Resistance to BRAF inhibition in BRAF-mutant colon cancer can be overcome with PI3K inhibition or demethylating agents. - Wikidata - wikimedia - TriplyDB

Resistance to BRAF inhibition in BRAF-mutant colon cancer can be overcome with PI3K inhibition or demethylating agents.

Resistance to BRAF inhibition in BRAF-mutant colon cancer can be overcome with PI3K inhibition or demethylating agents.

http://www.wikidata.org/entity/Q39224151

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Cancer genome landscapes One-Carbon Metabolism in Prostate Cancer: The Role of Androgen Signaling The Inositide Signaling Pathway As a Target for Treating Gastric Cancer and Colorectal Cancer The value of genomics in dissecting the RAS-network and in guiding therapeutics for RAS-driven cancers Serrated colorectal cancer: Molecular classification, prognosis, and response to chemotherapy Advances in targeted and immunobased therapies for colorectal cancer in the genomic era Somatic DNA mutation analysis in targeted therapy of solid tumours BRAF mutant colorectal cancer as a distinct subset of colorectal cancer: clinical characteristics, clinical behavior, and response to targeted therapies BRAF Mutation in Colorectal Cancer: An Update Toward a Molecular Classification of Colorectal Cancer: The Role of BRAF Time to re-consider the meaning of BRAF V600E mutation in papillary thyroid carcinoma Molecular alterations and biomarkers in colorectal cancer Molecular Technologies in the Clinical Diagnostic Laboratory The next steps in next-gen sequencing of cancer genomes Primary and acquired resistance to EGFR-targeted therapies in colorectal cancer: impact on future treatment strategies Dual pharmacological targeting of the MAP kinase and PI3K/mTOR pathway in preclinical models of colorectal cancer Discovery and SAR of Novel 2,3-Dihydroimidazo[1,2-c]quinazoline PI3K Inhibitors: Identification of Copanlisib (BAY 80-6946)Concomitant BRAF and PI3K/mTOR blockade is required for effective treatment of BRAF(V600E) colorectal cancer.Detailed imaging and genetic analysis reveal a secondary BRAF(L505H) resistance mutation and extensive intrapatient heterogeneity in metastatic BRAF mutant melanoma patients treated with vemurafenib.Combined BRAF and MEK Inhibition With Dabrafenib and Trametinib in BRAF V600-Mutant Colorectal Cancer.Phase II Pilot Study of Vemurafenib in Patients With Metastatic BRAF-Mutated Colorectal Cancer.Beyond RAS and BRAF: a target rich disease that is ripe for picking RAS and BRAF in metastatic colorectal cancer management Mechanisms of resistance to anti-epidermal growth factor receptor inhibitors in metastatic colorectal cancer Negative feedback regulation of the ERK1/2 MAPK pathway Prioritizing therapeutic targets using patient-derived xenograft models PI3K and cancer: lessons, challenges and opportunities Translating genomic profiling to gastrointestinal cancer treatment.A spatial simulation approach to account for protein structure when identifying non-random somatic mutations BRAF mutations: signaling, epidemiology, and clinical experience in multiple malignancies.Genomic sequencing: assessing the health care system, policy, and big-data implications.Resistance to Raf inhibition in cancer.Clinical responses to ERK inhibition in BRAFV600E-mutant colorectal cancer predicted using a computational model.Change or die: targeting adaptive signaling to kinase inhibition in cancer cells.Biological and molecular effects of small molecule kinase inhibitors on low-passage human colorectal cancer cell lines.Clinical development of dabrafenib in BRAF mutant melanoma and other malignancies.The MAPK pathway across different malignancies: a new perspective.Effects of BRAF mutations and BRAF inhibition on immune responses to melanoma Biology of colorectal cancer.Activating PIK3CA mutations coexist with BRAF or NRAS mutations in a limited fraction of melanomas.

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Resistance to BRAF inhibition in BRAF-mutant colon cancer can be overcome with PI3K inhibition or demethylating agents.

http://www.wikidata.org/entity/Q39224151

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Resistance to BRAF inhibition ...... ition or demethylating agents.

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Resistance to BRAF inhibition ...... ition or demethylating agents.

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Resistance to BRAF inhibition ...... ition or demethylating agents.

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Resistance to BRAF inhibition ...... ition or demethylating agents.

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Resistance to BRAF inhibition ...... ition or demethylating agents.

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Resistance to BRAF inhibition ...... ition or demethylating agents.

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Clinical Cancer Research

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Resistance to BRAF inhibition ...... ition or demethylating agents.

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Chun C Tsao

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Farshid Dayyani

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Feng Tian

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Gary E Gallick

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Gordon B Mills

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Jayesh Desai

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John M Mariadason

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Michael A Davies

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Muling Mao

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Robert Lemos

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P2860

Emergence of KRAS mutations and acquired resistance to anti-EGFR therapy in colorectal cancer

Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation

Improved survival with vemurafenib in melanoma with BRAF V600E mutation

Analysis of molecular inversion probe performance for allele copy number determination

The COSMIC (Catalogue of Somatic Mutations in Cancer) database and website

Discovery of a selective inhibitor of oncogenic B-Raf kinase with potent antimelanoma activity

Functional promoter upstream p53 regulatory sequence of IGFBP3 that is silenced by tumor specific methylation

Dissecting therapeutic resistance to RAF inhibition in melanoma by tumor genomic profiling.

Receptor tyrosine kinases exert dominant control over PI3K signaling in human KRAS mutant colorectal cancers.

Antitumor activity of BRAF inhibitor vemurafenib in preclinical models of BRAF-mutant colorectal cancer.

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657-667

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Ignacio I Wistuba

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23251002

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