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Articoli di riviste sul tema "Gastric cancer"

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Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 14 marzo 2023

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1

&NA;. "Gastrin and gastric cancer". European Journal of Gastroenterology & Hepatology 5, n. 3 (marzo 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 e Remo Naccarato. "Gastrin and gastric cancer". European Journal of Gastroenterology & Hepatology 5, n. 3 (marzo 1993): 184. http://dx.doi.org/10.1097/00042737-199303000-00012.

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3

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

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4

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

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

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Abstract (sommario):
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 e Tsutomu Chiba. "Involvement of cyclooxygenase-2 in gastric mucosal hypertrophy in gastrin transgenic mice". American Journal of Physiology-Gastrointestinal and Liver Physiology 290, n. 3 (marzo 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 e 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 gennaio 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 e Choon Jo Jin. "Early Gastric Cancer-Like Advanced Gastric Cancer versus Advanced Gastric Cancer-Like Early Gastric Cancer". Clinical Endoscopy 46, n. 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 e Linda C. Samuelson. "Gastrin induces parathyroid hormone-like hormone expression in gastric parietal cells". American Journal of Physiology-Gastrointestinal and Liver Physiology 312, n. 6 (1 giugno 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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10

Tian, Qing, Ying Guo, Dan Li e Liang Dong. "Hybrid Gastric Cancer Exosome as Potential Drug Carrier for Targeted Gastric Cancer Therapy". Journal of Biomaterials and Tissue Engineering 12, n. 11 (1 novembre 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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11

Miike, Tadashi, Shojiro Yamamoto, Yoshifumi Miyata, Tomoya Hirata, Yuko Noda, Takaho Noda, Sho Suzuki et al. "Surrounding Gastric Mucosa Findings Facilitate Diagnosis of Gastric Neoplasm as Gastric Adenoma or Early Gastric Cancer". Gastroenterology Research and Practice 2016 (2016): 1–5. http://dx.doi.org/10.1155/2016/6527653.

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Background and Aim. It is difficult to master the skill of discriminating gastric adenoma from early gastric cancer by conventional endoscopy or magnifying endoscopy combined with narrow-band imaging, because the colors and morphologies of these neoplasms are occasionally similar. We focused on the surrounding gastric mucosa findings in order to determine how to discriminate between early gastric cancer and gastric adenoma by analyzing the characteristics of the gastric background mucosa.Methods. We retrospectively examined 146 patients who underwent endoscopic submucosal dissection for gastric neoplasm between October 2009 and January 2015. The boundary of atrophic gastritis was classified endoscopically according to the Kimura-Takemoto classification system. Of 146 lesions, 63 early gastric cancers and 21 gastric adenomas were ultimately evaluated and assessed.Results. Almost all gastric adenomas were accompanied by open-type gastritis, whereas 47 and 16 early gastric cancers were accompanied by open-type and closed-type gastritis, respectively (p= 0.037).Conclusions. The evaluation of the boundary of atrophic gastritis associated with gastric neoplasms appears to be useful for discrimination between early gastric cancer and gastric adenoma. When gastric neoplasm is present in the context of surrounding localized gastric atrophy, gastric cancer is probable but not certain.
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Waldum, Helge, e Reidar Fossmark. "Gastritis, Gastric Polyps and Gastric Cancer". International Journal of Molecular Sciences 22, n. 12 (18 giugno 2021): 6548. http://dx.doi.org/10.3390/ijms22126548.

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Gastric cancer is still an important disease causing many deaths worldwide, although there has been a marked reduction in prevalence during the last few decades. The decline in gastric cancer prevalence is due to a reduction in Helicobacter pylori infection which has occurred for at least 50 years. The most probable mechanism for the carcinogenic effect of H. pylori is hypergastrinemia since H. pylori infected individuals do not have increased risk of gastric cancer before the development of oxyntic atrophy. When atrophy has developed, the carcinogenic process continues independent of H. pylori. Autoimmune gastritis also induces oxyntic atrophy leading to marked hypergastrinemia and development of ECL cell neoplasia as well as adenocarcinoma. Similarly, long-term treatment with efficient inhibitors of acid secretion like the proton pump inhibitors (PPIs) predisposes to ECL cell neoplasia of a different degree of malignancy. Contrasting the colon where most cancers develop from polyps, most polyps in the stomach have a low malignant potential. Nevertheless, gastric polyps may also give rise to cancer and have some risk factors and mechanisms in common with gastric cancer. In this overview the most common gastric polyps, i.e., hyperplastic polyps, adenomatous polyps and fundic gland polyps will be discussed with respect to etiology and particularly use of PPIs and relation to gastric carcinogenesis.
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Jaroenlapnopparat, Aunchalee, Khushboo Bhatia e Sahin Coban. "Inflammation and Gastric Cancer". Diseases 10, n. 3 (22 giugno 2022): 35. http://dx.doi.org/10.3390/diseases10030035.

