Tamoxifen-Associated Endometrial Cancer Is Affected by Prior Hormone Use
Women whose breast cancer was treated with tamoxifen have an increased risk for endometrial cancer, and the risk is highest for those women who had received estrogen replacement therapy or who are obese.
These results are presented by Leslie Bernstein, Ph.D., University of Southern California School of Medicine, and colleagues, in the October 6 issue of the Journal of the National Cancer Institute .
The authors used data on 324 case patients with endometrial cancer who had previously been treated for breast cancer. Control subjects671 in numberwere women with breast cancer who did not develop endometrial cancer and who were individually matched as closely as possible to the case subjects. The average age at breast cancer diagnosis was 65.9 years for case patients and 65.6 years for control subjects. The time interval between diagnosis of breast and endometrial cancers averaged 3.9 years. Data on breast cancer treatment and individual risk factors were collected for all participants through interviews and careful review of medical records.
Tamoxifen was of particular interest because of its use in treating breast cancer and in preventing recurrence because its use was associated in some studies with increased risk of endometrial cancer and because tamoxifen is being proposed for use in breast cancer prevention for women at high risk of the disease.
Overall, the authors report that tamoxifen therapy for breast cancer was associated with an increased risk of endometrial cancer with an odds ratio of 1.52 (that is, an increased risk of 52%). Women who had been on tamoxifen for more than 5 years had a fourfold greater chance of developing endometrial cancer. Prior use of estrogen increased the risk associated with tamoxifen use.
Tamoxifen has proven benefits in extending the disease-free and overall survival of women being treated for breast cancer, and it reduces the risk of developing breast cancer in women at high risk for the disease. However, the authors conclude that tamoxifen therapy for breast cancer does increase the risk for endometrial cancer and that the risk is higher for women who have used estrogen replacement therapy. The authors conclude that such women may need closer surveillance for endometrial cancer when they are using tamoxifen.
Contact: Brenda Maceo, University of Southern California (323) 442-2830; fax (323) 442-2832.
Only One in Three Medicare Patients With Blood in Stool Samples Receives the Recommended Follow-up Testing
About one third of the Medicare patients who tested positive for blood in their stool received the recommended follow-up testing, suggesting that population screening for colorectal cancer may be less effective and more costly than necessary.
These results, from Jon Lurie, M.D., M.S., Veterans Affairs Medical Center, White River Junction, VT, and Gilbert Welch, M.D., M.P.H., will appear in the October 6 issue of the Journal of the National Cancer Institute.
The fecal occult blood test (FOBT) has been shown to reduce mortality from colorectal cancer in controlled clinical trials, and Medicare now pays for such tests. The typical FOBT involves smearing a fecal sample onto cards after each of three bowel movements. The cards are then sent to a laboratory and tested for the presence of blood. Blood in the stool may be a sign of colorectal cancer.
In their study, the authors identified 24,246 people aged 65 years or older who had FOBT under Medicare. These people had no indication of colorectal cancer before their tests. For every 1000 people tested, 93 appeared to have blood in their stool and received follow-up testing. However, only about one third of the people who tested positive received the recommended follow-up tests that are considered standard for detecting colorectal cancercolonoscopy or flexible sigmoidoscopy and an air-contrast barium enema x-ray examination. Roughly one third received only partial colonic evaluation (flexible sigmoidoscopy only or barium enema only), and the remaining third were tested in a number of different ways, including an upper gastrointestinal series of x-rays, computed tomography, or magnetic resonance imaging of the abdomen, etc. Some individuals received a variety of tests. Of the 774 people who received a complete, recommended colon evaluation as a result of a positive FOBT, 241 had colonic polyps and 32 had colon cancer.
The authors note that the screening FOBT offers little benefit without proper follow-up testing and treatment. Their data analysis indicates that, with current patterns of practice, population screening with the FOBT may be less effective than estimated from controlled trials. Furthermore, the use of multiple tests increases the costs of screening, costs that are not revealed in controlled clinical trials.
Editorial writer John Bond, M.D., Veterans Affairs Medical Center and the University of Minnesota, Minneapolis, says screening the entire average-risk population for colorectal cancer would be very expensive. However, he notes, the cost of missing curable cancers or failing to prevent cancer by removing premalignant polyps may be even greater. A 1998 survey revealed that most people who had not been screened reported that no medical professional had ever recommended that they be screened, Bond says. A great deal of work remains in educating both the public and primary care physicians about the value of screening.
Contact: Nancy Serrell (603) 646-2117; fax (603) 646-2850. Editorial: Linda Duffy (612) 725-2102; fax (612) 725-2049.
Prostate-Specific Antigen May Retard Cancer Growth
Prostate-specific antigen (PSA), widely tested for in men as an indicator of potential prostate cancer, may actually slow the growth of cancers through inhibition of blood vessel formation.
These new results, which may explain the slow growth of prostate cancer and which call into question strategies to inhibit PSA expression as a cancer treatment, are presented by Anne Fortier, Ph.D., Barbara Nelson, Ph.D., Davida Grella, Ph.D., and John Holaday, Ph.D., of EntreMed, Inc., Rockville, MD, in the October 6 issue of the Journal of the National Cancer Institute.
Despite its name, PSA is not specific to prostate cancer, having been found in breast, lung, and uterine cancers as well. In one study, women whose breast cancer tested positive for PSA had a better prognosis than patients whose tumors were negative. These and other findings led the authors to test the hypothesis that increasing PSA values may not reflect bad news about cancer progression. Rather, increasing PSA values may indicate that the body is fighting the cancer by producing its own proteins that inhibit the growth of new blood vessels, a process termed "angiogenesis," which the tumor must have if it is to flourish.
To test the hypothesis that PSA may have antiangiogenic properties, the authors evaluated the effects of PSA on endothelial cell proliferation, migration, and invasion, three critical sequences in the orchestrated process of angiogenesis. The cells were stimulated with fibroblast growth factor or vascular endothelial growth factor, then treated with purified human PSA at concentrations ranging from 0.1 to 10µM . In these in vitro tests, PSA at concentrations of 0.3-5 µM significantly reduced endothelial cell functions. By contrast, PSA at these concentrations had no direct effect on prostate cancer cells or melanoma cells.
In other tests, mice were inoculated with melanoma cells, then starting 3 days later some of the mice received injections of purified human PSA for 11 consecutive days. Compared with control mice that did not receive PSA, those treated with PSA showed a 40% reduction in the number of lung metastases.
The authors note that their results suggest that PSA inhibits the growth of blood vessels associated with cancer progression. This may indicate that the elevation of PSA values in a variety of cancers is part of a normal process by which the body fights cancer progression. Therefore, they feel that their findings call into question various strategies to inhibit the expression of PSA in the treatment of prostate cancer and may indicate that PSA administration may be therapeutic in the treatment of a variety of cancers whose growth depends on angiogenesis.
Contact: Mary Sundeen, EntreMed, Inc., (301) 738-2490; fax (301) 217-9594.
Note: This memo to reporters is from the Journal staff and is not an official release of the National Cancer Institute (NCI) or Oxford University Press (OUP) nor does it reflect NCI or OUP policy. In addition, unless otherwise stated, all articles and items published in the Journal reflect the individual views of the authors and not necessarily the official points of view held by NCI, any other component of the U.S. government, OUP, or the organizations with which the authors are affiliated. Neither NCI nor any other component of the U.S. government nor OUP assumes any responsibility for the completeness of the articles or other items or the accuracy of the conclusions reached therein.
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