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Cancer is DEAD: Cancer cures from A to Z

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posted on Aug, 30 2010 @ 08:56 AM

Originally posted by IgnoranceIsntBlisss
reply to post by JohnnyCanuck

How nice of you to tell potentially terminal people to stick it out with the Doc's narrow approaches after they've been told they have a short time left to live. Rock on, eh.

Gee...I must have missed the part where I said that.

My point has always been that early treatment is essential, and that time spent self-medicating with complementary therapy might just lose you that window of opportunity. Unfortunately, the pay-off for that choice is generally either death or much more invasive/debilitating treatment. I don't hear you taking reponsibility for that.

You have plenty of folks on ATS that survived cancer using traditional medicine. How many have...themselves...beaten cancer using complementary means?

The sound of crickets chirping is indeed your answer.

posted on Aug, 30 2010 @ 11:52 AM
reply to post by JohnnyCanuck

You're like a big walking (Canadian) play-on-words...

Originally posted by JohnnyCanuck
Depriving people of that opportunity by distracting them with UNPROVEN therapies is morally reprehensible.

There you're insinuating that by listing a massive thing like I've done here I'm committing a moral crime...

...even though you can't quote me as saying people shouldn't listen to their doctors at all.

nd that time spent self-medicating with complementary therapy might just lose you that window of opportunity.

Now you're using the word "complimentary", while you've been insinuating that I'm telling people to go all out alternative / holistic. Perhaps you need a reminder of the meaning of the word 'complimentary'?

You have plenty of folks on ATS that survived cancer using traditional medicine. How many have...themselves...beaten cancer using complementary means?

The sound of crickets chirping is indeed your answer.

Gee... start a thread. Watch me: how many people have survived cancer? This deep in the thread, I'd be surprised if anyone notices me say that. Even if anyone does, then again you'll be hard pressed to find anyone that knew all of these in advance, knew how to use them in advance, applied it early stages and was willing to take the gamble.

The point isn't that people should gamble to appease your challenge... the point is your attack on my 'unscience' is itself unscientific.

Your words on the last page really seem like flannel chest pounding against complimentary treatments. Let me review your work in this thread...

Originally posted by JohnnyCanuck
It is far too easy to shout about medical conspiracies and the suppression of wonder drugs...when you're healthy.

Oh? They told my mom her tumor is inoperable, and she has about a year to live. What did they do when she was in the hospital getting charged $10,000 (USD) per day? Fed her boiled broccoli that she couldn't eat even though she likes broccoli. By the time she went home: they didn't even tell her to eat things like berries.

Originally posted by JohnnyCanuck
You are certainly not the only one on board with that story. One really big fear is that folks with their cancer at a treatable point ignore their oncologists and seek alternative means, instead...and when they don't work, it's too late to treat by any means.

In the couple of months between diagnosis of my prostate cancer and my radiation treatment I used complementary medicine to try and bring down my no avail. I had the brachytherapy and the cancer is gone...and because it was caught early and the treatment highly focused, there's none of that pesky incontinence and erectile dysfunction. They don't tell you that part when they're telling you to ignore your medical team and eat these apricot pits instead.

By the way, an herbal preparation called zyflamend is in clinical trials for cancer treatment right now. How does that factor into the conspiracy?

Hmm. So you attempted alternative therapy, over the period of a couple months, and it wasn't too late afterwards?

Tell us, what did you try, and how much?

It obviously wasn't too late for you. Did the cancer stop/slow in proliferation? That would be an item of discussion. If the alternative treatments actually slowed the growth, that is grounds for using them as complimentary treatment.

And what's that, an herbal concoction is in clinical trials? Not according to:
20 entries appear for the first one on my list that came to mind: curcumin.

Googling 'Zyflamend clinical trials' looked like a walk down pseudo alley. Let's try Google Scholar instead:

Zyflamend®, a Unique Herbal Preparation With Nonselective OX Inhibitory Activity, Induces Apoptosis of Prostate Cancer Cells That Lack COX-2 Expression

Cyclooxygenase (COX) inhibitors have suppressive effects on several types of cancer cells including prostate cancer. In this study, we considered the potential COX-inhibitory activity of a unique anti-inflammatory herbal preparation (Zyflamend; New Chapter, Inc., Brattleboro, VT) and analyzed its effects on the human prostate cancer cell line LNCaP. COX inhibitory activity of Zyflamend was determined by a spectrophotometric-based assay using purified ovine COX-1 and COX-2 enzymes. Effects of Zyflamend on LNCaP cell growth and apoptosis in vitro were assessed by cell counting, Western blot detection of poly ADP-ribose polymerase (PARP) cleavage, and measurement of caspase-3 activity in treated and control cell extracts.

Zyflamend®-Mediated Inhibition of Human Prostate Cancer PC3 Cell Proliferation: Effects on 12-LOX and Rb Protein Phosphorylation

The multiherb anti-inflammatory product Zyflamend was investigated for its antiproliferative effects on PC3 human prostate cancer cells and eicosanoid metabolism in this prostate cancer cell line. Zyflamend produced a concentration-dependent inhibition of cloned COX-1, COX-2, and 5-LOX enzyme activities, with inhibition of 5-HETE production being greater than that of PGE(2) formation. Applied to intact PC3 cells, Zyflamend was found to be most potent against 12-LOX, followed by 5-LOX and then COX activities. The concentration-dependent inhibition of PC3 cell proliferation was associated with a selective G(2)/M arrest of the cell cycle and induction of apoptosis, as evidenced by flow cytometric staining of PC3 cells with annexin V. Zyflamend also produced a concentration-dependent down-regulation of 5-LOX and 12-LOX expression.

Zyflamend, a polyherbal preparation, inhibits invasion, suppresses osteoclastogenesis, and potentiates apoptosis through down-regulation of NF-kappa B activation and NF-kappa B-regulated gene products.

Zyflamend, a polyherbal preparation, was designed based on constituents that exhibit antiproliferative, antiinflammatory, antioxidant, antiangiogenic, and apoptotic activities through a mechanism that is not well defined. Because the nuclear factor (NF)-kappaB has been shown to regulate proliferation, invasion, and metastasis of tumor cells, we postulated that Zyflamend modulates the activity of NF-kappa B. To test this hypothesis, we examined the effect of this preparation on NF-kappaB and NF-kappaB-regulated gene products. We found that Zyflamend inhibited receptor activator of NF-kappa B ligand-induced osteoclastogenesis, suppressed tumor necrosis factor (TNF)-induced invasion, and potentiated the cytotoxicity induced by TNF and chemotherapeutic agents, all of which are known to require NF-kappa B activation. Zyflamend suppressed NF-kappa B activation induced by both TNF and cigarette smoke condensate.

