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Identifying a Region of Interest in Site- and Stage-Specific Colon Cancer on Chromosome 13

From the Academic Surgical Unit (NSS, RB, JVT, JRTM) and Cell and Molecular Medicine (JG, LC), Division of Cancer, Postgraduate Medical Institute of the University of Hull, in association with the Hull and York Medical School, Castle Hill Hospital, Castle Road, Cottingham, United Kingdom.

Correspondence: Address correspondence and reprint requests to: L. Cawkwell, PhD, R&D Building, Castle Hill Hospital, Castle Road, Cottingham HU16 5JQ, UK; Fax: 01-48-262-2398; E-mail: l.cawkwell{at}hull.ac.uk

Background: The role of genes on chromosome 13q has not been confirmed in colorectal tumors, in part because most series that have been studied are heterogeneous in terms of tumor site, stage, and replication error (RER) status. Using a highly homogenous series of colon tumors, our aim was to identify areas of interest on 13q that are important in carcinogenesis.

Methods: Twenty-three RER-negative tumor specimens from patients with right-sided Dukes’ stage C colon tumors were selected for analysis with 10 microsatellite markers spanning 13q. The polymerase chain reaction–amplified products were analyzed by using a standard fluorescent loss of heterozygosity/allele imbalance assay.

Results: Markers showing the highest frequency of allelic imbalance were as follows: D13S175 (31%), D13S289 (27%), D13S263 (25%), and D13S265 (27%). The overall resolution of the map was approximately 11.4 to 11.7 cM.

Conclusions: This study of right-sided, RER-negative, Dukes’ stage C colon tumors showed the highest area of allelic imbalance corresponding to 13q11.2–11. This region includes LATS2 (large tumor suppressor 2 gene) and FGF9 (fibroblast growth factor 9), which may be involved in carcinogenesis.

Key Words: Colorectal cancer • Chromosome 13 • Loss of heterozygosity • Bowel tumorigenesis

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