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Gastric cancer remains a major killer globally, although its incidence has declined over the past century. It is the fifth most common cancer and the third most common reason for cancer-related deaths worldwide. Gastric cancer is the outcome of a complex interaction between environmental, host genetic, and microbial factors. There is significant evidence supporting the association between chronic inflammation and the onset of cancer. This association is particularly robust for gastrointestinal cancers in which microbial pathogens are responsible for the chronic inflammation that can be a triggering factor for the onset of those cancers. Helicobacter pylori is the most prominent example since it is the most widespread infection, affecting nearly half of the world’s population. It is well-known to be responsible for inducing chronic gastric inflammation progressing to atrophy, metaplasia, dysplasia, and eventually, gastric cancer. This review provides an overview of the association of the factors playing a role in chronic inflammation; the bacterial characteristics which are responsible for the colonization, persistence in the stomach, and triggering of inflammation; the microbiome involved in the chronic inflammation process; and the host factors that have a role in determining whether gastritis progresses to gastric cancer. Understanding these interconnections may improve our ability to prevent gastric cancer development and enhance our understanding of existing cases.
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Dias, Amanda de Araújo, Jamille Lopes Helmer, Sílvia Karinny Brito Calandrini de Azevedo, Cassio Caldato, Ciane Martins de Oliveira, Rodrigo Canto Moreira, Carla Viana Dendasck e Euzébio de Oliveira. "Genetic and environmental risk factors for gastric cancer". Revista Científica Multidisciplinar Núcleo do Conhecimento 10, n. 11 (9 novembre 2016): 63–72. http://dx.doi.org/10.32749/nucleodoconhecimento.com.br/health/gastric-cancer.

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Zheng, Guoqiao, Kristina Sundquist, Jan Sundquist, Tianhui Chen, Asta Försti, Akseli Hemminki e Kari Hemminki. "Second Primary Cancers After Gastric Cancer, and Gastric Cancer as Second Primary Cancer". Clinical Epidemiology Volume 13 (luglio 2021): 515–25. http://dx.doi.org/10.2147/clep.s304332.

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Kucukoner, Mehmet. "Helicobacter pylori in primary gastric lymphoma and gastric cancer: A clinicopathologic and prognostic assessment". Journal of Microbiology and Infectious Diseases 3, n. 2 (1 giugno 2013): 61–66. http://dx.doi.org/10.5799/ahinjs.02.2013.02.0082.

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Hange, Namrata, Manoj Reddy Somagutta, Sai Harsha Bobba, Narayana Reddy Bathula, Erkan Batti, Obumneme Jude Iloeje, Klodin Ghazarian, Gouthami Sajjanagandla, Ulhas Vasave e Bernard Emuze. "Visibility of gastric cancer awareness programs". International Journal Of Community Medicine And Public Health 8, n. 9 (27 agosto 2021): 4605. http://dx.doi.org/10.18203/2394-6040.ijcmph20213573.

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Gastric cancer is one of the most common and deadliest cancers known globally. Due to historically low survival rates and available few treatment modalities, especially in developing nations with high burden incidence of gastric cancers, reducing incidence seems to be the key to reducing mortality. This article has emphasized the planning and visibility of the gastric cancer awareness program. The gastric cancer awareness programs shall help people approach health care facilities if reported to be symptomatic and help to reduce the mortality burden through early detection and access to treatment. Stomach cancer awareness programs involve sensitization of the population regarding symptom recognition, screening, identification of vulnerable people, and preventive measures focused on disease control. Recognition of people at risk, symptom screening protocol along with prevention, and management of gastric cancer is meant to achieve this Gastric cancer control strategy. Gastric cancer awareness campaign, along with identification of risk factors, shall include prevention, early detection, and potential gastric cancer treatments through appropriate programs and activities. Targeting high-risk populations including males, aged more than 40 years, smokers, obese, alcoholic, red-meat eaters, population with low socioeconomic status, and people with a positive family history of gastric cancer along for health education shall be directed towards the annual gastric cancer screening programme either free or subsidized rate. Holistic gastric cancer awareness programs encompass the integrated lifestyle modification approach-addressing a healthy balanced diet; de-addiction for smoking and alcohol and stress-free life. Specific local, country-specific strategies tailored to each country's risk factor profile shall be considered while planning a gastric cancer awareness program.
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Kim, Gwang Ha. "Metachronous Gastric Cancer Occurring after Endoscopic Resection of Early Gastric Cancer". Korean Journal of Helicobacter and Upper Gastrointestinal Research 20, n. 4 (10 dicembre 2020): 295–99. http://dx.doi.org/10.7704/kjhugr.2020.0022.

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Endoscopic resection (ER) has been widely used as a curative treatment for early gastric cancers (EGCs). Especially endoscopic submucosal dissection has several merits such as high en bloc and curative resection rates for EGCs and preservation of the entire stomach. However, ER has the inevitable limitation that the possibility of newly developing gastric cancers in the preserved stomach is still present. Metachronous gastric cancer (MGC) is defined as a newly developed gastric cancer occurring at a previously uninvolved site ≥1 year after the index ER of EGCs. The incidence of MGC is 3.3~15.6% and increases over time after ER. Old age, male sex, current smoking, severe atrophy and intestinal metaplasia, persistent Helicobacter pylori (H. pylori) infection, differentiated-type histology, and multiple initial gastric cancers are risk factors of MGC. As H. pylori eradication could reduce the risk of MGC after ER of EGCs, H. pylori eradication is strongly recommended for the prevention of MGC after ER of EGCs. Most MGCs are found at an early stage on regular surveillance endoscopy after ER and successfully treated with ER, with excellent long-term outcomes.
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Jafari, Narjes, e Saeid Abediankenari. "MicroRNA-34 dysregulation in gastric cancer and gastric cancer stem cell". Tumor Biology 39, n. 5 (maggio 2017): 101042831770165. http://dx.doi.org/10.1177/1010428317701652.

