High frequency of p16 and p14 promoter hypermethylation and marked telomere instability in salivary gland tumors
Нема приказа
Аутори
Nikolić, NađaAničić, Boban
Čarkić, Jelena
Simonovic, Jelena
Toljic, Bosko
Tanić, Nasta
Tepavcevic, Zvezdana
Vukadinovic, Miroslav
Konstantinovic, Vitomir S.
Milašin, Jelena
Чланак у часопису (Објављена верзија)
Метаподаци
Приказ свих података о документуАпстракт
Objectives: to investigate p16(INK4a) and p14(ARF) tumor suppressor gene methylation status, determine telomere length and assess the importance of these epigenetic and genetic parameters in the development of pleomorphic adenoma and carcinoma ex pleomorphic adenoma of the parotid salivary glands. Materials and Methods: Genomic DNA from paraffin-embedded samples of 50 pleomorphic adenomas and 10 carcinomas ex pleomorphic adenoma was subjected to methylation specific polymerase chain reaction for hypermethylation analyses and real time polymerase chain reaction for the relative telomere length calculations. Results: Promoter hypermethylation of the two genes was a very frequent event in both neoplasms between 60% and 90% of samples were hypermethylated - but without significant difference between the groups. The mean relative telomere length in the pleomorphic adenoma group was significantly increased in comparison to the control group (P = 0.00), and significantly decreased in comparis...on to the carcinoma group (P = 0.05). Telomeres were also longer in myxoid and cellular histological subtypes of adenomas than in the classic type (P = 0.044 and P = 0.018, respectively). Longer telomeres were more frequent in tumors with hypermethylated p14(ARF) alleles (P = 0.013). Conclusion: Promoter hypermethylations seems to be an important mechanism of p16(INK4a) and Pl4(ARF) inactivation in parotid gland tumors. Telomeric lengthening appears to be involved in the pathogenesis of both benign and malignant tumors of the parotid glands. (C) 2015 Elsevier Ltd. All rights reserved.
Кључне речи:
Promoter hypermethylation / p16 / p14 / Telomere length / Parotid gland tumorsИзвор:
Archives of Oral Biology, 2015, 60, 11, 1662-1666Финансирање / пројекти:
- Генетичка контрола и молекуларни механизми у малигним, инфламаторним и развојним патологијама орофацијалне регије (RS-MESTD-Basic Research (BR or ON)-175075)
DOI: 10.1016/j.archoralbio.2015.08.011
ISSN: 0003-9969; 1879-1506
PubMed: 26351750
WoS: 000363080100010
Scopus: 2-s2.0-84941309502
Колекције
Институција/група
VinčaTY - JOUR AU - Nikolić, Nađa AU - Aničić, Boban AU - Čarkić, Jelena AU - Simonovic, Jelena AU - Toljic, Bosko AU - Tanić, Nasta AU - Tepavcevic, Zvezdana AU - Vukadinovic, Miroslav AU - Konstantinovic, Vitomir S. AU - Milašin, Jelena PY - 2015 UR - https://vinar.vin.bg.ac.rs/handle/123456789/778 AB - Objectives: to investigate p16(INK4a) and p14(ARF) tumor suppressor gene methylation status, determine telomere length and assess the importance of these epigenetic and genetic parameters in the development of pleomorphic adenoma and carcinoma ex pleomorphic adenoma of the parotid salivary glands. Materials and Methods: Genomic DNA from paraffin-embedded samples of 50 pleomorphic adenomas and 10 carcinomas ex pleomorphic adenoma was subjected to methylation specific polymerase chain reaction for hypermethylation analyses and real time polymerase chain reaction for the relative telomere length calculations. Results: Promoter hypermethylation of the two genes was a very frequent event in both neoplasms between 60% and 90% of samples were hypermethylated - but without significant difference between the groups. The mean relative telomere length in the pleomorphic adenoma group was significantly increased in comparison to the control group (P = 0.00), and significantly decreased in comparison to the carcinoma group (P = 0.05). Telomeres were also longer in myxoid and cellular histological subtypes of adenomas