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Prolactin inhibitors in oncology

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Published on Saturday, 25 February 2023

Di Bella Method and Prolactin (PRL) inhibitors (e.g. Bromocriptine, Cabergoline and so on) in oncology

Cabergoline and/or Bromocriptine negatively regulate Prolactin, the ubiquitary mitogenic hormone. This effect is reinforced by Somatostatin and/or its analogues (cfr. Somatostatin in oncology, the overlooked evidences) by negatively regulating highly mitogenic molecules such as GH and GH-dependent growth factors. By activating their respective membrane receptors (GHR, GFR and PRLR), the GH, GF and PRL molecules trigger chemical reactions of phosphorylation, transferring the signal from the cellular membrane to the nucleus. The larger the amount of GHR in a tumour cell, the greater its capacity to use the GH, and thus to grow, both locally and also to expand remotely.

The dose-dependent relationship between receptor expression of GH in tumour cells and their speed and ability to expand locally and to migrate and produce metastases has been extensively demonstrated. Since it has been definitively and scientifically proved that a tumour is a growth, and that this growth depends on GH, GF and PRL, the obvious main therapeutic objective for the cure of any tumour cannot logically exclude the inhibition of GH, GF and PRL by means of Somatostatin and the prolactin inhibitors Cabergoline and/or Bromocriptine. The inhibition of tumour growth by blocking the growth hormone through its biological antidote, Somatostatin (SST), thus follows a simple, linear, understandable and mathematical logic (figure below).

 

GH GFs PRL

 

In this figure growth hormone GH is in direct contact with the respective receptor GHR, at the level of the cellular membrane (in blue). The contact triggers transduction and amplification of the signal to the nucleus (in red). The reactions are protein-tyrosine kinase phosphorylation events. These reactions are blocked by somatostatin (SST) which, by activating its receptor SSTR, triggers OPPOSING enzymatic phosphatase systems which disactivate the protein-tyrosine kinase phosphorylation chain, inhibiting the neoplastic proliferation. This direct antitumoural action of SST on the tumour cell is combined with its equally potent indirect action, consisting of the reduction of the blood concentrations of GH and consequently of GF.

The same concept and the same therapeutic rationale apply to the pharmacological blocking of Prolactin by means of the relative inhibitors, such as Bromocriptine and Cabergoline. The same concept and the same therapeutic rationale apply in oncology to the blocking of estrogens and androgens in the respective hormone-dependent tumours. But oncology still does not understand the need to extend the same concept to the inhibition of the most potent ubiquitary oncogenes: GH (growth hormone), (GH-dependent) GFs (growth factors) and PRL.

The Di Bella Method (A Fixed Part) uses agonists Cabergoline and/or Bromocriptine.

Inhibitors of Prolactin have the following documented mitogenic activities with a great number of works published: In Vitro, In Vivo (Animal Only), Review, Editorial, Meta-analysis and In Vivo (Human Only).

 

 

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