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Gastric cancer is a major cause of cancer mortality worldwide, with a low survival rate for patients with advanced forms of the disease. Over the recent decades, the investigation of the pathophysiological mechanisms of tumourigenesis has opened promising avenues to understand some of the complexities of cancer treatment. However, tumour regeneration and metastasis impose great difficulty for gastric cancer cure. In recent years, cancer stem cells – a small subset of tumour cells in many cancers – have become a major focus of cancer research. Cancer stem cells are capable of self-renewal and are known to be responsible for tumour initiation, metastasis, therapy resistance and cancer recurrence. Recent studies have revealed the key role of microRNAs – small noncoding RNAs regulating gene expression – in these processes. MicroRNAs play crucial roles in the regulation of a wide range of biological processes in a post-transcriptional manner, though their expression is dysregulated in most malignancies, including gastric cancer. In this article, we review the consequences of aberrant expression of microRNA-34 in cancer and cancer stem cells, with a specific focus on the miR-34 dysregulation in gastric cancer and gastric cancer stem cells. We address the critical effects of the aberrant expression of miR-34 and its target genes in maintaining cancer stem cell properties. Information collection and discussion about the advancements in gastric cancer stem cells and microRNAs can be useful for providing novel insights into patient treatment.
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Jabbaripour, Pooneh, Mohammad Hossein Somi, Hossein Mashhadi Abdolahi e Roya Dolatkhah. "Gastric cancer in East Azerbaijan, Iran: Five-year survival analysis of population-based cancer registry results". Biomedical Research and Therapy 7, n. 11 (29 novembre 2020): 4114–21. http://dx.doi.org/10.15419/bmrat.v7i11.648.

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Introduction: Gastric cancer is the most common cancer with significant increasing trends during the last decade in Iran. The aim of this study was to evaluate the epidemiologic profile of gastric cancer along with gastric cancer-specific survival analysis. Methods: This was an analytical cross-sectional study in which all gastric cancer data were analyzed using the database of the East Azerbaijan Population-Based Cancer Registry (EA-PBCR). The incidents of definitive gastric cancer diagnosis were between the period of March 20th, 2015 to March 19th, 2017 ( = 3 Iranian solar years). The survival analysis was performed using the Kaplan-Meier method and life tables for 1- to 5-year survival data. The Log-rank test and Cox regression were computed to test the equality of survival function and mortality hazard. Results: Overall, 2,631 newly diagnosed gastric cancer cases were registered for 3 years. Gastric cancer was 2.35 times more common in men than women. The most common age group was the 7th decade- with 531 (31.2%) gastric cancer cases. Most of the gastric cancer cases were non-cardia (n = 2,244, 85.29%) cancer, and the proportion of non-cardia to cardia gastric cancer was 5.8:1. Overall survival was 60.1%, and 1- to 5-year survival proportions were 91.61%, 64.21%, 58.53%, 30.14% and 24.77%, respectively. Cardia cancers had a worse survival rate than non-cardia cancers, and the hazard of mortality was 1.33 times higher in cardia than non-cardia cancers (hazard ratio or HR = 1.33; 95% CI: 1.05 - 1.68; P = 0.017). Conclusion: Non-cardia gastric cancer is still the most dominant subsite in East Azerbaijan, Iran. There was a higher 1- to 5- year survival proportion in East Azerbaijan, with lower overall mortality rates, compared to other regions of Iran.
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Li, Na, Mingxuan Jia, Ce Yin e Ge Feng. "Effect of Hericium Evimaccus Alcohol Extracts on the Expression of Gastrin 17 and PKM2, and Cell Apoptosis in Rats with Gastric Cancer". Science of Advanced Materials 14, n. 1 (1 gennaio 2022): 155–61. http://dx.doi.org/10.1166/sam.2022.4180.

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The aim of this study was to study the effects of hericium evimaccus alcohol extracts on the expression of gastrin 17 and PKM2, and cell apoptosis in rats with gastric cancer. We selected 75 healthy ACL female rats, 15 healthy group, 15 gastric cancer group, 15 capecitabine group (drug control), 15 low-dose group (20 mg/kg), and high-dose group (40 mg/kg) of 15 rats, 2–4 months old, with body weight of 210–225 g, at average (213.25±12.37) g. Immunohistochemical staining was used to measure the pathological tissue morphology of gastric mucosa. MTT measured proliferation of gastric mucosa tissue cells, while flow cytometry was used to measure apoptosis. ELISA was used to detect the levels of motilin and gastrin, while Immunoblotting was used to detect the protein expression of PKM2, Caspase-3, PI3K, and AKT. The gastric mucosal tissue in the healthy group was normal, and cells were arranged in orderly and complete manner. The gastric mucosal tissues from rats in the gastric cancer group and low-dose group were infiltrated with inflammatory cells, which were arranged in disorderly manner. The infiltration of gastric mucosal cells in the high-dose group and capecitabine group were reduced, and their arrangement was more orderly. Compared with gastric cancer group, cell proliferation decreased and apoptosis increased in the low-dose group (P <0.05). Compared with low-dose group, the highdose group decreased proliferation and increased apoptosis (P <0.05). In comparison with high-dose group, the capecitabine group had increased proliferation and decreased apoptosis (P < 0.05). In comparison with healthy group, PKM2, Caspase-3, PI3K, and AKT increased, and levels of motilin and gastrin 17 decreased (P <0.05). In comparison with gastric cancer group, the PKM2, Caspase-3, PI3K, and AKT in the low-dose group decreased, and levels of motilin and gastrin 17 increased (P <0.05). In comparison with low-dose group, PKM2, Caspase-3, PI3K, and AKT in the high-dose group decreased, while levels of motilin and gastrin 17 increased (P <0.05). In comparison with high-dose group, KM2, Caspase-3, PI3K, and AKT in the capecitabine group increased, and levels of motilin and gastrin 17 decreased (P <0.05). The hericium evimaccus alcohol extract inhibited the expression of PKM2 protein by promoting the level of gastrin 17, thereby inhibiting the proliferation of cancer cells and promoting apoptosis.
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Waldum, Helge, e Patricia Mjønes. "Towards Understanding of Gastric Cancer Based upon Physiological Role of Gastrin and ECL Cells". Cancers 12, n. 11 (22 novembre 2020): 3477. http://dx.doi.org/10.3390/cancers12113477.

