Update artikel 17 oktober 2016:

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Hier links naar enkele studies met LDN - Low Dose Naltrexon. Klik op de links en u komt bij de studierapporten en zie ook gerelateerde artikelen:

Opioid growth factor improves clinical benefit and survival in patients with advanced pancreatic cancer

LDN bij gemzar

Grafiek van effecten van LDN bij gemzar bij alvleesklierkanker


OGF biotherapy improves the clinical benefit and prolongs survival in patients with pancreatic cancer by stabilizing disease or slowing progression. The effects of OGF did not adversely alter patient quality of life. The use of OGF biotherapy at earlier stages of disease or in combination with other chemotherapeutic agents may further improve the outcome of this malignancy.

LDN bj alvleesklierkankerpatienten

Scanbeelden tijdens behandeling van LDN bij alvleesklierkankerpatienten

Opioid growth factor and the treatment of human pancreatic cancer: a review.


Clinically, OGF is a safe, non-toxic biotherapy that extends survival and reduces tumor burden in patients with unresectable pancreatic cancer. In summary, the OGF-OGFr axis should be explored both as a primary therapy for pancreatic cancer, and as an adjuvant pathway with other chemotherapies.

LDN bij alvleesklierkanker

Grafiek boven: LDN bij alvleesklierkanker

Long-term remission of adenoid cystic tongue carcinoma with low dose naltrexone and vitamin D3--a case report.

Low-dose naltrexone therapy improves active Crohn's disease.

LDN bij ziekte van Crohn

A: Voor de behandeling met LDN
B: na de behandeling met LDN
LDN bij ziekte van Crohn 2

Low-dose naltrexone suppresses ovarian cancer and exhibits enhanced inhibition in combination with cisplatin.

The biology of the opioid growth factor receptor (OGFr).

Diabetic keratopathy and treatment by modulation of the opioid growth factor (OGF)-OGF receptor (OGFr) axis with naltrexone: a review.

Selective blockade of the OGF-OGFr pathway by naltrexone accelerates fibroblast proliferation and wound healing.

Mei 2002:

Naar naltrexone is wel onderzoek gedaan bij muizen ingespoten met menselijke kankercellen. Hier wordt een overzicht gegeven van wat er tot nu toe aan onderzoeksgegevens bekend zijn. Op de site kun je ook de abstract allemaal aanklikken en lezen. De nummers verwijzen naar de studies/referenties zoals die achter deze beschrijving zijn gegeven

  • Research History
    Ian Zagon, Ph.D., whose research group has done much of the basic animal work in the area of cancer treatment and endorphins, showed in 1981 in a mouse neuroblastoma model that very small doses (0.1 mg./kg) of naltrexone, given once a day, inhibit tumor growth, prolong survival in those mice that develop tumors and protect some mice from developing tumors altogether.2, 3 (abstract)

    Zagon had hypothesized that the small daily doses of naltrexone work to enhance the endorphin-related protective effect against cancer in mice by increasing the number and density of opiate receptors on tumor cells. He hypothesized as well that the increase in endorphins known to be induced by naltrexone might play a part in the protective effect of the small daily dose by working directly on the tumors' opiate receptors.4 (abstract)

    In 1996 and 1997, Zagon and his co-workers, reported on laboratory research using specially-bred mice that had no immune system (so-called "nude mice"). They transplanted, in separate experiments, human colon cancer and human pancreatic cancer into the animals and compared the growth of the cancer between those mice that received daily injections of metenkephalin and a control group that received placebo. In each experiment, metenkephalin acted as a negative regulator of tumorigenesis and was significantly able to suppress tumor appearance and growth in the treated group.5 (abstract)

