Cancer - possible cure?

[karnten07]

The drug DCA appears to be working in some cancer patients but it isn't receiving much funding since it can be manufactured generically and so pharmaceutical companies can't make money from it and are unwilling to invest in clinical trials. There are some clinical trials being carried out in Canada.

The way DCA works is that it targets the common mechanism in ALL cancers which is to get it's energy via glycolysis instead of the ordinary energy path way via the Kreb's cycle. The drug forces the cells to turn to non-glycolysis energy pathways and can induce apoptosis. Another alternative for cancer cells is fatty acid metabolism and so a strategy being suggested and tried by some is to take fat metabolism blockers which are apparently found in GREEN TEA. It is also being noticed that patients who drink caffeine beverages are doing better than non-caffeine drinkers and this is somethign to do with increasing efficacy of the DCA. Also vitamin B1 is meant to be a helpful supplement in treatment. I am a physics student and have little biology knowledge so I may have used terminology or explained some things incorrectly - but you can read for yourself at this website (which i have favorited): http://www.thedcasite.com/index.html

DCA is being hailed as the CURE for ALL CANCER and you yourself can purchase the chemical in its raw form from the internet, although i believe it can't be shipped into the United States but a friend or relative could bring you the chemical from abroad. Purchase from here:

http://www.buydca.com/index.html

The drug has been through CLINICAL TRIALS for a chronic disease often seen in children called lactic acidosis which is a buildup of lactic acid in the blood due to damaged or non-functioning mitochondria. It is safe, has low toxicity and is very cheap. The current cancer trials are trialling the drug in combination with traditional chemotherapy and radiation treatments on advanced stage or difficult to treat cancers so I'm unsure if the drug alone can treat cancer, although it may prove to be the case now that other developments have been found such as addition of CAFFEINE, GREEN TEA EXTRACT AND VITAMIN B1.

This treatment may save lives and people are recovering from terminal diagnoses. Spread the word and we may beat this thing yet. A video here:

I'm in the UK and may buy a batch since you never know when governments may adopt a US style ban on imports of the drug.

 

[Moonbear]

It's not very promising for treating cancer, because if you don't get the dose just right, it can actually have the opposite effect of promoting cancer.

Nutr Cancer. 2009;61(3):374-80.
Biphasic regulation of cell death and survival by hydrophobic bile acids in HCT116 cells.
Yui S, Kanamoto R, Saeki T.
A secondary bile acid, namely, deoxycholic acid (DCA), has been known to promote colon tumors; on the other hand, it also induces apoptosis in several human colon cancer cell lines. A hydrophobic primary bile acid, namely, chenodeoxycholic acid (CDCA), exhibits a similar property of apoptosis induction; DCA and CDCA also trigger some specific intracellular signal pathways in the human colon cancer cell line HCT116. In this article, we report that hydrophobic bile acids induce different cellular responses depending on their concentration, that is, a sublethal concentration of hydrophobic bile acids can suppress the apoptosis induced by a higher concentration of DCA. Pretreatment with DCA or CDCA at a concentration of < or = 200 microM for 8 h suppressed the apoptosis induced by 500 microM DCA in HCT116 cells. Under this condition, the association of caspase-9 and Apaf-1 and subsequent activation of caspase-9 were inhibited, but the release of cytochrome c from the mitochondria was not. At 200 microM, DCA and CDCA induced the phosphorylation of Akt and ERK1/2, although these phosphorylations do not appear to be indispensable for the cytoprotection. It is interpreted that prolonged exposure to sublethal concentrations of hydrophobic bile acids induces resistance to apoptosis, leading to promotion of colorectal tumorigenesis.

PMID: 19373611 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/pubmed/...nel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

Int J Cancer. 2009 May 15;124(10):2270-80.
Regulation of deoxycholate induction of CXCL8 by the adenomatous polyposis coli gene in colorectal cancer.

Rial NS, Lazennec G, Prasad AR, Krouse RS, Lance P, Gerner EW.

