Central Nervous System International Prognostic Index Impacts Overall Survival in Diffuse Large B-cell Lymphoma Treated with R-Chop in a third Level Cancer Center from Mexico: A Survey of 642 Patients

Abstract

Background: Central nervous system international prognosis index (CNS-IPI) is validated in European and the USA cancer databases. However, no validation has been done in Mexican population. Objective: The objective of the study was to assess the impact of the CNS-IPI on central nervous system (CNS) relapse and survival in Mexican patients with diffuse large B-cell lymphoma (DLBCL). Methods: In this retrospective analysis, clinical, biochemical, and histological variables and the CNS-IPI were analyzed. Results: Six hundred and forty-two patients with DBLCL were included in the study. The mean ± SD age was 56.8 ± 14.9 years. Most had an ECOG of 0-1: 75% (n = 484) had absence of B-symptoms and advanced disease (clinical stage: III-IV, n = 433, 67.4%). According to the CNS-IPI, almost one-half were in the low-risk category. According to the CNS-IPI, CNS relapse rate was 1.36% (95% CI: 83.2-92.8), 3.1% (95% CI: 132.4-162.8), and 7.4% (95% CI 61-91) for patients in the low-, intermediate-, and high-risk categories, respectively. The median overall survival in the high-risk group (CNS-IPI) was 22 months, and it has not been achieved after 80 months of follow-up for the other groups. Conclusions: CNS-IPI was associated with survival; therefore, we propose its use as a prognostic tool for prospective validation.

ct-DNA is useful to diagnose mutations at codon 641 of exon 16 of EZH2, which is a biomarker for relapse in patients with Diffuse Large B-cell Lymphoma treated with the R-CHOP scheme.

“…Lymphomas co-expressing MYC and BCL2 or BLC6 were considered double-expressors. Double-hit lymphomas were de ned as those with at least 10 % of MYC rearrangements were present by uorescence in situ hybridization (FISH) as previously described [21]. Regarding EZH2 status, they were classi ed as mutated or wild type.…”

“…The overexpression of EZH2 has been identi ed as a driver in lymphomagenesis [9]. In addition, the mutation at Y646 amino acid in the EZH2 gene is recurrently and signi cantly mutated in up to 40 % of B-cell lymphomas [10], and particularly in approximately [13][14][15][16][17][18][19][20][21][22][11][12]. The mutations of Tyr641 (Y641F, Y641N, Y641S, and Y641H) are de cient catalysts of unmodi ed H3K27 methylation relative to the wild type (wt) enzyme.…”