Chemokines are responsible for metastatic dissemination of cancers, including lymphomas. CCL3, a monocyte inflammatory protein-1 α, has been shown to be active as an inhibitor of primitive hematopoietic cell proliferation in vitro and in vivo. A dysfunction in this inhibitory process has been postulated to contribute to lymphomagenesis. The aim of this study was to measure the serum level of CCL3 and CCL3 mRNA in lymphoma patients compared with its expression during reactive lymphadenopathy; we also studied their effect on treatment response and survival of lymphoma patients.Materials and methods
The study included 53 lymphoma patients and 20 reactive lymphadenopathy patients. The serum level of CCL3 was assessed using the enzyme-linked immunosorbent assay technique, and CCL3 gene expression was measured using real time PCR.Results
There was a significant increase in the serum level of CCL3 in lymphoma patients (mean, 72.5±24.3 pg/ml) compared with reactive lymphadenopathy patients (mean, 31.5±12.6 pg/ml). Receiver–operator characteristic curve analysis showed a cutoff value of more than 55 pg/ml. There were positive and negative correlations with the lactate dehydrogenase level and time of follow-up (months), respectively. CCL3 expression was higher in lymphoma patients (90.5%) than in reactive lymphadenopathy patients (35%). Increased serum levels and expression of CCL3 were associated with treatment resistance. As regards survival, increased CCL3 expression was associated with decreased survival rate in lymphoma patients.Conclusion
CCL3 serum levels or gene expression could be a valuable prognostic marker and may provide insight into creating a new therapeutic modality.