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Pancreatic Neoplasms: HELP
Articles by Michael J. Thompson
Based on 2 articles published since 2010
(Why 2 articles?)
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Between 2010 and 2020, Michael Thompson wrote the following 2 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Pancreatic cancer patient survival correlates with DNA methylation of pancreas development genes. 2015

Thompson, Michael J / Rubbi, Liudmilla / Dawson, David W / Donahue, Timothy R / Pellegrini, Matteo. ·Department of Molecular, Cell, and Developmental Biology, University of California Los Angeles, Los Angeles, California, 90095, United States of America. · Department of Pathology and Laboratory Medicine, University of California Los Angeles, Los Angeles, California, 90095, United States of America; Jonsson Comprehensive Cancer Center, University of California Los Angeles, Los Angeles, California, 90095, United States of America. · Department of Surgery, University of California Los Angeles, Los Angeles, California, 90095, United States of America; Department of Molecular and Medical Pharmacology, University of California Los Angeles, Los Angeles, California, 90095, United States of America; Jonsson Comprehensive Cancer Center, University of California Los Angeles, Los Angeles, California, 90095, United States of America. ·PLoS One · Pubmed #26039411.

ABSTRACT: DNA methylation is an epigenetic mark associated with regulation of transcription and genome structure. These markers have been investigated in a variety of cancer settings for their utility in differentiating normal tissue from tumor tissue. Here, we examine the direct correlation between DNA methylation and patient survival. We find that changes in the DNA methylation of key pancreatic developmental genes are strongly associated with patient survival.

2 Article MGMT inhibition suppresses survivin expression in pancreatic cancer. 2015

Bobustuc, George C / Patel, Anand / Thompson, Michael / Srivenugopal, Kalkunte S / Frick, Jacob / Weese, James / Konduri, Santhi D. ·From the *Aurora Health Care, Milwaukee, WI; †Internal Medicine, Temple University Health Sciences Center, Philadelphia, PA; and †School of Pharmacy, Texas Tech University Health Sciences Center, Amarillo, TX. ·Pancreas · Pubmed #25875800.

ABSTRACT: OBJECTIVES: Survivin, an antiapoptotic gene inhibited by p53, is overexpressed in human cancers and correlates with chemotherapy resistance. Here, we investigated the mutual regulatory mechanism between MGMT (O-methylguanine DNA methyltransferase) and survivin. METHODS: This study used standard techniques for protein and messenger RNA levels, promoter activity, protein-DNA interaction, cell viability, and correlative animal model. RESULTS: O-benzylguanine (BG), a potent inhibitor of MGMT (a DNA repair protein), curtails the expression of survivin in pancreatic cancer. Silencing MGMT by small interfering RNA down-regulates survivin transcription. p53 inhibition enhances MGMT and survivin expressions. When p53 was silenced, BG-induced MGMT inhibition was not associated with the down-regulation of survivin, underscoring the regulatory role of p53 in the MGMT-survivin axis. O-benzylguanine inhibits survivin and PCNA (proliferating cell nuclear antigen) at messenger RNA and protein levels in PANC-1 and L3.6pl cells and decreases survivin promoter activity via increased p53 recruitment to the survivin promoter. In orthotopic pancreatic xenografts established in nude mice, BG ± gemcitabine (GEM) decrease survivin expression in tumor tissue; protein levels and immunohistochemistry show significant decrease in survivin and PCNA levels, which correlate with increased sensitivity to GEM. CONCLUSIONS: MGMT inhibition is associated with decrease in survivin expression and increase in sensitivity to GEM in pancreatic cancer.