Reverting estrogen-receptor-negative phenotype in HER-2-overexpressing advanced breast cancer patients exposed to trastuzumab plus chemotherapy - Wikidata - awgldk - TriplyDB

Reverting estrogen-receptor-negative phenotype in HER-2-overexpressing advanced breast cancer patients exposed to trastuzumab plus chemotherapy

Reverting estrogen-receptor-negative phenotype in HER-2-overexpressing advanced breast cancer patients exposed to trastuzumab plus chemotherapy

http://www.wikidata.org/entity/Q34480666

about

Phosphatidylinositol 3-kinase and antiestrogen resistance in breast cancer Putative biomarkers and targets of estrogen receptor negative human breast cancer Resistance to therapy in estrogen receptor positive and human epidermal growth factor 2 positive breast cancers: progress with latest therapeutic strategies The role of HER2 in cancer therapy and targeted drug delivery A phase I-II study of combined blockade of the ErbB receptor network with trastuzumab and gefitinib in patients with HER2 (ErbB2)-overexpressing metastatic breast cancer.Targeted Therapy in Breast Cancer.Adaptive changes result in activation of alternate signaling pathways and acquisition of resistance to aromatase inhibitors HER2: biology, detection, and clinical implications Headway in resistance to endocrine therapy in breast cancer.Molecular alterations between the primary breast cancer and the subsequent locoregional/metastatic tumor.Mutations in the phosphatidylinositol 3-kinase pathway: role in tumor progression and therapeutic implications in breast cancer.Different mechanisms for resistance to trastuzumab versus lapatinib in HER2-positive breast cancers--role of estrogen receptor and HER2 reactivation.Femara and the future: tailoring treatment and combination therapies with Femara.Does lapatinib work against HER2-negative breast cancers?BCAR4 induces antioestrogen resistance but sensitises breast cancer to lapatinib Potential use of humanized antibodies in the treatment of breast cancer.Mechanisms of endocrine resistance in breast cancer.Integration of endocrine therapy with targeted agents.Tamoxifen resistance in breast cancer.Resveratrol fuels HER2 and ERα-positive breast cancer behaving as proteasome inhibitor.Human epidermal growth factor receptor 2 (HER2)-positive and hormone receptor-positive breast cancer: new insights into molecular interactions and clinical implications.Therapeutic targeting of ERBB2 in breast cancer: understanding resistance in the laboratory and combating it in the clinic.Proteasome inhibitors prevent bi-directional HER2/estrogen-receptor cross-talk leading to cell death in endocrine and lapatinib-resistant HER2+/ER+ breast cancer cells.Correction: Reverting estrogen-receptor-negative phenotype in HER-2-overexpressing advanced breast cancer patients exposed to trastuzumab plus chemotherapy.Mechanisms for estrogen receptor expression in human cancer Clinical benefit of fulvestrant monotherapy in the multimodal treatment of hormone receptor and HER2 positive advanced breast cancer: a case series

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P2860

Reverting estrogen-receptor-negative phenotype in HER-2-overexpressing advanced breast cancer patients exposed to trastuzumab plus chemotherapy

http://www.wikidata.org/entity/Q34480666

description

2005 nî lūn-bûn

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2005 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

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2005 թվականի դեկտեմբերին հրատարակված գիտական հոդված

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2005年の論文

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2005年論文

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2005年論文

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2005年論文

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2005年論文

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2005年論文

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2005年论文

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name

Reverting estrogen-receptor-ne ...... trastuzumab plus chemotherapy

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Reverting estrogen-receptor-ne ...... trastuzumab plus chemotherapy

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Reverting estrogen-receptor-ne ...... trastuzumab plus chemotherapy

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Reverting estrogen-receptor-ne ...... trastuzumab plus chemotherapy

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Reverting estrogen-receptor-ne ...... trastuzumab plus chemotherapy

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Reverting estrogen-receptor-ne ...... trastuzumab plus chemotherapy

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Breast Cancer Research

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Reverting estrogen-receptor-ne ...... trastuzumab plus chemotherapy

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Andrea Rocca

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Aron Goldhirsch

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Elisabetta Munzone

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Franco Nolè

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Giuseppe Curigliano

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Giuseppe Renne

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Giuseppina Bonizzi

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P2860

Tamoxifen for early breast cancer: an overview of the randomised trials. Early Breast Cancer Trialists' Collaborative Group

Role of MAP kinase in the enhanced cell proliferation of long term estrogen deprived human breast cancer cells.

Changes in estrogen receptor, progesterone receptor, and pS2 expression in tamoxifen-resistant human breast cancer.

Constitutive activation of NF-kappaB during progression of breast cancer to hormone-independent growth.

HER-2/neu gene amplification characterized by fluorescence in situ hybridization: poor prognosis in node-negative breast carcinomas.

A cytoplasmic substrate of mitogen-activated protein kinase is responsible for estrogen receptor-alpha down-regulation in breast cancer cells: the role of nuclear factor-kappaB.

Inhibition of mitogen-activated protein kinase kinase selectively inhibits cell proliferation in human breast cancer cells displaying enhanced insulin-like growth factor I-mediated mitogen-activated protein kinase activation.

Demethylation of the estrogen receptor gene in estrogen receptor-negative breast cancer cells can reactivate estrogen receptor gene expression.

Hyperactivation of MAPK induces loss of ERalpha expression in breast cancer cells.

Phosphorylation of ERK1/2 mitogen-activated protein kinase is associated with poor response to anti-hormonal therapy and decreased patient survival in clinical breast cancer.

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10.1186/BCR1366

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