NDLI: A bcr-3 isoform of RARα-PML potentiates the development of PML-RARα-driven acute promyelocytic leukemia

Content Provider	PubMed Central
Author	Pollock, Jessica L. Westervelt, Peter Kurichety, Arun K. Giuseppe, Pelicci Pier Grisolano, Jay L. Ley, Timothy J.
Copyright Year	1999
Abstract	Acute promyelocytic leukemia (APML) most often is associated with the balanced reciprocal translocation t(15;17) (q22;q11.2) and the expression of both the PML-RARα and RARα-PML fusion cDNAs that are formed by this translocation. In this report, we investigated the biological role of a bcr-3 isoform of RARα-PML for the development of APML in a transgenic mouse model. Expression of RARα-PML alone in the early myeloid cells of transgenic mice did not alter myeloid development or cause APML, but its expression significantly increased the penetrance of APML in mice expressing a bcr-1 isoform of PML-RARα (15% of animals developed APML with PML-RARα alone vs. 57% with both transgenes, P < 0.001). The latency of APML development was not altered substantially by the expression of RARα-PML, suggesting that it does not behave as a classical “second hit” for development of the disease. Leukemias that arose from doubly transgenic mice were less mature than those from PML-RARα transgenic mice, but they both responded to all-trans retinoic acid in vitro. These findings suggest that PML-RARα drives the development of APML and defines its basic phenotype, whereas RARα-PML potentiates this phenotype via mechanisms that are not yet understood.
Starting Page	15103
File Format	PDF
ISSN	10916490
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	26
Volume Number	96
Language	English
Publisher	The National Academy of Sciences
Publisher Date	1999-12-21
Access Restriction	Open
Rights Holder	The National Academy of Sciences
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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Acute leukemia with promyelocytic features in PML/RARα transgenic mice

Expression of a bcr-1 isoform of RARα-PML does not affect the penetrance of acute promyelocytic leukemia or the acquisition of an interstitial deletion on mouse chromosome 2

Distribution of Different PML/RARα bcr Isoforms in Indian Acute Promyelocytic Leukemia (APL) Patients and Clinicohematological Correlation

Cell death induction by the acute promyelocytic leukemia-specific PML/RARα fusion protein

Catechins induced acute promyelocytic leukemia cell apoptosis and triggered PML-RARα oncoprotein degradation

UBE1L is a retinoid target that triggers PML/RARα degradation and apoptosis in acute promyelocytic leukemia

SMRT corepressor interacts with PLZF and with the PML-retinoic acid receptor α (RARα) and PLZF-RARα oncoproteins associated with acute promyelocytic leukemia

In acute promyelocytic leukemia NB4 cells, the synthetic retinoid CD437 induces contemporaneously apoptosis, a caspase-3-mediated degradation of PML/RARα protein and the PML retargeting on PML-nuclear bodies

PML-RARα and Dnmt3a1 Cooperate in vivo to Promote Acute Promyelocytic Leukemia

A bcr-3 isoform of RARα-PML potentiates the development of PML-RARα-driven acute promyelocytic leukemia

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