scholarly journals Acute Myeloid Leukemia with NUP98-RARG Gene Fusion Similar to Acute Promyelocytic Leukemia: Case Report and Literature Review

2020 ◽  
Vol Volume 13 ◽  
pp. 10559-10566
Author(s):  
Shandong Tao ◽  
Lixiao Song ◽  
Yuan Deng ◽  
Yue Chen ◽  
Yuye Shi ◽  
...  
2003 ◽  
Vol 4 (4) ◽  
pp. 289-291 ◽  
Author(s):  
Mario Annunziata ◽  
Salvatore Palmieri ◽  
Barbara Pocali ◽  
Mariacarla De Simone ◽  
Luigi Del Vecchio ◽  
...  

2021 ◽  
Vol 12 ◽  
pp. 204062072097698
Author(s):  
Xiaoyan Han ◽  
Chunxiang Jin ◽  
Gaofeng Zheng ◽  
Yi Li ◽  
Yungui Wang ◽  
...  

Some subtypes of acute myeloid leukemia (AML) share morphologic, immunophenotypic, and clinical features of acute promyelocytic leukemia (APL), but lack a PML–RARA (promyelocytic leukemia–retinoic acid receptor alpha) fusion gene. Instead, they have the retinoic acid receptor beta (RARB) or retinoic acid receptor gamma (RARG) rearranged. Almost all of these AML subtypes exhibit resistance to all-trans retinoic acid (ATRA); undoubtedly, the prognosis is poor. Here, we present an AML patient resembling APL with a novel cleavage and polyadenylation specific factor 6 ( CPSF6) –RARG fusion, showing resistance to ATRA and poor response to chemotherapy with homoharringtonine and cytarabine. Simultaneously, the patient also had extramedullary infiltration.


2014 ◽  
Vol 3 (1) ◽  
pp. 8 ◽  
Author(s):  
Jianling Ji ◽  
Eric Loo ◽  
Sheeja Pullarkat ◽  
Lynn Yang ◽  
Carlos A Tirado

Author(s):  
Manuel J. Arana Rosainz ◽  
Nghia Nguyen ◽  
Amer Wahed ◽  
Laura C. Lelenwa ◽  
Nfn Aakash ◽  
...  

2013 ◽  
Vol 13 (1) ◽  
pp. 93-96 ◽  
Author(s):  
Maro Ohanian ◽  
Gautam Borthakur ◽  
Alfonso Quintas-Cardama ◽  
Michael Mathisen ◽  
Jorge E. Cortés ◽  
...  

Blood ◽  
2006 ◽  
Vol 107 (8) ◽  
pp. 3330-3338 ◽  
Author(s):  
Beatrice U. Mueller ◽  
Thomas Pabst ◽  
José Fos ◽  
Vibor Petkovic ◽  
Martin F. Fey ◽  
...  

Abstract Tightly regulated expression of the transcription factor PU.1 is crucial for normal hematopoiesis. PU.1 knockdown mice develop acute myeloid leukemia (AML), and PU.1 mutations have been observed in some populations of patients with AML. Here we found that conditional expression of promyelocytic leukemia-retinoic acid receptor α (PML-RARA), the protein encoded by the t(15;17) translocation found in acute promyelocytic leukemia (APL), suppressed PU.1 expression, while treatment of APL cell lines and primary cells with all-trans retinoic acid (ATRA) restored PU.1 expression and induced neutrophil differentiation. ATRA-induced activation was mediated by a region in the PU.1 promoter to which CEBPB and OCT-1 binding were induced. Finally, conditional expression of PU.1 in human APL cells was sufficient to trigger neutrophil differentiation, whereas reduction of PU.1 by small interfering RNA (siRNA) blocked ATRA-induced neutrophil differentiation. This is the first report to show that PU.1 is suppressed in acute promyelocytic leukemia, and that ATRA restores PU.1 expression in cells harboring t(15;17).


Cancers ◽  
2021 ◽  
Vol 13 (23) ◽  
pp. 5883
Author(s):  
Zhan Su ◽  
Xin Liu

Acute promyelocytic leukemia (APL) is a unique and very deeply studied acute myeloid leukemia [...]


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