A two-step model for colon adenoma initiation and progression caused by APC loss. - Wikidata - wikimedia - TriplyDB

A two-step model for colon adenoma initiation and progression caused by APC loss.

A two-step model for colon adenoma initiation and progression caused by APC loss.

http://www.wikidata.org/entity/Q37251442

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FoxM1 promotes β-catenin nuclear localization and controls Wnt target-gene expression and glioma tumorigenesis β-Catenin-driven cancers require a YAP1 transcriptional complex for survival and tumorigenesis Molecular approach to genetic and epigenetic pathogenesis of early-onset colorectal cancer Role of retinoids in the prevention and treatment of colorectal cancer Similar but different: distinct roles for KRAS and BRAF oncogenes in colorectal cancer development and therapy resistance A fresh look at zebrafish from the perspective of cancer research Understanding phenotypic variation in rodent models with germline Apc mutations Smooth muscle tension induces invasive remodeling of the zebrafish intestine Crystal structures of human CtBP in complex with substrate MTOB reveal active site features useful for inhibitor design Cancer stem cells in basic science and in translational oncology: can we translate into clinical application?Mesalamine modulates intercellular adhesion through inhibition of p-21 activated kinase-1 Naked1 antagonizes Wnt signaling by preventing nuclear accumulation of β-catenin Beta-catenin phosphorylated at serine 45 is spatially uncoupled from beta-catenin phosphorylated in the GSK3 domain: implications for signaling.A quantitative proteomic approach of the different stages of colorectal cancer establishes OLFM4 as a new nonmetastatic tumor marker Integration of the beta-catenin-dependent Wnt pathway with integrin signaling through the adaptor molecule Grb2.A system-wide investigation of the dynamics of Wnt signaling reveals novel phases of transcriptional regulation Development of a mouse model for sporadic and metastatic colon tumors and its use in assessing drug treatment.Secreted frizzled-related protein 4: an angiogenesis inhibitor.Musashi-1 promotes a cancer stem cell lineage and chemoresistance in colorectal cancer cells.Transcription factor co-repressors in cancer biology: roles and targeting Krüppel-like factor 5 is a crucial mediator of intestinal tumorigenesis in mice harboring combined ApcMin and KRASV12 mutations.Cysteinyl leukotriene receptor 1 facilitates tumorigenesis in a mouse model of colitis-associated colon cancer.KRAS, Hedgehog, Wnt and the twisted developmental biology of pancreatic ductal adenocarcinoma.WNT signaling and distant metastasis in colon cancer through transcriptional activity of nuclear β-Catenin depend on active PI3K signaling.Vitamin D receptor deficiency enhances Wnt/β-catenin signaling and tumor burden in colon cancer.Apc(MIN) modulation of vitamin D secosteroid growth control Dvl2 promotes intestinal length and neoplasia in the ApcMin mouse model for colorectal cancer.The zebrafish as a model for cancer.DNA demethylase activity maintains intestinal cells in an undifferentiated state following loss of APC.SOST and DKK: Antagonists of LRP Family Signaling as Targets for Treating Bone Disease.The tumor suppressor adenomatous polyposis coli controls the direction in which a cell extrudes from an epithelium Adenomatous polyposis coli and hypoxia-inducible factor-1{alpha} have an antagonistic connection.Wnt signalling in adenomas of familial adenomatous polyposis patients.The absence of LPA receptor 2 reduces the tumorigenesis by ApcMin mutation in the intestine.Updating the Wnt pathways.Expression of CtBP family protein isoforms in breast cancer and their role in chemoresistance.Regulation of Nur77 expression by β-catenin and its mitogenic effect in colon cancer cells.Transcription factor Oct1 is a somatic and cancer stem cell determinant.FBXW7 influences murine intestinal homeostasis and cancer, targeting Notch, Jun, and DEK for degradation.Maslinic acid-enriched diet decreases intestinal tumorigenesis in Apc(Min/+) mice through transcriptomic and metabolomic reprogramming

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A two-step model for colon adenoma initiation and progression caused by APC loss.

http://www.wikidata.org/entity/Q37251442

description

article científic

@ca

article scientifique

@fr

articolo scientifico

@it

artigo científico

@pt

bilimsel makale

@tr

scientific article published on May 2009

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

A two-step model for colon adenoma initiation and progression caused by APC loss.

@en

A two-step model for colon adenoma initiation and progression caused by APC loss.

@nl

type

label

A two-step model for colon adenoma initiation and progression caused by APC loss.

@en

A two-step model for colon adenoma initiation and progression caused by APC loss.

@nl

prefLabel

A two-step model for colon adenoma initiation and progression caused by APC loss.

@en

A two-step model for colon adenoma initiation and progression caused by APC loss.

@nl

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J.CELL.2009.02.037

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A two-step model for colon adenoma initiation and progression caused by APC loss.

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David A Jones

http://www.w3.org/2001/XMLSchema#string

Imelda T Sandoval

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Jason Phelps

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Kunal Rai

http://www.w3.org/2001/XMLSchema#string

Randall W Burt

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Reid A Phelps

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Sharmistha Sarkar

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Somaye Dehghanizadeh

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Stephanie Chidester

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Talmage Broadbent

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P2860

Subcellular distribution of Wnt pathway proteins in normal and neoplastic colon

Identification of c-MYC as a target of the APC pathway

Activation of beta-catenin-Tcf signaling in colon cancer by mutations in beta-catenin or APC

Structural basis of the Axin-adenomatous polyposis coli interaction

A target-selected Apc-mutant rat kindred enhances the modeling of familial human colon cancer

A genetic model for colorectal tumorigenesis

Beta-catenin regulates expression of cyclin D1 in colon carcinoma cells

Wnt/beta-catenin signaling in development and disease

Lessons from hereditary colorectal cancer

beta-catenin signaling and cancer

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10.1016/J.CELL.2009.02.037

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