A meta‑analysis of serum p16 gene promoter methylation for diagnosis of nonsmall cell lung cancer.

OBJECTIVES: To evaluate the diagnostic value of serum p16 gene promoter methylation for diagnosis of nonsmall cell lung cancer (NSCLC). MATERIALS AND METHODS: By searching the databases of PubMed and CNKI, we included all the published articles related serum p16 gene promoter methylation and nonsmall lung cancer. The true positive, false positive, false negative, and true negative data for each included publication were extracted by the reviewers. The diagnostic sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, and area under the receiver operating characteristic (ROC) were pooled by MetaDiSc1.4 software. RESULTS: Finally, 13 manuscripts with 1440 subjects were involving in this diagnostic meta‑analysis. The pooled sensitivity and specificity were 0.25 (95% confidence interval [CI]: 0.18–0.32) and 0.95 (95% CI: 0.93–0.97), respectively, with randomized effect model. The pooled positive likelihood ratio and negative likelihood ratio were 5.08 (95% CI: 3.00–8.62) and 0.69 (95% CI: 0.62–0.77) with fixed effect model and randomized effect model, respectively. The diagnostic ROC curve for the included 13 publications was pooled by statistical software MetaDiSc14.0 according to the Bayes theorem. The pooled area under the ROC was 0.72 with its standard error of 0.10. CONCLUSION: According to the published articles, high specificity and low sensitivity were found in this meta‑analysis for the p16 gene promoter methylation in the diagnosis of NSCLC.

Noncoding RNA small nucleolar RNA host gene 1 promote cell proliferation in nonsmall cell lung cancer.

BACKGROUND: Nonsmall cell lung cancer (NSCLC) is the major cause of cancer death worldwide. Increasing evidence shows that noncoding RNAs (ncRNAs) are widely involved in the development and progression of NSCLC. ncRNA small nucleolar RNA host gene 1 (SNHG1) has not been studied in cancer, especially its role in lung cancer remains unknown. Our studies were designed to investigate the expression and biological significance of SNHG1 in lung cancer. SNHG1 may be a novel ncRNA in early diagnosis in lung cancer. METHODS: Noncoding RNA SNHG1 expression in 7 lung cancer cell lines was measured by quantitative real‑time polymerase chain reaction. RNA interference approaches were used to find the biological functions of SNHG1. The effect of SNHG1 on proliferation was evaluated by cell count and crystal violet stains. RESULTS: Noncoding RNA SNHG1 expression was significantly upregulated in lung cancer cells when compared with normal bronchial epithelial cells. In addition, in vitro assays our results indicated that knockdown of SNHG1 inhibited cell proliferation. CONCLUSIONS: Our data indicated that ncRNA SNHG1 is significantly upregulated in NSCLC cell lines and may represent a new biomarker and a potential therapeutic target for NSCLC intervention.

MicroRNA-449a inhibits cell growth in lung cancer and regulates long noncoding RNA nuclear enriched abundant transcript 1.

OBJECTIVE: Lung cancer has become the primary cause of cancer‑related death now. New therapies targeting the molecular regulatory machinery were required imperatively. MicroRNAs and long noncoding RNAs can respectively or cooperatively function as oncogenes or tumor suppressor genes in human cancers. The present study identified that miR‑449a was down‑regulated in tissue of human lung cancer. In this study, we aimed to investigate the function of miR‑449a in NL9980 and L9981 lung carcinoma cells lines and the relationship with lncRNA nuclear enriched abundant transcript 1 (NEAT1). MATERIALS AND METHODS: miR‑449a was profiled in several lung carcinoma cell lines by quantitative reverse transcription‑polymerase chain reaction RT‑PCR. We analyzed the effects of miR‑449a overexpression on proliferation, apoptosis and cell cycle in L9981 cells. The regulatory relationship between miR‑449a and NEAT1 was predicted in silico and further studied by miR‑449a inhibitor and mimics assay. RESULTS: miR‑449a was expressed in four cell lines, which we selected, however miR‑449a was in high level in NL9980 and in low level in L9981 (P < 0.05). When the miR‑449a was the overexpression in L9981 cells, the cell growth was suppressed, and the apoptosis cells were promoted compared with the control group (P < 0.05). The G1/G0 became longer and S, G2/M became shorter (P < 0.05) by miR‑449a overexpression. Further study of the interaction between miR‑449a and NEAT1 show that NEAT1 was up‑regulated when cells were transfected with miR‑449a inhibitor, and NEAT1 was down‑regulated when cells transfected with miR‑449a mimics. CONCLUSIONS: Our data indicate that miR‑449a may function as a suppressor of lung cancer, and affects the expression of NEAT1 in lung cancer cells.

