The Di Bella Method (DBM)

Published on Sunday, 25 November 2012

Introduction (full pdf)

The rationale, the aims, the components, the biochemical and physiological bases and the molecular biology mechanisms of action of the DBM are described. The tolerability, the clinical findings and the confirmation in the literature of the antitumoural efficacy of each individual component of the DBM, enhanced by the synergic factorial effect, are reported "The serious numerous irregularities that totally delegitimised the DBM experiments in 1998" (see below with complete transcription here) are also pointed out. The positive results achieved with the retrospective observational study on patients treated with the DBM are reported.



The current data in the literature on chemotherapy document a high degree of toxicity and a mortality percentage also reported by the Reuters Health Agency (Wesport, CT 2001-05-17): “Unexpected high mortality rates associated with chemotherapy regimen...”. This is confirmed by a study of the chemotherapy protocols for lymphoproliferative diseases (Atra et al. 1998) which reports a mortality rate of 11%, not caused by the tumour but solely by the chemotherapy.

The current survival of patients with tumours is mainly due to surgery, much less to radiotherapy, reaching 29% at 5 years (Richards et al. 2000). Of this 29%, only 2.1–2.5% is due to chemotherapy (Morgan et al. 2005). This fundamental publication is based on 14 years of observation, 225,000 patients and 22 types of tumour, aimed at ascertaining the true contribution of chemotherapy in achieving 5 years of survival (see "How effective is chemo therapy?").

Chemotherapy alone, without surgery, thus allows only 2.1–2.5% of patients to survive for 5 years, after which it has been ascertained that half of these patients who have survived for five years will die in the long-term as a result of their tumour (Lopez et al. 1998). Data from the recent conferences of the American Society of Clinical Oncology (ASCO) clearly show that in solid tumours monoclonal antibodies allow an average increase in survival of around two months, and only in rare cases, with or without associated chemotherapy, does this figure rise to or exceed four months.

Based on these data reported in the literature, we decided that it was appropriate to propose the new biological, physiological and rational therapy protocols of the DBM with greater efficacy and lower toxicity.


Treatment (components of the DBM)

The DBM consists of:


A fixed part

Consisting of the following components:

These molecules are mixed in solution form, a formulation that allows maximum bioavailability, in these ratios:

- All-Trans Retinoic Acid 0.5 gr;

- Axerophthol palmitate 0.5 gr;

- Betacarotene 2 gr;

- Alpha tocopheryl acetate 1,000 gr;

The daily dose is based on body weight decimals: an adult weighing 70 kg can take 7 grams of solution 3 times a day.

Melatonin tablets, Prof. Di Bella’s formulation, chemically complexed as follows: Melatonin 12% - Adenosine 51% - Glycin 37%, administered in doses of from 20 to 60 mg per day.

Bromocriptin 2.5 mg tablets, one tablet per day divided into ½ in the morning and ½ in the evening.

Cabergoline 0.5 mg tablets. This can be used with or instead of Bromocriptin, taking ½ a tablet twice a week.

Dihydrotachysterol, synthetic Vitamin D3, 10 drops before meals together with the retinoid solution 3 times a day.

Chondroitin sulfate, one 800 mg sachet morning and evening dissolved in water.

Cyclophosphamide 50 mg tablets, one or two per day.

Hydroxyurea 500 mg tablets, one or two per day as an alternative to cyclophosphamide.

Somatostatin, peptide with 14 amino acids, 3 mg per day, injected slowly in the evening after supper, subcutaneously or intravenously with a 12-hour timed syringe (evening administration is indispensable since this coincides with the nocturnal peak in GH and GH-dependent growth factors).

Octreotide, peptide with 8 amino acids, in a 1 mg ampoule/day administered as above (alternatively, the delayed formulation of Octreotide can be administered intramuscularly at the same doses).

Vitamin C, 2–4 grams per day, orally.

Calcium, 2 grams per day, orally.

A variable part

This includes the following components:

Androgen inhibitors in hormone-dependent tumours in males.

Estrogen inhibitors in hormone-dependent tumours in females (excluding Tamoxifen due to the possible thromboembolic and neoplastic induction complications).

Tetracosactide hexa-acetate, polypeptide with 24 amino acids, with the same indications as cortisone, used as a replacement of cortisone due to its better ratio between tolerability and efficacy. Dosage of 1 mg per week intramuscularly, depending on pressure, blood sugar and electrolytic homeostasis.

(N,N-Bis(phosphonomethyl)glycine) 200 mg capsules, twice a day, orally, in primary or secondary tumours of the osteocartilaginous tissue.

One 200 mg capsule a day, in lung tumours or cancer of the bladder.

10% watery solution, one dessert-spoon 3 times a day (at meals) in HCV-correlated hepatocarcinoma.

In thrombocythemia. Used in microdoses of about 30–40 mg, on alternate days.

At 20–25% in 50 ml intravenously in disproteinemia and in pleural and ascitic effusion.

White cell growth factors, in leucopenia, administered subcutaneously or intravenously until physiological values are restored.

In anemic conditions, associated in iron-deficiency anemia with iron orally or intravenously and folates.

500 mg tablets, 5–6 gram per day, in concomitant infectious diseases, for its antiviral, antibacterial and atoxic antiprotozoic effect and immunitary reinforcement.

5 ml intramuscularly per day (in concomitant infectious diseases) for immunitary reinforcement.

1,000 mg orally, morning and evening on the 1st day, one gram once a day on the 2nd and 3rd day, together with 2 litres per day of mineral water. At these doses, phenylquinoline-carbonic acid rapidly normalises uricemia with a decidedly more favourable toxicity/benefit ratio compared to the monoamine oxidase inhibitors commonly used in these situations. Chronic administration of these inhibitors blocks enzymatic chains with a high functional level and can cause other serious diseases.

200 mg capsules, twice a day to activate the choleretic and cholagogue effect and blood-tissue exchanges.

40 μg capsules, twice a day, with antioxidant free antiradical action.

22 mg capsules, one a day, for its differentiating and myeloprotective action.




Retinoids (see also All-trans-retinoic acid and cancer)



Vitamin A (Axerophthol or retinol):


Retinoic acid (All Trans Retinoic Acid – A.T.R.A.):


Vitamin E:

Inhibits the growth of various tumour cell lines, such as:


Melatonin (MLT - see also About Melatonin):


Somatostatin and analogues (see also Somatostatin in oncology, the overlooked evidences):


Vitamin D3 and analogues (see also Vitamin D and cancer):


Vitamin C:


Bromocriptine and/or Cabergoline:

Inhibitors of prolactin, which has the following documented mitogenic activities:



The DBM has 3 main objectives:

  1. Defence against neoplastic aggression;
  2. Inhibition of neoplastic proliferation;
  3. Contrasting the marked mutagenic tendency of the neoplastic phenotype.



