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Abstract
Vitamin C has been recognized and accepted by the US Food and Drug Administration (FDA) as one of 4 dietary antioxidants, the other 3 being vitamin E, the vitamin A precursor ß-carotene, and selenium, an essential component of the antioxidant enzymes glutathione peroxidase and thioredoxin reductase (Niki & Noguchi, 1997).
Several case-control and prospective cohort studies have investigated the association between plasma concentrations of vitamin C and cancer risk. Four studies found significantly higher concentrations of vitamin C in control subjects or survivors than in patients with cancer (Erhola et al., 1997).
Vitamin C concentrations >23 µmol/L were associated with a nonsignificant reduction in risk of cancer at all sites after 17 y. Nonsignificant reductions of 42% and 45% in colon cancer and lung cancer risk, respectively, were observed. No associations were observed for risk of stomach cancer or prostate cancer, the latter being a hormone-dependent cancer and hence less likely to be affected by diet, including vitamin C. It was suggested that plasma vitamin C concentrations >50 µmol/L are associated with protection against cancer, and an intake of 100 mg/d should be the recommended daily dose (Levine et al., 1996).
Chronic myeloid leukemia (CML) is a clonal myeloproliferative expansion of transformed, primitive hematopoietic progenitor cells. It involves myeloid, monocytic, erythroid, megakaryocytic, B-lymphoid, and occasionally T-lymphoid lineages (Faderl et al., 1999).
Imatinib, a BCR/ABL tyrosine kinase inhibitor, has shown remarkable clinical effects in chronic myelogenous leukemia. However, the leukemia cells become resistant to this drug in most blast crisis cases.