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1
Chan, On-on Annie, i 陳安安. "E-cadherin in gastric cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B29974082.
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Fung, Wai-Ki Vicki, i 馮慧琪. "Epigenetic alterations in gastric cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B45009995.
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Linnane, Emily. "Metabolic reprogramming in gastric cancer". Thesis, University of Liverpool, 2015. http://livrepository.liverpool.ac.uk/2014059/.
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Globally, gastric cancer claims around 800,000 lives per year. As many patients present at an advanced stage of disease, prognosis remains poor for most patients, with five-year survival rates of less than 30%. As many patients show only limited short-term benefits from current therapeutic regimes, there is a clear need for improved understanding of the molecular mechanisms that drive the development and spread of gastric cancer. In this context, the role of the tumour microenvironment in cancer development and the potential for new forms of therapeutic intervention has become a field of increasing interest in many areas of cancer research. It is now well established that the development and progression of gastric tumours is facilitated by reciprocal communication between cancer cells, and cells within the surrounding tissue. In this study we focus our investigation on the mechanisms and consequences of paracrine communication between gastric cancer cells and different populations of stromal myofibroblasts, which are prevalent within the cancer microenvironment and form a significant proportion of many solid tumours. Previous studies show that myofibroblasts derived from gastric tumours (CAMs) have inherently different profiles of gene expression, compared to patient matched adjacent tissue myofibroblasts (ATMs), or normal tissue myofibroblasts (NTMs). Given these differences, we were interested to know if specific myofibroblast populations respond differently to signals from cancer cells; or conversely, if they exhibit differential ability to facilitate pro- tumourogenic changes in gastric cancer cells. Using a combination of bioinformatics and experimental techniques we demonstrate that CAM-conditioned media induces distinct changes in the gene expression profiles and metabolic activity of AGS gastric cancer cells. Significantly, these changes were not observed following exposure to conditioned media derived from either ATM or NTM cells. Conversely, CAM cells were found to have higher levels of GLUT1 and MCT4 expression with a corresponding reduction in mitochondrial activity compared to NTM cell lines. Finally, initial analysis of CAM imposed changes in AGS gene-expression suggests changes may reflect patient prognosis or stage of tumour development, implying future potential for patient stratification. In conclusion, data from this study shows that activated CAMs are robustly programmed by cancer cells to facilitate optimal conditions for tumour growth. Therefore, further analysis of this system may provide much needed options for improved therapeutic intervention and precision medicine.
4
Inoue, Harutaka. "Risk of gastric cancer after Roux-en-Y gastric bypass". Kyoto University, 2008. http://hdl.handle.net/2433/124248.
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Cunningham, David. "Gastric cancer : natural history and treatment". Thesis, University of Glasgow, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293449.
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Selway, Simone Ann Marie. "Antisecretory agents and gastric morphology". Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386637.
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Paon, Lenaic Marie Pierre. "Gene expression profiling of metastatic gastric cancer". Thesis, University of Liverpool, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.490659.
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Gastric cancer is one of the main cancers in the world, and is responsible for a large number of deaths each year. In Europe, the main issue is that it is only detected at latter stages, when metastases have developed. Although metastasis is the main cause of death from such tumours, the process is a very complex one and still not fully understood. In order to unravel this mechanism, microarrays have been used to study the expression pattern of a large number of genes in primary tumours and metastatic samples. These studies aim at indentifying genes that may playa role in metastasis. A number of microarray studies have already been carried out on gastric cancer to pursue knowledge. However, they have been mainly carried out in Asian populations, which are thought to present different gastric tumours than Europeans, possibly due to genetic and environmental parameters. The present thesis therefore aimed to carry out the first microarray study on gastric tumours from a European population, to identify genes that might playa role in gastric cancer metastasis, and assess whether there were any differences between Asian and European samples. In order to achieve this aim, the printing of in-house microarrays and methods to amplify and hybridise the samples first needed to be developed. This included the development of a new amplification method, the SMARTff7 protocol. Results showed that this method allowed more genes to be amplified than with an .established protocol. In addition, a microarray study published in 2003 identified a metastasis specific gene expression signature that could differentiate between metastatic and nonmetastatic primary tumours from different sites. However, this study did not include samples from gastric cancer. It was thus decided to test whether this signature could be applied to primary gastric tumours, using the new MetriGenix® platform. Although the analysis seemed to indicate that the signature did not apply to gastric tumours, technical issues meant that the results were inconclusive. On the other hand, a larger microarray analysis using the techniques developed during this project allowed the indentification of a number of genes of interest which may playa role in the metastatic spread of gastric cancer.
8
Al-Dabbagh, S. A. "Nitrates in the aetiology of gastric cancer". Thesis, University of Oxford, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.353051.
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Lannigan, Alison Kerr. "Tyrosine kinase growth factors in gastric cancer". Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394975.
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Saunders, John. "Ex vivo modelling of oesophago-gastric cancer". Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/47574/.
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Introduction The response to neoadjuvant chemotherapy in oesophago-gastric (OG) cancer is only 40%, so over half of the patient’s disease will progress, whilst they also suffer the toxic chemotherapy side-effects. A model to predict chemotherapy response would provide a marked clinical benefit, by enabling personalised treatment of OG cancer. Methods Live chemo-naïve tumour biopsies were obtained following informed consent at staging endoscopy, before patients underwent their routine neoadjuvant chemotherapy. Tumour cells from the endoscopic biopsies were expanded, using an in vitro feeder layer system and supplemented medium. With ethics committee approval and under Home Office guidance, these individual patient cancer cells were engrafted into immuno-compromised mice, where they formed representative tumour xenografts. Primary patient tissue, the corresponding individual patient cancer cells and their matching xenografts were analysed using immunohistochemistry, demonstrating that the in vitro and in vivo cells had retained the characteristics of the original patient’s oesophageal adenocarcinoma. To model the human tumour micro-environment (TME), a three dimensional tumour growth assay (3D-TGA) was developed, whereby the individual patient’s primary tumour cells were grown as 3D cancer cell clusters. This was performed by seeding individual patient’s primary tumour cells within a biological basement membrane extract, rich in extracellular matrix (ECM) components, with and without human mesenchymal stem cells to provide stromal support. The individual patient cancer clusters in the 3D-TGA were subjected to detailed chemotherapeutic assessment, to quantify their chemo-sensitivity to the standard chemotherapy which was administered to the patient in the clinic. This 3D-TGA predicted chemo-sensitivity was then compared with the patient’s actual clinical chemotherapy response, as measured by the histological tumour regression grade, which directly relates to prognosis. In combination with standard platinum-based chemotherapy, the 3D-TGA was assessed as a platform for evaluating new chemotherapeutics: the novel emerging HDAC inhibitor Panobinostat, and the phosphodiesterase type 5 inhibitor Vardenafil, which has recently been shown to be active against cancer stroma, were evaluated. Results Individual patient tumours were grown from primary endoscopic biopsy tissue in over half of samples obtained within a clinically applicable timescale of 2-4 weeks. Incorporating human mesenchymal cells into the 3D-TGA significantly changed the growth and drug resistance profiles (p < 0.005). This 3D-TGA chemo-response in the presence of stroma reflected the clinical chemo-sensitivity, with an accurate correlation between the 3D-TGA predicted chemo-resistance and actual clinical response for the patients evaluated. As well as predicting potential chemo-sensitivity for individual patients, the method allows individual drugs and combinations to be evaluated, trends in chemo-sensitivity between patients to be appraised, and analysis of the effect of the TME on tumour growth and chemotherapy resistance. Combination with Panobinostat enhanced response and proved efficacious in otherwise chemo-resistant tumours. Addition of PDE5i demonstrated an overall significantly enhanced chemotherapeutic response (p=0.003), and consequently provided efficacy in 60% of the otherwise chemo-resistant tumours. Discussion The novel method of growing individual patient OG cancers, using a 3D model with specific components of the tumour micro-environment in particular ECM and mesenchymal cells, provides a clinically-relevant oesophageal cancer model with application for chemo-sensitivity testing. Mesenchymal cells have a significant effect enhancing chemotherapy drug resistance in OG cancer, and this 3D model allowed identification of patients in which stromal targeting using PDE5i provided a significant reduction in chemotherapy drug resistance. In these patients, addition of PDE5i to routine chemotherapy could result in a marked change in the clinical efficacy of their chemotherapy regimen. The 3D model’s chemo-response accurately reflects individual patients’ clinical chemo-sensitivity and so this research has direct clinical application: if this assay proves to be predictive across a wider patient population, then following clinical trials, it could potentially be used to routinely guide individual patient therapy in the clinic, with administration of tailored chemotherapy for individual patient benefit.