than in the classic type (P = 0.044 and P = 0.018, respectively). Longer telomeres were more frequent in tumors with hypermethylated p14(ARF) alleles (P = 0.013). Conclusion: Promoter hypermethylations seems to be an important mechanism of p16(INK4a) and Pl4(ARF) inactivation in parotid gland tumors. Telomeric lengthening appears to be involved in the pathogenesis of both benign and malignant tumors of the parotid glands. (C) 2015 Elsevier Ltd. All rights reserved. T2 - Archives of Oral Biology T1 - High frequency of p16 and p14 promoter hypermethylation and marked telomere instability in salivary gland tumors VL - 60 IS - 11 SP - 1662 EP - 1666 DO - 10.1016/j.archoralbio.2015.08.011 ER -
@article{ author = "Nikolić, Nađa and Aničić, Boban and Čarkić, Jelena and Simonovic, Jelena and Toljic, Bosko and Tanić, Nasta and Tepavcevic, Zvezdana and Vukadinovic, Miroslav and Konstantinovic, Vitomir S. and Milašin, Jelena", year = "2015", abstract = "Objectives: to investigate p16(INK4a) and p14(ARF) tumor suppressor gene methylation status, determine telomere length and assess the importance of these epigenetic and genetic parameters in the development of pleomorphic adenoma and carcinoma ex pleomorphic adenoma of the parotid salivary glands. Materials and Methods: Genomic DNA from paraffin-embedded samples of 50 pleomorphic adenomas and 10 carcinomas ex pleomorphic adenoma was subjected to methylation specific polymerase chain reaction for hypermethylation analyses and real time polymerase chain reaction for the relative telomere length calculations. Results: Promoter hypermethylation of the two genes was a very frequent event in both neoplasms between 60% and 90% of samples were hypermethylated - but without significant difference between the groups. The mean relative telomere length in the pleomorphic adenoma group was significantly increased in comparison to the control group (P = 0.00), and significantly decreased in comparison to the carcinoma group (P = 0.05). Telomeres were also longer in myxoid and cellular histological subtypes of adenomas than in the classic type (P = 0.044 and P = 0.018, respectively). Longer telomeres were more frequent in tumors with hypermethylated p14(ARF) alleles (P = 0.013). Conclusion: Promoter hypermethylations seems to be an important mechanism of p16(INK4a) and Pl4(ARF) inactivation in parotid gland tumors. Telomeric lengthening appears to be involved in the pathogenesis of both benign and malignant tumors of the parotid glands. (C) 2015 Elsevier Ltd. All rights reserved.", journal = "Archives of Oral Biology", title = "High frequency of p16 and p14 promoter hypermethylation and marked telomere instability in salivary gland tumors", volume = "60", number = "11", pages = "1662-1666", doi = "10.1016/j.archoralbio.2015.08.011" }
Nikolić, N., Aničić, B., Čarkić, J., Simonovic, J., Toljic, B., Tanić, N., Tepavcevic, Z., Vukadinovic, M., Konstantinovic, V. S.,& Milašin, J.. (2015). High frequency of p16 and p14 promoter hypermethylation and marked telomere instability in salivary gland tumors. in Archives of Oral Biology, 60(11), 1662-1666. https://doi.org/10.1016/j.archoralbio.2015.08.011
Nikolić N, Aničić B, Čarkić J, Simonovic J, Toljic B, Tanić N, Tepavcevic Z, Vukadinovic M, Konstantinovic VS, Milašin J. High frequency of p16 and p14 promoter hypermethylation and marked telomere instability in salivary gland tumors. in Archives of Oral Biology. 2015;60(11):1662-1666. doi:10.1016/j.archoralbio.2015.08.011 .
Nikolić, Nađa, Aničić, Boban, Čarkić, Jelena, Simonovic, Jelena, Toljic, Bosko, Tanić, Nasta, Tepavcevic, Zvezdana, Vukadinovic, Miroslav, Konstantinovic, Vitomir S., Milašin, Jelena, "High frequency of p16 and p14 promoter hypermethylation and marked telomere instability in salivary gland tumors" in Archives of Oral Biology, 60, no. 11 (2015):1662-1666, https://doi.org/10.1016/j.archoralbio.2015.08.011 . .