, Milena M.; Radojkovic, Milica; Davidović, Radoslav S.; Dimitrijević, Bogomir B.; Krtolica-Žikić, Koviljka

(2013)

TY  - JOUR
AU  - Krajnović, Milena M.
AU  - Radojkovic, Milica
AU  - Davidović, Radoslav S.
AU  - Dimitrijević, Bogomir B.
AU  - Krtolica-Žikić, Koviljka
PY  - 2013
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5388
AB  - In this study, methylation-specific polymerase chain reaction was used to investigate the role and potential prognostic significance of the methylation status of p16, p15, MGMT and DAPK genes in 32 specimens of follicular lymphoma (FL). Hypermethylation of p15 gene was associated with lower hemoglobin level (P = 0.020) and MGMT/DAPK comethylation with relapsed disease (P = 0.018). Among all patients with FL, there was no significant difference in the overall survival between those with hypermethylated and unmethylated of any examined genes. Therefore, we analyzed methylation in the different groups according to FL International Prognostic Index (FLIPI) and tumor grade. In the high-risk group, patients with hypermethylated p16 gene had significant lower overall survival than those with unmethylated p16 (P = 0.006) and trend toward shorter failure-free survival (P = 0.068). In the same risk group, there was a trend toward longer overall survival for patients with hypermethylated MGMT gene, compared to those with unmethylated MGMT gene (P = 0.066). p15 methylation had impact on shorter overall survival in grade I group of patients (P = 0.013), and DAPK methylation tended to have impact on shorter failure-free survival in the whole examined group (P = 0.079). Our results suggest that promotermethylation of p16 and MGMT genes could have prognostic value when used in combination with the FLIPI and p15 methylation in combination with tumor grade. Concurrent methylation of MGMT and DAPK genes could be the marker of tumor chemoresistance and disease recurrence.
T2  - Medical Oncology
T1  - Prognostic significance of epigenetic inactivation of p16, p15, MGMT and DAPK genes in follicular lymphoma
VL  - 30
IS  - 1
DO  - 10.1007/s12032-012-0441-3
ER  - 
@article{
author = "Krajnović, Milena M. and Radojkovic, Milica and Davidović, Radoslav S. and Dimitrijević, Bogomir B. and Krtolica-Žikić, Koviljka",
year = "2013",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5388",
abstract = "In this study, methylation-specific polymerase chain reaction was used to investigate the role and potential prognostic significance of the methylation status of p16, p15, MGMT and DAPK genes in 32 specimens of follicular lymphoma (FL). Hypermethylation of p15 gene was associated with lower hemoglobin level (P = 0.020) and MGMT/DAPK comethylation with relapsed disease (P = 0.018). Among all patients with FL, there was no significant difference in the overall survival between those with hypermethylated and unmethylated of any examined genes. Therefore, we analyzed methylation in the different groups according to FL International Prognostic Index (FLIPI) and tumor grade. In the high-risk group, patients with hypermethylated p16 gene had significant lower overall survival than those with unmethylated p16 (P = 0.006) and trend toward shorter failure-free survival (P = 0.068). In the same risk group, there was a trend toward longer overall survival for patients with hypermethylated MGMT gene, compared to those with unmethylated MGMT gene (P = 0.066). p15 methylation had impact on shorter overall survival in grade I group of patients (P = 0.013), and DAPK methylation tended to have impact on shorter failure-free survival in the whole examined group (P = 0.079). Our results suggest that promotermethylation of p16 and MGMT genes could have prognostic value when used in combination with the FLIPI and p15 methylation in combination with tumor grade. Concurrent methylation of MGMT and DAPK genes could be the marker of tumor chemoresistance and disease recurrence.",
journal = "Medical Oncology",
title = "Prognostic significance of epigenetic inactivation of p16, p15, MGMT and DAPK genes in follicular lymphoma",
volume = "30",
number = "1",
doi = "10.1007/s12032-012-0441-3"
}
Krajnović, M. M., Radojkovic, M., Davidović, R. S., Dimitrijević, B. B.,& Krtolica-Žikić, K. (2013). Prognostic significance of epigenetic inactivation of p16, p15, MGMT and DAPK genes in follicular lymphoma.
Medical Oncology, 30(1).
https://doi.org/10.1007/s12032-012-0441-3
Krajnović MM, Radojkovic M, Davidović RS, Dimitrijević BB, Krtolica-Žikić K. Prognostic significance of epigenetic inactivation of p16, p15, MGMT and DAPK genes in follicular lymphoma. Medical Oncology. 2013;30(1)
Krajnović Milena M., Radojkovic Milica, Davidović Radoslav S., Dimitrijević Bogomir B., Krtolica-Žikić Koviljka, "Prognostic significance of epigenetic inactivation of p16, p15, MGMT and DAPK genes in follicular lymphoma" Medical Oncology, 30, no. 1 (2013),
https://doi.org/10.1007/s12032-012-0441-3 .
18
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p14(ARF) methylation is a common event in the pathogenesis and progression of myxoid and pleomorphic liposarcoma

Davidović, Radoslav S.; Sopta, Jelena; Mandušić, Vesna; Krajnović, Milena M.; Stanojevic, Maja; Tulic, Goran; Dimitrijević, Bogomir B.