11
Porter, Timothy Robin. "Molecular genetics of gastrointestinal cancer". Thesis, University of Birmingham, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273741.
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Al-Marhoon, Mohammed Salem Ahmed. "The relationship between CagA Helicobacter pylori, gastric mucus gel thickness, hydrophobicity and gastric cancer". Thesis, University of Leeds, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.396542.
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13
Lu, Victor Ming Yuan. "A Decade Experience of Gastric Cancer Surgery at a High-Volume Tertiary Centre in Australia, a Low-Volume Country". Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/16316.
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Background: Gastrectomy is the mainstay curative treatment of gastric cancer. In Australia, the incidence of gastric cancer is much lower than other countries, especially the East. Consequently, there is a paucity of surgical outcomes reported for gastric cancer surgery in Australia. The aims of this study were 1) to report the surgical outcomes of all gastric cancer patients treated by gastrectomy at our single tertiary centre in Australia, 2) to compare the outcomes to other Australian and international centres and 3) to evaluate influence of time period, age and neoadjuvant chemotherapy (NAC) on surgical outcomes. Methods: A retrospective review of a prospectively maintained operations database identified 160 gastrectomy patients at a single tertiary centre in Australia between 2005 to 2014. They were screened against established inclusion and exclusion criteria. Demographic, preoperative, operative, postoperative and histopathological outcomes were compiled and analysed as categorical and continuous data. Results: Overall 102 gastrectomy patients curatively treated for gastric cancer satisfied criteria for inclusion into this study. Postoperative complications were observed in 29 (28%) patients. No mortality events were observed from operation to thirty days after hospital discharge. There was significantly increased postoperative stay in intensive care unit (p=0.00) and hospital (p=0.01) over time. NAC was administered to 39 (38%) patients and showed significant histopathological response (p=0.01) on specimen study. Conclusion: The surgical outcomes of the gastrectomy operations for gastric cancer performed at our centre compare favourably to the reported outcomes of other Australian and international centres. A prospective, long-term, multi-institutional
14
Bashash, Morteza. "Molecular epidemiology of gastric and esophageal cancer survival". Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/30666.
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Introduction: Gastric and esophageal cancers are among the deadliest forms of cancer. Studies of human cancer susceptibility examine factors associated with the incidence of disease. Studies of human cancer prognosis and prediction examine factors associated with disease outcomes. This dissertation is about molecular and other factors that affect survival of gastric and esophageal cancer patients. Methods: Population-based registry data linked with patient outcome data was used to describe the epidemiology of gastric and esophageal cancers in BC; to compare survival of cancer patients in BC, and Ardabil, Iran and to describe differences in survival of BC patients of different ethnicity. The ethnicity of patients was determined based on lists of names corresponding to each ethnic group. A prospective cohort study was conducted to examine the effect of genetic polymorphisms in TIMP (1-4) and MMP (2, 7 and 9) genes. Results: Analysis of cancer registry data points to several factors associated with gastric and esophageal cancer survival. Patients with gastric cardia experience worse survival compared to other gastric cancers. Ethnicity of gastric and esophageal cancer patients is associated with their survival. Gastric and esophageal cancer patients diagnosed in British Columbia have better survival compared to those daignosed in Adabil, Iran. Genetic polymorphisms are also associated with survival. My prospective study identified 4 genetic polymorphisms at TIMP-3 associated with survival of esophageal adenocarcinoma and gastroesophageal junction (GEJ). Conclusion: Besides established prognostic indicators, other factors affect survival of gastric and esophageal cancers. Differences in survival by ethnicity support the importance of ethnicity as a prognostic factor. Survival differences between BC and Ardabil are likely due to disease characteristics and patient factors, in addition to differences in healthcare systems. TIMP3 genetic polymorphisms are promising prognostic factors for adenocarcinoma of esophagus and GEJ. Modeling prognosis based on host factors, including ethnicity and genetic polymorphisms, is an emerging field of translational cancer research. More research is needed to fully explore the functional effects of TIMP3 polymorphisms, and to identify both genetic and lifestyle factors underlying the effect ethnicity on survival.
15
Webb, Penelope M. "The epidemiology of Helicobacter pylori and gastric cancer". Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.259836.
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樊曉明 i Xiaoming Fan. "Arachidonic acid metabolism in apoptosis of gastric cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31241633.
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Wang, Liyi. "MicroRNAs in gastric and oesophageal cancer-associated myofibroblasts". Thesis, University of Liverpool, 2013. http://livrepository.liverpool.ac.uk/11135/.
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MicroRNAs (miRNAs) are small RNAs of ~22 nucleotides in length that regulate gene expression post-transcriptionally. MicroRNAs regulate many biological processes, and may contribute to cancer initiation and progression. In the normal gastrointestinal mucosa, myofibroblasts are involved in wound healing, and in tumours, they play a role in cancer progression. The present study aimed to determine the miRNA expression profiles in different populations of myofibroblasts from gastric and oesophageal tissues, namely, cancer-associated myofibroblasts (CAMs), adjacent non-tumour tissue myofibroblasts (ATMs) and normal tissue myofibroblasts (NTMs), and to investigate the processes that are influenced by differential miRNA abundance in different myofibroblast populations. In addition, miRNA profiling of a putative myofibroblast precursor cell type, mesenchymal stromal cells (MSCs), was studied. Global miRNA expression profiling of a panel of previously characterised gastric and oesophageal myofibroblasts was determined using locked nucleic acid (LNA) miRNA arrays. The microarray data for hsa-miR-29b, hsa-miR-181d, hsa-miR-214 and hsa-miR-424 were validated by quantitative RT-PCR. Using unsupervised miRNA datasets, principal component analysis (PCA) segregated gastric and oesophageal NTMs, and CAMs from gastric and oesophageal carcinomas. Analysis of global miRNA expression showed distinct profile of MSCs in comparison to gastric and oesophageal NTMs. Hierarchical clustering analysis of miRNAs exhibiting significantly different abundance revealed distinct clusters between CAMs and ATMs, CAMs and NTMs and between ATMs and NTMs. In 12 paired samples of gastric CAMs and their corresponding ATMs, 12 miRNAs were significantly different with hsa-miR-181d being the most up-regulated miRNA in CAMs. Using already validated targets of 10 of these miRNAs, an analysis using MetaCore® indicated that the regulation of cell cycle progression and Wnt signalling were differentially affected. In a comparison of each CAM and its corresponding ATM, Wnt signalling was the only process that was significantly targeted by miRNAs that were different in abundance, in all 12 pairs. Using previously determined gene expression data, pairwise analysis of 20 transcripts associated with Wnt signalling showed a significant increase in WNT5A and TGFB2 mRNAs in CAMs compared to their ATMs. Additionally, Western blot analysis showed increased expression of Wnt-5a in CAMs. The results of migration and EdU incorporation assays indicated that Wnt-5a induced the migration and proliferation of both CAMs and ATMs. The abundance of hsa-miR-181d was significantly increased in CAMs by Wnt-5a. Migration of AGS (gastric cancer) cells was stimulated by Wnt-5a and was inhibited in the presence of TIMP-3, a validated target of the miR-181 family. After hsa-miR-181d knockdown, the migration and proliferation of CAMs were significantly decreased, and stimulation with Wnt-5a reversed the migratory inhibition of hsa-miR-181d knockdown CAMs. Conditioned medium from hsa-miR-181d knockdown CAMs inhibited the migration of AGS cells. The findings suggest that differential miRNA abundance is a feature of normal myofibroblasts from the stomach and oesophagus, and myofibroblasts from normal and cancer tissues. One consequence is increased Wnt-5a in gastric CAMs that is implicated in the regulation of cell migration, in health and disease, at least partly through modulation of hsa-miR-181d.
