Mucormycosis, a fungal infection caused by fungi from the order Mucorales, can cause severe disease, especially in immunocompromised subjects. These fungi are ubiquitous and can be found in environmental sources such as crop residues and soil. Among the multiple factors that increase the risk of mucormycosis infection are immunosuppression and diabetes mellitus.

Mucormycosis, a fungal infection caused by fungi from the order Mucorales, can cause severe disease, especially in immunocompromised subjects. These fungi are ubiquitous and can be found in environmental sources such as crop residues and soil. Among the multiple factors that increase the risk of mucormycosis infection are immunosuppression and diabetes mellitus.

Using ALK+ lung cancer patient-derived cell lines, researchers have performed phosphoproteomic screening and identified guanylate kinase 1 (GUK1) as a TKI sensitive metabolic molecule in ALK-driven lung cancer.

Using ALK+ lung cancer patient-derived cell lines, researchers have performed phosphoproteomic screening and identified guanylate kinase 1 (GUK1) as a TKI sensitive metabolic molecule in ALK-driven lung cancer. They reported their results online in Cell on Feb. 6, 2025.

Researchers from the University of Pittsburgh School of Medicine have linked pulmonary arterial hypertension (PAH), a progressive disease characterized by blood vessel remodeling, with lysosomal dysfunction and sterol metabolism. They reported their results on Jan. 23, 2025, in Science.

Chronic pain affects about 20% of the population worldwide. It is – inadequately – treated with nonsteroidal anti-inflammatory compounds and opioids that lack efficacy and that are associated with serious side effects. The signaling axis composed of nerve growth factor (NGF) and the receptor tropomyosin-related kinase A (TrkA) is one of the few nonopioid targets that have been validated for treating chronic pain in patients.

By comparing the transcriptomic profile of tissue regeneration after induced damage in the small intestine and colon with their transcriptomic landscape in their steady state, researchers have identified a pathway that unlinks tissue regeneration from tumorigenesis.

Currently, cancer therapy trial-and-error methodology is inefficient and unsustainable. Oncology is the worst therapeutic area for drug trial success; only 3.4% of drugs that enter phase I end up being FDA approved, and 57% fail due to poor drug efficacy in trials. Building tools that may aid in predicting an individual’s response to a specific therapy may help in reducing costs, guesswork, and importantly improve the outcome of patients and accelerate new drug development.

Currently, cancer therapy trial-and-error methodology is inefficient and unsustainable. Oncology is the worst therapeutic area for drug trial success; only 3.4% of drugs that enter phase I end up being FDA approved, and 57% fail due to poor drug efficacy in trials. Building tools that may aid in predicting an individual’s response to a specific therapy may help in reducing costs, guesswork, and importantly improve the outcome of patients and accelerate new drug development.

Breast cancer cells, when disseminated to other secondary organs such as the lungs, may stay in a dormant state for years, even decades. But the mechanisms that limit their expansion are not well understood. This is what researchers call a dormant mesenchymal-like phenotype before metastasis to the lungs. Now, scientists have shown in a study published Oct. 7, 2024, in Cell, that the limiting of disseminated breast cancer cells (DCCs) to metastasize in the lungs is due to alveolar macrophages, which activate signals that make DCCs stay dormant.