Following the publication of the above article, a concerned reader drew to the Editor's attention that, regarding the cell invasion assay data shown in Fig. 2B on p. 3469, the 'si‑NC (SGC7901)' and 'si‑NC (MGC803)' data panels appeared to show the same data, albeit the panels were presented in a different orientation with respect to each other (rotated through 180°). Moreover, the data in question had apparently already been submitted and published in an article in the journal Oncology Letters written by different authors, although from the same hospital. After having performed an internal investigation of these data in the Editorial Office, the Editor of Oncology Reports has confirmed the legitimacy of the reader's concerns. Therefore, the Editor has decided that this article should be retracted from the publication on the grounds of an overall lack of confidence in the data, and given that the same data appeared in an unrelated article in a different journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor sincerely apologizes to the readership for any incovenience caused, and we thank the reader for bringing this matter to our attention. [Oncology Reports 38: 3465‑3472, 2017; DOI: 10.3892/or.2017.6020].

Purpose: To investigate the effect of curcumin on gastric cancer cell proliferation and the mechanism of action involved. Methods: Viability of gastric cells following curcumin treatment was determined by 3 (4,5 dimethyl thiazol 2 yl) 2,5 diphenyl 2H tetrazollum bromide (MTT) assay. Flow cytometry was used for the assessment of apoptosis induction in SGC 7901 cells. Reverse transcriptase polymerase chain reaction (RT-PCR) and western blotting assay were used for the analysis of Znf139, survivin and Bcl 2 protein expressions. Results: The results showed that curcumin treatment reduced the viability of gastric cancer cell line SGC 7901 cells at 30 mu M concentration to 29.67 % after 48 h compared to 99.78 % for control culture. Apoptotic cell population increased significantly (p < 0.05) following treatment with curcumin. Zinc finger protein-139 mRNA and protein expression decreased significantly (p < 0.05) on treatment with curcumin. Furthermore, curcumin suppressed the levels of B cell lymphoma 2 (Bcl 2) and survivin protein. In the mice model of gastric cancer, treatment with 50 mg/kg dose of curcumin inhibited tumor growth and development significantly, compared to the untreated group (p < 0.05). Conclusion: The results demonstrate that curcumin treatment inhibits gastric cancer cell proliferation via down-regulation of zinc finger protein-139. It also suppresses tumor growth in mice. Therefore, curcumin is a promising gastric cancer inhibitor and should be further investigated for the management of gastric cancer.

Background: Chidamide (CS055/Tucidinostat/Epidaza®) is an oral subtype-selective HDAC inhibitor. An exploratory clinical study has demonstrated the encouraging antitumor activity of chidamide in combination with exemestane in hormone receptor (HR)-positive advanced breast cancer (ABC) patients. Methods: This randomized, double-blind, placebo-controlled study involved postmenopausal patients with HR-positive, HER2-negative ABC that had failed with tamoxifen and/or nonsteroidal aromatase inhibitor. Eligible patients were randomly assigned (2:1) to two arms (chidamide 30 mg twice a week plus exemestane 25 mg daily or placebo plus exemestane). The primary endpoint was progression-free survival (PFS), assessed by investigator. Secondary endpoints were overall survival (OS), objective response rate (ORR), clinical benefit rate (CBR), and safety. Results: 365 patients were enrolled at 22 centers in China, with 244 in the chidamide group and 121 in the placebo group. The median PFS was 7.4 months [95% confidence interval (CI), 5.5 to 9.2] with chidamide–exemestane and 3.8 months (95% CI, 3.7 to 5.5) with placebo–exemestane (hazard ratio for disease progression or death, 0.755; 95% CI, 0.582 to 0.978; P = 0.0336). ORR were 18.4% and 9.1% (P=0.026), and CBR were 46.7% and 35.5% (P = 0.034) in the chidamide group and placebo group, respectively. Overall survival results were not mature at the time of the analysis. The most common grade 3 or 4 adverse events (AE) in the chidamide group were neutropenia (50.8% vs. 2.5% in the placebo group), thrombocytopenia (27.5% vs. 2.5%), and leucopenia (18.8% vs. 2.5%). Serious adverse events occurred in 51 (20.9%) patients in the chidamide group and 7 (5.8%) patients in the placebo group. No treatment-related death was reported. Conclusions: This is the first oral HDAC inhibitor combined with exemestane in a pivotal clinical study to demonstrate PFS benefit and manageable adverse effect in HR–positive ABC patients progressed after prior endocrine therapy. Clinical trial identification: NCT02482753. Legal entity responsible for the study: Jiang Zefei. Funding: Chipscreen Biosciences Co., Ltd. Disclosure: All authors have declared no conflicts of interest.