18
Fan, Xiaoming. "Arachidonic acid metabolism in apoptosis of gastric cancer". Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B22805448.
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FOSCARINI, ALESSIA. "Functional characterization of Tribbles pseudokinases in gastric cancer". Doctoral thesis, Università degli studi di Pavia, 2022. http://hdl.handle.net/11571/1452907.
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Introduction: Gastric cancer (GC) is the fifth most common cancer and the fourth
leading cause of cancer-related deaths worldwide. It is often diagnosed at advanced
stages and is mostly resistant to conventional chemotherapy. To help GC
management, there is a need to develop new biomarkers: they are needed to
improve diagnosis, as well as novel therapeutic targets that may lead to the
development of effective therapies.
TRIB2 belongs to the Tribbles family of serine/threonine pseudokinases, scaffold
proteins involved in several cellular processes. In cancer, TRIB2 can act either as an
oncogene or a tumor suppressor gene, depending on the cellular context. TRIB2
also promotes drug resistance in different cancer types. Since this protein has never
been investigated in GC, our study aimed at addressing the significance of TRIB2
in this tumor.
Material & Methods: We performed data mining of The Cancer Genome Atlas
(TCGA) Stomach Adenocarcinoma (STAD) dataset and of the Broad Institute
Cancer Cell Line Encyclopedia (CCLE) GC dataset. Based on in silico results, we
then investigated the impact of lentiviral-mediated TRIB2 overexpression (OE) in
four GC cell lines (MKN45, KATO-III, MKN74 and NCI-N87) with chromosomal
instability phenotype (CIN). The impact of TRIB2 OE was evaluated by different
functional assays, including cell proliferation, motility, colony formation and cell
cycle analysis. Moreover, we investigated the mitogen-activated protein kinase
(MAPK) downstream pathway and the possible involvement of TRIB2 in drug
response, following cell treatments with two agents commonly used in GC
chemotherapy (5-fluorouracil and doxorubicin).
Results: Data mining of the TCGA STAD dataset and of the CCLE dataset
revealed a limited number of genetic and genomic alterations and a wide range of
mRNA expression levels of TRIBs in GC tissues, and in GC cell lines, respectively.
The analysis of TRIBs expression of STAD cases sorted by molecular phenotypes
showed that a lower TRIB2 mRNA expression was statistically significantly
associated with tumors characterized by chromosomal instability (CIN) compared
to tumors characterized by microsatellite instability (MSI). In addition, T4 stage in
CIN tumors was statistically significantly associated with low TRIB2 expression. In
vitro, TRIB2 OE was able to reduce proliferation and colony formation ability in
MKN45 and NCI-N87 cells. Furthermore, TRIB2 OE induced cell cycle arrest in
G2/M phase in MKN45 cells and reduced migration ability in NCI-N87 compared
to the control cells. On the other side, TRIB2 OE did not affect the MAPK pathway
and no differences were detected between TRIB2-overexpressing cells and control
cells treated both with 5-fluorouracil and doxorubicin.
20
Sara, Peri. "Chemotherapy resistance-associated epithelial to endothelial transition in gastric cancer". Doctoral thesis, Università di Siena, 2020. http://hdl.handle.net/11365/1096074.
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Gastric cancer (GC) is the fifth most common malignancy worldwide and the third leading cause of cancer-related death. Despite decreased incidence in the last decades and progress in early detection of the disease, most of GC cases are still diagnosed at advanced stages. The only curative treatment remains surgery, but chemo- and radio-therapy are widely used to downstage, prevent metastasis and recurrence. Chemoresistance is a major problem in GC due to limited therapeutic options and it is responsible for treatment failure.
We used a primary adenocarcinoma cell line (AGS) and made it resistant to three different chemotherapeutic drugs (5-fluorouracil, cisplatin and paclitaxel), separately. After evaluating the resistance of each line obtained to the different chemotherapy drugs and verifying that there was no cross-resistance, we tried to identify differences between resistant lines and the parental one that could be exploited to restore chemosensitivity. We evaluated factors associated with stemness and found an up-regulation in the resistant cell lines. This led us to investigate whether there was a greater propensity to vasculogenic mimicry in AGS resistant lines. The 5FU-resistant AGS cell line showed a marked capacity for vasculogenic mimicry, a phenomenon described and associated to bad prognosis in cancers like melanomas, but only recently discovered in gastric carcinoma. In addition, 5FU-resistant line acquired CD31 positivity, a marker that is normally associated with endothelial cells, demonstrating that 5FU-resistant AGS cells have undergone an epithelial-to-endothelial transition. We also tested an anti-angiogenic/anti-vasculogenic mimicry agent on 5FU-resistant AGS cells, that restored its chemosensitivity to 5-Fluorouracil.
Preliminary studies also investigated metabolic alterations occurring in AGS-chemoresistant cell lines with respect to the chemosensitive AGS-wt cell line. We have detected alterations in AGS-chemoresistant cell lines that could possibly be exploited to revert chemoresistance.
I also spent 8 months in the Netherlands, at the Hubrecht Institute, with the purpose of learning how to cultivate and manipulate stomach organoids derived from human biopsies. There I followed a project aimed to differentiate, in gastric organoids, endocrine cells (secreting somatostatin, ghrelin, serotonin, histamine and gastrin) that are found in the organ but only seldomly detected in organoid culture. For this purpose, it was necessary to transduce the pro-endocrine transcription factor Neurogenin 3 by lentivirus, which allowed a strong enrichment of the culture in endocrine cells but not for all lineages. New constructs were therefore cloned for the overexpression of other transcriptional factors that could be involved in endocrine differentiation. These were equally transduced into stomach organoid cultures. However, this approach did not lead to the desired result. Simultaneously, a gastric organoid line with an endogenous tagging for the gastrin gene was created by CRISPR/Cas9, so that when gastrin is expressed, the cell produces also a fluorescent protein that allows its easy identification. The realization of this cell line allowed a fast-screening of different culture conditions that could induce differentiation towards gastrin-secreting endocrine lineage. This led in a short time to the discovery of molecules that induced differentiation in gastrin-secreting cells, testifying the feasibility of the proposed method.
