PIK3CA mutations in in situ and invasive breast carcinomas. - Wikidata - wikimedia - TriplyDB

PIK3CA mutations in in situ and invasive breast carcinomas.

PIK3CA mutations in in situ and invasive breast carcinomas.

http://www.wikidata.org/entity/Q34001222

about

Mosaic overgrowth with fibroadipose hyperplasia is caused by somatic activating mutations in PIK3CA Somatic mutations in breast and serous ovarian cancer young patients: a systematic review and meta-analysis Phosphatidylinositol 3-kinase and antiestrogen resistance in breast cancer Appraisal of the technologies and review of the genomic landscape of ductal carcinoma in situ of the breast PIK3CA mutations in breast cancer: reconciling findings from preclinical and clinical data PAK1 is a breast cancer oncogene that coordinately activates MAPK and MET signaling Physiological levels of Pik3ca(H1047R) mutation in the mouse mammary gland results in ductal hyperplasia and formation of ERα-positive tumors ECM microenvironment regulates collective migration and local dissemination in normal and malignant mammary epithelium.PI3K pathway activation in high-grade ductal carcinoma in situ--implications for progression to invasive breast carcinoma.Recurrent inflammatory myofibroblastic tumors harboring PIK3CA and KIT mutations.Evolutionary pathways in BRCA1-associated breast tumors.PI3K pathway mutations and PTEN levels in primary and metastatic breast cancer.Cell-lineage heterogeneity and driver mutation recurrence in pre-invasive breast neoplasia.Genomic differences between pure ductal carcinoma in situ and synchronous ductal carcinoma in situ with invasive breast cancer.Mutations in the phosphatidylinositol 3-kinase pathway: role in tumor progression and therapeutic implications in breast cancer.Undifferentiated pleomorphic sarcoma with co-existence of KRAS/PIK3CA mutations Integrated molecular pathway analysis informs a synergistic combination therapy targeting PTEN/PI3K and EGFR pathways for basal-like breast cancer Immortalization of normal human mammary epithelial cells in two steps by direct targeting of senescence barriers does not require gross genomic alterations.An "elite hacker": breast tumors exploit the normal microenvironment program to instruct their progression and biological diversity.Single-cell genetic analysis of ductal carcinoma in situ and invasive breast cancer reveals enormous tumor heterogeneity yet conserved genomic imbalances and gain of MYC during progression.Initiating breast cancer by PIK3CA mutation PIK3CA mutation impact on survival in breast cancer patients and in ERα, PR and ERBB2-based subgroups.A Molecular Portrait of High-Grade Ductal Carcinoma In Situ.PIK3CA(H1047R)- and Her2-initiated mammary tumors escape PI3K dependency by compensatory activation of MEK-ERK signaling.Infiltrating epitheliosis of the breast: characterization of histological features, immunophenotype and genomic profile Genomic and mutational profiling of ductal carcinomas in situ and matched adjacent invasive breast cancers reveals intra-tumour genetic heterogeneity and clonal selection.Expression of PIK3CA mutant E545K in the mammary gland induces heterogeneous tumors but is less potent than mutant H1047R.Constitutively activated PI3K accelerates tumor initiation and modifies histopathology of breast cancer.Targeting mTOR pathway inhibits tumor growth in different molecular subtypes of triple-negative breast cancers.Targeting the PI3K signaling pathway in cancer therapy.Mouse models of PIK3CA mutations: one mutation initiates heterogeneous mammary tumors.Cellular evidence for selfish spermatogonial selection in aged human testes.Clinical management of breast cancer heterogeneity.Genomic tumor evolution of breast cancer.Ductal carcinoma in situ - update on risk assessment and management.Genome evolution in ductal carcinoma in situ: invasion of the clones.Oncogenic PIK3CA mutations in lobular breast cancer progression.PIK3CA mutations rarely demonstrate genotypic intratumoral heterogeneity and are selected for in breast cancer progression.Ductal Carcinoma In Situ Biology, Biomarkers, and Diagnosis.ndmaSNF: cancer subtype discovery based on integrative framework assisted by network diffusion model.

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PIK3CA mutations in in situ and invasive breast carcinomas.

http://www.wikidata.org/entity/Q34001222

description

2010 nî lūn-bûn

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2010 թուականի Յունիսին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի հունիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

PIK3CA mutations in in situ and invasive breast carcinomas.

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PIK3CA mutations in in situ and invasive breast carcinomas.

@en

PIK3CA mutations in in situ and invasive breast carcinomas.

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type

label

PIK3CA mutations in in situ and invasive breast carcinomas.

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PIK3CA mutations in in situ and invasive breast carcinomas.

@en

PIK3CA mutations in in situ and invasive breast carcinomas.

@nl

prefLabel

PIK3CA mutations in in situ and invasive breast carcinomas.

@ast

PIK3CA mutations in in situ and invasive breast carcinomas.

@en

PIK3CA mutations in in situ and invasive breast carcinomas.

@nl

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0008-5472.CAN-08-2660

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Cancer Research

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PIK3CA mutations in in situ and invasive breast carcinomas.

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Alexander Miron

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D Craig Allred

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Daniel Carrasco

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Deborah Dillon

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Eun Yoon Cho

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Gretchen Lewis

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Hailun Li

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Hee Jung Kim

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J Dirk Iglehart

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Kornelia Polyak

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P2860

Profiling critical cancer gene mutations in clinical tumor samples

A transforming mutation in the pleckstrin homology domain of AKT1 in cancer

High frequency of mutations of the PIK3CA gene in human cancers

Phosphatidylinositol-3-kinase and AKT1 mutations occur early in breast carcinoma.

PIK3CA mutations mostly begin to develop in ductal carcinoma of the breast.

A rapid, sensitive, reproducible and cost-effective method for mutation profiling of colon cancer and metastatic lymph nodes.

Recurrent gross mutations of the PTEN tumor suppressor gene in breast cancers with deficient DSB repair.

PI3-kinase and TOR: PIKTORing cell growth.

Oncogenic PI3K and its role in cancer.

Beyond PTEN mutations: the PI3K pathway as an integrator of multiple inputs during tumorigenesis.

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5674-5678

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