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.
Disrupted meiosis, the cell division process that leads to the production of reproductive cells in sexually reproducing organisms, led to a decline in overall health by triggering an accelerating aging signature in the roundworm Caenorhabditis elegans.
The work is “the first direct evidence that manipulating the health of reproductive cells leads to premature aging and a decline in healthspan,” senior author Arjumand Ghazi, an associate professor of pediatrics, developmental biology, and cell biology and physiology at the University of Pittsburgh and the University of Pittsburgh Medical Center (UPMC) Children’s Hospital, said in a press release.
The discovery of synthetic lethality between BRCA mutations and PARP inhibitors ranks has led to major advances in the treatment of BRCA-mutated cancers. Mutations in BRCA1 and BRCA2 can leave cells with a deficiency in homologous repair (HR). And that deficiency can make them vulnerable to PARP inhibitors, which block alternate DNA repair pathways, as well as platinum-based treatment, which induces DNA mutations that BRCA-deficient cells are unable to cope with.
The discovery of synthetic lethality between BRCA mutations and PARP inhibitors ranks has led to major advances in the treatment of BRCA-mutated cancers.