    Of especial importance, in 1996 the same group of researchers demonstrated that by utilizing LDN to induce an intermittent blockade of opioid receptors in similar laboratory animals (nude mice), the growth of inoculated human colon cancer was markedly retarded. "At the time (10 days) when all control mice had tumors, 80% of the mice in the 0.1 mg/kg NTX group had no signs of neoplasia." When measurements of metenkephalin plasma levels were made, the group that received LDN had metenkephalin levels that were elevated 2.5-fold compared with the control group. The researchers concluded that the results suggested "that daily intermittent opioid receptor blockade with NTX [low dose naltrexone] provokes the interaction of opioids and receptors in the interval following drug availability, with opioids serving to inhibit tumorigenicity of human colon cancer".6 (abstract)

    New findings by Zagon and colleagues at The Pennsylvania State University in Hershey were published in the December 1999 issue of the journal Brain Research. They had identified the specific cell receptor for one of the endorphins, metenkephalin (the levels of which are increased by LDN). Zagon stated that the opioids act as growth inhibitors, as well as neurotransmitters, and that this feature has implications for cancer treatment. Metenkephalin is found in all tissues, and appears to be associated with cells undergoing renewal or proliferation. Zagon's group was described as having mounted Phase I trials using metenkephalin in an attempt to control the growth of pancreatic cancer in humans. Pancreatic tumors appear to have low levels of the metenkephalin receptor. Low peptide or receptor levels may exist in cancer cells in general since they want to stimulate their own growth, Zagon said.7 (abstract)
  • De referenties zoals hier genoemd, en zoals gezegd op de site kunnen de abstracts direct worden aangeklikt.:
  • Referenties:
    Matthew, PM, Froelich CJ, Sibbitt WL, Jr., Bankhurst AD, Enhancement of natural cytotoxicity by beta-endorphin, J Immunol 130, pp.1658-1662, Apr 1983. Read the abstract. 
  • Zagon IS, McLaughlin PJ, Naltrexone prolongs the survival time of mice treated with neuroblastoma, Life Sci 28, pp. 1095-1102, 1981. (Abstract unavailable.) 
  • Zagon IS, McLaughlin PJ, Naltrexone modulates tumor response in mice with neuroblastoma, Science 221, pp.671-3, Aug 12, 1983. Read the abstract. 
  • Hytrek SD, McLaughlin PJ, Lang CM, Zagon IS, Inhibition of human colon cancer by intermittent opioid receptor blockade with naltrexone, Cancer Lett 101(2), pp. 159-64, Mar 29, 1996. Read the abstract. 
  • Zagon IS, Hytrek SD, Lang CM, Smith JP, McGarrity TJ, Wu Y, McLaughlin PJ, Opioid growth factor (enkephalin) prevents the incidence and retards the growth of human colon cancer, Am J Physiol 271(3 Pt 2), pp.R780-R786, Sep 1996. Read the abstract. 
  • Hytrek SD, et al. 1996. Zagon IS, Verderame MF, Allen SS, McLaughlin PJ, Cloning, sequencing, expression and function of a cDNA encoding a receptor for the opioid growth factor, [Met(5)]enkephalin, Brain Res 849(1-2), pp. 147-54, Dec 4, 1999. Read the abstract. 
  • Other References
    Recant L, Voyles NR, Luciano M, Pert CB, Naltrexone reduces weight gain, alters "beta-endorphin", and reduces insulin output from pancreatic islets of the genetically obese mice, Peptides1(4), pp. 309-313, Winter 1980. Read the abstract. 

    Zagon IS, McLaughlin PJ., Opioid antagonists inhibit the growth of metastatic murine neuroblastoma, Cancer Letters 21, pp. 89-94, 1983. Read the abstract. 

    Zagon IS, McLaughlin PJ, Duration of opiate receptor blockade determines tumorigenic response in mice with neuroblastoma: a role for endogenous opioid systems in cancer, Life Sci 35, pp. 409-416, 1984. Read the abstract. 

    Zagon IS, McLaughlin PJ, Opioid antagonist modulation of murine neuroblastoma: A profile of cell proliferation and opioid peptides and receptors, Brain Res 480, pp. 16-28, 1989. Read the abstract. 

    Zagon IS, Hytrek SD, Smith JP, McLaughlin PJ, Opioid growth factor (OGF) inhibits human pancreatic cancer transplanted into nude mice, Cancer Lett 112(2), pp.167-175, Jan 30, 1997. Read the abstract. 

Referentielijst van studies met LDN - Low Dose Naltrexone bij alvleesklierkanker


1. Rocha Lima CM, Centeno B. Update on pancreatic cancer. Curr Opin Oncol. 2002;14(4):424–430. [PubMed]
2. Jemal A, Siegel R, Ward E, et al. Cancer statistics, 2008. CA Cancer J Clin. 2008;58(2):71–96. [PubMed]
3. Bramhall S, Dunn JA, Neoptolemos JP. Epidemiology of pancreatic cancer. In: Beger HG, Warshaw AL, Buchler MW, et al., editors. The Pancreas. Cambridge, MA: Blackwell Science, Inc.; 1998.
4. Goldstein D, Carroll S, Apte M, et al. Modern management of pancreatic carcinoma. Intern Med J. 2004;34(8):475–481. [PubMed]
5. Heinemann V. Gemcitabine-based combination treatment of pancreatic cancer. Semin Oncol. 2002;29(1 Suppl 3):25–35. [PubMed]
6. McGinn CJ, Lawrence TS, Zalupski MM. On the development of gemcitabine-based chemoradiotherapy regimens in pancreatic cancer. Cancer. 2002;95(4 Suppl):933–940. [PubMed]
7. Oettle H, Riess H. Gemcitabine in combination with 5-fluorouracil with or without folinic acid in the treatment of pancreatic cancer. Cancer. 2002;95(4 Suppl):912–922. [PubMed]
8. Blackstock AW, Bernard SA, Richards F, et al. Phase I trial of twice-weekly gemcitabine and concurrent radiation in patients with advanced pancreatic cancer. J Clin Oncol. 1999;17(7):2208–2212. [PubMed]
9. Wolff RA. Novel therapies for pancreatic cancer. Cancer J. 2001;7(4):349–358. [PubMed]
10. Burris HA, III, Moore MJ, Andersen J, et al. Improvements in survival and clinical benefit with gemcitabine as first-line therapy for patients with advanced pancreas cancer: a randomized trial. J Clin Oncol. 1997;15(6):2403–2413. [PubMed]
11. Ozawa F, Friess H, Tempia-Caliera A, et al. Growth factors and their receptors in pancreatic cancer. Teratog Carcinog Mutagen. 2001;21(1):27–44. [PubMed]
12. Reddy SA. Signaling pathways in pancreatic cancer. Cancer J. 2001;7(4):274–286. [PubMed]
13. Shi X, Friess H, Kleeff J, et al. Pancreatic cancer: factors regulating tumor development, maintenance and metastasis. Pancreatology. 2001;1(5):517–524. [PubMed]
14. Zagon IS, Verderame MF, McLaughlin PJ. The biology of the opioid growth factor receptor (OGFr) Brain Res Brain Res Rev. 2002;38(3):351–376. [PubMed]
15. Zagon IS, Smith JP, McLaughlin PJ. Human pancreatic cancer cell proliferation in tissue culture is tonically inhibited by opioid growth factor. Int J Oncol. 1999;14(3):577–584. [PubMed]
16. Zagon IS, Smith JP, Conter R, et al. Identification and characterization of opioid growth factor receptor in human pancreatic adenocarcinoma. Int J Mol Med. 2000;5(1):77–84. [PubMed]
17. Zagon IS, Hytrek SD, Smith JP, et al. Opioid growth factor (OGF) inhibits human pancreatic cancer transplanted into nude mice. Cancer Lett. 1997;112(2):167–175. [PubMed]
18. Zagon IS, Roesener CD, Verderame MF, et al. Opioid growth factor regulates the cell cycle of human neoplasias. Int J Oncol. 2000;17(5):1053–1061. [PubMed]
19. Zagon IS, Ruth TB, Leure-duPree AE, et al. Immunoelectron microscopic localization of the opioid growth factor receptor (OGFr) and OGF in the cornea. Brain Res. 2003;967(1–2):37–47. [PubMed]
20. Zagon IS, Verderame MF, Allen SS, et al. Cloning, sequencing, chromosomal location, and function of cDNAs encoding an opioid growth factor receptor (OGFr) in humans. Brain Res. 2000;856(1–2):75–83. [PubMed]