Good find!

That looks an awful lot like many of my entries (except the part where under each entry each citation shows results in different types of cancer only).

This calls into question, what is in Zyflamend????

HOLY BASIL (Ocimum sanctum) Contains ursolic acid, which significantly enhances detoxification and promotes a healthy inflammation response.*
TURMERIC Unique curcumin phytonutrient complex, synergistic with green tea, significantly multiplying each herb's ability to promote healthy eicosanoid balance.*
GINGER Supercritical extract modulates both eicosanoid cascades and offers numerous anti-aging constituents*
GREEN TEA Proceedings of the National Academy of Sciences report green tea polyphenols exert a beneficial effect on healthy eicosanoid balance.* Major university database notes green tea contains 51 phytonutrients that promote a healthy inflammation response.*
ROSEMARY Dual extracts offer highly concentrated, full spectrum eicosanoid balance and support detoxification.*
HU ZHANG (Polygonum cuspidatum) Richest known resveratrol source, with each daily serving delivering the approximate equivelant of six glasses of resveratrol-rich wine.
CHINESE GOLDTHREAD AND BARBERRY Unique berberine phytonutrient complex naturally promotes a healthy inflammation response.*
OREGANO Source of large number of phytonutrient modulators (31) according to USDA database.*
BAIKAL SKULLCAP Unique baicalin phytonutrient complex, naturally promotes healthy inflammation response.*


Most of those are in my list!

Note that a great many of the entries in my list aren't merely in vitro successes.

Did you actually read my OP? I don;t think you did. You asked for a success story? Forget ATS, try NIH... I've been saving this for last:
Possible disease remission in patient with invasive bladder cancer with D-fraction regimen

This case study describes an invasive bladder cancer patient at a high risk for disease recurrence who only followed a D-fraction regimen (with vitamin C) refusing other medical interventions. The two-year follow-up yet indicated no clinical evidence of progression of residual disease or recurrence with possible disease remission.

That's in my OP. You should try reading it.

[edit on 30-8-2010 by IgnoranceIsntBlisss]

posted on Aug, 30 2010 @ 12:06 PM
reply to post by IgnoranceIsntBlisss

The bottom line is that the best bet we have in treating cancer is with the current medical practice. To postpone that treatment by using alternative therapies can be a death sentence. By all means, eat well, use preventative measures, but when the doctor says "This radiation treatment will cure you", in my estimation, only a fool will decline and keep sucking back the ol' essiac, et al.

That is the point that fails to come forward in discussions like this, and probably kills more cancer patients than alternative proponents would care to know about.

And if I have made that point, then that's all I need to say.

posted on Aug, 30 2010 @ 12:15 PM
reply to post by JohnnyCanuck

That point is in the thread. Your work on the last page directed towards me was totally unwarranted.

So now you're not going to describe for us the alternative regimen you self-medicated with, and whether or not it slowed / stopped the growth?

posted on Aug, 30 2010 @ 02:13 PM

Originally posted by IgnoranceIsntBlisss
So now you're not going to describe for us the alternative regimen you self-medicated with, and whether or not it slowed / stopped the growth?

No, because I have done that a number of times on this site. I adopted a regimen recommended by a naturopath, all good stuff, and if it slowed my prostate cancer in the time between a suspicion and the eventual procedure...well, it sure didn't show. I gave it 3 months then had the radioactive implants. Waiting longer would have lost me that therapy and left me with more invasive options that generally end up involving incontinence and ED.

As far as I'm concerned...that's a pretty good example of the kind of bet upon the table, and you don't hear it enough in threads of this nature. One final thought from me...unless one has actually faced a diagnosis of cancer, one has NO freakin' idea of what choice one would make. Over and out.

posted on Aug, 30 2010 @ 02:32 PM

Natural Sources: Peppercorns.
Concentrated Sources: Marketed as "Bioperine".
It's what gives "Black Pepper" its taste. I found studies talking about combining it with curcumin treatments because it's known to help nutrient uptake, and doing a scholar search I found multiple cancer studies using it alone.

Cytoprotective effect of piperine against benzoapyrene induced lung cancer with reference to lipid peroxidation and antioxidant system in Swiss albino mice

The cytoprotective effect of piperine on benzo[a]pyrene (B[a]P) induced experimental lung cancer was investigated in male Swiss albino mice. Oral administration of piperine (100 mg/kg body wt.) effectively suppressed lung cancer initiated with B[a]P as revealed by the decrease in the extent of lipid peroxidation with concomitant increase in the activities of enzymatic antioxidants (superoxide dismutase, catalase and glutathione peroxidase) and non-enzymatic antioxidant (reduced glutathione, vitamin E and vitamin C) levels when compared to lung cancer bearing animals. Our data suggest that piperine may extend its chemopreventive effect by modulating lipid peroxidation and augmenting antioxidant defense system.

Piperine Enhances the Bioavailability of the Tea Polyphenol Epigallocatechin-3-gallate in Mice

Epigallocatechin-3-gallate (EGCG), from green tea (Camellia sinensis), has demonstrated chemopreventive activity in animal models of carcinogenesis. Previously, we reported the bioavailability of EGCG in rats (1.6%) and mice (26.5%). Here, we report that cotreatment with a second dietary component, piperine (from black pepper), enhanced the bioavailability of EGCG in mice.