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Abstract (sommario):
The stomach is an ideal organ to study because the gastric juice kills most of the swallowed microbes and, thus, creates rather similar milieu among individuals. Combined with a rather easy access to gastric juice, gastric physiology was among the first areas to be studied. During the last century, a rather complete understanding of the regulation of gastric acidity was obtained, establishing the central role of gastrin and the histamine producing enterochromaffin-like (ECL) cell. Similarly, the close connection between regulation of function and proliferation became evident, and, furthermore, that chronic overstimulation of a cell with the ability to proliferate, results in tumour formation. The ECL cell has long been acknowledged to give rise to neuroendocrine tumours (NETs), but not to play any role in carcinogenesis of gastric adenocarcinomas. However, when examining human gastric adenocarcinomas with the best methods presently available (immunohistochemistry with increased sensitivity and in-situ hybridization), it became clear that many of these cancers expressed neuroendocrine markers, suggesting that some of these tumours were of neuroendocrine, and more specifically, ECL cell origin. Thus, the ECL cell and its main regulator, gastrin, are central in human gastric carcinogenesis, which make new possibilities in prevention, prophylaxis, and treatment of this cancer.
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Kale, Rohit Pralhadrao. "Epidemiological review on Gastric cancer". IP International Journal of Comprehensive and Advanced Pharmacology 7, n. 3 (15 agosto 2022): 131–33. http://dx.doi.org/10.18231/j.ijcaap.2022.027.

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The mortality rate of the patients with gastric cancer is reduced dramatically from past few years. Still the gastric cancer the major concern that is in front of health care professionals and is the second leading cause of cancer death across the world. But the trend of infection and the severity of infection differ as per location and histology. While there has been a marked decline in distal, intestinal type gastric cancers, the incidence of proximal, diffuse gastric carcinoma has been increasing, particularly in the Western countries. The severities of gastric cancer infection also differ by change in geographical location, social and economic status of the respective race as well. The main risk factors for distal gastric cancer include Helicobacter pylori infection and dietary factors; whereas gastro esophageal reflux disease and obesity play important roles in the development of proximal stomach cancer. The main aim of this review is to determine the epidemiology of gastric cancer and to discuss about available strategies for its prevention.
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Kitamura, K., T. Yamaguchi, S. Nishida, K. Yamamoto, K. Okamoto, H. Taniguchi, A. Hagiwara, K. Sawai e T. Takahashi. "Early gastric cancer mimicking advanced gastric cancer". British Journal of Cancer 75, n. 12 (giugno 1997): 1769–73. http://dx.doi.org/10.1038/bjc.1997.301.

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Jose, Tom, Vivek Kaul, Truptesh Kothari, Shivangi Kothari e Aron Blecher. "When Is Gastric Cancer Not Gastric Cancer?" American Journal of Gastroenterology 110 (ottobre 2015): S499. http://dx.doi.org/10.14309/00000434-201510001-01145.

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Smith, Jill P., Hong Cao, Wenqiang Chen, Kanwal Mahmood, Teresa Phillips, Lynda Youngpeter Sutton e Allen Cato. "Role of an anti-gastrin vaccine (PAS) alone and in combination with a PD-1 antibody on growth and metastases of gastric cancer." Journal of Clinical Oncology 40, n. 4_suppl (1 febbraio 2022): 334. http://dx.doi.org/10.1200/jco.2022.40.4_suppl.334.

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334 Background: Gastric cancer is a leading cause of cancer-related deaths worldwide. Many of those with advanced gastric cancer are responsive to immune checkpoint antibody therapy, although the median survival even with these new agents is less than 12 months. The gastrointestinal peptide, gastrin, has been shown to stimulate growth of gastric cancer through the cholecystokinin-B receptor (CCK-BR) and the inhibition of gastrin’s action results in decreased growth. In the current investigation we studied the effects of a cancer vaccine, Polyclonal Antibody Stimulator (PAS) that targets the gastrin peptide on growth of gastric cancer in mice. Methods: RNA was extracted from NCC-S1 and YTN-16 murine gastric cancers and analyzed by qRT-PCR for gastrin, CCK-BR, and PD-L1 expression. YTN-16 (5x106) cells were injected subcutaneously in (N = 40) syngeneic female C57BL/6 mice. Mice were divided into 4 groups of equal tumor size and treated with PBS (control), PD-1 antibody (PD-1 Ab) 50 μg, PAS 250μg, or the combination of the PD-1 Ab and PAS given at one week after tumor inoculation (week 0) and at weeks 1, 3, and 6. A PAS booster was also given at week 9.Tumor growth rate was monitored weekly with calipers. At the end of treatment, tumors were excised, weighed and analyzed with Masson’s trichrome stain for fibrosis, and for Ki67, CD8 T-cells, and M2-polarized macrophages by immunohistochemistry. Metastases were counted and confirmed by histology. Results: Gastrin, CCK-BR, and PD-L1 expression were confirmed by qRT-PCR in the gastric cancer cells. PAS monotherapy (P = 0.023) or PAS in combination with PD-1 Ab (P = 0.0003) resulted in significantly slowed tumor growth and with no metastases observed. Tumor weights were 40-52% smaller in mice treated with PAS or the combination therapy compared to PBS or PD-1 Ab, respectively, but this difference did not reach significance (P = 0.09). PD-1 Ab monotherapy did not change tumor size compared to PBS-treated control mouse tumors. Ki67 staining was decreased by 62-67% and fibrosis staining was decreased by 51-61% in tumors of mice treated with PAS monotherapy or in combination with PD-1 Ab, respectively (P < 0.0001). PAS monotherapy resulted in a 4-fold increase of CD8+ T-cells and a 56% decrease in M2-polarized macrophages (P = 0.0001) compared to control tumors. PAS and PD-1 Ab combination therapy resulted in an additive effect with 29% more CD8+ T-cells (P < 0.05) and 54% fewer M2-polarized macrophages (P < 0.0001) compared to tumors of PAS monotherapy-treated mice. Conclusions: Treatment of mice with an anti-gastrin vaccine, PAS, slows growth of gastric cancer and prevents metastases. PAS vaccination improves the effectiveness of PD-1 Ab therapy in part by decreasing tumor fibrosis and altering the tumor immune cell signature. This study suggests that addition of PAS to immune checkpoint antibody therapy in gastric cancer may be beneficial.
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Seo, Ji Yeon, Eun Hyo Jin, Hyuk Yoon, Hyun Jin Jo, Cheol Min Shin, Young Soo Park, Nayoung Kim, Hyun Chae Jung e Dong Ho Lee. "Characteristics and prognosis of gastric cancer according to Helicobacter pylori." Journal of Clinical Oncology 33, n. 3_suppl (20 gennaio 2015): 14. http://dx.doi.org/10.1200/jco.2015.33.3_suppl.14.

