Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bestatin, one of the biological response modifiers (BRMs), is an inhibitor of aminopeptidase B (AP-B), leucine aminopeptidase (LAP) and aminopeptidase M (AP-M). In this report, we investigated the direct effect of bestatin on the growth of cancer cells in vitro using established four choriocarcinoma cell lines. In vitro chemosensitivity was evaluated by the succinate dehydrogenase inhibition (SDI) test. Bestatin showed the growth-inhibitory effect on all the choriocarcinoma cell lines dose-dependently, especially on NaUCC-4 cells. Both an isomer of bestatin with no inhibitory activity against aminopeptidases, (2R, 3S)-AHPA-(R)-Leu, and another isomer with stronger inhibitory activity against AP-B than bestatin, (2S, 3S)-AHPA-(R)-Leu, did not show growth inhibition on NaUCC-4 cells. So it is suggested that one of the possible mechanisms responsible for the direct action of bestatin on the choriocarcinoma cells may be related to the inhibition of activity of LAP or AP-M rather than that of AP-B. Furthermore, cytotoxicity of actinomycin D on the choriocarcinoma cells was significantly enhanced by combination with bestatin. These results suggest that bestatin has not only an indirect host-mediated anti-tumor activity, but also a direct growth-inhibitory effect on some kinds of cancer cell lines.
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PMID:Growth inhibitory effect of bestatin on choriocarcinoma cell lines in vitro. 178 99

Alpha-glycerophosphate dehydrogenase (alpha-GPD) and succinate dehydrogenase (SD) activities were investigated in lymphocytes from peripheral blood of normal rats and rats bearing the Walker 256 carcinosarcoma. Computer analysis using an original algorithm revealed a hierarchy of biorhythmic patterns of dehydrogenase activities. In all rats, mean SD activity was higher than mean alpha-GPD activity. In rats without tumor, SD and alpha-GPD activities were both higher than in rats with the Walker tumor. Biorhythm spectra for both dehydrogenases were very similar in rats with or without tumor, but tumor implantation resulted in a change of the phase relationship between alpha-GPD and SD.
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PMID:Chronobiological analysis of peripheral lymphocyte dehydrogenase activities in rats with Walker 256 carcinosarcoma. 180 27

Chemosensitivity of hepatocellular carcinoma tissues from 72 patients to 6 antitumor agents was assayed using the succinate dehydrogenase inhibition test. Sensitivity was positive in 47.2% of tissues exposed to adriamycin, 53.5% to mitomycin C, 10.3% to 5-fluorouracil, 51.5% to cisplatin and aclacinomycin A. respectively, and 52.9% to carboquone. Eight percent of the tissues were sensitive to all 6 drugs, while the resistance rate to all drugs was 36.5%. The remaining 55.5% were sensitive to only some of the drugs. When a comparison of the sensitivity to the 6 drugs was made between two different areas of tumors in 16 patients, positive or negative sensitivity was in a range of 76.9-92.9%. The hypovascular masses seen on the angiography and the histologically well differentiated tumors were resistant to adriamycin, a drug most commonly prescribed to treat patients with liver cancer. For some of these tumors, mitomycin C or carboquone may be effective. Our observation shows that the succinate dehydrogenase inhibition test is useful for determining which drugs will be effective for a particular tumor.
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PMID:Human hepatocellular carcinoma sensitivity to antitumor drugs assayed using the succinate dehydrogenase inhibition test. 184 32

The in vitro succinate dehydrogenase inhibition (SDI) test was adapted to be used with microtiter plates and this microtiter SDI (mSDI) test was evaluated for clinical use of chemosensitivity testing, as compared to findings with the SDI test. The optimal conditions of the mSDI test were determined: (1) 2-5 x 10(4) cells/well; (2) enzymatic disaggregation of solid tumors with the use of a mixture of 0.2% pronase, 0.25% collagenase, 0.1% DNase for 20 min at 37 degrees C; (3) addition of 10 mM sodium succinate in the colorimetric reaction; and (4) use of dimethyl sulfoxide (DMSO) as a solvent for extraction of formazan product. Good correlations were observed between the mSDI and the SDI tests when S-180 cells (r = 0.890-0.996) or 16 human fresh tumor cells (r = 0.731-0.999) were exposed to six anti-cancer drugs (carboquone, adriamycin, mitomycin C, aclacinomycin A, cisplatin, 5-fluorouracil). Thus, the mSDI test facilitates testing of a large number of drugs with minimal amounts of specimens, and is expected to replace the SDI test for chemosensitivity testing of clinical tumor cells.
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PMID:The microtiter SDI test is more advantageous than the SDI test for assessing the chemosensitivity of human tumor cells. 195 59