Plinabulin (Plin) is a novel non-GCSF small molecule with anti-cancer activity, in development for prevention of Chemotherapy (Chemo)-Induced-Neutropenia (CIN) and under evaluation with induced by Docetaxel (Doc), Adriamycin, Cyclophosphamide, Irinotecan, Gemcitabine, Carboplatin, Abraxane). Plin is administered as a single IV infusion per cycle, and on the same day of Chemo, 30 minutes after Chemo. In contrast to G-CSF, Plin has anti-cancer, immune-enhancing activity due to dendritic cell activation and related T-cell proliferation, and Plin does not cause bone pain. Our randomized phase (Ph) 2 study 101 (NCT00630110) in lung cancer (NSCLC) with Docetaxel (Doc) 75 mg/M2 +/- Plin established the baseline for Grade 4 neutropenia without Plin. We recently completed the Ph2 portion of the Ph2/3 Study 105 (NCT03102606), comparing Plin with Pegfilgrastim (Peg) for Doc CIN prevention in NSCLC. The 20 mg/m2 Plin dose was equally effective as Peg for CIN, and this dose will be taken into Ph3. The CIN nadir was earlier with Peg, and occurrence of bone pain was higher with Peg vs Plin (33% vs 11%, resp), suggesting a different mechanism of action (MoA). To further understand Plin’s MoA, we analyzed hematology results with Plin and Peg treated subjects. Ph2 Study 105: NSCLC Pts were randomized to Doc 75 mg/ m2 day (D)1, and either Peg 6 mg D2 (n=14), or Plin at 5 (n=14),10 (n=13), 20 (n=14) mg/ m2 D1 (30 minutes after Doc). Blood for central hematology analysis was collected through Cycle 1. Grade (Gr) 4 neutropenia data without Plin (that is Plin 0 mg/ m2) data was taken from study 101. Docetaxel-induced Gr 4 Neutropenia was 14%, 23%, 14%, 33% when Doc was combined with Plin at a dose of 20, 10, 5, 0 mg/ m2 . At the highest Plin dose of 20 mg/ m2, Gr 4 Neutropenia frequency (14% for Plin or Peg) and Duration of Grade 4/Severe Neutropenia (DSN; 0.5 days for Plin or Peg) were similar for Plin and Peg, however Gr 4 thrombocytopenia frequency was 50% with Peg and 36% with Plin. All Grade thrombocytopenia was significantly higher (p=0.036) with Peg vs Plin. Plin appears to be equally effective as Peg against Doc CIN, however Plin, but not Peg, reduced Doc-induced thrombocytopenia. This is further indication of a difference in MoA for Plin vs Peg.