The DBM supports and enhances vital reactions and antitumoural homeostasis to allow them to counter the onset and progression of a tumour.

The tumour is a deviation from normal life, making it necessary to restore the altered reactions back to normal by reinforcing all the means that Physiology considers essential for life (Di Bella et al. 1969; Di Bella et al. 1971; Di Bella et al. 1974; Di Bella et al.1976; Di Bella et al. 1977; Di Bella et al. 1979; Di Bella et al. 1980; Di Bella et al. 1981; Di Bella et al. 1984; Di Bella et al. 1985; Di Bella et al. 1986; Di Bella et al. 1987; Di Bella et al. 1988; Di Bella et al. 1994; Di Bella 1997; Di Bella et al. 1998; Di Bella et al. 2002; Di Bella et al. 2006).

The DBM achieves this objective by means of innovative formulations and criteria for the use of Melatonin (complexed with Adenosine and Glycin), of Retinoids solubilized in Vitamin E, together with Vitamin C, Vitamin D3, and components of the ECM. Including apolar components such as Betacarotene and Vitamin E among the phospholipids of a cellular membrane stabilizes it and preserves it from oxidative damage and free radicals (Shklar et al. 1996; Israel et al. 2000; Khuri et al. 2001; Di Bella 2005; Dong et al. 2008; Lubin et al. 2008; Nesaretnam et al. 2008; Watters et al. 2009).

Both in situations that predispose to tumours and in actual neoplastic diseases, the structure and potential of the cellular membrane and, consequently, its expression and receptor functions, can be altered by deterioration of the oxidative processes and a consequent peak of free radicals. The doses foreseen by the DBM of retinoids and vit. E make it possible to achieve both a preventive and therapeutic effect, cancelling the possibility of damage caused by the free radicals (Odeleye et al. 1992; Launoy et al. 1998; Shimizu et al. 2004; Di Bella 2005; Elangovan et al. 2008; Neuzil et al. 2002; Frei et al. 2008).

The aim of optimizing vital reactions and defending them against neoplastic aggression is achieved with:

Retinoids and Melatonin have the ability to preserve and enhance the trophism, vitality and efficiency of healthy cells, at the same time depressing the progression, vitality and marked mutagenic tendency of the neoplastic phenotype (Di Bella et al. 1979; Di Bella et al. 1997; Onogi et al. 1998; Mediavilla et al. 1999; Bartsch et al. 1999; Wang et al. 1999; Khuri et al. 2001; Di Bella 2005; Di Bella et al. 2006; Garcia-Santos et al. 2006; Bogos et al. 2008; Martín-Renedo et al. 2008; Yap et al. 2008; Watters et al. 2009; Williams et al. 2009; Wu et al. 2009; Ginestier et al. 2009; Di Bella et al. 2009; Yin et al. 2009; Kim et al. 2009; Di Bella et al. 2009).

This apparent contradiction is based on the fact that retinoids are the most potent non-hormonal activators only of ordered, structural and functional growth for specific optimum biological equilibrium, while they decidedly inhibit disordered and non-specific neoplastic growth, causing apoptosis of the tumour cells.

Vitamins, on the other hand, are physiological catalysts between energy and matter.

Any change to living matter cannot exclude an adaptation of the energy status. Only slight variations in production quantity and absorption, i.e. the processing of the biological matter and its energy counterpart, are compatible with life: the reactions must take place gradually with minimal matter-energy variations, compensating each other over time. These reactions very gradually cause the production and absorption of energy and matter with material-energy equivalence. This continuous process, due to its exceptional purposes, must be gradually modulated and finely regulated, and would be impossible without vitamins, whose purpose is the conditioning and regulation of the matter-energy equilibrium on which life depends (Di Bella 2005).


The cellular membrane (in blue, containing the phospholipids layer in red) is a defence, a vital filter through which everything passes, from inside the cell outwards, where the stimuli and the conditionings are absorbed and analysed from the outside towards the inside and vice versa, communication takes place and impulses and signals are emitted and received. Optimising this process and making it efficient means making the cell capable of defending itself in optimum conditions: Vit. E and Betacarotene protect and stabilise the membrane, while MLT physiologically modulates its potentials, regulating the ionic channels and the entire receptorial dynamics and expression.


Complete knowledge of vitamins is the equivalent of knowledge of the most subtle energy-matter equilibriums and relationships and of all the reflections on life’s activities. Knowing the chemical composition, the formation, and the localisation of vitamins within a cell, the time of their intervention, the regulation and extent of their activity makes it possible to understand the essence of physiological life and to correct its pathological deviation. From their original biochemical-vital role, the rationale of vitamins in the DBM has risen to a therapeutic level that is essential both in preventing and curing various diseases. An in-depth knowledge of the regulatory mechanisms of normal physiological life thus makes it possible to devise effective countermeasures aimed at preventing degenerative or neoplastic deviations - Figure 1 (Di Bella 2005).

To understand the enormous importance of retinoids in biological economy, it is sufficient to consider that they provide the high energy cost both for growth and for the physiological order of growth, contributing to antitumoural homeostasis. The growth of living substance involves very high expenditure of energy, but physiological control of growth involves an equally high requirement of energy.



The ubiquitary receptorial expression of prolactin and GH (De Souza et al. 1974; Di Bella et al. 1979; Di Bella et al. 1981; Di Bella et al. 1997; Hooghe et al. 1998; Di Bella et al. 1998; Ben-Jonathan et al. 2002; Di Bella 2005; Di Bella 2009) represents one of the aspects of the direct and generalised mitogenic role of these molecules.

Cellular proliferation is strictly dependent on prolactin (Bonneterre et al. 1990; Di Bella et al. 1997; Di Bella et al. 1998;Tada et al. 1999; Gruszka et al. 2001; Di Bella 2005; Florio et al. 2008; Mouton et al. 2008; Di Bella 2009), on GH, the most important growth factor (De Souza et al. 1974; Di Bella et al. 1979; Di Bella et al. 1997; Di Bella L et al. 1998; Lincoln et al. 1998; Friend et al. 2000; Barnett et al. 2003; Anthony et al. 2009), and on GH-dependent mitogenic molecules positively regulated by GH, such as EGF, FGF, HGF, IGF1-2, NGF, PDGF, TGF, and VEGF (Szepesházi et al. 1999; Murray et al. 2004; Sall et al. 2004; Di Bella 2009; Hagemeister et al. 2008; Di Bella et al. 2009; Taslipinar et al. 2009), as well as on growth factors produced by the gastrointestinal system, such as VIP, CCK, and PG (Kath et al. 2000).

Both physiological and neoplastic cellular proliferation is triggered by these same molecules, which the neoplastic cell thus uses exponentially compared with a healthy cell. The loss of differentiation and uncontrolled proliferation, albeit to different extents, characterise all tumours.

