Somatostatin in oncology, the overlooked evidences

Published on Sunday, 22 December 2013

M.D. Ph.D Giuseppe Di Bella - Somatostatin (analogues and/or derivatives) in oncology, the overlooked evidences - 19/Jul/2010 - Bologna (Italy)

There are a great number of works published on the effectiveness of Somatostatin (analogues and/or derivatives, e.g. Octreotide, Sandostatin LAR, Pasireotide and so on) in different types of cancer: In Vitro, In Vivo (Animal Only), Review, Editorial, Meta-analysis and In Vivo (Human Only).

The Di Bella Method (A Fixed Part) mainly uses Somatostatin, Octreotide and/or Sandostatin LAR.


Somatostatin - 3D structure

Below a complete transcription:



Only In Vitro Research (Isolated organs, tissues, cells, or biochemical systems - IUPAC Gold Book definition)


In Vivo (Animal Only)




Commentary - Editorial - Letter to the Editor - Correspondence


Meta-Analysis, Pooled Analysis and Narrative Reviews


In Vivo (Human Only: Case Reports/Series, Clinical Trials, Comparative Studies, Randomized Controlled Trials and Retrospective Studies)



Somatostatin (analogues and/or derivatives) in oncology, the overlooked evidences:

So, the essential element of the Di Bella Therapy is the blocking of Growth Hormone (GH), the inhibition of Growth Hormone (GH).

It is worth pointing out that this therapy is not alternative in the meaning usually given to this word but is based on scientific data documented and verifiable! It is sufficient to access the international database Medline, the address is, 'medical publications dot government', therefore there is documentation about the effectiveness that each component of the Di Bella Method has in cancer therapy!

There is a fact that oncology has not yet adequately assessed and that is the inhibition of Growth Hormone (GH). The inhibition is done with the natural antidote that is Somatostatin. The product can be synthetic or biologic. Now on this, there are about 26,000 publications (e.g. Some pubblications about Somatostatin. The latest, of great interest, are from a Nobel, this Nobel is called Schally, he has a school of research very active in publishing. He published this: not only the Growth Hormone (GH), but the promoter of the growth hormone the Growth Hormone Releasing Factor (GHRF, GHRH or GRF), have a fundamental primary role in the induction, progression and metastasis of the tumor [e.g.: 1 - 2 - 3 - 4 - 5 - 6 - 7 - 8 and some additional publications of various authors].

Not only that, but this boost to the tumor occurs, either directly when the growth hormone acts on the tumor cell, and indirectly through the promotion of hormones that are produced by the various tissues, they are defined growth factors, they are produced by the various tissues under the effect of the Growth Hormone (GH). They are several tens, each of these has a very important role in the stimulation of tumor growth. Hence the Growth Hormone (GH) induces growth both physiological and tumoral. The difference is that cancer cell uses the same Growth Hormone (GH) needed by the healthy cell in exponential quantities! Somatostatin has this function: to drastically reduce the ability of the tumor cell to use the Growth Hormone (GH), not only, but also the use of growth factors induced by the Growth Hormone (GH).

Therefore the mechanism of action, the rational, the functioning are known and have a mathematical and understandable logic. Unfortunately they are not implemented: they are still trying to inactivate individual growth factors with monoclonal antibodies, when still they do not want to implement a fundamental concept, logical and very well documented. That is turn off the main switch: the main switch which gives energy to the tumor cell is the Growth Hormone (GH), because in turn induces a cascade of growth factors.

Growth Hormone (GH) is produced by the anterior pituitary, which is a gland that has central functions in our body, without which life would not exist. Still in the anterior pituitary, adjacent to the area of production of the Growth Hormone (GH), Prolactin (PRL) is produced which has a function slightly inferior to the Growth Hormone (GH). Growth Hormone (GH) and Prolactin (PRL) are ubiquitous. They are spread throughout the body and have central and primary functions in the growth of the physiological and tumoral cell. From this derives what: that if we want to inhibit tumor growth we must prevent cancer cell using the Growth Hormone (GH) and Prolactin (PRL).

At the World Congress of Singapore, held two weeks ago, I was invited to bring a report on the Di Bella therapy. And I brought a report presenting also the rationale of the therapy, mentioning the vast scientific validation available over these principles. I brought about 553 cases who responded to the therapy so widely better, we are not speaking of miracles, because so many people died even with the Di Bella therapy, however, they lived at least 3 times more with a quality of life ratio of 9 to 1, quality of life that can be quantified with a program. Not only that, from the Congress has emerged that they no longer use the word "cured" in solid tumors. Sometimes they are able to cure leukemia, but less than what they lead people to believe though. Not solid tumors, solid tumor is cured by surgery (e.g. How effective is chemo therapy?).

We presented a series of cases that have no equivalent in current therapies of solid tumors that were completely and permanently cured with the Di Bella therapy. No other cured case was brought to the world congress.

They speak of median survival: comparing in terms of median survival, for the same tumors, for the same stage, compared to their best and official results, we have a median survival, at least, three times better than theirs. At least! And a quality of life that is better by a ratio of 9 to 1, not only that, in some cases, we can document that they were healed. Stably and definitively healed. The others do not have healings and I repeat, in solid not operated tumors. Ours have not had surgery, they have not had chemo, they have not had radio. Why? Because we work with the Di Bella therapy on the causal elements of the tumor. They are mutations! These mutations either boost growth, thus acting by multiplying what are called oncogenes, and the fundamental one is the Growth Hormone (GH) and the growth factors induced by it, or in a mutation, there is blockage of tumor suppressor of the substances that must block the Growth Hormone (GH) and growth factors.

