Tumor microenvironment: becoming sick of Myc.
Several years ago, we described Myc as "the oncogene from hell", since evidence had just emerged that Myc, aside from being responsible for cell-cycle progression and tumor expansion, was also able to induce genomic instability in culture, wreaking havoc in tumor cells and accelerating tumor progression (Soucek and Evan, Cancer Cell 1:406-408, 2002; Vafa et al., Mol Cell 9:1031-1044, 2002). In this review, we discuss recent publications that expand Myc's evil armory to include coordination of the crosstalk between tumor and microenvironment. Indeed, endogenous Myc, acting as a client for upstream oncogenic lesions, instructs the tumor stroma, engages a complex inflammatory response and induces angiogenesis, thus allowing the tumor to thrive. This is highly topical in light of the fact that Hanahan and Weinberg have recently redefined the hallmarks of cancer and pointed out that genomic instability and inflammation are essential for both their acquisition and development (Hanahan and Weinberg, Cell 144:646-674, 2011). Myc, it seems, is behind it all.
Vall d'Hebron Institute of Oncology, Psg. Vall d'Hebron 119, Edifici Mediterranea, Laboratorio 20, 08035 Barcelona, Spain. jwhitfield@vhio.net
Jonathan R
JR
Whitfield
Laura
L
Soucek
D000818:Animals; D006801:Humans; D009369:Neoplasms / Q000209:etiology; D016271:Proto-Oncogene Proteins c-myc / Q000502:physiology*; D059016:Tumor Microenvironment
D016271:Proto-Oncogene Proteins c-myc