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.
Genome & Co. Ltd. has reported preclinical findings of its anti-CNTN4 antibody, GENA-104A16, and anti-APP antibody, 5A7 — stressing the contactin-4 (CNTN4) and amyloid precursor protein (APP) axis as a potential target for immuno-oncology. In the latest murine experiments, investigators led by Genome executives and researchers of Gwangju Institute of Science and Technology (GIST) found that blocking the interaction between CNTN4 and APP promoted cancer-destroying responses in mice, suggesting the pathway as a target for immunotherapy.
The inappropriate use of antibiotics over long periods of time has led to increasing bacterial drug resistance. Quinolones are among the most effective and widely used antibacterials, and there are ongoing efforts to develop new quinolone-based drugs able to overcome emerging bacterial drug resistance.
Researchers from the University of Minnesota have presented the discovery and preclinical characterization of a novel potent inhibitor of multidrug resistance-associated protein 1 (MRP1), ZW-1226, that is being developed as a therapeutic candidate for the treatment of multidrug resistant (MDR) cancers.
A study on the posttranslational modification through lactylation of non-histone proteins revealed a mechanism that participates in genome stability and provides resistance to chemotherapy. Scientists from The Second and The Seventh Affiliated Hospital of Sun Yat-sen University (SYSU) identified the lactation of the Nijmegen breakage syndrome 1 (NBS1) protein and the enzymes that participate in this process as a strategic point in cancer therapy.
The adaptation of cancer cells to therapies limits the effectiveness of treatments. However, understanding the mechanisms they use to do it could help reverse them or be used to design more powerful drugs. Scientists at New York University (NYU) have studied the transitions causing resistance and have observed how it develops through a gradual process they have called the “resistance continuum.”
Researchers from Contrafect Corp. have reported on the bactericidal activity of CF-370, a novel engineered lysin with broad-spectrum activity against gram-negative organisms, which are usually more resistant to antibacterial agents than gram-positive bacteria.
Bruton tyrosine kinase (BTK) enzyme inhibitors used to treat B-cell cancers, including chronic lymphocytic leukemia and non-Hodgkin lymphoma, also produce resistance by causing mutations in the protein. Now, a study on the BTK degrader NX-2127 showed the compound could be effective in eliminating BTK regardless of its mutations.
Bruton tyrosine kinase (BTK) enzyme inhibitors used to treat B-cell cancers, including chronic lymphocytic leukemia (CLL) and non-Hodgkin lymphoma, also produce resistance by causing mutations in the protein. Now, a study on the BTK degrader NX-2127 showed the compound could be effective in eliminating BTK regardless of its mutations.
Researchers have identified a new class of antibiotics that works by blocking the transportation of lipopolysaccharide (LPS) to the outer membrane of the gram-negative bacterium Acinetobacter baumannii. The most advanced member of the class, zosurabalpin (RG-6006, Roche AG), was effective against multiple A. baumannii strains, including carbapenem-resistant and multidrug-resistant strains.
RSS