I have emphasized the concept that these data are severely overlooked by the oncology, instead they should be evaluated, in light of the current failures. Because when we talk about survival of months, at best a few years, but without solving anything, it's a failure, these failures are essentially based on the fact that clinical medicine is ignoring a large part of the scientific data, of the scientific evidence!

The fact that the Growth Hormone (GH) is the general switch that must be turned off to block the tumor, has a very large documentation. There are publications of Lincoln DT [e.g.: 1 - 2 - 3 - 4 - 5 and some additional publications of various authors], who is an American researcher, who not only has proven, he has a whole school of research, there are several publications. He has identified the receptors, that is the point at which the cell receives the Growth Hormone (GH) and responds to this stimulus. They are called receptors. He saw that in the healthy cell they are a lot less, the growth hormone receptors, namely the ability to use the Growth Hormone (GH) in the healthy cell is dramatically lower than in the cancer cell!

Indeed continuing his studies he showed a dose-dependent relationship! The more the cancer cell expresses receptors, that is the more tumor cell is capable of using the growth hormone, the more it is aggressive, the more is its ability to give metastases, the faster it grows!

Therefore this is a fact scientifically documented and verifiable and not used in therapy, wich is of an exceptional gravity, from a point of view not only scientific but also ethical; because the patient has difficulty coping with the expense, to use what is the physiological inhibitor of the Growth Hormone (GH). The natural biological and non-toxic inhibitor which is Somatostatin. People have to pay for it! While the Italian government pays more than € 1 billion per year for monoclonal antibodies! The monoclonal antibody does not enable healing and does not grant survival because it goes to inhibit a single growth factor, whereas there are tens of them! And it does not inhibit the main switch namely that hormone growth from which all growth factors depend upon.



Lincoln DT et al.

[1] Lincoln DT, Temmin L, al-Jarallah MA, Mathew TC, Dashti H. - Primary Ki-1 lymphoma of the skin: expression of growth hormone receptors. Nutrition. 1995 Sep-Oct;11(5 Suppl):627-31;

[2] Lincoln DT, Sinowatz F, Temmim-Baker L, Baker HI, Kölle S, Waters MJ. - Growth hormone receptor expression in the nucleus and cytoplasm of normal and neoplastic cells. Histochem Cell Biol. 1998 Feb;109(2):141-59;

[3] Lincoln DT, Sinowatz F, Kölle S, Takahashi H, Parsons P, Waters M. - Up-regulation of growth hormone receptor immunoreactivity in human melanoma. Anticancer Res. 1999 May-Jun;19(3A):1919-31;

[4] Lincoln DT, Kaiser HE, Raju GP, Waters MJ. - Growth hormone and colorectal carcinoma: localization of receptors. In Vivo. 2000 Jan-Feb;14(1):41-9;

[5] Lincoln DT, Singal PK, Al-Banaw A. - Growth hormone in vascular pathology: neovascularization and expression of receptors is associated with cellular proliferation. Anticancer Res. 2007 Nov-Dec;27(6B):4201-18.



 Schally AV et al.

[1] Barabutis N, Siejka A, Schally AV. - Growth hormone releasing hormone induces the expression of nitric oxide synthase. J Cell Mol Med. 2011 May;15(5):1148-55. doi: 10.1111/j.1582-4934.2010.01096.x. Epub 2010 May 26;

[2] Barabutis N, Siejka A, Schally AV. - Effects of growth hormone-releasing hormone and its agonistic and antagonistic analogs in cancer and non-cancerous cell lines. Int J Oncol. 2010 May;36(5):1285-9;

[3] Guo J, Schally AV, Zarandi M, Varga J, Leung PC. - Antiproliferative effect of growth hormone-releasing hormone (GHRH) antagonist on ovarian cancer cells through the EGFR-Akt pathway. Reprod Biol Endocrinol. 2010 May 28;8:54. doi: 10.1186/1477-7827-8-54;

[4] Siejka A, Schally AV, Barabutis N. - Activation of Janus kinase/signal transducer and activator of transcription 3 pathway by growth hormone-releasing hormone. Cell Mol Life Sci. 2010 Mar;67(6):959-64. doi: 10.1007/s00018-009-0224-y. Epub 2009 Dec 13;

[5] Barabutis N, Siejka A, Schally AV, Block NL, Cai R, Varga JL. - Activation of mitogen-activated protein kinases by a splice variant of GHRH receptor. J Mol Endocrinol. J Mol Endocrinol. 2010 Feb;44(2):127-34. doi: 10.1677/JME-09-0121. Epub 2009 Nov 6;

[6] Pozsgai E, Schally AV, Zarandi M, Varga JL, Vidaurre I, Bellyei S. - The effect of GHRH antagonists on human glioblastomas and their mechanism of action. Int J Cancer. 2010 Nov 15;127(10):2313-22. doi: 10.1002/ijc.25259;

[7] Bellyei S, Schally AV, Zarandi M, Varga JL, Vidaurre I, Pozsgai E. - GHRH antagonists reduce the invasive and metastatic potential of human cancer cell lines in vitro. Cancer Lett. 2010 Jul 1;293(1):31-40. doi: 10.1016/j.canlet.2009.12.014. Epub 2010 Jan 12;

[8] Köster F, Engel JB, Schally AV, Hönig A, Schröer A, Seitz S, Hohla F, Ortmann O, Diedrich K, Buchholz S. - Triple-negative breast cancers express receptors for growth hormone-releasing hormone (GHRH) and respond to GHRH antagonists with growth inhibition. Breast Cancer Res Treat. 2009 Jul;116(2):273-9. doi: 10.1007/s10549-008-0120-4. Epub 2008 Jul 16.




Some additional publications about hGH/GH-GHRH/GHRF/GRF: