LncRNA SNHG11 accelerates the progression of lung adenocarcinoma via activating Notch pathways.

BACKGROUND: Numerous researches have emphasized that long non-coding RNAs (lncRNAs) have a close association with the biological process in multiple cancers including lung adenocarcinoma (LUAD). Nevertheless, the detailed function and potential mechanism of Small nucleolar RNA Host Gene 11 (SNHG11) in LUAD keep unknown. METHODS: Quantitative reverse transcription polymerase chain reaction (RT-qPCR) tested SNHG11, miR-193a-5p and notch receptor 3 (Notch3) expression. Functional assays tested the function of SNHG11 in LUAD cells. The relationship among SNHG11, miR-193a-5p and Notch3 was verified by mechanism assays. In vivo assays were implemented to reveal the role of SNHG11 in LUAD tumor growth. RESULTS: SNHG11 was evidently high expressed in LUAD cells in comparison to normal lung epithelial cells. Moreover, down-regulation of SNHG11 hindered viability, proliferation and migration of LUAD cells as well as tumor growth. As for the mechanisms, SNHG11 activated Notch pathway via regulating Notch3. In addition, SNHG11 competitively bound with miR-193a-5p to up-regulate Notch3. The last rescue assays displayed that SNHG11 affecting LUAD cell malignant behaviors via regulating miR-193a-5p/SNHG11. CONCLUSION: SNHG11 regulated miR-193a-5p/Notch3 axis to activate Notch pathway, consequently facilitating the proliferation and migration in LUAD.

Bone marrow mesenchymal stem cells-derived exosomal microRNA-19b-3p targets SOCS1 to facilitate progression of esophageal cancer.

OBJECTIVE: Exosomes can convey particular microRNAs (miRNAs) to affect biological functions of cancer cells. Nevertheless, the impact of bone marrow mesenchymal stem cells (BMSCs)-derived exosomes (BMSC-exos) transmitting miR-19b-3p on esophageal cancer (EC) progression remains scarcely studied. We aimed to explore the role of BMSC-exos mediating miR-19b-3p in EC cell growth. METHODS: Eighty-three cases of EC patients were included in this study and the expression of miR-19b-3p and suppressor of cytokine signaling 1 (SOCS1) in cancer and adjacent normal tissues from the patients were assessed. BMSCs were cultured and BMSC-exos were extracted, which were then transfected with altered miR-19b-3p and SOCS1 to assess their roles in proliferation, migration, invasion, epithelial-mesenchymal transition (EMT) and apoptosis of EC cells. Targeting relationship between miR-19b-3p and SOCS1 was verified by Targetscan and dual luciferase reporter gene assay. MiR-19b-3p and SOCS1 expression was assessed in TE-2 cells. RESULTS: MiR-19b-3p was upregulated and SOCS1 was downregulated in EC tissues. BMSC-exos or exosomal miR-19b-3p promoted malignant behaviors of EC cells. MiR-19b-3p was upregulated and targeted SOCS1 in EC cells. MiR-19b-3p inhibition or SOCS1 overexpression suppressed proliferation, migration, invasion and EMT, and induced apoptosis of EC cells. SOCS1 silencing abrogated these effect of miR-19b-3p inhibition on EC cells. CONCLUSION: BMSC-derived exosomal miR-19b-3p promotes progression of EC through targeting SOCS1. This study provides a novel understanding on molecular mechanisms of EC.

LINC01783 facilitates cell proliferation, migration and invasion in non-small cell lung cancer by targeting miR-432-5p to activate the notch pathway.