Effect of piperine on the inhibition of lung metastasis induced B16F-10 melanoma cells in mice

The effect of piperine on the inhibition of lung metastasis induced by B16F-10 melanoma cells was studied in C57BL/6 mice. Simultaneous administration of the compound with tumor induction produced a significant reduction (95.2%) in tumor nodule formation. Increased lung collagen hydroxyproline (22.37 μg/mg protein) in the metastasized lungs of the control animals compared to normal animals (0.95 μg/mg protein) was significantly reduced (2.59 μg/mg protein) in the piperine-treated animals. The high amount of uronic acid (355.83 μg/100 mg tissue) in the metastasized control animals was significantly reduced (65 μg/100 mg tissue) in the animals treated with piperine. Lung hexosamine content was also significantly reduced in the piperine-treated animals (0.98 mg/100 mg lyophilized tissue) compared to the untreated tumor-bearing animals (4.2 mg/100 mg lyophilized tissue). The elevated levels of serum sialic acid and serum gamma glutamyl transpeptidase activity in the untreated control animals was significantly reduced in the animals treated with piperine. The piperine-treated animals even survived the experiment (90 days). Histopathology of the lung tissue also correlated with the lifespan of the drug-treated animals. Our results demonstrate the antimetastatic activity of piperine, an alkaloid present in plants such as Piper nigrum and Piper longum.

Piperine, a major ingredient of black and long peppers, protects against AFB1-induced cytotoxicity and micronuclei formation in H4IIEC3 rat hepatoma cells

We studied the effect of piperine on the cytotoxicity and genotoxicity of aflatoxin B1 (AFB1) in rat hepatoma cells H4IIEC3/G-(H4IIE) using cellular growth and formation of micronuclei as endpoints. Piperine was earlier shown to inhibit cytochrome P-450-dependent aryl hydrocarbon hydroxylase and 7-methoxycoumarin demethylase activities in preparations of these cells with 1/2 maximum inhibition at 30-50 microM (Singh J. and Reen R.K., Current Science, 66, 365-369, 1994). The results of the present study showed that AFB1 inhibited the growth of H4IIE cells with an ED50 of 15 nM. Piperine markedly reduced the toxicity of the mycotoxin. Thus at 100 microM piperine largely restored the rate of growth of the cells. Likewise, piperine reduced the AFB1-induced formation of micronuclei in a concentration-dependent manner. Piperine itself was not toxic to the cells up to a concentration of almost 100 microM. The results suggest, that piperine is capable of counteracting AFB1 toxicity by suppressing cytochromes P-450 mediated bioactivation of the mycotoxin.

Targeting breast stem cells with the cancer preventive compounds curcumin and piperine

In order to determine whether the dietary polyphenols, curcumin, and piperine are able to modulate the self-renewal of normal and malignant breast stem cells, we examined the effects of these compounds on mammosphere formation, expression of the breast stem cell marker aldehyde dehydrogenase (ALDH), and Wnt signaling. ...Curcumin and piperine separately, and in combination, inhibit breast stem cell self-renewal but do not cause toxicity to differentiated cells. These compounds could be potential cancer preventive agents.

[edit on 30-8-2010 by IgnoranceIsntBlisss]

posted on Aug, 31 2010 @ 12:09 AM

Plant: Feverfew

Paclitaxel sensitivity of breast cancer cells with constitutively active NF-kappaB is enhanced by IkappaBalpha super-repressor and parthenolide

Parthenolide, an active ingredient of herbal remedies such as feverfew (tanacetum parthenium), mimicked the effects of IkappaBalpha by inhibiting NF-kappaB DNA binding activity and Mn-SOD expression, and increasing paclitaxel-induced apoptosis of breast cancer cells. These results suggest that active ingredients of herbs with anti-inflammatory properties may be useful in increasing the sensitivity of cancers with constitutively active NF-kappaB to chemotherapeutic drugs.

Critical roles of intracellular thiols and calcium in parthenolide-induced apoptosis in human colorectal cancer cells

Parthenolide is one of the main components responsible for the anti-inflammatory property of Feverfew. Recently, parthenolide has shown to induce apoptosis in cancer cells. Here we further studied the mechanism of parthenolide-induced apoptosis by focusing on the role of intracellular thiols and calcium in a human colorectal cancer cell, COLO 205. Parthenolide rapidly depleted intracellular thiols, including both free glutathione (GSH) and protein thiols. Concomitantly, there were dose- and time-dependent increases in intracellular reactive oxygen species (ROS) and calcium levels. Increased expression of GRP78 protein, a marker for endoplasmic reticulum stress was also detected. All these changes preceded parthenolide-induced apoptotic cell death. More importantly, pretreatment with N-acetylcysteine, a precursor of GSH synthesis, protected the cells from parthenolide-induced thiol depletion, ROS production, cytosolic calcium increase and completely blocked parthenolide-induced apoptosis. On the contrary, pretreatment of buthionine sulfoximine, an inhibitor of GSH synthesis sensitized the cell to apoptosis. These data clearly demonstrate that the intracellular thiols and calcium equilibrium play a critical role in parthenolide-induced apoptotic cell death.

Suppressed NF-kappaB and sustained JNK activation contribute to the sensitization effect of parthenolide to TNF-alpha-induced apoptosis in human cancer cells

Our study revealed a new mechanism that PN inhibits TNF-alpha-mediated NF-kappaB activation via disrupting the recruitment of the IkappaB kinases (IKK) complex to TNF receptor, which then blocked the subsequent signaling events including IKK kinase activation, IkappaBalpha degradation, p65 nuclear translocation, DNA binding and transactivation. Moreover, PN also markedly enhanced and sustained TNF-alpha-mediated JNK activation. A specific JNK inhibitor (SP600125), as well as over-expression of dominant-negative forms of JNK1 and JNK2 abolished the sensitization effect of PN on TNF-alpha-induced apoptosis. It is thus believed that suppressed NF-kappaB activation and sustained JNK activation contribute to the sensitization effect of PN to TNF-alpha-mediated cell death in human cancer cells.

Chemopreventive activity of parthenolide against UVB-induced skin cancer and its mechanisms

Parthenolide (PN) is a major sesquiterpene lactone of feverfew (Tanacetum parthanium) with known anti-inflammatory activity. However, the anticancer effects of PN have not been well studied. In the present investigation, we examined the cancer chemopreventive property of PN using a combination of in vivo and in vitro approaches. ...More importantly, we found that impaired AP-1, JNK and p38 signaling led to the sensitization of JB6 cells to UVB-induced apoptosis. Data from our study for the first time confirm the anticancer property of PN in an animal model, and provide evidence that the inhibitory effects on AP-1 and mitogen-activated protein kinases serve as one of the underlying mechanisms for the cancer chemopreventive property of PN.

