TLX1-Induced T-cell Acute Lymphoblastic Leukemia

Keersmaecker, Kim De; Ferrando, Adolfo A.

doi:10.1158/1078-0432.ccr-10-3037

Cited by 14 publications

(12 citation statements)

References 58 publications

(56 reference statements)

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“…3 ). Importantly, 64 transcription factors were exclusively detected by CEL-Seq+, including many with known relevance for leukemia (i.e., TLX 21 ), CML tumor stem cells (i.e., PPARG 20 ), CML cancer cell metabolism (i.e., SIX1 20 ), or response to treatment (i.e., PBX1 20 ). Accordingly, single cell studies aiming at a mechanistic understanding of tumor biology may broadly benefit from application of an enhanced T7 promoter in CEL-Seq+.…”

Section: Resultsmentioning

confidence: 99%

Maximizing transcription of nucleic acids with efficient T7 promoters

et al. 2020

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In vitro transcription using T7 bacteriophage polymerase is widely used in molecular biology. Here, we use 5′RACE-Seq to screen a randomized initially transcribed region of the T7 promoter for cross-talk with transcriptional activity. We reveal that sequences from position +4 to +8 downstream of the transcription start site affect T7 promoter activity over a 5-fold range, and identify promoter variants with significantly enhanced transcriptional output that increase the yield of in vitro transcription reactions across a wide range of template concentrations. We furthermore introduce CEL-Seq + , which uses an optimized T7 promoter to amplify cDNA for single-cell RNA-Sequencing. CEL-Seq+ facilitates scRNA-Seq library preparation, and substantially increases library complexity and the number of expressed genes detected per cell, highlighting a particular value of optimized T7 promoters in bioanalytical applications.

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Section: Resultsmentioning

confidence: 99%

Maximizing transcription of nucleic acids with efficient T7 promoters

et al. 2020

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“…[101][102][103][104] The prognostic significance of these alterations in childhood T-ALL remains largely unknown, although patients with TLX1 alterations appear to have more favorable outcomes (Table 1). 103,105 Mutations in X chromosome genes…”

Section: Chromosomal Translocationsmentioning

confidence: 99%

“…Gene expression profiling studies have classified T‐ALL into 4 molecular subtypes based on underlying genetic alterations and resulting oncogenic signaling pathway activation: 1) TLX1 /homeobox 11 ( TLX1‐HOX11) , 2) lymphoblastic leukemia‐associated hematopoiesis regulator 1 ( LYL1 ), 3) T‐cell acute leukemia 1/LIM domain only 2 (rhombotin‐like 1) ( TAL1/LMO2 ), and 4) T‐cell leukemia homeobox 1/homeobox 11‐like 2 ( TLX3/HOX11L2 ) . The prognostic significance of these alterations in childhood T‐ALL remains largely unknown, although patients with TLX1 alterations appear to have more favorable outcomes (Table ) …”

Section: Introductionmentioning

confidence: 99%

Childhood acute lymphoblastic leukemia: Integrating genomics into therapy

Tasian

Loh

Hunger

2015

Cancer

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Acute lymphoblastic leukemia (ALL), the most common malignancy of childhood, is a genetically complex entity that remains a major cause of childhood cancer-related mortality. Major advances in genomic and epigenomic profiling during the past decade have appreciably enhanced knowledge of the biology of de novo and relapsed ALL and have facilitated more precise risk stratification of patients. These achievements have also provided critical insights regarding potentially targetable lesions for development of new therapeutic approaches in the era of precision medicine. This review delineates the current genetic landscape of childhood ALL with emphasis upon patient outcomes with contemporary treatment regimens, as well as therapeutic implications of newly identified genomic alterations in specific subsets of ALL.

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“…TLX genes are normally not expressed in adult tissues[28]. Approximately 7%-20% of childhood T-ALL patientshave ectopic TLX1 and TLX3 expression [15,16].…”

Section: Discussionmentioning

confidence: 99%

Upregulation of T-Cell-Specific Transcription Factor Expression in Pediatric T-Cell Acute Lymphoblastic Leukemia (T-ALL)

Sayitoğlu

Erbilgin

et al. 2012

Turk J Hematol

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Objective: T-cell acute lymphoblastic leukemia (T-ALL) is associated with recurrent chromosomal aberrations andabnormal ectopic gene expression during T-cell development. In order to gain insight into the pathogenesis of T-ALLthis study aimed to measure the level of expression of 7 T-cell oncogenes (LMO2, LYL1, TAL1, TLX1, TLX3, BMI1, andCALM-AF10) in pediatric T-ALL patientsMaterial and Methods: LMO2, LYL1, TLX1, TLX3, BMI1, TAL1, and CALM-AF10 expression was measured usingquantitative real-time PCR in 43 pediatric T-ALL patients.Results: A high level of expression of LMO2, LYL1, TAL1, and BMI1 genes was observed in a large group of T-ALL.Several gene expression signatures indicative of leukemic arrest at specific stages of normal thymocyte development(LYL1 and LMO2) were highly expressed during the cortical and mature stages of T-cell development. Furthermore,upregulated TAL1 and BMI1 expression was observed in all phenotypic subgroups. In all, 6 of the patients had TLX1and TLX3 proto-oncogene expression, which does not occur in normal cells, and none of the patients had CALM-AF10fusion gene transcription. Expression of LYL1 alone and LMO2-LYL1 co-expression were associated with mediastinalinvolvement; however, high-level oncogene expression was not predictive of outcome in the present pediatric T-ALLpatient group, but there was a trend towards a poor prognostic impact of TAL1 and/or LMO2 and/or LYL1 protooncogeneexpression.Conclusion: Poor prognostic impact of TAL1 and/or LMO2 and/or LYL1 proto-oncogene expression indicate the needfor extensive study on oncogenic rearrangement and immunophenotypic markers in T-ALL, and their relationship totreatment outcome.Conflict of interest:None declared.

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TLX1-Induced T-cell Acute Lymphoblastic Leukemia

Cited by 14 publications

References 58 publications

Maximizing transcription of nucleic acids with efficient T7 promoters

Maximizing transcription of nucleic acids with efficient T7 promoters

Childhood acute lymphoblastic leukemia: Integrating genomics into therapy

Upregulation of T-Cell-Specific Transcription Factor Expression in Pediatric T-Cell Acute Lymphoblastic Leukemia (T-ALL)

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