Scientists demonstrate that partial knockdown of MAP4K4 replaces SV 40 small T antigen component of STRIPAK. Study suggests that MAP4K4 is a key substrate for serine/threonine phosphatase, PP2A, and promotes oncogenic transformation through activation of the Hippo pathway effector, YAP1.
Computational analysis of two large-scale independent CRISPR-Cas9 viability screens performed at the Broad and Sanger Institutes indicate reproducible findings in identifying gene dependencies.
Human pluripotent stem cells-derived natural killer cells have improved antibody-dependent cellular cytotoxicity and could be used to treat refractory malignancies.
Researchers identify that mechanistic target of rapamycin (mTOR) kinase inhibitor, PP242 induces cell death in glioblastoma cells by off-target inhibition of both protein kinase C alpha and Janus kinase 2 (JAK2).
Scientists compared performance of RNA-Seq processing pipelines for the expression quantification of long non-coding RNAs (lncRNAs) in cancer samples. This study indicates integrating pseudoalignment methods with transcriptome annotation is a recommended strategy for RNA-Seq analysis of lncRNAs.
CTD2 scientists at DFCI performed genome-scale open reading frame screens to identify mechanisms of resistance to androgen deprivation therapy. This study shows that transcription factor, CREB5, is overexpressed and mediates resistance to androgen receptor antagonists in prostate cancer.
Glioblastoma cells develop resistance to blockade the transcription factor STAT3. UCSF studies show that autocrine feedback loop among STAT3, EGFR and NF-KB mediates primary resistance and suggest combinatorial therapy to treat EGFR-amplified glioblastomas.
CTD2 scientists at Stanford University performed integrative analysis of early-stage breast cancer patient and cell line data to study the role of chromatin regulatory genes (CRG). These studies indicate, CRGs that promote DNA accessibility are associated with anthracycline sensitivity.
Neuroblastoma cells treated with RXDX-105, a small-molecule inhibitor of multiple kinases decreased cell viability and proliferation in vitro and in vivo.