K-ras Codon 12 Mutation Determines the Polypoid Growth of Colorectal Cancer
Resource
Cancer Research 58 (15): 3289-3293
Journal
Cancer Research
Journal Volume
58
Journal Issue
15
Pages
3289-3293
Date Issued
1998
Date
1998
Author(s)
Abstract
Colorectal carcinogenesis is widely thought to follow the adenoma- adenocarcinoma sequence. However, there are two morphologically distinct subtypes of colorectal cancer (CRC), polypoid and ulcerative. We conducted a comparative study to clarify whether different combinations of some commonly involved genetic alterations (including mutations in K-ras, p53, DCC, APC, and Rb genes) may exist between polypoid- and ulcerative-type CRCs, the two morphologically distinct types of CRC. By using PCR-based RFLP, single- strand conformational polymorphism, and loss of heterozygosity analysis, we found that K-ras codon 12 mutation was preferentially involved in polypoid tumor (P < 0.0001). There were no other significant correlations with p53 point mutation or loss of heterozygosity in chromosomes 5q, 17p, and 18q and Rb gene, which have been suggested to be involved in the progression of CRC of both morphological types. Therefore, different combinations of molecular genetic alterations may be involved in morphologically distinct types of colorectal carcinogenesis, and the K-ras codon 12 mutations may play an important role in polypoid growth of CRC. These results shed light on the function of K-ras oncogenes involved in colorectal carcinogenesis and may be important in the future design of genetic screening programs, determination of prognosis, and treatment for patients with CRC.
SDGs
Other Subjects
adult; aged; article; cancer growth; chromosome 17p; chromosome 18q; chromosome 5q; colon carcinogenesis; colorectal cancer; controlled study; female; gene mutation; genetic screening; heterozygosity loss; human; human tissue; major clinical study; male; oncogene k ras; priority journal; tumor suppressor gene; Codon; Colorectal Neoplasms; Genes, APC; Genes, DCC; Genes, p53; Genes, ras; Genes, Retinoblastoma; Humans; Mutation
Type
journal article
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