Background: Elevated absolute neutrophil (N) count (ANC) may suppress the immune system and the activation of cytotoxic T-Lymphocytes (L). An elevated N-to-L Ratio (NLR) of NLR ≥ 5, is an independent negative prognostic indicator for outcome in cancer patients (pts) (Zhou; Nature 2017). CIN is a common side effect with chemo for which G-CSF is used. Plin is a novel small molecule in development for CIN caused by myelosuppressive chemos. Plin is given as a single IV infusion per cycle, 30 minutes after chemo, vs 24 hours after chemo with G-CSF. Plin does not cause bone pain. In contrast to G-CSF, Plin has anti-cancer, immune-enhancing activity due to dendritic cell activation and related T-cell proliferation (Mohanlal, ASCO-SITC 2018). We completed the Phase (Ph)2 portion of the Ph 2/3 Study BPI-2358-105 (NCT03102606), comparing Plin (at different doses; n = 55) head-to-head with Pegfilgrastim (Peg) for prevention of Docetaxel (Doc) CIN. Duration of Severe Neutropenia (DSN) and incidence of Grade 4 neutropenia (Gr 4 NP) in Cycle 1 were the same for Plin (20 mg/m2) and Peg (6 mg): 0.5 days and 14% resp for DSN and Gr 4 NP (Blayney, ASCO 2018). Since Plin and Peg both mitigate CIN, we examined the effect on NLR. Methods: The Ph2 portion of study 105 was analyzed for NLR in Cycle 1 from NSCLC pts receiving Doc with either Plin (20 mg/m2; n = 14) or Peg (6 mg; n = 14q5). ANC and L were available through day (D) 15. Results: Median ANC with Plin remained within normal range, whereas Peg induced an overshoot in ANC, exceeding upper limit of normal after D6 (p < 0.001). Peg, but not Plin, significantly increased NLR to a ratio of > 5 after D6.Table: 1686PDBaselineD6D7D8D9D10D15Plin NLR2.633.011.831.261.131.151.96Peg NLR4.113.935.098.319.2112.28.11P-value NLRNSNS0.03<0.001<0.001<0.001<0.001 Open table in a new tab Conclusions: Plin is an equally effective, single-dose-per cycle agent as Peg for CIN, however in contrast to Peg, Plin does not increase NLR to immune-suppressive levels, and has immune-enhancing activity. For Chemo/Immunotherapy combinations, Plin could be the preferred option to prevent CIN. Clinical trial identification: NCT03102606. Legal entity responsible for the study: BeyondSpring Pharmaceuticals, Inc. Funding: BeyondSpring Pharmaceuticals, Inc. Disclosure: D. Blayney: Leadership: Artelo Biosciences; Stock and other ownership interests: PRM Pharmaceutical, Artelo Biosciences Madorra; Consulting or advisory role: OnQ Cascadian Therapeutics, Varian Medical Systems, Mylan, Creare, Heron Oncology Learning Center; Research funding: Amgen, BeyondSpring Pharmaceuticals, S. Ogenstad: Employment: Anida Pharma, BeyondSpring Pharmaceuticals, Black Swan, Ferring Pharmaceuticals, A/S G&L Sciences, IMS; Expert services: Jenner & Block, PQ Bypass, Rubin, Anders, Scientific Sensible Medical Innovations Ltd, Shahin Gharakhanian, MD Consulting, LLC Somahlution, Inc, L. Du, L. Huang, R. Mohanlal: Employee of BeyondSpring Pharmaceuticals, Inc. All other authors have declared no conflicts of interest.

The ubiquitin-specific peptidase 22 (USP22) belongs to the largest subfamily of deubiquitylases and recent studies indicate that overexpression of USP22 may promote gastric cancer progression and predict prognosis. But little is known about the interaction network of USP22 in gastric cancer. In this study, we applied bioinformatics methods and found that USP22 was correlated with the heat shock protein 90 (HSP90) which is now considered to be a biomarker to predict the prognosis of gastric cancer. Then the siRNA transfection and western blotting were used to testify the correlation of USP22 and HSP90 in gastric cancer cells. The immunohistochemistry staining of the microarrays was applied to confirm the correlation of USP22 and HSP90 expression in gastric cancer tissue and further analysis showed that co-expression of USP22 and HSP90 was related to lymph node metastasis and more effective in predicting the prognosis of gastric cancer. In summary, our data demonstrate that correlation exists between USP22 and HSP90 expressions in gastric cancer and co-expression of USP22 and HSP90 may be more effective in predicting prognosis of gastric cancer.

