The immune microenvironment of ovarian cancer is crucial in its progression. Recent studies highlight the significant role of MZB1 in shaping the tumor immune microenvironment (TIME), although its specific function in ovarian cancer remains unclear. We analyzed 381 ovarian cancer samples from the TCGA database, along with additional samples from GEO and single-cell datasets. Differentially expressed genes (DEGs) were identified using DESeq2. Various algorithms were applied to assess the relationship between MZB1 and the TIME. Cell proliferation was measured using the CCK-8 assay, while cell migration was evaluated using the wound healing assay. Furthermore, a nomogram predicting overall survival was developed based on multivariable Cox regression results. Our results indicated a positive correlation between high MZB1 expression and improved clinical prognosis. Additionally, higher MZB1 expression was linked to increased immune cell infiltration within the TIME. Elevated MZB1 levels inhibited the migration and proliferation of SKOV3 cells. The nomogram's C-index was 0.702, and its calibration curve demonstrated good calibration, indicating satisfactory discrimination and accuracy in predicting patient outcomes. This study comprehensively analyzes MZB1's role in the TIME of ovarian cancer. MZB1 is a promising prognostic marker and a potential target for personalized treatment.

Objective: Retrospective analysis: This study aimed to assess the expression and clinical relevance of Ecadherin and Survivin in primary and metastatic lymph nodes of advanced gastric carcinoma. Methods: A total of 47 cases of primary and metastatic lymph nodes in advanced gastric carcinoma were examined, and the expressions of e-cadherin and survivin were assessed using immunohistochemistry. We examined the disparities in e-cadherin and survivin expression between primary lesions and their metastases. Results: Among 47 cases, a highly positive expression of e-cadherin was observed in 14 cases, while survivin expression was down-regulated in 15 cases. This was more frequently associated with well-differentiated carcinoma than with poorly differentiated carcinoma. The three-year survival rate correlated with elevated e-cadherin expression in metastatic lymph nodes of advanced gastric carcinoma. Conclusions: Re-expression of E-cadherin is observed in tumor cells of certain metastatic lymph nodes, predominantly in those with low malignancy. E-cadherin facilitates the adhesion of tumor cells, potentially resulting in focal aggregation, which can subsequently proliferate at specific sites to form metastases, particularly in instances of high differentiation. In comparison to the primary tumors, Survivin expression in tumor cells of certain metastatic lymph nodes is diminished, particularly in tumor cells exhibiting low malignancy. However, it does not inherently signify the attenuation of malignant proliferation. The downregulation of Survivin expression shows no significant correlation with the 3-year survival rate of patients. E-cadherin and Survivin contribute to the composition of the tumor microenvironment. In metastatic lymph nodes, the re-expression of E-cadherin in certain tumor cells may facilitate the down-regulation of Survivin expression. The tumor microenvironment consists of various factors that interact with one another. Concomitant medication may enhance therapeutic efficacy. The 3-year survival rate of patients with metastatic lymph nodes is associated with the re-expression of E-cadherin in advanced gastric cancer. E-cadherin serves as an independent prognostic indicator for advanced gastric cancer.

Cancer stem cells (CSCs) often exhibit high expression of the p38/MAPK signaling pathway during therapy, leading to therapeutic stress-induced cellular escape (TSCE) and presenting a significant barrier to cancer treatment. Therefore, blocking the stress escape of CSCs or simultaneously targeting stress-escaping cells (TSCSCs) has become a crucial strategy in cancer therapy. However, the lack of specific markers for identifying TSCSCs has greatly limited the development of effective treatments. Cancer cell membranes exhibit selective binding and internalization by similar cancer cells. Herein, we report a nanoparticle with Fe3O4@SiO2 as the core, which serves as a carrier to load the p38 inhibitor and is subsequently coated with homologous CSCs membranes. Herein, we reported a CSC membrane-coated nanoparticles that effectively targeted to homologous cancer cells while minimizing off-target effects, inhibited TSCE and tumor growth by introducing p38 inhibitor and thermotherapy. The application of this nanomaterial holds promise in overcoming current treatment challenges and providing strategies for cancer therapy. Fluorescence colocalization and in vivo imaging demonstrate that this nanoparticle effectively targets TSCSCs homogeneously while minimizing off-target effects. Transwell and QPCR analyses show that this nanoparticle inhibits the motility of BCSCs by preventing microtubule reorganization, thereby limiting their therapeutic stress escape from TSCE. Additionally, by introducing the p38 inhibitor, the tumor growth was significantly inhibited through suppressing the p38/MAPK signaling pathway. The application of this nanomaterial holds promise in overcoming current treatment challenges and providing strategies for cancer therapy.

