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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The chemosensitivities of squamous cell carcinoma (SCC) tissues from the head and neck area were compared to findings of adenocarcinoma, mainly from digestive organs. The sensitivity of each tissue was determined using the in vitro succinate dehydrogenase (SD) inhibition test, which shares a common principle with the 3-(4,5-dimethyl-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay. Tumor tissues were obtained at surgery or biopsy. Anticancer drugs tested were carboquone, Adriamycin, mitomycin C, cisplatin (CDDP), aclacinomycin A, 5-fluorouracil and 1-hexylcarbamoyl-5-fluorouracil with 10 times the peak plasma concentration, respectively. The means +/- standard deviations of SD activities in SCC tissues were significantly lower than those in adenocarcinoma tissues (p less than 0.001), and the sensitivity rates of SD activity in SCC tissues had a higher value than those in adenocarcinoma tissues (p less than 0.05), against each drug. Our study showed that CDDP-based combination regimens might be effective for SCC tissues. The chemosensitivity of each excised tissue should be tested, in order to prescribe sensitive, effective drugs for each patient.
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PMID:Comparison of in vitro anticancer chemosensitivity between human squamous cell carcinoma and adenocarcinoma. 152 69

We obtained evidence that the cytotoxic effect of 5-fluorouracil (5-FU) is augmented when the drug is given in combination with hyperthermia (HYP) and dipyridamole (DP). Nontoxic levels of DP enhanced the combined cytotoxicity of 5-FU and HYP against B16 melanoma and human tumor cells in vitro as measured by the succinate dehydrogenase inhibition (SDI) test. Growth of B16 melanoma that had been subcutaneously implanted into the feet of C57 BL mice was inhibited by treatment with the combinations of 5-FU and HYP, of 5-FU and DP, and of 5-FU, HYP and DP as compared with the administration of 5-FU alone. Treatment with HYP plus DP did not alter the body weight of mice that received 5-FU. The administration of DP plus HYP seemed to render the tumor cells more sensitive to 5-FU. The combination of 5-FU, HYP and DP shows promise for the treatment of patients suffering from malignant disease.
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PMID:5-Fluorouracil's cytotoxicity is enhanced both in vitro and in vivo by concomitant treatment with hyperthermia and dipyridamole. 153 70

This study compares the toxic effects of the carotenoids, beta-carotene and canthaxanthin, and alpha-tocopherol (vitamin E) on human tumor cells and their normal counterparts in vitro. Seven different malignant cell lines were examined: oral carcinoma (two cell lines), breast (two cell lines), lung carcinoma (two cell lines), and malignant melanoma. The in vitro cell culture assays showed a consistent morphologic change in the affected tumor cells following treatment with carotenoid or vitamin E. A rounding of the tumor cells and eventual lifting off the tissue culture plate were observed. These changes were apparent after 1 to 5 hours of treatment depending on the tumor cell line. Associated with these observable cellular changes were quantitative reductions in proliferation (3H-thymidine proliferation) and succinic dehydrogenase activity (MTT assay). In addition, there was a noticeable change in protein expression, with an increased expression of a 70-kD protein following treatment with beta-carotene. This protein was associated with tumor cells showing a decrease in proliferation (oral carcinoma, malignant melanoma) but not with normal keratinocytes or melanocytes. These studies substantiate a selective cytotoxic effect on human tumor cell growth by carotenoids and alpha-tocopherol in vitro, and may provide an explanation of the therapeutic activity of these agents and their possible use in the treatment of premalignancy or early oral carcinoma.
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PMID:The selective cytotoxic effect of carotenoids and alpha-tocopherol on human cancer cell lines in vitro. 154 92

We compared the cytotoxic effects of two anthracycline derivatives, epirubicin (EPI) and adriamycin (ADM), against human tumor cells in vitro. Various tumor specimens, obtained at surgery, included 57 liver, 19 lung, 16 gastric, 10 colorectal and 7 breast cancer specimens. These tumor cells were exposed to the same concentration of EPI or ADM for 3 days. The chemosensitivity of each tumor cell type to each drug was then assayed using the in vitro succinate dehydrogenase inhibition (SDI) test. Sensitivity to the treatment was defined as a 50% or greater reduction in the succinate dehydrogenase (SD) activity of the tumor cells, relative to that of the control (untreated) cells. Each cell type, except for gastric cancer cells, was equally sensitive to EPI and ADM. Gastric cancer cells were more sensitive to EPI than to ADM (P less than 0.05). The rate of coincidence, the sum of the co-sensitive and co-resistant rates of all the tumors, was quite high (90.8%). Thus, these findings indicate that EPI and ADM are equally cytotoxic to each tumor cell type, but EPI is more cytotoxic than ADM to gastric cancer cells. Since EPI is reported to be less cardiotoxic than ADM, EPI may replace ADM in cancer chemotherapy.
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PMID:Epirubicin is equivalent to adriamycin in vitro against many cancer cells but more effective against gastric cancer cells. 158 May 55

