PMID- 12817431
OWN - NLM
STAT- MEDLINE
DCOM- 20030702
LR  - 20151119
IS  - 0002-9173 (Print)
IS  - 0002-9173 (Linking)
VI  - 119
IP  - 6
DP  - 2003 Jun
TI  - Chronic myeloid leukemia following therapy with imatinib mesylate (Gleevec). Bone 
      marrow histopathology and correlation with genetic status.
PG  - 833-41
AB  - We evaluated bone marrow pathologic features and cytogenetic and molecular 
      genetic status of 13 patients with interferon-resistant, chronic-phase chronic 
      myeloid leukemia (CML), treated with imatinib mesylate (Gleevec). All had 
      morphologic evidence of CML in the blood and bone marrow and were positive for 
      bcr-abl by reverse transcriptase-polymerase chain reaction, fluorescence in situ 
      hybridization (FISH), or both. Follow-up marrow biopsies, interphase FISH for 
      bcr-abl, and conventional cytogenetics were performed at 3-month intervals (up to 
      24 months) after therapy initiation. All patients exhibited a reduction in bone 
      marrow cellularity with decreases in myeloid/erythroid ratios at 3 to 6 months 
      after therapy. The percentage of bcr-abl-positive cells by FISH decreased in all 
      patients (pretherapy median, 73%; 3 months median, 47%). Cytogenetic and FISH 
      data defined 2 groups after 6 months of follow-up: 5 patients became negative for 
      bcr-abl by FISH; 8 remained positive, 4 of whom developed signs of clonal 
      cytogenetic evolution. Patients who became negative for bcr-abl had no 
      morphologic evidence of CML at 15 to 24 months of follow-up, whereas patients who 
      remained positive redeveloped morphologic features of CML as cellularity 
      increased. Some bcr-abl-positive patients showed signs of progression, including 
      2 patients who developed myeloid blast phase. Although all patients demonstrated 
      an initial decrease in bone marrow cellularity after imatinib mesylate therapy, 
      continued follow-up showed that histopathologic findings correlated with genetic 
      response.
FAU - Frater, John L
AU  - Frater JL
AD  - Department of Pathology, Northwestern Memorial Hospital, Northwestern University 
      Feinberg School of Medicine, Chicago, IL, USA.
FAU - Tallman, Martin S
AU  - Tallman MS
FAU - Variakojis, Daina
AU  - Variakojis D
FAU - Druker, Brian J
AU  - Druker BJ
FAU - Resta, Debra
AU  - Resta D
FAU - Riley, Mary Beth
AU  - Riley MB
FAU - Hrisinko, Mary Ann
AU  - Hrisinko MA
FAU - Peterson, LoAnn C
AU  - Peterson LC
LA  - eng
PT  - Clinical Trial
PT  - Clinical Trial, Phase II
PT  - Journal Article
PT  - Multicenter Study
PL  - England
TA  - Am J Clin Pathol
JT  - American journal of clinical pathology
JID - 0370470
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Benzamides)
RN  - 0 (Piperazines)
RN  - 0 (Pyrimidines)
RN  - 0 (Reticulin)
RN  - 8A1O1M485B (Imatinib Mesylate)
RN  - 9008-11-1 (Interferons)
RN  - EC 2.7.10.2 (Fusion Proteins, bcr-abl)
SB  - IM
MH  - Antineoplastic Agents/*therapeutic use
MH  - Benzamides
MH  - Biopsy
MH  - Bone Marrow/*pathology
MH  - Cytogenetic Analysis
MH  - Drug Resistance
MH  - Fibrosis
MH  - Fusion Proteins, bcr-abl/genetics
MH  - Histiocytes/pathology
MH  - Humans
MH  - Hyperplasia
MH  - Imatinib Mesylate
MH  - In Situ Hybridization, Fluorescence
MH  - Interferons
MH  - Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*drug 
      therapy/*genetics/pathology
MH  - Leukocyte Count
MH  - Megakaryocytes/pathology
MH  - Piperazines/*therapeutic use
MH  - Pyrimidines/*therapeutic use
MH  - Reticulin/analysis
MH  - Reverse Transcriptase Polymerase Chain Reaction
EDAT- 2003/06/24 05:00
MHDA- 2003/07/03 05:00
CRDT- 2003/06/24 05:00
PHST- 2003/06/24 05:00 [pubmed]
PHST- 2003/07/03 05:00 [medline]
PHST- 2003/06/24 05:00 [entrez]
AID - 10.1309/A4RG-P4LF-12GG-H8MW [doi]
PST - ppublish
SO  - Am J Clin Pathol. 2003 Jun;119(6):833-41. doi: 10.1309/A4RG-P4LF-12GG-H8MW.