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)

Erythromycin has recently been shown to exert a great effect on gastroduodenal motor activity. This prokinetic action may be clinically useful in patients with gastrointestinal hypomotility such as diabetic or postsurgical gastroparesis. The case of a diabetic patient who underwent antrectomy Billroth II for gastric cancer is presented. Severe gastroparesis appeared after surgery and nasogastric aspiration could not be removed, although the patient was treated with metoclopramide, and glucose levels, hydroelectrolytic balance and nutritional status were corrected. Forty-one days after the first operation, a second gastrectomy with Bilroth II reconstruction was performed because of supposed anastomotic narrowing, which was not confirmed at surgery. Fourteen days later, i.v. erythromycin (200 mg/4h) was started owing to gastroparesis persistence. Six days after treatment the patient tolerated oral ingestion. Prokinetic drugs constitute the specific therapy for gastroparesis. Metoclopramide is the most used, although its efficacy is limited. In the last few years, erythromycin has proved to have a powerful effect on gastroduodenal motility. This effect is mediated, at least in part, by its motilin stimulating activity accelerating gastric emptying. Our patient completely recovered from gastroparesis after erythromycin treatment. Recent results of erythromycin therapy in these patients have been promising, despite the difficult management involved.
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PMID:[Usefulness of erythromycin in severe postoperative gastroparesis]. 776 43

A gastric cancer with liver metastases was associated with low morning levels of plasma glucose (24 mg/dl), insulin (< 2.5 microU/ml) and growth hormone (0.23 ng/ml). Primary and metastatic tumour tissue stained positively with anti-insulin-like growth factor II (IGF-II) monoclonal antibody. Western immunoblot analysis revealed a high molecular weight IGF-II in the serum: 15 kDa (normal: 7.5 kDa). Postmortem reverse transcription polymerase chain reaction on mRNA from both sites revealed 471 base pairs size cDNA encoding prepro-IGF-II. These results suggest that the gastric carcinoma encoded, expressed, and secreted IGF-II, probably causing the extrapancreatic tumour hypoglycaemia.
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PMID:Expression of insulin-like growth factor II by a gastric carcinoma associated with hypoglycaemia. 820 58

We have developed a chemosensitivity assay of human tumors growing on collagen-sponge-gel-supported histoculture. This assay is thus termed the Histoculture Drug Response Assay (HDRA). In the HDRA, the end points of [3H]thymidine incorporation measured by histological autoradiography and tetrazolium dye reduction were initially used and found to have good in vitro-in vivo correlations, including that determined in clinical trials. We have now developed glucose consumption as an endpoint in histoculture. We have monitored glucose consumption for 11 weeks with histocultured stomach cancer tissue that was obtained from a patient with stomach cancer metastatic to the lymph node. The histocultured lymph node specimens were treated with various concentrations of doxorubicin and cisplatinum. The glucose-consumption rate decreased with greater concentrations of both drugs. The results correlated with the thymidine labeling index. From these results, we conclude that the glucose-consumption-rate endpoint in histocultured cancer tissue is non-destructive, unlike the [3H]thymidine and tetrazolium dye end points, allowing serial determinations over extended periods in culture. Thus, the glucose consumption end point may enhance the development of optimal treatment doses and schedules. We also conclude that long-term histoculture drug response studies of metastatic stomach cancer are possible.
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PMID:The measurement of glucose consumption in histoculture to determine effects of doxorubicin and cisplatinum on human gastric carcinoma. 823

