Loss of heterozygosity of the retinoblastoma and adenomatous polyposis susceptibility gene loci and in chromosomes 10p, 10q and 16q in human prostate cancer

Phillips, S. M. A.; Morton, Dion; Lee, S. J.; Wallace, David; Neoptolemos, John P.

doi:10.1111/j.1464-410x.1994.tb07602.x

Cited by 98 publications

(46 citation statements)

References 20 publications

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“…Data regarding 16p status revealed no alterations, in accordance with previously reported studies (Carter et al, 1990;Kunimi et al, 1991;Philip et al, 1994). Nevertheless, our pilot study led to the identification of 25% microsatellite alterations at 16q22.1.…”

Section: Chromosome 16q Analysissupporting

confidence: 76%

“…These investigators identified deletions at the 16q22-24 region in only 3 of 21 (15%) informative cases. Philip et al (1994) found comparable results, detecting 16q24 deletions in 3 of 17 (18%) prostate carcinomas. In another study, 52 prostatic tumors were analyzed and an overall 16q deletion rate of 36% was reported .…”

supporting

confidence: 69%

“…Common sites of deletions have been reported for chromosomes 7q, 8p, 10q and 16q (Carter et al, 1990;Kunimi et al, 1991;Macoska et al, 1994). Nevertheless, the most frequent site of chromosomal losses in prostate cancer, together with 8p deletions, appears to be chromosome 16q Massenkeil et al, 1994;Philip et al, 1994). Loss of heterozygosity (LOH) at 16q was reported in 5 of 16 (31%) prostate cancer samples analyzed by restriction fragment length polymorphism (RFLP) and Southern blot (SB) analysis (Carter et al, 1990).…”

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confidence: 99%

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Chromosome 16 in primary prostate cancer: A microsatellite analysis

et al. 1997

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Cytogenetic and molecular genetic analyses of prostate cancer specimens have revealed nonrandom chromosomal deletions, affecting chromosomes 7q, 8p, 10q and 16q. Based on these data, we designed this study to further characterize the altered region(s) on chromosome 16 by evaluating 16 microsatellite markers on a population composed of 32 paired normal and primary prostatic tumor samples. The 16 microsatellites selected mapped to 11 distinct loci on 16q and 5 loci on 16p. No alterations were identified affecting 16p. However, 16 of 31 (51%) informative cases showed molecular alterations in at least one of the loci analyzed on 16q, consisting of 18 deletions and 11 bandshifts. Moreover, most of the deletions clustered at 6 microsatellite loci, mapping to the 16q22. Cytogenetic and molecular genetic analyses of prostate cancer have revealed consistent chromosomal alterations (Lundgren et al., 1992). Common sites of deletions have been reported for chromosomes 7q, 8p, 10q and 16q (Carter et al., 1990;Kunimi et al., 1991;Macoska et al., 1994). Nevertheless, the most frequent site of chromosomal losses in prostate cancer, together with 8p deletions, appears to be chromosome 16q Massenkeil et al., 1994;Philip et al., 1994). Loss of heterozygosity (LOH) at 16q was reported in 5 of 16 (31%) prostate cancer samples analyzed by restriction fragment length polymorphism (RFLP) and Southern blot (SB) analysis (Carter et al., 1990). These losses mapped to the 16q22.1-22.2 and 16q24.2 regions. Subsequently, Kunimi et al. (1991) reported 16q LOH in 6 of 10 (60%) informative prostatic carcinomas, mapping the losses to the HP locus at 16q22.1. Similarly, Bergerheim et al. (1991) reported that 10 of 18 prostate cancer cases (56%) studied had 16q deletions. However, a lower incidence of deletions was reported by Massenkeil et al. (1994). These investigators identified deletions at the 16q22-24 region in only 3 of 21 (15%) informative cases. Philip et al. (1994) found comparable results, detecting 16q24 deletions in 3 of 17 (18%) prostate carcinomas. In another study, 52 prostatic tumors were analyzed and an overall 16q deletion rate of 36% was reported . Moreover, this study also revealed that 16q losses were more commonly detected in metastatic lesions than in primary tumors. Taken together, these data suggest that the long arm of chromosome 16 harbors a candidate tumor suppressor gene (TSG) involved in prostate cancer progression. The chromosomal deletions described above were further confirmed using microsatellite repeat amplification. Sakr et al. (1994) identified allelic losses at 16q22.1 in a subset of primary prostate cancer (42% of informative cases). Gao et al. (1994) reported a high frequency of the mutator phenotype at 18 microsatellite marker loci on 12 chromosomes. A proximal locus on 16q11.2 showed alterations in 7 of 31 cases (23%). In addition, analysis of chromosome 16q using fluorescence in situ hybridization (FISH) and comparative genomic hybridization (CGH) revealed a higher incidence of deletions (Cher et al., 1...

