Can telomere alterations predict biochemical recurrence in prostate adenocarcinoma? A preliminary study

被引:11
作者
Baydar, Dilek Ertoy [1 ]
Ozen, Haluk [1 ]
Geyik, Pinar O. [1 ]
Gurel, Bora [1 ]
机构
[1] Hacettepe Univ Hosp, Dept Pathol, TR-06100 Ankara, Turkey
关键词
Prostate cancer; Telomere; FISH; Prognosis; PSA recurrence; COLORECTAL-CARCINOMA; CANCER-CELLS; DNA-CONTENT; IN-VITRO; LENGTH; EXPRESSION; ASSOCIATION; FIBROBLASTS; DYSFUNCTION; SENESCENCE;
D O I
10.1016/j.prp.2010.05.009
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Telomeres function in human somatic tissues to stabilize chromosome ends. Telomere shortening can be one of the ways that cause chromosomal instability in the pathogenesis of prostatic carcinoma. In the current study, we evaluated telomere length (TL) in normal and malignant prostate tissues, and its association with prognostic factors and with time to biochemical tumor recurrence. Tissue microarrays constructed from paraffin blocks from radical prostatectomy specimens containing 61 randomly selected cases were used. Sections were hybridized with a Cy3-labeled telomere-specific peptide nucleic acid probe. TL, proportional to probe fluorescence intensity, was visually evaluated. Statistical analysis was done to relate TL clinical and pathological prognostic variables. The majority (49/61) of prostate cancers displayed abnormally short telomeres. Univariate analysis revealed inverse correlation between telomere shortening in tumor and Gleason scores (p = 0.017). Multivariate analyses pointed to TL as an independent predictor in addition to serum pre-operative PSA for reduced biochemical progression-free survival (p = 0.035). Telomere shortening is a common alteration in prostatic adenocarcinoma. Normal or long telomeres are rarely seen and, when present, seem to provide a growth advantage for the tumor as being an advocate for poor differentiation. (C) 2010 Elsevier GmbH. All rights reserved.
引用
收藏
页码:700 / 704
页数:5
相关论文
共 31 条
[1]   Telomere dysfunction promotes non-reciprocal translocations and epithelial cancers in mice [J].
Artandi, SE ;
Chang, S ;
Lee, SL ;
Alson, S ;
Gottlieb, GJ ;
Chin, L ;
DePinho, RA .
NATURE, 2000, 406 (6796) :641-645
[2]   Telomere states and cell fates [J].
Blackburn, EH .
NATURE, 2000, 408 (6808) :53-56
[3]  
Braakhuis BJM, 2003, CANCER RES, V63, P1727
[4]   Small molecule, oligonucleotide-based telomerase template inhibition in combination with cytolytic therapy in an in vitro androgen-independent prostate cancer model [J].
Canales, BK ;
Li, YM ;
Thompson, MG ;
Gleason, JM ;
Chen, Z ;
Malaeb, B ;
Corey, DR ;
Herbert, BS ;
Shay, JW ;
Koeneman, KS .
UROLOGIC ONCOLOGY-SEMINARS AND ORIGINAL INVESTIGATIONS, 2006, 24 (02) :141-151
[5]   Association between outcome and telomere DNA content in prostate cancer [J].
Donaldson, L ;
Fordyce, C ;
Gilliland, F ;
Smith, A ;
Feddersen, R ;
Joste, N ;
Moyzis, R ;
Griffith, J .
JOURNAL OF UROLOGY, 1999, 162 (05) :1788-1792
[6]   Opinion - Telomere dysfunction and the initiation of genome instability [J].
Feldser, DM ;
Hackett, JA ;
Greider, CW .
NATURE REVIEWS CANCER, 2003, 3 (08) :623-627
[7]   Association between cancer-free survival and telomere DNA content in prostate tumors [J].
Fordyce, CA ;
Heaphy, CM ;
Joste, NE ;
Smith, AY ;
Hunt, WC ;
Griffith, JK .
JOURNAL OF UROLOGY, 2005, 173 (02) :610-614
[8]   Correlations of telomere length, telomerase activity, and telomeric-repeat binding factor 1 expression in colorectal carcinoma - Prognostic indications [J].
Garcia-Aranda, C ;
de Juan, C ;
Diaz-Lopez, A ;
Sanchez-Pernaute, A ;
Torres, AJ ;
Diaz-Rubio, E ;
Balibrea, JL ;
Benito, M ;
Iniesta, P .
CANCER, 2006, 106 (03) :541-551
[9]   Telomere length and human telomerase reverse transcriptase expression as markers for progression and prognosis of colorectal carcinoma [J].
Gertler, R ;
Rosenberg, R ;
Stricker, D ;
Friederichs, J ;
Hoos, A ;
Werner, M ;
Ulm, K ;
Holzmann, B ;
Nekarda, H ;
Siewert, JR .
JOURNAL OF CLINICAL ONCOLOGY, 2004, 22 (10) :1807-1814
[10]  
Hirashima T, 2000, ANTICANCER RES, V20, P2181