(2013)

TY  - JOUR
AU  - Davidović, Radoslav S.
AU  - Sopta, Jelena
AU  - Mandušić, Vesna
AU  - Krajnović, Milena M.
AU  - Stanojevic, Maja
AU  - Tulic, Goran
AU  - Dimitrijević, Bogomir B.
PY  - 2013
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5646
AB  - Liposarcoma represents the most frequent group of soft tissue sarcomas. The group can be divided into three different classes: (1) differentiated/undifferentiated (WDLPS/DDLPS), (2) myxoid/round cell (MLPS/RCLPS) and (3) pleomorphic liposarcoma (PLS). It has become apparent that p53-p14 and Rb-p16 pathways play important roles in the pathogenesis of various sarcoma types. Molecular studies of the genes involved in these two pathways showed wide variations between the liposarcoma subtypes or even within the same subtype. We sought to examine mutational status of p53 and methylation status of p16(INK4a)/p14(ARF) genes in primary and recurrent liposarcoma tumors. There were twelve myxoid (12/18, 66.7 %) and six pleomorphic liposarcoma (6/18, 33.3 %) samples. Immunohistochemical analysis revealed that p53 protein was overexpressed in 3/12 MLPS (25 %) and 6/6 PLS (100 %). Mutational analysis showed that 2/11 MLPS (18.2 %) and 2/6 PLS (33.3 %) contained mutated p53 gene. On the other hand, 3/18 samples (16.7 %) had methylated p16 promoter. However, the frequencies of the p14(ARF) gene methylation were 83.3 % (10/12) and 50 % (3/6) in myxoid and pleomorphic group, respectively. Overall, 15 out of 18 (83.3 %) samples had either p53 gene mutation or methylated p14(ARF) promoter. The results from the current study suggest significant impact of the p14(ARF) gene methylation on the pathogenesis and progression of myxoid and to a lesser extent pleomorphic liposarcoma. Despite the limited number of samples, our study points to necessity of further investigation of p53-p14 and Rb-p16 pathways in liposarcoma.
T2  - Medical Oncology
T1  - p14(ARF) methylation is a common event in the pathogenesis and progression of myxoid and pleomorphic liposarcoma
VL  - 30
IS  - 3
DO  - 10.1007/s12032-013-0682-9
ER  - 
@article{
author = "Davidović, Radoslav S. and Sopta, Jelena and Mandušić, Vesna and Krajnović, Milena M. and Stanojevic, Maja and Tulic, Goran and Dimitrijević, Bogomir B.",
year = "2013",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5646",
abstract = "Liposarcoma represents the most frequent group of soft tissue sarcomas. The group can be divided into three different classes: (1) differentiated/undifferentiated (WDLPS/DDLPS), (2) myxoid/round cell (MLPS/RCLPS) and (3) pleomorphic liposarcoma (PLS). It has become apparent that p53-p14 and Rb-p16 pathways play important roles in the pathogenesis of various sarcoma types. Molecular studies of the genes involved in these two pathways showed wide variations between the liposarcoma subtypes or even within the same subtype. We sought to examine mutational status of p53 and methylation status of p16(INK4a)/p14(ARF) genes in primary and recurrent liposarcoma tumors. There were twelve myxoid (12/18, 66.7 %) and six pleomorphic liposarcoma (6/18, 33.3 %) samples. Immunohistochemical analysis revealed that p53 protein was overexpressed in 3/12 MLPS (25 %) and 6/6 PLS (100 %). Mutational analysis showed that 2/11 MLPS (18.2 %) and 2/6 PLS (33.3 %) contained mutated p53 gene. On the other hand, 3/18 samples (16.7 %) had methylated p16 promoter. However, the frequencies of the p14(ARF) gene methylation were 83.3 % (10/12) and 50 % (3/6) in myxoid and pleomorphic group, respectively. Overall, 15 out of 18 (83.3 %) samples had either p53 gene mutation or methylated p14(ARF) promoter. The results from the current study suggest significant impact of the p14(ARF) gene methylation on the pathogenesis and progression of myxoid and to a lesser extent pleomorphic liposarcoma. Despite the limited number of samples, our study points to necessity of further investigation of p53-p14 and Rb-p16 pathways in liposarcoma.",
journal = "Medical Oncology",
title = "p14(ARF) methylation is a common event in the pathogenesis and progression of myxoid and pleomorphic liposarcoma",
volume = "30",
number = "3",
doi = "10.1007/s12032-013-0682-9"
}
Davidović, R. S., Sopta, J., Mandušić, V., Krajnović, M. M., Stanojevic, M., Tulic, G.,& Dimitrijević, B. B. (2013). p14(ARF) methylation is a common event in the pathogenesis and progression of myxoid and pleomorphic liposarcoma.
Medical Oncology, 30(3).
https://doi.org/10.1007/s12032-013-0682-9
Davidović RS, Sopta J, Mandušić V, Krajnović MM, Stanojevic M, Tulic G, Dimitrijević BB. p14(ARF) methylation is a common event in the pathogenesis and progression of myxoid and pleomorphic liposarcoma. Medical Oncology. 2013;30(3)
Davidović Radoslav S., Sopta Jelena, Mandušić Vesna, Krajnović Milena M., Stanojevic Maja, Tulic Goran, Dimitrijević Bogomir B., "p14(ARF) methylation is a common event in the pathogenesis and progression of myxoid and pleomorphic liposarcoma" Medical Oncology, 30, no. 3 (2013),
https://doi.org/10.1007/s12032-013-0682-9 .
6
4
4

