IPT is an integrative oncology technique that is used with sucess to shrink tumors. It is not a cure-all, the the evidence does show tumor shrinkage, improvement of cancer markers and extra quality of life.  However, when the cancer is advanced, or metastatic, IPT will not be sufficient to reverse the cancer.  Here’s how it works: The patient consumes no food the night before.  Insulin is then administrated the following morning, before the chemo so that  the cancer cells open up, which makes sense because there are many more insulin receptors on cancer cells. Once the patient is hypoglycemic and the cancer cells are opened up thanks to the insulin, a low dose of chemo is injected, about 10 percent. It is claimed that the insulin also increases the cell membrane’s permeability for cytotoxic drugs, as well as the S-phase fraction of tumour cells. This explanation also makes sense because increasing the number of cells with active DNA replication, makes the tumour more vulnerable for the action of cytotoxic drugs, in particular cell-cycle-phase-specific agents. One of the big advantages of this technique in relation to conventional chemotherapy is that there are fewer genotoxic drugs that damage the healthy cells.   See Integrative Oncology Protocol for this approach


IPT.  Lodi


Brad. Stem…

ISRN Urol. 2012;2012:140182. doi: 10.5402/2012/140182. Epub 2012 May 8.

Low-dose chemotherapy with insulin (insulin potentiation therapy) in combination with hormone therapy for treatment of castration-resistant prostate cancer.

Damyanov C1, Gerasimova D, Maslev I, Gavrilov V.

Author information



To evaluate the results and quality of life of patients with resistant of castration-resistant tumors previously treated with Insulin-potentiation therapy (IPT) combined with hormone therapy.


Sixteen patients with metastasis prostate tumors after bilateral castration, androgenic blockade, and progression of the disease were observed during the study. The patients were divided into two groups: group A consisting of 8 patients treated with low-dose chemotherapy Epirubicin, Vinblastine, and Cyclophosphamide combined with LHRH agonist and group B consisting of another 8 patients treated with low-dose chemotherapy Docetaxel combined with LHRH agonist.


The overall (groups A and B) results concerning PSA after the sixth IPT show partial effect in 8 out of 16 (50%) patients, stabilization in 4 out of 16 (25%), and progression in 4 out of 16 (25%). The median survival for all treated patients is 11,7 months (range 3-30 months). During the treatment no significant side effects were observed, and no lethal cases occurred.


In spite of the small number of the treated patients with castration-resistant prostate tumors, the preliminary results are promising and this gives us hope and expectations for future serious multicenter research over the possibilities for routine implementation of IPTLD.

PMID: 22649741 PMCID: PMC3357525 DOI: 10.5402/2012/140182

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Chemotherapy is the only option for oncologists when a cancer has widely spread to different body sites. However, almost all currently available chemotherapeutic drugs will eventually encounter resistance after their initial positive effect, mainly because cancer cells develop genetic alterations, collectively coined herein as mutations, to adapt to the therapy. Some patients may still respond to a second chemo drug, but few cases respond to a third one. Since it takes time for cancer cells to develop new mutations and then select those life-sustaining ones via clonal expansion, “run against time for mutations to emerge” should be a crucial principle for treatment of those currently incurable cancers. Since cancer cells constantly change to adapt to the therapy whereas normal cells are stable, it may be a better strategy to shift our focus from killing cancer cells per se to protecting normal cells from chemotherapeutic toxicity. This new strategy requires the development of new drugs that are nongenotoxic and can quickly, in just hours or days, kill cancer cells without leaving the still-alive cells with time to develop mutations, and that should have their toxicities confined to only one or few organs, so that specific protections can be developed and applied.

Keywords: Cancer, Chemotherapy, Chemoresistance, Mutation, Metastasis

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Cancer prognosis has been greatly improved these days, compared to 1971 when the US president Nixon declared the war on cancer 1. Some cancer types are basically curable, such as testicular cancer, gestational choriocarcinoma, and some subtypes of leukemia. Certain cancers, including lung, colorectal, breast, and prostate cancers, have a greatly diverse prognosis, with some early-diagnosed cases curable simply by surgical removal while many other cases, especially those that miss an early diagnosis, having a dolorous outcome. Skin melanoma and nasopharyngeal cancer may also belong to this group as they may be killed by high dose of interleukin-2 2–4 and by radiotherapy with or without chemotherapy 5–7, respectively. There are some other types of cancer that may not be curable but are indolent and may take over a decade to progress to the terminal stage, such as thyroid cancer 8–10. Unfortunately, there are still certain cancers, such as pancreatic, liver, or gastric cancer, that basically have no cure and are difficult to diagnose earlier; even those cases that are diagnosed at an early stage by serendipity are very likely to die from metastases eventually. A huge number of chemotherapeutic drugs (“chemo drugs” hereafter for brevity) have been developed in the past decades. However, although some of them have magical efficacy initially, especially those having specific targets and so-called magic bullets 1,11,12, basically all of them will eventually encounter resistance 13 after having given an initial high to the patient and sometimes also to the oncologist. Even worse, these drugs will induce resistance via not only quick, nongenetic mechanisms 14–16 but also genetic mutations and ensuing clonal selections of the cells that basically resist all kinds of remedies 17,18. After a long cogitation, we have come up with a new strategy for those currently incurable cancers and present it in this essay for peers to debate.