Identification of the genes involved in enhanced fenretinide-induced apoptosis by parthenolide in human hepatoma cells (liver cancer)

Fenretinide (N-4-hydroxyphenyl retinamide, 4HPR) is a synthetic anticancer retinoid that is a well-known apoptosis-inducing agent. Recently, we observed that the apoptosis induced by fenretinide could be effectively enhanced in hepatoma cells by a concomitant treatment with parthenolide, which is a known inhibitor of nuclear factor-kappaB (NF-kappaB). ...Compared with controls treated with an empty vector or with antisense cDNA, the ectopic expression of ANKRD1 led to reduced colony formation and to enhanced apoptotic cell death in hepatoma cells. These results suggest that ANKRD1 and the other genes, whose expressions were substantially modulated by the parthenolide-mediated inhibition of NF-kappaB activation, play roles in the enhanced drug-induced apoptosis. In addition, this study suggests that those identified genes may be useful in anticancer strategies against hepatoma.

Parthenolide and sulindac cooperate to mediate growth suppression and inhibit the nuclear factor-κB pathway in pancreatic carcinoma cells

Activation of the transcription factor nuclear factor-κB (NF-κB) has been implicated in pancreatic tumorigenesis. We evaluated the effect of a novel NF-κB inhibitor, parthenolide, a sesquiterpene lactone isolated from the herb feverfew, in three human pancreatic tumor cell lines (BxPC-3, PANC-1, and MIA PaCa-2). Parthenolide inhibited pancreatic cancer cell growth in a dose-dependent manner with substantial growth inhibition observed between 5 and 10 μmol/L parthenolide in all three cell lines.

Antiproliferative activity of parthenolide against three human cancer cell lines and human umbilical vein endothelial cells

Parthenolide is a major sesquiterpene lactone derived from feverfew (Tanacetum parthenium) with known anti-inflammatory activity. Moreover, the anticancer potential of this compound was suggested. In this study, we determined the effect of parthenolide on proliferation of three human cancer cell lines: human lung carcinoma (A549), human medulloblastoma (TE671), human colon adenocarcinoma (HT-29) and human umbilical vein endothelial cells (HUVEC) in vitro. Cell proliferation was assessed by means of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The IC(50) value (the concentration of drug necessary to induce 50% inhibition) together with confidence limits was calculated. Parthenolide inhibited proliferation of all three types of cancer cells (A549, TE671, HT-29) and HUVEC with the following IC(50) values (in muM): 4.3, 6.5, 7.0 and 2.8, respectively. Thus, the antiproliferative potential of parthenolide was confirmed.

The sesquiterpene lactone parthenolide induces selective apoptosis of B-chronic lymphocytic leukemia cells in vitro

We have studied the in vitro actions of the sesquiterpene lactone parthenolide (PTL) on cells isolated from patients with chronic lymphocytic leukemia (CLL). Dye reduction viability assays showed that the median LD50 for PTL was 6.2 M (n=78). Fifteen of these isolates were relatively resistant to the conventional agent chlorambucil but retained sensitivity to PTL. Brief exposures to PTL (1–3 h) were sufficient to induce caspase activation and commitment to cell death. Chronic lymphocytic leukemia cells were more sensitive towards PTL than were normal T lymphocytes or CD34+ haematopoietic progenitor cells. The mechanism of cell killing was via PTL-induced generation of reactive oxygen species, resulting in turn in a proapoptotic Bax conformational change, release of mitochondrial cytochrome c and caspase activation. Parthenolide also decreased nuclear levels of the antiapoptotic transcription factor nuclear factor-kappa B and diminished phosphorylation of its negative regulator IB. Killing of CLL cells by PTL was apparently independent of p53 induction. This is the first report showing the relative selectivity of PTL towards CLL cells. The data here warrant further investigation of this class of natural product as potential therapeutic agents for CLL.

Restoring chemotherapy and hormone therapy sensitivity by parthenolide in a xenograft hormone refractory prostate cancer model

Parthenolide at low micromolar concentration inhibited proliferation of CWR22Rv1 and HUVEC cells, promoted apoptosis and abrogated NFkappaB-DNA binding. Parthenolide downregulated anti-apoptotic genes under NFkappaB control, TRAF 1 and 2, and promoted sustained activation of c-jun-NH2 kinase (JNK). Parthenolide also augmented the in vivo efficacy of docetaxel and restored sensitivity to anti-androgen therapy.

parthenolide suppresses tumor growth in a xenograft model of renal cell carcinoma by inhibiting the activation of NF-κB

Immunohistochemistry and Western blot analysis showed decreased nuclear localization of NF-κB and phosphorylated NF-κB protein and subsequently expression of MMP-9, Bcl-xL and Cox-2 in response to parthenolide treatment. These results indicate that parthenolide is a useful in the treatment of renal cell carcinoma and acts via inhibition of NF-κB.

posted on Aug, 31 2010 @ 01:33 AM

Plant family: Celastrus (Bittersweet or Staff Vine)

One notable species: Celastrus Orbiculatus

The roots, stems and leaves are antiphlogistic, antirheumatic, depurative and tonic[147, 218]. A decoction of the roots and stems is used internally whilst the crushed fresh leaves are used for external applications[147]. The plant is used in the treatment of paralysis, numbness of the four extremities, headache, toothache, spontaneous abscess formation and snake bites[147]. Many plants in this genus contain compounds of interest for their antitumour activity[218].
Plants for a Future Database

Several active ingredients: one being Celastrol, which is also found in the related Chinese vine: Tripterygium Wilfordii.

A New Sesquiterpene Ester from Celastrus orbiculatus Reversing Multidrug Resistance in Cancer Cells

In a search for revertants of multidrug-resistance in cancer cells, a novel (1) and two known (2, 3) sesquiterpene esters were isolated from the root of Celastrus orbiculatus. The structure of 1 was elucidated as 1β,2β-diacetoxy-6α,9α-bis(benzoyloxy)dihydro-β-agarofuran. Compounds 1−3 partially or completely reversed resistance to adriamycin, vinblastine, and paclitaxel of multidrug-resistant KB-V1 and MCF7/ADR cells.

