Lineage ambiguity in acute leukemia

Roberts, George T.; Badawi, Saad B. El; Sackey, Kwesi; Spence, David; Sheth, Kirtikant V.; Aur, Rhomes J. A.

doi:10.1002/1097-0142(19861001)58:7<1473::aid-cncr2820580716>3.0.co;2-0

Cited by 8 publications

(1 citation statement)

References 24 publications

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“…When classification could not be achieved by light microscopy alone, the blast cells were examined by electron microscopy in a Jeol 100B electron microscope, either untreated or after treatment for myeloperoxidase or platelet peroxidase using standard methods [8]. Since 1984, the blast cells of transformants were studied for surface immunophenotype using commercially obtained monoclonal antibodies derived from mouse ascitic fluid, using a previously described method [9].…”

Section: Methodsmentioning

confidence: 99%

Morphological and Immunological Pattern of Blastic Transformation in Chronic Myeloid Leukemia in Saudi Arabia: Study of 90 Transformations Among 248 Patients

et al. 1991

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We examined the pattern of blastic transformation in 90 of 248 patients (36%) with chronic myeloid leukemia who were seen at the King Faisal Specialist Hospital and Research Centre between 1975 and1988. The mean and median ages of all patients were 38.2 and 36.0 years, respectively. Four of the 90 transformants (4.4%) presented in blastic transformation, and 86 cases (95.5%) evolved from a well-defined chronic phase. Twenty-nine (32.2%) of the patients underwent lymphoid blastic transformation, while 28 (31.1%) were myeloid, seven (7.8%) were myelomonocytic, four (4.4%) were monocytic or erythroblastic, six (6.7%) were megakaryoblastic, ten (11.1%) were of mixed lineage, and two (2.2%) were unclassifiable. The lymphoid blast cells were uniformly common acute lymphocytic leukemia (i.e., Ia and CD10 positive), whereas the myeloid transformations were predominantly Ia negative. Mixed phenotype blasts were also predominantly Ia positive (i.e., 8 of 10), with varying positivity for CD10 and myeloid/monocytic markers. We conclude that blast crisis in chronic myeloid leukemia occurs in Saudi patients in a pattern similar to that seen in patients elsewhere, and that surface Ia antigen positivity in lymphoblast cells is a reliable marker for differentiating lymphoid from nonlymphoid crisis, in which the Ia antigen is not usually demonstrable.

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Section: Methodsmentioning

confidence: 99%

Morphological and Immunological Pattern of Blastic Transformation in Chronic Myeloid Leukemia in Saudi Arabia: Study of 90 Transformations Among 248 Patients

et al. 1991

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Hairy cell leukemia cells express CD1A antigen

Panfilis¹,

Manara²,

Torresani³

et al. 1988

Cancer

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Five patients with hairy cell leukemia (HCL) were studied. Peripheral blood leukocytes, rosette-forming cells (T) and non-T-cells were stained in immunofluorescence by a panel of monoclonal antibodies to investigate the phenotype of HCL cells (HCLC). In all patients HCLC showed B-lymphocyte phenotype, although they were not stained by antibodies reactive for monocytes, natural killer cells, or T-cells. However, in all instances the large majority of HCLC were unexpectedly stained with an antibody (anti-CD1a) usually detectable only in early thymocytes and on Langerhans cells. This finding was further confirmed by immunoelectron microscopy. This type of ambiguity in the lineage of HCL could imply that HCLC might arise from cells differentiated towards the B-cell lineage, still sustaining an early antigen of a different (T) lineage. These results, moreover, extend the range of the known distribution of the CD1a antigen, which could be useful in diagnosing HCL.

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Surface marker analysis and karyotype distinguish acute biphenotypic leukemia from acute myelogenous leukemia expressing terminal deoxynucleotidyl transferase

Moscinski

Nowell̀

Hoxie

et al. 1991

Cancer

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Surface phenotyping by flow cytometry and cytochemical study were used to identify 15 adult patients with acute leukemia displaying ambiguous phenotypes. Differences were found in the blast cell karyotype and immunoglobulin gene rearrangements of terminal deoxynucleotidyl transferase (TdT)‐positive acute myelogenous leukemia (AML) and biphenotypic leukemia expressing B lymphoid and myeloid markers. The karyotypic abnormalities, t(9;22) and t(4;11), were noticed in acute biphenotypic leukemia, and were consistently associated with rearrangement at the immunoglobulin locus. Furthermore, coexpression of CD19/CD20 and either myeloperoxidase or myeloid surface markers were predictive of finding the t(9;22) or t(4;11) karyotype. Patients with TdT‐positive AML, on the other hand, were less likely to show rearrangement at the immunoglobulin locus, and did not have the t(9;22) or t(4;11). Instead, a variety of nonrandom karyotypic abnormalities were seen, including trisomy 13. Unlike common AML, the majority of TdT‐positive cases demonstrated an abnormal karyotype with duplications and/ or deletions present in all cases. In no instance was trisomy 8, t(8;21), t(15;17), or any other isolated translocation identified. The authors therefore suggest that immunophenotyping, when combined with cytochemical analysis of TdT and myeloperoxidase or Sudan black B, may aid in the characterization of subgroups of atypical acute leukemia, such that alternate approaches to therapy can be evaluated. Cancer 68:2161–2168, 1991.

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Lineage ambiguity in acute leukemia

Cited by 8 publications

References 24 publications

Morphological and Immunological Pattern of Blastic Transformation in Chronic Myeloid Leukemia in Saudi Arabia: Study of 90 Transformations Among 248 Patients

Morphological and Immunological Pattern of Blastic Transformation in Chronic Myeloid Leukemia in Saudi Arabia: Study of 90 Transformations Among 248 Patients

Hairy cell leukemia cells express CD1A antigen

Surface marker analysis and karyotype distinguish acute biphenotypic leukemia from acute myelogenous leukemia expressing terminal deoxynucleotidyl transferase

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