21
Al, Khathami Ali Gaithan. "Towards gastric cancer immunotherapy : assessment of cancer immunity and potential immune targets". Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8855/.
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Gastric cancer (GC), the fourth most common malignancy worldwide, has poor prognosis and treatment innovation is needed. The aims of this project were to investigate immune targets and treatment strategies for GC. I identified new T-cell epitopes in three Epstein-Barr virus (EBV) tumor antigens, LMP1, LMP2 and BARF1, expressed in the 10% of GC cases positive for EBV. T-cell clones showed that a BARF1-specific CD4 T-cell epitope restricted by HLA-DR51, an allele common in the population, was presented by an EBV-positive epithelial cancer cell line. Analysing blood and fresh tumor from newly diagnosed GC patients, I detected T-cell responses to MAGEA1, MAGEA4 and NY-ESO-1 tumour antigens in blood but not tumor. Compared to healthy donors, patients had: higher frequencies of LAG3 or CTLA4 positive CD8 T-cells, TIM-3 or CTLA4 CD4+ T-cells, T-regs, NKT-cells and gamma-delta T-cells in blood and tissue. Patients also had high granulocytic MDSC frequencies in PBMC. The CD4:CD8 ratio was low in some patients' blood, potentially indicating immunosenesence, but was always higher in tumor tissue. I successfully generated tumour infiltrating lymphocytes (TILs) from nine patients' tumors. These comprised high T-cells and NK-cells and low T-reg and MDSC. LAG-3 was increased, but PD1, was decreased on TIL T-cells. Using 3-dimensional organoids established from two patients, I showed that TIL NK-cells, but not TIL T-cells, recognized autologous tumor organoids. My results are the first proof of principle that TILs can readily be generated from gastric tumors, can target tumors cells and therefore be used to treat gastric cancer.
22
Ng, Ada Kar Key. "Clinical and pathological outcomes in patients undergoing chemotherapy and resection for oesophageal and gastric adenocarcinoma in a newly established oesophago-gastric cancer centre". Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/17335.
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Background: The incidence of oesophageal carcinoma (OCa) is increasing globally. In the world, it is the 8th most commonly diagnosed cancer, and 6th most common cause of cancer death. In Australia, oesophageal cancer is the 12th most commonly diagnosed cancer in males, and the 8th most common cause of cancer death. Historically, oesophageal and gastric adenocarcinomas (GCa) were two separate entities based on their anatomical location and histological features. However, the Western world has seen a rise in distal oesophageal adenocarcinoma, adenocarcinoma of the oesophagogatsric junction (OGJ), and intestinal-type gastric adenocarcinoma of the cardia. Subsequently much uncertainty now surrounds the characterization and management of these tumours, in particular, whether there is a link between oesophageal adenocarcinoma, and that of intestinal-type gastric adenocarcinoma. Furthermore OGJ adenocarcinomas are less well understood and it is unclear whether they fall into the spectrum of a similar condition, or are indeed an entity of their own. Multi-modality treatment has evolved to become standard of care, with surgery remaining a key component. The optimal surgical approach to oesophagectomy remains controversial. Minimally invasive oesophagectomy (MIO) has the theorectical benefit of reducing surgical trauma without compromising oncological outcome compared to traditional open surgery. Aims: The aims of this dissertation are two fold: 1. To review the current standard of care for the treatment of oesophageal cancer, with a focus on the trend towards multi-modality treatment, and operative strategies. I review our local protocols and present an audit of a single high-volume surgical unit. 2. Secondly to undertake SELDI-TOF analysis on tumour samples, comparing the protein profiles of OGJ tumours with oesophageal and gastric adenocarcinomas. Methods: 1. A retrospective review of a prospectively collected database was performed to audit the results of a single institution presented in Chapter 2. A prospectively maintained database was established in 2001. Data fields were based on those of the Association of Upper GI Surgeons of the UK and Ireland (AUGIS). Clinical, operative and pathological data for patients undergoing OG resection at our institution were recorded prospectively using datafields modelled on the AUGIS (Association of Upper Gastrointestinal Surgeons of Great Britain and Ireland) database. Key parameters of care standards were examined including peri-operative mortality and morbidity, unscheduled return to operating theatre, anastomotic failure, lymph node count and circumferential margin positivity. These were compared to “acceptable” rates in the literature. 2. Ethical approval for this study was obtained from Northern Sydney Local Health District Human Research Ethics Committee (Reference number 1310-342M) in conjunction with approved protocol for access of tumour tissue from tumour bank. All patients with adenocarcinoma of the oesophagus and stomach were prospectively recorded in an electronic database and tumour bank was notified of each surgical procedure. Patient consent was obtained prior to surgical procedures. Each sample’s clinical details and histopathological report were reviewed and collated in a de-identified database. Any discrepancies were then discussed with the clinican/surgeon and a pathologist. A total of 53 samples were selected, 15 samples that were truly oesophageal adenocarcinoma without involvement of the OGJ, 17 samples were OGJ tumours with histological involvement of the OGJ and evidence of intestinal metaplasia, and 21 gastric adenocarcinomas which were at least 5cm away from the OGJ without involvement of the OGJ or the oesophagus. Specimens were prepared according to protocol and assessed using the SELDI-TOF MS method. Differential protein profiles were compared between the three groups of adenocarcinomas. Results: 1. Between December 2002 and May 2012, 134 patients were identified from our database as undergoing resection for oesophageal cancer by two surgeons or trainees under supervision in our specialised unit. Ninety-day mortality rate was 2.2%, with other key surgical performance indicators all falling within international acceptable standards. When comparing the two surgical approaches, post-operative mortality rates were 2.8% and 1.7% respectively for Open and MIO with no statistically significant difference in surgical and medical complications between the two procedures. We have not been able to demonstrate a benefit of one technique over the other. In terms of oncological outcomes, margin positivity and lymph node yield were not different between MIO and open oesophagectomy. The one significant finding we demonstrated was the higher stricture rate from MIO requiring dilatation. Our rate of 33% is consistent with other reported series of cervical anastomoses. Overall median survival for all patients was 42.6 months. When comparing the two operative techniques, there is no difference in overall or disease-specific survival. 2. The protein profiles of OCa, OGJ Ca and intestinal-type GCa have 34 peaks in common. Proteins with m/z8773 and 3046 can be used to differentiate between oesophageal and gastric adenocarcinoma. Using m/z8773 alone, it was able to predict oesophageal samples from gastric samples with accuracy of 82.8%, with the addition of m/z3046, the accuracy of differentiating the two tumours reached 100%. Applying this panel of two proteins to OGJ Ca, the junctional tumours demonstrated a pattern more closely resembling GCa, with the exception of one outlying specimen. Conclusion: Oesophagectomy can be performed at our institution with acceptable operative mortality and morbidity rates, furthermore, there were no differences in disease-specific or overall survival between the two surgical techniques. We have shown that oesophageal, OGJ and gastric cancers have differential protein profiles. Ongoing further studies with validation may prove beneficial in characterising OGJ cancers, and allow for improved staging, and potentially management strategies.
23
Yip, Bon-ham, i 葉邦瀚. "Immunoglobulin gene translocations in gastric lymphoma". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B37345321.
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Kaurah, Pardeep Kaur. "Hereditary diffuse gastric cancer : cancer risk and the personal cost of preventive surgery". Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/60293.
