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If YOU got diagnosed with melanoma...

melanoma cancer supplements ip-6

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#1 Rolf

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Posted 17 April 2012 - 05:53 PM


...what supplement would be the cornerstone for your (complementary) treatment?

Dear all,

Indeed, new to this -very interesting!- forum, and like many before me posing an urgent question on behalf of a loved one.

My father has been diagnosed with a small and unfortunately hidden melanoma behind his ear. Unfortunately, it has already metastasised - at least to lymph nodes - and as he has been fatigued and losing weight I fear to internal organs as well.

As I'm sure you are all very aware melanoma can strike very quickly and very deadly - and does not respond well to conventional (chemo etc) cancer therapies.

This week my father will receive scan results. After that he may get some surgery, and immunotherapy (Ipilimumab, perhaps TIL), hopefully genetic medication as well (if he tests positive for mutations).

I want to back this therapy line up with a forceful complementary approach, with the primary aim to halt all tumor growth and the ambitious [I feel you simply have to try your luck as hard you can] end goal of complete tumor necrosis.

For lifestyle routes I'm trying my father to cut down on carbs (and completely on processed sugared foods), rid all dairy (milk especially), add soy (to keep protein up and for fytonutrient benefits) and increase fibres (and of course veggies). Next to that I want him to do at least one hour of walking each morning.

This should lay a foundation for immuno stimulation and hopefully decrease some tumor growth factors.

Next it comes to supplements - and that's where I get to my above question. I do hope there are specialists around, because -as you'll understand- much needs to be achieved in a short time span. Making supplement mistakes can be fatal...

I simply wonder what you - if YOU received melanoma diagnosis - based on knowledge, scientific insights and your personal gut-feeling - would feel & think could help you most...

For my father I'm assembling a supplement programme with the aim of blocking as many growth routes - and (unfortunately mostly based on in vitro studies) fingers-crossed routes to promote melanoma apoptosis (and anti-angiogenese, anti-metastase).

Many of the dosages I would suggest are sub-clinical. That is mainly because I fear (liver) toxicity. I do hope they will still be high enough to succesfully encircle the melanoma - cutting of its supply, while stuff like Vemurafenib goes for the actual kill... (which would depend on luck with the BRAF mutation - 55% chance).

I think the programme should include DIM/I3C (50mg), genistein (25-50mg - in isoflavones complex, soy), ECGC (300mg - in catechin complex, green tea), curcumin (400mg), vit D3 (75mcg/3000iu), melatonin (6mg), OPCs (150mg), resveratrol (100mg), IP-6 (1500mg) - and 4g of fish oil.

So, what do you think? Where would you agree - and where do you not? Am I dosing too 'safe' - or perhaps too high? What would you do differently?

I'm particularly interested to hear if people here have faith in IP-6 (irt melanoma). Is it as potent as it sounds? I understand it could cut off iron supply to tumor cells, but fear high doses could hurt general health - where should the balance be sought?

I'm also particularly interested to hear which you would choose, if you could choose only one supplement (to combat metastasised melanoma).

Next to this I'm interested to hear anyone's views on DCA - and on CoQ10 (to me there is no evidence of supplementation benefit in simply noting low levels in patients) and anything important that I may have overlooked.

Any help in this fight would be an encouragement in itself and deeply, greatly appreciated......

Rolf
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#2 hippocampus

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Posted 17 April 2012 - 07:11 PM

search about milk thistle - it may be helpful against non-melanoma skin cancer, but I dunno about melanoma. I don't think it can't hurt, though ...

also: if you're planning to give him curcumin, use curcumin with (bio)piperine - it's much more bioavailable.

Edited by hippocampus, 17 April 2012 - 07:12 PM.

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#3 Rolf

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Posted 17 April 2012 - 09:11 PM

Thanks hippocampus. I do intend to include piperine as bioavailability for curcumine is indeed a concern.

Not sure about the milk thistle. Non-melanoma skin cancers are very different from melanoma - the latter being far more aggressive.

