TAS::75 0849::TAS CONTINUATION OF FOLLOW-UP OF DES-EXPOSED COHORTS
TAS::75 0849::TAS CONTINUATION OF FOLLOW-UP OF DES-EXPOSED COHORTS
批准号:
8179001
负责人:
WILLIAM STROHSNITTER
金额:
$39.77万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2010
资助国家:
美国
项目状态:
已结题
起止时间:
2010-09-30 至 2011-09-29
关键词:
AdenocarcinomaAnimal ModelBehavioralClear CellCohort StudiesCollaborationsCollectionDaughterDiethylstilbestrolDiseaseEstrogensEuropeExposure toFemaleFollow-Up StudiesImmune System and Related DisordersLinkMailsMalignant NeoplasmsMalignant neoplasm of prostateMedical RecordsMedical centerMothersPathology ReportPharmaceutical PreparationsPhasePopulation StudyPregnancyPregnant WomenPremature BirthPreneoplastic ConditionsPreventionQuestionnairesReportingResearchRiskSonSpontaneous abortionSupport ContractsVaginaWorkcancer riskcohortfollow-uphigh riskin uteromalemalignant breast neoplasmmemberoffspringreproductive
中文摘要
己烯雌酚(DES)是1938年首次合成的一种药物,在美国和欧洲被用于数百万孕妇预防自然流产和早产。1971年,Herbst报告了妊娠期使用DES与暴露雌性后代发生阴道透明细胞腺癌(CCA)之间的强相关性。动物模型已经证明DES对子宫内暴露的后代的一系列影响,包括生殖功能障碍,免疫系统变化,行为和性异常,以及男性和女性各种生殖癌症的增加。NCI与五个现场中心合作,重新组装了以前研究过的DES暴露和未暴露的母亲,女儿和儿子的队列,并通过队列内的家庭联系确定了以前未研究过的记录暴露状态的受试者。标准化的基线问卷被邮寄给队列成员,以确定癌症和其他疾病的风险。收集了报告的癌症和肿瘤前疾病的病理学报告。已经进行了三个不同阶段的后续行动。本研究的目的是通过邮寄问卷和收集病历的方式继续随访,这是在研究的第一阶段开始的。人们担心,接触DES的女儿患乳腺癌的风险可能更高。在子宫内暴露于高水平的内源性雌激素被认为会增加乳腺癌的风险,DES是一种有效的雌激素。儿子的癌症风险也将继续评估,特别是前列腺癌风险的增加。由于在子宫内暴露于DES的后代目前已接近40岁,此时癌症发病率开始上升,因此继续随访这些群体以确定癌症风险是否长期增加是重要的。
英文摘要
Diethylstilbestrol (DES), a drug first synthesized in 1938, was administered to several million pregnant women in the U.S. and Europe for the prevention of spontaneous abortion and premature delivery. In 1971, Herbst reported a strong association between DES use in pregnancy and the occurrence of vaginal clear cell adenocarcinoma (CCA) in exposed female offspring. Animal models have demonstrated a range of DES effects on offspring exposed in utero, including reproductive dysfunction, immune system changes, behavioral and sexual abnormalities, and increases in various reproductive cancer in males and females. NCI, in collaboration with five field centers, reassembled previously studied cohorts of DES-exposed and unexposed mothers, daughters and sons, and identified subjects with documented exposure status who had not been studied previously, through familial links within the cohorts. Standardized baseline questionnaires were mailed to cohort members to ascertain the risk of cancer and other disorders. Pathology reports were collected for reported cancers and preneoplastic conditions. Three separate phases of follow-up have been conducted. The purpose of this study is to continue the follow-up, by means of mailed questionnaires and medical record collection, which was begun during the the first phase of the study. Concern has arisen that DES-exposed daughters may be at higher risk of breast cancer. Exposure to high levels of endogenous estrogen in utero has been hypothesized to increase the risk of breast cancer and DES is a potent estrogen. Cancer risk in the sons will also continue to be assessed, especially for increased risks of prostate cancer. since the offspring who were exposed to DES in utero are currently reaching their late forties, when cancer rates begin to rise, it is important to continue the follow-up of these cohorts to determine if there are long-term increases in cancer risk.
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