Management of thyroid carcinoma relies upon the tumour cells maintaining th
e differentiated functions that are typical of normal thyroid follicular ce
lls, such as: dependence upon thyrotropin for growth, production of thyrogl
obulin and effective transport of iodine. Likewise, differentiated thyroid
carcinomas often exhibit an auspicious clinical behaviour with a slow rate
of growth and low potential for invasion and distant metastasis. These feat
ures permit therapy of disseminated tumour, effective follow-up surveillanc
e and the assumption of a good prognosis. As each of these features are los
t, the opportunities for both disease status assessment and therapeutic int
ervention diminish accordingly. A major obstacle is our failure to define e
ffective systemic treatments to replace radioiodine therapy, whose loss is
consonant with the loss of iodine transport and retention. The extreme of u
ndifferentiated clinical behaviour is epitomized by anaplastic thyroid carc
inoma, a rare, terminally dedifferentiated malignancy that is rapidly and i
nvariably fatal. It is important to be attuned to clinical clues suggesting
the presence of dedifferentiated tumour and related prognostic signs. This
allows the application of currently limited therapeutic options and define
s the need for research to develop new systemic treatments.