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Cell Mol Life Sci. 2012 Mar;69(6):931-4. doi: 10.1007/s00018-011-0860-x. Epub 2011 Oct 28.

Tumor microenvironment: becoming sick of Myc.

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Vall d'Hebron Institute of Oncology, Psg. Vall d'Hebron 119, Edifici Mediterranea, Laboratorio 20, 08035 Barcelona, Spain.


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.

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