This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Chiang, J.-M. Articles by Chou, T.-B. Search for Related Content PubMed PubMed Citation Articles by Chiang, J.-M. Articles by Chou, T.-B.

K-ras Codon 12 Mutation Determines the Polypoid Growth of Colorectal Cancer¹

Human Molecular Genetics Laboratory [J-M. C., Y-H. W. C.], and Division of Colon and Rectal Surgery [J-M. C.], Chang Gung Memorial Hospital, Taipei, Taiwan 333; and Department of Zoology, National Taiwan University, Taipei, Taiwan 106 [T-B. C.]

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.

¹ Supported by National Health Research Institute Grant DOH 86-HR-637 and Chang Gung Memorial Hospital Grant CMRP 567.

² To whom requests for reprints should be addressed, at Department of Zoology, National Taiwan University, No. 1 Section 4, Roosevelt Road, Taipei, Taiwan 106, Phone: 886-2-363-0231 ext. 2262; Fax: 886-2-363-6837; E-mail: tbchou@ccms.ntu.edu.tw.

Received 1/14/98. Accepted 6/ 3/98.

This article has been cited by other articles:

				K. Fransen, M. Klintenas, A. Osterstrom, J. Dimberg, H.-J. Monstein, and P. Soderkvist Mutation analysis of the BRAF, ARAF and RAF-1 genes in human colorectal adenocarcinomas Carcinogenesis, April 1, 2004; 25(4): 527 - 533. [Abstract] [Full Text] [PDF]

				J.-H. Lee, S. C. Abraham, H.-S. Kim, J.-H. Nam, C. Choi, M.-C. Lee, C.-S. Park, S.-W. Juhng, A. Rashid, S. R. Hamilton, et al. Inverse Relationship between APC Gene Mutation in Gastric Adenomas and Development of Adenocarcinoma Am. J. Pathol., August 1, 2002; 161(2): 611 - 618. [Abstract] [Full Text] [PDF]

				H. Tsunozaki, K. Yoshinaga, J. Kumagai, and K. Sugihara Cyclooxygenase-2 Overexpression in Colorectal Cancer is Associated with Non-polypoid Growth Jpn. J. Clin. Oncol., May 1, 2002; 32(5): 167 - 171. [Abstract] [Full Text] [PDF]

				E Hidaka, A Yanagisawa, M Seki, T Setoguchi, and Y Kato Genetic alterations and growth pattern in biliary duct carcinomas: loss of heterozygosity at chromosome 5q bears a close relation with polypoid growth Gut, May 1, 2001; 48(5): 656 - 659. [Abstract] [Full Text] [PDF]

				M. Yashiro, J. M. Carethers, L. Laghi, K. Saito, P. Slezak, E. Jaramillo, C. Rubio, K. Koizumi, K. Hirakawa, and C. R. Boland Genetic Pathways in the Evolution of Morphologically Distinct Colorectal Neoplasms Cancer Res., March 1, 2001; 61(6): 2676 - 2683. [Abstract] [Full Text]