I have just received good news about my father btw. To my surprise and of course great relief the scans revealed that the melanoma has not yet visibly infected other organs. There was another infected lymf node found, but that too is scheduled for surgery.

After radiotherapy the hospital does now no longer offer immune therapy. The good news is - as it is melanoma - very relative of course, as the chance of recurrence is very high still.

Therefore I do plan to continue assembling a decent supplement scheme - although at somewhat lower dosages - and preferably without stuff like IP-6 and DCA - which may still be useful should new metastases develop...

Any advice on a moderate version of the plan would still be greatly appreciated!!
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#4 tlm884

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Posted 18 April 2012 - 05:07 AM

I would make sure my Vitamin D status was adequate. One thing that comes to mind is topical caffeine application. Here is a journal article in Photobiology about topical caffeine.

http://www.pnlab.org...documents/f.pdf

#5 arska

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Posted 18 April 2012 - 12:02 PM

I definitively would include at least these mushrooms: Ganoderma lucidum (reishi, lingzhi) and Inonotus obliquus (chaga).

Edited by arska, 18 April 2012 - 12:04 PM.

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#6 Rolf

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Posted 18 April 2012 - 03:12 PM

@tlm884: thanks. D3 is definitely high on my list. I've read about topical caffeine before, but that seems much more effective against non-melanoma - and I'm looking for something to combat internal metastases, not skin lesions. (Besides, oddly enough, my father has never been much out in the sun...)

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#7 Rolf

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Posted 18 April 2012 - 04:30 PM

@arska: thanks, I've heard them being mentioned before, but I've overlooked this. Perhaps I had some bias against it. But this study especially looks promising:

http://www.ncbi.nlm....pubmed/19041933

So very interesting indeed!

Do you have any experience with extracts in supplement form? Would you know anything about cost, dosage etc? (I am afraid I will have to prioritise at some point...)

#8 Rolf

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Posted 18 April 2012 - 08:37 PM

I am now considering at least the following - daily dosages:

- 200 mg EGCG
- 50 mg genistein
- 160 mg anthocyanidins
- 20 mg resveratrol
- 2000 mg curcumin
- 75 mcg vit D3
- 1.5 mg melatonin
- 6 grams of fish oil (standard DHA/EPA)

I think I'll leave out the DIM as I find it controversial. As you can see the above dosages are quite moderate.

I'm currently considering to also include a moderate dose of quercetin, at some 250 mg daily.

Does anyone have comments, criticism about my dose/substance choices - or think something crucial is left out?

Remember, the above scheme is in between melanoma prevention and melanoma treatment. After pending surgery there are no visible metastases...

Again, thanks a bunch!

#9 tlm884

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Posted 19 April 2012 - 12:53 AM

I wouldn't bother with such a low dose of resveratrol with such an aggressive disease. I would personally consume between 500mg and 1000mg of resveratrol a day.

#10 niner

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Posted 19 April 2012 - 12:02 PM

I agree with tlm884 regarding resveratrol. There is some talk in the literature that a low dose of resveratrol might be counterproductive with cancer, to the extent that it would inhibit apoptosis. On the other hand, high doses of resveratrol are said to enhance apoptosis, which is what you want with cancer. The upshot of this is to go big or not at all, in this case. I'd raise EGCG. 6g is getting to be a pretty large dose of fish oil. I don't know the evidence for a dose like this with cancer, but it's more than I would give to a healthy person.
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#11 Rolf

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Posted 19 April 2012 - 12:33 PM

@ tlm884 & niner: thanks, both of you! This is substantial...

To first of all explain the above scheme: the philosophy behind it is to add a spectrum of chemicals that encircle the tumor, and hinder its possible escape routes. Then a couple of most potent ones (selected based on melanoma research studies) are added in a higher dose to hopefully achieve tumor necrosis (through recovery of mitochondrial apoptosis).

It may sound odd, but some chemicals - indeed like resveratrol - are simply added to improve general health. To me it sounds much more likely resveratrol would hinder the melanoma treatment when added in a higher dose, as it could then compete with the selected substances that should go for the kill.