Increasing evidence suggests that the glutathione peroxidase 2 may actually play important roles in tumorigenesis and progression in various human cancers such as colorectal carcinomas and lung adenocarcinomas. However, the role of glutathione peroxidase 2 in gastric carcinoma remains to be determined. In this study, the expression and prognostic significance of glutathione peroxidase 2 in gastric carcinoma were investigated and the well-known prognostic factor Ki-67 labeling index was also assessed as positive control. Glutathione peroxidase 2 expression levels in the tumor tissue specimens, the matched adjacent normal tissue specimens, and the lymph node metastases of 176 patients with gastric carcinoma were evaluated by quantitative polymerase chain reaction, western blotting, and immunohistochemical staining. The associations between glutathione peroxidase 2 expression levels, as determined by immunohistochemical staining, and multiple clinicopathological characteristics were determined by Pearson's chi-square test and Spearman's correlation analysis. The relationships between glutathione peroxidase 2 expression and other clinicopathological variables and patient prognoses were analyzed further by the Kaplan-Meier method, the log-rank test, and Cox multivariate regression. The quantitative polymerase chain reaction, western blotting, and immunohistochemical staining results showed that glutathione peroxidase 2 expression levels were upregulated in both the primary tumor foci and the lymph node metastases of patients with gastric carcinoma (all p values<0.05). Furthermore, Pearson's chi-square tests, as well as Spearman's correlation analysis, revealed that glutathione peroxidase 2 expression levels were strongly correlated with the Ki-67 labeling index, differentiation, histological patterns, Lauren classifications, lymph node metastasis, vascular invasion, tumor-node-metastasis stages, Helicobacter pylori infection, and overall survival (all p values<0.05). Kaplan-Meier analysis, as well as the log-rank test and multivariate Cox regression analysis, showed that multiple clinicopathological risk factors and glutathione peroxidase 2 expression were novel independent prognostic factors for gastric carcinoma (all p values<0.05). Glutathione peroxidase 2 expression is a novel independent prognostic biomarker for gastric carcinoma that may be used to devise personalized therapeutic regimens and precision treatments for this disease.

T-LAK (lymphokine-activated killer T) cell-originated protein kinase (TOPK) is a MAPKK (mitogen-activated protein kinase kinase)-like protein kinase, which interacts with some tumor suppressor proteins and may play some important roles in the activation of T-LAK cells and signaling for the mediation of their cytotoxic functions against cancer cells. Here, in this study, a retrospective analysis of 79 resected gastric cancer patients was carried out to examine TOPK expression by immunohistochemistry. SGC7901 cell lines with depletion of endogenous TOPK were used to investigate if TOPK could promote cell migration. We found that the positive frequency of TOPK in cancer cells was 92.4%, whereas no TOPK expression was detected in non-cancerous mucosa. With increasing expression of TOPK, there was a significant increase in pT classification (P=0.0319) and pN classification (P=0.0337). In univariate analyses, AJCC stage (P<0.0001), pT classification (P<0.0001), pN classification (P<0.0001), differentiation (P=0.0268), peritoneal metastasis (P=0.0002) and gross features (P=0.0100) were significant prognostic factors. In multivariate analysis, AJCC stage was an independent predictor of survival (P<0.0001). Reductions of TOPK in SGC7901 cells were associated with decreases in cell invasion (P=0.0102) and migration (P=0.0278). Taken together, TOPK overexpression is associated with poor prognosis in GC. TOPK promotes gastric cancer cell migration.

Gastric cancer (GC) is one of the most common malignant diseases worldwide. Although significant progress has been made in the early detection and treatment of GC over the past decades, the prognosis is still not satisfactory and the underlying mechanisms of carcinogenesis remain unknown. Long non-coding RNA MIAT has been established as a key player in the regulation of various biological and pathological processes including chronic lymphocytic leukemias, acute myocardial infarction and neuroendocrine prostate cancer. However, the function of MIAT in GC remains largely unknown. The expressions of lncRNA MIAT, miR-29a-3p and HDAC4 mRNA were analysed using quantitative real-time PCR (qRT-PCR). RNA interference approach was used to investigate the cellular functions of MIAT and miR-29a-3p. Cell Counting Kit-8 (CCK-8) assay and flow cytometry assay were performed to detect cell proliferation and apoptosis. Cell migration and invasion abilities were evaluated by Transwell assays. In the present study, we first confirmed the high expression level of MIAT in GC tissues and cell lines. In addition, knockdown of MIAT suppressed the proliferation, migration and invasion of GC cells in vitro. Furthermore, our results demonstrated that MIAT competitively binds to miR-29a-3p and consequently upregulates the expression of HDAC4, which is a downstream target of miR-29a-3p. In conclusion, the present study highlighted the involvement of the MIAT/miR-29a-3p/HDAC4 axis in the development of GC, which provided potential diagnostic and therapeutic targets for GC.