We report a 91-year-old man who had a stroke and died of renal failure. He had been treated for hypertension since 20 years before the onset of the present illness. In addition, he was operated on a gastric cancer 17 years previously. Otherwise he was doing well until May 29, 1991 (when he was 87-year-old) when he had sudden onset of dysarthria and right facial weakness. He was admitted to our hospital. On admission, general physical examination was unremarkable, and neurologic examination revealed a mentally sound man with slight dysarthria, right facial weakness, orolingual dyskinesia, and dysequilibrium in which he showed difficulty in tandem gait; however, no cerebellar ataxia was noted. A cranial CT scan revealed leukoaraiosis with multiple low density areas in the cerebral white matter. His BUN was 37 mg/dl and Cr 2.2 mg/dl. His neurologic symptoms cleared within the next few weeks and he was discharged with ticlopidine 100 mg q.d.. He had been doing well after the discharge except for gradual worsening of his renal function; his BUN was 65 mg/dl and Cr 3.27 mg/dl in April of 1994. On March 10, 1995, he fell down and hit his back; he became unable to walk because of pain, and he was admitted again on March 16, 1995. On admission, his blood pressure was 170/80 mmHg. There was an 1 + pitting pretibial edema; otherwise general physical examination was unremarkable. Neurologic examination revealed an alert and oriented man, however, Hasegawa's dementia scale was 23/30. Higher cerebral functions as well as cranial nerves were intact. He showed some unsteadiness of gait, however, no motor weakness or ataxia was noted. Deep tendon reflexes were diminished, but Chaddock sign was positive bilaterally. Vibration was diminished in the feet, however, pain and touch sensations were intact. Laboratory examination revealed a compression fracture of the twelfth thoracic vertebra. Blood count and chemistries were as follows; Hb 7.6 g/dl, Hct 23.3%, TP 6.0 g/dl, Alb 3.6 g/dl, BUN 87 mg/dl, Cr 4.53 mg/dl, T-Chol 174 mg/dl, HDL-Chol 49 mg/dl, Glu 156 mg/dl, Na 142 mEq/L, K 5.4 mEq/L, Cl 115 mEq/L. A urine specimen contained 1 + protein and 1 + glucose, and the sediments contained hyaline casts. A cranial CT scan was essentially same as that taken four years ago. His hospital course was complicated with pneumonia, congestive heart failure, and progressive renal failure. He was treated with intravenous fluid, chemotherapy, and other supportive measures, however, he expired from respiratory failure on April 30, 1995. He was discussed in a neurologic CPC, and the chief discussant arrived at the conclusion that the patient had Binswanger's disease in the brain, benign nephrosclerosis from arteriolosclerosis due to hypertension, congestive heart failure, and pneumonia. Opinions were divided regarding the question as to whether or not this patient had Binswanger's disease. Although his cranial CT scan revealed leukoaraiosis, his dementia and gait disturbance was only mild until his fall on March, 1995. Clinical features did not conform to those of Binswanger's disease. Postmortem examination of the right hemisphere revealed wide spread atherosclerosis and arteriolosclerosis. The kidney showed benign nephrosclerosis due to arteriolosclerosis. Sclerotic changes were also seen in the coronary arteries and the left middle cerebral artery with 70% stenosis. Myelin stain showed diffuse myelin pallor of the cerebral white matters with scattered small infarcts. Arterioles in the white matter showed arteriolosclerosis. Small infarcts were also seen in the putamen and in the thalamus. This patient appeared to have had circulatory disturbance of the white matter which is the basic abnormality causing Binswanger's disease. However, white matter changes in this patient were not quite severe enough to make a pathologic diagnosis of Binswanger's disease.
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PMID:[A 91-year-old man with a stroke, hypertension, and renal failure]. 899 Apr 84

Cisplatinum is currently used as a front line agent in many important tumors, but its dose-limiting nephrotoxicity prevents potential efficacy. There is therefore great interest in developing new platinum agents that have less toxicity. We have synthesized new platinum analogues containing DACH as a carrier ligand and DPPE as a leaving group. Previously we showed that these new platinum complexes have much less nephrotoxicity than cisplatinum. In the present study, the efficacy of one new platinum complex was evaluated with human patient bladder tumor specimens in three-dimensional histoculture as well as with monolayer cultures of cancer cell lines. The efficacy end points used were glucose consumption and thymidine incorporation on the histocultured specimens and MTT reduction on monolayer cell cultures. Our results showed that the new platinum complex was more effective at high concentration (10(-3) M) but less effective at low concentration (10(-4) M) compared to cisplatinum on histocultured bladder tumor specimens. The compound demonstrated higher efficacy than cisplatinum on P-388, and L-1210 leukemic cell lines. The new analog demonstrated similar efficacy to cisplatinum on the MKN-45 human stomach cancer cell line. The PC-14 human lung cancer cell line, MH1C1 rat hepatoma cell line, NIH-OV3, SKOV-3 ovarian cancer cell lines were as sensitive to the new analog as to cisplatinum at high concentrations of the new platinum analogue. The cisplatinum-resistant M-14 melanoma cell line was not sensitive to either the new analog or cisplatinum. Based on these results, this novel platinum compound appears to be a valuable lead compound with high efficacy and low nephrotoxicity.
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PMID:Efficacy of the platinum analog [Pt(cis-dach)(DPPE)-2NO3] on histocultured human patient bladder tumors and cancer cell lines. 904 1

