Jaromira Kovarova

TL;DR: This paper showed that tumor cells without mitochondrial DNA (mtDNA) showed delayed tumor growth, and that tumor formation is associated with acquisition of mtDNA from host cells, leading to partial recovery of mitochondrial function in cells derived from primary tumors grown from cells without mtDNA and a shorter lag in tumor growth.

TL;DR: Results show that intact mitochondria with their mtDNA payload are transferred in the developing tumour, and provide functional evidence for an essential role of oxidative phosphorylation in cancer.

TL;DR: It is shown that pyrimidine biosynthesis dependent on respiration-linked dihydroorotate dehydrogenase (DHODH) is required to overcome cell-cycle arrest, while mitochondrial ATP generation is dispensable for tumorigenesis, pointing to inhibitors of DHODH as potential anti-cancer agents.

TL;DR: Evidence that mitochondrial DNA transfer occurs in vivo has now been published and it is possible that intercellular mitochondrial transfer is a fundamental physiological process with a role in development and tissue homeostasis.

TL;DR: In the current review, the contributions of both intracellular and intercellular mitochondrial dynamics to the etiology of PD will be discussed.