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Old 11-29-2009, 02:07 AM   #1
Rich66
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Insulin potentiated therapy (IPT)

Med Hypotheses. 2000 Oct;55(4):330-4.
Insulin, chemotherapy, and the mechanisms of malignancy: the design and the demise of cancer.


FULL TEXT (PDF attached below)

Ayre SG, Garcia y Bellon DP, Garcia DP Jr.
The endogenous molecular biology of cancer cells involves autocrine and paracrine secretion of insulin and insulin-like growth-factors I and II, which subserve energy production and growth stimulation, respectively, in these cells. These activities confer on cancer its malignant potential, working as they do autonomously, free from higher levels of integrated control. Taking advantage of cancer's mechanisms of malignancy by employing exogenous insulin as a biologic response modifier, it is possible to potentiate the cytotoxic effects of chemotherapeutic agents for improved treatment of cancer. A synergy between certain membrane and metabolic effects of insulin on cancer cell molecular biology increases anticancer drug efficacy, and it does so with reduced doses of the drugs, enhancing their safety. This treatment strategy has been applied abroad over the last five decades with very promising clinical results. Copyright 2000 Harcourt Publishers Ltd.

PMID: 11000062 [PubMed - indexed for MEDLINE]


Quote:
In clinical applications of IPT, pharmacologic doses of insulin - 0.4 units per kilogram body weight (Humalog, Lilly) - are administered to manipulate the endogenous mechanisms of malignancy in cancer cells via the mechanisms described. Naturally, insulin delivery is done in conjunction with glucose monitoring and appropriate hypertonic glucose administration. Drug potentiation results from an insulin-induced increase in transmembrane passage and intracellular accumulation of drug, along with a recruitment of cells into S-phase of the cell replicative cycle by cross-reaction of insulin with IGF receptors. A synergy between these two effects of insulin and the pharmacokinetics of anticancer drug
therapy greatly enhances cytotoxicity, particularly for the cell cycle phase-specific anticancer drugs.


As well as improved efficacy, this regimen also increases safety because of the lower total doses that may be effectively used, with corresponding reduced drug side effects. Typically, reductions of seventy-five to ninety percent of the usual and customary doses of anticancer medication are given, employing combinations of chemotherapy agents standard for the diagnosis and stage of the particular disease. Augmenting both elements of safety and efficacy here is IPT's "smart bomb" effect caused by the relative selectivity of insulin action on cancer cells, as compared to normal somatic cells, due to the excess of insulin and IGF receptors on their cell membranes.


Conclusion

Insulin Potentiation Therapy is an empirically derived innovation for which good scientific evidence now exists to affirm its formulation. Being consistent with the natural biology of cancer cells, the operative mechanisms in IPT make it an ideal process for the medical treatment of cancer. In its turn, IPT strongly affirms the appropriateness of chemotherapy in cancer management, creating the possibility of expanding the scope of application for chemotherapy as primary treatment for certain malignancies. These are two important affirmations. First, the strong anecdotal and supporting scientific evidence for IPT makes this a potential boon for the medical profession to be able to manage cancer more effectively. Second, relying as it does on chemotherapy there is little that is truly "alternative" about Insulin Potentiation Therapy, a similar boon for important sectors of the medical industry that provide us with the tools for treating cancer.


Dr. Ayer's website (treatment/training near Chicago):
http://contemporarymedicine.net/index.php?md=105
Contemporary Medicine
322 Burr Ridge Parkway
Burr Ridge, IL 60527
630.321.9010


Claimed success stories from Garcia Jr.:
http://www.iptldmd.com/Patient%20Stories.html

http://en.wikipedia.org/wiki/Insulin...iation_therapy


Cancer Chemother Pharmacol (2004) 53: 220–224
Insulin-induced enhancement of antitumoral response to methotrexate in breast cancer patients.
Full Text (PDF) Archived full text

Lasalvia-Prisco E, Cucchi S, Vazquez J, Lasalvia-Galante E, Golomar W, Gordon W.

Department of Medicine, School of Medicine, University of Uruguay, Montevideo, Uruguay.

