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Melanoma: HELP
Articles by Michael R. Grever
Based on 2 articles published since 2010
(Why 2 articles?)

Between 2010 and 2020, Michael R. Grever wrote the following 2 articles about Melanoma.
+ Citations + Abstracts
1 Article Cotreatment of hairy cell leukemia and melanoma with the BRAF inhibitor dabrafenib. 2015

Blachly, James S / Lozanski, Gerard / Lucas, David M / Grever, Michael R / Kendra, Kari / Andritsos, Leslie A. ·From the Division of Hematology, Department of Internal Medicine, Department of Pathology, and Division of Oncology, Department of Internal Medicine, The Ohio State University, Columbus, Ohio. ·J Natl Compr Canc Netw · Pubmed #25583765.

ABSTRACT: The activating BRAF mutation p.V600E has been identified in many cancers, including colon and lung adenocarcinomas, papillary thyroid cancer, malignant melanoma, and hairy cell leukemia (HCL). Malignant melanoma and HCL are of particular interest because of both the high proportion of cases harboring the mutation and the dramatic responses to BRAF inhibitor therapy reported in the literature. This report presents a patient with HCL and malignant melanoma with the BRAF p.V600E mutation, and discusses the successful treatment of both cancers with the BRAF inhibitor dabrafenib.

2 Article PRMT5 is upregulated in malignant and metastatic melanoma and regulates expression of MITF and p27(Kip1.). 2013

Nicholas, Courtney / Yang, Jennifer / Peters, Sara B / Bill, Matthew A / Baiocchi, Robert A / Yan, Fengting / Sïf, Saïd / Tae, Sookil / Gaudio, Eugenio / Wu, Xin / Grever, Michael R / Young, Gregory S / Lesinski, Gregory B. ·Department of Internal Medicine, Division of Medical Oncology, The Ohio State University Comprehensive Cancer Center, Columbus, Ohio, United States of America. ·PLoS One · Pubmed #24098663.

ABSTRACT: Protein arginine methyltransferase-5 (PRMT5) is a Type II arginine methyltransferase that regulates various cellular functions. We hypothesized that PRMT5 plays a role in regulating the growth of human melanoma cells. Immunohistochemical analysis indicated significant upregulation of PRMT5 in human melanocytic nevi, malignant melanomas and metastatic melanomas as compared to normal epidermis. Furthermore, nuclear PRMT5 was significantly decreased in metastatic melanomas as compared to primary cutaneous melanomas. In human metastatic melanoma cell lines, PRMT5 was predominantly cytoplasmic, and associated with its enzymatic cofactor Mep50, but not STAT3 or cyclin D1. However, histologic examination of tumor xenografts from athymic mice revealed heterogeneous nuclear and cytoplasmic PRMT5 expression. Depletion of PRMT5 via siRNA inhibited proliferation in a subset of melanoma cell lines, while it accelerated growth of others. Loss of PRMT5 also led to reduced expression of MITF (microphthalmia-associated transcription factor), a melanocyte-lineage specific oncogene, and increased expression of the cell cycle regulator p27(Kip1). These results are the first to report elevated PRMT5 expression in human melanoma specimens and indicate this protein may regulate MITF and p27(Kip1) expression in human melanoma cells.