title: B-lymphoid/myeloid stem cell origin in Ph-positive acute leukemia with myeloid markers.
abstract: We report two cases of Philadelphia chromosome (Ph)-positive acute leukemia with definite myeloid markers. Ph was the sole chromosomal abnormality at presentation, and neither eosinophilia, basophilia, thrombocytosis nor hepatosplenomegaly was present. In both cases, Ph+ myeloblasts showed positive stain for myeloperoxidase and naphthol ASD chloroacetate esterase, which fulfilled the FAB criteria of acute myelogenous leukemia (AML). Ph+ myeloblasts co-expressed myeloid and B-lymphoid antigens (CD10, CD13, CD19 and CD33). In case 1, myeloblasts rearranged M-BCR, and the expression of M-BCR/ABL chimeric RNA was demonstrated by using the reverse transcription polymerase chain reaction (RT-PCR). They also clonally rearranged IGH. Ph clone disappeared on cytogenetic analysis in remission, and granulocytes in remission did not have rearranged M-BCR. In case 2, morphocytochemically distinct myeloid and lymphoid blast populations were seen. Myeloblasts and lymphoblasts were enriched > 96% as CD19-/CD33+ and CD19+/CD33- populations, respectively. Both of them possessed the identical rearrangement of IGH and M-BCR, indicating a common leukemic progenitor cell origin. Furthermore, m-BCR/ABL was detected in addition to M-BCR/ABL on RT-PCR. Accordingly, both cases were diagnosed as de novo Ph+ acute leukemia rather than as chronic myelogenous leukemia in blastic crisis. Their mixed B-lymphoid/myeloid characteristics strongly suggest that so-called 'Ph+ AML' is derived from Ph+ myeloid/B-lymphoid stem cells.
authors.affiliation: Harasanshin General Hospital, Fukuoka, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Akashi
authors.forename: S
authors.initials: S
authors.lastname: Taniguchi
authors.forename: K
authors.initials: K
authors.lastname: Nagafuji
authors.forename: M
authors.initials: M
authors.lastname: Harada
authors.forename: T
authors.initials: T
authors.lastname: Shibuya
authors.forename: S
authors.initials: S
authors.lastname: Hayashi
authors.forename: H
authors.initials: H
authors.lastname: Gondo
authors.forename: Y
authors.initials: Y
authors.lastname: Niho
mesh_terms: D000293:Adolescent; D000328:Adult; D015703:Antigens, CD / Q000032:analysis; D000951:Antigens, Neoplasm / Q000032:analysis; D001402:B-Lymphocytes / Q000473:pathology*; D001483:Base Sequence; D016044:Fusion Proteins, bcr-abl / Q000235:genetics; D015321:Gene Rearrangement / Q000235:genetics; D016313:Genes, abl / Q000235:genetics; D006801:Humans; D016130:Immunophenotyping; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics / Q000276:immunology / Q000473:pathology*; D015470:Leukemia, Myeloid, Acute / Q000235:genetics / Q000276:immunology / Q000473:pathology*; D008297:Male; D008969:Molecular Sequence Data; D010641:Phenotype; D011505:Protein-Tyrosine Kinases; D011518:Proto-Oncogene Proteins / Q000235:genetics; D051562:Proto-Oncogene Proteins c-bcr; D012333:RNA, Messenger / Q000235:genetics
chemical_list: D015703:Antigens, CD; D000951:Antigens, Neoplasm; D011518:Proto-Oncogene Proteins; D012333:RNA, Messenger; D011505:Protein-Tyrosine Kinases; D016044:Fusion Proteins, bcr-abl; C496613:BCR protein, human; D051562:Proto-Oncogene Proteins c-bcr