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Updated: Feb 21, 2026
Spontaneous Murine Model of Anaplastic Thyroid Cancer
Published on: February 3, 2023
cMYC expression in thyroid follicular cell-derived carcinomas: a role in thyroid tumorigenesis
Hany I Sakr1, Deborah J Chute1, Christian Nasr2
1Cleveland Clinic, Department of Pathology and Laboratory Medicine, 9500 Euclid Avenue, L25, Cleveland, OH, 44195, USA.
Background:
cMYC 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.
Methods:
Immunohistochemical 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.
Results:
cMYC 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 BRAF V600E 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.
Conclusions:
Our 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.
Insights
Overexpression of nuclear cMYC (myelocytomatosis oncogene) is linked to dedifferentiation in thyroid cancers. This study clarifies cMYC expression patterns in various thyroid carcinomas, revealing its role in tumor progression.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- cMYC is a key regulator of human genes, implicated in a significant portion of human cancers.
- Existing literature presents conflicting data regarding cMYC protein expression patterns in thyroid carcinomas.
- Understanding cMYC's role is crucial for differentiating thyroid cancer subtypes and progression.
Purpose of the Study:
- To elucidate cMYC expression patterns and intensity in follicular cell-derived thyroid carcinomas.
- To correlate cMYC expression with BRAFV600E mutation status.
- To investigate the potential role of cMYC in the dedifferentiation of well-differentiated thyroid carcinomas.
Main Methods:
- Immunohistochemistry (IHC) was employed to detect cMYC and BRAFV600E protein expression.
- Tissue microarrays and whole tissue sections from various thyroid carcinoma subtypes (papillary, follicular, oncocytic, undifferentiated) were analyzed.
- Nodular hyperplasia served as a non-neoplastic control group.
Main Results:
- cMYC exhibited predominantly nuclear localization in both neoplastic and hyperplastic thyroid tissues.
- Weak cMYC expression was observed in nodular hyperplasias and well-differentiated carcinomas.
- Strong nuclear cMYC positivity was prevalent in undifferentiated carcinomas (UDCs), correlating with tumor size and dedifferentiation from well-differentiated precursors.
Conclusions:
- Nuclear overexpression of cMYC is associated with tumorigenesis and dedifferentiation in follicular cell-derived thyroid carcinomas.
- This finding provides novel insights into the role of cMYC in thyroid cancer progression, particularly in the transition to less differentiated forms.
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