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(American Journal of Pathology. 1998;153:1977-1984.)
© 1998 American Society for Investigative Pathology

Regular Articles

Loss of Heterozygosity and Microsatellite Instability in De Novo versus Ex-Adenoma Carcinomas of the Colorectum

James D. Mueller* , Nina Haegle{dagger} , Gisela Keller{dagger} , Elke Mueller{dagger} , Gabriele Saretzky{ddagger} , Birgit Bethke§ , Manfred Stolte§ and Heinz Höfler{dagger}

From the Department of Surgery* and the Institute of Pathology,{dagger} Klinikum rechts der Isar, Technische Universität München, Munich; the Institute of Pathology,{ddagger} University Hospital Charite', Humbolt Universität, Berlin; and the Institute of Pathology,§ Klinikum Bayreuth, Bayreuth, Germany

Small adenocarcinomas of the colorectum showing no evidence of origin from an adenoma have been called de novo carcinomas, a name that implies an origin via a different molecular genetic mechanism than the usual colorectal carcinoma which develops from an adenoma. Using microsatellite analysis, 35 early (pT1) de novo and 36 pT1 ex-adenoma carcinomas were compared using 8 microsatellite loci at 6 different chromosomal loci (1p, 2p, 8p, 5q, 17p, and 18q) known or hypothesized to be important for colorectal carcinogenesis. The rate of loss of heterozygosity (LOH) at the 17p locus (near the p53 gene) was significantly higher in the de novo than in the ex-adenoma group (73 vs. 37%, P = 0.004). The rates of LOH at the other loci (including the APC and DCC genes) and the rate of MSI were not significantly different in the two groups. These results indicate that de novo carcinomas of the colorectum develop via a similar carcinogenetic pathway as conventional ex-adenoma carcinomas; however, their higher rate of LOH at 17p is evidence for a biologically more advanced lesion with more frequent p53 mutations, consistent with clinicopathological data indicating that de novo carcinomas are more aggressive than ex-adenoma carcinomas.




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