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[PMID]: 29392424
[Au] Autor:Shahkarami S; Mehrasa R; Younesian S; Yaghmaie M; Chahardouli B; Vaezi M; Rezaei N; Nikbakht M; Alimoghaddam K; Ghavamzadeh A; Tavakkoly-Bazzaz J; Ghaffari SH
[Ad] Address:Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
[Ti] Title:Minimal residual disease (MRD) detection using rearrangement of immunoglobulin/T cell receptor genes in adult patients with acute lymphoblastic leukemia (ALL).
[So] Source:Ann Hematol;97(4):585-595, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:MRD detection with allele-specific oligonucleotide-quantitative polymerase chain reaction (ASO-qPCR) and using clone-specific immunoglobulin/T cell receptor rearrangements is considered as a powerful prognostic factor in acute lymphoblastic leukemia (ALL). In the present study, we evaluated an ASO-qPCR assay for MRD quantification in peripheral blood (PB) samples of adult patients with ALL. DNA was isolated from PB samples of patients with newly diagnosed ALL. They were first investigated by multiplex-PCR assay to identify V/J usage. An ASO-qPCR technique was then applied for 2.5-year monthly MRD quantification for detection of patient-specific Ig/TCR receptor rearrangements as a molecular target. From 98 patients who were diagnosed as ALL, 72 (73.5%) were enrolled in the present study for MRD detection. MRD was successfully quantified in patients with 1-month interval time. MRD level at the end of induction therapy up to day 88 was the only significant prognostic factor. Regarding MRD level, patients were categorized into two groups of low and high-risk. 2.5-year OS in all three time points (days 28, 58 and 88) were significantly lower in high-risk group (P < 0.008). The results of the 2.5-year MRD detection indicate that MRD level at the end of induction up to about 6 months after the first diagnosis was associated with clinical outcome. This study may highlight the usefulness of PB and the definitions of cut-off level for early prediction of relapse and for stratifying ALL patients. Short-interval time points and frequent PB sampling to monitor MRD level is suggested for early clinical relapse prediction and clinical management of the disease.
[Mh] MeSH terms primary: Gene Rearrangement, T-Lymphocyte/drug effects
Induction Chemotherapy
Precursor Cell Lymphoblastic Leukemia-Lymphoma/diagnosis
[Mh] MeSH terms secundary: Adult
Alleles
Female
Follow-Up Studies
Hospitals, University
Humans
Iran
Male
Multiplex Polymerase Chain Reaction
Neoplasm Proteins/chemistry
Neoplasm Proteins/genetics
Neoplasm Proteins/metabolism
Neoplasm, Residual/diagnosis
Neoplasm, Residual/genetics
Neoplasm, Residual/metabolism
Neoplasm, Residual/pathology
Oligonucleotides/chemistry
Oligonucleotides/metabolism
Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy
Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics
Precursor Cell Lymphoblastic Leukemia-Lymphoma/pathology
Prognosis
Prospective Studies
Real-Time Polymerase Chain Reaction
Reverse Transcriptase Polymerase Chain Reaction
Risk Assessment
Survival Analysis
Tumor Burden/drug effects
[Pt] Publication type:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Name of substance:0 (Neoplasm Proteins); 0 (Oligonucleotides)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180203
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-018-3230-z

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[PMID]: 29429164
[Au] Autor:Zhang F; Luo DL; Chen Y; Wu HM; Yan JH; Luo XL; He J; Luo LQ; Liu YH
[Ad] Address:Department of Pathology, Guangdong General Hospital/Guangdong Academy of Medical Sciences, Guangzhou 510080, China.
[Ti] Title:[Expression of ßF1 and T cell receptor γ in T lymphoblastic lymphoma/leukemia].
[So] Source:Zhonghua Bing Li Xue Za Zhi;47(2):119-122, 2018 Feb 08.
