Colorectal Cancer
Copyright ©2007 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Aug 7, 2007; 13(29): 3932-3938
Published online Aug 7, 2007. doi: 10.3748/wjg.v13.i29.3932
Involvement of Krüppel-like factor 6 (KLF6) mutation in the development of nonpolypoid colorectal carcinoma
Shinichi Mukai, Toru Hiyama, Shinji Tanaka, Masaharu Yoshihara, Koji Arihiro, Kazuaki Chayama
Shinichi Mukai, Kazuaki Chayama, Department of Medicine and Molecular Science, Division of Frontier Medical Science, Program for Biomedical Research, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan
Toru Hiyama, Masaharu Yoshihara, Health Service Center, Hiroshima University, Higashihiroshima, Japan
Shinji Tanaka, Department of Endoscopy, Hiroshima University Hospital, Hiroshima, Japan
Koji Arihiro, Department of Anatomical Pathology, Hiroshima University Hospital, Hiroshima, Japan
Author contributions: All authors contributed equally to the work.
Correspondence to: Dr. Shinji Tanaka, Department of Endoscopy, Hiroshima University Hospital, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan. colon@hiroshima-u.ac.jp
Telephone: +81-82-2575538 Fax: +81-82-2575538
Received: January 16, 2007
Revised: February 20, 2007
Accepted: April 4, 2007
Published online: August 7, 2007
Abstract

AIM: To examine Krüppel-like factor 6 (KLF6) mutations in nonpolypoid-type tumors and alterations of K-ras, p53, and B-raf in relation between mutation and morphologic type, particularly nonpolypoid-type colorectal carcinomas.

METHODS: Fifty-five early nonpolypoid colorectal carcinomas were analyzed. Loss of heterozygosity (LOH) of KLF6 and p53 was determined by microsatellite assay. Mutations of KLF6, K-ras, and B-raf were examined by polymerase chain reaction-single-strand conformation polymorphism followed by direct sequencing. In LOH-positive and/or mutation-positive tumors, multiple (4-7) samples in each tumor were microdissected and examined for genetic alterations. p53 expression was evaluated by immunohistochemistry.

RESULTS: LOH of KLF6 and p53 was found in 14 of 29 (48.3%) and 14 of 31 (45.2%) tumors, respectively. In 10 of the 14 (71.4%) KLF6 LOH-positive tumors and 9 of the 14 (64.3%) p53 LOH-positive tumors, LOH was found in all of the microdissected samples. In 1 of the 10 (10.0%) KLF6 LOH-positive tumors, a single missense mutation was identified. K-ras and B-raf mutations were found in 5 of 55 (9.1%) and 6 of 55 (10.9%) tumors, respectively. However, these mutations were detected only in subsets of microdissected tumor samples.

CONCLUSION: These data suggest that KLF6 and p53 mutations are involved in the development of nonpolypoid colorectal carcinoma, whereas K-ras and B-raf mutations are not.

Keywords: Nonpolypoid colorectal carcinoma; KLF6; p53; K-ras; B-raf