title: Expression of myeloid-associated and lymphoid-associated cell-surface antigens in acute myeloid leukemia of childhood: a Pediatric Oncology Group study.
abstract: OBJECTIVE
  Although the expression of both myeloid- and lymphoid-associated cell-surface antigens in acute myeloid leukemia (AML) has been described, the clinical significance of such antigen expression remains unknown in the pediatric population. We sought to define an antibody panel for optimal diagnostic antigenic analysis and to test associations among antigen expression and a number of clinical features at presentation and prognosis in pediatric AML.
  
  
  METHODS
  We reviewed the extensive immunophenotypic analysis performed at the time of diagnosis on 132 assessable patients registered on a single Pediatric Oncology Group AML protocol between 1984 and 1988.
  
  
  RESULTS
  Eighty-eight percent of patients were identified by testing for expression of CD33 and CD13. Overall, 61% of patients expressed at least one lymphoid-associated antigen, most commonly CD4, CD7, or CD19. Expression of CD5, CD10, CD20, or CD22, commonly detected in T- or B-lineage pediatric acute lymphoid leukemia (ALL), was uncommon; coexpression of multiple lymphoid-associated antigens was also uncommon. Expression of the monocyte-associated antigen CD14 correlated with French-American-British (FAB) M4 or M5 morphology. Otherwise, no correlation between antigen expression and FAB classification was noted. None of the myeloid, lymphoid, natural-killer (NK), or progenitor-associated antigens were associated with significant differences in the likelihood of remission induction or event-free survival when expressor versus nonexpressor groups were compared.
  
  
  CONCLUSIONS
  The distribution of cell-surface antigen expression in pediatric acute leukemia usually permitted the discrimination of AML from ALL by using a limited panel of antibodies. Although the expression of lymphoid-associated antigens was common, such expression did not seem to be associated with an adverse prognosis in pediatric AML.
authors.affiliation: Johns Hopkins Oncology Center, Baltimore, MD.
authors.forename: S J
authors.initials: SJ
authors.lastname: Kuerbitz
authors.forename: C I
authors.initials: CI
authors.lastname: Civin
authors.forename: J P
authors.initials: JP
authors.lastname: Krischer
authors.forename: Y
authors.initials: Y
authors.lastname: Ravindranath
authors.forename: C P
authors.initials: CP
authors.lastname: Steuber
authors.forename: H J
authors.initials: HJ
authors.lastname: Weinstein
authors.forename: N
authors.initials: N
authors.lastname: Winick
authors.forename: A H
authors.initials: AH
authors.lastname: Ragab
authors.forename: M V
authors.initials: MV
authors.lastname: Gresik
authors.forename: W M
authors.initials: WM
authors.lastname: Crist
mesh_terms: D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D000911:Antibodies, Monoclonal; D000951:Antigens, Neoplasm / Q000032:analysis*; D000954:Antigens, Surface / Q000032:analysis*; D002648:Child; D015870:Gene Expression; D006801:Humans; D016130:Immunophenotyping; D007951:Leukemia, Myeloid / Q000175:diagnosis / Q000378:metabolism*; D015993:Life Tables; D011379:Prognosis; D016016:Proportional Hazards Models
chemical_list: D000911:Antibodies, Monoclonal; D000951:Antigens, Neoplasm; D000954:Antigens, Surface