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)

A newly established cancer marker, the PFK inhibition test, has been further examined for its capacity to detect malignant neoplasms irrespective of the organs in which cancer cells start proliferating. We tested 1,160 sera from cancer patients and compared them with 756 normal sera, using histograms and normal paper for analysis of accumulated frequency. PFK activity through the influence of normal sera showed normal distribution, and cancerous sera shifted to the inhibitory site with an irregular shape. From these analyses, the patients were classified into the following types: normal range: PFK greater than SD (standard deviation of PFK activity in normal sera); suspicious range: SD greater than PFK greater than 2SD, must be given the PFK test again; and dangerous range: PFK less than 2SD, further examination must be carried out to detect cancer. Fifty percent of the sera from all the cancer patients inhibited PFK beyond 2 SD of normal sera. We also analyzed organ-associated PFK distribution, eg, gastric, colorectal, and mammary cancer. In gastric cancer, PFK inhibition was stronger in accordance with how far a particular stage of cancer had progressed. However, 50% of sera from stage I gastric cancer patients was positive beyond the cut-off line of 2 SD. We examined 104 sera from patients diagnosed as benign prostatic hypertrophy and found malignant cells in 10 patients whose sera tended to be positive in PFK inhibition. The PFK inhibitory factor in the body fluids of cancer patients was fractionated by Sephadex G-75 gel filtration and DEAE ion exchange chromatography. The approximate molecular weight of this factor was 13,000 daltons. The factor was resistant to heat and acid (0.1 N HCl and H2SO4) and was sensitive to 0.1 N NaOH and phosphate buffer. Diluted sulfuric acid and ammonium sulfate made an inactive NaOH-treated sample active when lyophilized following dialysis against distilled water. PFK inhibition by cancerous sera was eliminated by fructose-2,6-bisphosphate (the strongest activator of PFK) in a dose-dependent manner. PFK attached to agarose beads was found to be reversible even after being inhibited by cancerous body fluids and ATP water solution. Although PFK is apt to decay in a low pH range, the established procedure did not destroy PFK, but induced a direct inhibition of PFK by ATP through the ATP inhibition site on the PFK molecule. The PFK inhibitor may possibly function as a proton carrier and release protons to activate the ATP inhibition site.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:PFK inhibition test for cancer detection: clinical applications and mechanisms of PFK inhibition. 295 72

Hyperthermic treatment using ACNU combined with a thermosensitizing drug, methylglyoxal-bis-guanylhydrazone (MGBG), was studied in human gastric cancer xenotransplanted into nude mice. In order to increase the intra-cellular MGBG content, intraperitoneal injection of alpha-difluoromethylornithine(DFMO) 1000 mg/kg was performed twice with an interval of 6 hours and 50 mg/kg of MGBG was given at the time of the second administration of DFMO. After 6 hours of MGBG administration, ACNU 20 mg/kg was given intraperitoneally and, subsequently a 23-minute hyperthermia was carried out in a water bath at 43.5 degrees C. After 48 hours a second hyperthermia was performed by the same method. Tumor weight was estimated using Battelle's Columbus Institute protocol and the inoculated tumors, which were extirpated 60 minutes after 3H-thymidine injection at a prescribed interval after cessation of hyperthermia, were assayed biochemically for the determination of DNA biosynthesis. In mice given ACNU, DFMO, MGBG plus heat, considerably superior results were obtained. Although the DFMO plus MGBG group was inferior in antitumor activity to the ACNU only or heat only group, the DFMO, MGBG plus heat group showed much the same antitumor effects, compared to the ACNU plus heat group. These data suggest that the thermosensitizing efficacy of MGBG may be applicable for clinical use.
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PMID:[Studies on hyperthermia by the use of a thermosensitizing drug]. 307 89

The influence of fat emulsification of N1-(2-tetrahydrofuryl)-5-fluorouracil (FT-207) on lymphatic transport was studied in seven postoperative gastric cancer patients. The water-in-oil-type of emulsion of FT-207 (FT-w/o), the oil-in-water-type emulsion of FT-207 (FT-o/w) and an enteric-coated granule of FT-207 (FT-G) each in 1-g doses, calculated in terms of FT-207, were administered orally. Lymph from a thoracic duct fistula, prepared in advance, and from the blood of a peripheral vein was collected simultaneously along a time course after administration to measure the concentrations of FT-207 and 5-fluorouracil (5-FU). For FT-w/o, FT-207, and 5-FU, concentrations were significantly higher, both in the lymph and in the blood, than those for FT-G and FT-o/w. However, no significant differences in FT-207 and 5-FU concentrations were observed between FT-o/w and FT-G. It was concluded that FT-w/o can be useful as an adjuvant chemotherapeutic drug in the postoperative treatment of gastric cancer.
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PMID:N1-(2 tetrahydrofuryl)-5-fluorouracil (FT-207) in the postoperative adjuvant chemotherapy of gastric cancer. Delivery of a fat-emulsified agent to the lymph. 308 Feb 17

