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A physiologically-based quantitative systems pharmacology model for mechanistic understanding of the response to alogliptin and its application in patients with renal impairment.
J Pharmacokinet Pharmacodyn
January 2025
Department of Clinical Pharmacy and Pharmacy Administration, West China school of Pharmacy, Sichuan University, Chengdu, 610064, China.
Alogliptin is a highly selective inhibitor of dipeptidyl peptidase-4 and primarily excreted as unchanged drug in the urine, and differences in clinical outcomes in renal impairment patients increase the risk of serious adverse reactions. In this study, we developed a comprehensive physiologically-based quantitative systematic pharmacology model of the alogliptin-glucose control system to predict plasma exposure and use glucose as a clinical endpoint to prospectively understand its therapeutic outcomes with varying renal function. Our model incorporates a PBPK model for alogliptin, DPP-4 activity described by receptor occupancy theory, and the crosstalk and feedback loops for GLP-1-GIP-glucagon, insulin, and glucose.
View Article and Find Full Text PDFRANK/RANKL Signaling Pathway in Breast Development and Cancer.
Adv Exp Med Biol
January 2025
Molecular Oncology, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
RANK pathway has attracted increasing interest as a promising target in breast cancer, given the availability of denosumab, an anti-RANKL drug. RANK signaling mediates progesterone-driven regulation of mammary gland development and favors breast cancer initiation by controlling mammary cell proliferation and stem cell fate. RANK activation promotes luminal mammary epithelial cell senescence, acting as an initial barrier to tumorigenesis but ultimately facilitating tumor progression and metastasis.
View Article and Find Full Text PDFMechanisms of Regulation of Cell Fate in Breast Development and Cancer.
Adv Exp Med Biol
January 2025
Laboratory of Stem Cells and Cancer (LSCC), Université Libre de Bruxelles (ULB), Brussels, Belgium.
This chapter focuses on the mechanisms of regulation of cell fate in breast development, occurring mainly after birth, as well as in breast cancer. First, we will review how the microenvironment of the breast, as well as external cues, plays a crucial role in mammary gland cell specification and will describe how it has been shown to reprogram non-mammary cells into mammary epithelial cells. Then we will focus on the transcription factors and master regulators which have been established to be determinant for basal (BC) and luminal cell (LC) identity, and will describe the experiments of ectopic expression or loss of function of these transcription factors which demonstrated that they were crucial for cell fate.
View Article and Find Full Text PDFMitotic chromatin marking governs the segregation of DNA damage.
Nat Commun
January 2025
Laboratory of Epigenome Integrity, Epigenetics & Cell Fate Centre, UMR7216 CNRS, Université Paris Cité, Paris, France.
The faithful segregation of intact genetic material and the perpetuation of chromatin states through mitotic cell divisions are pivotal for maintaining cell function and identity across cell generations. However, most exogenous mutagens generate long-lasting DNA lesions that are segregated during mitosis. How this segregation is controlled is unknown.
View Article and Find Full Text PDFComplex p53 dynamics regulated by miR-125b in cellular responses to reactive oxidative stress and DNA damage.
Brief Bioinform
November 2024
Department of Translational Research, Dasman Diabetes Institute, Dasman 15462, Kuwait City, Kuwait.
In response to distinct cellular stresses, the p53 exhibits distinct dynamics. These p53 dynamics subsequently control cell fate. However, different stresses can generate the same p53 dynamics with different cell fate outcomes, suggesting that the integration of dynamic information from other pathways is important for cell fate regulation.
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