Nuclear transfer experiments show that normal cytoplasm/mitochondria suppress tumorigenicity even in the presence of an abnormal cancer nucleus, challenging the somatic mutation theory.
"I'm somebody who really thinks the nuclear transfer experiments are enough to rock your world. If you believe in the, you know, sort of somatic mutation theory, like that should just stop you dead in your tracks and make you say like, "Wait, how is this? This really undoes everything in the most simple, beautiful way."" (said at 0:05:13)
Nuclear-cytoplasm transfer and cybrid cell experiments demonstrate that combining a cancer nucleus with normal cytoplasm/mitochondria can suppress tumorigenic phenotypes and restore normal differentiation in cell and animal models. Proponents of the metabolic theory of cancer use these findings to challenge the prevailing somatic mutation theory. However, the available body of evidence consists primarily of in vitro cybrid assays, animal nuclear transfer studies, and narrative reviews, meaning clinical certainty remains very low.
- supports: Inter-genomic cross talk between mitochondria and the nucleus plays an important role in t… (Gene 2005)
"Interestingly we found that altered expression of APE1 in rho0 cells and tumorigenic phenotype can be reversed by exogenous transfer of wild type mitochondria in rho0 cells." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Cancer as a mitochondrial metabolic disease. (Frontiers in cell and developmental biology 2015)
"The findings are reviewed from nuclear cytoplasm transfer experiments that relate to the origin of cancer. The evidence from these experiments is difficult to reconcile with the somatic mutation theory, but is consistent with the notion that cancer is primarily a mitochondrial metabolic disease." (abstract, conclusions, passage verified)
pubmedfull study (doi)