OBJECTIVES: We sought to determine the association between changes in unemployment, healthcare spending and stomach cancer mortality. METHODS: Multivariate regression analysis was used to assess how changes in unemployment and public-sector expenditure on healthcare (PSEH) varied with stomach cancer mortality in 25 member states of the European Union from 1981 to 2009. Country-specific differences in healthcare infrastructure and demographics were controlled for 1- to 5-year time-lag analyses and robustness checks were carried out. RESULTS: A 1% increase in unemployment was associated with a significant increase in stomach cancer mortality in both men and women [men: coefficient (R)=0.1080, 95% confidence interval (CI)=0.0470-0.1690, P=0.0006; women: R=0.0488, 95% CI=0.0168-0.0809, P=0.0029]. A 1% increase in PSEH was associated with a significant decrease in stomach cancer mortality (men: R=-0.0009, 95% CI=-0.0013 to -0.005, P|0.0001; women: R=-0.0004, 95% CI=-0.0007 to -0.0001, P=0.0054). The
BioAssay record AID 95314 submitted by ChEMBL: Compound was tested in vitro for cytotoxic activity against KATO III human stomach cancer cell line by MTT assay.
TY - JOUR. T1 - Differential response to gamma radiation of human stomach cancer cells in vitro. AU - Jenkins, V. K.. AU - Barranco, S. C.. AU - Townsend, Courtney. AU - Perry, R. R.. AU - Ives, K. L.. PY - 1986. Y1 - 1986. N2 - In vitro effects of radiation were studied in two permanent cell lines (AGS and SII) from two patients with adenocarcinoma of the stomach and three permanent sublines from each cell line. Radiation survival parameters for AGS and SII parent cell lines and sublines were determined after in vitro irradiation of their cells with 0·5 to 10 Gy of 60Co gamma rays. The AGS and SII cell lines had different growth properties, DNA contents and radiation survival curves. Surviving fractions of SII parent cells (76 chromosomes) after 2·0 and 10 Gy were 1·22 and 17·8 times greater, respectively, than values for AGS parent cells (47 chromosomes). Sensitivities (D0) were 1·08 and 1·45 Gy for AGS and SII parent lines, respectively. The D0 values for AGS parent cells and sublines ...
Human Stomach Cancer Stem Cell (Plated cells are also available). 120 Population doublings or up to 12 passages. One million viable cells upon thawing of frozen cells, frozen vial of cells shipped in dry-ice. Cell Cultures from single donors, 1000 different cell cultures available, please indicate which lots you require from the 1000 donors. Source: Human Stomach Cancer tissue. Positive Markers: CD44, CD 133, SSEA3/4, Oct4, Tumorigenicity (,1000 cells), Alkaline Phosphatase, Aldehyde Dehydrogenase, Telomerase For non-academic use, please inquire for pricing. Cells are only guaranteed with purchase of Creative Bioarray Media and Creative Bioarray Extra Cellular Matrix for appropriate cell culture, for 30 days from the date of shipment ...
TY - JOUR. T1 - Abnormal expression and function of the E-cadherin-catenin complex in gastric carcinoma cell lines. AU - Jawhari, A. U.. AU - Noda, M.. AU - Farthing, M. J.G.. AU - Pignatelli, M.. PY - 1999/1/1. Y1 - 1999/1/1. N2 - Dysfunction of the cadherin-catenin complex, a key component of adherens junctions, is thought to confer invasive potential to cells. The aim of this study is to examine the expression and function of the E-cadherin/catenin complex in gastric carcinoma cell lines. Expression of E-cadherin, α, β and γ-catenin and p120(ctn), and of the adenomatous polyposis coil protein (APC), together with function of the cadherin-catenin complex was examined in a panel of gastric carcinoma cell lines, using immunocytochemistry, Western blotting and a cell-cell aggregation assay. Protein interactions were examined by sequential immunoprecipitation and immunoblotting with antibodies to E-cadherin, α, β and γ-catenin, p120(ctn) and APC. Abnormalities of E-cadherin, α- and ...
Saitama Cancer Center Research Institute. It is now well accepted that (-)-epigallocatechin gallate (EGCG) inhibits carcinogenesis in the digestive tract in rodents. To understand the mechanisms of anticarcinogenesis, we first studied growth inhibition by EGCG in human stomach cancer cell lines established at Seoul National University (SNU cell lines). Inhibition by EGCG of [3H]thymidine incorporation into eight SNU cell lines was examined, in relation to transforming growth factor-beta (TGF-beta) responsiveness. Various tea polyphenols derived from green tea and black tea induced growth inhibition and apoptosis of human stomach cancer cell line KATO III, and inhibition of tumor necrosis factor-alpha (TNF-alpha) release from the cells, in the order of (-)-epicatechin gallate (ECG), EGCG, (-)-epigallocatechin (EGC), teaflavins (TF) and (-)-epicatechin (EC). In addition, we demonstrated that EGCG inhibited TNF-alpha gene expression in KATO III cells, as well as okadaic acid-induced AP-1 and ...
