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However, leukemia cells studied to date have shown variable susceptibility to TRAIL.

Our study demonstrates that cells of acute T-lymphoblastic leukemia MOLT-4 are resistant to TRAIL and that ionizing radiation in the therapeutically achievable dose of 1 Gy sensitizes TRAIL-resistant cells MOLT-4 to the TRAIL-induced apoptosis by increase in death receptors for TRAIL DR5.

When TRAIL is applied after the irradiation in the time of increased DR5 positivity more efficient cell killing is achieved.

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(PMID = 28550838.001).

[ISSN] 1211-4286

[Journal-full-title] Acta medica (Hradec Kralove)

[ISO-abbreviation] Acta Medica (Hradec Kralove)

[Language] eng

[Publication-type] Journal Article

[Publication-country] Czech Republic

[Keywords] NOTNLM ; Apoptosis / DR5 / Ionizing radiation / Leukemia / TRAIL

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The molecular mechanisms involved in disease progression and relapse in T-cell acute lymphoblastic leukemia (T-ALL) are poorly understood.

This analysis showed that diagnosis and relapsed cases have common genetic alterations, but also that relapsed samples frequently lose chromosomal markers present at diagnosis, suggesting that relapsed T-ALL emerges from an ancestral clone different from the major leukemic population at diagnosis.

[MeSH-major] Genes, Wilms Tumor. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

[MeSH-minor] Adult. Child. Chromosome Aberrations. Clone Cells / chemistry. DNA Methylation. DNA Mutational Analysis. DNA, Neoplasm / genetics. Disease Progression. Genes, Homeobox. Humans. Kaplan-Meier Estimate. Neoplasm Proteins / chemistry. Neoplasm Proteins / genetics. Oncogenes. Polymorphism, Single Nucleotide. Prognosis. Recurrence. WT1 Proteins / chemistry. WT1 Proteins / genetics. Zinc Fingers / genetics

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(PMID = 19494353.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Databank-accession-numbers] GEO/ GSE15931

[Grant] United States / NCI NIH HHS / CA / CA114737; United States / NCI NIH HHS / CA / R01 CA129382; United Kingdom / Medical Research Council / / ; United Kingdom / Medical Research Council / / MRC/ MC/ U137686856; United States / NCI NIH HHS / CA / CA02111; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; United Kingdom / Medical Research Council / / MRC/ G0500389; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / U24 CA114737; United States / NCI NIH HHS / CA / R01 CA120196-03

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / WT1 Proteins

[Other-IDs] NLM/ PMC2721784

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

BACKGROUND: Glucocorticoid (GC) resistance is frequently seen in acute lymphoblastic leukemia of T-cell lineage (T-ALL).

METHODS: Cell proliferation was detected by 3-(4,5-dimethylthiazol-2-yl)- 2,5-diphenyltetrazolium bromide (MTT) assay.

Fluorescence-activated cell sorting (FACS) analysis was used to analyze apoptosis and cell cycles.

Western blot analysis was performed to test the expression of the downstream effector proteins of mammalian target of rapamycin (mTOR), the cell cycle regulatory proteins, and apoptosis associated proteins.

Cell cycle arrest was associated with modulation of G1-S phase regulators.

Rapamycin enhanced GC-induced apoptosis and this was not achieved by modulation of glucocorticoid receptor (GR) expression, but synergistically up-regulation of pro-apoptotic proteins like caspase-3, Bax, and Bim, and down-regulation of anti-apoptotic protein of Mcl-1.

CONCLUSION: Our data suggests that rapamycin can effectively reverse GC resistance in T-ALL and this effect is achieved by inducing cell cycles arrested at G0/G1 phase and activating the intrinsic apoptotic program.

[MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Dexamethasone / pharmacology. Drug Resistance, Neoplasm / drug effects. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Sirolimus / pharmacology

[MeSH-minor] Blotting, Western. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Separation. Drug Synergism. Flow Cytometry. Humans

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(PMID = 21083937.001).

[ISSN] 1756-9966

[Journal-full-title] Journal of experimental & clinical cancer research : CR

[ISO-abbreviation] J. Exp. Clin. Cancer Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 7S5I7G3JQL / Dexamethasone; W36ZG6FT64 / Sirolimus

[Other-IDs] NLM/ PMC2998469

   

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[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Mutations in NOTCH1 are frequently detected in patients with T-cell acute lymphoblastic leukemia (T-ALL) and in mouse T-ALL models.

Treatment of mouse or human T-ALL cell lines in vitro with gamma-secretase inhibitors (GSIs) results in growth arrest and/or apoptosis.

T-ALL cell lines also exhibit PI3K/mTOR pathway activation, indicating that rapamycin may also have therapeutic benefit.

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(PMID = 19246562.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA096899; United States / NCI NIH HHS / CA / CA096899; United States / NIDDK NIH HHS / DK / P30DK32529

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Carrier Proteins; 0 / Cyclic S-Oxides; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / MRK 003; 0 / Proto-Oncogene Proteins; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse; 0 / Thiadiazoles; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 3.4.- / Amyloid Precursor Protein Secretases

[Other-IDs] NLM/ PMC2699237

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Effects of triptolide on proliferation and apoptosis of Jurkat cell line in acute T lymphocytic leukemia].

The aim of this study was to investigate the anti-proliferation and pro-apoptosis of triptolide on Jurkat cell line in acute T lymphocytic leukemia.

The inhibitory ratio was measured by Cell Counting Kit-8 assay.

The translocation of phosphatidylserine at the outer surface of the cell plasma membrane could be induced by triptolide.

Moreover, these pro-apoptosis effects were in time-dependent manner.

This study provides experimental basis for clinical use of triptolide in leukemia therapy.

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(PMID = 18549618.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Diterpenes; 0 / Epoxy Compounds; 0 / Phenanthrenes; 19ALD1S53J / triptolide

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The t(11;14)(p13;q11) is presumed to arise from an erroneous T-cell receptor delta TCRD V(D)J recombination and to result in LMO2 activation.

We performed combined in vivo, ex vivo, and in silico analyses on 9 new t(11;14)(p13;q11)-positive T-cell acute lymphoblastic leukemia (T-ALL) as well as normal thymocytes.

[MeSH-major] Chromosome Breakage. DNA-Binding Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Metalloproteins / genetics

[MeSH-minor] Adaptor Proteins, Signal Transducing. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 14. Genes, T-Cell Receptor delta. Humans. LIM Domain Proteins. Proto-Oncogene Proteins / genetics. Translocation, Genetic

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(PMID = 17360939.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LMO2 protein, human; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The identification of activating mutations in NOTCH1 in over 50% of T-cell acute lymphoblastic leukemias (T-ALL) has generated major interest in the elucidation of the mechanisms of transformation downstream of oncogenic NOTCH and in the targeting of the NOTCH signaling pathway in this disease.

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(PMID = 20008221.001).

[ISSN] 1520-4383

[Journal-full-title] Hematology. American Society of Hematology. Education Program

[ISO-abbreviation] Hematology Am Soc Hematol Educ Program

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA120196-03; United States / NCI NIH HHS / CA / CA129382-02; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / CA120196-03; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / R01 CA129382-02

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Glucocorticoids; 0 / NOTCH1 protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptor, Notch1; EC 3.4.- / Amyloid Precursor Protein Secretases

[Number-of-references] 40

[Other-IDs] NLM/ NIHMS168983; NLM/ PMC2847371

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Recent studies have demonstrated that most patients with T-cell acute lymphocytic leukemia (T-ALL) have activating mutations in NOTCH1.

