Context.— Melanotic neuroectodermal tumor of infancy, albeit rare and generally regarded as benign, is an important tumor to recognize because of its rapid growth, potential for local recurrence, and small round blue cell morphology, which can lead to misdiagnosis of a malignant neoplasm. Objective.— To review its clinical presentation and immunomorphologic findings, and discuss common entities in the differential diagnosis. Data Sources.— The study involved PubMed searches, including multiple review articles, case studies, retrospective studies, selected book chapters, and University of Michigan cases. Conclusions.— Melanotic neuroectodermal tumor of infancy most commonly occurs in the bones of the head and neck region during the first year of life, but it can also present in other locations, including the central nervous system, testes, ovaries, and subcutaneous soft tissues. Histologically, it is composed of a biphasic population of cells, consisting of epithelioid melanin-producing cells and primitive neurogenic cells in a fibrocollagenous stroma. These microscopic findings, especially in small biopsies, can lead to a broad differential diagnosis that includes malignant small round blue cell tumors and malignant melanoma. Melanotic neuroectodermal tumor of infancy commonly has an infiltrative growth pattern, and anatomic constraints often lead to incomplete resection and local recurrence, requiring multiple surgical operations. Because melanotic neuroectodermal tumor of infancy can mimic a more aggressive and aggressively treated malignancy, recognition of this rare tumor is very crucial for pathologists.

Introduction The rate of malignancy (ROM) in thyroid fine needle aspirations (FNA) classified under “atypia of undetermined significance (AUS)/follicular lesion of undetermined significance (FLUS), including Hürthle cell type (HLUS)” category of The Bethesda system for reporting thyroid cytopathology (TBSRTC) in literature is highly variable. The 2018 TBSRTC was updated to note a preferred categorization of AUS cases into subcategories. This study evaluates the impact of AUS subclassification on rates of neoplasia (RON), rates of malignancy (ROM), and cytopathologist (CP) concordance. Methods 93 thyroid FNAs previously diagnosed as FLUS or HLUS from January 1, 2013 to December 31, 2014 with subsequent surgical resection were identified. Four CPs reclassified these cases using TBSRTC AUS subcategories of follicular cells with architectural and/or cytologic atypia, predominantly Hürthle cells, and atypical lymphocytes. RON and ROM were calculated for each diagnostic subcategory for each CP. Results The original RON and ROM for FLUS cases were 31.4% and 15.1% and were 77.8% and 22.2% for HLUS cases. 10.8% of cases showed diagnostic concordance amongst the four CPs. The most frequently utilized subcategory was architectural atypia. RON ranges for architectural atypia, cytologic atypia, architectural and cytologic atypia, and predominantly Hürthle cells were 28.1% to 35.7%, 0% to 33.3%, 35.3% to 66.7%, and 57.1% to 87.5%. The range of ROM was 13.9% to 16.7%, 0% to 33%, 0% to 42.9%, and 0% to 25%, respectively. Conclusion RON for AUS predominantly Hürthle cells subcategory was higher than previously reported, which may indicate use for tailored patient management pathways. AUS subclassification can result in significant interobserver variability. Therefore, institutions may consider consensus/quality control sessions to optimize diagnostic concordance.

Purpose: The purpose of our project is to determine the presence of Merkel cell polyomavirus (MCPyV) in different tumor types and sarcoidosis. Introduction: MCPyV was recently shown to be present in 80%-100% of Merkel cell carcinomas (MCC) and is considered an oncogenic driver of this tumor. Our goal is to survey a variety of tumor types with a novel antibody (Ab3), which has been shown in literature to have increased sensitivity in detection of MCPyV. We also examined if the virus plays a role in the development of sarcoidosis. Methods: We collected 107 FFPE samples using the electronic medical record at UTMC. There were 24 endometrial carcinomas, 20 intraductal breast carcinomas, 18 neuroendocrine tumors, 15 gastrointestinal stromal tumors, 11 Merkel cell tumors, 8 lobular breast carcinomas, 8 myxomas, and 3 sarcoid granulomas. Hematoxylin and eosin stained slides from the tumors were reviewed, and tissue microarrays were assembled. A cell line (MS-1) extracted from adrenal metastases of MCC was used as a control. The Ab3 mouse antibody that targets fragments of the large T antigen was used to detect presence of MCPyV through immunohistochemistry (IHC) staining method. Results: Upon review of IHC staining 90.9 %( 10/11) of Merkel cell carcinomas, 5.6% (1/18) of neuroendocrine carcinomas, and 4.2% (1/24) of endometrial carcinomas were positive for MCPyV, and there was no detection of MCPyV in GIST, sarcoid, intraductal, or lobular breast carcinoma, or myxomas. Conclusions: MCPyV is strongly associated with MCC and was present in 2 other tumors. While mechanisms of how this virus causes cancer are still being elucidated, such a ubiquitous virus may also be associated with other tumors. Our study, while small in sample size, showed that other neuroendocrine tumors and endometrial carcinomas might also have an association with MCPyV virus.

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