Abstract
BackgroundcMYC regulates approximately 15% of human genes and is involved in up to 20% of all human cancers. Reports discussing cMYC protein expression in thyroid carcinomas are limited, with controversies pertaining to cMYC expression patterns noted in the literature. The aims of the current study were to clarify patterns and intensities of cMYC expression in follicular cell-derived thyroid carcinomas across a spectrum of cancer morphologies and disease aggressivities, to correlate cMYC with BRAFV600E expression, and to evaluate the potential role of cMYC in progression of well-differentiated thyroid carcinomas into less well-differentiated carcinomas.MethodsImmunohistochemical studies using specific monoclonal antibodies for cMYC and BRAFV600E were performed on tissue microarrays built from follicular cell-derived thyroid carcinomas (25 papillary, 24 follicular, 24 oncocytic variant of follicular, and 21 undifferentiated). In addition, cMYC IHC testing was also performed on whole tissue tumor sections from a subset of patients. Nodular hyperplasia cases were used as non-neoplastic controls. Appropriate positive and negative controls were included.ResultscMYC was expressed almost exclusively in a nuclear fashion in both thyroid carcinomas and nodular hyperplasias. cMYC expression was weakly positive in both nodular hyperplasias and well-differentiated carcinomas. The majority of undifferentiated carcinomas (UDCs) showed strong nuclear cMYC positivity. PTC cases that were positive for cMYC (6/25) harbored the BRAFV600E mutation. A correlation was confirmed between cMYC intensity and tumor size in UDCs. UDC cases that developed out of well-differentiated thyroid carcinomas showed frank overexpression of cMYC in the undifferentiated tumor components.ConclusionsOur study suggests that nuclear overexpression of cMYC correlates with tumorigenesis / dedifferentiation in follicular cell derived thyroid carcinomas, a concept that has not been shown before on whole tissue sections.
Highlights
CMYC regulates approximately 15% of human genes and is involved in up to 20% of all human cancers
In summary, we demonstrated a nuclear staining pattern of cMYC IHC in tissue microarray (TMA) of follicular cell-derived thyroid carcinomas. cMYC expression in undifferentiated thyroid carcinomas was statistically significantly greater than in nodular hyperplasia (NH) and well-differentiated carcinomas. cMYC positivity was identified in undifferentiated carcinoma (UDC) cases (16/21, 76%) with strong positivity in more than half (57%) of all UDC cases
UDC cases that developed in association with or out of well-differentiated thyroid carcinomas showed frank overexpression of cMYC upon dedifferentiation
Summary
CMYC regulates approximately 15% of human genes and is involved in up to 20% of all human cancers. The aims of the current study were to clarify patterns and intensities of cMYC expression in follicular cell-derived thyroid carcinomas across a spectrum of cancer morphologies and disease aggressivities, to correlate cMYC with BRAFV600E expression, and to evaluate the potential role of cMYC in progression of well-differentiated thyroid carcinomas into less well-differentiated carcinomas. We utilized IHC for cMYC in a tissue microarray (TMA) study performed on a spectrum of follicular cell-derived thyroid carcinomas, including papillary (n = 25), follicular (n = 25), oncocytic variant of follicular (n = 25), and undifferentiated (n = 22) carcinomas. Aims of this study were to further clarify patterns of cMYC expression in thyroid carcinomas across the spectrum of morphology and disease aggressivity, to evaluate potential cMYC diagnostic usefulness, to find a correlation (if any) between cMYC and BRAFV600E expression in thyroid carcinomas, and to determine the extent to which cMYC may contribute to carcinogenesis
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