title: CD66c expression in B-cell acute lymphoblastic leukemia: strength and weakness.
abstract: BACKGROUND
  In B-cell acute lymphoblastic leukemia (B-ALL), testing at diagnosis for BCR/ABL1 gene rearrangements is mandatory for prognostic stratification and treatment decisions. Several diagnostic methods have been proposed using flow cytometry to identify BCR/ABL1(+) B-ALL.
  
  
  METHODS
  We evaluated expression of the myeloid antigen CD66c by flow cytometry in B-ALL. We studied 94 patients with B-ALL. The t(9;22)(q34;q11) or BCR/ABL1 rearrangement was detected by cytogenetic analysis or RT/PCR. Myeloid antigens CD66c, CD13, CD33, CD117, Myeloperoxidase, CD15 and CD65 were determined by flow cytometry.
  
  
  RESULTS
  Of these 94 cases, 17 (18%) cases displayed BCR/ABL1 gene rearrangements and 38 (40%) cases were CD66c positive. CD66c was the most common myeloid antigen expressed on malignant lymphoblasts. Its expression was correlated with BCR/ABL1 rearrangements (P = 0.0001): sensitivity 82%, specificity 69%, positive predictive value 37% and negative predictive value 95%. Co-expression of CD66c(+) CD13(+) was more frequent in BCR/ABL1(+) B-ALL (29%) than BCR/ABL1(-) cases (4%) (P = 0.0044). Some BCR/ABL1(-) B-ALL cases (including hyperdiploid or cases with normal karyotype) were CD66c positive (31%).
  
  
  CONCLUSIONS
  CD66c expression is correlated, but not specifically, with BCR/ABL1 rearrangement. It would seem better to interpret the absence of CD66c expression with a lack of BCR/ABL1 rearrangement. This myeloid antigen could be interesting in the detection of minimal residual disease.
authors.affiliation: Laboratoire d'Hématologie, Centre Hospitalier Universitaire, Amiens, France. guillaume.nicolas@chu-amiens.fr
authors.forename: N
authors.initials: N
authors.lastname: Guillaume
authors.forename: D
authors.initials: D
authors.lastname: Penther
authors.forename: I
authors.initials: I
authors.lastname: Vaida
authors.forename: B
authors.initials: B
authors.lastname: Gruson
authors.forename: V
authors.initials: V
authors.lastname: Harrivel
authors.forename: J F
authors.initials: JF
authors.lastname: Claisse
authors.forename: J C
authors.initials: JC
authors.lastname: Capiod
authors.forename: J J
authors.initials: JJ
authors.lastname: Lefrere
authors.forename: G
authors.initials: G
authors.lastname: Damaj
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD / Q000235:genetics* / Q000378:metabolism*; D015815:Cell Adhesion Molecules / Q000235:genetics* / Q000378:metabolism*; D002648:Child; D002675:Child, Preschool; D015331:Cohort Studies; D005260:Female; D016044:Fusion Proteins, bcr-abl / Q000235:genetics / Q000378:metabolism; D058851:GPI-Linked Proteins / Q000235:genetics / Q000378:metabolism; D015972:Gene Expression Regulation, Neoplastic; D015321:Gene Rearrangement / Q000235:genetics; D006801:Humans; D008297:Male; D008875:Middle Aged; D018365:Neoplasm, Residual / Q000235:genetics; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000235:genetics* / Q000378:metabolism*; D055815:Young Adult
chemical_list: D015703:Antigens, CD; C504117:CEACAM6 protein, human; D015815:Cell Adhesion Molecules; D058851:GPI-Linked Proteins; D016044:Fusion Proteins, bcr-abl