Transcription factors of the ETS family govern a cohort of key cancer-associated regulators of malignancy in squamous cell carcinomas.

Genome-wide CRISPR/Cas9 screens enable the identification of actionable vulnerabilities of oral squamous cell carcinoma, and their unique dependencies on YAP1 and WWTR1 of the Hippo pathway.

Fibrolamellar carcinoma results from a genetic lesion that produces the DNAJ-PKAc fusion kinase, which is recruited into macromolecular complexes and is sensitive to combinations of signal transduction inhibitor drugs.

A single-cell RNA profiling analysis has delineated the molecular changes driving the progression from actinic keratosis to cutaneous squamous cell carcinoma.

Deletion and small-molecule inhibition of ubiquitin-specific protease 28 destabilizes the oncogenes c-MYC, c-JUN, and Δp63, and elicits regression of squamous cell lung carcinoma, a major cancer type with currently limited treatment options.

UPF1 mutations were reportedly present at high frequencies in a cohort of pancreatic adenosquamous carcinoma patients, but these lesions are unlikely to be functional drivers of this cancer subtype.

PHAROH lncRNA is upregulated in hepatocellular carcinoma and functions by sequestering the translational suppressor TIAR via a 71 nucleotide hairpin to regulate c-MYC translation.

A new mechanism connects the loss of TGFβ signaling with invasion and metastasis in highly malignant transition zone tumors.

Faithful models of RMC require SMARCB1 loss for survival, and genetic and small-molecule screens identify inhibition of the ubiquitin-proteasome system (UPS) as a potential therapeutic approach for SMARCB1 deficient cancers.

High levels of nuclear YAP are sufficient to drive squamous cell carincoma formation and frequently also drive progression to spindle cell carcinoma by promoting epithelial-to-mesenchymal transition after tissue damage.