BRAF fusions identified in melanomas have variable treatment responses and phenotypes

MEK drives BRAF activation through allosteric control of KSR proteins

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Identification of NTRK3 Fusions in Childhood Melanocytic Neoplasms

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ALK Inhibitor Response in Melanomas Expressing EML4-ALK Fusions and Alternate ALK Isoforms

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Targeting the MAPK Signaling Pathway in Cancer: Promising Preclinical Activity with the Novel Selective ERK1/2 Inhibitor BVD-523 (Ulixertinib)

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Oncogenic BRAF fusions in mucosal melanomas activate the MAPK pathway and are sensitive to MEK/PI3K inhibition or MEK/CDK4/6 inhibition

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Feedback activation of neurofibromin terminates growth factor-induced Ras activation

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BRAFV600E Mutations in High-Grade Colorectal Neuroendocrine Tumors May Predict Responsiveness to BRAF-MEK Combination Therapy

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Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies

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Structural and Thermodynamic Properties of Septin 3 Investigated by Small-Angle X-Ray Scattering

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The role ofBRAFmutations in primary melanoma growth rate and survival

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Colorectal Cancer Heterogeneity and Targeted Therapy: A Case for Molecular Disease Subtypes

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Pathogenetic Implications of BRAF Mutation Distribution in Stage IV Melanoma Patients

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The distribution ofBRAFgene fusions in solid tumors and response to targeted therapy

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Targeted Therapy for Patients with BRAF-Mutant Lung Cancer Results from the European EURAF Cohort

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Clinical activity of the MEK inhibitor trametinib in metastatic melanoma containingBRAFkinase fusion

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Clonal status of actionable driver events and the timing of mutational processes in cancer evolution

(2015) Nicholas McGranahan et al.   Science Translational Medicine

Sustained proliferation in cancer: Mechanisms and novel therapeutic targets

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Tissue invasion and metastasis: Molecular, biological and clinical perspectives

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An Efficient Method for Identifying Gene Fusions by Targeted RNA Sequencing from Fresh Frozen and FFPE Samples

(2015) Jonathan A. Scolnick et al.   PLoS One

BRAF Fusions Define a Distinct Molecular Subset of Melanomas with Potential Sensitivity to MEK Inhibition

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Cancer immunotherapies, their safety and toxicity

(2013) Gheath Alatrash et al.   Expert Opinion On Drug Safety

Recurrent BRAF kinase fusions in melanocytic tumors offer an opportunity for targeted therapy

(2013) Thomas Botton et al.   Pigment Cell & Melanoma Research

Paradoxical activation and RAF inhibitor resistance of BRAF protein kinase fusions characterizing pediatric astrocytomas

(2013) A. J. Sievert et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

Concurrent MEK2 Mutation and BRAF Amplification Confer Resistance to BRAF and MEK Inhibitors in Melanoma

(2013) Jessie Villanueva et al.   Cell Reports

RET, ROS1 and ALK fusions in lung cancer

(2012) Kengo Takeuchi et al.   NATURE MEDICINE

NIH Image to ImageJ: 25 years of image analysis

(2012) Caroline A Schneider et al.   NATURE METHODS

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(2012) John J. Tentler et al.   Nature Reviews Clinical Oncology

Oncogenic B-Raf signaling in melanoma cells controls a network of microRNAs with combinatorial functions

(2012) K L Couts et al.   ONCOGENE

Transmembrane helix dimerization: Beyond the search for sequence motifs

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

(2011) Poulikos I. Poulikakos et al.   NATURE

Regulation of RAF Activity by 14-3-3 Proteins

(2008) Andreas Fischer et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

AberrantBRAFsplicing as an alternative mechanism for oncogenic B-Raf activation in thyroid carcinoma

(2008) Essa Y Baitei et al.   JOURNAL OF PATHOLOGY