Serum Creatine Kinase as a Biomarker to Predict Wooden Breast in vivo for Chicken Breeding.

The present study aimed to find a blood marker for the prediction of wooden breast (WB) in live broiler to assist the genetic selection of fast-growing chickens. The experiments were carried out with two chicken flocks: 250 male broilers in flock 1 and 100 male and female broilers in flock 2. Both flocks were slaughtered and measured. The breast filets were assessed by combining subjective scoring and compression force at 28 (flock 1 only) and 42 days of age. The enzyme activity in serum and breast tissue (flock 1 only) of normal and affected groups was tested. The results showed that the compression force was significantly different between the normal and affected groups at 28 and 42 days of age (P < 0.001), and it increased significantly with rising WB and WS scores. The serum creatine kinase (CK) value increased significantly with rising compression force at 42 days of age (P < 0.001). The serum CK positively correlated with compression force (r = 0.608; P < 0.001) and the linear regression equation (serum CK = 0.9960∗compression force + 1.884) was established for the line studied. The association between serum CK and compression force is consistent between flocks 1 and 2. In conclusion, our study confirmed that compression force could be the quantitative indicator to differentiate breast filets and found that serum CK could be a candidate biomarker to predict WB in live broilers and assist genetic selection in broiler breeding.

Targeted silencing of TEM8 suppresses non­small cell lung cancer tumor growth via the ERK/Bcl­2 signaling pathway.

Non­small cell lung cancer (NSCLC) is one of the most common malignancies with high rates of mortality. Although great progress has been made with the development of novel immunotherapies and targeted therapeutic strategies, the 5­year total survival rate of lung cancer has remained unchanged over the past few decades. Therefore, more effective therapeutics are urgently needed. Tumor endothelial marker 8 (TEM8) is an integrin­like cell surface transmembrane protein that has been demonstrated to be upregulated in numerous cancer types and previously showed promise for targeted cancer therapy. However, the role of TEM8 in NSCLC remains poorly understood. The present study aimed to investigate the effects of silencing TEM8 on expression and regulation of extracellular signal­regulated kinase (ERK)1/2 signaling pathways in NSCLC. In the present study, a lentiviral vector that encoded a short hairpin RNA targeting TEM8 was designed and transfected into Xuanwei Lung Cancer (XWLC)­05 lung cancer cells to silence TEM8 expression. Male BALB/c­nu/nu mice were then given subcutaneous injections in the right dorsal flank with XWLC­05 cells. Microvessel density was measured using an anti­CD34 antibody. The mRNA and protein levels of ERK1/2 and Bcl­2 in XWLC­05 cells or xenograft tumor tissues were detected by reverse transcription­quantitative polymerase chain reaction and western blotting. TEM8 knockdown was found to significantly inhibit tumor growth and conferred an anti­angiogenic ability in vivo. Furthermore, TEM8 knockdown suppressed the expression of Bcl­2 mediated by ERK1/2 activity in XWLC­05 cells or tissues from mice with NSCLC. To conclude, these results suggest that the targeted silencing of TEM8 may serve as an effective method of treating NSCLC.

Integrated analysis of the methylome and transcriptome of chickens with fatty liver hemorrhagic syndrome.

BACKGROUND: DNA methylation, a biochemical modification of cytosine, has an important role in lipid metabolism. Fatty liver hemorrhagic syndrome (FLHS) is a serious disease and is tightly linked to lipid homeostasis. Herein, we compared the methylome and transcriptome of chickens with and without FLHS. RESULTS: We found genome-wide dysregulated DNA methylation pattern in which regions up- and down-stream of gene body were hypo-methylated in chickens with FLHS. A total of 4155 differentially methylated genes and 1389 differentially expressed genes were identified. Genes were focused when a negative relationship between mRNA expression and DNA methylation in promoter and gene body were detected. Based on pathway enrichment analysis, we found expression of genes related to lipogenesis and oxygenolysis (e.g., PPAR signaling pathway, fatty acid biosynthesis, and fatty acid elongation) to be up-regulated with associated down-regulated DNA methylation. In contrast, genes related to cellular junction and communication pathways (e.g., vascular smooth muscle contraction, phosphatidylinositol signaling system, and gap junction) were inhibited and with associated up-regulation of DNA methylation. CONCLUSIONS: In the current study, we provide a genome-wide scale landscape of DNA methylation and gene expression. The hepatic hypo-methylation feature has been identified with FLHS chickens. By integrated analysis, the results strongly suggest that increased lipid accumulation and hepatocyte rupture are central pathways that are regulated by DNA methylation in chickens with FLHS.