The use of somatostatin and its analogues, by acting on growth, the common denominator of every tumour, must be based on a rational indication in every tumour (Di Bella et al. 1979; Di Bella et al. 1981; Di Bella et al. 1997; Pollak et al. 1997; Di Bella et al. 1998; Pawlikowski et al. 1998; Friend et al. 2000; Lachowicz et al. 2000; Friend et al. 2000; Schally et al. 2001; Massa et al. 2004; Di Bella 2005; Arena et al. 2007; Guillermet-Guibert et al. 2007; Di Bella 2008; Lee et al. 2008; Verhoef et al. 2008; Vieira Neto et al. 2008; Volante et al. 2008; Ben-Shlomo et al. 2009; Di Bella et al. 2009; Bellyei et al. 2010).

In many tumours, not just neuroendocrine types, a receptorial expression for somatostatin has been documented (Moertel et al. 1994; Sestini et al. 1996; Kogner et al. 1997; Briganti et al. 1997; Van Eijck et al. 1998; Borgström et al. 1999; Friend et al. 2000; Albérini et al. 2000; Florio et al. 2000; Cattaneo et al. 2000; Steták et al. 2001; Orlando et al. 2001; Faggiano et al. 2008; Florio et al. 2008; Fusco et al. 2008; Kwekkeboom et al. 2008; Hubalewska-Dydejczyk et al. 2008; Ioannou et al. 2008; Khanna et al. 2008; Li et al. 2008; Corleto et al. 2009; Edelman et al. 2009; Hassaneen et al. 2009; He et al. 2009; Laklai et al. 2009; Luboldt et al. 2009; Pisarek et al. 2009; Ruscica et al. 2010).


The doses and methods of administration of Somatostatin foreseen by the DBM make it possible to lower the plasma concentrations of circulating GH, while maintaining a sufficient level to ensure the indispensable use by the various physiological districts.


The causal relationship between the receptorial expression of GH (of which SST is the biological antidote) and tumoural induction and progression has been demonstrated (Friend et al. 2000; Zeitler et al. 2000; Gruszka et al. 2001), showing much higher histochemical concentrations of GHR in tumoural tissues with respect to healthy tissue. The powerful mitogenic role of GH is therefore known and amply documented, as is the fact that the proliferative index and the speed at which the tumour populations progress are directly proportional to the receptorial expression of GH - Figure 2 (Lincoln et al. 1998).

The inhibition of various oncogenes, including MIC, by SST and the other components of the DBM has been reported (Degli Uberti et al. 1991; Peverali et al. 1996; Sun et al. 2002; Gumireddy et al. 2003; Durand et al. 2008; Aktas et al. 2010).

The known causal factors of oncogenesis also include chromosomal damage, leading, to varying extents, to inactivation of oncosuppressor genes: CD44, Bcl-2, P53, as well as Caspases 3–8, key elements in the apoptotic cascade. The negative regulation of oncosupressors is antagonised by the components of the DBM, such as Retinoic acid, which inhibits the inactivation of the caspases (Piedrafita et al. 1997; Takada et al. 2001; Jiang et al. 2008) and MLT which preserves P53 and Bcl-2 from degradation (Mediavilla et al. 1999). The inactivation of oncosuppressors can take place at the same time as amplification of oncogenes such as the N-myc gene and the proto-oncogene TRK, considered one of the neoplastic cytogenic causes. Components of the DBM such as Somatostatin and the Retinoids (Giannini et al. 1997; Witzigmann et al. 2008; Quan et al.2008) antagonize the proliferative incentive of these molecules. Among the pathogenetic factors, the alteration of the GF-TRK ligand-receptor system and the altered response to the differential stimulus are effectively countered by the retinoids (Hassan et al. 1990; Giannini et al. 1997; Peverali et al. 1996; Voigt et al. 2000, Kulikov et al. 2007; Huang et al. 2009; Wu et al. 2009; Witzigmann et al. 2008). Differentiation is synergically reinforced by other components of the DBM, such as Melatonin (Cos et al. 1996; Garcia-Santos et al. 2006; McMillan et al. 1999), Vitamin D3 (Lange et al. 2007; Gocek et al. 2009), Vitamin E (Turley et al. 1995; Swettenham et al. 2005), Vitamin C (Carosio et al. 2007), and Chondroitin Sulfate (Batra et al. 1997; Liang et al. 2009). It is known how the GH-IGF1 axis has a determining influence on biological neoplastic development (Murray et al. 2004). The IGFR respond mitogenically to IGF. The suppressive effect of SST and its analogues on serum levels of IGF1 is both direct, through inhibition of the IGF gene (Cascinu et al. 1997), and indirect, by suppression of GH and thus of its hepatic induction of IGF1 (Sall et al. 2004; Murray et al. 2004; Taslipinar et al. 2009).

The tumour cells are characterised, albeit to different extents, by various levels of expression of tyrosine kinase receptors. The protein kinase activity is effectively inhibited by SST and its analogues (Reardon et al. 1996; Pawlikowski et al. 1998; Lachowicz-Ochedalska et al. 2000; Cattaneo et al. 2000; Florio et al.2001Massa et al. 2004; Lee et al. 2008; Florio et al. 2008). The expression of TRK-B and the amplification of N-Myc, together with the high telomerasic activity, common to various tumours, are negatively regulated by SST (Degli Uberti et al. 1991; Sun et al. 2002; Durand et al. 2008). Biological antidotes of GH, such as Somatostatin and its analogues, reduce the expression and transcription of highly mitogenic growth factors, such as IGF 1-2 (Sall et al. 2004), FGF (Held-Feindt et al. 1999), VEGF (Albini et al. 1999; Vidal et al. 2000). The inhibitory activity of SST on another potent mitogenic growth factor, EGF, has also been reported (Watt et al. 2009), acting through multiple mechanisms such as the dose-dependent inhibition of tyrosine phosphorylation induced by the activation of EGFR by EGF (Mishima et al. 1999), the reduction of EGFR in tumour cells (Szepesházi et al. 1999), the reduction of the expression of EGF (Held-Feindt et al. 2001), and the depletion of the plasma concentrations of EGF (Cascinu et al. 1997; Mishima et al. 1999; Szepesházi et al. 1999; Held-Feindt et al. 1999).

Somatostatin and its analogues extend their negative regulation to the respective receptors with evident antiproliferative and antiangiogenic repercussions (Manni et al. 1989; Barrie et al. 1993; Klijn et al. 1996; Pollak et al. 1997; Pawlikowski et al. 1998; Mishima et al. 1999; Lachowicz-Ochedalska et al. 2000; Friend et al. 2000; Schally et al. 2001; Watson et al. 2001; Schally et al. 2003; Massa et al. 2004; Di Bella 2005; Arena et al. 2007; Guillermet-Guibert et al. 2007; Bocci et al. 2007; Di Bella 2008; Lee et al. 2008; Di Bella et al. 2009).

