Identification of a 1‐cM region of common deletion on 13q14 associated with human prostate cancer

Ueda, Takeshi; Emi, Mitsuru; Suzuki, Hiroyoshi; Komiya, Akira; Akakura, Koichiro; Ichikawa, Tomohiko; Watanabe, Masatoshi; Shiraishi, Taizo; Masai, Motoyuki; Igarashi, Tatsuo; Itô, Haruo

doi:10.1002/(sici)1098-2264(199903)24:3<183::aid-gcc2>3.3.co;2-a

Cited by 5 publications

(6 citation statements)

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“…Despite the presence of two important tumour suppressor genes at 13q, namely BRCA2 and RB1, no correlation between LOH and down-regulation of these genes has been observed (Latil et al 1999(Latil et al , 2002. A detailed analysis of microsatellite markers on 13q identified a minimal region of loss of 800 kb at 13q14.2-q14.3 (Ueda et al 1999, Yin et al 1999, Chen et al 2001. This allelic imbalance is observed in about 65% of prostate tumours and has been found to be associated with early biochemical relapse (Brookman-Amissah et al 2007).…”

Section: Focusing On Single Mirs: Starting From Geneticsmentioning

confidence: 99%

MicroRNAs and prostate cancer

Coppola¹,

Maria²,

Bonci³

2010

Endocrine-Related Cancer

137

126

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Despite much progress in prostate cancer management, new diagnostic, prognostic and therapeutic tools are needed to predict disease severity, choose among the available treatments and establish more effective therapies for advanced prostate cancer. In the last few years, compelling evidence has documented the role of microRNAs as new broad-spectrum oncogenes or tumour suppressor genes, thus their use as diagnostic, prognostic and therapeutic biomolecules is envisaged. This review extensively and critically summarizes the current knowledge about microRNA deregulation in prostate cancer disease, underlining present limits and future perspectives.Endocrine-Related Cancer (2010) 17 F1-F17

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Section: Focusing On Single Mirs: Starting From Geneticsmentioning

confidence: 99%

MicroRNAs and prostate cancer

Coppola¹,

Maria²,

Bonci³

2010

Endocrine-Related Cancer

137

126

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“…Loss of 13q sequences is a recurrent finding in LOH and CGH studies of prostate cancer (Cher et al, 1996;Cooney et al, 1996b;Hyytinen et al, 1999;Melamed et al, 1997;Nupponen et al, 1998;Ueda et al, 1999;Visakorpi et al, 1995b). Chromosome 13q contains at least three putative tumor suppressor genes: RB1 (13q14), BRCA2 (13q12-q13), and DBM (13q14).…”

