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BACKGROUND Low-dose computed tomography (LDCT) screening is effective in reducing lung cancer mortality in smokers; however, the evidence in nonsmokers is scarce. OBJECTIVE This study aimed to evaluate the participant rate and effectiveness of one-off LDCT screening for lung cancer among smokers and nonsmokers. METHODS A population-based prospective cohort study was performed to enroll participants aged between 40 and 74 years from 2013 to 2019 from 4 cities in Zhejiang Province, China. Participants who were evaluated as having a high risk of lung cancer from an established risk score model were recommended to undergo LDCT screening. Follow-up outcomes were retrieved on June 30, 2020. The uptake rate of LDCT screening for evaluated high-risk participants and the detection rate of early-stage lung cancer (stage 0-I) were calculated. The lung cancer incidence, lung cancer mortality, and all-cause mortality were compared between the screened and nonscreened groups. RESULTS At baseline, 62.56% (18,818/30,079) of smokers and 6% (5483/91,455) of nonsmokers were identified as high risk (PPPP=.005), whereas no significance was found (42/44, 96% vs 10/12, 83%; P=.20) among nonsmokers. Compared with participants who were not screened, LDCT screening in smokers significantly increased lung cancer incidence (hazard ratio [HR] 1.39, 95% CI 1.09-1.76; P=.007) but reduced lung cancer mortality (HR 0.52, 95% CI 0.28-0.96; P=.04) and all-cause mortality (HR 0.47, 95% CI 0.32-0.69; PP=.06), all-cause mortality (P=.89), and lung cancer mortality (P=.17). CONCLUSIONS LDCT screening effectively reduces lung cancer and all-cause mortality among high-risk smokers. Further efforts to define high-risk populations and explore adequate lung cancer screening modalities for nonsmokers are needed.

Background: Esophageal cancer (EC) often occurs in the elderly, and approximately 40% of patients are 70 years or older. To investigate the long-term survival of esophageal cancer in elderly patients, to provide a theoretical direction for better management and predicting survival of EC based on the hospital-based multi-center study in China.Methods: The study was conducted in eighteen hospitals including 6 provincial hospitals, 8 municipal hospitals, and 4 county hospitals. We extracted information from medical record homepage, records of admission and discharge, and pathological diagnosis reports from the medical record department of the elderly patients at 70-84 years to further obtain the 3-year and 5-year overall survival (OS), and main associated factors, and to analyze the current therapeutic effect of different treatment options for elderly patients. Results: The 3-year and 5-year OS rate of the 1013 elderly patients was 44.8% and 32.8%, respectively. Their median survival was 28.00 months. The median survival of patients with squamous cell carcinoma was longer than that of other pathological type (squamous vs. other types: 31.00 vs. 20.00 months, P = 0.018). The median survival of patients with surgery only or combined therapy was longer than that of radiotherapy, chemotherapy, no therapy (surgery only vs. combined therapy vs. radiotherapy vs. chemotherapy vs. no therapy: 56.00 vs. 33.00 vs. 26.00 vs.18.00 vs. 16.00 months, PConclusions: The survival rate of the elderly EC patients was still low in China. Age, therapy method, and pathological stage were mainly associated with the survival rate of EC in elderly patients.

Purpose In prostate cancer, castration resistance is a factor that frequently leads to death in individuals with this disease. Recent studies have suggested that prostate cancer stem cells (PCSCs) are pivotal regulators in the establishment of castration resistance. The nanog homeobox (NANOG) and the transforming growth factor (TGF)-β1/drosophila mothers against decapentaplegic protein (SMAD) signaling pathways are involved in several cancer stem cells but are not involved in PCSCs. The purpose of this study is to investigate the effect of NANOG on the proliferation of PCSCs regulated by the TGF-β1/SMAD signaling pathway. Methods In this study, we used flow cytometry to isolate CD44+/CD133+/NANOG+ PCSCs from DU145 prostate cancer cells. Then we used short hairpin RNA to silence NANOG and observed the biological behavior and the TGF-β1/SMAD signal of PCSCs. Results NANOG decreased PCSC proliferation, increased apoptosis, and blocked cell cycling at G0/G1. Furthermore, reduction in the TGF-β1, p15, and p-SMAD2 expression was observed. Conclusion These findings suggest that NANOG positively regulates the growth of PCSCs through the TGF-β1/SMAD signaling pathway.