It is now a confirmed fact that neoplastic progression is strictly dependent on angiogenesis and that this represents an obligatory and essential phase. Acquisition of an angiogenic phenotype is decisive for expansion of the tumour (Longo 2002). Somatostatin and its analogues negatively regulate the “angiogenic inductors” and all the phases of angiogenesis (Jia et al. 2003; Kunert-Radek et al. 2008) such as the cascade of monocytes (Wiedermann et al. 1993), interleukin 8, Prostaglandin E 2 and VIP, endothelial nitric oxide synthase (e-Nos) (Florio et al. 2003) as well as growth factors whose synergism is essential for angiogenesis, such as VEGF-A (Cascinu et al. 2001; Mentlein et al. 2001), TGF, (Murray et al. 2004; Hagemeister et al. 2008), FGF, HGF (Jia et al.. 2003; Hagemeister et al. 2008), and PDGF (Cattaneo et al. 1999). The inhibition of angiogenesis induced by SST is synergically and factorially reinforced by the other components of the DBM, such as Melatonin (Lissoni et al. 2001), Retinoids (Majewski et al. 1994; McMillan et al. 1999; Kini et al. 2001; Liu et al. 2005), Vitamin D3 (Mantell et al. 2000; Kisker et al. 2003), Vitamin E (Shklar et al. 1996; Tang et al. 2001), Vitamin C (Ashino et al. 2003), prolactin inhibitors (Turner et al. 2000), and components of the extracellular matrix (Ozerdem et al. 2004; Liu et al. 2005). The cytostatic, antiproliferative, and antimetastatic effects of Somatostatin have also been documented (Di Bella et al. 1979; Di Bella et al. 1981; Kogner et al. 1997; Di Bella et al. 1997; Schally et al. 1998; Di Bella et al. 1998; Orlando et al. 2001; Schally et al. 2003; Di Bella 2005; Arena et al. 2007; Krysiak et al. 2006; Guillermet-Guibert et al. 2007; Barbieri et al. 2008; Colucci et al. 2008; Di Bella 2008; Gambini et al. 2008; Li et al. 2008; Watt et al. 2008; Shima et al. 2008; Quan et al.2008; Van Keimpema et al.2008; Chen et al. 2009; Di Bella et al. 2009; Liu et al. 2009; Oberg et al. 2009; Hauser et al. 2009; Jia et al. 2009; Kaprin et al. 2009; Songgang et al. 2009; Nakashima et al. 2009; Zou et al. 2009; Ruscica et al. 2010). These effects are effectively synergised by the other components of the DBM.

The literature has therefore confirmed the differentiating antineoplastic and cytostatic, antiproliferative, antiangiogenic and antimetastatic mechanisms of action of all the components of the DBM.

Without the contribution of the growth hormone (GH) and the growth factors (GF) produced by the tissues by GH activity, no physiological or tumoural growth can take place. Cellular mutations are caused by various physical, chemical and infectious agents. Several components of the DBM (MLT, Vit. D3, C, E, Retinoids, components of the ECM) have a differentiating effect.

The growth of hormone-dependent tumours also involves estrogen (tumours of the breast and uterus) and testosterone (prostate and testicular cancer).



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.


The 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.


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 3.

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, (GH-dependent) GF and PRL.

Oncology continues to play about with the somatostatin receptor (SSTR), limiting its use to situations in which the receptor is identified in the tumour cells.

The test generally carried out for this search is Octreoscan. This test consists of an intravenous injection of a radiolabelled somatostatin analogue, usually Octreotide, and scintigraphy to detect the presence of SSTR in the tissues. This technique is not particularly reliable as it is not always capable of identifying even two of the seven receptors of somatostatin, numbers 2 and 5, and has proved to give a high percentage of false negatives. More reliable procedures, such as immunohistochemistry and reverse transcriptase, have in fact ascertained the presence of SSTR in many situations which gave completely negative results with Octreoscan (Schaer et al. 1997; Van Eijck et al. 1998; Held-Feindt et al. 1999; Mishima et al. 1999; Pinzani et al. 2001; Watson et al. 2001; Barnett et al. 2003). The conviction that Octreoscan helps in ascertaining the usefulness of somatostatin is therefore obsolete. Octreoscan has no effect whatsoever on the rationale of treatment with somatostatin for a number of reasons: all tumour cells have dose-dependent growth indices relative to the expression of the growth hormone receptor (GHR) inhibited by somatostatin (Lincoln et al. 1998). GH also promotes tumour growth by means of an indirect mechanism: induction of “Growth factors" (GF), highly mitogenic molecules which can be produced by tissues if activated by GH.


The GH-dependent growth factors that carry out a leading role in neoplastic induction and progression include epidermal growth factor (EGF), fibroblast growth factor (FGF), hepatocyte growth factor (HGF), IGF 1-2 produced by the liver, nerve growth factor (NGF), platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF) and transforming growth factor (TGF), etc...


In the absence of growth hormone (GH), no tissue can produce Growth factors. GH thus has an essential, powerful and dual mitogenic role:

Using somatostatin to negatively regulate GH and GH-dependent GF thus acts directly on tumour growth, regardless of whether somatostatin receptors (SSTR) are present or not in the tumour cells. The presence of SSTR on the membrane of the tumour cell can accelerate or intensify the response to SST, but this response would in any case occur for the reasons stated above.

The concept of restricting the use of somatostatin to the detection of one of its receptors in the tumour is therefore irrational. In addition, even when somatostatin receptors are not found in the tumour, they are in any case always present in the vessels around the tumour.

By blocking GH and the relative GF, SST is thus the most powerful inhibitor of tumoural proliferation and represents a necessary and essential component, albeit not sufficient, in the treatment of all tumours, with or without the presence of somatostatin receptors, and limiting, therefore, the therapeutic indications for using monoclonal antibodies. Monoclonal antibodies inhibit the kinases activated by the GF, but it has been extensively documented that SST inhibits the gene expression of all the GF, blocks their transcription and extends the block to the expression and transcription of their respective receptors. By reducing the rate of circulating GH with SST, the basic molecule necessary for the synthesis of GF is already eliminated. The toxicity of monoclonal antibodies is due to the fact that the receptor of the cellular membrane on which the monoclonal antibody acts does not consist only of the GF gene to be blocked, but of an entire family of genes all inactivated by the monoclonal antibody. It is precisely this unwanted but unavoidable blocking of all the other genes connected to the GF receptor that causes toxicity. Monoclonal antibodies are often used together with or following chemotherapy, with a logic that is difficult to understand: chemotherapy is in fact cytotoxic and cytolytic, it eliminates and/or intoxicates the cells, but in the large percentage of cells that it does not eliminate it destroys to a greater or lesser extent the more exposed fragile surface layer of the cell, the cellular membrane, the site of the receptors on which the monoclonal antibodies act, thus eliminating or destroying the receptor sites on which the MA should act, or severely denaturing membrane potentials, the ionic channels and the transduction chain of the signal to the nucleus.


