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proven to kill cancer tumors in mice in 1 hit, They have said 18 months in the daily mail to start clinical trials, Why then fecikn wait that long!Its a bloody flower!! The government have no intention on curing cancer and never will have! ''conspiracy'' how much money would they lose if the cured it! billions, greedy wankers... why give people hope just another load of bollocks.. Just like that guy on the run who proved that cannabis cures cancer in oil form, why's he on the run? from curing people of cancer,......... after watching my dad the last 6 months suffer going through endless chemo sessions i get so angry when i see stuff like this say 18 months before clinical trials start and 7-8 years b4 it comes out!! although it has proven results! 100's of thousands of terminal cancer patients will be dead before they pull there greedy fat cat fingers out there arses, sorry rant over just makes me so angry! my dad and my best friend both suffering and they say 7-8 years b4 it will even be realised with a proven record of killing 90% of most tumors !

CD40L - a multipotent molecule for tumor therapy. Loskog A, Tötterman TH. Endocr Metab Immune Disord Drug Targets. 2007 Mar;7(1):23-8. Review. PMID: 17346201

D structure of the virus, known as Seneca Valley Virus-001, reveals that it is unlike any other known member of the Picornaviridae viral family, and confirms its recent designation as a separate genus "Senecavirus." The new study reveals that the virus's outer protein shell looks like a craggy golf ball¬-one with uneven divets and raised spikes-and the RNA strand beneath it is arranged in a round mesh rather like a whiffleball. "It is not at all like other known picornaviruses that we are familiar with, including poliovirus and rhinoviruses, which cause the common cold," says the study's senior author, Associate Professor Vijay S. Reddy, Ph.D., of The Scripps Research Institute. "This crystal structure will now help us understand how Senecavirus works, and how we can take advantage of it." The Senecavirus is a "new" virus, discovered several years ago by Neotropix Inc., a biotech company in Malvern, Pennsylvania. It was at first thought to be a laboratory contaminant, but researchers found it was a pathogen, now believed to originate from cows or pigs. Further investigation found that the virus was harmless to normal human cells, but could infect certain solid tumors, such as small cell lung cancer, the most common form of lung cancer.

This month, the authoritative International Agency for Research into Cancer (IARC) have weighed in on the issue. By gathering a group of expert scientists, they have looked at all the available evidence and published a detailed report on vitamin D and cancer. The massive tome weighs in at 465 pages, but we'll take a look at the key points in the first of two posts looking at the vitamin D debate. It is impossible for us to get more than about five percent of the vitamin D we need from our diet - unless, like Eskimos, we eat oily fish three times a day.

What if we didn't try to cure cancer, but simply kept tumors from growing too big? That's what radiologist Robert Gatenby of the Moffitt Cancer Center proposes this week in the journal Nature. Gatenby argues that high doses of powerful chemotherapies wreak havoc on a patient's immune system and foster the rapid regrowth of chemoresistant cancers that doctors have no hope of fighting.  So instead of curing cancer, he suggests doctors aim to stabilize the tumor at a tolerable size. In practice, this would mean that doctors identify a target size for an individual tumor that gives the patient the best quality of life.  Then, they will regularly monitor the tumor's growth with medical imaging equipment like a PET/CT scanner (see photo), and regulate doses of anticancer drugs to maintain it at a precise volume.

In vitro and in vivo immunomodulating and immunorestorative effects of Astragalus membranaceus. Cho WC, Leung KN. J Ethnopharmacol. 2007 Aug 15;113(1):132-41. Epub 2007 May 31. PMID: 17611061 doi:10.1016/j.jep.2007.05.020    

The influence of processing and preservation on the retention of health-promoting compounds in broccoli. Galgano F, Favati F, Caruso M, Pietrafesa A, Natella S. J Food Sci. 2007 Mar;72(2):S130-5. PMID: 17995854 DOI: 10.1111/j.1750-3841.2006.00258.x

Heating decreases epithiospecifier protein activity and increases sulforaphane formation in broccoli. Matusheski NV, Juvik JA, Jeffery EH. Phytochemistry. 2004 May;65(9):1273-81. PMID: 15184012 doi:10.1016/j.phytochem.2004.04.013