p14ARF methylation is a common event in the pathogenesis and progression of mixoid and pleomorphic liposarcoma

Sopta, J.; Davidović, Radoslav S.; Kovacevic, R.; Lujic, N.; Ristic, D.

(2013)

TY  - CONF
AU  - Sopta, J.
AU  - Davidović, Radoslav S.
AU  - Kovacevic, R.
AU  - Lujic, N.
AU  - Ristic, D.
PY  - 2013
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/2742
C3  - European Journal of Cancer
T1  - p14ARF methylation is a common event in the pathogenesis and progression of mixoid and pleomorphic liposarcoma
VL  - 49
SP  - S15
EP  - S16
ER  - 
@conference{
author = "Sopta, J. and Davidović, Radoslav S. and Kovacevic, R. and Lujic, N. and Ristic, D.",
year = "2013",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/2742",
journal = "European Journal of Cancer",
title = "p14ARF methylation is a common event in the pathogenesis and progression of mixoid and pleomorphic liposarcoma",
volume = "49",
pages = "S15-S16"
}
Sopta, J., Davidović, R. S., Kovacevic, R., Lujic, N.,& Ristic, D. (2013). p14ARF methylation is a common event in the pathogenesis and progression of mixoid and pleomorphic liposarcoma.
European Journal of Cancer, 49, S15-S16.
Sopta J, Davidović RS, Kovacevic R, Lujic N, Ristic D. p14ARF methylation is a common event in the pathogenesis and progression of mixoid and pleomorphic liposarcoma. European Journal of Cancer. 2013;49:S15-S16
Sopta J., Davidović Radoslav S., Kovacevic R., Lujic N., Ristic D., "p14ARF methylation is a common event in the pathogenesis and progression of mixoid and pleomorphic liposarcoma" European Journal of Cancer, 49 (2013):S15-S16

The impact of PTEN tumor suppressor gene on acquiring resistance to tamoxifen treatment in breast cancer patients

Tanić, Nikola; Milovanović, Zorka M.; Tanić, Nasta; Dzodic, Radan; Juranic, Zorica; Šušnjar, Snežana; Plesinac-Karapandzic, Vesna; Tatic, Svetislav; Dramićanin, Tatjana; Davidović, Radoslav S.; Dimitrijević, Bogomir B.

(2012)

