التفاصيل البيبلوغرافية
العنوان:
Expression of p16(INK4A) and alterations of the 9p21-23 chromosome region in non-small-cell lung carcinomas: Relationship with tumor growth parameters and ploidy status
المؤلفون:
Athanassios Kotsinas , M. Veslemes , Dina Tiniakos , Thelxiopi Vogiatzi , G. Mariatos , George Z. Rassidakis , Nikos Angelou , Panayotis Zacharatos , Christos Kittas , Triantaphyllos Liloglou , Vassilis G. Gorgoulis , Evangelos N. Manolis , Pericles Foukas , John K. Field
المصدر:
Scopus-Elsevier
مصطلحات موضوعية:
Cancer Research , Pathology , medicine.medical_specialty , Tumor suppressor gene , Proliferation index , Cancer , Aneuploidy , Chromosome 9 , Biology , medicine.disease , medicine.disease_cause , Oncology , CDKN2A , Allelic Imbalance , medicine , Cancer research , Carcinogenesis
الوصف:
The 9p21-23 chromosome region harbors a number of known and putative tumor-suppressor genes (TSGs). The best characterized gene in this area is p16INK4A (CDKN2A). Alterations of its product have been observed in various malignancies, including non-small-cell lung carcinomas (NSCLCs). We earlier investigated the mechanisms underlying p16INK4A inactivation. In the present study, we examined, in a series of 87 NSCLCs, its relationship with the kinetic parameters [proliferation index (PI) and apoptotic index (Al)] and the ploidy status of the tumors. In addition, we extended our previous LOH analysis of the 9p21-23 region by examining flanking areas of p16INK4A. Aberrant p16 expression was observed in 41.4% of the carcinomas. A significant association was found with increased PI (p = 0.037), but not with apoptosis. Aneuploid tumors were more frequently correlated with abnormal p16 staining (p = 0.05). A high frequency of allelic imbalance (Alm) was noticed at the D9S161 (51.3%) and D9S157 (64.5%) loci, which lie approximately 4cM centromeric and 7cM telomeric, respectively, to CDKN2A. Abnormal p16INK4A expression was strongly correlated with Alm at D9S161 (p = 0.004). Allelic losses at D9S157 occurred more frequently in early stages (p = 0.018) and were significantly associated with deletions at D9S161 (p = 0.035). We conclude that, in a sub-set of NSCLCs, (i) abnormal p16 expression contributes to tumor growth mainly by increasing the proliferative activity in the initial stages of carcinogenesis; (ii) the association with aneuploidy merely reflects the impact of aberrant p16 on proliferative activity; and (iii) other putative TSGs possibly reside within the 9p21-23 region that possibly co-operate in certain cases with CDKN2A in the development of NSCLCs. Int. J. Cancer (Pred. Oncol.) 89:133–141, 2000. © 2000 Wiley-Liss, Inc.
URL الوصول:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9da1dce26ada06f983c7497c6fa2cac3 http://www.scopus.com/inward/record.url?eid=2-s2.0-0034688939&partnerID=MN8TOARS
Rights:
OPEN
رقم الانضمام:
edsair.doi.dedup.....9da1dce26ada06f983c7497c6fa2cac3
قاعدة البيانات:
OpenAIRE