TS-1 is an oral anticancer drug approved in Japan consisting of tegafur (a pro-drug of fluorouracil, 5-FU), gimeracil and oteracil potassium. The response rate of TS-1 in the untreated advanced gastric cancer patients was 44.6% in the late phase II study. In 2007, efficacy of the adjuvant therapy using TS-1 in the resected gastric cancer patients was demonstrated by ACTS-GC study group conducted in Japan. PSK is an oral anticancer drug approved in Japan consisting of protein-bound polysaccharide extracted from mycelium of Trametes (Coriolus) versicolor, a kind of mushroom. Even though survival benefit by PSK in combination with adjuvant chemotherapy using 5-FU or tegafur in the postoperative gastric cancer patients was already demonstrated, it is not uncertain about efficacy of combination therapy with PSK and TS-1 in gastric cancer. In this study, we compare efficacy and safety of postoperative adjuvant therapy using TS-1 or TS-1+PSK in the stage II or III gastric cancer patients ...
Long-term cigarette smoking increases the risk of gastric cancer mortality. Nicotine and NNK, tobacco-specific mitogens, were reported to correlate with cancer progression on gastric cancer. Since metastasis is the major cause of cancer death, the influence of nicotine on the migration of gastric cancer cells remains to be determined. In addition, how to improve the therapeutic efficacy is the important issue for gastric cancer. Our preliminary results indicated that nicotine or NNK treatment can enhance the migratory ability on gastric cancer. The enhancement effect was mediated through nicotinic acetylcholine receptor (nAChR). Silence of alpha7-nAChR expression may inhibit the enhanced effect by nicotine or NNK treatment, indicating that nAChR may be the target for preventing gastric cancer migration. Further, we also found that down-regulation of nAChR increased the sensitivity to chemo-therapy. Those result suggested that nAChR may be the novel therapeutic target for gastric cancer therapy. ...
NMDA receptor Type 2B (NMDAR2B) is a candidate TSG first identified in esophageal squamous cell carcinoma (ESCC). To evaluate NMDAR2B methylation in gastric cancer progression, we performed quantitative methylation-specific PCR (MSP), RTPCR and immnunohistochemistry (IHC) in primary gastric tissues and colony formation assays in gastric cancer cell lines. We found that the expression of NMDAR2B was reactivated by the demethylating agent, 5-aza-20-deoxycytidine, with or without trichostatin A in gastric cancer cell lines. Moreover, inactivation of NMDAR2B was found to be closely correlated with promoter methylation status in gastric cell lines and primary gastric tumors. IHC data also showed that NMDAR2B was specifically expressed in gastric epithelial cells and its expression was diminished or absent in gastric cancer epithelium. Quantitative analysis of NMDAR2B promoter methylation showed 61% (17/28) hypermethylation in primary gastric tumors versus 5% (1/20) in normal gastric tissues from ...
Angiogenesis is essential for tumor growth and metastasis and depends on the production of angiogenic factors by host and/or tumor cells. The role of angiogenesis and angiogenic factor expression in intestinal- and diffuse-type gastric cancer are undefined. Archival specimens of 51 intestinal-type and 38 diffuse-type human gastric carcinomas were examined for tumor vessel counts, angiogenic factor expression, and the presence or absence of angiogenic factor receptors on tumor endothelium using antibodies against vascular endothelial growth factor (VEGF) and its receptors (KDR and flt-1), basic fibroblast growth factor (bFGF) and its receptors (bek and flg), and factor VIII (endothelial cells). Vessel count and VEGF and bFGF expression were higher in intestinal-type than in diffuse-type gastric cancers (P = 0.01, P , 0.001, and P , 0.001, respectively). Similarly, vessel count and VEGF expression were higher in patients with liver metastasis than in patients with peritoneal dissemination (P = ...
Diffuse-type gastric carcinoma (DGC) cell lines with robust overexpression of Met are sensitive to Met inhibitors. (a) DGC and other gastric carcinoma cell line
TY - JOUR. T1 - Depth of response is a significant predictor for long-term outcome in advanced gastric cancer patients treated with trastuzumab. AU - Lee, Choong kun. AU - Kim, Seung seob. AU - Park, Saemi. AU - Kim, Chan. AU - Heo, Su Jin. AU - Lim, Joon Seok. AU - Kim, Hyunki. AU - Kim, Hyo Song. AU - Rha, Sun Young. AU - Chung, Hyun Cheol. AU - Park, Sohee. AU - Jung, Minkyu. PY - 2017/1/1. Y1 - 2017/1/1. N2 - Purpose: We aimed to determine and compare the predictive values of depth of response (DpR) and early tumor shrinkage (ETS) on long-term outcomes in gastric cancer patients treated with trastuzumab. Results: From a total of 368 computed tomography examinations, DpR and ETS were evaluated. DpR was a significant tumor-size metric in predicting PFS and OS, and showed better discriminatory ability (higher Ct indices, 0.6957 for PFS; 0.7191 for OS) than ETS. DpR ≥ 45% (vs. , 45%) was the optimal cutoffvalue, as it was best able to identify patients with longer PFS (median 9.0 vs. 6.3 ...
