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Forecasting Asparaginase Need and Cost for Childhood Cancer Using ACCESS FORxECAST.
JCO Glob Oncol
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Division of Haematology/Oncology, The Hospital for Sick Children, Toronto, Canada.
Purpose: Asparaginase (ASN) is a critical component of pediatric ALL protocols. Until recently, ASN was available in three formulations: native Escherichia coli, PEGylated E. coli (PEG), and Erwinase, with native E.
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Epics Therapeutics SA, rue Adrienne Bolland 47, Gosselies 6041, Belgium.
METTL3 is the RNA methyltransferase predominantly responsible for the addition of N-methyladenosine (mA), the most abundant modification to mRNA. The prevalence of mA and the activity and expression of METTL3 have been linked to the appearance and progression of acute myeloid leukemia (AML), thereby making METTL3 an attractive target for cancer therapeutics. We report herein the discovery and optimization of small-molecule inhibitors of METTL3, culminating in the selection of as an proof-of-concept compound.
View Article and Find Full Text PDFEvaluation of the practical application of the category-imbalanced myeloid cell classification model.
PLoS One
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School of Medical Technology and Engineering, Henan University of Science and Technology, Luoyang, China.
The incidence of acute myeloid leukemia (AML) is increasing annually, and timely diagnostic and treatments can substantially improve patient survival rates. AML typing traditionally relies on manual microscopy for classifying and counting myeloid cells, which is time-consuming, laborious, and subjective. Therefore, developing a reliable automated model for myeloid cell classification is imperative.
View Article and Find Full Text PDFHoxBlinc lncRNA reprograms CTCF-independent TADs to drive leukemic transcription and HSC dysregulation in NUP98-rearranged leukemia.
J Clin Invest
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Division of Pediatric Hematology/Oncology, Department of Pediatrics, Pennsylvania State University College of Medicine, Hershey, United States of America.
Although nucleoporin 98 (NUP98) fusion oncogenes often drive aggressive pediatric leukemia by altering chromatin structure and expression of HOX genes, underlying mechanisms remain elusive. Here, we report that a Hoxb-associated lncRNA HoxBlinc was aberrantly activated in NUP98-PHF23 fusion-driven leukemias. HoxBlinc chromatin occupancies led to elevated MLL1 recruitment and aberrant homeotic topologically associated domains (TADs) that enhanced chromatin accessibilities and activated homeotic/hematopoietic oncogenes.
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