Nomogram For The Prediction Of Malignancy In Small (8-20 mm) Indeterminate Solid Solitary Pulmonary Nodules In Chinese Populations.

PURPOSE: This study aimed to develop and validate a nomogram for predicting the malignancy of small (8-20 mm) solid indeterminate solitary pulmonary nodules (SPNs) in a Chinese population by using routine clinical and computed tomography data. METHODS: The prediction model was developed using a retrospective cohort that comprised 493 consecutive patients with small indeterminate SPNs who were treated between December 2012 and December 2016. The model was independently validated using a second retrospective cohort comprising 216 consecutive patients treated between January 2017 and May 2018. The investigated variables included patient characteristics (e.g., age and smoking history), nodule parameters (e.g., marginal spiculation and significant enhancement), and tumor biomarker levels (e.g., carcinoembryonic antigen). A prediction model was developed by using multivariable logistic regression analysis, and the model's performance was presented as a nomogram. The model was evaluated based on its discriminative ability, calibration, and clinical usefulness. RESULTS: The developed nomogram was ultimately based on age, marginal spiculation, significant enhancement, and pleural indentation. The Harrell concordance index values were 0.869 in the training cohort (95% confidence interval: 0.837-0.901) and 0.847 in the validation cohort (95% confidence interval: 0.792-0.902). The Hosmer-Lemeshow test revealed good calibration in each of the training and validation cohorts. Decision curve analysis confirmed that the nomogram was clinically useful (risk threshold from 0.10 to 0.85). CONCLUSION: Patient age, marginal spiculation, significant enhancement, and pleural indentation are independent predictors of malignancy in small indeterminate solid SPNs. The developed nomogram is easy-to-use and may allow the accurate prediction of malignancy in small indeterminate solid SPNs among Chinese patients.

Progress on the role of miRNA in the development of lung cancer and its mechanisms / 中国肿瘤生物治疗杂志

@#肺癌的发病机制非常复杂，目前仍未明确。研究发现miRNA是肿瘤中的一组重要的调节因子，与肺癌的发生发展密 切相关，异常表达后可作为致癌miRNA或抑癌miRNA参与调控信号通路基因的表达，影响肺癌细胞的增殖、迁移、侵袭、转移等 过程。本文就miRNA作为抑癌或致癌基因在肺癌发生发展中机制的最新研究进展进行综述。

Effect of exosome-derived lncRNAin tumor and its microenvironment / 中国肿瘤生物治疗杂志

@# 外泌体是一种纳米级别的生物膜结构，由机体的多种细胞分泌，广泛分布于唾液、血浆、乳汁等体液中。外泌体中含 有蛋白质、mRNA、miRNA、lncRNA、细胞因子、转录因子受体等多种生物活性物质。肿瘤细胞或肿瘤旁细胞分泌的外泌体可将 一些肿瘤特有的生物信息转移到邻近细胞，甚至远处细胞，并且通过这种细胞间通信传递肿瘤的特性，从而促进肿瘤的发生发 展。本综述旨在着重讨论肿瘤细胞及癌旁细胞分泌的含lncRNA的外泌体对肿瘤微环境，肿瘤的生物学特性的影响，为肿瘤的基 础研究及临床诊断治疗提出新的思路。

The Correlation of Visfatin and Its Gene Polymorphism with Non-Small Cell Lung Cancer.