Long non‑coding RNAs (lncRNAs) are involved in the pathogenesis of prostate cancer (PCa) as competitive endogenous RNA. The present study aimed to investigate the molecular mech--anisms of lncRNA small nucleolar RNA host gene 16 (SNHG16) in the proliferation and metastasis of PCa cells. Cancer tissues and adjacent normal tissues were collected from 80 patients with PCa who did not receive any treatment. Reverse transcription‑quantitative PCR analysis was performed to detect the expression levels of SNHG16, hsa‑microRNA (miRNA/miR)‑373‑3p and transforming growth factor‑β receptor type 2 (TGF‑β‑R2), and Spearman's correlation coefficient analysis was performed to assess the correlations between these molecules. Furthermore, the effects of SNHG16 knockdown and overexpression on the biological functions of DU‑145 PCa cells and TGF‑β‑R2/SMAD signaling were analyzed. The dual‑luciferase reporter assay was performed to assess the associations between SNHG16 and miR‑373‑3p, and TGF‑β‑R2 and miR‑373‑3p, the effects of which were verified via rescue experiments. The results demonstrated that the expression levels of SNHG16 and TGF‑β‑R2 were significantly upregulated in PCa tissues, whereas miR‑373‑3p expression was significantly downregulated (P

Previous studies have reported that the expression levels of microRNA (miR)-28-3p are downregulated in prostate cancer (PCa) compared with those in adjacent normal tissues. However, to the best of our knowledge, the function and underlying mechanisms of miR-28-3p in PCa have not been reported. The present study aimed to explore the role of miR-28-3p and its mechanism in the development of PCa. In the present study, miR-28-3p and ADP-ribosylation factor 6 (ARF6) expression levels were analyzed using reverse transcription-quantitative PCR (RT-qPCR). Cell proliferation, colony formation, apoptosis, migration and invasion were determined using Cell Counting Kit-8, colony forming, flow cytometry and Transwell assays, respectively. The association between miR-28-3p and ARF6 was investigated using a dual luciferase reporter assay. ARF6, Rac1, Erk1/2 and phosphorylated (p)-Erk1/2 protein expression levels were analyzed using western blotting. The results of the present study revealed that miR-28-3p expression levels were downregulated, whereas ARF6 expression levels were upregulated in PCa cell lines (LNCaP, 22Rv-1, PC-3 and DU145) compared with those in the normal prostate line RWPE-1. The overexpression of miR-28-3p promoted cell apoptosis, and inhibited cell proliferation, colony formation, migration and invasion. However, the knockdown of miR-28-3p exerted the opposite results. The results of the dual luciferase reporter assays, RT-qPCR and western blotting indicated that ARF6 was a target gene of miR-28-3p. Finally, rescue experiments demonstrated that ARF6 overexpression attenuated the effects of the miR-28-3p mimic by upregulating Rac1 and p-Erk1/2 expression in PCa cells. In conclusion, these findings indicated that miR-28-3p may inhibit the biological behaviors of PCa cells by targeting ARF6, and therefore may represent a novel therapeutic candidate for PCa.

IMPORTANCE: Most older patients with esophageal cancer cannot complete the standard concurrent chemoradiotherapy (CCRT). An effective and tolerable chemoradiotherapy regimen for older patients is needed. OBJECTIVE: To evaluate the efficacy and toxic effects of CCRT with S-1 vs radiotherapy (RT) alone in older patients with esophageal cancer. DESIGN, SETTING, AND PARTICIPANTS: A randomized, open-label, phase 3 clinical trial was conducted at 23 Chinese centers between June 1, 2016, and August 31, 2018. The study enrolled 298 patients aged 70 to 85 years. Eligible participants had histologically confirmed esophageal cancer, stage IB to IVB disease based on the 6th edition of the American Joint Committee on Cancer (stage IVB: only metastasis to the supraclavicular/celiac lymph nodes) and an Eastern Cooperative Oncology Group performance status of 0 to 1. Data analysis was performed from August 1, 2020, to March 10, 2021. INTERVENTIONS: Patients were stratified according to age (

