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== Proposed mechanisms ==
== Proposed mechanisms ==


Antineoplastons, being investigational drugs, have never been FDA approved as "safe and effective" in treating human cancer. Independent tests at the [[National Cancer Institute]] have never been positive.<ref name="mayo">{{cite journal |author=Burzynski SR |title=Efficacy of antineoplastons A10 and AS2-1 |journal=Mayo Clin. Proc. |volume=74 |issue=6 |pages=641–2 |year=1999 |pmid=10377942}}</ref> A 1995 [[Phase I trial]] by Japanese researchers showed promise, but [[Phase II trial]]s were never initiated.<ref>{{cite news|url=http://www.houstonpress.com/2009-01-01/news/cancer-doctor-stanislaw-burzynski-sees-himself-as-a-crusading-researcher-not-a-quack/2|date=January 1, 2009|title=Cancer Doctor Stanislaw Burzynski Sees Himself as a Crusading Researcher, Not a Quack|author=Craig Malisow|newspaper=Houston Press}}</ref>
Antineoplastons, being investigational drugs, have never been FDA approved as "safe and effective" in treating human cancer. Independent tests at the [[National Cancer Institute]] have never been positive.<ref name="mayo">{{cite journal |author=Burzynski SR |title=Efficacy of antineoplastons A10 and AS2-1 |journal=Mayo Clin. Proc. |volume=74 |issue=6 |pages=641–2 |year=1999 |pmid=10377942}}</ref> A 1995 [[Phase I trial]] by Japanese researchers showed promise, and [[Phase II trial]]s were initiated.<ref>{{PubMed|url=http://www.ncbi.nlm.nih.gov/pubmed/12579278|date=2003|title=The preventive effect of antineoplaston AS2-1 on HCC recurrence|author=Tsuda H, Sata M, Kumabe T, Uchida M, Hara H.|publication=PubMed}}</ref>


Burzynski suggests that antineoplastons A10 and AS2-1 both work by inhibiting oncogenes, promoting [[apoptosis]], and activating tumor suppressor genes. <ref name="mechanism" /> Several other mechanisms of action have been proposed.
Burzynski suggests that antineoplastons A10 and AS2-1 both work by inhibiting oncogenes, promoting [[apoptosis]], and activating tumor suppressor genes. <ref name="mechanism" /> Several other mechanisms of action have been proposed.

Revision as of 18:39, 22 June 2010

Antineoplaston (ANP) is a name coined by Stanislaw Burzynski for a group of peptides, derivatives, and mixtures that he uses as an alternative cancer treatment.[1] These compounds are not licensed as drugs but are instead sold and administered by Burzynski as part of clinical trials that he runs at his own establishments, the Burzynski Clinic [2] and the Burzynski Research Institute, Inc.[3] in Houston, Texas. [4][5] The clinical efficacy of antineoplastons combinations for various diseases have been the subject of many such trials by Burzynski and his associates, but these have not produced any clear evidence of efficacy. Oncologists have described these studies as flawed, with one doctor stating that they are "scientific nonsense".[6]

There is no convincing evidence from randomized controlled trials in the scientific literature that antineoplastons are useful treatments of cancer and the U.S. Food and Drug Administration (FDA) has not approved these products for the treatment of any disease.[4] The American Cancer Society has stated that there is no evidence that these products have any beneficial effects in cancer and have recommended that people do not buy these products.[7] A recent medical review described this treatment as a "disproven therapy".[8]

Although no randomized controlled clinical trials have yet been performed, in Phase II FDA-supervised clinical trials for patients with high-grade, recurrent, and progressive brainstem glioma, "Antineoplastons contributed to more than a 5-year survival in recurrent diffuse intrinsic glioblastomas and anaplastic astrocytomas of the brainstem in a small group of patients". [9]

Background

Stanislaw Burzynski has stated that he began investigating the use of antineoplastons after detecting what he considered significant differences in peptides between the blood of cancer patients and a control group.[10]. Burzynski first identified antineoplastons from human blood. Since similar peptides had been isolated from urine, in 1970 Burzynski initially purified urine as a bulk source of antineoplastons. Since 1980 he has been reproducing his compounds synthetically.[11] Since his initial discovery, Burzynski has isolated dozens of peptide and derivatives, some of which he states are active against cancer with low toxicity.

The first active peptide fraction identified was called antineoplaston A-10 (3-phenylacetylamino-2,6-piperidinedione). From A-10, antineoplaston AS2-1, a 4:1 mixture of phenylacetic acid and phenylacetylglutamine, was derived [12]. The website of the Burzynski clinic states that the active ingredient of antineoplaston A10-I is phenylacetylglutamine [13].

Phenylacetic acid is a toxic compound that the body produces during normal metabolism. It is detoxified in the liver to phenylacetyl glutamine. The "antineoplaston A-10" compound is an isolation artifact resulting from heating the urine under acidic conditions. The "antineoplaston AS2-1" mixture is the result of an alkaline hydrolysis of "antineoplaston A-10". All compounds are widely available cheap chemicals.

