{"title":"生命历程流行病学与乳腺癌:将风险转化为预防","authors":"M. Sherman","doi":"10.1158/1538-7755.CARISK16-IA11","DOIUrl":null,"url":null,"abstract":"Molecular histology may be conceptualized as the microscopic and molecular characteristics of normal tissues that are required for physiologic function. Over the life course, the molecular histology of the breast changes in response to physiological alterations, imparting spatial and temporal heterogeneity within the breasts of individuals and among women. These transitions contribute to the enormous range and imprecisely defined limits of what pathologists consider normal. Appreciation that molecular histology may reflect the cumulative influence of prior exposures linked to breast cancer risk, and may provide information about risk of developing breast cancer in the future, has stimulated interest in this topic. Unlike the study of breast cancer or its precursors, which represents a focal pathophysiologic deviation from normal, molecular histology, if assessable, would represent the state of the entire at-risk organ, based upon examination of a small tissue sample. The adult breast is characterized by well-developed terminal duct lobular units (TDLUs), which comprise the functional unit of milk production and represent the source of nearly all breast cancer precursors. Physiological changes in human breasts are likely driven by paracrine mechanisms, suggesting that tissue context and cellular topography are critical elements in physiology and pathophysiology. The breast undergoes profound changes with completion of childbearing and aging. Age-related TDLU involution may be conceptualized as a protective mechanism that lowers breast cancer risk following completion of childbearing, and in this context, delayed or incomplete involution is a breast cancer risk factor. With aging, the percent of the breast comprised of fibroglandular tissue declines, which is associated with a reduction in mammographic density, a strong breast cancer risk factor. Mammographic density is also imperfectly correlated with epithelial content in the breast. Women with benign breast disease whose surrounding normal breast tissue does not undergo age-appropriate TDLU involution are at increased risk of developing breast cancer, and both breast density and TDLU involution are independent markers of breast cancer risk. However, an important challenge is to understand the markers and mechanisms that underlie breast involution with aging, including both the epithelial and non-epithelial components, and to learn why both density and TDLU content decline with aging as breast cancer incidence rises. The thesis of this presentation is that understanding the amount of epithelium at-risk, the insults it sustains and the mechanisms that lead to its elimination, persistence or expansion may provide a window into the development of integrative biomarkers of risk that can translate into improved screening and prevention. However, progress towards this goal is quite early. Citation Format: Mark E. Sherman. Life course epidemiology and breast cancer: translating risk into prevention. [abstract]. In: Proceedings of the AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; Nov 16-19, 2016; Orlando, FL. 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These transitions contribute to the enormous range and imprecisely defined limits of what pathologists consider normal. Appreciation that molecular histology may reflect the cumulative influence of prior exposures linked to breast cancer risk, and may provide information about risk of developing breast cancer in the future, has stimulated interest in this topic. Unlike the study of breast cancer or its precursors, which represents a focal pathophysiologic deviation from normal, molecular histology, if assessable, would represent the state of the entire at-risk organ, based upon examination of a small tissue sample. The adult breast is characterized by well-developed terminal duct lobular units (TDLUs), which comprise the functional unit of milk production and represent the source of nearly all breast cancer precursors. Physiological changes in human breasts are likely driven by paracrine mechanisms, suggesting that tissue context and cellular topography are critical elements in physiology and pathophysiology. The breast undergoes profound changes with completion of childbearing and aging. Age-related TDLU involution may be conceptualized as a protective mechanism that lowers breast cancer risk following completion of childbearing, and in this context, delayed or incomplete involution is a breast cancer risk factor. With aging, the percent of the breast comprised of fibroglandular tissue declines, which is associated with a reduction in mammographic density, a strong breast cancer risk factor. Mammographic density is also imperfectly correlated with epithelial content in the breast. Women with benign breast disease whose surrounding normal breast tissue does not undergo age-appropriate TDLU involution are at increased risk of developing breast cancer, and both breast density and TDLU involution are independent markers