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Michael Goggins

Researcher at Johns Hopkins University

Publications -  378
Citations -  52451

Michael Goggins is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Pancreatic cancer & Cancer. The author has an hindex of 111, co-authored 358 publications receiving 45785 citations. Previous affiliations of Michael Goggins include Johns Hopkins University School of Medicine & Fred Hutchinson Cancer Research Center.

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Nuclear Localization of Dpc4 (Madh4, Smad4) in Colorectal Carcinomas and Relation to Mismatch Repair/Transforming Growth Factor-β Receptor Defects

TL;DR: Nuclear localization of Dpc4 can be maintained in cells with inactivated TGF-beta type II receptors, suggesting the persistence of tumor-suppressive action of an upstream signaling input, most likely a ligand/receptor complex distinct from TGF -beta.
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Cyclooxygenase-Deficient Pancreatic Cancer Cells Use Exogenous Sources of Prostaglandins

TL;DR: It is shown that pancreatic cancer stromal cells, such as fibroblasts expressing COX-1 andCOX-2, are a likely source of prostaglandins for Pancreatic cancer cells deficient in COX, and blocking multidrug resistance–associated protein-4 in fibroBlasts suppresses the proliferation of cocultured pancreatic cancers lacking COX.
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Increased expression of cytoplasmic HuR in familial adenomatous polyposis

TL;DR: HuR is increasingly expressed in the cytoplasmic epithelial compartment in consecutive stages of the adenoma-carcinoma sequence in FAP and in sporadic colorectal cancer specimens, where it may contribute to the increased cyclooxygenase-2 (COX-2) expression observed during tumorigenesis.
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Risk of Pancreatic Cancer Among Individuals With Pathogenic Variants in the ATM Gene

TL;DR: In this article, a multicenter cohort study of pancreatic cancer family registries in the US and Canada using pedigree data from 130 pancreatic cancers kindreds with a pathogenic germlineATMvariant was performed from January 2020 to February 2021.
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Mutant KRAS and GNAS DNA Concentrations in Secretin-Stimulated Pancreatic Fluid Collected from the Pancreatic Duct and the Duodenal Lumen.

TL;DR: Comparing concentrations of mutant DNA in pancreatic fluid from patients who had samples collected from both the pancreatic duct and duodenal lumen found that KRAS and GNAS mutation concentrations are significantly lower in secretin-stimulated pancreatic fluids collected from the duodenum compared with samples Collected from the Pancreas.