Endocrine Abstracts (2010) 22 P407

Expression of Ki-67, RET and p53 in papillary thyroid microcarcinomas with or without autoimmune thyroid diseases

Zsuzsanna Szanto1, Imre Zoltan Kun1, Simona Gurzu2, Janos Jung2 & Angela Borda2

1Endocrinology Clinic, UMPh, Targu Mures, Romania; 1Institute of Pathology, UMPh, Targu Mures, Romania.

Our objective was to investigate the expression of Ki-67, RET and p53 in papillary thyroid micro–carcinomas (PTMCs) with or without autoimmune thyroid diseases. We included in the study 36 patients thyroidectomized between 2002 2007 for benign or malignant thyroid lesions, registered at Endocrinology Clinic and/or Institute of Pathology Targu Mureş, at whom the histology diagnosed PTMC. This cohort was divided into two groups: 19 PTMCs only and 17 PTMCs associated with Hashimoto’s disease. All cases were analysed immunohistochemically for Ki-67, RET and p53. Our results showed that PTMCs expressed Ki-67 two-times more frequent in cases without autoimmune thyroid disease (52% versus 23.5%), indicating a higher proliferative activity. Similarly, PTMCs harboring potential risk to transform into clinical overt forms showed a 4-times higher proliferative activity in absence of thyroid autoimmunity (54.5% versus 12.5%). 69.4% of PTMCs were immunomarked with RET. PTMCs associated with Hashimoto’s thyroiditis expressed RET more frequent and with greater intensity than those without this autoimmune disease (88.2% versus 52.6%). In PTMCs associated with extensive chronic auto-immune thyroiditis the dense inflammatory infiltration was situated mainly around the malignant microlesions. In RET-positive microcarcinomas coexisting with autoimmune thyroiditis, malignant thyrocytes were intensively marked with RET if they were surrounded by lymphocytic infiltration. We did not obtain considerable differences in p53-immunoreactivity between the two studied groups.

Chronic autoimmune thyroiditis associated with thyroid microcarcinomas might be a defense reaction, arising when normal thyrocytes transform into pre–cancerous/cancerous cells. When PTMCs have already developed, autoimmune thyroid phenomena seem to have a protective role againts progression towards clinical overt PTCs, reducing proliferative activity and spread of tumor cells. This inter-pre-tation is in concordance with clinical studies that sustain an improved disease-free survival if autoimmune thyroid diseases are associated.

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