Objective: To investigate the protein expression of visfatin and its gene polymorphism in non-small cell lung cancer (NSCLC) patients. Methods: The plasma level of visfatin was detected by enzyme-linked immunosorbent assay, and the genotypes rs59744560, rs9770242, and rs61330082 in the visfatin gene were detected by gene sequencing. Result: This study revealed that plasma levels of visfatin in NSCLC patients were significantly higher than the levels in healthy people (p < 0.01). The high level of plasma visfatin was found to be significantly correlated with TNM stage (p < 0.05). No mutations were detected in rs59744560 and rs9770242 loci. Three genotypes (CC, CT, and TT) were detected in rs61330082 locus, and the differences in the frequency distribution of these genotypes were significant in the two groups (p < 0.05). Central obesity and the CC genotype were independent risk factors in the pathogenesis of NSCLC (p < 0.05). Conclusion: The plasma visfatin level in NSCLC patients significantly increased, and high plasma visfatin levels were correlated with tumor stage. Gene polymorphism was found in the visfatin gene rs61330082 locus. The CC genotype might increase the risk for patients suffering from NSCLC, while the CT genotype, TT genotype, and T allele may reduce the risk of NSCLC. The rs61330082 locus can be used as genetic markers of high-risk populations.

Effect of silencing TEM8 gene on proliferation, apoptosis, migration and invasion of XWLC­05 lung cancer cells.

Currently, the role of tumor endothelial marker 8 (TEM8) in the occurrence, development, invasion and metastasis of lung cancer and its mechanism are poorly understood. The present study aimed to investigate the effects of TEM8 on proliferation, apoptosis, migration and invasion of XWLC­05 lung cancer cells. The expression of TEM8 in human lung cancer and adjacent tissues was detected by reverse transcription­quantitative polymerase chain reaction and western blotting. An interference vector coding a short hairpin RNA (shRNA) targeting TEM8 was designed and transfected into XWLC­05 lung cancer cells. MTT assay was used to detect cell proliferation. Flow cytometry was employed to detect cell cycle and apoptosis. Cell scratch assay was used for cell migration detection. Cell invasion ability was detected by the Transwell method. The expression of TEM8 in lung cancer tissues was significantly increased compared with adjacent tissues (P<0.05). Following the silencing of TEM8 by shRNA interference, cell proliferation was inhibited and the apoptosis rate increased. The cell cycle was arrested at G1 phase, while the migration and invasion ability of cancer cells was decreased. Silencing TEM8 may inhibit proliferation of XWLC­05 lung cancer cells, promote cell apoptosis, arrest the cell cycle at G1 phase and decrease the migration and invasive ability. Thus, TEM8 may be a potential target in therapy for lung cancer.

The role of long non-coding RNA PANDAR in the occurrence and development of malignant tumors / 中国肿瘤生物治疗杂志

@# 长链非编码RNA（long non-coding RNA，lncRNA）最初被认为是不具有功能的“转录噪声”，但越来越多的研究发现， lncRNA的失调在很多肿瘤中起着癌基因或抑癌基因的作用，是癌症发展的关键分子。PANDAR作为一种重要的lncRNA受到了 诸多关注。有研究证明，PANDAR在许多肿瘤中特异性表达，在大多数肿瘤中上调，但在非小细胞肺癌中显著下调，PANDAR的 特异性表达与肿瘤大小、TNM分期和总生存率显著相关。本文通过对lncRNAPANDAR在恶性肿瘤细胞中的主要作用模式、 表 达情况、作用机制及对各类肿瘤发生发展的影响进行综述，旨在为临床恶性肿瘤生物学诊治疗提供新的靶标。

Advances in research of peripheral blood miRNAs in early diagnosis of tumors / 中国肿瘤生物治疗杂志

@#[Abstract] MicroRNA (miRNA) is non-coding RNA molecule consisting of 20-25 nucleotides. It plays an important role in regulation of tumorigenesis and progression, including proliferation, differentiation and apoptosis of cancer cells, which directly affect the progress of tumors. Peripheral blood miRNA is relatively more stable, and easier to acquired and detected than tissue miRNA. It is a new generation biomarker for early detection and early diagnosis of tumors. It is also one of the main development directions of research and application in precision medicine. Methods commonly used in peripheral blood miRNA detection are RT-PCR, electrochemical detection, NanoString Technologies, genechip and high-throughput sequencing etc. Multiple miRNAs in peripheral blood are the early diagnostic markers for non-small cell lung cancer, esophageal squamous cell carcinoma, pancreatic cancer, squamous cell carcinoma of the head and neck, ovarian cancer, colorectal cancer, breast cancer, prostate cancer and hematological malignancies. Combined detection of multiple peripheral blood miRNAs, as well as combined detection of tumor-specific miRNAand serological, imaging and other auxiliary methods, can improve the sensitivity and specificity of tumor diagnosis at early stage.

