The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
The biology of CML blast crisis
Open accessAbstract
Chronic myelogenous leukemia (CML) evolves from a chronic phase characterized by the Philadelphia chromosome as the sole genetic abnormality into blast crisis, which is often associated with additional chromosomal and molecular secondary changes. Although the pathogenic effects of most CML blast crisis secondary changes are still poorly understood, ample evidence suggests that the phenotype of CML blast crisis cells (enhanced proliferation and survival, differentiation arrest) depends on cooperation of BCR/ABL with genes dysregulated during disease progression. Most genetic abnormalities of CML blast crisis have a direct or indirect effect on p53 or Rb (or both) gene activity, which are primarily required for cell proliferation and survival, but not differentiation. Thus, the differentiation arrest of CML blast crisis cells is a secondary consequence of these abnormalities or is caused by dysregulation of differentiation-regulatory genes (ie, C/EBPα). Validation of the critical role of certain secondary changes (ie, loss of p53 or C/EBPα function) in murine models of CML blast crisis and in in vitro assays of BCR/ABL transformation of human hematopoietic progenitors might lead to the development of novel therapies based on targeting BCR/ABL and inhibiting or restoring the gene activity gained or lost during disease progression (ie, p53 or C/EBPα).
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Cites
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Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis
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Separation of C/EBPα-mediated proliferation arrest and differentiation pathways
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Cited by
The cancer stem cell: premises, promises and challenges
Clevers, H. (2011) · Nature Medicine · doi:10.1038/nm.2304 · Cited by 1,923
Translation of the Philadelphia chromosome into therapy for CML
Druker, B. J. (2008) · Blood · doi:10.1182/blood-2008-07-077958 · Cited by 668
Gene expression changes associated with progression and response in chronic myeloid leukemia
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Protein phosphatase 2A: a target for anticancer therapy
Perrotti, D., & Neviani, P. (2013) · The Lancet Oncology · doi:10.1016/s1470-2045(12)70558-2 · Cited by 400
Self-citationThe p53 family in differentiation and tumorigenesis
Stiewe, T. (2007) · Nature Reviews Cancer · doi:10.1038/nrc2072 · Cited by 306
Metadata
- Authors
- Calabretta, B., & Perrotti, D.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2004-06-01
- Volume
- 103
- Issue
- 11
- Pages
- 4010-4022
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2058576674
- Cited by
- 592
- References
- 9
- FWCI
- 25.29
- Type
- journal article
- Language
- en
- Open access
- green
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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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