Brief Reports
Copyright ©2005 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Mar 21, 2005; 11(11): 1668-1672
Published online Mar 21, 2005. doi: 10.3748/wjg.v11.i11.1668
Detailed deletion mapping of loss of heterozygosity on 22q13 in sporadic colorectal cancer
Hai-Tao Zheng, Zhi-Hai Peng, Chong-Zhi Zhou, Da-Peng Li, Zhao-Wen Wang, Guo-Qiang Qiu, Lin He
Hai-Tao Zheng, Zhi-Hai Peng, Chong-Zhi Zhou, Da-Peng Li, Zhao-Wen Wang, Guo-Qiang Qiu, Department of General Surgery, Shanghai First People Hospital, Shanghai 200080, China
Lin He, Shanghai Institutes for Nutritional Sciences, Chinese Academy of Science, 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 First People Hospital, 85 Wujin Road, Shanghai 200080, China. pengpzhb@online.sh.cn
Telephone: +86-21-63240090-4312
Received: November 2, 2004
Revised: November 3, 2004
Accepted: November 24, 2004
Published online: March 21, 2005
Abstract

AIM: Both development and progression of malignancies occur as a multistep process, requiring the activation of oncogenes and the inactivation of several tumor suppressor genes. The loss of heterozygosity (LOH) of tumor suppressor genes is believed to play a key role in carcinogenesis of colorectal cancer (CRC). In this study, we analyzed the LOH of seven loci on chromosome 22q13 in an effort to identify candidate tumor suppressor genes involved in colorectal carcinogenesis.

METHODS: Matched tumor and normal tissue DNA were analyzed by PCR using fluorescence-labeled polymorphic microsatellite markers in 83 CRC patients. PCR products were eletrophoresed and LOH was determined by calculating the peak height acquired through computer software. Comparisons between LOH frequency and clinicopathological features were performed by χ2 test. P<0.05 was considered as statistical significance.

RESULTS: The average LOH frequency of chromosome 22q13 was 28.38%. The highest LOH frequency was 64.71% on D22S1160 locus, and the lowest was 21.43% on D22S1141 locus. We detected two obvious minimal deletion regions: one between markers D22S1171 and D22S274, the other flanked by markers D22S1160 and D22S1149, each about 2.7 and 1.8 cm, respectively. None had lost in all informative loci. LOH frequency on D22S1171 is 50% on distal colon, which was higher than that on proximal one (P = 0.020); on D22S114 locus, none LOH event occurred in patients with liver metastasis, whilst 46.94% occurred in patients without liver metastasis (P = 0.008); on D22S1160 locus, LOH frequency in lymph nodes metastasis patients was 83.33%, which was much higher than 43.75% without lymph nodes metastasis ones (P = 0.016). There was no statistical significance between clinicopathological features and other loci.

CONCLUSION: This study provides evidence of two minimal deletion regions, which may harbor putative tumor suppressor genes related to progression and metastasis in sporadic colorectal carcinoma on chromosome 22q13.

Keywords: Heterozygosity; Chromosome 22; Sporadic colorectal cancer; Gene mapping