PURPOSE. It has been reported that insulin increases the cytotoxic effect in vitro of methotrexate by as much as 10,000-fold. The purpose of this study was to explore the clinical value of insulin as a potentiator of methotrexate. PATIENTS AND METHODS. Included in this prospective, randomized clinical trial were 30 women with metastatic breast cancer resistant to fluorouracil + Adriamycin + cyclophosphamide and also resistant to hormone therapy with measurable lesions. Three groups each of ten patients received two 21-day courses of the following treatments: insulin + methotrexate, methotrexate, and insulin, respectively. In each patient, the size of the target tumor was measured before and after treatment according to the Response Evaluation Criteria In Solid Tumors. The changes in the size of the target tumor in the three groups were compared statistically. RESULTS. Under the trial conditions, the methotrexate-treated group and the insulin-treated group responded most frequently with progressive disease. The group treated with insulin + methotrexate responded most frequently with stable disease. The median increase in tumor size was significantly lower with insulin + methotrexate than with each drug used separately. DISCUSSION. Our results confirmed in vivo the results of previous in vitro studies showing clinical evidence that insulin potentiates methotrexate under conditions where insulin alone does not promote an increase in tumor growth. Therefore, the chemotherapy antitumoral activity must have been enhanced by the biochemical events elicited in tumor cells by insulin. CONCLUSIONS. In multidrug-resistant metastatic breast cancer, methotrexate + insulin produced a significant antitumoral response that was not seen with either methotrexate or insulin used separately.

PMID: 14655024 [PubMed - as supplied by publisher]



Metabolic Modification by Insulin Enhances Methotrexate Cytotoxicity in MCF-7 Human
Breast Cancer Cells: http://www.insulinbeikrebs.at/pdf/alabaster1981.pdf

Abstract—Insulin, which activates and modifies metabolic pathways in MCF-1 human breast cancer cells, is shown to increase the cytotoxic effect of methotrexate up to ten thousand-fold in vitro. This enhanced Cytotoxicity is not due to an increased bound intracellular drug level, an increased growth rate or an increase in S phase cells, but may involve the modification or activation of biochemical pathways associated with cell growth, even in cells not undergoing DNA synthesis. This observation supports the hypothesis that tumor cell sensitivity to chemotherapy could be increased by using agents that can activate the biochemical or metabolic pathways that determine the cytotoxic process




Acta Pharmacol Sin. 2007 May;28(5):721-30.
Pretreatment with insulin enhances anticancer functions of 5-fluorouracil in human esophageal and colonic cancer cells.

Zou K, Ju JH, Xie H.
Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
AIM: To investigate the effects of insulin on enhancing 5-fluorouracil (5-FU) anticancer functions and its mechanisms in the human esophageal cancer cell line (Eca 109) and human colonic cancer cell line (Ls-174-t). METHODS: The effect of insulin/5-FU combination treatment on the growth of Eca 109 and Ls-174-t cells was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay. After insulin treatment or insulin/5-FU treatment, cell cycle distribution of both cell lines was analyzed by flow cytometry. Western blot assay was used to assess the expression of caspase-3 and thymidylate synthase (TS). Apoptosis was detected by flow cytometry, DNA fragmentation assay, and terminal transferase dUTP nick end labeling assay (TUNEL). Moreover, the changes of 5-FU uptake after insulin pretreatment were detected by HPLC assay and Western blot analysis. RESULTS: We found that insulin enhanced the inhibitory effect of 5- FU on cell proliferation when Eca 109 cells and Ls-174-t cells were pretreated with insulin for the appropriate time. Insulin increased the cell number of the S phase and the uptake of 5-FU. Insulin/5-FU treatment enhanced apoptosis of tumor cells and upregulated the expression of cleaved caspase-3 compared with 5-FU treatment. Moreover, insulin/5-FU treatment induced the changes of free TS and the TS ternary complex level compared with 5-FU treatment in Eca 109 and Ls-174-t cells. CONCLUSION: These data suggest that insulin enhances anticancer functions of 5- FU when it is treated before 5-FU for the appropriate time in human esophageal and colonic cancer cell lines.

PMID: 17439729 [PubMed - indexed for MEDLINE]


Cancer Res. 1984 Aug;44(8):3570-5.
Perturbation by insulin of human breast cancer cell cycle kinetics.

