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.

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.

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.”

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.