Abstract:
:It has been proposed that the structural and numerical chromosome abnormalities recorded in breast cancer could be the result of telomere dysfunction and that telomerase is activated de novo to provide a survival mechanism curtailing further chromosomal aberrations. However, recent in vivo and in vitro data show that the ectopic expression of telomerase promotes tumorigenesis via a telomere length-independent mechanism. In this study, the relation between telomerase expression and the extent of chromosomal aberrations was investigated in 62 primary breast carcinomas. Telomerase activity was measured using a polymerase chain reaction-based telomeric repeat amplification protocol assay and 92% of the tumors were found to express telomerase with a relative activity ranging from 0 to 3839.6. Genetic alterations were determined by G-banding and comparative genomic hybridization analysis and 97% of the tumors exhibited chromosomal aberrations ranging from 0 to 44 (average: 10.98). In the overall series, the relationship between telomerase activity levels and genetic changes could be best described by a quadratic model, whereas in tumors with below-average genetic alteration numbers, a significant positive association was recorded between the two variables (coefficient=0.374, P=.017). The relationship between telomerase activity levels and the extent of genetic alteration may reflect the complex effect of telomerase activation upon tumor progression in breast carcinomas.
journal_name
Neoplasiajournal_title
Neoplasia (New York, N.Y.)authors
Papadopoulou A,Trangas T,Teixeira MR,Heim S,Dimitriadis E,Tsarouha H,Andersen JA,Evangelou E,Ioannidis P,Agnantis NJ,Pandis Ndoi
10.1016/s1476-5586(03)80009-xkeywords:
subject
Has Abstractpub_date
2003-03-01 00:00:00pages
170-8issue
2eissn
1522-8002issn
1476-5586journal_volume
5pub_type
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