The role and mechanism of miR-32 in occurrence and development of malignant tumors / 中国肿瘤生物治疗杂志

@#微小RNA（microRNA，miRNA）是一种内源性的长度为18~25个核苷酸的非编码RNA，通过与蛋白质编码基因的 mRNA结合来发挥重要的基因调控作用，与恶性肿瘤的发生发展密切相关。miR-32作为miRNA家族的重要成员，在不同肿瘤中 表达水平存在明显差异，因其与恶性肿瘤的相关性及本身表达的正反作用双向性， 在miRNA领域受到了更多的关注。近年来研 究发现，miR-32对恶性肿瘤细胞的增殖、迁移与侵袭、自噬和凋亡均有影响。此外，miR-32与其上游靶基因、肿瘤代谢及临床诊 断和治疗也有密切的关系。本文就miR-32在恶性肿瘤发生发展中的作用及其机制、临床诊治中应用等最新研究进展作一综述。

MicroRNA-370 inhibits the growth and metastasis of lung cancer by down-regulating epidermal growth factor receptor expression.

Abnormal microRNA-370 (miR-370) expression has been frequently reported in several types of cancers, including lung cancer. However, the role and molecular mechanisms of miR-370 in regulating the growth and metastasis of lung cancer have not been clarified. Here, we show higher levels of epidermal growth factor receptor (EGFR), but lower levels of miR-370 expression in most human lung cancer cells and non-tumor cells. Induction of miR-370 over-expression significantly reduced the levels of EGFR expression and the EGFR 3'untranslated region (UTR)-regulated luciferase activity in XWLC-05 and H157 cells, suggesting that miR-370 may bind to the 3'UTR of EGFR mRNA. Compared with the control cells, induction of miR370 overexpression significantly inhibited the proliferation, clone formation capacity, migration and invasion of XWLC-05 and H157 cells while miR-370 inhibitor over-expression enhanced their tumor behaviors in vitro. Furthermore, miR-370 over-expression down-regulated the EGFR and hypoxia-inducible factor (HIF)-1α expression, and attenuated the extracellular single-regulated kinase (ERK)1/2 and AKT phosphorylation in XWLC-05 and H157 cells. In contrast, miR370 inhibitor over-expression increased the EGFR and HIF-1α expression as well as the ERK1/2 and AKT phosphorylation in XWLC-05 and H157 cells. Moreover, miR-370 over-expression significantly reduced the levels of EGFR and CD31 expression and inhibited the growth and lung metastasis of xenograft NSCLC tumors in mice. Our study indicates that miR-370 may bind to the 3'UTR of EGFR to inhibit EGFR expression and the growth, angiogenesis and metastasis of non-small cell lung cancer by down-regulating the ERK1/2 and AKT signaling.

Acquired resistance to HSP90 inhibitor 17-AAG and increased metastatic potential are associated with MUC1 expression in colon carcinoma cells.

