Bibliografías temáticas / Gastric cancer

Literatura académica sobre el tema "Gastric cancer"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 14 de marzo de 2023

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Artículos de revistas sobre el tema "Gastric cancer"

1

&NA;. "Gastrin and gastric cancer". European Journal of Gastroenterology & Hepatology 5, n.º 3 (marzo de 1993): 183. http://dx.doi.org/10.1097/00042737-199303000-00011.

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Farinati, Fabio, Gianni Delia Libera, Flavio Valiante, Maria Cristina Fanton, Mario Plebani, Francesco Di Mario y Remo Naccarato. "Gastrin and gastric cancer". European Journal of Gastroenterology & Hepatology 5, n.º 3 (marzo de 1993): 184. http://dx.doi.org/10.1097/00042737-199303000-00012.

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Waldum, Helge L. "Gastrin and gastric cancer". European Journal of Gastroenterology & Hepatology 5, n.º 3 (marzo de 1993): 185–86. http://dx.doi.org/10.1097/00042737-199303000-00013.

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Smith, Jill P., Sandeep Nadella y Nick Osborne. "Gastrin and Gastric Cancer". Cellular and Molecular Gastroenterology and Hepatology 4, n.º 1 (julio de 2017): 75–83. http://dx.doi.org/10.1016/j.jcmgh.2017.03.004.

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Waldum, Helge y Reidar Fossmark. "Types of Gastric Carcinomas". International Journal of Molecular Sciences 19, n.º 12 (18 de diciembre de 2018): 4109. http://dx.doi.org/10.3390/ijms19124109.

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Gastric cancer has reduced prevalence, but poor prognoses. To improve treatment, better knowledge of carcinogenesis and cells of origin should be sought. Stomach cancers are typically localized to one of the three mucosae; cardial, oxyntic and antral. Moreover, not only the stem cell, but the ECL cell may proliferate and give rise to tumours. According to Laurén, the classification of gastric carcinomas seems to reflect biological important differences and possible different cell of origin since the two subtypes, intestinal and diffuse, do not transform into the other and show different epidemiology. The stem cell probably gives rise to the intestinal type, whereas the ECL cell may be important in the diffuse type. Elevation of gastrin may be the carcinogenic factor for Helicobacter pylori as well as the recently described increased risk of gastric cancer due to proton pump inhibitor treatment. Therefore, it is essential to determine the role of the gastrin target cell, the ECL cell, in gastric carcinogenesis. Clinical trials with gastrin antagonists could improve prognoses in those with gastrin receptor positive tumours. However, further studies on gastric carcinomas applying relative available methods and with the highest sensitivity are warranted to improve our knowledge of gastric carcinogenesis.
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Kanda, Naoki, Hiroshi Seno, Mayumi Kawada, Tateo Sawabu, Yoshito Uenoyoma, Toshio Nakajima, Yoshitaka Konda, Hirokazu Fukui, Toshiyuki Takeuchi y Tsutomu Chiba. "Involvement of cyclooxygenase-2 in gastric mucosal hypertrophy in gastrin transgenic mice". American Journal of Physiology-Gastrointestinal and Liver Physiology 290, n.º 3 (marzo de 2006): G519—G527. http://dx.doi.org/10.1152/ajpgi.00113.2005.

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Gastrin promotes gastric mucosal growth, and hypergastrinemia induces gastric mucosal hypertrophy. Recently, it has been reported that gastrin induces cyclooxygenase-2 (COX-2) in human gastric and colorectal cancer cell lines. However, whether COX-2 is involved in gastrin-induced gastric mucosal growth in vivo is unknown. We investigated the role of COX-2 in gastrin-induced gastric mucosal hypertrophy using gastrin transgenic mice. Hypergastrinemic mice [mice with mutated gastrin under the control of the β-actin promoter (ACT-GAS mice)] received the COX-2 inhibitor celecoxib (0, 200, or 500 mg/kg of diet) from 5 wk of age and were killed at 16 or 24 wk. Some ACT-GAS mice received celecoxib from 16 wk and were killed at 24 wk. Eighty-week-old ACT-GAS mice without celecoxib treatment were also examined. The thickness of the gastric mucosa, cell populations, COX-2 expression, and PGE2levels were evaluated. All ACT-GAS mice showed gastric mucosal hypertrophy, and four of six 80-wk-old ACT-GAS mice developed gastric cancer. COX-2 was expressed in interstitial cells of the hypertrophic gastric mucosa and gastric cancers. Moreover, PGE2levels in the gastric mucosa of ACT-GAS mice were significantly higher than those of normal mice. With treatment with celecoxib, PGE2levels, the gastric mucosal thickness, and the number of total gastric cells per gastric gland of ACT-GAS mice were significantly decreased. The decrease in gastric mucosal thickness was caused by a reduction of foveolar hyperplasia. The thickness of glandules and the number of Ki67-positive cells were not significantly changed. In conclusion, COX-2 contributes to gastrin-induced mucosal hypertrophy of the stomach.
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Xue, Huiguang, Aihua Yang, Fuguo Liu, Xueguo Sun y Xishuang Liu. "Clinical significance of Serum Pepsinogen I/II and gastrin-17 determination in gastric cancer diagnosis and prognosis". European Journal of Inflammation 16 (1 de enero de 2018): 205873921878129. http://dx.doi.org/10.1177/2058739218781291.

