scholarly journals Myeloid/T-cell acute lymphoblastic leukemia in children and adults

2011 ◽  
Vol 3 (2s) ◽  
pp. 3 ◽  
Author(s):  
Sabina Chiaretti ◽  
Monica Messina ◽  
Simona Tavolaro ◽  
Robin Foà
Keyword(s):  
Gene Expression ◽  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Lymphoblastic Leukemia ◽  
Age Groups ◽  
Cell Receptor ◽  
Large Set ◽  
Cell Acute Lymphoblastic Leukemia

Until recently, few molecular aberrations were recognized in T-cell acute lymphoblastic leukemia (T-ALL) and they were restricted to aberrations involving the T-cell receptor (TCR). The introduction of powerful technologies has allowed to identify novel rearrangements. In this context, we have performed a gene expression profiling analysis on a relatively large cohort (n=69) of adult patients with a diagnosis of T-ALL. By unsupervised clustering, we identified 5 subgroups. Of these, one branch included 7 patients (10%) whose gene expression profile resembled that of AML. These cases were characterized by the overexpression of a large set of myeloid-related genes, as well as of miR-223. Finally, these patients appear to have an unfavorable clinical course. This newly identified subset of T-ALL cases partly resembles the so-called ETP (early T-precursor) pediatric subgroup: both age groups have in fact a peculiar gene expression profile, an unfavorable outcome and an incidence of about 10%.

scholarly journals Comparative gene expression profiling of T-cell acute lymphoblastic leukemias (T-ALL) expressing the T-cell receptor 𝛂β or γδ (T-ALL𝛂β / T-ALLγδ)

2019 ◽  
Author(s):  
Shahan Mamoor
Keyword(s):  
Gene Expression ◽  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
T Cell Receptor ◽  
Expression Profiling ◽  
Lymphoblastic Leukemia ◽  
Cell Receptor ◽  
Differentially Expressed ◽  
Aggressive Form ◽  
Cell Acute Lymphoblastic Leukemia

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive form of leukemia with inferior treatment outcomes. The T-cell receptor (TCR) exists in two major forms: the 𝛂βTCR or the γδTCR, and 20-35% of T-ALL cases express either the 𝛂βTCR or the γδTCR (T-ALL𝛂β or T-ALLγδ). Using a published dataset from a cohort of 14 TCR+ T-ALL patients, I found a series of genes that are differentially expressed among patients T-ALL𝛂β or T-ALLγδ. Any number of these differentially expressed genes may be a scientifically and/or clinically actionable target in TCR+ T-ALL.

scholarly journals Progenitor B-1 B-cell acute lymphoblastic leukemia is associated with collaborative mutations in 3 critical pathways

2017 ◽  
Vol 1 (20) ◽  
pp. 1749-1759 ◽  
Author(s):  
Sheryl M. Gough ◽  
Liat Goldberg ◽  
Marbin Pineda ◽  
Robert L. Walker ◽  
Yuelin J. Zhu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Acute Lymphoblastic Leukemia ◽  
B Cells ◽  
B Cell ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Lymphoblastic Leukemia ◽  
Critical Pathways ◽  
Key Points ◽  
Cell Acute Lymphoblastic Leukemia

Key Points An NUP98-PHF23 fusion collaborates with acquired Bcor and Jak/Stat mutations to produce a pro–B-1 ALL. Gene expression profile of murine pro–B-1 ALL resembles that of a subset of human ALL, suggesting some human ALLs arise from pro–B-1 B cells.

scholarly journals Prognostic significance of protein-coding and long non-coding RNA expression profile in T-cell acute lymphoblastic leukemia

2021 ◽  
Author(s):  
Deepak Verma ◽  
Shruti Kapoor ◽  
Disha Sharma ◽  
Jay Singh ◽  
Gunjan Sharma ◽  
...  
Keyword(s):  
Gene Expression ◽  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Expression Profile ◽  
Lymphoblastic Leukemia ◽  
High Expression ◽  
Protein Coding ◽  
Non Coding Rna ◽  
Cell Acute Lymphoblastic Leukemia ◽  
Long Non Coding Rna