In the above scheme this is primarily the curcumin. ECGC has a role somewhere in between, so I also don't want to dose that any higher. I do now [the latest addition] plan to add 500 mg of quercetine.

The rationale is partially based on this (somewhat older, 2000) comparison study:
http://findarticles...._5/ai_68727260/

To my surprise it showed quercetine is more effective than ECGC (and ECGC is more effective than resveratrol). All these compounds do however (in several in vitro and in vivo (human melanoma in mice) studies) show pro-apoptosis action.

Other stuff that seems to be relatively potent is the genistein (mostly anti-metastatic) and vit D3.

Also, I do not want to raise the total anti-oxidant and phytonutrient intake to extremely unnatural levels, as I fear it could backfire on general health - for instance through lowered blood pressure, stroke risk and liver toxicity. By aiming for a synergistic approach of several compounds, these could add benefits in rather low dosages - in my opinion - as for the 20 mg of resveratrol.

I have not heard about resveratrol's possible inhibition of apoptosis before. Was this witnessed in case of melanoma? What were the additional circumstances? Would you consider it a genuine risk?

The idea behind the indeed very large fish oil dose is the delayed benefit. My father has been taking 1 gram daily. I find that insufficient. But to have immediate (within weeks) effect of elevated blood and tissue levels one has to kick start, don't you agree? So for instance empty a big jar at 6 grams daily, and then maintain at 3 grams afterwards. Do you see risks at the 6g dose? (The same should actually apply to the vitamine D3, btw...)

Again thanks a lot for your help and best to all of you!
Rolf

#12 Rolf

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Posted 21 April 2012 - 01:31 PM

So what do you people think of fish oil suppletion?

I've just completedly removed it (from 1g to 6g to now 0g daily) from the programme. I may include a low dose later on, but first I'll have to become wiser on the subject.

Several studies indicate (especially DHA) could be anti-melanoma. But there is also indication it lowers T-cell count, while increasing macrophages. What do people think of that effect in relation to cancer and melanoma specifically? T-cells of course we would want, but aren't macrophages detrimental in case of cancer?

(I do know there are some counter-indications for using fish oil during platinum-based chemo. I think this is irrelevant - my father is not offered any chemo therapy. Immuno responses are of course crucial though.)

I've including daily consumption of oat fibres to my father's diet (do hope he follows religiously). As these contain bèta-glucans these may be helpful as T-cell activators - much like the above-mentioned mushrooms. Another is daily medium-intensity exercise (walking, cycling).

But perhaps this immune focus is flawed anyway - as perhaps direct cellular effects of supplements (pro-apoptosis, anti-angiogenisis etc) are of greater importance? What do you people think?

Any more comments on the above-mentioned supplements? (To name one I am considering a 150 mcg front load for the vitamin D, just two weeks or something, before settling at 75 mcg - which should be high enough in the long run...)

Many thanks..!

#13 rubegoldberg

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Posted 22 April 2012 - 04:14 AM

fisetin can be a useful agent for slowing the progression of melanoma. Bioactive FoodComponents for Melanoma: An Overview lists fisetin as well as the other flavonoids posted previously.
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#14 arska

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Posted 22 April 2012 - 06:47 PM

Do you have any experience with extracts in supplement form? Would you know anything about cost, dosage etc? (I am afraid I will have to prioritise at some point...)


I take daily 6g of equivalent double extracted (ethanol and water) Ganoderma ticnture. I make them at home. My source for Gandoerma is [ https://www.mountainroseherbs.com/ ] . The most prominent USA mycologist is Paul Stamets and he has a business that also sells fungi extracts [http://www.fungi.com/mycotech/] . You might find the info on his site interesting and a starting point for your further study. I would like to recommend also this book: http://amzn.to/IxkLtA

Usually the amount of Ganodrema for treatment of different cancers vary between 2-9 g/day. There seems to be synergistic effect if taken with vitamin C.

