Spotlight

Abstract

Iijima et al., pp. 797–801 Damage to the short arm of chromosome 3 frequently occurs in lung cancer. The gene for lactotransferrin (LTF), an avid iron-binding protein, lies in the section of chromosome 3 that is often deleted. LTF scavenges free iron in fluids, suppressing damage from free radicals and decreasing the access of iron to invading microorganisms. The protein has been reported to inhibit the growth of solid tumors in humans and prevent metastasis in rodents. In this study, the authors looked at expression of LTF in lung cancer lines and some primary tumors. More than half the small cell lung cancer lines examined lacked expression of LTF, as did 77% of non-small cell lung carcinoma lines. Among the 77%, all subtypes were represented. Of the 13 primary NSCLCs tested, 7 failed to express LTF. To determine whether promoter hypermethylation caused the lack of expression, the authors tested a demethylating agent and found that it restored LTF expression in 4 of 7 lines tested. The team also found that the LTF gene is silenced in some cases by hypermethylation of CpG sites, and that inhibiting histone deacetylation restored LTF expression in 4 of the 7 lines. Finally, they identified several mutations in the LTF gene that have not been previously reported, which could have resulted in gene inactivation. Whether silenced by mutation, methylation, or histone deacetylation, LTF certainly seems to play a key role in lung cancer of various types. Cho et al., pp. 970–978 Vitamins C and E, with their antioxidant properties; vitamin A, which regulates differentiation; and folate, with its role in DNA repair—naturally, these helpful molecules make the list of possible cancer blockers. But do they really help? Probably not, at least in the case of lung cancer, according to this report. The authors looked at a pooled analysis of 8 cohort studies from Europe and North America, each of which provided intake data for vitamins from foods-only sources, as well as food plus supplements. They found that total intakes of vitamins A, C, E, and folate were not associated with a lower risk of lung cancer after adjusting for various risk factors, such as smoking habits. Few previous studies have suggested that vitamin A reduces risk, and few studies have examined the effect of vitamin E intake. Neither vitamin A nor vitamin E helped prevent lung cancer in clinical trials. Some studies have suggested that vitamin C intake reduces risk, but others have found no statistically significant associations. Similarly, few epidemiological studies have examined folate intake in relation to lung cancer risk, and those that exist reveal no association. A case-control study looking at dietary folate consumption indicated that folate could reduce lung cancer risk among former smokers, but because the association did not apply to total folate intake, the benefit could have come from other cancer-preventive compounds in fruit. The effect of vitamin C intake also intertwines with the effect of fruit intake, which could reflect activity of other active components in fruit, specifically beta-cryptoxanthin, which is found in citrus fruits and which reduces cancer risk. The authors conclude that intakes of vitamins A, C, E, and folate do not reduce the risk of lung cancer. Friis et al., pp. 998–1003 For decades, breast implants have been suspected of causing cancer, since silicone and other foreign materials cause cancer in rodents. Yet no evidence points to the same effect in humans. The accumulated epidemiological evidence does not support a link between breast implants and cancer. Still, only few data exist regarding cancers other than breast cancer, and only few studies have looked at risk more than about 15 years after implantation. In this article, the authors report on their extension of an earlier cohort study, which now provides up to 30 years' worth of cancer data on women who had received breast implants. Women with cosmetic breast implants, the authors found, have a lower risk of breast cancer than the general population, results that support prior epidemiological findings. The authors suggest several possible explanations for this finding. They caution that it is unlikely that the silicone itself prevents cancer, but rather that women with a family history of breast cancer might be less likely to seek implants, or that detection of cancer during the preoperative phase, which would preclude implantation, reduces the frequency of cancer among women receiving implants. Implant recipients do, however, have an increased risk of non-melanoma skin cancer, which the authors suggest could result from increased sun exposure. They found no other increase or decrease in cancer risk at other sites. Furthermore, the study found no evidence that implants impede diagnosis of breast cancer, results which are, again, in agreement with earlier reports.