Antiinflammatory Constituents of Celastrus orbiculatus Inhibit the NF-κB Activation and NO Production

Two new sesquiterpene esters, 1β,8β-diacetoxyl-6α,9α-difuroyloxydihydro-β-agarofuran (1) and 1β-acetoxyl-2β,6α,9α-trifuroyloxydihydro-β-agarofuran (2), together with four known sesquiterpene esters (3−6), celastrol (7), and celaphanol A (8) were isolated from the roots of Celastrus orbiculatus in a search for inhibitors of NF-κB activation and nitric oxide production. Compound 7 was the most active, while compounds 1, 2, 4, and 8 showed moderate inhibition in both NF-κB activation and nitric oxide production.

Antitumor effects of novel triterpene from Celastrus hypoleucus on human colorectal cancer cell line RKO in vitro

Novel triterpene (12-oleanene-3beta, 6alpha-diol) from C. hypoleucus significantly inhibited proliferation of RKO cells in dose-dependent and time-dependent manner, the IC50 was (12.20 +/- 0.79) microg x mL(-1) at 48 h. Typical apoptotic changes were observed in RKO cells under the fluorescence microscope and the light microscope. DNA ladder was detected on agarose gels at concentrations from 10 microg x mL(-1) to 20 microg x mL(-1) at 48 h. With FCM methods, dose-dependent apoptosis-induced effect was observed in RKO cell line after treatment of triterpene for 48 h, and the apoptotic rates were increased from(2.93 +/- 0.84) % to (50.79 +/- 6.61) % at concentrations from 2.5 microg x mL(-1) to 20 microg x mL(-1). DNA histograms data from FCM analysis showed that the number of cells was obviously reduced during G0-G1 phase and G2-M phase, but not during S phase for RKO cell line after treatment with various concentrations of the triterpene for 48 hours.

Apoptosis of Gastric Cancer SGC-7901 Cells Induced by Celastrus orbiculatus Thunb Extract

Conclusion Both the extracts from Celastrus orbiculatus thunb with ethyl acetate and n-butanol induced the apoptosis of SGC-7901 cells in vitro by a potential mechanism of up-regulating the expression of P53 gene.

Celastrol, a Triterpene Extracted from the Chinese “Thunder of God Vine,” Is a Potent Proteasome Inhibitor and Suppresses Human Prostate Cancer Growth in Nude Mice

Celastrol, an active compound extracted from the root bark of the Chinese medicine “Thunder of God Vine” (Tripterygium wilfordii Hook F.), was used for years as a natural remedy for inflammatory conditions. Although Celastrol has been shown to induce leukemia cell apoptosis, the molecular target involved has not been identified. Furthermore, whether Celastrol has antitumor activity in vivo has never been conclusively shown. Here, we report, for the first time, that Celastrol potently and preferentially inhibits the chymotrypsin-like activity of a purified 20S proteasome (IC50 = 2.5 μmol/L) and human prostate cancer cellular 26S proteasome (at 1-5 μmol/L). ...Multiple assays using the animal tumor tissue samples from both early and end time points showed in vivo inhibition of the proteasomal activity and induction of apoptosis after Celastrol treatment. Our results show that Celastrol is a natural proteasome inhibitor that has a great potential for cancer prevention and treatment.

A novel Hsp90 inhibitor to disrupt Hsp90/Cdc37 complex against pancreatic cancer cells

Here, we reported that celastrol disrupted Hsp90-Cdc37 interaction in the superchaperone complex to exhibit antitumor activity in vitro and in vivo. Molecular docking and molecular dynamic simulations showed that celastrol blocked the critical interaction of Glu33 (Hsp90) and Arg167 (Cdc37). Immunoprecipitation confirmed that celastrol (10 μmol/L) disrupted the Hsp90-Cdc37 interaction in the pancreatic cancer cell line Panc-1. In contrast to classic Hsp90 inhibitor (geldanamycin), celastrol (0.1-100 μmol/L) did not interfere with ATP binding to Hsp90. However, celastrol (1-5 μmol/L) induced Hsp90 client protein degradation (Cdk4 and Akt) by 70% to 80% and increased Hsp70 expression by 12-fold.

The NF-kappa B inhibitor, celastrol, could enhance the anti-cancer effect of gambogic acid on oral squamous cell carcinoma

The results showed that GA could inhibit the proliferation and induce the apoptosis of the oral squamous cell carcinoma cell lines and that the NF-kappa B pathway was simultaneously activated by GA treatment. The minimal cytotoxic dose of celastrol was able to effectively suppress the GA-induced NF-kappa B pathway activation. Following the combined treatment with GA and the minimal cytotoxic dose of celastrol or the dominant negative mutant SR-IκBα, proliferation was significantly inhibited, and the apoptotic rate of Tca8113 cells was significantly increased. Conclusion
The combination of GA and celastrol has a synergistic antitumor effect. The effect can be primarily attributed to apoptosis induced by a decrease in NF-kappa B pathway activation. The NF-kappa B signaling pathway plays an important role in this process. Therefore, combining GA and celastrol may be a promising modality for treating oral squamous cell carcinoma.

Celastrol Synergistically Enhances Temozolomide Cytotoxicity in Melanoma Cells

The TMZ/CEL combination induced the phosphorylation of c-Jun NH2-terminal kinase, implicating the mitogen-activated protein kinase pathway in the treatment effects. Our data suggest that CEL may be effective in sensitizing resistant melanoma cells to the effects of TMZ.

[edit on 31-8-2010 by IgnoranceIsntBlisss]

posted on Sep, 1 2010 @ 12:47 AM

Source: Citrus Fruit & Peels

Dietary Supplementation of the Citrus Antioxidant Auraptene Inhibits N,N-Diethylnitrosamine-Induced Rat Hepatocarcinogenesis

In the first experiment, feeding with AUR at both doses during DEN exposure decreased the mean numbers of GST-P-positive and TGF-alpha-positive EAF/cm(2), and the reduction in the number of TGF-alpha-positive EAF by feeding 500 ppm AUR was statistically significant (p < 0.005). In the second experiment, the 'initiation' feeding with 500 ppm AUR significantly inhibited the incidence (33 vs. 83%, p = 0.000511) and multiplicity (0.67 +/- 1.09 vs. 1.96 +/- 1.85, p < 0.005) of liver cell carcinoma. Also, the 'post-initiation' feeding with AUR at both doses significantly reduced the development of hepatocellular carcinoma (100 ppm: incidence, 15%, p = 0.000006; multiplicity: 0.25 +/- 0.64, p < 0.001; 500 ppm: incidence, 11%, p = 0.000002; multiplicity, 0.26 +/- 0.81, p < 0.001). In addition, AUR feeding reduced cell proliferation and the apoptotic index in liver cell neoplasms.