We report a 64-year-old woman who developed nausea, headache, and consciousness disturbance. She was well until four years before the onset of her neurologic illness when (April of 1990 at her 59 years of the age) she was found to have an early cancer in her anterior wall of the lower stomach. Subtotal gastrectomy was performed and the operative result was reported as curative. Four years after the surgery (December of 1994 at her 64 years of the age), she noted suboccipital headache and nausea which had become progressively worse and she was admitted to our service on May 24, 1995. On admission, she appeared chronically ill but general physical examination was unremarkable with normal vital signs. Neurologically she was alert and not demented, and the higher cerebral functions were intact. Cranial nerves were also unremarkable. She was able to walk in tandem and on heels. No motor weakness or ataxia was noted. Deep tendon reflexes were moderately increased, however, no Babinski sign was noted. Although she had headache, no meningeal signs were seen. Slight superficial and vibratory sensory loss was noted in both feet. Routine blood work was again unremarkable except for slight increase in CEA to 8.3 ng/dl (N < 5 ng/dl). The opening pressure of lumbar CSF was 180 mm H2O and the CSF contained 39 cells/microliter, 79 mg of protein, and 10 mg/dl of glucose. Approximately half of the cells were atypical malignant cells. Plain CT was unremarkable, however, tentorial border showed enhancement after contrast infusion. FGS showed no malignant tumors in the stomach. She was treated with intravenous glycerol and whole brain radiation, however, she continued to complain of severe headache, and her sensorium started to be disturbed one month after the admission. Follow-up cranial CT scan revealed enlargement of the lateral and the third ventricles. Her consciousness progressively deteriorated and she became comatose three months after the admission. Repeated cranial CT scan showed enlargement of the ventricles, but no mass lesions were seen within the brain. She developed respiratory arrest on September 25 of the same year. She was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had a gastric cancer with meningeal seeding developing meningeal carcinomatosis. The cause of deep coma was ascribed to damage of cerebral cortical areas secondary to metastatic carcinoma cells and fibrinous materials in the surface of the brain. Postmortem examination revealed thickening and clouding of leptomeninges of the cerebral convexity. On histologic observation, patchy areas of fibrous thickening were seen in the cerebral leptomeninges; in such areas, adenocarcinomatous cells were seen scattered. The basal meninges were free of carcinoma cells, however, leptomeninges of the cerebellum and brain stem tegmentum contained scattered carcinoma cells. The lateral and the third ventricles were enlarged, however, insides of the brain were free of pathologies; the ependymal layer were intact. In the stomach no carcinoma cells were remaining. Pneumonic changes were seen in the right upper and the left lower lobes which appeared to be the direct cause of her death. No evidence of tentorial herniation was noted. The cause of her deep coma was not clearly determined, however, combination of hydrocephalus and cortical malfunction due to leptomeningeal carcinoma cell infiltration and fibrinous material accumulation appeared to have played a role.
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PMID:[A 64-year-old woman with severe headache and progressive disturbance of consciousness]. 919 1