Nanoparticular drug delivery system (NDDS) has great potential for enhancing the efficacy of traditional chemotherapeutic drugs. However, it is still a great challenge to fabricate a biocompatible NDDS with simple structure capable of optimizing therapeutic efficacy, such as high tumor accumulation, suitable drug release profile (e.g. no premature drug leakage in normal physiological conditions while having a rapid release in cancer cells), low immunogenicity, as well as good biocompatibility. In this work, a simple core/shell structured nanoparticle was fabricated for prostate cancer treatment, in which a mesoporous silica nanoparticle core was applied as a container to high-efficiently encapsulate drugs (doxorubicin, DOX), CaCO3 interlayer was designed to act as sheddable pH-sensitive gatekeepers for controlling drug release, and cancer cell membrane wrapped outlayer could improve the colloid stability and tumor accumulation capacity. In vitro cell experiments demonstrated that the as-prepared nanovehicles (denoted as DOX/MSN@CaCO3@CM) could be efficiently uptaken by LNCaP-AI prostate cancer cells and even exhibited a better anti-tumor efficiency than free DOX. In addition, Live/Dead cell detection and apoptosis experiment demonstrated that MSN/DOX@CaCO3@CM could effectively induce apoptosis-related death in prostate cancer cells. In vivo antitumor results demonstrated that DOX/MSN@CaCO3@CM administration could remarkably suppress the tumor growth. Compared with other tedious approaches to optimize the therapeutic efficacy, this study provides an effective drug targeting system only using naturally biomaterials for the treatment of prostate cancer, which might have great potential in clinic usage.

Background: Long noncoding RNAs (lncRNAs) are one of the major causes of tumorigenesis. However, the roles and mechan­­isms of lncRNA SNHG16 in prostate cancer (PCa) remain unknown. The purpose of this study was to elucidate the mech­­anisms of lncRNA SNHG16 in the proliferation and metastasis of human PCa cells.Material and Methods: First, the quantitative polymerase chain reaction (qPCR) was used to measure SNHG16 expression in PCa tissues and adjacent normal tissues (n=80). Down-regulate and over-express SNHG16 in human PCa DU-145 cell. Then cell proliferation was detected by CCK8 assay, cell apoptosis was analyzed by flow cytometry, cell migration were determined by wound healing, and cell invasion was examined by transwell. Western blot assays were used to examine the expression of the TGFBR2, c-MYC, E2F4, SMAD2, p-SMAD2, SMAD3, and p-SMAD3. Second, the targeting relationship between SNHG16 and hsa-miR-373-3p was verified by dual-luciferase reporter assay and rescue experiments. Third, the targeting relationship between hsa-miR-373-3p and TGFBR2 was verified by dual-luciferase reporter assay and rescue experiments. Results: The expression of SNHG16 was significant increase in PCa tissues (Z=-8.405, P P=0.007). Silencing SNHG16 inhibited DU-145 cell proliferation, migration, and invasion, while induced cell apoptosis significantly (PPPZ=-8.344, P7, P = 0.024). Hsa-miR-373-3p expression of hsa-miR-373-3p was negatively correlated with SNHG16 (r=-0.544, PZ=-5.945, PPConclusion: LncRNA SNHG16 might act as a ceRNA to regulate the proliferation and migration of DU-145 cells by modulating the hsa-miR-373-3p/TGFBR2/SMAD axis.

