Results and Conclusion
Taurolidine induces cancer cell death through a variety of mechanisms. Even now, all the antineoplastic pathways it employs
are not completely elucidated. It has been shown to enhance apoptosis, inhibit angiogenesis, reduce tumor adherence, downregulate
proinflammatory cytokine release, and stimulate anticancer immune regulation following surgical trauma. Apoptosis is activated
through both a mitochondrial cytochrome-c-dependent mechanism and an extrinsic direct pathway. A lot of in vitro and animal
data support taurolidine’s tumoricidal action. Taurolidine has been used as an antimicrobial agent in the clinical setting
since the 1970s and thus far appears nontoxic. The nontoxic nature of taurolidine makes it a favorable option compared with
current chemotherapeutic regimens. Few published clinical studies exist evaluating the role of taurolidine as a chemotherapeutic
agent. The literature lacks a gold-standard level 1 randomized clinical trial to evaluate taurolidine’s potential antineoplastic
benefits. However, these trials are currently underway. Such randomized control studies are vital to clarify the role of taurolidine
in modern cancer treatment.