Three distinct commonly deleted regions of chromosome arm 16q in human primary and metastatic prostate cancers

Suzuki, Hiroyoshi; Komiya, Akira; Emi, Mitsuru; Kuramochi, Hiroaki; Shiraishi, Taizo; Yatani, Ryuichi; Shimazaki, Jun

doi:10.1002/(sici)1098-2264(199612)17:4<225::aid-gcc4>3.3.co;2-s

Cited by 9 publications

(17 citation statements)

References 24 publications

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“…Chromosome 16q is another region commonly affected in prostate cancer; the candidate TSG E‐cadherin is located on 16q22.1 [25]. Two candidates for TSGs, DCC and DPC4 (also termed Smad4 ) have been reported on the long arm of chromosome 18 [26].…”

Section: Discussionmentioning

confidence: 99%

Genetic changes in stage pT2N0 prostate cancer studied by comparative genomic hybridization

Wolter¹,

Gottfried

Mattfeldt³

2002

BJU International

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Objective To identify chromosomal regions important for progression in clinically organ-con®ned prostate cancer, as the genetic changes underlying the development and progression of prostate cancer are poorly understood. Materials and methods Comparative genomic hybridization (CGH) was used to search for DNA sequence copy-number changes in a series of 50 primary organcon®ned prostate adenocarcinomas (pT2N0) removed by radical prostatectomy. Results CGH analysis indicated that 23 (46%) of the primary prostate adenocarcinomas showed chromosome alterations. The percentage of tumours with losses (38%) was higher than with gains (28%). Losses of 13q (24%), 8p (18%), 6q (10%), 16q (8%), 18q (6%) and 5q (6%) and gains of 17q (12%), 20q (12%), 9q (10%), 17p (8%) and 8q (6%) were the most frequent alterations. Ampli®cations were found at 8q24-qter. Minimal overlapping regions of loss, indicative of the presence of tumour-suppressor genes, were mapped to 13q21.1-q21.3 and 8p21.2, and minimal overlapping regions of gain, indicative of the presence of oncogenes, were found at 9q34.4-qter, 17q25-qter and 20q13.3-qter. There was a signi®cant association between Gleason score and losses and gains (P=0.003), and an association between chromosomal imbalance and high histological grade (P=0.008). Conclusion These results suggest that losses or gains of DNA in these regions are important for prostate cancer progression, and document the spectrum of chromosomal alterations in stage pT2N0 of clinically organ-con®ned prostate cancer.

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Section: Discussionmentioning

confidence: 99%

Genetic changes in stage pT2N0 prostate cancer studied by comparative genomic hybridization

Wolter¹,

Gottfried

Mattfeldt³

2002

BJU International

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“…Loss of function in E-cadherin and/or other collaborating proteins contributes to increased proliferation, invasion and metastasis in many malignant epithelial tumours [22,23]. Mutations in E-cadherin , which encodes a transmembrane protein, have been described in cancers of the endometrium and ovary [11], signet ring cell carcinoma of the stomach [24,25], the diffuse sclerosing variant of papillary thyroid carcinoma [26], invasive lobular breast cancer [5,19,27,28], and diffuse and mixed gastric cancer [24,28,29,30].…”

Section: Introductionmentioning

confidence: 99%

Low frequency of E-cadherinalterations in familial breast cancer

et al. 2001

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In order to explore the possible role of E-cadherin in familial cancer, 19 familial breast cancer patients, whose tumours demonstrated loss of heterozygosity (LOH) at the E-cadherin locus, were screened for germline mutations. No pathogenic germline alterations were detected in these individuals. However, a somatic mutation was found (49-2A→C) in one of the tumours. This tumour showed a pattern of both ductal and lobular histology. Another 10 families with cases of breast, gastric and colon cancer were also screened for germline mutations, and no mutations were found. A missense mutation in exon 12 of E-cadherin (1774G→A; Ala592Thr) was previously found in one family with diffuse gastric cancer, and colon and breast cancer. An allelic association study was performed to determine whether the Ala592Thr alteration predisposes to breast cancer. In total, we studied 484 familial breast cancer patients, 614 sporadic breast cancer patients and 497 control individuals. The frequencies of this alteration were similar in these groups. However, a correlation between the Ala592Thr alteration and ductal comedo-type tumour was seen. These results, together with previously reported studies, indicate that germline mutations and, more commonly, somatic mutations in E-cadherin may have an influence on the behaviour of the tumours, rather than predispose to breast cancer.

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“…Loss of heterozygosity (LOH) studies in breast and prostate cancer have identified chromosome region 16q24.3 as the probable position of a tumour suppressor gene (Suzuki et al 1996;Brenner and Aldaz 1997). We have previously described a detailed physical and transcription map encompassing a region of approximately 940 kb within this 16q24.3 LOH region, from which a number of known genes and potential transcripts have been localized (Whitmore et al 1998).…”

Section: Introductionmentioning

confidence: 99%

Genomic structure and expression analysis of the spastic paraplegia gene, SPG7

Settasatian¹,

Whitmore²,

Crawford³

et al. 1999

Human Genetics

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SPG7 is a newly identified gene involved in an autosomal recessive form of hereditary spastic paraplegia (HSP), a genetically heterogeneous group of neurodegenerative disorders. This gene encodes a protein characterized as a nuclear-encoded mitochondrial metalloprotease. The present report describes the genomic structure of the SPG7 gene. It is organized into 17 exons ranging from 78 to 242 bp and spans approximately 52 kb within three overlapping cosmids. The exon/intron boundaries and all splice junctions are consistent with the published consensus sequences for donor and acceptor sites. The provided genomic structure of SPG7 should facilitate the screening for mutations in this gene in patients with HSP and other related mitochondrial disease syndromes. SPG7 has been mapped to chromosome 16q24.3, a region of frequent loss of heterozygosity (LOH) seen in sporadic breast and prostate cancer. We have performed single-strand conformation polymorphism analysis of ten exons of this gene in a number of sporadic breast cancer samples showing LOH at 16q24.3. No mutations were detected; only single nucleotide polymorphisms were observed in exon 11, intron 7, intron 10 and intron 12. An expression analysis study has revealed the differential expression of SPG7 mRNA in various tissues and at different developmental stages.

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Three distinct commonly deleted regions of chromosome arm 16q in human primary and metastatic prostate cancers

Cited by 9 publications

References 24 publications

Genetic changes in stage pT2N0 prostate cancer studied by comparative genomic hybridization

Genetic changes in stage pT2N0 prostate cancer studied by comparative genomic hybridization

Low frequency of E-cadherinalterations in familial breast cancer

Genomic structure and expression analysis of the spastic paraplegia gene, SPG7

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