Regards,

Edited by arska, 22 April 2012 - 06:49 PM.

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#15 arska

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Posted 22 April 2012 - 07:49 PM

Rolf,

Sorry I forgot to mention the Chaga related stuff:

Traditionally in Baltic and Russia it is prepared as tea. Use 100g (about 3 oz) of dried chaga in powder form in 1.5 litres of water. Simmer it for 1.5-2 hours at around 80 degrees celcius (175 F). Let it continue to infuse over night preferably in a thermos bottle.
Take 4 x 30 ml per day.



Further reading:

[http://www.ncbi.nlm....ubmed/20607061]
"To test this hypothesis, the growth inhibition of each subfraction isolated from I. obliquus (chaga) on human carcinoma cell lines (lung carcinoma, stomach adenocarcinoma, breast adenocarcinoma, and cervical adenocarcinoma, was tested in vitro...significantly inhibited tumor growth in mice bearing S-180 as compared with the control mouse tumor...The results suggest that I. obliquus...could be used as natural anticancer ingredients in the food and/or pharmaceutical industry."

[http://www.ncbi.nlm....pubmed/21820502 ]
"CONCLUSIONS: We suggest that IO(chaga) modulates immune responses through secretion of Th1/Th2 cytokines in immune cells and regulates antigen-specific antibody production."

[http://www.ncbi.nlm....ubmed/20532760]
"Chemical investigations show that I. obliquus produces a diverse range of secondary metabolites including phenolic compounds, melanins, and lanostane-type triterpenoids. Among these are the active components for antioxidant, antitumoral, and antiviral activities and for improving human immunity against infection of pathogenic microbes."

[http://www.ncbi.nlm....ubmed/19627197]
"Chaga extracts were examined for cytotoxic effects against normal and cancer cell lines.... extract of the fruiting body showed significant cytotoxicity towards tumor cell lines without affecting normal cells."



Kind regards,

#16 DbCooper

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Posted 22 April 2012 - 09:46 PM

I personally would be on 300-500mg of Alpha Lipoic Acid and a daily dose of low dose Naltrexone (inclining up to 4.5 mg). As mentioned by a previous poster, Milk Thistle would be a great addition to this.

#17 stponky

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Posted 22 April 2012 - 11:25 PM

There is a drug for melanoma now. Watch the BBC documentary "Defeating Cancer"

#18 Rolf

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Posted 22 April 2012 - 11:27 PM

@ rubegoldberg: thanks for mentioning fisetine! Besides, that U Wisconsin overview study was very interesting as well. Hadn't seen that one before. From what I understand fisetine may inhibit tumor proliferation via a unique route. If so, I'll definately try and include a dose. Thanks again!

#19 Rolf

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Posted 22 April 2012 - 11:33 PM

@ arska: you have been more than helpful. Many, many thanks! I'll read all these studies and articles you suggest. The 'mushroom route' is all novel to me. Do you think/know it is down to the immune activating unique fibres (somewhat similar to oat beta glucans) - or are there other chemicals at play?

I read you take a daily dose yourself. From this I understand you may be battling cancer yourself. I wish you all the strength, wisdom and luck!

#20 Rolf

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Posted 22 April 2012 - 11:36 PM

@DbCooper: thanks for mentioning ALA and [as indeed others before] milk thistle/silymarin. Both seem worth including [at conservative dose] as additional growth inhibitors. That liver will be overjoyed for one! ;)

#21 Rolf

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Posted 22 April 2012 - 11:46 PM

@ stponky: indeed, it's called Vemurafenib - and I happen to indeed have seen that BBC documentary as well. Many thanks! The drug is no life saver on its own, but definitely effective in hurting melanoma cells - but only for those ~55% of melanoma sufferers that are fortunate enough to have a specific gene mutation (the BRAF gene), which signals a growth factor that the drug succesfully blocks - for some time. [I feel it's a medical crime to use that drug as a stand-alone treatment - as you would allow the tumor time to evolve around it. It should be part of an integrate approach, which could (theoretically) really remove the cancer. But go tell that to an oncologist 'kind enough' to include you in a trial...]