Background: Survival of patients with stage I non-small cell lung cancer (NSCLC) varies greatly. We sought to explore whether presence of oncogenic alterations in histologically-negative lymph nodes (LNs) can be of prognostic significance in stage I lung adenocarcinoma (LUAD). Methods: Genomic analysis of oncogenic alterations was applied to 123 stage I LUAD tumors. The same genomic variants identified in primary tumors were examined in corresponding histologically-negative LNs. Results: A total of 102 (82.9%) patients had at least one canonical oncogenic alteration detected in primary tumors, and 57 LNs from 12 patients (11.8%) were found to carry the identical oncogenic alterations detected in the corresponding primary tumor tissues, including EGFR mutations (six cases), KRAS mutations (three cases), ALK fusion (one case), BRAF mutation (one case) and HER2 & NRAS co-mutations (one case). None of these LNs was found to have occult tumor cells by routine pathological assessment or immunohistochemistry staining using antibodies against pan-cytokeratins (AE1/AE3) and the epithelial marker Ber-EP4. The detection rate of oncogenenic alterations in LN was significantly higher in RAS-mutant tumors than EGFR mutant tumors (36.36% verse 7.41%, p = 0.017). Patients with oncogenic alterations in LN showed inferior disease-free survival (DFS, p = 0.025) and overall survival (OS, p = 0.027). Furthermore, patients with RAS-mutations detected in LN had the worst DFS and OS (p = 0.001). Among the 11 patients with RAS mutation in primary tumors, DFS and OS in the four patients with mutations detected in LN were significantly shorter than the remaining seven patients without mutations LN (DFS, p = 0.001, OS, p = 0.002). Conclusions: Genomic analysis has the potential to detect oncogenic alterations in regional LNs for localized LUAD and presence of oncogenic alterations in regional LN may be associated with inferior clinical outcome of stage I LUAD, particularly for certain molecular subgroups. ClinicalTrials.gov ID NCT04266691

Objective MTDH/AEG-1 could act as an oncogene by regulating cellular transformation, proliferation, invasion, metastasis, and angiogenesis. This study aims to explore the mechanism by which MTDH/AEG-1 inhibits cancer growth and metastasis and enhances chemosensitivity. Methods Mouse model was established using orally immunized mice exposed to attenuated Salmonella containing vectors carrying full length MTDH/AEG-1 gene, and we were able to enhance the immune response and inhibit the growth and metastasis of prostate cancer through activation of cellular and humoral immunities and induction of CD8+ T cells. Immunohistochemistry and TUNEL assay, CD4+ and CD8+ T cell analysis by flow cytometry, HE staining, RT-PCR analysis, Western-blot analysis and quantitative polymerase chain reaction were performed. Results The MTDH/AEG-1 gene vaccine induced the anti-tumor function of cytotoxic T lymphocytes and CD8+ T cells and inhibited tumor growth and metastasis of prostate cancer. In the therapy model, the MTDH/AEG-1 gene vaccine significantly enhanced chemosensitivity to paclitaxel, inhibited tumor growth, promoted tumor cell apoptosis, and prolonged the survival time of tumor-bearing mice without any apparent side effects. Conclusions Our results demonstrated that MTDH/AEG-1-based DNA vaccines could used for the treatment of prostate cancer in terms of the inhibition of tumor growth, the lifespan of tumor-bearing animals. Combined with chemotherapy, MTDH/AEG-1-based DNA vaccines may produce highly favorable outcomes in the prevention and treatment of prostate cancer, suggesting the immune efficacy of MTDH/AEG-1-based DNA should be further analyzed in other cancers.

Prostate cancer is the second leading cause of cancer deaths among men in Western counties and has increased in incidence also in China in recent years. Although diagnosis modalities for primary prostate cancer have markedly improved, there are still no effective therapies for metastatic prostate cancer. SU6668 is an inhibitor of the tyrosine kinase activity of three angiogenic receptors VEGFR2, PDGFRβ and FGFR1. There is strong experimental evidence that SU6668 can induce growth inhibition of various primary tumors. However, the function and molecular mechanism of SU6668 in prostate cancer has not been fully elucidated. In the present study, we found that SU6668 inhibited the proliferation and invasion of prostate cancer cells. Functional studies also demonstrated that SU6668 inhibited epithelial-mesenchymal transition in DU145 and LNCap cells. After treatment with SU6668, MTDH protein, which has been reported to be significantly overexpressed in many human tumor tissues, was downregulated in DU145 and LNCap cells. siRNA-mediated silencing of MTDH in prostate cancer cells decreased their proliferation and invasive capabilities, suggesting that SU6668 may inhibit cell proliferation and invasion of prostate cancer cells partly through downstream targeting of MTDH. Mechanistic investigations showed that AKT signaling pathway was inhibited after SU6668 treatment in prostate cancer cells. Moreover, a combination of SU6668 and PI3K-AKT pathway inhibitor LY29004 resulted in increased inhibition of cell proliferation and invasion in DU145 cells. Taken together, our findings revealed that SU6668 suppressed prostate cancer progression by downregulating MTDH/AKT signaling pathway and identified a promising therapeutic strategy for prostate cancer.

