PMID- 7694687
OWN - NLM
STAT- MEDLINE
DCOM- 19940104
LR  - 20210216
IS  - 0006-4971 (Print)
IS  - 0006-4971 (Linking)
VI  - 82
IP  - 11
DP  - 1993 Dec 1
TI  - Expression of MDR1 gene in acute leukemia cells: association with CD7+ acute 
      myeloblastic leukemia/acute lymphoblastic leukemia.
PG  - 3445-51
AB  - MDR1 gene expression was examined in acute leukemia cells from 75 Japanese 
      patients at diagnosis (50 with acute myeloblastic leukemia [AML]: 10 M1, 18 M2, 5 
      M3, 8 M4, 9 M5; 25 with acute lymphoblastic leukemia [ALL]: 13 B-precursor, 12 
      T-lineage). The results of MDR1 mRNA expression by reverse transcriptase 
      polymerase chain reaction were confirmed by immunostaining using the 
      anti-P-glycoprotein monoclonal antibody UIC2 and by a functional study using the 
      rhodamine efflux test. Morphologically, AML M1 cases had the highest incidence of 
      MDR1 gene expression (6 of 10 patients). Phenotypically, CD7 and CD34 were the 
      only surface markers that were significantly associated with MDR1 gene expression 
      (P < .01). In CD7+CD4-CD8- ALL, which is thought to originate from the 
      lymphohematopoietic stem cell, expressed the MDR1 gene with a high incidence (six 
      of eight patients), whereas three surface CD3+ and one CD4+CD8+ T-cell ALL 
      (T-ALL) did not have detectable MDR1 transcripts. Only two cases of 13 
      B-precursor ALL had MDR1 mRNA, one of which had the Philadelphia (Ph1) 
      chromosome. No association was observed between MDR1 gene expression and CD34 
      positivity in ALL. Our results that MDR1 mRNA was frequently expressed in CD7+ 
      AML and CD7+CD4-CD8- ALL, together with the previous reports indicating clinical 
      similarities between these leukemias, provides a clue to clarify a relationship 
      between CD7+ AML and CD7+CD4-CD8- ALL. In addition, MDR1 expression in CD7+ 
      AML/ALL might be responsible for the poor response to conventional chemotherapies 
      of these types of leukemia.
FAU - Miwa, H
AU  - Miwa H
AD  - Second Department of Internal Medicine, Mie University School of Medicine, Tsu, 
      Japan.
FAU - Kita, K
AU  - Kita K
FAU - Nishii, K
AU  - Nishii K
FAU - Morita, N
AU  - Morita N
FAU - Takakura, N
AU  - Takakura N
FAU - Ohishi, K
AU  - Ohishi K
FAU - Mahmud, N
AU  - Mahmud N
FAU - Kageyama, S
AU  - Kageyama S
FAU - Fukumoto, M
AU  - Fukumoto M
FAU - Shirakawa, S
AU  - Shirakawa S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Blood
JT  - Blood
JID - 7603509
RN  - 0 (Antigens, CD)
RN  - 0 (Antigens, CD7)
RN  - 0 (Antigens, Differentiation, T-Lymphocyte)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Adult
MH  - Antigens, CD/*analysis
MH  - Antigens, CD7
MH  - Antigens, Differentiation, T-Lymphocyte/*analysis
MH  - Base Sequence
MH  - Drug Resistance/*genetics
MH  - *Gene Expression
MH  - Humans
MH  - Leukemia, Myeloid, Acute/drug therapy/*genetics/immunology
MH  - Molecular Sequence Data
MH  - Phenotype
MH  - Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy/*genetics/immunology
MH  - RNA, Messenger/analysis
EDAT- 1993/12/01 00:00
MHDA- 1993/12/01 00:01
CRDT- 1993/12/01 00:00
PHST- 1993/12/01 00:00 [pubmed]
PHST- 1993/12/01 00:01 [medline]
PHST- 1993/12/01 00:00 [entrez]
AID - S0006-4971(20)67957-5 [pii]
PST - ppublish
SO  - Blood. 1993 Dec 1;82(11):3445-51.