Publications

CTD² scientists at UCSF (1) identified two major subtypes of KRAS mutant cancers of the lung, pancreas, and the large intestine which differentially engage effector pathways. These findings can be used to develop effective combination of therapies.

Researchers at UCSF (2) discovered that antisecretory factor decreases osmotic adaptation, increases drug uptake, and promotes anti-tumor activity in glioblastoma.

Studies demonstrated that epithelial-to-mesenchymal transition-inducing transcription factor, Snail, represses tumor suppressive RNA splicing regulatory protein, ESRP1, and promotes tumorigenesis in lung cancer.

CTD² investigators developed an orthogonal CRISPR screening method that can quantify loss- and gain-of-function phenotypes in the same cell. This method is useful to determine gene dependencies and direction of genetic interactions.

CTD² researchers engineered T cell receptor with oncogenic mutation BRAF^V600E- specific CD4⁺ T cells in a patient with acral melanoma. These engineered T cells may have antitumor effects and enhance CD8⁺ T cell responses in patients with BRAF mutated cancers.

Review on using patient-derived three-dimensional “organoid” models as a personal cancer model to develop effective treatment options.

CTD² review focused on signaling pathways mediated by the epidermal growth factor receptor (EGFR) and mutant EGFRvIII and novel therapies to overcome treatment resistance in glioblastoma.

Loss-of-function CRISPR/Cas9-based cancer dependency screes in MYCN-amplified neuroblastoma identified polycomb repressive complex 2 as a druggable pathway.