Immunophenotyping

Behm, Frederick G.

doi:10.1017/cbo9780511471001.008

Cited by 7 publications

(5 citation statements)

References 448 publications

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“…A minority of the cases carry t(2;8)(p11;q24) or t(8;22)(q24;q11) chromosomal rearrangements. These three rearrangements share the juxtaposition of MYC proto-oncogene on chromosome 8 and either the heavy or light chain immunoglobulin genes 27 . MYC rearrangement was also reported to involve a non-immunoglobulin chromosomal locus t(4;8)(q31.1;q24.1) in the B-lymphoblasts of a 4-year-old boy 19 .…”

Section: Discussionmentioning

confidence: 99%

B Lymphoblastic Leukemia/Lymphoma With Burkitt-like Morphology and IGH/MYC Rearrangement

Gupta

Molofsky

et al. 2018

American Journal of Surgical Pathology

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Isolated MYC rearrangement without other recurrent genetic abnormalities is rare in B lymphoblastic leukemia/lymphoma (B-ALL/LBL), with most cases reported in pediatric patients. We report 3 adult cases with lymphoblasts showing a precursor B cell immunophenotype, and isolated MYC/IGH translocation. All 3 cases occurred in male patients with initial presentation of diffuse lymphadenopathy. Cases 1 and 2 had B-ALL with significantly increased lymphoblasts in peripheral blood and bone marrow. Case 3, a patient with human immunodeficiency virus infection, had the diagnosis of B-LBL made on a retroperitoneal lymph node biopsy and had no peripheral blood or bone marrow involvement. The leukemic and lymphoma cells in all 3 cases demonstrated Burkitt lymphoma-like morphology with deeply basophilic cytoplasm and numerous cytoplasmic vacuoles. However, all 3 had immature immunophenotypes including expression of terminal deoxynucleotidyl transferase (TdT), absence of BCL6, and dim-to-negative CD45. CD20 was largely negative in 2 of 3 cases. All 3 had confirmed MYC/IGH translocation, but lacked rearrangements of BCL2 or BCL6. EBV was negative by Epstein-Barr virus encoded small RNA in situ hybridization. Treatment protocols varied, including both high-risk ALL-type (protocol 8707) and high-grade lymphoma regimens (hyper-CVAD [cyclophosphamide, vincristine, adriamycin, and dexamethasone]), but no patient achieved continuous complete remission. These cases seem to represent a distinct biological phenomenon, in which a MYC translocation may be acquired at an immature stage of differentiation, thus manifesting features of both B-ALL/LBL and Burkitt lymphoma.

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Section: Discussionmentioning

confidence: 99%

B Lymphoblastic Leukemia/Lymphoma With Burkitt-like Morphology and IGH/MYC Rearrangement

Gupta

Molofsky

et al. 2018

American Journal of Surgical Pathology

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“…Immunophenotyping of leukemic cells at diagnosis was performed by standard methods. 24 Leukemic and normal mononuclear cells were collected after centrifugation on a Lymphoprep density gradient (Nycomed, Oslo, Norway) and were washed 3 times in phosphate-buffered saline. For the microarray experiments, CD19 ϩ leukemic cells were enriched using a magnetic cell separation system (Miltenyi Biotec, Bergisch Gladbach, Germany), yielding more than 98% CD19 ϩ cell purity.…”

Section: Cellsmentioning

confidence: 99%

Identification of novel markers for monitoring minimal residual disease in acute lymphoblastic leukemia