Citrus Auraptene Exerts Dose-dependent Chemopreventive Activity in Rat Large Bowel Tumorigenesis: The Inhibition Correlates with Suppression of Cell Proliferation and Lipid Peroxidation and with Induction of Phase II Drug-metabolizing Enzymes

These findings suggest that the inhibitory effects of auraptene on AOM-induced colon tumorigenesis at the initiation level might be associated, in part, with increased activity of Phase II enzymes, and those at the postinitiation stage might be related to suppression of cell proliferation and lipid peroxidation in the colonic mucosa.

Citrus Antioxidant Auraptene on Lung Metastasis of Melanoma Cells in Mice

The modifying effects of the organoselenium 1,4-phenylenebis(methylene)selenocyanate (p-XSC) and the Citrus antioxidant auraptene as dietary supplements on experimental pulmonary metastasis of B16BL6 murine melanoma cells were investigated in an i.v. injection model in mice. ...These results indicate that in mice, diet supplementation with p-XSC and auraptene reduces pulmonary metastasis of B16BL6 melanoma cells and inhibits the growth of these metastatic tumors in lung, in part, by inducing apoptosis. We suggest that these agents, especially p-XSC, may be valuable in preventing metastatic diseases in future studies in the clinic.

Suppression by citrus auraptene of phorbol ester- and endotoxin-induced inflammatory responses: role of attenuation of leukocyte activation

Auraptene (AUR), a citrus coumarin derivative, is one of the promising chemopreventive agents against skin, tongue, esophagus and colon carcinogenesis in rodents. We reported previously that AUR suppresses superoxide anion (O2–) generation from inflammatory leukocytes in in vitro experiments. ...This contrasting activity profile between AUR and UMB was rationalized to be a result of their distinct differences in cellular uptake efficiencies, i.e. the geranyloxyl group in AUR was found to play an essential role in incorporation. Thus, our findings indicate that AUR is an effective agent to attenuate the biochemical responsiveness of inflammatory leukocytes, which may be essential for a greater understanding of the action mechanism that underlies its inhibition of inflammation-associated carcinogenesis.

Protective effects of citrus nobiletin and auraptene in transgenic rats developing adenocarcinoma of the prostate (TRAP) and human prostate carcinoma cells

We here investigated the influence of nobiletin and auraptene on prostate carcinogenesis using transgenic rats developing adenocarcinoma of the prostate (TRAP) bearing the SV40 T antigen transgene under control of the probasin promoter and human prostate cancer cells. ... A further experiment demonstrated that growth of androgen sensitive LNCaP and androgen insensitive DU145 and PC3 human prostate cancer cells, was suppressed by both nobiletin and to a lesser extent auraptene in a dose-dependent manner, with significant increase in apoptosis. In conclusion, these compounds, particularly nobiletin, may be valuable for prostate cancer prevention.

In Vitro Absorption and Metabolism of a Citrus Chemopreventive Agent, Auraptene, and Its Modifying Effects on Xenobiotic Enzyme Activities in Mouse Livers

Oral administration of AUR by gavage at 50-200 mg/kg body wt dose dependently induced glutathione S-transferase (GST) activity in mouse livers without affecting cytochrome P-450 activity. Using 10 coumarin-related compounds, we found that only those coumarins having a 7-alkyloxyl group induced GST, but not cytochrome P-450, activity. The present study presumes that AUR accumulates in the epithelial cells of the small intestine and then gradually permeates into the portal vein. Stable localizability of AUR in the colon and liver may be associated with the induction of GST activity, which is important as the action mechanism for suppression of rodent chemical carcinogenesis.

Chemoprevention of 4-nitroquinoline 1-oxide-induced oral carcinogenesis by citrus auraptene in rats

Dietary administration of auraptene significantly decreased BrdU-labelling index and polyamine concentrations in the oral mucosa (P < 0.05). In addition, auraptene administration significantly increased the activities of GST and QR in the liver and tongue. Although dose-dependent effect was not found, citrus auraptene is effective in inhibiting the development of oral neoplasms induced by 4-NQO. Thus, suppression by the initiation-feeding of auraptene might relate to elevation in the phase II enzymes GST and QR of the liver and tongue, and inhibition occurring during the post- initiation might be related to suppression of increased cell proliferation caused by 4-NQO in the oral mucosa.

Auraptene, a Citrus Coumarin, Inhibits 12-0-Tetradecanoylphorbol-13-acetate-induced Tumor Promotion in ICR Mouse Skin, Possibly through Suppression of Superoxide Generation in Leukocytes

Coumarin-related compounds, auraptene and umbelliferone, have been isolated from the cold-pressed oil of natsumikan (Citrus natsudaidai HAYATA), and tested as inhibitors of tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced Epstein-Barr virus activation in Raji cells. ...Quantitative analyses using high-performance liquid chromatography showed the occurrence of auraptene not only in both the peels and sarcocarps of natsumikan, but also in those of hassaku orange (C. hassaku) and grapefruit (C. paradisi,) and even in their bottled fresh juice form. These results indicate that auraptene is a chemopreventer of skin tumorigenesis, and implies that suppression of leukocyte activation might be the mechanism through which it inhibits tumor promotion.

[edit on 1-9-2010 by IgnoranceIsntBlisss]

posted on Sep, 3 2010 @ 01:17 AM
Damn, is this thread dead?

Should I stop taking the extra tine to launch new entries here before my own site?

posted on Sep, 3 2010 @ 01:16 PM

Originally posted by JohnnyCanuck
reply to post by IgnoranceIsntBlisss

The bottom line is that the best bet we have in treating cancer is with the current medical practice. To postpone that treatment by using alternative therapies can be a death sentence. By all means, eat well, use preventative measures, but when the doctor says "This radiation treatment will cure you", in my estimation, only a fool will decline and keep sucking back the ol' essiac, et al.

That is the point that fails to come forward in discussions like this, and probably kills more cancer patients than alternative proponents would care to know about.

And if I have made that point, then that's all I need to say.

Your Joking right??

Lets say I own a Auto Shop, I have tons of people coming in for work which keeps me employed and I want to make sure it STAYS THAT WAY.