article{28d6110c-5d57-42d8-9243-f7ea1c6d6398, abstract = {This analysis of DNA-ploidy heterogeneity in advanced gastric carcinomas is consistent with the hypothesis of the emergence of a single aneuploid cell clone as a crucial mechanism in the progression from early gastric carcinoma to advanced gastric cancer. The prognostic value of DNA-ploidy in gastric cancers has been a matter of controversy. Tumour DNA-ploidy heterogeneity, the presence within the same tumour of multiple stemlines differing in DNA content, has been described in various tumours including gastric cancers. The occurrence of such heterogeneity has been accepted as an explanation for the divergent DNA-ploidy results in this type of tumours. A previous study of early gastric cancers suggested that in pure diploid superficial carcinomas, genetic instability might lead to a cell clone which has undergone a ploidy shift and is more aggressive. If so, this would initially result in DNA-ploidy heterogeneity. Proliferative dominance ...
This study is a single arm, single center phase II study of AZD5363 in combination with paclitaxel in patients with advanced gastric adenocarcinoma harboring
Principal Investigator:YAMAGUCHI Koji, Project Period (FY):2000 - 2001, Research Category:Grant-in-Aid for Scientific Research (C), Section:一般, Research Field:Digestive surgery
TY - JOUR. T1 - Nicotine promotes cell migration through alpha7 nicotinic acetylcholine receptor in gastric cancer cells. AU - Lien, Yung Chang. AU - Wang, Weu. AU - Kuo, Li Jen. AU - Liu, Jun Jen. AU - Wei, Po Li. AU - Ho, Yuan Soon. AU - Ting, Wen Chien. AU - Wu, Chih Hsiung. AU - Chang, Yu Jia. PY - 2011/9. Y1 - 2011/9. N2 - Background: The objective was to study the mechanism of nicotine-enhanced migration of gastric cancer cells. Long-term cigarette smoking increases the risk of gastric cancer mortality. Tobacco-specific mitogen, nicotine, was reported to correlate with cancer progression on gastric cancer. Since metastasis is the major cause of cancer death, the influence of nicotine on the migration of gastric cancer cells remains to be determined. Materials and Methods: The influence of nicotine on migration of gastric cancer cells was evaluated by transwell assay and wound-healing migration assay. Receptor-mediated migration was studied by both inhibitor and small interfering RNA. ...
PAX8 was not only a mitotic factor, but identified as a transcription factor involved in the prognosis of human tumor patients. Elucidating the function of PAX8 on the pathology of stomach cancer was meaningful. PAX8 was found to be upregulated in primary stomach cancer tissue and the TCGA stomach cancer dataset. Interestingly, SOX13 and PAX8 showed consistent expression patterns, and the combined high PAX8 and SOX18 expression induced a worse prognosis of stomach cancer patients. SOX13 was further identified as a transcription factor of PAX8, and further affect Aurora B and Cyclin B1 expression, two cell cycle related factors of the downstream of PAX8, including. Furthermore, PAX8 depletion inducted G1-phase arrest and the decrease of EdU incorporation, cell viability and colony formation can be rescued by SOX13 overexpression. SOX13 participated in the elevated expression of PAX8, which promote the proliferation of stomach cancer cells. Therefore, SOX13 mediated PAX8 expression was recognized as a
PAX8 was not only a mitotic factor, but identified as a transcription factor involved in the prognosis of human tumor patients. Elucidating the function of PAX8 on the pathology of stomach cancer was meaningful. PAX8 was found to be upregulated in primary stomach cancer tissue and the TCGA stomach cancer dataset. Interestingly, SOX13 and PAX8 showed consistent expression patterns, and the combined high PAX8 and SOX18 expression induced a worse prognosis of stomach cancer patients. SOX13 was further identified as a transcription factor of PAX8, and further affect Aurora B and Cyclin B1 expression, two cell cycle related factors of the downstream of PAX8, including. Furthermore, PAX8 depletion inducted G1-phase arrest and the decrease of EdU incorporation, cell viability and colony formation can be rescued by SOX13 overexpression. SOX13 participated in the elevated expression of PAX8, which promote the proliferation of stomach cancer cells. Therefore, SOX13 mediated PAX8 expression was recognized as a
In this study, we determined the role of COX-2 inhibition in the prevention of sodium chloride enhanced gastric carcinogenesis induced by MNNG in Wistar rats. MNNG induced gastric cancer is a well established animal model of stomach carcinogenesis.16 The mutagen, when given in drinking water, induces intestinal metaplasia and adenocarcinoma in the pyloric mucosa of Wistar rats.1620 The histology of this induced gastric malignancy resembles the differentiated type of stomach cancer in humans. To enhance the carcinogenic effects of MNNG, highly concentrated sodium chloride solution was given to these animals in the initial six weeks.17 In the present study, 75% of MNNG treated animals developed gastric cancer at the end of 48 weeks, confirming that this is a highly successful model of gastric tumorigenesis.. Although the exact mechanism underlying MNNG induced gastric cancer remains poorly understood, previous studies showed that the genetic makeup of the animals may play a role.21 For example, ...