[Is] ISSN:0529-5807
[Cp] Country of publication:China
[La] Language:chi
[Ab] Abstract:To evaluate the expression of ßF1 and T cell receptor (TCR)γ in T lymphoblastic lymphoma/leukemia(T-LBL/ALL), and investigate the clinicopathological features. Fifty-one cases of T-LBL/ALL were collected at Guangdong General Hospital from 2010 to 2016, the expression of ßF1 and TCRγ was assessed by immunohistochemistry. There were 13 cases of children and adolescents, and 38 cases of adults. The expression rates of ßF1 and TCRγ were 27.5%(14/51) and 15.7%(8/51) respectively. The proportion of adults in αß T-LBL/ALL, TCR-silent T-LBL/ALL and γδ T-LBL/ALL was 7/14, 79.3%(23/29)and 8/8 respectively, and the difference was significant ( =0.023). There was no statistical difference in sex, LDH, bone marrow involvement and Ann arbor stage among these three groups( >0.05). γδ T-LBL/ALLs included 6 cases of CD4(-)/CD8(-) phenotype, whereas αß T-LBL/ALL included 7 cases of CD4(+) /CD8(+) phenotype. There was significant difference in CD4/CD8 expression among these three groups( <0.01). γδ T-LBL/ALL occurred only in adults, with predominantly CD4(-)/CD8(-) phenotype. αß T-LBL/ALL occurred more common in children and adolescents, with predominantly CD4(+) /CD8(+) phenotype.
[Mh] MeSH terms primary: Lymphoma, T-Cell/metabolism
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/metabolism
Receptors, Antigen, T-Cell/metabolism
[Mh] MeSH terms secundary: Adolescent
Adult
Child
Humans
Immunohistochemistry
Phenotype
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Receptors, Antigen, T-Cell)
[Em] Entry month:1803
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[Js] Journal subset:IM
[Da] Date of entry for processing:180213
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0529-5807.2018.02.008

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[PMID]: 29184402
[Au] Autor:Wu X; Wang L; Qiu Y; Zhang B; Hu Z; Jin R
[Ad] Address:Department of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan.
[Ti] Title:Cooperation of IRAK1/4 inhibitor and ABT-737 in nanoparticles for synergistic therapy of T cell acute lymphoblastic leukemia.
[So] Source:Int J Nanomedicine;12:8025-8034, 2017.
[Is] ISSN:1178-2013
[Cp] Country of publication:New Zealand
[La] Language:eng
[Ab] Abstract:T cell acute lymphoblastic leukemia (T-ALL) is caused by clonal expansion of variant T cell progenitors and is considered as a high risk leukemia. Contemporary single chemotherapy has a limited effect due to dynamic and versatile properties of T-ALL. Here IRAK1/4 inhibitor and ABT-737 were co-encapsulated into polyethylene glycol modified poly (lactic-co-glycolic acid) nanoparticles (IRAK/ABT-NP) to enhance synergistic therapy of T-ALL. The formulation was optimized to achieve high drug loading using Box-Behnken design and response surface methodology. The optimal parameter comprised 2.98% polymer in acetonitrile, a ratio of oil phase to water phase of 1:8.33, and 2.12% emulsifier concentration. High drug loading and uniform spherical shape was achieved. In vitro release study showed sustained release of IRAK1/4 inhibitor for 72 hours as well as sustained release of ABT-737 for more than 120 hours. Uptake efficiency of IRAK/ABT-NP and induced apoptotic T-ALL fraction by IRAK/ABT-NP were much higher than the IRAK1/4 and ABT-737 combined solution. IC of IRAK/ABT-NP was two-fold lower than free drug combination in Jurkat cells. Additionally, we conducted in vivo experiments in which IRAK/ABT-NP exhibited greater cytotoxicity toward T-ALL cells, the capacity to significantly restore white blood cell number in peripheral blood, and improved survival time of T-ALL mouse model compared to the IRAK1/4 and ABT-737 combined solution.
