Scientists in the Czech Republic and Australia have found that tumor cells without mitochondrial DNA (mtDNA) show delayed tumor growth and that tumor formation is associated with acquisition of mtDNA from host cells. Professor Jiří Neužil and his team at the Institute of Biotechnology CAS and Griffith University, Australia made the discovery. It leads to a partial recovery of mitochondrial function in cells derived from primary tumors grown from cells without mtDNA and a shorter lag in tumor growth. Cell lines from circulating tumor cells showed further recovery of mitochondrial respiration and an intermediate lag to tumor growth, while cells from lung metastases exhibited full restoration of respiratory function and no lag in tumor growth. Stepwise assembly of mitochondrial respiratory (super)complexes was correlated with acquisition of respiratory function. Findings of 25 scientists, including Professor Neužil’s team, indicate horizontal transfer of mtDNA from host cells in the tumor microenvironment to tumor cells with compromised respiratory function to re-establish respiration and tumor-initiating efficacy. These results suggest pathophysiological processes for overcoming mtDNA damage and support the notion of high plasticity of malignant cells. Cell Metabolism of Jan. 6, 2015, describes the significant discovery in full.