Researchers at the University of California San Diego have uncovered a key mechanism underlying the treatment resistance of melanoma with the BRAF V600E mutation through pathways involved in focal adhesion and extracellular matrix (ECM) remodeling. These two processes remodel the tumor cell environment in melanoma through the RAF/MEK cell signaling pathway. However, the combined use of FAK inhibitors with a RAF-MEK clamp overcame this resistance.

RAS G12D is one of the most frequent mutations in RAS, and when it occurs, it leaves RAS in a permanently active state, causing the cell to proliferate uncontrollably. Examples of the so-called RAS-addicted cancers are colorectal cancer or pancreatic ductal adenocarcinoma.

Human antigen R (HuR) controls the stability and translation of several transcripts that are key for metabolism, inflammation and cancer, including TNF-α or MYC. Previous findings have shown the pro-tumorigenic role of HuR in hepatocellular carcinoma (HCC), and its inhibition to be involved in metabolic dysfunction-associated steatohepatitis (MASH).

Multiple endogenous retroviruses (ERVs) in human DNA may be programmed to activate as cancer therapy. A recent study, led by scientists at the Dana-Farber Cancer Institute, expanded on a previously reported case of kidney cancer cure after hematopoietic stem cell transplantation attributed to the expression of an ERV driven by the hypoxia-inducible factor 2 (HIF2). The question was whether this finding might play out with different ERVs and different types of cancer through HIF.

The map of cystic fibrosis (CF) research is being redrawn in the U.K. as improvements in treatment, and in particular the introduction of CF modulator drugs, mean people with the rare inherited disease are living much longer.