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)

CDF1 mice receiving Adriamycin, 12 mg/kg IP develop a toxic GI mucositis. The mean survival in CDF1 mice after Adriamycin injection was found to be 6.5 +/- 2.0 weeks and could be increased by alcohol or acetate Vitamin E pretreatment (with 2 g/kg qDx7d) to 22.06 +/- 12.3 weeks or by treatment with Venoruton after Adriamycin (qDx7 with 1.5 g/kg) to 23.7 +/- 12.7 weeks. Other schedules were ineffective or harmful. The ability of Venoruton to enhance survival when given after Adriamycin encouraged us to proceed to tumor bearing mice. The maximum survival with CDF1 mice bearing 5 X 10(6) L1210 cells was 1 +/- 0.2 week which could be increased to 2.17 +/- 0.8 weeks with optimal dose Adriamycin (10 mg/kg). Optimum survival with Venoruton and a single dose of Adriamycin was 2.45 +/- 0.91 weeks with Venoruton, 1.5 g, qd X 14, and 12 mg/kg Adriamycin. Treatment of L1210 bearing mice with Adriamycin, 10 mg/kg on days 1 and 8, yielded a survival of 2.23 +/- 0.7 weeks. An equitoxic regimen of Adriamycin, 11 mg/kg on days 1 and 9, plus Venoruton, 1.5 g, qd X 14, increased survival 30% to 3.08 +/- 2.9 weeks. Venoruton is a promising agent to increase the therapeutic index of Adriamycin.
 ...
PMID:Effect of dose schedule of vitamin E and hydroxethylruticide on intestinal toxicity induced by adriamycin. 377 91

The effects of various forms of tocopherol (vitamin E) on the growth and differentiation of mouse melanoma (B-16) and mouse fibroblast (L-cells) cells in culture were studied. D-alpha-tocopherol acid succinate induced morphological alterations and growth inhibition in melanoma cells. When vitamin E acid succinate was removed 4 days after treatment, the above changes remained irreversible for a period of 24 hr, after which resistant cells and partially affected cells renewed cell division and eventually reached confluency. The relative efficacy of D and DL forms of vitamin E acid succinate remains to be evaluated. However, other forms of vitamin E such as DL-alpha-tocopherol free alcohol, Aquasol DL-alpha-tocopherol acetate, DL-alpha-tocopherol nicotinate, or sodium succinate with an equivalent volume of ethanol, at similar concentrations, were ineffective. Vitamin E acid succinate at similar concentrations did not induce morphological changes in fibroblasts. Melanoma cells were about 2-fold more sensitive to vitamin E acid succinate than were fibroblasts for the criterion of growth inhibition. Vitamin E acid succinate-induced morphological changes and growth inhibition in melanoma cells were expressed in hormone-supplemented serum-free medium, but the concentration requirement was about 5 times less than that needed in serum-supplemented medium. Although cyclic adenosine 3': 5'-monophosphate-stimulating agents are known to cause growth inhibition and morphological changes in melanoma cells in culture, vitamin E acid succinate-induced morphological alterations in melanoma cells are no mediated by a rise in cellular cyclic adenosine 3':5'-monophosphate. Ethanol was sufficient to increase the melanin content in melanoma cells. These data show that vitamin E acid succinate may be a potentially useful tumor therapeutic agent.
 ...
PMID:Effects of tocopherol (vitamin E) acid succinate on morphological alterations and growth inhibition in melanoma cells in culture. 627 80