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  1. Hanahan D. Rethinking the war on cancer. Lancet. 2014;383:558–563. [PubMed]
  2. Kaufman HL, Wong MK, Daniels GA, McDermott DF, Aung S, Lowder JN, et al. The use of registries to improve cancer treatment: a national database for patients treated with interleukin-2 (IL-2) J. Pers. Med. 2014;4:52–64. [PMC free article] [PubMed]
  3. Rosenberg SA. IL-2: the first effective immunotherapy for human cancer. J. Immunol. 2014;192:5451–5458. [PubMed]
  4. Ledford H. Old cancer drug gets fresh look. Nature. 2014;509:541–542. [PubMed]
  5. Rottey S, Madani I, Deron P. Van BS. Modern treatment for nasopharyngeal carcinoma: current status and prospects. Curr. Opin. Oncol. 2011;23:254–258. [PubMed]
  6. Tao CJ, Lin L, Zhou GQ, Tang LL, Chen L, Mao YP, et al. Comparison of long-term survival and toxicity of cisplatin delivered weekly versus every three weeks concurrently with intensity-modulated radiotherapy in nasopharyngeal carcinoma. PLoS ONE. 2014;9:e110765. . doi: 10.1371/journal.pone.0110765. [PMC free article] [PubMed]
  7. Zhang L, Chen QY, Liu H, Tang LQ. Mai HQ. Emerging treatment options for nasopharyngeal carcinoma. Drug Des. Devel. Ther. 2013;7:37–52. [PMC free article] [PubMed]
  8. Curry HL, Parkes SE, Powell JE. Mann JR. Caring for survivors of childhood cancers: the size of the problem. Eur. J. Cancer. 2006;42:501–508. [PubMed]
  9. Perri F, Pezzullo L, Chiofalo MG, Lastoria S, Di GF, Scarpati GD, et al. Targeted therapy: a new hope for thyroid carcinomas. Crit. Rev. Oncol. Hematol. 2014;94:55–63. . doi: 10.1016/j.critrevonc.2014.10.012. [PubMed]
  10. Kim TY, Kim WG, Kim WB. Shong YK. Current status and future perspectives in differentiated thyroid cancer. Endocrinol. Metab. (Seoul) 2014;29:217–225. [PMC free article] [PubMed]
  11. Azmi AS. Adopting network pharmacology for cancer drug discovery. Curr. Drug Discov. Technol. 2013;10:95–105. [PubMed]
  12. Duffy MJ. The war on cancer: are we winning? Tumour Biol. 2013;34:1275–1284. [PubMed]
  13. Huang S. The war on cancer: lessons from the war on terror. Front. Oncol. 2014;4:293. . doi: 10.3389/fonc.2014.00293. [PMC free article] [PubMed]
  14. Pisco AO, Brock A, Zhou J, Moor A, Mojtahedi M, Jackson D, et al. Non-Darwinian dynamics in therapy-induced cancer drug resistance. Nat. Commun. 2013;4:2467. . doi: 10.1038/ncomms3467. [PMC free article] [PubMed]
  15. Brock A, Chang H. Huang S. Non-genetic heterogeneity–a mutation-independent driving force for the somatic evolution of tumours. Nat. Rev. Genet. 2009;10:336–342. [PubMed]
  16. Huang S. Tumor progression: chance and necessity in Darwinian and Lamarckian somatic (mutationless) evolution. Prog. Biophys. Mol. Biol. 2012;110:69–86. [PubMed]
  17. Zhang J, Lou XM, Zellmer L, Liu SQ, Xu NZ. Liao DJ. Just like the rest of evolution in Mother Nature, the evolution of cancers may be driven by natural selection, and not by haphazard mutations. Oncoscience. 2014;1:580–590. [PMC free article] [PubMed]
  18. Zhang J, Lou XM, Jin LY, Zhou RJ, Liu SQ, Xu NZ, et al. Necrosis, and then stress induced necrosis-like cell death, but not apoptosis, should be the preferred cell death mode for chemotherapy: clearance of a few misconceptions. Oncoscience. 2014;1:407–422. [PMC free article] [PubMed]
  19. Nauts HC. The beneficial effects of bacterial infections on host resistance to cancer. End results in 449 cases. A study and abstracts of reports in the world medical literature (1775–1980) and personal communication. Cancer Res. Inst. Monogr. 1980;8:1–225.
  20. Busch W. Uber den Einfluss welche heftigere Erysipeln zuweilig auf organisierte Neubildungenausuben. Vrh. Naturhist. Preuss. Rhein. Westphal. 1866;23:28–30.
  21. Busch W. Aus der sitzung der medicinischen section. Berl. Klin. Wochenschr. 1868;5:137–138.
  22. Hobohm U. Fever and cancer in perspective. Cancer Immunol. Immunother. 2001;50:391–396. [PubMed]


Seed Brad part 2


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