![]() ![]() The likely reason for the inconsistency is the diverse histological types and multivariate nature of melanoma, making consensus view about melanoma gene expression behaviour, a challenge, which also hinders development of novel anti-melanoma therapies. Īfter the advent of the ‘ omics’ era, despite several attempts to identify gene signatures and genetic changes in melanoma, inconsistencies in the results still exists. Melanoma initiation is followed by its proliferation to different layers of skin via multiple growth phases (cutaneous metastasis CM) and finally to lymph nodes (LN), which metastasize tumour to different organs. In general, melanoma initiates with marked disruption of cellular homeostatic mechanisms leading to a malignant transformation of skin melanocytes (cutaneous non-metastatic CnM). AK received research fellowship from Council of Scientific and Industrial Research (CSIR)-India.Ĭompeting interests: The authors have declared that no competing interests exist.Īdvance malignant melanoma represents a deadly cancer state due to its high dissemination potential and increasing therapy resistance. įunding: DG conceived and received a grant from the Department of Biotechnology (DBT)-India grants (Grant no. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are creditedĭata Availability: Processed Data are available at. Received: JAccepted: OctoPublished: November 11, 2015Ĭopyright: © 2015 Kaushik et al. ![]() PLoS ONE 10(11):Įditor: Roger Chammas, Universidade de São Paulo, BRAZIL The web-based database resource consists of results from the analysis presented here, integrated with cytoscape web and user-friendly tools for visualization, retrieval and further analysis.Ĭitation: Kaushik A, Bhatia Y, Ali S, Gupta D (2015) Gene Network Rewiring to Study Melanoma Stage Progression and Elements Essential for Driving Melanoma. The study results are also presented as a freely available database at. Our analysis also reveals presence of distinct network hubs in different stages of metastasizing tumor for the same set of pathways in the statistically conserved gene sets. Moreover, the deviated network properties of the disease gene sets allow ranking/prioritization of different enriched, dysregulated and conserved pathway terms in metastatic melanoma, in agreement with previous findings. We found that the shortlisted disease genes in the study show strong and abnormal network connectivity, which enhances with the disease progression. Intriguingly, a majority of the melanoma network-rewired genes are not differentially expressed and the disease genes involved in melanoma progression consistently modulate its activity by rewiring network connections. We meta-analysed 642 microarray samples to generate melanoma reconstructed networks representing four different stages of melanoma progression to extract genes with altered molecular circuitry wiring as compared to a normal cellular state. ![]() In this study, we have performed systems biology studies to enhance our knowledge about the conserved property of disease genes or gene sets among mutually exclusive datasets representing melanoma progression. ![]() Systems biology offers an alternative approach to re-explore the genes or gene sets that display dysregulated behaviour without being differentially expressed. These characteristics of melanoma also make the development of drugs and identification of novel drug targets for metastatic melanoma a daunting task. Metastatic melanoma patients have a poor prognosis, mainly attributable to the underlying heterogeneity in melanoma driver genes and altered gene expression profiles. ![]()
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