Posted: May 14, 2011 8:23 am
Mononoke wrote:
http://hubpages.com/hub/Scientists_cure ... kes_notice
read the article it sounds too good to be true.
The illustration is full of fail, here is why...
[1] In hypoxic conditions, cancer cells don't switch to glycolysis as another way of making energy. Glycolysis is an integral part of cellular metabolism regardless of whether a cell is cancerous or not. In normal cells under normoxic conditions, glycolysis is followed by the tricarboxylic acid cycle. In hypoxic conditions, lactic acid fermentation occurs instead of the tricarboxylic acid cycle. There is no dichotomy between glycolysis and something else.
[2] Mitochondria switching off or the ability to evade apoptosis per se does NOT make the cells immortal, cell immortality is linked to the activation of telomere maintenance mechanisms such as the telomerase pathway or the ALT pathway. Cells that cannot do this cannot be immortal.
[3] The idea that one may turn mitochondria back "on" is a bit bollocks too, and so is the idea that reactivating mitochondrial apoptotic signalling in cancerous cells (as opposed to turning mitochondria back on) will invariably trigger apoptosis, since there are many possible ways for cancer cells to evade apoptosis even if the mitochondrial components of apoptosis signalling pathways are active.
For a detailed review of how cancer cells may evade apoptosis through various pathways, at premitochondrial, mitochondrial and postmitochondrial levels, please check this.
One of the hallmarks of human cancers is the intrinsic or acquired resistance to apoptosis. Evasion of apoptosis can be part of a cellular stress response to ensure the cell's survival upon exposure to stressful stimuli. Apoptosis resistance may contribute to carcinogenesis, tumor progression, and also treatment resistance, since most current anticancer therapies including chemotherapy as well as radio- and immunotherapies primarily act by activating cell death pathways including apoptosis in cancer cells. Hence, a better understanding of the molecular mechanisms regarding how cellular stress stimuli trigger antiapoptotic mechanisms and how this contributes to tumor resistance to apoptotic cell death is expected to provide the basis for a rational approach to overcome apoptosis resistance mechanisms in cancers.
http://www.hindawi.com/journals/ijcb/2010/370835/
It looks like the illustrators of that popular science article that you linked to have been less than rigorous, Mononoke.
None of this however means that dicholoroacetate may not be able to trigger apoptosis in certain cancers with certain mechanisms of evading apoptosis, as always, though, one must start to account for heterogeneity in cancer cells and the very real possibility of ending up with a population of resistant cells.