To evaluate and compare the effectiveness of double Endobutton technique and suture anchor combined Endobutton plate in the treatment of Tossy type III acromioclavicular joint dislocation.Between May 2010 and March 2014, a retrospective study was preformed on 56 patients with Tossy type III acromioclavicular joint dislocation. The coracoclavicular ligament was reconstructed with double Endobutton technique in 31 cases (Endobutton group), and with suture anchor combined Endobutton plate in 25 cases (Anchor group). There was no significant difference in age, gender, injury causes, injury side, associated injury, medical comorbidities, and disease duration between 2 groups (P0.05). The operation time, medical device expenses, postoperative complications, preoperative and postoperative Constant-Murley scores, and postoperative Karlsson grading of the injured shoulder were compared between 2 groups.The average operation time in Endobutton group was significantly greater than that in Anchor group (t = 4.285, P = 0.000); there was no significant difference in the medical device expenses between 2 groups (t = 1.555, P = 0.126). Primary healing of incision was obtained in all patients of 2 groups; no early complications of infection and skin necrosis occurred. All patients were followed up 15.6 months on average (range, 11-35 months). During follow-up, some loss of reduction and ectopic ossification in the coracoclavicular gap were observed in 1 case and 6 cases of Endobutton group, respectively. No recurrence of acromioclavicular joint dislocation, implant fixation loosening and broken, and secondary fractures occurred in the other patients. There was significant difference in the incidence of postoperative complications between 2 groups (P = 0.013). Constant-Murley scores of the injured shoulder significantly increased at 9 months after operation when compared with preoperative values in 2 groups (P0.05), but no significant difference was observed between 2 groups (P0.05). At last follow-up, there was no significant difference in Karlsson grading between 2 groups (Z = -0.628, P = 0.530).Both double Endobutton technique and suture anchor combined Endobutton plate have good effectiveness in the treatment of Tossy type III acromioclavicular joint dislocation. But the latter is associated with easier operation, less operation time, and less complications.

The gene MTDH/AEG-1 is overexpressed in more than 40% of breast cancer patients, and it is associated with poor clinical outcomes. Previous studies have indicated that MTDH/AEG-1 could promote metastatic lung-seeding and enhance chemoresistance. Therefore, MTDH/AEG-1 could be a candidate target against breast cancer lung metastasis. We demonstrated that MTDH/AEG-1-based DNA vaccine, delivered by attenuated Salmonella typhimurium, could evoke strong CD8(+) cytotoxic-T-cell mediated immune responses against breast cancer. This vaccine showed anti-tumor growth and metastasis efficacy in a prophylactic setting. Importantly, in a therapeutic model, MTDH/AEG-1 vaccine was proved to increase chemosensitivity to doxorubicin and inhibit breast cancer lung metastasis. This vaccine could also prolong the life span of tumor-bearing mice without significant side effects in vivo. These results suggested that this novel DNA vaccine was effective in the inhibition of breast cancer growth and metastasis, and this vaccine in combination with chemotherapies offered new strategies for the clinical therapeutics of breast cancer metastasis.