BACKGROUND: Non-small cell lung cancer (NSCLC) is a common malignancy around the globe. Increasing long non-coding RNAs (lncRNAs) have been confirmed to be associated with the progression of cancers, including NSCLC. Long intergenic non-protein coding RNA 1783 (LINC01783) is a novel lncRNA and its regulatory function as competing endogenous RNA (ceRNA) has not been studied in NSCLC. METHODS: RT-qPCR measured the expression level of LINC01783 in NSCLC cells. CCK-8, EdU, transwell and wound healing assays were conducted to detect cell proliferation, migration and invasion in NSCLC. The relationship between miR-432-5p and LINC01783 along with delta like 1 (DLL-1) was illustrated by RNA pull down, RIP and luciferase reporter assays. RESULTS: LINC01783 was found remarkably increased in NSCLC cell lines, and down-regulation of LINC01783 suppressed cell proliferation, migration and invasion. Then, we discovered Notch pathway was related to the progression of NSCLC, and DLL-1 expression was reduced by LINC01783 knockdown. Furthermore, DLL-1 overexpression could counteract the suppressive effects of LINC01783 down-regulation on the growth of NSCLC cells. MiR-432-5p was observed to be the mutual miRNA that could bind with both LINC01783 and DLL-1. Overexpression of miR-432-5p inhibited DLL-1 expression. In the rescue assays, miR-432-5p depletion offset the impacts of LINC01783 knockdown, and then DLL-1 silence recovered the influence of miR-432-5p down-regulation on NSCLC cell growth. CONCLUSION: LINC01783 aggravates NSCLC cell growth by regulating Notch pathway and sponging miR-432-5p, being a potential target in the treatment for NSCLC.

Diosmetin induces apoptosis and enhances the chemotherapeutic efficacy of paclitaxel in non-small cell lung cancer cells via Nrf2 inhibition.

BACKGROUND AND PURPOSE: Non-small-cell lung cancer (NSCLC) accounts for up to 80-85% of all lung cancers and has a disappointing prognosis. Flavonoids exert anticancer properties, mostly involving stimulation of ROS production without significant toxicity to normal cells. This study was aimed to delineate the effect of diosmetin, a natural flavonoid, on NSCLC cells and its ability to enhance the antitumour activity of paclitaxel. EXPERIMENTAL APPROACH: NSCLC cells, normal cell lines HLF-1 and BEAS-2B, and immunodeficient mice were chosen as models to study the effects of diosmetin. Changes in cell viability, apoptosis, and ROS were analysed by MTT assay, flow cytometry assay, and fluorescent probe DCFH-DA. Expression of proteins and mRNA was determined by Western blotting and real-time RT-PCR. Growth of xenografted tumours was measured. Spleens and other vital organs were analysed with histological and immunohistochemical techniques. KEY RESULTS: Diosmetin induced selective apoptotic death in NSCLC cells but spared normal cells, via ROS accumulation. Diosmetin induced ROS production in NSCLC cells probably via reducing Nrf2 stability through disruption of the PI3K/Akt/GSK-3ß pathway. The in vitro and in vivo xenograft studies showed that combined treatment of diosmetin and paclitaxel synergistically suppressed NSCLC cells. Histological analysis of vital organs showed no obvious toxicity of diosmetin, which matched our in vitro findings. CONCLUSIONS AND IMPLICATIONS: Diosmetin selectively induced apoptosis and enhanced the efficacy of paclitaxel in NSCLC cells via ROS accumulation through disruption of the PI3K/Akt/GSK-3ß/Nrf2 pathway. Therefore, diosmetin may be a promising candidate for adjuvant treatment of NSCLC.

Tumoral NOX4 recruits M2 tumor-associated macrophages via ROS/PI3K signaling-dependent various cytokine production to promote NSCLC growth.

