Gwangju Institute of Science & Technology, National Cancer Center of Korea and Seoul National University have jointly divulged new PreS1 (hepatitis B virus, HBV) derivatives for the treatment of HBV infection.
The University of Kansas has synthesized TNF-α (ARE sequence)/ELAV-like protein 1 (HuR) interaction inhibitors. They are reported to be useful for the treatment of cancer, kidney fibrosis, liver fibrosis, pulmonary fibrosis and myocardial fibrosis.
Akari Therapeutics plc has unveiled a new pipeline candidate, AKTX-102, an antibody-drug conjugate (ADC) directed against CEACAM5, a novel target highly relevant in gastrointestinal and lung cancers.
Breast cancer is the most frequently diagnosed malignancy worldwide. Inhibiting PARP-mediated DNA repair has emerged as a promising anticancer strategy, with PARP inhibitors (PARPis) demonstrating clinical efficacy particularly in tumors with defective homologous recombination repair, such as BRCA-deficient cancers.
Starkage Therapeutics SAS has established a research collaboration with Gustave Roussy to characterize cellular senescence induced by standard-of-care treatments in a series of digestive cancers.
Programmed death-ligand 1 (PD-L1) is a crucial immune checkpoint ligand that inhibits antitumor immunity by engaging PD-1 on T cells, and checkpoint blockade has become a pillar of anticancer therapy. However, many patients show limited treatment responses.
Researchers at the Biodonostia Health Research Institute reported on the role of KLF15 in cholangiocarcinogenesis and its potential as a therapeutic target in this disease.
Intratumoral regulatory T cells (Tregs) suppress antitumor immunity and are linked to poor prognosis across many cancers. These tumor-infiltrating Tregs express high levels of cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), making them attractive targets for immunotherapy. However, systemic Treg depletion carries the risk of severe autoimmune toxicity.
Liver fibrosis in the course of metabolic dysfunction-associated steatohepatitis (MASH) could be significantly reduced using CAR T-cells generated in vivo. Scientists at the Icahn School of Medicine at Mount Sinai have developed an experimental cell therapy that eliminates only one type of liver cell, the stellate cells that express fibroblast activation protein alpha (FAP). This strategy not only reduced fibrosis but also reversed liver damage.
Cancer cells expand through mutations – but not just through mutations. They also change their behavior in the absence of underlying genetic alterations. Such plasticity helps the cells both adapt to the cellular stress fueled by out-of-control growth and resist targeted and chemotherapies alike. Investigators from Memorial Sloan Kettering Cancer Center and Huazhong Agricultural University have gained new insights into the underlying mechanisms of plasticity.
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