We sequenced the heterodimerization domain and the PEST domain of Notch1 in our mouse model of TAL1-induced leukemia and found that 74% of the tumors harbor activating mutations in Notch1.

Cell lines derived from these tumors undergo G(0)/G(1) arrest and apoptosis when treated with a gamma-secretase inhibitor.

Thus, Notch1 mutations are often acquired as a part of the molecular pathogenesis of T-ALLs that develop in mice with known predisposing genetic alterations.

[MeSH-major] Disease Models, Animal. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma / genetics. Mutation / genetics. Receptor, Notch1 / genetics. Thymus Neoplasms / genetics

[MeSH-minor] Amyloid Precursor Protein Secretases. Animals. Apoptosis. Aspartic Acid Endopeptidases. Basic Helix-Loop-Helix Transcription Factors / genetics. Basic Helix-Loop-Helix Transcription Factors / physiology. DNA-Binding Proteins / genetics. DNA-Binding Proteins / physiology. Endopeptidases / chemistry. Enzyme Inhibitors / pharmacology. Female. G0 Phase. G1 Phase. Histones / genetics. Histones / physiology. Humans. Male. Mice. Mice, Transgenic. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / physiology. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / physiology

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[Cites] Mol Cell Biol. 2000 Jun;20(11):3831-42 [10805726.001]

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(PMID = 16166587.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Grant] United States / NCI NIH HHS / CA / R01 CA096899

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / H2AX protein, mouse; 0 / Histones; 0 / NOTCH1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Rag2 protein, mouse; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse; 0 / Tumor Suppressor Protein p53; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.- / Endopeptidases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / BACE1 protein, human; EC 3.4.23.46 / Bace1 protein, mouse

[Other-IDs] NLM/ PMC1895623

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Previously, we found that the H1 histamine receptor antagonist diphenhydramine induces apoptosis in human acute T-lymphocytic leukemia cells.

Since histamine has been shown to act as a growth factor in malignant melanoma cells, we decided to evaluate the in vitro effect of diphenhydramine and other H1 histamine receptor antagonists, such as terfenadine, astemizol and triprolidine on four malignant human melanoma cell lines.

These antagonists were found to induce apoptotic cell death in all four melanoma cell lines.

[MeSH-minor] Caspase 2. Cell Line, Tumor. Cytosol / metabolism. DNA Damage. Enzyme Activation. Fibroblasts / metabolism. Histamine / metabolism. Humans. Melanocytes / metabolism. Mutagens / pharmacology

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(PMID = 16569656.001).

[ISSN] 0143-3334

[Journal-full-title] Carcinogenesis

[ISO-abbreviation] Carcinogenesis

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Histamine H1 Antagonists; 0 / Mutagens; 820484N8I3 / Histamine; EC 3.4.22.- / Caspase 2; EC 3.4.22.- / Caspases

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Expression of survivin and its location in bone marrow cells of childhood acute leukemia: relationship to therapeutic efficacy].

OBJECTIVE: Survivin, a unique member of the inhibitor of apoptosis protein (IAP) family, plays an important role in regulating both apoptosis and cell division.

METHODS: The expression of survivin protein was detected by immunohistochemical assay in bone marrow cells from 62 children with acute leukemia and 40 hospitalized children who did not have leukemia (Control group), and in a human acute T lymphocytic leukemia cell line (Molt-4 cells) treated in vitro with daunorubicin (DNR).

Cell apoptosis was detected using flow cytometry.

RESULTS: Survivin protein was expressed in 41.9% of the 62 children with acute leukemia but in only 5.0% of the Control group (chi(2)=16.66; P < 0.01).

The expression rate of survivin was 46.2% in cytoplasm and 53.9% in nucleus in the children with acute leukemia (chi(2)0.3077; P> 0.05).

DNR treatment also induced survivin transllocation from cytoplasm to nucleus and cell apoptosis in a time and dosage-dependent manner.

CONCLUSIONS: Survivin may play an important role in the development and prognosis of childhood acute leukemia.

The different expression pattern of survivin in the cytoplasm and the nucleus may be associated with therapeutic efficacy and prognosis in acute leukemia.

DNR may reduce the survivin expression in leukemic cells and induce cell apoptosis.

[MeSH-major] Bone Marrow Cells / chemistry. Daunorubicin / therapeutic use. Leukemia, Myeloid, Acute / metabolism. Microtubule-Associated Proteins / analysis. Neoplasm Proteins / analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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(PMID = 16613699.001).

[ISSN] 1008-8830

[Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics

[ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; ZS7284E0ZP / Daunorubicin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Present status in studying immunotherapy for acute leukemia and its perspective--Editorial].

One of the important approaches for further prolonging remission duration and eradicating minimal residual disease in acute leukemia is immunotherapy.

Four kinds of immunotherapy for acute leukemia are under investigation:.

(1) monoclonal antibodies, among them, Mylotarg (cytotoxic antibiotic calicheamicin linked to CD33 Mab) is given for the treatment of refractory or relapsed acute myeloid leukemia and molecular relapse in acute promyelocytic leukemia with good results, Campath-1H (antiCD52 Mab) is administered in the treatment of prolymphocytic leukemia and Rituximab (anti-CD20 Mab) in B-PLL with high complete remission rates.

Other Mabs under preclinical and clinical trials include anti-IL-2 receptor Mab for the treatment of acute T lymphocytic leukemia, anti-220 kD Mab-6G7 for acute leukemias, recombinant immune toxin BL22 (anti-CD22) for hairy cell leukemia and Mabs labeled with radio-isotopes for different types of acute leukemias;.

(2) adoptive cellular immunotherapy using cytokine-induced killer cell, alloreactive NK cells, allogeneic or autologous leukemic-specific CD8(+) cytotoxic T lymphocytes, and other immune effector cells;.

(4) leukemia vaccines of several different formulations including antigen-specific, leukemia cell-based, leukemia antigen-pulsed dendritic cell (DC) and leukemia-derived DC vaccines, the latter two formulations are more attractive.

In conclusion, up to now, the most effective example of immunotherapy in acute leukemia is provided by the administration of Mabs, and the majority of other approaches in immunotherapy for acute leukemia although promising, need further studies.

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(PMID = 15854271.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] Editorial; English Abstract

[Publication-country] China

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Cancer Vaccines

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive subset of ALL with poor clinical outcome compared to B-ALL.

Therefore, to improve treatment, it is imperative to delineate the molecular blueprint of this disease.

In addition to the activating mutations of Notch previously described, this review will outline combinations of mutations in pathways that contribute to Notch signaling and appear to drive T-ALL development by 'mimicking' Notch effects on cell cycle and apoptosis.

[MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Neoplasm Proteins / physiology. Receptors, Notch / physiology. T-Lymphocytes / pathology

[MeSH-minor] Animals. Apoptosis / physiology. Cell Cycle / physiology. F-Box Proteins / physiology. Gene Expression Regulation, Leukemic. Genes, Tumor Suppressor. Humans. Ikaros Transcription Factor / genetics. Ikaros Transcription Factor / physiology. Ligands. Mice. Mice, Transgenic. Oncogenes. PTEN Phosphohydrolase / deficiency. PTEN Phosphohydrolase / genetics. PTEN Phosphohydrolase / physiology. Signal Transduction / physiology. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / physiology. Tumor Suppressor Proteins / physiology. Ubiquitin-Protein Ligases / physiology

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(PMID = 18758476.001).

[ISSN] 1476-5594

[Journal-full-title] Oncogene

[ISO-abbreviation] Oncogene

[Language] eng

[Grant] United States / NCI NIH HHS / CA / T32 CA09171

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review

[Publication-country] England

[Chemical-registry-number] 0 / F-Box Proteins; 0 / Fbxw7 protein, mouse; 0 / IKZF1 protein, human; 0 / Ligands; 0 / Neoplasm Proteins; 0 / Receptors, Notch; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 148971-36-2 / Ikaros Transcription Factor; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.3.2.19 / Ubiquitin-Protein Ligases

[Number-of-references] 84

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Recent studies have highlighted the role of Notch signalling in the development of T cell acute lymphoblasic leukaemia (T-ALL).

The aims of this study were to determine the effect of Notch signalling on apoptosis in human T-ALL cell lines and to identify targets of Notch signalling that may mediate this effect.

Microarray analysis revealed that GIMAP5, a gene coding for an anti-apoptotic intracellular protein, is upregulated by Notch in T-ALL cell lines.

[MeSH-major] Apoptosis. GTP-Binding Proteins / biosynthesis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptor, Notch1 / metabolism. Receptors, Notch / metabolism. Signal Transduction

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[Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.

(PMID = 20817506.001).

[ISSN] 1096-0961

[Journal-full-title] Blood cells, molecules & diseases

[ISO-abbreviation] Blood Cells Mol. Dis.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / GIMAP5 protein, human; 0 / Glucocorticoids; 0 / NOTCH1 protein, human; 0 / NOTCH3 protein, human; 0 / Protease Inhibitors; 0 / Receptor, Notch1; 0 / Receptors, Notch; EC 3.6.1.- / GTP-Binding Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Results of a phase I study of clofarabine (CLO) plus cyclophosphamide (CY) in adult patients (pts) with relapsed and/or refractory acute lymphoblastic leukemia (ALL).

The continual reassessment method (CRM) was used to determine the maximum tolerated dose (MTD) from 4 pre-defined dose levels.

Twenty-one pts had pre-B ALL, 5 pts pre-T/T ALL, 1 pt mature B ALL, and 3 pts biphenotypic acute leukemias.

All pts had pre-B ALL.

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(PMID = 27961382.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

: e14623 Background: Notch signaling is an evolutionary-conserved pathway in vertebrates and invertebrates which is involved many developmental processes, including cell fate decisions, apoptosis, proliferation, and stem-cell self renewal.

Increasing evidence suggests that the Notch signaling pathway is frequently up regulated in many forms of cancer including acute T-cell lymphoblastic leukemia, cervical, prostate, lung, breast and others.

RESULTS: Our data show that ANTP/DN MAML fusion protein, TR4 contains signals for proper cell targeting, internalization and nuclear transport.

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(PMID = 27964214.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

METHODS: PD-L1 expression was analyzed in 16 NHL cell lines by flow cytometry (FC) and in 111 lymphoma specimens by immunohistochemistry (IHC) (n=92) or FC (n=19).

In functional studies, irradiated anaplastic large cell lymphoma (ALCL) cells were co-cultured with allogeneic T cells in the presence of anti-PD-L1 blocking antibody, and IFNγ secretion and thymidine incorporation was used to assess T cell function and proliferation.

To further test tumor-T cell interactions, malignant ascites from a patient with ALK+ ALCL and peripheral blood mononuclear cells from a patient with leukemic mantle cell lymphoma, both containing PD-L1-expressing tumor cells and tumor-associated T cells, were stimulated with phytohemagglutinin (a polyclonal T cell activator) and incubated with anti-PD-L1 antibody.

Levels of 16 inflammatory cytokines were measured as an assessment of T cell activity.

RESULTS: All 9 B cell lymphoma lines were negative for PD-L1, while all 5 ALCL cell lines were strongly positive.

One T-cell ALL line was positive, and one peripheral T cell lymphoma was negative.

Strong PD-L1 staining was detected by IHC in all 14 ALCL specimens and in 83% of diffuse large B cell lymphomas (DLBCL) analyzed (n=35).

In the autologous setting using cultures of ALCL and mantle cell lymphoma specimens containing host T cells, secretion of inflammatory cytokines by tumor-associated T cells, including GMCSF, IFNγ, IL-1, IL-6, IL-8, TNFα, and MIP1α, were increased by incubation with anti-PD-L1 antibody.

PD-L1 may play a role in thwarting an effective anti-tumor immune response and represents an attractive target for lymphoma immunotherapy.

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(PMID = 27960901.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cytogenetic abnormalities in mesenchymal stem cells in chronic lymphocytic leukemia (CLL) patients and normal subjects.

: e22002 Background: Mesenchymal stem cells (MSC) residing in the marrow support hematopoiesis and protect cancer cells from undergoing cell death induced by chemotherapy.

Recent reports have described clonal cytogenetic abnormalities in the MSC of acute myeloid leukemia and myelodysplastic syndrome patients.

After 3-4 non-stimulated cell culture passages, the karyotype was analyzed in 5-40 metaphase cells from each subject Abnormalities were considered clonal using the accepted convention of the same chromosomal gain or rearrangement in 2 or more cells or loss in at least 3 cells.

CONCLUSIONS: Marrow MSC derived from CLL patients and normal subjects do show an array of cytogenetic abnormalities including clonal chromosomal abnormalities.

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(PMID = 27963169.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Result of adolescent acute lymphoblastic leukemia protocol (MCP 841) from a developing country.

: 10046 Background: Acute Lymphatic Leukemia is a curable disease in the range of 80 - 90% in developed countries by aggressive protocol like BFM, St. Judes' but result is much less in adolescence age group (60-70%).

In a follow-up period of 24 - 88 months (with an average of 54 months) the disease-free survival ( DFS) was 42 (56%) patients with an overall survival of 46 (61.34%) patients.

The major cause of the mortality was infection 18% (24.0% patients) followed progressive disease 9 (12.0%) and hemorrhage 2 (2.7%).

CONCLUSIONS: The data of acute lymphatic leukemia in adolescent is not satisfactory as compared to other pediatric patients.

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(PMID = 27962472.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Transliterated title] Arthroplastie de resurfaçage métal/métal en cas d’anatomie de hanche anormale.

These patients were defined to have abnormal coxanatomy by virtue of previous dysplastic disease of hip in three cases, previous Legg-Calve-Perthes disease, multiple epiphyseal dysplasia, T cell acute lymphoblastic leukaemia, trauma and sepsis in one case each.

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(PMID = 28755114.001).