In an attempt to enhance the antitumor effects of hyperthermochemotherapy, methylglyoxal-bis-guanylhydrazone (MGBG) and alpha-difluoromethylornithine (DFMO) were used in combination with hyperthermochemotherapy of 1-(4-amino-2-methyl-5-pyrimidinyl)-methyl-3-(2-chloroethyl)-3-nitrosoure a (ACNU) against human gastric cancer (ST-2) xenotransplanted into nude mice. After priming with DFMO and MGBG, ACNU was given ip and subsequently, a 23 minute-hyperthermia was carried out by placing the leg with the tumor into a water bath of a temperature of 43.5 +/- 0.1 degrees C. The second hyperthermic treatment was given in the same manner after 48 hours. MGBG and DFMO were administered for 4 successive days from the previous day of the first hyperthermia. In mice treated with DFMO plus MGBG, either tumor growth or tumor tripling time was much the same as in the control, while in mice given MGBG, DFMO plus heat, there was a diminution in tumor growth. Hyperthermia together with MGBG, DFMO plus ACNU brought about remarkable antiproliferative effects on ST-2 tumor growth, compared to three regimens with MGBG, DFMO plus heat, MGBG, DFMO plus ACNU, as well as ACNU plus heat. These data suggest that a combination of MGBG with DFMO leads to a favorable thermosensitization to the antitumor efficacy of ACNU.
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PMID:Enhanced antitumor efficacy with a combination of hyperthermochemotherapy and thermosensitization with polyamine antimetabolites in nude mice. 311 28

Hyperthermochemotherapy with hypoxic cell radiosensitizers has been carried out using human gastric cancer xenotransplanted into the nude mouse. Misonidazole (MIS) and metronidazole (MTR), hypoxic cell radiosensitizers, were administered singularly or in combination with an ip dose of 500 mg/kg each, and after 60 minutes, an ip dose of MMC of 2.0 mg/kg was given. Subsequently, hyperthermia was applied, twice at a 48-hour interval, by a water bath at 43.5 +/- 0.1 degrees C for 23 minutes. The antitumor activity of hyperthermia with MTR was similar to that of hyperthermia alone, whereas hyperthermia with MIS surpassed hyperthermia alone, at 0.03237 less than p less than 0.05038. Hyperthermia combined with MIS and MMC enhanced the antitumor effects, as compared to hyperthermia with MMC, and with MMC plus MTR. Tumor volumetric tripling times in case of MMC plus heat, MTR, MMC plus heat, and MIS, MMC plus heat were about 229, 213, and 398 hours, respectively, compared to about 110 hours in the control and 160 hours in the case of hyperthermia alone. Thus, these data suggest that the antitumor efficacy of hyperthermochemotherapy with MIS may be the result of a synergistic phenomenon of thermo-chemosensitization.
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PMID:[Enhancement of hyperthermochemotherapy with hypoxic cell radiosensitizers]. 312 68

We studied the effect of inhibition of polyamine biosynthesis by alpha-difluoromethylornithine on the growth of a human gastric adenocarcinoma (CLEES) xenotransplanted in nude mice. CLEES is a well-differentiated gastric adenocarcinoma of the intestinal type. The doubling time has ranged from 7 to 10 days through 11 passages. Electron microscopic and immunohistochemical studies comparing the original tumor and xenotransplants showed similar structure and similar amounts of carcinoembryonic antigen. Polyamine biosynthesis is required for cell division. alpha-Difluoromethylornithine inhibits ornithine decarboxylase, the rate-limiting enzyme in polyamine biosynthesis. In this study, 48 athymic mice were used in two experiments. In the first experiment, two groups of 12 mice each were inoculated with CLEES tumor cells and received either tap water or a 3% alpha-difluoromethylornithine solution as drinking water. Tumor size was measured twice weekly. Tumor size was significantly decreased from controls by the fourth week of treatment and at all points of analysis thereafter for 7 wk. In the second experiment, alpha-difluoromethylornithine significantly reduced tumor concentrations of the polyamines putrescine and spermidine. In addition, the tumor content of DNA was significantly reduced in treated mice (0.64 +/- 0.16 mg) compared to controls (4.76 +/- 0.92 mg). Our data suggest that inhibition of polyamine biosynthesis may be a useful component of multidrug chemotherapy for human gastric adenocarcinoma. Establishment of tumor lines such as this gastric adenocarcinoma will facilitate further studies on the biological behavior of human gastric cancer and its response to chemotherapeutic manipulation in vivo.
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PMID:Inhibition of human gastric adenocarcinoma xenograft growth in nude mice by alpha-difluoromethylornithine. 313 Jan 88

