Abstract
BackgroundAdrenocortical carcinoma (ACC) is a rare but highly malignant neoplasm with limited treatment options.MethodsIn this study, the clinicopathological features of 22 ACCs and 22 adrenocortical adenomas (ACA) were analyzed, and the EGFR protein expression, EGFR gene mutation status and EGFR gene copy number alteration of all tumors were examined using immunohistochemistry, fluorescence in situ hybridization (FISH), and the Scorpion Amplification Refractory Mutation System (ARMS), respectively.ResultsEGFR protein expression was detected in 63.6% of the ACC samples, and EGFR FISH was positive in 50% of the ACC samples (all were high polysomy on chromosome 7). In contrast, 27.3% of the ACA samples demonstrated EGFR expression, and none of the ACA samples tested positive by FISH. There were significant differences between the ACC and ACA in terms of protein expression (P = 0.035) and gene copy number alterations (P < 0.001).ConclusionsEGFR protein expression and high polysomy on chromosome 7 are frequent abnormalities in ACC than in ACA.Virtual slidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/2068470757103500.
Highlights
Adrenocortical carcinoma (ACC) is a rare but highly malignant neoplasm with limited treatment options
We have found that epidermal growth factor receptor (EGFR) protein expression was more frequent in myxoid ACC than in myxoid adrenocortical adenomas (ACA) [17]
We have investigated EGFR protein expression, EGFR mutations, and EGFR gene copy number variations in adrenocortical neoplasms, in 22 conventional ACC cases and 22 conventional ACA cases
Summary
Adrenocortical carcinoma (ACC) is a rare but highly malignant neoplasm with limited treatment options. The vast majority of these tumors are benign adrenocortical adenomas (ACA), and only a small subset constitutes malignant adrenocortical carcinomas (ACC) [2]. These tumor entities are discriminated according to gross and microscopic criteria, such as the Weiss score [3]. EGFR belongs to the ErbB family of tyrosine kinase receptors, which have strong regulatory effects on cell proliferation, differentiation, survival, and migration [7]. Treatment with the monoclonal anti-EGFR antibody cetuximab and the EGFR tyrosine kinase inhibitor erlotinib (in monotherapy or in combination with cytotoxic drugs) has resulted in improved survival in patients with colorectal cancer and non-small-cell lung cancer [10,11]
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