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Currently, the diagnosis of atrophic gastritis and gastric cancer are mainly made by endoscopy and histopathology. Our study aimed to explore the practical value of Serum Pepsinogen I/II and gastrin-17 in gastric cancer diagnosis and prognosis. We collected 60 cases of gastric ulcer from February 2015 to November 2016 as gastric ulcer group, and 40 cases of gastric cancer treated in the same period as gastric cancer group. In 3 years after gastric cancer, 20 patients were served as postoperative gastric cancer group, and 70 healthy subjects as control group. The results showed that serum Pepsinogen I/II, gastrin-17, and other serum gastric function indexes were tested by enzyme-linked immunosorbent assay (ELISA). The serum PGI level of gastric ulcer group was higher than control group ( P < 0.05). The serum G-17 concentrations in gastric ulcer group, gastric cancer group, and postoperative gastric cancer group were all higher than control group ( P < 0.05). The area under receiver operating characteristic (ROC) curve of PGI screening was 0.905 and the best cutoff point was PGI < 75 µg/L. Their sensitivity and specificity were 87.2% and 75.1%; the area under ROC curve of PGI/PGII rate screening was 0.761 and the best cutoff point was PGI/PGII < 4. Their sensitivity and specificity were 88.9% and 62.3%. Multi logistical regression showed that the level of serum PGI, PGI, and G-17 and the odds ratio (OR) level of gastric cancer risk were 2.093, 2.653, and 0.494 ( P < 0.05). The examination of Serum Pepsinogen I/II, gastrin-17, and other serum gastric function indexes can be used in the diagnosis and prognosis of gastric cancer and has a rather high practical value in monitoring recurrence in postoperative gastric cancer patients.
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Park, Hyun Sik, Sun-Young Lee, Sung Noh Hong, Jeong Hwan Kim, In-Kyung Sung, Hyung Seok Park, Chan Sup Shim y Choon Jo Jin. "Early Gastric Cancer-Like Advanced Gastric Cancer versus Advanced Gastric Cancer-Like Early Gastric Cancer". Clinical Endoscopy 46, n.º 2 (2013): 155. http://dx.doi.org/10.5946/ce.2013.46.2.155.

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Al Menhali, Asma, Theresa M. Keeley, Elise S. Demitrack y Linda C. Samuelson. "Gastrin induces parathyroid hormone-like hormone expression in gastric parietal cells". American Journal of Physiology-Gastrointestinal and Liver Physiology 312, n.º 6 (1 de junio de 2017): G649—G657. http://dx.doi.org/10.1152/ajpgi.00366.2016.

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Parietal cells play a fundamental role in stomach maintenance, not only by creating a pathogen-free environment through the production of gastric acid, but also by secreting growth factors important for homeostasis of the gastric epithelium. The gastrointestinal hormone gastrin is known to be a central regulator of both parietal cell function and gastric epithelial cell proliferation and differentiation. Our previous gene expression profiling studies of mouse stomach identified parathyroid hormone-like hormone (PTHLH) as a potential gastrin-regulated gastric growth factor. Although PTHLH is commonly overexpressed in gastric tumors, its normal expression, function, and regulation in the stomach are poorly understood. In this study we used pharmacologic and genetic mouse models as well as human gastric cancer cell lines to determine the cellular localization and regulation of this growth factor by the hormone gastrin. Analysis of PthlhLacZ/+ knock-in reporter mice localized Pthlh expression to parietal cells in the gastric corpus. Regulation by gastrin was demonstrated by increased Pthlh mRNA abundance after acute gastrin treatment in wild-type mice and reduced expression in gastrin-deficient mice. PTHLH transcripts were also observed in normal human stomach as well as in human gastric cancer cell lines. Gastrin treatment of AGS-E gastric cancer cells induced a rapid and robust increase in numerous PTHLH mRNA isoforms. This induction was largely due to increased transcriptional initiation, although analysis of mRNA half-life showed that gastrin treatment also extended the half-life of PTHLH mRNA, suggesting that gastrin regulates expression by both transcriptional and posttranscriptional mechanisms. NEW & NOTEWORTHY We show that the growth factor parathyroid hormone-like hormone (PTHLH) is expressed in acid-secreting parietal cells of the mouse stomach. We define the specific PTHLH mRNA isoforms expressed in human stomach and in human gastric cancer cell lines and show that gastrin induces PTHLH expression via transcription activation and mRNA stabilization. Our findings suggest that PTHLH is a gastrin-regulated growth factor that might contribute to gastric epithelial cell homeostasis.
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Tian, Qing, Ying Guo, Dan Li y Liang Dong. "Hybrid Gastric Cancer Exosome as Potential Drug Carrier for Targeted Gastric Cancer Therapy". Journal of Biomaterials and Tissue Engineering 12, n.º 11 (1 de noviembre de 2022): 2228–32. http://dx.doi.org/10.1166/jbt.2022.3167.

