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Melanoma: HELP
Articles by Christin E. Burd
Based on 7 articles published since 2009
(Why 7 articles?)
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Between 2009 and 2019, Christin E. Burd wrote the following 7 articles about Melanoma.
 
+ Citations + Abstracts
1 Clinical Trial Targeted next generation sequencing identifies clinically actionable mutations in patients with melanoma. 2014

Jeck, William R / Parker, Joel / Carson, Craig C / Shields, Janiel M / Sambade, Maria J / Peters, Eldon C / Burd, Christin E / Thomas, Nancy E / Chiang, Derek Y / Liu, Wenjin / Eberhard, David A / Ollila, David / Grilley-Olson, Juneko / Moschos, Stergios / Neil Hayes, D / Sharpless, Norman E. ·Department of Genetics, University of North Carolina School of Medicine, Chapel Hill, NC, USA. ·Pigment Cell Melanoma Res · Pubmed #24628946.

ABSTRACT: Somatic sequencing of cancers has produced new insight into tumorigenesis, tumor heterogeneity, and disease progression, but the vast majority of genetic events identified are of indeterminate clinical significance. Here, we describe a NextGen sequencing approach to fully analyzing 248 genes, including all those of known clinical significance in melanoma. This strategy features solution capture of DNA followed by multiplexed, high-throughput sequencing and was evaluated in 31 melanoma cell lines and 18 tumor tissues from patients with metastatic melanoma. Mutations in melanoma cell lines correlated with their sensitivity to corresponding small molecule inhibitors, confirming, for example, lapatinib sensitivity in ERBB4 mutant lines and identifying a novel activating mutation of BRAF. The latter event would not have been identified by clinical sequencing and was associated with responsiveness to a BRAF kinase inhibitor. This approach identified focal copy number changes of PTEN not found by standard methods, such as comparative genomic hybridization (CGH). Actionable mutations were found in 89% of the tumor tissues analyzed, 56% of which would not be identified by standard-of-care approaches. This work shows that targeted sequencing is an attractive approach for clinical use in melanoma.

2 Article Co-targeting BET and MEK as salvage therapy for MAPK and checkpoint inhibitor-resistant melanoma. 2018

Echevarría-Vargas, Ileabett M / Reyes-Uribe, Patricia I / Guterres, Adam N / Yin, Xiangfan / Kossenkov, Andrew V / Liu, Qin / Zhang, Gao / Krepler, Clemens / Cheng, Chaoran / Wei, Zhi / Somasundaram, Rajasekharan / Karakousis, Giorgos / Xu, Wei / Morrissette, Jennifer Jd / Lu, Yiling / Mills, Gordon B / Sullivan, Ryan J / Benchun, Miao / Frederick, Dennie T / Boland, Genevieve / Flaherty, Keith T / Weeraratna, Ashani T / Herlyn, Meenhard / Amaravadi, Ravi / Schuchter, Lynn M / Burd, Christin E / Aplin, Andrew E / Xu, Xiaowei / Villanueva, Jessie. ·Molecular & Cellular Oncogenesis Program, The Wistar Institute, Philadelphia, PA, USA. · College of Computing Sciences, New Jersey Institute of Technology, Newark, NJ, USA. · Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA, USA. · Department of Surgery, Hospital of the University of Pennsylvania, Philadelphia, PA, USA. · Center for Personalized Diagnostics, Hospital of the University of Pennsylvania University of Pennsylvania, Philadelphia, PA, USA. · Department of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania, Philadelphia, PA, USA. · Department of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. · Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA, USA. · Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. · Melanoma Research Center, The Wistar Institute, Philadelphia, PA, USA. · Immunology, Microenvironment and Metastasis Program, The Wistar Institute, Philadelphia, PA, USA. · Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, PA, USA. · Departments of Molecular Genetics and Cancer Biology and Genetics, Ohio State University, Columbus, OH, USA. · Department of Cancer Biology and Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USA. · Molecular & Cellular Oncogenesis Program, The Wistar Institute, Philadelphia, PA, USA jvillanueva@wistar.org. ·EMBO Mol Med · Pubmed #29650805.

ABSTRACT: Despite novel therapies for melanoma, drug resistance remains a significant hurdle to achieving optimal responses. NRAS-mutant melanoma is an archetype of therapeutic challenges in the field, which we used to test drug combinations to avert drug resistance. We show that BET proteins are overexpressed in NRAS-mutant melanoma and that high levels of the BET family member BRD4 are associated with poor patient survival. Combining BET and MEK inhibitors synergistically curbed the growth of

3 Article Ultraviolet radiation accelerates NRas-mutant melanomagenesis: A cooperative effect blocked by sunscreen. 2017

Hennessey, Rebecca C / Holderbaum, Andrea M / Bonilla, Anamaria / Delaney, Conor / Gillahan, James E / Tober, Kathleen L / Oberyszyn, Tatiana M / Zippin, Jonathan H / Burd, Christin E. ·Department of Cancer Biology and Genetics, Biomedical Research Tower, The Ohio State University, Columbus, OH, USA. · Department of Molecular Genetics, Biomedical Research Tower, The Ohio State University, Columbus, OH, USA. · Department of Pathology, The Ohio State University, Columbus, OH, USA. · Department of Dermatology, Joan and Sanford I. Weill Medical College of Cornell University, New York, NY, USA. ·Pigment Cell Melanoma Res · Pubmed #28544727.

