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Article

Functional KRAS mutations and a potential role for PI3K/AKT activation in Wilms tumors.

Molecular oncology - 1 Apr 2017

Polosukhina Dina, Love Harold D, Correa Hernan, Su Zengliu, Dahlman Kimberly B, Pao William, Moses Harold L, Arteaga Carlos L, Lovvorn Harold N, Zent Roy, Clark Peter E

Abstract excerpt

Wilms tumor (WT) is the most common renal neoplasm of childhood and affects 1 in 10 000 children aged less than 15 years. These embryonal tumors are thought to arise from primitive nephrogenic rests that derive from the metanephric mesenchyme during kidney development and are characterized partly by increased Wnt/β-catenin signaling. We previously showed that coordinate activation of Ras and β-catenin accelerates...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 28188683
DOI: 10.1002/1878-0261.12044
PMCID: PMC5378659

Genes

KRAS

Provenance

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Functional KRAS mutations and a potential role for PI3K/AKT activation in Wilms tumors.PMID 28188683Read ↗

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Hyperactivation of Ha-ras oncogene, but not Ink4a/Arf deficiency, triggers bladder tumorigenesis.Semantic proximity Read ↗

KrasP34R and KrasT58I mutations induce distinct RASopathy phenotypes in mice.Semantic proximity Read ↗

The tumor suppressor WT1 drives progenitor cell progression and epithelialization to prevent Wilms tumorigenesis in human kidney organoidsSemantic proximity Read ↗

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Wilms tumor cells with WT1 mutations have characteristic features of mesenchymal stem cells and express molecular markers of paraxial mesoderm.Semantic proximity Read ↗

Mutational activation of the beta-catenin proto-oncogene is a common event in the development of Wilms' tumors.Semantic proximity Read ↗

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