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Gastric cancer is among the leading lethal cancer types in the world. However, its five year survival rate is far from satisfactory. Therefore, the development of targeted cancer gastric cancer therapy is a promising way to cure gastric cancer. Gastric cancer exosome is reported to have high caner targeting efficacy, but its yield is relatively low. Herein, we proposed a facile way to construct hybrid gastric cancer exosome (HGCE) with high yield as potential drug carrier for targeted gastric cancer therapy. The doxorubicin (Dox) loaded HGCE (Dox/HGCE) was developed as drug delivery system (DDS) to treat gastric cancer. In vitro and in vivo results demonstrated that Dox/HGCE showed not only high and specific homing ability to the gastric cancer cells (SGC7901) but also good anticancer performance which can be a promising DDS for gastric cancer therapy.
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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.

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Fung, 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.

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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.
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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.
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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.
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Libros sobre el tema "Gastric cancer"

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Gastric cancer. Cambridge, UK: Cambridge University Press, 2010.

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Nishi, Mitsumasa, Heizaburo Ichikawa, Toshifusa Nakajima, Keiichi Maruyama y Eiichi Tahara, eds. Gastric Cancer. Tokyo: Springer Japan, 1993. http://dx.doi.org/10.1007/978-4-431-68328-5.

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Shiotani, Akiko, ed. Gastric Cancer. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-1120-8.

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Gore, Richard M., ed. Gastric Cancer. Cambridge: Cambridge University Press, 2009. http://dx.doi.org/10.1017/cbo9780511691751.

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Strong, Vivian E., ed. Gastric Cancer. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15826-6.

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Takashi, Sugimura y Sasako Mitsuru, eds. Gastric cancer. Oxford: Oxford University Press, 1997.

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M, Gore Richard, ed. Gastric cancer. Cambridge: Cambridge University Press, 2010.

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Mitsumasa, Nishi, ed. Gastric cancer. Tokyo: Springer-Verlag, 1993.

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O, Douglass Harold, ed. Gastric cancer. New York: Churchill Livingstone, 1988.

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de Castria, Tiago Biachi y Rodrigo Santa Cruz Guindalini, eds. Diffuse Gastric Cancer. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95234-5.

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Capítulos de libros sobre el tema "Gastric cancer"

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Tsugawa, Hitoshi y Hidekazu Suzuki. "Gastric Carcinogenesis". En Gastric Cancer, 51–62. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1120-8_4.

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Magalhães, Helena Sofia Azevedo de Oliveira. "Gastric Cancer". En Principles of Specialty Nursing, 255–60. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-76457-3_16.

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Chang, Jennifer S., Mekhail Anwar y Hans T. Chung. "Gastric Cancer". En Handbook of Evidence-Based Radiation Oncology, 423–40. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-62642-0_19.

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Baack, Tobias, Sabine Mai y Frederik Wenz. "Gastric Cancer". En Target Volume Definition in Radiation Oncology, 161–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-45934-8_9.

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Calvo, Felipe A., Manuel Santos, Fernando Pardo, José L. Hernández, Javier Alvarez-Cienfuegos y Juan Voltas. "Gastric Cancer". En Intraoperative Radiotherapy, 51–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84183-5_7.

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Taguchi, Tetsuo. "Gastric Cancer". En Induction Chemotherapy, 163–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-18173-3_12.

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Martinez-Monge, Rafael, Miren Gaztañaga, Javier Álvarez-Cienfuegos, Robert C. Miller y Felipe A. Calvo. "Gastric Cancer". En Intraoperative Irradiation, 223–48. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-015-7_12.