Numerous studies showed that drug resistance of gastric cancer cells could be modulated by the abnormal expression of microRNAs (miRNAs) which target multiple cell signaling pathways. The possible function of miR-1271 in the formation of cisplatin resistance in gastric cancer cells has been investigated in this study. miR-1271 was significantly down-regulated in gastric cancer tissues and various gastric cancer cell lines. Moreover, it was down-regulated in the cisplatin-resistant gastric cancer cell line SGC7901/cisplatin (DDP) and the down-regulation of miR-1271 in SGC7901/DPP cells was accompanied by the up-regulation of insulin-like growth factor 1 receptor (IGF1R)/insulin receptor substrate 1 (IRS1) pathway-related proteins, i.e., IGF1R, IRS1, serine/threonine-protein kinase mTOR (mTOR), and the apoptosis regulator Bcl-2 (BCL2), compared with the parental SGC7901 cells. Over-expression of miR-1271 sensitized SGC7901/DDP cells to cisplatin. Changes in the luciferase activity of reporter ...
Occurrence of metastatic cancer to the stomach is rare, particularly in patients with prostate cancer. Gastric metastasis generally presents as a solitary and submucosal lesion with a central depression. We describe a case of gastric metastasis arising from prostate cancer, which is almost indistinguishable from the undifferentiated-type gastric cancer. A definitive diagnosis was not made until endoscopic resection. On performing both conventional and magnifying endoscopies, the lesion appeared to be slightly depressed and discolored area and it could not be distinguished from undifferentiated early gastric cancer. Biopsy from the lesion was negative for immunohistochemical staining of prostate-specific antigen, a sensitive and specific marker for prostate cancer. Thus, false initial diagnosis of an early primary gastric cancer was made and endoscopic submucosal dissection was performed. Pathological findings from the resected specimen aroused suspicion of a metastatic lesion. Consequently,
A mouse model of metastasis of human gastric cancer is one of the most important tools for studying the biological mechanisms underlying human gastric cancer metastasis. In this paper, we established a mouse model of metastatic human gastric cancer in nude mice that has a higher rate of tumor formation and metastasis than existing models. To generate the mouse model of metastatic human gastric cancer, fresh tumor tissues from patients that have undergone surgery for gastric cancer were subcutaneously implanted in the right and left groins of nude mice. When the implanted tissue grew to 1 cubic centimeter, the mice were killed, and the tumor tissues were examined and resected. The tumor tissues were implanted into nude mice and subjected to pathological examination, immunohistochemical staining, and real-time PCR for cytokeratin 8/18 (CK8/18), E-cadherin, vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). The mice were also analyzed for metastasis in their
To examine toxicity and outcomes for patients treated with preoperative chemoradiotherapy (CRT) for gastric cancer. Patients with gastroesophageal (GE) junction (Siewert type II and III) or gastric adenocarcinoma who underwent neoadjuvant CRT followed by planned surgical resection at Duke University between 1987 and 2009 were reviewed. Overall survival (OS), local control (LC) and disease-free survival (DFS) were estimated using the Kaplan-Meier method. Toxicity was graded according to the Common Toxicity Criteria for Adverse Events version 4.0. Forty-eight patients were included. Most (73%) had proximal (GE junction, cardia and fundus) tumors. Median radiation therapy dose was 45 Gy. All patients received concurrent chemotherapy. Thirty-six patients (75%) underwent surgery. Pathologic complete response and R0 resection rates were 19% and 86%, respectively. Thirty-day surgical mortality was 6%. At 42 months median follow-up, 3-year actuarial OS was 40%. For patients undergoing surgery, 3-year OS, LC and
In the present study, we examined the expression of Cyr-61 and COX-2 in 82 gastric cancer specimens and 43 non-tumor gastric mucosa specimens, and the results demonstrated the clinical significance of the expressions of Cyr-61 and COX-2 in determining the clinicopathologic features of gastric cancer and predicting its prognostic value.. Our results showed that Cyr-61 expression in gastric cancer tissues was significantly higher than that in the non-tumor gastric mucosa tissues. Furthermore, gastric cancer with higher Cyr-61 expression was associated with stronger invasion and metastasis abilities, advanced TNM stage and shorter survival time, suggesting that Cyr-61 plays an important role in the progression of gastric cancer. These results were consistent with the findings of Lin et al. [15]. They found Cyr-61 expression level was closely related to stages of gastric cancers, lymph node metastasis, and histological type. The 5-year survival time of patients with high Cyr-61 expression was ...
The expression of metallothionein (MT)-3 is often markedly reduced in gastric carcinoma (GC). The molecular mechanism of this MT-3 downregulation is unknown. Transcriptional silencing of MT-3 by methylation of CpG island was investigated by nucleotide sequencing and denaturing high performance liquid chromatography (DHPLC) analyses. We found that normal brain tissue and a xenografted GC that expressed MT-3 mRNA had unmethylated regions of the CpG island in intron1 of this gene. On the other hand, gastric cancer cell lines AGS and MKN445, a xenografted GC, and a representative primary gastric cancer that had no expression of MT-3 mRNA demonstrated hypermethylation of the MT-3 intron1 CpG island. Treatment of the gastric cancer cell lines with 5-azacytidine resulted in new expression of MT-3 mRNA in these cells. A quantifying DHPLC assay was developed to determine the methylation status of this specific region of the MT-3 gene.. Fifty-eight primary GC and their corresponding normal gastric ...