[ISSN] 1633-8065

[Journal-full-title] European journal of orthopaedic surgery & traumatology : orthopedie traumatologie

[ISO-abbreviation] Eur J Orthop Surg Traumatol

[Language] eng

[Publication-type] Journal Article

[Publication-country] France

[Keywords] NOTNLM ; Anatomy / Arthroplasty / Hip / Metal-on-metal

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia.

: 10048 Background: T-cell acute lymphoblastic leukemia (T-ALL) is representing 10-15% of pediatric ALL.

Our published data showed that T-ALL phenotype patients fared poorly with 5 year survival of 27% versus 83% for precursor B-ALL (Recent Advances Research Update: 2006, 7; 1, P 51-56).

OBJECTIVES: We reviewed all patients diagnosed with T-ALL to assess risk classification according to NCI criteria, type of therapy received, overall survival and causes of mortality.

METHODS: Retrospective review of all patients files diagnosed with T-ALL from 1989 until now with data collection including; sex, age, white cell count (WBCs), CNS disease, type of protocol used, length of survival, overall survival, cause of death (toxic, disease).

Median WBCs 50,000/Cmm (range: 1.500-619,000/Cmm) and positive CNS at diagnosis 10/52 (20%).

Overall survival 27/52 (52%) and 25 pts. died (48%); 15 secondary to disease recurrence (9 on UKALL, 4 BFM, 2 CCG 1961); 4 during induction, 1 fulminant hepatic failure, 1 tumor lysis syndrome, and 4 due to toxicities (mucormycosis, staphylococcal toxic shock syndrome, CMV pneumonia, pseudomonas sepsis).

Further risk and response stratification in addition to intensification of therapy for T-cell ALL in our center may prove to be beneficial.

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(PMID = 27962474.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive neoplastic disorder, in which multiple genetic abnormalities cooperate in the malignant transformation of thymocytes.

[MeSH-major] Chromosome Aberrations. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Sequence Deletion

[MeSH-minor] Cell Cycle Proteins / genetics. Child. DNA Mutational Analysis. F-Box Proteins / genetics. Gene Dosage. Gene Rearrangement. Genome, Human. Humans. In Situ Hybridization, Fluorescence. Ubiquitin-Protein Ligases / genetics. WT1 Proteins / genetics

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(PMID = 18185524.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Homeodomain Proteins; 0 / TLX3 protein, human; 0 / WT1 Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Downregulation of Notch signaling by gamma-secretase inhibition can abrogate chemotherapy-induced apoptosis in T-ALL cell lines.

Activation of Notch1 signaling plays an important role in the pathogenesis of precursor T-cell lymphoblastic leukemia (T-ALL).

In this study, we analyzed the response of four T-ALL cell lines to compound E, a potent gamma-secretase inhibitor, and to the combination of compound E with vincristine, daunorubicin, L-asparaginase (L-ASP), and dexamethasone (DEX).

We identified two distinct types of responses: In type 1 cell lines, represented by TALL1 and HSB2, GSI-induced apoptosis followed cell cycle arrest and enhanced the induction of apoptosis caused by DEX and L-ASP.

In type 2 cell lines, represented by CEM and Jurkat J6, GSI caused neither cell cycle block nor cell death.

In type 2 cells, GSI induced the upregulation of Bcl-xl mRNA and protein, which was thus identified as a candidate mechanism for the inhibition of apoptosis.

[MeSH-major] Amyloid Precursor Protein Secretases / physiology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Receptor, Notch1 / antagonists & inhibitors

[MeSH-minor] Asparaginase / pharmacology. Benzodiazepinones / pharmacology. Cell Line, Tumor. Daunorubicin / pharmacology. Dexamethasone / pharmacology. Down-Regulation. Humans. Signal Transduction. Vincristine / pharmacology

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(PMID = 19057901.001).

[ISSN] 1432-0584

[Journal-full-title] Annals of hematology

[ISO-abbreviation] Ann. Hematol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / 2-(((3,5-difluorophenyl)acetyl)amino)-N-(1-methyl-2-oxo-5-phenyl-2,3-dihydro-1H-1,4-benzodiazepin-3-yl)propanamide; 0 / Benzodiazepinones; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.5.1.1 / Asparaginase; ZS7284E0ZP / Daunorubicin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Ligand-driven activation of the notch pathway in T-ALL and solid tumors: why Not(ch)?

The Notch pathway is an evolutionally conserved cell-cell interaction signalling system involved in several key aspects of cell life, ranging from differentiation and proliferation to apoptosis.

The clearest example of oncogenic Notch signalling is observed in T acute lymphoblastic leukemia (T-ALL), an aggressive neoplasm of immature T-cells, due to genetic alterations leading to ligand-independent increased Notch1 receptor signalling.

In solid tumors, however, extrinsic regulation through canonical cell-cell interactions appears to drive activation of the pathway.

[MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptors, Notch / metabolism

[MeSH-minor] Animals. Humans. Intracellular Signaling Peptides and Proteins. Leukemia / metabolism. Membrane Proteins / metabolism. Models, Biological. Neovascularization, Pathologic / metabolism. Signal Transduction / genetics. Signal Transduction / physiology

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(PMID = 20016278.001).

[ISSN] 1551-4005

[Journal-full-title] Cell cycle (Georgetown, Tex.)

[ISO-abbreviation] Cell Cycle

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / Receptors, Notch; 0 / delta protein

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Prognostic influence of immunological subtypes of T-cell acute lymphoblastic leukemia. Study of 81 patients].

[Transliterated title] Significado pronóstico de los subtipos inmunológicos de la leucemia aguda linfoblástica T del adulto. Estudio de 81 pacientes.

BACKGROUND AND OBJECTIVE: T-cell acute lymphoblastic leukemia (ALL) includes 4 immunological subtypes: pro-T, pre-T, thymic or cortical and mature.

In some studies, pro-T and mature subtypes have a poor prognosis.

The objective of this study was to describe the clinical characteristics, the result of treatment and the prognosis of the immunological subtypes of T-cell ALL in 81 adult patients included in 2 protocols of the Spanish PETHEMA group (ALL-96 and ALL-93).

The main clinical and biological parameters as well as the rate of response to treatment, the frequency of complete remission , disease free survival and overall survival were compared in each T-cell ALL subtype.

RESULTS: Of the 64 evaluable patients the distribution of the immunological subtypes was: 3 pro-T, 17 pre-T, 22 thymic or cortical and 22 mature.

Patients with mature T-cell ALL had a slow rate of response to treatment in comparison with patients wit pre-T and mature T-cell ALL but this did not translate to significant differences in frequency of complete remission (77% vs 94%), disease free survival (42% vs 46%) and overall survival (29% vs 47%).

CONCLUSIONS: Although patients with mature T-cell ALL had a slow rate of response to treatment and their survival tended to be shorter, in the present study there were no statistically significant differences in the prognosis of the different subtypes of T-cell ALL.

[MeSH-major] Leukemia-Lymphoma, Adult T-Cell / mortality

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(PMID = 16426542.001).

[ISSN] 0025-7753

[Journal-full-title] Medicina clínica

[ISO-abbreviation] Med Clin (Barc)

[Language] spa

[Publication-type] English Abstract; Journal Article

[Publication-country] Spain

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Limited but potential efficacy by graft-versus-leukemia (GVL) for Pro T-ALL].

We present a 22-year-old male diagnosed with pro T-acute lymphoblastic leukemia (ALL).