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Germline CDH1 mutation carriers are at risk for early-onset diffuse gastric cancer and female carriers have an additional risk of lobular breast cancer. Reliable estimates of cancer risk are essential for genetic counselling and clinical management of mutation carriers. Prophylactic total gastrectomy (PTG) to eliminate the gastric cancer risk is an option for mutation carriers. Current information on post-surgical outcomes and quality of life is limited. The objectives of this research were 1) To improve the evidentiary basis of genetic counselling by deriving reliable estimates of cancer risk in CDH1 mutation carriers; 2) To catalogue a comprehensive list of all novel and previously reported germline mutations to date; and 3) To provide data on post-surgical clinical outcomes and to describe the impact of the surgery on participants’ quality of life. Methods: Penetrance was derived from 67 mutation-positive families comprising 4031 individuals (350 affected with gastric cancer and 99 with breast cancer). Participants were recruited through multiple sources for clinical outcomes and quality of life study. Hospital records provided information on clinical outcomes. All participants were asked to complete validated questionnaires measuring generic and condition specific QOL (PROMIS, EORTC and SF 36v.II) at a single point. Results: By age 75 years, the cumulative incidence of gastric cancer was 70% (95% confidence interval [CI], 40%-94%) for males and 56% (95% CI, 27%-90%) for females. The risk of breast cancer for females was 42% (95% CI, 23%-68%) by 75 years. The mutational landscape of CDH1 did not reveal mutational hotspots but several shared mutations are seen in unrelated families. The 53 participants who had undergone PTG reported frequent symptoms of fatigue (59%), abdominal pain (55%), and diarrhea (45%). Cognitive, role and social function plus the symptoms anxiety, pain, taste, dyspnea and diarrhea were significant predictor variables for quality of life (p<0.05). Conclusions: Our more precise and robust penetrance figures will improve genetic counselling of unaffected carriers. Although this study reveals good overall QOL for individuals after PTG, attention should be given to managing symptoms as part of long term care to further enhance quality of life.Medicine, Faculty of
Graduate
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Jiménez, Flores Lizbeth Minerva. "The Role of Protein Kinase N in Gastric Cancer". Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/664078.
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Gastric cancer (GC) is one of the most common types of cancer in the Western World and accounts for over 700,000 deaths every year worldwide. The prognosis is dismal, with an average 5-year survival rate of less than 20%, mainly because of late diagnosis, due to the early stages are clinically silent. The cause of GC is multifactorial, as infectious agents, enviromental or/and genetic factors. Based on Lauren’s histologic classification, there are 2 types of GC: intestinal (IGC) and diffuse (DGC). Diffuse carcinoma cells lacks cohesion and invade tissues independently or in small clusters, is more common in young patients and behaves more aggressively than the intestinal type. Recent findings published in Nature and Nature Genetics identified frequent hotspots (14-24%) mutations in the small GTPase RHOA in the diffuse type of gastric tumors. To investigate the mechanism that underlies downstream of RHOA we analyzed the capacity of the mutations more commonly found in gastric tumors to bind to different effectors. We observed that the mutations found in gastric tumors specifically affect the capacity of RHOA to bind to PKN effector family. Therefore, in this thesis we study and characterized the role of PKN1 in GC. We demonstrated that the downregulation of PKN1 with shRNA or the deletion mediated by CRISPR/Cas9 results in the increase of proliferation in the diffuse gastric cell lines “in vitro” and “in vivo”. Moreover, the opposite effect is observed when we overexpress the constitutively active form of PKN1 in diffuse gastric cell lines with moderate or low levels of PKN1. In addition, we use a novel mouse model with conditional expression in the gastric mucosa of the RHOA-Y42C mutation (the most frequent mutation found in DGC) to investigate the role of RHOA in gastric tumorogenesis initiated by either N-methyl-N-nitrosourea (MNU) or Apc mutations. The mice with expression of the RHOA- Y42C have a significant increase in the number of tumors indicating that RhoA-Y42C is important for progression of the gastric tumors. Finally, we performed a preclinical testing of a new therapeutic approach, such as dietary supplements of arachidonic acid, a well- established activator of PKN1. The work carried out in this thesis will shed light on the newly identified deregulation of RHOA-PKN signaling in gastric cancer and provide a solid rationale for therapeutic targeting of this pathway.
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Vickery, Craig William. "The quality of life of patients with gastric cancer". Thesis, University of Bristol, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.412853.
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Tse, Tak-fong. "Role of RON activation on chemoresistance in gastric cancer". Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38592253.
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Fall, Katja. "Medical interventions and gastric cancer risk : an observational approach /". Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-905-6/.
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Lindblad, Mats. "Aspects on the etiology of esophageal and gastric cancer /". Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-110-5/.
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Lagergren, Jesper. "Cancer of the esophagus and gastric cardia etiological aspects /". Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3397-9/.
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KONDO, TATSUHEI, HIDEO KAMEI i KEISUKE TERABE. "Histopathological Study on the Prognosis of pT2 Gastric Cancer". Nagoya University School of Medicine, 1986. http://hdl.handle.net/2237/17488.
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Jennings, Neil Andrew. "The Role of Oestrogen in Diffuse Type Gastric Cancer". Thesis, University of Newcastle Upon Tyne, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.525099.
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Morgan, C. "Molecular analysis of the mechanisms leading to gastric cancer". Thesis, Swansea University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.638240.
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It is now widely accepted that reactive oxygen species (ROS), generated as a consequence of chronic inflammation, can be both mutagenic and carcinogenic and are believed to play an important role in the initiation of gastric carcinogenesis. In this study the Electron Spin Resonance (ESR) spectroscopy technique and Restriction Site Mutation (RSM) assay were used to investigate the role of ROS in gastric cancer. ESR was employed to directly measure the levels of free radicals in precancerous and cancerous gastric tissue. My findings showed a significant difference in free radical concentration between gastritis and tumour samples and an overall trend towards increased radical levels in gastritis tissue. When radical levels in gastritis samples were analysed with regards to Helicobacter pylori infection, no clear link could be established. RSM was used for mutation detection analysis on the p53 gene and the elucidation of a mutational fingerprint for ROS. RSM was able to detect hydrogen peroxide mediated DNA damage in a gastric cell line. The majority of these mutations were GC (r) AT transitions, which were also the mutation types detected in biopsy samples. My results also showed that p53 was mutated in a large proportion of gastritis and intestinal metaplasia samples. These findings suggest that ROS induced mutations of p53 are involved in the initiation of gastric cancer. When the ROS induced p53 mutations in gastritis samples were matched to Helicobacter pylori status and strain virulence, only a tenuous relationship appeared to exist. Therefore, oxidative damage is an important risk factor in gastric cancer, with H. pylori contributing to genetic instability in a sub population of individuals.
34
Tse, Tak-fong, i 謝德芳. "Role of RON activation on chemoresistance in gastric cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B38592253.
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Corso, Giovanni. "Searching for novel diagnostic-prognostic biomarkers in gastric cancer". Doctoral thesis, Faculdade de Medicina da Universidade do Porto, 2011. http://hdl.handle.net/10216/62210.
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Costa, Susana Correia da. "Pathogenesis of Gastric Cancer". Master's thesis, 2016. https://repositorio-aberto.up.pt/handle/10216/89191.
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Costa, Susana Correia da. "Pathogenesis of Gastric Cancer". Dissertação, 2016. https://repositorio-aberto.up.pt/handle/10216/89191.
