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The mechanisms by which in vivo expression of the Yamanaka transcription factors (OSKM) renders somatic cells permissive for differentiation remain unclear. Here, the authors show that in vivo reprogramming using OSKM generates germ cell tumors and drives acquisition of totipotency-like features in somatic cells through DMRT1.
There is some evidence of a hereditary risk for developing testicular germ cell tumours. Here, the authors use whole-exome sequencing and identify a risk variant for the disease in DNAAF1, a gene involved in microtubule-based cilia.