Abstract: |
Our previous work identified a chromosomal translocation t(4;6) in prostate cancer cell lines and primary tumors. Using probes located on 4q22 and 6q15, the breakpoints identified in LNCaP cells, we performed fluorescence in situ hybridization analysis to detect this translocation in a large series of clinical localized prostate cancer samples treated conservatively. We found that t(4;6)(q22;q15) occurred in 78 of 667 cases (11.7%). The t(4;6)(q22;q15) was not independently associated with patient outcome. However, it occurs more frequently in high clinical T stage, high tumor volume specimens and in those with high baseline PSA (P=0.001, 0.001 and 0.01, respectively). The t(4;6)(q22;q15) occurred more frequently in samples with two or more TMPRSS2:ERG fusion genes caused by internal deletion than in samples without these genomic alterations, but this correlation is not statistically significant (P=0.0628). The potential role of this translocation in the development of human prostate cancer is discussed. © 2010 Nature Publishing Group. All rights reserved. |
Keywords: |
adult; controlled study; human tissue; aged; gene mutation; major clinical study; gene deletion; cancer staging; prostate specific antigen; in situ hybridization, fluorescence; disease association; tumor volume; genetic association; cancer cell culture; carcinogenesis; cancer hormone therapy; prostate cancer; prostatic neoplasms; fluorescence in situ hybridization; gene rearrangement; conservative treatment; prostatectomy; genomic instability; antigen detection; fusion gene; oncogene proteins, fusion; outcomes research; chromosome breakage; chromosome translocation; chromosomes, human, pair 6; translocation, genetic; tissue microarray; transurethral resection; molecular probe; chromosome 6q; chromosome 4q; cell strain lncap; chromosome identification; chromosome translocation 4; chromosome translocation 6; chromosomes, human, pair 4
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