[Mh] MeSH terms primary: Antineoplastic Combined Chemotherapy Protocols/pharmacology
Interleukin-1 Receptor-Associated Kinases/antagonists & inhibitors
Nanoparticles/chemistry
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/drug therapy
[Mh] MeSH terms secundary: Animals
Antineoplastic Combined Chemotherapy Protocols/administration & dosage
Biphenyl Compounds/administration & dosage
Biphenyl Compounds/pharmacology
Drug Liberation
Drug Synergism
Female
Humans
Jurkat Cells
Lactic Acid/chemistry
Mice
Nanoparticles/administration & dosage
Nitrophenols/administration & dosage
Nitrophenols/pharmacology
Piperazines/administration & dosage
Piperazines/pharmacology
Polyglycolic Acid/chemistry
Sulfonamides/administration & dosage
Sulfonamides/pharmacology
Xenograft Model Antitumor Assays
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (ABT-737); 0 (Biphenyl Compounds); 0 (Nitrophenols); 0 (Piperazines); 0 (Sulfonamides); 0 (polylactic acid-polyglycolic acid copolymer); 26009-03-0 (Polyglycolic Acid); 33X04XA5AT (Lactic Acid); EC 2.7.11.1 (IRAK1 protein, human); EC 2.7.11.1 (IRAK4 protein, human); EC 2.7.11.1 (Interleukin-1 Receptor-Associated Kinases)
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[Js] Journal subset:IM
[Da] Date of entry for processing:171130
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S146875

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[PMID]: 28465412
[Au] Autor:Severson E; Arnett KL; Wang H; Zang C; Taing L; Liu H; Pear WS; Shirley Liu X; Blacklow SC; Aster JC
[Ad] Address:Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
[Ti] Title:Genome-wide identification and characterization of Notch transcription complex-binding sequence-paired sites in leukemia cells.
[So] Source:Sci Signal;10(477), 2017 May 02.
[Is] ISSN:1937-9145
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Notch transcription complexes (NTCs) drive target gene expression by binding to two distinct types of genomic response elements, NTC monomer-binding sites and sequence-paired sites (SPSs) that bind NTC dimers. SPSs are conserved and have been linked to the Notch responsiveness of a few genes. To assess the overall contribution of SPSs to Notch-dependent gene regulation, we determined the DNA sequence requirements for NTC dimerization using a fluorescence resonance energy transfer (FRET) assay and applied insights from these in vitro studies to Notch-"addicted" T cell acute lymphoblastic leukemia (T-ALL) cells. We found that SPSs contributed to the regulation of about a third of direct Notch target genes. Although originally described in promoters, SPSs are present mainly in long-range enhancers, including an enhancer containing a newly described SPS that regulates expression. Our work provides a general method for identifying SPSs in genome-wide data sets and highlights the widespread role of NTC dimerization in Notch-transformed leukemia cells.
[Mh] MeSH terms primary: Enhancer Elements, Genetic
Gene Expression Regulation, Leukemic
Genome, Human
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/genetics
Receptors, Notch/metabolism
Transcription Factors/metabolism
[Mh] MeSH terms secundary: Animals
Gene Expression Profiling
Humans
Mice
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/metabolism
Promoter Regions, Genetic
Protein Binding
Receptors, Notch/genetics
Signal Transduction
Transcription Factors/genetics
Tumor Cells, Cultured
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Receptors, Notch); 0 (Transcription Factors)
[Em] Entry month:1802
[Cu] Class update date: 180303
[Lr] Last revision date:180303
[Js] Journal subset:IM
[Da] Date of entry for processing:170504
[St] Status:MEDLINE

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Clinical Trials Registry
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[PMID]: 29385376
[Au] Autor:Park JH; Rivière I; Gonen M; Wang X; Sénéchal B; Curran KJ; Sauter C; Wang Y; Santomasso B; Mead E; Roshal M; Maslak P; Davila M; Brentjens RJ; Sadelain M
[Ad] Address:From the Leukemia Service, Department of Medicine (J.H.P., C.S., P.M., R.J.B.), the Michael G. Harris Cell Therapy and Cell Engineering Facility (I.R., X.W., B. Sénéchal, Y.W.), the Center for Cell Engineering (J.H.P., I.R., X.W., R.J.B., M.S.), and the Departments of Epidemiology and Biostatistics
[Ti] Title:Long-Term Follow-up of CD19 CAR Therapy in Acute Lymphoblastic Leukemia.
[So] Source:N Engl J Med;378(5):449-459, 2018 02 01.
