Robust Calibration of High Dimension Nonlinear Dynamical Models for Omics Data: An Application in Cancer Systems Biology

2020 ◽  
Vol 28 (1) ◽  
pp. 196-207 ◽  
Author(s):  
Fortunato Bianconi ◽  
Chiara Antonini ◽  
Lorenzo Tomassoni ◽  
Paolo Valigi
2020 ◽  
Vol 10 (4) ◽  
pp. 180
Author(s):  
Gizem Damla Yalcin ◽  
Nurseda Danisik ◽  
Rana Can Baygin ◽  
Ahmet Acar

Over the past decade, we have witnessed an increasing number of large-scale studies that have provided multi-omics data by high-throughput sequencing approaches. This has particularly helped with identifying key (epi)genetic alterations in cancers. Importantly, aberrations that lead to the activation of signaling networks through the disruption of normal cellular homeostasis is seen both in cancer cells and also in the neighboring tumor microenvironment. Cancer systems biology approaches have enabled the efficient integration of experimental data with computational algorithms and the implementation of actionable targeted therapies, as the exceptions, for the treatment of cancer. Comprehensive multi-omics data obtained through the sequencing of tumor samples and experimental model systems will be important in implementing novel cancer systems biology approaches and increasing their efficacy for tailoring novel personalized treatment modalities in cancer. In this review, we discuss emerging cancer systems biology approaches based on multi-omics data derived from bulk and single-cell genomics studies in addition to existing experimental model systems that play a critical role in understanding (epi)genetic heterogeneity and therapy resistance in cancer.


Aging Cell ◽  
2015 ◽  
Vol 14 (6) ◽  
pp. 933-944 ◽  
Author(s):  
Jonas Zierer ◽  
Cristina Menni ◽  
Gabi Kastenmüller ◽  
Tim D. Spector

2018 ◽  
Vol 17 ◽  
pp. 117693511879975 ◽  
Author(s):  
Abdallah K Alameddine ◽  
Frederick Conlin ◽  
Brian Binnall

Background: Frequently occurring in cancer are the aberrant alterations of regulatory onco-metabolites, various oncogenes/epigenetic stochasticity, and suppressor genes, as well as the deficient mismatch repair mechanism, chronic inflammation, or those deviations belonging to the other cancer characteristics. How these aberrations that evolve overtime determine the global phenotype of malignant tumors remains to be completely understood. Dynamic analysis may have potential to reveal the mechanism of carcinogenesis and can offer new therapeutic intervention. Aims: We introduce simplified mathematical tools to model serial quantitative data of cancer biomarkers. We also highlight an introductory overview of mathematical tools and models as they apply from the viewpoint of known cancer features. Methods: Mathematical modeling of potentially actionable genomic products and how they proceed overtime during tumorigenesis are explored. This report is intended to be instinctive without being overly technical. Results: To date, many mathematical models of the common features of cancer have been developed. However, the dynamic of integrated heterogeneous processes and their cross talks related to carcinogenesis remains to be resolved. Conclusions: In cancer research, outlining mathematical modeling of experimentally obtained data snapshots of molecular species may provide insights into a better understanding of the multiple biochemical circuits. Recent discoveries have provided support for the existence of complex cancer progression in dynamics that span from a simple 1-dimensional deterministic system to a stochastic (ie, probabilistic) or to an oscillatory and multistable networks. Further research in mathematical modeling of cancer progression, based on the evolving molecular kinetics (time series), could inform a specific and a predictive behavior about the global systems biology of vulnerable tumor cells in their earlier stages of oncogenesis. On this footing, new preventive measures and anticancer therapy could then be constructed.


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