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

Eighty young adult male Syrian hamsters were divided into four equal groups. Group 1 animals had the right buccal pouches painted with a 0.1% solution of 7,12 dimethylbenz(a)anthracene (DMBA) three times per wk for 28 wk. Group 2 animals were similarly painted with DMBA for 28 wk but were also given 140 micrograms vitamin E in 0.4 ml mineral oil three times weekly on days alternate to DMBA painting. Group 3 animals were used as DMBA-vehicle controls. Group 4 animals were vitamin E controls. Animals were killed after 28 wk, the pouches photographed and tumors counted, measured. The pouches were fixed in formalin, sectioned in paraffin and studied histologically and histochemically for tumor necrosis factors alpha and beta. All animals in Group 1 and 3 had gross tumors of the right buccal pouch. None of the animals in Group 2 had grossly visible tumors. Microscopic studies revealed that, while no gross tumors were seen in the Group 2 animals, there was histologic evidence of dysplasia and early carcinoma-in-situ undergoing degeneration. Immunohistochemical staining revealed a dense infiltrate of mononuclear cells adjacent to tumor sites with a large number of cytotoxic T lymphocytes and macrophages. Vitamin E appears to prevent tumor formation by stimulating a potent immune response to selectively destroy tumor cells as they begin to develop into recognizable microscopic foci of carcinoma.
 ...
PMID:Prevention of experimental cancer and immunostimulation by vitamin E (immunosurveillance). 211 3

Vitamin E succinate inhibited proliferation of C4#1 cells, an established avian retrovirus [reticuloendotheliosis virus (REV)]-transformed immature lymphoid tumor cell line, in a dose-dependent manner. The cytostatic effects of vitamin E succinate were reversible in that treated cells regained their ability to divide after vitamin E succinate removal. Possible mechanism(s) for the antiproliferative actions of vitamin E succinate were investigated. Analyses of C4#1 cell surface membrane antigen profiles and morphology indicated that vitamin E succinate was not inducing differentiation of the tumor cells to a more mature, differentiated, nonproliferative state. Five antioxidants, including a synthetic analogue of vitamin E, Trolox, as well as the active vitamin form, DL-alpha-tocopherol, were incapable of inhibiting C4#1 tumor cell growth, indicating that a mechanism of action other than or in addition to functions as an antioxidant may be operating. Cell cycle analyses suggested that C4#1 tumor cells treated with vitamin E succinate were blocked in the G0G1/early S phases of the cell cycle. Tumor growth arrested by vitamin E succinate did not affect the expression of the REV-encoded oncogene, v-rel, at either the RNA or protein level. These studies demonstrated that vitamin E, in the form of vitamin E succinate, inhibited the growth of retrovirus-transformed tumor cells in vitro and suggested that the antiproliferative effects of vitamin E succinate did not involve antioxidant properties but rather, as yet, unidentified mechanisms leading to cell cycle blockage.
 ...
PMID:Growth-inhibitory effects of vitamin E succinate on retrovirus-transformed tumor cells in vitro. 236 34

Vitamin E(dl-alpha-tocopherol) dissolved in ethanol with polyethylene glycol as the vehicle and administered by intraperitoneal injections of 0.1 mg/gm body weight at two day intervals, was demonstrated to be a potent immunomodulating reagent in young chickens challenged with avian reticuloendotheliosis virus-transformed tumor cells. Vitamin E treatment enhanced the mitogen-induced proliferative responses of spleen cells from age matched, unchallenged chickens; reduced the tumor cell-induced suppression of host splenic lymphocyte mitogen responses; and eliminated tumor cell-induced suppressor cell activity. However, inspite of an improved immune status the vitamin E treated-tumor cell challenged chickens exhibited enhanced tumorigenesis.
 ...
PMID:Modulation of immune suppression and enhanced tumorigenesis in retrovirus tumor challenged chickens treated with vitamin E. 256 27

