Article

Paradoxical role of AT-rich interactive domain 1A in restraining pancreatic carcinogenesis

2019-11-08

Abstract excerpt

<h4>Background & Aims</h4> ARID1A is postulated to be a tumor suppressor gene owing to loss-of-function mutations in human pancreatic ductal adenocarcinomas (PDAC). However, its role in pancreatic pathogenesis is not clear despite recent studies using genetically engineered mouse (GEM) models. We aimed at further understanding of its direct functional role in PDAC, using a combination of GEM model, PDAC cell line...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work: 47c2e94d-5b3b-5488-a243-23c10e8c7359
DOI: 10.1101/835793

Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest

Paradoxical role of AT-rich interactive domain 1A in restraining pancreatic carcinogenesisDOI 10.1101/835793Read

Paradoxical Role of AT-rich Interactive Domain 1A in Restraining Pancreatic CarcinogenesisSemantic proximity Read

ARID1A suppresses malignant transformation of human pancreatic cells via mediating senescence-associated miR-503/CDKN2A regulatory axisSemantic proximity Read

Loss of ARID1A Expression Correlates With Tumor Differentiation and Tumor Progression Stage in Pancreatic Ductal Adenocarcinoma.Semantic proximity Read

A CRISPR/Cas9-Engineered ARID1A-Deficient Human Gastric Cancer Organoid Model Reveals Essential and Nonessential Modes of Oncogenic Transformation.Semantic proximity Read

Molecular biology of pancreatic neuroendocrine tumors: From mechanism to translationSemantic proximity Read

Loss of p53 tumor suppression function drives invasion and genomic instability in models of murine pancreatic cancerSemantic proximity Read

Ring1b-dependent epigenetic remodelling is an essential prerequisite for pancreatic carcinogenesisSemantic proximity Read

Targeting DNA Damage Repair Mechanisms in Pancreas CancerSemantic proximity Read

Loss of ATM accelerates pancreatic cancer formation and epithelial–mesenchymal transitionSemantic proximity Read

Loss of ARID1A Promotes Epithelial–Mesenchymal Transition and Sensitizes Pancreatic Tumors to Proteotoxic StressSemantic proximity Read

A Genetically Engineered Human Organoid Model Reveals Distinct Genetic and Epigenetic Barriers of Lineage Plasticity in Early PDAC TransformationSemantic proximity Read

ARF6 and AMAP1 are major targets of KRAS and TP53 mutations to promote invasion, PD-L1 dynamics, and immune evasion of pancreatic cancerSemantic proximity Read