The combination drug ceftazidime-avibactam (CZA) is a last line of defense against the common Pseudomonas aeruginosa hospital bug: It’s the drug that gets called in when nothing else works, but there’s now evidence that it may not keep working for long.

Based on an analysis of two critically ill patients with P. aeruginosa infections, the bacteria are developin g genetic mutations that change the enzymes they produce – and can ward off an attack from CZA.

Researchers led by a team from Tongji University in China have now published a new paper in Microbiology Spectrum detailing the mutations and what it might mean for fighting P. aeruginosa in the future.

A study led by the Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), working in collaboration with an international research team, has identified a new molecular mechanism involved in hypertrophic cardiomyopathy, the most common inherited cardiovascular disease.

The research, published in Nature Cardiovascular Research, also demonstrates that mavacamten—the first targeted therapy available for this condition—is effective across different types of genetic mutations.

Hypertrophic cardiomyopathy is the most common inherited heart disease and the leading cause of sudden cardiac death in young people and athletes.

Inhibiting menin, a protein that supports leukemia growth and is already targeted to treat some forms of leukemia, also holds promise for treating myeloproliferative neoplasms. A new study from scientists at St. Jude Children’s Research Hospital showed that inhibiting menin significantly extended survival and reversed multiple disease features in preclinical models. The findings were published today in Cancer Cell.

Menin is best known as a therapeutic vulnerability in certain types of acute leukemia, including those with KMT2A gene rearrangements or NPM1 mutations. Menin inhibitors, such as revumenib, have greatly improved treatment for these cancers and are approved by the Food and Drug Administration (FDA). However, menin inhibition can reduce megakaryocytes (normal platelet-forming cells) and decrease platelet counts. Producing too many megakaryocytes is a hallmark of diseases called myeloproliferative neoplasms, which are slow-developing, rare blood cancers.

John Crispino, Ph.D., MBA, St. Jude Division of Experimental Hematology director and Department of Hematology member, tested whether inhibiting menin could be a viable therapeutic strategy for myeloproliferative neoplasms.