Aspirin use is not associated with an increase or a decrease in mortality from pancreatic cancer, a new study has found.
Previous epidemiologic studies have reported mixed and limited results regarding a possible association between aspirin use and pancreatic cancer risk. Eric J. Jacobs, Ph.D., of the American Cancer Society, and colleagues examined self-reported aspirin use in a cohort of 987,590 adults in the United States Cancer Prevention Study II. In this group, aspirin use has previously been found to be associated with reduced risk of mortality from cancers of the colon, stomach, and esophagus.
During the 18-year follow-up period, 2,434 men and 2,143 women died from pancreatic cancer. The authors found no association between aspirin use and pancreatic cancer mortality, even among participants who reported aspirin use equal to or greater than 30 times per month or who had used aspirin for 20 or more years.
Contact: Eric Miller, American Cancer Society, (404) 417-5839, eric.miller@cancer.org
Indicator of Insulin Production Associated With Colorectal Cancer Risk
A new study has found that elevated insulin production--a condition called hyperinsulinemia--is associated with an increased risk of colorectal cancer.
Colorectal cancer and type 2 diabetes share many risk factors, such as a diet high in calories, animal fat, and refined carbohydrates; a sedentary lifestyle; and a high body mass index. Hyperinsulinemia--a presence of excess insulin in the blood, which is associated with type 2 diabetes--also appears to be associated with an increased risk of colorectal cancer.
To determine whether insulin and insulin resistance are associated with the risk of developing colorectal cancer, Jing Ma, M.D., Ph.D., of the Brigham and Women's Hospital, Boston, measured the plasma concentration of C-peptide (an indicator of insulin production) of 176 men with colorectal cancer and 294 healthy control men. They found that elevated insulin production was associated with an increased risk of colorectal cancer, independent of body mass index, factors related to insulin resistance, or vigorous exercise.
"Our data not only support the hypothesis that elevated long-term insulin production is one underlying mechanism to link dietary and lifestyle risk factors with colorectal cancer risk but also provide a strong biologic argument that avoiding or reducing the modifiable risk factors … could effectively decrease the risk of colorectal cancer and the risk of type 2 diabetes and cardiovascular disease … " the authors conclude.
Contact: Melanie Franco, Brigham and Women's Hospital, (617) 534-1605, mfranco1@partners.org
Study Finds Association Between Primary, Contralateral Breast Cancers
The estrogen receptor (ER) status of a primary breast cancer is associated with the receptor status of a breast cancer in the opposite breast for women who do not take tamoxifen, a new study has found. In addition, patients with an ER-positive primary cancer who receive tamoxifen have fewer ER-positive contralateral breast cancers, possibly as a result of tamoxifen treatment.
About 6% to 9% of women with breast cancer will develop breast cancer in the opposite breast (called contralateral breast cancer). Tamoxifen reduces the risk of contralateral breast cancer and primarily benefits women with ER-positive disease. Sandra Swain, M.D., of the National Cancer Institute, and colleagues examined data from earlier breast cancer clinical trials to determine the relationship between the ER status of primary and contralateral breast cancers and whether tamoxifen treatment affects this relationship.
Among patients who did not receive tamoxifen, 89% with an ER-positive primary cancer had an ER-positive contralateral breast cancer and 70% with an ER-negative primary cancer had an ER-negative contralateral breast cancer. Among patients who received tamoxifen, 56% with an ER-positive primary cancer had an ER-positive contralateral breast cancer and 78% with an ER-negative primary cancer had an ER-negative contralateral breast cancer.
Contact: National Cancer Institute Press Office, 301-496-6641, ncipressofficers@mail.nih.gov
Study Examines PSA as Intermediate End Point for Death After Hormonal Therapy
The response of prostate-specific antigen (PSA) levels to salvage hormonal therapy can serve as an intermediate end point for prostate cancer-specific mortality in patients with a rising PSA level after surgery or radiation therapy, a new study concludes.
PSA levels decline in almost all patients following the initiation of salvage hormonal therapy; however, the rates of the rise prior to therapy and the subsequent decline following therapy can vary among patients. Anthony V. D'Amico, M.D., Ph.D., and colleagues from the Brigham and Women's Hospital, Boston, evaluated whether PSA response--the ratio of the rate of PSA change after salvage hormonal therapy to the rate of PSA change before salvage therapy--is associated with prostate cancer-specific mortality.
They found that PSA response was associated with time to prostate cancer-specific mortality following salvage hormonal therapy; however, there was no association between prostate cancer-specific mortality and the rates of change in PSA either before or after hormonal therapy. They also found that patients with a PSA response less than or equal to 1 had a shorter time to prostate cancer-specific mortality than patients with a PSA response of more than 1.
Contact: Melanie Franco, Brigham and Women's Hospital, (617) 534-1605, mfranco1@partners.org
Also in the April 7 JNCI:
- Immediate Mammogram Reading May Decrease Stress Associated With Abnormal Results: http://www.eurekalert.org/emb_releases/2004-04/jotn-imr040104.php
- Exposure to Famine Associated With Increased Breast Cancer Risk: http://www.eurekalert.org/emb_releases/2004-04/jotn-etf040104.php
Note: The Journal of the National Cancer Institute is published by Oxford University Press and is not affiliated with the National Cancer Institute. Attribution to the Journal of the National Cancer Institute is requested in all news coverage. Visit the Journal online at http://jncicancerspectrum.oupjournals.org/.
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