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CONTI, LAURA. "Risk of gastric neoplasms in autoimmune atrophic gastritis and its relationship with gastric microbiota and immune pathways". Doctoral thesis, 2023. https://hdl.handle.net/11573/1666843.
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Autoimmune atrophic gastritis (AAG) is a slowly progressive organ-specific, immune-mediated condition, characterized by atrophy of the oxyntic mucosa with subsequent hypochlorhydria and hypergastrinemia. When this pathological process occurs, the subsequent reduced mass of specialized parietal cells can lead to impaired gastric acid and intrinsic factor secretion, eventually resulting in malabsorption of iron and vitamin B12 with consequent iron deficiency and/or pernicious anemia as well as an impairment of gastric microbiota composition and an increased risk of gastric tumours. The prevalence of AAG in the general population is estimated to be as high as 2-5%. Patients affected by AAG are likely to develop several neoplasms, in particular type-1 neuroendocrine tumors in percentage variable from 0.4% to 7% and gastric cancer (GC) with an incidence ranging between 0% and 1.8% per year. In AAG, the development towards GC depends on several factors such as conditions leading to an increased intragastric pH and oxidative stress, gastric microbiota composition, host factors such as the immune pathway, rather than environmental risk factors like smoke, alcohol, body mass index and diet. The increased GC risk associated to AAG emphasizes the importance of diagnosing and monitoring these patients, as recommended by the last European guidelines on diagnosis and management of precancerous gastric conditions (MAPS II). Many questions regarding the natural history of AAG and the risk factors for the development of GC in patients affected by AAG are still opened. On the basis of this scenario, several monocentric and multicentric studies were conducted within this PhD project with the aim to in-depth assess several clinical, biochemical, histological and immunological aspects, not previously investigated, that may contribute to better understand the natural history of AAG as well as the risk factors involved in gastric carcinogenesis and the best management of this gastric precancerous condition. Considering the studies performed on gastric microbiota and immunological pathways in AAG, we can consider them as the first pieces of evidence, and they certainly cannot be interpreted as a point of arrival but should rather be viewed as a starting point for future research in this very complex and intriguing field in which much work is yet to be done.
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Wei-HsinHsiao i 蕭微炘. "The First-Degree Relatives of Gastric Cancer Patients have Genomic Predisposition to Gastric Cancer Pre-cancer Change". Thesis, 2013. http://ndltd.ncl.edu.tw/handle/34354900066230524876.
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碩士國立成功大學
臨床醫學研究所
101
Helicobacter pylori (H. pylori) is a WHO type I carcinogen of gastric cancer with familial clustering predisposing to precancerous change, such as intestinal metaplasia (IM). Spasmolytic polypeptide-expressing metaplasia (SPEM) is a new precancerous lesion, may be earlier than IM after H. pylori infection, and related with trefoil factor2 (TFF2) expression. Previous studies had found that the origin of SPEM is through transdifferentiation from mature chief cell following parietal cell loss. RUNX3, a tumor suppressor, is a member of the runt-domain transcription factor family that regulates the transcription of several genes involved in the decrease of cancer development, differentiation, and proliferation. RUNX3 is expressed in gastric epithelial cells and particularly in chief cell. And the epigenetic change of RUNX3 had found to be associate with gastric cancer. It is interested to validate whether the RUNX3 and TFF2 host genomic predisposition can determine the presence of SPEM after H. pylori infection. H. pylori may interact with integrin α5β1 to translocate virulence factor into cell, and expression of integrin α5β1 is also highly associated with IM. Thereforee, it is wotth investigating the the relationship between integrin α5β1 expression and SPEM development. Furthermore, it should be highly significant to validate if the integrin α5β1 expression and host genomic predisposition correlate with the novel issue SPEM. In this study, we found the first-degree relatives of gastric cancer families (1st- GCFs) have higher SPEM expression pattern than duodenal ulcer (DU) patients after H. pylori infection, and 1st-GCFs in gastric surface epithelium had abnormal integrin α5β1 expression location, which are closedly associated with advanced SPEM deveopment. 1st-GCFs have host genomic predisposition in RUNX3 single nucleotide polymorphisms (SNP)s at -1714 CC, -1582 CC, -1166 TT, +492 TT. However, the significance of the association between RUNX3 and TFF2 SNPs and SPEM expression level needs furtherer clarification. The 1st- GCFs have higher proportions of ITGA5-1160 TT homozygous and ITGB1-1949 T, -1575 C, +31804 C, +32492 G compared with DU patients. The 1st-GCFs with abnormal integrin α5β1 expression pattern patients have higher proportions of ITGB1-1660 AATTT/AATTT and ITGB1-685 GG homozygous compared with DU patients. Subsequently, we explored whether the different SNPs carrying type could affect the ITGA5 and ITGB1 promoter activity in AGS and GES-1 cell or not. In vitro transfection study in both the AGS and GES-1 cell lines have shown that ITGA5 promoter with -1160 G have higher promoter activity than -1160 T. interestingly, in AGS cells H. pylori can up-regulate the ITGA5 promoter activity with -1160 T. On the other hand, the different ITGB1 promoter SNPs composed and H. pylori infection have dramatic changes in the AGS and GES-1 cells with different regulatory capabilities. The summarized results of this study: 1) H. pylori-infected 1st-GCFs have higher proportion of precancerous lesion SPEM expression and abnormal integrin α5β1 expression pattern compared with DU patients. Sevral SNPs and haplotype of RUNX3, ITGA5 and ITGB1 are significantly associated with 1st-GCFs compared with DU patients; 2 ) After comprehensive analysis, we speculated that 1st-GCFs stomach tissue changes may occur from abnormal integrin α5β1 expression, followed by SPEM expression and progress to advanced SPEM, and then the IM formed after H. pylori infection; 3) ITGA5 and ITGB1 promoter SNPs may affect promoter activities and H. pylori infection could further influence the promoter activity. Both in AGS or GES-1 cell line experimental modes, the ITGA5 and ITGB1 promoter SNPs may show the different activity trends. These phenomena may be affected by the transcription factors involved; however their detailed mechanisms remain to be clarified. In this study, the contributions of these clinical studies are: 1) to gain more understanding of the gastric cancer high-risk population ie, 1st-GCFs, precancerous lesions pattern and propose a possible change process; 2) The 1st-GCFs have genetic predisposition to the gastric cancer and gastric cancer precancerous changes in integrin α5β1 may provide the diagnostic and therapeutic indices in gastric cancer prevention and management.
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Lume, Maria João Cardoso. "Controvérsias sobre Early Gastric Cancer". Master's thesis, 2014. https://repositorio-aberto.up.pt/handle/10216/74321.
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Lume, Maria João Cardoso. "Controvérsias sobre Early Gastric Cancer". Dissertação, 2014. https://repositorio-aberto.up.pt/handle/10216/74321.
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Rocha, Sara Jorge Moreira da. "Deconstructing gastric cancer colonization: the interplay between immune cells, gastric cancer cells and extracellular vesicles". Doctoral thesis, 2020. https://hdl.handle.net/10216/128647.
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Rocha, Sara Jorge Moreira da. "Deconstructing gastric cancer colonization: the interplay between immune cells, gastric cancer cells and extracellular vesicles". Tese, 2020. https://hdl.handle.net/10216/128647.
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LIU, CHENG-YING, i 劉增應. "Multistate and Multifactorial Progression of Gastric Cancer : Commity-Based Mass Screening for Gastric Cancer in Matzu". Thesis, 2003. http://ndltd.ncl.edu.tw/handle/17389882773761859231.
