New research from Memorial Sloan Kettering Cancer Center (MSK) uncovers new details of the immune response against leptomeningeal metastasis; develops a grading system to assess the risk of developing thrombocytopenia after CAR T cell therapy; outlines a method for scientists to estimate metabolic characteristics from challenging clinical samples; and probes CRISPR’s anti-viral capabilities.

The demand for the widely used cancer drug Taxol is increasing, but it’s difficult and expensive to produce because it hasn’t been possible to do it biosynthetically. Until now, that is. Researchers from the University of Copenhagen have cracked the last part of a code that science has struggled with for 30 years. The breakthrough could halve the price of the drug and make production far more sustainable.

Deep-penetration light-triggered pyroptosis based on nanomedicine for tumor precision therapy still remains challenging. Towards this goal, Scientist in China reported a supramolecular engineering strategy to construct Pt(IV)-coordinated supra-(carbon dots) with NIR-activated photocatalytic capacity to trigger tumor pyroptosis, thereby evoking anti-tumor immune responses to suppress distant tumor and prevent cancer metastasis. The finding will open new avenues for precision phototherapy in future clinical oncology by supramolecular-mediated nanomedicine with deep-penetration light triggered pyroptosis.

Albert Einstein College of Medicine has appointed Britta Will, Ph.D., associate professor of oncology, of medicine and of cell biology, and the Diane and Arthur B. Belfer Scholar in Cancer Research, as the permanent director of the Ruth L. and David S. Gottesman Institute for Stem Cell Research and Regenerative Medicine.

With mitochondrial DNA (mtDNA) base editing tools, this study controlled the nuclear background to investigate the causal effect of mtDNA mutations. Co-existence of wild-type and mutant mtDNA (heteroplasmy) in MT-ND5 was introduced.  Enhanced oncogenic potential was confirmed with in vitro and in vivo assays. They reported compromised mitochondrial respiration and increased glycolytic activity, often termed as the Warburg effect following the mutations. By tracking cellular phenotypes during the MT-ND5 heteroplasmy decay, they reasoned that the increased glycolytic activity was to rescue NAD⁺ depreciation. Increased ROS level, genome instability, altered NAD⁺ epigenetics are the likely factors drove oncogenesis post MT-ND5 mutations.