Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypoxia-inducible factors (HIFs) are transcription factors that activate the transcription of target genes involved in crucial aspects of cancer development. This study investigated the expression of HIFs and their contribution to the regulation of target genes related to angiogenesis and glucose metabolism in gastric cancer. The data showed that HIFs were over-expressed in gastric cancer and that activation of the target genes was observed mainly in the early stages. Moreover, the results of the present study revealed that only HIF-1alpha, but not HIF-2alpha dimerizes with HIF-1beta and then regulates expression of target genes in response to hypoxia. The results of the present study demonstrate that HIF-1alpha and HIF-1beta enhances expression of VEGF and glucose metabolism-related genes in response to hypoxia in gastric cancer. These data offer important information regarding HIF pathways in the development of gastric cancer.
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PMID:Regulation of glucose metabolism-related genes and VEGF by HIF-1alpha and HIF-1beta, but not HIF-2alpha, in gastric cancer. 1928

The patient was a 67-year-old man under follow-up after gastric cancer surgery. An abdominal CT scan performed 1 year earlier had shown an approximately 14-mm hypovascular mass in the pancreatic body; however, he did not consent to treatment and was followed up for 1 year. A blood workup showed that the fasting blood glucose level, which had been within normal limits, was elevated to 174 mg/dl (normal, 70-109 mg/dl), and the HbA1c level was 12.0% (normal, 4.3-5.8%). Abdominal CT revealed an approximately 20-mm mass in the pancreatic body and an approximately 12-mm mass in the pancreatic tail, and magnetic resonance imaging cholangiopancreatography (MRCP) showed discontinuity of the main pancreatic duct (MPD). Since these findings led to the suspicion of invasive ductal carcinoma (IDC) of the pancreas developing in the pancreatic body and tail, we performed distal pancreatectomy with splenectomy. Histologically, IDCs were observed in the pancreatic body and tail. However, PanIN was not observed in the MPD between the two carcinomas. They were diagnosed as independent invasive ductal carcinomas of the pancreas.
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PMID:Multi-centric pancreatic cancer without PanIN lesion. 1933 39

Noninvasive tumor imaging could lead to the early detection and timely treatment of cancer. Optical coherence tomography (OCT) has been reported as an ideal diagnostic tool for distinguishing tumor tissues from normal tissues based on structural imaging. In this study, the capability of OCT for functional imaging of normal and tumor tissues based on time- and depth-resolved quantification of the permeability of biomolecules through these tissues is investigated. The orthotopic graft model of gastric cancer in nude mice is used, normal and tumor tissues from the gastric wall are imaged, and a diffusion of 20% aqueous solution of glucose in normal stomach tissues and gastric tumor tissues is monitored and quantified as a function of time and tissue depth by an OCT system. Our results show that the permeability coefficient is (0.94+/-0.04)x10(-5) cms in stomach tissues and (5.32+/-0.17)x10(-5) cms in tumor tissues, respectively, and that tumor tissues have a higher permeability coefficient compared to normal tissues in optical coherence tomographic images. From the results, it is found that the accurate and sensitive assessment of the permeability coefficients of normal and tumor tissues offers an effective OCT image method for detection of tumor tissues and clinical diagnosis.
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PMID:Application of hyperosmotic agent to determine gastric cancer with optical coherence tomography ex vivo in mice. 1940 58

Focal gastrointestinal 2-deoxy-2-[(18)F]-fluoro-D: -glucose (FDG) uptake can frequently be found on FDG-PET/CT even in patients without known gastrointestinal malignancy. The aim of this study was to evaluate whether increased gastrointestinal FDG uptake without CT correlate is an early indicator of patients developing gastrointestinal malignancies. A total of 1,006 patients without esophagogastric or anorectal malignancies underwent FDG-PET/CT. The esophagogastric junction, the stomach and the anorectum were evaluated for increased FDG uptake. Patients without elevated uptake were assigned to group A, patients with elevated uptake were allocated to group B. The SUVmax values of both groups were tested for significant differences using the U test. A follow-up of longer than 1 year (mean 853 +/- 414 days) served as gold standard. A total of 460 patients had to be excluded based on insufficient follow-up data. For the remaining 546 patients the mean SUVmax was as follows: (a) esophagogastric junction, group A 3.1 +/- 0.66, group B 4.0 +/- 1.11, p < 0.01; (b) stomach, group A 2.8 +/- 0.77, group B 4.1 +/- 1.33, p < 0.01; (c) rectal ampulla, group A 2.8 +/- 0.83, group B 3.9 +/- 1.49, p < 0.01; (d) anal canal, group A 2.7 +/- 0.55, group B 3.9 +/- 1.59, p < 0.01. Only one patient developed gastric cancer. In the case of an unremarkable CT, elevated esophagogastric or anorectal FDG uptake does not predict cancer development and does not have to be investigated further.
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PMID:Gastrointestinal 18F-FDG accumulation on PET without a corresponding CT abnormality is not an early indicator of cancer development. 1941 94