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碩士國立臺灣大學
預防醫學研究所
91
Abstract Background Notwithstanding multistate and multifactorial model for gastric cancer was proposed in early studies quantitative models for throwing light on the mechanism of disease progression were barely addressed. Aims The present study was therefore (1) to elucidate risk factors accounting for gastric cancer and its precursor and; (2) to model the progression rates from superficial gastritis to gastric cancer. Material and Methods Data used in this study were derived from a community-based screening for gastric cancer in Matzu with high prevalence of gastric cancer. A total of 2201 residents participated in a two-stage screening project using H pylori infection, PGI, and PGII as screening criteria. Those who had positive results were referred to receive endoscopy and biopsy. We identified 434 biopsy-proven precursors and gastric cancers, including 229 superficial gastrisits, 53 atrophy gastritis, 119 intestinal meta-plasia, and 33 gastric cancers. Serum samples for testing anti-HP, PGI, PGII were collected. Information on life-style factors, family history, personal disease, dietary factors were obtained from a structured questionnaire. Cox regression model was used to assess the effect of risk factors on the severity of gastric neoplasm. Markov model was proposed to estimate the progression rates from superficial gastritis to gastric cancer. Results In the multivariate analysis, H pylori infection (OR=3.10, 95% CI: 1.10-3.72), family history of gastric cancer or esophageal ca (OR=3.39, 95% CI: 2.42-4.75), history of UGI disease (OR=4.72, 95% CI: 3.57-6.26), cooked seafood intake (OR=3.48, 95% CI: 1.49-8.15) were significant factors for occurrence of SG. The effects of PGIon SG were modified by smoking or drinking. H pylori infection (OR=11.17, 95% CI: 4.32-28.90), family history of gastric cancer or esophageal ca (OR=3.31, 95% CI: 1.51-7.22), history of UGI disease (OR=4.87, 95% CI: 2.68-8.85), salted meat intake (OR=3.00, 95% CI: 0.71-12.73) were also statistically significant for AG. H pylori infection (OR=1.66, 95% CI: 1.13-2.43), level of PGI(OR=2.63, 95% CI: 1.74-3.95), family history of gastric cancer or esophageal ca (OR=5.02, 95% CI: 3.08-8.20), history of UGI disease (OR=4.35, 95% CI: 2.93-6.46), and fermented bean intake (OR=3.06, 95% CI: 1.24-7.56) remained statistically significant for IM. For gastric cancer, only leaf vegetable intake (OR=0.16, 95% CI: 0.04-0.78), and meat intake (OR=6.94, 95% CI: 2.04-23.65) remained statistically significant (Table 4.14). Annual progression rate from SG to AG was 2.45% (95% CI: 1.57%-3.33%). Annual progression rates from AG to IM or from IM to gastric cancer were 12.70% (95% CI: 5.23%-20.16%) and 11.95% (95% CI: 3.49%-20.41%), respectively. This gives average dwelling times for staying at AG and IM were 7.87 years and 8.37 years, respectively. The effects of H pylori, PGI&II or other dietary factors on different stages of precursor and gastric cancer were also modeled. Annual rates of malignant transformation for IM, AG and GS were 0.63%, 0.44% and 0%. Intervention efficacy for treating precursors can be calculated. Conclusions The present study elucidated risk factors associated with precursor and invasive carcinoma of stomach. The findings fit in with Correa multi-factor and multi-stage carcinogenesis model, indicating the initiator role of H pylori and the promoter of salty food and inhibitor of vegetables in late stage of carcinogenesis. Progression rates from superficial gastritis to invasive carcinoma were also quantified. The results have significant implications for early detection of precursor of gastric cancer.
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"Comprehensive Genomic Characterization of Gastric Cancer". 2016. http://repository.lib.cuhk.edu.hk/en/item/cuhk-1292462.
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Faria, Lídia Maria Azevedo. "Gastric cancer screening : a systematic review". Master's thesis, 2020. https://hdl.handle.net/10216/128792.
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Introdução e objetivo: O rastreio de base populacional para cancro gástrico (CG) é recomendado em populações de alto risco, apesar dos métodos e intervalos do mesmo variarem. Em populações de risco intermédio, as guidelines da Sociedade Europeia de Endoscopia Gastrointestinal sugerem que o rastreio por esofagogastroduodenoscopia (EGD) deve ser considerado dependendo dos recursos disponíveis. O objetivo deste estudo foi caracterizar os programas de rastreio de CG a nível mundial.
Métodos: Foram procurados estudos acerca do rastreio de base populacional para CG na MEDLINE e Scopus. Estudos com pacientes sintomáticos, lesões pré-malignas, CG hereditários e CG em vigilância foram excluídos. Os seguintes outcomes foram analisados: taxa de adesão, taxa de deteção precoce de CG e taxa de deteção de CG. Adicionalmente, foi enviado um questionário acerca do rastreio de cancro digestivo para sociedades de Endoscopia e Gastroenterologia.
Resultados: 44 estudos foram incluídos. O Japão e a Coreia oferecem um rastreio de base populacional por trânsito gastroduodenal (TG) ou EGD, com taxas de adesão a variar entre 14.31-58.01% e 7.40-74.8%, respetivamente. O Japão reportou taxas de deteção precoce de 0.02-0.21% e 0.35-0.66% e taxas de deteção entre 0.05-0.52% e 0.40-0.87%, em TG e EGD, respetivamente. A Coreia reportou uma taxa de deteção precoce de CG de 0.22% por EGD e taxas de deteção entre 0.01-0.29% e 0.07-0.08%, para EGD e para o TG, respetivamente. A China oferece rastreio por EGD, com uma taxa de adesão de 18.4% e taxa de deteção precoce CG e deteção de 0.23-0.67% e 0.09-0.85%, respetivamente. No ocidente, vários métodos de rastreio foram utilizados em estudos pilotos. Em relação ao questionário, apenas a Sérvia e a Suécia reportaram a existência de um programa de rastreio para CG.
Discussão: O rastreio em massa para o CG está disponível no Japão, Coreia e China. Os programas endoscópicos tendem a alcançar taxas de deteção precoce e de deteção de CG superiores aos programas TG, com taxas de adesão variáveis.Background and Aims: Population-based gastric cancer (GC) screening is recommended in high-risk populations, although screening methods and intervals vary. In intermediate-risk populations, European Society of Gastrointestinal Endoscopy guidelines suggest that esophagogastroduodenoscopy (EGD) screening may be considered depending on resources. The aim of this study was to characterize GC screening programs worldwide. Methods: Studies regarding population-based GC screening were searched through MEDLINE and Scopus. Studies on symptomatic patients, premalignant lesions, hereditary GC and GC surveillance were excluded. The following outcomes were analysed: adherence rate, early-GC detection rate and GC detection rate. Additionally, a survey on digestive cancer screening was sent to Endoscopy/Gastroenterology societies. Results: 44 studies were included. Population-based screening by upper gastrointestinal series (UGIS) or EGD is offered in Japan and Korea, with adherence rates between 14.31-58.01% and 7.40-74.8%, respectively. Japan reported early-GC detection rates of 0.02-0.21% and 0.35-0.66% and detection rates of 0.05-0.52% and 0.40-0.87%, for UGIS and EGD, respectively. Korea reported an EGD early-GC detection of 0.22% and detection rates between 0.01-0.29% and 0.07-0.08%, for EGD and UGIS, respectively. China offers EGD screening, with an adherence rate of 18.41% and early-GC and detection rates of 0.23-0.67% and 0.09-0.85%, respectively. In Western, several screening methods were used in pilot studies. Regarding the survey, only Serbia and Sweden reported the existence of a screening program. Discussion: Mass screening for GC is available in Japan, Korea and China. Endoscopy-based programs seem to achieve higher early-GC and GC detection rates rather than UGIS, with variable adherence rates.