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Section: Chromosome 16q Analysissupporting

confidence: 76%

supporting

confidence: 69%

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confidence: 99%

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Chromosome 16 in primary prostate cancer: A microsatellite analysis

et al. 1997

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“…In prostate cancer, there are several deletions at various chromosomal regions (Cannon-Albright and Eeles, 1995;Lundgren et al, 1992). More specifically, LOH on chromosomes 8p (50%), 10p (55%), 10q (30%), 17q (52%), 16q (30%) and 18q (40%) have been reported in prostate cancer tissues (Emmert-Buck et al, 1995;Gray et al, 1995;Phillips et al, 1994;Cannon-Albright and Eeles, 1995;Carter et al, 1994;Egawa et al, 1995;Gao et al, 1995). We have identified LOH on 3p24-25 and 3p22-12 regions of the short arm of chromosome 3 in human prostate cancer, indicating 2 discrete areas of deletion on chromosome 3p (Dahiya et al, 1997).…”

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confidence: 99%

Deletion of chromosome 11p15, p12, q22, q23-24 loci in human prostate cancer

et al. 1997

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Loss of heterozygosity (LOH) on chromosome 11 is frequently altered in various epithelial cancers. The present study was designed to investigate LOH on chromosome 11 in microdissected samples of normal prostatic epithelium and invasive carcinoma from the same patients. For this purpose, DNA was extracted from the microdissected normal and tumor cells of 38 prostate cancers, amplified by polymerase chain reaction PCR and analyzed for LOH on chromosome 11 using 9 different polymorphic DNA markers (D11S1307, D11S989, D11S1313, D11S898, D11S940, D11S1818, D11S924, D11S1336 and D11S912). LOH on chromosome 11 was identified in 30 of 38 cases (78%) with at least one marker. Four distinct regions of loss detected were: 1) at 11p15, at loci between D11S1307 and D11S989; 2) at 11p12, on locus D11S131 (11p12); 3) at 11q22, on loci D11S898, D11S940 and D11S1818; and 4) at 11q23-24, on loci between D11S1336 and D11S912. We found 25% of the tumors with LOH at 11p15; 39% had LOH at 11p12; 66% had LOH at 11q22; and 47% had LOH at 11q23-24. These deletions at 11p15, 11p12, 11q22 and 11q23-24 loci were not related to the stage or grade of the tumor. Int.

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“…[46][47][48][49] Two other sites on chromosome 10, 10p and 10q26, are also deleted in association with or independent of 10q22-24 losses. 39,[43][44][45] In our study, two loci on 10q, 10q25.1 and 10q25, were examined, but neither showed a significant difference between the relapse and non-relapse groups.…”

Section: Discussionmentioning

confidence: 99%

Allelic imbalance and biochemical outcome after radical prostatectomy

Bott

Masters

Parkinson

et al. 2006

Prostate Cancer Prostatic Dis

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Objective: To compare the incidence of allelic imbalance (AI) in men with rapid disease progression with those who remained disease free after radical prostatectomy, with the aim of identifying genetic markers to predict prognosis and guide further treatment. Patients and methods: Tumour and normal DNA were extracted from two matched groups of 31 men with extracapsular node-negative (pT3N0) prostate cancer who had undergone radical prostatectomy. One group comprised men who developed biochemical recurrence within 2 years of surgery and one group were prostate-specific antigen (PSA) free for at least 3 years. Men were matched for Gleason grade, preoperative PSA and pathological stage. Analysis was performed by genotyping. Results: Allelic imbalance was analysed using 30 markers, and was seen in at least one marker in 57 (92%) of the cases. Deletion at marker D10S211 (10p12.1) was significantly more common in the relapse group than the non-relapse group (35 vs 5%, P ¼ 0.03). Conclusions: This study demonstrates significant association between AI on chromosome 10 and biochemical progression after radical prostatectomy.

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Loss of heterozygosity of the retinoblastoma and adenomatous polyposis susceptibility gene loci and in chromosomes 10p, 10q and 16q in human prostate cancer

Abstract: These findings suggest that losses of the RB1 and APC tumour suppressor genes and suspected tumour suppressor genes on 10p, 10q and 16q may be important events in the genesis of prostatic tumours.

Cited by 98 publications

References 20 publications

Chromosome 16 in primary prostate cancer: A microsatellite analysis

Chromosome 16 in primary prostate cancer: A microsatellite analysis

Deletion of chromosome 11p15, p12, q22, q23-24 loci in human prostate cancer

Allelic imbalance and biochemical outcome after radical prostatectomy

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