Mutant KRAS promotes hyperplasia and alters differentiation in the colon epithelium but does not expand the presumptive stem cell pool. - Wikidata - wikimedia - TriplyDB

Mutant KRAS promotes hyperplasia and alters differentiation in the colon epithelium but does not expand the presumptive stem cell pool.

Mutant KRAS promotes hyperplasia and alters differentiation in the colon epithelium but does not expand the presumptive stem cell pool.

http://www.wikidata.org/entity/Q38271066

about

Molecular pathological classification of colorectal cancer Similar but different: distinct roles for KRAS and BRAF oncogenes in colorectal cancer development and therapy resistance Reserve stem cells: Differentiated cells reprogram to fuel repair, metaplasia, and neoplasia in the adult gastrointestinal tract Adult mammalian stem cells: the role of Wnt, Lgr5 and R-spondins Animal models of colorectal cancer Cancer stemness in Apc- vs. Apc/KRAS-driven intestinal tumorigenesis A genetic progression model of Braf(V600E)-induced intestinal tumorigenesis reveals targets for therapeutic intervention.Assessment of the mode of action underlying development of rodent small intestinal tumors following oral exposure to hexavalent chromium and relevance to humans Role of the protein tyrosine phosphatase Shp2 in homeostasis of the intestinal epithelium Impaired coordination between signaling pathways is revealed in human colorectal cancer using single-cell mass cytometry of archival tissue blocks Expression of Abelson interactor 1 (Abi1) correlates with inflammation, KRAS mutation and adenomatous change during colonic carcinogenesis.Colorectal carcinogenesis--update and perspectives.Interleukin-17 receptor a signaling in transformed enterocytes promotes early colorectal tumorigenesis.The MEK/ERK pathway promotes NOTCH signalling in pancreatic cancer cells.Promotion of Intestinal Epithelial Cell Turnover by Commensal Bacteria: Role of Short-Chain Fatty Acids Oncogenic K-Ras promotes proliferation in quiescent intestinal stem cells RasGRP1 opposes proliferative EGFR-SOS1-Ras signals and restricts intestinal epithelial cell growth.Correlation between Gene Variants, Signaling Pathways, and Efficacy of Chemotherapy Drugs against Colon Cancers Clinicopathologic and genetic characterization of traditional serrated adenomas of the colon The mysterious human epidermal cell cycle, or an oncogene-induced differentiation checkpoint.Pathology of rodent models of intestinal cancer: progress report and recommendations Genetic reconstitution of tumorigenesis in primary intestinal cells Sox9 induction, ectopic Paneth cells, and mitotic spindle axis defects in mouse colon adenomatous epithelium arising from conditional biallelic Apc inactivation Serrated polyposis associated with a family history of colorectal cancer and/or polyps: The preferential location of polyps in the colon and rectum defines two molecular entities BRAFV600E cooperates with CDX2 inactivation to promote serrated colorectal tumorigenesis.Shp2/MAPK signaling controls goblet/paneth cell fate decisions in the intestine c-Cbl mediates the degradation of tumorigenic nuclear β-catenin contributing to the heterogeneity in Wnt activity in colorectal tumors.Proteomics in studying cancer stem cell biology.K-ras Mutations as the Earliest Driving Force in a Subset of Colorectal Carcinomas.Biased competition between Lgr5 intestinal stem cells driven by oncogenic mutation induces clonal expansion.Inflammatory response in serrated precursor lesions of the colon classified according to WHO entities, clinical parameters and phenotype-genotype correlation.KRAS mutation associated with CD44/CD166 immunoexpression as predictors of worse outcome in metastatic colon cancer.A role for the epidermal growth factor receptor signaling in development of intestinal serrated polyps in mice and humans Apc inactivation, but not obesity, synergizes with Pten deficiency to drive intestinal stem cell-derived tumorigenesis.KRAS and cancer stem cells in APC-mutant colorectal cancer.Interaction between Wnt/β-catenin and RAS-ERK pathways and an anti-cancer strategy via degradations of β-catenin and RAS by targeting the Wnt/β-catenin pathway.KLF5 mediates the hyper-proliferative phenotype of the intestinal epithelium in mice with intestine-specific endogenous K-RasG12D expression.Colorectal cancer: genetic abnormalities, tumor progression, tumor heterogeneity, clonal evolution and tumor-initiating cells.

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P2860

Mutant KRAS promotes hyperplasia and alters differentiation in the colon epithelium but does not expand the presumptive stem cell pool.

http://www.wikidata.org/entity/Q38271066

description

2011 nî lūn-bûn

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2011年の論文

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2011年学术文章

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2011年学术文章

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2011年学术文章

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2011年学术文章

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2011年学术文章

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2011年學術文章

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2011年學術文章

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2011年學術文章

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Mutant KRAS promotes hyperplas ...... he presumptive stem cell pool.

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J.GASTRO.2011.05.007

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Gastroenterology

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Mutant KRAS promotes hyperplas ...... he presumptive stem cell pool.

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Aaron Burberry

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Eric R Fearon

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Evan Sands

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Jenny Zhao

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Kathleen R Cho

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Kelly Brown

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Maranne Green

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Yali Zhai

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Ying Feng

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P2860

The beta-catenin/TCF-4 complex imposes a crypt progenitor phenotype on colorectal cancer cells

Cre reporter strains produced by targeted insertion of EYFP and ECFP into the ROSA26 locus

A genetic model for colorectal tumorigenesis

The genomic landscapes of human breast and colorectal cancers

Identification of stem cells in small intestine and colon by marker gene Lgr5

Genetic alterations during colorectal-tumor development

Notch/gamma-secretase inhibition turns proliferative cells in intestinal crypts and adenomas into goblet cells

Paneth cells constitute the niche for Lgr5 stem cells in intestinal crypts

Expression of Musashi-1 in human normal colon crypt cells: a possible stem cell marker of human colon epithelium.

Identification of a putative intestinal stem cell and early lineage marker; musashi-1.

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