In case of my father no additional treatment is offered as after surgery all visible metastases will be removed. Statistics tell us this is likely far from the microscopic reality - and it's simply matter of time before new ones show up, unless you treat them aggresively. Vemurafenib could be useful, but I wouldn't know how to obtain it. One other essential step is for my father to be tested for the BRAF mutation. He may not even have it.

Again, thanks to you all!

#22 brunotto

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Posted 23 April 2012 - 10:49 AM

Celecoxib + Fluvastatin

http://www.ncbi.nlm....pubmed/21205474

OBJECTIVE:

To evaluate effects of celecoxib (a selective cox-2 inhibitor)combined with fluvastatin (a HMG-CoA reductase inhibitor) on tumor growth and cell apoptosis in hepatocellular carcinoma xenograft in nude mice.
METHODS:

Hepatocellular carcinoma BEL-7402 cells were inoculated subcutaneously into the left armpit of nude mice, the mice (n = 32) were then randomly divided into 4 groups: the control group, the celecoxib group,the fluvastatin group and the combination group. At the end of the study, Tumor Tissues were collected for analysis. Cell apoptosis was determined by flow cytometry analysis and TUNEL assay. Akt, p-Akt and survivin protein levels were measured by Western blot. Statistical comparisons were made using factorial analysis of variance (ANOVA) and multiple comparisons between each two groups were calculated using SNK-q test.
RESULTS:

The combination of Celecoxib and fluvastatin resulted in a greater inhibition of tumor growth than either agent alone, the tumor inhibitory rate was 34.0% in the Celecoxib group, 25.0% in the fluvastatin group and 72.2% in the combination group. The percentages of TUNEL--positive cancer cells in the celecoxib and fluvastatin alone treatment groups were 8.5%+/-1.4% and 9.4%+/-1.7% respectively as compared to the control group which was 3.5%+/-0.8%. Combination therapy showed a significantly greater increase in tumor cell apoptosis in comparison with the control and single-therapy groups (apoptotic index: 19.4%+/-3.0%; P value is less than 0.01 versus celecoxib or fluvastatin groups). The results of flow cytometry analysis also showed the same tendency. a small number of apoptotic cells were detected in the control tumours (4.1%+/-1.6%), whereas a large number of apoptotic cells were detected in tumours treated with celecoxib (9.1%+/-2.1%) or fluvastatin (10.1%+/-2.3%) alone; and the combination therapy resulted in even more apoptotic cells (23.6%+/-5.8%; P value is less than 0.01 versus celecoxib or fluvastatin groups). Western blot analysis demonstrated that the combination of celecoxib and fluvastatin significantly down-regulated p-Akt (0.23+/-0.08 versus 1.12+/-0.07 and surviving (0.50+/-0.07 versus 1.47+/-0.19) in BEL-7402 tumours compared with the control (P value is less than 0.01 for all).
CONCLUSION:

The present study provided evidence that treatment with celecoxib in combination with fluvastatin resulted in the inhibition of HCC tumour growth in an in vivo mouse model.

Edited by brunotto, 23 April 2012 - 10:54 AM.

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#23 brunotto

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Posted 23 April 2012 - 11:03 AM

Fluvastatin enhances sorafenib cytotoxicity in melanoma cells via modulation of AKT and JNK signaling pathways.

The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, 560 First Avenue, New York, NY 10016, U.S.A.

