Surface marker analysis of acute myeloblastic leukemia: identification of differentiation-associated phenotypes

Abstract A series of monoclonal antibodies reactive with normal myeloid cells at different stages of differentiation (anti-MY4, -MY7, -MY8, -Mo1, -Ia) were used to characterize the leukemic cells of 70 patients with acute myeloblastic leukemia (AML). Sixty-two of the leukemias expressed a phenotype corresponding to a recognizable immature normal myeloid cell. These 62 cases could be divided into 4 phenotype groups, corresponding approximately to the normal CFU-C (group I, 21%), myeloblast (group II, 26%), promyelocyte (group III, 8%), and promonocyte (group IV, 45%). Morphological subtyping of these leukemias tended to agree with the immunologic phenotype, particularly with more “differentiated” morphological subtypes, such as acute monocytic leukemia or acute promyelocytic leukemia. However, each phenotype group contained more than one morphological type of AML, indicating that the level of differentiation of the surface membrane of AML cells may not always be concordant with morphology. The phenotype groups were also analyzed with respect to cytochemical staining patterns, age, the presence of Auer rods, and complete remission rates. Statistically significant differences among the groups were noted in the distribution of myeloperoxidase staining, nonspecific esterase staining, and Auer rods. The complete remission rates varied from 60% (groups III and IV) to 88% (group II). These results suggest that surface marker analysis in AML may be used as a highly reproducible classification system that will provide additional information about the leukemic cells in conjunction with morphological analysis.

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Surface marker analysis of acute myeloblastic leukemia: identification of differentiation-associated phenotypes

Blood ◽

10.1182/blood.v62.3.557.bloodjournal623557 ◽

1983 ◽

Vol 62 (3) ◽

pp. 557-563

Author(s):

JD Griffin ◽

RJ Mayer ◽

HJ Weinstein ◽

DS Rosenthal ◽

FS Coral ◽

...

Keyword(s):

Complete Remission ◽

Surface Marker ◽

Acute Myeloblastic Leukemia ◽

Leukemic Cells ◽

Nonspecific Esterase ◽

Marker Analysis ◽

Group I ◽

Remission Rates ◽

Group Ii ◽

Surface Marker Analysis

A series of monoclonal antibodies reactive with normal myeloid cells at different stages of differentiation (anti-MY4, -MY7, -MY8, -Mo1, -Ia) were used to characterize the leukemic cells of 70 patients with acute myeloblastic leukemia (AML). Sixty-two of the leukemias expressed a phenotype corresponding to a recognizable immature normal myeloid cell. These 62 cases could be divided into 4 phenotype groups, corresponding approximately to the normal CFU-C (group I, 21%), myeloblast (group II, 26%), promyelocyte (group III, 8%), and promonocyte (group IV, 45%). Morphological subtyping of these leukemias tended to agree with the immunologic phenotype, particularly with more “differentiated” morphological subtypes, such as acute monocytic leukemia or acute promyelocytic leukemia. However, each phenotype group contained more than one morphological type of AML, indicating that the level of differentiation of the surface membrane of AML cells may not always be concordant with morphology. The phenotype groups were also analyzed with respect to cytochemical staining patterns, age, the presence of Auer rods, and complete remission rates. Statistically significant differences among the groups were noted in the distribution of myeloperoxidase staining, nonspecific esterase staining, and Auer rods. The complete remission rates varied from 60% (groups III and IV) to 88% (group II). These results suggest that surface marker analysis in AML may be used as a highly reproducible classification system that will provide additional information about the leukemic cells in conjunction with morphological analysis.

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Surface Marker Analysis of Acute Myeloblastic Leukemia

Cancer Treatment and Research - Chronic and Acute Leukemias in Adults ◽

10.1007/978-1-4613-2581-9_4 ◽

1985 ◽

pp. 113-145 ◽

Cited By ~ 1

Author(s):

James D. Griffin

Keyword(s):

Surface Marker ◽

Acute Myeloblastic Leukemia ◽

Marker Analysis ◽

Surface Marker Analysis

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The importance of cell size and surface marker analysis in childhood acute myeloblastic leukemia

Leukemia Research ◽

10.1016/s0145-2126(99)00053-3 ◽

1999 ◽

Vol 23 (8) ◽

pp. 701-707 ◽

Cited By ~ 1

Author(s):

Lale Olcay ◽

Ulya Ertem ◽

Hamza Okur ◽

A.Murat Tuncer

Keyword(s):

Cell Size ◽

Surface Marker ◽

Acute Myeloblastic Leukemia ◽

Marker Analysis ◽

Surface Marker Analysis

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Use of surface marker analysis to predict outcome of adult acute myeloblastic leukemia

Blood ◽

10.1182/blood.v68.6.1232.bloodjournal6861232 ◽

1986 ◽

Vol 68 (6) ◽

pp. 1232-1241

Author(s):

JD Griffin ◽

R Davis ◽

DA Nelson ◽

FR Davey ◽

RJ Mayer ◽

...

