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Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors
Published on: September 20, 2016
Malignancy: Tumor Suppressor Gene Aberrations in Acute Myelogenous Leukemia
DEREK L. Stirewalt1, JERALD P. Radich
1Clinical Research Division, Fred Hutchinson Cancer Research Center, and the Division of Oncology, University of Washington, Seattle, Washington.
Hematology (Amsterdam, Netherlands)
|June 16, 2001
Summary
Tumor suppressor genes play a role in acute myelogenous leukemia (AML) development. While mutations in p53 and Retinoblastoma (Rb) genes are uncommon in AML, expression abnormalities in several related genes are observed.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Acute myelogenous leukemia (AML) is a complex blood cancer.
- Cancer development often involves the disruption of tumor suppressor genes.
- Understanding these disruptions is key to comprehending AML pathogenesis.
Purpose of the Study:
- To review the current literature on tumor suppressor genes in AML.
- To explore the potential involvement of these genes in AML development.
Main Methods:
- Literature review of studies on tumor suppressor genes in AML.
- Analysis of mutation and expression data for key genes.
Main Results:
- Mutations in p53 and Retinoblastoma (Rb) genes are infrequent in AML compared to solid tumors.
- Expression abnormalities are noted in several tumor suppressor genes and related genes, including MDM2, p73, Rb, p14(ARF), p15(INK4B), and p16(INK4A).
Conclusions:
- Despite uncommon mutations in p53 and Rb, altered expression of other tumor suppressor genes is significant in AML.
- These genetic alterations likely contribute to the evasion of normal regulatory controls in AML pathogenesis.
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