Loss of Heterozygosity on Chromosome 10p14–p15 in Colorectal Carcinoma

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Abstract

High frequencies of loss of heterozygosity (LOH) on chromosome 10p14–p15 have been reported in various tumors, including gliomas, pulmonary carcinoid tumors and cervical, hepatic, prostatic and esophageal carcinomas. However, LOH on chromosome 10p14–p15 in colorectal tumors has not been reported. Therefore, we examined LOH on chromosome 10p14–p15 in 60 colorectal carcinomas (21 superficial and 39 advanced types) by microsatellite assay. Three microsatellite loci, D10S191 (10p14), D10S558 and D10S249 (10p15) were examined by polymerase chain reaction [early colorectal carcinomas, LOH of markers D10S191 (36%), D10S558 (7%) and D10S249 (11%), and in advanced colorectal carcinomas, LOH of markers D10S191 (20%), D10S558 (13%) and D10S249 (33%)]. There were no significant associations between LOH on chromosome 10p14–p15 and clinicopathologic features, including patient age, sex, tumor location, depth of invasion, histologic type, lymph node metastasis and prognosis. These data suggest that a putative tumor suppressor gene associated with colorectal carcinogenesis may be located on chromosome 10p14–p15 and that alteration of this gene may be involved in the development but not progression of colorectal tumors.

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Allelotype of colorectal carcinomas.

B Vogelstein, A C Preisinger, Rodrigo Nakamura … (1989)

To examine the extent and variation of allelic loss in a common adult tumor, polymorphic DNA markers were studied from every nonacrocentric autosomal arm in 56 paired colorectal carcinoma and adjacent normal colonic mucosa specimens. This analysis was termed an allelotype, in analogy with a karyotype. Three major conclusions were drawn from this analysis: (i) Allelic deletions were remarkably common; one of the alleles of each polymorphic marker tested was lost in at least some tumors, and some tumors lost more than half of their parental alleles. (ii) In addition to allelic deletions, new DNA fragments not present in normal tissue were identified in five carcinomas; these new fragments contained repeated sequences of the variable number of tandem repeat type. (iii) Patients with more than the median percentage of allelic deletions had a considerably worse prognosis than did the other patients, although the size and stage of the primary tumors were very similar in the two groups. In addition to its implications concerning the genetic events underlying tumorigenesis, tumor allelotype may provide a molecular tool for improved estimation of prognosis in patients with colorectal cancer.

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Identification of a chromosome 18q gene that is altered in colorectal cancers

E Fearon, K K Cho, J Nigro … (1990)

Allelic deletions involving chromosome 18q occur in more than 70 percent of colorectal cancers. Such deletions are thought to signal the existence of a tumor suppressor gene in the affected region, but until now a candidate suppressor gene on this chromosomal arm had not been identified. A contiguous stretch of DNA comprising 370 kilobase pairs (kb) has now been cloned from a region of chromosome 18q suspected to reside near this gene. Potential exons in the 370-kb region were defined by human-rodent sequence identities, and the expression of potential exons was assessed by an "exon-connection" strategy based on the polymerase chain reaction. Expressed exons were used as probes for cDNA screening to obtain clones that encoded a portion of a gene termed DCC; this cDNA was encoded by at least eight exons within the 370-kb genomic region. The predicted amino acid sequence of the cDNA specified a protein with sequence similarity to neural cell adhesion molecules and other related cell surface glycoproteins. While the DCC gene was expressed in most normal tissues, including colonic mucosa, its expression was greatly reduced or absent in most colorectal carcinomas tested. Somatic mutations within the DCC gene observed in colorectal cancers included a homozygous deletion of the 5' end of the gene, a point mutation within one of the introns, and ten examples of DNA insertions within a 0.17-kb fragment immediately downstream of one of the exons. The DCC gene may play a role in the pathogenesis of human colorectal neoplasia, perhaps through alteration of the normal cell-cell interactions controlling growth.

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Frequent loss of SMAD4/DPC4 protein in colorectal cancers.

P Sistonen, Tero Järvinen, R Salovaara … (2002)

Loss of DNA sequences from chromosome 18q21 is a major genetic change in colorectal tumorigenesis. Multiple genes have been identified in this area. One of these, DPC4 (deleted in pancreatic cancer 4, also known as SMAD4), is mutated in a minor subset of colorectal carcinomas as well as in germlines of humans predisposed to colon tumours. The involvement of SMAD4 in sporadic colorectal neoplasia was evaluated by immunohistochemistry in 53 unselected cases and 27 cases displaying microsatellite instability. SMAD4 expression was absent in 20 of 53 (38%) unselected colorectal carcinomas, and reduced in another 15 (28%) cases. However, 26 of 27 cancers displaying microsatellite instability and TGF-betaIIR mutations were positive for SMAD4 immunostaining. Loss of SMAD4 expression may play a more prominent role in colon cancer than anticipated based on genetic evidence, but not in mutator phenotype tumours.

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Author and article information

Journal

Journal ID (publisher-id): PAT

Journal ID (nlm-ta): Pathobiology

Journal ID (doi): 10.1159/issn.1015-2008

Title: Pathobiology

Publisher: S. Karger AG

ISSN (Print): 1015-2008

ISSN (Electronic): 1423-0291

Publication date Subscription-year: 2005

Publication date (Print): September 2005

Publication date (Electronic): 02 September 2005

Volume: 72

Issue: 4

Pages: 220-224

Affiliations

^aDepartment of Medicine and Molecular Science, Division of Frontier Medical Science, Program for Biomedical Research, Graduate School of Biomedical Sciences, Hiroshima University, and Departments of ^bEndoscopy and ^cAnatomical Pathology, Hiroshima University Hospital, Hiroshima, and ^dHealth Service Center, Hiroshima University, Higashihiroshima, Japan

Article

Publisher ID: 86792 Other ID: Pathobiology 2005;72:220–224

DOI: 10.1159/000086792

PubMed ID: 16127298

SO-VID: 7e54ea47-4941-4ac8-8cf4-9152f7a03378

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Loss of Heterozygosity on Chromosome 10p14–p15 in Colorectal Carcinoma

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Karger: Oncology

Most cited references 28

Allelotype of colorectal carcinomas.

Identification of a chromosome 18q gene that is altered in colorectal cancers

Frequent loss of SMAD4/DPC4 protein in colorectal cancers.

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Cited by 4

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