The clinical significance of the expression of CD7 antigen on the blas
ts of 207 consecutive patients with de novo acute myeloid leukemia (AM
L) was evaluated. For this purpose, fifty-three CD7+ patients (23 fema
les and 30 males; mean age 52 years) were analyzed and classified into
the following subtypes according to French-American-British (FAB) cla
ssification: 7 MD, 13 M1, 9 M2, 1 M3, 9 M4, 14 M5. Immunophenotypic st
udies were carried out by flow cytometry and blast cells were selected
on the basis of forward light scatter gating and pan-myeloid marker,
either CD13 or CD33. All the CD7+ patients were negative for surface C
D3 and T-cell-receptor (TCR) molecules. We found no correlation betwee
n CD7 expression and sex, age, hepatosplenomegaly and/or central nervo
us system involvement. The immaturity of CD7+leukemic cells was suppor
ted by the high expression of CD34 (P = 0.001), CD7 positivity was sig
nificantly associated with a white blood cell count (WBC) greater than
100 x 10(9)/L (P = 0.003). P-Glycoprotein (P-170) expression was also
evaluated in 135 patients by a flow-cytometric assay: there was a clo
se relationship between CD7 and P-170 positivity (P < 0.001), For remi
ssion induction, all patients received therapeutic regimens routinely
used for AML, The complete remission (CR) rate was significantly lower
in CD7+ cases (32% vs 74%, P = 0.001). The overall survival and disea
se free survival rate of CD7+ AML was lower than those of CD7- patient
s (P < 0.001 and = 0.002, respectively). CD7+ AML with coexpression of
CD14 had a particularly unfavourable response and prognosis in compar
ison with CD7+ patients without CD14. These clinical findings in CD7AML subtype could be explained by the convergence of the following unf
avourable prognostic factors: 1) co-expression of immaturity markers (
CD34); 2) frequent monocytic differentiation (CD14); 3) strict correla
tion with P-170 phenotype. These findings may require an effort to dra
w up a more useful diagnostic formulation of AML in clinical managemen
t.