Blue indicates the cellular membrane with the somatostatin receptors (SSTR), while green represents the cytoplasm of the cell inside the membrane, in which the chemical reactions activated by the contact between SST (ligand) and the SSTR take place. These reactions (phosphatase), indicated with the white arrows, block the protein-tyrosine kinase phosphorylation reactions of the tumoural proliferation induced by GH and GF. On the right side of the figure is a schematic representation of the blood vessels surrounding the tumour and giving it nutritional support with a high and constant expression of SSTR.


It is as if a switch were put out of action or the wire connecting the switch to a bulb were cut and one still expected the light to work - Figure 5.

The blood vessels around the tumour do in fact present a constant concentration of SSTR which, if activated by somatostatin, negatively regulate angiogenesis, and consequently the progression of the tumour. It has in fact been documented that even in cases in which no SSTR is detected in the tumour, somatostatin acts directly and effectively, blocking the growth of the tumour through inhibition of angiogenesis, and without angiogenesis no tumour can develop. In the cells of Kaposi’s sarcoma, in which SSTR were found to be totally absent, growth was completely blocked by somatostatin. The blood vessels around Kaposi’s sarcoma, however, have been shown to contain a high density of SSTR, and the cytostatic effect of SST is therefore a result of the antiangiogenic effect (Albini et al. 1999).

Until the cells that form the first tumoural aggregate measuring just a few millimetres are able to create their own system of blood vessels (neoplastic angiogenesis), they grow very slowly and remain at the “carcinoma in situ" stage. Expansion of the tumour only takes place when angiogenesis occurs, i.e. when the tumour succeeds in creating a network of blood vessels to ensure the supply of nutritional substances and eliminate metabolic waste. The literature has shown that all the stages of angiogenesis are negatively regulated by somatostatin and its analogues and, albeit to a lesser extent, by all the other components of the DBMS.


Molecules which contribute to the promotion of angiogenesis and synergically inhibited by somatostatin and every other component of the DBM:
Endothelial nitric oxide synthase (eNOS), Interleukin 8 (Il8), GH-induced monocyte chemotaxis (MC), Prostaglandin 2 (PG2), Fibroblast growth factor (FGF), Hepatocyte growth factor (HGF), Hepatic-derived insulin growth factor (IGF 1-2), Platelet-derived growth factor (PDGF), Vascular endothelial growth factor (VEGF), Transformation growth factor (TGF).


If angiogenesis is an obligatory phase of neoplastic expansion and if angiogenesis is totally inhibited by somatostatin, then its indication in all tumours, regardless of the presence of SSTR, is additionally supported.Even local situations of anoxia and acidosis favour angiogenesis and can often be corrected by the improvement of the blood-tissue exchanges induced by the differentiating components of the DBM - Figure 6.




Inhibition of the tumour cell mutations


The differentiating receptor sites are indicated on the blue cellular membrane: RAR the retinoic acid receptors, with 3 subgroups (alpha, beta and gamma), MELR the melatonin receptor, ECMR the extracellular matrix receptor. In the nucleus, in red, are the nuclear receptors: RXR the retinoic acid receptor, VDR the vitamin D3 receptor, ROR and RZR alpha and beta the Melatonin receptors. The ligands of these receptors, both membrane and nuclear, are components of the DBM, and combine a differentiating synergic response with the antiproliferative reinforcement of SST and prolactin inhibitors. If activated promptly and synergically, all these receptor blockades of the tumour mutationand proliferations are difficult to overcome. In the enlarged membrane area with the + and – signs above and below, are the ionic channels of calcium, sodium and potassium, vitally important for biological equilibrium and to contrast the tumour: modulated by melatonin by controlling the membrane potentials, they carry out their differentiating effect by activating reactions of Phosphorylation, Methylation and Acetylation.


The other fundamental aspect of neoplastic progression, and thus an objective of the therapeutic rationale of the DBM, consists of the tumour cell mutations. With every mutation, the cell selects and acquires a series of advantages. Differentiating properties of DBM components, such as Melatonin, Retinoids, VIT E, C, D3, and components of the extracellular matrix (ECM), contrast the marked mutagenic tendency of the neoplastic phenotype - Figure 7.

The strategic objectives of an antiblastic treatment cannot, therefore, exclude control of the mutations, which represent an essential feature and a common denominator of tumour cells, not least because of their dependence for growth on GH, PRL, and GF.

Tumour cells are characterised by an increasing frequency of mutations, followed by a predefined programme of survival inherited from bacteria (Radman et al. 1975) (transferred from prokaryotes) defined by Radman as the “SOS" system, which is repressed in healthy cells and accessed in conditions of acute stress.

This survival programme triggers a predefined process that allows the cell that has become neoplastic to adapt very rapidly and efficiently to the adverse conditions, with a modulated progression by means of a predetermined development mechanism.

The model which continues to dominate the official standards of oncology has still not assimilated this essential aspect of neoplastic evolution, a necessary stage in understanding oncological biology and interpreting the evolutionary processes involved in the progression of tumour diseases (not to be confused with a Darwinian concept). The protagonists of this development are in fact natural selection and genetic variation. Natural selection acts on genetic variation by providing evolutional advantages to phenotypes and genotypes which have adapted best to the environment.

The source of the genetic diversity is the mutation in the DNA sequences, and the mutation is a phenomenon, by definition, which is totally casual, managed totally by chance.

Within the framework of evolution, in which mutations and natural selection occur, it is thus clear that everything is guided by chance.

Cancer also follows this evolutional path and it is certainly a somatic process totally guided by chance that leads to carcinogenesis. In man this is a genetic process, the dynamics being regulated by the interaction between mutation, selection and the mechanisms of antiblastic homeostasis of tissue organisation, a process specific and obviously limited to higher multicellular complex organisms. The evolution of a cell towards malignancy starts with one or more casual mutations.These mutations obviously provide the cell with an advantage in proliferative terms and are thus in some way used by the selection. A tumoural disease is therefore currently interpreted as being evolutional. The accumulation of mutations will naturally produce subsequent waves of clonal expansion.

According to the prevailing model of the orthodox vision of cancer, it is a genetic disease, originating above all from the mutation of 2 classes of genes, oncogenes and oncosuppressors, thus from mutations of genes that regulate differentiation and growth, and directly involved in evolution, and of those in charge of maintaining the integrity of the DNA, ensuring the constancy of DNA synthesis and its repair by means of the many mechanisms that have appeared during evolution. Among the genes that regulate antiblastic homeostasis, a fundamental role is played by those that generate apoptosis. Every time one or more mutations occur in these genes, the tumour disease progresses. When a mutation occurs in the DNA damage repair genes, then what has been defined as genetic instability takes place, i.e. the mutant phenotype. A simple mutation of a healthy cell would not be able to explain this accumulation of mutations and thus the presence of a much more unstable phenotype is called for.