Flow cytometry analysis of the leukemic cells showed cCD3+, CD7+, CD2+, CD1a-, CD3-, CD5-, CD4-, CD8-, CD34+, and HLA-DR+ as a pro T-cell phenotype.

He underwent up-front stem cell transplantation (SCT) from an HLA-full matched sibling, with early relapse just before transplantation.

Based on the immature T cell phenotype frequently with myeloid markers, a graft-versus- leukemic effect might be expected after allogeneic SCT for Pro T-ALL and a positive indication of SCT for this disease should be considered.

[MeSH-major] Graft vs Leukemia Effect / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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(PMID = 19011341.001).

[ISSN] 0385-0684

[Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy

[ISO-abbreviation] Gan To Kagaku Ryoho

[Language] jpn

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Japan

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Leukemia-associated antigenic isoforms induce a specific immune response in children with T-ALL.

The potential immunogenicity of acute lymphoblastic leukemia of the T cell (T-ALL), a small subgroup of childhood leukemia with increased risk for treatment failure and early relapse, was addressed by serological identification of leukemia-derived antigens by recombinant expression cloning (SEREX).

Further characterization of the 4 novel isoforms revealed that 3 (HECTD1Delta, CX-ORF-15Delta and hCAP-EDelta) had restricted mRNA expression in more than 70% of T-ALLs (n = 22) and that specific antibodies against these isoforms were detected in up to 30% of patients (n = 16), with the highest frequency for HECTD1Delta.

The latter protein was present at high abundance in T-ALLs but not in normal hematopoietic tissues.

Given that the leukemia-associated antigens detected in this study have an intracellular localization, the generation of immune effector responses most likely requires antigen presentation.

To test this assumption, dendritic cells were loaded with HECTD1Delta protein and used for T cell stimulation.

A specific T cell response was induced in vitro in all 3 healthy donors studied, including a former T-ALL patient.

[MeSH-major] Antigens, Neoplasm / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology

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[Copyright] Copyright 2006 Wiley-Liss, Inc.

(PMID = 17016825.001).

[ISSN] 0020-7136

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies; 0 / Antigens, Neoplasm; 0 / DNA, Complementary; 0 / Protein Isoforms; 0 / RNA, Messenger; 82115-62-6 / Interferon-gamma

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Recent studies have demonstrated that the MYB oncogene is frequently duplicated in human T cell acute lymphoblastic leukemia (T-ALL).

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(PMID = 18070937.001).

[ISSN] 1540-9538

[Journal-full-title] The Journal of experimental medicine

[ISO-abbreviation] J. Exp. Med.

[Language] ENG

[Databank-accession-numbers] GEO/ GSE7615

[Grant] United States / NCI NIH HHS / CA / P01 CA109901; United States / NIGMS NIH HHS / GM / R37 GM050237; United States / NCI NIH HHS / CA / CA11560; United States / NIGMS NIH HHS / GM / GM067055; United States / NIGMS NIH HHS / GM / R01 GM067055; United States / NIGMS NIH HHS / GM / R01 GM050237; United States / NCI NIH HHS / CA / R01 CA111560; United States / NCI NIH HHS / CA / R21 CA115853; United States / NIGMS NIH HHS / GM / GM050237; United States / NCI NIH HHS / CA / CA115853; United States / NCI NIH HHS / CA / CA68484-11; United States / NCI NIH HHS / CA / P01 CA068484; United States / NCI NIH HHS / CA / CA109901

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myb

[Other-IDs] NLM/ PMC2150982

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Our analyses indicate that the PI3K/Akt pathway is constitutively active in the four T-ALL cell lines tested.

PTEN expression was not detected in 3/4 cell lines tested, suggesting the loss of PTEN-mediated Akt activation.

We analysed the relationship between Notch-1 and the PI3K/Akt signalling and show that inhibition of the Akt pathway changes Notch expression; Notch-1 protein decreased in all the cell lines upon treatment with the inhibitor.

[MeSH-major] Phosphatidylinositol 3-Kinases / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptor, Notch1 / metabolism. Signal Transduction

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[Copyright] 2007 Wiley-Liss, Inc.

(PMID = 17849443.001).

[ISSN] 1097-4644

[Journal-full-title] Journal of cellular biochemistry

[ISO-abbreviation] J. Cell. Biochem.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / bcl-2-Associated X Protein; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 3.6.5.2 / ras Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Frequency and clinical relevance of DNA microsatellite alterations of the CDKN2A/B, ATM and p53 gene loci: a comparison between pediatric precursor T-cell lymphoblastic lymphoma and T-cell lymphoblastic leukemia.

Although deletions of cell cycle regulatory gene loci have long been reported in various malignancies, little is known regarding their relevance in pediatric T-cell lymphoblastic lymphoma (T-LBL) and T-cell lymphoblastic leukemia (TALL).

[MeSH-major] Cell Cycle Proteins / genetics. Cyclin-Dependent Kinase Inhibitor p15 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. DNA-Binding Proteins / genetics. Genetic Loci / genetics. Leukemia, T-Cell / genetics. Microsatellite Repeats / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Protein-Serine-Threonine Kinases / genetics. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Proteins / genetics

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(PMID = 19586936.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] Italy

[Chemical-registry-number] 0 / CDKN2B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / Genetic Markers; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases

[Other-IDs] NLM/ PMC2805736

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Notch-1 regulates Akt signaling pathway and the expression of cell cycle regulatory proteins cyclin D1, CDK2 and p21 in T-ALL cell lines.

Gain-of-function mutations in Notch-1 are common in T-cell lymphoblastic leukemia (T-ALL), making this receptor a promising target for drugs such as gamma-secretase inhibitors (GSIs).

However, GSIs seem to be active in only a small fraction of T-ALL cell lines with constitutive Notch-1 activity and the downstream response of Notch signaling is only partially understood.

To further investigate the molecular mechanisms underlying proliferation suppression and apoptosis and explore effective downstream target genes, we used RNA interference (RNAi) technology to down-regulate the expression of Notch-1 in GSIs-resistant T-ALL cell lines.

Results showed that down-regulation of Notch-1 by transfection of a small interfering RNA (siRNA) could cause SupT1 cells proliferation inhibition by inducing G(0)/G(1) cell cycle arrest and apoptosis.

The proliferation inhibitory and apoptotic effects resulting from down-regulation of Notch-1 may be mediated through regulating the expression of cell cycle regulatory proteins cyclin D1, CDK2 and p21 and the activity of Akt signaling.

Taken together, cell cycle regulatory proteins and Akt signaling may be attractive targets in T-ALL.

[MeSH-major] CDC2 Protein Kinase / genetics. Cyclin D1 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-akt / metabolism. Receptor, Notch1 / physiology. Signal Transduction / physiology

[MeSH-minor] Apoptosis. Base Sequence. Cell Cycle. Cell Line, Tumor. Cell Proliferation. Down-Regulation / physiology. Humans. Mutation. RNA Interference. RNA, Small Interfering. Reverse Transcriptase Polymerase Chain Reaction

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(PMID = 19091404.001).

