Disorders of the cell cycle regulatory machinery play a key role in the pathogenesis of cancer. Over-expression of cyclin D1 protein has been reported in several solid tumors and certain lymphoid malignancies, but little is known about the effect of its expression on clinical behavior and outcome in B-cell Non-Hodgkin lymphoma (NHL). In this study, we investigated the expression of cyclin Dl in group of patients with NHL and correlated the results with the clinical and laboratory data. The degree of expression of cyclin Dl protein was evaluated by flow cytometry in a group of NHL patients (n = 46) and in normal control group (n = 10). Cyclin Dl over expression was detected in 10 out of 46 (21.7%) patients; they were 5/5-mantle cell lymphoma (MCL) (100%) and 5/28 large B-cell lymphoma (17.8%). All other NHL subtypes showed normal cyclin D1 expression. The clinical signs (hepatomegaly, splenomegaly and B-symptoms, clinical staging) and laboratory data (hemoglobin, white cell count (WBCs), platelet count, and bone marrow infiltration) were not significantly different between NHL subgroup with cyclin Dl over expression and that with normal cyclin Dl expression. Serum lactic dehydrogenase (LDH) levels and lymphadenopathy were significantly higher in NHL group with cyclin D1 over expression as compared to those without. Also, cyclin D1 over expression is associated with poor outcome of NHL patients. Cyclin Dl over expression was evident among all cases of MCL and few cases of large B-cell lymphoma. Cyclin Dl over expression might be used as adjuvant tool for diagnosis of MCL; has role in NHL biology and is bad prognostic index in NHL.

Background: Classical Hodgkin's lymphoma (cHL) represents the majority of HLs with a relatively good prognosis. In 20% of patients, primary treatment fails. Prediction of treatment failure is critical. A gene signature of tumour associated macrophages (TAM) correlated with response to treatment as CD68 positive TAM was found to be associated with shortened survival. We aim to investigate the relation CD68+TAM infiltration to patients' outcome. Patients and Methods: Pathological materials of 115 patients with cHL were used. Clinical characteristics of patients were collected from the records. CD68 immunostaining was performed to determine the number of infiltrating TAM and subsequently followed by stratification of results. Results of CD68 immunostaining were statistically analysed to correlate the extent of CD68+ TAM infiltration with clinicopathological characteristics, treatment outcome, and patients' survival. Results: High CD68+TAM infiltration was observed in more patients of cHL (96/115 of patients = 83.5%). High CD68+TAM infiltration was associated with extranodal presentation (P = .001), and higher stage (P = .022). No associations with other clinicopathological parameters were found. High CD68+TAM infiltration was not found to be an independent predictor of treatment outcome. High CD68+TAM infiltration correlated with disease free survival (DFS) (log-rank = 4.505, P = .034) but not with disease specific survival (DSS) (log-rank = 1.371, P = .242). Conclusions:The results of our study support the adverse prognostic effect of high TAM in cHL. Technical standardisation of CD68 immunostaining is required to establish TAM infiltration as a prognostic predictor. Also in vivo and in vitro cHL models have to be established for proper understanding of the role of CD68 in modulating the TAM in cHL.