Heat shock protein 90 (HSP90) is a molecular chaperone required for the stability and function of many proteins. The chaperoning of oncoproteins by HSP90 enhances the survival, growth, and invasive potential of cancer cells. HSP90 inhibitors are promising new anticancer agents, in which the benzoquinone ansamycin 17-allylamino-17-demethoxygeldanamycin (17-AAG) is currently in clinical evaluation. However, the implications of acquired resistance to this class of drug remain largely unexplored. In the present study, we have generated isogenic human colon cancer cell lines that are resistant to 17-AAG by continued culturing in the compound. Cross-resistance was found with another HSP90 inhibitor 17-dimethylaminoethylamino-17-demethoxygeldanamycin. The resistant cells showed obvious morphology changes with a metastatic phenotype and significant increases in migration and adhesion to collagens. Western blotting analysis of epithelial-mesenchymal transition molecular markers found that expression of E-cadherin downregulated, whereas expression of N-cadherin and ß-catenin upregulated in the resistant cells. Mucin 1 (MUC1) has been reported to mediate metastasis as well as chemical resistance in many cancers. Here, we found that MUC1 expression was significantly elevated in the acquired drug resistance cells. 17-AAG treatment could decrease MUC1 more in parental cells than in acquired 17-AAG-resistant cells. Further study found that knockdown of MUC1 expression by small interfering RNA could obviously re-sensitize the resistant cells to 17-AAG treatment, and decrease the cell migration and adhesion. These were coupled with a downregulation in N-cadherin and ß-catenin. The results indicate that HSP90 inhibitor therapies in colon carcinomas could generate resistance and increase metastatic potential that might mediated by upregulation of MUC1 expression. Findings from this study further our understanding of the potential clinical effects of HSP90-directed therapies in colon carcinomas.

Modification of cytokine-induced killer cells with chimeric antigen receptors (CARs) enhances antitumor immunity to epidermal growth factor receptor (EGFR)-positive malignancies.

Epidermal growth factor receptor (EGFR, ErbB1, Her-1) is a cell surface molecule overexpressing in a variety of human malignancies and, thus, is an excellent target for immunotherapy. Immunotherapy targeting EGFR-overexpressing malignancies using genetically modified immune effector cells is a novel and promising approach. In the present study, we have developed an adoptive cellular immunotherapy strategy based on the chimeric antigen receptor (CAR)-modified cytokine-induced killer (CAR-CIK) cells specific for the tumor cells expressing EGFR. To generate CAR-CIK cells, a lentiviral vector coding the EGFR-specific CAR was constructed and transduced into the CIK cells. The CAR-CIK cells showed significantly enhanced cytotoxicity and increased production of cytokines IFN-γ and IL-2 when co-cultured with EGFR-positive cancer cells. In tumor xenografts, adoptive immunotherapy of CAR-CIK cells could inhibit tumor growth and prolong the survival of EGFR-overexpressing human tumor xenografts. Moreover, tumor growth inhibition and prolonged survival in mice with EGFR(+) human cancer were associated with the increased persistence of CAR-CIK cells in vivo. Our study indicates that modification with EGFR-specific CAR strongly enhances the antitumor activity of the CIK cells against EGFR-positive malignancies.

Down-regulated SOX4 expression suppresses cell proliferation, metastasis and induces apoptosis in Xuanwei female lung cancer patients.

The transcription factor SOX4 has functional importance in foetal lung maturation and tumorigenesis in a number of cancers. However, its biological functions in the progression of lung tumorigenesis remain unclear. In this study, we found that the expression levels of SOX4 mRNA and protein were significantly higher in Xuanwei female lung cancer tissues than in benign lung lesions. The patients with high expression of the SOX4 protein had a higher pathological grade, lymph node (LN) metastasis, poor tumor differentiation and worse prognosis than those patients with low expression of SOX4. Knockdown of the SOX4 gene in the Xuanwei female lung cancer cell line XWLC-05 resulted in apoptotic morphological changes, decreased cell proliferation, invasion and migration. Furthermore, knockdown of the SOX4 gene resulted in obvious sub-G1 peaks and induction of apoptosis through upregulation of caspase-3 expression, while in cells treated with a caspase-3 inhibitor, apoptosis induced by silencing SOX4 expression was inhibited. In vivo analysis in nude mice further confirmed that knockdown of SOX4 suppressed tumor growth. In conclusion, SOX4 appears to be an important tumor suppressor gene in the regulation of Xuanwei female lung cancer cell proliferation, apoptosis and metastases, and it may be a potential target for effective lung cancer therapy.

Impact of cellular immune function on prognosis of lung cancer patients after cytokine-induced killer cell therapy.