M2-type tumor-associated macrophages (TAMs) infiltration contributes to cancer malignant progression. However, the mechanisms for controlling recruitment and M2 polarization of macrophages by cancer cells are largely unclear. NADPH oxidase 4 (NOX4) is abundantly expressed in non-small cell lung cancer (NSCLC) and mediates cancer progression. NOXs are in close relation with cancer-related inflammation, nevertheless, whether tumoral NOXs influence microenvironmental macrophages remains undentified. This study found that there was a close association between NOX4 expression and macrophage chemotaxis in patients with NSCLC analyzed using TCGA RNA-sequencing data. NOX4 in NSCLC cells (A549 and Calu-1 cell lines) efficiently enhanced murine peritoneal macrophage migration and induces M2 polarization. Immunohistochemical analysis of clinical specimens confirmed the positive correlation of NOX4 and CD68 or CD206. The mechanical study revealed that tumoral NOX4-induced reactive oxygen species (ROS) stimulated various cytokine production, including CCL7, IL8, CSF-1 and VEGF-C, via PI3K/Akt signaling-dependent manner. Blockade of the function of these cytokines reversed NOX4 effect on macrophages. Specifically, the results showed that tumoral NOX4-educated M2 macrophages exhibited elevated JNK activity, expressed and released HB-EGF, thus facilitating NSCLC proliferation in vitro. Pretreatment of macrophages with JNK inhibitor blocked tumoral NOX4-induced HB-EGF production in M2 macrophages. Finally, in a xenograft mouse model, overexpression of NOX4 in A549 cells enhanced the tumor growth. Elimination of ROS by NAC or inhibition of NOX4 activity by GKT137831 suppressed tumor growth accompanied by reduction in macrophage infiltration and the percentage of M2 macrophages. In conclusion, our study indicates that tumoral NOX4 recruits M2 TAMs via ROS/PI3K signaling-dependent various cytokine production, thus contributing NSCLC cell growth.

Inhibition of PDGFR by CP-673451 induces apoptosis and increases cisplatin cytotoxicity in NSCLC cells via inhibiting the Nrf2-mediated defense mechanism.

Platelet-derived growth factor receptors (PDGFRs) are abundantly expressed by stromal cells in the non-small cell lung cancer (NSCLC) microenvironment, and in a subset of cancer cells, usually with their overexpression and/or activating mutation. However, the effect of PDGFR inhibition on lung cancer cells themselves has been largely neglected. In this study, we investigated the anticancer activity of CP-673451, a potent and selective inhibitor of PDGFRß, on NSCLC cell lines (A549 and H358) and the potential mechanism. The results showed that inhibition of PDGFRß by CP-673451 induced a significant increase in cell apoptosis, accompanied by ROS accumulation. However, CP-673451 exerted less cytotoxicity in normal lung epithelial cell line BEAS-2B cells determined by MTT and apoptosis assay. Elimination of ROS by NAC reversed the CP-673451-induced apoptosis in NSCLC cells. Furthermore, CP-673451 down-regulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) probably through inhibition of PI3K/Akt pathway. Rescue of Nrf2 activity counteracted the effects of CP-673451 on cell apoptosis and ROS accumulation. Silencing PDGFRß expression by PDGFRß siRNA exerted similar effects with CP-673451 in A549 cells, and when PDGFRß was knockdowned by PDGFRß siRNA, CP-673451 produced no additional effects on cell viability, ROS and GSH production, Nrf2 expression as well as PI3K/Akt pathway activity. Specifically, Nrf2 plays an indispensable role in NSCLC cell sensitivity to platinum-based treatments and we found that combination of CP-673451 and cisplatin produced a synergistic anticancer effect and substantial ROS production in vitro. Therefore, these results clearly demonstrate the effectiveness of inhibition of PDGFRß against NSCLC cells and strongly suggest that CP-673451 may be a promising adjuvant chemotherapeutic drug.

Increased expression of circRNA_102231 in lung cancer and its clinical significance.

