A hypermutation phenotype and somatic MSH6 mutations in recurrent human malignant gliomas after alkylator chemotherapy. - Wikidata - wikimedia - TriplyDB

A hypermutation phenotype and somatic MSH6 mutations in recurrent human malignant gliomas after alkylator chemotherapy.

A hypermutation phenotype and somatic MSH6 mutations in recurrent human malignant gliomas after alkylator chemotherapy.

http://www.wikidata.org/entity/Q48582050

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Mutational profiling of kinases in glioblastoma.Recent advances in the molecular understanding of glioblastoma An integrated genomic analysis of human glioblastoma multiforme Integrated genomic analysis identifies clinically relevant subtypes of glioblastoma characterized by abnormalities in PDGFRA, IDH1, EGFR, and NF1 Comprehensive genomic characterization defines human glioblastoma genes and core pathways Deciphering intratumor heterogeneity and temporal acquisition of driver events to refine precision medicine Tumour heterogeneity and the evolution of polyclonal drug resistance Role of Deficient Mismatch Repair in the Personalized Management of Colorectal Cancer Hypermutation in human cancer genomes: footprints and mechanisms Deciphering signatures of mutational processes operative in human cancer Signatures of mutational processes in human cancer The cancer genome Patterns of somatic mutation in human cancer genomes Targeting the phosphoinositide 3-kinase pathway in cancer The causes and consequences of genetic heterogeneity in cancer evolution Advances in the genetics of glioblastoma: are we reaching critical mass?Realizing the promise of cancer predisposition genes.Changes in allelic imbalances in locally advanced breast cancers after chemotherapy.Mutation analysis of BRAF, MEK1 and MEK2 in 15 ovarian cancer cell lines: implications for therapy.Mismatch repair deficiency does not mediate clinical resistance to temozolomide in malignant glioma Targetable signaling pathway mutations are associated with malignant phenotype in IDH-mutant gliomas.Loss of the mismatch repair protein MSH6 in human glioblastomas is associated with tumor progression during temozolomide treatment.HOXA10 is associated with temozolomide resistance through regulation of the homologous recombinant DNA repair pathway in glioblastoma cell lines.Cancer driver mutations in protein kinase genes Specific biomarkers of receptors, pathways of inhibition and targeted therapies: clinical applications.Recurrent somatic mutation of FAT1 in multiple human cancers leads to aberrant Wnt activation.Mutational analysis reveals the origin and therapy-driven evolution of recurrent glioma Alkylation sensitivity screens reveal a conserved cross-species functionome.Intraclonal diversity in follicular lymphoma analyzed by quantitative ultradeep sequencing of noncoding regions Mismatch repair deficiency is an uncommon mechanism of alkylator resistance in pediatric malignant gliomas: a report from the Children's Oncology Group.Antibody-directed enzyme prodrug therapy (ADEPT) for cancer.Major differences between tumor and normal human cell fates after exposure to chemotherapeutic monofunctional alkylator Tousled-like kinase-dependent phosphorylation of Rad9 plays a role in cell cycle progression and G2/M checkpoint exit.Whole-genome and multisector exome sequencing of primary and post-treatment glioblastoma reveals patterns of tumor evolution Combined Flt3L/TK gene therapy induces immunological surveillance which mediates an immune response against a surrogate brain tumor neoantigen.Our changing view of the genomic landscape of cancer.Ultradeep analysis of tumor heterogeneity in regions of somatic hypermutation Physiologic MRI for assessment of response to therapy and prognosis in glioblastoma.A transcriptomic signature mediated by HOXA9 promotes human glioblastoma initiation, aggressiveness and resistance to temozolomide Evolution of DNA repair defects during malignant progression of low-grade gliomas after temozolomide treatment.

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P2860

A hypermutation phenotype and somatic MSH6 mutations in recurrent human malignant gliomas after alkylator chemotherapy.

http://www.wikidata.org/entity/Q48582050

description

2006 nî lūn-bûn

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2006年の論文

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年學術文章

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2006年學術文章

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name

A hypermutation phenotype and ...... after alkylator chemotherapy.

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A hypermutation phenotype and ...... after alkylator chemotherapy.

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type

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A hypermutation phenotype and ...... after alkylator chemotherapy.

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A hypermutation phenotype and ...... after alkylator chemotherapy.

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A hypermutation phenotype and ...... after alkylator chemotherapy.

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A hypermutation phenotype and ...... after alkylator chemotherapy.

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A hypermutation phenotype and ...... after alkylator chemotherapy.

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Adam Butler

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