Colorectal Cancer
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. May 15, 2004; 10(10): 1431-1435
Published online May 15, 2004. doi: 10.3748/wjg.v10.i10.1431
Loss of heterozygosity on hromosome 1 in sporadic colorectal carcinoma
Chong-Zhi Zhou, Guo-Qiang Qiu, Fang Zhang, Lin He, Zhi-Hai Peng
Chong-Zhi Zhou, Guo-Qiang Qiu, Fang Zhang, Zhi-Hai Peng, Department of General Surgery, Shanghai Jiaotong University, First People’s Hospital, Shanghai 200080, China
Lin He, Shanghai Institute for Biological Science, Chinese Academy of Sciences, Shanghai 200031, China
Author contributions: All authors contributed equally to the work.
Supported by the National Natural Science Foundation of China, No. 30080016
Correspondence to: Dr. Zhi-Hai Peng, Department of General Surgery, Shanghai Jiaotong University, First People’s Hospital, 85 Wujin Road, Shanghai 200080, China.
Telephone: +86-21-63240090 Ext 3102
Received: June 10, 2003
Revised: August 9, 2003
Accepted: August 16, 2003
Published online: May 15, 2004

AIM: Loss of heterozygosity (LOH) on tumor suppressor genes is believed to play a key role in carcinogenesis of colorectal cancer. When it occurs at a tumor suppressor gene locus with abnormal allele, neoplastic transformation happens. In this study, we analyzed the LOH at 21 loci on chromosome 1 in sporadic colorectal cancer to identify additional loci involved in colorectal tumorigenesis.

METHODS: Twenty-one polymorphic micro-satellite DNA markers were analyzed with PCR both in 83 cases of colorectal cancer and in normal tissues. PCR products were eletrophoresed on an ABI 377 DNA sequencer. Genescan 3.1 and Genotype 2.1 software were used for LOH scanning and analysis. χ2 test was used to compare LOH frequency with clinicopathological data. P < 0.05 was considered as statistically significant.

RESULTS: The average LOH frequency of chromosome 1, short arm and long arm was 19.83%, 18.00% and 21.66%, respectively. The 2 highest LOH loci with a frequency of 36.54% and 32.50% were identified on D1S468 (1p36.33-p36.31) and D1S413 (1q31.3), respectively. On D1S2726 locus, LOH frequency of rectal cancer was 28.57% (6/21), which was higher than that of colon cancer (0.00%, 0/33) (P = 0.002), suggesting that the mechanism of carcinogenisis was different in both groups.

CONCLUSION: Putative tumor suppressor genes on chromosome 1 may relate to sporadic colorectal carcinomas. Tumor-suppressor-genes might locate on 1p36.33-36.31 and/or 1q31.3.

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