T-cell prolymphocytic leukemia with an unusual phenotype CD4+ CD8+

Kluin-Nelemans, Hanneke C.; Gmelig-Meyling, F.H.J.; Kootte, A. M. M.; Ottolander, G. J. den; Termijtelen, A.; Kluin, Philip M.; Beverstock, Geoffrey C.; Brand, Anneke

doi:10.1002/1097-0142(19870815)60:4<794::aid-cncr2820600415>3.0.co;2-r

Cited by 8 publications

(2 citation statements)

References 51 publications

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“…Both cases of ALL were immunophenotyped in suspension and on cytocentrifuge preparations (6) . Primary antibodies used were : goat or burro FITC and TRITC-conjugated anti-Ig antisera (Kallestad, Nordic), for detection of cell surface Ig and cytoplasmic Fr chains, rabbit anti-terminal transferase (TdT) (Bethesda Research Laboratories, Gaithersburg, MD), CD10 (BA3) (Hybritech, Luik, Belgium), CD19 (B4), and CD20 (Bl), CD24 (BAI) (Hybritech), CD2 (Leu-5) (Becton Dickinson & Co.), and CD7 (WT1) (Sanbio, Uden, The Netherlands) .…”

Section: Immunophenotypic Analysismentioning

confidence: 99%

Translocation t(14;18) in B cell lymphomas as a cause for defective immunoglobulin production.

Jong¹,

Voetdijk²,

Ommen³

et al. 1989

The Journal of Experimental Medicine

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Although follicle center cell (FCC) lymphomas represent mature B cells, a considerable percentage do not have detectable Ig production. We have used Southern blotting and the polymerase chain reaction (PCR) to study the involvement of translocations t(14;18) and t(8;14) in causing defective Ig production in 16 Ig- FCC-derived lymphomas and three Ig- B cell acute lymphoblastic leukemias. In 6 of 19 cases, a t(14;18) was present with the other allele either deleted or in germline. In two cases a t(14;18) and a t(8;14) affected both Ig alleles, as confirmed by karyotyping. In two other cases, rearrangement of both bcl-2 on chromosome 18 and c-myc on chromosome 8 were found as well. Although cytogenetic proof was not available, the latter was probably involved in t(8;14). Restriction map analysis of one more case showed rearrangement on the pseudo-JH3 gene on one allele and t(14;18) on the other. Thus, in 11 of 19 cases, defective Ig H chain production could be explained by the inactivation of both Ig H chain genes due to translocation of one allele, in combination with deletions or defective rearrangements of the other allele. In contrast, in 28 of 30 Ig+ lymphomas, one functional Ig H chain allele was found, either in, or not in, combination with t(14;18). In two cases a single rearranged Ig H chain allele was found in combination with rearrangement of bcl-2. No comigration of the single Ig rearrangement with bcl-2, however, was found both by Southern blotting and PCR, suggesting a variant bcl-2 translocation, which leaves the Ig H chain allele functionally intact.

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Section: Immunophenotypic Analysismentioning

confidence: 99%

Translocation t(14;18) in B cell lymphomas as a cause for defective immunoglobulin production.

Jong¹,

Voetdijk²,

Ommen³

et al. 1989

The Journal of Experimental Medicine

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“…Mononuclear cells were obtained from heparinized venous blood and bone marrow by Ficoll-Hypaque gradient centrifugation. The peripheral blood contamination in the aspirates, calculated according to Holdrinet et a1 (1980) phenotypes were determined by immunoluorescense microscopy as described (Kluin-Nelemans et al, 1987). At least 200 nucleated cells were scored.…”

Section: Red Blood Cells Complement Sensitivity Of Rbcs Was Tested Bmentioning

confidence: 99%

Haematopoietic and immunologic abnormalities in severe aplastic anaemia patients treated with anti‐thymocyte globulin

et al. 1989

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Summary. Thirty‐five patients with severe aplastic anaemia (SAA) were extensively evaluated 0.3‐12.4 years (median 3.8) after anti‐thymocyte globulin (ATG) treatment. All but one were transfusion independent. Most patients revealed a normal Hb level and a granulocyte count over 1.5 × 109/1 but were still thrombocytopenic due to decreased platelet production. Lymphocytopenia and/or monocytopenia was found in about 30%. Two patients had a monocytosis. Although there was a great range in degree of recovery at various time intervals after ATG. patients tested more than 4 years after ATG tended to have higher cell counts. Lymphocyte counts correlated with the interval between ATG and evaluation, and with haematopoietic recovery. Qualitative abnormalities were found in all cell lines. Most patients showed a homogeneous macrocytic RBC population, and almost 50% a positive sucrose lysis test: only three patients showed evidence of haemolysis and only two of these showed a positive Ham test. Mean platetet volumes were reduced out of proportion to their number. Platelet function, determined by bleeding time and aggregometry, was impaired in over 30%. The granulocytic series showed a shift to the left in about 30%. Hypersegmentation and pseudo Pelger‐Huet anomaly were seen in some patients. Lymphocyte subset distribution in blood and bone marrow was within the normal range but absolute blood levels of CD4 cells in particular were slightly decreased, and tended to increase gradually with time after ATG. IgG and IgA levels were significantly decreased. In only one patient cytogenetic analysis of unstimulated bone marrow cells revealed an abnormal karyotype, but in eight of eight patients an increased sensitivity of lymphocytes to X‐rays was found. These data suggest impairment at the level of the very early haematopoietic progenitor cell in all patients up to 10 years after ATG. Since similar findings have been reported in clonal (pre‐)malignant disease, SAA, improved after ATG treatment, might be prone to clonal (malignant) evolution.

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2021

Flow Cytometry of Hematological Malignancies

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T-cell prolymphocytic leukemia with an unusual phenotype CD4+ CD8+

Cited by 8 publications

References 51 publications

Translocation t(14;18) in B cell lymphomas as a cause for defective immunoglobulin production.

Translocation t(14;18) in B cell lymphomas as a cause for defective immunoglobulin production.

Haematopoietic and immunologic abnormalities in severe aplastic anaemia patients treated with anti‐thymocyte globulin

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