{"title":"雌二醇对早期乳腺癌DNA损伤反应及G1/S过渡期调控影响的数学模型","authors":"Mayang Fati Kusuma, F. Adi-Kusumo","doi":"10.1063/1.5139158","DOIUrl":null,"url":null,"abstract":"Breast cancer is a malignant disease that triggers the anomalies of the cells proliferation in breast tissue. There are some known factors that have ability to increase someone risk to suffer this disease, i.e., hormone, genetics, lifestyle, etc. One of the important hormone for the growth of breast tissue is estrogen, but it also contributes to breast cancer via DNA damage induced by producing the oxidative metabolites. Also, estrogen can provoke excessive proliferation that triggers the tumorigenesis process, where the key effectors are C-Myc and Cyclin D1 (CycD1). In this paper, we introduce a new mathematical model of the DNA damage as the response of the estrogen involving the G1/S transition phase in cell cycle. The model is a 15-dimensional system of the first order of ODE that shows the chemical reactions between proteins and hormones that play important roles in cell cycle regulations. The model could be a foundation to understand the initial behavior of the breast cancer. We use numerical simulations by using fourth order Runge Kutta method to study the molecular behavior of the normal cells and the anomalies on the abnormal cells that initially lead breast cancer.Breast cancer is a malignant disease that triggers the anomalies of the cells proliferation in breast tissue. There are some known factors that have ability to increase someone risk to suffer this disease, i.e., hormone, genetics, lifestyle, etc. One of the important hormone for the growth of breast tissue is estrogen, but it also contributes to breast cancer via DNA damage induced by producing the oxidative metabolites. 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引用次数: 2

摘要

乳腺癌是一种引起乳腺组织细胞增生异常的恶性疾病。有一些已知的因素能够增加患这种疾病的风险,即激素、遗传、生活方式等。雌激素是乳腺组织生长的重要激素之一,但它也会通过产生氧化代谢物引起的DNA损伤而导致乳腺癌。此外,雌激素可引起过度增殖,从而触发肿瘤发生过程,其中关键效应物是C-Myc和Cyclin D1 (CycD1)。在本文中,我们提出了一个新的数学模型,用于描述雌激素在细胞周期G1/S过渡阶段对DNA损伤的反应。该模型是一阶ODE的15维系统,显示了在细胞周期调节中起重要作用的蛋白质和激素之间的化学反应。该模型可以为了解乳腺癌的初始行为奠定基础。采用四阶Runge - Kutta方法进行数值模拟,研究了正常细胞的分子行为以及异常细胞在早期导致乳腺癌的异常情况。乳腺癌是一种引起乳腺组织细胞增生异常的恶性疾病。有一些已知的因素能够增加患这种疾病的风险,即激素、遗传、生活方式等。雌激素是乳腺组织生长的重要激素之一,但它也会通过产生氧化代谢物引起的DNA损伤而导致乳腺癌。此外,雌激素可引起过度增殖,从而触发肿瘤发生过程,其中关键效应物是C-Myc和Cyclin D1 (CycD1)。在本文中,我们提出了一个新的数学模型,用于描述雌激素在细胞周期G1/S过渡阶段对DNA损伤的反应。该模型是一阶ODE的15维系统,显示了在细胞周期调节中起重要作用的蛋白质和激素之间的化学反应。该模型可以为了解乳腺癌的初始行为奠定基础。我们使用数值模拟…
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A mathematical modelling for estradiol influence on DNA damage response and G1/S transition phase regulations in early stage of breast cancer
Breast cancer is a malignant disease that triggers the anomalies of the cells proliferation in breast tissue. There are some known factors that have ability to increase someone risk to suffer this disease, i.e., hormone, genetics, lifestyle, etc. One of the important hormone for the growth of breast tissue is estrogen, but it also contributes to breast cancer via DNA damage induced by producing the oxidative metabolites. Also, estrogen can provoke excessive proliferation that triggers the tumorigenesis process, where the key effectors are C-Myc and Cyclin D1 (CycD1). In this paper, we introduce a new mathematical model of the DNA damage as the response of the estrogen involving the G1/S transition phase in cell cycle. The model is a 15-dimensional system of the first order of ODE that shows the chemical reactions between proteins and hormones that play important roles in cell cycle regulations. The model could be a foundation to understand the initial behavior of the breast cancer. We use numerical simulations by using fourth order Runge Kutta method to study the molecular behavior of the normal cells and the anomalies on the abnormal cells that initially lead breast cancer.Breast cancer is a malignant disease that triggers the anomalies of the cells proliferation in breast tissue. There are some known factors that have ability to increase someone risk to suffer this disease, i.e., hormone, genetics, lifestyle, etc. One of the important hormone for the growth of breast tissue is estrogen, but it also contributes to breast cancer via DNA damage induced by producing the oxidative metabolites. Also, estrogen can provoke excessive proliferation that triggers the tumorigenesis process, where the key effectors are C-Myc and Cyclin D1 (CycD1). In this paper, we introduce a new mathematical model of the DNA damage as the response of the estrogen involving the G1/S transition phase in cell cycle. The model is a 15-dimensional system of the first order of ODE that shows the chemical reactions between proteins and hormones that play important roles in cell cycle regulations. The model could be a foundation to understand the initial behavior of the breast cancer. We use numerical simula...
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