PMID- 9916508
OWN - NLM
STAT- MEDLINE
DCOM- 19990322
LR  - 20181201
IS  - 0047-1860 (Print)
IS  - 0047-1860 (Linking)
VI  - 46
IP  - 12
DP  - 1998 Dec
TI  - [Progress in laboratory medicine in chronic myeloid leukemia].
PG  - 1226-31
AB  - Chronic myeloid leukemia (CML) is a hematopoietic stem cell disorder that is 
      characterized by splenomegaly and marked elevation of the blood leukocyte count 
      with granulocyte in maturity. Ph chromosome was identified in CML in 1960 and was 
      found to clearly result from reciprocal translocation between chromosome 9 and 
      chromosome 22 (t(q;22)) (q34;q11). CML arises from a single pluripotent 
      hematopoietic stem cell with the Ph chromosome and demonstration of the Ph 
      chromosome in blood or marrow cells establishes and unequivocal diagnosis of CML. 
      The Ph chromosome is recognized as the cytogenetic result of a rearrangement of 
      the ABL gene on chromosome 9 and the BCL gene on chromosome 22, which leads to 
      the creation of a BCR/ABL fusion gene on chromosome 22. Abnormal ABL-related 
      protein with increased tyrosine kinase activity suggested a molecular mechanism 
      of CML. The BCR/ABL fusion gene can be found not only in the chromosome but in 
      interphase nuclei by fluorescence in situ hybridization (FISH). We employed both 
      fluorescence activated cell sorter (FACS) and FISH to study the lineage 
      involvement of individual stem cells and progenitor cells in patients with CML. 
      Evidence of BCR/ABL fusion was found in pluripotent stem cells (CD34+, Thy1+), 
      myeloid cells, B progenitor cells (CD34+, CD19+) and T/NK progenitor cells 
      (CD34+, CD7+, CD5+) but not mature T cells (CD3+) or natural killer cells (CD3-, 
      CD56+). These data suggested that BCR/ABL gene fusion occurs in pluripotent stem 
      cells and that Ph+ T cells and natural killer cells are eliminated during 
      differentiation.
FAU - Miura, A
AU  - Miura A
AD  - Third Department of Internal Medicine, Akita University School of Medicine.
LA  - jpn
PT  - Journal Article
PT  - Lecture
PT  - Review
PL  - Japan
TA  - Rinsho Byori
JT  - Rinsho byori. The Japanese journal of clinical pathology
JID - 2984781R
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
RN  - EC 2.7.10.2 (Fusion Proteins, bcr-abl)
SB  - IM
MH  - Artificial Gene Fusion
MH  - Cell Differentiation
MH  - Chromosomes, Human, Pair 22
MH  - Chromosomes, Human, Pair 9
MH  - Fusion Proteins, bcr-abl/genetics
MH  - Gene Rearrangement
MH  - Hematopoietic Stem Cells/cytology
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - *Leukemia, Myelogenous, Chronic, BCR-ABL Positive/diagnosis/genetics
MH  - Philadelphia Chromosome
MH  - Protein-Tyrosine Kinases/metabolism
MH  - Translocation, Genetic
RF  - 5
EDAT- 1999/01/23 00:00
MHDA- 1999/01/23 00:01
CRDT- 1999/01/23 00:00
PHST- 1999/01/23 00:00 [pubmed]
PHST- 1999/01/23 00:01 [medline]
PHST- 1999/01/23 00:00 [entrez]
PST - ppublish
SO  - Rinsho Byori. 1998 Dec;46(12):1226-31.