الفهرس 
LymphomaOnly 14 pages are availabe for public view
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Abstract
ABSTRACT
Background: Non-Hodgkin Lymphoma (NHL) comprises an extremely heterogeneous group of mature lymphoid neoplasm that might be derived from either B-cell or T/NK cell lineages. Within this broad term of NHL, numerous disease entities with variable clinical behavior and diverse molecular features were included. The p53 protein is a transcription factor known as the ”guardian of the genome” because of its critical function in preserving genomic integrity. The TP53 gene is mutated in approximately half of all human malignancies and in 10 to 20% of NHL patients. Investigating TP53 mutation assists in risk stratification, guiding treatment decisions, and exploring targeted therapies.
Objective: To identify the association between TP53 mutation and clinical, standard laboratory profile, morphological, other cytogenetic findings in B-NHL patients and assess the prognostic impact of TP53 on B-NHL patients’ outcome.
Methods: The present study is two phases, cross sectional study then Cohort study. It included 37 newly diagnosed B-NHL patients. The B- NHL patients on therapy and T-NHL cases were excluded from the study. The patients selected for the study were attending the Hematology Unit of Ain Shams University Hospitals for diagnosis. Mutation analysis of the TP53 gene was performed using real-time polymerase chain reaction (PCR), alongside fluorescence in situ hybridization (FISH) with a routine panel for NHL and the LSI 17p13 probe to detect deletion of the 17p (TP53) gene.
Results: Mutation analysis of the TP53 gene revealed that 13.5% of patients were positive for the mutation. Analysis of the characteristics of TP53-positive patients showed a significant association with adverse cytogenetic anomalies, predominantly del 17p13. Concerning the impact of TP53 mutation on the outcome of B-NHL, 5/5 (100%) of positive patients had poor outcome, although that was not statistically confirmed may be attributed to the sample size. To study patient outcomes, they were subdivided into two groups: those with favorable and poor outcomes. Both groups were compared regarding various prognostic factors. A significant relation was found in the poor outcome group regarding B symptoms, Ann Arbor staging, high LDH level, BM infiltration, extra nodal involvement and IPI. However, no statistically significant difference was found in between favorable or poor outcome groups, regarding clinical features, age, hemoglobin level, cytogenetic abnormalities and immunophenotypes.
Conclusion: A significant association was detected between TP53 mutation and adverse cytogenetic anomalies, predominantly del 17p13. Although TP53 mutation-positive patients demonstrated a poor therapeutic response, no notable association confirmed between TP53 mutation and the clinical outcome of B-NHL patients, potentially due to the limited sample size. No significant relationship was found between TP53 mutation and specific clinical presentations or standard laboratory test results rather than cytogenetic analysis. Additionally, a significant association was detected between the poor outcome of NHL patients and B-symptoms, extra nodal involvement, high LDH, international prognostic index.