Circular RNAs (circRNAs) are a type of endogenous non-coding RNAs which implicated in the progression of cancers. However, the role of circRNA_102231 in lung cancer remains unclear. Gene Expression Omnibus (GEO) datasets were used to investigate aberrantly expressed circRNAs in lung cancer. CircRNA_102231 expression in lung adenocarcinoma (LAC) tissues was dertermined by qRT-PCR. Furthermore, we explored the functions of circRNA_102231 on lung cancer cells progression. In the present study, circRNA_102231 was found to be one of the most significantly upregulated circRNAs in the GEO datasets analysis (GSE101586). QRT-PCR showed that circRNA_102231 expression was significantly upregulated in LAC tissues and associated with the advanced TNM stage, lymph node metastasis, and poor overall survival of lung cancer patients. The area under the receiver operating characteristic curve (ROC) was 0.897. in addition, function assays showed that circRNA_102231 inhibition significantly suppressed lung cancer cells proliferation and invasion ability in vitro. In conclusion, our study demonstrated that circRNA_102231 could act as a potential biomarker and therapeutic target for lung cancer patients.

Paracrine signaling by VEGF-C promotes non-small cell lung cancer cell metastasis via recruitment of tumor-associated macrophages.

High expression of tumoral vascular endothelial growth factor C (VEGF-C) is correlated with clinical non-small cell lung cancer (NSCLC) metastasis and patient survival. Nevertheless, the comprehensive mechanisms accounting for VEGF-C-mediated cancer progression remain largely unclear. The present study found that VEGF-C expression was upregulated in various NSCLC cell lines. By utilizing transwell migration assay, we found that both recombinant VEGF-C protein and overexpression of VEGF-C in NSCLC cells (A549 and H441 cell lines) could efficiently enhance RAW264.7 cell (murine macrophages) migration. However, recombinant VEGF-C treatment had no effects on both CD206 (an M2 macrophage marker) expression and M1/M2 cytokine profiles of macrophages. Furthermore, additional treatment of recombinant Flt-4/Fc, the specific VEGFR-3 inhibitor or the specific VEGFR-2 inhibitor significantly suppressed macrophage migration compared with A549-CM (conditioned medium) or H441-CM alone group, confirming that NSCLC cells-derived VEGF-C is sufficient to promote macrophage migration. Interestingly, VEGF-C could stimulate the Src/p38 signaling via VEGFR-2/3 axis in macrophages, and inhibition of Src/p38 signaling obviously reversed the enhancement effect of VEGF-C on macrophage migration. Finally, the functional importance of macrophage infiltration induced by tumoral VEGF-C in promoting metastasis was established in a mouse model. In conclusion, our results highlight a novel function of tumoral VEGF-C that paracrinely induces macrophage recruitment, and resultantly promotes NSCLC cell metastasis. Therefore, VEGF-C/VEGFR-2/3 axis may be a promising microenvironmental target against progression of NSCLC.

A 10­microRNA prognosis scoring system in esophageal squamous cell carcinoma constructed using bioinformatic methods.

MicroRNA (miR) signatures may aid the diagnosis and prediction of cancer; therefore, miRs associated with the prognosis of esophageal squamous cell carcinoma (ESCC) were screened. miR­sequencing (seq) and mRNA­seq data from early­stage ESCC samples were downloaded from The Cancer Genome Atlas (TCGA) database, and samples from subjects with a >6­month survival time were assessed with Cox regression analysis for prognosis­associated miRs. A further two miR expression datasets of ESCC samples, GSE43732 and GSE13937, were downloaded from the Gene Expression Omnibus database. Common miRs between prognosis­associated miRs, and miRs in the GSE43732 and GSE13937, datasets were used for risk score calculations for each sample, and median risk scores were applied for the stratification of low­ and high­risk samples. A prognostic scoring system of signature miRs was subsequently constructed and used for survival analysis for low­ and high­risk samples. Differentially­expressed genes (DEGs) corresponding to all miRs were screened and functional annotation was performed. A total of 34 prognostic miRs were screened and a scoring system was created using 10 signature miRs (hsa­miR­140, ­33b, ­34b, ­144, ­486, ­214, ­129­2, ­374a and ­412). Using this system, low­risk samples were identified to be associated with longer survival compared with high­risk samples in the TCGA and GSE43732 datasets. Age, alcohol and tobacco use, and radiotherapy were prognostic factors for samples with different risk scores and the same clinical features. There were 168 DEGs, and the top 20 risk scores positively­correlated and the top 20 risk scores negatively­correlated DEGs were significantly enriched for six and 10 functional terms, respectively. 'Tight junction' and 'melanogenesis' were two significantly enriched pathways of DEGs. miR­214, miR­129­2, miR­37a and miR­486 may predict ESCC patient survival, although further studies to validate this hypothesis are required.

