June 12, 2012 at 3:20 am #3546
I have not posted in a long time. I am fine, feel well and just returned from a months vacation in Europe.
I have Metastatic Colon Cancer and self medicated with DCA from May 2009 till November 2010 with good results. Then I looked for a clinical trial for five months before going on first line chemo, Folfiri. I then took three months off before starting back on DCA but adding the chemo Vidaza. This took place from 1/1/2012 till 3/30/2012.
The off label use of Vidaza with DCA for three months produced stable disease. My oncologist says that one of my tumors shrank some. I have taken three months off since and now have to decide if I will go on with DCA and Vidaza or go back on regular chemo again. If I do go back on DCA and Vidaza I will add Celebrex to the mix and try to add Dopamine. Have no idea how to do that. If I go back to using Folfiri I will consider dropping Avastin and adding Dopamine.
Dopamine does the exact opposite of Avastin. It repairs and normalizes the blood vessels that supply your tumor. The reason to do this is to get more chemo to the tumor and maybe reduce the area of the tumor that is hypoxic by getting more oxygen to the tumor. It may be that DCA actually promotes cancer in hypoxic areas.
One study says that in mice with human colon cancer Dopamine caused the increase in one drug, 5-FU, by 100% and for tumors to decrease by three times the rate they decreased by in mice with no Dopamine.
A study at MD Anderson was done with Vidaza and Celebrex to see it they would help those predisposed to getting Colon Canc from actually getting the disease. A surprise finding was that mice with actual colon cancer tumors saw major reductions in tumor size with the mix. Since I have already used Vidaza with DCA with NO side affects and stable to better than stable results I want to add Celebrex.
Have a number of other ideas I am looking at also.June 12, 2012 at 7:51 am #4344
Hi, i'm very sorry to hear that, check this link as th word has been spoken about the cancer helping theory in colorectal cancers..colorectal as far as i know is any cancer in colon areas..
so maybe you are best off dca than on. i found another more recent page but i can't find it anymore…July 4, 2012 at 3:40 pm #4372
I'm very happy to hear you are doing so well. Just a word of caution about Celebrex and all of the other NSAIDs. I save my nephrologist for the first time a week ago this morning. Seems I have lost 50% of my kidney function, which is 2x the amount for a person my age, according to him. His first question to me was "How long have you been on Naprosyn?" I told him "about a decade." His reply "you took your last one this morning, because that is the cause of your accelerated kidney function loss."
Having been in the pharmaceutical business since 1972, I asked him if this was true for all the NSAIDs. He said "Yes."
Also, with the use of any NSAID, Cytotec 1 QID should be standard therapy. Cytotec replaces the prostaglandins in the stomach lining which the NSAIDs deplete leaving the stomach far more susceptible to ulceration. Generic drugs of today are not the same as generic drugs of the 1980's when it was a very real gamble to take them. Cytotec is dirt checp, and far better than treating an ulcer.
Just a word of caution on the non-reverseable kidney damage I now have to live with as well as the use of Cytotec. There is a lot of Motrin and Aleve sold and taken on a daily basis.
Snuffy said it
Snuffy meant itJuly 7, 2012 at 2:28 pm #4379
Thanks Snuffy for the info on Celebrex. However when you are told that you have nine months to live the longer term is less relevant. I was told that someone in my condition could expect nine months, that was the end of last September. Statistically I should be dead now or soon.
But I am in very good health and my latest CT scan shows NO growth, stable disease, after three months of doing NOTHING and I am continueing to do NOTHING for maybe another three months.
That is after being on DCA and Vidaza for three months, January thru March. Since the treatments with Vidaza start with five days on and three weeks off that means I have not had Vidaza for four months, DCA for three months.
I credit this to Vidaza which imparts a memory to my cancer cells telling them not to grow for some extended period. Study at John Hopkins suggest this.
When I start treating my Colon Cancer again, in three months, my latest ideas are to take DCA and Vidaza again but add Celebrex and Xeloda. Why? This report from Illinois.
Their results are incredible and in real Colon Cancer patients.
The neat thing is the combinations of information about what works with these drugs. I know DCA worked/works for me at least to keep my cancers from growing or metastasizing (after initially reducing my tumor by 65%). Then there is a study that shows that DCA and Xeloda (5-FU) works well for Colon Cancer.