The usefulness of an in vitro human tumor culture system using a specialized collagen gel matrix derived from pig skin was retrospectively evaluated as a chemosensitivity test for human gastric carcinomas. Seven xenograft tumors derived from human gastric cancers were examined by this system (CGM assay) and compared with the data obtained by a nude mice assay (NM assay) and a succinic dehydrogenase inhibition test (SDI test). Xenograft tumors had three-dimensional growth on the collagen gel matrix like that in vivo. There was increasing cell kill with rising cytotoxic drug concentration. When drug sensitivity was evaluated as effective based on an inhibition rate of 40% or more in the CGM assay, drug sensitivity as measured by the CGM assay corresponded with that measured by the NM assay for all xenograft tumors but not the SDI test. This system could be applied for chemosensitivity test of scirrhous gastric carcinomas. It was suggested that the CGM assay may be more like an in vivo like chemosensitivity test and clinically useful testing for the patients with gastric cancer, including scirrhous one.
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PMID:[In vitro chemosensitivity test using collagen gel matrix for human gastric carcinomas]. 196 Nov 82

The activity of the mitochondrial glycerol phosphate dehydrogenase (EC 1.1.99.5), the enzyme unique to the glycerol phosphate hydrogen shuttle, was measured in normal human tissues and tumors and compared with the activity of succinate dehydrogenase, another enzyme that transfers electrons to ubiquinone at site II of the electron transport chain. Six of 7 insulinomas and 10 of 12 carcinoid tumors showed high glycerol phosphate dehydrogenase activity. The activity was also increased in 3 of 4 gastrinomas, 2 paraganglionomas, 1 of 4 thyroid nodules, and 1 parathyroid tumor. These tissues belong to the amine precursor uptake decarboxylation system. The activity of glycerol phosphate dehydrogenase was generally unremarkable in non-amine precursor uptake decarboxylation system tumors and in normal tissues studied. However, 1 of 2 breast carcinomas, 1 submandibular tumor, and 2 of 3 melanomas were enriched in glycerol phosphate dehydrogenase activity. In general, succinate dehydrogenase activity exceeded that of glycerol phosphate dehydrogenase in all tissues except some of the tissues in which glycerol phosphate dehydrogenase activity was high. Normal tissues, such as the pancreatic beta-cell, which aerobically metabolize glucose rapidly utilize the glycerol phosphate shuttle to oxidize the large amount of NADH formed from glucose metabolism in the cytosol. Whether this is the reason for the enriched activity of the glycerol phosphate dehydrogenase in certain amine precursor uptake decarboxylation system tumors is unknown.
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PMID:High activity of mitochondrial glycerol phosphate dehydrogenase in insulinomas and carcinoid and other tumors of the amine precursor uptake decarboxylation system. 197 16

The chemosensitivities of 26 lung adenocarcinoma tissues were compared to those of 110 gastric adenocarcinoma tissues, using the in vitro succinate dehydrogenase inhibition (SDI) test. Tumour tissues obtained at surgery were exposed to five different anticancer drugs: carboquone (CQ), adriamycin (ADM), mitomycin C (MMC), cisplatin (DDP) and 5-fluorouracil (5-FU). The lung adenocarcinomas showed a statistically significant reduction in succinate dehydrogenase (SD) activity, compared to the gastric adenocarcinomas, after exposure to each drug. The chemosensitivity was defined as a reduction in SD activity to 50% of control or less. Lesser degrees of reduction in SD activity were defined as drug resistance. The sensitivity rates to ADM, MMC and DDP, respectively, were significantly higher in the lung than in the gastric adenocarcinomas. Tumour cells from 22 (84.6%) of the 26 lung adenocarcinoma tissues showed a sensitivity to more than three drugs, whereas the rate was only 46.4% (51/110) for the gastric adenocarcinomas. The rate of resistance to all the drugs tested was 3.8% (1/26) for the lung adenocarcinomas, in contrast to the 20.9% (23/110) seen with the gastric adenocarcinomas. Thus, while adenocarcinomas of the lung and stomach both show clinical resistance to anticancer agents, the chemosensitivity of the lung tissues is greater. In the light of these observations, attention must be directed to improving specific drug delivery systems.
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PMID:Lung adenocarcinoma is more sensitive than gastric adenocarcinoma to anticancer drugs in vitro. 199 57