Ecological Studies Of Ultraviolet B, Vitamin D And Cancer Since 2000. Grant WB, Mohr SB. Ann Epidemiol. 2009 Mar 6. [Epub ahead of print] PMID: 19269856 doi:10.1016/j.annepidem.2008.12.014

Arginine deprivation as a targeted therapy for cancer. Feun L, You M, Wu CJ, Kuo MT, Wangpaichitr M, Spector S, Savaraj N. Curr Pharm Des. 2008;14(11):1049-57. Review. PMID: 18473854

Review article: vitamin D acquisition and breast cancer risk. Pérez-López FR, Chedraui P, Haya J. Reprod Sci. 2009 Jan;16(1):7-19. Review. PMID: 19144887 DOI: 10.1177/1933719108327595 Conclusions: Although there are controversial results, it seems plausible that sufficient endogenous vitamin D levels may have a protective function on mammary cells, reducing breast cancer risk.

Vitamin D and prevention of breast cancer: pooled analysis. Garland CF, Gorham ED, Mohr SB, Grant WB, Giovannucci EL, Lipkin M, Newmark H, Holick MF, Garland FC. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):708-11. PMID: 17368188 CONCLUSIONS: Intake of 2000 IU/day of Vitamin D(3), and, when possible, very moderate exposure to sunlight, could raise serum 25(OH)D to 52 ng/ml, a level associated with reduction by 50% in incidence of breast cancer, according to observational studies.

Mechanisms of berberine (natural yellow 18)-induced mitochondrial dysfunction: interaction with the adenine nucleotide translocator. Pereira CV, Machado NG, Oliveira PJ. Toxicol Sci. 2008 Oct;105(2):408-17. Epub 2008 Jul 3. PMID: 18599498 doi: 10.1124/jpet.107.128017 The data from the present work appear to show that berberine also presents some degree of toxicity to "nontumor" systems, which should be carefully understood. ANT inhibition in nontumor cells by berberine would be responsible for a decrease in energy production and could also result in MPT induction. To the best of our knowledge, no full toxicity assessment exists for berberine in humans, although its use in several commercially available supplements suggests that the compound may present a relatively wide safety interval. In fact, a study with patients with congestive heart failure treated with 1.2 g/day of oral berberine revealed low toxicity and resulted into an average plasma concentration of 0.11 mg/l which would translate into 0.3µM (Zeng and Zeng, 1999Go). Repeated cumulative treatments, alternative forms of formulation (e.g., topical application vs. injection) or more importantly, active mitochondrial accumulation due to its positive charge would be expected to increase its concentration in cells into the range of concentrations used in this study. Empirical data from nontraditional medicines plus the use of extensive clinical assays would allow the use of berberine as a promising antimelanoma agent while maintaining its safety for humans. In radial/vertical forms of melanoma, a possible topical application of berberine would also be possible, thus minimizing side effects on other organs. In conclusion, the present work identifies the ANT as an important target for berberine, with clear relevance for its proposed antitumor effects.

Berberine and Coptidis rhizoma as novel antineoplastic agents: a review of traditional use and biomedical investigations. Tang J, Feng Y, Tsao S, Wang N, Curtain R, Wang Y. J Ethnopharmacol. 2009 Oct 29;126(1):5-17. Epub 2009 Aug 15. PMID: 19686830 doi:10.1016/j.jep.2009.08.009 Conclusions The modern evidences of treating cancer with Huanglian and berberine have a strong linkage with traditional concept and rules of using Huanglian in CM practice. As anticancer candidates with low toxicity, berberine and its altered structure, as well as Huanglian and its formulae, will attract scientists to pursue the potential anticancer effects and the mechanisms by using technologies of genomics, proteomics and other advanced approaches. On the other hand, relatively few in vivo studies have been conducted on anticancer effects of Huanglian and berberine. The clinical application of berberine or Huanglian as novel cancer therapeutic agents requires in vivo validations and further investigations of their anticancer mechanisms.