Oncogenic PI3K/AKT promotes the step-wise evolution of combination BRAF/MEK inhibitor resistance in melanoma

Overall Survival and Durable Responses in Patients WithBRAFV600–Mutant Metastatic Melanoma Receiving Dabrafenib Combined With Trametinib

(2016) Georgina V. Long et al.   JOURNAL OF CLINICAL ONCOLOGY

Tunable-Combinatorial Mechanisms of Acquired Resistance Limit the Efficacy of BRAF/MEK Cotargeting but Result in Melanoma Drug Addiction

(2015) Gatien Moriceau et al.   CANCER CELL

Non-genomic and Immune Evolution of Melanoma Acquiring MAPKi Resistance

(2015) Willy Hugo et al.   CELL

Acquired BRAF inhibitor resistance: A multicenter meta-analysis of the spectrum and frequencies, clinical behaviour, and phenotypic associations of resistance mechanisms

(2015) Douglas B. Johnson et al.   EUROPEAN JOURNAL OF CANCER

MITF and c-Jun antagonism interconnects melanoma dedifferentiation with pro-inflammatory cytokine responsiveness and myeloid cell recruitment

(2015) Stefanie Riesenberg et al.   Nature Communications

The Molecular Signatures Database Hallmark Gene Set Collection

(2015) Arthur Liberzon et al.   Cell Systems

Loss of NF1 in Cutaneous Melanoma Is Associated with RAS Activation and MEK Dependence

(2014) Moriah H. Nissan et al.   CANCER RESEARCH

BRAF Inhibitor Resistance Mechanisms in Metastatic Melanoma: Spectrum and Clinical Impact

(2014) H. Rizos et al.   CLINICAL CANCER RESEARCH

Differential activity of MEK and ERK inhibitors in BRAF inhibitor resistant melanoma

(2014) Matteo S. Carlino et al.   Molecular Oncology

A Melanoma Cell State Distinction Influences Sensitivity to MAPK Pathway Inhibitors

(2014) D. J. Konieczkowski et al.   Cancer Discovery

Tumor Genetic Analyses of Patients with Metastatic Melanoma Treated with the BRAF Inhibitor Dabrafenib (GSK2118436)

(2013) K. L. Nathanson et al.   CLINICAL CANCER RESEARCH

Pharmacodynamic Effects and Mechanisms of Resistance to Vemurafenib in Patients With Metastatic Melanoma

(2013) Kerstin Trunzer et al.   JOURNAL OF CLINICAL ONCOLOGY

MEK162 for patients with advanced melanoma harbouring NRAS or Val600 BRAF mutations: a non-randomised, open-label phase 2 study

(2013) Paolo A Ascierto et al.   LANCET ONCOLOGY

A Novel AKT1 Mutant Amplifies an Adaptive Melanoma Response to BRAF Inhibition

(2013) H. Shi et al.   Cancer Discovery

Acquired Resistance and Clonal Evolution in Melanoma during BRAF Inhibitor Therapy

(2013) H. Shi et al.   Cancer Discovery

Resistance to Irreversible EGF Receptor Tyrosine Kinase Inhibitors through a Multistep Mechanism Involving the IGF1R Pathway

(2012) A. B. Cortot et al.   CANCER RESEARCH

Tumour micro-environment elicits innate resistance to RAF inhibitors through HGF secretion

(2012) Ravid Straussman et al.   NATURE

The crossregulation between ERK and PI3K signaling pathways determines the tumoricidal efficacy of MEK inhibitor

(2012) Jae-Kyung Won et al.   Journal of Molecular Cell Biology

Dissecting Therapeutic Resistance to RAF Inhibition in Melanoma by Tumor Genomic Profiling

(2011) Nikhil Wagle et al.   JOURNAL OF CLINICAL ONCOLOGY

Concurrent loss of the PTEN and RB1 tumor suppressors attenuates RAF dependence in melanomas harboring V600EBRAF

(2011) F Xing et al.   ONCOGENE

The Ras-ERK and PI3K-mTOR pathways: cross-talk and compensation

(2011) Michelle C. Mendoza et al.   TRENDS IN BIOCHEMICAL SCIENCES

Recovery of phospho-ERK activity allows melanoma cells to escape from BRAF inhibitor therapy

(2010) K H T Paraiso et al.   BRITISH JOURNAL OF CANCER

Akt3-Mediated Resistance to Apoptosis in B-RAF-Targeted Melanoma Cells

(2010) Y. Shao et al.   CANCER RESEARCH

Oncogene-Induced Senescence Does Not Require the p16INK4a or p14ARF Melanoma Tumor Suppressors

(2009) Sebastian Haferkamp et al.   JOURNAL OF INVESTIGATIVE DERMATOLOGY

Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1

(2009) David A. Barbie et al.   NATURE

V600EBRAF is associated with disabled feedback inhibition of RAF-MEK signaling and elevated transcriptional output of the pathway

(2009) C. A. Pratilas et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA