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HOX Loci Focused CRISPR/sgRNA Library Screening Identifying Critical CTCF Boundaries

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Hoxa9 collaborates with E2A-PBX1 in mouse B cell leukemia in association with Flt3 activation and decrease of B cell

Mona Hassawi¹, Elena A Shestakova, Marilaine Fournier

¹Hospital Maisonneuve-Rosemont Research Center, Montreal, QC.

Developmental Dynamics : an Official Publication of the American Association of Anatomists

|September 3, 2013

Summary

Hoxa9 collaborates with E2A-PBX1 to accelerate B cell leukemia development in mice. This involves Flt3 signaling, suggesting potential relevance to human pediatric leukemia.

Keywords:

Hox genes oncogenes transcription factors transgenic mouse model

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Area of Science:

Oncology
Molecular Biology
Hematology

Background:

E2A-PBX1 fusion protein is implicated in pediatric B cell leukemia.
Homeobox (Hox) genes interact with E2A-PBX1 in T cell leukemia.
Hoxa genes were identified as potential collaborators in E2A-PBX1 B cell leukemia.

Purpose of the Study:

To investigate if Hoxa9 enhances E2A-PBX1-induced leukemogenesis.
To understand the collaborative oncogenic mechanisms between Hoxa9 and E2A-PBX1.

Main Methods:

Proviral insertional mutagenesis screen in a mouse model.
Transplantation experiments using bone marrow chimeras.
Quantitative-reverse transcriptase polymerase chain reaction (qRT-PCR) analysis.

Main Results:

Hoxa9 overexpression confers a proliferative advantage to E2A-PBX1 B cells.
Hoxa9 accelerates leukemia generation but cannot transform B cells alone.
Leukemias showed repression of B cell genes and Flt3 activation, indicating impaired differentiation and enhanced proliferation.

Conclusions:

Hoxa9 collaborates with E2A-PBX1 in B cell oncogenic transformation.
The collaboration involves Flt3 signaling.
This mouse model offers insights into human B cell leukemia.