Nuclear Localization of Dpc4 (Madh4, Smad4) in Colorectal Carcinomas and Relation to Mismatch Repair/Transforming Growth Factor-β Receptor Defects Elizabeth.

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Nuclear Localization of Dpc4 (Madh4, Smad4) in Colorectal Carcinomas and Relation to Mismatch Repair/Transforming Growth Factor-β Receptor Defects Elizabeth Montgomery, Michael Goggins, Shibin Zhou, Pedram Argani, Robb E. Wilentz, Manju Kaushal, Susan Booker, Katharine Romans, Parul Bhargava, Ralph H. Hruban, Scott E. Kern The American Journal of Pathology Volume 158, Issue 2, Pages 537-542 (February 2001) DOI: 10.1016/S0002-9440(10)63995-8 Copyright © 2001 American Society for Investigative Pathology Terms and Conditions

Figure 1 Diagram showing interrelationships between TGF-β superfamily members. Although TGF-β itself is known to lead to activation of Dpc4 in some systems, the data presented here support the presence of other input as well. The figure is schematic; the receptor is heterodimeric and requires additional proteins for efficient signaling, and the Smad complex also comprises multiple proteins to accomplish specific functions. The American Journal of Pathology 2001 158, 537-542DOI: (10.1016/S0002-9440(10)63995-8) Copyright © 2001 American Society for Investigative Pathology Terms and Conditions

Figure 2 A: The tumors prepared from HCT116 cells (which are known to have a truncating mutation of TGFBR2 but are DPC4+/+) have both nuclear (arrow) and cytoplasmic labeling for Dpc4. Immunohistochemistry using anti-Dpc4 antibody, counterstained with hematoxylin. B: A xenograft prepared from cell line 5-60 cells (lacking intact TGFBR2 but DPC4+/−) has both nuclear (arrow) and cytoplasmic labeling with the Dpc4 antibody. Immunohistochemistry using anti-Dpc4 antibody, counterstained with hematoxylin. C:Xenografted tumor prepared from cell line 5-18 cells (lacking intact TGFBR2 and DPC4−/−) showed neither cytoplasmic nor nuclear labeling with the anti-Dpc4 antibody. The labeled cells in this photograph are ingrown stromal cells from the host animal; the large tumor cells (arrow) are unlabeled. Immunohistochemistry using anti-Dpc4 antibody, counterstained with hematoxylin. The American Journal of Pathology 2001 158, 537-542DOI: (10.1016/S0002-9440(10)63995-8) Copyright © 2001 American Society for Investigative Pathology Terms and Conditions

Figure 3 A: Colon carcinoma from a patient with HNPCC. This patient was shown to have a TGFBR2 mutation. Tumor cells contain both nuclear and cytoplasmic Dpc4. Immunohistochemistry using anti-Dpc4 antibody, counterstained with hematoxylin. B: A sporadic colorectal carcinoma completely lacking expression of Dpc4. The stromal and inflammatory cells within the desmoplastic stroma serve as internal controls that express Dpc4. Immunohistochemistry using anti-Dpc4 antibody, counterstained with hematoxylin. C: Sporadic colorectal adenocarcinoma with strong expression of Dpc4 in tumor cell nuclei and cytoplasm. The lymphoid cells (arrow) in the lamina propria also label for Dpc4. The American Journal of Pathology 2001 158, 537-542DOI: (10.1016/S0002-9440(10)63995-8) Copyright © 2001 American Society for Investigative Pathology Terms and Conditions