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Updated: Aug 8, 2026
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Multiplexed Fluorescent Immunohistochemical Staining, Imaging, and Analysis in Histological Samples of Lymphoma
Published on: January 9, 2019
High throughput tissue microarray analysis of FHIT expression in diffuse large cell B-cell lymphoma from Saudi Arabia
Khawla Al Kuraya1, Abdul Khalid Siraj, Prashant Bavi
1Cancer Genomics, Research Centre, King Faisal Specialist Hospital and Research Centre, Riyadh, Kingdom of Saudi Arabia.
Summary
Fragile histidine triad (FHIT) gene alterations in diffuse large B-cell lymphoma (DLBCL) were studied. Promoter hypermethylation, not protein loss, correlated with poor prognosis in non-germinal center DLBCL.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Alterations in the fragile histidine triad (FHIT) gene are implicated in diffuse large B-cell lymphoma (DLBCL).
- Understanding FHIT inactivation mechanisms and prognostic significance is crucial for DLBCL patient outcomes.
Purpose of the Study:
- To investigate FHIT gene inactivation mechanisms (promoter hypermethylation and protein expression) in DLBCL.
- To clarify the prognostic relevance of FHIT alterations in DLBCL patients.
Main Methods:
- Analysis of 114 DLBCL cases with clinical follow-up.
- Immunohistochemistry for FHIT protein expression on tissue microarrays.
- FHIT promoter hypermethylation analysis on DNA samples.
Main Results:
- Reduced or absent FHIT protein expression observed in 66% of DLBCL cases, unrelated to prognosis.
- FHIT promoter hypermethylation detected in 23% of cases.
- Hypermethylation associated with poor prognosis and more frequent in non-germinal center DLBCL (27%) vs. germinal center DLBCL (13%).
Conclusions:
- FHIT promoter hypermethylation, not protein loss alone, is a significant mechanism for FHIT inactivation in a subset of DLBCL.
- FHIT promoter hypermethylation serves as a negative prognostic marker in DLBCL, particularly in the non-germinal center subtype.
