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)

Glycylprolyl beta-naphthylamidase activities in sera from 40 normal subjects (18-81 years) were: 22.6 +/- 0.9 (S.E.) (11.8-38.2) I.U./1 serum at 37 degrees C. The enzyme activities did not differ significantly with age between the younger group under 40-years-old and the older group over 40-years-old. Males, especially under 40-years-old, had slight but significantly higher activities than females. The levels were decreased in patients with gastric cancer. The levels were elevated in patients with hepatobiliary diseases, and had significant correlations with the results of the serum tests in hepatic diseases such as glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, alkaline phosphatase and total bilirubin, but had no correlation with serum lactate dehydrogenase. In cellulose acetate electrophoresis, normal sera had a single peak at the beta-globulin region, but the sera in hepatitis or liver cirrhosis showed not only an increase in the normal peak at the beta-globulin region but also the appearance of the other one or two new peaks in the alpha1 and alpha2-globulin regions.
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PMID:Glycylprolyl beta-naphthylamidase activity in human serum. 114 81

We recently reported the isolation of the K-sam complementary DNA (cDNA), which was amplified preferentially in poorly differentiated types of stomach cancer and codes for one of the heparin-binding growth factor or fibroblast growth factor (FGF) receptor families. The K-sam-related gene, N-sam (NCC-IT-cell-derived sam), was isolated by screening of the cDNA libraries of human immature teratoma cells, NCC-IT. Sequence analysis of the N-sam cDNAs showed that N-sam encodes a human FGF receptor, the FLG protein. N-sam was expressed in lymphocytic leukemia/lymphoma cells, predominantly in the thymic T-cell phenotype. In a T-cell leukemia line, MOLT3, N-sam mRNA expression was markedly enhanced by 12-O-tetradecanoylphorbol-13-acetate treatment and was also up-regulated by basic FGF exposure. These results indicate that N-sam expression is regulated during T-cell ontogeny and modulated by its putative ligand exposure. The results also suggested that interaction between immature T-cell and marrow or thymic interstitial cells might be mediated by N-sam and basic FGF stored in the extracellular matrix of stromal cells.
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PMID:K-sam-related gene, N-sam, encodes fibroblast growth factor receptor and is expressed in T-lymphocytic tumors. 131 50

The effect of s.c. administration of deoxycorticosterone acetate (DOCA) plus p.o. treatment with NaCl solution on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine and the effect of p.o. potassium supplementation on the enhanced induction of gastric carcinogenesis in DOCA-NaCl rats were investigated in Wistar rats. After 25 weeks of p.o. treatment with the carcinogen, rats received s.c. injections of DOCA (50 mg/kg) twice a week and were given 1% NaCl solution with and without 1% KCl as drinking water. In Week 52, the blood pressure, the incidence of gastric cancer, and the number of cancers per rat were significantly greater in DOCA-NaCl rats than in the untreated group. Prolonged p.o. treatment of DOCA-NaCl hypertensive rats with potassium significantly reduced their blood pressure, the incidence of gastric cancers, and their number per rat. All gastric tumors were in the glandular portions of the stomach. The norepinephrine concentration in the gastric wall and the labeling indices of gastric mucosa were significantly greater in DOCA-NaCl hypertensive rats than in the untreated group, but p.o. potassium supplementation significantly reduced the norepinephrine concentration in the gastric wall and the labeling indices of the gastric mucosa in DOCA-NaCl rats. Thus, administration of DOCA and NaCl increased the norepinephrine concentration in the gastric wall and promoted gastric carcinogenesis, and p.o. potassium supplementation decreased the norepinephrine concentration in the gastric rats. Inasmuch as the norepinephrine concentration has been used as a marker of sympathetic nervous activity, these findings suggest that the sympathetic nervous system plays an important role in gastric carcinogenesis, probably associated with cell proliferation of antral epithelial cells.
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PMID:Enhanced induction of gastric carcinogenesis by N-methyl-N'-nitro-N-nitrosoguanidine in deoxycorticosterone acetate-NaCl hypertensive rats and its inhibition by potassium chloride. 203 26

