HLA-DR antigen-negative acute myeloid leukemia

M. Wetzler, B. K. McElwain, C. C. Stewart, L. Blumenson, A. Mortazavi, L. A. Ford, James L Slack, M. Barcos, S. Ferrone, M. R. Baer

Research output: Contribution to journalArticle

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Abstract

Human leukocyte antigen (HLA) Class II antigens are variably expressed on acute myeloid leukemia (AML) blasts. The biological and clinical significance of HLA Class II antigen expression by AML cells is not known. Therefore, we sought to characterize cases of AML without detectable HLA-DR expression. Samples from 248 consecutive adult AML patients were immunophenotyped by multiparameter flow cytometry at diagnosis. HLA-DR antigens were not detected on AML cells from 43 patients, including 20 with acute promyelocytic leukemia (APL), and 23 with other subtypes of AML. All APL cases had t(15;17), but there were no characteristic chromosome abnormalities in non-APL cases. No direct expression of other antigens was identified in HLA-DR-negative APL and non-APL cases. Interestingly, cells from three HLA-DR-negative non-APL patients had similar morphology to that of the hypogranular variant of APL. This morphology, however, was not present in any HLA-DR-positive AML cases. Treatment response was similar in the 23 HLA-DR-negative non-APL and the 205 HLA-DR-positive patients. Finally, relapse was infrequently associated with changes in HLA-DR antigen expression, as the HLA-DR antigen was lost at relapse in only 4% of HLA-DR-positive cases, and was gained at relapse in only 17% of HLA-DR-negative cases. We conclude that HLA-DR-negative AML includes approximately equal numbers of APL and non-APL cases, and that the morphology of HLA-DR-negative non-APL cases can mimic the hypogranular variant of APL. The diagnosis of APL cannot be based on morphology and lack of HLA-DR antigen expression; rather, it requires cytogenetic or molecular confirmation.

Original languageEnglish (US)
Pages (from-to)707-715
Number of pages9
JournalLeukemia
Volume17
Issue number4
DOIs
StatePublished - Apr 1 2003
Externally publishedYes

Fingerprint

HLA Antigens
Acute Myeloid Leukemia
Antigens
Acute Promyelocytic Leukemia
Leukemia
Histocompatibility Antigens Class II
Myeloid Cells
Recurrence
Cytogenetics
Chromosome Aberrations

Keywords

  • Acute myeloid leukemia
  • HLA-DR
  • Immunophenotype

ASJC Scopus subject areas

  • Hematology
  • Cancer Research

Cite this

Wetzler, M., McElwain, B. K., Stewart, C. C., Blumenson, L., Mortazavi, A., Ford, L. A., ... Baer, M. R. (2003). HLA-DR antigen-negative acute myeloid leukemia. Leukemia, 17(4), 707-715. https://doi.org/10.1038/sj.leu.2402865

HLA-DR antigen-negative acute myeloid leukemia. / Wetzler, M.; McElwain, B. K.; Stewart, C. C.; Blumenson, L.; Mortazavi, A.; Ford, L. A.; Slack, James L; Barcos, M.; Ferrone, S.; Baer, M. R.

In: Leukemia, Vol. 17, No. 4, 01.04.2003, p. 707-715.

Research output: Contribution to journalArticle

Wetzler, M, McElwain, BK, Stewart, CC, Blumenson, L, Mortazavi, A, Ford, LA, Slack, JL, Barcos, M, Ferrone, S & Baer, MR 2003, 'HLA-DR antigen-negative acute myeloid leukemia', Leukemia, vol. 17, no. 4, pp. 707-715. https://doi.org/10.1038/sj.leu.2402865
Wetzler M, McElwain BK, Stewart CC, Blumenson L, Mortazavi A, Ford LA et al. HLA-DR antigen-negative acute myeloid leukemia. Leukemia. 2003 Apr 1;17(4):707-715. https://doi.org/10.1038/sj.leu.2402865
Wetzler, M. ; McElwain, B. K. ; Stewart, C. C. ; Blumenson, L. ; Mortazavi, A. ; Ford, L. A. ; Slack, James L ; Barcos, M. ; Ferrone, S. ; Baer, M. R. / HLA-DR antigen-negative acute myeloid leukemia. In: Leukemia. 2003 ; Vol. 17, No. 4. pp. 707-715.
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AU - Mortazavi, A.

AU - Ford, L. A.

AU - Slack, James L

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AB - Human leukocyte antigen (HLA) Class II antigens are variably expressed on acute myeloid leukemia (AML) blasts. The biological and clinical significance of HLA Class II antigen expression by AML cells is not known. Therefore, we sought to characterize cases of AML without detectable HLA-DR expression. Samples from 248 consecutive adult AML patients were immunophenotyped by multiparameter flow cytometry at diagnosis. HLA-DR antigens were not detected on AML cells from 43 patients, including 20 with acute promyelocytic leukemia (APL), and 23 with other subtypes of AML. All APL cases had t(15;17), but there were no characteristic chromosome abnormalities in non-APL cases. No direct expression of other antigens was identified in HLA-DR-negative APL and non-APL cases. Interestingly, cells from three HLA-DR-negative non-APL patients had similar morphology to that of the hypogranular variant of APL. This morphology, however, was not present in any HLA-DR-positive AML cases. Treatment response was similar in the 23 HLA-DR-negative non-APL and the 205 HLA-DR-positive patients. Finally, relapse was infrequently associated with changes in HLA-DR antigen expression, as the HLA-DR antigen was lost at relapse in only 4% of HLA-DR-positive cases, and was gained at relapse in only 17% of HLA-DR-negative cases. We conclude that HLA-DR-negative AML includes approximately equal numbers of APL and non-APL cases, and that the morphology of HLA-DR-negative non-APL cases can mimic the hypogranular variant of APL. The diagnosis of APL cannot be based on morphology and lack of HLA-DR antigen expression; rather, it requires cytogenetic or molecular confirmation.

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