Abstract

Most metastatic melanomas are refractory to current available therapy, underscoring the need to identify new effective treatments. Sorafenib, a multikinase inhibitor of the mitogen-activated protein kinase signaling pathway, showed promise in earlier stages of clinical development, but ultimately failed to demonstrate efficacy as a single agent in the treatment of melanoma. In order to enhance the efficacy of sorafenib in the treatment of melanoma, we tested over 2,000 naturally occurring compounds and marketed drugs in the presence of sorafenib in chemoresistant human melanoma cell lines also resistant to sorafenib-induced apoptosis. Of the 9 compounds identified as sorafenib sensitizers, we prioritized the cholesterol-lowering agent fluvastatin, based on its favorable pharmacokinetics and safety profile. Our results demonstrate that fluvastatin at 1 μM, a level safely achieved through oral administration, dramatically enhances the growth-inhibitory activity of clinically achievable concentrations of sorafenib in M14 and SKM-173 melanoma cells, with a 3.2- and 3.6-fold reduction in sorafenib 50% growth inhibition (GI50), respectively. Similar effects were observed for other melanoma cell lines. Combination indices analysis revealed a synergistic relationship between the two agents. Fluvastatin enhances sorafenib-mediated apoptosis as revealed through enhanced cleavage of poly (ADP-ribose) polymerase. In combination with sorafenib, fluvastatin treatment results in reduced levels of activated murine thymoma viral oncogene homolog along with enhanced levels of activated c-Jun N-terminal kinase. Sensitization to sorafenib is unique to fluvastatin, as other statins (pravastatin and simvastatin) do not enhance sorafenib-mediated growth inhibition. These promising results warrant further investigation into the clinical applicability of fluvastatin as an agent for enhancing the efficacy of sorafenib in the treatment of melanoma.

http://www.ncbi.nlm....pubmed/21965734

#24 arska

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Posted 23 April 2012 - 12:04 PM

Sorry, few of the links were outdated so here are the valid ones:


"To test this hypothesis, the growth inhibition of each subfraction isolated from I. obliquus"
http://www.ncbi.nlm....les/PMC2895696/

"Chemical investigations show that I. obliquus produces"
http://www.ncbi.nlm....pubmed/20532760

"Cancer cell cytotoxicity of extracts and small phenolic compounds from Chaga [Inonotus obliquus (persoon) Pilat]."
http://www.ncbi.nlm....pubmed/19627197

#25 brunotto

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Posted 23 April 2012 - 12:39 PM

Protective effect of pentoxyfilline in renal toxicity after methotrexate administration.

Asvadi I, Hajipour B, Asvadi A, Asl NA, Roshangar L, Khodadadi A.

Source

Hematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.

Abstract

INTRODUCTION:

Nephrotoxicity is an important side-effect of treatment with Methotrexate (MTX). Pentoxifylline (PTX) is an anti-inflmmatory and anti-oxidant agent. We hypothesized that pentoxifylline may affords renal protection by downregulating TNF-alpha as well as by improving cellular anti-oxidant activity.
MATERIALS AND METHODS:

Forty five male Wistar rats were assigned to 3 groups of 15 animals each: Group 1: control group (0.9% saline). Group 2: MTX; injected with 20 mg/kg MTX intraperitoneally (i.p.). Group 3: MTX + PTX injected i.p. MTX (20 mg/kg) + PTX (50 mg/kg) i.p. PTX was administered since 3 days before MTX administration and continued for 6 days. After 6 days rats were anesthetized and serum sampled and renal tissue removed for biochemical and histological evaluation.
RESULTS:

Data showed that glutathione peroxidase (GPx), superoxide dismutase (SOD) activities were lower in PTX + MTX group comparing to MTX group significantly (p < 0.05). Renal tissue injury index and percent of TUNEL positive cells, renal tissue malondialdehyde (MDA) levels, serum BUN (Blood Urea Nitrogen), creatinine (Cr) and TNF-alpha levels were higher in MTX group comparing to MTX+PTX group significantly (p < 0.05).
CONCLUSIONS:

In this study, the increased level of tissue MDA and serum TNF-alpha level together may be suggested that the underlying mechanism is related to direct toxicity of MTX rather than blockage in folate synthesis in kidneys. PTX administration also attenuated renal tissue injury and number of apoptic cells and suppressed the elevation of BUN and Cr levels. However, further studies are essential to elucidate the exact mechanisms of MTX-induced renal toxicity, and protection and the effect of PTX

http://www.ncbi.nlm....pubmed/22013722

Sensitization of cervix cancer cells to Adriamycin by Pentoxifylline induces an increase in apoptosis and decrease senescence...