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Hasson, Brian F., Brandon J. Fisher, Larry C. Daugherty, Brandon J. Fisher, Larry C. Daugherty, Filip T. Troicki, Jaganmohan Poli et al. "Gastric Cancer". En Encyclopedia of Radiation Oncology, 296. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_1129.

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Faigel, Douglas O. y Sarah A. Rodriguez. "Gastric Cancer". En Atlas of Endoscopic Ultrasonography, 59–63. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444346305.ch13.

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Macdonald, John S., Scott Hundahl, Stephen R. Smalley, Denise O’Dea y Edith P. Mitchell. "Gastric Cancer". En Gastrointestinal Oncology, 101–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-13306-0_5.

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Actas de conferencias sobre el tema "Gastric cancer"

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Dixon, T. Michael y Huan Vu. "Laparoscopic ultrasound and gastric cancer". En BiOS 2001 The International Symposium on Biomedical Optics, editado por R. Rox Anderson, Kenneth E. Bartels, Lawrence S. Bass, C. Gaelyn Garrett, Kenton W. Gregory, Abraham Katzir, Nikiforos Kollias et al. SPIE, 2001. http://dx.doi.org/10.1117/12.427805.

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Kharnas, Sergey S., N. M. Kuzin, Victor Y. Zavodnov, Olga A. Sclyanskaya, Kirill G. Linkov, Victor B. Loschenov, Gennadii A. Meerovich, Nadezgda L. Torshina, Alexander A. Stratonnikov y Rudolf W. Steiner. "Photodynamic therapy of gastric cancer". En BiOS Europe '95, editado por Benjamin Ehrenberg, Giulio Jori y Johan Moan. SPIE, 1996. http://dx.doi.org/10.1117/12.230992.

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In, Haejin, Marisa Langdon-Embry, Judith Wylie-Rosett y Bruce Rapkin. "Abstract A01: Gastric cancer pre-screener project: Development of a comprehensive gastric cancer risk questionnaire". En Abstracts: AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; November 16-19, 2016; Orlando, FL. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7755.carisk16-a01.

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Brassard, P., Z. Ante y P. Ernst. "Risk of Gastric Cancer in COPD". En American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3137.

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Saidi, S. y S. Ghomari. "879 Krukenberg tumors: gastric cancer metastasis". En ESGO 2021 Congress. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/ijgc-2021-esgo.488.

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Li, Yuexiang, Xuechen Li, Xinpeng Xie y Linlin Shen. "Deep learning based gastric cancer identification". En 2018 IEEE 15th International Symposium on Biomedical Imaging (ISBI 2018). IEEE, 2018. http://dx.doi.org/10.1109/isbi.2018.8363550.

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"Metastatic Breast Cancer to Stomach Mimicking Primary Gastric cancer". En 2nd Hawler Pharmaceutical Sciences Conference. Hawler Medical University, 2020. http://dx.doi.org/10.15218/hpsc.02.07.

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Huber, Anne, Christine Dijkstra, Matthias Ernst y Moritz Eissmann. "Abstract PO-014: DNA methyltransferases drive gastric cancer growth and present a therapy target for gastric cancer". En Abstracts: AACR Special Virtual Conference on Epigenetics and Metabolism; October 15-16, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.epimetab20-po-014.

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Путова, Мария Вадимовна y Николай Евгеньевич Семенов. "THE CYTOLOGICAL DIAGNOSIS FOR THE DETECTION OF PERITONEAL FREE CANCER CELLS IN GASTRIC CANCER PATIENTS". En Наука. Исследования. Практика: сборник избранных статей по материалам Международной научной конференции (Санкт-Петербург, Февраль 2021). Crossref, 2021. http://dx.doi.org/10.37539/srp295.2021.91.51.009.

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Детекция свободных опухолевых клеток (СОК) в перитонеальных смывах больных раком желудка - единственный эффективный метод для диагностики микроканцероматоза брюшины и стадирования заболевания. Комбинированный морфологический метод (световая микроскопия и иммуноцитохимическое исследование) позволяет выявлять СОК со специфичностью 98%, чувствительностью 95%, общей точностью метода 98%. The detection of free cancer cells (FCC) in the materials of peritoneal washing of patients with gastric cancer allows to identify peritoneal microscopic carcinomatosis and to determine the disease’s stage for appropriate treatment decision making. With the combined use of all those methods (conversion microscopy and immunocytochemical study) of preparation and assessment of the material, the specificity of cytological diagnosis was 98%, and the sensitivity was 95%, the overall accuracy of the method reached 98%.
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Adhisty, Karolin, Mutia Nadra Maulida y Nabilla Rizki Oktadini. "Gastric Acid Detection Device for Cancer Patients". En 2nd Sriwijaya International Conference of Public Health (SICPH 2019). Paris, France: Atlantis Press, 2020. http://dx.doi.org/10.2991/ahsr.k.200612.038.

