190 results found
    1. Cancer Biology
    2. Chromosomes and Gene Expression

    Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells

    Ana Filipa Domingues, Rashmi Kulkarni ... Cristina Pina
    Histone acetyl-transferase Kat2a preserves leukemia stem cells through frequent transcriptional firing of metabolic and regulatory gene promoters and maintenance of a largely invariant self-renewal program.
    1. Developmental Biology
    2. Chromosomes and Gene Expression

    lncRNA requirements for mouse acute myeloid leukemia and normal differentiation

    M Joaquina Delás, Leah R Sabin ... Gregory J Hannon
    A comprehensive analysis of long noncoding RNAs in the hematopoietic system reveals their dynamic regulation and a loss-of-function screen identifies some required for leukemia progression and involved in normal myeloid differentiation.
    1. Cancer Biology

    Convergent organization of aberrant MYB complex controls oncogenic gene expression in acute myeloid leukemia

    Sumiko Takao, Lauren Forbes ... Alex Kentsis
    Definition of leukemia gene expression mechanisms reveals general principles of cancer gene control and offers a pharmacologic strategy for its therapeutic reprogramming.
    1. Cancer Biology

    Therapeutic resistance in acute myeloid leukemia cells is mediated by a novel ATM/mTOR pathway regulating oxidative phosphorylation

    Hae J Park, Mark A Gregory ... James DeGregori
    Cellular and molecular analyses of human AML cells reveal a novel pathway activated by the bone marrow microenvironment that confers resistance to FLT3 inhibition and can be exploited to improve the efficacy of FLT3 inhibitor therapy for AML.
    1. Biochemistry and Chemical Biology
    2. Cancer Biology

    Overcoming myelosuppression due to synthetic lethal toxicity for FLT3-targeted acute myeloid leukemia therapy

    Alexander A Warkentin, Michael S Lopez ... Kevan M Shokat
    Anti-targets are proteins that cause problems when inhibited along with an intended target and our novel chemical strategy affords unprecedented selectivity in the context of FLT3 vs. KIT inhibition for treatment of a devastating blood cancer.
    1. Biochemistry and Chemical Biology
    2. Cancer Biology

    Intrinsic OXPHOS limitations underlie cellular bioenergetics in leukemia

    Margaret AM Nelson, Kelsey L McLaughlin ... Kelsey H Fisher-Wellman
    Across a physiological span of ATP-free energy, leukemic mitochondria primarily consume, rather than produce, ATP.
    1. Structural Biology and Molecular Biophysics

    Detection of human disease conditions by single-cell morpho-rheological phenotyping of blood

    Nicole Toepfner, Christoph Herold ... Jochen Guck
    The morphology and deformability of all blood cells can be measured continuously and with high throughput directly in whole blood without prior enrichment or separation.
    1. Cancer Biology
    2. Developmental Biology

    Fetal and neonatal hematopoietic progenitors are functionally and transcriptionally resistant to Flt3-ITD mutations

    Shaina N Porter, Andrew S Cluster ... Jeffrey A Magee
    Age-specific transcriptional responses to Flt3-ITD and cooperating Flt3/Runx1 mutations cause hematopoietic stem cell depletion and myeloid progenitor expansion during adult, but not fetal/neonatal, stages of development.
    1. Biochemistry and Chemical Biology
    2. Cancer Biology

    Crosstalk between AML and stromal cells triggers acetate secretion through the metabolic rewiring of stromal cells

    Nuria Vilaplana-Lopera, Vincent Cuminetti ... Paloma Garcia
    Interplay between AML and stromal cells can initiate a mechanism involving gap junctions where ROS is transferred from cancer cells to stromal cells which then produce acetate which can in return be absorbed/utilised by the cancer cells.
    1. Cancer Biology
    2. Chromosomes and Gene Expression

    Non-canonical H3K79me2-dependent pathways promote the survival of MLL-rearranged leukemia

    William F Richter, Rohan N Shah, Alexander J Ruthenburg
    FLT3-ITD/STAT5A signaling is more sensitive to Dot1L inhibition than the canonical MLL-fusion activated drivers of leukemogenesis, providing a potential therapeutic avenue for one of the most frequent lesions in leukemia.

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