Background: Laryngeal cancer is the one of the most prevalent cancer of the upper respiratory tract. Aiming to get a better understanding of the epidemiological characteristics and trends of laryngeal cancer in Zhejiang cancer registry in China during 2000–2011, we used the standardized quality control and statistical methods to analyze the incidence and mortality that were vital for making decision about laryngeal cancer prevention and control. Materials and Methods: Comparably high-quality data from eight population-based cancer registries in Zhejiang from 2000 to 2011 were qualified for analysis. The pooled data were stratified by area, sex, and age group. All incidence and mortality rates were age-standardized to the 2000 Chinese standard population and Segi's population, which were expressed per 100,000 populations. Average annual percent changes (AAPCs) and 95% confidence intervals of laryngeal cancer incidence and mortality were calculated for the temporal trends. The logarithmic trend line was also drawn to reflect the time trends of incidence and mortality. Results: During the 12 years, the 8 cancer registries covered a total of 81,758,277 person-year population (65,500,842 in urban and 16,257,435 in rural areas) including 41,315,911 person-year males and 40,442,366 person-year females. The age-standardized incidence rates were 1.10/10 5 by Chinese population and 1.12/10 5 by world population, respectively. The incidence of laryngeal cancer was relatively low in subjects under 44 years old. Then, it increased sharply after 45 years old and finally reached the peak in subjects of 75–79 years old. The age-standardized mortality rates of the Chinese population and world population were 0.28/10 5 and 0.35/10 5 , respectively. The mortality of laryngeal cancer was at a low level in subjects under 49 years old. The rate dramatically increased in subjects over 50 years old, and then peaked in the age group of 80–84 years. The crude incidence of laryngeal cancer in Zhejiang cancer registration areas in 2000 was approximately 1.39/10 5 , and it reached 1.78/10 5 in 2011, with the AAPC of 2.47%; the temporal trend line indicates that the incidence remained steady during the 12 years. The crude mortality of laryngeal cancer in Zhejiang registration areas in 2000 was about 0.30/10 5 and increased to 0.66/10 5 , with the AAPC of 4.24% which showed no statistical significance; the temporal trend line indicates that mortality was going up to a certain extent, but not evident. Conclusions: Laryngeal cancer significantly influenced the quality of life for the patients. The comprehensive measures should be carried out to prevent the upward trend of laryngeal cancer.

To investigate the cervical cancer incidence and mortality in cancer registries of Zhejiang province during 2000 to 2009.The data of cervical cancer incidence and mortality were collected from six cancer registries in Zhejiang province. Staff of Zhejiang Provincial Cancer Prevention and Control Office checked, sorted and analyzed the data to calculate crude, standardized rate and trend. Chinese census in 1982 and Segi's population were used for age-standardized incidence and mortality rates.The incidence rate of cervical cancer in Zhejiang cancer registration areas was 11.78/100 000 during 2000 to 2009, and age-standardized incidence rates by Chinese standard population and by world standard population were 7.05/100 000 and 8.62/100 000, respectively. The mortality rate was 1.89/100 000, and age-standardized mortality rates by Chinese standard population and by world standard population were 0.95/100 000 and 1.23/100 000, respectively. The age-specific incidence rates showed different trends, increased significantly after the age of 25, peaked at 45-year-old group, which was 23.03/100 000 (578/2 510 099) , and decreased at the age of 50, while the age-specific mortality rates gentlely increased, peaked at 85 years of age group, which was 11.94/100 000 (33/276 414) . The cervical Cancer Incidence from 5.96/100 000 (86/1 443 589) in 2000, increased to 18.90/100 000 (898/4 751 426) in 2009, the annual percent change (APC) was 16.64% (95%CI:11.87%-21.61%). The mortality showed a gentle upward trend from 1.45/100 000 (21/1 443 589) , increased to 2.53/100 000 (120/4 751 426) in 2009, the APC was 6.63% (95%CI:1.73%-11.77%).Cervical cancer showed younger trend, the incidence and mortality trends showed an increasing trend, should strengthen the prevention and control of cervical cancer.

