Abstract
Testicular germ cell cancers are subdivided into seminomas and non-seminomas. Here, we summarize how different cellular microenvironments affect the cell fate of seminomas. Further, we describe the molecular mechanisms driving a reprogramming into an embryonal carcinoma (the stem cell population of the non-seminomas) and differentiation into a mixed non-seminoma. Our results may explain how non-seminomas develop that contain a seminoma component, which are often observed in clinical routine.
Similar content being viewed by others
Literatur
Oosterhuis JW, Looijenga LHJ (2005) Testicular germ-cell tumours in a broader perspective. Nat Rev Cancer 5:210–222
Berney DM, Looijenga L, Idrees M et al. (2016) Germ cell neoplasia in situ (GCNIS): evolution of the current nomenclature for testicular pre-invasive germ cell malignancy. Histopathology 69:7–10
Eckert D, Nettersheim D, Heukamp LC et al. (2008) TCam-2 but not JKT-1 cells resemble seminoma in cell culture. Cell Tissue Res 331:529–538
Nettersheim D, Westernströer B, Haas N et al. (2012) Establishment of a versatile seminoma model indicates-cellular plasticity of germ cell tumor cells. Genes Chromosom Cancer 51:717–726
Nettersheim D, Jostes S, Sharma R et al. (2015) BMP inhibition in seminomas initiates acquisition of pluripotency via NODAL signaling resulting in reprogramming to an embryonal carcinoma. PLoS Genet 11:e1005415
Nettersheim D, Heimsoeth A, Jostes S et al. (2016) SOX2 is essential for in vivo reprogramming of seminoma-like TCam-2 cells to an embryonal carcinoma-like fate. Oncotarget 7:47095–47110
Nettersheim D, Heukamp LC, Fronhoffs F et al. (2013) Analysis of TET expression/activity and 5mC oxidation during normal and malignant germ cell development. PLoS One 8:e82881
Wermann H, Stoop H, Gillis AJ et al. (2010) Global DNA methylation in fetal human germ cells and germ cell tumours: association with differentiation and cisplatin resistance. J Pathol 221:433–442
Nettersheim D, Gillis AJM, Looijenga LHJ et al. (2011) TGF-β1, EGF and FGF4 synergistically induce differentiation of the seminoma cell line TCam-2 into a cell type resembling mixed non-seminoma. Int J Androl 34:e189–203
Author information
Authors and Affiliations
Corresponding author
Additional information
Daniel Nettersheim Jahrgang 1980. 2000–2005 Bioingenieurwesenstudium an der Fachhochschule Jülich. 2005–2006 wissenschaftlicher Mitarbeiter an der Fachhochschule Bonn-Rhein-Sieg. Seit 2006 wissenschaftlicher Mitarbeiter in der Abteilung für Entwicklungspathologie am Institut für Pathologie, Uniklinikum Bonn. 2006–2010 Promotion (Dr. rer. nat., Molekulare Biomedizin) an der Universität Bonn. 2011–2016 Habilitation an der Medizinischen Fakultät der Universität Bonn (Molekulare Pathologie).
Hubert Schorle Jahrgang 1962. 1983–1989 Biologiestudium an der Universität Würzburg. 1989–1991 Promotion. 1992–1996 Postdoc am Whitehead Institute/Massachusetts Institute of Technology, Boston, MA, USA. 1997–2001 Gruppenleiter am Karlsruher Institut für Technologie (KIT). 2001–2004 Oberassistent am Institut für Pathologie, Uniklinikum Bonn. 2004 Professor am Zentrum für Medizinische Biotechnologie (ZMB), Universität Duisburg-Essen. Seit 2005 Professor und Leiter der Abteilung Entwicklungspathologie am Institut für Pathologie, Uniklinikum Bonn.
Rights and permissions
About this article
Cite this article
Nettersheim, D., Schorle, H. Das Mikromilieu beeinflusst das Zellschicksal von Keimzelltumoren. Biospektrum 23, 779–781 (2017). https://doi.org/10.1007/s12268-017-0873-6
Published:
Issue Date:
DOI: https://doi.org/10.1007/s12268-017-0873-6