There is probably a positioning error as regards the concept of genetic instability. According to Radman’s theory (based on a survival system named SOS and supported by professor Israel and Italian authors), two fundamental players are the LexA gene and the RecA gene, together with the relative proteins.

The LexA gene is a transcriptional repressor, while the RecA gene is a positive regulator. The relative publications should be referred to for more details.

In conditions of stability, the “SOS” survival programme is not active but is repressed by the Lex A gene. The “SOS” system consists of around twenty genes and when the DNA is damaged or the survival of the cell is in danger, the Lex A protein is somehow inactivated by the production of another protein, Rec A, and at this point the genes are activated. This system is undoubtedly triggered by casual mutations, favourably selected and acquired by the cell that has access to this information in particular conditions.

There is strong evidence to support the idea that this system, acquired by evolution and present in eukaryotes, has been transmitted to human cells.

The search for an “SOS” programme in eukaryotes and in multicellular organisms such as ours has already produced positive results. Professor Israel’s studies have led to a search for homologies between the proteins and genes of the bacterial “SOS” system and those contained in our cells (Israel 1996).

One of these genes has already been identified. There is a very marked homology between the RecA bacterial protein and a protein present in our cells, Rad 51. We thus have justified reasons for believing that the “SOS” system can also exist in our cells, even in a much more developed version. On closer examination, the current dominant model of malignant development being the result solely of chance, i.e. produced by a number of subsequent but always casual mutations, does not hold good due to the fairly predictable nature of the malignant development. Except for the initial events, certainly due to casual mutations, the progression of the tumoural disease is undoubtedly a stereotype, closely following a predefined script.

The tumour cells gradually acquire more and more properties and characteristics and “learn” to carry out a series of activities. Such a phenotype requires around one thousand generation cycles to develop. Considering that each generation cycle takes around 48 hours, in a relatively short period of time the tumour cells are able to produce growth factors that their non-endocrine homologues are unable to synthesize. The tumour cells express receptors to these factors, which influence selective proliferation limited to these neoplastic populations.

The tumour cells also become increasingly mobile and deformable in order to better reach the capillaries and increase their metastatic potential; they also acquire the ability to survive and proliferate in different types of parenchymal tissue, and to coat themselves with molecules that protect them from the immune system. They then become able to secrete proteases which, by dissolving the membranes, allow the invasion of adjacent cells as well as inducing angiogenesis and local and systemic immunodepression. A study published in 2003 in “Nature” reports how a melanoma cell attacked by a lymphocyte can produce “apoptosis” of the lymphocyte; the neoplastic populations thus gradually acquire the ability to eliminate the cells of the immune system that attempt to attack the tumour cell.

Lastly, the tumour cell is able to modify the surrounding cellular environment, inducing the adjacent cells to support its proliferation.

The very fact that the tumour cell can easily encode the essential steps of its progression towards malignancy, and gradually increase its aggressiveness, proliferation and adaptation, contradicts the concept of a strictly casual development of the tumoural disease.

There are additional aspects which support this theory; the paraneoplastic syndromes, a sort of litmus paper of the progression towards malignancy. One significant particular consists of the fact that if these mutations were governed by chance, or better if their progression were totally governed by chance, then we would see both favourable and unfavourable mutations, or in any case mutations that were neutral compared with development of the tumour. But this is not in fact the case. The paraneoplastic syndromes show that tumour cells only produce substances that are of biological use to the tumour (Israel 1996).

This is in strong opposition to the official oncology concept of casual progression, since in this case we would also see the production of substances that are neutral or at least unfavourable to the progression of the tumour. There are some genetic events that characterise the progression of the tumour which are not mutations but merely reactivations and repressions or amplifications of genes that are not mutant but silent.

This inevitably leads us to conclude that the more evolved multicellular organisms such as ours have certainly inherited parts of a genome from bacteria, as clearly reported by recent studies of molecular genetics which show that certain bacterial genes have been totally preserved in our cells.

In the evolution of multicellular organisms towards increasingly more complex forms, the destiny of every cell is linked to the destiny of the community to which it belongs.

Evolution towards complexity, towards a multicellular organism, foresees a sort of cellular community cooperation and thus the introduction of new rules. In this sense, evolution has set up a kind of counter-programme or system that controls tissue homeostasis, something which is obviously not possible or necessary in a bacterial or unicellular environment.

This is the system of the oncosuppressors, which ensures antiblastic cellular homeostasis and prevents each individual cell from freeing itself and becoming independent, a process which could put the entire tissue community at risk.

Evolution produced this oncosuppressor system which is certainly still young, and thus more imperfect with certain deficiencies.

As a result, research has not yet found the homologues of oncosuppressors in the eukaryotes, and we thus have reason to believe that oncosuppressors are genes which evolved at a later stage.

One particularly interesting oncosuppressor is the p53 gene, the guardian of the genome, directly involved in activation of a cellular programme that is fundamental for antiblastic homeostasis, apoptosis.

I have talked at length about Radman’s survival programme in order to highlight, also in view of the subsequent findings, the rationality of the criteria, the molecular mechanisms and the objectives of the DBM. The research carried out by Radman, accepted and developed by Professors Israel and Truc, presented at the 1st National DBM Conference in May 2004 (Di Bella 2005), and reported here, provide greater awareness that the protein-like ability of the tumour cell to adapt, to mutate and recover, and its formidable vitality, all features unknown to physiological human biology, have been seriously underestimated. An exact and realistic evaluation of the practically unlimited neoplastic biological potential leads to a therapeutic logic which conforms exactly to the claims and rationale of the DBM: only an early synergic and concentric multitherapy attack, without interruption, can stand up to, limit and prevail over a form of life which is different and dramatically superior to physiological life, and which has an extremely high capacity to adapt to and overcome every single adverse condition that medicine can invent to fight it. The neoplastic cell therefore easily overcomes any obstacle, however efficient it is, and only the simultaneous activation of a series of blockades against the neoplastic mutations can prevent the tumour cell’s most deadly mechanism of defence: mutation. Only the synergic factorial effect of the cytostatic and antiproliferative differentiating multitherapy components of the DBM can counter the exponential proliferation of the neoplastic phenotype and its very high mutagenic ability, an extremely efficient defence system that is difficult to penetrate. It is necessary to act on critical elements of the neoplastic process such as differentiation by the simultaneous activation of multiple differentiating receptor targets like the VDR (Vit D3 nuclear receptors), RXR (retinoic acid nuclear receptor), RAR–alpha, beta, gamma (retinoic acid membrane receptors), and Mel-1,2 RZR/ROR (Melatonin membrane and nuclear receptors). At the same time it is necessary to eliminate the greatest possible variety and amount of energy from the neoplastic cell, represented by GH, GF, and PRL, and in hormone-dependent tumours by estrogens and androgens. This objective is achieved by inhibiting the incretion of hypophysial GH and the relative GF by means of SST and its analogues, and of PRL with Bromocriptine and/or Cabergoline. An extensive review of the relative literature (around 2000 papers) is included in the volume “The Di Bella Method” (Di Bella 2005). MLT has a particular, determining and multifunctional effect, negatively regulating angiogenesis by inhibiting an essential component, PDGF, and by regulating (with a homeostatic mechanism of serotoninergic modulation also made possible by its binding of hydrogen with adenosine) the rate of thrombocythemia, platelet aggregation (synergically to Alfa MSH), vasal tone and endothelial permeability (through modulation of EDRF and EDCF), essential factors for the release of PDGF.

