Experimental drugs that directly inhibit the NSD2 enzyme have shown potential as an effective strategy against hard-to-treat cancers, such as lung and pancreatic tumors driven by KRAS mutations. The therapeutic mechanism involves reversing a histone H3 methylation that promotes open chromatin and the expression of oncogenes.
Dana Farber Cancer Institute Inc. and Stanford University have patented new molecular glue degraders comprising cereblon (CRBN) binding moiety acting as casein kinase 1 isoform α and/or wee1-like protein kinase (Wee1) degradation inducers reported to be useful for the treatment of cancer.
The first patent from Palo Alto, Calif.-headquartered Updoc Inc. provides protection for their development of an artificially intelligent, voice-based method for prescribing, managing and administering at least one medication for management of type 2 diabetes to a patient.
Immune checkpoint inhibitors (ICIs) are monoclonal antibodies activating the immune system to kill tumor cells, representing a major advancement in cancer treatment. However, by activating T-cell immunity, ICI treatment can lead to immune-related adverse events affecting the several organs, including the heart.
A combination of Epstein-Barr virus (EBV) antibodies and genetic factors may be linked to an increased risk of multiple sclerosis (MS), according to a study led by scientists at Karolinska Institutet and Stanford University. “The Epstein-Barr virus has been a suspect for many years for having a role in causing MS. The evidence for it has increased though one has not really reached complete proof of its role,” Tomas Olsson told BioWorld.
At the BioFuture 2024 conference held in New York in November, Seema Kumar, the CEO of Cure, described women’s health as something that has been directed at the “bikini area.” That “bikini” bias extended to both diseases and their causes – women’s health covered the breasts and reproductive system, and its causes were hormonal. Both concepts are far too narrow.
Cancer therapies can eliminate specific tumors based on their genetic content. However, some cancer cells survive. How do they do it? Part of the answer lies in extrachromosomal DNA (ecDNA), an ace up the tumors’ sleeve to adapt and evade attack. Three simultaneous studies in the journal Nature lay all the cards on the table, revealing ecDNAs’ content, their origin, their inheritance, their influence in cancer, and a way to combat them.
Cancer therapies can eliminate specific tumors based on their genetic content. However, some cancer cells survive. How do they do it? Part of the answer lies in extrachromosomal DNA (ecDNA), an ace up the tumors’ sleeve to adapt and evade attack. Three simultaneous studies in the journal Nature lay all the cards on the table, revealing ecDNAs’ content, their origin, their inheritance, their influence in cancer, and a way to combat them.