Tesis sobre el tema "Gastric cancer"
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Chan, On-on Annie y 陳安安. "E-cadherin in gastric cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B29974082.
Texto completoFung, Wai-Ki Vicki y 馮慧琪. "Epigenetic alterations in gastric cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B45009995.
Texto completoLinnane, Emily. "Metabolic reprogramming in gastric cancer". Thesis, University of Liverpool, 2015. http://livrepository.liverpool.ac.uk/2014059/.
Texto completoInoue, Harutaka. "Risk of gastric cancer after Roux-en-Y gastric bypass". Kyoto University, 2008. http://hdl.handle.net/2433/124248.
Texto completoCunningham, David. "Gastric cancer : natural history and treatment". Thesis, University of Glasgow, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293449.
Texto completoSelway, Simone Ann Marie. "Antisecretory agents and gastric morphology". Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386637.
Texto completoPaon, 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.
Texto completoAl-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.
Texto completoLannigan, 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.
Texto completoSaunders, John. "Ex vivo modelling of oesophago-gastric cancer". Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/47574/.
Texto completoPorter, Timothy Robin. "Molecular genetics of gastrointestinal cancer". Thesis, University of Birmingham, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273741.
Texto completoAl-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.
Texto completoLu, 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.
Texto completoBashash, Morteza. "Molecular epidemiology of gastric and esophageal cancer survival". Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/30666.
Texto completoWebb, 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.
Texto completo樊曉明 y 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.
Texto completoWang, Liyi. "MicroRNAs in gastric and oesophageal cancer-associated myofibroblasts". Thesis, University of Liverpool, 2013. http://livrepository.liverpool.ac.uk/11135/.
Texto completoFan, 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.
Texto completoFOSCARINI, ALESSIA. "Functional characterization of Tribbles pseudokinases in gastric cancer". Doctoral thesis, Università degli studi di Pavia, 2022. http://hdl.handle.net/11571/1452907.
Texto completoSara, Peri. "Chemotherapy resistance-associated epithelial to endothelial transition in gastric cancer". Doctoral thesis, Università di Siena, 2020. http://hdl.handle.net/11365/1096074.
Texto completoAl, 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/.
Texto completoNg, 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.
Texto completoYip, Bon-ham y 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.
Texto completoKaurah, 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.
Texto completoMedicine, Faculty of
Graduate
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.
Texto completoVickery, 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.
Texto completoTse, 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.
Texto completoFall, Katja. "Medical interventions and gastric cancer risk : an observational approach /". Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-905-6/.
Texto completoLindblad, Mats. "Aspects on the etiology of esophageal and gastric cancer /". Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-110-5/.
Texto completoLagergren, Jesper. "Cancer of the esophagus and gastric cardia etiological aspects /". Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3397-9/.
Texto completoKONDO, TATSUHEI, HIDEO KAMEI y KEISUKE TERABE. "Histopathological Study on the Prognosis of pT2 Gastric Cancer". Nagoya University School of Medicine, 1986. http://hdl.handle.net/2237/17488.
Texto completoJennings, 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.
Texto completoMorgan, 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.
Texto completoTse, Tak-fong y 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.
Texto completoCorso, 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.
Texto completoCosta, Susana Correia da. "Pathogenesis of Gastric Cancer". Master's thesis, 2016. https://repositorio-aberto.up.pt/handle/10216/89191.
Texto completoCosta, Susana Correia da. "Pathogenesis of Gastric Cancer". Dissertação, 2016. https://repositorio-aberto.up.pt/handle/10216/89191.
Texto completoCONTI, 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.
Texto completoWei-HsinHsiao y 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.
Texto completo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.
Lume, Maria João Cardoso. "Controvérsias sobre Early Gastric Cancer". Master's thesis, 2014. https://repositorio-aberto.up.pt/handle/10216/74321.
Texto completoLume, Maria João Cardoso. "Controvérsias sobre Early Gastric Cancer". Dissertação, 2014. https://repositorio-aberto.up.pt/handle/10216/74321.
Texto completoRocha, 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.
Texto completoRocha, 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.
Texto completoLIU, CHENG-YING y 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.
Texto completo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.
"Comprehensive Genomic Characterization of Gastric Cancer". 2016. http://repository.lib.cuhk.edu.hk/en/item/cuhk-1292462.
Texto completoFaria, Lídia Maria Azevedo. "Gastric cancer screening : a systematic review". Master's thesis, 2020. https://hdl.handle.net/10216/128792.
Texto completoBackground 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.
Lima, Gabriel Trovão Pereira de. "Deep Learning For Gastric Cancer Detection". Master's thesis, 2021. https://hdl.handle.net/10216/138746.
Texto completoFaria, Lídia Maria Azevedo. "Gastric cancer screening : a systematic review". Dissertação, 2020. https://hdl.handle.net/10216/128792.
Texto completoBackground 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.
Huang, Kuo-Hung y 黃國宏. "Biomarkers investigation of gastric cancer progression". Thesis, 2018. http://ndltd.ncl.edu.tw/handle/nkva9y.
Texto completo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.
"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.
Texto completoThesis (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.