Other highlights in the May 18 JNCI
Study Examines Effect of Increasing the Recall Rate in Breast Screening Program
Lowering the threshold for recalling patients for additional assessment after a mammogram can detect more breast cancers earlier, but the benefit levels off, according to a new study.
Breast cancer screening programs aim to improve patient mortality and decrease morbidity by detecting high numbers of early-stage cancers without increasing the number of false positives--women recalled for additional assessment who do not have cancer. There is a relationship between the recall rate and the false-positive rate, but it has remained unclear.
To estimate the effect of changes in the recall rate on the earlier detection of breast cancers, Johannes D. M. Otten, M.Sc., of Radboud University Nijmegen Medical Centre in Nijmegen, the Netherlands, and colleagues conducted a blinded review of interval and screen-detected cancers in the Dutch screening program. Because the recall rate in the Netherlands is the lowest worldwide--less than 1%--the researchers were able to estimate how changing this rate might change both detection and false-positive rates.
They found that increasing the recall rate in the Dutch program to 2% would increase the detection rate from 4.20 cancers per 1,000 women to 4.52 cancers per 1,000 women due to the earlier detection of interval cancers. Increasing the recall rate to 3% or 4% would increase the detection rate to 4.58 cancers per 1,000 women and 4.63 cancers per 1,000 women, respectively. For each 1% increase in the recall rate above 5%, the detection rate would increase by 0.03 cancers per 1,000 women, but less than 10% of the women recalled for further assessment would actually have cancer.
Contact: Ms. Joke Groeneveld, Communications Office, Radboud University Nijmegen Medical Centre, (+31)243610625
Hormone Levels Associated With Breast Cancer Risk in Premenopausal Women
A new study has found that premenopausal women who had elevated blood levels of the androgens testosterone or androstenedione or low levels of progesterone had an increased risk of breast cancer.
Sex steroids have been implicated in the development of breast cancer. Studies have shown that postmenopausal women who have elevated blood levels of androgens of adrenal and/or ovarian origin or of estrogens have an increased risk of breast cancer. Studies of premenopausal women, however, have produced unclear results.
To examine the relationship between premenopausal blood concentrations of sex steroids and subsequent breast cancer risk, Dr. Rudolf Kaaks, of the International Agency for Research on Cancer in Lyon, France, and colleagues conducted a case–control study of 370 case subjects (premenopausal women with breast cancer) and 726 control subjects (premenopausal women without breast cancer) drawn from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort.
Elevated blood concentrations of testosterone, androstenedione, and an adrenal androgen were associated with an increased risk of breast cancer, whereas elevated blood concentrations of progesterone were associated with a decreased risk of breast cancer. Breast cancer risk was not associated with blood levels of other hormones.
The estimated absolute risk of breast cancer among women younger than age 40 after 10 years of follow-up was 2.6% for those in the highest quartile of blood testosterone versus 1.5% for those in the lowest quartile and 1.7% for those in the highest quartile of blood progesterone versus 2.6% for those in the lowest quartile.
Contact: Dr. Rudolf Kaaks, International Agency for Research on Cancer, 33-4-72-73-85-53, firstname.lastname@example.org
Study Identifies Potential Strategy for Inducing Tumor Cell Death
Inhibiting the enzyme acyl-CoA synthetase may be a novel strategy for inducing cell death in p53-defective tumors, according to a new study.
How to induce apoptosis in tumor cells, especially those that do not have a functioning p53 tumor suppressor gene, is unclear. Takashi Tsuruo, Ph.D., of the Japanese Foundation for Cancer Research in Tokyo, and colleagues measured p53 status and activity of the apoptosome, a protein complex that forms when cytochrome c is released from the mitochondria and initiates cell death, in a series of normal tissues and cancer cell lines.
They found that many p53-defective tumor cell lines had higher apoptosome activity than the normal cell lines and tissues. In addition, the authors identified Triacsin c as an inhibitor of acyl-CoA synthetase, an enzyme that regulates cytochrome c release. Triacsin c induced apoptosome-mediated cell death in tumor cells and suppressed the growth of lung tumors in a mouse model. The authors conclude that acyl-CoA synthetase inhibition may be a novel strategy to induce p53-defective tumor cell death.
Contact: Tetsuo Mashima, Japanese Foundation for Cancer Research, 81-3-3520-0111, email@example.com
Commentary Identifies Strengths, Weaknesses of Cancer Prediction Models
Models designed to predict the occurrence of cancer have become popular for use by cancer researchers, clinicians, and the public. But interest has also been increasing in ensuring that these models are correctly developed, rigorously evaluated, and appropriately applied. In a commentary, Andrew N. Freedman, Ph.D., of the National Cancer Institute, and colleagues report on a 2004 workshop sponsored by the NCI in which experts identified the strengths and limitations of cancer and genetic susceptibility prediction models, including those currently in use and in development. Participants also identified research priorities and resources.
Contact: National Cancer Institute Press Office, 301-496-6641, NCIPressOfficers@mail.nih.gov
Also in the May 18 JNCI:
Iodine Deficiency, Supplements Affect Thyroid Cancer Risk in Children Exposed to Radioactive Iodine: http://www.eurekalert.org/emb_releases/2005-05/jotn-ids051205.php Protein Targets Tumor Vasculature, Delays Tumor Growth in Animal Study: http://www.eurekalert.org/emb_releases/2005-05/jotn-ptt051205.php
Source: Eurekalert & othersLast reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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