ABSTRACT: To mitigate melanoma risk, sunscreen use is widely advocated; yet, the ability of sunscreens to prevent melanoma remains controversial. Here, we test the tenet that sunscreens limit melanoma risk by blocking ultraviolet radiation (UV)-induced DNA damage using murine models that recapitulate the genetics and spontaneous evolution of human melanoma. We find that a single, non-erythematous dose of UV dramatically accelerates melanoma onset and increases tumor multiplicity in mice carrying an endogenous, melanocyte-specific NRas

4 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

5 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.,

6 Article An oncogenic Ezh2 mutation induces tumors through global redistribution of histone 3 lysine 27 trimethylation. 2016

Souroullas, George P / Jeck, William R / Parker, Joel S / Simon, Jeremy M / Liu, Jie-Yu / Paulk, Joshiawa / Xiong, Jessie / Clark, Kelly S / Fedoriw, Yuri / Qi, Jun / Burd, Christin E / Bradner, James E / Sharpless, Norman E. ·Department of Genetics, University of North Carolina (UNC) School of Medicine, Chapel Hill, North Carolina, USA. · Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina, USA. · Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA. · Department of Pathology and Laboratory Medicine, University of North Carolina School of Medicine, Chapel Hill, North Carolina, USA. · Department of Molecular Genetics, Ohio State University, Columbus, Ohio, USA. · Department of Molecular Virology, Immunology and Medical Genetics, Ohio State University, Columbus, Ohio, USA. · Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA. ·Nat Med · Pubmed #27135738.

ABSTRACT: B cell lymphoma and melanoma harbor recurrent mutations in the gene encoding the EZH2 histone methyltransferase (EZH2), but the carcinogenic role of these mutations is unclear. Here we describe a mouse model in which the most common somatic Ezh2 gain-of-function mutation (EZH2(Y646F) in human; Ezh2(Y641F) in mouse) is conditionally expressed. Expression of Ezh2(Y641F) in mouse B cells or melanocytes caused high-penetrance lymphoma or melanoma, respectively. Overexpression of the anti-apoptotic protein Bcl2, but not the oncoprotein Myc, or loss of the tumor suppressor protein p53 (encoded by Trp53 in mice) further accelerated lymphoma progression. Expression of the mutant Braf but not the mutant Nras oncoprotein further accelerated melanoma progression. Although expression of Ezh2(Y641F) globally increased the abundance of trimethylated Lys27 of histone H3 (H3K27me3), it also caused a widespread redistribution of this repressive mark, including a loss of H3K27me3 that was associated with increased transcription at many loci. These results suggest that Ezh2(Y641F) induces lymphoma and melanoma through a vast reorganization of chromatin structure, inducing both repression and activation of polycomb-regulated loci.

7 Article Mutation-specific RAS oncogenicity explains NRAS codon 61 selection in melanoma. 2014

Burd, Christin E / Liu, Wenjin / Huynh, Minh V / Waqas, Meriam A / Gillahan, James E / Clark, Kelly S / Fu, Kailing / Martin, Brit L / Jeck, William R / Souroullas, George P / Darr, David B / Zedek, Daniel C / Miley, Michael J / Baguley, Bruce C / Campbell, Sharon L / Sharpless, Norman E. ·Department of Molecular Genetics, The Ohio State University, Columbus, Ohio. Department of Molecular and Cellular Biochemistry, The Ohio State University, Columbus, Ohio. · Department of Genetics, University of North Carolina School of Medicine, Chapel Hill, North Carolina. The Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina. · Department of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill, North Carolina. · Department of Molecular Genetics, The Ohio State University, Columbus, Ohio. · Department of Dermatology, University of North Carolina School of Medicine, Chapel Hill, North Carolina. · Department of Pharmacology, University of North Carolina School of Medicine, Chapel Hill, North Carolina. · Auckland Cancer Society Research Centre, University of Auckland, Auckland, New Zealand. · The Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina. Department of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill, North Carolina. · Department of Genetics, University of North Carolina School of Medicine, Chapel Hill, North Carolina. The Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina. NES@med.unc.edu. ·Cancer Discov · Pubmed #25252692.

ABSTRACT: SIGNIFICANCE: This work explains the curious predominance in human melanoma of mutations of codon 61 of NRAS over other oncogenic NRAS mutations. Using conditional "knock-in" mouse models, we show that physiologic expression of NRASQ61R, but not NRASG12D, drives melanoma formation.