Pancreatic cancer is a leading cause of cancer-related death, with a five-year survival rate of 13%. The high mortality is largely due to a lack of effective therapy options. In a recent paper publish...

A study of human and mouse models of pancreatic cancer finds that inhibiting the lipid kinase PIKfyve interferes with the cancer’s lipid homeostasis, making it a potential target for drug development.

As proof of principle, an analysis using a suite of human-aligned immunocompetent mouse models of hepatocellular carcinoma identifies a promising therapeutic candidate, cladribine, which acts in ...

As proof of principle, an analysis using a suite of human-aligned immunocompetent mouse models of hepatocellular carcinoma identifies a promising therapeutic candidate, cladribine, which acts in a highly effective subtype-specific manner in combination with standard-of-care therapy.

Recognition Award for Cancer Researchers of Colour.

Recognition Award for Cancer Researchers of Colour.

In 1982, the RAS genes HRAS and KRAS were discovered as the first human cancer genes, with KRAS later identified as one of the most frequently mutated oncogenes. Yet, it took nearly 40 years to develop clinically effective inhibitors for RAS-mutant cancers. The discovery in 2013 by Shokat and colleagues of a druggable pocket in KRAS paved the way to FDA approval of the first covalently binding KRASG12C inhibitors, sotorasib and adagrasib, in 2021 and 2022, respectively. However, rather than marking the end of a successful assault on the Mount Everest of cancer research, this landmark only revealed new challenges in RAS drug discovery. In this review, we highlight the progress on defining resistance mechanisms and developing combination treatment strategies to improve patient responses to KRAS therapies.

Clare Lappin, 54, is in remission after surgery, radiotherapy and the hormone therapy drug Tamoxifen, was at Glasgow Forge to officially open the 5,000 square foot superstore

The kinases MARK2 and MARK3 are identified as requirements for the function of the YAP and TAZ oncogenes, thus providing a druggable vulnerability in Hippo-dysregulated carcinomas and sarcomas.