Infant leukemia: An analysis of nine chinese patients

Abstract

A study was made of the cellular and molecular characteristics of nine Chinese infants, consecutively presenting with acute leukemia. Five cases were acute lymphoblastic leukemia (ALL); four were acute nonlymphoblastic leukemia (ANLL). Hyperleukocytosis, hepatosplenomegaly, and poor response to conventional therapy were common features, and CNS involvement was detected at diagnosis in three cases. The blast cells from all five cases with ALL expressed early B-cell markers, i.e., HLA-DR+, CD19+, but CD10-. Terminal deoxynucleotidyl transferase (TdT) was present in blasts from four of the five cases and periodic acid-Schiff staining in blasts from two patients only. The leukemic cells of one patient also showed positive nonspecific esterase activity and expressed myeloid-associated antigens CD33 (My9), CD11 (OkM1), and CD14 (My4 and Mo2). Molecular analysis of leukemic cell DNA from this and two other patients showed rearrangement of the immunoglobulin (Ig) heavy-chain genes, but without any evidence of kappa light-chain gene rearrangement. T-cell receptor (TCR) genes remained in the germline configuration in these cases. Cytogenetic analysis showed translocation t(4;11) (q21;q23) in all four cases studied. In the group of ANLL, three cases belonged to the M4 and one to the M2 subtype. Chromosomal abnormality involving 11q23 was also detected in two patients: t(11;17)(q23;q11) and del(11)(q14q23) in each case respectively. Neither Ig nor TCR gene rearrangement was present in blast cells from patients with ANLL. The data indicate that chromosomal rearrangement of band 11q23 was quite common in Chinese infants with either form of leukemia, a finding that may have pathogenetic implications.

Molecular cloning and analysis of chromosome band 11q23 involved in leukaemia‐associated translocations

“…The frequency of this family of translocations affecting chromosome band llq23 has been estimated to be approximately 5% in adult and childhood acute leukaemias (Abe and Sandberg, 1984;Raimondi et al, 1989). By contrast, the incidence of llq23 abnormalities in leukaemias in infants of under 12 months of age has been found to be much higher (75% or greater) (Abe et al, 1983;Kaneko et al, 1988Chuu et al, 1990Gibbons et al, 1990). In addition to such findings in "de novo" leukaemias, evidence is emerging to link epipodophyllotoxin treatment of malignant disorders to the occurrence of secondary leukaemias with llq23 abnormalities (Pui et al, 1989;Prieto et al, 1990;Pedersen-Bjergaard and Philip, 1991;Whitlock et al, 1991).…”

Unexpected mortality from the use of E. coli L-asparaginase during remission induction therapy for childhood acute lymphoblastic leukemia: a report from the Taiwan Pediatric Oncology Group

“…Immunophenotypic studies were performed by previously described methods. 10 Standard-risk ALL was defined by the following criteria: (1) leukocyte count Ͻ10 × 10 9 /l for patients aged 1 to 2 years or 7 to 10 years; Ͻ50 × 10 9 /l for those aged 2 to 7 years; and (2) non-T, non-B immunophenotype, no central nervous system (CNS) leukemia, as defined by the presence of any leukemic lymphoblasts identified on cytocentrifuged smears of cerebrospinal fluid, 11 or the presence of cranial nerve palsies and the lack of expression of two or more myeloid-associated antigens (CD11, CD13, CD14, CD15 or CD33).…”

Structure and expression of the human trithorax-like gene 1 involved in acute leukemias.

“…These rearrangements are observed in acute leukemias, especially-t(4;11), t(1;11), and t(11;19) translocations (2,3) in acute lymphoid leukemias (ALL) and t(1;11), t(2;11), t(6;11), t(9;11), t(10;11), t(l1;l17), and t(X;ll) in acute myeloid leukemias (AML) (4)(5)(6)(7)(8). The frequency of translocations involving this region is notably higher in infants (estimated to be 75%) (9)(10)(11) than in children and adults (=5%) (12,13). It has been shown that this region of the genome contains the human trithorax-like gene 1 (Htrxl gene), which is interrupted in the translocation event in infant leukemic patients and in the cell line RS4;11 (14).…”