Background: Chemotherapeutic drugs like Adriamycin (ADR) induces apoptosis or senescence in cancer cells but these cells often develop resistance and generate responses of short duration or complete failure. The methylxantine drug Pentoxifylline (PTX) used routinely in the clinics setting for circulatory diseases has been recently described to have antitumor properties. We evaluated whether pretreatment with PTX modifies apoptosis and senescence induced by ADR in cervix cancer cells. Methods: HeLa (HPV 18+), SiHa (HPV 16+) cervix cancer cells and non-tumorigenic immortalized HaCaT cells (control) were treated with PTX, ADR or PTX + ADR. The cellular toxicity of PTX and survival fraction were determinated by WST-1 and clonogenic assay respectively. Apoptosis, caspase activation and ADR efflux rate were measured by flow cytometry, senescence by microscopy. IκBα and DNA fragmentation were determinated by ELISA. Proapoptotic, antiapoptotic and senescence genes, as well as HPV-E6/E7 mRNA expression, were detected by time real RT-PCR. p53 protein levels were assayed by Western blot. Results: PTX is toxic (WST-1), affects survival (clonogenic assay) and induces apoptosis in cervix cancer cells. Additionally, the combination of this drug with ADR diminished the survival fraction and significantly increased apoptosis of HeLa and SiHa cervix cancer cells. Treatments were less effective in HaCaT cells. We found caspase participation in the induction of apoptosis by PTX, ADR or its combination. Surprisingly, in spite of the antitumor activity displayed by PTX, our results indicate that methylxantine, per se does not induce senescence; however it inhibits senescence induced by ADR and at the same time increases apoptosis. PTX elevates IκBα levels. Such sensitization is achieved through the up-regulation of proapoptotic factors such as caspase and bcl family gene expression. PTX and PTX + ADR also decrease E6 and E7 expression in SiHa cells, but not in HeLa cells. p53 was detected only in SiHa cells treated with ADR.

Conclusion: PTX is a good inducer of apoptosis but does not induce senescence. Furthermore, PTX reduced the ADR-induced senescence and increased apoptosis in cervix cancer cells.

http://www.mendeley....ase-senescence/

#26 arska

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Posted 23 April 2012 - 12:50 PM

Cannabinoids are a novel treatment option for skincancers. There are interesting reports on this site: http://www.cannabiss...aking-news.html

Regards,

#27 arska

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Posted 23 April 2012 - 01:15 PM

Do you think/know it is down to the immune activating unique fibres (somewhat similar to oat beta glucans) - or are there other chemicals at play?




Chaga and other medicinal mushrooms contain a non-linear complex polysaccharides (beta-glucans) that produce potent immune supporting properties. Different medicinal mushrooms have beta-glucans that match up with a specific type of cells in the immune system promoting a different immune response. Chaga has rather high ORAC value as well. The betulin and betulinic acid compounds, similar to the triterpenes found in Reishi, also have immune supporting properties.


Regards,

#28 Logic

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Posted 30 April 2012 - 12:49 AM

http://www.longecity...y-kills-cancer/

#29 tintinet

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Posted 30 April 2012 - 08:04 AM

Definitely get his melanoma tested for the BRAF mutation. It's his best probable established therapy at this time.





"A benefit of vemurafenib was seen in all subgroups in the trial, including patients with metastatic disease (stage M1c) and high levels of lactate dehydrogenase, conditions that are usually associated with poor prognosis.


Vemurafenib had a "manageable" safety profile and there were few drug-related discontinuations from the trial, noted Dr. Chapman.


"Vemurafenib is the first single drug for melanoma to improve response rate, PFS, and OS compared with standard chemotherapy," he said. "It is a promising new therapy for patients with metastatic BRAFV600E-mutated melanoma and a foundation upon which to build combination therapies in the future."


