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R.B. · 06-24-2007, 03:32 PM

The flow of events is sometimes beguiling.

I ask a question raised by your post go off to look for something else and up it pops or at least part.

It does recognise BC lines have abnormal energy utilisation.

There are several trials on fats and BC herceptin consideration of lipid rafts etc. So it would look as if fats and particularly omega three and six are part of this some how.

I have only skimmed this but it seems to be saying that the boundaries between non-oxygen and fat burning cancer is not as clear cut as commonly suggested - AND that whilst some may be irreparably damaged some my just have had the fat supply line cut / higher demand / insufficient supply.

More questions than answers - There are not enough hours in the day to read everything!

RB

http://content.febsjournal.org/cgi/c...ull/274/6/1393

"In early studies on energy metabolism of tumor cells, it was proposed that the enhanced glycolysis was induced by a decreased oxidative phosphorylation. Since then it has been indiscriminately applied to all types of tumor cells that the ATP supply is mainly or only provided by glycolysis, without an appropriate experimental evaluation".....................

"All tumor cell types show an enhanced glycolytic flux; however, not all have a diminished mitochondrial metabolic capacity. Therefore, the take-home message is that not all tumor cell types depend exclusively on glycolysis for ATP supply; some may equally or predominantly rely on oxidative phosphorylation. In consequence, the driving force for the enhanced glycolysis in tumor cells cannot be an energy deficiency induced only by a damaged oxidative phosphorylation. The accelerated cellular proliferation may also impose an energy deficiency (as well as a higher demand for glycolytic and Krebs cycle biosynthetic intermediaries), which can only be covered by an increased glycolysis together with an unperturbed oxidative phosphorylation."

06-24-2007, 03:32 PM	#20
R.B. Senior Member Join Date: Mar 2006 Posts: 1,843	The flow of events is sometimes beguiling. I ask a question raised by your post go off to look for something else and up it pops or at least part. It does recognise BC lines have abnormal energy utilisation. There are several trials on fats and BC herceptin consideration of lipid rafts etc. So it would look as if fats and particularly omega three and six are part of this some how. I have only skimmed this but it seems to be saying that the boundaries between non-oxygen and fat burning cancer is not as clear cut as commonly suggested - AND that whilst some may be irreparably damaged some my just have had the fat supply line cut / higher demand / insufficient supply. More questions than answers - There are not enough hours in the day to read everything! RB http://content.febsjournal.org/cgi/c...ull/274/6/1393 "In early studies on energy metabolism of tumor cells, it was proposed that the enhanced glycolysis was induced by a decreased oxidative phosphorylation. Since then it has been indiscriminately applied to all types of tumor cells that the ATP supply is mainly or only provided by glycolysis, without an appropriate experimental evaluation"..................... "All tumor cell types show an enhanced glycolytic flux; however, not all have a diminished mitochondrial metabolic capacity. Therefore, the take-home message is that not all tumor cell types depend exclusively on glycolysis for ATP supply; some may equally or predominantly rely on oxidative phosphorylation. In consequence, the driving force for the enhanced glycolysis in tumor cells cannot be an energy deficiency induced only by a damaged oxidative phosphorylation. The accelerated cellular proliferation may also impose an energy deficiency (as well as a higher demand for glycolytic and Krebs cycle biosynthetic intermediaries), which can only be covered by an increased glycolysis together with an unperturbed oxidative phosphorylation."