The in vitro drug sensitivity of gastric cancer tissues obtained from 40 patients with advanced cancer was compared in terms of the pathological classifications which were assigned according to the General Rules for the Gastric Cancer Study in Surgery and Pathology in Japan. Cases of poorly differentiated adenocarcinoma which had penetrated the serosa were evaluated using the succinate dehydrogenase inhibition (SDI) test for determining the in vitro chemosensitivity. The sensitivity of the stage III group to cisplatin was higher than that of the stage IV group. Although there were no statistical differences in drug sensitivities according to macroscopic findings (Borrmann's classification), the expanding growth type was more susceptible that the infiltrating type to cisplatin, aclacinomycin A (ACR) and carboquone (CQ) microscopically. In cases of lymph node metastasis [n(+)] the sensitivity to cisplatin, ACR, CQ, adriamycin and mitomycin C was less than in those with or without primary lymph node metastasis [n(-)]; lymphatic invasion in the gastric wall (ly) was a significant factor linked to drug resistance. Our findings indicate that the evaluation of tumor pathology is important in predicting the chemosensitivity of poorly differentiated gastric cancers.
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PMID:Relationship between tumor histopathology and in vitro sensitivity to antitumor drugs in gastric cancer. 162 13

We investigated whether tumor cell lysis by lymphokine-activated killer (LAK) cells was enhanced by treatment of the tumor cells with cisplatin (CDDP) in vitro. Tumor cells were treated with CDDP in vitro, and the cytotoxic activity for LAK cells was measured by 4-h 51Cr-release assay. The alterations of succinate dehydrogenase (SD) activity, and DNA,RNA synthesis of tumor cells were analysed. The susceptibility of CDDP-treated (2 micrograms/ml, 2h) Daudi and KATO-III cells to lysis by short term-cultured LAK cells was enhanced, as was the susceptibility of CDDP-treated (2 micrograms/ml, 12h) autologous tumor and Daudi cells to lysis by long term-cultured LAK cells. SD activity and DNA synthesis in tumor cells were impaired by 12-h treatment with 2 micrograms/ml of CDDP, whereas those were not altered by 2-h treatment with 2 micrograms/ml of CDDP. The enhancement of the susceptibility of CDDP-treated tumor cells to long term-cultured LAK cells was thus elucidated; it was shown to be due to alterations of the tumor cells with regard to their SD activity and DNA synthesis. It is suggested that the combined therapy with CDDP and LAK cells offers hope for increasing the response rate and the long-term survival of cancer patients.
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PMID:Cisplatin treatment renders tumor cells more susceptible to attack by lymphokine-activated killer cells. 166 52

Well-coupled mitochondria were isolated from a HuH13 line of human hepatoma cells and human liver tissue. The liver mitochondria showed a feeble glutamine oxidation activity in contrast to the hepatoma mitochondria, whereas they utilized glutamate well for the oxidative phosphorylation. In the liver mitochondria, glutamate was oxidized via the routes of transamination and deamination. On the other hand, glutamate oxidation was initiated preferentially via transamination pathway in the tumor mitochondria. In the liver mitochondria, bicarbonate nearly at a physiological concentration inhibited oxygen uptake with glutamate as substrate. The interaction of bicarbonate with the pathway of glutamate oxidation occurred primarily at the level of succinate dehydrogenase, due to competitive inhibition of the enzyme by the compound. In contrast to the liver mitochondria, glutamate oxidation was not affected by bicarbonate in the tumor mitochondria. These results indicate that the aberrations in the glutamate metabolism and its regulation observed in the hepatoma mitochondria may be favorable to the respiration utilizing glutamine and/or glutamate as an energy source.
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PMID:Pathway of glutamate oxidation and its regulation in the HuH13 line of human hepatoma cells. 167 60