Patients with previously untreated, unresectable stage IIIC or IV melanoma who tested positive for the BRAFV600Emutation on a real-time polymerase chain reaction assay were randomly assigned to twice-daily 60 mg oral vemurafenib or standard chemotherapy with dacarbazine for 3 weeks. Of the patients screened, 47% were mutation positive.


Dr. Chapman explained that, as the trial enrollment was proceeding in 2010, emerging data from a phase II study made it clear that the phase III trial design, as originally conceived, had underestimated the treatment effect of vemurafenib. A revised statistical plan was established in October 2010 before any data in the trial were analyzed.



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When the study’s independent Data and Safety Monitoring Board (DSMB) reviewed the data in January 2011, it determined that there was compelling evidence of vemurafenib’s treatment benefit over dacarbazine. The DSMB recommended that patients in the chemotherapy arm be allowed to cross over to treatment with vemurafenib and this change was quickly implemented, explained Dr. Chapman.



The revised statistical plan included two primary endpoints: OS, with a lower number of required events than originally planned (196, reduced from 468), and PFS. The revised plan called for one interim analysis at 50% of the number of deaths needed for final analysis, and the data announced on Sunday were from this analysis.


Of the 675 patients enrolled at 104 centers worldwide, 337 received vemurafenib and 338 received dacarbazine. At the planned interim analysis, the hazard ratio for OS was 0.37 (95% CI [0.26, 0.55]; p < 0.0001) and the hazard ratio for PFS was 0.26 (95% CI [0.20, 0.33]; p < 0.0001), both were in favor of vemurafenib (Fig. 1).


Estimated 6-month survival was 84% for vemurafenib and 64% for dacarbazine. In the 65% of patients who were evaluable, the overall response rate was 48.4% for vemurafenib and 5.5% for dacarbazine.


The most frequent adverse events in patients receiving vemurafenib included arthralgia, rash, and diarrhea. Dr. Chapman noted that cutaneous squamous cell carcinomas and other cutaneous tumors, which are associated with vemurafenib and other drugs in its class, were seen in the patients receiving the drug and all of them were excised by dermatologists. None of the lesions were associated with metastases.


During a discussion of the study, Kim Margolin, MD, of the University of Washington and the Fred Hutchinson Cancer Research Center, praised the "excellent early results of a challenging but transformative study." She said the work was "based on a rational approach to molecular biology and therapeutic drug development" and showed "a strong survival benefit of vemurafenib over dacarbazine" in patients with melanoma whose tumor had the BRAFV600Emutation.


Dr. Margolin said the drug is already being made available through an expanded access program to patients with qualifying BRAF mutations, and it is anticipated that it may be approved by the U.S. Food and Drug Administration later this year.


Dr. Margolin said the drug’s rapid relief for symptomatic patients was "something melanoma specialists have never been able to offer," and she is excited by the implications of this development. She noted, however, that the median progression-free duration in the study was 7 months, and that the nature of relapse from this form of molecularly targeted therapy is still being investigated."



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#30 Orthorexic

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Posted 02 May 2012 - 06:34 PM

"Tuberculosis jabs cut 60pc off risk of melanoma"

http://www.theaustra...f-1225793355003

This seems mostly or perhaps even exclusively for preventive purposes, but you could look into a tuberculosis vaccination. This is highly speculative, but perhaps it helps his immune system fight the disease.

And you could also look into a ketogenic diet, which seems to help somewhat according to some trials.

http://www.nutrition.../content/8/1/54

http://www.livestron...t-brain-cancer/

But then again, I'm really no cancer specialist, so take my advice with a big grain of salt. These were just some reports I've found on the internet. As always, following the treatment as prescribed by professionals is the best bet.

And since you're from the Netherlands, I'm not sure in which hospital your father is treated, but we've got two specialized cancer centres: de Daniël den Hoedkliniek en het Antoni van Leeuwenhoek Ziekenhuis. You could ask for a second opinion over there. Who knows, perhaps they've got additional treatment options than the more general hospitals, which have no cancer specialisation.

Edited by Orthorexic, 02 May 2012 - 06:54 PM.






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