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Analysis of the p16INK4A, p15INK4B and p18INK4C genes in multiple myeloma
T Tasaka1, J Berenson, R Vescio
1Department of Medicine, UCLA School of Medicine, Cedars-Sinai Research Institute 90048, USA.
Abstract:
To study the structural integrity of the cyclin-dependent kinase inhibitors known as INK4A (p16), INK4B (p15) and INK4C (p18) in multiple myeloma, we examined 20 primary myeloma samples (including one case of plasma cell leukaemia) using polymerase chain reaction-single strand conformation polymorphism, and 17 samples were examined by Southern blot analysis. The plasma cell leukaemia sample had homozygous deletions of the p15 and p16 genes (6%). One myeloma case had a p15 gene homozygous deletion (6%) with an intact p16 gene. This sample also had a p18 homozygous deletion, suggesting that the deletion of both genes may be important in either the development or progression of myeloma. No point mutations of these INK4 genes were found in the 20 samples. This is the first report that indicates that deletions of p15, p16 and p18 genes occur in some individuals with multiple myeloma (2/17 cases).
Insights
Gene deletions of p15, p16, and p18 (INK4 family) occur in multiple myeloma. These genetic alterations may play a role in the development and progression of this blood cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Multiple myeloma is a cancer of plasma cells.
- Cyclin-dependent kinase inhibitors (INK4 family) regulate cell cycle progression.
- The role of INK4A (p16), INK4B (p15), and INK4C (p18) in multiple myeloma is not well understood.
Purpose of the Study:
- To investigate the structural integrity of INK4A (p16), INK4B (p15), and INK4C (p18) genes in multiple myeloma.
- To determine the frequency and type of genetic alterations in these genes in myeloma patients.
Main Methods:
- Analysis of 20 primary multiple myeloma samples.
- Utilized polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and Southern blot analysis.
- Examined gene deletions and point mutations in p15, p16, and p18 genes.
Main Results:
- Homozygous deletions of p15 and p16 genes were observed in one plasma cell leukaemia sample (6%).
- One myeloma case exhibited a homozygous deletion of the p15 gene and a p18 homozygous deletion, with an intact p16 gene.
- No point mutations were detected in the INK4 genes across all 20 samples.
- Deletions of p15, p16, and p18 genes were identified in 2 out of 17 myeloma cases.
Conclusions:
- Gene deletions of p15, p16, and p18 occur in a subset of multiple myeloma patients.
- These deletions may be significant in the pathogenesis or progression of multiple myeloma.
- Further research is warranted to elucidate the functional impact of these genetic alterations.
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