Xeloda (5-FU) is one of the drugs I was given as part of my chemo last year and worked very well for me at least in reducing tumor size if not killing CSCs. Then there is the evidence that Vidaza worked with DCA for me from January till now (and still working though I have had no Vidaza for four months). That is one of my tumors shank some but more important, after stopping DCA the first time, after using if for 18 months, my tumors grew aggressively in the next few months. This time with DCA and Vidaza they did not continue to grow and continue not to grow. Vidaza imparts a memory to tumor cells telling them not to grow. I may go for three months doing nothing to see how far Vidaza will take me before progression.
Then there is the report from a study at MD Anderson showing that Celebrex and Vidaza work very well for Colon Cancer in mice. Inflamation causes DNA Methylation so combining an anti DNA Methylation drug, Vidaza, with and anti inflamatory drug, Celebrex might work.
and now this fantastic report that Celebrex and Xeloda work wonders.
All these interconnections between these drugs and my own results. Of course I have no idea what they would do if I took them together. Could be the perfect storm for cancer or me. Nothing ventured…
At the moment I am feeling really smart…. and very lucky. If I can keep the smarty pants feeling under control maybe I can live awhile longer
Feel great, going swimming now.
BobJuly 23, 2012 at 3:47 am #4398
WOW! Thanks for all the great links and treatment strategies. The Lin ADAPT study is most interesting. Have you tried to contact the lab doing this phase 2 study?
I have been researching colon cancer for my father. He is stage 4 mesentary, and now with a tumor in the liver as well. Our first three months of chemo (oxylaplatin based) along with curcumin, metformin, and a range of vitamins including lipo vitamin C, had reduced his tumors by a third.
However it all came roaring back during the second 2 month chemo session plus a two month break.
He has KRAS 13D, which is a pretty aggressive cancer.July 23, 2012 at 1:55 pm #4399
A bump in the Celebrex road ..July 23, 2012 at 9:04 pm #4401
Interesting. I did some follow-up searches and found an approximately equal number of papers suggesting that Celebrex induces MRP proteins and that it downregulates them. It also inactivates STAT3, which contributes to chemoresistance.
Anyway there's good evidence that it has direct anticancer action in patients, so I'm personally going to take it up until the point I may need chemotherapy, and then re-evaluate.July 23, 2012 at 9:09 pm #4402
Do not get me wrong .. I'm also very interested in Celebrex and Xeloda for my father. Your Marketwatch link allowed me to put two and two together. I follow an excellent Onco blob (IMO) and you might like to browse thru it.July 24, 2012 at 2:22 am #4405
BTW, have you looked into sodium butyrate?July 25, 2012 at 2:34 pm #4407
The FIRST thing to do is to get some advocates to help you make sould decisions. Minocycline is an antibiotic and could in the end actually make you more vulnerable. In your situation look for local cancer centers, independent and hospital affiliated and CAMP OUT AT THIER DOOR. Fully explain your situation. If there is aid out there they can guide you to some agency that can help.
Cancer is not something to be triffled with and seek out real medical help ASAP. Taking some drug because someone gave it to you is worse than no good. There is a lot of research and "alternative" treatments for breast cancer but conventional medicine is desperately needed as well. Speed is of the essence. Quite lucky if you haven't metasisized by now. ACT IMMEDIATELY!July 25, 2012 at 6:47 pm #4410
IMO: Breast cancer is very treatable. Do whatever your doctors say (unless they ever say something defeatist like "get your affairs in order").
Get whatever type of genetic testing on the tumor is available.
Read "Life Over Cancer", preferably before you have surgery.
DCA is worth investigating but is far from the only alternative treatment available. You can read about numerous drugs and nutrients which may be helpful in books like "Anticancer: A New Way of Life" and "Beyond the Magic Bullet". I could mention curcumin, melatonin, fish oil, quercetin, lactoferrin, selenate, gamma-tocotrienols, medicinal mushrooms, garlic, ginger, mustard, broccoli, blueberries, pomegranate, EGCG (green tea), celebrex, statin drugs, proton pump inhibitors, etc. You might want to do some reading before adopting any of them, as they may be incompatible with chemotherapy and they may be contraindicated for your type of breast cancer because of estrogenic involvement. Every doctor has told me to be sure to take lots of vitamin D, so that should be at the top of your list.
