Further mechanistic studies show that CUDC-101 triggers caspase-dependent degradation of the promyelocytic leukemia-retinoic acid receptor alpha fusion protein.
APL is a model for oncogene-targeted therapies: <i>all-trans</i> retinoic acid (ATRA) and arsenic both target and degrade its ProMyelocytic Leukemia/Retinoic Acid Receptor α (PML/RARA) driver.
They are also commonly deficient for expression of ATRX protein, a repressor of ALT activity, and a component of promyelocytic leukemia nuclear bodies (PML NBs) that are required for intrinsic immunity to various viruses.
In this experimental study, human SSCs were isolated and their identities were confirmed by tracking their promyelocytic leukemia zinc finger (PLZF) protein.
However, flourescence in situ hybridization (FISH) and reverse transcriptase polymerase chain reaction (RT-PCR) studies were negative for transcripts promyelocytic leukemia (<i>PML</i>) gene and retinoic acid receptor alpha (<i>RARA</i>) or <i>PML-RARA</i> fusion.
Arsenic trioxide (ATO) is another anti-cancer agent that promotes autophagy-dependent clearance of promyelocytic leukemiaretinoic acid receptor alpha gene (PML-RARα) in APL cells.
The expression of senescence-associated beta-galactosidase (SA-β-gal), cell senescence-related markers (p16, p21, and promyelocytic leukemia; PML), and a growth marker (MCM2) was immunohistochemically examined.
Currently, more than 11 fusion partners of RARα have been identified, of which PML accounts for 95%, promyelocytic leukemia zinc finger (PLZF) take up2%, and the remaining are other variants.
The promyelocytic leukemia (PML)-retinoic acid receptor α (RARA) fusion is hypothesized to serve a vital role in the pathogenesis of acute promyelocytic leukemia (APL), which results from a reciprocal translocation between chromosomes 15 and 17, t(15;17)(q24;q21).
The promyelocytic leukemia (PML)/retinoic acid receptor-alpha (RARα) onco-fusion protein that is generated from t(15;17) chromosome translocation is crucial for the leukemogenesis of acute promyelocytic leukemia (APL) and is well documented as a transcriptional repressor.
Furthermore, crocetin suppressed the expression of clinical marker promyelocytic leukemia/retinoic acid receptor-α ( PML/RARα) in NB4 and primary APL cells, and reduced the expression of histone deacetylase 1 ( HDAC1) in all leukemic cells.
Among them, members of the tripartite motif (TRIM) family have emerged as important players endowed with both antiviral effects and modulatory capacity of the innate immune response.TRIM5α and TRIM19 (i.e. promyelocytic leukemia, PML) are among the best-characterized family members; however, in this review we will focus on the potential role of another family member, i.e.
In addition, under steady-state conditions, DP T cells expressed eomesodermin (Eomes) and promyelocytic leukemia zinc finger (PLZF) proteins, both of which act as transcription factors in innate/memory-like T cells.
We present a case of an 18-year-old female who was diagnosed with AML (FLT3 (Fms like tyrosine kinase 3) and PML-RARA (promyelocytic leukemia-retinoic acid receptor alpha) translocation-negative) and after initial treatment with a standard induction regimen of cytarabine and daunorubicin (3+7 regimen), her bone marrow showed blast cells less than 5% and dense aggregates/sheets of atypical/immature mast cells with immunohistochemical stain CD117+ve and toluidine blue positive in mast cell aggregates.
Although the role of promyelocytic leukemia/retinoic acid receptor α (PML/RARA) fusion protein is well recognized in acute promyelocytic leukemia (APL), its contribution to initiation and maintenance of leukemogenesis is not completely understood.
Several host gene products, including the nuclear domain 10 (ND10) components PML (promyelocytic leukemia) and Daxx (death domain-associated protein 6), as well as IFI16 (interferon-inducible protein 16), have been shown to restrict herpes simplex virus 1 (HSV-1) replication.
However, few studies have investigated whether BRD4 influenced acute promyelocytic leukemia (APL), and whether BRD4 had interaction with promyelocytic leukemia-retinoic acid receptor α (PML/RARα) fusion protein to some extent.
The As2O3-mediated degradation of PML-RARA (promyelocytic leukemia-retinoic acid receptor-α) oncoprotein via the proteasome pathway appears to be critical for such distinguished sensitivity.
The As2O3-mediated degradation of PML-RARA (promyelocytic leukemia-retinoic acid receptor-α) oncoprotein via the proteasome pathway appears to be critical for such distinguished sensitivity.
Although the role of promyelocytic leukemia/retinoic acid receptor α (PML/RARA) fusion protein is well recognized in acute promyelocytic leukemia (APL), its contribution to initiation and maintenance of leukemogenesis is not completely understood.