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Microsatellite instability and k-ras, p53 mutations in thyroid lymphoma
T Takakuwa1, T Hongyo, M Syaifudin
1Departments of Pathology, Osaka University Medical School, Suita, Osaka 565-0871, Japan.
Japanese Journal of Cancer Research : Gann
|April 13, 2000
Summary
Chronic inflammation may drive thyroid cancer through replication errors. Microsatellite instability, a marker of genomic instability, was found in diffuse large B-cell lymphoma, suggesting a role in tumor progression.
Area of Science:
- Oncology
- Genetics
- Pathology
Background:
- Thyroid lymphoma (TL) is linked to chronic lymphocytic thyroiditis (CLTH).
- Replication error (RER) in inflammatory lesions suggests a role in cancer development.
- The role of RER in TL pathogenesis requires clarification.
Purpose of the Study:
- To investigate the involvement of RER in TL pathogenesis.
- To analyze microsatellite instability (MSI) in CLTH and various TL subtypes.
- To examine p53 and k-ras gene mutations in relation to RER.
Main Methods:
- Analyzed MSI in 16 microsatellite repeats across 9 CLTH and 19 TL cases (including DLBL, follicular, MALT, lymphoplasmacytic types).
- Assessed p53 and k-ras gene mutations.
- Defined MSI as alterations at 2 or more microsatellite loci.
Main Results:
- MSI was detected in 5 of 10 diffuse large B-cell lymphoma (DLBL) cases, significantly higher than other TL types and CLTH (P < 0.05).
- Four cases (21.1%) exhibited k-ras mutations, strongly associated with RER in DLBL.
- p53 mutations were found in 2 TL cases but not CLTH; no significant RER-p53 association was observed.
Conclusions:
- Genomic instability, indicated by MSI, contributes to the progression of TL from low to high grade.
- RER and k-ras mutations are closely associated in DLBL.
- RER does not appear to drive the development of low-grade lymphoma within CLTH lesions.