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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Formation of ribothymidine by the ribose exchange reaction between thymine and uridine with the cell-free extract of mouse Ehrlich ascites tumor cells was demonstrated. Since phosphate ions appear to be not required for this reaction, perhaps it proceeds by the mechnism of direct exchange of nucleoside N-ribosyltransferase. The transfer activity was found in the precipitates when the crude extract was fractionated with 30-60% saturated ammonium sulfate. Ribothymidine formation was also demonstrated between thymine and ribonucleosides other than uridine with this tumor extract. Production of ribothymidine from thymine and uridine was detected also by the use of extracts from lung, brain, and regenerating liver of normal rats, and from newborn rats (whole body). An extract of Rhodamine sarcoma exhibited the ribose exchange activity, while that of human gastric cancer did not.
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PMID:Formation of ribothymidine from thymine and ribonucleosides by the cell-free extract of tumors and rat tissues. 34 Apr 51

The total binding capacity of the cell receptors and not only the fraction required to elicit physiological response was detected and it is shown that specific receptors filled by endogenous estradiol were detected along with the unfilled sites. Changing the temperature of the incubation media altered intracellular distribution of bound estradiol. Late nucleolar retention of estradiol was shown after its release from nuclear protein. This unexpected finding may be a key event. Tumor tissues were obtained from 40 primary breast cancers, 2 endometrial carcinomas, and 1 lung and 1 gastric cancer; 2 normal human spleens, 2 mouse livers, and 1 breast from a 5-month pregnant women were processed. Tissue samples were transferred to a cold flask containing phosphate-buffered balanced salt solution. Further details of preparation are given to show typical estradiol-target cells containing variable amounts of specific estradiol-receptors. For immunofluorescence staining and indirect technique was used to show the in situ estradiol localization. The fluorescence staining showed 3 patterns. Cells incubated in the cold mostly displayed a bright, homogeneously diffuse fluorescence of the cytoplasm with the nuclear area unstained. There were some negative cells. The 2nd pattern of fluorescence was shown by those incubated at room temperature. Cytoplasmic staining was more marked and nuclear areas showed bright-fluorescent light stippling. A 3rd staining pattern was seen after slow postincubation warming up to 37 degrees C when increased nuclear staining occurred. Some cells did not show any nuclear labeling despite the clear cytoplasmic fluorescence. Preparations of human spleen, nontarget tumors, or mouse liver had no fluorescent cells. All fluorescent stainings were prevented by preincubation and washing in media containing Nafoxidine and N-ethylmaleimide. Control experiments confirmed the immune specificity of the detection of estradiol. Breast tissue cells from a pregnant women showed moderate cytoplasmic and faint nuclear fluorescence before incubation with estradiol, after which cytoplasmic staining was reinforced. Cells from the premenstrual beast cancers sometimes showed fluorescence without exposure to estradiol.
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PMID:Detection and dynamic localisation of estradiol-receptor complexes in intact target cells by immunofluorescence technique. 78 84

Gastric juice was neutralized (nGJ) in vivo by 80 ml of a phosphate buffer containing radiolabelled vitamin B12 as dilution indicator. Unprocessed nGJ was analyzed in the double gel diffusion technique for the presence of serum proteins using monospecific antisera. Alpha1-Acid glycoprotein (AGP) was found in a high incidence (36 out of 38 subjects) in nGJ of gastric cancer patients. AGP was also observed less frequently in nGJ of patients with Billroth II resections (6/15), metaplasia (11/52), gastric ulcer (3/24), chronic atrophic gastritis (2/26) and chronic gastritis (3/63). AGP was absent in the control group (0/21), in patients with surface gastritis (0/38) and in subjects with normal acid secretion (0/45). Immunochemical studies demonstrated no identity of AGP with human "gastrointestinal tumor associated antigens." In 7 out of 17 AGP positive samples immunochemical differences between gastric and serum AGP were observed.
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PMID:Alpha 1-acid glycoprotein in gastric cancer juice. 80 43

