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Short Communication |
From the Departments of Pathology,* InternalMedicine, and HumanGenetics, and The Comprehensive CancerCenter, The University of Michigan MedicalSchool, Ann Arbor, Michigan
In various cancers, inactivating mutations in the
adenomatous polyposis coli or Axin tumor suppressor proteins or
activating mutations in ß-catenin’s amino-terminal domain elevate
ß-catenin levels, resulting in marked effects on T-cell
factor (TCF)-regulated transcription. Several candidate
ß-catenin/TCF-regulated genes in cancer have been proposed.
Expression of a few of these genes has been studied in primary human
cancers, but most studies have focused on colon cancers and not
on other cancer types that harbor mutational defects in adenomatous
polyposis coli, AXIN, or ß-catenin. Mutations leading
to ß-catenin deregulation are found in nearly half of ovarian
endometrioid adenocarcinomas (OEAs). We report here on the expression
of 6 candidate ß-catenin/TCF-regulated genes in a panel of 44 primary
OEAs, more than a third of which carry demonstrable defects in
ß-catenin regulation. Using quantitative assays of gene
expression, we found significantly elevated expression of the
MMP-7, CCND1 (Cyclin
D1), CX43 (Connexin
43), PPAR-
, and
ITF2 genes in OEAs with deregulated ß-catenin. This
correlation was not observed for c-myc, another
putative ß-catenin/TCF-regulated gene. Immunohistochemical studies
confirmed that overexpression of cyclin D1 and MMP-7 was highly
associated with nuclear accumulation of ß-catenin and mutational
defects of the Wnt/ß-catenin/TCF-signaling pathway. Our findings
indicate cyclin D1, MMP-7, connexin 43,
PPAR-, and ITF-2, likely play important roles in the
pathogenesis of those OEAs that manifest defects in ß-catenin
regulation.
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