[ISSN] 1873-5835

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / NOTCH1 protein, human; 0 / RNA, Small Interfering; 0 / Receptor, Notch1; 136601-57-5 / Cyclin D1; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.22 / CDC2 Protein Kinase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Adult patients with acute lymphoblastic T cell leukemia (T-ALL) have a very poor prognosis and few effective therapeutic options.

In addition, treatment of malignant T-cell lines with peg-Arg I significantly impaired their proliferation, which correlated with a decreased progression into the cell cycle, followed by the induction of apoptosis.

The results suggest the potential benefit of L-Arginine depletion by peg-Arg I in the treatment of T-cell malignancies.

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(PMID = 20407034.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCRR NIH HHS / RR / P20RR021970; United States / NCRR NIH HHS / RR / P20 RR021970; United States / NCI NIH HHS / CA / R01 CA082689; United States / NIGMS NIH HHS / GM / P20 GM103501; United States / NCI NIH HHS / CA / R01 CA107974

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CCND3 protein, human; 0 / Cyclin D3; 04079A1RDZ / Cytarabine; 30IQX730WE / Polyethylene Glycols; 94ZLA3W45F / Arginine; EC 3.5.3.1 / Arginase

[Other-IDs] NLM/ PMC2892956

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

NOTCH1 mutations are common in T-lineage acute lymphoblastic leukemia (T-ALL).

Twin studies and retrospective screening of neonatal blood spots provide evidence that fusion genes and other chromosomal abnormalities associated with pediatric leukemias can originate prenatally.

[MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics

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(PMID = 17901244.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis.

Neurofibromatosis type 1 (NF1) is an autosomal dominant genetic disorder caused by mutations in the NF1 gene.

Patients with NF1 have a higher risk to develop juvenile myelomonocytic leukemia (JMML) with a possible progression toward acute myeloid leukemia (AML).

In an oligo array comparative genomic hybridization-based screening of 103 patients with pediatric T-cell acute lymphoblastic leukemia (T-ALL) and 71 patients with MLL-rearranged AML, a recurrent cryptic deletion, del(17)(q11.2), was identified in 3 patients with T-ALL and 2 patients with MLL-rearranged AML.

Since the NF1 protein is a negative regulator of the RAS pathway (RAS-GTPase activating protein), homozygous NF1 inactivation represent a novel type I mutation in pediatric MLL-rearranged AML and T-ALL with a predicted frequency that is less than 10%.

NF1 inactivation may provide an additional proliferative signal toward the development of leukemia.

[MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation / genetics. Neurofibromatoses / genetics. Neurofibromin 1 / genetics

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(PMID = 18172006.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Neurofibromin 1; 0 / RNA, Messenger

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The C-MYB locus is involved in chromosomal translocation and genomic duplications in human T-cell acute leukemia (T-ALL), the translocation defining a new T-ALL subtype in very young children.

The C-Myb transcription factor is essential for hematopoiesis, including in the T-cell lineage.

Here, we identified 2 types of genomic alterations involving the C-MYB locus at 6q23 in human T-cell acute leukemia (T-ALL).

Expression analysis, including allele-specific approaches, showed stronger C-MYB expression in the MYB-rearranged cases compared with other T-ALLs, and a dramatically skewed C-MYB allele expression in the TCRB-MYB cases, which suggests that a translocation-driven deregulated expression may overcome a cellular attempt to down-regulate C-MYB.

Strikingly, profiling of the T-ALLs by clinical, genomic, and large-scale gene expression analyses shows that the TCRB-MYB translocation defines a new T-ALL subtype associated with a very young age for T-cell leukemia (median, 2.2 years) and with a proliferation/mitosis expression signature.

[MeSH-major] Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 7 / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Proto-Oncogene Proteins c-myb / genetics. Translocation, Genetic

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(PMID = 17452517.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Grant] United States / NCI NIH HHS / CA / R01 CA101859

[Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myb

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Pediatric T-cell acute lymphoblastic leukemia (T-ALL) is characterized by chromosomal rearrangements possibly enforcing arrest at specific development stages.

We studied the relationship between molecular-cytogenetic abnormalities and T-cell development stage to investigate whether arrest at specific stages can explain the prognostic significance of specific abnormalities.

HOX11 cases were CD1 positive consistent with a cortical stage, but as 4/5 cases lacked cytoplasmatic-beta expression, developmental arrest may precede beta-selection.

HOX11L2 was especially confined to immature and pre-AB developmental stages, but 3/17 HOX11L2 mature cases were restricted to the gammadelta-lineage.

Classification into T-cell developmental subgroups was not predictive for outcome.

[MeSH-major] Gene Rearrangement / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Neoplasm Recurrence, Local / genetics. Receptor, Notch1 / genetics

[MeSH-minor] Basic Helix-Loop-Helix Transcription Factors / genetics. Cell Lineage. Child. Female. Homeodomain Proteins / genetics. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Mutation / genetics. Oncogene Proteins, Fusion / genetics. Prognosis. Proto-Oncogene Proteins / genetics. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Receptors, Antigen, T-Cell, alpha-beta / genetics. Receptors, Antigen, T-Cell, gamma-delta / genetics. Reverse Transcriptase Polymerase Chain Reaction

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(PMID = 17928886.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / AF10-CALM fusion protein, human; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Homeodomain Proteins; 0 / NOTCH1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Antigen, T-Cell, gamma-delta; 0 / TLX3 protein, human; 135471-20-4 / TAL1 protein, human

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The NUP214-ABL1 fusion gene in T-cell acute lymphoblastic leukemia (T-ALL) has recently been identified as a possible target for imatinib and related tyrosine kinase inhibitors, but exact data regarding the prognostic impact and frequency of the several putative NUP214-ABL1 mRNA transcripts are still missing.

Eleven (3.9%) patients were NUP214-ABL1 positive, and 5 different transcripts were observed; 8 patients had a thymic immunophenotype, 1 had an early T-cell immunophenotype, and 2 had a mature T-cell immunophenotype.

[MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-abl / genetics

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(PMID = 16873673.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Benzamides; 0 / NUP214 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Molecular cytogenetic study of 126 unselected T-ALL cases reveals high incidence of TCRbeta locus rearrangements and putative new T-cell oncogenes.

Chromosomal aberrations of T-cell receptor (TCR) gene loci often involve the TCRalphadelta (14q11) locus and affect various known T-cell oncogenes.

Therefore, we initiated a screening of 126 T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma cases and 19 T-ALL cell lines using FISH break-apart assays for the different TCR loci.

Some of these chromosome aberrations target new putative T-cell oncogenes at chromosome 11q24, 20p12 and 6q22.

Five patients and one cell line carried chromosomal rearrangements affecting both TCRbeta and TCRalphadelta loci.

In conclusion, this study presents the first inventory of chromosomal rearrangements of TCR loci in T-ALL, revealing an unexpected high number of cryptic chromosomal rearrangements of the TCRbeta locus and further broadening the spectrum of genes putatively implicated in T-cell oncogenesis.

[MeSH-major] Gene Rearrangement, T-Lymphocyte / genetics. Genes, T-Cell Receptor beta / genetics. Leukemia-Lymphoma, Adult T-Cell / epidemiology. Leukemia-Lymphoma, Adult T-Cell / genetics

[MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Genes, T-Cell Receptor alpha / genetics. Genes, T-Cell Receptor delta / genetics. Humans. In Situ Hybridization, Fluorescence. Incidence. Male. Middle Aged. Retrospective Studies. Translocation, Genetic

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(PMID = 16673021.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't

[Publication-country] England

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Genetic alterations determine chemotherapy resistance in childhood T-ALL: modelling in stage-specific cell lines and correlation with diagnostic patient samples.