Ultrastructural and histochemical studies on human gastric cancer cells disclosed the presence of native and synthesized glycogen particles. The glycogen particles were investigated in the histochemical synthesis of glycogen particles from glucose 1-phosphate by the phosphorylase-branching glycosyltransferase system and non-incubated native glycogen in human gastric adenocarcinoma tubulare. It was observed that focal synthesis localized inthe intracytoplasmic matrix and intranucleus. Intranuclear synthesized glycogen appeared as a rosette form ranging from 1100 to 1300 A in diameter and free particles ranging from 325 to 900 A in diagmeter. The synthesis of glycogen appeared in the nucleus as well as in the cytoplasm of the human gastric cancer cells, and the synthesized glycogen was observed as a group of particles. Newly formed glycogen particles appeared occasionally in the interchromatin area as a large macromolecular structure of rosette form. Native glycogen appeared as a free-particle (250-333 A, medium =300 A) and aggregated rosette from (694-1050 A, medium=917 A) in the autophagosome of gastric cancer cells. There was not, however, a native glycogen particle in the nuclei of gastric cancer cells. Under certain conditons the nuclei of gastric cancer cells can acquire the capacity to synthesize glycogen.
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PMID:Intranuclear synthesized and native glycogen particles in human gastric cancer: ultrastructure and histochemistry. 83 12

Uninvolved gastric mucosa from duodenal ulcer, gastric ulcer, and gastric cancer patients was incubated with [1-14C]glucose and [6-14C]glucose in order to assess the relative contributions of the pentose phosphate pathway and Krebs cycle to glucose metabolism. [14C]Glucose counts retained by the tissue, glycolysis, and pyruvate formation were also measured. Tumor tissue from the cancer patients was included in the study. Less than 1.2% of the glucose entering the tissues was metabolized via the pentose phosphate pathway; suggesting that this pathway plays a minor role in energy production from glucose. The major determinant of energy production was the Krebs cycle. Its contribution to glucose metabolism was greatest in the body mucosa of duodenal ulcer patients, less in the uninvolved body mucosa of gastric ulcer patients, and lower still in the corresponding body mucosa of gastric cancer patients. The low levels of Krebs cycle activity seen in the latter tissue resembled those of uninvolved antral mucosa. The smallest Krebs cycle contribution was seen in tumor tissue. [14C]Glucose counts retained by the tissue and glycolysis both tended to vary inversely with Krebs cycle activity among the tissues studied. Thus, both were small in the body mucosa of noncancer patients and somewhat larger in the body mucosa of cancer patients, in uninvolved antral mucosa and in tumor tissue.
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PMID:Krebs cycle, pentose phosphate pathway, and glycolysis in the uninvolved gastric mucosa of peptic ulcer and gastric cancer patients. 91 74

Sera from cancer patients specifically suppressed phosphofructokinase (fructose-6-phosphate kinase [PFK], EC 2.7.1.11), a rate-limiting enzyme in the glycolysis pathway. Among 418 cancerous sera, 68.7% evidence suppression; there was no organ specificity. Among 42 sera from early gastric cancer patients, 29 (69.0%) were positive, as were advanced gastric cancer, 14/19 (73.3%) pancreas cancer, and 75/101 (74.3%) lung cancer sera. In contrast 6/50 (12.0%) sera from patients with gastroduodenal ulcer, 3/23 (13.0%) with myoma uteri, and 0/6 with lung tuberculosis were positive. Patients with diabetes mellitus and those receiving steroid hormone therapy showed strong positive suppression. Comparative studies using other tumor markers (immunosuppressive acid protein, carcinoembryonic antigen, alpha-fetoprotein, beta 2-microglobulin, and ferritin) and the same sera used from PFK assay showed that the PFK method was two to three times more sensitive. Sephadex G-200 column chromatography revealed that the PFK-suppressive activity was retained in the postalbumin fraction. The PFK method may represent a promising new cancer screening method.
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PMID:A new cancer marker: a possible cancer screening method based on the suppression of phosphofructokinase by sera from cancer patients. 293 46