Chen

Coustan‐Smith

Suzuki

et al. 2001

Blood

144

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To identify new markers of minimal residual disease (MRD) in B-lineage acute lymphoblastic leukemia (ALL), gene expression of leukemic cells obtained from 4 patients with newly diagnosed ALL was compared with that of normal CD19 ؉ CD10 ؉ B-cell progenitors obtained from 2 healthy donors. By cDNA array analysis, 334 of 4132 genes studied were expressed 1.5-to 5.8-fold higher in leukemic cells relative to both normal samples; 238 of these genes were also overexpressed in the leukemic cell line RS4;11. Nine genes were selected among the 274 overexpressed in at least 2 leukemic samples, and expression of the encoded proteins was measured by flow cytometry. Two proteins (caldesmon and myeloid nuclear differentiation antigen) were only weakly expressed in leukemic cells despite strong hybridization signals in the array. By contrast, 7 proteins (CD58, creatine kinase B, ninjurin1, Ref1, calpastatin, HDJ-2, and annexin VI) were expressed in B-lineage ALL cells at higher levels than in normal CD19 ؉ CD10 ؉ B-cell progenitors (P < .05 in all comparisons). IntroductionIn B-lineage acute lymphoblastic leukemia (ALL), the most common form of leukemia in children, the level of minimal (ie, submicroscopic) residual disease (MRD) during clinical remission is one of the most powerful prognostic indicators. 1 Correlative studies have demonstrated that detection of MRD by flow cytometric or polymerase chain reaction (PCR) analysis of leukemiaspecific markers is strongly associated with subsequent relapse. 2-10 Therefore, MRD assays are being introduced into treatment protocols as a tool to gauge treatment response and aid in the selection of therapeutic strategies.The greatest remaining obstacle to the routine use of MRD studies in ALL therapy protocols is that none of the techniques currently available for MRD detection can be applied to all patients. PCR amplification of chromosomal breakpoints can be applied to fewer than half of all children with ALL, that is, those whose leukemic cells express nonrandom genetic abnormalities. 11 The success rate of PCR analysis of antigen-receptor genes ranges from 80% to 90% because of lack of sufficiently specific leukemia sequences, oligoclonality, and clonal evolution. [12][13][14][15] This method is also laborious and can be performed only in a few specialized centers. Flow cytometry is widely used for the diagnosis and classification of leukemia but can monitor MRD in only 80% to 85% of cases of B-lineage ALL because of lack of leukemiaspecific immunophenotypes. 16 Moreover, MRD studies by this technique require extensive panels of complex antibody combinations to distinguish leukemic lymphoblasts from their normal counterparts, the B-lymphoid progenitors of the bone marrow, and to prevent false-negative findings due to immunophenotypic changes during the course of the disease. 16 Thus, the identification of new leukemia markers that are easily detectable and are stably expressed in a large proportion of B-lineage cases would greatly simplify the application of MRD studies and help...

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“…Early myeloblasts of undifferentiated AML (AML-M0), AML with minimal maturation (AML-M1), AML with maturation (AML-M2) and acute myelomonocytic leukemia (AML-M4) express CD34 and HLA-DR but these are lost by the pathologic promyelocytes which are typical for acute promyelocytic leukemia (APL or AML-M3) [89]. Similar to normal myelo-monoblasts, leukemic blasts have intermediate FSC, low SSC and low or intermediate CD45 [90].…”

Section: Cd96mentioning

confidence: 99%

“…Expression of monocyteassociated markers CD4, CD14, CD64 is related to monocyte progenitors of acute myelomonocytic leukemia (AML-M4). Other myeloid associated markers CD11b, CD11c, CD13, CD33, CD15, CD65, CD66, and CD117 are also frequently expressed in various combinations on leukemic blasts but are not useful for distinguishing the different subtypes of AML [89]. The AML-M1 subtype is usually associated with asynchronous coexpression of T-cell markers -CD7 and CD4 [92,93].…”

Section: Cd96mentioning

confidence: 99%

Immunophenotype characterization of hematopoietic stem cells, progenitor cells restricted to myeloid lineage and their leukemia counterparts

Fajtova¹,

Babušíková²

2010

neo

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The aim of this review is to evaluate recent immunophenotype knowledge of hematopoietic stem cells and their restricted progenies committed to myeloid lineage -common myeloid progenitors, myelo-monocytic progenitors, megakaryo-erythroid progenitors and granulocyte progenitors up to mature neutrophil granulocyte. This study evaluates also recent knowledge of immunophenotype of leukemic stem cells and their more differentiated progeny committed to myeloid lineage -acute myeloid leukemia blast cells with regard to their phenotypic similarity to normal stem and granulocyte committed progenitor cells. Improved knowledge of normal stem and progenitor cells phenotypes, identifying new leukemia-specific markers, searching for aberrant marker expression and evaluation of aberrant intensity or combination of various marker expressions is important for distinguishing normal cells from their malignant counterpart in view of the diagnostics of leukemias or follow-up of minimal residual disease.

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Immunophenotyping

Cited by 7 publications

References 448 publications

B Lymphoblastic Leukemia/Lymphoma With Burkitt-like Morphology and IGH/MYC Rearrangement

B Lymphoblastic Leukemia/Lymphoma With Burkitt-like Morphology and IGH/MYC Rearrangement

Identification of novel markers for monitoring minimal residual disease in acute lymphoblastic leukemia

Immunophenotype characterization of hematopoietic stem cells, progenitor cells restricted to myeloid lineage and their leukemia counterparts

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