ABSTRACT
National Human Genome Research Institute, National Institutes of Health, Building 50, MSC8000, Bethesda, MD 20892, USA. aEmail: belldaph@mail.nih.gov *Corresponding author
There are several defi ned “hallmarks” or acquired functional attributes shared by cancer cells; namely, their ability to propagate their own growth signals, insensitivity to anti-growth signals, ability to evade apoptosis, capacity for unlimited replication, acquired angiogenic properties, and acquired invasive and metastatic potential (Hanahan and Weinberg 2000), as well as two recently added hallmarks, i.e., ability to avoid immune destruction and reprogram energy metabolism (Hanahan and Weinberg 2011). Furthermore, interactions between cancer cells and surrounding normal cells are believed to create supportive “tumor microenvironments” (Hanahan and Weinberg 2011), which add an additional level of complexity to the quest for cancer therapeutics. It is now well established that alterations in the tumor genome, epigenome, transcriptome, proteome, and metabolome, as well as the tumor microenvironment, all underlie the pathogenesis of human cancer (reviewed in Kolch and Pitt 2010; Brower 2011; Gilbertson 2011; Nagrath et al. 2011; Stratton 2011).