PDF of full text

Gross GE, Boldt DH, Osborne CK.
The growth of cultured human breast cancer cells is sensitive to physiological concentrations of insulin suggesting that it may regulate breast cancer growth in vivo. The mechanisms for the growth effects of insulin are poorly defined. In the present study, we examine the effects of insulin on the cell cycle kinetics of asynchronous MCF-7 human breast cancer cells growing in serum-free medium. When the [3H]thymidine labeling index is used to estimate the S-phase fraction, insulin added to asynchronously growing cells results in a time-dependent increase in the proportion of cells engaged in DNA synthesis. Computer analysis of DNA histograms obtained by flow cytometry of mithramycin-stained cells also shows a time-dependent progression of cells into and through the S-phase compartment. Sixteen hr after adding insulin to asynchronous cells, 66% of cells are in S-phase compared to 37% in controls. The effect of insulin on the cell cycle progression of MCF-7 cells is also dose dependent. Stimulation is observed with physiological insulin concentrations of 0.1 to 1.0 nM; maximal effects are observed with 1.0 to 10 nM insulin. Various insulin analogues enhance the progression of cells into S phase in proportion to their ability to bind to the insulin receptor in MCF-7 cells (porcine greater than or equal to chicken greater than guinea pig greater than deoctapeptide insulin), while unrelated peptide hormones have no effect on the cell cycle kinetics. Cell cycle analysis after the addition of colchicine to prevent mitosis and the reentry of cells into G1 demonstrates a shortened G1 in response to insulin. Continuous [3H]thymidine-labeling studies after the addition of colchicine suggest that the growth fraction is about 88% with or without insulin. In summary, insulin causes a marked perturbation of the cell cycle kinetics of MCF-7 human breast cancer cells by facilitating the transit of cells through G1. The data also suggest that this effect is mediated via the insulin receptor.

PMID: 6378371 [PubMed - indexed for MEDLINE]



SGA, Donato Perez Garcia y Bellon and Donato Perez Garcia, Jr
European Journal of Cancer 1990; 26(11-12):1262-3
Published on IPTQ by permission from Donato Perez Garcia, M.D.
WE HAVE developed a neoadjuvant chemohormonal therapy for breast carcinomas without surgery or radiotherapy. Cyclophosphamide, methotrexate, and 5-fluorouracil are administered, with insulin as a biological response modifier to potentiate anticancer drug effects [1]. This regimen affords maximum breast conservation and minimum patient discomfort.
Breast malignancies are histologically verified by fine needle biopsy. Insulin/chemotherapy cycles are repeated twice a week for 3 weeks, and then weekly for another 3—6 weeks depending on clinical findings. Fasting subjects receive insulin (0.3 U/kg) and, at onset of hypoglycaemia, cyclophosphamide 8 mg/rn2, methotrexate 3 mg/rn2, and 5-fluorouracil 50 mg/rn2 with 50% hypertonic glucose, intravenously. On non-treatment days, patients are given oral cyclophosphamide 50 mg and rnethotrexate 2.5 mg.
A 32-year-old woman found a lump in her right breast in November 1988. Xeromammography confirmed the presence of a lesion (Fig. 1), and a biopsy revealed an infiltrating ductal adenocarcinoma. After 8 weeks of chemohormonal therapy, the breast mass was no longer palpable. A xeromammogram at 3 months showed no evidence of tumour (Fig. 1).
Insulin and insulin-like growth factor-1 (IGF-1) have been identified as autocrine and/or paracrine growth factors in human breast cancer cells [2—4]. We administer pharmacological doses of insulin to manipulate membrane and metabolic activities of these endogenous growth-promoting mechanisms, thereby potentiating anticancer drug effects. Drug potentiation results from an insulin-induced increase in the transmembrane passage of anticancer drugs in human breast cancer cells [5, 6], and a recruitment of cell populations into S-phase of the replicative cycle by cross-reaction of insulin with IGF-1 receptors [7]. The cell-killing effects of anticancer drugs, particularly the chemotherapy agents specific for cell cycle phase, are greatly augmented [8]. Therefore, ideal pharmacokinetic circumstances for the chemotherapy of breast cancer are created. As well as improved efficacy, this regimen increases safety because of lower total doses administered and reduced side-effects.
Chemohormonal therapy with oestrogen has shown promising results in preliminary trials [9]. However, insulin and chemotherapy is more efficacious, as not only can insulin mimic oestrogen’s cell-recruiting effects in oestrogen receptor positive human breast cancer cells [10], but insulin also stimulates recruitment in oestrogen receptor negative cells. Unlike oestrogen, insulin can increase the transmembrane passage and intracellular accumulation of anticancer drugs. The administration of low-dose anticancer drug therapy with insulin can produce complete and long-term regression of tumour masses in treated subjects. Therapy is tolerated without adverse effect and in our case produced excellent cosmetic results.
Fig. 1. Patient 1: xeromammogram on 3 February (left)
and 15 June (right) 1989.
1. SGA, Perez Garcia y Bellon D, Perez Garcia D Jr. Insulin potentiation therapy: a new concept in the management of chronic degenerative disease. Med Hypotheses 1986,20, 199—210.
2. Hilf R. The actions of insulin as a hormonal factor in breast cancer. In: Pike MC, Siiteri PK, Welsch CW, eds. Hormones and Breast Cancer. Cold Spring Harbor, Cold Spring Harbor Laboratory, 1981, 317—337.
3. Lippman ME, Dickson RB, Kasid A, et al. Autocrine and paracrine growth regulation of human breast cancer. J Steroid Biochem 1986, 24, 147—154.
4. Cullen JK, Yee D, Sly WS, et al. Insulin-like growth factor receptor expression and function in human breast cancer. Cancer Res 1990, 50,48—53.
5. Alabaster 0, Vonderhaar BK, Shafie SM. Metabolic modification by insulin enhances methotrexate cytotoxicity in MCF-7 human breast cancer cells. Eur J Cancer Clin Oncol 1981, 17, 1223—1228.
6. Oster JB, Creasey WA. Enhancement of cellular uptake of ellipticine by insulin preincubation. Eur 3 Cancer Clin Oncol 1981, 17, 1097—1103.
7. Van Wyk JJ, Graves DC, Casella SJ, Jacobs S. Evidence from monoclonal antibody studies that insulin stimulates deoxyribonucleic acid synthesis through the type 1 somatomedin receptor. 3 Clin Endocrinol Metab 1985, 61,639—643.
8. Shackney SE, Cell kinetics and cancer chemotherapy. In: Calabresi
P, Schein PS, Rosenberg SA, eds. Medical Oncology: Basic Principles and Clinical Management of Cancer, New York, Macmillan, 1985, 41—60.
9. Paridaens R, Klijn JGM, Julien JP, et al. Chemotherapy with estrogenic recruitment in breast cancer: experimental background and clinical studies conducted by the EORTC breast cancer cooperative group. Eur J Cancer Clin Oncol 1986,22,728.
10. Van der Burg B, de Laat SW, van Zoelen EJJ. Mitogenic stimulation of human breast cancer cells in a growth-factor defined medium: synergistic action of insulin and estrogens. In: Brescani F, King RJB, Lippman ME, Raynaud JP, eds. Progress in Cancer Research and Therapy, vol. 35: Hormones and Cancer 3. New York, Raven Press, 1988,231—233.