Nrf2 mediates redox adaptation in NOX4-overexpressed non-small cell lung cancer cells.

The redox adaptation mechanisms in cancer cells are very complex and remain largely unclear. Our previous studies have confirmed that NADPH oxidase 4 (NOX4) is abundantly expressed in non-small cell lung cancer (NSCLC) and confers apoptosis resistance on NSCLC cells. However, the comprehensive mechanisms for NOX4-mediated oxidative resistance of cancer cells remain still undentified. The present study found that NOX4-derived H2O2 enhanced the nuclear factor erythroid 2-related factor 2 (Nrf2) stability via disruption of redox-dependent proteasomal degradation and stimulated its activity through activation of PI3K signaling. Specifically, the results showed that ectopic NOX4 expression did not induce apoptosis of A549 cells; however, inhibition of Nrf2 resulted in obvious apoptotic death of NOX4-overexpressed A549 cells, accompanied by a significant increase in H2O2 level and decrease in GSH content. Besides, inhibition of Nrf2 could suppress cell growth and efficiently reverse the enhancement effect of NOX4 on cell growth. The in vivo data confirmed that inhibition of Nrf2 could interfere apoptosis resistance in NOX4-overexpressed A549 tumors and led to cell growth inhibition. In conclusion, these results reveal that Nrf2 is critically involved in redox adaptation regulation in NOX4-overexpressed NSCLC cells. Therefore, NOX4 and Nrf2 may be promising combination targets against malignant progression of NSCLC.

[Risk Factors for Post-surgery Recurrence of Multiple Pulmonary Cystic Echinococcosis].

Clinical information of patients with multiple pulmonary cystic echinococcosis who received surgery in the Department of Thoracic Surgery of the Hospital from January 2005 to October 2014 was collected. Multivariate logistic regression analysis was used to analyze the predisposing factors for post-surgery recurrence of multiple pulmonary cystic echinococcosis. Among the 73 cases of multiple pulmonary cystic echinococcosis, 40 were males and 33 were females, with a male-to-female ratio of 1.21 : 1. The average age of patients was 37.6 years. All the patients reported a living history in pastoral areas or contacts with dogs. Thirty-eight patients were administered with albendazole tablets or liposomal albendazole for 3 to 12 months after surgery. Recurrence occurred in 6 cases, with a rate of 8.2%. Multivariate logistic regression analysis revealed the preoperative rupture of hydatid cyst to be the risk factor for post-surgery recurrence. The administration of anti-hydatid drugs after surgery plays a protective role against recurrence, and may reduce the risk of recurrence.

Screening aberrant methylation profile in esophageal squamous cell carcinoma for Kazakhs in Xinjiang area of China.