21. Smith JP, Conter RL, Bingaman SI, et al. Treatment of advanced pancreatic cancer with opioid growth factor: phase I. Anticancer Drugs. 2004;15(3):203–209. [PubMed]
22. Karnofsky DA, Abelmann WH, Craver LF, et al. Performance status in cancer patients. Cancer. 1948;1:634–656.
23. Bergner M. Development, testing, and the use of the Sickness Impact Profile. In: Walker SR, Rosser RM, editors. Quality of Life: Assessment and Application. Boston, MA: MTP Press Limited; 1987.
24. Beck AT, Ward CH, Medelson M, et al. An inventory for measuring depression. Arch Gen Psychiatry. 1961;4:561–571. [PubMed]
25. Melzack R. The McGill Pain Questionnaire: major properties and scoring methods. Pain. 1975;1(3):277–299. [PubMed]
26. National Cancer Institute. Version 2.0 DCTD. Bethesda, MD: National Cancer Institute, National Institutes of Health; 1998. [3-23-1998]. Cancer Therapy Evaluation Program: Common toxicity criteria.
27. Therasse P, Arbuck SG, Eisenhauer EA, et al. New guidelines to evaluate the response to treatment in solid tumors. European Organization for Research and Treatment of Cancer, National Cancer Institute of the United States, National Cancer Institute of Canada. J Natl Cancer Inst. 2000;92(3):205–216. [PubMed]
28. National Cancer Institute. Common Terminology Criteria for Adverse Events v3.0 (CTCAE) Bethesda, MD: National Cancer Institute, National Institutes of Health; 2006. [8-9-2006].
29. Kaplan EL, Meier P. Nonparametric estimation from incomplete observations. J Am Stat Assoc. 1958;53:457–481.
30. Burris H, Storniolo AM. Assessing clinical benefit in the treatment of pancreas cancer: gemcitabine compared to 5-fluorouracil. Eur J Cancer. 1997;33 Suppl 1:S18–S22. [PubMed]
31. Crippa S, Dominguez I, Rodriguez JR, et al. Quality of life in pancreatic cancer: analysis by stage and treatment. J Gastrointest Surg. 2008;12(5):783–793. [PMC free article] [PubMed]
32. Green MR. Gemcitabine safety overview. Semin Oncol. 1996;23(5 Suppl 10):32–35. [PubMed]
33. Sonis ST. Mucositis as a biological process: a new hypothesis for the development of chemotherapy-induced stomatotoxicity. Oral Oncol. 1998;34(1):39–43. [PubMed]
34. Cartwright TH, Cohn A, Varkey JA, et al. Phase II study of oral capecitabine in patients with advanced or metastatic pancreatic cancer. J Clin Oncol. 2002;20(1):160–164. [PubMed]
35. Sack GH, Jr, Levin J, Bell WR. Trousseau’s syndrome and other manifestations of chronic disseminated coagulopathy in patients with neoplasms: clinical, pathophysiologic, and therapeutic features. Medicine (Baltimore) 1977;56(1):1–37. [PubMed]
36. Stein PD, Beemath A, Meyers FA, et al. Pulmonary embolism as a cause of death in patients who died with cancer. Am J Med. 2006;119(2):163–165. [PubMed]
37. Smith JP, Conter RL, Demers LM, et al. Elevated levels of opioid growth factor in the plasma of patients with pancreatic cancer. Pancreas. 2000;21(2):158–164. [PubMed]
38. Zagon IS, Jaglowski JR, Verderame MF, et al. Combination chemotherapy with gemcitabine and biotherapy with opioid growth factor (OGF) enhances the growth inhibition of pancreatic adenocarcinoma. Cancer Chemother Pharmacol. 2005;56(5):510–520. [PubMed]

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