Helicobacter pylori can utilise amino acids as the sole carbon energy source. The present study demonstrated that H. pylori grown in continuous culture in a defined medium containing glucose and amino acids utilised alanine, arginine, asparagine, aspartate, glutamine, glutamate, proline and serine. Specific asparaginase and glutaminase enzymes deaminated asparagine and glutamine respectively to aspartate and glutamate, with the production of ammonia. The glutaminase activity was inhibited by 6-diazo-5-oxo-L-norleucine. All the 13 strains of H. pylori tested produced both glutaminase and asparaginase activities. Glutamine is important in the health of the gastric and intestinal mucosa and is a primary energy source for lymphocytes. Depletion of glutamine at the site of H. pylori infection may be of significance in the pathogenesis of H. pylori-associated diseases such as peptic ulcer and gastric cancer.
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PMID:Amino acid utilisation and deamination of glutamine and asparagine by Helicobacter pylori. 929 92

A number of causes of malnutrition after total gastrectomy have been proposed. The purpose of this study was to assess nutritional status and to determine the cause of malnutrition after total gastrectomy. We studied 20 gastric cancer patients who had undergone total gastrectomy and immunochemotherapy and 6 normal controls. Nutritional status was assessed by dietary history, anthropometric methods, and serologic measurements. Malabsorption tests included the fecal fat excretion test, D-xylose absorption test, glucose tolerance test, vitamin B12 absorption test using dual isotopes, bacterial culture of jejunal aspirates, and jejunal biopsy. Weight loss was compared to the preoperative status in all patients (average 15%: 59.0 +/- 9.9 vs. 50.2 +/- 7.8 kg, preoperatively vs. postoperatively). Average daily calorie intake was 1586.2 kcal, which is lower than the normal intake of Korean adults (1838 kcal). Malnutrition of skeletal and visceral protein was not found. There was, however, severe fat malnutrition and a deficit of body fat. Postoperatively the body mass index was considerably lower than that preoperatively (22.2 +/- 0.4 vs. 18.9 +/- 0.4 kg/m2; preoperatively vs. postoperatively). With malabsorption tests, the daily excreted amount of fecal fat was 28.6 +/- 3.4 g (mean +/- SD) in patients and 6.9 +/- 0.2 g in controls. There was no significant malabsorption of carbohydrates. In 64.3% (9/14) of patients, vitamin B12 absorption was abnormal; and the serum concentration of vitamin B12, which was significantly related to malabsorption of this vitamin, was lower than normal in 73.7% (14/19). Bacterial overgrowth was not found, and there were no abnormal histologic findings in the jejunal mucosa. These results suggest that poor oral intake and fat malabsorption following total gastrectomy cause malnutrition and that fat malabsorption may be related to relative pancreatic insufficiency.
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PMID:Nutritional status of gastric cancer patients after total gastrectomy. 1044 33

The present study has examined the glycoconjugate profile in plasma and erythrocyte membranes of 24 adult male gastric cancer patients and an equal number of age and sex-matched controls. Protein-bound hexose, hexosamine and sialic acid were significantly increased in plasma and erythrocytes of gastric cancer patients compared to controls. Elevation of glycoconjugates in circulation is suggested to be a result of increased shedding by the tumor cells or increased synthesis by liver, due to acute phase response.
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PMID:Glycoconjugate profile in plasma and erythrocytes of gastric cancer patients. 951 4

Malignancy is one of the most common causes of exudative effusions and increases in incidence in the elderly. Lung cancer is the most common cause of malignant effusion caused by contiguous spread and its propensity to invade the pulmonary vasculature and embolize to the visceral pleura. Lung, breast, ovary, and gastric cancer and lymphomas account for about 80% of all malignant effusions. Dyspnea and cough are the most common symptoms at presentation. Thirty percent of patients have a low pleural fluid pH (> or = 7.30) and glucose (> 60 mg/dL) at presentation, which predicts a decreased survival, an increase yield on diagnostic studies, and a poor response to chemical pleurodesis. Talc by poudrage or slurry is the most successful pleurodesis agent. Pleural peritoneal shunt is an option for patients with an intractable, symptomatic malignant effusion who cannot undergo or who have failed pleurodesis.
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PMID:Malignancy metastatic to the pleura. 964 86


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