目的 探讨Nell-1基因启动子区不同甲基化位点与胃癌预后有关联的各种因素之间的相关性.方法 收集2012年哈尔滨医科大学附属第四医院肿瘤外科25例接受胃癌根治术的患者资料,运用混合效应线性模型分析Nell-1基因启动子区不同甲基化位点与胃癌预后有关的各种因素之间的相关性.结果 Nell-1基因启动子区第26号甲基化位点的胃癌组织组甲基化率与胃正常组织组甲基化率之间的差别有统计学意义,混合效应线性模型分析显示胃癌预后有关的因素(癌胚抗原、糖蛋白抗原199)对Nell-1基因启动子区第26号甲基化位点的甲基化率有影响,相同影响因素下该位点胃癌组织组甲基化率受到的影响程度高于胃正常组织组.结论 不同甲基化位点其甲基化率不同,其与胃癌患者肿瘤标记物之间存在一定相关性.

目的:明确胃癌原发灶与其转移淋巴结中Her2过表达或扩增的差异性,为临床胃癌治疗方案的选择提供参考依据.方法:选择112例经术后病理检查证实为胃癌原发灶Her2强阳性(Her2阳性表达为3+)表达并伴有淋巴结转移的患者样本,应用免疫组化方法并参照《胃癌Her2检测指南》中规定的检测流程重新判定有Her2过表达或扩增的胃癌原发病灶其相应的转移淋巴结中Her2有无过表达或扩增,再将检测结果进行比较.结果:112例患者中,胃癌组织Her2的阳性率为74.11％,淋巴结Her2的阳性表达为66.07％,二者共同阳性表达率为61.61％,差异无统计学意义(P=0.064).两,二者一致率为83.04％,kappa检验结果为(Z=6.452,P＜0.001).胃癌组织Her2的基因表达与年龄、性别、肿瘤位置和肿瘤大小以及远端转移均无显著相关性,而与Lauren分型、组织学分级、浸润深度、淋巴结转移以及TNM分期有关(P＜0.05).结论:胃癌原发病灶中Her2过表达或扩增与其相应的转移淋巴结中Her2过表达或扩增具有一致性.胃癌组织Her2状态与Lauren分型、组织学分级、浸润深度、淋巴结转移以及TNM分期有关.

Slightly increased pressure stimulates tumor cell adhesion and proliferation. In the present study, we aimed to evaluate the effects of high pressure on gene expression and the biological behavior of gastric cancer cells. After incubation for 30 min at 37˚C under ambient and increased pressure, one portion of SGC7901 cells was used for cell proliferation and apoptosis assays, cell cycle analysis, adhesion invasion or migration assays. The other portion of cells was harvested for detection of matrix metalloproteinase-2 (MMP-2), inhibitor of DNA binding-1 (ID1), sonic Hedgehog (SHH) and E-cadherin expression by western blotting or RT-PCR. In addition, we investigated the effects of high pressure on SGC7901 cell ultrastructure by transmission electron microscopy. We found that the adhesion fold under increased pressure of 760 and 1,520 mmHg was 2.39±1.05 (P<0.05) and 2.47±0.85 (P<0.01) as compared with the control, respectively. The invasion fold was 3.42±2.06 (P<0.05) and 5.13±2.49 (P<0.01) as compared with the control, respectively. The migration was 1.65±0.20 (P<0.001) and 2.53±0.50 (P<0.001) as compared with the control, respectively. At increased pressure, MMP-2 and ID1 expression increased significantly, while the expression of SHH decreased significantly. However, we did not find significant change in proliferation, apoptosis, cell cycle or ultrastructure of the SGC7901 cells under high pressure. In conclusion, high pressure promoted the adhesion, invasion and migration of SGC7901 cells. Moreover, the present study suggests that the pressure-augmented invasion and migration may be related to the increase in MMP-2 expression. Moreover, high pressure may suppress SGC7901 cell differentiation, which may result from the change in SHH and ID1 expression.

目的:探讨Nell-1基因启动子区不同甲基化位点与胃癌患者术后病理分期及淋巴结转移度之间相关性.方法:收集2012年4月至2012年9月在哈尔滨医科大学附属第四临床医院肿瘤外科25例接受胃癌根治术的病人资料,运用配对t检验及线性回归统计方法,分析Nell-1基因启动子区不同甲基化位点与胃癌患者临床病理资料之间的相关因素.结果:Nell-1基因启动子区不同甲基化位点的胃癌组织组和胃正常组织组甲基化率之间的差别有统计学意义(第1号位点及第38号位点),简单线性回归结果分析显示在第1号位点随着患者术后病理分期逐渐降低,胃癌组织组和胃正常组织组甲基化率之间的差值会逐渐增大(负相关);而在第38号位点随着淋巴结转移度的逐渐增大,胃癌组织组和胃正常组织组甲基化率之间的差值会逐渐增大(正相关).结论:胃癌的发生受诸多因素的影响,不同甲基化位点其甲基化率不同,其与胃癌患者临床病理资料之间存在一定相关性.

