Thyroid Growth and XXXX .

@entity3557 @entity1 @entity8958 @entity1377 @entity5 @entity189 @entity105 @entity259
It is proposed that most @entity3557 originate in infancy and childhood, based on the early rise in sporadic @entity259 incidence, the pattern of radiation-induced risk (highest in those exposed as @entity1 ), and the high prevalence of sporadic @entity3557 in @entity1 and adolescents (ultrasound screening after the Fukushima accident). The early origin can be linked to the growth pattern of follicular cells, with a high mitotic rate in infancy falling to very low replacement levels in adult life. The cell of origin of @entity259 , the differentiated follicular cell, has a limited growth potential. Unlike @entity5 originating in stem cells, loss of the usually tight link between differentiation and replicative senescence is required for immortalisation. It is suggested that this loss distinguishes larger clinically significant @entity3557 from @entity3557 of little clinical significance. @entity105 can then be divided into 3 stages: (1) initiation, the first mutation in the carcinogenic cascade, for radiation-induced @entity3557 usually a @entity8958 rearrangement, (2) progression, acquisition of the additional mutations needed for low-grade malignancy, and (3) escape, further mutations giving immortality and a higher net growth rate. Most @entity3557 will not have achieved full immortality by adulthood, and remain as so-called micro- @entity189 with a very low growth rate. The use of the term ' @entity5 ' to describe @entity3557 in older @entity1 encourages overtreatment and alarms @entity1 . Invasive @entity3557 show a spectrum of malignancy, which at its lowest poses no threat to life. The treatment protocols and nomenclature for small @entity1377 need to be reconsidered in the light of the new evidence available, the continuing discovery of smaller lesions, and the model of @entity105 proposed.
