Aside from cancer, it would also be interesting to see how triclosan may have affected a more dedicated inflammatory bowel disease (IBD) mouse model. The underlying etiology to explain IBD is not fully understood and there are some data to implicate a role for dietary and environmental factors. If this link were established in the IBD mouse model, evaluating whether or not triclosan placed those mice at even more risk of developing colorectal cancer would be important to determine.

Although much of the literature is dominated by the pro-oncogenic associations with triclosan, there are also scattered data to support the use of triclosan in treating certain types of cancer.  One example includes the use of triclosan in prostate cancer. As a fatty acid synthase inhibitor, triclosan has shown some anticancer effects in certain prostate cancer cell lines and has been shown to induce apoptosis in these prostate cancer cell lines.6

As more research is conducted on fatty acid synthase inhibitors in the future, triclosan will undoubtedly be evaluated in in vitro and animal models, at minimum. Triclosan has also been used to treat patients with cancer who develop radiation-induced oral mucositis.7 As these patients may have more “leaky” oral mucosa, it could be possible that more triclosan may be systemically absorbed. There are limited long-term follow-up studies looking at specific serum levels in this patient population, which would be needed to determine if the benefits of mucositis healing would outweigh any potential risks associated with long-term use.


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At this point, it is very difficult to discern the true oncogenic potential of triclosan. It is important to realize that much of the published data include in vitro and animal model data. More thorough clinical data in humans, both retrospective and prospective, is needed in the future to further clarify triclosan’s potential oncogenic properties.

References

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  2. Darbre PD. Environmental oestrogens, cosmetics and breast cancer. Best Pract Res Clin Endocrinol Metab. 2006;20(1):121-143.
  3. Gee RH, Charles A, Taylor N, et al. Oestrogenic and androgenic activity of triclosan in breast cancer cells. J Appl. Toxicol. 2008;28(1):78-91.
  4. Kim JY, Yi BR, Go RE, et al. Methoxychlor and triclosan stimulates ovarian cancer growth by regulating cell cycle-and apoptosis-related genes via an estrogen receptor-dependent pathway. Environ Toxicol Pharmacol. 2014;37(3):1264-1274.
  5. Yang H, Wang W, Romano KA, et al. A common antimicrobial additive increases colonic inflammation and colitis-associated colon tumorigenesis in mice. Sci Transl Med. 2018;10(443). doi: 10.1126/scitranslmed.aan4116
  6. Sadowski MC, Pouwer RH, Gunter JH, et al. The fatty acid synthase inhibitor triclosan: repurposing an anti-microbial agent for targeting prostate cancer.  Oncotarget. 2014;5(19):9362-9381.
  7. Satheeshkumar PS, Chamba MS, Balan A, et al. Effectiveness of triclosan in the management of radiation-induced oral mucositis: a randomized clinical trial. J Cancer Res Ther. 2010;6(4):466-472.