© 2001 by Oxford University Press
Journal of the National Cancer Institute, Vol. 93, No. 9, 661,
May 2, 2001
© 2001 Oxford University Press
IN THIS ISSUE |
The National Surgical Adjuvant Breast and Bowel Project B-14 trial, a large, randomized, placebo-controlled trial of women with estrogen receptor-positive, lymph node-negative breast cancer, demonstrated that 5 years of tamoxifen treatment improves disease-free survival and overall survival. In this issue of the Journal, Fisher et al. (p. 684) present new results from the trial, based on 7 years of follow-up after the initial 5-year treatment period, that address whether tamoxifen treatment for more than 5 years provides additional benefit. The authors found that women who did not continue tamoxifen treatment beyond 5 years had a slight advantage in disease-free survival over those who did. The authors conclude that continuing tamoxifen treatment beyond 5 years provides no additional benefit to breast cancer patients with estrogen receptor-positive, node-negative disease.
In an editorial (p. 662), Abrams discusses the history of randomized trials of tamoxifen duration and notes that, although the updated results of Fisher et al. do not completely resolve the issue, 5 years of tamoxifen is a reasonable standard outside of the clinical trial setting.
RASSF1A and Lung and Breast Cancers
Because the recently identified RASSF1 locus frequently undergoes allele loss from chromosome 3p21.3 both in lung and breast cancers, Burbee et al. (p. 691) tested the hypothesis that RASSF1 encodes a tumor suppressor gene. The authors assessed expression of two RASSF1 gene products, RASFF1A and RASSF1C, in lung and breast cancers and cell lines. They found that RASSF1A was expressed in nonmalignant cell cultures but not in a majority of small-cell lung carcinoma (SCLC), non-small-cell carcinoma (NSCLC), or breast cancer cell lines. RASSF1A promoter hypermethylation was detected in 100% of SCLCs, 63% of primary resected NSCLCs, and 49% of primary breast cancers and was associated with impaired survival for NSCLC patients. Introducing RASSF1A into a cell line that lacked endogenous RASSF1A expression suppressed the malignant cell phenotype both in vitro and in vivo. The authors conclude that RASSF1A is a potential 3p21.3 tumor suppressor gene in lung and breast cancers.
In an editorial, Baylin and Herman (p. 664) discuss promoter hypermethylation in the context of characterizing tumor suppressor genes. The authors stress that promoter hypermethylation and location in a region of loss of heterozygosity is not sufficient to define a tumor suppressor gene and that proof of tumorigenic function is essential.
Trends in Melanoma Incidence
It is unclear whether the increasing trend in melanoma incidence is real or whether it reflects improved diagnosis. Jemal et al. (p. 678) examined recent age-adjusted melanoma incidence patterns among the U.S. white population stratified by sex, age, tumor stage, and tumor thickness by using the Surveillance, Epidemiology, and End Results Program data. Melanoma incidence increased in females born since the 1960s. From 1974–1975 through 1988–1989, upward trends for the incidence of localized tumors and downward trends for the incidence of distant-stage tumors occurred in the age group under 40 years. In general, incidence rates statistically significantly increased for thin tumors among females and for both thin and thick tumors among males. The authors speculate that the recent trends may reflect increased sunlight exposure and that incidence may continue to rise until the current middle-aged population ages.
Socioeconomic Status and Prostate Cancer Incidence
Socioeconomic status (SES) affects many aspects of health and health care. Using a measurement of SES that considered the combined impact of education and income, Liu et al. (p. 705) examined census tract-specific population data to determine prostate cancer incidence rates before and after prostate-specific antigen (PSA) testing came into widespread use. The authors found no association between SES and prostate cancer incidence in any racial/ethnic group or between SES and the stage of disease for men diagnosed with prostate cancer in the 16-year period before PSA testing was widely available. However, for men diagnosed in the 10-year period after PSA testing was introduced, higher SES was associated with increased prostate cancer incidence and with earlier stage cancers at diagnosis. The authors conclude that SES has a substantial impact on prostate cancer incidence rates mediated through access to and use of PSA testing.
p53 Missense Mutations in Ductal Carcinoma In Situ
Mutation of the tumor suppressor gene p53 (TP53) is one of the most frequent somatic alterations in sporadic breast cancer and occurs at least as early as the ductal carcinoma in situ (DCIS) stage. To understand in what histologic grade of DCIS the p53 mutations occur, Done et al. (p. 700) studied 94 patients with DCIS but without invasive breast cancer. DCIS from 10 of 94 patients contained p53 missense mutations. All 10 were of a solid or a comedo histologic pattern and showed cells of nuclear grade 2 or 3. The authors noted statistically significant differences between the mutation frequencies in three histologic grade categories (0% in low grade to 40.9% in high grade). The authors conclude that p53 mutations can occur before the development of invasive breast cancer, particularly in DCIS of high histologic grade.
In an editorial, Simpson et al. (p. 666) point out the importance of using cases of DCIS with no invasive carcinoma that were carefully selected from clinically relevant categories by grade and size. This, they say, lends support to the important concept that DCIS is not a single disease.
Alcohol and Breast Cancer
Some epidemiologic studies have found an association between alcohol consumption and increased risk of breast cancer, but results are inconsistent for women who consume lower amounts of alcohol. Dorgan et al. (p. 710) studied whether alcohol consumption by postmenopausal women elevates serum levels of steroid hormones associated with an increased risk of breast cancer. Women were rotated in random order through three 8-week periods in which they consumed alcohol equivalent to zero, one, or two alcoholic drinks per day, and serum levels of hormones were measured at the end of each period. The authors found that, when women consumed alcohol, serum levels of two hormones, estrone sulfate and dehydroepiandrosterone sulfate, increased. The authors suggest that the increases in these two hormones provide a possible mechanism by which consumption of small amounts of alcohol per day by postmenopausal women could increase their risk of breast cancer.
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