In 2005, a Japanese epidemiological study showed that increase in plasma glucose levels is a risk factor for gastric cancer. However, no animal model has hitherto shown any association between diabetes mellitus and neoplasia in the stomach. Diabetic (db/db) mice have obese and diabetic phenotypes, including hyperglycemia, because of disruption of the leptin receptor. In the present study, effects of hyperglycemia and/or hyperinsulinemia on the development of proliferative lesions were therefore examined in db/db mice given N-methyl-N-nitrosourea (MNU). A total of 120 mice were assigned to four groups: Group A, 40 db/db mice with MNU; Group B, 40 + /db mice with MNU; Group C, 30 misty (wild-type) mice with MNU; Group D, 10 db/db mice without MNU. MNU was given at 60 ppm in drinking water for 20 weeks. Subgroups of animals were sacrificed at weeks 21 and 30 and blood samples were collected to measure glucose, insulin, leptin, and adiponectin concentrations. The removed stomachs were fixed in formalin, and embedded in paraffin for histological examination and immunohistochemistry. At week 30 in Groups A, B, C and D, hyperplasia was observed in 100, 79, 57, and 0%, and dysplasia in 91, 43, 71, and 0%, respectively. Adenocarcinomas and pepsinogen-altered pyloric glands (PAPG), putative preneoplastic lesions, were observed only in Group A, at an incidence of 45%. The serum levels of insulin and leptin were also elevated in Group A. Gastric carcinogenesis by MNU was enhanced in db/db mice, possibly in association with hyperinsulinemia and hyperleptinemia.
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PMID:Gastric carcinogenesis by N-Methyl-N-nitrosourea is enhanced in db/db diabetic mice. 1943 3

Most cancer cells predominantly produce energy by glycolysis rather than oxidative phosphorylation via the tricarboxylic acid (TCA) cycle, even in the presence of an adequate oxygen supply (Warburg effect). However, little has been reported regarding the direct measurements of global metabolites in clinical tumor tissues. Here, we applied capillary electrophoresis time-of-flight mass spectrometry, which enables comprehensive and quantitative analysis of charged metabolites, to simultaneously measure their levels in tumor and grossly normal tissues obtained from 16 colon and 12 stomach cancer patients. Quantification of 94 metabolites in colon and 95 metabolites in stomach involved in glycolysis, the pentose phosphate pathway, the TCA and urea cycles, and amino acid and nucleotide metabolisms resulted in the identification of several cancer-specific metabolic traits. Extremely low glucose and high lactate and glycolytic intermediate concentrations were found in both colon and stomach tumor tissues, which indicated enhanced glycolysis and thus confirmed the Warburg effect. Significant accumulation of all amino acids except glutamine in the tumors implied autophagic degradation of proteins and active glutamine breakdown for energy production, i.e., glutaminolysis. In addition, significant organ-specific differences were found in the levels of TCA cycle intermediates, which reflected the dependency of each tissue on aerobic respiration according to oxygen availability. The results uncovered unexpectedly poor nutritional conditions in the actual tumor microenvironment and showed that capillary electrophoresis coupled to mass spectrometry-based metabolomics, which is capable of quantifying the levels of energy metabolites in tissues, could be a powerful tool for the development of novel anticancer agents that target cancer-specific metabolism.
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PMID:Quantitative metabolome profiling of colon and stomach cancer microenvironment by capillary electrophoresis time-of-flight mass spectrometry. 1945 66

Two new complexes ZnL(2)x2H(2)O (1) and CuL(2)x2H(2)O (2) (HL=1-hydroxy-6-(2-(1-piperidinyl)ethoxy)xanthone) have been synthesized and characterized. Their interactions with calf thymus DNA (ct DNA) were investigated by absorption spectroscopy, fluorescence spectroscopy, ethidium bromide (EB) displacement experiments, circular dichroism spectroscopy and viscosity measurements. Experimental results suggested that there were intercalative interactions of the complexes with DNA. The binding affinity of complex 2 was higher than that of 1. In addition, the cytotoxic effects of both complexes were evaluated with lung adenocarcinoma (GLC-82), esophagus squamous cancer (ECA109) and human gastric cancer (SGC7901) cells using MTT assay. Both were potent exhibiting significant cytotoxicity in vitro.
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PMID:Synthesis and characterization of the Zn(II) and Cu(II) piperidinyl isoeuxanthone complexes: DNA-binding and cytotoxic activity. 1960 5

