T lymphoid/myeloid bilineal crisis in chronic myelogenous leukemia.
We describe 2 cases of "bilineal" crisis in chronic myelogenous leukemia (CML) with T cell and myeloid phenotypes. In both cases, morphocytochemically distinct myeloid and T lymphoid blast populations proliferated simultaneously in the phase of blastic crisis--myeloperoxidase (MPO)-positive, CD7+/CD33+ myeloblasts in the peripheral blood, and MPO-negative, periodic acid Schiff (PAS)-positive lymphoblasts in the lymph nodes. In each case, common karyotypes containing Ph1 translocation were demonstrated in both the peripheral blood and the lymph node samples. In Case 1, the lymph nodes were occupied by > 90% lymphoblasts, which were positive for CD2, cytoplasmic CD3 (cCD3), CD5 and CD7 and terminal deoxynucleotidyl transferase (TdT), but negative for myeloid antigens. Myeloblasts and T lymphoblasts showed an identical rearrangement of the bcr gene by Southern blotting analysis, although the clonal rearrangement of the T cell receptor (TcR)-delta gene was seen only in T lymphoblasts. In Case 2, simultaneous proliferation of myeloblasts and lymphoblasts was documented morphocytochemically in the lymph node, and a flow cytometric analysis revealed the coexistence of CD7+/CD33+ and CD7+/CD33- blast populations. Each blast population was enriched by antibody-conjugated immunomagnetic beads; the former was positive for MPO by 64% but negative for cCD3 and TdT, whereas the latter was positive for cCD3 and TdT but negative for MPO (< 1%). CD7+/CD33+ myeloblasts and CD7+/CD33- lymphoblasts showed an identical rearrangement of the bcr gene. Neither TcR-beta, TcR-gamma nor the TcR-delta gene was clonally rearranged in either population. These observations clearly indicate that T lymphoid and myeloid blasts share common Ph1-positive progenitors, and that Ph1-positive T lymphoid/myeloid progenitors are probably involved in the development of blastic transformation in some percentage of CML patients.
Akashi
K
K
Department of Hematology, Harasanshin General Hospital, Fukuoka, Japan.
Mizuno
S
S
Harada
M
M
Kimura
N
N
Kinjyo
M
M
Shibuya
T
T
Shimoda
K
K
Takeshita
M
M
Okamura
S
S
Matsumoto
I
I
D000328:Adult; D015703:Antigens, CD / Q000032:analysis; D019011:Antigens, CD7; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D000945:Antigens, Differentiation, T-Lymphocyte / Q000032:analysis; D001752:Blast Crisis / Q000235:genetics / Q000473:pathology*; D015139:Blotting, Southern; D001853:Bone Marrow / Q000473:pathology*; D018801:CD2 Antigens; D017252:CD3 Complex / Q000032:analysis; D018956:CD5 Antigens; D002471:Cell Transformation, Neoplastic / Q000235:genetics / Q000473:pathology*; D002499:Centrifugation, Density Gradient; D005260:Female; D005434:Flow Cytometry; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics; D015334:Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor / Q000235:genetics; D006801:Humans; D007621:Karyotyping; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics / Q000473:pathology*; D008221:Lymphoid Tissue / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D011233:Precipitin Tests; D011505:Protein-Tyrosine Kinases; D011518:Proto-Oncogene Proteins / Q000235:genetics; D051562:Proto-Oncogene Proteins c-bcr; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000235:genetics; D011971:Receptors, Immunologic / Q000032:analysis; D063268:Sialic Acid Binding Ig-like Lectin 3; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology* / Q000648:ultrastructure
D015703:Antigens, CD; D019011:Antigens, CD7; D015214:Antigens, Differentiation, Myelomonocytic; D000945:Antigens, Differentiation, T-Lymphocyte; D018801:CD2 Antigens; D017252:CD3 Complex; C571163:CD33 protein, human; D018956:CD5 Antigens; D011518:Proto-Oncogene Proteins; D016692:Receptors, Antigen, T-Cell, gamma-delta; D011971:Receptors, Immunologic; D063268:Sialic Acid Binding Ig-like Lectin 3; D011505:Protein-Tyrosine Kinases; C496613:BCR protein, human; D051562:Proto-Oncogene Proteins c-bcr