Although cancer types differ substantially, many cancers share common gene expression signatures. Consistent with this observation, we find convergent and representative distributions and correlation vectors that are distinct in cancer and noncancer ensembles. These differences originate in many genes, but comparatively few genes account for the major differences. We identify genes with different combinatorial regulation in cancer and noncancer as indicated by significant differences in their correlation vectors. Among the identified genes are many established oncogenes and apoptotic genes (such as members of the Bcl-2, the MAPK, and the Ras families) and new candidate oncogenes. Our findings expand and complement the tumorigenic role of up and down regulation of these genes by emphasizing cancer-specific changes in their couplings and correlation patterns at genome-wide level that are independent from their mean levels of expression in cancer cells. Given the central role of these genes in defining the cancerous state it may be worth investigating them and the differences in their combinatorial regulation for developing wide-spectrum anticancer drugs.
slavovLabI have always hated the career building aspects of pursuing an academic career, and yet I do not have good ideas how to sidestep them.
These aspects aren't unique to academia (seem worse in politics) but are particularly incongruous with what inspired many of us to do research.
slavovLab@skryazhi@NSF I strongly dislike invoking "competition with China" as a motivation -- this is misguided on many levels.
It's hard to predict that this will evolve, and I do not know enough to make an informed prediction. It sounds more promising than menacing.