Capecitabine maintenance therapy in patients with recurrent or metastatic breast cancer

Our objective was to investigate the efficacy and safety of capecitabine maintenance therapy (CMT) after capecitabine-based combination chemotherapy in patients with metastatic breast cancer. The clinical data of 139 metastatic breast cancer patients treated from March 2008 to May 2012 with capecitabine-based combination chemotherapy were retrospectively analyzed. When initial disease control was achieved by the combination chemotherapy, we used CMT for 50 patients, while 37 patients were treated with a different (non-CMT) maintenance therapy. We compared time to progression (TTP), objective response rate, disease control rate, clinical benefit rate, and safety of the two groups, and a sub-group analysis was performed according to pathological characteristics. Sixty-four percent of the patients received a median of six cycles of a docetaxel+capecitabine combination chemotherapy regimen (range 1-45); the median TTP (MTTP) for the complete treatment was 9.43 months (95%CI=8.38-10.48 months) for the CMT group and 4.5 months (95%CI=4.22-4.78 months; P=0.004) for the non-CMT group. The MTTPs for the maintenance therapies administered after the initial capecitabine combined chemotherapy were 4.11 months (95%CI=3.34-4.87 months) for the CMT group and 2.0 months (95%CI=1.63-2.38 months) for the non-CMT group. Gastrointestinal side effects, decreased white blood cells and palmar-plantar erythrodysesthesia were the main adverse reactions experienced with the combination chemotherapies, CMT and non-CMT treatments. No significant differences in the incidence of adverse reactions were detected in the CMT and non-CMT patients. After initial disease control was achieved with the capecitabine-based combination chemotherapy, CMT can significantly prolong TTP rates with a favorable safety profile.

Experimental studies on early treatment of schistosomal infection with artemether.

An early treatment with artemether given in appropriate regimens was tested in mice, rabbits and dogs for prevention purposes. Artemether was administered intragastrically (ig) to the hosts on day 7 after infection with Schistosoma japonicum cercariae at a single dose, and the same dose of artemether was repeated every 1 or 2 weeks for 2-4 times. As a result, most of the female worms were killed before their oviposition with female worm reduction rates of 90-100%, resulting in protection of the host from damage induced by schistosome eggs. When rabbits were treated ig with artemether 10 mg kg-1 on day 7 after infection, followed by repeated dosing every week for 4 times, some parameters related to acute schistosomiasis, such as temperature, eosinophil count and eggs in the feces were negative, and low specific antigen and antibody levels in serum were seen. Further study showed that the appropriate regimens of Artemether were also effective in early treatment of reinfection with cercariae. When rabbits infected with 48-52 cercariae once every other day for 5 times were treated ig with artemether 15 mg kg-1, followed by repeated dosing every 1 or 2 week for 2- 3 times, the female worm reduction rates were 92.1-98.4%. Histopathological examination of the livers showed that the above-mentioned early treatment with Artemether exhibited a promising protective effect on dogs and rabbits. The major features included normal appearance of the liver resembling those of uninfected dogs and rabbits; few or no dispersed miliary egg tubercles appeared on the surface of the liver; the structure of the hepatic lobules was normal with normal arrangement of the liver bundles; few or no eggs appeared in the portal vein area and there was apparent diminution of total egg granuloma, comprising inflammatory, fibrous or scarred egg granuloma. On the basis of above-mentioned results, early treatment with Artemether could be recommended for field trial for controlling acute schistosomiasis, reducing infection rate and intensity of infection.