Influence of Cobalamin on the Survival of Mice Bearing Ascites Tumor

Tsao, Constance S.; Myashita, Koichi

doi:10.1159/000163770

Cited by 5 publications

(2 citation statements)

References 8 publications

(9 reference statements)

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“…Methylcobalamin inhibited tumor growth of SC-3 injected into mice [111], and caused SC-3 mouse mammary tumor cells to undergo apoptosis, even when stimulated to grow by the presence of growth-inducing androgen [112]. Methylcobalamin, but not cyanocobalamin, increased the survival time of mice bearing implanted leukemia tumor cells [113]. 5'-deoxyadenosylcobalamin and methylcobalamin, but not cyanocobalamin, were shown to be effective cytotoxic agents [114].…”

Section: Reviewmentioning

confidence: 99%

Nutrition and cancer: A review of the evidence for an anti-cancer diet

Donaldson¹

2004

Nutr J

553

344

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It has been estimated that 30–40 percent of all cancers can be prevented by lifestyle and dietary measures alone. Obesity, nutrient sparse foods such as concentrated sugars and refined flour products that contribute to impaired glucose metabolism (which leads to diabetes), low fiber intake, consumption of red meat, and imbalance of omega 3 and omega 6 fats all contribute to excess cancer risk. Intake of flax seed, especially its lignan fraction, and abundant portions of fruits and vegetables will lower cancer risk. Allium and cruciferous vegetables are especially beneficial, with broccoli sprouts being the densest source of sulforophane. Protective elements in a cancer prevention diet include selenium, folic acid, vitamin B-12, vitamin D, chlorophyll, and antioxidants such as the carotenoids (α-carotene, β-carotene, lycopene, lutein, cryptoxanthin). Ascorbic acid has limited benefits orally, but could be very beneficial intravenously. Supplementary use of oral digestive enzymes and probiotics also has merit as anticancer dietary measures. When a diet is compiled according to the guidelines here it is likely that there would be at least a 60–70 percent decrease in breast, colorectal, and prostate cancers, and even a 40–50 percent decrease in lung cancer, along with similar reductions in cancers at other sites. Such a diet would be conducive to preventing cancer and would favor recovery from cancer as well.

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Section: Reviewmentioning

confidence: 99%

Nutrition and cancer: A review of the evidence for an anti-cancer diet

Donaldson¹

2004

Nutr J

553

344

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“…Several previous studies have described associations between cobalamins and cancer. Other studies showed that cobalamins were selectively cytotoxic to fastgrowing malignant cells in culture (7) and were able to increase significantly the survival time of tumor-bearing mice (8). A second study showed that the atypical bronchial squamous metaplasia, frequently present in the lungs of smokers before the development of lung cancer, was improved by supplementation with folate and vitamin B-12 (6).…”

Section: Introductionmentioning

confidence: 99%

Methylcobalamin Decreases mRNA Levels of Androgen-Induced Growth Factor in Androgen-Dependent Shionogi Carcinoma 115 Cells

Nishizawa¹,

Yamamoto²,

Tanigaki³

et al. 1999

Nutrition and Cancer

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Methylcobalamin (MeCbl) is an important enzyme cofactor required for methionine synthase activity. It also inhibits, in a dose-dependent manner, the proliferation of an androgen-dependent cell line, SC-3, derived from an androgen-dependent mouse mammary tumor (Shionogi carcinoma 115). In SC-3 cells, androgen induces the production of androgen-induced growth factor (AIGF), an autocrine growth factor increasing the proliferation of SC-3 cells. MeCbl treatment suppressed the androgen-induced, AIGF-mediated growth of SC-3 cells, as well as the androgen-induced increase of AIGF mRNA. In SC-3 cells, androgen receptors linked with androgen form complexes that tightly bind DNA and act as transcription factors in the nucleus to regulate the expression of specific genes such as AIGF. The number and dissociation constants of androgen receptors in control and MeCbl-treated SC-3 cells were the same. Similarly, the extent of binding of normal androgen receptors in nuclei from control and MeCbl-treated cells was virtually identical. The androgen receptors from control and MeCbl-treated cells showed similar capacities for conversion to a form that tightly binds to DNA on heat activation. These results suggest that the reduction of AIGF mRNA, subsequent to the nuclear binding of androgen receptors, may be a partial cause of the growth-inhibitory activity of MeCbl in SC-3 cells.

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