What would I do;
A. Fix problem and send them on their way never coming back for the same problem because I "Fixed" it.
B. "Fix" it only to make to make sure;
1: I "Fix" it and tell them later on that I tried by best when they return to spend more $$ due to failure.

2: Make it look like I fixed it but in reality issue a temporary fix insuring they will return for another fix, Certainly keeping a flow of income for me.

Now replace Auto shop with Your Doctor or Cancer treatment facility/Cancer Treatment Centers of America and you have yourself a
never ending supply of Customers waiting to spend thousands and thousands of Dollars for your "Treatment"

Amazing Topic btw OP.

posted on Sep, 3 2010 @ 02:29 PM
reply to post by IgnoranceIsntBlisss

This is a very well put together post.....A definite S+F.

posted on Sep, 3 2010 @ 03:35 PM
Incredible thread. Thank you very much!...

posted on Sep, 3 2010 @ 06:35 PM
Thanks guys! This project is never ending...

More on damaging Ethylene Vinyl Acetate (found in fire safe cigarettes):

Chromosome Damage Induced by Vinyl Acetate through in Vitro Formation of Acetaldehyde in Human Lymphocytes and Chinese Hamster Ovary Cells

A 48-h treatment with vinyl acetate (0.05–1 mm) induced a drastic increase in sister chromatid exchanges (SCEs) and (in first division cells) structural chromosome aberrations in cultured human lymphocytes. The effects were more pronounced in cultures of isolated lymphocytes than in whole-blood cultures. A distinct dose-dependent induction of SCEs similarly occurred in Chinese hamster ovary cells after a 24-h vinyl acetate treatment (0.125–1 mm). A pulse treatment of Chinese hamster ovary cells for 4 h also yielded a clear increase in SCEs, but at higher concentrations (0.3–5 mm). The presence of rat liver S9 mix enhanced the SCE-inducing effect of vinyl acetate in Chinese hamster ovary cells. Gas chromatographic analysis of human whole-blood lymphocyte cultures treated for 10 s-20 min with vinyl acetate (5.4 mm) revealed a rapid degradation of vinyl acetate and formation of acetaldehyde. During the 20-min observation period, no degradation of vinyl acetate or formation of acetaldehyde were observed in complete culture medium without blood, which suggested that the reaction was enzymatic. Acetaldehyde induced SCEs in human whole-blood lymphocyte cultures at concentrations (0.125–2 mm) comparable to those used for vinyl acetate. The results indicate that vinyl acetate induces chromosome damage in cell cultures through enzyme-mediated hydrolysis to acetaldehyde.

A biologically based risk assessment for vinyl acetate-induced cancer and noncancer inhalation toxicity

Benchmark dose methods were used to estimate the ED10 and LED10 for olfactory degeneration, the precursor lesion thought to drive cellular proliferation and eventually tumor development at excess cellular acetaldehyde levels. A concentration x time adjustment was applied to the benchmark dose values. Human-equivalent concentrations were calculated by using the human PBPK model to predict concentrations that yield similar cellular levels of acetic acid, acetaldehyde, and pHi. After the application of appropriate uncertainty factors, an ambient air value of 0.4 to 1.0 ppm was derived. The biologically based approach supports a workplace standard of 10 ppm.

Differentiating between local cytotoxicity, mitogenesis, and genotoxicity in carcinogen risk assessments: the case of vinyl acetate

Vinyl acetate is carcinogenic at portals of entry (nasal cavity and upper gastrointestinal tract). Local metabolism of vinyl acetate produces DNA-reactive acetaldehyde but also produces acetic acid and protons, which contribute to intracellular acidification, cytotoxicity and cell proliferation.

Mode-of-action-based dosimeters for interspecies extrapolation of vinyl acetate inhalation risk

Vinyl acetate is used in the manufacture of many polymers. The Clean Air Act Amendments of 1990 require that an inhalation risk assessment be conducted to assess risks to human health from ambient exposures. Vinyl acetate is a nasal carcinogen in rats and induces olfactory degeneration in rats and mice.

Physiologically Based Modeling of Vinyl Acetate Uptake, Metabolism, and Intracellular pH Changes in the Rat Nasal Cavity

Chronic inhalation exposure to vinyl acetate (VA) causes lesions in the nasal cavity of the rat. This effect appears to be related to tissue exposure to either acetaldehyde (AAld) or acetic acid (AA) metabolites of VA or both. ...The dosimetry model was applied to data from a series of experiments designed to measure the uptake and metabolism of VA in the isolated upper respiratory tract of the rat at exposure concentrations ranging from 73 to 2190 ppm. ...In addition, based on measured tissue hydrolysis rates, sufficient acid should be formed by the metabolism of VA to cause significant changes in pHi. VA exposures of 200 and 600 ppm were predicted to result in a pHi of less than 7.2 and 6.7, respectively. This model provides nasal dosimetry estimates needed to develop mechanistically based risk assessment approaches for human exposures to VA vapor.

Chronic toxicity and oncogenicity inhalation study with vinyl acetate in the rat and mouse

Vinyl acetate was evaluated for chronic toxicity and oncogenicity in male and female rats and mice in a 104-week study. Target concentrations were 0, 50, 200, and 600 ppm. The study included interim terminations at approximately 53 and 83 weeks and a group whose exposure was terminated at 70 weeks and allowed a 15-week recovery period. Over the course of the exposures, body weight gain was consistently depressed in all 600 ppm groups and in the 200 ppm mice. Except for female rats of the 600 ppm exposure group, recovery animals showed significant improvements in weight gain relative to controls. There were no changes in hematological parameters of either species that could be unequivocally related to treatment. The only effect noted on clinical chemical parameters during the study were decreases in blood glucose in the 600 ppm females. There were no adverse effects on survival in either species. Increases in lung weight were noted in rats and mice primarily in the 600 ppm groups. These changes were associated with bronchial exfoliation, macrophage accumulation, and fibrous plaques and buds extending into the airway lumen, and bronchial/bronchiolar epithelial disorganization. The most significant histopathological changes were noted in the nasal cavity. In the olfactory epithelium of both rats and mice, the main nonneoplastic changes included epithelial atrophy, regenerative effects (squamous metaplasia and respiratory metaplasia of olfactory epithelium), basal cell hyperplasia, and epithelial nest-like infolds. No nonneoplastic changes were observed in the respiratory epithelium of rats, while squamous metaplasia at the naso/maxilloturbinate region was prevalent in mice. Nonneoplastic changes were similar in the recovery groups. Oncogenic responses to vinyl acetate exposure were mainly confined to the nasal cavity in rats and included endo- and exophytic papillomas, squamous cell carcinoma, carcinoma in situ in olfactory regions, and endophytic papilloma in respiratory regions. Squamous cell carcinomas were also found either in areas normally covered by cuboidal epithelium or areas of unknown origin. One squamous cell carcinoma was found in the larynx of a rat of the 600 ppm groups. One squamous cell carcinoma was found in the lung of a mouse of the 600 ppm group. The no-observable- adverse-effect level for all effects was 50 ppm in both species. The tumorigenic response appears to be nonlinear. The nonlinear dose response and the unique nature of the rodent nasal cavity suggest that specific risk extrapolation models should be developed for vinyl acetate.

