Clinical and Pathological Implications of Concurrent Autoimmune Thyroid Disorders and Papillary Thyroid Cancer
Figure 3
Putative links between RET/PTC rearrangement and concurrent thyroid inflammation. (a) RET/PTC could drive expression of several proinflammatory molecules that may elicit concurrent inflammation. Another possibility (b) is inflammation propitiating RET/PTC rearrangement. Inflammation produces reactive oxygen species and free radicals that may facilitate DNA damage and chromosomal abnormities, like RET/PTC rearrangement. (c) Molecules released by inflammation could sustain the survival of thyroid cells in which RET/PTC rearrangements randomly occur, thereby allowing the selection of clones that acquire additional genetic lesions and thus become resistant to oncogene-induced apoptosis.
