ArticleScientific reports2019
Novel strategy for rapid functional in vivo validation of oncogenic drivers in haematological malignancies.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Tet2 is a tumor suppressor in the preleukemic phase of T-cell acute lymphoblastic leukemia.Blood advances · 2024Article
- Article
- Direct and indirect anti-leukemic properties of activity-on-target interferons for the treatment of T-cell acute lymphoblastic leukemia.Haematologica · 2022Article
- Myb drives B-cell neoplasms and myeloid malignancies in vivo.Blood advances · 2022Article
- Cyclin D2 overexpression drives B1a-derived MCL-like lymphoma in mice.The Journal of experimental medicine · 2021Article
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Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In cancer research, it remains challenging to functionally validate putative novel oncogenic drivers and to establish relevant preclinical models for evaluation of novel therapeutic strategies. Here, we describe an optimized and efficient pipeline for the generation of novel conditional overexpression mouse models in which putative oncogenes, along with an eGFP/Luciferase dual reporter, are expressed from the endogenous ROSA26 (R26) promoter. The efficiency of this approach was demonstrated by the generation and validation of novel R26 knock-in (KI) mice that allow conditional overexpression of Jarid2, Runx2, MN1 and a dominant negative allele of ETV6. As proof of concept, we confirm that MN1 overexpression in the hematopoietic lineage is sufficient to drive myeloid leukemia. In addition, we show that T-cell specific activation of MN1 in combination with loss of Pten increases tumour penetrance and stimulates the formation of Lyl1
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