Bromodomain-containing protein 4 (BRD4) is an epigenetic regulator that promotes transcription of oncogenic drivers such as MYC and contributes to tumor growth and therapy resistance in colorectal cancer, making it a promising therapeutic target. Researchers from Hangzhou Kexing Biochem Co. Ltd. described the discovery and preclinical characterization of compound [I], a potent BRD4 inhibitor.
Harbour Biomed is spinning out newco Solstice Oncology and is outlicensing its CTLA-4 antibody, porustobart (HBM-4003), to the newco in a cash and equity deal worth more than $1.2 billion.
Harbour Biomed is spinning out newco Solstice Oncology and is outlicensing its CTLA-4 antibody, porustobart (HBM-4003), to the newco in a cash and equity deal worth more than $1.2 billion.
In a recent study, researchers from Stony Brook University Renaissance School of Medicine and Cold Spring Harbor Laboratory investigated whether in vivo targeting of gastrointestinal tissues via foodborne delivery of Lm-based cancer vaccines could control tumor growth in murine models of colorectal cancer.
Mutations in GTPase KRAS, concretely KRAS G12D, are predominant in pancreatic and colorectal cancers and targeting them is still a challenge. Researchers have published results from studies of a new KRAS G12D inhibitor, LPM-5140276, for the potential treatment of these cancer types harboring this mutation.
Kahimmune Therapeutics SAS has signed an exclusive licensing agreement with Gustave Roussy and SATT Paris-Saclay. Created at the end of last year as a spin-off of Gustave Roussy and SATT Paris-Saclay, Kahimmune builds on the latest discoveries in immunology relating to the dark genome.
Chemotherapy is often seen solely as a tumor-targeting treatment, yet new evidence reveals a paradox: the tissue injury it causes can reprogram the body’s defenses, influencing the risk of metastasis. Researchers from the University of Lausanne and collaborators reported that chemotherapy reshapes the gut-immune axis by inducing microbiota-derived indole-3-propionic acid, which reprograms myelopoiesis to curb monocyte-driven immunosuppression and metastasis in colorectal cancer.
Chemotherapy is often seen solely as a tumor-targeting treatment, yet new evidence reveals a paradox: the tissue injury it causes can reprogram the body’s defenses, influencing the risk of metastasis. Researchers from the University of Lausanne and collaborators reported that chemotherapy reshapes the gut-immune axis by inducing microbiota-derived indole-3-propionic acid (IPA), which reprograms myelopoiesis to curb monocyte-driven immunosuppression and metastasis in colorectal cancer (CRC).
Cardiff Oncology Inc. welcomed Mani Mohindru as interim CEO and simultaneously provided what the company dubbed a “positive” but stock-denting clinical update. The firm rolled out data from the 113-patient phase II trial called CRDF-004, designed to test the oral Polo-like kinase 1 (PLK1) inhibitor onvansertib in first-line, RAS-mutated metastatic colorectal cancer (mCRC). Shares (NASDAQ:CRDF) closed Jan. 27 at $2, down 94 cents, or 32%, as Wall Street took in the results.
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.