Experimental cancer drug resurfaces
Small clinical trial yields promising results for controversial molecule.
A compound shown to shrink tumours in rats by correcting metabolic oddities found in cancer cells has now been tested in five patients with brain cancer.
The results, published today in Science Translational Medicine, provide clues as to how the drug, a small molecule called dichloroacetate (DCA), works. But it is too soon to say whether it will provide an effective treatment against cancer in humans, says lead author Evangelos Michelakis, a cardiologist at the University of Alberta in Edmonton.
DCA has had a stormy history. In 2007, Michelakis and his colleagues reported that feeding the chemical to rats slowed the growth of tumours without any apparent side effects. They suggested that it might work by stimulating glucose metabolism in energy-producing cellular structures called mitochondria.
http://hubpages.com/hub/Scientists_cure ... kes_notice
read the article it sounds too good to be true.
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.
The unique metabolism of most solid tumours (aerobic glycolysis, i.e., Warburg effect) is not only the basis of diagnosing cancer with metabolic imaging but might also be associated with the resistance to apoptosis that characterises cancer. The glycolytic phenotype in cancer appears to be the common denominator of diverse molecular abnormalities in cancer and may be associated with a (potentially reversible) suppression of mitochondrial function. The generic drug dichloroacetate is an orally available small molecule that, by inhibiting the pyruvate dehydrogenase kinase, increases the flux of pyruvate into the mitochondria, promoting glucose oxidation over glycolysis. This reverses the suppressed mitochondrial apoptosis in cancer and results in suppression of tumour growth in vitro and in vivo. Here, we review the scientific and clinical rationale supporting the rapid translation of this promising metabolic modulator in early-phase cancer clinical trials.
mitochondria, metabolism, apoptosis, potassium channels, positron emission tomography, glycolysis
Mononoke wrote:sorry guys. I have zero biology knowledge.
quisquose wrote:As far as I am concerned, scientists have cured cancer. At least the ones that me and my daughter had.
katja z wrote:Thanks for the comments GenesForLife, the article did seem to be a bit fishy (mitochondria cells, wtf?) so I was suspicious, but it's good to know just what it got wrong and why I shouldn't tell everyone with cancer that they can be magically cured by this drug. This has just come up on FB as well, may I repost your response there? Properly attributed of course
Goldenmane wrote:PZ haz your back: http://scienceblogs.com/pharyngula/2011/05/dichloroacetate_and_cancer.php
lordshipmayhem wrote:Goldenmane wrote:PZ haz your back: http://scienceblogs.com/pharyngula/2011/05/dichloroacetate_and_cancer.php
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