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DNMT3B7, a Truncated DNMT3B Isoform Expressed in Human Tumors, Disrupts Embryonic Development and Accelerates Lymphomagenesis
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Abstract
Epigenetic changes are among the most common alterations observed in cancer cells, yet the mechanism by which cancer cells acquire and maintain abnormal DNA methylation patterns is not understood. Cancer cells have an altered distribution of DNA methylation and express aberrant DNA methyltransferase 3B transcripts, which encode truncated proteins, some of which lack the COOH-terminal catalytic domain. To test if a truncated DNMT3B isoform disrupts DNA methylation in vivo, we constructed two lines of transgenic mice expressing DNMT3B7, a truncated DNMT3B isoform commonly found in cancer cells. DNMT3B7 transgenic mice exhibit altered embryonic development, including lymphopenia, craniofacial abnormalities, and cardiac defects, similar to Dnmt3b-deficient animals, but rarely develop cancer. However, when DNMT3B7 transgenic mice are bred with Eμ-Myc transgenic mice, which model aggressive B-cell lymphoma, DNMT3B7 expression increases the frequency of mediastinal lymphomas in Eμ-Myc animals. Eμ-Myc/DNMT3B7 mediastinal lymphomas have more chromosomal rearrangements, increased global DNA methylation levels, and more locus-specific perturbations in DNA methylation patterns compared with Eμ-Myc lymphomas. These data represent the first in vivo modeling of cancer-associated DNA methylation changes and suggest that truncated DNMT3B isoforms contribute to the redistribution of DNA methylation characterizing virtually every human tumor. Cancer Res; 70(14); 5840–50. ©2010 AACR.
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“Genomic DNA was hydrolyzed and analyzed in triplicate for the relative levels of 5-hydroxymethylcytosine by liquid chromatography-electrospray ionization tandem mass spectrometry (Shah et al., 2010).”
From Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation (2011) · cites this paper as Shah et al., 2010
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Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation
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Metadata
- Authors
- Shah, M. Y., Vasanthakumar, A., Barnes, N. Y., Figueroa, M. E., Kamp, A., Hendrick, C., Ostler, K. R., Davis, E. M., Lin, S., Anastasi, J., Le Beau, M. M., Moskowitz, I. P., Melnick, A., Pytel, P., & Godley, L. A.
- Affiliations
- Authors' Affiliations: 1Section of Hematology/Oncology, Department of Medicine; 2Institute of Molecular Pediatric Science, Department of Pediatrics; 3Biostatistics Core Facility; 4The University of Chicago Comprehensive Cancer Center; 5Department of Pathology, The University of Chicago, Chicago, Illinois; and 6Department of Hematology/Oncology, Weill Cornell Medical College, New York, New York
- Venue
- Cancer Research
- Published
- 2010-07-14
- Volume
- 70
- Issue
- 14
- Pages
- 5840-5850
- ISSN
- 0008-5472
- 1538-7445
- PMC
- PMC2905468
- Cited by
- 63
- References
- 48
- Language
- en
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