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There are certain very well defined groups of genes that you would expect to be co-expressed, e.g. ribosomal proteins, proteosome subunits, splicesome components, VHATPase subunits; and each of these groups are co-expressed in different circumstances. It therefore looks to me that either your different tumour tissues (if that is the situation) are in similar ...


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Check the beautiful publication of Daniel Ramsk├Âld et al. 2009, which holds the numbers for generally anticipated co-expression. The specific level of co-expression, which applies to your scenario, will depend upon your tissue, your thresholds, and your definition of co-expression. It you look for a co-change of some genes across different specimen (rather ...


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This is a very interesting question, and one that has been at the heart of cancer research for a long time. I think it separates into three issues. Are there non-genetic mechanisms that can induce uncontrolled cell proliferation? Yes, at least in experimental settings. There are many viruses that induce proliferation in its host cell, and viral genes / ...


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Given the incidence rate of cancer, it is likely that usually multiple somewhat independent events have to occur, so that cancer forms (see the famous interpretation of the underlying data/thinking by Hanahan et Weinberg 2000 ) Epigenetic changes seem to be a likely factor contributing to cancer ( summary of an experiment, where they are also causal/inducing ...


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To directly respond to the quote presented, Segmented copy number profiles represent the summed outcome of all the SCNAs [somatic copy number alterations] that occurred during cancer development. As a tumor progresses, genomic instability can often increase. That is, more and more SCNAs occur. Because of this, one SCNA can overlap another. For ...



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