Acquired drug resistance eventually leads to treatment failure in T-cell acute lymphoblastic leukaemia (T-ALL).

Immunophenotypic and cytogenetic heterogeneities within T-ALL influence susceptibility to cytotoxic therapy, and little is known about the mechanisms of drug resistance at specific stages of T-cell ontogeny.

We developed tolerance to therapeutic concentrations of daunorubicin (DNR) and L-asparaginase (L-asp) in Jurkat (CD1a(-), sCD3(+)) and Sup T1 (CD1a(+), sCD3(-)) cell lines, having respective 'mature' and 'cortical' stages of developmental arrest.

Microarray analysis identified upregulation of asparagine synthetase (ASNS) and argininosuccinate synthase 1 (ASS1) to cell lines with acquired resistance to L-asp, and in the case of DNR, upregulation of ATP-binding cassette B1 (ABCB1).

This study expands the pool of available drug resistant cell lines having cortical and mature stages of developmental arrest, introduces three new drug resistant T-ALL cell lines, and identifies gene interactions leading to L-asp and DNR resistance.

[MeSH-major] Cell Line, Tumor. Drug Resistance, Neoplasm / genetics. Gene Expression Regulation, Leukemic. Genes, MDR. Leukemia-Lymphoma, Adult T-Cell / genetics

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(PMID = 17854304.001).

[ISSN] 0007-1048

[Journal-full-title] British journal of haematology

[ISO-abbreviation] Br. J. Haematol.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / 1 R01 CA114589; United States / NCI NIH HHS / CA / U10 CA98543-03-14305

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / P-Glycoprotein; 0 / RNA, Small Interfering; 5J49Q6B70F / Vincristine; 9PHQ9Y1OLM / Prednisolone; EC 3.5.1.1 / Asparaginase; EC 6.3.1.1 / Aspartate-Ammonia Ligase; EC 6.3.4.5 / Argininosuccinate Synthase; ZS7284E0ZP / Daunorubicin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The NRR includes the 3 Lin12/Notch repeats and the juxtamembrane heterodimerization domain, the region of Notch1 most frequently mutated in T-cell acute lymphoblastic leukemia lymphoma (T-ALL).

[MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Receptor, Notch1 / chemistry. Receptor, Notch1 / metabolism. Regulatory Sequences, Nucleic Acid. Signal Transduction

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(PMID = 19075186.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Grant] United States / NCI NIH HHS / CA / R56 CA092433; United States / NCI NIH HHS / CA / P01 CA119070-030003; United States / NCI NIH HHS / CA / R01 CA092433-05S1; United States / NCI NIH HHS / CA / CA092433; United States / NCI NIH HHS / CA / R56 CA092433-06A1; United States / NCI NIH HHS / CA / R01 CA092433; United States / NCI NIH HHS / CA / P01 CA119070-03; United States / NCI NIH HHS / CA / P01 CA119070-039001; United States / NCI NIH HHS / CA / P01 CA119070-029001; United States / NCI NIH HHS / CA / P01 CA119070-020003; United States / NCI NIH HHS / CA / R01 CA092433-05; United Kingdom / Medical Research Council / / MRC/ G0500389; United States / NCI NIH HHS / CA / R01 CA092433-04; United States / NCI NIH HHS / CA / P01 CA119070

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / NOTCH2 protein, human; 0 / Receptor, Notch1; 0 / Receptor, Notch2; EC 1.13.12.- / Luciferases

[Other-IDs] NLM/ PMC2676092

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The Ikaros (Ikzf1) gene, encoding a transcription regulator, is a major tumor suppressor in B-cell acute lymphoblastic leukemia (B-ALL).

[MeSH-major] Gene Silencing. Ikaros Transcription Factor / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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[Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.

[CommentIn] Leuk Res. 2010 Apr;34(4):416-7 [19892402.001]

(PMID = 19796813.001).

[ISSN] 1873-5835

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / IKZF1 protein, human; 0 / Protein Isoforms; 148971-36-2 / Ikaros Transcription Factor

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

T-cell acute lymphoblastic leukemia (T-ALL) is the hematological malignancy of bone marrow characterized by the rapid proliferation and subsequent accumulation of immature T lymphocyte and mainly occurs in children and adolescents.

This review briefly discusses the four main subtypes of Notch 1 activating mutations, also focuses on how these mutations change the normal signaling pathways and genes expression during their participation in the pathogenesis of T-ALL, and how these insights will promote the development of newly targeting therapies for patients with this aggressive form of leukemia.

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(PMID = 20137156.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] China

[Chemical-registry-number] 0 / Receptor, Notch1

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The Notch pathway is frequently activated in T-cell acute lymphoblastic leukemias (T-ALLs).

Of the Notch receptors, Notch1 is a recurrent target of gain-of-function mutations and Notch3 is expressed in all T-ALLs, but it is currently unclear how these receptors contribute to T-cell transformation in vivo.

While deletion of Notch3 has little effect, T cell-specific deletion of floxed Notch1 promoter/exon 1 sequences significantly accelerates leukemogenesis.

Further, spontaneous deletion of 5' Notch1 sequences occurs in approximately 75% of Ikaros-deficient T-ALLs.

[MeSH-major] Ikaros Transcription Factor / physiology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic / genetics. Receptor, Notch1 / genetics. Transcriptional Activation / physiology

[MeSH-minor] Animals. Blotting, Northern. Blotting, Western. Cell Transformation, Neoplastic. DNA Primers / chemistry. DNA Primers / genetics. Flow Cytometry. Gene Expression Regulation, Neoplastic. Immunoglobulin J Recombination Signal Sequence-Binding Protein / physiology. Mice. Mice, Knockout. Mutation / genetics. RNA, Messenger / genetics. Receptors, Notch / physiology. Reverse Transcriptase Polymerase Chain Reaction. Sequence Deletion. Survival Rate

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(PMID = 20829372.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Grant] United States / NICHD NIH HHS / HD / R01 HD034883

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / DNA Primers; 0 / Immunoglobulin J Recombination Signal Sequence-Binding Protein; 0 / Notch1 protein, mouse; 0 / Notch3 protein, mouse; 0 / RNA, Messenger; 0 / Rbpj protein, mouse; 0 / Receptor, Notch1; 0 / Receptors, Notch; 0 / Zfpn1a1 protein, mouse; 148971-36-2 / Ikaros Transcription Factor

[Other-IDs] NLM/ PMC3100247

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Point mutations that trigger ligand-independent proteolysis of the Notch1 ectodomain occur frequently in human T-cell acute lymphoblastic leukemia (T-ALL) but are rare in murine T-ALL, suggesting that other mechanisms account for Notch1 activation in murine tumors.

Here we show that most murine T-ALLs harbor Notch1 deletions that fall into 2 types, both leading to ligand-independent Notch1 activation.

