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P53 tumor suppressor gene in chronic myelogenous leukemia: a sequential study
A Rovira1, A Urbano-Ispizua, F Cervantes
1Postgraduate School of Hematology, Hematology Department, Hospital Clínic i Provincial, Barcelona, Spain.
Annals of Hematology
|March 1, 1995
Summary
Alterations in the p53 gene, specifically loss of one allele, were observed in chronic myeloid leukemia (CML) patients during accelerated or blast crisis phases. This suggests a role for p53 gene mutations in CML progression.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm characterized by the Philadelphia chromosome (Ph) and BCR-ABL fusion gene.
- The progression of CML from chronic phase to accelerated phase and blast crisis involves genetic alterations.
- The p53 tumor suppressor gene plays a critical role in maintaining genomic stability.
Purpose of the Study:
- To investigate the loss of p53 gene alleles in patients with Ph+, BCR/ABL+ chronic myeloid leukemia (CML).
- To determine the correlation between p53 gene alterations and the progression of CML to advanced phases.
Main Methods:
- Polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP) analysis using the AccII enzyme.
- Analysis of peripheral blood and bone marrow samples from 26 CML patients at different disease phases.
- Cytogenetic study including i(17q) chromosome analysis.
Main Results:
- Loss of one p53 gene allele was observed in 4 out of 12 informative cases.
- Allelic deletion of p53 coincided with the development of accelerated phase or blast crisis in all affected cases.
- One patient showed p53 allele loss in accelerated and blastic phases but not in the chronic phase.
Conclusions:
- Monoallelic deletion of the p53 gene is relatively frequent in advanced CML.
- p53 gene alterations may play a significant role in the evolution of CML to blast crisis.
- Further investigation into p53's role in CML pathogenesis is warranted.