TY - JOUR
T1 - Mosaic analysis with double markers reveals tumor cell of origin in glioma
AU - Liu, Chong
AU - Sage, Jonathan C.
AU - Miller, Michael R.
AU - Verhaak, Roel G.W.
AU - Hippenmeyer, Simon
AU - Vogel, Hannes
AU - Foreman, Oded
AU - Bronson, Roderick T.
AU - Nishiyama, Akiko
AU - Luo, Liqun
AU - Zong, Hui
N1 - Funding Information:
We thank A. Henner and M. Valle for technical support; J. Dugas for his help with the immunopanning method; and B. Bowerman, C. Doe, R. Galvao, W. Hong, M. Kohwi, M. Raff, R. Read, B. Tasic, X. Wu, and Y. Zhu for critical comments on the manuscript. This work is supported by NIH grants (R55-CA136495, R01-CA136495). M.R.M was supported by an NSF predoctoral fellowship. S.H. was supported by postdoctoral fellowships from the European Molecular Biology Organization (ALTF 851-2005), Human Frontier Science Program Organization (LT00805/2006-L), and Swiss National Science Foundation (PA00P3_124160). H.Z. is a Pew Scholar in Biomedical Sciences, supported by The Pew Charitable Trusts.
PY - 2011/7/22
Y1 - 2011/7/22
N2 - Cancer cell of origin is difficult to identify by analyzing cells within terminal stage tumors, whose identity could be concealed by the acquired plasticity. Thus, an ideal approach to identify the cell of origin is to analyze proliferative abnormalities in distinct lineages prior to malignancy. Here, we use mosaic analysis with double markers (MADM) in mice to model gliomagenesis by initiating concurrent p53/Nf1 mutations sporadically in neural stem cells (NSCs). Surprisingly, MADM-based lineage tracing revealed significant aberrant growth prior to malignancy only in oligodendrocyte precursor cells (OPCs), but not in any other NSC-derived lineages or NSCs themselves. Upon tumor formation, phenotypic and transcriptome analyses of tumor cells revealed salient OPC features. Finally, introducing the same p53/Nf1 mutations directly into OPCs consistently led to gliomagenesis. Our findings suggest OPCs as the cell of origin in this model, even when initial mutations occur in NSCs, and highlight the importance of analyzing premalignant stages to identify the cancer cell of origin.
AB - Cancer cell of origin is difficult to identify by analyzing cells within terminal stage tumors, whose identity could be concealed by the acquired plasticity. Thus, an ideal approach to identify the cell of origin is to analyze proliferative abnormalities in distinct lineages prior to malignancy. Here, we use mosaic analysis with double markers (MADM) in mice to model gliomagenesis by initiating concurrent p53/Nf1 mutations sporadically in neural stem cells (NSCs). Surprisingly, MADM-based lineage tracing revealed significant aberrant growth prior to malignancy only in oligodendrocyte precursor cells (OPCs), but not in any other NSC-derived lineages or NSCs themselves. Upon tumor formation, phenotypic and transcriptome analyses of tumor cells revealed salient OPC features. Finally, introducing the same p53/Nf1 mutations directly into OPCs consistently led to gliomagenesis. Our findings suggest OPCs as the cell of origin in this model, even when initial mutations occur in NSCs, and highlight the importance of analyzing premalignant stages to identify the cancer cell of origin.
UR - http://www.scopus.com/inward/record.url?scp=79960809488&partnerID=8YFLogxK
U2 - 10.1016/j.cell.2011.06.014
DO - 10.1016/j.cell.2011.06.014
M3 - Article
C2 - 21737130
AN - SCOPUS:79960809488
SN - 0092-8674
VL - 146
SP - 209
EP - 221
JO - Cell
JF - Cell
IS - 2
ER -