Special Issue "System Biology in Cancer Research"

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A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (20 September 2012)

Special Issue Editor

Guest Editor
Dr. Bernard Corfe (Website)

Department of Oncology, The Medical School, Beech Hill Road, Sheffield, S10 2RX, UK

Special Issue Information

Dear Colleagues,

Systems biology is an emerging interdisciplinary approach to biological research deliberately embracing a suite of divergent approaches. It seeks to incorporate substantive bodies of literature, high throughput (omics)data, mathemetical modelling to generate in silico models with predictive capacity to improve understanding of biology. In essence it is anti-reductionist. Systems biology is being applied to cancer research at a number of levels and from a number of perspectives, network modelling is applied to large datasets to reveal novel markers or targets of disease (1,2) and also from a ground-up perspective in the modelling of pathways previously described purely qualitatively (3). It is perhaps naive to treat a cancer as behaving like the host organism and the application of models of competition in ecosystems and game theory have also been applied to modelling the behaviour of tumours (4,5).

This special edition of Cancers gives an opportunity to describe recent original research in the application of any systems-biology approach in cancer research, the development or application of new platforms or insights, and is open to reviews of the field and benefits of application. If you would like to discuss an idea for a paper before committing please contact the guest editor.

Dr. Bernard Corfe
Guest Editor

Keywords

  • systems biology
  • network analysis
  • pathways analysis
  • data integration
  • strategies
  • genomics
  • proteomics
  • metabolomics
  • epigenomics
  • modelling

Published Papers (3 papers)

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Open AccessArticle Annotating Cancer Variants and Anti-Cancer Therapeutics in Reactome
Cancers 2012, 4(4), 1180-1211; doi:10.3390/cancers4041180
Received: 8 October 2012 / Revised: 31 October 2012 / Accepted: 2 November 2012 / Published: 8 November 2012
Cited by 72 | PDF Full-text (1361 KB) | HTML Full-text | XML Full-text
Abstract
Reactome describes biological pathways as chemical reactions that closely mirror the actual physical interactions that occur in the cell. Recent extensions of our data model accommodate the annotation of cancer and other disease processes. First, we have extended our class of protein [...] Read more.
Reactome describes biological pathways as chemical reactions that closely mirror the actual physical interactions that occur in the cell. Recent extensions of our data model accommodate the annotation of cancer and other disease processes. First, we have extended our class of protein modifications to accommodate annotation of changes in amino acid sequence and the formation of fusion proteins to describe the proteins involved in disease processes. Second, we have added a disease attribute to reaction, pathway, and physical entity classes that uses disease ontology terms. To support the graphical representation of “cancer” pathways, we have adapted our Pathway Browser to display disease variants and events in a way that allows comparison with the wild type pathway, and shows connections between perturbations in cancer and other biological pathways. The curation of pathways associated with cancer, coupled with our efforts to create other disease-specific pathways, will interoperate with our existing pathway and network analysis tools. Using the Epidermal Growth Factor Receptor (EGFR) signaling pathway as an example, we show how Reactome annotates and presents the altered biological behavior of EGFR variants due to their altered kinase and ligand-binding properties, and the mode of action and specificity of anti-cancer therapeutics. Full article
(This article belongs to the Special Issue System Biology in Cancer Research)
Open AccessArticle Relative Expression of Vitamin D Hydroxylases, CYP27B1 and CYP24A1, and of Cyclooxygenase-2 and Heterogeneity of Human Colorectal Cancer in Relation to Age, Gender, Tumor Location, and Malignancy: Results from Factor and Cluster Analysis
Cancers 2012, 4(3), 763-776; doi:10.3390/cancers4030763
Received: 22 May 2012 / Revised: 6 July 2012 / Accepted: 13 July 2012 / Published: 26 July 2012
Cited by 4 | PDF Full-text (207 KB) | HTML Full-text | XML Full-text
Abstract
Previous studies on the significance of vitamin D insufficiency and chronic inflammation in colorectal cancer development clearly indicated that maintenance of cellular homeostasis in the large intestinal epithelium requires balanced interaction of 1,25-(OH)2D3 and prostaglandin cellular signaling networks. The [...] Read more.
Previous studies on the significance of vitamin D insufficiency and chronic inflammation in colorectal cancer development clearly indicated that maintenance of cellular homeostasis in the large intestinal epithelium requires balanced interaction of 1,25-(OH)2D3 and prostaglandin cellular signaling networks. The present study addresses the question how colorectal cancer pathogenesis depends on alterations of activities of vitamin D hydroxylases, i.e., CYP27B1-encoded 25-hydroxyvitamin D-1a-hydroxylase and CYP24A1-encoded 25-hydroxyvitamin D-24-hydroxylase, and inflammation-induced cyclooxygenase-2 (COX-2). Data from 105 cancer patients on CYP27B1, VDR, CYP24A1, and COX-2 mRNA expression in relation to tumor grade, anatomical location, gender and age were fit into a multivariate model of exploratory factor analysis. Nearly identical results were obtained by the principal factor and the maximum likelihood method, and these were confirmed by hierarchical cluster analysis: Within the eight mutually dependent variables studied four independent constellations were found that identify different features of colorectal cancer pathogenesis: (i) Escape of COX-2 activity from restraints by the CYP27B1/VDR system can initiate cancer growth anywhere in the colorectum regardless of age and gender; (ii) variations in COX-2 expression are mainly responsible for differences in cancer incidence in relation to tumor location; (iii) advancing age has a strong gender-specific influence on cancer incidence; (iv) progression from well differentiated to undifferentiated cancer is solely associated with a rise in CYP24A1 expression. Full article
(This article belongs to the Special Issue System Biology in Cancer Research)
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Open AccessCommentary Cancer Cachexia: Muscle Physiology and Exercise Training
Cancers 2012, 4(4), 1247-1251; doi:10.3390/cancers4041247
Received: 11 September 2012 / Revised: 17 November 2012 / Accepted: 21 November 2012 / Published: 29 November 2012
Cited by 3 | PDF Full-text (308 KB) | HTML Full-text | XML Full-text
Abstract
Cachexia in cancer patients is a condition marked by severe tissue wasting and a myriad of quality of life and health consequences. Cachexia is also directly linked to the issues of morbidity and survivability in cancer patients. Therapeutic means of mitigating cachexia [...] Read more.
Cachexia in cancer patients is a condition marked by severe tissue wasting and a myriad of quality of life and health consequences. Cachexia is also directly linked to the issues of morbidity and survivability in cancer patients. Therapeutic means of mitigating cachexia and its effects are thus critical in cancer patient treatment. We present a discussion on the use of physical exercise activities in the context of such treatment as a means to disruption the tissue wasting effects (i.e., muscle tissue losses via anorexigenic pro-inflammatory cytokines) of cachexia. In addition we propose a theoretical model (Exercise Anti-Cachectic Hypothetical—“EACH” model) as to how exercise training may promote a disruption in the cycle of events leading to advancing cachexia and in turn promote an enhanced functionality and thus improved quality of life in cancer patients. Full article
(This article belongs to the Special Issue System Biology in Cancer Research)

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