<b><i>Background:</i></b> The chemokine receptor CXCR5 is selectively expressed on B cells; it is involved in lymphocyte homing and the development of normal lymphoid tissue. Its principle ligand is CXCL13 or B lymphocyte chemoattractant. Three polymorphisms in the <i>CXCR5</i> gene, rs148351692 C/G, rs6421571 C/T, and rs78440425 G/A, have been identified. <b><i>Objective:</i></b> To assess the genetic polymorphisms of <i>CXCR5</i> and evaluate their possible contribution to the susceptibility and response to therapy of diffuse large B-cell lymphoma (DLBCL). <b><i>Patients and Methods:</i></b> Fifty DLBCL (not otherwise specified) patients and 50 control subjects were included in this study. <i>CXCR5</i> genotypes were determined by PCR-RFLP. <b><i>Results:</i></b> Our study revealed that the <i>CXCR5</i> rs148351692 C/G and rs6421571 C/T gene polymorphisms are associated with an increased risk of developing DLBCL (OR 28.57 [95% CI 8.96–96.56] and 3.45 [1.67–11.83] respectively), while CXCR5 rs78440425 G/A showed no association with the risk of lymphoma. Moreover, the double and triple combined gene polymorphisms are associated with an increased risk of developing DLBCL of approximately 120-fold and 105-fold, respectively. <i>CXCR5</i> gene polymorphisms had no significant impact on disease outcome or response to therapy. <b><i>Conclusions:</i></b> <i>CXCR5</i> gene polymorphisms could be considered a potential risk factor for the development of DLBCL.
Background: Primary extranodal diffuse large B-Cell lymphoma (PE-DLBCL) accounts for about one-third of all cases of DLBCL. We reviewed the clinical and pathological characteristics of cases with PE-DLBCL presented to NCI, Egypt. Patients and methods: We retrospectively studied patients with pathologically documented PE-DLBCL presented to the National Cancer Institute between January 2008 and December 2010. Revision of histopathology and sub-classification of patients to germinal centre (GC) DLBCL and non-GC-DLBCL through immunostaining of CD10, BCL-6 and MUM-1 were done. Cases that were CD10+/BCL-6±/ MUM-1- were categorised as GC-DLBCL, while cases that were CD10-/BCL-6±/MUM-1+ were categorised as non-GC-DLBCL. Clinical data regarding baseline characteristics, chemotherapy given and the response to chemotherapy was collected. Results: A total of 57 patients of PE-DLBCL were included in the study. Mean age was 48.9 years (range 21-78), and 32 patients (56.1%) were females. Most frequent locations were gastrointestinal and liver (29.9% and 22.9 %; respectively). Forty-two patients (73.7%) were sub-classified as non-GC-DLBCL. The patients who were stage III/IV were more common (52.6%). Fifty-two patients received CHOP, 5 received CVP, and 6 patients received radiotherapy after finishing chemotherapy. Complete response rate (CR) was 64.9%, there was no difference in the CR (66.7%, 64.3%) and Overall Survival (53.3%, 52.4%) in GC-DLBCL group in comparison to non-GC-DLBCL group (p = 0.24 and 0.6; respectively). The CR and OS for patients with low international prognostic index (IPI) were significantly better than patients with intermediate or high IPI (p = 0.008 and 0.08, respectively). Conclusion: Non-GC-DLBCL is more common than GC-DLBCL in PE-DLBCL in Egyptian population. The most affected sites are gastrointestinal and liver reflecting the association between high frequency of hepatitis B and C and hepatic non-Hodgkin’s lymphoma (NHL). Stage of the disease and IPI remains the most important prognostic factor for PE-DLBCL.
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