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14 Background: Different features of gastric cancer according to Helicobacter pylori(Hp) infection is still under debate. The aim of this study was to compare clinical, pathologic characteristics and prognosis of gastric cancer between Hp-positive (HpP) and Hp-negative (HpN) gastric cancer. Methods: Patients diagnosed as gastric cancer in Seoul National University Bundang hospital from June 2003 to December 2010 were reviewed. Status of Hp was evaluated by histology and rapid urease test (RUT). Patients who had positive histology and/or positive RUT were classified as HpP. Patients who had atrophic gastritis and/or intestinal metaplasia from histology were also classified as HpP. Patients who had both negative histology and RUT were defined as HpN. Results: The number of patients with HpP and HpN were 852 (62.6%) and 509 (37.4%), respectively. Antral location was more common in gastric cancer with HpP than in those with HpN (51.8% vs 44.9%, P = 0.003). Stage of gastric cancer was higher in patients with HpN than in patients with HpP (stage IV 17.9% vs 9.6%, P < 0.001). Age, sex of patients and Lauren classification of gastric cancer was not different according to Hp status. Recurrence and mortality was significantly higher in patients with HpN gastric cancer than those in HpP gastric cancer (P = 0.002 and P= 0.001). Conclusions: Gastric cancers have different clinical and pathologic features according to the Hp status. Patients with HpN gastric cancers have poorer prognosis than those with HpC or HpP gastric cancers.
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Miura, Ko, Tadayuki Oshima, Akio Tamura, Ken Hara, Takuya Okugawa, Masashi Fukushima, Toshihiko Tomita, Hirokazu Fukui e Hiroto Miwa. "Gastric Xanthoma Is Related to the Rapid Growth of Gastric Cancer". Journal of Clinical Medicine 10, n. 23 (5 dicembre 2021): 5704. http://dx.doi.org/10.3390/jcm10235704.

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Early detection of gastric cancer is important. However, rapid growth of gastric cancers that cannot be resected endoscopically occurs even with periodic check-ups. Accordingly, we assessed factors associated with the speed of gastric cancer growth by examining historical endoscopic images. A total of 1996 gastric cancer cases were screened, and characteristics of lesions with slow and rapid growth were assessed. A total of 114 lesions from 114 patients were included in the assessment. Sixty slow-growing and fifty-four rapidly growing gastric cancers were compared. Female sex and incidence of lesions in the lower part of the stomach were significantly less frequent in the rapid-growth group than in the slow-growth group. History of endoscopic treatment tended to be more frequent in the rapid-growth group. Age, body mass index, histology, Helicobacter pylori status, and medications did not differ significantly between groups. Xanthoma was significantly related to rapid growth of gastric cancer, and map-like redness tended to be more frequent in the rapid-growth group in univariate analysis. Xanthoma was significantly related to rapid growth of gastric cancer on multivariate analysis. Further studies are warranted to clarify the pathophysiological mechanisms involved in the speed of gastric cancer growth.
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Wang, Sheng-Fan, Kuo-Hung Huang, Wei-Chuan Tseng, Jeng-Fan Lo, Anna Fen-Yau Li, Wen-Liang Fang, Chian-Feng Chen et al. "DNAJA3/Tid1 Is Required for Mitochondrial DNA Maintenance and Regulates Migration and Invasion of Human Gastric Cancer Cells". Cancers 12, n. 11 (20 novembre 2020): 3463. http://dx.doi.org/10.3390/cancers12113463.

