Flinders University and Flinders Medical Centre researchers have found a critical link between having two types of polyps, common growths found in the bowel, and an increased risk of developing cancer, according to a new study published in Clinical Gastroenterology and Hepatology (CGH) journal.

The use of immune checkpoint inhibitors (ICIs) has significantly improved the efficacy of cancer therapy, but their associated immune-related adverse events (irAEs) can severely compromise treatment safety. This review systematically summarizes the core mechanisms underlying irAEs, which include multi-organ damage resulting from T-cell dysfunction, B-cell-mediated autoantibody abnormalities, cytokine network dysregulation, and monocyte-driven inflammatory cascades. Identified risk factors encompass a range of elements, including host clinical characteristics and underlying diseases, gut microbiota dysbiosis, characteristics of the treatment regimen, tumor type and its histological features, genetic factors and immunogenetic polymorphisms, pre-existing autoimmune conditions or a history of autoimmunity, and a history of previous exposures alongside various environmental factors. The grading criteria, their clinical context and incidence rates, and clinical management strategies for irAEs affecting various organ systems are detailed herein. Future research should aim to deeply analyze the shared mechanisms and temporal dynamics between irAEs and anti-tumor effects, develop targeted irAE prediction and monitoring systems, and optimize strategies for irAE prevention and treatment.

A new discovery by Van Andel Institute scientists reveals that glucose, an essential cellular fuel that powers immune cells, also aids in T cells’ internal communication and boosts their cancer-fighting properties. The findings may help optimize T cells’ ability to combat cancer and other diseases.

Chinese researchers have identified key immune checkpoints on natural killer (NK) cells that enable tumors to evade immune destruction. This systematic review reveals how inhibitory receptors like TIGIT, NKG2A, and PD-1 suppress NK cell function in the tumor microenvironment, and demonstrates that blocking these checkpoints – through monoclonal antibodies, gene editing (CRISPR-Cas9), or engineered CAR-NK cells – significantly enhances anti-tumor immunity. The findings provide a roadmap for next-generation immunotherapies targeting solid tumors and blood cancers.

The 48th Annual UNC Lineberger Scientific Symposium, is a day-and-a-half meeting exploring advances across the cancer research continuum—from molecular discovery to clinical application to population impact—that are improving cancer outcomes. The meeting features 16 talks by leaders in cancer research that bridge basic, translational and population sciences.

New research has revealed that perilipin 2 protein modulates aggressive cancer progression in advanced lung adenocarcinoma, the most common type of lung cancer, by regulating lipid droplet accumulation, which plays an important role in lipid metabolism by making cancer cells store more fat, acting as a fuel source. Findings from this new study in The American Journal of Pathology, published by Elsevier, suggest that perilipin 2 could serve as a prognostic factor to help predict the likely outcome (prognosis) of the disease and point to new potential lipid-based targets for treating lung adenocarcinoma.

Patients with microsatellite instability-high (MSI-H) tumors are likely to have better clinical outcomes than other patients. Recently, researchers from Yonsei University College of Medicine have proposed MSI-SEER, a novel AI model for accurate MSI prediction as well as immune checkpoint inhibitor responsiveness prediction. The innovative technology is expected to help battle gastric and colorectal cancers and further cancer research in general.

Researchers discovered that interleukin-6 (IL-6) in colorectal cancer triggers a STAT3-to-PI3K signaling switch in cancer stem cells (CSCs), enabling potent PD-L1 upregulation and immune evasion. While non-CSCs use the STAT3-FRA1 pathway for PD-L1 expression, CSCs activate the PI3K-AKT-ZEB1 axis, explaining why some tumors resist immunotherapy. In mouse models, triple therapy (PI3Ki + STAT3i + anti-PD-L1) synergistically shrank IL-6-high tumors by blocking both pathways and boosting T-cell infiltration. The study proposes IL-6/PD-L1 as biomarkers for patient stratification.