T-acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy associated with poor outcome. To unravel gene-expression profile of immunophenotypic subtypes of T-ALL, we did transcriptome analysis in 35 cases. We also analyzed the prognostic relevance of 23 targets: protein-coding genes, histone modifiers and long non-coding RNA (lncRNA) expression profile, identified on RNA sequencing, on an independent cohort of 99 T-ALL cases. We found high expression of MEF2C to be associated with prednisolone resistance (p=0.048) and CD34 expression (p=0.012). BAALC expression was associated with expression of CD34 (p=0.032) and myeloid markers (p=0.021). XIST and KDM6a expression levels were higher in females (p=0.047 and 0.011, respectively). Post-induction minimal residual disease (MRD) positivity was associated with high lncRNA PCAT18 (p=0.04), HHEX (p=0.027) and MEF2C (p=0.007). Early thymic precursor (ETP-ALL) immunophenotype was associated with high expression of MEF2C (p=0.003), BAALC (p=0.003), LYL1 (p=0.01), LYN (p=0.01), XIST (p=0.02) and low levels of ST20 (p=0.007) and EML4 (p=0.03). On survival analysis, MEF2C high expression emerged as significant predictor of 3-year event free survival (EFS) (low 71.78+6.58% vs high 36.57+10.74%, HR 3.5, p=0.0003) and overall survival (OS) (low 94.77+2.96% vs high 78.75+8.45%, HR 4.88, p=0.016) in our patients. LncRNA MALAT1 low expression also emerged as predictor inferior OS (low 76.02+10.48 vs high 94.11+3.31, HR 0.22, p=0.027). Keywords: RNA-Sequencing, T-cell acute lymphoblastic Leukemia, Early thymic precursor, LncRNA, Gene expression profile.

scholarly journals Clinical characterization and prognosis of T cell acute lymphoblastic leukemia with high CRLF2 gene expression in children

PLoS ONE ◽  
2019 ◽  
Vol 14 (12) ◽  
pp. e0224652
Author(s):  
Mingmin Wang ◽  
Jinquan Wen ◽  
Yuxia Guo ◽  
Yali Shen ◽  
Xizhou An ◽  
...  
Keyword(s):  
Gene Expression ◽  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Lymphoblastic Leukemia ◽  
Cell Acute Lymphoblastic Leukemia

Crosslineage T-Cell Receptor Genes Rearrangements and Active Receptor Editing in B-Cell Acute Lymphoblastic Leukemia.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4259-4259
Author(s):  
Hanna Makuch-Lasica ◽  
Miroslaw Majewski ◽  
Grazyna Nowak ◽  
Iwona Kania ◽  
Monika Lewandowska ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
B Cell ◽  
T Cell Receptor ◽  
Light Chain ◽  
Lymphoblastic Leukemia ◽  
Cell Receptor ◽  
Heteroduplex Analysis ◽  
Receptor Editing ◽  
Cell Acute Lymphoblastic Leukemia

Abstract B-cell acute lymphoblastic leukemia (B-ALL) results from clonal expansion of B-lymphocytes derived at different stage of differentiation. Immunoglobulin (Ig) heavy chain genes (IGH), light chain kappa (IGK) and lambda (IGL) genes rearrange during early B-lymphocyte differentiation. T-cell receptor (TCR) genes are considered to rearrange exclusively in normal T lymphocytes, but malignant B lymphoblasts often contain crosslineage rearranged TCR genes. The clonal leukemic cell population, carrying identical copies of rearranged Ig and/or TCR genes, can be identified above 95% of B-ALL patients. In our study Ig/TCR genes rearrangements were detected by multiplex PCR with heteroduplex analysis according to BIOMED-2 protocol. DNA was isolated by column method from mononuclear cells isolated from the peripheral blood/bone marrow samples obtained at initial diagnosis from 36 B-ALL patients. Monoclonal rearrangements of Ig genes were detected in 100% (36/36) of patients. The most frequent rearrangements were observed in IGH genes (94%), including complete IGHV-IGHJ in 83% (30/36) and incomplete IGHD-IGHJ in 22% (8/36) of patients. Among complete IGH rearrangements 2 biallelic rearrangements in IGHV1-7 and IGHJ genes (FR3) were found. Ig light chain genes rearrangements were identified in 26 patients (72%) (including 64% of IGKV-IGKJ, 47% IGKV/intron-Kde, and 22% IGLV-IGLJ) what indicates active receptor editing occurring during B lymphoblasts leukemogenesis. Crosslineage TCR genes rearrangements were found in 97% (35/36) of patients. TCR beta genes rearrangements were detected in 47% (17/36) of patients (complete TRBV-TRBJ in 25% (9/36), TRBD-TRBJ in 6/36 patients - 17%). TRGV-TRGV in 58% (21/36), TRDV-TRDJ in 58% (21/36); 17 monoallelic and 4 biallelic were found. The inactivation of potentially functional IGKV-IGKJ by secondary rearrangements indicates active receptor editing. Our data describe IGK and IGL genes rearrangements incidence, present allelic exclusion and active receptor editing in B-ALL patients. B-ALL lymphoblast undergoes rearrangement on the same IGK allele before IGL genes rearrangement occur. The data may suggest the possible of antigens in B-ALL immunopathogenesis. The results indicate also rearranged IGK, IGL and TCR genes as stable molecular marker for monitoring MRD in B-ALL.

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