ArticleThe Journal of experimental medicine2001
BCL-2 cooperates with promyelocytic leukemia retinoic acid receptor alpha chimeric protein (PMLRARalpha) to block neutrophil differentiation and initiate acute leukemia.
Article in The Journal of experimental medicine, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 106 citations in OpenAlex.
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- A systems genetics approach delineates the role of Bcl2 in leukemia pathogenesis.Leukemia research · 2022Article
- Roles and Regulation of BCL-xL in Hematological Malignancies.International journal of molecular sciences · 2022Review
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- Oncogenic role of lncRNA CRNDE in acute promyelocytic leukemia and NPM1-mutant acute myeloid leukemia.Cell death discovery · 2020Article
- miR-125b regulates cell progression in chronic myeloid leukemia via targeting BAK1.American journal of translational research · 2016Article
- Hepatocyte-specific Bid depletion reduces tumor development by suppressing inflammation-related compensatory proliferation.Cell death and differentiation · 2015Article
- Transcription and methylation analyses of preleukemic promyelocytes indicate a dual role for PML/RARA in leukemia initiation.Haematologica · 2015Article
- BCL-xL/MCL-1 inhibition and RARγ antagonism work cooperatively in human HL60 leukemia cells.Experimental cell research · 2014Article
- Notch signaling in acute promyelocytic leukemia.Leukemia · 2013Article
- Inhibition of apoptosis by BCL2 prevents leukemic transformation of a murine myelodysplastic syndrome.Blood · 2012Article
- The significance of low PU.1 expression in patients with acute promyelocytic leukemia.Journal of hematology & oncology · 2012Article
- Sequencing a mouse acute promyelocytic leukemia genome reveals genetic events relevant for disease progression.The Journal of clinical investigation · 2011Article
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- Evidence of functional interaction between NuMA-RARalpha and RXRalpha in an in vivo model of acute promyelocytic leukemia.Oncogene · 2008Article
- Review: genetic models of acute myeloid leukaemia.Oncogene · 2008Review
- Hematopoietic developmental pathways: on cellular basis.Oncogene · 2007Review
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9 authors at 5 institutions in 2 countries.
Funding
Abstract
The promyelocytic leukemia retinoic acid receptor alpha (PMLRARalpha) chimeric protein is associated with acute promyelocytic leukemia (APL). PMLRARalpha transgenic mice develop leukemia only after several months, suggesting that PMLRARalpha does not by itself confer a fully malignant phenotype. Suppression of apoptosis can have a central role in tumorigenesis; therefore, we assessed whether BCL-2 influenced the ability of PMLRARalpha to initiate leukemia. Evaluation of preleukemic animals showed that whereas PMLRARalpha alone modestly altered neutrophil maturation, the combination of PMLRARalpha and BCL-2 caused a marked accumulation of immature myeloid cells in bone marrow. Leukemias developed more rapidly in mice coexpressing PMLRARalpha and BCL-2 than in mice expressing PMLRARalpha alone, and all mice expressing both transgenes succumbed to leukemia by 7 mo. Although both preleukemic, doubly transgenic mice and leukemic animals had abundant promyelocytes in the bone marrow, only leukemic mice exhibited thrombocytopenia and dissemination of immature cells. Recurrent gain of chromosomes 7, 8, 10, and 15 and recurrent loss of chromosome 2 were identified in the leukemias. These chromosomal changes may be responsible for the suppression of normal hematopoiesis and dissemination characteristic of the acute leukemias. Our results indicate that genetic changes that inhibit apoptosis can cooperate with PMLRARalpha to initiate APL.
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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.