The serine protease inhibitor clade E member 1 (SERPINE1) has been studied as a potential biomarker in a variety of cancers, but poorly studied in gastric cancer (GC). The purpose of this study was to explore the prognostic value of SERPINE1 in GC and primarily analyze its functions. We analyzed the the prognostic value of SERPINE1 and studied the relationship with clinicopathologic biomarkers in gastric cancer. The expression of SERPINE1 was analyzed by GEO and TCGA databases. Moreover, we validated the results by immunohistochemistry. Next, the correlation analysis between SERPINE1 and the cuproptosis-related genes was analyzed by the “Spearman” method. CIBERSORT and TIMER algorithms were used to analyze the correlation of SERPINE1 with immune infiltration. Furthermore, GO and KEGG gene enrichment analyses were used to study the functions and pathways that SERPINE1 might be involved in. Then, drug sensitivity analysis was performed using CellMiner database. Finally, a cuproptosis-immune-related prognostic model was constructed using genes related to immune and cuproptosis, and verified against external datasets. SERPINE1 was up-regulated in gastric cancer tissues, which tends toward poor prognosis. Using immunohistochemistry experiment, the expression and prognostic value of SERPINE1 were verified. Then, we found that SERPINE1 was negatively correlated with cuproptosis-related genes FDX1, LIAS, LIPT1, and PDHA1. On the contrary, SERPINE1 was positively correlated with APOE. This indicates the effect of SERPINE1 on the cuproptosis process. Furthermore, by conducting immune-related analyses, it was revealed that SERPINE1 may promote the inhibitory immune microenvironment. The infiltration level of resting NK cells, neutrophils, activated mast cells, and macrophages M2 was positively correlated with SERPINE1. However, B cell memory and plasma cells were negatively correlated with SERPINE1. Functional analysis showed that SERPINE1 was closely related to angiogenesis, apoptosis, and ECM degradation. The KEGG pathway analysis showed that SERPINE1 may be associated with P53, Pi3k/Akt, TGF-β, and other signaling pathways. Drug sensitivity analysis showed that SERPINE1 could be also seen as a potential treatment target. The risk model based on SERPINE1 co-expression genes could better predict the survival of GC patients than SERPINE1 alone. We also verified the prognostic value of the risk score by GEO external datasets. SERPINE1 is highly expressed in gastric cancer and related to poor prognosis. SERPINE1 may regulate cuproptosis and the immune microenvironment by a series of pathways. Therefore, SERPINE1 as a prognostic biomarker and potential therapeutic target deserves further study.