Hyperthermia for human gastric cancer xenotransplanted into the hindlegs of nude mice was performed to determine whether misonidazole (MISO) or metronidazole (MTR), derivatives of nitroimidazole, would intensify the antitumour effects of hyperthermia only, or combined with mitomycin C (MMC). MISO, MTR and MMC were given i.p. at doses of 500 mg kg-1, 500 mg kg-1 and 2.0 mg kg-1 respectively, and MISO or MTR was administered 45 min before MMC. Hyperthermia was applied twice at 48 h intervals, by means of a water bath at 43.5 +/- 0.1 degrees C for 23 min. Tumour tripling times following heat alone, MTR plus heat, and MISO plus heat were about 6.7, 8.0 and 7.9 days respectively, compared with 4.6 days for the control, but tumour regression occurred in the heat plus MISO group only. Tumour tripling times for MMC plus heat, MMC plus MTR plus heat, and MMC plus MISO plus heat were 9.6, 11.6 and 17.1 days respectively, compared to 4.6 days for the control and 6.7 days for heat alone. These data suggest that the antitumour activity of MMC plus MISO plus heat is an additive phenomenon.
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PMID:Enhancement of hyperthermochemotherapy for human gastric cancer in nude mice by thermosensitization with nitroimidazoles. 316 92

Epidemiologic studies have reported associations between gastrointestinal cancer mortality and exposure to cutting fluids and abrasives in metal machining and precision grinding operations. Two previous studies found excess stomach cancer among workers exposed to water-based cutting fluids in bearing plants. This study reports similar findings in a third and larger population. Cause of death and work histories were determined for 1,766 bearing plant workers who died between Jan 1, 1950 and June 30, 1982. Mortality odds ratios (SMOR) and proportional mortality ratios (PMR) revealed significant excesses of gastrointestinal malignancies. The proportional mortality excess for stomach cancer among white men was greatest among those with more than 10 years' exposure in the major grinding group (PMR = 13/3.8 = 3.39; P less than .001). The SMOR by logistic regression for stomach cancer among white men was 2.3 (P = .02) for 25 years' grinding experience. For cancer of the pancreas among white men, there were significant associations with both machining and grinding jobs in straight oil (SMOR = 9.9 and 3.2, respectively, for 25 years duration). These findings could not be explained by confounding due to the ethnic background of the decedents. This study confirms previous evidence that grinding operations using water-based cutting fluids increase the risk for stomach cancer and provides moderate evidence that exposures to straight oil-cutting fluids increase the risk for cancer of the pancreas. There were indications, meriting further investigation, that non-malignant liver disease is associated with cutting fluid exposures and that lung cancer is associated with oil smoke from operations such as forging or heat treating.
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PMID:Mortality among bearing plant workers exposed to metalworking fluids and abrasives. 318 87

General mortality analysis showed an increasing tendency of circulatory diseases in two villages examined. Respiratory diseases and suicide were more frequent in the village with greater pesticide use (village I). The relative risk (RR) of gastric cancer for men is significantly higher in village I (high rate of pesticide use) than in the county as a whole (RR, 1.65; 95% confidence interval (CI), 0.96-2.83) and also in relation to the national data (RR, 3.20; 95% CI, 1.91-5.36). Since the nitrate concentration in the drinking water, the drug consumption, smoking and eating habits are similar in the two villages, and since alcohol consumption is higher in village II (moderate rate of pesticide use), it seems that nitrosable pesticides may play a role in the etiology of stomach cancer. This is supported by the fact that a higher number of gastric cancer cases was found where larger quantities of nitrosable pesticides had been used.
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PMID:Pesticide use related to cancer incidence as studied in a rural district of Hungary. 321 55

To study the relationship between thermotolerance and post-thermal phenomenon, tumor pO2 (TpO2) in xenoplanted gastric cancer tissue (H-23) has been measured by a polarographic method. The heat treatment was done in a water bath at 43.5 +/- 0.1 degrees C for 23 minutes. In order to produce thermotolerance, the second treatment was carried out at an interval of 24 hours, or, alternatively at 72 hours, or at 5 days or at 7 days. The thermotolerance of the H-23 tumor reached its maximum at the 72 hour-interval and was seen to disappear completely at 7 days. The TpO2 in the H-23 tumor decreased immediately after a single heat treatment and returned to its pre-treated value after 10 hours. In cases of the second heat treatment, the 72-hour interval group returned to its pre-treated value in 2-6 hours, whereas the 24-hour, 5-day, and 7-day interval groups showed a longer recovery time. The relationship between thermotolerance and TpO2 recovery was inverse at r = -0.858 and p = 0.035. Thus, our study suggests that not only is the thermotolerance affected by the alteration of the intra-cellular components, but also by the post-thermal changes in the tumor vessels.
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PMID:[The relationship between thermotolerance and the tissue oxygen tension in human gastric cancer tissue]. 323 Jun 39


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