Dear Colleagues,

Thyroid carcinoma is the most common endocrine malignancy with a raising incidence in developed countries likely to be related to the greater use of imaging methods, although environmental causes cannot be excluded. Management of these incidentally discovered tumors is not consensual.

Depending on the cell of origin, thyroid carcinoma is further subdivided into follicular-cell derived or C-cell derived. The embryological origin and the enzymatic machinery of these two cell types are different with an impact on clinical presentation and therapeutic approach. Follicular cells are able to uptake iodine and synthesize thyroid hormones whereas C cells secrete calcitonin. On the other hand, follicular-cell derived carcinomas range from differentiated, the most frequent histological subtype, to poorly differentiated or even, more rarely, to undifferentiated.

Thyroid carcinoma has attracted the attention of several researchers for different reasons.

The first historical landmark, at the end of the 1940s, was the use of 131I for the treatment of well-differentiated metastatic carcinomas originating in the follicular epithelium. The rationale for its use was based on the knowledge that follicular cells had the potential to capture iodine. Since this is a specific property of this type of cell, we can say that 131I was probably one of the first targeted therapies to be used. So far, the 131I remains the adjuvant therapy of choice for patients with metastatic disease. However, issues such as appropriate use and dosage remain controversial.

Medullary thyroid carcinoma, the specific type arising from C-cells, can be familial in 25% of cases with an autosomal dominant mode of transmission. It is among the first cancers whose features were exploited for prevention. In 1993, the identification of germline mutations in the RET proto-oncogene as the underlying cause of familial medullary thyroid carcinoma made possible the genetic screening of affected families. Almost thirty years after starting prophylactic thyroidectomies guided by genetic screening, it would be interesting to reevaluate data with a focus on long term outcomes.

Despite a general good response to the standard treatment (surgery with or without 131I), a few cases have an aggressive behavior and are refractory to 131I or, as is the case for medullary thyroid carcinoma, are not candidates for this treatment. A better understanding of the genetic alterations and of the dysregulated pathways in thyroid cancer led to the use of targeted therapies. In the past 8 years tyrosine kinase inhibitors became the mainstay of treatment for these cases. Whom, When, and How to treat remain evolving questions.

The latest advance relates to the approval, in May 2018, by the Food and Drug Administration of dabrafenib and trametinib administered together for the treatment of anaplastic thyroid cancer with BRAF V600E mutation. The first reports suggest that this combination is a highly promising targeted therapy with a potential to transform the outcome of some patients with anaplastic thyroid carcinoma one of the most aggressive solid cancers.

We invite physicians and researchers with an interest in the field of thyroid cancer to share their results and views toward an integrative knowledge.

Dr. Maria João Bugalho
Guest Editor

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• radioiodine-refractory cancer
• sodium/iodide symporter
• targeted therapies
• familial forms
• undifferentiated cancer
• biomarkers
• genetics