To investigate the incidence and mortality rates of thyroid cancer in Zhejiang province during 2000 to 2009.The data of thyroid cancer were collected from six cancer registries in Zhejiang province and the incidence and mortality rates of thyroid cancer were analysed.The mean annual incidence rate of thyroid cancer in Zhejiang cancer registration areas was 6.93/100 000 during 2000 to 2009, and male/female ratio was 1: 3.43. The incidence rate was 3.62/100 000 in 2000 and it increased to 11.42/100 000 in 2009, with the annual percent change (APC) of 16.32% (95% confidence interval: 12.90%-19.85%). The mean annual mortality rate of thyroid cancer was 0.27/100 000 during 2000 to 2009, and male/female ratio was 1: 1.12. The mortality showed a rising trend without a distinct fluctuation from 2000 to 2009, the APC was 2.14% (95% confidence interval: from -7.10% to 12.30%). The incidence showed a rising trend with the increase of ages after 15 years old, and peaked at 55-60 years old. The mortality was low before 54 years old, but showed a rising trend with a distinct fluctuation after 55 years old, and peaked at 85-90 years old.The prevention and control of risk factors for thyroid cancer in young and middle-aged people is key to decrease the incidence and mortality of thyroid cancer.

Objective: The Zhejiang Provincial Cancer Prevention and Control Office collected cancer registration data during 2000 to 2009 from 6 cancer registries in Zhejiang province of China in order to analyze the cancer incidence. Methods: Descriptive analysis included cancer incidence stratified by sex, age and cancer site group. The proportions and cumulative rates of 10 common cancers in different groups were also calculated. Chinese population census in 1982 and Segi’s population were used for calculating age-standardized incidence rates. The log-linear model was used for fitting to calculate the incidence trends. Results: The 6 cancer registries in Zhejiang province in China covered a total of 60,087,888 person-years during 2000 to 2009 (males 30,445,904, females 29,641,984). The total number of new cancer cases were 163,104 (males 92,982, females 70,122). The morphology verified cases accounted for 69.7%, and the new cases verified only by information from death certification accounted for 1.23%. The crude incidence rate in Zhejiang cancer registration areas was 271.5/10 5 during 2000 to 2009 (male 305.41/10 5 , female 236.58/10 5 ), age-standardized incidence rates by Chinese standard population (ASIRC) and by world standard population (ASIRW) were 147.1/10 5 and 188.2/10 5 , the cumulative incidence rate (aged from 0 to 74) being 21.7%. The crude incidence rate was 209.6/10 5 in 2000, and it increased to 320.20/10 5 in 2009 (52.8%), with an annual percent change (APC) of 4.51% (95% confidence interval, 3.25%-5.79%). Age-specific incidence rate of 80-84 age group was achieved at the highest point of the incidence curve. Overall with different age groups, the cancer incidences differed, the incidence of liver cancer being highest in 15-44 age group in males; the incidence of breast cancer was the highest in 15-64 age group in females; the incidences of lung cancer were the highest in both males and females over the age of 65 years. Conclusions: Lung cancer, digestive system malignancies and breast cancer are the most common cancers in Zhejiang province in China requiring an especial focus. The incidences of thyroid cancer, prostate cancer, cervical cancer and lymphoma have increased rapidly. Prevention and control measures should be implemented for these cancers.

To investigate the incidence and mortality of brain tumor in Zhejiang cancer registration areas from 2000 to 2009.Data from 6 Cancer registration areas of Zhejiang province were collected. Number of cases, crude rates, proportions, age standardized rates, cumulate rates, cut rates, age-specific rates and annual percentage change (APC, 95% CI) of brain tumor incidence and mortality were analyzed.There were 5 123 new diagnosed brain tumor cases in Zhejiang cancer registration areas, accounting for 3.14% of all the new cancer cases. The incidence rate of brain tumor was 8.53/100 000, and the standardized incidence rate by Chinese population was 5.72/100 000, ranking the 7th????? in cancer incidence spectrum of anatomic sites. Agespecific incidence of brain tumor increased along with age, and peaked among 70-74 age groups (24.09/100 000). The annual incidence rate of brain tumor increased from 2000 (6.87/100 000) to 2009(8.35/100 000), with APC as 1.58% (95%CI: -2.17%-5.47%, no statistical significance). A total of 2 357 deaths caused by brain tumor were reported from 2000-2009, accounting for 2.47% of all the cancer death cases. Mortality rate on brain tumor appeared to be 3.92/100 000, with the standardized mortality rate by Chinese population as 2.45/100 000, ranking the 7th????? in cancer mortality spectrum of anatomic sites. The age-specific mortality of brain tumor remained low among 0-39 year-olds, and reached the peak at 80-84 age groups (17.64/100 000). The annual mortality rate of brain tumor decreased from 2000(4.30/100 000)to 2009 (3.83/100 000) with minor fluctuation, and the APC was -0.65% (95%CI: -3.35%-2.12%, no statistical significance).Brain tumors incidence and mortality in Zhejiang cancer registration areas were at a relatively high level. People who were at middle-age, especially above 70 years old should be the key targets for protection on this disease. Brain tumor incidence rates increased annually in Zhejiang, which should be called for attention.

