Acquired resistance to BRAF inhibition can confer cross-resistance to combined BRAF/MEK inhibition. (Q39375855)

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26 January 2020

title

Acquired resistance to BRAF inhibition can confer cross-resistance to combined BRAF/MEK inhibition (English)

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4

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26 January 2020

Richard F. Kefford

5

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26 January 2020

author name string

Kavitha Gowrishankar

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26 January 2020

Stephanie Snoyman

2

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26 January 2020

Gulietta M Pupo

3

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26 January 2020

Helen Rizos

6

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26 January 2020

language of work or name

English

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publication date

22 March 2012

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Journal of Investigative Dermatology

26 January 2020

published in

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volume

132

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issue

7

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26 January 2020

page(s)

1850-1859

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describes a project that uses

26 January 2020

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Reversing melanoma cross-resistance to BRAF and MEK inhibitors by co-targeting the AKT/mTOR pathway.

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7 January 2021

Clinical efficacy of a RAF inhibitor needs broad target blockade in BRAF-mutant melanoma

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Improved survival with vemurafenib in melanoma with BRAF V600E mutation

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BRAF gene amplification can promote acquired resistance to MEK inhibitors in cancer cells harboring the BRAF V600E mutation

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Mutations of the BRAF gene in human cancer

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Transcriptional pathway signatures predict MEK addiction and response to selumetinib (AZD6244)

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In melanoma, RAS mutations are accompanied by switching signaling from BRAF to CRAF and disrupted cyclic AMP signaling

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MEK1 mutations confer resistance to MEK and B-RAF inhibition

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Inhibition of Mutated, Activated BRAF in Metastatic Melanoma

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Enforced expression of p14ARF induces p53-dependent cell cycle arrest but not apoptosis.

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GSK1120212 (JTP-74057) Is an Inhibitor of MEK Activity and Activation with Favorable Pharmacokinetic Properties for Sustained In Vivo Pathway Inhibition

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Oncogene-induced senescence does not require the p16(INK4a) or p14ARF melanoma tumor suppressors.

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Phase I/II study to assess safety, pharmacokinetics, and efficacy of the oral MEK 1/2 inhibitor GSK1120212 (GSK212) dosed in combination with the oral BRAF inhibitor GSK2118436 (GSK436)

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Combined targeting of BRAF and CRAF or BRAF and PI3K effector pathways is required for efficacy in NRAS mutant tumors

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MEK-independent survival of B-RAFV600E melanoma cells selected for resistance to apoptosis induced by the RAF inhibitor PLX4720.

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COT drives resistance to RAF inhibition through MAP kinase pathway reactivation

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7 January 2021

Amplification of the driving oncogene, KRAS or BRAF, underpins acquired resistance to MEK1/2 inhibitors in colorectal cancer cells.

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Elevated CRAF as a potential mechanism of acquired resistance to BRAF inhibition in melanoma

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7 January 2021

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

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7 January 2021

The "SWOT" of BRAF inhibition in melanoma: RAF inhibitors, MEK inhibitors or both?

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PTEN loss confers BRAF inhibitor resistance to melanoma cells through the suppression of BIM expression

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7 January 2021

RAF inhibitor resistance is mediated by dimerization of aberrantly spliced BRAF(V600E)

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7 January 2021

Dual inhibition of V600EBRAF and the PI3K/AKT/mTOR pathway cooperates to induce apoptosis in melanoma cells through a MEK-independent mechanism

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7 January 2021

IGFBP7 is not required for B-RAF-induced melanocyte senescence

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7 January 2021

Combinatorial treatments that overcome PDGFRβ-driven resistance of melanoma cells to V600EB-RAF inhibition

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7 January 2021

Understanding melanoma signaling networks as the basis for molecular targeted therapy

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7 January 2021

BRAF mutation predicts sensitivity to MEK inhibition

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7 January 2021

The mammalian MAPK/ERK pathway exhibits properties of a negative feedback amplifier

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7 January 2021

Acquired resistance to BRAF inhibitors mediated by a RAF kinase switch in melanoma can be overcome by cotargeting MEK and IGF-1R/PI3K

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7 January 2021

Mechanism of activation of the RAF-ERK signaling pathway by oncogenic mutations of B-RAF

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7 January 2021

Comprehensive dissection of PDGF-PDGFR signaling pathways in PDGFR genetically defined cells

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7 January 2021