This study was carried out to evaluate whether the preoperative levels of serum glycoproteins (CEA, SCC, TPA, IAP, ACT, ASP and sialic acid) and HLA antigens (class I and II) could be potential aids in the selection of suitable gastric and esophageal cancer patients for postoperative adjuvant immunotherapy of PSK. Gastric cancer patients underwent gastrectomy and received postoperative adjuvant chemotherapy (MMC, FT and ADR) with or without PSK. One hundred and forty esophageal cancer patients in cooperative study groups (organizing chairman; Dr. Hiroshi Satoh) underwent esophagectomy and received postoperative adjuvant radiotherapy and chemotherapy (FT, BLM) with or without PSK. The efficacy of PSK was recognized in the patients with normal levels of all glycoproteins in gastric cancer, and with normal levels of CEA or SCC or TPA and abnormal levels of one or more APRs in both gastric and esophageal cancer, and with positive HLA-B40 antigen. The combination of tumor-associated factors, such as CEA, SCC and TPA and various non-specific reactants such as APRs was useful as a prognostic indicator. In addition, some of HLA antigens were also valuable. The pretreatment levels of glycoproteins and HLA antigens have potential aids in the selection of patients with gastric and esophageal cancer for PSK treatment.
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PMID:[Clinical effects of PSK on esophageal and gastric cancer patients and usefulness of serum levels of glycoproteins and HLA antigens as prognostic indicators]. 258 37

Tumor promoting phorbol esters, 12-O-tetradecanoylphorbol-13-acetate (TPA) and phorbol-12,13-dibutyrate (PDBu), significantly enhanced the growth of human gastric cancer cell line TMK-1, whilst activating protein kinase C. The time course of 125I-epidermal growth factor (EGF) binding to TMK-1 cells after TPA treatment showed a decrease in the number of EGF receptors on TMK-1 cells within 3 hr. Autophosphorylation of EGF receptor decreased in accordance with the decrease of EGF binding by TPA treatment. Scatchard plot analysis of TMK-1 cells after TPA treatment showed that high affinity EGF receptor disappeared at 3hr but the number of EGF receptors increased at 24 hr. These findings suggest that tumor promoting phorbol esters stimulate the cell growth through activation of protein kinase C and modification of EGF receptor of human gastric cancer cell line TMK-1.
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PMID:The effect of phorbol esters on cell growth and epidermal growth factor receptor modulation in a human gastric carcinoma cell line TMK-1. 263 48

We produced the chelated Adriamycin-Aluminum complex (ADM-Al complex) for experimented evaluation. Human gastric cancer was transplanted into nude mice divided into 4 groups for drug injections; 1) Control (0.9% NaCl), 2) Al acetate (1 mg/ml), 3) ADM only (1 mg/ml) and 4) ADM-Al complex (ADM 1 mg/ml + Al 1 mg/ml), 0.2 ml of each was administered through several injections simultaneously into the tumor periphery. Long term retention of ADM in the tumor was observed pathologically in Group 4. The concentration (microgram/g) of ADM after injection (5, 7, 28 days) was 22.3, 12.6, and 3.5 in Group 4, against 8.4, 2.0, and 0.0 in Group 3 (p less than 0.01). The estimated tumor weight inhibition rate was 66.6% in Group 4, compared with 21.4% in Group 3, and only 3% in Group 2. DNA tritium thymidine uptake inhibition rate was 43.8% in Group 4, compared with 21.2% in Group 3, and in 9.4% Group 2. No side-effect due to Al-chelation was observed. These results demonstrate the effectiveness of ADM-Al complex as a topical anticancer agent. Clinical use must be explored.
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PMID:[Experimental study on an adriamycin-aluminum complex modified anticancer agent]. 273 41

Serum tissue polypeptide antigen (TPA) levels were measured in 33 patients with esophageal cancer, 39 with stomach cancer and 50 with colon cancer. At the same time five glycoproteins, namely immunosuppressive acidic glycoprotein (IAP), alpha 1-antichymotripsin (alpha 1-ACT), acid soluble glycoproteins (ASP), sialic acid and carcinoembryonic antigen (CEA), were measured for comparison. The mean TPA values were 59.0 +/- 15.4 U/l in 61 normal subjects, 103.6 +/- 104.2 U/l (positive rate, 24.2%) in esophageal cancer patients, 111.9 +/- 49.8 U/l (71.8%) in stomach cancer patients and 124.8 +/- 195.5 U/l (40%) in colon cancer patients. The serum TPA levels in patients with stomach cancer rose with an increased number of involved lymph nodes and with a higher degree of infiltrative growth and increased with the advancement of tumor growth postoperatively. Serum TPA levels correlated well with those of alpha 1-ACT, IAP and ASP in stomach cancer patients and with those of CEA, ASP and sialic acid in colon cancer, but not in esophageal cancer patients. It is suggested that the serum TPA might represent one of the reactant proteins and/or tumor-associated antigens that appear to be dependent upon the cancer status.
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PMID:[Clinical evaluation of tissue polypeptide antigen in patients with esophageal, stomach and colon cancer]. 648 66