The present study showed that vitamin E, although ineffective by itself, was able to potentiate the ability of selenium to inhibit the development of mammary tumors induced by dimethylbenz(a)anthracene (DMBA) in rats. Animals were maintained on a high-polyunsaturated fat (20% corn oil) diet in order to increase the degree of oxidant stress; additional selenium and/or vitamin E were present at a concentration of 2.5 and 1000 mg/kg of diet, respectively. It should be noted that rats tolerated these levels of supplementation very well with no obvious undesirable effect. Furthermore, our results indicated that vitamin E facilitated the anticarcinogenic action of selenium only when it was present during the proliferative phase. We then proceeded to examine whether DMBA administration would lead to any persistent damage in tissue peroxidation or changes in activities of enzymes associated with peroxide metabolism. It was found that DMBA resulted in an acute but modest increase in lipid peroxidation at 24 hr after carcinogen treatment. This perturbation was only of a transient nature. By comparing the response in a target tissue (mammary fat pad) and a non-target tissue (liver), it can be inferred that DMBA may have a differential effect on the degree of oxidant stress. The antagonistic effect of selenium and vitamin E in suppressing lipid peroxidation was then evaluated. Several conclusions can be drawn regarding the antioxidant potency of these agents in conjunction with their efficacies in cancer prevention. First, although vitamin E is a more effective antioxidant than selenium, it is apparent that systemic suppression of lipid peroxidation by vitamin E subsequent to a carcinogenic insult is not sufficient to inhibit tumor formation. Vitamin E supplementation increases significantly the microsomal hydroperoxidase activity. At the present time, it is unclear what role, if any, this enzyme plays in the synergistic effect of vitamin E and selenium in the inhibition of tumorigenesis. Secondly, the anticarcinogenic action of high levels of selenium is not related to its biochemical function in the regulation of the selenium-dependent glutathione peroxidase. The explanation for this is that the enzyme is already operating at near maximal capacity under normal physiological conditions. Additional selenium will not further increase its activity, since the enzyme protein becomes the limiting factor. Finally, vitamin E may be able to provide a more favorable climate against oxidant stress, thereby potentiating the action of selenium via some other mechanism.
 ...
PMID:Synergistic effect of vitamin E and selenium in the chemoprevention of mammary carcinogenesis in rats. 641 56

Epidemiological studies suggest a causal relationship of dietary polyunsaturated fatty acids (PUFA's) with the morbidity and mortality from breast cancer. In order to reveal possible underlying mechanisms of these findings, we studied the influence of n-3 and n-6 PUFA's in comparison to oleic acid on the proliferation of well characterized estrogen dependent (MCF-7, ZR-75, T-47-D) and estrogen independent (MDA-MB-231, HBL-100) breast cancer cells in culture. The cell growth inhibitory effect was related to the formation of lipid peroxidation products. Normal human skin fibroblasts served as a control. In fibroblasts, the addition of 20 micrograms/ml of exogenous fatty acids either had no effect or caused an insignificant increase of proliferation. Similar results were obtained with MCF-7 cells. In all other breast cancer cell types, n-3 long-chain PUFA's, eicosapentaenoic and docosahexaenoic acids, were the most effective fatty acids in arresting the cell growth. Alpha-linolenic and gamma-linolenic acid exerted a variable effect on cell proliferation depending on the cell line investigated. Oleic acid significantly stimulated the proliferation of hormone-independent breast cancer cells while it had no effect on the proliferation of hormone-dependent cells. Viability studies by trypan blue excretion indicated that the arrest in cell growth was not due to major cytotoxic effects. The addition of PUFA's to breast cancer cells caused a significant increase in the formation of conjugated dienes and lipid hydroperoxides in the cellular lipids; their content was significantly correlated with the capacity of arresting cell growth. In contrast, the addition of PUFA's to fibroblasts did not increase lipid hydroperoxide formation. The addition of Vitamin E to cancer cells at a concentration of 10 microM to the PUFA-supplemented medium almost completely restored cell growth. Our data indicate that PUFA's significantly interfere with cell proliferation of breast cancer cells in vitro due to the formation of oxidation products. In addition to that, there must be other factors involved, most probably related to the differential metabolism of PUFA's in tumor cells. Our findings may have some impact on treatment and prevention of breast cancer.
 ...
PMID:Influence of n-3 fatty acids on the growth of human breast cancer cells in vitro: relationship to peroxides and vitamin-E. 757 84

