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Melanoma: HELP
Articles by Reena Shakya
Based on 2 articles published since 2008
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Between 2008 and 2019, Reena Shakya wrote the following 2 articles about Melanoma.
 
+ Citations + Abstracts
1 Article The Exportin-1 Inhibitor Selinexor Exerts Superior Antitumor Activity when Combined with T-Cell Checkpoint Inhibitors. 2017

Farren, Matthew R / Hennessey, Rebecca C / Shakya, Reena / Elnaggar, Omar / Young, Gregory / Kendra, Kari / Landesman, Yosef / Elloul, Sivan / Crochiere, Marsha / Klebanov, Boris / Kashyap, Trinayan / Burd, Christin E / Lesinski, Gregory B. ·Department of Hematology and Medical Oncology, Winship Cancer Institute of Emory University, Atlanta, Georgia. · Department of Molecular Genetics, The Ohio State University, Columbus, Ohio. · Department of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University, Columbus, Ohio. · Target Validation Shared Resource, The Ohio State University, Columbus, Ohio. · Division of Internal Medicine, The Ohio State University, Columbus, Ohio. · Center for Biostatistics, The Ohio State University, Columbus, Ohio. · Karyopharm Therapeutics, Newton, Massachusetts. · Department of Hematology and Medical Oncology, Winship Cancer Institute of Emory University, Atlanta, Georgia. gregory.b.lesinski@emory.edu. ·Mol Cancer Ther · Pubmed #28148715.

ABSTRACT: Selinexor, a selective inhibitor of nuclear export (SINE) compound targeting exportin-1, has previously been shown to inhibit melanoma cell growth

2 Article Stromal Senescence By Prolonged CDK4/6 Inhibition Potentiates Tumor Growth. 2017

Guan, Xiangnan / LaPak, Kyle M / Hennessey, Rebecca C / Yu, Christina Y / Shakya, Reena / Zhang, Jianying / Burd, Christin E. ·Department of Molecular Genetics, The Ohio State University, Columbus, Ohio. · Department of Cancer Biology and Genetics, The Ohio State University, Columbus, Ohio. · Department of Biomedical Informatics, The Ohio State University, Columbus, Ohio. · The Ohio State University Comprehensive Cancer Center - Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, Columbus, Ohio. · Department of Molecular Genetics, The Ohio State University, Columbus, Ohio. burd.25@osu.edu. ·Mol Cancer Res · Pubmed #28039358.

ABSTRACT: Senescent cells within the tumor microenvironment (TME) adopt a proinflammatory, senescence-associated secretory phenotype (SASP) that promotes cancer initiation, progression, and therapeutic resistance. Here, exposure to palbociclib (PD-0332991), a CDK4/6 inhibitor, induces senescence and a robust SASP in normal fibroblasts. Senescence caused by prolonged CDK4/6 inhibition is DNA damage-independent and associated with Mdm2 downregulation, whereas the SASP elicited by these cells is largely reliant upon NF-κB activation. Based upon these observations, it was hypothesized that the exposure of nontransformed stromal cells to PD-0332991 would promote tumor growth. Ongoing clinical trials of CDK4/6 inhibitors in melanoma prompted a validation of this hypothesis using a suite of genetically defined melanoma cells (i.e.,