http://iptq.com/

http://www.iptforcancer.com/

http://en.wikipedia.org/wiki/Insulin...iation_therapy

http://www.contemporarymedicine.net/...emotherapy.htm


IPTLD™ vs. Traditional Chemotherapy Treatment

One outstanding advantage IPTLD™ has over traditional treatment is that a much lower dose of chemotherapeutic drugs is required. IPTLD™ more selectively targets cancer cells while affecting relatively few normal cells. Therefore, patients do not suffer the severe side effects that commonly occur with conventional chemotherapy, such as hair loss, vomiting, fatigue and depression. Thus, the quality of a patient's life is significantly improved in comparison to that many patients experience when undergoing conventional treatment experience.

A Closer Look at How it Works


Cancer cells derive energy from an unlimited supply of glucose, which they get by secreting their own insulin. They also stimulate their own growth by producing insulin-like growth factors (IGF). These are the mechanisms of malignancy.
Insulin and IGF each work by attaching to specific cell membrane receptors, which are much more concentrated on cancer cell membranes than on normal ones. Attachment to these receptors is key to the success of IPTLD™ and helps explain why it is able to use lower doses of drugs that mainly target the cancer cells, kill them more effectively, and avoid the dose-related side effects of traditional chemotherapy.
In effect, IPTLD™ kills cancer cells by using the same mechanisms that cancer cells use to kill people.
A One-Two Punch

Insulin, in addition to its ability to help deliver higher-levels of the chemotherapy drugs into the cancer cells, also causes these cells to go into their growth phase where they actually become more vulnerable to the chemotherapy drugs. The cells are hit harder and at a time when they are most vulnerable to the assault, thus maximizing results.
In 1981, a study conducted at George Washington University showed that the chemotherapy drug, methotrexate, when used with insulin, increased the drug's cell-killing effect by a factor of 10,000!
This study was done in conjunction with the Laboratory of Pathophysiology at NCI which studied the impact of methotrexate on breast cancer with and without insulin. The study concluded that 10-10 methotrexate without insulin was equivalent to 10-6 when combined with insulin. This 1981 study found a specific enhancement of a particular carrier system for methotrexate, but launched additional interest in studying IPTLD™ and its broader applications. Additional research found that because insulin recruits resting cancer cells to become active in protein and DNA synthesis, they become more vulnerable to the targeted activity of chemotherapy. As an added advantage, insulin assists debilitated cancer patients appetite and metabolism, helping to resolve the wasting that accompanies the disease and its therapy Alabaster, O. Metabolic modification by insulin enhances methotrexate cytotoxicity in MCF-7 human breast cancer. Europ J Cancer Oncol. 1981; 17:1223-1228.