Section: Chromosomal Lossesmentioning

confidence: 99%

Identification of Genetic Markers for Prostatic Cancer Progression

Alers

Rochat

Krijtenburg

et al. 2000

Laboratory Investigation

164

126

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SUMMARY:Despite the high incidence of prostate cancer, only limited data are available on genes or chromosomes specifically involved in its initiation and progression. We have applied comparative genomic hybridization to routinely processed, paraffin-embedded, tissues at different times in prostatic tumor progression to screen the tumor genome for gains and losses. Our panel included specimens derived from 56 different patients: 23 patients with primary, prostate-confined carcinomas; 18 patients with regional lymph node metastases; and 15 patients with distant metastases. Chromosome arms that most frequently showed losses, included 13q (55%), 8p (48%), 6q (43%), 5q (32%), 16q (25%), 18q (20%), 2q (18%), 4q (18%), 10q (18%), and Y (16%). Gains were often seen of chromosome arms 8q (36%), 17q (23%), Xq (23%), 7q (21%), 3q (18%), 9q (18%), 1q (16%), Xp (16%). Furthermore, specific high-level amplifications, eg, of 1q21, 1q25, and Xq12 to q13, were found in metastatic cancers. A significant accumulation of genetic changes in distant metastases was observed, eg, loss of 10q (p ϭ 0.03) and gain of 7q (p ϭ 0.03) sequences. In addition, investigation of a potential biomarker identified in previous studies by our group, ie, extra copies of #7 and/or #8, revealed a high prevalence of 7pq and/or 8q gain in the distant metastases (p ϭ 0.02). Importantly, gains were observed more frequently in tumors derived from progressors after radical prostatectomy, than in nonprogressors (mean time of follow-up, 74 months). Specifically, gain of chromosome 7pq and/or 8q sequences appeared an accurate discriminator between the progressors and nonprogressors. Multivariate analysis showed a significant correlation between progressive disease and the number of chromosomes with gains. This correlation also held true when stage (p ϭ 0.007) or grade (p ϭ 0.002) were taken into account. Likewise, this applied for gain of chromosome 7pq and/or 8q sequences (p ϭ 0.03 and p ϭ 0.005 for stage or grade, respectively). Additionally, an increase in the number of chromosomes with gains per case was related to a decrease in biochemical progression-free survival (P trend Ͻ0.001). More specifically, the gain of 7pq and/or 8q sequences markedly reduced the biochemical progression-free survival (p Ͻ 0.001). In conclusion, this study has, firstly, documented the spectrum of chromosomal alterations in subsequent stages of prostate cancer, a number of which had not been described previously. It allowed us to identify chromosomal regions related to advanced tumor stage, ie, loss of 10q24 and gain of 7q11.2 and/or 7q31 sequences. Secondly, gain of 7pq and/or 8q was identified as a potential genetic discriminator between progressors and nonprogressors after radical surgery. (Lab Invest 2000, 80:931-942). P rostate cancer is the most commonly diagnosed, male noncutaneous malignancy and the second leading cause of cancer-related death in men in Western industrialized countries. Its incidence is continuously rising, with over 200,000 new cases diagnosed each year, r...

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“…[4][5][6] We have investigated several regions of chromosomal loss in prostate cancer using LOH analysis. [7][8][9][10][11][12][13][14][15] CGH is a molecular technique that allows screening of the whole genome for DNA sequence copy number alterations. Regions of increased copy number may contain oncogenes, whereas regions of decreased copy number may contain putative TSGs.…”

Section: Introductionmentioning

confidence: 99%

Genetic changes in pT2 and pT3 prostate cancer detected by comparative genomic hybridization

Fukasawa

Kino

Kobayashi

et al. 2007

Prostate Cancer Prostatic Dis

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Prostate-specific antigen (PSA) screening has led to a remarkable increase in prostate cancer cases undergoing operative therapy. Over half of patients with locally advanced cancer (^pT3) develop rising PSA levels (biochemical failure) within 10 years. It is very difficult to predict which patients will progress rapidly to advanced disease following biochemical failure (BF). Therefore, a more useful prognostic factor is needed to suggest the most appropriate therapies for each patient. To determine chromosomal aberrations, we examined 30 patients with stage pT2 or pT3 primary prostate adenocarcinomas and no metastases (pN0M0) by comparative genomic hybridization (CGH). Laser capture microdissection (LCM) was used to gather cancer cells from frozen prostate specimens. Common chromosomal alterations included losses on 2q23-24, 4q26-28, 6q14-22, 8p12-22 and 13q21-31, as well as gains on 1p32-36, 6p21 and 17q21-22. Losses at 8p12-22 and 13q21-31 were observed more frequently in pT3 than pT2 tumors (Po0.05 and Po0.01, respectively). Losses at 8p12-22 were more frequent in tumors with BF (Po0.05), and those at 13q12-21 were more frequent in tumors with Gleason score (GS) 7 or more than lower GS (Po0.05). These findings suggest that losses of 8p12-22 and 13q21-31 are important determinants of prostate cancer progression.

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Identification of a 1‐cM region of common deletion on 13q14 associated with human prostate cancer

Cited by 5 publications

References 0 publications

MicroRNAs and prostate cancer

MicroRNAs and prostate cancer

Identification of Genetic Markers for Prostatic Cancer Progression

Genetic changes in pT2 and pT3 prostate cancer detected by comparative genomic hybridization

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