In this study we evaluated the effect of dietary administration of a high-fat, low-fiber diet (HRD) supplemented with Vitamin E, beta-carotene or folic acid and wheat bran on the growth of pre-existing aberrant crypt foci (ACF) that had been induced in Fischer-344 rats exposed to azoxymethane (AOM) and a HRD for 10 weeks. The rats (25 rats/dietary group) were fed a HRD for 2 weeks and were then given 2 subcutaneous injections of AOM (15 mg/kg body weight) while the rats continued on the HRD. After 6 weeks, rats were either maintained on the HRD (control) or crossed over to a HRD containing non-toxic levels of either Vitamin E, beta-carotene, folic acid or wheat bran. At 10, 14 and 18 weeks after the initiation of the experiment, 5 rats from each group were killed and the number of aberrant crypt foci (ACF) with different multiplicities were compared between groups. The dietary intervention was continued for 30 weeks to determine whether the inhibitory effect on the growth of ACF influenced the subsequent development of colonic tumors. The results revealed that vitamin E and beta-carotene caused a significant decrease in the number of ACF of different multiplicities when compared to the effect of the HRD alone. The decrease in the number of ACF due to folic acid and wheat bran appeared to be much smaller and in most cases was not significant. However, there was also a significant decrease in the incidence of colonic tumors and tumor multiplicity in both the vitamin E and beta-carotene groups that was not seen in the control group. The reports clearly demonstrates the ability of vitamin E and beta-carotene to inhibit the growth of colonic ACF, even in the presence of the strong promoting effect of high levels of dietary fat, using a post-initiation experimental design.
 ...
PMID:Inhibition of progression of aberrant crypt foci and colon tumor development by vitamin E and beta-carotene in rats on a high-risk diet. 775 87

Thirty-two typical patients with breast cancer, aged 32-81 years and classified 'high risk' because of tumor spread to the lymph nodes in the axilla, were studied for 18 months following an Adjuvant Nutritional Intervention in Cancer protocol (ANICA protocol). The nutritional protocol was added to the surgical and therapeutic treatment of breast cancer, as required by regulations in Denmark. The added treatment was a combination of nutritional antioxidants (Vitamin C: 2850 mg, Vitamin E: 2500 iu, beta-carotene 32.5 iu, selenium 387 micrograms plus secondary vitamins and minerals), essential fatty acids (1.2 g gamma linolenic acid and 3.5 g n-3 fatty acids) and Coenzyme Q10 (90 mg per day). The ANICA protocol is based on the concept of testing the synergistic effect of those categories of nutritional supplements, including vitamin Q10, previously having shown deficiency and/or therapeutic value as single elements in diverse forms of cancer, as cancer may be synergistically related to diverse biochemical dysfunctions and vitamin deficiencies. Biochemical markers, clinical condition, tumor spread, quality of life parameters and survival were followed during the trial. Compliance was excellent. The main observations were: (1) none of the patients died during the study period. (the expected number was four.) (2) none of the patients showed signs of further distant metastases. (3) quality of life was improved (no weight loss, reduced use of pain killers). (4) six patients showed apparent partial remission.
 ...
PMID:Apparent partial remission of breast cancer in 'high risk' patients supplemented with nutritional antioxidants, essential fatty acids and coenzyme Q10. 775 35

Vitamin E was quantified in renal cell carcinomas (RCC) and in 'intact' renal cortex, obtained from 31 patients subjected either to unilateral nephrectomy or to partial resection of the only kidney. Histologically, 14 tumors consisted predominantly of clear cells (group 1) and 17 of other cell types (group 2). In both groups, a significant increase in vitamin E concentration, as compared to the 'intact' cortex, was observed: 167.8 +/- 27.9 and 68.2 +/- 15.2 micrograms/g wet tissue weight (mean +/- SEM) for groups 1 and 2, respectively, versus 10.1 +/- 0.53 micrograms/g wet tissue weight for the cortex. Although the total lipid content was also increased in tumors (especially in group 1), the vitamin E concentration in tumor tissue, calculated per milligram of total lipids, proved to be much higher in both groups than in 'intact' cortex. A significant positive correlation was observed between vitamin E and total lipid content in group 1 and 2 carcinomas. It was also found that vitamin E accumulation in RCC is unlikely to be attributed to an enhanced lipid deposit in the tumor cells. Thus, in 8 tumors of group 2 the vitamin E levels were markedly enhanced although these tumors did not differ from the cortex in total lipid concentrations. Vitamin A content determined in 17 carcinomas, when calculated per milligram of total lipids, was the same as in 'intact' cortex.
 ...
PMID:Liposoluble vitamins E and A in human renal cortex and renal cell carcinomas. 777 11