Growth of normal and malignant mouse mammary epithelial cells (MMEC) on a biomatrix of substrate-attached material from 3T3-L1 preadipocytes was evaluated to devise culture conditions that are suitable for transformation studies but do not involve embedding cells in a gel. The biomatrix was prepared as described by Levine and Stockdale, and serum-free medium contained bovine serum albumin, insulin, progesterone, prolactin, and linoleic acid. Each cell type produced a distinctive pattern of colony architecture in this culture system. Cells from virgin mice (vMMEC) usually formed elaborate, three-dimensional structures resembling ducts and alveoli; cells from pregnant mice (pMMEC) grew as flat monolayers; and tumor cells grew in multilayered clusters. Cell growth was monitored by an assay for succinate dehydrogenase. Similar growth rates were found through Day 8 in cultures of vMMEC and D2 carcinoma cells. Growth of vMMEC slowed thereafter, whereas tumor cells typically continued growing through Day 14 to 18. Increase in cell number during 18 days in culture was 3-, 7-, 9-, and 11-fold for cells from pregnant and virgin mice, BALB/cfC3H and D2 carcinomas, respectively. The percent cells in S phase on Day 2 of culture was 9% for pMMEC, 4 to 11% for BALB/cfC3H tumor cells, 20% for vMMEC, and 24% for D2 tumor cells. Thus, this culture system promotes extended growth of MMEC and offers several advantages over embedding cells in a collagen gel. It may therefore be applicable to in vitro transformation studies with MMEC.
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PMID:Comparative growth of normal and malignant mouse mammary epithelium cultured serum-free on a biomatrix from preadipocytes. 171 54

We describe our experience with succinic dehydrogenase inhibition (SDI) test for solid tumors as a chemosensitivity test using 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide. Specimens were obtained from 76 surgical resected tumors, including 32 colon cancers, 24 stomach cancers and 16 lung cancers. Following enzymatic dissociation of scissors-minced tumors, viable cells were cultured in serum free medium (S-Clone SF-B) for 4 days with eight drug concentrations obtained by 2-fold dilution of drugs. Among 76 specimens tested, 48 specimens including 15 colon cancers, 18 stomach cancers and 15 lung cancers were successfully evaluated. For the purpose of judgement, 50% inhibitory concentration (IC50) was calculated in each case. Tumor specimen was regarded as sensitive to a given agent when the IC50 value was the same or smaller than the cut-off concentrations (1 microgram/ml for mitomycin C, 5 micrograms/ml for cisplatin, 2 micrograms/ml for adriamycin and 50 micrograms/ml for 5-fluorouracil), and was regarded as resistant when it was larger than these levels. In vitro vs in vivo drug sensitivity was successfully evaluated in 23 cases. The overall predicting accuracy rate was 78% (18/23), with one true positive, 5 false positive and 17 true negative cases. This test appeared to be useful to tailor effective agents for patients because of its relatively high successful and predictive rates.
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PMID:[Comparison between clinical response and in vitro chemosensitivity of solid tumors in the succinic dehydrogenase inhibition test]. 172 63

The sunergic effects on sarcoma-180 (S-180) cells and on human malignant tumor cells between 1-hexylcarbamoyl-5-fluorouracil (HCFU), a lipophilic masked compound of 5-fluorouracil (5-FU), and hyperthermia were investigated. After the S-180 cells had been exposed to 77 microM of the drug for 3 days, with or without heat (43 degrees C) treatment for 2 hr, the succinate dehydrogenase (SD) activity was assayed to determine cell viability. The SD activity of S-180 cells treated with HCFU combined with heat decreased to about 7.8% of findings in the control cells. When the S-180 cells were implanted in a pad of the left posterior inferior foot of a mouse, the size of the tumor markedly decreased in case of exposure to HCFU and heat, compared with findings in other groups. Body weight of the mice remained stable after these procedures. Decrease in the SD activity of 6 human gastric cancers and 7 colorectal cancers exposed to HCFU combined with heat was compared with findings in the other groups. The SD activity markedly decreased when the cells were exposed to HCFU combined with heat. These results suggest that HCFU plus hyperthermia treatment is effective in the host with a malignancy and that the toxicity is minimal.
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PMID:Hyperthermia potentiates the cytotoxic activity of 1-hexylcarbamoyl-5-fluorouracil in sarcoma-180 cells and human malignant tumor cells. 177 28


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