A variant c-KITmutation, D816H, fundamental to the sequential development of an ovarian mixed germ cell tumor and systemic mastocytosis with chronic myelomonocytic leukemia

Author:

Mitchell Sarah G.1,Bunting Silvia T.2,Saxe Debra3,Olson Thomas1,Keller Frank G.1

Affiliation:

1. Department of Pediatric Hematology/Oncology; Children's Healthcare of Atlanta, Emory University School of Medicine; Atlanta Georgia

2. Department of Pathology; Children's Healthcare of Atlanta, Emory University School of Medicine; Atlanta Georgia

3. Department of Pathology and Laboratory Medicine; Emory University School of Medicine; Atlanta Georgia

Publisher

Wiley

Subject

Oncology,Hematology,Pediatrics, Perinatology, and Child Health

Reference13 articles.

1. Activating c-kit gene mutations in human germ cell tumors;Tian;Am J Pathol.,1999

2. Mastocytosis: A mutated KIT receptor induced myeloproliferative disorder;Chatterjee;Oncotarget.,2015

3. Pathology and molecular biology of teratomas in childhood and adolescence;Harms;Klin Padiatr.,2006

4. Somatic KIT mutations occur predominantly in seminoma germ cell tumors and are not predictive of bilateral disease: Report of 220 tumors and review of literature;Coffey;Genes Chromosomes Cancer.,2008

5. A c-KIT codon 816 mutation, D816H, in the testicular germ cell tumor: Case report of a Japanese patient with bilateral testicular seminomas;Tate;Acta Med Okayama.,2005

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