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The estimate of new cancer cases reached 18.1 million worldwide in 2018 [1], with a constantly growing trend that needs to be contrasted by efficacious (chemo) preventive strategies able to counteract the dreadful global burden of this disease [2]. Several preclinical, epidemiological and clinical studies proposed nonsteroidal anti-inflammatory drugs (NSAIDs) as one of the most promising class of compounds for the prevention of different cancer types, including mammary tumors [3], even if their use in long-term treatment is limited by side effects due to cyclooxygenase (COX) inhibition. Recently, we identified SIRT1 as a novel target for NSAID chemopreventive activity, independent from COX [4]. SIRT1 is the mammalian homolog of yeast silent information regulator 2 (Sir2), member of the NAD+-dependent class III histone deacetylases. SIRT1 deacetylates various protein substrates including histones, DNA-repair, intracellular signaling and transcription factors; because of this pleiotropic action, SIRT1 has been implicated in the regulation of several biological processes related with cancer such as energetic metabolism, proliferation, inflammation, apoptosis and hypoxia [5]. Our work demonstrated that NSAIDs with different chemical structures can directly interact with the enzyme and inhibit its deacetylase activity. Because of the SIRT1 inhibition, the oncosuppressor p53/P21 pathway is activated and counteracts the cell hyperproliferation occurring during initial tumorigenesis steps in preclinical breast cancer models and in patients [4]. Although several studies reported a controversial role for SIRT1 inhibition in tumorigenesis, a recent phase III clinical trial investigating the effects of nicotinamide (vitamin B3, the physiological inhibitor of SIRT1) in non-melanoma skin cancer demonstrated the ability of this vitamin to reduce the rates of new tumorigenic events in high-risk patients characterized by immunosuppression and DNA repair defect. In these patients, nicotinamide administration increased the level of pro-inflammatory cytokines and stimulated DNA repair, thus significantly reducing the risk of tumor onset [6]. This clinical result, substantiated by several preclinical studies [7], points to SIRT1 inhibition as a potential strategy for cancer prevention using a candidate drug of natural origin, nicotinamide, particularly attractive for a non-toxic, cheap chemopreventive treatment. Editorial

Nicotinamide in the prevention of breast cancer recurrences?