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Functional Evidence for a Colorectal Cancer Tumor Suppressor Gene at Chromosome 8p22-23 by Monochromosome Transfer¹

The Queensland Institute of Medical Research, The Bancroft Centre, Royal Brisbane Hospital Post Office, Brisbane, QLD 4029, Australia [C. E. G., P. J. W., G. C-T.]; Kanematsu Laboratories, Royal Prince Alfred Hospital, Sydney, QLD 2000 Australia [R. L. L. H.]; Department of Cytogenetics and Molecular Genetics, Women's and Children's Hospital, Adelaide, QLD 5006, Australia [E. B., E. W.]; and Laboratory of Molecular Carcinogenesis, NIEHS, Research Triangle Park, North Carolina 27709 [L. A., J. C. B.]

Chromosome 8p is considered, from loss of heterozygosity analysis, to be a strong candidate for the location of a tumor suppressor gene inactivated in colorectal cancer. We have found a 53% (27 of 51) rate of allelic loss at the LPL locus on 8p22, with the smallest region of overlap of deletions including the region D8S258 to D8S277. Using microcell-mediated monochromosome 8 transfer into three colorectal cancer cell lines, SW480, SW620 and HT29, we have demonstrated a reduction of tumorigenicity in SW620 hybrids. Partial deletions of chromosome 8 in some SW620/8 hybrids further delineate the critical region(s) to 8p22–23. Hybrids of the colorectal cancer cell lines SW480 and HT29 containing chromosome 8 did not show suppression of tumorigenesis, but the H29/8 hybrid showed total suppression of soft agar clonicity. This indicates an alternate pathway of mutational progression in these three lines, despite the fact that SW480 was derived from the same patient as SW620.

¹ This work was supported by the National Health and Medical Research Council of Australia and the Queensland Cancer Fund. G.C.T. is an National Health and Medical Research Council Research Fellow.

² To whom requests for reprints should be addressed. Phone: 61 7 3362 0390; Fax: 61 7 3362 0105; E-mail: georgiaT@qimr.edu.au.

Received 4/30/96. Accepted 9/16/96.

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