[Is] ISSN:1533-4406
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: CD19-specific chimeric antigen receptor (CAR) T cells induce high rates of initial response among patients with relapsed B-cell acute lymphoblastic leukemia (ALL) and long-term remissions in a subgroup of patients. METHODS: We conducted a phase 1 trial involving adults with relapsed B-cell ALL who received an infusion of autologous T cells expressing the 19-28z CAR at the Memorial Sloan Kettering Cancer Center (MSKCC). Safety and long-term outcomes were assessed, as were their associations with demographic, clinical, and disease characteristics. RESULTS: A total of 53 adults received 19-28z CAR T cells that were manufactured at MSKCC. After infusion, severe cytokine release syndrome occurred in 14 of 53 patients (26%; 95% confidence interval [CI], 15 to 40); 1 patient died. Complete remission was observed in 83% of the patients. At a median follow-up of 29 months (range, 1 to 65), the median event-free survival was 6.1 months (95% CI, 5.0 to 11.5), and the median overall survival was 12.9 months (95% CI, 8.7 to 23.4). Patients with a low disease burden (<5% bone marrow blasts) before treatment had markedly enhanced remission duration and survival, with a median event-free survival of 10.6 months (95% CI, 5.9 to not reached) and a median overall survival of 20.1 months (95% CI, 8.7 to not reached). Patients with a higher burden of disease (≥5% bone marrow blasts or extramedullary disease) had a greater incidence of the cytokine release syndrome and neurotoxic events and shorter long-term survival than did patients with a low disease burden. CONCLUSIONS: In the entire cohort, the median overall survival was 12.9 months. Among patients with a low disease burden, the median overall survival was 20.1 months and was accompanied by a markedly lower incidence of the cytokine release syndrome and neurotoxic events after 19-28z CAR T-cell infusion than was observed among patients with a higher disease burden. (Funded by the Commonwealth Foundation for Cancer Research and others; ClinicalTrials.gov number, NCT01044069 .).
[Mh] MeSH terms primary: Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy
Receptors, Antigen, T-Cell/therapeutic use
T-Lymphocytes/immunology
[Mh] MeSH terms secundary: Adult
Aged
Cytokines/metabolism
Follow-Up Studies
Humans
Middle Aged
Precursor Cell Lymphoblastic Leukemia-Lymphoma/mortality
Recurrence
Remission Induction
Survival Analysis
[Pt] Publication type:CLINICAL TRIAL, PHASE I; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (CD19-specific chimeric antigen receptor); 0 (Cytokines); 0 (Receptors, Antigen, T-Cell)
[Em] Entry month:1802
[Cu] Class update date: 180222
[Lr] Last revision date:180222
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180201
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMoa1709919

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[PMID]: 29384978
[Au] Autor:Nishiwaki S; Sugiura I; Miyata Y; Saito S; Sawa M; Nishida T; Miyamura K; Kuwatsuka Y; Kohno A; Yuge M; Kasai M; Iida H; Kurahashi S; Osaki M; Goto T; Terakura S; Murata M; Nishikawa H; Kiyoi H
[Ad] Address:Center for Advanced Medicine and Clinical Research, Nagoya University Hospital, Nagoya.
[Ti] Title:Efficacy and safety of autologous peripheral blood stem cell transplantation for Philadelphia chromosome-positive acute lymphoblastic leukemia: A study protocol for a multicenter exploratory prospective study (Auto-Ph17 study).
