Molecular pathogenesis of acute promyelocytic leukaemia and APL variants

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Major nucleolar proteins shuttle between nucleus and cytoplasm

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Crystal structure of the RAR-γ ligand-binding domain bound to all-trans retinoic acid

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Role of the histone deacetylase complex in acute promyelocytic leukaemia

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Deconstructing a Disease: RAR, Its Fusion Partners, and Their Roles in the Pathogenesis of Acute Promyelocytic Leukemia

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Function of retinoic acid receptor γ in the mouse

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The Role of PML in Tumor Suppression

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Distinct interactions of PML-RARα and PLZF-RARα with co-repressors determine differential responses to RA in APL

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PML is induced by oncogenic <i>ras</i> and promotes premature senescence

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Nucleophosmin regulates the stability and transcriptional activity of p53

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Role of PML in Cell Growth and the Retinoic Acid Pathway

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The function of PML in p53-dependent apoptosis

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The t(5;17) variant of acute promyelocytic leukemia expresses a nucleophosmin-retinoic acid receptor fusion

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A PMLRAR α transgene initiates murine acute promyelocytic leukemia

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Anaplastic large cell lymphomas expressing the novel chimeric protein p80NPM/ALK: a distinct clinicopathologic entity

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The role of Stat5a and Stat5b in signaling by IL-2 family cytokines

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Altered Myeloid Development and Acute Leukemia in Transgenic Mice Expressing PML-RARα Under Control of Cathepsin G Regulatory Sequences

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Clinical and molecular characterization of a rare syndrome of acute promyelocytic leukemia associated with translocation (11;17)

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

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PML/RARα and FLT3-ITD induce an APL-like disease in a mouse model

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Retinoic Acid and Arsenic Synergize to Eradicate Leukemic Cells in a Mouse Model of Acute Promyelocytic Leukemia

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Histone deacetylase inhibitors induce remission in transgenic models of therapy-resistant acute promyelocytic leukemia

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Reduced Retinoic Acid-Sensitivities of Nuclear Receptor Corepressor Binding to PML- and PLZF-RARα Underlie Molecular Pathogenesis and Treatment of Acute Promyelocytic Leukemia

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Histone deacetylase associated with mSin3A mediates repression by the acute promyelocytic leukemia-associated PLZF protein

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Plzf regulates limb and axial skeletal patterning

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Fusion of retinoic acid receptor α to NuMA, the nuclear mitotic apparatus protein, by a variant translocation in acute promyelocytic leukaemia

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Signal Transducer and Activator of Transcription (STAT)5 Activation by BCR/ABL Is Dependent on Intact Src Homology (SH)3 and SH2 Domains of BCR/ABL and Is Required for Leukemogenesis

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The Signal Transducer and Activator of Transcription STAT5b Gene Is a New Partner of Retinoic Acid Receptor in Acute Promyelocytic-Like Leukaemia

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Genomic variability and alternative splicing generate multiple PML/RAR alpha transcripts that encode aberrant PML proteins and PML/RAR alpha isoforms in acute promyelocytic leukaemia.

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Translocation breakpoint of acute promyelocytic leukemia lies within the retinoic acid receptor alpha locus.

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Localization of nascent RNA and CREB binding protein with the PML-containing nuclear body

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Acquisition of Oncogenic Potential by RAR Chimeras in Acute Promyelocytic Leukemia through Formation of Homodimers

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Deconstructing PML‐induced premature senescence

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A dominant negative retinoic acid receptor blocks neutrophil differentiation at the promyelocyte stage.

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Rearrangements of the retinoic acid receptor alpha and promyelocytic leukemia zinc finger genes resulting from t(11;17)(q23;q21) in a patient with acute promyelocytic leukemia.

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Primary structure of NuMA, an intranuclear protein that defines a novel pathway for segregation of proteins at mitosis.

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NuMA is required for the proper completion of mitosis.

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Critical Residues within the BTB Domain of PLZF and Bcl-6 Modulate Interaction with Corepressors

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Translocations of the RARα gene in acute promyelocytic leukemia

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Acute promyelocytic leukemia: a model for the role of molecular diagnosis and residual disease monitoring in directing treatment approach in acute myeloid leukemia

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Retinoic acid (RA) and As 2 O 3 treatment in transgenic models of acute promyelocytic leukemia (APL) unravel the distinct nature of the leukemogenic process induced by the PML-RARα and PLZF-RARα oncoproteins

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PML RING suppresses oncogenic transformation by reducing the affinity of eIF4E for mRNA

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Normal development and growth of mice carrying a targeted disruption of the alpha 1 retinoic acid receptor gene.

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CCAAT/enhancer binding protein ε is a potential retinoid target gene in acute promyelocytic leukemia treatment

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