Gastric cancer is the second leading cause of death from malignant disease worldwide and most frequently discovered in advanced stages. Because curative surgery is regarded as the only option for cure, early detection of resectable gastric cancer is extremely important for good patient outcomes. Therefore, noninvasive diagnostic modalities such as evolutionary endoscopy and positron emission tomography are utilized as screening tools for gastric cancer. To date, early gastric cancer is being treated using minimally invasive methods such as endoscopic treatment and laparoscopic surgery, while in advanced cancer it is necessary to consider multimodality treatment including chemotherapy, radiotherapy, and surgery. Because of the results of large clinical trials, surgery with extended lymphadenectomy could not be recommended as a standard therapy for advanced gastric cancer. Recent clinical trials had shown survival benefits of adjuvant chemotherapy after curative resection compared with surgery alone. In
Stomach tumors can have a genetic basis and hereditary diffuse gastric cancer (HDGC) represents approximately 1-3% of all gastric tumors.
... (HDGC) is a type of stomach (gastric) cancer that runs through families. HDGC is different from other types of stomach cancer because the cancer cells do not form into a solid tumor. Instead, HDGC cancer cells disperse or scatter throughout the stomach tissue. Because of this, this type of cancer spreads (metastasizes) more easily to other parts of the body.. Symptoms of this condition are often not recognized until the cancer is in later stages. These symptoms may include stomach pain, vomiting, and weight loss. Unfortunately, this type of cancer is difficult to catch in early stages. Therefore, if you have a history of HDGC in your family, it is important to get regular and frequent stomach (endoscopy) exams to detect for any cancer cell formation.. HDGC is caused by a genetic mutation in the CDH1 gene which is located on chromosome 16. When a mutation is present in the gene, the gene is unable to pass along the correct instructions to the rest of the cells of ...
Early gastric carcinoma (GC) is considered to be a curable cancer, as it progresses to the advanced stage following varying durations. Understanding the early stage of GC may provide an insight into its pathogenesis and contribute to reducing the mortality rate of this disease. To investigate the genomic aberrations associated with 22 cases of early GC, high-density microarray comparative genomic hybridization was performed in the present study. The most notable finding was copy number gains (log2 ratio >0.25) on the long arm of chromosome 8, which occurred in 77.3% (17/22) of GC cases, and the delineated minimal common region was 8q22.1-q24.3. More specifically, two amplified (log2 ratio >1) loci in the 8q22.1-q24.3 region were detected in 18.2% (4/22) of GC cases. The first loci covered a region of 102.4-107.9 kb, mapping on 8q22.3-q23.1, and comprised the transcription factor CP2-like 3 gene. The second loci, spanning 128.7-145.7 kb on 8q24.21-q24.3, comprised the representative oncogene of ...
PIT is a highly selective cancer therapy, which is based on a molecular-targeted mAb conjugated to the photosensitizer IR700 and the use of NIR light. We have previously reported that HER2 target-specific cell death was achieved with a single dose of Tra-IR700 administration followed by NIR light irradiation. However, some cancer cells survived after PIT, and recurrences eventually developed in our in vivo model [12, 13]. Generally, mAb distribution is heterogeneous in most tumors, especially in peripheral locations where the tumors receive good blood supply [13, 20-22]. In addition, tumor heterogeneity is relatively common in human epithelial carcinomas, including in gastric cancer [9, 16, 17]. Taken together, this suggests that the antitumor effects of PIT alone on human gastric cancer may be limited. To solve this problem, we here examined whether the antitumor effect was enhanced by combining PIT with chemotherapy, as compared with PIT alone, in human gastric cancer cells. Our findings ...
Another factor associated with gastric cancer in certain populations is a high frequency of infection with H. pylori. Although it is not fully understood how H. pylori might increase the risk of gastric cancer, this rod-shaped helical bacterium has been classified since 1994 as a type I carcinogen by both the International Agency for Research on Cancer and the World Health Organization.11,14 Notably, H. pylori infection is most often associated with gastric cancers of the intestinal histologic subtype, which are observed more frequently in some areas of the world than others. Additionally, infection with H. pylori is not associated with all types of gastric cancer. H. pylori infection is only an independent risk factor for distal gastric cancer, and is not an independent risk factor for proximal forms of gastric cancer.5 Finally, although H. pylori infection is associated with 3- to 6-fold increase in the risk of developing gastric cancer, the vast majority of individuals infected with H. ...
