Tumor regionality in the mouse intestine reflects the mechanism of loss of Apc function. - Wikidata - wikimedia - TriplyDB

Tumor regionality in the mouse intestine reflects the mechanism of loss of Apc function.

Tumor regionality in the mouse intestine reflects the mechanism of loss of Apc function.

http://www.wikidata.org/entity/Q36448895

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Understanding phenotypic variation in rodent models with germline Apc mutations In utero and neonatal sensitivity of ApcMin/+ mice to radiation-induced intestinal neoplasia Potential implication of the chemical properties and bioactivity of nitrone spin traps for therapeutics Anti-cancer activity of nitrones in the Apc(Min/+) model of colorectal cancer Distinguishing between cancer driver and passenger gene alteration candidates via cross-species comparison: a pilot study.Polyclonality of familial murine adenomas: analyses of mouse chimeras with low tumor multiplicity suggest short-range interactions Krüppel-like factor 5 is a crucial mediator of intestinal tumorigenesis in mice harboring combined ApcMin and KRASV12 mutations.Genetic basis of variation in adenoma multiplicity in ApcMin/+ Mom1S mice.Inflammatory cues acting on the adult intestinal stem cells and the early onset of cancer (review).A locus on chromosome 8 controlling tumor regionality-a new type of tumor diversity in the mouse lung Complete deletion of Apc results in severe polyposis in mice.The modifier of Min 2 (Mom2) locus: embryonic lethality of a mutation in the Atp5a1 gene suggests a novel mechanism of polyp suppression.Advanced Intestinal Cancers often Maintain a Multi-Ancestral Architecture.Atm is a negative regulator of intestinal neoplasia.Transcriptional recapitulation and subversion of embryonic colon development by mouse colon tumor models and human colon cancer.Helicobacter hepaticus infection promotes colon tumorigenesis in the BALB/c-Rag2(-/-) Apc(Min/+) mouse.More than two decades of Apc modeling in rodents The pleiotropic phenotype of Apc mutations in the mouse: allele specificity and effects of the genetic background.Cyp1b1 exerts opposing effects on intestinal tumorigenesis via exogenous and endogenous substrates NHERF1/EBP50 Suppresses Wnt-β-Catenin Pathway-Driven Intestinal Neoplasia.APC and its modifiers in colon cancer.Role of beta-catenin in the adult liver.Lung tumor location and lymphocyte infiltration in mice are genetically determined.Chir99021 and Valproic acid reduce the proliferative advantage of Apc mutant cells.Cytoskeleton out of the cupboard: colon cancer and cytoskeletal changes induced by loss of APC.

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Tumor regionality in the mouse intestine reflects the mechanism of loss of Apc function.

http://www.wikidata.org/entity/Q36448895

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2004 nî lūn-bûn

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2004年の論文

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2004年学术文章

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2004年学术文章

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2004年学术文章

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2004年学术文章

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2004年學術文章

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2004年學術文章

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2004年學術文章

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Tumor regionality in the mouse intestine reflects the mechanism of loss of Apc function.

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Tumor regionality in the mouse intestine reflects the mechanism of loss of Apc function.

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Tumor regionality in the mouse intestine reflects the mechanism of loss of Apc function.

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Tumor regionality in the mouse intestine reflects the mechanism of loss of Apc function.

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Tumor regionality in the mouse intestine reflects the mechanism of loss of Apc function.

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Tumor regionality in the mouse intestine reflects the mechanism of loss of Apc function.

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PNAS.0403338101

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Proceedings of the National Academy of Sciences of the United States of America

P1476

Tumor regionality in the mouse intestine reflects the mechanism of loss of Apc function.

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Alanna White

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Alex R Shoemaker

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Kevin M Haigis

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Peter D Hoff

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Richard B Halberg

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William F Dove

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P2860

A targeted chain-termination mutation in the mouse Apc gene results in multiple intestinal tumors

The human mutator gene homolog MSH2 and its association with hereditary nonpolyposis colon cancer

Involvement of mouse Mlh1 in DNA mismatch repair and meiotic crossing over

Inactivation of the mouse Msh2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancer

Tumour susceptibility and spontaneous mutation in mice deficient in Mlh1, Pms1 and Pms2 DNA mismatch repair

Mlh1 deficiency enhances several phenotypes of Apc(Min)/+ mice

Tumorigenesis in Mlh1 and Mlh1/Apc1638N mutant mice

Mom1 is a semi-dominant modifier of intestinal adenoma size and multiplicity in Min/+ mice

A dominant mutation that predisposes to multiple intestinal neoplasia in the mouse

Multiple intestinal neoplasia caused by a mutation in the murine homolog of the APC gene

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