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PMID: 10623651 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Immunohistochemical labeling for dpc4 mirrors genetic status in pancreatic adenocarcinomas : a new marker of DPC4 inactivation.

The American journal of pathology ·Vol. 156 ·No. 1 ·2000-01-00 ·Pages 37-43

Wilentz RE, Su GH, Dai JL, Sparks AB, Argani P, Sohn TA, Yeo CJ, Kern SE, Hruban RH

Abstract

DPC4 (MADH4, SMAD4) is a tumor suppressor gene inactivated by allelic loss in approximately 55% of pancreatic adenocarcinomas. Unfortunately, it can be technically very difficult to detect the inactivation of DPC4 at the genetic level because genetic analyses require the microdissection of relatively pure samples of neoplastic and normal tissues. This is especially true for pancreatic adenocarcinomas, which elicit vigorous, non-neoplastic, stromal responses. Immunohistochemical labeling can overcome this hurdle because it preserves morphological information. We therefore studied the expression of the DPC4 gene product in 46 cancers, including 5 cancer cell lines by Western blot analysis and 41 primary periampullary adenocarcinomas by immunohistochemistry. The status of exons 1-11 of the DPC4 gene in all 46 of the cancers had been previously characterized at the molecular level, allowing us to correlate Dpc4 expression directly with gene status. Three cell lines had wild-type DPC4 genes, and Dpc4 expression was detected in all three by Western blot. The two cell lines with homozygously deleted DPC4 genes did not show Dpc4 protein by Western blot analysis. Immunohistochemical labeling revealed that 17 (94%) of the 18 primary adenocarcinomas with wild-type DPC4 genes expressed the DPC4 gene product, whereas 21 (91%) of 23 primary adenocarcinomas with inactivated DPC4 genes did not. Cases in which there was discordance between the immunohistochemical labeling and the genetic analyses were reanalyzed genetically, and we identified a deletion in exon 0 of DPC4 in one of these cases. This is the first report of a mutation in exon 0 of DPC4 in a pancreatic cancer. The contrast between the strong expression of Dpc4 by normal tissues and the loss of expression in the carcinomas was highlighted in several cases in which an infiltrating cancer was identified growing into a benign duct. These observations suggest that immunohistochemical labeling for the DPC4 gene product is an extremely sensitive and specific marker for DPC4 gene alterations in pancreatic carcinomas. The sensitivity and specificity of immunohistochemical labeling for Dpc4 in other periampullary carcinomas has yet to be determined.

MeSH Terms
Adenocarcinoma/genetics,metabolism,pathology Biomarkers Blotting, Western DNA-Binding Proteins/metabolism Gene Expression Regulation/physiology Humans Immunohistochemistry Pancreatic Neoplasms/genetics,metabolism,pathology Sensitivity and Specificity Smad4 Protein Trans-Activators/metabolism
Chemicals
Biomarkers DNA-Binding Proteins SMAD4 protein, human Smad4 Protein Trans-Activators
Authors & Affiliations
9 authors, click to expand affiliations / ORCID
Wilentz R E
Departments of Pathology, Oncology, and Surgery, The Johns Hopkins Medical Institutions, Baltimore, Maryland.
Su G H
Dai J L
Sparks A B
Argani P
Sohn T A
Yeo C J
Kern S E
Hruban R H
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Article Info
Journal
The American journal of pathology
Abbr.
Am J Pathol
ISSN
0002-9440
Published
2000-01-00
Pages
37-43
Language
English
Region
United States
NLM ID
0370502
PMCID
PMC1868651
Subset
IM
Grants
NCI NIH HHS · T32 CA067751 · United States
NCI NIH HHS · P50 CA062924 · United States
NCI NIH HHS · CA62924 · United States
NCI NIH HHS · CA67751-03 · United States
NCI NIH HHS · CA68228 · United States
NCI NIH HHS · R01 CA068228 · United States
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