Malignant Mixed Mullerian Tumor with an Endometrioid Adenocarcinoma with a Component of Giant Cell Carcinoma: A Case Report and Literature ReviewEric Johannesen* and Van Nguyen
Department of Pathology and Anatomical Sciences, University of Missouri Columbia, One Hospital Drive, USA
- *Corresponding Author:
- Eric Johannesen
University of Missouri Columbia
Columbia, MO, USA
E-mail: [email protected]
Received date: February 10, 2015, Accepted date: February 23, 2015, Published date: February 28, 2015
Citation: Johannesen E, Nguyen V (2015) Malignant Mixed Mullerian Tumor with an Endometrioid Adenocarcinoma with a Component of Giant Cell Carcinoma: A Case Report and Literature Review. J Clin Exp Pathol 5:212. doi:10.4172/2161-0681.1000212
Copyright: © 2015 Johannesen E, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
A 70 year old female underwent a hysterectomy due to a diagnosis of high grade endometrioid adenocarcinoma. Pathological examination revealed a Malignant Mixed Mullerian Tumor (MMMT) along with a conventional endometrioid adenocarcinoma with a component of giant cell carcinoma. Giant cell carcinoma of the endometrium is a rare tumor consisting of sheets of discohesive appearing cells with numerous anaplastic looking giant cells. Only 13 cases of giant cell carcinoma have been described and the majority present as a component of endometrioid carcinoma. The giant cells are often positive for keratin markers and are negative for CD68 and HCG which can help distinguish them from other tumors with multinucleate giant cells. Malignant Mixed Mullerian Tumors (MMMT) were once thought to originate from two separate neoplasms that underwent collision. But recently studies have found that these malignancies appear to arise from a malignant epithelial type cell that undergoes Epithelial to Mesenchymal Transition (EMT). Studies suggest that mutations in AKT2 and p53 result in increased levels of SLUG and ZEB, which represses E-cadherin. It is the loss of e-cadherin that is believed to be a central player in EMT. It is widely believed that tumors frequently display intra-tumoral heterogeneity that can result in neoplasms with striking variations in their characteristics. This case can make a nice example of how tumors can develop strikingly different characteristics.