Oncogenic rearrangements driving ionizing radiation–associated human cancer
Massimo Santoro, Francesca Carlomagno
Massimo Santoro, Francesca Carlomagno
Published October 25, 2013
Citation Information: J Clin Invest. 2013;123(11):4566-4568. https://doi.org/10.1172/JCI72725.
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Commentary

Oncogenic rearrangements driving ionizing radiation–associated human cancer

Abstract

The Chernobyl nuclear disaster has caused a remarkable increase in radiation-induced papillary thyroid carcinoma in children and young adults. In this issue of the JCI, Ricarte-Filho and colleagues demonstrate that chromosomal rearrangements are the oncogenic “drivers” in most post-Chernobyl carcinomas and that they often lead to unscheduled activation of the MAPK signaling pathway. These findings represent a major step forward in our understanding of radiation-induced carcinogenesis and suggest various hypotheses about the mechanisms underlying the formation and selection of gene rearrangements during cancer cell evolution.

Authors

Massimo Santoro, Francesca Carlomagno

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Figure 1

Filho study (red) (12).

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Filho study (red) (12). Most of them target components of the MAPK sig...
Most of them target components of the MAPK signaling cascade and include rearrangements of RET (RET/PTC) or NTRK1 and NTRK3 receptor tyrosine kinases (RTKs), or BRAF kinase. An exception is represented by rearrangements affecting the PPARG steroid hormone receptor.