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Background: Gastric cancer is a common health issue. Deregulated cellular energetics is regarded as a cancer hallmark and mitochondrial dysfunction might contribute to cancer progression. Tid1, a mitochondrial co-chaperone, may play a role as a tumor suppressor in various cancers, but the role of Tid1 in gastric cancers remains under investigated. Methods: The clinical TCGA online database and immunohistochemical staining for Tid1 expression in tumor samples of gastric cancer patients were analyzed. Tid1 knockdown by siRNA was applied to investigate the role of Tid1 in gastric cancer cells. Results: Low Tid1 protein-expressing gastric cancer patients had a poorer prognosis and higher lymph node invasion than high Tid1-expressing patients. Knockdown of Tid1 did not increase cell proliferation, colony/tumor sphere formation, or chemotherapy resistance in gastric cancer cells. However, Tid1 knockdown increased cell migration and invasion. Moreover, Tid1 knockdown reduced the mtDNA copy number of gastric cancer cells. In addition, the Tid1-galectin-7-MMP-9 axis might be associated with Tid1 knockdown–induced cell migration and invasion of gastric cancer cells. Conclusions: Tid1 is required for mtDNA maintenance and regulates migration and invasion of gastric cancer cells. Tid1 deletion may be a poor prognostic factor in gastric cancers and could be further investigated for development of gastric cancer treatments.
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Liu, Yan, Jihai Zhu, Jun Liu, Xueman Ma, Jun Zhao e Zhanhai Su. "Knockdown of Gastrin Promotes Apoptosis of Gastric Cancer Cells by Decreasing ROS Generation". BioMed Research International 2021 (14 aprile 2021): 1–12. http://dx.doi.org/10.1155/2021/5590037.

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Overexpressed gastrin is reported to promote oncogenesis and development of gastric cancer by inhibiting apoptosis of cancer cells; however, the underlying mechanism remains unclear. Our study is aimed at revealing the mechanism underlying the effect of gastrin on apoptosis of gastric cancer cells. Gastrin-interfering cell line was constructed by stably transfecting gastrin-specific pshRNA plasmid to gastric cancer cell line BGC-823. Then, differentially expressed proteins between untreated BGC-823 and gastrin-interfering BGC-823 cell lines were detected by the iTRAQ technique. GO and KEGG analysis was used to analyze the differentially expressed genes that code these differentially expressed proteins. The Annexin V-FITC staining assay was used to detect gastric cancer cell apoptosis. The DCFH-DA fluorescent probe staining assay was used to measure intracellular ROS. Mitochondrial membrane potential was detected by flow cytometry. Western blot was used to analyze the mitochondria respiratory chain proteins and apoptosis-related proteins. A total of 107 differentially expressed proteins were identified by iTRAQ. GO and KEGG analysis showed that proteins coded by the corresponding differentially expressed genes were mainly enriched in the mitochondrial oxidative respiratory chain, and the expression of three proteins (COX17, COX5B, ATP5J) was upregulated. The three proteins with higher scores were verified by Western blot. The apoptosis rate of the gastrin knockdown cancer cell was significantly increased; meanwhile, gastrin knockdown leads to increase of membrane potential and decrease of intracellular ROS production. Additionally, Bax was significantly increased, whereas NF-κB-p65 and Bcl-2 were downregulated after knockdown of gastrin. Concomitantly, pretreatment with NAC reversed the effect of gastrin on the Bax and Bcl-2 expression. Gastrin promotes the production of ROS from mitochondria, activates NF-κB, and inhibits apoptosis via modulating the expression level of Bcl-2 and Bax.
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Kim, Dae Hwan, Nari Shin, Gwang Ha Kim, Geum Am Song, Tae-Yong Jeon, Dong-Heon Kim, Gregory Y. Lauwers e Do Youn Park. "Mucin Expression in Gastric Cancer: Reappraisal of Its Clinicopathologic and Prognostic Significance". Archives of Pathology & Laboratory Medicine 137, n. 8 (1 agosto 2013): 1047–53. http://dx.doi.org/10.5858/arpa.2012-0193-oa.

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Context.—The clinical validity of mucin expression in gastric cancer is debated. Whereas several reports demonstrate a correlation between mucin expression and prognosis, others deny such an association. Objectives.—This survival analysis study aims to elucidate the prognostic significance of mucin expression in gastric cancer. Design.—A retrospective survival analysis was done with 412 cases of gastric cancer characterized on the basis of MUC immunohistochemistry using MUC2, MUC5AC, MUC6, and CD10 antibodies; the cases were divided into those with a gastric, an intestinal, or a null mucin phenotype based on the predominant mucin. Results.—There was no association between mucin expression and survival when considering overall gastric cancers or the advanced gastric cancer subtype. However, early gastric cancers with a gastric mucin phenotype showed longer survival than those with an intestinal mucin phenotype (P = .01) or a null phenotype (P = .01). In particular, MUC5AC-positive early gastric cancers resulted in longer survival than did those that did not express MUC5AC (P = .009). The loss of MUC5AC expression was identified as an independent, poor prognostic factor in early gastric cancers using the Cox regression proportional hazard model (hazard ratio, 3.50; P = .045). Conclusions.—MUC5AC expression is significantly associated with patient survival and can be used to predict outcomes in the gastric cancers, especially in the early gastric cancers.
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Saito, Shin, Yoshinori Hosoya, Takashi Ui, Joji Kitayama, Rihito Kanamaru, Hidenori Haruta, Kentaro Kurashina, Shiro Matsumoto, Naohiro Sata e Alan Lefor. "PS02.150: SEVEN PATIENTS WITH GASTRIC-TUBE CANCER AFTER ESOPHAGECTOMY". Diseases of the Esophagus 31, Supplement_1 (1 settembre 2018): 163–64. http://dx.doi.org/10.1093/dote/doy089.ps02.150.

