Приказ основних података о документу
TP53 AND C-MYC CO-ALTERATIONS - A HALLMARK OF ORAL CANCER PROGRESSION
dc.creator | Tanić, Nasta | |
dc.creator | Milašin, Jelena | |
dc.creator | Dramićanin, Tatjana | |
dc.creator | Bošković, Maja | |
dc.creator | Vukadinovic, Miroslav | |
dc.creator | Milošević, Verica | |
dc.creator | Tanić, Nikola | |
dc.date.accessioned | 2018-03-01T23:47:11Z | |
dc.date.available | 2018-03-01T23:47:11Z | |
dc.date.issued | 2013 | |
dc.identifier.issn | 1452-8258 | |
dc.identifier.issn | 1452-8266 | |
dc.identifier.uri | https://vinar.vin.bg.ac.rs/handle/123456789/5747 | |
dc.description.abstract | Background: Head and neck squamous cell carcinoma, including oral cancer, is the sixth most common cancer worldwide. Despite advances in surgery and treatment, the 5-year survival rate has not improved significantly. There fore, reliable molecular markers for oral cancer progression are badly needed. Methods: We conducted a copy number analysis to estimate amplification status of c-myc, cycD1 and EGFR oncogenes, mutational PCR-SSCP analysis to determine activation of H-ras oncogene and inactivation of TP53 tumour suppressor gene and methylation specific PCR analysis to evaluate hypermethylation of p16 and MGMT genes. Results: c-myc oncogene was amplified in 56.7%, cycD1 in 20% and EGFR in 16.7% of Oral Squamous Cell Carcinoma (OSCC) cases while H-ras was activated in 33.3% of samples. Amplification of c-myc was significantly associated with the tumour grade 2. Interestingly, EGFR and H-ras alterations were mutually exclusive. p16 and MGMT were inactivated by hypermethylation in 30% and 13.3% of cases. Co-alteration of cycD1 and p16 were not observed in any of the analyzed samples. TP53 was inactivated in 56.7% of samples and was significantly associated with progression of OSCC, grade 2 and stage 2. Moreover, TP53 and c-myc oncogene were simultaneously altered in grade 2 OSCC. Conclusions: The most promising marker of OSCC progression remains the TP53 tumour suppressor, which is the most frequently mutated gene in oral cancers. Since there is synergism between TP53 and c-myc, it seems that co-alteration of these two genes could be also a good marker of OSCC progression from grade1 to grade 2 tumours. | en |
dc.relation | info:eu-repo/grantAgreement/MESTD/Integrated and Interdisciplinary Research (IIR or III)/41031/RS// | |
dc.relation | info:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/173049/RS// | |
dc.rights | openAccess | en |
dc.source | Journal of Medical Biochemistry | en |
dc.subject | c-myc | en |
dc.subject | oncogenes | en |
dc.subject | oral squamous cell carcinoma | en |
dc.subject | TP53 | en |
dc.subject | tumour progression | en |
dc.subject | tumour suppressors | en |
dc.title | TP53 AND C-MYC CO-ALTERATIONS - A HALLMARK OF ORAL CANCER PROGRESSION | en |
dc.type | article | en |
dcterms.abstract | Таниц, Наста; Миласин, Јелена; Драмићанин Татјана; Вукадиновиц, Мирослав; Таниц, Никола; Милосевиц, Верица; Босковиц, Маја; | |
dc.citation.volume | 32 | |
dc.citation.issue | 4 | |
dc.citation.spage | 380 | |
dc.citation.epage | 388 | |
dc.identifier.wos | 000326577800011 | |
dc.identifier.doi | 10.2478/jomb-2014-0009 | |
dc.citation.rank | M23 | |
dc.identifier.scopus | 2-s2.0-84887485612 | |
dc.identifier.fulltext | https://vinar.vin.bg.ac.rs//bitstream/id/13535/5743.pdf |