© 2000 by Oxford University Press
Journal of the National Cancer Institute, Vol. 92, No. 17, 1365,
September 6, 2000
© 2000 Oxford University Press
IN THIS ISSUE |
Advances in surgery, including breast-conserving or reconstructive approaches, offer improved cosmetic options to women undergoing treatment of breast cancer. However, few studies have comprehensively compared the effects of different surgical options on physical symptoms and emotional health. Rowland et al. (p. 1422) evaluated women who underwent lumpectomy, mastectomy alone, or mastectomy with reconstruction. They found that women with either type of mastectomy experienced more physical symptoms than those who underwent lumpectomy. Women undergoing lumpectomy had the best outcomes in the areas of body image and feelings of attractiveness, while women who had mastectomy with reconstruction experienced the most negative impact of surgery on their sex lives. The authors also reported that, beyond the first year after diagnosis, a woman’s overall quality of life is more closely related to her age and exposure to adjuvant therapy than to her breast surgery.
"As interest in long-term cancer survivorship grows, studies such as this can provide a benchmark against which to measure our continued progress toward improving not just women’s survival from, but importantly, their quality of life after breast cancer."
—Rowland et al.
The GC79 Gene and Apoptosis in Prostate Cells
To determine the mechanism by which androgen-dependent prostate cancer cells become androgen independent, differentially expressed genes in these cells have been identified. Chang et al. (p. 1414) characterize one of these genes, GC79, which is more highly expressed in androgen-dependent prostate cancer cells than in androgen-independent prostate cancer cells. They report that the DNA sequence indicates that GC79 encodes a zinc-finger protein, possibly a transcription factor. The prostate regresses (shrinks) when androgen is withdrawn; the authors report that GC79 messenger RNA expression is increased in the regressing rat ventral prostate. When they inserted GC79 complementary DNA into both COS-1 monkey kidney cells and LNCaP human prostate cancer cells, the number of apoptotic cells in cultures was eight times higher than in corresponding control cell cultures. They conclude that GC79 is an androgen-repressible gene that is potentially involved in apoptosis and may have implications for the development of androgen-independent prostate cancer.
In an accompanying editorial, Isaacs (p. 1367) notes that the failure to express GC79 or other "death-signaling" genes is just one of several potential mechanisms that could cause prostate cancer cells to become androgen independent. Depending on the mechanism by which androgen independence arises, he notes, it may be possible to induce apoptosis in such cells. He adds that a variety of approaches to do just that are in preclinical and clinical testing.
Protective Mechanisms of Vitamin E
Vitamin E is a naturally occurring antioxidant that may protect against cancer, although studies in humans have been inconclusive and its anticancer mechanism of action is not well understood. Using the Mutatect mouse model, in which cancer cells are injected into mice to form tumors, Sandhu et al. (p. 1429) examined whether dietary vitamin E administered to mice would reduce the frequency of mutations or the number of oxidant-producing neutrophils in the tumors. They found that vitamin E reduced the frequency of mutations by as much as 84%, and it reduced myeloperoxidase levels—a measure of neutrophil infiltration—by about 75%. The authors conclude that vitamin E could protect against cancer by two mechanisms: scavenging reactive oxygen or nitrogen species and preventing neutrophil infiltration into tumors.
"Our report is the first, to our knowledge, to show an unequivocal protective effect of dietary vitamin E supplements . . . on mutation frequency in an experimental tumor."
—Sandhu et al.
p21-Mediated Activation of the Estrogen-Signaling Pathway
Estrogens are important regulators of growth and differentiation in normal breast tissue. About 10% of estrogen receptor (ER)-negative breast cancers are responsive to hormonal stimulation. Chen et al. (p. 1403) investigated whether p21, a cyclin-dependent kinase inhibitor that arrests cells in the G1 phase of the cell cycle, is a component of the ER-signaling pathway and if it can mediate estrogen’s actions in ER-negative breast cancer. They found a strong positive association between the expression of p21 and ER in nine breast cancer cell lines and in tumor samples from 60 patients with breast cancer. When they overexpressed p21 in a p21-negative, ER-negative breast cancer cell line, p21 mediated activation of the estrogen-signaling pathway and expression of ER-related molecules. The authors conclude that p21 may play a novel role in the estrogen-signaling pathway.
Early Development of Nevi
Sun exposure in childhood and the presence of nevi, or moles, are associated with risk of melanoma, but few studies have longitudinally examined the development of nevi in young children. Harrison et al. (p. 1436) followed two cohorts of Caucasian children from birth to age 3 years in cities with contrastingly high and low levels of ambient ultraviolet radiation—Townsville, Australia, and Glasgow, Scotland—to compare the development of nevi. They found that nevi first developed in Australian children between 6 and 12 months of age and in Scottish children before 2 years of age, accelerating rapidly thereafter in both cases. The authors also observed that the number of nevi was substantially higher in Australian children from age 12 months onward. Although early nevus development appeared to be associated with higher numbers of nevi at 3 years of age in the Australian children, the authors note that longer follow-up will confirm whether the association holds over time.
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