Learning community provides learners and teachers a new type to organize their learning and teaching. For English majors, it is feasible and applicable to form a learning community, especially with the Internet as the assisted base. In the author’s course, 52 students majoring in English take part in the practice of building and running the learning communities. Some problems and advantages are analyzed, with the suggestions given in the conclusion. Keywords—learning community, Internet-based, English

FAT4 plays a crucial role in carcinogenesis as a key component of the Hippo signaling pathway. We hypothesized that potential functional polymorphisms in the FAT4 gene may modify the risk of esophageal cancer. To test this hypothesis, we evaluated the association between four nonsynonymous polymorphisms (rs1039808, rs12508222, rs1567047 and rs1014867) in FAT4 and esophageal cancer risk in a case-control study of 2,139 esophageal cancer cases and 2,273 controls in a Chinese population. We found that the T allele of rs1014867 (Pro4972Ser) was significantly associated with a decreased risk of esophageal cancer (odds ratio [OR]=0.77, 95% confidence interval [95% CI]=0.66-0.90; p=1.42 × 10(-3)). We also observed a borderline significant association between rs1039808 (Ala807Val) and esophageal cancer risk (OR=0.90, 95% CI=0.82-1.00; p=0.050), which was more prominent in non-drinkers (OR=0.82, 95% CI=0.71-0.94; p=6.53 × 10(-3)). Furthermore, we detected a significant interaction between rs1039808 genotypes and alcohol drinking on esophageal cancer risk (p=0.013). These findings indicate that the nonsynonymous variants rs1014867 (Pro4972Ser) and rs1039808 (Ala807Val) of FAT4 may contribute to esophageal cancer susceptibility.

The transforming growth factor (TGF)-β is a potent growth inhibitor primarily responsible for cell growth, differentiation, and apoptosis, and frequently perturbed during development of tumors, including gastric cancer. TGF-β receptor type I (TGFβR1) may be a modifier of cancer risk by constitutively decreasing the TGF-β inhibitory signals during early tumorigenesis and increasing the TGF-β signals in tumor progression. In this study, we hypothesized that genetic variants of TGFBR1 may influence the risk of gastric cancer. We conducted a two-stage case-control study of gastric cancer, including 650 cases and 683 controls in the first stage and 484 cases and 348 controls in the second stage, and genotyped five tagging single nucleotide polymorphisms (SNPs) to represent common variants in the whole TGFBR1 gene. In the first stage, two SNPs rs6478974 and rs10512263 were found to be potentially associated with risk of gastric cancer (P = 3.35 × 10(-3) for rs6478974 AT vs. TT and P = 0.033 for rs10512263 CT vs. TT), which were further confirmed in the second stage with similar effects (P = 0.144 and 0.049, respectively). After combining the two stages, we found that these two SNPs were associated with a significantly increased risk of gastric cancer in dominant models [adjusted odds ratio (OR) = 1.36, 95% confidence interval (CI): 1.14-1.63 for rs6478974 AT/AA vs. TT; adjusted OR = 1.26, 95% CI: 1.05-1.50 for rs10512263 CT/CC vs. TT] or additive model (adjusted OR = 1.23, 95% CI: 1.08-1.40 for rs6478974). These findings indicate that TGFBR1 polymorphisms may be implicated with the development of gastric cancer in Han-Chinese population.