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.

In keratinocytes, the BRAF and RAF1 proteins work independently to balance the activity of mitogenic and stress kinase cascades and uphold the mechanical and immunological barrier functions of the epidermis.

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.

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

Adult muscle progenitors evade differentiation by expressing a short RNA isoform of Zfh1 which is insensitive to regulation by a micro-RNA.

Spontaneous growth arrest of transformed melanocytes (resulting in benign “moles”) does not result from cell-autonomous oncogene-induced senescence, but can be explained by collective mechanisms used in normal tissue size control.

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.

An area of visual-motor cortex called the lateral intraparietal area encodes eye position signals that support visually-guided behaviors and image stabilization.

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