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Abstract Background The prolonged survival of patients receiving surgery for esophageal cancer has led to an increased incidence of adenocarcinoma arising in the gastric tube used for reconstruction (gastric tube cancer). The incidence of gastric tube cancer after esophagectomy has been reported to be 1.3–6.3% in Japan. Patients with early stage gastric tube cancer can be treated by endoscopic resection, however patients with advanced gastric tube cancer need to undergo the resection of the gastric tube. Methods A total of 497 patients underwent esophagectomy with gastric tube reconstruction between 2001 and 2015 at our institution. During the same period, gastric tube cancer was detected in seven patients including three by endoscopic submucosal dissection (ESD) and three by surgery. We investigated the clinicopathological study of these seven patient with gastric tube cancer. Results The incidence of gastric tube cancer was 1.4% (7/497) at our hospital. Average age was 73 years old (range, 62–84). Six patients were men and one was women. Average interval from esophagectomy to initial treatment was 78.3 ± 61.0 (months). Among seven patients with gastic tube cancer, three were treated by ESD and 3 underwent surgery. One patient went to a palliative therapy. All seven patient with gastric tube cancer, who didn’t have specific complains, were detected by regular upper gastrointestinal endoscopy. We observed a very high proportion of patients with H. pylori infection (at least five patients among seven). Conclusion ESD for gastric tube cancer after esophagectomy is a technically difficult procedure because of the limited working space and unusual fluid-pooling area in the reconstructed gastrictube as well as the presence of severe gastric fibrosis with staples under the suture line. A highly skilled endoscopist can perform the procedure successfully. An operative technique for the resection of gastric tube cancer by means of lifting the anterior chest wall and video scope-assisted surgery enabled the resection of gastric tube without performing a sternotomy. Disclosure All authors have declared no conflicts of interest.
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Ebert, Matthias P. A., Jun Yu, Juliane Hoffmann, Alba Rocco, Christoph Röcken, Sabine Kahmann, Oliver Müller, Murray Korc, Joseph J. Sung e Peter Malfertheiner. "Loss of Beta-Catenin Expression in Metastatic Gastric Cancer". Journal of Clinical Oncology 21, n. 9 (1 maggio 2003): 1708–14. http://dx.doi.org/10.1200/jco.2003.10.017.

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Purpose: Beta-catenin (β-catenin) participates in intercellular adhesion and is an integral part of the Wnt signaling pathway. The role of β-catenin in the pathogenesis of gastric cancer and its metastasis is largely unknown. Patients and Methods: Immunohistochemistry and Western blot analysis were used to analyze the expression of β-catenin in 87 human gastric cancers, in metastasis and cancer cell lines. The β-catenin and the adenomatous polyposis coli (APC) genes were analyzed for gene mutations. Furthermore, methylation of the β-catenin promoter in cell lines was assessed by treatment with 5′-azadeoxycytidine and sodium bisulfite genomic sequencing. Results: β-Catenin expression was present at either the cell membrane or the cytoplasm in 34 of 75 primary gastric cancers. Expression of β-catenin was significantly more frequent in intestinal-type (P = .0049) and well-differentiated gastric cancers (P < .001). There were no quantitative differences between gastric cancers and the nonmalignant gastric tissues, as determined by Western blot analysis. One of 18 metastatic cancer lesions and four of five gastric cancer cell lines expressed β-catenin protein. N87 cells, derived from the liver metastasis of a gastric cancer, did not express β-catenin. Treatment with 5′-azadeoxycytidine restored β-catenin protein levels in this cell line, which exhibited significantly more 5-methylcytosines in the β-catenin promoter compared with the other cell lines. Conclusion: β-Catenin expression is lost in a subgroup of primary gastric cancers, is frequently absent in metastases, and exhibits nuclear localization in cancers with either β-catenin or APC gene mutations. Interestingly, the loss of β-catenin expression in metastatic gastric cancers may result from hypermethylation of the β-catenin promoter.
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Xicola, Rosa M., Shuwei Li, Nicolette Rodriguez, Patrick Reinecke, Rachid Karam, Virginia Speare, Mary Helen Black, Holly LaDuca e Xavier Llor. "Clinical features and cancer risk in families with pathogenic CDH1 variants irrespective of clinical criteria". Journal of Medical Genetics 56, n. 12 (11 luglio 2019): 838–43. http://dx.doi.org/10.1136/jmedgenet-2019-105991.

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BackgroundThe clinical phenotype of CDH1 pathogenic variant carriers has mostly been studied in families that fulfil criteria of hereditary diffuse gastric cancer (HDGC). We aimed at determining cancer phenotype and cancer risk estimation among families with CDH1 pathogenic variants not selected by HDGC clinical criteria.MethodsPatients were all consecutively identified CDH1 pathogenic variant carriers from a clinical laboratory tested with multigene panel testing and from an academic cancer genetics programme. Clinical and demographic features, cancer phenotypes and genotype–phenotype correlations were determined among CDH1 families. Age-specific cumulative cancer risks (penetrance) were calculated based on 38 families with available pedigrees.ResultsWithin the 113 CDH1 pathogenic variant probands and 476 relatives, 113 had gastric cancer, 177 breast cancer and 196 other cancers. Mean age at diagnosis was 47 for gastric and 54 for breast cancer. Forty-six per cent fulfilled criteria of HDGC. While 36% of families had both gastric and breast cancers, 36% had breast but no gastric cancers and 16% had gastric but not breast cancers. Cumulative risk of cancer by age 80 was 37.2% for gastric and 42.9% for breast cancer.ConclusionIn unselected CDH1 pathogenic variant carrier families, gastric cancer risks were lower and age at diagnosis higher than previously reported in families pre-selected for HDGC criteria. A substantial proportion of families did not present with any gastric cancers and their cancers were limited to breast. Thus, clinical criteria for CDH1 testing should be widened, including breast cancer families only, and a consideration for delayed prophylactic gastrectomy/surveillance should be evaluated.
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Wilkinson, N. W., J. Howe, L. Patel-Parekh, B. Smith, C. Scott-Conner e J. Donohue. "Differences in the patterns of presentation and treatment between proximal and distal gastric cancers". Journal of Clinical Oncology 24, n. 18_suppl (20 giugno 2006): 4022. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.4022.

