Distribution of lymphomas subtypes in Jiangsu Province: a multicenter analysis of 5 147 cases / 中华血液学杂志

<p><b>OBJECTIVE</b>To investigate the epidemiological characteristics of lymphoma in Jiangsu province.</p><p><b>METHODS</b>A total of 5 147 consecutive lymphoma samples collected from 18 hospitals in Jiangsu province from January 2007 to December 2013 and diagnosed according to the WHO classification were enrolled in this study. Basic epidemiological information including age, gender and lymphoma subtypes was analyzed.</p><p><b>RESULTS</b>The median age of all lymphoma cases was 59(2-96) years, and gender ratio (M/F) was 1.6:1. The subtypes distribution analysis revealed that Hodgkin lymphoma (HL) accounted for 5.19% (n=241), whereas non-Hodgkin's lymphoma (NHL) accounted for 94.81% (n=4 400). Further analysis displayed B-NHL formed 75.44% (n=3 501) of all cases and T/NK-NHL 16.51% (n=766), diffuse large B-cell lymphoma and NK/T-cell lymphoma were the major subtypes of B-NHL and T/NK-NHL (53.50%, 1 873/3 501 and 31.85%, 244/766), respectively.</p><p><b>CONCLUSION</b>Unique epidemiological characteristics of lymphoma in Jiangsu province was different from other regions in China and western country, which can provide strong theoretical basis for public health, clinical and basic research.</p>

Influx of extracellular calcium participates in rituximab-enhanced ionizing radiation-induced apoptosis in Raji cells.

We have previously shown that rituximab has a significant radiosensitizing effect on Raji cells in vitro. To investigate whether calcium signals participate in rituximab- and radiation-induced cell death in Raji cells, confocal laser scanning microscopy was used to detect kinetic changes in intracellular free calcium concentration ([Ca2+]i). Cell survival, the rates of apoptosis in Raji cells and the kinetics of γ-H2AX foci induction and loss were also evaluated. X-irradiation of Raji cells induced an initial increase of [Ca2+]i in both the presence and absence of extracellular calcium, followed by a decrease in [Ca2+]i over time. Rituximab enhanced both the amplitude and the duration of intracellular calcium signals in the irradiated cells. EGTA significantly inhibited radiation- or radiation/rituximab combination treatment-induced apoptosis. However, the calcium chelators EGTA and BAPTA/AM conferred no survival advantage on the irradiated cells. Furthermore, although no significant difference was seen after 1h, the treatment of cells with a combination of irradiation and rituxiamb caused an increase of γ-H2AX foci when compared with irradiated cells after 8h. Both EGTA and BAPTA/AM suppressed the number of γ-H2AX foci induced by either radiation or radiation combined with rituximab. Our results suggest that rituximab increases the level of [Ca2+]i in irradiated Raji cells. The entry of calcium from the extracellular space plays an essential role in [Ca2+]i-dependent radiation-induced apoptosis in Raji cells. The calcium chelators inhibited the formation of γ-H2AX foci, which are thought to prevent the activation of Ca2+/Mg(2+)-dependent endonucleases and subsequent DNA fragmentation. The calcium chelators most likely modulate only particular features of apoptosis and fail to change the fates of cells that are already committed to die.

Rituximab sensitizes a Burkitt lymphoma cell line to cell killing by X-irradiation.

Clinical trials with rituximab in combination with chemotherapeutic regimens have shown promising results. Data on the effects of rituximab treatment in combination with irradiation are, however, limited and inconsistent. This study aims to investigate the effects of rituximab (R) on cell death induced by X-irradiation in Raji lymphoma cells and to evaluate its mechanisms. We found the cell growth inhibition by irradiation was enhanced by additional rituximab exposure both in cells precultured with rituximab followed by irradiation (R + irradiation) or in cells treated in the reverse sequence (irradiation + R). R + irradiation combination treatment induced more apoptotic cells than irradiation and irradiation + R treatment as early as 12 h after treatment. At 24 h, both combination treatments, R + irradiation and irradiation + R, showed apoptotic cells, which were significantly different from irradiation alone. G2/M cell cycle arrest was observed after irradiation alone and the combination treatment. The combination treatment revealed an elevation in reactive oxygen species (ROS) generation in a radiation dose-dependent manner. In addition, rituximab enhanced the cell growth inhibition and apoptotic cell death induced by the oxidative agent, H(2)O(2). We propose that rituximab mediates a significant in vitro radiosensitizing effect and induces cell cycle changes and apoptosis in Raji cells. ROS probably play an important role in these events.