Keyword(s):

T Cell ◽

Complete Remission ◽

Clinical Significance ◽

Total Population ◽

Cell Lineage ◽

Antigen Expression ◽

Acute Myeloblastic Leukemia ◽

Myeloid Antigens ◽

Hla Dr ◽

Surface Marker Analysis

In order to investigate the clinical significance of surface antigen analysis in acute myeloblastic leukemia (AML), the blasts from 196 patients with AML were analyzed prospectively with a panel of 16 monoclonal antibodies. The antibodies were selected to identify differentiation-associated antigens of either the myeloid lineage (MY9, PM-81, AML-2–23, MY7, MCS-1, MY8, Mo1, MY1, MY4, Mo2), T cell lineage (T101, T11), B cell lineage (B1, B4) or multiple lineages [J5 (CALLA), HLA-DR]. Independent morphological review and classification by French- American-British (FAB) criteria was performed in 161 of the 196 cases. One or more myeloid surface antigens were detected on the blasts of 195 cases, while B and T cell markers were detected on 0% to 2% of cases. When both blood and marrow samples were studied on the same patient, very few differences were noted between the antigenic profiles of the paired specimens. The frequency of expression of individual myeloid antigens ranged from 91% (PM-81) to 29% (Mo2). Expression of individual antigens was found to correlate significantly with several clinical parameters including FAB classification, cytochemical staining for alpha naphthyl acetate esterase, leukocyte count, and the presence of extramedullary disease at presentation. Two myeloid antigens (MY4 and MY7) predicted for a low rate of complete remission (CR) to standard induction chemotherapy. MY4+ cases (37% of the total population) had a CR rate of 53%, while M4- cases had a CR rate of 69% (P = .03). MY7+ cases (57% of the total population) had a CR rate of 55% while MY7- cases had a CR rate of 73% (P = .01). Neither MY4 nor MY7 antigen expression was correlated with patient age. Paired combinations of antigens were also examined. The [MY4- MY7-] phenotype was exhibited by 32% of all cases and was associated with an 82% CR rate while the CR rate of all other cases was 54% (P = .001). The expression of three antigens (HLA-DR, MY8, Mo1) was associated with a decreased continuous complete remission (P less than .05, median follow-up time of 19 months). Expression of MY8 antigen was also associated with decreased survival (P = .03). These results confirm earlier reports of antigenic heterogeneity in AML, and indicate that immunologically defined subgroups of AML patients which are of potential clinical significance can be identified.

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A unique surface marker profile in T-cell acute lymphocytic leukemia

Blood ◽

10.1182/blood.v55.4.702.bloodjournal554702 ◽

1980 ◽

Vol 55 (4) ◽

pp. 702-705

Author(s):

ER Richie ◽

MP Sullivan ◽

J van Eys

Keyword(s):

T Cell ◽

Peripheral Blood ◽

Acute Lymphocytic Leukemia ◽

Early Stage ◽

Mixed Lymphocyte Culture ◽

Lymphocyte Culture ◽

Surface Marker ◽

Lymphocytic Leukemia ◽

Leukemic Cells ◽

Surface Marker Analysis

A 5-yr-old girl with acute lymphocytic leukemia presented with moderate hepatomegaly, marked splenomegaly, but no evidence of a mediastinal mass. The peripheral blood white count was 270 x 10(9)/liter with 99% leukemic cells. Surface marker analysis showed the lymphoblasts to be E- rosette negative and complement receptor positive. The patient's leukemic cells were unreactive with anti-p23,30, which detects Ia-like antigens, and strongly reactive with A99 anti-T-cell serum, which reacts with normal human thymocytes and peripheral blood T cells. The percentage of leukemic cells bearing complement receptors diminished during relapse. The leukemic cells obtained at diagnosis and during relapse were nonreactive to mitogens and alloantigens and failed to stimulate proliferation of normal lymphocytes in mixed lymphocyte culture. There was no evidence for active suppression of normal lymphocyte reactivity mediated by the leukemic cells. The surface marker and functional profile of these leukemic cells is consistent with that of an early stage in T-cell maturation.

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