Background: HNSCC patients who progress after first-line platinum-based CT for R/M disease have few treatment options. In the Phase III LUX-H&N1 trial, afatinib, an irreversible ErbB family blocker, significantly improved progression-free survival (PFS) and health-related quality of life (HRQoL) compared with MTX in this patient population (Machiels et al, Lancet Oncol 2015). The LUX-H&N3 trial, sharing a similar study design, evaluates afatinib vs MTX in the same treatment setting in patients in Asia/Middle East/North Africa. Trial design: LUX-H&N3 is a Phase III, open-label, randomized trial evaluating efficacy and safety of afatinib vs MTX in R/M HNSCC patients progressing on/after first-line platinum-based CT (NCT01856478). Key eligibility criteria: age ≥18 years; ECOG PS 0 or 1; histologically or cytologically confirmed R/M HNSCC not amenable for salvage surgery or radiotherapy; documented progressive disease (PD) after ≥2 cycles of cisplatin/carboplatin for R/M disease (>1 systemic therapy not allowed). Prior treatment with EGFR-targeted antibody therapy but not EGFR-targeted small molecules is allowed. Patients are randomized 2:1 to afatinib (40 mg/day orally) or MTX (40 mg/m2 IV weekly), stratified by ECOG PS (0/1) and prior EGFR-targeted antibody therapy in the R/M setting (Yes/No). The initial afatinib dose must be escalated to 50 mg after ≥4 weeks with minimal drug-related adverse events (AEs), or reduced by 10 mg decrements to a minimum of 20 mg in case of drug-related grade ≥3 or selected grade 1/2 AEs. The MTX dose can be escalated to 50 mg/m2, or reduced by 10 mg/m2 decrements to a minimum of 20 mg/m2 in case of drug-related grade ≥2 or selected grade >1 AEs. Treatment will continue until PD or intolerable AEs. Treatment may continue beyond PD in case of clinical benefit as judged by the investigator. The primary endpoint is PFS; secondary endpoints include overall survival, objective response, HRQoL, and safety. Target enrollment is 300 patients; recruitment is ongoing. Clinical trial identification: NCT01856478 Disclosure: M.-J. Ahn: involvement with an advisory board for BMS, ARIAD and Lilly. A. Chan: advisory board involvement with Merck and Pfizer and research funding from Merck, Eli Lilly, Boehringer Ingelheim and Amgen. J.H. Kang: advisory board involvement with Boehringer Ingelheim, Eli Lilly, Pfizer and ONO Pharmaceutical Co.; corporate-sponsored research for Eli Lilly; and honoraria from Pfizer, Novartis and Boehringer Ingelheim. E. Cohen: involvement with an advisory board for Merck and Pfizer and honoraria from Eisai and Bayer. G.-Q. Hu, Y. Geng, E. Ehrnrooth: employment with Boehringer Ingelheim. All other authors have declared no conflicts of interest.

MicroRNAs (miRNAs) are small non-coding RNAs that function as regulators of gene expression. MiR-125 is a family of miRNAs that have been shown to be involved in various cancer types. In this study, for the first time, we showed that miR-125a-5p was specifically down-regulated in both colon cancer tissue and colon cancer cell lines. The tumor suppressor role of miR-125a-5p in colon cancer was supported by the observation that overexpression of miR-125a-5p inhibited cell proliferation and induced cell apoptosis in colon cancer cells. We also confirmed that in colon cancer cells, anti-apoptotic genes BCL2, BCL2L12 and Mcl-1 were direct targets of miR-125a-5p, and they were down-regulated by miR-125a-5p overexpression. Furthermore, restoration of BCL2, BCL2L12 and Mcl-1 expression in colon cancer cells could partially reverse the cell proliferation inhibition and apoptosis stimulation caused by miR-125a-5p overexpression, indicating that miR-125a-5p inhibits cell proliferation and induces apoptosis in colon cancer cells via targeting BCL2, BCL2L12 and Mcl-1.