To screen the aberrant methylation genes in esophageal squamous cell carcinoma (ESCC) for Kazakh nationality in Xinjiang, and the aberrant DNA methylation genes pattern provides a clue for deeply study on ESCC mechanism. Illumina Human Methylation 450 K chip was used to screen the genome-wide methylation on six cancer tissues and six adjacent normal tissues of ESCC in Kazakh people. Meanwhile, mRNA library was constructed by scanning the RNA expression on two cancer tissues and two adjacent normal tissues by Hiseq2000. After association study between the methylation profile and expression profile, aberrant DNA methylated genes were screened out and were uploaded to the GoMiner and the KEGG, completing the bioinformatic analysis. There were 227 hypermethylation genes and 6 hypomethylated genes in cancer tissue, mRNA expression varied from 0.0312 to 8,192 in cancer tissues compared with 0.0312-1,024 in adjacent normal tissues. The correlation study indicated that there were 10 loci in 10 down-regulated genes of hypermethylated in negative correlation group. Additionally, there were 11 loci in 10 up-regulated genes in negative group. Using GoMiner to do GO analysis on aberrant DNA methylation genes, RAPGEFL1, TP53AIP1, KIAA1522, DUOXA2 were identified not involved in any biological processes. ALDH1L1 participated in folinic acid catabolism and CAPN1 positively regulated the cell proliferation. And ALDH1L1 involved in one carbon metabolism and CAPN1 participate in the apoptosis process by applying pathway analysis. The aberrant DNA methylation profiles were established and provided a clue for deeply study on ESCC of Kazakh nationality.

Human papillomavirus promotes esophageal squamous cell carcinoma by regulating DNA methylation and expression of HLA-DQB1.

AIMS: Esophageal cancer (EC) is one of the most prevalent and deadly cancers worldwide. Along with nutrition, smoking and alcohol consumption, human papillomavirus (HPV) infection is one of the major risk factors, which is modulated by host immune response. This study is aimed at elucidating how HPV modifies host immune system in the EC pathogenesis. METHODS: The HPV and HLA-DQB1 levels in primary esophageal squamous cell (ESC) cancer cells from Han, Khazak and Uygur patients were analyzed by quantitative real-time PCR and immunoblotting. The ability of HPV16 E6/E7 to transform normal primary ESCs was investigated by infecting ESC with pMSCVpuro-carried E6 or E7. The shRNA against HPV16 E6 or E7 was delivered by adenovirus into esophageal squamous cell carcinoma (ESCC) cells with high HPV content. The DNA methylation level of HLA-DQB1 was measured by methylation-specific PCR. RESULTS: The HLA-DQB1 expression level was correlated with the levels of HPV and inversely related to DNA methylation level of HLA-DQB1. Overexpressing HPV16 E6 or E7 alone was enough to transform normal primary ESCs. However, single knockdown of either E6 or E7 in ESC cancer cells did not reduce HLA-DQB1 expression. CONCLUSIONS: Oncogenic HPV E6 and E7 genes promoted ESCC pathogenesis by upregulating susceptible HLA-DQB1 via DNA demethylation.

[Expression of MCP-1 in the patients of chronic hepatitis B complicated with nonalcoholic fatty liver disease].

AIM: To investigate the expression level of monocyte chemoattractant protein-1 (MCP-1) in the liver of the patients with chronic hepatitis B (CHB) complicated with non-alcoholic fatty liver diseases (NAFLD). METHODS: The study enrolled 21 CHB with NAFLD patients and 46 CHB without NAFLD patients as the controls. Real-time quantitative reverse transcriptase-polymerase chain reaction (QRT-PCR) and immunohistochemistry (IHC) were applied to detect the expression of MCP-1 at the mRNA and protein levels in the liver tissues, respectively. Non-parametric Mann-Whitney test was used to analyze the difference between the CHB patients with and without NAFLD. RESULTS: The mRNA relative expression level of MCP-1 in CHB+NAFLD group was 0.034 (0.024-0.058), higher than that in the control group 0.016 (0.012-0.024). The immunohistochemical score was 8.7±2.5 in CHB+NAFLD group and 6.2±3.5 in the control group. The difference in MCP-1 expression at the both protein and mRNA levels was significant statistically between the two groups (P<0.01). CONCLUSION: MCP-1 expression level in the liver is higher in CHB with NAFLD patients than that in CHB without NAFLD patients.

Relationship between HLA-G gene polymorphism and the susceptibility of esophageal cancer in Kazakh and Han nationality in Xinjiang.

