CML with an e1a3 BCR-ABL fusion: Rare, benign, and a potential diagnostic pitfall [1]

Blood

Volumn 100, Issue 3, 2002, Pages 1092-1093

  Al Ali, Haifa Kathria ^a   Leiblein, Sabine ^a   Kovacs, Ines ^a   Hennig, Evelin ^a   Niederwieser, Dietger ^a   Deininger, Michael W N ^a  

^a UNIVERSITY OF LEIPZIG   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

ALPHA INTERFERON; BCR ABL PROTEIN; HYBRID PROTEIN; HYDROXYUREA; IMATINIB; MESSENGER RNA;

ADULT; AGED; CANCER CYTODIAGNOSIS; CASE REPORT; CHROMOSOME REARRANGEMENT; CHRONIC MYELOID LEUKEMIA; CYTOGENETICS; FLUORESCENCE IN SITU HYBRIDIZATION; HUMAN; HUMAN CELL; LETTER; LEUKEMIA; LEUKEMIA CELL; PRIORITY JOURNAL; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION;

EID: 0036682497     PISSN: 00064971     EISSN: None     Source Type: Journal    
DOI: 10.1182/blood-2002-03-0930     Document Type: Letter

References (9)

1. P190BCR-ABL chronic myeloid leukaemia: The missing link with chronic myelomonocytic leukaemia?
2. The diversity of BCR-ABL fusion proteins and their relationship to leukemia phenotype
3. Lack of SH3 domain does not imply a more severe clinical course in Ph+ chronic myeloid leukemia patients
4. A novel variant of the bcr-abl fusion product in Philadelphia chromosome-positive acute lymphoblastic leukemia
5. Are aberrant BCR-ABL transcripts more common than previously thought?
6. E1A3 as a unique, naturally occurring BCR-ABL transcript in an indolent case of chronic myeloid leukaemia
7. An optimized multiplex polymerase chain reaction (PCR) for detection of BCR-ABL fusion mRNAs in haematological disorders
8. The SH3 domain contributes to BCR/ABL-dependent leukemogenesis in vivo: Role in adhesion, invasion, and homing
9. 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