Cancer cells do not exist as pure homogeneous populations in vivo. Instead they 
are embedded in "cancer cell nests" that are surrounded by stromal cells, 
especially cancer associated fibroblasts. Thus, it is not unreasonable to 
suspect that stromal fibroblasts could influence the metabolism of adjacent 
cancer cells, and visa versa. In accordance with this idea, we have recently 
proposed that the Warburg effect in cancer cells may be due to culturing cancer 
cells by themselves, out of their normal stromal context or tumor 
microenvironment. In fact, when cancer cells are co-cultured with fibroblasts, 
then cancer cells increase their mitochondrial mass, while fibroblasts lose 
their mitochondria. An in depth analysis of this phenomenon reveals that 
aggressive cancer cells are "parasites" that use oxidative stress as a "weapon" 
to extract nutrients from surrounding stromal cells. Oxidative stress in 
fibroblasts induces the autophagic destruction of mitochondria, by mitophagy. 
Then, stromal cells are forced to undergo aerobic glycolysis, and produce 
energy-rich nutrients (such as lactate and ketones) to "feed" cancer cells. This 
mechanism would allow cancer cells to seed anywhere, without blood vessels as a 
food source, as they could simply induce oxidative stress wherever they go, 
explaining how cancer cells survive during metastasis. We suggest that stromal 
catabolism, via autophagy and mitophagy, fuels the anabolic growth of tumor 
cells, promoting tumor progression and metastasis. We have previously termed 
this new paradigm "The Autophagic Tumor Stroma Model of Cancer Metabolism", or 
the "Reverse Warburg Effect". We also discuss how glutamine addiction 
(glutaminolysis) in cancer cells fits well with this new model, by promoting 
oxidative mitochondrial metabolism in aggressive cancer cells.