scholarly journals Cancer systems biology: signal processing for cancer research

2011 ◽  
Vol 30 (4) ◽  
pp. 221-225 ◽  
Author(s):  
Olli Yli-Harja ◽  
Antti Ylipaa ◽  
Matti Nykter ◽  
Wei Zhang
Author(s):  
Lieven Verbeke ◽  
Steven Van Laere

Cancer systems biology encompasses the application of systems biology approaches to cancer research. Historically, systems biology was first applied in cancer research to enable a pathway-oriented interpretation of gene expression data and this strategy has undoubtedly delivered relevant insights with respect to many aspects of cancer biology. Nowadays, cancer is regarded as a complex system that integrates signals from different levels (i.e. (epi)genomics, transcriptomics, micro-environment) through a network of interconnected proteins to generate a biological response. This holistic approach not only allows the identification of new and relevant signal transduction pathways, but also provides a better understanding of several key properties of cancer cells that can be best understood from a network-level perspective: robustness, evolvability, and plasticity. This chapter provides an overview of several key concepts of systems biology, including reference gene set libraries, network topology, and available strategies to establish biological networks. Next, these concepts are utilized to explain gene set and gene network analysis with particular focus on cancer biology. Finally, the caveats and challenges that are facing cancer systems biology are summarized.


2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Sajib Chakraborty ◽  
Md. Ismail Hosen ◽  
Musaddeque Ahmed ◽  
Hossain Uddin Shekhar

The acquisition of cancer hallmarks requires molecular alterations at multiple levels including genome, epigenome, transcriptome, proteome, and metabolome. In the past decade, numerous attempts have been made to untangle the molecular mechanisms of carcinogenesis involving single OMICS approaches such as scanning the genome for cancer-specific mutations and identifying altered epigenetic-landscapes within cancer cells or by exploring the differential expression of mRNA and protein through transcriptomics and proteomics techniques, respectively. While these single-level OMICS approaches have contributed towards the identification of cancer-specific mutations, epigenetic alterations, and molecular subtyping of tumors based on gene/protein-expression, they lack the resolving-power to establish the casual relationship between molecular signatures and the phenotypic manifestation of cancer hallmarks. In contrast, the multi-OMICS approaches involving the interrogation of the cancer cells/tissues in multiple dimensions have the potential to uncover the intricate molecular mechanism underlying different phenotypic manifestations of cancer hallmarks such as metastasis and angiogenesis. Moreover, multi-OMICS approaches can be used to dissect the cellular response to chemo- or immunotherapy as well as discover molecular candidates with diagnostic/prognostic value. In this review, we focused on the applications of different multi-OMICS approaches in the field of cancer research and discussed how these approaches are shaping the field of personalized oncomedicine. We have highlighted pioneering studies from “The Cancer Genome Atlas (TCGA)” consortium encompassing integrated OMICS analysis of over 11,000 tumors from 33 most prevalent forms of cancer. Accumulation of huge cancer-specific multi-OMICS data in repositories like TCGA provides a unique opportunity for the systems biology approach to tackle the complexity of cancer cells through the unification of experimental data and computational/mathematical models. In future, systems biology based approach is likely to predict the phenotypic changes of cancer cells upon chemo-/immunotherapy treatment. This review is sought to encourage investigators to bring these different approaches together for interrogating cancer at molecular, cellular, and systems levels.


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.


2006 ◽  
pp. 353-366
Author(s):  
Jackie L. Stilwell ◽  
Yinghui Guan ◽  
Richard M. Neve ◽  
Joe W. Gray

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