TY - JOUR. T1 - Decreased Expression of MicroRNA-143 and-145 in Human Gastric Cancers. AU - Takagi, Takeshi. AU - Iio, Akio. AU - Nakagawa, Yoshihito. AU - Naoe, Tomoki. AU - Tanigawa, Nobuhiko. AU - Akao, Yukihiro. PY - 2009/7/1. Y1 - 2009/7/1. N2 - Objective: Downregulation of specific microRNAs (miRNAs) occurs in human tumors, which suggests a function for miRNAs in tumor suppression. We investigated the role of the miRNAs miR-143 and miR-145 in gastric cancers. Methods: The expression levels of miR-143 and miR-145 in the samples from 43 patients with gastric cancer were determined by real-time PCR using TaqMan assay. The growth inhibitory effect was estimated by the transfection of human gastric cancer cells with the miRNA. Results: The expression levels of miR-143 and-145 were decreased in most human gastric cancers examined, as previously reported to occur in colon tumors. The transfection of human gastric MKN-1 cells with miR-145 resulted in a greater growth inhibitory effect than that ...
1. McLean MH, El-Omar EM. Genetics of gastric cancer. Nature reviews Gastroenterology & hepatology. 2014;11:664-74 2. Torre LA, Bray F, Siegel RL, Ferlay J, Lortet-Tieulent J, Jemal A. Global cancer statistics, 2012. CA: a cancer journal for clinicians. 2015;65:87-108 3. Hu Y, Huang C, Sun Y, Su X, Cao H, Hu J. et al. Morbidity and Mortality of Laparoscopic Versus Open D2 Distal Gastrectomy for Advanced Gastric Cancer: A Randomized Controlled Trial. J Clin Oncol. 2016 4. Liu H, Li F, Zhu Y, Li T, Huang H, Lin T. et al. Whole-exome sequencing to identify somatic mutations in peritoneal metastatic gastric adenocarcinoma: A preliminary study. Oncotarget. 2016;7:43894-906 5. Zhang J, Huang JY, Chen YN, Yuan F, Zhang H, Yan FH. et al. Whole genome and transcriptome sequencing of matched primary and peritoneal metastatic gastric carcinoma. Scientific reports. 2015;5:13750 6. Huang B, Sun Z, Wang Z, Lu C, Xing C, Zhao B. et al. Factors associated with peritoneal metastasis in non-serosa-invasive ...
In the present study, we examined the expression of IL-8 receptors in human gastric carcinomas. Both IL-8RA and IL-8RB were constitutively expressed by all human gastric cancer cell lines examined. IHC analysis of surgical specimens of human gastric carcinomas showed that IL-8 receptors were expressed by tumor cells, microvascular endothelial cells, and inflammatory cells. IL-8 is expressed by a variety of malignant tumor cells, including pancreas (26) , lung (27) , prostate (28) , bladder (29) , head and neck squamous carcinomas (30) , and melanoma (5) . IL-8 produced by lung carcinoma cells has actually been shown to stimulate angiogenesis (27 , 31) . More recently, IL-8 has been shown to act as an autocrine growth stimulator for lung (32) , liver, and pancreatic carcinomas (26) , and melanoma cells (5 , 33) . Our recent data have revealed that IL-8 mRNA levels in gastric carcinoma tissues directly correlated with tumor vascularity (11) , and transfection of the IL-8 gene into gastric ...
List of Tables and Figures Figure Global Gastric Cancer Drugs Market Size (Million USD) Status and Outlook (2013-2018) Table Global Gastric Cancer Drugs Revenue (Million USD) Comparison by Regions (2013-2018) Figure Global Gastric Cancer Drugs Market Share by Regions (2013-2018) Figure United States Gastric Cancer Drugs Market Size (Million USD) and Growth Rate by Regions (2013-2018) Figure Europe Gastric Cancer Drugs Market Size (Million USD) and Growth Rate by Regions (2013-2018) Figure China Gastric Cancer Drugs Market Size (Million USD) and Growth Rate by Regions (2013-2018) Figure Japan Gastric Cancer Drugs Market Size (Million USD) and Growth Rate by Regions (2013-2018) Figure Southeast Asia Gastric Cancer Drugs Market Size (Million USD) and Growth Rate by Regions (2013-2018) Figure India Gastric Cancer Drugs Market Size (Million USD) and Growth Rate by Regions (2013-2018) Table Global Gastric Cancer Drugs Revenue (Million USD) and Growth Rate (%) Comparison by Product (2013-2018) Figure ...
The immunohistochemical expression of tenascin was examined in the normal adult mucosa of the stomach, primary tumours and lymph node metastases of gastric cancer patients. In normal gastric tissue tenascin was expressed in the muscularis mucosae, muscularis propria and vessel walls, however it was not expressed in either the mucosal connective tissue or the stromal tissue in the submucosal layer. In gastric cancer, tenascin was expressed in 35 of 85 primary tumours, and in 8 of 25 metastases in lymph nodes. Tenascin was located in the fibrous stroma surrounding foci of cancer. The expression of tenascin in the primary tumour did not correlate with the depth of invasion, lymph node metastasis or prognosis. Tenascin appears during the process of either malignant transformation or tumour progression in gastric cancer, and the positive expression of tenascin may be useful as a stromal marker for the early detection of gastric cancer.
