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RAS

Auris Medical to Develop KRAS-Targeting RNA Treatment for Colorectal Cancer as First Therapeutic Indication for OligoPhore™ Technology

[Auris Medical Holding Ltd.] Auris Medical Holding Ltd. announced the selection of mutant KRAS-driven colorectal cancer as the first therapeutic indication for its OligoPhore™ oligonucleotide delivery platform, based on outcomes from studies with OligoPhore™ enabled KRAS silencing, and a well-defined regulatory and development pathway.

Cell-Based Regenerative Medicine for Renovascular Disease

[Trends in Molecular Medicine] Several regenerative approaches involving the delivery of reparative cells or products have achieved kidney repair in experimental models of renal artery stenosis (RAS) and the delivery of mesenchymal stem/stromal cells has already been translated to human subjects with RAS with promising results.

Highly Metastatic Claudin-Low Mammary Cancers Can Originate from Luminal Epithelial Cells

[Nature Communications] The authors showed that persistent oncogenic RAS signaling caused highly metastatic triple-negative mammary tumors in mice. The continuous signaling of oncogenic RAS played a crucial role in the cellular plasticity and maintenance of the mesenchymal and stem cell characteristics of claudin-low mammary cancer cells.

Single-Cell RNA Sequencing Reveals the Mechanism of Sonodynamic Therapy Combined with a RAS Inhibitor in the Setting of Hepatocellular Carcinoma

[Journal of Nanobiotechnology] To dissect the mechanism of a combined tumoricidal therapeutic strategy, scientists investigated the scRNA-seq transcriptional profiles of an hepatocellular carcinoma xenograft following treatment.

Acrolein Contributes to Human Colorectal Tumorigenesis through the Activation of RAS-MAPK Pathway

[Scientific Reports] Scientists found that acrolein induced oncogenic transformation, including faster cell cycling, proliferation, sphere formation and cell migration, in fibroblast cells, and acrolein-induced DNA damages were higher in colorectal cancer (CRC) tumor tissues than in normal epithelial cells in CRC patients.

Depalmitoylation Rewires FLT3-ITD Signaling and Exacerbates Leukemia Progression

[Blood] Investigators discovered that FLT3-ITD, one of the most frequent mutations in acute myeloid leukemia, was S-palmitoylated by the ZDHHC6 palmitoyl acyltransferase. Disruption of palmitoylation redirected FLT3-ITD to the plasma membrane and rewired its downstream signaling by activating AKT and ERK pathways in addition to STAT5.

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