%0 Journal Article
%T Structural and functional properties of genes involved in human cancer
%A Simon J Furney
%A Desmond G Higgins
%A Christos A Ouzounis
%A N¨²ria L¨®pez-Bigas
%J BMC Genomics
%D 2006
%I BioMed Central
%R 10.1186/1471-2164-7-3
%X We have conducted an analysis of a set of genes known to be involved in cancer in order to unveil their unique features that can assist towards the identification of new candidate cancer genes.We have detected key patterns in this group of genes in terms of the molecular function or the biological process in which they are involved as well as sequence properties. Based on these features we have developed an accurate Bayesian classification model with which human genes have been scored for their likelihood of involvement in cancer.All cancers are caused by alterations in DNA that affect the biochemical function or expression of certain genes providing expansion capabilities to the cell with the mutations. Generally this is a multi-step process, requiring mutations in several genes that ultimately result in the uncontrolled growth of a clone derived from the cells with the mutations[1]. A main aim in cancer research is to identify the causative genes and mutations leading to carcinogenesis. This knowledge can then be translated into new targets for diagnosis and treatment. The continuing investigation into the genetic basis of cancer has revealed a number of genes whose individual or concerted actions, when mutated, result in oncogenesis. Cancer-causing genes have been classified into three distinct groups: proto-oncogenes, tumour-suppressor genes, and stability genes, according to the biological roles they fulfil in a normal cell and hence, the aberrant process they effect in an oncogenic state[2]. Proto-oncogenes, when mutated, unleash their oncogenic potential primarily by remaining in a permanently activated state. On the other hand, oncogenic induction by tumour-suppressor genes occurs through the inactivation of the gene/protein. Stability genes are responsible for processes including DNA repair and chromosomal segregation. Mutations in these genes lead to a higher mutation rate in the genome[3].The computational era of cancer research has revolved around the id
%U http://www.biomedcentral.com/1471-2164/7/3