Background: Gastric adenocarcinoma is the fifth most common cancer and third leading cause of cancer mortality in the world. In the US, outcomes for gastric cancer are dismal with only 28% surviving to 5 years. Upper gastrointestinal endoscopy is the gold standard for early detection of gastric tumors and used in countries with high prevalence for mass screening. However, due to the low prevalence of gastric cancer in the general U.S. population, a national screening program is not cost effective. Tools to identify patients at higher risk of gastric cancer may help identify subpopulations that should be referred for opportunistic screening.. Purpose: To characterize the questionnaire development of a comprehensive gastric cancer risk assessment survey instrument that will be used to collect primary data in a large-scale case-control study. This primary data will be used to create a predictive model and determine items that best discriminate between gastric cases and controls, to ultimately ...
A human gastric adenocarcinoma cell line, HGT-1, was established in vitro from the primary tumor of a 60-year-old patient. Histological examination of the tumor revealed a poorly differentiated adenocarcinoma. Primary tumor cells were cloned in soft agarose and gave rise to tumor colonies. The procedures enabling us to form a continuous cell line from the agarose colonies are described. The cultured cells grew as monolayers of closely apposed polygonal cells with a population-doubling time of 19.48 ± 1.20 (S.E.) hr during exponential growth at passage 59. They had an epithelial morphology. Ultrastructural studies revealed the presence of microvilli and tight junctions. The HGT-1 cell line is tumorigenic in nude mice and has a hyperdiploid karyotype with a modal number of 57 chromosomes. It exhibits numerous marker chromosomes. These human gastric epithelial cells do not secrete mucus or carcinoembryonic antigen. They exhibit functional histamine H2-receptors mediating cellular cyclic adenosine ...
A cancer predisposition syndrome with increased susceptibility to diffuse gastric cancer. Diffuse gastric cancer is a malignant disease characterized by poorly differentiated infiltrating lesions resulting in thickening of the stomach. Malignant tumors start in the stomach, can spread to the esophagus or the small intestine, and can extend through the stomach wall to nearby lymph nodes and organs. It also can metastasize to other parts of the body ...
Introduction : Gastric cancer is the second most common cause of cancer-related mortality worldwide. 5-fluorouracil (5-FU) is a commonly used anti-cancer drug. Various polyunsaturated fatty acids (PUFAs) are known to have tumoricidal action both in vitro and in vivo. Though PUFAs are known to...
According to a large European study, men who average more than four alcoholic beverages per day are more likely than light drinkers to develop stomach cancer. These results were published in the American Journal of Clinical Nutrition.. Cancer of the stomach is called gastric cancer. Gastric adenocarcinoma is the most common type of stomach cancer. It arises from cells that line the surface of the stomach.. Risk factors for stomach cancer include infection with the Helicobacter pylori (H. pylori) bacterium, smoking, high consumption of smoked or salted foods, and low intake of fruits and vegetables. Poor drinking water and a lack of refrigeration appear to contribute to the development of gastric cancer.. To explore how alcohol affects stomach cancer risk, researchers evaluated information from the European Prospective Investigation into Cancer and Nutrition (EPIC) study. More than 400 cases of stomach cancer were diagnosed among study participants.. ...
BioAssay record AID 95322 submitted by ChEMBL: Inhibitory concentration against stomach adenocarcinoma KATO-III cell line for cytotoxicity was determined.
A genome-wide study performed in a Japanese population identified a strong association between SNP rs2294008 (Met1Thr) in the Prostate Stem Cell Antigen gene (PSCA) and diffuse-type gastric cancer (GC). This association was validated in different Asian populations, and, very recently, a study has been published in Caucasians. In this study, we analyzed the association between PSCA variation and GC risk in Caucasians from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Six tagSNPs covering the PSCA gene region were genotyped in 411 incident gastric adenocarcinoma cases and 1530 matched controls from a nested case-control study in the EPIC cohort. Associations were analyzed by unconditional logistic regression, adjusting for age, sex and country. The T allele of rs2294008 in PSCA was found to be a highly significant risk factor for GC (per allele OR = 1.42, 95% CI: 1.23-1.66, p-value = 6.5 × 10(-6) ), particularly of the noncardia-type (per allele OR = 1.47, 95% CI: 1.19-1
We characterized the oxidative stress (OS) status by the levels of reduced/oxidized glutathione (GSH/GSSG), malondialdehyde (MDA) and the mutagenic base 8-oxo-78-dihydro-2-deoxyguanosine (8-oxo-dG) in human gastric carcinoma (HGC) samples and compared the results with normal tissue from the same patients. We also analyzed 8-oxo-dG in peripheral mononuclear cells (PMNC) and urine from healthy control subjects and in affected patients in the basal state and one, three, six, nine and twelve months after tumor resection. The levels of DNA repair enzyme mRNA expression (hOGG1, RAD51, MUYTH and MTH1) were determined in tumor specimens and compared with normal mucosa. Tumor specimens exhibited increased levels of MDA and 8-oxo-dG compared with normal gastric tissue. GSH levels were also increased, while GSSG levels remained stable. DNA repair enzyme mRNA expression was induced in the tumor tissues. Levels of 8-oxo-dG were significantly elevated in both urine and PMNC of gastric cancer patients compared with