Innovative therapeutic targets of the DBM also include the homeostasis of the environment in which the tumour cell lives, the physiological regulation of the cellular membrane potentials, the basal membranes, which have proven differentiating activity, the adhesion proteins, the layers restricting expansion of the tumour, the entire extracellular matrix, the trophism and efficiency of the parenchyma, tissues, and endothelia with relative re-establishment at physiological level of the vasal permeability, and of the blood-tissue exchanges and perfusion. The formulations, posology and doses of MLT and the vitamin components of the DBM also enhance immunity.

The aims of the DBM include physiological recovery of the circadian biological rhythms that are destroyed in tumours, by modulating the bioavailability of the pineal indoles in a context of temporal therapeutic continuity, in the sense of a continuous assault on a tumour cell already sensitized by the numerous differentiating agents and from which hormones and growth factors have also been eliminated, without (unlike chemotherapy cycles) allowing it pauses in which to recover, all supplemented by minimal apoptotic, non-cytotoxic and non-mutagenic doses of chemotherapy, made more tolerant by the MLT (Pacini 2009) and the vitamins contained in the DBM.




Basis of this retrospective observational study

Since the end of the 1970s, a growing number of tumour patients in Italy have chosen to be treated with the Di Bella Method (DBM), conceived and progressively refined and supplemented by Prof. Luigi Di Bella, a doctor and scientist with additional degrees in chemistry and pharmacology, and a university lecturer in general physiology, human physiology and biochemistry, preferring this method to chemotherapy. The tolerability of this method and the positive results in terms of survival and quality of life led to an increasingly widespread use of the DBM (practised by thousands of patients), creating serious disputes between public opinion and health institutions, which tried to evade the growing request for the DBM to be made available free-of-charge with a phase II trial, the planning, conduction and conclusion of which were the cause of harsh criticism and discomposure, not only in public opinion but also among politicians, doctors and the media, up to the point of investigations by magistrates. The irregularities of this trial were also the subject of more than fifty parliamentary questions, published in the Official Gazette of the Italian Parliament. Regardless of the numerous and serious irregularities that were documented and also reported in the international literature, the Italian Institute of Health, which is responsible for medical trials, claimed that: «It was necessary to carry out a study without a control group since, in the situation that existed at the start of 1998, this was not conceivable...».

It was not conceivable to carry out this type of study which is generally performed throughout the world, and also in Italy (but not for the DBM!?).

This reasoning does not hold up: in fact, when the DBM trial was published in the British Medical Journal, the editor, Marcus Muller, strongly criticised the design of the study (a very unusual occurrence), claiming that: The authors (of the trial report) state also that they would not have been able to perform a randomised clinical study for ethical reasons, but these reasons are not clear. In actual fact, it could be claimed that it was precisely the poor planning of the study that was anti-ethical.

And as regards the lack of a control group, this is what the researcher, Rey M.D., had to say in a letter to the B.M.J.: «What was the Di Bella treatment compared to? Nothing! It would have been much more useful to compare the Di Bella treatment and conventional treatment». As we can see, the study design was considered to be poor, since two fundamental characteristics which give a study scientific proof were missing, i.e. randomisation and a control group.

The definitive denial of the conclusions reached by this study is further confirmed by the increasing number of reports in the literature on the antitumoural efficacy of the active ingredients of the DBM (somatostatin, retinoids, vitamin D3, Melatonin, etc.), declared to be ineffective by the trial.

The numerous and serious irregularities of this trial include:

Those responsible for the trial were tried but not charged as it was thought that the numerous and serious irregularities, not denied by the magistrates, were not due to criminal intent but to the hurried design of the trial, under the pressure of public opinion. The fact remains, and was not denied by the magistrates, that these irregularities deprived the trial of all scientific significance and clinical indications. They were denounced not only by the 50 parliamentary questions (reported in the Official Gazette of the Italian Republic) but also by the Italian press and television. They are fully documented in the book by Vincenzo BrancatisanoUn po’ di verità sulla cura Di Bella“ (A bit of truth about the Di Bella treatment), Ed Travel Factory, 1999. An analysis of the entire design, conduction and conclusion of the trial, supported by original documents, ministerial reports, findings and checks is published in the monograph “Il Metodo Di Bella”, Mattioli Editore, 3rd Edition, 2005 by the undersigned. This documentation totally delegitimises the trial.

I believe that this somewhat lengthy introduction was necessary because the objection could be raised that the trial in Italy in 1998 declared the DBM to be ineffective, and to explain the reasons that led to the first spontaneous, retrospective observational clinical study in Italy, set up solely as a result of public initiative to contest the results of the trial and vindicate freedom of choice for treatment. Thousands of patients in Italy have presented appeals to the magistrates for the right to receive the Di Bella treatment free-of-charge, and many still continue to present such appeals. Following the trial, more than two thousand rulings ordered the Italian Health Service to provide the DBM, on the basis of sworn experts’ reports which certified the positive effects of the treatment in patients in whom chemotherapy and/or monoclonal antibodies had proved ineffective. We believe this should be pointed out, not only for its social importance, and the total lack of precedents, but also for the considerable amount of scientific and clinical data that has emerged.

We now report the data relative to 124 oncological patients examined by three doctors, appointed as “Technical Experts” by the Public Prosecutor’s Office of Lecce, while another 104 cases are already present in the literature and reported in journals reviewed by Med-Line. Other cases, approximately 325, divided into homogeneous groups according to disease, will be published on when the statistics are complete.

After the trial, in addition to the administrative appeals aimed at obtaining the drugs free-of-charge, many patients also spontaneously sent their clinical notes to the Public Prosecutor’s Office of Lecce which, being the first to order the Health Service to provide the DBM, had become a reference point. The technical experts divided the cases as follows:

  1. Patients who presented appeals to the Public Prosecutor’s Office of Lecce to obtain the treatment;
  2. Patients who, angry about the evident and serious irregularities of the trial, had spontaneously sent their clinical notes to the Public Prosecutor’s Office of Lecce to document the positive effects obtained with the DBM.

