The fight against cancer often begins with uncovering hidden players, and this study reveals one such key player: an unexpected class of abbreviated N-glycans. These molecules, upregulated in cancer cells, are excreted through a surprising mechanism—lysosomal exocytosis. Even more fascinating is the intricate relationship between lysosomal exocytosis and focal adhesions, structures critical for cell anchoring and communication. By decoding how focal adhesions regulate lysosomal exocytosis, researchers are opening new doors to understanding cancer cell adhesion and migration and exploring innovative therapies targeting these molecular interactions.

The possibility of a new therapy for colorectal cancer could be achieved by blocking DUSP6, a protein that is important for cell growth, survival, and repair. 

Obesity, recognized as a complex and growing health issue, is associated with an increased risk of various cancers. A comprehensive review provides insights into the mechanisms linking obesity to cancer risk and discusses potential clinical implications. Inflammation, hormonal imbalances, gut microbiota dysregulation, adipokine level disruptions, and physical and biochemical stimuli are identified as key mechanisms through which obesity influences cancer development. Chronic low-grade inflammation in adipose tissue, marked by increased proinflammatory immune cell infiltration and cytokine release, is a significant characteristic of obesity and plays a role in carcinogenesis. Hormonal disturbances, such as elevated estrogen levels, contribute to the development of obesity-related cancers, especially in postmenopausal women. The gut microbiota is also dysregulated in obesity, promoting inflammation and carcinogenesis. Adipose tissue, an active endocrine organ, secretes adipokines like leptin and adiponectin, which can either promote or inhibit cancer development when their levels are altered in obesity. Additionally, physical stimuli such as increased abdominal pressure and interstitial fibrosis contribute to the risk of obesity-associated cancer.

Salk scientists discover protein first identified at Salk in 1996 called PIN1 encourages tumor growth in bladder cancer, then find treatment that pairs a PIN1-blocker and popular cholesterol-controlling statins to halt tumor growth in mice—pointing to possible new, optimized bladder cancer treatments.

Salk scientists link bile acids and immune cell performance in liver cancer, finding that supplementing the bile acid UDCA—already a current treatment for liver disease—and inhibiting bile acid-forming protein BAAT could boost liver cancer patient response to immunotherapy. Future research may reveal dietary choices that would favorably alter the gut microbiome to promote immune-boosting bile acids.

A phase 1 clinical trial co-led by researchers at Washington University School of Medicine in St. Louis found that a new type of cell-based immunotherapy was safe for patients with several types of B-cell lymphoma, a type of blood cancer. Larger studies are needed to assess efficacy, but the approach shows promise.

Researchers at Case Western Reserve University School of Medicine have discovered how specific protein regions contribute to breast cancer.

Study identifies a novel mechanism driving osteosarcoma and provides insights to help predict patient outcomes