And stay positive. This is beatable.July 25, 2012 at 7:41 pm #4415
I think you'll also find that B vitamins are critical in treatment of breast cancer, and then there's always megadosing of vitamin C. There are so many things that can help but curing vitamin defeciencies is a big first step. Take 10,000 units of vitamin D3 daily, along with vitamin k for absorbtion. Ask for a vitamin D level test if you can get it. BTW it takes a long time to raise vitamin D levels. Homemade lipo C is worth checking out too.July 25, 2012 at 9:10 pm #4418
Here's one thing I have learned that applies to most cancers: Primary cancer (where it first appears, before it spreads) is treatable and can frequently be completely cured or controlled. As long as your doctors have promising, evidence-based treatments to offer you, I would listen to them.
Once they are out of options, or they only have low-probability high-toxicity treatments like secondary chemotherapies to offer you, then is the time to consider saying no. There are a lot of alternative ways to attack cancer, but at this stage your doctors probably have the best weapons. STAY ALIVE, then you'll have lots of time to work on your qi.July 27, 2012 at 12:32 pm #4422
Last May Michelakis' study ("Mitochondrial activation by inhibition of PDKII suppresses HIF1a signaling and angiogenesis in cancer" , http://www.nature.com/onc/journal/vaop/ncurrent/full/onc2012198a.html ) mentions DCA-Vidaza increased therapeutic efficacy: "Another mechanism of potential resistance maybe the recently reported decrease of the DCA transporter SLC5A8, via methylation, is cancer tissues.75 Babu et al. reversed this by increasing the expression of SLC5A8 with the DNA
methylation inhibitor 50-Azadc, potentiating the anticancer effects of DCA."
In fact the referred Babu et al. document ("Role of SLC5A8, a plasma membrane transporter and a tumor suppressor, in the antitumor activity of dichloroacetate" , http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3140604/?tool=pubmed ) reports "The findings that dichloroacetate induces cell death selectively in tumor cells at low concentrations but only if SLC5A8 is expressed have clinical and therapeutic significance. The ability of dichloroacetate to activate PDC via inhibition of PDK in cancer cells provides a mechanistically rational basis for the antitumor activity of the compound. But cancer cells are resistant to the drug because of the absence of an effective transporter for the drug, necessitating requirement of high concentrations of the compound to induce cell death, which unfortunately causes detrimental side effects such as neuropathy. We have demonstrated in the present study that SLC5A8 serves as an active transporter for dichloroacetate. However, since the expression of the transporter is silenced in tumor cells, how can the present findings be relevant to the potential therapeutic use of the drug? The silencing of SLC5A8 in cancer cells occurs via epigenetic mechanisms involving DNA methylation; treatment of cancer cells with 5′-azacytidine, an inhibitor of DNA methylation, re-activates the expression of the gene (Li et al., 2003; Ueno et al., 2004; Hong et al., 2005; Porra et al., 2005; Thangaraju et al., 2006; Park et al., 2007, 2008). DNA methylation plays a critical role in silencing tumor suppressor genes in a variety of cancers, and DNA methylation inhibitors hold promise as anticancer drugs (Baylin, 2005). Two compounds with DNA methylation inhibition activity are in clinical use for treatment of hematologic malignancies. These are 5′-aza-2′-deoxycytidine, also known as decitabine (trade name, Dacogen) and 5′-azacytidine (trade name, Vidaza). In vitro studies have shown that treatment of a variety of cancer cell lines with these compounds re-activates the expression of SLC5A8. We speculate that the same phenomenon would also occur in vivo. Therefore, a combination of a DNA methylation inhibitor and dichloroacetate is likely to be effective for treatment of cancer because the DNA methylation inhibitor would induce the expression of SLC5A8 in tumors, which would then effectively transport dichloroacetate into tumor cells to elicit its antitumor activity. This mode of treatment would reduce considerably the concentration of dichloroacetate necessary for in vivo efficacy as an anticancer agent, thus potentially providing tumor selectivity and also avoiding the detrimental side effects such as neuropathy. The findings of the present study provide a rational basis for such a combination therapy."
You may find info about also in these robmx's posts: http://www.thedcasite.com/dca-forum/topic/new-idea-on-making-dca-work-better-at-lower-doses#post-17
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