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4022 Background: While the overall incidence of gastric cancer has declined in the United States, the incidence of proximal gastric cancers has increased. Understanding the differences between proximal and distal gastric cancer, may enable us to identify important risk factors and treatment patterns. Methods: Data on 6099 patients diagnosed with gastric adenocarcinoma were collected as a Patient Care Evaluation under the auspices of the American College of Surgeons Commission on Cancer. Clearly defined proximal and distal cancers were compared using the Pearson chi-square test and logistic regression. Results: The proximal cancer group included 1924 patients (87% cardia; 13% fundus) and the distal cancer group included 1312 patients (85% antrum; 15% pylorus). Proximal gastric cancers occurred more often in men (p<0.0001), whites (compared to Black, Hispanic, Native American and Asian races) (p<0.0001), and at younger age (p<0.0001) compared to distal cancers. Risk factors for proximal presentation included tobacco use (Hazard ratio (HR) 1.9, p= 0.002) alchohol use (HR 1.5, p= 0.038) and Barretts (HR 2.7, p<0.0001). Risk factors for distal presentation included H. Pylori (HR 2.3, p= 0.001). Despite increased use of multi-modality therapy, fewer proximal gastric cancers underwent resection compared to distal cancers (p<0.0001). Conclusions: Different risk factors can be identified for proximal and distal gastric cancers, which can impact on risk reduction, screening efforts and help define the pathogenesis of gastric cancer. While proximal cancer patients receive more aggressive multimodality treatments, including adjuvant and neoadjuvant therapy, fewer undergo surgical resection. Long term survival based upon proximal and distal tumor differences will be explored when follow-up data become available.Key Words: gastric adenocarcinoma, proximal gastric cancer, distal gastric cancer, risk factors, treatment. [Table: see text] No significant financial relationships to disclose.
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Hur, Chin. "Gastric Cancer:". Gastrointestinal Endoscopy Clinics of North America 31, n. 3 (luglio 2021): xv—xviii. http://dx.doi.org/10.1016/j.giec.2021.04.002.

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HUR, CHIN. "Gastric Cancer". Gastrointestinal Endoscopy Clinics of North America 31, n. 3 (luglio 2021): i. http://dx.doi.org/10.1016/s1052-5157(21)00039-8.

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Ajani, Jaffer A., James S. Barthel, Tanios Bekaii-Saab, David J. Bentrem, Thomas A. D'Amico, Prajnan Das, Crystal Denlinger et al. "Gastric Cancer". Journal of the National Comprehensive Cancer Network 8, n. 4 (aprile 2010): 378–409. http://dx.doi.org/10.6004/jnccn.2010.0030.

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Latif, Alaa. "Gastric cancer". Postgraduate Medicine 102, n. 4 (ottobre 1997): 231–41. http://dx.doi.org/10.3810/pgm.1997.10.343.

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Gore, Richard M. "GASTRIC CANCER". Radiologic Clinics of North America 35, n. 2 (marzo 1997): 295–310. http://dx.doi.org/10.1016/s0033-8389(22)00709-6.

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Gore, Richard M., Marc S. Levine, Gary G. Ghahremani e Frank H. Miller. "GASTRIC CANCER". Radiologic Clinics of North America 35, n. 2 (marzo 1997): 311–29. http://dx.doi.org/10.1016/s0033-8389(22)00710-2.

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Miller, Frank H., Michael L. Kochman, Mark S. Talamonti, Gary G. Ghahremani e Richard M. Gore. "GASTRIC CANCER". Radiologic Clinics of North America 35, n. 2 (marzo 1997): 331–49. http://dx.doi.org/10.1016/s0033-8389(22)00711-4.

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Norwood, Dalton A., Eleazar E. Montalvan, Ricardo L. Dominguez e Douglas R. Morgan. "Gastric Cancer". Gastroenterology Clinics of North America 51, n. 3 (settembre 2022): 501–18. http://dx.doi.org/10.1016/j.gtc.2022.05.001.

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Lawrence, W. "Gastric Cancer". CA: A Cancer Journal for Clinicians 36, n. 4 (1 luglio 1986): 216–36. http://dx.doi.org/10.3322/canjclin.36.4.216.

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Carlson, Robert H. "Gastric Cancer". Oncology Times 36, n. 16 (agosto 2014): 20–21. http://dx.doi.org/10.1097/01.cot.0000453662.42790.6a.

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Carlson, Robert H. "Gastric Cancer". Oncology Times 36, n. 17 (settembre 2014): 58–59. http://dx.doi.org/10.1097/01.cot.0000454167.88634.f9.

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Carlson, Robert H. "Gastric Cancer". Oncology Times 29, n. 3 (febbraio 2007): 28. http://dx.doi.org/10.1097/01.cot.0000266373.45591.5c.

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Susman, Ed. "Gastric Cancer". Oncology Times 26, n. 5 (marzo 2004): 15. http://dx.doi.org/10.1097/01.cot.0000291491.09483.4e.

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Susman, Ed. "Gastric Cancer". Oncology Times 26, n. 5 (marzo 2004): 58–60. http://dx.doi.org/10.1097/01.cot.0000291506.16214.a3.

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Mann, G. Bruce. "Gastric cancer". ANZ Journal of Surgery 74, n. 10 (ottobre 2004): 827–28. http://dx.doi.org/10.1111/j.1445-1433.2004.03240.x.

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