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Study of the gene expression and microRNA expression profiles of malignant rhabdoid tumors originated in the brain (AT/RT) and in the kidney (RTK)

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Abstract

Purpose

Malignant rhabdoid tumors (MRT) can occur in a variety of anatomical sites. The most frequent locations are the brain, where they are named atypical teratoid/rhabdoid tumors (AT/RT), and the kidney, where they are named rhabdoid tumors of the kidney (RTK). MRTs at all sites are recognized as the same entity due to their similar morphology, aggressive behavior, and a common genetic abnormality, an inactivating mutation of the SMARCB1/INI-1/hSNF5/BAF47 gene. We aim to investigate potential molecular differences between AT/RT and RTK.

Methods

We analyzed the microRNA (miRNA) and gene expression (GE) profiles of 10 RTK, 13 AT/RT, and 2 human MRT cell lines (G401-RTK and MON-AT/RT). Illumina V2 MicroRNA Chips (Illumina, Inc., CA, USA) were used for miRNA analysis, and Illumina HT-12 whole genome expression arrays were used for GE analysis.

Results

The distribution of p values from GE showed a significant difference between RTK and AT/RT, with 20 % of the genes having p values ≤0.05 and the principal component analysis of the GE data showed separation between RTK and AT/RT. However, the miRNA expression failed to identify the different tumor groups. Among the 122 genes significantly differentially expressed between AT/RT and RTK, we found both genes related to brain development (i.e., FABP7, 22-fold increase in AT/RT) and genes related to kidney development (i.e., TCF21, sixfold increase in RTK).

Conclusion

Based on our results, we hypothesized that although MRT are indeed the same tumor, independent of the site of origin, the GE differences reflect the influence of microenvironment over tumor development.

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Acknowledgments

This project was supported by the Rally Foundation for Childhood Cancer Research in memory of Haley Trainer and Dr. Ralph and Marian C. Falk Medical Research Trust. Samples were provided by The Falk Brain Tumor Bank—Chicago, IL and the Children’s Oncology Group–COG. MON cell line was kindly provided by Dr. Delattre, Intitut Curie—Paris.

Conflict of interest

The authors declare that they have no conflicts of interest.

Author information

Authors and Affiliations

  1. Division of Pediatric Neurosurgery, Ann and Robert H. Lurie Children’s Hospital of Chicago, 225 E. Chicago Avenue, Box # 28, Chicago, IL, 60611, USA

    Alex T. Grupenmacher, Abby L. Halpern, Tadanori Tomita & Simone T. Sredni

  2. Feinberg School of Medicine, Northwestern University, 420 East Superior Street, Chicago, IL, 60611, USA

    Maria de Fátima Bonaldo, Tadanori Tomita & Simone T. Sredni

  3. Ann and Robert H. Lurie Children’s Hospital of Chicago Research Center—Cancer Biology and Epigenomics Program, 2430 North Halted Street, Chicago, IL, 60614, USA

    Abby L. Halpern, Maria de Fátima Bonaldo, Christopher A. Hamm, Alexandre de Andrade & Simone T. Sredni

  4. Joseph J. Zilber School of Public Health, University of Wisconsin-Milwaukee, 1240 N. 10th Street, Milwaukee, WI, 53205, USA

    Chiang-Ching Huang

  5. Federal University of Paraña, School of Medicine, Rua Padre Camargo, 280, Curitiba, 80060-240, PR, Brazil

    Alex T. Grupenmacher

Authors
  1. Alex T. Grupenmacher
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  2. Abby L. Halpern
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  3. Maria de Fátima Bonaldo
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  4. Chiang-Ching Huang
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  5. Christopher A. Hamm
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  6. Alexandre de Andrade
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  7. Tadanori Tomita
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  8. Simone T. Sredni
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Corresponding author

Correspondence to Simone T. Sredni.

Additional information

Alex T. Grupenmacher and Abby L. Halpern—these two authors contributed equally to the manuscript and project.

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Grupenmacher, A.T., Halpern, A.L., Bonaldo, M.d.F. et al. Study of the gene expression and microRNA expression profiles of malignant rhabdoid tumors originated in the brain (AT/RT) and in the kidney (RTK). Childs Nerv Syst 29, 1977–1983 (2013). https://doi.org/10.1007/s00381-013-2268-4

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  • DOI: https://doi.org/10.1007/s00381-013-2268-4

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