Literature DB >> 7868749

Immunohistochemical expression of BCL-2 in melanomas and intradermal nevi.

M C Saenz-Santamaría1, J A Reed, N S McNutt, C R Shea.   

Abstract

The BCL-2 gene is the prototype of a newly described family of oncogenes involved in tumorigenesis by blocking apoptosis, or programmed cell death. Overexpression of BCL-2 protein was originally described in follicular B-cell lymphomas bearing the 14;18 translocation. BCL-2 overexpression has also been described in other lymphomas and more rarely in neoplasms outside the lymphoid tissue. The aim of this paper is to determine the immunohistochemical expression of BCL-2 in intradermal nevi and primary invasive and metastatic melanoma. Formalin-fixed and paraffin-embedded tissues from 4 cutaneous melanoma metastases, 10 primary invasive melanomas, and 10 intradermal melanocytic nevi were immunolabeled with monoclonal antibodies directed against BCL-2 protein (Dako, clone 124) and Ki-67 antigen (Amac, clone MIB-1), after antigen retrieval techniques. Morphologically normal epidermal melanocytes expressed BCL-2, as did nevi and melanomas in virtually all cells. However, whereas the labeling in normal melanocytes and nevus cells showed a uniformly strong reactivity, melanoma cells showed a variable but mainly weak reactivity. Ki-67 antigen expression was restricted to melanomas. The widespread expression of BCL-2 suggests that this oncoprotein cannot be involved in the malignant transformation of melanocytic cells. It seems likely that the decreased BCL-2 expression detected in melanomas may reflect one further step of tumor progression in melanocytic neoplasms.

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Year:  1994        PMID: 7868749     DOI: 10.1111/j.1600-0560.1994.tb00278.x

Source DB:  PubMed          Journal:  J Cutan Pathol        ISSN: 0303-6987            Impact factor:   1.587


  9 in total

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2.  Proliferation, apoptosis, and survivin expression in a spectrum of melanocytic nevi.

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Review 4.  Melanoma in immunosuppressed patients.

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8.  Clinical profiling of BCL-2 family members in the setting of BRAF inhibition offers a rationale for targeting de novo resistance using BH3 mimetics.

Authors:  Dennie T Frederick; Roberto A Salas Fragomeni; Aislyn Schalck; Isabel Ferreiro-Neira; Taylor Hoff; Zachary A Cooper; Rizwan Haq; David J Panka; Lawrence N Kwong; Michael A Davies; James C Cusack; Keith T Flaherty; David E Fisher; James W Mier; Jennifer A Wargo; Ryan J Sullivan
Journal:  PLoS One       Date:  2014-07-01       Impact factor: 3.240

9.  Overexpression of Mcl-1 confers resistance to BRAFV600E inhibitors alone and in combination with MEK1/2 inhibitors in melanoma.

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  9 in total

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