Follicular Thyroid Tumor

Thyroid tumors of follicular cell origin serve as a good model for studying possible genetic events regarding tumor origin, transformation, and progression. Multiple genetic events appear to be responsible for the progression from adenoma to carcinoma in some tumors (see Fig. 36-1).1,2,22,23 Follicular adenomas have close cytologic and morphologic similarity to follicular carcinomas; the defining difference is the presence of capsular invasion and/or vascular invasion in carcinomas. Because of this similarity, it has been proposed that follicular carcinomas originate from preexisting adenomas. Follicular adenomas could represent premalignant tumors that could transform into carcinomas, through copy number changes in critical genes controlling invasion, angiogenesis, and metastasis. Clinical evidence that follicular carcinomas are obviously larger than follicular adenomas supports this theory.

Hemmer and coworkers24 found that copy number changes were more frequent in follicular carcinomas (9 [69%] of 13) than in histologically benign follicular adenomas (14 [48%] of 29) using CGH. However, the average number of copy number changes was less in follicular carcinoma (1.6 changes per case, range 0 to 6) than in follicular adenoma (2.5 changes, range 0 to 12). On the other hand, Frisk and associates25 subsequently described that the frequency of aberrations was similar in follicular adenomas (8 adenomas, 1.9 changes/mean) and follicular carcinomas (13 carcinomas, 1.5 changes/mean), as well as in 8 minimally invasive follicular carcinomas (1.5 changes/mean) and 5 widely invasive follicular carcinomas (1.6 changes/mean). Hemmer and colleagues24 reported that a loss of chromosome 22 or 22q was particularly common in carcinomas (6 [46%] of 13) whereas a loss of chromosome 22 was found in only 2 (7%) of 29 adenomas. Moreover, loss of the chromosome 22 was present in 7 (54%) of the 13 widely invasive follicular carcinomas but in none of the 7 minimally invasive carcinomas (P = 0.04).10 Loss of chromosome 22 was also common in older than in younger patients (P = 0.01). A loss of lp was frequent in follicular carcinomas (20%), whereas gains in chromosomes 5, 7, 12, 14, and X were common in follicular adenomas but not found in follicular carcinomas.24 A DNA copy number loss was also common in 13q in follicular carcinomas (25%).10 The common regions for DNA copy number gain were in lq (25%) and in 17q (20%) for follicular carcinomas. Papillary carcinomas that also arise from follicular cells have fewer chromosomal aberrations, especially losses, than follicular carcinomas.10 One candidate for the tumor suppressor gene in chromosome 22q is neurofibromatosis type 2 (NF2) located at 22ql2, and there may be another putative suppressor gene distal to NF2. The significance of these and other suppressor genes located in 22q in the genesis of follicular carcinoma is currently unknown. Although formation of fusion genes PAX8-PPARyl caused by a t(2;3)(ql3;p25) has been observed in several cases of follicular carcinomas,26 unfortunately it is difficult to identify these chromosomal translocations using CGH.

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