[So] Source:Medicine (Baltimore);96(52):e9568, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:INTRODUCTION: The prognosis of Philadelphia chromosome positive acute lymphoblastic leukemia (Ph + ALL) has been dramatically improved since the introduction of tyrosine kinase inhibitors (TKIs). Although allogeneic hematopoietic cell transplantation (allo-HCT) is a major treatment option, the role of autologous peripheral blood stem cell transplantation (auto-PBSCT) has been reconsidered, especially in patients who achieved early molecular remission. METHODS AND ANALYSIS: This is a multicenter exploratory study for Ph + ALL patients aged between 55 and 70 years who achieved complete molecular remission within 3 cycles of chemotherapy. The target sample size is 5, and the registration period is 2 years. The primary endpoint is Day100- mortality after transplantation, and the secondary endpoints are survival, relapse rate, nonrelapse mortality, and adverse events.This study is divided into 3 phases: peripheral blood stem cell harvest, transplantation, and maintenance. Chemomobilization is performed using a combination of cyclophosphamide (CPM), doxorubicin, vincristine (VCR), and prednisolone (PSL). As a preparative regimen, the LEED regimen is used, which consists of melphalan, CPM, etoposide, and dexamethasone. Twelve cycles of maintenance therapy using a combination of VCR, PSL, and dasatinib are performed.In association with relapse, the minimal residual disease (MRD) of BCR-ABL chimeric gene and T-cell subsets are analyzed both before and after auto-PBSCT. ETHICS AND DISSEMINATION: The protocol was approved by the institutional review board of Nagoya University Hospital and all the participating hospitals. Written informed consent was obtained from all patients before registration, in accordance with the Declaration of Helsinki. Results of the study will be disseminated via publications in peer-reviewed journals. TRIAL REGISTRATION: Trial registration number UMIN000026445.
[Mh] MeSH terms primary: Peripheral Blood Stem Cell Transplantation/mortality
Peripheral Blood Stem Cell Transplantation/methods
Philadelphia Chromosome
Precursor Cell Lymphoblastic Leukemia-Lymphoma/mortality
Precursor Cell Lymphoblastic Leukemia-Lymphoma/therapy
[Mh] MeSH terms secundary: Aged
Disease Progression
Female
Genes, abl/physiology
Humans
Immunosuppressive Agents/administration & dosage
Male
Middle Aged
Peripheral Blood Stem Cell Transplantation/adverse effects
Prospective Studies
Proto-Oncogene Proteins c-bcr/biosynthesis
Research Design
Survival Analysis
[Pt] Publication type:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Name of substance:0 (Immunosuppressive Agents); EC 2.7.11.1 (BCR protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins c-bcr)
[Em] Entry month:1802
[Cu] Class update date: 180220
[Lr] Last revision date:180220
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009568

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[PMID]: 29278703
[Au] Autor:Miyashita K; Kitajima K; Goyama S; Kitamura T; Hara T
[Ad] Address:Stem Cell Project, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan; Division of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
[Ti] Title:Overexpression of Lhx2 suppresses proliferation of human T cell acute lymphoblastic leukemia-derived cells, partly by reducing LMO2 protein levels.
[So] Source:Biochem Biophys Res Commun;495(3):2310-2316, 2018 01 15.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:T cell acute lymphoblastic leukemia (T-ALL) is a malignant cancer with poor prognosis. The transcriptional co-factor LIM domain only 2 (LMO2) and its target gene HHEX are essential for self-renewal of T cell precursors and T-ALL etiology. LMO2 directly associates with LDB1 in a large DNA-containing nuclear complex and controls the transcription of T-ALL-related genes. Recently, we reported that overexpression of the LIM-homeodomain transcription factor, Lhx2, results in liberation of the Lmo2 protein from the Lmo2-Ldb1 complex, followed by ubiquitin proteasome mediated degradation. Here, we found that proliferation of five human T-ALL-derived cell lines, including CCRF-CEM, was significantly suppressed by retroviral overexpression of Lhx2. The majority of Lhx2-transduced CCRF-CEM cells arrested in G phase and subsequently underwent apoptosis. Expression of LMO2 protein as well as HHEX, ERG, HES1 and MYC genes was repressed in CCRF-CEM cells by transduction with Lhx2. Lhx2-mediated growth inhibition was partially rescued by simultaneous overexpression of Lmo2; however, both the C-terminal LIM domain and the homeodomain of Lhx2 were required for its growth-suppressive activity. These data indicate that Lhx2 is capable of blocking proliferation of T-ALL-derived cells by both LMO2-dependent and -independent means. We propose Lhx2 as a new molecular tool for anti-T-ALL drug development.
