PMID- 22749039
OWN - NLM
STAT- MEDLINE
DCOM- 20120910
LR  - 20220408
IS  - 2210-7762 (Print)
VI  - 205
IP  - 6
DP  - 2012 Jun
TI  - Acute promyelocytic leukemia with a STAT5b-RARalpha fusion transcript defined by 
      array-CGH, FISH, and RT-PCR.
PG  - 327-31
LID - 10.1016/j.cancergen.2012.02.007 [doi]
AB  - Acute promyelocytic leukemia (APL) is characterized by the generation of the 
      PML-RARalpha fusion transcript as a result of a reciprocal chromosomal rearrangement, 
      t(15;17)(q22;q12), with breakpoints within the PML gene and the RARalpha gene. In a 
      small proportion of APL cases, RARalpha is fused with a number of alternative partner 
      genes. The signal transducer and activator of transcription 5 beta (STAT5b) is 
      one of the variant partners. Here, we describe one rare case with all-trans 
      retinoic acid (ATRA) -unresponsive APL characterized by the STAT5b-RARalpha fusion 
      transcript. Morphology and immunophenotypic analyses indicated the typical 
      features of APL; however, cytogenetic analysis exhibited a normal karyotype, and 
      importantly, results of interphase fluorescence in situ hybridization (FISH) or 
      reverse transcriptase-polymerase chain reaction (RT-PCR) analysis indicated that 
      PML-RARalpha expression was negative. FISH analysis with the RARalpha dual-color 
      break-apart rearrangement probe indicated a submicroscopic deletion of the 3' end 
      of one RARA gene. Indeed, the STAT5b-RARalpha fusion transcript was found in this 
      case by array-based comparative genomic hybridization and nested RT-PCR. To the 
      best of our knowledge, we report here only the sixth APL patient in the world 
      with the STAT5b-RARalpha fusion transcript. Additional clinical studies concerning 
      the prognosis, response to therapy, and pathogenesis of APL patients with 
      STAT5b-RARalpha fusion are necessary.
CI  - Copyright (c) 2012 Elsevier Inc. All rights reserved.
FAU - Chen, Haoyue
AU  - Chen H
AD  - Jingjiang People's Hospital, the Seventh Affiliated Hospital of Yangzhou 
      University, Jiangsu Province, PR China.
FAU - Pan, Jinlan
AU  - Pan J
FAU - Yao, Li
AU  - Yao L
FAU - Wu, Lingyu
AU  - Wu L
FAU - Zhu, Jianqin
AU  - Zhu J
FAU - Wang, Wei
AU  - Wang W
FAU - Liu, Chunhua
AU  - Liu C
FAU - Han, Qiaoyan
AU  - Han Q
FAU - Du, Guibin
AU  - Du G
FAU - Cen, Jiannong
AU  - Cen J
FAU - Xue, Yongquan
AU  - Xue Y
FAU - Wu, Depei
AU  - Wu D
FAU - Sun, Miao
AU  - Sun M
FAU - Chen, Suning
AU  - Chen S
LA  - eng
PT  - Case Reports
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cancer Genet
JT  - Cancer genetics
JID - 101539150
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Oncogene Proteins, Fusion)
RN  - 0 (RARA protein, human)
RN  - 0 (Receptors, Retinoic Acid)
RN  - 0 (Retinoic Acid Receptor alpha)
RN  - 0 (STAT5 Transcription Factor)
RN  - 0 (STAT5B protein, human)
RN  - 5688UTC01R (Tretinoin)
SB  - IM
MH  - Adult
MH  - Antineoplastic Agents/therapeutic use
MH  - Chromosome Aberrations
MH  - Comparative Genomic Hybridization
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Karyotype
MH  - Leukemia, Promyelocytic, Acute/drug therapy/*genetics
MH  - Male
MH  - Neoplasm Proteins/genetics
MH  - Oncogene Proteins, Fusion/*genetics
MH  - Receptors, Retinoic Acid/*genetics
MH  - Retinoic Acid Receptor alpha
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - STAT5 Transcription Factor/*genetics
MH  - Translocation, Genetic
MH  - Tretinoin/therapeutic use
EDAT- 2012/07/04 06:00
MHDA- 2012/09/11 06:00
CRDT- 2012/07/04 06:00
PHST- 2012/01/12 00:00 [received]
PHST- 2012/02/14 00:00 [revised]
PHST- 2012/02/20 00:00 [accepted]
PHST- 2012/07/04 06:00 [entrez]
PHST- 2012/07/04 06:00 [pubmed]
PHST- 2012/09/11 06:00 [medline]
AID - S2210-7762(12)00051-8 [pii]
AID - 10.1016/j.cancergen.2012.02.007 [doi]
PST - ppublish
SO  - Cancer Genet. 2012 Jun;205(6):327-31. doi: 10.1016/j.cancergen.2012.02.007.