Supplementary Figure 1. High-throughput small-molecule screen in ovarian cancer cells. Supplementary Figure 2. Inhibition of ovarian cancer cell viability by JQ1 and THZ1. Supplementary Figure 3. Cell cycle and apoptosis analysis upon THZ1 treatment. Supplementary Figure 4. Impact of THZ1 on tumor xenograft models, normal cells and lung cancer cells. Supplementary Figure 5. Effects of CDK7 depletion in ovarian cancer cell lines. Supplementary Figure 6. Effects of individual CDK depletion in ovarian cancer cell lines. Supplementary Figure 7. Hazard ratio for each CDK as a predictor of overall survival in ovarian cancer. Supplementary Figure 8. Gene set enrichment analysis in THZ1 versus DMSO treated ovarian cancer cells. Supplementary Figure 9. Super-enhancer-associated genes identified in COV 413B, OVCA420 and SKOV3 cells. Supplementary Table 1. Percentage of viability inhibition with 181 inhibitors. Supplementary Table 2. IC50 of THZ1 in ovarian cancer cell lines. Supplementary Table 3. EOC patient cohort for CDK7 IHC. Supplementary Table 4. THZ1-inhibited gene transcripts. Supplementary Table 5. Functional annotation analysis by DAVID. Supplementary Table 6. Super-enhancer analysis of COV 413B. Supplementary Table 7. Super-enhancer analysis of OVCA420. Supplementary Table 8. Super-enhancer analysis of SKOV3.

Objective . The aim of this study is to explore the expressions and clinical significance of melanoma-associated antigen-A9 (MAGE-A9) in cervical cancer tissues and peripheral blood mononuclear cells (PBMC). Methods . 108 patients who were scheduled to undergo cervical conization or extensive hysterectomy between March 2019 and January 2021 due to cervical lesions were selected by convenient sampling. According to postoperative pathological results, the patients were divided into a cervical cancer group ( n = 64) and cervical intraepithelial neoplasia (CIN) group ( n = 44). The expression levels of MAGE-A9 mRNA in cervical lesion tissues and PBMC were detected by real-time fluorescence quantitative PCR, and the expression of MAGE-A9 protein in lesion tissues was detected by immunohistochemistry. The correlation between MAGE-A9 mRNA expressions in cancer tissues and PBMC and serum tumor markers in patients with cervical cancer and the relationship between MAGE-A9 protein expression in cancer tissues and clinicopathological characteristics were analyzed, and a receiver operating characteristic curve (ROC curve) was drawn to explore the diagnostic value of MAGE-A9 mRNA expressions in cancer tissues and PBMC on cervical cancer. Results . The expression levels of MAGE-A9 mRNA in cervical lesion tissues and PBMC in the cervical cancer group were significantly higher than those in the CIN group ( P < 0.05), and the levels of serum SCC-Ag, CA-125, and CEA were significantly higher than those in the CIN group ( P < 0.05). The positive rate of the MAGE-A9 protein expression in cervical lesion tissues in the cervical cancer group was significantly higher than that in the CIN group ( P < 0.05). The expression levels of MAGE-A9 mRNA in cancer tissues and PBMC of patients with cervical cancer were positively correlated with serum SCC-Ag, CA-125, and CEA ( P < 0.05). The positive rate of the MAGE-A9 protein expression in cervical cancer tissues was related to FIGO stage, tumor diameter, degree of differentiation, lymph node metastasis, and high-risk HPV infection ( P < 0.05) and was not correlated with age and pathological type ( P > 0.05). The areas under the ROC curves of MAGE-A9 mRNA in lesion tissue and MAGE-A9 mRNA in PBMC were 0.925 and 0.900 in the diagnosis of cervical cancer ( P < 0.05). Conclusion . The expressions of MAGE-A9 in cancer tissues and PBMC of patients with cervical cancer are upregulated, which is related to the levels of serum tumor markers and the progression of disease. MAGE-A9 is expected to become an important marker for the diagnosis of early cervical cancer.

