Britschgi, Christian; Fey, Martin F (2009). Tumor suppressor genes in myeloid differentiation and leukemogenesis. Future oncology, 5(2), pp. 245-57. London: Future Medicine Ltd. 10.2217/14796694.5.2.245
Full text not available from this repository. (Request a copy)Tumor suppressor genes, such as p53, RB, the INK4-ARF family and PML, suppress malignant transformation by regulating cell cycle progression, ensuring the fidelity of DNA replication and chromosomal segregation, or by inducing apoptosis in response to potentially deleterious events. In myeloid leukemia, hematopoietic differentiation resulting from highly coordinated, stage-wise expression of myeloid transcription and soluble signaling factors is disrupted leading to a block in terminal differentiation and uncontrolled proliferation. This virtually always involves functional inactivation or genetic disruption of one or several tumor suppressor genes in order to circumvent their checkpoint control and apoptosis-inducing functions. Hence, reactivation of tumor suppressor gene function has therapeutic potential and can possibly enhance conventional cytotoxic chemotherapy. In this review, we focus on the role of different tumor suppressor genes in myeloid differentiation and leukemogenesis, and discuss implications for therapy.
Item Type: |
Journal Article (Further Contribution) |
|---|---|
Division/Institute: |
04 Faculty of Medicine > Department of Haematology, Oncology, Infectious Diseases, Laboratory Medicine and Hospital Pharmacy (DOLS) > Clinic of Medical Oncology |
UniBE Contributor: |
Britschgi, Christian, Fey, Martin |
ISSN: |
1479-6694 |
Publisher: |
Future Medicine Ltd. |
Language: |
English |
Submitter: |
Factscience Import |
Date Deposited: |
04 Oct 2013 15:11 |
Last Modified: |
05 Dec 2022 14:21 |
Publisher DOI: |
10.2217/14796694.5.2.245 |
PubMed ID: |
19284382 |
Web of Science ID: |
000264469800017 |
URI: |
https://boris.unibe.ch/id/eprint/31373 (FactScience: 195866) |
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