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Cited by 192

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Tumorigenic activity of the BCR-ABL oncogenes is mediated by BCL2.

Open access
Sánchez-García, I, Grütz, G·1995·Proceedings of the National Academy of Sciences

Abstract

BCR-ABL is a chimeric oncogene generated by translocation of sequences from the c-abl protein-tyrosine kinase gene on chromosome 9 into the BCR gene on chromosome 22. Alternative chimeric proteins, p210BCR-ABL and p190BCR-ABL, are produced that are characteristic of chronic myelogenous leukemia and acute lymphoblastic leukemia, respectively. Their role in the etiology of human leukemia remains to be defined. Transformed murine hematopoietic cells can be used as a model of BCR-ABL function since these cells can be made growth factor independent and tumorigenic by the action of the BCR-ABL oncogene. We show that the BCR-ABL oncogenes prevent apoptotic death in these cells by inducing a Bcl-2 expression pathway. Furthermore, BCR-ABL-expressing cells revert to factor dependence and nontumorigenicity after Bcl-2 expression is suppressed. These results help to explain the ability of BCR-ABL oncogenes to synergize with c-myc in cell transformation.

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Metadata

Authors
Sánchez-García, I., & Grütz, G.
Venue
Proceedings of the National Academy of Sciences
Published
1995-06-06
Volume
92
Issue
12
Pages
5287-5291
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2038588592
Cited by
192
References
3
FWCI
6.99
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Tumorigenic activity of the BCR-ABL oncogenes is mediated by BCL2. https://app.cochat.ai/papers/10.1073/pnas.92.12.5287
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Sánchez-García, I., & Grütz, G. (1995). Tumorigenic activity of the BCR-ABL oncogenes is mediated by BCL2. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.92.12.5287

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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