What Are the Risks?

If hypoglycemia is unchecked by glucose administration, it can lead to insulin shock, which can bring about anemia, kidney, liver, or heart damage, loss of consciousness or coma. This is easily managed, however, during the treatment.


A treatment that capitalizes on the PET/Glucose mechanism:

http://www.antiagingmedicine.com/procedures_insulin.htm

Controlling Cancer Growth
At the Nevada Center we use a form of chemotherapy called Insulin Potentiation Therapy (IPT). IPT is a simple, safe medical treatment that exploits the fact that cancer cells, unlike healthy cells, are not able to metabolize fat for energy. They rely completely on glucose (sugar/carbohydrates) for their energy supply. This is a weakness of cancer cells, and we use this weakness to control them. We use the hormone insulin to do this.
When insulin is injected it has the effect of causing the patient’s blood sugar to drop. As the blood sugar drops, the patient’s healthy cells simply shift over to fat metabolism, but the patient’s cancer cells become seriously compromised. Since they rely entirely on sugar metabolism, they go into an emergency mode and open all of their membranes in an effort to get sugar. In this state they are very vulnerable to chemotherapy drugs.
Once the blood sugar has reached a low enough level for the treatment to be effective, we then inject the chemotherapy drugs. This is immediately followed by an intravenous infusion of large amounts of sugar. What happens next is that the cancer cells, weakened and starved for sugar, take up the chemotherapy drugs in large amounts as they take up the sugar they so desperately need.
The effect of this technique is two-fold. First, the cancer cells will take up much larger amounts of chemotherapy medications than they ordinarily would without the insulin application. Secondly, since they are in such a weakened and vulnerable state from the lack of sugar, they are much more sensitive to the toxic effects of the drugs. The result is a level of cancer cell death and growth control comparable to standard chemotherapy. But there is one very big difference.
IPT Is Gentle
Because the IPT technique results in a higher concentration of the chemo-therapeutic drugs in the cancer cells, we are able to use much lower chemo-therapy doses than are normally used to get the same intracellular levels. In general, we usually use about one tenth of the standard dose. A recent soon to be published review of patients treated with IPT shows that the cancer growth controlling effect of IPT isequal to that of standard chemotherapy.
The fact that we can use a lower dose of medication and yet have the same results leads to two very important advantages to IPT. First, the lower dose means that there are little to no side effects. Our patients typically feel as good as ever – even immediately after the treatments. Secondly, and perhaps more importantly, because the doses are so low, IPT treatments can be used as long as they are needed without the concern of long-term toxicity to healthy cells and tissues.


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Quackwatch warning on IPT: http://www.quackwatch.com/01Quackery...ancer/ipt.html

includes pricing at time it was written.


ACS basically denouncement:
http://www.cancer.org/docroot/ETO/co...on_Therapy.asp



Sloan Kettering's posted take on it:
http://www.mskcc.org/mskcc/html/69265.cfm

Clinical Summary
Insulin Potentiation Therapy (IPT) is a questionable cancer therapy that uses insulin as an adjunct agent to potentiate the effect of chemotherapy and other medications. This therapy was developed in Mexico by Dr. Donato Perez Garcia in the 1930's and has been used together with other unconventional therapies for many years (1). Advocates of IPT believe that cancer cells consume more sugar than healthy cells and therefore cancer cells are more sensitive to insulin and insulin-like growth factor (IGF) (2) (7). Insulin is also believed to increase the permeability of cell membranes, increasing the intracellular concentration and cytotoxic effect of anticancer drugs (1). According to the theory behind the therapy, if cancer cells can be activated by exogenous insulin, a reduced dose (up to one-tenth the normal dose) of a chemo drug can provide the same cytotoxic effects with less severe adverse reactions. No clinical trials have been performed to validate these claims. In addition, the pharmacokinetic profiles on concurrent use of insulin and chemo drugs are lacking and it is unclear whether the insulin also potentiates the toxic effects of chemotherapy on healthy cells. Although proponents have cited many anecdotal case reports suggest that IPT may be effective, currently there is no data comparing the efficacy of IPT to conventional chemotherapy. Most of the medications used, such as insulin and other chemo drugs, are approved by the FDA, but the IPT clinics administer them 'off-label.' Some clinics that administer IPT are not operated or staffed by oncologists. Side effects of IPT include hypoglycemic reaction. A systematic review of 21 studies showed a correlation between circulating levels of IGF-I, IGFBP3 (IGF-binding protein) and an increased risk of common cancers (8). IPT remains an unproven cancer therapy until there are more studies available to validate its benefit.