Ovarian cancer was one of the most common malignant tumors in female reproductive organs. Moreover, epithelial ovarian cancer showed the highest mortality rate in gynecological tumors, posing serious threats to women's life and health. Transient Receptor Potential Cation Channel Subfamily V Member 2 (TRPV2) and matrix metalloproteinase-2 MMP-2 have been found to play important roles in regulating the pathogenesis of most tumors, but there were few studies exploring the relationships of TRPV2 and MMP-2 in OC. Therefore, we evaluated the expression of TRPV2 and MMP-2 proteins in cancer tissues and adjacent normal tissues of OC patients. Immunohistochemistry was used to analyze the expressions of TRPV2 and MMP-2 in cancer tissues (N = 70) and adjacent normal tissues (N = 70) of OC patients, and the correlation of TRPV2 and MMP-2 with the occurrence and development of OC was analyzed with the combination of clinicopathological parameters of OC patients. The results showed that the expressions of TRPV2 and MMP-2 in OC tissues were significantly higher than those in adjacent normal tissues, and there were significant differences in TRPV2 and MMP-2 expressions in terms of tumor stage, differentiation, and lymph node metastasis of OC. Taken together, our results showed that protein expressions of TRPV2 and MMP-2 were closely related associated with the occurrence and development of OC.

PURPOSE:Ovarian cancer is a devastating gynecological disease which is considered the major cause of cancer fatality around the world. The down-regulation of microRNA-33b (miR-33b) was reported in some malignancies. Hence, we transfected the miR-33b mimic into SKOV3 cells and evaluated the impacts of this interference on the growth and migration repression of these tumor cells as well as on targeted genes expression.METHODS:In our study, transfecting the miR-33b mimic and inhibitor, negative control (NC), and NC inhibitor were established using Lipofectamine 2000. The cytotoxic effects of miR-33b were evaluated by MTT. To assess the miR-33b effects on cell migration, a scratching test was applied. The expression levels of miR-33b, ADAMTS, C-Myc, MMP9, K-Ras, and CXCR4 were evaluated using qRT-PCR.RESULTS:These findings indicate that transfection of miR-143 mimic had no marked effects on the SKOV3 cell line. As expected, miR-33b relative expression levels were as follows: miR-33b mimic >NC and NC inhibitor >miR-33b inhibitor (p < 0.01). Moreover, transfected miR-33b mimic could suppress SKOV3 cells' proliferation, whereas transfected miR-33b inhibitor could promote cell proliferation (p < 0.01). MiR-33b overexpression significantly down-regulated the MMP9, CXCR-4, c-Myc, ADAMTS, and K-Ras mRNA levels (p < 0.05).CONCLUSION:As expected, these results confirm the tumor-suppressive effect of miR-33b in the SKOV3 ovarian cancer cell line by reducing cell survival, proliferation, and migration.

Cyclophosphamide (CP) is very well-known anticancer drug and commonly used against various cancers. CP therapy is related to female ovarian cancer and causes female infertility. The ovarian cancer associated with the increase oxidative stress and inflammatory reaction. Syringic acid (SA) is very well phyto-constituent and already proof antioxidant and anti-inflammatory effects on various diseases. We investigated the chemoprotective impact of SA on CP mediated ovarian damage, and the underlying mechanism. CP (75 mg/kg) was used to cause ovarian damage and rats were randomly divided into separate groups and received a different dose of SA for 14-day. Body weight, food and water intake were determined. Ovarian weight and tumor index was measured. Antioxidant parameters were determined in the serum and ovarian tissue. Pro-inflammatory cytokines, apoptosis parameters and inflammatory mediators were estimated in the serum. Hormonal parameters and Histomorphometry were estimated. Dose dependently treatment of SA significantly (p < 0.001) decreased the levels of biochemical parameter such as nitric oxide (NO), myeloperoxidase (MPO) and augmented the antioxidant parameters include catalase (CAT), glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD) and reduced malondialdehyde (MDA) level in serum and ovarian tissue. SA treatment significantly (p < 0.001) suppressed the level of luteinizing hormones (LH), anti-mullerian hormone (AMH), estradiol (E2) and folliclestimulating hormone (FSH) as well as ovarian follicles. SA significantly (p < 0.001) down-regulated cytokines, inflammatory mediator and caspase-3 parameters. Taken altogether, we conclude that SA considerably reduced ovarian damage via reduced oxidative stress and inflammatory reaction.