of breast cancer risk. However, an important challenge is to understand the markers and mechanisms that underlie breast involution with aging, including both the epithelial and non-epithelial components, and to learn why both density and TDLU content decline with aging as breast cancer incidence rises. The thesis of this presentation is that understanding the amount of epithelium at-risk, the insults it sustains and the mechanisms that lead to its elimination, persistence or expansion may provide a window into the development of integrative biomarkers of risk that can translate into improved screening and prevention. However, progress towards this goal is quite early. Citation Format: Mark E. Sherman. Life course epidemiology and breast cancer: translating risk into prevention. [abstract]. In: Proceedings of the AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; Nov 16-19, 2016; Orlando, FL. 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引用次数: 0
摘要
分子组织学可以被定义为生理功能所需的正常组织的微观和分子特征。在整个生命过程中,乳房的分子组织学随着生理变化而变化,赋予个体和女性乳房内的空间和时间异质性。这些转变导致了病理学家认为正常的范围和不精确定义的限制。认识到分子组织学可能反映与乳腺癌风险相关的先前暴露的累积影响,并可能提供有关未来患乳腺癌风险的信息,这激发了人们对这一主题的兴趣。不同于对乳腺癌或其前体的研究,它代表了对正常的局部病理生理偏差,分子组织学,如果可评估,将代表整个危险器官的状态,基于对小组织样本的检查。成人乳房的特征是发育良好的末端导管小叶单位(TDLUs),它包括产乳的功能单位,代表了几乎所有乳腺癌前体的来源。人类乳房的生理变化可能是由旁分泌机制驱动的,这表明组织环境和细胞地形是生理和病理生理的关键因素。随着生育的完成和年龄的增长,乳房发生了深刻的变化。与年龄相关的TDLU复旧可以被理解为一种降低生育结束后乳腺癌风险的保护机制,在这种情况下,延迟或不完全复旧是乳腺癌的危险因素。随着年龄的增长,由纤维腺组织组成的乳房比例下降,这与乳房x光检查密度的降低有关,这是一个强烈的乳腺癌风险因素。乳腺x线摄影密度与乳腺上皮细胞含量也不完全相关。患有良性乳腺疾病的妇女,其周围的正常乳腺组织没有发生与年龄相适应的TDLU复发,其患乳腺癌的风险增加,乳房密度和TDLU复发都是乳腺癌风险的独立标志。然而,一个重要的挑战是了解乳腺衰老背后的标志物和机制,包括上皮和非上皮成分,以及为什么密度和TDLU含量随着乳腺癌发病率的上升而随着年龄的增长而下降。本次演讲的主题是了解处于危险中的上皮细胞的数量,它所承受的损害以及导致其消除、持续或扩大的机制,可能为开发风险的综合生物标志物提供了一个窗口,可以转化为改进的筛查和预防。然而,实现这一目标的进展还为时尚早。引文格式:Mark E. Sherman。生命历程流行病学与乳腺癌:将风险转化为预防。[摘要]。摘自:AACR特别会议论文集:改进癌症风险预测以预防和早期发现;2016年11月16日至19日;费城(PA): AACR;癌症流行病学杂志,2017;26(5增刊):摘要11 - 11。
Abstract IA11: Life course epidemiology and breast cancer: translating risk into prevention
Molecular histology may be conceptualized as the microscopic and molecular characteristics of normal tissues that are required for physiologic function. Over the life course, the molecular histology of the breast changes in response to physiological alterations, imparting spatial and temporal heterogeneity within the breasts of individuals and among women. These transitions contribute to the enormous range and imprecisely defined limits of what pathologists consider normal. Appreciation that molecular histology may reflect the cumulative influence of prior exposures linked to breast cancer risk, and may provide information about risk of developing breast cancer in the future, has stimulated interest in this topic. Unlike the study of breast cancer or its precursors, which represents a focal pathophysiologic deviation from normal, molecular histology, if assessable, would represent the state of the entire at-risk organ, based upon examination of a small tissue sample. The adult breast is characterized by well-developed terminal duct lobular units (TDLUs), which comprise the functional unit of milk production and represent the source of nearly all breast cancer precursors. Physiological changes in human breasts are likely driven by paracrine mechanisms, suggesting that tissue context and cellular topography are critical elements in physiology and pathophysiology. The breast undergoes profound changes with completion of childbearing and aging. Age-related TDLU involution may be conceptualized as a protective mechanism that lowers breast cancer risk following completion of childbearing, and in this context, delayed or incomplete involution is a breast cancer risk factor. With aging, the percent of the breast comprised of fibroglandular tissue declines, which is associated with a reduction in mammographic density, a strong breast cancer risk factor. Mammographic density is also imperfectly correlated with epithelial content in the breast. Women with benign breast disease whose surrounding normal breast tissue does not undergo age-appropriate TDLU involution are at increased risk of developing breast cancer, and both breast density and TDLU involution are independent markers of breast cancer risk. However, an important challenge is to understand the markers and mechanisms that underlie breast involution with aging, including both the epithelial and non-epithelial components, and to learn why both density and TDLU content decline with aging as breast cancer incidence rises. The thesis of this presentation is that understanding the amount of epithelium at-risk, the insults it sustains and the mechanisms that lead to its elimination, persistence or expansion may provide a window into the development of integrative biomarkers of risk that can translate into improved screening and prevention. However, progress towards this goal is quite early. Citation Format: Mark E. Sherman. Life course epidemiology and breast cancer: translating risk into prevention. [abstract]. In: Proceedings of the AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; Nov 16-19, 2016; Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(5 Suppl):Abstract nr IA11.