Microsatellite instability is associated with the histological features of the tumor in nonfamilial colorectal cancer

Mauro Risio, Gigliola Reato, Paola Francia Di Celle, Marco Fizzotti, Francesco Paolo Rossini, Robin Foà

Research output: Contribution to journalArticle

Abstract

Replication errors (RERs) at microsatellite loci were examined in 46 specimens of nonfamilial colorectal cancer. Somatic microsatellite alterations in at least two genetic loci, D11S904, D13S175, D2S123, and D10S197, consistent with a RER(+) phenotype were found in four cases (8.7%). Six additional cases (13%) showed alterations at a single locus. Mutinous differentiation was observed in 3 of 4 (75%) adenocarcinomas with a RER(+) phenotype and only in 19% (8 of 42) of RER(-) adenocarcinomas (P <0.05). A distinct cap of inflammatory cells at the advancing edge of the tumor and Crohn's-like reaction in peritumoral stroma were histologically identified in 50 and 25% of RER(+) and in 5 and 0% of RER(-) tumors, respectively (P <0.05). Also, the plexiform pattern of growth of carcinoma turned out to be significantly associated with the RER(+) phenotype (P <0.05). Mucinous differentiation and stromal inflammatory reactions are frequent features of hereditary nonpolyposis colorectal cancer in which germ-line mutations of mismatch repair genes cause genetic instability. Our results indicate that a link exists between such histological features and somatic genetic instability consistent with a RER(+) phenotype also in nonfamilial colorectal cancer.

Original languageEnglish
Pages (from-to)5470-5474
Number of pages5
JournalCancer Research
Volume56
Issue number23
Publication statusPublished - Dec 1 1996

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

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    Risio, M., Reato, G., Di Celle, P. F., Fizzotti, M., Rossini, F. P., & Foà, R. (1996). Microsatellite instability is associated with the histological features of the tumor in nonfamilial colorectal cancer. Cancer Research, 56(23), 5470-5474.