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Immunohistochemical stain using SMAD4/6309R showing loss of SMAD4 expression in pancreatic ductal adenocarcinoma. Note adjacent benign ductal epithelium and background stroma as internal control showing positive / retained SMAD4 staining.
Formalin-fixed, paraffin-embedded human small intestine stained with SMAD4 / DPC4 Recombinant Rabbit Monoclonal Antibody (SMAD4/6309R). HIER: Tris/EDTA, pH9.0, 45min. 2°: HRP-polymer, 30min. DAB, 5min.
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Signaling from the ligand-activated membrane receptor serine/threonine kinases to nuclear targets is mediated by a set of evolutionarily conserved proteins known as DPC4. Upon ligand binding, the receptors of the TGF-β family phosphorylate SMAD proteins (SMAD1 and SMAD2). These proteins then move into the nucleus, where they activate transcription. To carry out this function, the receptor activated SMAD1 and 2 require association with the product of deleted in pancreatic carcinoma, locus 4 (DPC4), also known as SMAD4. SMAD4/DPC4 is also implicated as a tumor suppressor, since it is inactivated in more than half of pancreatic carcinomas and to a lesser extent in a variety of other cancers. The lack of SMAD4 expression is present in approximately 80% of cases of pancreatic adenocarcinoma, but rarely in endometrial (0%), colorectal (0%), ovarian (3%), lung (0%), breast (2%) adenocarcinomas, and malignant melanoma (4%). SMAD4is an important marker for confirming a diagnosis of pancreatic adenocarcinoma.
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