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Supportive Studies
- Published clinical and in-vitro studies that support the use of insulin as a biologic response modifier.

Metabolic Modification by Insulin Enhances Methotrexate Cytotoxicity in MCF-7 Human Breast Cells. Alabaster, O. Vonderhaar, B. and Shafie, S. Eur J Cancer Clin Oncol. Vol 17, No. 11, pp 1223-1228. 1961.

Insulin treatment in cancer cachexia: effects on survival, metabolism, and
physical functioning. Lundholm K, Körner U, Gunnebo L, Sixt-Ammilon P, Fouladiun M, Daneryd P, Bosaeus I. Clin Cancer Res. 2007 May 1;13(9):2699 706.


Long-Term Effect of Diabetes and Its Treatment on Cognitive Function. Jacobson, Alan, et.al. N Engl J Med 2007; 356:1842-52.

Pretreatment with insulin enhances anticancer functions of 5-fluorouracil in human esophageal and colonic cancer cells. Zou K, Ju JH, Xie H. Acta Pharmacol Sin. 2007 May; 28(5):721-30.

Preclinical safety and antitumor efficacy of insulin combined with irradiation. Bénédicte F. Jordan, Nelson Beghein, Nathalie Crokart, Christine Baudelet, Vincent Gregoire, Bernard Gallez. Radiotherapy and Oncology 81 (2006) 112–117.

Insulin-induced enhancement of antitumoral response to methotrexate in breast cancer patients. Lasalvio-Prisco, Eduardo, et.al. Cancer Chemother Pharmacol (2004) 53: 220–224.

The effect of insulin on chemotherapeutic drug sensitivity in human esophageal and lung cancer cells. Zhonghua Yi Xue Za Zhi. 2003 Feb 10;83(3):195-7.


RESOURCES
Insulin Potentiation Therapy


Links

The Elka Best Foundation - The Elka Best Foundation funds education and research to provide kinder, gentler chemotherapy

International Organization of IPT Physicians - The IOIP was established to coordinate the efforts and communication of the over 300 trained IPTLD™ providers world-wide.


Articles


The effect of insulin on chemotherapeutic drug sensitivity in human esophageal and lung cancer cells
- Department of Oncology, General Hospital of People's Liberation Army Beijing 100853, China
Pretreatment with insulin enhances anticancer functions of 5-fluorouracil in human esophageal and colonic cancer cells - Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Insulin for Cancer
- TIME Magazine Monday, Mar. 09, 1925
IPT: A New Concept in the Management of Chronic Degenerative Disease - S. G. Ayre, D. Perez Garcia y Bellon and D. Perez Garcia, Jr.
IPT and Cachexia: A Dual-Purpose Approach to Cancer Management - Ayre and Tisdale
New Approaches to the Delivery of Drugs to the Brain - S.G. Ayre
Blood Brain-Barrier - Ayre, Skaletski and Mosnaim
Neoadjuvant Low-Dose Chemotherapy with Insulin in Breast Carcinomas - S. G. Ayre, D. Perez Garcia y Bellon and D. Perez Garcia, Jr.
Insulin, Chemotherapy and the Mechanisms of Malignancy: The Design and the Demise of Cancer - S. G. Ayre, D. Perez Garcia y Bellon and D. Perez Garcia, Jr.
Long-term effect of diabetes and its treatment on cognitive function - New England Journal of Medicine
Insulin-induced enhancement of antitumoral response to methotrexate in breast cancer patients - Uruguay Study
The risk of developing uterine sarcoma after tamoxifen use - International Journal of Gynecological Cancer
THE INSULIN POTENTIATED THERAPY(IPT) IN THE TREATMENT OF CHRONICAL AND ONCOLOGICAL DISEASES - Journal MED

Attached Files
File Type: pdf Insulin Potentian Therapy_introduction_Ayres.pdf (26.3 KB, 1506 views)
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Mom's treatment history (link)
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