men may choose not to compound their already increased risk."
When DES, a synthetic estrogen, was developed in 1938, physicians believed that low levels of estrogen in pregnant women led to spontaneous abortions or premature deliveries. In 1953, a clinical trial indicated no benefit with regard to miscarriage prevention. However, use continued in the U.S. until 1971 when researchers determined that DES greatly increased the risk of developing rare cancers of the vagina and cervix in DES daughters; the federal Food and Drug Administration subsequently banned use of the drug in pregnant women.
Later research demonstrated that DES increased the risk of breast cancer development in the mothers who used it.
To see if DES daughters and sons were also at greater risk of cancer or other serious illnesses, in 1992 the National Cancer Institute (NCI) funded a long-term study that assembled all known "cohorts," or groups of DES daughters that were already being studied (some since the 1970s), as well as a collection of unexposed women. This particular analysis included 4,817 exposed and 2,073 unexposed daughters, and, to date, 102 cases of invasive breast cancer have occurred in the combined group.
Factoring out other breast cancer risk variables such as the age when these women first gave birth, or their number of children, did not change DES daughters' relative risk of developing breast cancer, Palmer said. She adds that the breast cancer cases "tracked the normal range" of breast cancer subtypes, so are expected to be neither more nor less lethal than is commonly seen.
Only a few deaths have occurred in the combined group due to breast cancer, so survival statistics are not yet available, she said.
Scientifically, the study may be the first to provide direct evidence that prenatal exposure to excess estrogen may be a risk factor for development of breast cancer, Palmer said. "That theory has been aroundPage: 1 2 3 Related medicine news :1
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