ArticleProceedings of the National Academy of Sciences of the United States of America1998
BCR/ABL-mediated leukemogenesis requires the activity of the small GTP-binding protein Rac.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
38 citing papers in PubMed, 97 citations in OpenAlex.
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- Critical Requirement of SOS1 for Development of BCR/ABL-Driven Chronic Myelogenous Leukemia.Cancers · 2022Article
- Impact of the Breakpoint Region on the Leukemogenic Potential and the TKI Responsiveness of AtypicalFrontiers in pharmacology · 2021Article
- The signaling axis atypical protein kinase C λ/ι-Satb2 mediates leukemic transformation of B-cell progenitors.Nature communications · 2019Article
- Phosphorylation of SOS1 on tyrosine 1196 promotes its RAC GEF activity and contributes to BCR-ABL leukemogenesis.Leukemia · 2018Article
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- ELMO1 is upregulated in AML CD34+ stem/progenitor cells, mediates chemotaxis and predicts poor prognosis in normal karyotype AML.PloS one · 2014Article
- Rho GTPases modulate malignant transformation of tumor cells.Small GTPases · 2014Review
- Activation of Rac1 GTPase promotes leukemia cell chemotherapy resistance, quiescence and niche interaction.Molecular oncology · 2013Article
- CBL-B is required for leukemogenesis mediated by BCR-ABL through negative regulation of bone marrow homing.Leukemia · 2013Article
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- Extensive gene-specific translational reprogramming in a model of B cell differentiation and Abl-dependent transformation.PloS one · 2012Article
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- Drosophila Abelson kinase mediates cell invasion and proliferation through two distinct MAPK pathways.Oncogene · 2010Article
- Regulation of phagocyte NADPH oxidase by hydrogen peroxide through a Ca(2+)/c-Abl signaling pathway.Free radical biology & medicine · 2010Article
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Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The phenotype of hematopoietic cells transformed by the BCR/ABL oncoprotein of the Philadelphia chromosome is characterized by growth factor-independent proliferation, reduced susceptibility to apoptosis, and altered adhesion and motility. The mechanisms underlying this phenotype are not fully understood, but there is evidence that some of the properties of BCR/ABL-expressing cells are dependent on the activation of downstream effector molecules such as RAS, PI-3k, and bcl-2. We show here that the small GTP-binding protein Rac is activated by BCR/ABL in a tyrosine kinase-dependent manner. Upon transfection with a vector carrying the dominant-negative N17Rac, BCR/ABL-expressing myeloid precursor 32Dcl3 cells retained the resistance to growth factor deprivation-induced apoptosis but showed a decrease in proliferative potential in the absence of interleukin-3 (IL-3) and markedly reduced invasive properties. Moreover, compared with BCR/ABL-expressing cells, fewer BCR/ABL plus N17Rac double transfectants were capable of homing to bone marrow and spleen. Consistent with these findings, survival of SCID mice injected with the BCR/ABL plus N17Rac double transfectants was markedly prolonged as compared with that of mice injected with BCR/ABL-expressing cells. Together, these data support the important role of a Rac-dependent pathway(s) controlling motility in BCR/ABL-mediated leukemogenesis.
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