[Mh] MeSH terms primary: Adaptor Proteins, Signal Transducing/metabolism
Cell Proliferation
LIM Domain Proteins/metabolism
LIM-Homeodomain Proteins/metabolism
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/metabolism
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/pathology
Proto-Oncogene Proteins/metabolism
Transcription Factors/metabolism
[Mh] MeSH terms secundary: Cell Line, Tumor
Down-Regulation
Gene Expression Regulation, Neoplastic
Humans
Up-Regulation
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Adaptor Proteins, Signal Transducing); 0 (LHX2 protein, human); 0 (LIM Domain Proteins); 0 (LIM-Homeodomain Proteins); 0 (LMO2 protein, human); 0 (Proto-Oncogene Proteins); 0 (Transcription Factors)
[Em] Entry month:1802
[Cu] Class update date: 180214
[Lr] Last revision date:180214
[Js] Journal subset:IM
[Da] Date of entry for processing:171227
[St] Status:MEDLINE

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[PMID]: 29326336
[Au] Autor:Leong WZ; Tan SH; Ngoc PCT; Amanda S; Yam AWY; Liau WS; Gong Z; Lawton LN; Tenen DG; Sanda T
[Ad] Address:Cancer Science Institute of Singapore, National University of Singapore, 117599 Singapore.
[Ti] Title:ARID5B as a critical downstream target of the TAL1 complex that activates the oncogenic transcriptional program and promotes T-cell leukemogenesis.
[So] Source:Genes Dev;31(23-24):2343-2360, 2017 12 01.
[Is] ISSN:1549-5477
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The oncogenic transcription factor induces an aberrant transcriptional program in T-cell acute lymphoblastic leukemia (T-ALL) cells. However, the critical factors that are directly activated by TAL1 and contribute to T-ALL pathogenesis are largely unknown. Here, we identified ( ) as a collaborating oncogenic factor involved in the transcriptional program in T-ALL. expression is down-regulated at the double-negative 2-4 stages in normal thymocytes, while it is induced by the TAL1 complex in human T-ALL cells. The enhancer located 135 kb upstream of the gene locus is activated under a superenhancer in T-ALL cells but not in normal T cells. Notably, ARID5B-bound regions are associated predominantly with active transcription. ARID5B and TAL1 frequently co-occupy target genes and coordinately control their expression. ARID5B positively regulates the expression of TAL1 and its regulatory partners. ARID5B also activates the expression of the oncogene Importantly, ARID5B is required for the survival and growth of T-ALL cells and forced expression of ARID5B in immature thymocytes results in thymus retention, differentiation arrest, radioresistance, and tumor formation in zebrafish. Our results indicate that ARID5B reinforces the oncogenic transcriptional program by positively regulating the TAL1-induced regulatory circuit and in T-ALL, thereby contributing to T-cell leukemogenesis.
[Mh] MeSH terms primary: Carcinogenesis/genetics
DNA-Binding Proteins/metabolism
Gene Expression Regulation, Neoplastic
T-Cell Acute Lymphocytic Leukemia Protein 1/metabolism
Transcription Factors/metabolism
[Mh] MeSH terms secundary: Animals
Cell Line, Tumor
Cell Survival/genetics
DNA-Binding Proteins/genetics
Enhancer Elements, Genetic/genetics
Gene Expression Profiling
Genes, myc/genetics
HEK293 Cells
Humans
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
Protein Binding
Protein Domains/genetics
Thymocytes/metabolism
Thymus Gland/growth & development
Transcription Factors/genetics
Transcriptional Activation/genetics
Zebrafish
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (ARID5B protein, human); 0 (DNA-Binding Proteins); 0 (T-Cell Acute Lymphocytic Leukemia Protein 1); 0 (Transcription Factors); 135471-20-4 (TAL1 protein, human)
[Em] Entry month:1802
[Cu] Class update date: 180208
[Lr] Last revision date:180208
[Js] Journal subset:IM
[Da] Date of entry for processing:180113
[St] Status:MEDLINE
[do] DOI:10.1101/gad.302646.117

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[PMID]: 29303717
[Au] Autor:Yaqub F
[Ti] Title:2017: a year in review.
[So] Source:Lancet;390(10114):2753-2754, 2018 12 23.