Aims: Glycolysis is an important process for cervical carcinoma development. Previous studies have indicated that stress-induced phosphoprotein 1 (STIP1) is associated with development of multiple tumors. Nevertheless, the role and mechanism of STIP1 in glycolysis of cervical carcinoma remain unclear. Main methods: The association between STIP1 and survival probability and the correlation between STIP1 expression and pyruvate kinase M2 (PKM2) as well as lactate dehydrogenase isoform A (LDHA) levels in cervical carcinoma were analyzed via The Cancer Genome Atlas (TCGA). The expression of STIP1, PKM2, LDHA, and cytochrome c (Cyt C) was measured via western blot or quantitative reverse transcription polymerase chain reaction. Cell viability and apoptosis were examined via cell counting kit 8 and flow cytometry, respectively. Glycolysis was assessed via detection of glucose consumption and lactate production. The protein involved in the Wnt/beta-catenin pathway was measured via western blot. Key findings: STIP1 abundance was elevated in cervical carcinoma cells. High expression of STIP1 indicated poor survival probability. Knockdown of STIP1 inhibited cervical carcinoma cell viability and promoted apoptosis. STIP1 expression was positively correlated with PKM2 and LDHA levels in cervical carcinoma. Silence of STIP1 inhibited glycolysis and decreased PKM2 and LDHA expression. Down-regulation of STIP1 repressed the Wnt/beta-catenin pathway. Overexpression of beta-catenin reversed the effect of STIP1 silence on viability, apoptosis, glycolysis, and levels of PKM2 and LDHA. Significance: STIP1 knockdown suppressed glycolysis in cervical carcinoma by inhibiting PKM2 and LDHA expression and activation of the Wnt/beta-catenin pathway.

Prostate cancer is an urogenital malignancy which is common in older men.Androgen deprivation therapy is an usual treatment for metastatic prostate cancer significantly inhibiting the progression of advanced prostate cancer via blocking androgen synthesis,or competitive binding to androgen receptors.Nevertheless,most of the patients end up with metastatic castration-resistant prostate cancer (mCRPC) on the account of androgen resistance.It has been shown that androgen receptor splice variant 7 is strongly associated with the development of mCRPC and its drug resistance to androgen receptor signal transduction inhibitors (enzalutamide and abiraterone) in studies of recent years.

We designed a hand-assisted device for laparoscopic D2 dissection for gastric cancer that allows the placement in peritoneal cavity of surgical instrument and the entry and maneuvering of the left hand of a surgeon. Here, we describe the surgical technique for radical resection of gastric cardia cancer using the hand-assisted laparoscopic technique. Our preliminary experience with three gastric cardia cancer patients shows that this new approach is safe, feasible and effective and may offer a cost-effective to other.

目的 观察胃癌患者手术前后血清胰岛素样生长因子Ⅰ( IGF-Ⅰ)、IGF-Ⅰ受体( IGF-ⅠR)、胰岛素样生长因子Ⅱ( IGF-Ⅱ)水平变化,并探讨其临床意义. 方法 选择行胃癌根治术的胃癌患者50例(观察组)、体检健康者50例(对照组) ,检测观察组手术前后、对照组体检日血清IGF-Ⅰ、IGF-ⅠR、IGF-Ⅱ. 分析各指标与胃癌患者临床病理特征的关系. 结果 观察组术前血清IGF-Ⅰ、IGF-ⅠR、IGF-Ⅱ水平均高于术后及对照组(P均<0.05),但术后各指标与对照组比较差异均无统计学意义(P均>0.05). 单因素分析显示,低分化者血清IGF-Ⅰ、IGF-ⅠR、IGF-Ⅱ水平明显高于高分化、中分化者,TNM分期Ⅲ、Ⅳ期者明显高于Ⅰ、Ⅱ期者,有淋巴结转移者明显高于无淋巴结转移者(P均<0.05). 结论 胃癌患者术前血清IGF-Ⅰ、IGF-ⅠR、IGF-Ⅱ水平明显升高,其水平变化与肿瘤的组织分化程度、淋巴结转移、TNM分期有关.

