© 2001 by Oxford University Press
Journal of the National Cancer Institute, Vol. 93, No. 11, 797,
June 6, 2001
© 2001 Oxford University Press
IN THIS ISSUE |
Every year for the past 4 years, the American Cancer Society, National Cancer Institute, North American Association of Central Cancer Registries, and Centers for Disease Control and Prevention, including the National Center for Health Statistics, have collaborated to produce the Report to the Nation, an update on trends in cancer incidence and mortality in the United States. In this year’s report, Howe et al. (p. 824) present data showing that, from 1992 through 1998, total cancer death rates declined in both males and females, as did total cancer incidence in males. Total cancer incidence increased in females over this period because of breast cancer incidence increases in certain age groups. In contrast to the overall declines, mortality or incidence increased for 12 cancers, most of which are relatively uncommon. The authors discuss a number of strategies to reduce the future cancer burden in the United States: prevention, early detection, improved diagnosis and treatment, and reduction of disparities in access to cancer care.
"Although it is encouraging that overall cancer incidence and mortality rates continue to decline in the United States, measures to sustain this progress must address the entire spectrum of prevention, early detection, and improved treatment and quality of life and must be aimed at reducing mortality among all populations."
—Howe et al.
Detecting Colorectal Cancer Mutations in Stool DNA
Cells lining the colon and rectum are shed into stool, offering the possibility of examining stool DNA for mutations known to occur during the development of colorectal cancer. In this issue, Dong et al. (p. 858) describe procedures that allowed them to isolate sufficient DNA from the stool of colorectal cancer patients to detect tumor-associated mutations present in only a small fraction of stool DNA molecules. The authors compared the mutation status of three genetic targets (TP53, K-RAS, and BAT26) in tumor and stool DNA. Together, the three markers detected 36 (71%) of 51 patients with colorectal cancer. In every case, if a mutation was found in the stool, it was also found in the corresponding primary tumor. The authors point out that the specificity of the markers and the timing of mutation detectability need to be assessed in a large sample of cancer-free individuals.
In an editorial, Atkin (p. 798) notes that future studies should focus on the ability of existing genetic markers to detect early, asymptomatic cancers and advanced adenomas in a screening setting. She also suggests that new markers of abnormal function might be more efficient than markers based on mutations in the genes involved in the adenoma-to-carcinoma sequence.
Telomerase Repression and HPV Immortalization
Infection with high-risk human papillomavirus (HPV) types can result in cervical cancer development in vivo and lead to immortalization of primary human epithelial cells in vitro in a process that appears to involve the activation of telomerase in the host cell. Losses of alleles from human chromosome 6 have been observed in premalignant cervical lesions, so Steenbergen et al. (p. 865) used microcell-mediated chromosome transfer to investigate whether this chromosome might harbor a telomerase repressor locus. The introduction of chromosome 6 into an HPV-immortalized keratinocyte cell line or an in vivo-derived cervical cancer cell line led to the induction of growth arrest after a marked lag period, a reduction in telomerase activity, and a reduction in the expression of the telomerase gene hTERT in both cell lines. The authors conclude that chromosome 6 may harbor a repressor of hTERT expression (or an inducer of such a repressor) and suggest that the loss of this locus may be involved in HPV-mediated immortalization.
"The present demonstration of a telomeric shortening-based growth arrest by chromosome 6 in two HPV-containing cell lines indicates that dysregulation of a gene on this chromosome is involved in immortalization of at least a subset of cells transformed by HPV in vitro and in vivo."
—Steenbergen et al.
Anal Squamous Intraepithelial Lesions in HIV-Positive Women
Anal cancers are thought to arise from squamous intraepithelial lesions in the anal canal, and women infected with human immunodeficiency virus-1 (HIV) may be at higher risk of anal cancer. Holly et al. (p. 843) determined the prevalence of human papillomavirus (HPV)-related abnormalities of the anal canal in women, particularly those infected with HIV, and evaluated potential risk factors. Abnormal anal cytology was diagnosed in 26% of HIV-positive and 8% of HIV-negative women. HIV-positive women had an increased risk of anal disease. Abnormal anal cytology in HIV-positive women was associated with detection of anal HPV, lower CD4 counts, history of anal intercourse, and concurrent abnormal cervical cytology. The authors suggest anoscopic and histologic assessment and careful follow-up of HIV-positive women.
Chemotherapy for Colon Cancer in the Elderly
Adjuvant chemotherapy based on 5-fluorouracil has been demonstrated in randomized trials to be effective at reducing mortality from stage III colon cancer. It is not known, however, how widely such treatment is used outside clinical trials, particularly among elderly patients. Schrag et al. (p. 850) addressed this question by examining linked Medicare and Surveillance, Epidemiology, and End Results data for patients aged 65 years and older. They found that, even in the absence of important comorbidity, rates of adjuvant chemotherapy use in advanced colon cancer declined dramatically with increasing age of patients. The authors suggest that chemotherapy may be underutilized among older patients and that underepresentation of the elderly in randomized trials generates confusion regarding optimal treatment strategies. They recommend further investigation of whether such factors as patient preference and physicians’ attitudes might explain this phenomenon.
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