Combination of Vitamin E in a single megadose of 20 units per 200 gram rat and chemotherapy was performed. The results revealed that Vitamin E treatment does indeed reduce Adriamycin toxicity and adds to tumor reduction and decrease metastasis. Vitamin E also enhances the efficacy of Cyclophosphamide, Adriamycin and Methotrexate.
 ...
PMID:Chemotherapy and vitamin E in treatment of Nb rat prostate tumors. 297 62

The influences of vitamin C and vitamin E on cancer reported in the literature are reviewed. Several correlational studies and case-control studies suggest that the consumption of vitamin C-containing foods is associated with lower risk for certain cancers, particularly gastric and esophageal cancer. No definite links between dietary vitamin E and human cancer have been demonstrated. Animal and in vitro studies have shown that vitamins C and E can effectively inhibit the formation of carcinogenic nitrosamines. However, animal studies examining the effects of these two vitamins on other chemically-induced cancers are not conclusive. Vitamin C supplementation has been reported to inhibit skin, nerve, lung and kidney carcinogenesis. Vitamin E has been shown to inhibit skin, liver, oral, ear duct, and forestomach carcinogenesis; and to enhance, to have no effect on, or to inhibit mammary gland or colon carcinogenesis, depending upon the method of administration, the level of dietary selenium or fat, and the species and strain of animals used. Both vitamin C and vitamin E can inhibit mutagenesis and carcinogenesis in vitro. Each of the vitamins has been shown to inhibit tumor cell growth and carcinogen-induced DNA damage. The mechanism of action of the two vitamins against carcinogens is not clearly understood. Several suggested mechanisms of action include modification of the metabolism of polycyclic hydrocarbons, reduction of mutagenic activity and reaction with genotoxic free radicals. It is concluded that the potential usefulness of vitamin C and vitamin E in the prevention and treatment of cancer should not be ignored because under certain experimental conditions these two vitamins exert inhibitory effects on chemical carcinogenesis. More carefully standardized and controlled experiments are required to adequately evaluate this potential.
 ...
PMID:Vitamin C, vitamin E and cancer (review). 305 51

Combined effects of vitamin E (alpha-tocopherol) and cisplatin on the growth of two murine neuroblastomas (C1300, NS-20) was investigated in vivo. Five groups of mice were prepared; group 1 were fed the control diet, group 2 were fed a vitamin E-deficient diet, group 3 were fed a vitamin E-supplemented diet, group 4 were fed the control diet and plus vitamin E solution given intraperitoneally during the treatment (solvent i.p. group), and group 5 were given vitamin E in the same manner (20 mg/kg/day; vitamin E i.p. group). Cisplatin (6 mg/kg) was injected intraperitoneally into the mice of each group during the treatment. In case of the C1300 neuroblastoma, the antitumor activity of cisplatin was most enhanced in the mice receiving vitamin E i.p., and the intra-tumor vitamin E and platinum levels were significantly higher in this group than in the other groups (P less than 0.01, and P less than 0.05 respectively). In contrast, in animals transplanted with the NS-20 murine neuroblastoma, which proved to be a cisplatin-tolerant tumor in separate experiments, no combined effect of those drugs was observed, although the intra-tumor level of platinum was elevated. The possibility was that vitamin E increases the influx of cisplatin into the tumor cells and acts after incorporation of cisplatin through the plasma membrane. Vitamin E did not accentuate the cisplatin-induced renal impairment in vitamin E-loaded groups. Those results suggested that vitamin E should be considered as a co-agent of cisplatin for the treatment of neuroblastoma.
 ...
PMID:Combined effects of vitamin E (alpha-tocopherol) and cisplatin on the growth of murine neuroblastoma in vivo. 320 17

Adriamycin used in combination with vitamin E (Tocopherol) was evaluated in the treatment of Nb rat prostate adenocarcinoma. Vitamin E has been shown to enhance the growth-inhibitory effects of adriamycin on human prostatic carcinoma cells in vitro. The adriamycin-vitamin E treatment groups had the lowest average final tumor volume, but the mortality rate was 57% (17/30). These results suggest that vitamin E may play a role in enhancing the cytotoxic effects of adriamycin, but may not have any protective effect on normal cells as previously suggested through in vitro methods.
 ...
PMID:Adriamycin-vitamin E combination therapy for treatment of prostate adenocarcinoma in the Nb rat model. 341 71

