Transcription factors in myeloid development: balancing differentiation with transformation

In recent years, great progress has been made in elucidating the progenitor-cell hierarchy of the myeloid lineage. Transcription factors have been shown to be key determinants in the orchestration of myeloid identity and differentiation fates. Most transcription factors show cell-lineage-restricted and stage-restricted expression patterns, indicating the requirement for tight regulation of their activities. Moreover, if dysregulated or mutated, these transcription factors cause the differentiation block observed in many myeloid leukaemias. Consequently, therapies designed to restore defective transcription factor functions are an attractive option in the treatment of myeloid and other human cancers

The Janus-faced Nature of miR-22 in Hematopoiesis: Is It an Oncogenic Tumor Suppressor or Rather a Tumor-Suppressive Oncogene?

10.1371/journal.pgen.1006505PLoS Genetics131e100650

RNA Editome imbalance in hepatocellular carcinoma

10.1158/0008-5472.CAN-13-3485Cancer Research7451301-1306CNRE

Mapping Distinct Bone Marrow Niche Populations and Their Differentiation Paths

10.1016/j.celrep.2019.06.031Cell Reports282302-3110000

Hematopoietic stem cell and multilineage defects generated by constitutive beta-catenin activation

Gain of Wnt signaling through beta-catenin has been ascribed a critical function in the stimulation of hematopoietic stem cell self-renewal, whereas loss of beta-catenin is reportedly dispensable for hematopoiesis. Here we have used conditional mouse genetics and transplantation assays to demonstrate that constitutive activation of beta-catenin blocked multilineage differentiation, leading to the death of mice. Blood cell depletion was accompanied by failure of hematopoietic stem cells to repopulate irradiated hosts and to differentiate into mature cells. Activation of beta-catenin enforced cell cycle entry of hematopoietic stem cells, thus leading to exhaustion of the long-term stem cell pool. Our data suggest that fine-tuned Wnt stimulation is essential for hematopoiesis and is thus critical for therapeutic hematopoietic stem cell population expansion

BIM mediates EGFR tyrosine kinase inhibitor-induced apoptosis in lung cancers with oncogenic EGFR mutations

10.1371/journal.pmed.0040315PLoS Medicine4101669-168

Styryl quinazolinones as potential inducers of myeloid differentiation via upregulation of C/EBPα

10.3390/molecules23081938Molecules238193