Treatment

Since antineoplastons are not licensed as treatments for any disease, Burzynski can only sell his products as part of clinical trials. Patients receiving cancer treatment with antineoplastons must therefore first qualify for one of the currently available clinical trials. In order to qualify for most of the trials, a patient must have first failed standard treatment for the condition being treated, or it must be a condition that is unlikely to respond to currently available therapy and for which no curative therapy exists.

Antineoplastons may be administered intravenously or orally. Patients who respond positively to initial treatment with intravenous antineoplastons sometimes transition to the oral form. Intravenous antineoplastons are administered continuously with a portable programmable pump that the patient carries on a shoulder strap in a canvas bag.

Treatment with antineoplastons can be very costly to patients without insurance coverage, exceeding $100,000 for the first year of intravenous treatment. Many insurance companies consider antineoplaston therapy to be investigational and unproven and do not cover the cost.[14][15]

The "antineoplastons," natural peptides and metabolites, are not generally cytotoxic like many historical (and current) antineoplastic agents; rather the highest usage levels carry a very high sodium load that require careful attention to fluid and electrolyte balance.

Proposed mechanisms

Antineoplastons, being investigational drugs, have never been FDA approved as "safe and effective" in treating human cancer. Independent tests at the National Cancer Institute have never been positive.[16] A 1995 Phase I trial by Japanese researchers showed promise, and Phase II trials were initiated.[17]

Burzynski suggests that antineoplastons A10 and AS2-1 both work by inhibiting oncogenes, promoting apoptosis, and activating tumor suppressor genes. [13] Several other mechanisms of action have been proposed.

One of the factors that allows some cancers to grow out of control is the presence of abnormal enzymes, a byproduct of DNA methylation. In the presence of these enzymes, the normal life cycle of the cells is disrupted and they replicate continuously. Antineoplastons have been shown in the laboratory to inhibit these enzymes [18].

Recent studies have shown that inhibiting histone deacetylase (HDAC) promotes the activation of tumor suppressor genes p21 and p53. Phenylacetic acid contained in the AS2-1 mixture has been shown to be a weak HDAC inhibitor[19].

References

  1. ^ Block KI (2004). "Antineoplastons and the challenges of research in integrative care". Integr Cancer Ther. 3 (1): 3–4. doi:10.1177/1534735404263274. PMID 15035867. {{cite journal}}: Unknown parameter |month= ignored (help)
  2. ^ http://www.burzynskiclinic.com
  3. ^ http://www.burzynskiresearch.com
  4. ^ a b Antineoplastons National Cancer Institute
  5. ^ "Lessons from antineoplaston". Lancet. 349 (9054): 741. 1997. doi:10.1016/S0140-6736(97)21011-1. PMID 9091754. {{cite journal}}: Unknown parameter |month= ignored (help)
  6. ^ Terri Langford Oncologists criticize methods of controversial cancer treatment Associated press October 1998
  7. ^ Antineoplastic, A. (1983). "Antineoplastons". CA Cancer J Clin. 33 (1): 57–9. doi:10.3322/canjclin.33.1.57. PMID 6401577.
  8. ^ Vickers A (2004). "Alternative cancer cures: "unproven" or "disproven"?". CA Cancer J Clin. 54 (2): 110–8. doi:10.3322/canjclin.54.2.110. PMID 15061600.
  9. ^ Targeted therapy with antineoplastons A10 and AS2-1 of high-grade, recurrent, and progressive brainstem glioma, [1] PUB MED March 2006
  10. ^ Burzynski SR (1986). "Antineoplastons: history of the research (I)". Drugs under experimental and clinical research. 12 Suppl 1: 1–9. PMID 3527634.
  11. ^ Ralph Moss (1996), The Cancer Industry ISBN 1881025098
  12. ^ NCI Drug Dictionary, Definitions of antineoplastons A10 and AS2-1
  13. ^ a b S.R. Burzynski, The Proposed Mechanism of Antitumor Activity of Antineoplastons (ANPs) in High Grade Glioma Pathology (HBSG) Integrative Cancer Therapies 2006; 40-47
  14. ^ Aetna Clinical Policy Bulletin, Antineoplaston Therapy and Sodium Phenylbutyrate
  15. ^ Blue Cross/Blue Shield Medical Policy, Antineoplaston Therapy
  16. ^ Burzynski SR (1999). "Efficacy of antineoplastons A10 and AS2-1". Mayo Clin. Proc. 74 (6): 641–2. PMID 10377942.
  17. ^ Parameter error in {{PMID}}: Missing PMID.
  18. ^ Liau MC, Burzynski SR (1986). "Altered methylation complex isozymes as selective targets for cancer chemotherapy". Drugs under experimental and clinical research. 12 Suppl 1: 77–86. PMID 3743383.
  19. ^ Jung M (2001). "Inhibitors of histone deacetylase as new anticancer agents". Curr. Med. Chem. 8 (12): 1505–11. PMID 11562279.
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