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Informes sobre el tema "Gastric cancer"

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Deng, Chun, Zhenyu Zhang, Zhi Guo, Hengduo Qi, Yang Liu, Haimin Xiao y Xiaojun Li. Assessment of intraoperative use of indocyanine green fluorescence imaging on the number of lymph node dissection during minimally invasive gastrectomy: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, noviembre de 2021. http://dx.doi.org/10.37766/inplasy2021.11.0062.

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Review question / Objective: Whether is indocyanine green fluorescence imaging-guided lymphadenectomy feasible to improve the number of lymph node dissections during radical gastrectomy in patients with gastric cancer undergoing curative resection? Condition being studied: Gastric cancer was the sixth most common malignant tumor and the fourth leading cause of cancer-related death in the world. Radical lymphadenectomy was a standard procedure in radical gastrectomy for gastric cancer. The retrieval of more lymph nodes was beneficial for improving the accuracy of tumor staging and the long-term survival of patients with gastric cancer. Indocyanine green(ICG) near-infrared fluorescent imaging has been found to provide surgeons with effective visualization of the lymphatic anatomy. As a new surgical navigation technique, ICG near-infrared fluorescent imaging was a hot spot and had already demonstrated promising results in the localization of lymph nodes during surgery in patients with breast cancer, non–small cell lung cancer, and gastric cancer. In addition, ICG had increasingly been reported in the localization of tumor, lymph node dissection, and the evaluation of anastomotic blood supply during radical gastrectomy for gastric cancer. However, it remained unclear whether ICG fluorescence imaging would assist surgeons in performing safe and sufficient lymphadenectomy.
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Chen, Jiuzhou, Yaru Guo, Yan Yuan, Miao Fan y Yong Xin. Neoadjuvant chemoradiotherapy for resectable gastric cancer: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, marzo de 2022. http://dx.doi.org/10.37766/inplasy2022.3.0164.

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Meng, Wenwen, Haiyan Shi, Jie Liu, Xiaohui Ge, Yafeng Xu, Shiqi Shan, Lin Wang, Juwei Liu, Lin Zha y Jun Niu. NF-κB expression and survival outcomes in gastric cancer: A meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, agosto de 2020. http://dx.doi.org/10.37766/inplasy2020.8.0037.

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Fu, Shifeng, Jin Yan, Yuyong Tan y Deliang Liu. Prognostic value of SII in survival outcome in gastric cancer: A meta-analysis. International Platform of Registered Systematic Review and Meta-analysis Protocols, mayo de 2020. http://dx.doi.org/10.37766/inplasy2020.5.0021.

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Sun, Xiaoxi, Huiqin Wen, Bingxiang Zhan y Peng Yang. Prognostic Significance of Pretreatment Systemic Immune-Inflammation Index in Gastric Cancer: A Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, diciembre de 2020. http://dx.doi.org/10.37766/inplasy2020.12.0110.

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Yilihamu, Ailimulatijiang y Bin Cai Ying. Prevalence of lymph nodes in early gastric cancer: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, octubre de 2022. http://dx.doi.org/10.37766/inplasy2022.10.0064.

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Li, Jian, Qinyu Xu, Yanyan Zhang, Yaqiong Zhang, Songhua Bei, Ying Ding, Xiaohong Zhang y Li Feng. Diagnostic Value of Circulating LncRNAs for Gastric Cancer: A Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, noviembre de 2022. http://dx.doi.org/10.37766/inplasy2022.11.0024.

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Jin, Yuanyang y Zhimin Suo. Immunocheckpoint inhibitors for advanced gastric cancer or gastroesophageal junction cancer with different microsatellite stability: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, octubre de 2022. http://dx.doi.org/10.37766/inplasy2022.10.0106.

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Li, Tian y Min Sun. Associations between hepatectomy and survival of gastric cancer patients with liver metastases: A network pooling analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, diciembre de 2020. http://dx.doi.org/10.37766/inplasy2020.12.0009.

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Zhang, Tianqi, Tiefeng Zhang, Chuancheng Li, Xixi Zhai y Qing Huo. Complementary and alternative therapies for precancerous lesions of gastric cancer: A Bayesian network meta-analysis protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, diciembre de 2020. http://dx.doi.org/10.37766/inplasy2020.12.0077.

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