Elevated deoxycholic acid (DCA), mutations in the adenomatous polyposis coli (APC) gene and chronic inflammation are associated with increased risk of colorectal cancer. APC status was manipulated to determine whether DCA mediates inflammatory molecules in normal or initiated colonic mucosa. DCA increased steady state mRNA and protein levels of CXCL8 in cells which do not express wild-type APC. Steady-state CXCL8 mRNA and protein were suppressed when cells with conditional expression of wild-type APC were exposed to DCA. Immunostaining did not detect CXCL8 in normal human colonic mucosa. CXCL8 was expressed in adenomatous polyps and adenocarcinomas. CXCL8 expression correlated with nuclear beta-catenin localization in epithelial cells of adenomas, but was associated with endothelial cells and neutrophils in the adenocarcinomas. DCA-mediated CXCL8 promoter-reporter activity was elevated in a mutant APC background. Wild-type APC suppressed this effect. Mutation of activator protein-1 (AP-1) or nuclear factor kappa B (NF-kappaB) sites suppressed the activation of the CXCL8 promoter-reporter by DCA. Chromatin immunoprecipitation revealed that AP-1 and NF-kappaB binding to the 5'-promoter of CXCL8 was induced by DCA. The beta-catenin transcription factor was bound to the 5'-promoter of CXCL8 in the absence or presence of DCA. Phenotypic assays determined that DCA-mediated invasion was blocked by antibody-directed against CXCL8 or wild-type APC. CXCL8 exposure led to matrix metalloproteinase-2 production and increased invasion on laminin-coated filters. These data suggest that DCA-mediated CXCL8 occurs in initiated colonic epithelium and neutralizing CXCL8 could reduce the invasive potential of tumors. (c) 2008 Wiley-Liss, Inc.
PMID: 19173296 [PubMed - indexed for MEDLINE]

http://www3.interscience.wiley.com/journal/121575427/abstract?CRETRY=1&SRETRY=0

 

[Coin]

karnten posted this twice so I'm going to post my reply twice:

DCA is a neurotoxin and can potentially kill you, especially when prepared by non-professionals like the people running thedcasite/buydca. DCA could possibly be effective as a chemotherapy drug at some point in the future. However this is only the case if testing is done to determine how it interacts with cancer in humans, what the correct dosages are, how it should be prepared and delivered, etc. The people running thedcasite/buydca have done none of these things and are running an incredibly dangerous scam, exploiting the desperate.

More information on buydca/thedcasite can be found linked here:

http://scienceblogs.com/insolence/2007/02/slumming_around_the_dca_site_thedcasitec.php [Broken]

 

[karnten07]

ALL drugs have associated toxicities but first off DCA has been trialled extensively to treat chronic lactic acidosis and is used routinely to treat this disorder therefore has been approved by the FDA for human use. Clinical trials take a long time and people could be using DCA now as an alternative LAST RESORT therapy when they are given terminal diagnosis. IT'S worth a try and it is best to do your research such as the dosages given in the current trials and such. I do think that anyone who was told that there were no other treatments approved that could help recover WOULD try this unproven therapy.

I appreciate your guys well informed views on this topic since as i say I am not particularly biology literate. But you do agree that it is SAE in humans at particular dosages for certain treatment periods as found in clinical trials and that there is reason to BELIEVE it may be a VIABLE treatment. People with cancer need HOPE and i sincerely hope that if you had friends or relatives severely affected by the disease that you would approach them with this alternative and engage with the patient's medical professionals handling their care.

 

[Moonbear]

"Hope" is not a good reason to justify a drug trial with something that seems to be causing the very disease it is being purported to treat. It is not helpful if one makes someone even worse by giving them a drug that hastens the progression of their disease rather than treating it.

You are being VERY speculative in your arguments, not supporting them by sound science (the science contradicts your assertions that it is useful), and are peddling quackery to suggest people should use a drug for an unapproved purpose when it is more likely to do harm than help.