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[Cancer Research 53, 5849-5852, December 15, 1993]
© 1993 American Association for Cancer Research

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Genomic Instability in Colorectal Cancer: Relationship to Clinicopathological Variables and Family History1

Ragnhild A. Lothe2, Päivi Peltomäki, Gunn Iren Meling, Lauri A. Aaltonen, Minna Nyström-Lahti, Lea Pylkkänen, Ketil Heimdal, Tone I. Andersen, Pål Møller, Torleiv O. Rognum, Sophie D. Fosså, Tor Haldorsen, Frøydis Langmark, Anton Brøgger, Albert de la Chapelle and Anne-Lise Børresen

Department of Genetics, Institute for Cancer Research [R. A. L., K. H., T. I. A., P. M., A. B., A-L. B.], and Department of Medical Oncology and Radiotherapy [S. D. F.], The Norwegian Radium Hospital, 0310 Oslo, Norway; Department of Medical Genetics, P. O. Box 21, University of Helsinki, SF-00014 Helsinki, Finland [P. P., L. A. A., M. N-L., L. P., A. d. l. C.]; Institute of Forensic Medicine, The National Hospital, University of Oslo, 0027 Oslo, Norway [G. I. M., T. O. R.]; Surgical Department, Norwegian Lutheran Hospital, 0319 Oslo, Norway [G. I. M.]; Section of Medical Statistics, University of Oslo, 0317 Oslo, Norway [T. H.]; and the Norwegian Cancer Registry, Fritjof Nansens v.17, Oslo, Norway [F. L.]

Recent reports have suggested that one or more genes may cause replication errors (RER) during colorectal tumorigenesis. Additional alleles are seen in the tumors when analyzing random microsatellite loci. We have studied seven dinucleotide repeat loci, located on seven different chromosomes, by use of polymerase chain reaction amplification and denaturing polyacrylamide gel electrophoresis. We found that 16.5% (40 of 243) colorectal cancers showed RER at one or several loci (RER+). This includes 31% (4 of 13) among cases with a strong positive family history according to previously published criteria and 17% (35 of 207) among cases with no history of familial cancer. Interestingly, no significant association was found between RER+ tumors and a general familial clustering of cancer. Microsatellite instability was significantly associated with DNA diploid status of the tumor (P < 0.001), with the location of the tumor in the proximal colon (P < 0.001), and with poorly differentiated tumor phenotype (P < 0.001). Patients with RER+ at ≥ 2 loci tumors had an increased survival (P = 0.05).

We further analyzed 84 breast cancers and 86 male germ cell cancers using the same seven markers. None of the tumors were RER+, indicating that this phenomenon may be specific to certain types of tumors.

1 Supported by grants from the Norwegian Research Council for Science and Humanities, the Norwegian Cancer Society, the Academy of Finland, the Finnish Cancer Society, and the Sigrid Juselius Foundation. Part of this study was done at the Folkhalsan Institute of Genetics.

2 To whom requests for reprints should be addressed.

Received 10/ 9/93. Accepted 11/ 2/93.




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