It will be banned in the USA due to being a National Security risk.

get a plant and grow it in your garden. find out how the native chinses use it, so you know how to safely ingest it... no need to wait for pharma to synthisize it to cure yourself of cancer.

LoP Guest  Wrote:

The top 10% of the 1% has access to cancer cures and to a whole slew of other cures/procedures not available to the rest of us.
There is a cure for cancer. It's just not available to YOU.
Factual info is hard to come by, and is from second and third sources*, but look at the empirical evidence: The members of the super elite live to ridiculous ages, none of them have, had, (or die) of cancer. Heart disease seems to be non-existent, and even Cheney is alive even though by all conventional medical estimates he should have died of heart failure a long time ago.
It's stroke or brain hemorrhage which seems to be taking them out eventually.

*They are under the threat of death (and their families) if they tell.
A relative, who is a senior oncologist in a major hospital in a European capital, said, that during the trips he/she made to oncology conventions around the world (courtesy of drug companies), heard in passing, whispered/veiled references to the existence of universal or almost universal cure. It's kind of a puzzlement... (or is it?)

They believe if they give the universal cure(s) to cancer and other diseases/illnesses the population will explode exponentially and without additional resources we will quickly finish off our natural resources and go extinct. Think about it. No-one dies, and people keep being born. It would be a disaster - this is the crux of the problem

LoP Guest  Wrote:

The top 10% of the 1% has access to cancer cures and to a whole slew of other cures/procedures not available to the rest of us.
There is a cure for cancer. It's just not available to YOU.
Factual info is hard to come by, and is from second and third sources*, but look at the empirical evidence: The members of the super elite live to ridiculous ages, none of them have, had, (or die) of cancer. Heart disease seems to be non-existent, and even Cheney is alive even though by all conventional medical estimates he should have died of heart failure a long time ago.
It's stroke or brain hemorrhage which seems to be taking them out eventually.

*They are under the threat of death (and their families) if they tell.
A relative, who is a senior oncologist in a major hospital in a European capital, said, that during the trips he/she made to oncology conventions around the world (courtesy of drug companies), heard in passing, whispered/veiled references to the existence of universal or almost universal cure. It's kind of a puzzlement... (or is it?)

I don't believe that - many of the super rich/powerful have died of cancer (such as Steve Jobs and Ted Kennedy). The difference is they have the resources to search out the best nutritionists, herbalists, personal trainers, preventative medicine and general healthcare - unlike the rest of us. It's not like the rest of us can't find the same information, but we have to do the research ourselves and most don't have the background knowledge or the willpower to bother with it. I mean, look at how fat and unhealthy the population at-large is. Take curcumen, for example. Most people haven't even heard of it let alone its many health benefits.

Cancer Now Leading Cause of Death in China
Janet Larsen
Cancer is now the leading cause of death in China. Chinese Ministry of Health data implicate cancer in close to a quarter of all deaths countrywide. As is common with many countries as they industrialize, the usual plagues of poverty—infectious diseases and high infant mortality—have given way to diseases more often associated with affluence, such as heart disease, stroke, and cancer.
http://www.earth-policy.org/plan_b_updat...1/update96

LoP Guest  Wrote:

The top 10% of the 1% has access to cancer cures and to a whole slew of other cures/procedures not available to the rest of us.
There is a cure for cancer. It's just not available to YOU.
Factual info is hard to come by, and is from second and third sources*, but look at the empirical evidence: The members of the super elite live to ridiculous ages, none of them have, had, (or die) of cancer. Heart disease seems to be non-existent, and even Cheney is alive even though by all conventional medical estimates he should have died of heart failure a long time ago.
It's stroke or brain hemorrhage which seems to be taking them out eventually.

*They are under the threat of death (and their families) if they tell.
A relative, who is a senior oncologist in a major hospital in a European capital, said, that during the trips he/she made to oncology conventions around the world (courtesy of drug companies), heard in passing, whispered/veiled references to the existence of universal or almost universal cure. It's kind of a puzzlement... (or is it?)

They believe if they give the universal cure(s) to cancer and other diseases/illnesses the population will explode exponentially and without additional resources we will quickly finish off our natural resources and go extinct. Think about it. No-one dies, and people keep being born. It would be a disaster - this is the crux of the problem

Quote:Discussion
We conclude from our findings that triptolide at low nanomolar concentrations down-regulates XIAP and Mcl-1, potently inhibits cell growth, and promotes cell death through the mitochondrial pathway in various leukemic cell lines. It also induced significant cell death in leukemic blasts isolated from the bone marrow and peripheral blood of patients with AML. The responses do not seem to depend on cytogenetics or previous treatments and responses. Additional data may identify patient groups with increased/decreased sensitivity to triptolide, but the data presented here do not identify such groups. Although triptolide decreased XIAP and Mcl-1 levels, and induced activation of caspase-3 and cell death in all leukemic cells tested, some cell lines are less sensitive than others. The reason for this is not clear at this point. However, it seems that the faster-growing cells are more responsive than the slower-growing cells.

Triptolide-induced cell death in AML patient samples was observed in both short-term in vitro cultures, as shown by annexin V staining, and long-term cultures, as shown by colony-forming assays. After 24 hours of treatment, blasts from patients with AML were much more sensitive to triptolide than were CD34+ cells from normal bone marrow (Figure 2A). However, triptolide indistinguishably decreased clonogenic survival in AML blasts and normal bone marrow samples. Nonetheless, even though it is preferable for therapeutic agents to eliminate or reduce the colony formation of leukemic blasts and spare that of normal bone marrow progenitor cells, this cannot be the single determinant of the potential clinical applicability of a drug. In fact, Ara-C, the most commonly used chemotherapeutic agent in the treatment of AML, also shows little or no selectivity for malignant cells over normal cells in colony-forming assays.35 It was reported that PG490-88, a water-soluble derivative of triptolide, at 0.25 mg/kg markedly decreased tumor growth and at 0.5- and 0.75-mg/kg doses caused profound tumor regression without apparent toxicities in nude mouse human tumor xenograft models.36 A decrease in white blood cells was reported in clinical trials with triptolide or extracts of Tripterygium wilfordii.37,38 A phase 1 clinical trial with a water-soluble derivative of triptolide on solid tumors is presently ongoing in Europe.

