ArticleLeukemia2011
Differential requirements for c-Myc in chronic hematopoietic hyperplasia and acute hematopoietic malignancies in Pten-null mice.
Article in Leukemia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- Myc-Miz1 signaling promotes self-renewal of leukemia stem cells by repressing Cebpα and Cebpδ.Blood · 2020Article
- Leukemogenic nucleophosmin mutation disrupts the transcription factor hub that regulates granulomonocytic fates.The Journal of clinical investigation · 2018Article
- CALR mutational status identifies different disease subtypes of essential thrombocythemia showing distinct expression profiles.Blood cancer journal · 2017Article
- Control of amino acid transport coordinates metabolic reprogramming in T-cell malignancy.Leukemia · 2017Article
- Necroptosis in spontaneously-mutated hematopoietic cells induces autoimmune bone marrow failure in mice.Haematologica · 2017Article
- Oncogenic PTEN functions and models in T-cell malignancies.Oncogene · 2016Review
- Glucose and glutamine fuel protein O-GlcNAcylation to control T cell self-renewal and malignancy.Nature immunology · 2016Article
- FAK mediates a compensatory survival signal parallel to PI3K-AKT in PTEN-null T-ALL cells.Cell reports · 2015Article
- Article
- Article
- Targeting the PI3K/Akt/mTOR signaling pathway in B-precursor acute lymphoblastic leukemia and its therapeutic potential.Leukemia · 2014Article
- Cytogenomics of hexavalent chromium (Cr 6+) exposed cells: a comprehensive review.The Indian journal of medical research · 2014Review
- Connection between Tumor Suppressor BRCA1 and PTEN in Damaged DNA Repair.Frontiers in oncology · 2014Review
- Regulation of T cell homeostasis and responses by pten.Frontiers in immunology · 2012Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Myeloproliferative disorders (MPDs), lymphoproliferative disorders (LPDs), acute T-lymphocytic or myeloid leukemia and T-lymphocytic lymphoma were developed in inducible Pten (phosphatase and tensin homolog, deleted on chromosome ten)-knockout mice (Pten(-/-)). The appearance of these multiple diseases in one animal model provides an opportunity to study the pathogenesis of multiple diseases simultaneously. To study whether Myc function is required for the development of these hematopoietic disorders in Pten(-/-) mice, we generated inducible Pten/Myc double-knockout mice (Pten(-/-)/Myc(-/-)). By comparing the hematopoietic phenotypes of these double-knockout mice with those of Pten(-/-) mice, we found that both sets of animals developed MPDs and LPDs. However, none of the compound-mutant mice developed acute leukemia or lymphoma. Interestingly, in contrast to the MPDs that developed in Pten(-/-) mice, which are dominated by granulocytes, megakaryocytes predominate in the MPDs of Pten(-/-)/Myc(-/-) mice. Our study suggests that the deregulation of phosphoinositide 3-kinase/Akt signaling in Pten(-/-) hematopoietic cells protects these cells from apoptotic cell death, resulting in chronic proliferative disorders. However, owing to the differential requirement for Myc in granulocyte as compared to megakaryocyte proliferation, Myc deletion converts Pten(-/-) MPDs from granulocyte- to megakaryocyte-dominated conditions. Myc is absolutely required for the development of acute hematopoietic malignancies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.