The effect of thalidomide in preventing delayed nausea and vomiting induced by GP regimen of chemotherapy for non-small cell lung cancer / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To observe the effect of thalidomide in preventing nausea and vomiting induced by emetogenic cisplatin (CDDP) chemotherapy in patients with advanced non-small cell lung cancer.</p><p><b>METHODS</b>This study was carried out as a prospective, randomized control clinical trial. 61 patients with advanced non-small cell lung cancer were scheduled to receive chemotherapy (gemcitabin 1000 mg/m(2) i.v. gtt d1, 8 and CDDP 75 mg/m(2) i.v. gtt d1, GP regimen). The patients were randomly divided into a treatment and control groups. All patients in both groups received ramosetron 0.3 mg intravenously (i.v.) and metoclopramide 20 mg intramuscularly (i.m.) 30 min prior to chemotherapy to prevent nausea and emesis on day 1. In the treatment group, addition of thalidomide (50 mg p.o. bid) were administered on days 1 to 5 after the start of chemotherapy.</p><p><b>RESULTS</b>Acute nausea was effectively controlled in 74.2% of the patients in the control group and in 90.0% of treatment group. Acute vomiting was effectively controlled in 90.3% of the patients in the control group and in 93.3% of treatment group. No statistically significant differences showed in effective control of acute nausea and vomiting between the 2 groups (P = 0.108; P = 1.000). Delayed nausea was effectively controlled in 19.4% of the patients in control group and in 56.7% in the treatment group. Delayed vomiting was effectively controlled in 48.4% of the patients in control group and 76.7% in treatment group. Statistically there was a significant differences in effective control of delayed nausea and vomiting between the 2 groups (P = 0.003, P = 0.023). Both antiemetic regimens were well tolerated, and no significant difference was observed in adverse events between the 2 groups (P > 0.05).</p><p><b>CONCLUSION</b>Our results demonstrate that thalidomide is highly effective in controlling delayed nausea and vomiting episodes in patients induced by moderately emetogenic chemotherapy. Moreover, no serious toxic effects are induced by this treatment.</p>

Expression of survivin gene in apoptosis induced by dexamethasone in CEM cells / 中国当代儿科杂志

<p><b>OBJECTIVE</b>The precise mechanism of glucocorticoid-induced apoptosis has not yet been elucidated. Survivin, a member of the inhibitors of apoptosis protein family, correlates with inhibition of apoptosis, proliferation, angiogenesis and multiple drugs resistance. This study aimed to investigate the variation of the survivin gene expression in apoptosis induced by dexamethasone (Dex) in the human T-lineage acute lymphoblastic leukemia (ALL) cell line, CEM-WT cells.</p><p><b>METHODS</b>The logarithmically growing CEM cells cultured in vitro (cell density 2 x10(5)/mL) were exposed to 0.1, 0.5, 1, 5, and 10 microM Dex, then were collected 24, 48 and 72 hrs later. Untreated CEM cells were used as Controls. The cell viability was determined by trypan blue dye exclusion. Apoptosis was evaluated by morphology and flow cytometry. Survivin protein and gene were analyzed by Western Blot and RT-PCR.</p><p><b>RESULTS</b>CEM cells growth was obviously inhibited by 0.1, 0.5, 1, 5, and 10 microM Dex from 48 hrs. The inhibition effect was dose- and time-dependent. CEM cells treated with Dex (> or = 5 microM) exhibited typical apoptotic features. The apoptosis increased after 5 microM Dex treatment in a time-dependent manner, with the apoptosis percentage increasing from 14.9% (12 hrs) to 46.2% (48 hrs). Compared with that of the Control group, the expression of survivin protein was down-regulated, with the expression rate of 54.6%, 45.5%, 15.8% and 9.7% respectively at 12, 24, 48 and 72 hrs after 5 microM Dex treatment. 5 microM Dex treatment also resulted in a decrease of survivin mRNA expression. The survivin mRNA expression was 76.4%, 67.3%, 55.0%, 49.9%, 38.3% and 18.3% of the Control respectively at 6, 12, 24, 48 and 72 hrs after Dex treatment.</p><p><b>CONCLUSIONS</b>Apoptosis induced by Dex in CEM cells is associated with downregulation of the survivin expression.</p>