OBJECTIVE: To explore the association between polymorphism of the human leukocyte antigen G (HLA-G) and susceptibility of esophageal carcinoma (EC) in Kazakh and Han nationality in Xinjiang. METHODS: The 14 bp deletion/insertion (rs16375) and 0105N (rs41557518) of HLA-G genotyping were determined by PCR and PCR-RFLP, respectively in 239 patients and 467 controls. RESULTS: There was a 2.69-fold (P(c) = 0.04, 95% CI: 1.30-5.55) increased risk of developing EC in individuals with the -14 bp/-14 bp genotype (rs16375) compared with those carrying +14 bp/+14 bp genotype in Kazakh after Bonferroni correction, there was no association of 0105N (rs41557518) both in Kazak and Han population. And there was a 2.82-fold (P(c) = 0.04, 95% CI: 1.32-6.04) increased risk of developing EC in individuals with -14 bp/-14 bp and C/C genotypes compared with those who had +14 bp/+14 bp and C/C genotypes in Kazakh. CONCLUSIONS: The study demonstrates that EC is associated with polymorphism of HLA-G14 bp in Chinese Kazak population. The 14 bp deletion/insertion of HLA-G gene may play a role in EC susceptibility of Kazakh.

Study on the relationship between TagSNPs and haplotype of hCHK2 and esophageal cancer in Kazakh and Han in Xinjiang.

AIM OF THE STUDY: To determine the association of hCHK2 rs2278022, rs2602431, and rs2970077 polymorphisms and haplotypes with susceptibility to esophageal cancer in Kazakh and Han in Xinjiang Uygur Autonomous Region. MATERIAL AND METHODS: Molecular epidemiology was carried out on 239 cases of esophageal cancer (132 Kazakh, 107 Han) and 513 controls (309 Kazakh, 204 Han) of Xinjiang. Polymorphisms of hCHK2 at rs2278022, rs2602431 and rs2970077 were analyzed by polymerase chain reaction-ligase detection reaction (PCR-LDR). Haplotypes were estimated by the SHEsis software. Statistical differences in genotype/haplotype frequencies, and frequencies between the case group and the control group were estimated. RESULTS: 1) No significant difference was observed in the frequency of hCHK2 at rs2278022, rs2602431 and rs2970077 between the cases and controls in Kazakh and Han (P > 0.05); 2) In Kazakh and Han, the distribution of haplotypes was not significantly different between esophageal cancer cases and controls (P > 0.05). CONCLUSIONS: Polymorphisms of hCHK2 at rs2278022, rs2602431 and rs2970077 and haplotypes are unlikely to be associated with the susceptibility to esophageal cancer in Kazakh and Han.

[The clinical analysis of 93 children with pulmonary echinococcus].

OBJECTIVE: To approach the clinical characteristics and surgical treatment of children with pulmonary echinococcus. METHODS: Retrospective analysis of child patients with pulmonary echinococcus from January 1980 to December 2008 was carried out, associated with clinical manifestations, diagnosis and treatment, operation methods (complete removal of endocyst and cystectomy with needle aspiration), prognosis and recurrence. There were 93 patients (54 male and 39 female) aged from 2 to 14 years. There were 82 cases lived in the echinococcosis pulmonary endemic areas, accounting for 88.1% (82/93), and 79 cases of patients had obvious contact with dogs or sheep, accounting for 84.9% (79/93). There were 68 cases with simple pulmonary echinococcus accounted for 73.1% (68/93), 25 cases suffered from complexity pulmonary hydatid, accounting for 26.9% (25/93). RESULTS: All patients were cured or improved after surgery except one dead. Six cases got postoperative pulmonary infection, 3 cases had wound infection, 1 case suffered from bile-pleura fistula. There were 76 patients (81.7%) followed up for 1 to 10 years after surgery. Five cases had recurrence, the recurrence rate was 5.4% (5/93). CONCLUSIONS: The clinical symptoms of pulmonary echinococcus in children is not typical, misdiagnosis and missed diagnosis take place easily. Complete removal of endocyst has low postoperative complications and lower relapse rate.