The isoform of protein kinase C responsible for the inhibition of histamine-stimulated adenylate cyclase by the phorbol ester, 12-O-tetradecanoylphorbol 13-acetate (TPA), has been investigated in a particulate fraction prepared from the human gastric cancer cell line HGT-1. The alpha and epsilon isoforms of protein kinase C were detected in HGT-1 cells and in a 40,000 x g particulate fraction by immunoblotting procedures. The inhibitory effect of TPA on histamine-stimulated adenylate cyclase was enhanced by the presence of Ca2+, but decreased in a concentration-dependent manner by anti-peptide antibody to protein kinase C alpha, but not to protein kinase C epsilon. Addition of Ca2+ and TPA to the 40,000 x g particulate fraction stimulated the phosphorylation of the protein kinase C substrate myelin basic peptide 4-14. Protein kinase C alpha is probably the isoform responsible for inhibition of histamine-stimulated adenylate cyclase in HGT-1 cells.
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PMID:The alpha isoform of protein kinase C inhibits histamine-stimulated adenylate cyclase activity in a particulate fraction of the human gastric cancer cell line HGT-1. 754 78

Certain Lilium plants contain (25S)-spirost-5-ene-3 beta,27-diol glycosides embracing 3-hydroxy-3-methylglutaric acid at the C-27 hydroxy position. One of their derivatives, methyl ester of (25R)-27-O-[(S)-3-hydroxy-3-methylglutaryl]-spirost-5-ene-3 beta,27-diol 3-O-(O-alpha-L-rhamnopyranosyl-(1-->2)-O-[beta-D-glucopyranosyl-(1-->4)] - beta-D-glucopyranoside) was found to inhibit 12-O-tetradecanoylphorbol-13-acetate (TPA)-stimulated 32P-incorporation into the phospholipids of human cervical cancer (HeLa) cells and also to inhibit the proliferation of various kinds of human malignant tumor cells, pancreatic cancer (PANC-1), osteosarcoma (OST), human gastric cancer (HGC-27), pheochromocytoma (PC-12) and HeLa cells, in vitro.
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PMID:Inhibitory effects of steroidal saponins on 12-O-tetradecanoylphorbol-13-acetate (TPA)-enhanced 32P-incorporation into phospholipids of HeLa cells and proliferation of human malignant tumor cells. 755 Jan 6

The human platelet-activating factor receptor (PAFR) gene is transcribed by two distinct promoters (promoter 1 and promoter 2) to generate two transcripts (designated as PAFR transcript 1 and PAFR transcript 2), though their open reading frames are identical. By primer extension analysis to discriminate two transcripts, we found that the levels of PAFR transcript 1 (leukocyte-type), but not PAFR transcript 2 (tissue-type), are upregulated by PAF as well as by 12-O-tetradecanoylphorbol-13-acetate (TPA) in the human stomach cancer cell line (JR-St cells) which expresses both functional PAFR transcript 1 and PAFR transcript 2 endogenously. Functional analysis of the promoter 1 with a transient expression assay using chloramphenicol acetyltransferase (CAT) gene as a reporter showed that both PAF and TPA activated the promoter 1 but not the deleted promoter lacking the three consensus binding sites for NF-kappa B located from -571 bp to -459 bp. These findings suggest a molecular mechanism of positive regulation of PAFR gene expression by PAF through NF-kappa B, possibly by a phosphorylation reaction involving protein kinase C by PAF.
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PMID:Platelet-activating factor (PAF) positively auto-regulates the expression of human PAF receptor transcript 1 (leukocyte-type) through NF-kappa B. 780 42


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