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Pancreatic Neoplasms: HELP
Articles by Marta Dzyadyk
Based on 2 articles published since 2010
(Why 2 articles?)
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Between 2010 and 2020, Marta Dzyadyk wrote the following 2 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Functional characterization of a multi-cancer risk locus on chr5p15.33 reveals regulation of TERT by ZNF148. 2017

Fang, Jun / Jia, Jinping / Makowski, Matthew / Xu, Mai / Wang, Zhaoming / Zhang, Tongwu / Hoskins, Jason W / Choi, Jiyeon / Han, Younghun / Zhang, Mingfeng / Thomas, Janelle / Kovacs, Michael / Collins, Irene / Dzyadyk, Marta / Thompson, Abbey / O'Neill, Maura / Das, Sudipto / Lan, Qi / Koster, Roelof / Anonymous1181133 / Anonymous1191133 / Anonymous1201133 / Stolzenberg-Solomon, Rachael S / Kraft, Peter / Wolpin, Brian M / Jansen, Pascal W T C / Olson, Sara / McGlynn, Katherine A / Kanetsky, Peter A / Chatterjee, Nilanjan / Barrett, Jennifer H / Dunning, Alison M / Taylor, John C / Newton-Bishop, Julia A / Bishop, D Timothy / Andresson, Thorkell / Petersen, Gloria M / Amos, Christopher I / Iles, Mark M / Nathanson, Katherine L / Landi, Maria Teresa / Vermeulen, Michiel / Brown, Kevin M / Amundadottir, Laufey T. ·Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. · Department of Molecular Biology, Radboud Institute for Molecular Life Sciences, Radboud University, Nijmegen 6500 HB, The Netherlands. · Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. · Cancer Genomics Research Laboratory, National Cancer Institute, Division of Cancer Epidemiology and Genetics, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, Maryland 21702, USA. · Department of Community and Family Medicine, Geisel School of Medicine, Dartmouth College, Lebanon, New Hampshire 03756, USA. · Protein Characterization Laboratory, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Frederick, Maryland 21701, USA. · Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts 02115, USA. · Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts 02115, USA. · Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA. · Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02215, USA. · Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York City, New York 10065, USA. · Department of Cancer Epidemiology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA. · Section of Epidemiology and Biostatistics, Leeds Institute of Cancer and Pathology, University of Leeds, Leeds LS9 7TF, UK. · Department of Oncology, University of Cambridge, Cambridge CB2 0XZ, UK. · Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota 55905, USA. · Translational Medicine and Human Genetics, Department of Medicine and Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ·Nat Commun · Pubmed #28447668.

ABSTRACT: Genome wide association studies (GWAS) have mapped multiple independent cancer susceptibility loci to chr5p15.33. Here, we show that fine-mapping of pancreatic and testicular cancer GWAS within one of these loci (Region 2 in CLPTM1L) focuses the signal to nine highly correlated SNPs. Of these, rs36115365-C associated with increased pancreatic and testicular but decreased lung cancer and melanoma risk, and exhibited preferred protein-binding and enhanced regulatory activity. Transcriptional gene silencing of this regulatory element repressed TERT expression in an allele-specific manner. Proteomic analysis identifies allele-preferred binding of Zinc finger protein 148 (ZNF148) to rs36115365-C, further supported by binding of purified recombinant ZNF148. Knockdown of ZNF148 results in reduced TERT expression, telomerase activity and telomere length. Our results indicate that the association with chr5p15.33-Region 2 may be explained by rs36115365, a variant influencing TERT expression via ZNF148 in a manner consistent with elevated TERT in carriers of the C allele.

2 Article CLPTM1L promotes growth and enhances aneuploidy in pancreatic cancer cells. 2014

Jia, Jinping / Bosley, Allen D / Thompson, Abbey / Hoskins, Jason W / Cheuk, Adam / Collins, Irene / Parikh, Hemang / Xiao, Zhen / Ylaya, Kris / Dzyadyk, Marta / Cozen, Wendy / Hernandez, Brenda Y / Lynch, Charles F / Loncarek, Jadranka / Altekruse, Sean F / Zhang, Lizhi / Westlake, Christopher J / Factor, Valentina M / Thorgeirsson, Snorri / Bamlet, William R / Hewitt, Stephen M / Petersen, Gloria M / Andresson, Thorkell / Amundadottir, Laufey T. ·Authors' Affiliations: Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics; Pediatric Oncology Branch; Laboratory of Pathology; Division of Cancer Control and Population Sciences; Laboratory of Experimental Carcinogenesis, National Cancer Institute, NIH, Department of Health and Human Services, Bethesda; Laboratory of Proteomics and Analytical Technologies, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research; Laboratory of Protein Dynamics and Signaling and Laboratory of Cell & Developmental Signaling, NCI-Frederick, Frederick, Maryland; Keck School of Medicine, University of Southern California, Los Angeles, California; University of Hawaii Cancer Center, Honolulu, Hawaii; Department of Epidemiology, College of Public Health, University of Iowa, Iowa City, Iowa; and Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota. · Authors' Affiliations: Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics; Pediatric Oncology Branch; Laboratory of Pathology; Division of Cancer Control and Population Sciences; Laboratory of Experimental Carcinogenesis, National Cancer Institute, NIH, Department of Health and Human Services, Bethesda; Laboratory of Proteomics and Analytical Technologies, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research; Laboratory of Protein Dynamics and Signaling and Laboratory of Cell & Developmental Signaling, NCI-Frederick, Frederick, Maryland; Keck School of Medicine, University of Southern California, Los Angeles, California; University of Hawaii Cancer Center, Honolulu, Hawaii; Department of Epidemiology, College of Public Health, University of Iowa, Iowa City, Iowa; and Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota amundadottirl@mail.nih.gov. ·Cancer Res · Pubmed #24648346.

ABSTRACT: Genome-wide association studies (GWAS) of 10 different cancers have identified pleiotropic cancer predisposition loci across a region of chromosome 5p15.33 that includes the TERT and CLPTM1L genes. Of these, susceptibility alleles for pancreatic cancer have mapped to the CLPTM1L gene, thus prompting an investigation of the function of CLPTM1L in the pancreas. Immunofluorescence analysis indicated that CLPTM1L localized to the endoplasmic reticulum where it is likely embedded in the membrane, in accord with multiple predicted transmembrane domains. Overexpression of CLPTM1L enhanced growth of pancreatic cancer cells in vitro (1.3-1.5-fold; PDAY7 < 0.003) and in vivo (3.46-fold; PDAY68 = 0.039), suggesting a role in tumor growth; this effect was abrogated by deletion of two hydrophilic domains. Affinity purification followed by mass spectrometry identified an interaction between CLPTM1L and non-muscle myosin II (NMM-II), a protein involved in maintaining cell shape, migration, and cytokinesis. The two proteins colocalized in the cytoplasm and, after treatment with a DNA-damaging agent, at the centrosomes. Overexpression of CLPTM1L and depletion of NMM-II induced aneuploidy, indicating that CLPTM1L may interfere with normal NMM-II function in regulating cytokinesis. Immunohistochemical analysis revealed enhanced staining of CLPTM1L in human pancreatic ductal adenocarcinoma (n = 378) as compared with normal pancreatic tissue samples (n = 17; P = 1.7 × 10(-4)). Our results suggest that CLPTM1L functions as a growth-promoting gene in the pancreas and that overexpression may lead to an abrogation of normal cytokinesis, indicating that it should be considered as a plausible candidate gene that could explain the effect of pancreatic cancer susceptibility alleles on chr5p15.33.