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.

A long non-coding RNA molecule called cherub is a driver of tumor development.

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

Genetic and biochemical approaches identify a new component of the cellular signaling machinery driving migration of limb muscle precursor cells during mouse embryogenesis and reveal the underlying molecular mechanism.

Overexpression of PLK1 triggers oncogenic transformation and transcriptional reprogramming of prostate epithelial cells, which stimulates cell migration and invasion.

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.

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.