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. 2021 Aug 25;11(9):572. doi: 10.3390/metabo11090572

Figure 1.

Figure 1

Role of the nucleus and mitochondria in the origin of tumors. Normal cells are shown in green with nuclear and mitochondrial morphology indicative of normal gene expression and OxPhos function, respectively. Tumor cells are shown in red with abnormal nuclear and mitochondrial morphology indicative of genomic instability and abnormal OxPhos function, respectively. “(1) Normal cells beget normal cells with regulated growth. (2) Tumor cells beget tumor cells with dysregulated growth. (3) Transfer of a tumor cell nucleus into a normal cytoplasm begets normal cells that have regulated growth, despite the presence of the tumor-associated genomic abnormalities. (4) Transfer of a normal cell nucleus into a tumor cell cytoplasm begets dead cells or tumor cells with dysregulated growth”. The general reproducibility of the findings across a broad range of tumor types, animal species, and experimental techniques is notable in light of major concerns regarding the irreproducibility of scientific results published in prestigious journals [40,48,49]. “The results of these experiments are profound in showing that nuclear genomic defects alone cannot account for the origin of tumors and that normal-functioning mitochondria can suppress tumorigenesis”. Original diagram from Jeffrey Ling and Thomas N. Seyfried with permission [41].