The AF4·MLL fusion protein is capable of inducing ALL in mice without requirement of MLL·AF4

Bursen, Adelheid, Schwabe, Karen, Rüster, Brigitte, Henschler, Reinhard, Ruthardt, Martin ORCID: https://orcid.org/0000-0003-1021-3811, Dingermann, Theo and Marschalek, Rolf 2010. The AF4·MLL fusion protein is capable of inducing ALL in mice without requirement of MLL·AF4. Blood 115 (17) , 3570–3579. 10.1182/blood-2009-06-229542

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Abstract

The chromosomal translocation t(4;11)(q21;q23) is the most frequent genetic aberration of the human MLL gene, resulting in high-risk acute lymphoblastic leukemia (ALL). To elucidate the leukemogenic potential of the fusion proteins MLL.AF4 and AF4.MLL, Lin(-)/Sca1(+) purified cells (LSPCs) were retrovirally transduced with either both fusion genes or with MLL.AF4 or AF4.MLL alone. Recipients of AF4.MLL- or double-transduced LSPCs developed pro-B ALL, B/T biphenotypic acute leukemia, or mixed lineage leukemia. Transplantation of MLL.AF4- or mock-transduced LSPCs did not result in disease development during an observation period of 13 months. These findings indicate that the expression of the AF4.MLL fusion protein is capable of inducing acute lymphoblastic leukemia even in the absence of the MLL.AF4 fusion protein. In view of recent findings, these results may imply that t(4;11) leukemia is based on 2 oncoproteins, providing an explanation for the very early onset of disease in humans.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Medicine
Publisher:	American Society of Hematology
ISSN:	0006-4971
Date of Acceptance:	4 February 2010
Last Modified:	22 Feb 2024 14:45
URI:	https://orca.cardiff.ac.uk/id/eprint/166082

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