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  • Open Access

    ARTICLE

    Changes in DNA Damage Repair Gene Expression and Cell Cycle Gene Expression Do Not Explain Radioresistance in Tamoxifen-Resistant Breast Cancer

    Annemarie E. M. Post*†, Johan Bussink*, Fred C. G. J. Sweep, Paul N. Span*

    Oncology Research, Vol.28, No.1, pp. 33-40, 2020, DOI:10.3727/096504019X15555794826018

    Abstract Tamoxifen-induced radioresistance, reported in vitro, might pose a problem for patients who receive neoadjuvant tamoxifen treatment and subsequently receive radiotherapy after surgery. Previous studies suggested that DNA damage repair or cell cycle genes are involved, and could therefore be targeted to preclude the occurrence of cross-resistance. We aimed to characterize the observed cross-resistance by investigating gene expression of DNA damage repair genes and cell cycle genes in estrogen receptor-positive MCF-7 breast cancer cells that were cultured to tamoxifen resistance. RNA sequencing was performed, and expression of genes characteristic for several DNA damage repair pathways was… More >

  • Open Access

    ARTICLE

    Cancer Cell(s) Cycle Sequencing Reveals Universal Mechanisms of Apoptosis

    R. M. Ardito Marretta*, F. Ales

    Molecular & Cellular Biomechanics, Vol.7, No.4, pp. 225-266, 2010, DOI:10.3970/mcb.2010.007.225

    Abstract In this paper, cell cycle in higher eukaryotes and their molecular networks signals both inG1/SandG2/Mtransitions are replicatedin silico. Biochemical kinetics, converted into a set of differential equations, and system control theory are employed to design multi-nested digital layers to simulate protein-to-protein activation and inhibition for cell cycle dynamics in the presence of damaged genomes. Sequencing and controlling the digital process of four micro-scale species networks (p53/Mdm2/DNA damage, p21mRNA/cyclin-CDK complex, CDK/CDC25/wee1/ SKP2/APC/CKI and apoptosis target genes system) not only allows the comprehension of the mechanisms of these molecule interactions but paves the way for unraveling the… More >

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