Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin A is attracting increasing attention as a potential cancer chemopreventative agent. To investigate the effect of vitamin A on tumor establishment, growth and metastasis, rats were fed diets containing zero, adequate or excess (100X adequate) amounts of vitamin A prior to subcutaneous injection with transplantable hepatocellular carcinomas derived from solid tumors induced by N-2-fluorenylacetamide. When rats were injected at the same time the dietary regimen was begun, tumor growth was similar in both the deficient and adequate vitamin A groups with 20% less in the excess vitamin A group. However, when rats were injected 2 weeks post-initiation of the dietary regimen, tumors were fewer and appeared later under conditions of either vitamin A deficiency or excess. When rats were injected with a metastatic line 2 weeks following initiation of the dietary regimen, no metastases were observed in the animals fed excess vitamin A, but 60% had metastases in the deficient group and 75% in the adequate group. Results suggest that dietary extremes of vitamin A affect tumor establishment and growth and excess amounts prevent metastasis of transplantable hepatomas in the rat.
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PMID:Chemoprevention of tumor development and metastasis of transplantable hepatocellular carcinomas in rats by vitamin A. 624 1

Vitamin A possesses both wound-healing and antitumor actions. Vitamin A-induced fibroplasia results in subsequent increased collagen production and deposition. This effect of vitamin A has been shown to result in the production of collagenous capsules around several murine breast and lung tumor systems. This tumor encapsulation process can potentially convert a systemic disease to a local one that can be easily treated by tumor excision. The goal of the present study was to determine whether supplemental vitamin A could promote the encapsulation of a murine melanoma. Sixty DBA/2J male mice were inoculated intracutaneously with 1 x 106 Cloudman S91 melanoma cells using a 30-gauge needle. The mice were divided into three groups: a control group, a pre-vitamin A group, and a post-vitamin A group. The control mice were fed a commercial chow containing 15,000 IU of vitamin A and 6.4 mg of beta-carotene per kilogram diet, considerably more than the National Research Council's recommended daily allowance of vitamin A for normal mice. The control diet was, therefore, not vitamin A-deficient. The pre-vitamin A mice were fed the basal chow supplemented with 150,000 IU of vitamin A per kilogram diet for 10 days before inoculation and for the remainder of the study. The post-vitamin A mice were fed the vitamin A-supplemented diet beginning on the day of inoculation and continuing for the remainder of the study. Sixty days after inoculation, tumor growth was assessed and the five mice remaining in each group were euthanized. Ventral skin at the site of inoculation was harvested for histologic assessment of local tumor growth and invasiveness. The liver and lungs of each of these mice were also harvested for histologic assessment of tumor metastasis. Sixty days after tumor inoculation, a 60 percent survival rate was observed in the control group as opposed to the vitamin A-supplemented animals, which demonstrated a 100 percent survival rate in both groups (n = 5 in each group). Decreased mean tumor size and gross tumor in most vitamin A-supplemented animals were statistically significant when compared with the control animals. The control animals had a mean tumor size of 26.1 mm, whereas the post-vitamin A group had a mean tumor size of 5.7 mm. One hundred percent of the control group exhibited tumor; one animal had distant metastases. The pre-vitamin A group did not exhibit any tumor growth, and the post-vitamin A group exhibited tumor growth in 40 percent of animals. Neither vitamin A-supplemented group showed any evidence of distant metastases. The animals supplemented with vitamin A demonstrated decreased tumor growth and metastasis. This in vivo model may indicate a potential prophylactic and therapeutic role for supplemental vitamin A in the treatment of malignant melanoma.
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PMID:Investigation of the growth and metastasis of malignant melanoma in a murine model: the role of supplemental vitamin A. 1283 88

Clinical, epidemiological and experimental findings have provided evidence supporting a role of free radicals in the etiology of cancer. Free radical production is enhanced in many disease states, by carcinogen exposure, and under conditions of stress contributing widely to cancer development in humans. We have established an experimental breast cancer model to examine the effects of all-trans-retinol (retinol/vitamin A) on the production of free radicals in human breast epithelial cells induced by high linear energy transfer (LET)-radiation in the presence of 17beta estradiol. The following cell lines were used in these studies: the MCF-10F cell line, a spontaneously immortalized human breast epithelial cell line. Alpha 5 derived from MCF-10F cells irradiated with two separated doses of 60 cGy alpha particles in the presence of estrogens (60E/60E). Tumor 2, from a tumor formed in nude mice after injection with the cell line alpha 5. Tumor 3, from secondary tumor formed from injecting tumor 2 cells into nude mice. Each of the cell types examined had significantly elevated H(2)O(2) production levels compared to MCF-10F control cells (p<0.001). Retinol (1 microl/ml) significantly (p<0.05) decreased H(2)O(2) production in all cell types examined. Retinol significantly decreased (p<0.05) invasive capabilities of cells across matrigel coated invasion chambers and significantly reduced (p<0.05) PCNA, Fra-1, mutant p53 and increased Rb protein expression levels in comparison to non-retinol-treated ones when assayed using immunofluorescent staining coupled with confocal microscopy. The reduced H(2)O(2) production, decrease in cell invasive capabilities and alterations in protein expression levels suggest that retinol can be used as a chemopreventive agent in human breast cancer.
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PMID:Effect of retinol on radiation- and estrogen-induced neoplastic transformation of human breast epithelial cells. 1587 Sep 16