© 2000 by Oxford University Press
Journal of the National Cancer Institute, Vol. 92, No. 2, 89,
January 19, 2000
© 2000 Oxford University Press
IN THIS ISSUE |
Cigarette designs have changed over the past 40 years, with average tar and nicotine smoke yields more than 60% lower than they were previously. To compensate, smokers of modern low-yield and medium-yield cigarettes have modified their smoking behavior to obtain the desired level of nicotine. Djordjevic et al. (p. 106) tested whether yields of tar and nicotine in cigarette smoke measured using a Federal Trade Commission (FTC) protocol accurately reflect amounts of toxins and carcinogens delivered to smokers of modern cigarettes. They found that these smokers took larger puffs at shorter intervals and drew larger volumes of smoke from their cigarettes compared with the parameters specified in the FTC protocol. They conclude that smokers today receive about twice the level of tar, nicotine, and carcinogens estimated using the FTC protocol.
"The FTC protocol underestimates the nicotine and carcinogen dosages to smokers and overestimates the proportional benefit of low-yield cigarettes."—Djordjevic et al.
In an accompanying editorial, Wilken-feld et al. (p. 90) emphasize the importance of this study and discuss its relevance to the current debate about tobacco. They elaborate on the history of the FTC method of testing cigarettes and they urge that changes in the current system of testing cigarettes be swift and comprehensive.
Bcar1/p130Cas, Antiestrogen Resistance, and Breast Cancer
Two studies in this issue focus on a newly characterized gene that, when overexpressed, confers antiestrogen resistance on breast cancer cells. The first study, by Brinkman et al. (p. 112), describes the isolation of the gene, Bcar1/p130Cas (breast cancer antiestrogen resistance/p130 Crk-associated substrate), which causes antiestrogen resistance in estrogen-dependent breast cancer cells in vitro. In the second study, van der Flier et al. (p. 120) investigated whether Bcar1/p130Cas has a role in clinical breast cancer. In this latter study, the researchers measured Bcar1/p130Cas protein levels in extracts of 937 primary breast carcinomas and then explored associations of this protein with various clinical and patient characteristics. They found that patients with primary breast cancers that expressed high levels of Bcar1/p130Cas protein experienced more rapid disease recurrence, had shorter overall survival, and had a greater risk of resistance to the anties-trogen drug tamoxifen than patients whose tumors expressed no Bcar1/p130Cas protein.
In an accompanying editorial (p. 92), Jordan further considers the implications of these findings for future research in the area of antiestrogen resistance. He noted that knowledge of the BCAR1 gene may someday help better identify those breast cancer patients who stand to benefit from antiestrogen therapy.
Early Stages of Angiogenesis
Li et al. (p. 143) have monitored the early events of angiogenesis (the formation of new blood vessels) in vivo by using two rodent mammary tumor cell lines genetically engineered to produce an enhanced version of green fluorescence protein (GFP). The investigators monitored the movement of GFP-labeled cells and angiogenesis-related changes for up to 4 weeks after tumor cell implantation. Modification of the host vasculature was evident when tumor masses reached approximately 60-80 cells, and functional new blood vessels were seen when tumor masses reached approximately 100-300 cells. Individual tumor cells exhibited a directional growth pattern toward the pre-existing host vasculature. When an anti-angiogenic protein, ex-flk1, was injected with the tumor cells, this early angiogenic activity and tumor growth were inhibited considerably, suggesting that angiogenesis inhibitors may halt tumor growth even before the onset of angiogenesis.
In an accompanying editorial, Folkman (p. 94) points out that this report enlarges our understanding of the mechanism of antiangiogenic therapy. He says that Li et al. clearly show that at least one angiogenesis inhibitor can operate before a tumor has become vascularized and can lead to inhibition or eradication of a nascent tumor.
p53 Mutations and Hepatocellular Carcinoma in The Gambia
Mutation of the p53 gene at codon 249, which is found frequently in hepatocellular carcinoma (HCC), can be detected in populations that are exposed to aflatoxins and have a high proportion of hepatitis B virus carriers. The Gambia in western Africa has such a population. Kirk et al. (p. 148) evaluated whether this mutation could be detected in cell-free DNA isolated from the plasma of Gambian subjects and thus be used to detect HCC. They found the mutation in 36% of plasma DNA samples from Gambian patients with HCC and at lower rates in Gambian patients with cirrhosis and in Gambian control subjects. The mutation was not present in a similar population of patients from Europe with various liver pathologies. The authors conclude that the presence of this mutation in plasma DNA is strongly associated with HCC in Gambian patients and that its low-level presence in patients with cirrhosis and control subjects from that country may lead to earlier detection of HCC.
Physical Activity and Breast Cancer
Studies of the relationship between physical activity and risk of breast cancer have produced inconsistent results, perhaps because of differences in how physical activity was measured. To assess the relationship between risk of breast cancer and lifetime physical activity, Verloop et al. (p. 128) interviewed 918 women with breast cancer and the same number of age-matched control subjects. The women were asked about their physical activity at ages 10-12 years and 13-15 years, lifetime recreational activity, and occupational physical activity. They found that women who engaged in recreational physical activity had a decreased risk of breast cancer and that physical activity during any period of life appeared to be relevant. However, they emphasize that, for public health recommendations, more research needs to be done to determine at what point in a woman's life the initiation of physical activity can still have an impact on the risk of breast cancer.
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