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

DNAs from 21 human stomach cancers, 16 metastatic stomach cancers to lymph nodes, and 21 apparently noncancerous specimens of stomach mucosae from a total of 26 patients with stomach cancer were tested for their ability to induce neoplastic transformation of NIH 3T3 cells on transfection by the calcium phosphate precipitation technique. Three samples of DNA were shown to have transforming activity; one was from a primary stomach cancer of one patient, the second was from a noncancerous portion of stomach mucosa of the same patient, and the third was from a lymph node metastasis of stomach cancer from another patient. These transformants were tumorigenic in nude mice, and DNAs from the cells could induce secondary transformants. A portion of the transforming gene from the stomach cancer of one patient, which contained the sequences expressed in the NIH 3T3 transformants, was cloned. The transforming gene did not have any homology with the transforming sequences reported previously. We have applied the term hst to this novel human transforming gene. The transforming gene, hst, was found to be present in all the primary and secondary transformants induced by the other two samples of DNA.
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PMID:Transforming gene from human stomach cancers and a noncancerous portion of stomach mucosa. 345 65

In vitro chemosensitivity was evaluated by SDI test in various human tumors including 1 lymph node metastasis of esophageal cancer, 10 gastric cancers, 4 colo-rectal cancers, 1 hepatoma, 2 lung cancers, 2 breast cancers and 1 gallbladder cancer. Tumor fragments cut with scissors were exposed to twelve kinds of antitumor drugs at five to ten times peak plasma concentration. After 3 days at 37 degrees C, each tumor fragment suspension was washed with phosphate-buffered saline and assayed for succinate dehydrogenase (SD) activity using 3-(4,5- dimethyl-2-thiazolyl)-2, 5-diphenyl-2H tetrazolium bromide (MTT) as a hydrogen acceptor. When the SD activity of the drug-treated cells was reduced to below 50% that of control cells, the chemosensitivity to the antitumor drug was considered positive. The chemosensitivity of each tumor varied individually. Mitomycin C or 5-fluorouracil are regularly used to treat gastric cancer patients, but, some specimens of gastric cancer in this study showed a resistance to these drugs and an unexpected sensitivity to other drugs. Our results show that the SDI test is a convenient method for clinical use and gives significant information about drug sensitivity.
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PMID:[In vitro chemosensitivity of various human tumors evaluated by the SDI (succinate dehydrogenase inhibition) test]. 405 18

Fava beans are prominent in the diet of the Colombian population at high gastric cancer risk. Upon nitrite treatment under simulated gastric conditions, a potent mutagen was formed as detected by a forward mutation assay using Salmonella typhimurium TM677 without microsomal activation. The promutagen was partially purified by preparative t.l.c. and normal phase h.p.l.c. of the acetone-soluble portion of a dried aqueous extract. The nitrosated promutagen fully accounted for the mutagenicity observed with whole fava beans. One gram of fresh fava beans yielded approximately 0.35 nmol of mutagen. Mutagenicity data indicated that this mutagen was more potent than N-methyl-N'-nitro-N-nitrosoguanidine. The characteristics of the mutagen were typical of an activated N-nitroso compound, that is a compound in which the N-nitroso moiety is attached to an activating group, such as a carbonyl group. Irradiation of the mutagen yielded a Griess positive reaction. By reverse-phase h.p.l.c. photohydrolysis, a single peak could be ascribed to the mutagen. Its stability varied as a function of pH, being most unstable under alkaline conditions. Cysteine and phosphate concentration had no effect on its rate of decomposition, thereby strongly suggesting that the mutagen is an N-nitrosourea. The results obtained in this study support the hypothesis of carcinogenesis via the intragastric production of activated N-nitroso compounds.
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PMID:Formation of an activated N-nitroso compound in nitrite-treated fava beans (Vicia faba). 715 Dec 53


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