Introduction

Our understanding of the molecular pathways controlling tumor growth, survival, and metastasis has increased at a staggering pace over the last decades. Large-scale institutional efforts such as The Cancer Genome Atlas projects have identified previously unknown mutations with high frequencies in various cancers (1). These data, when combined with pathway analysis tools, point us towards genetic events most likely to be important “drivers” of cancer and to those that may be simply “passenger” mutations (2,3). In addition, the widespread availability of functional genomic tools, such as siRNA, shRNA vectors, and genetically engineered mouse models (GEM models), and anti-sense technology, has allowed individual laboratories to carefully evaluate the role of selected genes and pathways, defining their contributions to various aspects of tumorigenesis. Importantly, from these efforts, novel ideas about the fundamentals of the cancer process itself have recently emerged. These include the supporting role of non-tumor cells in the tumor micro-environment, the concept of cancer stem cells, epithelial-to-mesenchymal transitions, the various mechanisms that tumors employ to ensure immune evasion, the principle of oncogene addiction, and the increasingly interesting contribution of non-coding RNAs, to name only a few (4–7). These insights have given us hope that the recent migration of cancer treatment away from untargeted cytotoxic therapy to selective molecular-targeted therapies will ultimately be translated into novel life-saving cancer treatments.