Cancer Treatment Today

About 25% of undifferentiated thyroid cancers have BRAF mutations, and this proportion is probably higher in tumors with documented evidence of progression from a pre-existing well-differentiated PTC. In the latter case, the BRAF mutation is present in both components of the tumor–well-differentiated and undifferentiated–suggesting a role for oncogenic BRAF in disease progression. What to do about those mutations is not clear. At least two clinical trials of multikinase inhibitors with strong activity against RAF (BAY 43-9006, Bayer Health Care, West Haven, CT and AMG706, Amgen, Thousand Oaks, CA) are ongoing in differentiated thyroid cancer. The results of these studies should pave the way for a new era in thyroid cancer therapy, in which the genetic basis of tumor development is used to tailor the best treatment for each patient. A recent phase II trial evaluated patients with differentiated (n = 27), medullary (n = 1), and poorly differentiated (n = 2) thyroid cancers treated with sorafenib (400 mg twice daily), a drug that affects BRAF. Twenty-three percent had a partial response and 53% had stable disease, with an overall median progression-free survival duration of 79 weeks.

Clear Decision:

Was BRAF testing (81210) performed on 02/23/15 medically necessary for the treatment of this member’s condition?

No. Targeting BRAF in thyroid cancer is experimental at this time.

References

Mark Yarchoan, RAF Mutation and Thyroid Cancer Recurrence. JCO November 24, 2014JCO.2014.59.3657

Elisei R, et al.  (2012) The BRAF(V600E) mutation is an independent, poor prognostic factor for the outcome of patients with low-risk intrathyroid papillary thyroid carcinoma: Single-institution results from a large cohort study. J Clin Endocrinol Metab 97:4390–4398

Gupta-Abramson V. Phase II trial of sorafenib in advanced thyroid cancer. J Clin Oncol 2008;26:4714-4719.