Results 261 to 270 of about 950,400 (402)
Using celastrol as a case study, this review summarizes various target discovery strategies for natural products, including chemical proteomics, protein microarray, degradation‐based protein profiling, proteome‐wide label‐free approaches, network pharmacology, target‐based drug screening, and indirect strategies.
Yanbei Tu+5 more
wiley +1 more source
Modulation of copper homeostasis and cuproptosis by PDHA1 in acute myeloid leukemia. [PDF]
Chen T+8 more
europepmc +1 more source
A comparative study of dibromomannitol and busulfan in the treatment of chronic myeloid leukemia. A study of cancer and leukemia group B [PDF]
Richard T. Silver+7 more
openalex +1 more source
Phenylethanoid Glycosides in Cistanches: Chemistry, Pharmacokinetic, and Antitumor Properties
This review systematically summarizes the representative PhGs found in CH species, their pharmacokinetic parameters, and primary metabolites in humans and rats. Additionally, it examines the antitumor activities of PhGs in CH and their associated signaling pathways against various malignancies.
Jie Li+7 more
wiley +1 more source
Multimodal spatial proteomic profiling in acute myeloid leukemia. [PDF]
Ly CP+19 more
europepmc +1 more source
Genomic Profile and Clinical Outcomes in Acute Myeloid Leukemia with Monosomal Karyotype. [PDF]
Wangulu C+7 more
europepmc +1 more source
8;21 Translocation in acute myeloid leukemia an ultrastructural study [PDF]
Guido Tricot, A. Broeckaert van Orshoven
openalex +1 more source
Mechanisms of enhancer‐driven oncogene activation
Abstract An aggressive subtype of acute myeloid leukemia (AML) is caused by enhancer hijacking resulting in MECOM overexpression. Several chromosomal rearrangements can lead to this: the most common (inv(3)/t(3;3)) results in a hijacked GATA2 enhancer, and there are several atypical MECOM rearrangements involving enhancers from other hematopoietic ...
Joyce Vriend+2 more
wiley +1 more source
Targeting the Menin–KMT2A interaction in leukemia: Lessons learned and future directions
Abstract Chromosomal rearrangements involving the Mixed Lineage Leukemia gene (MLL1, KMT2A) are defining a genetically distinct subset in about 10% of human acute leukemias. Translocations involving the KMT2A‐locus at chromosome 11q23 are resulting in the formation of a chimeric oncogene, where the N‐terminal part of KMT2A is fused to a variety of ...
Florian Perner+3 more
wiley +1 more source