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Slowing Down Metastatic Thyroid Cancer

Conquest - Fall 2008

Videographer/editor: Deborah E. Thomas
Producer: Scott Merville
New Drug Active Against Advanced Thyroid Cancer

Thyroid cancer that has spread to distant sites has a poor prognosis. But an experimental drug that inhibits tumor blood vessel formation can slow disease progression in some patients, a research team led by M. D. Anderson investigators reports.

The investigational drug, motesanib diphosphate, is a VEGF inhibitor, a biologic agent that targets receptors on a protein known as vascular endothelial growth factor. VEGF is instrumental in angiogenesis (formation of new blood vessels), a process that allows tumors to grow and spread.

Study lead author Steve Sherman, M.D., chair of M. D. Anderson’s Department of Endocrine Neoplasia and Hormonal Disorders, noted strong evidence that VEGF receptors play an important role in metastatic thyroid cancer, a disease with few treatment options.

“There’s no standard accepted chemotherapy for advanced metastatic differentiated thyroid cancer, and response rates have typically been 25% or less,” Sherman says. “Most patients are not treated with systemic chemotherapy because the limited benefit rarely justifies the side effects.”

Steve Sherman, M.D., chair of the Department of Endocrine Neoplasia and Hormonal Disorders, headed a study that may lead to improved treatments for patients with metastatic thyroid cancer

Sherman, colleagues in 10 countries and scientists from Amgen, which is developing motesanib diphosphate (AMG 706), planned and conducted one of the largest clinical trials ever done for metastatic thyroid cancer.

Of the 93 patients with rapidly progressing cancer who were enrolled in the study, 49% had a positive response. From that group 14% had their tumors shrink and 35% had their tumors stabilize for more than 24 weeks. Median progression-free survival was estimated to be 40 weeks.

Genetic analyses of 25 patients indicated that those with a specific mutation known as BRAF V600E in their tumors had a better response to motesanib diphosphate than did those without the mutation. Additional research is needed on this genetic connection, but the early results are a good start, Sherman says.

Reported in the July 3 issue of the New England Journal.

Conquest - Fall 2008

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