PUBLICATION

Heritable T-cell malignancy models established in a zebrafish phenotypic screen

Authors
Frazer, J.K., Meeker, N.D., Rudner, L., Bradley, D.F., Smith, A.C., Demarest, B., Joshi, D., Locke, E.E., Hutchinson, S.A., Tripp, S., Perkins, S.L., and Trede, N.S.
ID
ZDB-PUB-090616-53
Date
2009
Source
Leukemia   23(10): 1825-1835 (Journal)
Registered Authors
Demarest, Bradley, Frazer, Kimble, Hutchinson, Sarah, Trede, Nick
Keywords
lymphoma, zebrafish, T lymphocyte, genetic screen
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Disease Models, Animal*
  • Flow Cytometry
  • Genetic Predisposition to Disease*
  • Green Fluorescent Proteins/genetics
  • Green Fluorescent Proteins/metabolism
  • Humans
  • Immunoenzyme Techniques
  • Incidence
  • Mutagenesis
  • Phenotype
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/genetics*
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/pathology
  • RNA, Messenger/genetics
  • RNA, Messenger/metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Transgenes/genetics*
  • Zebrafish/genetics*
PubMed
19516274 Full text @ Leukemia
Abstract
T-cell neoplasias are common in pediatric oncology, and include acute lymphoblastic leukemia (T-ALL) and lymphoblastic lymphoma (T-LBL). These cancers have worse prognoses than their B-cell counterparts, and their treatments carry significant morbidity. Although many pediatric malignancies have characteristic translocations, most T-lymphocyte-derived diseases lack cytogenetic hallmarks. Lacking these informative lesions, insight into their molecular pathogenesis is less complete. Although dysregulation of the NOTCH1 pathway occurs in a substantial fraction of cases, many other genetic lesions of T-cell malignancy have not yet been determined. To address this deficiency, we pioneered a phenotype-driven forward-genetic screen in zebrafish (Danio rerio). Using transgenic fish with T-lymphocyte-specific expression of enhanced green fluorescent protein (EGFP), we performed chemical mutagenesis, screened animals for GFP(+) tumors, and identified multiple lines with a heritable predisposition to T-cell malignancy. In each line, the patterns of infiltration and morphological appearance resembled human T-ALL and T-LBL. T-cell receptor analyses confirmed their clonality. Malignancies were transplantable and contained leukemia-initiating cells, like their human correlates. In summary, we have identified multiple zebrafish mutants that recapitulate human T-cell neoplasia and show heritable transmission. These vertebrate models provide new genetic platforms for the study of these important human cancers.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping