期刊
ONCOTARGET
卷 8, 期 21, 页码 34141-34163出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.9388
关键词
Ewing sarcoma; EWS-FLI1; EWS-FLI1 driven transgenic mouse model
资金
- Deutsche Forschungsgemeinschaft Collaborative Research Centre 1149 [INST 40/492-1, SPP 1468 Tu220/6-2]
- Children's Cancer Foundation
- St. Baldrick's Foundation
- Go4theGoal
- Burroughs Wellcome Clinical Scientist Award in Translational Research
- NIH [RC4CA156509, R01CA133662, R01CA138212]
- National Cancer Institute [P30 CA51008]
- Institut National de la Sante et de la Recherche Medicale
- Institut Curie
- Institut National du Cancer
- Ligue Nationale contre le Cancer
- Reseau National des Genopoles, Agence National de la Recherche
- societe Francaise des Cancers de l'Enfant
- Grants-in-Aid for Scientific Research [26250029, 16H02676] Funding Source: KAKEN
Ewing sarcoma (ES) involves a tumor-specific chromosomal translocation that produces the EWS-FLI1 protein, which is required for the growth of ES cells both in vitro and in vivo. However, an EWS-FLI1-driven transgenic mouse model is not currently available. Here, we present data from six independent laboratories seeking an alternative approach to express EWS-FLI1 in different murine tissues. We used the Runx2, Col1a2.3, Col1a3.6, Prx1, CAG, Nse, NEFL, Dermo1, P0, Sox9 and Osterix promoters to target EWS-FLI1 or Cre expression. Additional approaches included the induction of an endogenous chromosomal translocation, in utero knock-in, and the injection of Cre-expressing adenovirus to induce EWS-FLI1 expression locally in multiple lineages. Most models resulted in embryonic lethality or developmental defects. EWS-FLI1-induced apoptosis, promoter leakiness, the lack of potential cofactors, and the difficulty of expressing EWS-FLI1 in specific sites were considered the primary reasons for the failed attempts to create a transgenic mouse model of ES.
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