Google’s AI Evolution: How Machine Learning is Revolutionizing Scientific Software Development
The New Frontier of Scientific Programming Google researchers have pioneered an innovative approach that uses artificial intelligence to evolve and…
The New Frontier of Scientific Programming Google researchers have pioneered an innovative approach that uses artificial intelligence to evolve and…
Scientists have identified why acute myeloid leukemia resists proteasome inhibitors that work well in multiple myeloma. By combining these drugs with autophagy blockers, researchers effectively killed AML cells and extended survival in models, offering hope for broader patient benefit regardless of genetic mutations.
Researchers have uncovered the mechanism behind acute myeloid leukemia’s resistance to a class of drugs effective against other blood cancers, according to a new study from UC San Diego School of Medicine. The findings, published in Blood journal, reveal how AML cells activate backup systems to survive proteasome inhibitor treatment, which has long frustrated attempts to expand use of these medications beyond multiple myeloma.