The present study aimed to explore the expression of microRNA (miRNA or miR) in drug-resistant and drug-sensitive ovarian cancer cell lines, and to seek the potential therapeutic target of ovarian cancer drug-resistant mechanism in order to improve drug resistance by altering miRNA levels. The drug-resistant characteristics of SKOV3/DDP, SKOV3, COC1/DDP and COC1 cell lines were studied. The miRNAs that were differentially expressed between cisplatin-resistant cells and its parental cells in ovarian cancer were screened with a miRNA chip. The effect of miRNAs was detected, and their drug-resistant mechanism was investigated by transfection and 3-(4,5-dimethylthiazol-2-yl) 2,5-diphe-nyltetrazolium bromide methods. Among the expression screening of miRNAs, 41 mRNAs, including Homo sapiens (hsa) -miR-30a-5p and hsa-miR-34c-5p, were highly expressed in the drug-resistant cells, whereas 44 miRNAs, including hsa-miR-96-5p and hsa-miR-200c-3p, were lowly expressed. The expression levels of hsa-miR-30a-5p in two types of ovarian cancer chemotherapy-resistant cell lines were significantly higher than those in chemotherapy-sensitive cell lines, which was associated with ovarian cancer chemotherapy resistance. In conclusion, high expression of miRNA-30a-5p was able to promote cell growth and colony forming ability, and enhance cell migration and invasion. Thus, miRNA-30a-5p is expected to become a meaningful novel target for ovarian cancer resistant treatment.

目的：探讨改良入路腹腔镜手术或三联合外科手术在胃贲门癌根治术中的可行性。方法河北医科大学第二医院胃肠外科设计了一种能够将开腹手术、手辅助或腹腔镜手术结合在同一台手术的专利装置（腹腔镜手助器），并将这3种手术结合在一起的方式称为TULS。回顾性分析2014年6—8月行TULS贲门癌根治术治疗的8例患者临床资料。结果本组8例患者均顺利完成手术，无中转开腹患者，平均手术时间为186（155～218） min，术中出血量为110（80～200） ml，清扫淋巴结数目为27（19～38）枚／例，无术中及术后严重并发症的发生，于术后9～14（中位数11） d痊愈出院。术后随访5（4～6）月，均无明显不适。结论 TULS应用于贲门癌根治术，安全可行，短期疗效满意。

Objective To analyze the effect of the treatment of ovarian epithelial carcinoma by using the sustained release implant.Methods From January 2012 to December 2013,60 patients with ovarian epithelial carcinoma were randomly divided into observation group and control group,each of 30 cases.The observation group was treated with the sustained release implant,and the control group was treated by chemotherapy,and the effi cacy of the two patients was compared.Results The recurrence rate of the observation group was signifi cantly better than the control group,the difference was statistically signifi cant(P0.05).Conclusion For ovarian epithelial cancer patients,the use of sustained-release implant therapy,can signifi cantly reduce the recurrence rate of ovarian epithelial cancer,worthy of promotion in clinical.

