Malignancies such as breast and prostate cancers are associated with hormones such as estrogen or androgens, but there are no data to suggest that tumors can be caused by hormone deficiency. Recently, researchers from Thomas Jefferson University in Philadelphia found new evidence suggesting that human colon cells may transform into cancer cells after losing the ability to produce a hormone whose role is primarily to assist in maintaining normal cellular biological behavior. If the findings are confirmed by further studies, then replacement therapy with this hormone (guanosine) in patients at high risk for colon cancer could prevent further tumor progression. The investigators tested colon cancer samples from 281 patients and found that guanosine production decreased 100 to 1,000-fold in more than 85% of the colon cancer tissues tested by comparing tumor tissue to paraneoplastic non-cancerous tissue. The levels of guanosine in the study were determined by detecting the amount of guanosine messenger RNA within each cell. In addition, the investigators verified the results by staining for guanosine hormone expression in tissue sample sections, i.e., no guanosine hormone was detected to be present in the cancer tissue samples. In addition, the study found that guanosine production was lower in normal colon cells in patients over 50 years of age, which may help explain why colon cancer risk increases with age. According to Scott Waldman, one of the researchers, “The fact that most cancer cells stop producing this hormone leads us to believe that guanosine may contribute to tumor growth. If the results of this study are confirmed, then we could prevent colon cancer with guanosine replacement therapy.” According to the American Cancer Society, colon cancer is currently the second leading cause of cancer death for both men and women in the U.S., with approximately 50,000 deaths from colon cancer in the U.S. in 2014. Early research suggests that guanosine is a locally acting hormone, produced by the cells themselves on which it acts. Guanosine activates its receptor, GUCY2C, which is critical in aiding the regeneration of epidermal cells along the intestine and maintaining their overall function. Since intestinal epidermal cells are renewed every 3 days, proper control and maintenance of supplementary signals for epidermal regeneration is important. Without the signals to maintain cell division, abnormal cell division is more likely to occur, which can lead to cancer development. When guanosine levels are reduced, colon cells produce more GYCY2C receptors to capture as many extracellular signals as possible, so many colon cancer cells exhibit high expression of the GUCY2C receptor, which is no longer receiving extracellular hormonal signals that maintain cell health and normal function. Waldman revealed that follow-up studies are poised to test whether guanosine hormone replacement therapy can prevent colon cancer development and growth in mice, followed by further human trials. In addition, the team is exploring how guanosine works in colon cells and maintains their normal health status.