47
Lima, Gabriel Trovão Pereira de. "Deep Learning For Gastric Cancer Detection". Master's thesis, 2021. https://hdl.handle.net/10216/138746.
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Faria, Lídia Maria Azevedo. "Gastric cancer screening : a systematic review". Dissertação, 2020. https://hdl.handle.net/10216/128792.
Pełny tekst źródłaStreszczenie:
Introdução e objetivo: O rastreio de base populacional para cancro gástrico (CG) é recomendado em populações de alto risco, apesar dos métodos e intervalos do mesmo variarem. Em populações de risco intermédio, as guidelines da Sociedade Europeia de Endoscopia Gastrointestinal sugerem que o rastreio por esofagogastroduodenoscopia (EGD) deve ser considerado dependendo dos recursos disponíveis. O objetivo deste estudo foi caracterizar os programas de rastreio de CG a nível mundial.
Métodos: Foram procurados estudos acerca do rastreio de base populacional para CG na MEDLINE e Scopus. Estudos com pacientes sintomáticos, lesões pré-malignas, CG hereditários e CG em vigilância foram excluídos. Os seguintes outcomes foram analisados: taxa de adesão, taxa de deteção precoce de CG e taxa de deteção de CG. Adicionalmente, foi enviado um questionário acerca do rastreio de cancro digestivo para sociedades de Endoscopia e Gastroenterologia.
Resultados: 44 estudos foram incluídos. O Japão e a Coreia oferecem um rastreio de base populacional por trânsito gastroduodenal (TG) ou EGD, com taxas de adesão a variar entre 14.31-58.01% e 7.40-74.8%, respetivamente. O Japão reportou taxas de deteção precoce de 0.02-0.21% e 0.35-0.66% e taxas de deteção entre 0.05-0.52% e 0.40-0.87%, em TG e EGD, respetivamente. A Coreia reportou uma taxa de deteção precoce de CG de 0.22% por EGD e taxas de deteção entre 0.01-0.29% e 0.07-0.08%, para EGD e para o TG, respetivamente. A China oferece rastreio por EGD, com uma taxa de adesão de 18.4% e taxa de deteção precoce CG e deteção de 0.23-0.67% e 0.09-0.85%, respetivamente. No ocidente, vários métodos de rastreio foram utilizados em estudos pilotos. Em relação ao questionário, apenas a Sérvia e a Suécia reportaram a existência de um programa de rastreio para CG.
Discussão: O rastreio em massa para o CG está disponível no Japão, Coreia e China. Os programas endoscópicos tendem a alcançar taxas de deteção precoce e de deteção de CG superiores aos programas TG, com taxas de adesão variáveis.Background and Aims: Population-based gastric cancer (GC) screening is recommended in high-risk populations, although screening methods and intervals vary. In intermediate-risk populations, European Society of Gastrointestinal Endoscopy guidelines suggest that esophagogastroduodenoscopy (EGD) screening may be considered depending on resources. The aim of this study was to characterize GC screening programs worldwide. Methods: Studies regarding population-based GC screening were searched through MEDLINE and Scopus. Studies on symptomatic patients, premalignant lesions, hereditary GC and GC surveillance were excluded. The following outcomes were analysed: adherence rate, early-GC detection rate and GC detection rate. Additionally, a survey on digestive cancer screening was sent to Endoscopy/Gastroenterology societies. Results: 44 studies were included. Population-based screening by upper gastrointestinal series (UGIS) or EGD is offered in Japan and Korea, with adherence rates between 14.31-58.01% and 7.40-74.8%, respectively. Japan reported early-GC detection rates of 0.02-0.21% and 0.35-0.66% and detection rates of 0.05-0.52% and 0.40-0.87%, for UGIS and EGD, respectively. Korea reported an EGD early-GC detection of 0.22% and detection rates between 0.01-0.29% and 0.07-0.08%, for EGD and UGIS, respectively. China offers EGD screening, with an adherence rate of 18.41% and early-GC and detection rates of 0.23-0.67% and 0.09-0.85%, respectively. In Western, several screening methods were used in pilot studies. Regarding the survey, only Serbia and Sweden reported the existence of a screening program. Discussion: Mass screening for GC is available in Japan, Korea and China. Endoscopy-based programs seem to achieve higher early-GC and GC detection rates rather than UGIS, with variable adherence rates.
49
Huang, Kuo-Hung, i 黃國宏. "Biomarkers investigation of gastric cancer progression". Thesis, 2018. http://ndltd.ncl.edu.tw/handle/nkva9y.
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博士國立陽明大學
臨床醫學研究所
106
In Taiwan, gastric cancer is ranked the sixth common cancer and the fifth cancer mortality. Surgical resection with radical lymph nodes dissection still plays an important role for gastric cancer. Our studies found that gastric cancer patients with SIRT3 expression have better prognosis than those without. SIRT3 expression is an independent better prognostic marker for overall survival. Besides, we also found that Caspase-3 expression in gastric cancer patients is related to favorable clinicopathological features and a positive prognosis after curative surgery. Furthermore, RhoA expression is associated with poor prognosis in gastric cancer patients, expecially diffuse type gastric cancer. SIRT3, Caspase-3 and RhoA may act as prognostic markers in human gastric cancer. With regard to signaling pathway in gastric cancer cells, we found that gastric cancer patients with positive c-Met expression had poorer overall survival than patients without c-Met expression (P = 0.043) and that Jagged1 expression significantly correlated with c-Met expression (r = 0.301; P = 0.004). In addition, Jagged1 activity increased after HGF stimulation, which in turn increased the downstream expression of cyclooxygenase 2 (COX-2) in a time dependent manner. After knockdown of receptor, HGF was found to increase the proliferation and migration ability in human gastric cancer cells. However, overexpression of N1IC still had no effect after HGF stimulation. Our study found a feedback loop between the HGF/c-Met and Jagged1/Notch1 signaling. Furthermore, both HGF/c-Met and Notch1 signaling triggered the COX-2 activity. In terms of histone modification, we found that gastric cancer patients with higher H3K4ac and H3K4me3 expression have favorable prognosis than those with lower expression. In vitro and in vivo study showed that gastric cancer cell proliferation, migration and tumor growth were inhibited by histone deacetylase (HDAC) inhibitor. H3K4ac expression is associated with better clinicopathological appearances and may act as a potential biomarkers in human gastric cancer. These results suggest that gastric cancer progression is not associated with a unique signaling pathway and that a feedback loop may exist between the HGF/c-Met and Notch1 signaling pathways, which may result in therapeutic resistance. Therefore, multi-modality therapies should be considered for treating gastric cancer. Besides, our studies found several predictive biomarkers for the prognosis of gastric cancer patients. We hope our studies could be helpful for the biological classification in the future.
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"DACT1 is silenced by CpG methylation in gastric cancer and contributes to the pathogenesis of gastric cancer". Thesis, 2011. http://library.cuhk.edu.hk/record=b6075505.
Pełny tekst źródłaStreszczenie:
Wang, Shiyan.Thesis (Ph.D.)--Chinese University of Hong Kong, 2011.
Includes bibliographical references (leaves 123-139).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstract also in Chinese.