Patients with hereditary diffuse gastric cancer (HDGC), a cancer predisposition syndrome associated with germline mutations of the CDH1 (E-cadherin) gene, have few effective treatment options. Despite marked differences in natural history, histopathology, and genetic profile to patients afflicted by sporadic gastric cancer, patients with HDGC receive, in large, identical systemic regimens. The lack of a robust preclinical in vitro system suitable for effective drug screening has been one of the obstacles to date which has hampered therapeutic advances in this rare disease. In order to identify therapeutic leads selective for the HDGC subtype of gastric cancer, we compared gene expression profiles and drug phenotype derived from an oncology library of 1912 compounds between gastric cancer cells established from a patient with metastatic HDGC harboring a c.1380delA CDH1 germline variant and sporadic gastric cancer cells. Unsupervised hierarchical cluster analysis shows select gene expression alterations
TY - JOUR. T1 - Osteopontin, E-cadherin, and β-catenin expression as prognostic biomarkers in patients with radically resected gastric cancer. AU - Di Bartolomeo, M.. AU - Pietrantonio, F.. AU - Pellegrinelli, A.. AU - Martinetti, A.. AU - Mariani, L.. AU - Daidone, M.G.. AU - Bajetta, Emillio. AU - Pelosi, G.. AU - de Braud, F.. AU - Floriani, I.. AU - Miceli, R.. N1 - Cited By :3 Export Date: 8 March 2017. PY - 2016. Y1 - 2016. U2 - 10.1007/s10120-015-0495-y. DO - 10.1007/s10120-015-0495-y. M3 - Article. VL - 19. SP - 412. EP - 420. JO - Gastric Cancer. JF - Gastric Cancer. SN - 1436-3291. IS - 2. ER - ...
TY - JOUR. T1 - Prognostic factors in metastatic gastric cancer. T2 - results of a population-based, retrospective cohort study in Ontario. AU - Dixon, Matthew. AU - Mahar, Alyson L.. AU - Helyer, Lucy K.. AU - Vasilevska-Ristovska, Jovanka. AU - Law, Calvin. AU - Coburn, Natalie G.. PY - 2016/1/1. Y1 - 2016/1/1. N2 - Background: Stage IV gastric cancer is lethal, and little population-based research on prognostic factors has been performed in low-incidence countries. Therefore, we investigated the consistency of the associations of patient, disease and healthcare system factors identified in previous population-based research to understand their generalizability to other low-incidence populations. Methods: A population-based, retrospective cohort study of patients diagnosed with Stage IV gastric cancer in Ontario between 1 April 2005 and 31 March 2008 was performed. Kaplan-Meier methodology and the log-rank test were used for bivariate analysis. Multivariate Cox proportional hazard regression ...
Gastric cancer is the second most typical reason behind cancer-related death world-wide (1). features for tumorigenesis investigations to discover a great predictive biomarker for targeted therapy have already been undertaken lately to be able to improve present therapeutics (1 3 The PI3K/AKT pathway may play an integral function in regulating several cellular processes such as for example proliferation development apoptosis cytoskeletal rearrangement and cell fat burning capacity (4 5 In gastric cancers the PI3K/AKT signaling is normally inappropriately turned on through mutation or alteration of several the different parts of the PI3K pathway. Until now the systems observed broadly for PI3K/AKT activation in gastric cancers consist of somatic activating mutations and amplifications in p110α (6-8) lack of the PTEN tumor suppressor (8) and hereditary amplifications of AKT1 (9). Preclinical research of human gastric cancer cell lines Proparacaine HCl manufacture has demonstrated the ...
In an attempt to elucidate the role played by neoplastic epithelial cells in the formation of stromal collagen, the synthesis of collagen by two cloned human gastric carcinoma cell lines was studied.. The presence of antigenicity of procollagen α1(I) chain in the cytoplasms of both carcinoma cell lines growing in culture was demonstrated by an immunocytochemical technique using specific antibodies. After denaturation of the radiolabeled collagenous proteins extracted from the combined cells and culture media, two components comigrating with authentic α1(I) and α2 chains on sodium dodecyl sulfate:polyacrylamide gel electrophoresis were found. Electrophoretogram analysis revealed further a dense band slightly slower than the α1(I) chain, most likely representing α1(I) trimer. These radioactive components disappeared after exposure of the samples to bacterial collagenase. The relative activity of collagen synthesis determined by using purified collagenase was slightly higher than that of ...
A drug commonly used to treat acid reflux is linked to a more than doubled risk of developing stomach cancer," reports The Guardian. Researchers wanted to investigate whether theres a link between medicines known as proton pump inhibitors (PPIs) and stomach cancer. Widely used PPIs include esomeprazole, lansoprazole, omeprazole, pantoprazole and rabeprazole.. PPIs are used to treat acid reflux and protect the stomach lining, have been linked to stomach cancer before. But theyre also used to treat H. pylori, a bacterial infection that can also cause reflux-like symptoms and is known to raise the risk of stomach cancer. This somewhat complicates the picture.. Researchers from Hong Kong studied 63,397 people whod been treated for stomach infection with H. pylori bacteria. Even after the bacteria had been killed, those who took PPIs on a long-term basis were more likely to be diagnosed with stomach cancer in the following 7 to 8 years of follow-up. Because of the study design, we cant tell if ...