In terms of its mechanism, triptolide was shown here to effectively inhibit XIAP expression at both the protein and RNA levels (Figure 4A and 4B, respectively). In addition, we found that the decrease in XIAP protein levels caused by triptolide was mediated through both caspase degradation of XIAP protein and transcriptional inhibition of XIAP mRNA, but not through proteasome degradation (Figure 4A-B). NFκB39-41 and both the phosphatidylinositol-3 kinase (PI3K) and the mitogen-activated protein kinase kinase/extracellular-signal regulated kinase (MEK/ERK) pathways24,42,43 have been shown to regulate XIAP expression. Since triptolide has been shown to inhibit NFκB,13,14 this finding suggests that the transcriptional down-regulation of XIAP by triptolide is mediated, at least in part, through NFκB inhibition. We did not, however, detect any changes in AKT and ERK phosphorylation up to 4 hours in OCI-AML3 and Jurkat cells treated with triptolide (data not shown). The notion that triptolide induces cell death through XIAP inhibition is further supported by the finding that forced XIAP overexpression attenuated triptolide-induced cell death (Figure 4C).

The inhibition of caspases by the broad-spectrum caspase inhibitor IDN-1965 blocked cell death induced by triptolide, suggesting that it was caspase-dependent. On the other hand, MEFs deficient in caspase-9 were resistant to triptolide, indicating that mitochondrial pathway–mediated caspase-9 activation leading to effector caspase-3 cleavage is critical to triptolide's action. This was further supported by the finding that triptolide decreased Mcl-1 levels, enhanced cytochrome C release, and induced changes in MMP and that overexpression of Bcl-2 suppressed the cell death induced by triptolide. Mcl-1 is a member of the antiapoptotic Bcl-2 family of proteins that inhibits cell death at the mitochondrial level, and XIAP is a potent caspase-9 and caspase-3 inhibitor that blocks cell death, both upstream and downstream of the apoptotic cell death cascade. Since Mcl-1 and XIAP are frequently overexpressed in leukemias,22,44,45 the ability of triptolide to reduce the levels of both Mcl-1 and XIAP makes it a powerful inducer of apoptosis.

Even though triptolide was very effective as a single agent in killing various leukemic cell lines and blasts from patients with AML, its benefits would be even greater if it could enhance the efficacy of various drugs currently used clinically in treating hematologic malignancies or solid tumors. In this regard, others and we have shown that triptolide is a potent XIAP inhibitor. Here, we demonstrate for the first time that triptolide also decreased Mcl-1 protein level. By decreasing both XIAP, an IAP family protein, and Mcl-1, an antiapoptotic Bcl-2 family protein, triptolide can lower the apoptotic threshold and thereby enhance cell death induced by chemotherapeutic agents. However, the combination of triptolide and Ara-C in OCI-AML3 cells did not increase cell death over that induced by Ara-C alone. This may be due to the fact that since OCI-AML3 cells are relatively resistant to Ara-C, the decrease in XIAP and Mcl-1 induced by triptolide at low nanomolar concentration (≤ 10 nM) did not lower the apoptotic threshold enough to overcome cellular resistance to Ara-C. Starting at a concentration of 15 nM, triptolide by itself can induce cell death in OCI-AML3 cells after 48 hours. Nevertheless, we observed sensitization by triptolide of Ara-C–induced cell death in 2 samples from Ara-C–resistant patients with AML. Triptolide at low concentrations was found to synergistically induce cell death in cell lines but not in AML blasts when combined with Dox or gemtuzumab ozogamicin. The mechanism of this effect is not clear. It may be important to point out that triptolide also decreased levels of survivin and cdc2 (not shown). Survivin is an IAP that plays important roles in both cell proliferation and cell death,46,47 and its expression is cell-cycle dependent, with the highest level in G2M.48 Cdc2, a cyclin B1–dependent kinase (Cdk1), is essential for the progression from the G2 phase to mitosis.49,50 Studies have shown that survivin is phosphorylated by cdc2–cyclin B1. Therefore, the inhibition of cyclin-dependent kinase decreases survivin levels and induces cell death.51-53 Triptolide's inhibition of cdc2, resulting in a decrease in survivin, could, at least in part, explain the synergistic effects on cell survival of triptolide in combination with G2 blockers such as Dox and gemtuzumab ozogamicin. The lack of synergistic effects of triptolide and Dox or gemtuzumab ozogamicin on primary AML blasts is probably due to the low proliferative rate of primary leukemic cells in vitro. Therefore, when testing the efficacy of therapeutic agents in vitro, we need to consider that leukemic cells may respond differently to treatment outside their bone marrow microenvironment.54

The potent effects of triptolide in leukemic cells reported in this study warrant further investigations of this compound for the treatment of leukemia. As noted, a phase 1 clinical trial of a water-soluble derivative of the drug is ongoing.

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Acknowledgments
We would like to thank Rosemarie Lauzon for assistance in the preparation of the paper, Dr Christian Bailly from Pierre-Fabre for valuable comments, and Wenjing Chen for help in collecting patient information.

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Notes
Prepublished online as Blood First Edition Paper, March 23, 2006; DOI 10.1182/blood-2005-09-3898.


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1895484/