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Bob Argiropoulos

Researcher at Alberta Children's Hospital

Publications -  46
Citations -  2831

Bob Argiropoulos is an academic researcher from Alberta Children's Hospital. The author has contributed to research in topics: Myeloid leukemia & Leukemia. The author has an hindex of 21, co-authored 46 publications receiving 2586 citations. Previous affiliations of Bob Argiropoulos include University of Calgary & University of British Columbia.

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Identification of miR-145 and miR-146a as mediators of the 5q– syndrome phenotype

TL;DR: Deletes chromosome 5q and identifies Toll–interleukin-1 receptor domain–containing adaptor protein (TIRAP) and tumor necrosis factor receptor–associated factor-6 (TRAF6) as respective targets of these miRNAs.
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Hox genes in hematopoiesis and leukemogenesis

TL;DR: It is proposed that Hox-dependent pathways are closely linked to the self-renewal program crucial to the origin and function of leukemic stem cells.
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In-depth characterization of the microRNA transcriptome in a leukemia progression model

TL;DR: The potential for miRNA-mediated release of oncogenes that facilitates leukemic progression from the preleukemic to leukemia inducing state is revealed and the finding of extensive sequence variations (isomiRs) for almost all miRNA and miRNA species adds additional complexity to the miRNA transcriptome.
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Disruption of the ASTN2/TRIM32 locus at 9q33.1 is a risk factor in males for autism spectrum disorders, ADHD and other neurodevelopmental phenotypes

Anath C. Lionel, +94 more
TL;DR: The 3'-terminal ASTN2 deletions were significantly enriched compared with controls in males with NDDs, but not in females, and new light is shed on the role of the astrotactins in psychopathology and their interplay in human neurodevelopment.
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MN1 overexpression induces acute myeloid leukemia in mice and predicts ATRA resistance in patients with AML.

TL;DR: It is demonstrated using retroviral gene transfer and bone marrow transplantation that MN1 overexpression rapidly induces lethal AML in mice, and MN1 is a unique oncogene in hematopoiesis that both promotes proliferation/self-renewal and blocks differentiation, and may become useful as a predictive marker in AML treatment.