In cancer cells, glucose is often converted into lactic acid, which is known as the 'Warburg effect'. The reason that cancer cells have a higher rate of aerobic glycolysis, but not oxidative phosphorylation, remains largely unclear. Herein, we proposed an epigenetic mechanism of the Warburg effect. Fructose-1,6-bisphosphatase-1 (FBP1), which functions to antagonize glycolysis was downregulated through NF-kappaB pathway in Ras-transformed NIH3T3 cells. Restoration of FBP1 expression suppressed anchorage-independent growth, indicating the relevance of FBP1 downregulation in carcinogenesis. Indeed, FBP1 was downregulated in gastric carcinomas (P<0.01, n=22) and gastric cancer cell lines (57%, 4/7). Restoration of FBP1 expression reduced growth and glycolysis in gastric cancer cells. Moreover, FBP1 downregulation was reversed by pharmacological demethylation. Its promoter was hypermethylated in gastric cancer cell lines (57%, 4/7) and gastric carcinomas (33%, 33/101). Inhibition of NF-kappaB restored FBP1 expression, partially through demethylation of FBP1 promoter. Notably, Cox regression analysis revealed FBP1 promoter methylation as an independent prognosis predicator for gastric cancer (hazard ratio: 3.60, P=0.010). In summary, we found that NF-kappaB functions downstream of Ras to promote epigenetic downregulation of FBP1. Promoter methylation of FBP1 can be used as a new biomarker for prognosis prediction of gastric cancer. Such an important epigenetic link between glycolysis and carcinogenesis partly explains the Warburg effect.
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PMID:Warburg effect revisited: an epigenetic link between glycolysis and gastric carcinogenesis. 1988 51

Change in glucose metabolism after bariatric operations may be credited to duodenal bypass. This study aims to evaluate the effect of duodenal bypass on glucose levels in lean individuals submitted to gastrectomy for gastric cancer. We reviewed 56 non-diabetic and 6 diabetic patients submitted to gastrectomy and Roux-en-Y for gastric cancer (partial gastrectomy in 66%/total gastrectomy in 34%). Glucose levels were not significantly altered after operation (P = 0.5). Diabetes control was improved in one patient with oral medication. In conclusion, duodenal bypass do not decrease glucose levels in lean individuals treated for gastric cancer.
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PMID:Duodenal bypass does not decrease glucose levels of lean individuals with gastric cancer submitted to partial or total gastrectomy. 1991 92

Adiponectin is a peptide hormone secreted from the adipose tissue, affecting the proliferation and insulin sensitivity in different cell types. The levels of adiponectin have been found to be decreased in hyperinsulinemia and insulin resistant states, such as obesity. The previous studies have suggested that plasma adiponectin levels are decreased in patients with endometrial and breast cancer. In our study, the relationship among serum adiponectin levels, demographic features and histopathological variables was evaluated in gastric cancer patients. Forty consecutive patients with gastric cancer who underwent gastrectomy with standard lymph node dissection were included and 43 healthy controls were included in this study. The serum levels of glucose, insulin, C-peptide, HbA1c and adiponectin were measured in both groups. We analyzed the correlation among these parameters and patients' demographic features, such as age, gender, body mass index (BMI) and histopathological variables such as tumor localization, stage, nodal status, histological grade, vascular and lymphatic invasion. The mean age was 60.05+9.72 in patients, while it was 38.6+12.73 in controls. The mean serum adiponectin levels were 12.62+7.9 and 10.07+6.72 ng/ml, respectively, in groups. There was no different in terms of adiponectin, C-peptide, HOMA-R level in both groups. On the other hand, BMI, glucose and insulin levels were significantly different in gastric cancer patients in comparison with the controls. There was no correlation among the levels of adiponectin, BMI, insulin and c-peptide levels in patient group (P>0.05). The adiponectin levels of woman were significantly lower than male patients (P=0.002). No relations were detected among tumor stage, tumor localization, nodal status, lymphatic and vascular invasion, and the levels of serum adiponectin (P>0.05). Interestingly, a positive correlation was found between tumor grade and plasma adiponectin levels (r=0.372; P=0.018). Our results suggest that plasma adiponectin levels were similar in both patients with gastric cancer and the controls. In addition, no correlation was found between adiponectin levels and demographic features and histopathological variables of patients. But, in undifferentiated tumors, plasma adiponectin level was significantly higher than well-differentiated grade tumors.
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PMID:The association of serum adiponectin levels with histopathological variables in gastric cancer patients. 2001 20


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