AIMS: To investigate changes in cellular immune function of patients with lung cancer before and after cytokine- induced killer (CIK) cell therapy and to identify variation effects on overall survival (OS) and progression-free survival (PFS). MATERIALS AND METHODS: A total of 943 lung cancer patients with immune dysfunction were recruited from January 2002 to January 2010, 532 being allocated to conventional therapy and 411 to CIK therapy after a standard treatment according to the NCCN Clinical Practice Guidelines. All the patients were investigated for cellular immune function before and after therapy every three months. and clinical prognostic outcomes were analyzed. RESULTS: After six courses of treatment, immune function was much improved in patients receiving CIK cells therapy as compared to controls. The percentages of recurrence and/or metastases for patients undergoing CIK cell therapy was 56.2% and 49.1% respectively but 78.6% and 70.3% among controls (p<0.001). The median OS times for CIK cell therapy and control groups were 48 and 36 months respectively. The OS rates at 12, 36, 60, 84 months in CIK treated patients were 97.8%, 66.9%, 27.7%, and 4.1% while they were 92.3%, 44.5%, 9.2%, and 1.5% in controls. OS and PFS were significantly different by log rank test between the two groups and across the three immune improvement classes. CONCLUSIONS: The immune function of lung cancer patients was improved by CIK cell therapy, associated with an increase in the OS rate and extension of the time to recurrence and/or metastasis.

[Targeted Sox4 gene-knock-down suppresses xenograft growth of Xuanwei female lung cancer cell line XWLC-05 cells in nude mice].

OBJECTIVE: To study the effect of targeted Sox4 gene-knock-down on the growth of xenografts of Xuanwei female lung cancer cell line XWLC-05 cells in nude mice. METHODS: Recombinant plasmid pGFP-V-RS-Sox4 shRNA was constructed and transfected into XWLC-05 cells. Real-time quantitative PCR and Western blot were applied to confirm the effect of Sox4 gene-knock-down. XWLC-05 cells stably transfected with the plasmids were inoculated into nude mice to establish the xenograft model. The nude mouse status, tumor formation and tumor growth were observed, and the tumor inhibition rate was calculated. CT scan was performed to assess the metastasis of xenografts. Immunohistochemical staining was applied to detect Sox4 and ki-67 protein expression. RESULTS: Recombinant plasmid pGFP-V-RS-A-Sox4 shRNA which can effectively knocking-down Sox4 gene was successfully constructed and the stable transfected cells were selected by puromycin-screening. The success rate of tumor cell inoculation was 100% in the mice of all groups except those inoculated with saline. The body weight of all mice inoculated with parental XWLC-05 cells (blank control), pGFP-V-RS-scram shRNA trsfected XWLC-05 cells (negative control), and pGFP-V-RS-Sox4 shRNA transfected XWLC-05 cells was increased to a varying degree, but there was no significant difference among the groups (P > 0.05 ). The growth of xenografts was significantly inhibited after silencing the Sox4 gene expression when compared with that of the blank and negative controls (P < 0.05) . The volume of removed tumors of the Sox4 gene-inhibited mice was (2.30 ± 0.34) cm(3) , significantly smaller than that of the negative control (3.99 ± 0.45) cm(3) and the blank control (4.03 ± 0.42) cm(3) (P < 0.05) . The weight of removed tumors of Sox4 gene-inhibited mice was (0.86 ± 0.14) g, significantly lower than that of the negative control (1.84 ± 0.27) g and blank control (1.86 ± 0.22) g, (P < 0.05). Immunohistochemical staining showed that Sox4 and ki-67 proteins mainly expressed in cell nuclei. The staining was significantly decreased in xenografts of Sox4-inhibited mice when compared with the negative and blank controls (P < 0.05). No distant metastasis was found in any mouse by CT imaging and pathological examination during the observation period. CONCLUSIONS: The xenograft model of Xuanwei female lung cancer cell line XWLC-05 cells in nude mice is successfully established. Knocking-down of Sox4 gene can suppress the xenograft tumor growth.

[Expression of transcription factor SOX4 and its clinical significance in female lung cancer patients in Xuanwei area, Yunnan Province].

