PMID- 8547645
OWN - NLM
STAT- MEDLINE
DCOM- 19960216
LR  - 20210216
IS  - 0006-4971 (Print)
IS  - 0006-4971 (Linking)
VI  - 87
IP  - 1
DP  - 1996 Jan 1
TI  - Probing the pathobiology of response to all-trans retinoic acid in acute 
      promyelocytic leukemia: premature chromosome condensation/fluorescence in situ 
      hybridization analysis.
PG  - 218-26
AB  - The response of acute promyelocytic leukemia (APL) peripheral blood and bone 
      marrow cells to trans-retinoic acid (RA) was cytogenetically characterized during 
      RA treatment using the techniques of premature chromosome condensation (PCC) and 
      fluorescence in situ hybridization (FISH). Before treatment, the predominant 
      immature bone marrow cells were found to have t(15;17), whereas the residual 
      mature granulocytes were diploid and lacked evidence of the translocation. In 
      response to RA treatment, an increase in the leukocyte count was noted. The 
      majority of these cells exhibited a t(15;17). Subsequently (eg, between days 6 
      and 23), 32% to 91% of the maturing myeloid cells still exhibited t(15;17). The 
      appearance of t(15;17) in gradually maturing elements suggests that RA 
      contributed to a release of the maturation block of the leukemic elements. As 
      responding patients obtained complete remission, diploid elements without 
      evidence of the translocation prevailed in the blood and bone marrow. In 16 
      patients studied after 1 month in complete remission, all but 2 showed all 
      diploid cells. The residual t(15;17) cells disappeared 18 days later in 1 
      patient, whereas the second patient exhibited clinical evidence of relapse 20 
      days later. These results suggest that response of patients with APL to RA is 
      associated with maturation, subsequent loss of the mature leukemic elements, and 
      preferential regeneration of normal diploid hematopoietic elements.
FAU - Vyas, R C
AU  - Vyas RC
AD  - Department of Clinical Investigation, University of Texas M.D. Anderson Cancer 
      Center, Houston, USA.
FAU - Frankel, S R
AU  - Frankel SR
FAU - Agbor, P
AU  - Agbor P
FAU - Miller, W H Jr
AU  - Miller WH Jr
FAU - Warrell, R P Jr
AU  - Warrell RP Jr
FAU - Hittelman, W N
AU  - Hittelman WN
LA  - eng
GR  - CA-27931/CA/NCI NIH HHS/United States
GR  - CA-57645/CA/NCI NIH HHS/United States
GR  - P01 CA-55164/CA/NCI NIH HHS/United States
GR  - etc.
PT  - Clinical Trial
PT  - Clinical Trial, Phase II
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Blood
JT  - Blood
JID - 7603509
RN  - 0 (Immunologic Factors)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Oncogene Proteins, Fusion)
RN  - 0 (promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein)
RN  - 5688UTC01R (Tretinoin)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Animals
MH  - Blood Cells/pathology
MH  - Bone Marrow/pathology
MH  - Cell Differentiation
MH  - Child
MH  - Chromosomes, Human/*drug effects/ultrastructure
MH  - Chromosomes, Human, Pair 15/ultrastructure
MH  - Chromosomes, Human, Pair 17/ultrastructure
MH  - Cricetinae
MH  - Cricetulus
MH  - Diploidy
MH  - Female
MH  - Humans
MH  - Hybrid Cells/drug effects/ultrastructure
MH  - Immunologic Factors/*pharmacology/therapeutic use
MH  - In Situ Hybridization, Fluorescence
MH  - Leukemia, Promyelocytic, Acute/genetics/pathology/*therapy
MH  - Male
MH  - Middle Aged
MH  - Neoplasm Proteins/analysis/genetics
MH  - Neoplasm, Residual
MH  - Neoplastic Stem Cells/*drug effects/ultrastructure
MH  - Oncogene Proteins, Fusion/analysis/genetics
MH  - Remission Induction
MH  - Translocation, Genetic
MH  - Tretinoin/*pharmacology/therapeutic use
EDAT- 1996/01/01 00:00
MHDA- 2001/03/28 10:01
CRDT- 1996/01/01 00:00
PHST- 1996/01/01 00:00 [pubmed]
PHST- 2001/03/28 10:01 [medline]
PHST- 1996/01/01 00:00 [entrez]
AID - S0006-4971(20)66211-5 [pii]
PST - ppublish
SO  - Blood. 1996 Jan 1;87(1):218-26.