The chemosensitivities of 62 human colon cancer tissues, 67 rectal cancer tissues and 31 tumor-adjacent normal mucosal tissues were determined using the in vitro succinate dehydrogenase inhibition (SDI) test. These tissues obtained at the time of surgery were exposed to carboquone (CQ), adriamycin (ADM), mitomycin C (MMC), aclacinomycin A (ACR), cisplatin (DDP) and 5-fluorouracil (5-FU). The chemosensitivity was considered as positive when succinate dehydrogenase (SD) activity of the drug-treated cells decreased to below 50% of that of control cells, on day 3 of exposure. Decrease in the SD activity was noted in the colon cancer tissues, compared to the rectal cancer tissues, exposed to six antitumor drugs and in particular, to CQ (p less than 0.05), DDP (p less than 0.01) and ACR (p less than 0.05, one-sided paired t test). Decrease in the SD activity was noted in the tumor tissues, compared to the tumor-adjacent normal tissues, exposed to CQ, MMC and ACR (p less than 0.01). The sensitive rates were higher in the colon cancer tissues than the rectal cancer tissues, against all six antitumor drugs. Our findings show that the rectal cancer tissues are resistant to antitumor drugs, compared to the colon cancer tissues in vitro. When selecting antitumor drugs to treat patients with a rectal cancer, the assessment for chemosensitivity of the related tissues is crucial.
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PMID:Human colon cancer tissues are more sensitive than rectal cancer tissues to antitumor drugs in vitro. 199 40

In order to determine the most effective anticancer agent for individual human tumor, we have performed several chemosensitivity tests, such as human tumor clonogenic assay (HTCA), succinic dehydrogenase inhibition test (SDI-T), nude mouse isotope assay (NM-IA) and subrenal capsule assay (SRCA). In this study, an novel in vitro chemosensitivity test (ATP-assay) measuring ATP amounts of cancer cells was carried out in 69 fresh gastro-intestinal tumors obtained at surgery. As the results, the evaluable rate of ATP assay was 87.0%. The positive rate of ATP assay against all tumors were 13.3% in mitomycin-C (MMC), 11.7% in adriamycin (ADM), 13.3% in 5-fluorouracil (5-FU) and 18.3% in cis-diamminedichloroplatinum (CDDP), respectively. Overall predictive accuracy rate was 82.8%. The comparative study of the survival rates of the patients with stage IV gastric cancer, receiving sensitive anticancer agents assayed by ATP assay, and those receiving negative anticancer agents revealed that the survival rate of the patients treated with sensitive drugs was longer with Kaplan-Meier analysis. From these results, it seems reasonable to conclude that ATP assay is of value in determining the chemosensitivity of gastrointestinal cancer in each patient.
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PMID:[Clinical studies of in vitro chemosensitivity test evaluated by ATP assay of gastrointestinal cancer]. 212 11

For the chemosensitivity for carcinoma of digestive organs, gastric, colorectal, and hepatic cancer tissues were examined using in vitro succinate dehydrogenase inhibition (SDI) test and in vivo subrenal capsule (SRC) assay. The chemosensitivity varied in the tissue. The origin of an organ tumor, histological differentiation, and difference of primary or metastatic lesions are critical for determining chemosensitivity. Biochemical analysis shows that antitumor drugs have an increased susceptibility in tissues with high activity of pyrimidine nucleotide synthesis.
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PMID:Chemosensitivity test for carcinoma of digestive organs. 215 26


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