Easing the brunt of thyroid cancer

The enzyme’s overexpression is often found in papillary thyroid cancers with BRAF^V600E mutations. It eventually leads to therapy resistance. 

These findings prompted researchers to dig deeper into the role CYP24A1 plays in aggravating the most common type of thyroid cancer. 

To learn how, Yufei Shi at King Faisal Specialized Hospital and Research Centre in Riyadh, Saudi Arabia, and his colleagues induced thyroid cancer in mice and tracked the effect of overexpressing Cyp24a1. The overexpression resulted in the activation of multiple signalling pathways and induced resistance to PLX4720, a BRAF^V600E inhibitor used for antitumor therapy. 

To confirm their findings, the authors removed Cyp24a1 from a group of mice carrying mutated Braf^V600E. Its deletion reduced thyroid cancer growth by fourfold. They also found that calcitriol, the active form of vitamin D, can enhance the effect of PLX4720. 

This makes Cyp24a1 a potentially good candidate for targeted cancer therapy, Shi says. “We are considering a trial to combine vitamin D and PLX4720 for thyroid cancer patients.” 

This can open the door for the use of Vitamin D as a supplement for cancer patients with elevated levels of Cyp24a1, not just thyroid cancer patients. Future research will be directed towards discovering drugs to inhibit its overexpression, the author says.

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