Inactivation of both APC alleles in human and mouse tumors
about
Localized gene action controlling intestinal neoplasia in miceApc1638T: a mouse model delineating critical domains of the adenomatous polyposis coli protein involved in tumorigenesis and developmentAnti-cancer activity of nitrones in the Apc(Min/+) model of colorectal cancerPolyclonality of familial murine adenomas: analyses of mouse chimeras with low tumor multiplicity suggest short-range interactionsThe adenomatous polyposis coli protein.Striking the target in Wnt-y conditions: intervening in Wnt signaling during cancer progression3,3'-diindolylmethane enhances the efficacy of butyrate in colon cancer prevention through down-regulation of survivinAltered dynamics of intestinal cell maturation in Apc1638N/+ mice.Reduced rates of gene loss, gene silencing, and gene mutation in Dnmt1-deficient embryonic stem cells.Apc(MIN) modulation of vitamin D secosteroid growth controlThe activating mutation R201C in GNAS promotes intestinal tumourigenesis in Apc(Min/+) mice through activation of Wnt and ERK1/2 MAPK pathways.Generation of a transgenic mouse for colorectal cancer research with intestinal cre expression limited to the large intestineMbd4 inactivation increases Cright-arrowT transition mutations and promotes gastrointestinal tumor formation.A continuum model for tumour suppression.Shmt1 heterozygosity impairs folate-dependent thymidylate synthesis capacity and modifies risk of Apc(min)-mediated intestinal cancer risk.Bim1p/Yeb1p mediates the Kar9p-dependent cortical attachment of cytoplasmic microtubules.A Sleeping Beauty transposon-mediated screen identifies murine susceptibility genes for adenomatous polyposis coli (Apc)-dependent intestinal tumorigenesisNewly defined aberrant crypt foci as a marker for dysplasia in the rat colon.Colonic crypt changes during adenoma development in familial adenomatous polyposis: immunohistochemical evidence for expansion of the crypt base cell population.Non-steroidal anti-inflammatory drugs and colorectal cancer preventionDiscovery of potent, orally bioavailable, small-molecule inhibitors of WNT signaling from a cell-based pathway screen.The angiogenic switch molecule, secreted FGF-binding protein, an indicator of early stages of pancreatic and colorectal adenocarcinoma.The modifier of Min 2 (Mom2) locus: embryonic lethality of a mutation in the Atp5a1 gene suggests a novel mechanism of polyp suppression.BRCA2 is inactivated late in the development of pancreatic intraepithelial neoplasia: evidence and implicationsA Drosophila homolog of the tumor suppressor gene adenomatous polyposis coli down-regulates beta-catenin but its zygotic expression is not essential for the regulation of Armadillo.Conditional deletion of beta1 integrins in the intestinal epithelium causes a loss of Hedgehog expression, intestinal hyperplasia, and early postnatal lethality.Decreased RXRα is Associated with Increased β-Catenin/TCF4 in (56)Fe-Induced Intestinal Tumors.Mast cells are an essential hematopoietic component for polyp development.Synergy between Apc min and an activated ras mutation is sufficient to induce colon carcinomas.Effects of p53 mutations on apoptosis in mouse intestinal and human colonic adenomas.Cyclooxygenase 2 is up-regulated and localized to macrophages in the intestine of Min mice.Helicobacter hepaticus infection promotes colon tumorigenesis in the BALB/c-Rag2(-/-) Apc(Min/+) mouse.Epigenetic regulation of colon cancer and intestinal stem cellsAdenoma development in familial adenomatous polyposis and MUTYH-associated polyposis: somatic landscape and driver genes.DNA Hypomethylation Contributes to Genomic Instability and Intestinal Cancer Initiation.Tumor angiogenesis: initiation and targeting - therapeutic targeting of an FGF-binding protein, an angiogenic switch molecule, and indicator of early stages of gastrointestinal adenocarcinomas -APC mutations in colorectal tumors with mismatch repair deficiency.An APC:WNT Counter-Current-Like Mechanism Regulates Cell Division Along the Human Colonic Crypt Axis: A Mechanism That Explains How APC Mutations Induce Proliferative Abnormalities That Drive Colon Cancer Development.NSAIDs: Old Drugs Reveal New Anticancer Targets.NSAIDs and Cell Proliferation in Colorectal Cancer.
P2860
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P2860
Inactivation of both APC alleles in human and mouse tumors
description
1994 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած
@hyw
1994 թվականի նոյեմբերին հրատարակված գիտական հոդված
@hy
artículu científicu espublizáu en 1994
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im November 1994 veröffentlichter wissenschaftlicher Artikel
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scientific journal article
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vedecký článok (publikovaný 1994/11/15)
@sk
vědecký článek publikovaný v roce 1994
@cs
wetenschappelijk artikel (gepubliceerd op 1994/11/15)
@nl
наукова стаття, опублікована в листопаді 1994
@uk
مقالة علمية (نشرت في 15-11-1994)
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name
Inactivation of both APC alleles in human and mouse tumors
@ast
Inactivation of both APC alleles in human and mouse tumors
@en
Inactivation of both APC alleles in human and mouse tumors
@nl
type
label
Inactivation of both APC alleles in human and mouse tumors
@ast
Inactivation of both APC alleles in human and mouse tumors
@en
Inactivation of both APC alleles in human and mouse tumors
@nl
prefLabel
Inactivation of both APC alleles in human and mouse tumors
@ast
Inactivation of both APC alleles in human and mouse tumors
@en
Inactivation of both APC alleles in human and mouse tumors
@nl
P2093
P1433
P1476
Inactivation of both APC alleles in human and mouse tumors
@en
P2093
D. B. Levy
K. J. Smith
S. R. Hamilton
Y. Beazer-Barclay
P304
P407
P577
1994-11-15T00:00:00Z