The V600E mutation in BRAF is a cancer hot spot because it opens the activation segment through destabilization of autoinhibitory interactions, but it does not significantly impair folding of the inactive or active kinase domain.

Genetic analyses reveal how CDX2 and BRAF defects seen in serrated colorectal cancer (CRCs), a poor prognosis CRC subset, cooperate in tumorigenesis in humans and in a mouse cancer model.

Oncogenic BRAF causes genome duplication and reversible growth arrest in human melanocytes that is conditional on microRNA expression and differentiation state.

Two of the most commonly mutated growth factor pathways induce a deadly feature of lung adenocarcinoma.

Pre-clinical and patient data show that inhibition of autophagy with an approved, inexpensive, well-tolerated drug can overcome resistance to BRAF^V600E inhibition in multiple brain tumor subtypes with different resistance mechanisms.

RNF43 interacts with receptor complexes of the Wnt/PCP signaling and its enzymatic activity results in the reduced cells sensitivity to WNT5A what translates in melanoma into decreased invasive properties and increased response to targeted therapies of this skin cancer.

Transformation mediated by oncogenic BRAF requires transcriptional activation of TWIST at the earliest stage of neoplastic transformation.

Genetically engineered murine models reveal novel mechanisms of cell identity regulation in lung cancer and provide insights into the complex interplay between lineage specifiers and oncogenic signaling pathways in this disease.

The temporal patterns of MAPK activity differentially regulate cell autonomous and non-cell autonomous effects of oncogene expression.