Could space help advance brain cancer research? Results from the University of Notre Dame, published in PNAS, show that glioblastoma organoids grown in microgravity on the ISS more closely mimic human tumors than those grown on Earth, creating more realistic models for studying disease progression and testing new therapies.

A new study from Mayo Clinic suggests checkpoint immunotherapy may reshape the immune environment within lymph nodes after melanoma has spread to them. Researchers found that treatment reorganized several types of immune cells and changed the behavior of certain cells, called macrophages, that can either support or suppress an immune response depending on their environment.

Hyperactive YAP and TAZ, cancer-promoting proteins regulated by the Hippo pathway, were associated with genomic instability that may make cancer cells more recognizable to the immune system, while also increasing PD-L2, which helps the cells evade T cell attack. That combination may help explain why certain Hippo pathway alterations were linked to better outcomes among cancer patients treated with immune checkpoint inhibitors, which can block inhibitory signals that restrain T cell activity.

This study demonstrates that cytokine IL-33 alleviates the immunosuppressive tumor microenvironment in hepatocellular carcinoma, activates the STING/IRF axis, increases functional CD8⁺ T cells and TLSs, and synergizes with anti-PD-L1 to boost antitumor immunity, offering a promising strategy to enhance HCC immunotherapy.

Fox Chase Cancer Center researchers identified a potential therapeutic target for pancreatic cancer after showing that tumor growth can be slowed and immune suppression can be reduced in preclinical trials by blocking a particular protein, called anoctamin 6 (ANO6). The study, published in Nature Cancer, found that ANO6 helps pancreatic cancer cells obtain nutrients from surrounding cells while suppressing the immune system’s ability to fight tumors

Tracking a protein that drives cell division could help doctors tell which breast cancers are likely to respond to CDK4/6 inhibitors, a widely used class of targeted drugs.

Gastric cancer is a major cause of cancer mortality, with epigenetic silencing of tumor-suppressor genes playing a central role in its pathogenesis. The role of psiTPTE22-HERV, a recently evolved human-specific gene resulting from the fusion of human endogenous retrovirus (HERV) DNA and adjacent non-HERV DNA, in gastric carcinogenesis has remained unclear.

Gastric cancer (GC) remains one of the leading causes of cancer-related mortality worldwide, with metastasis accounting for the majority of patient deaths. Although advances in molecular profiling have improved our understanding of gastric tumorigenesis, the mechanisms driving invasion and metastatic spread remain incompletely understood. Pseudogenes, once considered nonfunctional genomic relics, are increasingly recognized as important regulators of cancer biology. However, the functions of many pseudogenes in gastric cancer progression have yet to be defined.