Background: The incidence and mortality rates of cancer in patients with Bipolar Disorder (BD) is higher
compared with the general population. The role of Lithium (Li) in cancer proliferation/inhibition is still a controversial
issue in the literature.
Objective: Based on a clinical case with lithium intake and development of a renal tumor, we aimed to explore the
relationship between Li use and tumor proliferation, with regard to the mechanism of action of Li.
Method: We present evidence of a female patient with bipolar disorder I, who had been on Li for several years, either
as monotherapy or in combination with Valproate (VPA). While on Li monotherapy, the patient had undergone unilateral
nephrectomy due to a chromophobe cell renal tumor. A literature search was performed using keywords
bipolar disorder, medical comorbidity, cancer, renal tumor, lithium, mood stabilizers, valproate and mechanism of
Results: The limited data on the relationship between Li and cancer proliferation in clinical populations support
neither a positive relationship between long-term Li use and increased urinary tract cancers nor an overall cancer
risk. Growing evidence identifies effects of Li on cancer proliferation through inhibition of glycogen synthase
kinase-3β (GSK-3β), modulations of redox status, inflammatory changes, pro-/anti-apoptotic mechanisms, and mitochondrial
Conclusion: Despite the presence of contradictory data, a substantial body of evidence mainly from molecular studies
points to Li’s anti-carcinogenic effects. However, the underlying mechanistic pathways remain unclear. Mitochondrial
dysfunction and redox modulations are potential areas for research on the relationship between Li and