Articles tagged with Tumor Suppressive Immunity
Researchers have identified complement factor B as a promising target for pancreatic cancer treatment. Inhibiting this enzyme suppresses cancer growth, induces cellular senescence, and remodels the tumor immune microenvironment. The combination of CFB inhibition with chemotherapy and immunotherapy showed the greatest tumor suppression.
The Alliance QUANTUM trial is testing whether post-transplant consolidation therapy with teclistamab improves survival in patients with primary plasma cell leukemia. Plasma cell leukemia is a rare but aggressive blood cancer with poor long-term survival rates.
Researchers discover enzyme ANKIB1 crucial for innate immune signalling, driving type I and type III interferon induction. This finding solves a long-standing puzzle in innate immunity and provides opportunities for new therapies for devastating diseases.
A specific protein, RASH3D19, activates the RAS signaling pathway involved in aggressive tumor growth and resistance to KRAS inhibitors. Blocking RASH3D19 improves outcomes in preclinical models, suggesting a potential therapeutic strategy.
Researchers have discovered that rhesus macaques shed TIGIT from immune cell surfaces when exposed to plasmin, a natural enzyme involved in blood clot breakdown. This creates a soluble form of TIGIT that can still bind anti-TIGIT monoclonal antibodies, potentially leading to misleading safety and efficacy data for human trials.
Researchers have identified distinct immune profiles for different subtypes of pediatric germ cell tumors, which could lead to more targeted therapies. The study found that certain tumor subtypes respond well to immunotherapy and others exhibit an immunosuppressive environment, making them more aggressive.
Scientists at Salk Institute discovered that removing bile acid-creating protein BAAT and adding bile acid UDCA controls tumor growth in mice with liver cancer. UDCA supplements may be a quick solution to improving liver cancer patient outcomes.
The study identified 72 genes commonly expressed in chronically activated CD8+ T cells across seven types of cancer. One gene, CXCR6, supports the survival of these cells by promoting CD28 signaling. This finding may inform targets for broadly active cancer therapies and treatments.
Researchers at TUM have uncovered a mechanism by which tumor cells prevent the formation of immune responses, including cytotoxic T cells. This discovery provides rationales for new cancer immunotherapies and could enhance existing treatments.