Vinyl acetate (CASRN 108-05-4)

In rats exposed to the high concentration of VA (600 ppm), Owen (1988) noted lesions at different levels in the respiratory tract. In the histopathology report of Dreef-van der Meulen (1988) on Owen's animals, olfactory epithelial metaplasia/atrophy and nest-like epithelial folds (hyperplastic, regenerative epithelial structures) were noted in the nasal cavity, exfoliation of bronchial epithelium, fibrous intraluminal projections (also termed tags, indicative of regeneration of exfoliated areas) in the bronchi, and pigmented histiocyte accumulation in the lungs. No alterations were noted in the trachea. Data presented in the study showed that these respiratory tract lesions all occurred in the high-exposure animals with increased severity or at incidences significantly greater than in controls (p

posted on Sep, 3 2010 @ 06:43 PM
reply to post by gpena

Interesting analogy.

While it isn't that mechanics need to operate like that, all too many of them do.

Everyone who owns a car has experienced that, even if they don't know it.

Why would this be any different with the medical establishment?

I don't know about anyone else, but I regularly tell my customers where to find the info that they can figure out how to fix a better part of the niche machines after we sell it to them or do a major overhaul for them. Nobody wants to buy money pits... but then again mechanics and doctors know we need automobiles and health, regardless. While it doesn't cost $10,000 a day for me to work on someones machine, from my point of view it's still expensive. I feel grimy if they're paying for the most menial marginal things, while eventually sorts of things will break that they have to bring it in to the pros.

[edit on 3-9-2010 by IgnoranceIsntBlisss]

posted on Sep, 3 2010 @ 06:47 PM

Originally posted by gpena
Your Joking right??

I don't joke much about cancer and if one has never faced the beast, one never knows the road they'll take. Your analogies are all very well and good until things get serious. If you should happen to get to that point...

...lemme know how it all works out.

posted on Sep, 3 2010 @ 08:46 PM
Didn't you know?

There is no cure!

posted on Sep, 3 2010 @ 10:50 PM

House Plants

If you have lung or related respiratory types of cancer then house plants should be a must. Plants filter toxic agents such as benzene, formaldehyde and trichloroethylene from the air, and emit oxygen which may help with Tumor Hypoxia.

NASA's Clean Air Study helped identify many good air filtering house plants:
English Ivy , Spider plant, Golden pothos, Peace lily, Chinese evergreen, Bamboo palm, Snake plant, Heartleaf philodendron, Selloum philodendron, Elephant ear philodendron, Red-edged dracaena, Cornstalk dracaena, Janet Craig dracaena, Warneck dracaena, Weeping Fig, Gerbera Daisy, Pot Mum, Rubber Plant, Boston fern, Kimberly queen fern, Dwarf date palm, Areca palm, Dendrobium orchid, Dumb cane (Camilla), Dumb cane (Exotica), King of hearts and Moth orchid.

posted on Sep, 4 2010 @ 12:30 AM
reply to post by IgnoranceIsntBlisss

Thanks for being on with Conspiracy Chicks, just finished listening and glad you are bringing this important information on cancer cures to our members and am sure beyond.

posted on Sep, 4 2010 @ 07:57 AM
Great post!
A couple of points:

1. There are physicians willing to work with patients in using natural products alone or in conjunction with conventional surgery, chemotherapy, etc. You can find them via various websites. One I like is the American Academy of Antiaging Medicine's fellowship on Integrative Cancer Treatment. They can refer you to a graduate of their program.

2. The problem with poor adoption of these natural chemicals is that they are not patentable. Politically, I think it would greatly improve cancer care if we were to grant companies the ability to patent such products for a limited time period, say 20 years, providing that they actually sold it on the market-not just held the patent and prevented others from making it. Companies are not intrinsically evil; they just want to make money. If you make it profitable, the big pharma companies will jump right onto the natural product manufacturing business and doctors will use them. Patent law is the problem; there is no conspiracy. Doctors are mostly trained to use what is promoted by drug companies.

3. What works in a lab does not always work in a human being. Many things kill cancer cells in a petrie dish, but due to lack of absorption or other factors when they are eaten, they may do nothing in a living human. So, when evaluating compounds, one must look for substances that have shown results in actual living cancer patients, such as melatonin, fish oil, curcumin, etc. Perhaps if they could be given intravenously a better effect would be seen. However, most of these products are only available as oral preparations.

4. I am a physician and use many of these products in my practice of integrative medicine. The are are best for prevention and post-surgery/post-chemo recurrence prevention. They are not magic bullets. The best option, in my experience, is to combine them with a rigid diet/juicing regimen such as Gerson therapy, a detox program including removal of heavy metals etc which is quite complex and beyond the scope of this site, and low dose targeted chemotherapy using a variety of natural or synthetic drugs chosen via sophisticated chemo-sensitivity testing, not available in the US, and then IPT (insulin-potentiation therapy), and enhancement of immune functioning with things like D-fraction, Beta-glucan, etc. I have seen complete cures of "terminal" cancer patients, including the physician to whom I refer patients for all of this(cured his own lung cancer). It works, but is currently very expensive and mostly not paid by insurance, and requires the patient to drastically change their diet and lifestyle forever-or the cancer may recur. Most people get cancer because of their terrible diet and lifestyle choices; they may be willing to change for a short time, but not long term in most cases. If they can't maintain the new diet/supplements, the cancer recurs as it is a systemic condition, not just an isolated thing that can be plucked out.

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