Purpose: To investigate the activity and mechanisms of Tanshinones in inhibiting the growth of gastric cancer cells. Methods: PI3K, PDK1 and AKT phosphorylation and expression of cell cycle related markers in gastric cancer cells were determined by western blotting. The cell-cycle distribution was analyzed by flow cytometry. Results and Conclusions: The growth of gastric cancer cells was inhibited by Tanshinones dose-dependently. TIIA inhibited cell cycle progression, which was accompanied by regulating the expression of p21 and cyclin D1 and Rb phosphorylation. Activation of PI3K/PDK1/AKT signaling pathway was confirmed in gastric cancer cells as compared with normal gastric epithelial cells. Tanshinones significantly attenuated the elevation of PI3K and PDK1 phosphorylation, but only the changes of PDK1 phosphorylation showed the most consistent pattern with the activity with Tanshinones. Overexpression of PDK1 remarkably attenuated TIIA-inhibited cell cycle transition, and subsequently reversed the growth-inhibition activity of TIIA in MKN45 cells. Conversely, knockdown of PDK1 further augmented the effects of TIIA on cell growth, cell cycle transition and related molecular markers. Collectively, our study provides a novel mechanism by which TIIA prevents gastric cancer cell proliferation, and thus TIIA may be a promising anti-cancer agent for the treatment of gastric cancer.

A new technique has successfully established the non-obese diabetic/severely combined immunodeficiency (NOD/SCID) mouse model of ovarian cancer. Under 4% chloral hydrate (0.1 mL/g dose) anesthesia, female mice were inoculated with tumor-cell suspension. The expression rate of OVCAR3 to CA125 was assessed using flow cytometry. The inoculated site was hand palpated and the signs and symptoms related to tumor growth were observed with the naked eye. The allophycocyanin (APC) indirectly labeled mouse-antihuman CA125 and fluorescein isothiocyanate (FITC)-labeled anti-mouse MHC Class I molecule (H-2Kd/H-2Dd) were observed using a confocal laser scanning microscope. The animal model of ovarian cancer constructed using this method can more directly reflect the characteristics of cancer cells. It provides reliable experimental results and presents a technical platform for the research of ovarian cancer stem cells.

Epidermal growth factor (EGF) plays an important role in tumorigenesis. The association between the +61 A/G polymorphism of the EGF gene and colon cancer risk remains controversial and unclear. The objective of this study was to investigate the association between EGF +61 A/G polymorphism and colon cancer risk in a Chinese population. A hospital-based case-control study was conducted to assess the possible association between EGF +61 A/G polymorphism and colon cancer risk. A total of 180 colon cancer patients and 180 cancer-free healthy controls were recruited in the Chinese population. Genomic DNA was isolated from peripheral blood, and gene polymorphisms were analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Colon cancer patients had a significantly higher frequency of +61 GG genotype (odds ratio [OR]=1.93, 95% confidence interval [CI]=1.07, 3.50; p=0.03) than that of controls. When stratified by the tumor location, tumor size, growth pattern, differentiation, and tumor-node-metastasis (TNM) stage of colon cancer, no statistically significant results were observed. Our study revealed that EGF +61 GG genotype was associated with a higher risk of colon cancer in Chinese population.

目的 证实并比较胃癌自体肿瘤组织总RNA转染树突状细胞(dendritic cell,DC)诱导的细胞毒性T淋巴细胞(cytotoxic T-lymphocytes,CTL)对肿瘤组织和正常组织总RNA转染DC的致伤作用.方法 用脂质体转染的方法将3例胃癌患者肿瘤组织总RNA和正常组织总RNA转染到其自体单个核细胞源性DC中,以肿瘤组织总RNA转染DC(DC/Tumor RNA)致敏T淋巴细胞得到CTL,以calcein-AM细胞毒试验和酶联免疫斑点法测定干扰素-γ(interferon-γ,IFN-γ)分泌来检测CTL对肿瘤组织和正常组织总RNA转染DC的溶细胞效果.结果 CTL对DC/Tumor RNA杀伤率与对转染正常组织总RNA的DC(DC/Normal RNA)杀伤率比较差异有统计学意义(P<0.05).DC/Tumor RNA组CTL分泌IFN-γ较DC/Normal RNA组高出近2倍(P<0.05).结论 转染肿瘤组织总RNA的DC提高了抗肿瘤CTL的细胞毒作用,同时也诱导CTL对正常组织的致伤作用,以期降低DC为基础的肿瘤免疫治疗对正常组织的致伤作用提供理论依据.