Lithium has anticancer effects.

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Lithium is a drug used to reduce the severity of various mood disorders such as bipolar depression, mania, and schizoaffective disorder. Several retrospective studies have shown that psychiatric patients undergoing lithium therapy for bipolar disorder have a lower incidence of cancer than those not receiving the lithium therapy in a matched group. 

One piece of experimental evidence for lithium’s potential as a cancer therapeutic modality is that it has been observed to inhibit prostate tumor growth, presumably through its ability to inhibit glycogen synthase kinase (GSK3), in both cell line studies and animal models. 

With respect to other cancers, lithium has been found to selectively kill neuroblastoma cells over normally differentiated neurons. A similar effect was achieved in a similar study involving ovarian cancer cells; however, the results were inconsistent when the experiment was repeated. The disparity between the two studies has not yet been resolved. 

With respect to colorectal cancers, one study suggested that lithium inhibits proliferation of colorectal cancer cells, while another one showed that lithium specifically induced a reversal of the epithelial-to-mesenchymal transition characteristic of colon cancer cells. 

Lithium therapy is usually systemic rather than topical or local; therefore, it has been suggested that it might inhibit metastasis in the entire body. Evidence supporting this hypothesis this is that lithium inhibits metastasis-inducing factors in colon cancer cell lines and reduces metastasis in animal models. 

In addition, lithium has been shown to induce autophagy by inhibiting inositol monophosphatase. Autophagy is a key cellular process in decelerating cancer growth and maintaining homeostasis. The full range of lithium effects on autophagy is complicated, as expected, due to multiple targets within the organism, which further have multiple substrates. A statistical study on correlating the interactomes of lithium-sensitive enzymes with cellular pathways implicated in cancer illustrated a mutual enrichment among them. This study also showed secondary lithium sensitivity to already known cancer-related genes and highlighted new possible targets. 

The evidence above suggests that lithium may significantly inhibit cancer occurrence and progress. Our primary goal is to develop a logically coherent collection and bring together evidence and logical arguments relevant to understanding the relationship between lithium intake and cancer as a foundation for possible lithium therapy. As with all cancer research, fundamental advances in the basic biology of cell differentiation, cell duplication, and apoptosis must go hand in hand with advances in cancer therapy. 

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