The difference between the two groups was above all the fact that group A, the great majority, consisted of patients wanting to try the DBM after the failure of chemotherapy, while in the second group, apart from a few exceptions, the patients had chosen the DBM as their first line therapy. This explains the appropriateness, for a realistic and reliable assessment of the DBM, of evaluating only group B, not “contaminated” by previous chemotherapy.

The report of the ruling issued by the Court of Lecce indicates an observation period which lasted for several years. Of the initial 126 cases, two died during treatment and 124 were monitored for more than 3 years, with a significant percentage of patients observed for more than 5 years. An analysis of the clinical records and the reports by the doctors who treated the 124 patients in group B provided the following data:





Overall results: Leukemia and Lymphoma


Overall results: Breast Cancer


Overall results: Brain Cancer


Overall results: Pancreas Cancer


Overall results: Lung Caner


Overall results: It was also possible to measure the data on the quality of life of these 124 patients!





The conclusions and reports of the 3 experts of the Court of Lecce on the total number of fully documented cases led to a clear declaration of efficacy and tolerability of the DBM.

On the basis of these sworn reports, the Magistrate declared that:

The considerable amount of clinical documentation acquired during these proceedings unquestionably show that many patients, not included in the trial, have obtained positive results with the DBM, not only as regards an improvement in quality of life, but also in terms of blocking or regression of the disease.

The reports by doctors, patients and relatives of patients on the total or partial recovery of health following application of the Di Bella treatment (..and) the technical experts’ reports (…show that) all (the patients) had an improvement in their quality of life (…) and are having positive results thanks to the considerable extension in survival with respect to the initial unfavourable short-term prognosis (just a few weeks of life).

In conclusion, the DBM seems to have determined an improvement in the quality of life in most of the treated cases. No side effects of the DBM have ever been noted.

We are not unaware of the contrast between the results of the technical experts and the conclusions of the official trial (...). The improvement in the conditions of life of the tumour patients as a result of taking the drugs prescribed by the DBM is a fact that is more than sufficient to justify the administration of this treatment, and this is related to protection of the absolute legal right to health, referred to in Art. 32 of the Constitution, which would otherwise be seriously and irreparably compromised.

These conclusions of a magistrate, based on clinical reports, witness statements and data validated by sworn experts‘ reports, are scientifically significant and merit careful and detailed examination. They are in radical contrast to and belie the conclusions of the DBM trial, the irregularities of which and the completely unreliable design, conduction and conclusions are by now well known and fully documented.

Adding the following data to these 124 cases certified by the experts of the Court of Lecce provides an overall picture of the statistics:


Number of cases: Pathologies:
23 Non-Hodgkin’s lymphoma
26 Breast cancer
2 Small cell lung cancer
1 Osteogenic sarcoma
1 Pleural mesothelioma
1 Brain tumour


Reports on the results of the DBM presented at the 1st and 2nd National DBM Conferences, at the Conference on Biological treatment of neoplastic and degenerative diseases and at the 95th National Conference (or this pdf version High Resolution, approx. 170MB!) of the SIO (Italian Society of Otorhinolaringology), Turin 2008:


Number of cases: Pathologies:
78 Lung cancer
13 Pleural mesothelioma
6 Non-Hodgkin’s lymphoma
3 Gastric cancer
2 Metastatic breast cancer
2 Adenocarcinoma of the pancreas
2 Rectal colon cancer
2 Sarcoma
1 Multiple myeloma
1 Astrocytoma
1 Mucinous adenocarcinoma of the ovary
1 Metastatic adenocarcinoma of the sigmoid colon
1 Cholangiocellular adenocarcinoma
1 Hepatocarcinoma
1 Ovarian cancer
1 Multiple adenomatosis of the liver
1 Leiomyosarcoma
1 Cancer of the larynx
1 Pleomorphic liposarcoma
1 Gastric lymphoma
1 Non-small-cell pulmonary adenocarcinoma
1 Epidermoid lung cancer
1 Hepato-pancreatic cancer
1 Pleuropulmonary undifferentiated cancer
1 Breast cancer


Number of cases:   
28 Non-Small-Cell lung cancer
46 Small-Cell lung cancer
17 Pancreatic cancer
6 Breast cancer
4 Metastatic breast cancer
10 Non-Hodgkin’s lymphoma
4 Exocrine pancreatic cancer
3 Sarcoma
1 Multiple myeloma
1 Chronic lymphatic leukemia
1 Anaplastic lung cancer
1 Hepatocarcinoma
1 Breast cancer with pulmonary disssemination



A series of data can be pointed out that, albeit with different frequencies, times, methods and intensity in the various types of tumour, are common or relatively frequent findings.



The number of clinical cases monitored, the period of observation, which in many cases was more than five years, and the great variety of neoplastic histotypes make it possible to draw preliminary conclusions limited to the median survival rates, the quality of life and the tolerability of the DBM. We consider these data as preliminary, even though they are documented, since they are the results of a retrospective observational study and because the division into homogeneous diseases and the statistical processing of the objective responses of the individual diseases are still in progress, although close to publication. We do point out, however, that the National Cancer Institute puts survival of the tumour patient in first place and quality of life in second place in the objectives of a clinical study. These data are not, therefore, without dignity and scientific importance.

A review of the overall statistics shows and evident uniformity of data relative to median survival and quality of life. The results published in the proceedings of the 4 conferences, in Italian journals (not reviewed by Med Line), international journals reviewed in Med Line, and of the case series certified by the Court of Lecce are substantially identical.

In all the tumours treated with the DBM, albeit with important differences between them, a net increase can be seen in life expectation and an improvement in quality of life, without any significant toxicity compared with the data in the literature relative to the same types of tumour and at the same stages.

It is clearly demonstrated that the response to the DBM is directly proportional to the timeliness of the treatment and inversely proportional to the number and intensity of chemo-radiotherapy sessions carried out.

If the DBM precedes such treatment, recurrences are a much rarer event compared with the data in the literature.

We believe that a comparison of the documented scientific bases, the linear and mathematical logic of the rationale of the DBM, and the significant results with the severe and known limits of the current antitumoural treatments can lead to a greater interest in the prospects opened up by the DBM. A tumour is a deviation from normal life, which can be corrected by the DBM, supporting and enhancing vital reactions. The Di Bella Method is not, therefore, an "alternative", in the common meaning of the term, but a rational integration and the convergence of definitively acquired medical-scientific knowledge and emerging scientific evidence in clinical medicine liberated from political-financial contamination.


The Di Bella Method (DBM)


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