New study finds metastatic colorectal cancer’s immune defenses may begin outside the cancer cell, challenging view held for decades
Peer-Reviewed Publication
Updates every hour. Last Updated: 20-Oct-2026 16:16 ET (20-Oct-2026 20:16 GMT/UTC)
Researchers at the University of South Florida, Tampa General Hospital and Hokkaido University have uncovered an important mechanism behind immune evasion in metastatic colorectal cancer (mCRC). The finding challenges a 30-year-old theory in cancer research and identifies a molecular pathway that offers a new target for treatment.
Experts from the University of Nottingham have discovered how a common genetic mutation disrupts the positioning of a key protein during cell division, revealing a new mechanism behind acute myeloid leukaemia and a potential avenue for future treatment.
Acute myeloid leukaemia (AML) is an aggressive blood cancer that disrupts the production of healthy blood cells. Around one-third of patients carry a mutation in a gene called NPM1, which causes its protein to accumulate in the wrong part of the cell and plays a key role in driving the disease.
Until now, research has largely focused on how the mutated protein moves between the cell's nucleus and the surrounding cytoplasm. But a new study, led by Dr Daniel Booth and Dr Claire Seedhouse at the University of Nottingham's School of Medicine, reveals that what happens during cell division itself is also critical.
A team from IRB Barcelona, in collaboration with the Sant Joan de Déu Research Institute and the Pediatric Cancer Center Barcelona at Sant Joan de Déu Hospital, has described a mechanism by which a cancer-related protein can activate regions of DNA that normally remain silenced.
Using the Drosophila fruit fly, the researchers demonstrated that this activation depends on collaboration with another protein, enabling the study of a mechanism that is difficult to isolate in human cells.
The study, published in G3: Genes|Genomes|Genetics, may help explain previous observations in prostate cancer and B-cell acute lymphoblastic leukemia.
A genetic switch that activates immune cells as they fight tumours: this is the new strategy developed by an international research team coordinated by Velia Siciliano at the Istituto Italiano di Tecnologia (IIT – Italian Institute of Technology) in Naples and described in the scientific journal Nature Communications. The study marks another step towards engineering precise and more effective synthetic immunotherapies against solid tumours, such as melanoma and breast cancer.
Cirrhosis once viewed as irreversible, can improve after effective treatment, but recovery may not be complete or permanent. Researchers from China propose recognizing recompensation as a distinct treatment-related disease state and distinguishing stable from unstable recovery. Evidence across liver diseases shows that recompensation improves outcomes compared with persistent decompensation, while some patients later relapse. The framework could support more consistent research, clinical assessment, and long-term surveillance for patients recovering after cirrhosis treatment.
This authoritative review synthesizes 5 years of pivotal clinical and translational advances in esophageal cancer (EC), encompassing molecular pathogenesis, genomic and epigenetic landscapes, targeted therapeutic modalities and the tumor immune microenvironment. It underscores breakthroughs of immunotherapy in EC management while acknowledging slower progress in targeted treatments. Promising future directions include TKIs, CDK4/6 inhibitors, PI3K/AKT/mTOR pathway modulators, epigenetic regulators, ADCs, and rational combination strategies to overcome drug resistance and improve long-term patient survival outcomes.
CSHL Assistant Professor Semir Beyaz and colleagues have shown that transcription factor PPARD can promote the fitness of both cancer and immune cells. Their research could help make CAR T-cell therapy effective against colorectal cancer and lead to new treatment strategies for endometriosis, among other conditions.