The present study was designed to evaluate whether vitamin E could be a useful chemopreventive agent to reduce spontaneous lung tumorigenesis in mice. Starting at 6 weeks of age, groups were divided into three groups, i.e. A/J mice fed a control diet (A/J control), A/J mice fed a vitamin E-supplemented diet (A/J vitamin E) and ddY mice fed a control diet (ddY control). At the 28th experimental week, nuclear NADPH-driven active oxygen generation, thiobarbituric acid reactive substances (TBARS) and DNA single strand breaks (DNA-SSB) in A/J mice fed a control diet were significantly higher than those in the ddY control group. A/J mice fed Vitamin E for 28 weeks could decrease the levels of TBARS and DNA-SSB with a significant difference, as compared with those in A/J control mice. The nuclear alpha-tocopherol levels in A/J controls were significantly lower than those in ddY controls, on the contrary, the vitamin feeding to A/J mice increased nuclear alpha-tocopherol levels more than that in the ddY controls. At the 40th experimental week, lung tumor incidence and tumor multiplicity (percentage of mice with tumors) in A/J controls were reduced and brought close to those in ddY control mice by vitamin E. Then the alpha-tocopherol level in plasma of A/J controls was significantly lower than the level in plasma of ddY controls, and the level in tumor-bearing mice in A/J controls also showed a lower level with significant difference as compared to that in non-tumor-bearing mice of A/J controls. These results suggest that the difference in susceptibility to spontaneous lung tumorigenesis between A/J and ddY mice partly depends on the difference of oxidative stress on the pulmonary nuclei, and vitamin E can act as a useful chemopreventive agent to reduce spontaneous lung tumorigenesis in mice.
 ...
PMID:Vitamin E acts as a useful chemopreventive agent to reduce spontaneous lung tumorigenesis in mice. 781 42

Oxidative stress may play a partial role in chemically induced tumorigenesis in mice. Herein, we investigated the preventive effect of vitamin E on 4-nitroquinoline 1-oxide (4NQO)-induced oxidative damage on pulmonary nuclei and lung tumorigenesis in mice. At 4 weeks after 4NQO injection, the levels of nuclear thiobarbituric acid substances (TBARS) and DNA single strand breaks (DNA-SSB) in the lungs of mice treated with 4NQO were significantly higher than those in the control mice. The 4NQO-induced oxidative stress on the nuclei and DNA-SSB were significantly inhibited by vitamin E treatment. The nuclear alpha-tocopherol level in the 4NQO-treated group was significantly lower than that in the control, but the plasma alpha-tocopherol level in the former was slightly lower than that in the latter. Vitamin E feeding compensated the decrease of the level in the nuclei and plasma. The feeding on excessive vitamin E for 23 weeks after 4NQO injection could partly reduce the lung tumor incidence as well as lung tumor multiplicity in mice. These findings suggest that vitamin E could partly suppress 4NQO-induced lung tumorigenesis in mice, probably through the inhibition of 4NQO-induced oxidative damage on the nuclei.
 ...
PMID:Effect of vitamin E on 4-nitroquinoline 1-oxide-induced lung tumorigenesis in mice. 781 32

Vitamin E was quantified in tumor tissue obtained from 17 patients with renal cell carcinoma (RCC). The tumors consisted of two groups: (I) represented primarily by clear cells (10 cases) and (II) without predominant appearance of those cells (7 cases). Vitamin E concentration in tumor tissue was compared with that in intact tissue sites of the kidney. The vitamin content in intact renal medulla was shown to be 1.5 times higher than in intact cortex. Vitamin E level in group I tumors was shown to be on average 15 and 10 times as much as in intact renal cortex and medulla, respectively. The vitamin concentration in group II tumors, as compared with the above intact renal tissues, was 7- and 5-fold higher, respectively. In spite of the high tumor total lipids levels, the vitamin E concentration, calculated per mg total lipids, was still higher in tumor tissue than in the normal renal tissues. This finding was especially demonstrable for the group I tumors. In the benign renal tumor angiomyolipoma vitamin E concentration, calculated on a wet weight basis, was higher than in intact renal tissue, but no differences were observed when a per total lipids calculation was performed. Vitamin A concentration determined in the tumor samples obtained from 6 patients was the same as in intact cortex.
 ...
PMID:[Content of vitamins E and A in tumor tissue in kidney cancer]. 805 29


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