Vitamin E was shown to regress established epidermoid carcinomas of Syrian hamster buccal pouch in 20 experimental animals following tumor induction by applications three times a week of 0.5% 7,12-dimethylbenz[a]anthracene (CAS: 57-97-6) in mineral oil for 13 weeks. The vitamin E was injected into the tumor-bearing buccal pouch twice weekly for 4 weeks in a dose of 250 micrograms in minimum essential medium. Twenty animals were maintained as untreated controls, and another 20 animals were sham-inoculated vehicle controls. Microscopic examination of buccal pouches with regressed tumor showed small epidermoid carcinomas with degeneration of tumor cells and a dense infiltrate of leukocytes, lymphocytes, and histiocytes. Buccal pouches of control animals showed large well-differentiated or moderately differentiated epidermoid carcinomas. The hamster buccal pouch cancer model presents many similarities to human oral cancer, including expression of the same oncogene, and these results offer hope for the chemotherapy of human oral cancer with the use of a relatively nontoxic agent injected locally.
 ...
PMID:Regression by vitamin E of experimental oral cancer. 347 5

The effects of cabbage and vitamin E on colon carcinogenesis were investigated in Swiss mice treated with 1,2-dimethylhydrazine. Throughout the experiment the mice were fed a laboratory chow diet (46 mg vitamin E per kg) or chow containing 13 g cabbage per 100 g or 180 mg vitamin E per kg. Starting after 31 days of diet treatment the mice received 7 weekly s.c. injections of DMH. They were sacrificed 17 weeks after the first dose of DMH. While diet did not significantly alter colon tumor response, some trends were observed. Female mice given cabbage had a higher incidence (percent of mice with a tumor) and multiplicity (tumors per tumor bearing mouse) of colon tumors. Males were little affected by cabbage apart from a lower incidence of adenocarcinomas. Compared with mice fed the control diet those given vitamin E had a higher colon tumor incidence. This effect, which was stronger in females, was due to an increased incidence of adenomas. Vitamin E had little apparent affect on tumor multiplicity apart from a reduction in adenocarcinomas in females and adenomas in males. The data do not support the view that cabbage and vitamin E are protective against colon cancer.
 ...
PMID:Cabbage and vitamin E: their effect on colon tumor formation in mice. 356 89

Vitamin E (tocopherol) enhances the growth inhibitory effects of adriamycin (ADR) on a variety of cancer cells in vitro. The role of vitamin E (d-alpha-tocopheryl) acid succinate in adjuvant chemotherapy with ADR was assessed in DU-145 human prostatic carcinoma cells in culture. Adriamycin produced a dose-dependent growth inhibition of DU-145 cells. The ID50 of DU-145 cells on the criteria: of clonal assay was 13 ng./ml. and of cell count assay was 14 ng./ml. Vitamin E succinate also inhibited the growth of DU-145 human prostatic carcinoma cells in a dose-dependent manner. 4.4 micrograms./ml. and 5.4 micrograms./ml. vitamin E succinate in the culture medium produced inhibition of growth to 50 per cent of control (ID50) in the clonal and the cell count assays respectively. When adriamycin and vitamin E succinate were used in combination, both additive and synergistic effects were observed, depending on the concentration of vitamin E succinate used. Doses of vitamin E succinate greater than its ID50 had a synergistic effect while doses smaller than its ID50 had an additive effect. In either case, the presence of vitamin E succinate caused an enhancement of tumor cell cytotoxicity of adriamycin while decreasing its ID50. Equivalent concentrations of sodium succinate and ethanol used to dissolve vitamin E succinate did not have any effect on DU-145 cells. Thus, it is concluded that the effect of vitamin E succinate is due to vitamin E and not due to succinate or ethanol. These results suggest that vitamin E may have a role in the treatment of human prostatic cancer as an adjuvant agent to adriamycin.
 ...
PMID:Vitamin E enhances the chemotherapeutic effects of adriamycin on human prostatic carcinoma cells in vitro. 373 28


1 2 3 4 5 6 7 8 9 10 Next >>