PMID- 9643569 OWN - NLM STAT- MEDLINE DCOM- 19980929 LR - 20190116 IS - 1042-8194 (Print) IS - 1026-8022 (Linking) VI - 29 IP - 5-6 DP - 1998 May TI - Minimal residual disease in acute myelogenous leukemia with PML/RAR alpha or AML1/ETO mRNA and phenotypic analysis of possible T and natural killer cells in bone marrow. PG - 553-61 AB - Here we studied minimal residual disease (MRD) of patients with acute myeloid leukemia (AML) who have PML/RAR alpha or AML1/ETO as well as the phenotypic analysis of lymphocyte subsets involved in antitumor immunity. Eight patients in long-term (LT; 3 to 15 years) and 15 patients in short-term (ST; up to 3 years) remission were studied. Using the reverse transcription-polymerase chain reaction (RT) assay, the limit of detection was 10(-5) to 10(-6) for PML/RAR alpha transcript and 10(-4) to 10(-5) for the AML1/ETO transcript. Simultaneously, T lymphocyte subsets and NK cells from the peripheral blood (PB) and bone marrow (BM) were investigated by flow cytometric analysis. Four of the eight patients in LT and 7 of the 15 patients in ST remission were MRD-positive. Although all MRD-positive patients in LT remission are still until now event-free, 3 of the 7 MRD-positive (MRD+) patients in ST remission soon relapsed. The total populations of CD4+, CD8+ and CD56+ [possible T-cell and natural killer (T/NK) populations] in the BM of ST patients and MRD+/LT patients were significantly (p < .01) low. The CD8+ CD28+ population showed the same tendency (p < .01-.02). The T/NK subsets in the BM of MRD-negative (MRD-) LT (MRD-/LT) patients showed similar numbers of cells as normal volunteers. Basically, the total percentage of the CD4+, CD8+ and CD56+ cell populations in the BM was increased and in the following order: MRD-/LT patients, normal volunteers, MRD+/LT patients and MRD+ or -/ST patients. The percentages of the T/NK-cell subsets in the PB were not significantly different among these groups. Thus, the difference of the possible T/NK-cell phenotype in the BM may strongly influence clinical and molecular remission. These results still remain to be confirmed by further studies of the functional anti-tumor immunity of T/NK cells of AML in remission. FAU - Inokuchi, K AU - Inokuchi K AD - Division of Hematology, Department of Internal Medicine, Nippon Medical School, Tokyo, Japan. FAU - Iwakiri, R AU - Iwakiri R FAU - Futaki, M AU - Futaki M FAU - Hanawa, H AU - Hanawa H FAU - Tanosaki, S AU - Tanosaki S FAU - Nomura, T AU - Nomura T FAU - Dan, K AU - Dan K LA - eng PT - Comparative Study PT - Journal Article PL - United States TA - Leuk Lymphoma JT - Leukemia & lymphoma JID - 9007422 RN - 0 (AML1-ETO fusion protein, human) RN - 0 (Core Binding Factor Alpha 2 Subunit) RN - 0 (DNA, Neoplasm) RN - 0 (Neoplasm Proteins) RN - 0 (Oncogene Proteins, Fusion) RN - 0 (RUNX1 Translocation Partner 1 Protein) RN - 0 (Recombinant Fusion Proteins) RN - 0 (Transcription Factors) RN - 0 (promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein) SB - IM MH - Core Binding Factor Alpha 2 Subunit MH - DNA, Neoplasm/analysis MH - Disease-Free Survival MH - Flow Cytometry MH - Humans MH - Immunophenotyping MH - Killer Cells, Natural/*pathology MH - Leukemia, Myeloid, Acute/genetics/mortality/*pathology MH - Leukemia, Promyelocytic, Acute/genetics/mortality/*pathology MH - Neoplasm Proteins/*analysis/genetics MH - Neoplasm, Residual MH - Oncogene Proteins, Fusion/*analysis/genetics MH - Polymerase Chain Reaction MH - Predictive Value of Tests MH - RUNX1 Translocation Partner 1 Protein MH - Recombinant Fusion Proteins/analysis/genetics MH - Remission Induction MH - T-Lymphocyte Subsets/*pathology MH - Time Factors MH - Transcription Factors/*analysis/genetics EDAT- 1998/06/27 00:00 MHDA- 1998/06/27 00:01 CRDT- 1998/06/27 00:00 PHST- 1998/06/27 00:00 [pubmed] PHST- 1998/06/27 00:01 [medline] PHST- 1998/06/27 00:00 [entrez] AID - 10.3109/10428199809050915 [doi] PST - ppublish SO - Leuk Lymphoma. 1998 May;29(5-6):553-61. doi: 10.3109/10428199809050915.