Targets Thymidylate Synthase and Oncogenic Ras Signaling in Ras Mutant Tumors
This combination strategy contains inhibitors and pharmaceutically acceptable excipients for the treatment of various forms of cancer, such as breast cancer, prostate cancer, brain cancer, or pancreatic cancer. Cancer is the second leading cause of death in the United States. As a result, the United States spends the most on cancer drugs worldwide, accounting for 42.2 percent of global spending in 2014. In the same year, the global market for cancer drugs hit $100 billion in annual sales, and is expected to reach $147 billion in annual sales by 2018. Although cancer treatment continues to make improvements, and cancer patients are living longer with treatment, more innovation is needed to better understand the disease and to more effectively treat patients. Researchers at the University of Florida have discovered a way to inhibit cancer growth by simultaneously targeting thymidylate synthase and oncogenic Ras signaling. Human thymidylate synthase is responsible for significantly accelerating the spread of cancer. This drug improvement has the potential to treat various forms of cancer by inhibiting cancer growth.
Combination strategy that inhibits cancer growth for the treatment of various forms of cancer
- Utilizes combination strategy, resulting in striking synergy in Ras mutant tumors
- Inhibits cancer growth, targeting thymidylate synthase and oncogenic Ras signaling
Simultaneously targeting human thymidylate synthase and oncogenic Ras signaling inhibits cancer growth. This combination strategy results in striking synergy in Ras mutant tumors. The combination of inhibitors and pharmaceutically acceptable excipients results in anti-tumor activity that is greater than that observed with either drug alone. Researchers at the University of Florida have discovered an improved method of treating various forms of cancer. Experimental results indicate that there are potential benefits in treating cancer patients that harbor mutant Ras and show overexpression of thymidylate synthase.