OBJECTIVE: To investigate the expression of transcription factor SOX4 in lung cancer tissues of female patients in Xuanwei area, Yunnan Province, and explore its correlation with clinicopathological characteristics and prognosis of the female patients. METHODS: Real-time PCR was applied on lung cancer specimens and their corresponding normal lung tissues from 96 female cases of Xuanwei area to assess the expression of SOX4 mRNA. Immunohistochemical staining was performed to investigate the SOX4 protein expression, and further to elucidate its correlation with clinicopathological characteristics and prognosis. RESULTS: The expression level of SOX4 mRNA in the cancer tissues (2.53 ± 1.65) was significantly higher than that of matched normal tissues (1.43 ± 1.14, P = 0.003). Immunohistochemical staining showed that there were 53.1% (51/96) positive expression of SOX4 protein in the cancer tissue and only 26.0% (25/96) in matched normal tissue (P < 0.001). The expression of SOX4 protein had a significant correlation with clinical stage, lymph node metastasis and differentiation of tumor (P < 0.05). The survival analysis by Kaplan-Meier method showed that patients with positive expression of SOX4 protein, lymph node metastasis and advanced tumor stage had a significantly shorter median survival time (P < 0.05). Cox regression survival analysis showed that pathological grade was a significant independent factor affecting prognosis. CONCLUSIONS: The expressions of SOX4 mRNA and protein are significantly up-regulated in Xuanwei female lung cancer patients. Patients with positive SOX4 expression have a shorter median survival time. SOX4 protein expression level combined with pathological grade can be used as a prognostic indicator of female lung cancer patients in Xuanwei area, Yunnan Province.

Moderating effects and maintenance of lung cancer cellular immune functions by CIK cell therapy.

AIMS: To study the CIK cell treatment effects on regulation of cellular immune function disorders in patients with lung cancer, and to analyze the time characteristics. METHODS: Cellular immune function was assessed by FCM, and patients with functional disorders were randomly divided into two groups, one given CIK cell therapy within 18 months (5 courses) and the other the controls, which were followed up for 1 year with cellular immune functions tested once a month. RESULTS: There were 5 types of cellular immunity, 4 of which are disorders; after CIK treatment, the improvement rate of the 4 groups were 79.1%, 70.8%, 76.0% and 70.0%, intergroup differences not being statistically significant (P=0.675), all significantly higher than in the control group (P=0.000). The median maintenance times for the 4 groups were 10.4 months (9.76-11.04), 8.4 months (7.86-8.94), 9.8 months (9.20-10.4) and 7.9 months (6.25-9.55), respectively. CONCLUSIONS: CIK cells were able to improve the immune functions of patients with lung cancer, the rate of improvement and maintenance time being related to the immune function before the treatment and CIK-cell-therapy courses.

[Evaluation of effects of quality scale for removable partial dentures in clinical application].

PURPOSE: To evaluate the effects of quality scale for removable partial dentures (RPD)in clinical application. METHODS: Quality scale for removable partial dentures was designed. Twelve items were devised for visual survey and try-in in base, artificial teeth, clasp, rest, connector and adjustment. The assessments were divided into 3 grades A, B and C. Four commercial dental laboratories were divided into experimental group and control group randomly. All RPD made in two groups were given score with the quality scale by single-blind method. In the experimental group,the technicians were familiar with the quality scale. The assessments were periodically feedbacked to administrative staffs and exchanges were carried out between doctors and technicians by telephone. No feedback information was provided in the control group. The assessments were compared between the two groups. The data was analyzed with SPSS17.0 software package. RESULTS: The scores of assessments for base, artificial teeth, clasp, rest, connector and adjustment in the experimental group were greater than that in the control group. The difference was significant between the two groups by analysis of variance (P<0.01). The grade A and C for RPD used acrylic resin, flexible resin and cast framework in the experimental group was 27.2%,39.5%,40.6% and 9.2%, 7.9%,7.2%, respectively. The grade B was in the majority. In the control group, the grade A and C was 9.4%,15.6%,15% and 40.6%,23.6%,25%,respectively. The majority was grade B and the grade C was significantly higher than the experimental group(P<0.05). CONCLUSION: Applying the quality scale of RPD can improve the fabricating quality of prosthesis.