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

Data-driven systems biology models of signaling predict cellular response to untested perturbations and can nominate drug combinations to overcome drug resistance in cancer cells.

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.

Two receptors have been identified that can be targeted in melanocytes with selective small molecule agonists to modulate human skin color.

The protein IFI6 regulates DNA replication via the transcription factor E2F2, which is necessary for transformation and growth of melanomas induced by the NRASQ61K mutant oncogene product.

The microRNA, miR-146a, is regulated by mutant BRAF/NRAS proteins, and promotes the development of melanoma via increasing Notch signaling pathway, suggesting that combining drugs targeting BRAF/NRAS and Notch may provide an effective melanoma treatment.

Mice studies show that the 'just-right' balance optimal for BRAF^V600E-induced cecal tumor formation can be achieved through FAK alteration.

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.