[Is] ISSN:1474-547X
[Cp] Country of publication:England
[La] Language:eng
[Mh] MeSH terms primary: Armed Conflicts
Child Nutrition Disorders/epidemiology
Cholera/epidemiology
Epidemics
Human Rights
Immunotherapy, Adoptive/methods
Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/therapy
Refugees
Sex Offenses
Sexual Harassment
[Mh] MeSH terms secundary: Bangladesh
Child, Preschool
China
Economic Recession
Ethiopia/epidemiology
Food Supply
Health Policy
Humans
Myanmar
Nuclear Weapons
Politics
Somalia/epidemiology
T-Lymphocytes/transplantation
Transplantation, Autologous
United States
Venezuela
World Health Organization
Yemen/epidemiology
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180117
[Lr] Last revision date:180117
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180106
[St] Status:MEDLINE

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[PMID]: 29200162
[Au] Autor:Valliyammai N; Nancy NK; Sagar TG; Rajkumar T
[Ad] Address:Departments of Molecular Oncology.
[Ti] Title:Study of NOTCH1 and FBXW7 Mutations and Its Prognostic Significance in South Indian T-Cell Acute Lymphoblastic Leukemia.
[So] Source:J Pediatr Hematol Oncol;40(1):e1-e8, 2018 Jan.
[Is] ISSN:1536-3678
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:NOTCH1/FBXW7 mutations trigger oncogenic NOTCH1 signaling and its downstream target genes play crucial roles in the molecular pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL). In the present study, NOTCH1 and FBXW7 mutations were studied in 25 primary T-ALL samples. All 34 exons of NOTCH1 and hotspot exons (exon 9 and exon 10) of FBXW7 were polymerase chain reaction amplified and sequenced for mutations. Our results showed that 13/25 (52%) were NOTCH1-mutated, of which 11 patients (44%) showed mutation in the hotspot exons. Four patients (16%) had mutations in non-hotspot exons of NOTCH1. Notably, 2 T-ALL patients (8%) harbored mutations in both hotspot and non-hotspot exons of NOTCH1, whereas 2 patients (8%) had mutations in the hotspot exons of FBXW7. In all, 7 mutations were identified which were not previously reported. The real-time polymerase chain reaction study in 15 patients revealed that increased expression of activated NOTCH1 was found in NOTCH1/FBXW7 hotspot exon-mutated cases. In addition, NOTCH1/FBXW7-mutated patients had showed upregulated HES1, c-MYC, NOTCH3 gene expression. When survival analysis was performed including samples (n=50) from our previous study, an early treatment response and better survival was observed in NOTCH1/FBXW7 hotspot-mutated patients. Our study suggests that NOTCH1/FBXW7 hotspot-mutated T-ALL cases had better response to ALL BFM-95 protocol.
[Mh] MeSH terms primary: F-Box-WD Repeat-Containing Protein 7/genetics
Mutation
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/genetics
Prognosis
Receptor, Notch1/genetics
[Mh] MeSH terms secundary: Adolescent
Adult
Antineoplastic Combined Chemotherapy Protocols
Asparaginase
Child
Child, Preschool
Cyclophosphamide
Cytarabine
DNA Mutational Analysis
Female
Gene Expression Regulation, Neoplastic
Humans
India/epidemiology
Infant
Infant, Newborn
Male
Mercaptopurine
Methotrexate
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/diagnosis
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/epidemiology
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/mortality
Prednisone
Survival Analysis
Vincristine
Young Adult
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (F-Box-WD Repeat-Containing Protein 7); 0 (FBXW7 protein, human); 0 (NOTCH1 protein, human); 0 (Receptor, Notch1); 04079A1RDZ (Cytarabine); 5J49Q6B70F (Vincristine); 8N3DW7272P (Cyclophosphamide); E7WED276I5 (Mercaptopurine); EC 3.5.1.1 (Asparaginase); VB0R961HZT (Prednisone); YL5FZ2Y5U1 (Methotrexate)
[Em] Entry month:1801
[Cu] Class update date: 180112
[Lr] Last revision date:180112
[Js] Journal subset:IM
[Da] Date of entry for processing:171205
[St] Status:MEDLINE
[do] DOI:10.1097/MPH.0000000000001006


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