Insulin and insulin-like growth factor-1 (IGF-1) have been identified as autocrine and/or paracrine growth factors in human breast cancer cells [2ó4]. We administer pharmacological doses of insulin to manipulate membrane and metabolic activities of these endogenous growth-promoting mechanisms, thereby potentiating anticancer drug effects. Drug potentiation results from an insulin-induced increase in the transmembrane passage of anticancer drugs in human breast cancer cells [5, 6], and a recruitment of cell populations into S-phase of the replicative cycle by cross-reaction of insulin with IGF-1 receptors . The cell-killing effects of anticancer drugs, particularly the chemotherapy agents specific for cell cycle phase, are greatly augmented . Therefore, ideal pharmacokinetic circumstances for the chemotherapy of breast cancer are created. As well as improved efficacy, this regimen increases safety because of lower total doses administered and reduced side-effects.
Chemohormonal therapy with oestrogen has shown promising results in preliminary trials . However, insulin and chemotherapy is more efficacious, as not only can insulin mimic oestrogenís cell-recruiting effects in oestrogen receptor positive human breast cancer cells , but insulin also stimulates recruitment in oestrogen receptor negative cells. Unlike oestrogen, insulin can increase the transmembrane passage and intracellular accumulation of anticancer drugs. The administration of low-dose anticancer drug therapy with insulin can produce complete and long-term regression of tumour masses in treated subjects. Therapy is tolerated without adverse effect and in our case produced excellent cosmetic results.