TY  - JOUR
AU  - Tanić, Nikola
AU  - Milovanović, Zorka M.
AU  - Tanić, Nasta
AU  - Dzodic, Radan
AU  - Juranic, Zorica
AU  - Šušnjar, Snežana
AU  - Plesinac-Karapandzic, Vesna
AU  - Tatic, Svetislav
AU  - Dramićanin, Tatjana
AU  - Davidović, Radoslav S.
AU  - Dimitrijević, Bogomir B.
PY  - 2012
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5073
AB  - Tamoxifen is a standard therapeutical treatment in patients with estrogen receptor positive breast carcinoma. However, less than 50% of estrogen receptor positive breast cancers do not respond to tamoxifen treatment whereas 40% of tumors that initially respond to treatment develop resistance over time. The underlying mechanisms for tamoxifen resistance are probably multifactorial but remain largely unknown. The primary aim of this study was to investigate the impact of PTEN tumor suppressor gene on acquiring resistance to tamoxifen by analyzing loss of heterozygosity (LOH) and immunohystochemical expression of PTEN in 49 primary breast carcinomas of patients treated with tamoxifen as the only adjuvant therapy. The effect of PTEN inactivation on breast cancer progression and disease outcome was also analyzed. Reduced or completely lost PTEN expression was observed in 55.1% of samples, while 63.3% of samples displayed LOH of PTEN gene. Inactivation of PTEN immunoexpression significantly correlated with the PTEN loss of heterozygosity, suggesting LOH as the most important genetic mechanism for the reduction or complete loss of PTEN expression in primary breast carcinoma. Most importantly, LOH of PTEN and consequential reduction of its immunoexpression showed significant correlation with the recurrence of the disease. Besides, our study revealed that LOH of PTEN tumor suppressor was significantly associated with shorter disease free survival, breast cancer specific survival and overall survival. In summary, our results imply that LOH of PTEN could be used as a good prognostic characteristic for the outcome of breast cancer patients treated with tamoxifen.
T2  - Cancer Biology and Therapy
T1  - The impact of PTEN tumor suppressor gene on acquiring resistance to tamoxifen treatment in breast cancer patients
VL  - 13
IS  - 12
SP  - 1165
EP  - 1174
DO  - 10.4161/cbt.21346
ER  - 
@article{
author = "Tanić, Nikola and Milovanović, Zorka M. and Tanić, Nasta and Dzodic, Radan and Juranic, Zorica and Šušnjar, Snežana and Plesinac-Karapandzic, Vesna and Tatic, Svetislav and Dramićanin, Tatjana and Davidović, Radoslav S. and Dimitrijević, Bogomir B.",
year = "2012",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5073",
abstract = "Tamoxifen is a standard therapeutical treatment in patients with estrogen receptor positive breast carcinoma. However, less than 50% of estrogen receptor positive breast cancers do not respond to tamoxifen treatment whereas 40% of tumors that initially respond to treatment develop resistance over time. The underlying mechanisms for tamoxifen resistance are probably multifactorial but remain largely unknown. The primary aim of this study was to investigate the impact of PTEN tumor suppressor gene on acquiring resistance to tamoxifen by analyzing loss of heterozygosity (LOH) and immunohystochemical expression of PTEN in 49 primary breast carcinomas of patients treated with tamoxifen as the only adjuvant therapy. The effect of PTEN inactivation on breast cancer progression and disease outcome was also analyzed. Reduced or completely lost PTEN expression was observed in 55.1% of samples, while 63.3% of samples displayed LOH of PTEN gene. Inactivation of PTEN immunoexpression significantly correlated with the PTEN loss of heterozygosity, suggesting LOH as the most important genetic mechanism for the reduction or complete loss of PTEN expression in primary breast carcinoma. Most importantly, LOH of PTEN and consequential reduction of its immunoexpression showed significant correlation with the recurrence of the disease. Besides, our study revealed that LOH of PTEN tumor suppressor was significantly associated with shorter disease free survival, breast cancer specific survival and overall survival. In summary, our results imply that LOH of PTEN could be used as a good prognostic characteristic for the outcome of breast cancer patients treated with tamoxifen.",
journal = "Cancer Biology and Therapy",
title = "The impact of PTEN tumor suppressor gene on acquiring resistance to tamoxifen treatment in breast cancer patients",
volume = "13",
number = "12",
pages = "1165-1174",
doi = "10.4161/cbt.21346"
}
Tanić, N., Milovanović, Z. M., Tanić, N., Dzodic, R., Juranic, Z., Šušnjar, S., Plesinac-Karapandzic, V., Tatic, S., Dramićanin, T., Davidović, R. S.,& Dimitrijević, B. B. (2012). The impact of PTEN tumor suppressor gene on acquiring resistance to tamoxifen treatment in breast cancer patients.
Cancer Biology and Therapy, 13(12), 1165-1174.
https://doi.org/10.4161/cbt.21346
Tanić N, Milovanović ZM, Tanić N, Dzodic R, Juranic Z, Šušnjar S, Plesinac-Karapandzic V, Tatic S, Dramićanin T, Davidović RS, Dimitrijević BB. The impact of PTEN tumor suppressor gene on acquiring resistance to tamoxifen treatment in breast cancer patients. Cancer Biology and Therapy. 2012;13(12):1165-1174
Tanić Nikola, Milovanović Zorka M., Tanić Nasta, Dzodic Radan, Juranic Zorica, Šušnjar Snežana, Plesinac-Karapandzic Vesna, Tatic Svetislav, Dramićanin Tatjana, Davidović Radoslav S., Dimitrijević Bogomir B., "The impact of PTEN tumor suppressor gene on acquiring resistance to tamoxifen treatment in breast cancer patients" Cancer Biology and Therapy, 13, no. 12 (2012):1165-1174,
https://doi.org/10.4161/cbt.21346 .
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