ISSN: 2161-0681

Journal de pathologie clinique et expérimentale

Accès libre

Notre groupe organise plus de 3 000 séries de conférences Événements chaque année aux États-Unis, en Europe et en Europe. Asie avec le soutien de 1 000 autres Sociétés scientifiques et publie plus de 700 Open Access Revues qui contiennent plus de 50 000 personnalités éminentes, des scientifiques réputés en tant que membres du comité de rédaction.

Les revues en libre accès gagnent plus de lecteurs et de citations
700 revues et 15 000 000 de lecteurs Chaque revue attire plus de 25 000 lecteurs

Indexé dans
  • Index Copernic
  • Google Scholar
  • Sherpa Roméo
  • Ouvrir la porte J
  • JournalSeek de génamique
  • JournalTOC
  • Annuaire des périodiques d'Ulrich
  • Recherche de référence
  • Université Hamdard
  • EBSCO AZ
  • OCLC-WorldCat
  • Publons
  • Fondation genevoise pour l'enseignement et la recherche médicale
  • Euro Pub
  • ICMJE
Partager cette page

Abstrait

Malignant Mixed Mullerian Tumor with an Endometrioid Adenocarcinoma with a Component of Giant Cell Carcinoma: A Case Report and Literature Review

Eric Johannesen and Van Nguyen

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.

Avertissement: Ce résumé a été traduit à l'aide d'outils d'intelligence artificielle et n'a pas encore été examiné ni vérifié.