We aimed to assess the efficacy and safety of S-1 combined with cisplatin (SC) over cisplatin alone (C) for the treatment of advanced gastric cancer in China. Between July 2009 and June 2011, 72 eligible patients with advanced gastric cancer were selected and divided randomly into two groups. Thirty-six patients received SC, with S-1 on days 1 through 14 of a 21-day cycle and cisplatin (60mg/m(2) on day 1) every 4 weeks for two cycles. The other 36 patients were administered only cisplatin (in the same manner as SC). The primary outcome was overall survival. The secondary outcomes were progression-free survival and adverse events. The 2-year overall response rate was 51.5 and 42.3% for the SC and C groups, respectively, and the difference was statistically significant, whereas the median overall survival was 9.4 months (range, 1.9-24.4 months) and 7.6 months (range, 1.7-21.4 months), respectively (P=0.039). The median progression-free survival was 7.7 months for SC (range, 1.8-19.4 months), whereas it was 6.5 months (range, 1.5-16.4 months) for C (P=0.047). The toxicity profile was similar in both groups. In summary, we have shown that S-1 combined with cisplatin is more effective, with acceptable toxicity in comparison with cisplatin alone in Chinese patients with advanced gastric cancer. Chinese Clinical Trials Register: ChiCTR-TRC-13003993.

目的:探讨热疗联合放疗在复发性卵巢癌治疗中的协同增敏作用.方法:68例晚期复发性卵巢癌患者,将其随机分为单纯放疗组(对照组)和热疗联合放疗组(实验组).两组盆腔三维适形放疗单次剂量为200 cGy,1次/日,5次/周.实验组在放疗结束后2小时内进行热疗,2次/周,共5周.治疗前及治疗结束后1个月均通过超声及CT检查对两组患者肿瘤体积的变化进行疗效评估,同时观察两组患者治疗后3年的生存情况.结果:近期疗效中发现,实验组11例完全缓解,17例部分缓解,对照组3例完全缓解,15例部分缓解,两组总有效率及完全缓解率差异均有统计学意义(P＜0.05).实验组3年总的生存率明显高于对照组,差异有统计学意义(P＜0.05).结论:热疗联合放疗可有效的杀灭复发的卵巢恶性肿瘤细胞,可缓解放疗副反应,明显提高患者的生存率.

Sperm-associated antigen 9 (SPAG9) has been reported to express in several cancers and have clinical significance. Using immunohistochemistry, we found that there was a strong association among SPAG9 expression and tumor size, TNM stage, histological grade, lymph node metastasis, and recurrence. It suggested that SPAG9-elevated expression was an independently prognostic indicator for both OS and DFS. Furthermore, the selected treatment of chemotherapy with Taxol/non-Taxol significantly affects OS and DFS. To sum up, SPAG9-elevated expression contributes to malignant behavior and poor prognosis of breast cancer and may support a potential indicator in treatment selection.

Mass spectrometry (MS) enables rapid and sensitive qualitative and quantitative analyses of biomolecules (proteins, peptides, oligosaccharides, lipids, DNA, and RNA), drugs, and metabolites. MS has become an essential tool in modern biomedical research, including the analysis of DNA methylation. DNA methylation has been reported in many cancers, suggesting that it can be utilized as an early biomarker to improve the early diagnosis rate. Using matrix-assisted laser desorption/ionization time-of-flight MS and MassCLEAVE reagent, we compared Nell-1 hypermethylation levels among tumor tissues, paracarcinoma tissues, and normal tissues from gastric cancer patients. Almost 80% of the CpG sites in the amplicons produced were covered by the analysis. Our results indicate a significant difference in methylation status between gastric cancer tissue (a higher level) and normal tissue. The same trend was identified in gastric cancer tissue versus paracarcinoma tissue. We also detected lower relative expression of Nell-1 by real-time PCR. Furthermore, immunohistochemical analyses revealed that Nell-1 staining was less intense in cancer tissue relative to normal tissue and that the tumor cells had spread to the muscle layer. These findings may serve as a guide for the early diagnosis of gastric cancer.