Type 1 deletions remove exon 1 and the proximal promoter, appear to be RAG-mediated, and are associated with mRNA transcripts that initiate from 3' regions of Notch1.

Type 2 deletions remove sequences between exon 1 and exons 26 to 28 of Notch1, appear to be RAG-independent, and are associated with transcripts in which exon 1 is spliced out of frame to 3' Notch1 exons.

[MeSH-major] Homeodomain Proteins / physiology. Peptide Chain Initiation, Translational / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic / genetics. Receptor, Notch1 / genetics. Transcriptional Activation / physiology

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[Cites] Cell. 2010 Apr 30;141(3):419-31 [20398922.001]

[Cites] Blood. 2010 Dec 16;116(25):5443-54 [20829372.001]

[CommentIn] Blood. 2010 Dec 16;116(25):5436-8 [21163932.001]

(PMID = 20852131.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Grant] United States / NCI NIH HHS / CA / R01 CA096899

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Notch1 protein, mouse; 0 / RNA, Messenger; 0 / Receptor, Notch1; 0 / Zfpn1a1 protein, mouse; 128559-51-3 / RAG-1 protein; 148971-36-2 / Ikaros Transcription Factor

[Other-IDs] NLM/ PMC3031398

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Disruption of the BCL11B gene through inv(14)(q11.2q32.31) results in the expression of BCL11B-TRDC fusion transcripts and is associated with the absence of wild-type BCL11B transcripts in T-ALL.

T-cell acute lymphoblastic leukemia (T-ALL) is associated with chromosomal aberrations characterized by juxtaposition of proto-oncogenes to T-cell receptor gene loci (TCR), resulting in the deregulated transcription of these proto-oncogenes.

The TRDV1-BCL11B joining region was 1344 bp long and contained fragments derived from 20q11.22, 3p21.33 and from 11p12, indicating the complex character of this aberration.

A strong expression of in-frame transcripts with truncated BCL11B and TCRD constant region (TRDC) were observed, but in contrast to normal T cells and other T-ALL samples, no wild-type BCL11B transcripts were detected in the T-ALL sample.

Screening of 37 other T-ALLs revealed one additional case with expression of the BCL11B-TRDC fusion transcript.

As BCL11B appears to play a key role in T-cell differentiation, BCL11B disruption and disturbed expression may contribute to the development of T-cell malignancies in man.

[MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 14. Leukemia-Lymphoma, Adult T-Cell / genetics. Translocation, Genetic

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(PMID = 15668700.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / BCL11B protein, human; 0 / DNA-Binding Proteins; 0 / Repressor Proteins; 0 / Tumor Suppressor Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] NOTCH1/FBXW7 mutation identifies a large subgroup with favorable outcome in adult T-cell acute lymphoblastic leukemia (T-ALL): a Group for Research on Adult Acute Lymphoblastic Leukemia (GRAALL) study.

Many somatic genetic abnormalities have been identified in T-cell acute lymphoblastic leukemia (T-ALL) but each individual abnormality accounts for a small proportion of cases; therapeutic stratification consequently still relies on classical clinical markers.

We screened 141 adult diagnostic T-ALL samples from patients treated on either the Lymphoblastic Acute Leukemia in Adults (LALA)-94 (n = 87) or the GRAALL-2003 (n = 54) trials.

In 88 cases (62%) there were demonstrated NOTCH1 mutations (42% heterodimerization [HD], 10% HD+proline glutamate serine threonine [PEST], 6% PEST, 2% juxtamembrane mutations, 2% transactivation domain [TAD]) and 34 cases (24%) had FBXW7 mutations (21 cases had both NOTCH1 and FBXW7 mutations); 40 cases (28%) were wild type for both.

[MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics. Ubiquitin-Protein Ligases / genetics

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(PMID = 19109228.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Receptor, Notch1; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Clinical, cytogenetic and molecular characteristics of 14 T-ALL patients carrying the TCRbeta-HOXA rearrangement: a study of the Groupe Francophone de Cytogénétique Hématologique.

Recently, we and others described a new chromosomal rearrangement, that is, inv(7)(p15q34) and t(7;7)(p15;q34) involving the T-cell receptor beta (TCRbeta) (7q34) and the HOXA gene locus (7p15) in 5% of T-cell acute lymphoblastic leukemia (T-ALL) patients leading to transcriptional activation of especially HOXA10.

To further address the clinical, immunophenotypical and molecular genetic findings of this chromosomal aberration, we studied 330 additional T-ALLs.

In conclusion, this study defines TCRbeta-HOXA rearranged T-ALLs as a distinct cytogenetic subgroup by clinical, immunophenotypical and molecular genetic characteristics.

[MeSH-major] Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Receptors, Antigen, T-Cell, alpha-beta / genetics

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(PMID = 17039236.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Homeodomain Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell, alpha-beta; 140441-81-2 / HOXA10 protein, human

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Aggressive Langerhans cell histiocytosis following T-ALL: clonally related neoplasms with persistent expression of constitutively active NOTCH1.

Langerhans cell histiocytosis (LCH) and related entities are neoplasms of unknown pathogenesis.

Here, we describe studies assessing the role of NOTCH1 mutations in LCH, which were based on a case of fatal Langerhans cell tumor after T-cell acute lymphoblastic leukemia (T-ALL).

Although the two types of neoplasm in this patient were temporally and pathologically distinct, molecular analyses showed that they harbored the same T-cell receptor gene rearrangements and two activating NOTCH1 mutations involving exons 27 and 34.

Analysis of cDNA prepared from the aggressive Langerhans cell tumor showed that the NOTCH1 mutations were aligned in cis, a configuration that caused synergistic increases in NOTCH1 signal strength in reporter gene assays.

Immunohistochemistry confirmed that the Langerhans cell tumor also expressed NOTCH1 protein.

Although these data suggested that NOTCH1 mutations might contribute to the pathogenesis of typical sporadic LCH and related neoplasms occurring in the absence of T-ALL, an analysis of 24 cases of LCH and Rosai-Dorfman Disease occurring in patients without an antecedent history of T-ALL revealed no mutations.

Thus, activating NOTCH1 mutations appear to be unique to aggressive Langerhans cell tumors occurring after T-ALL.

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(PMID = 17874453.001).

[ISSN] 0361-8609

[Journal-full-title] American journal of hematology

[ISO-abbreviation] Am. J. Hematol.

[Language] ENG

[Grant] United States / NIAID NIH HHS / AI / AI050225; United States / NCI NIH HHS / CA / CA082308; United States / NCI NIH HHS / CA / CA119070-02; United States / NCI NIH HHS / CA / P01 CA119070-02; United States / NCI NIH HHS / CA / P01 CA119070

[Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Precursor T-cell acute lymphoblastic leukemia (T-ALL) in children represents a clinical challenge, because relapses are usually fatal.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Deletion. Chromosomes, Human, Pair 6 / genetics. Neoplasm Proteins / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Signal Transduction / genetics

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(PMID = 19406988.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Databank-accession-numbers] GEO/ GPL5713/ GSE8738

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / NOTCH1 protein, human; 0 / Neoplasm Proteins; 0 / Receptor, Notch1; 0 / Transforming Growth Factor beta; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Hexamethylene bisacetamide inhibits malignant phenotype in T-ALL cell lines.

T acute lymphoblastic leukemia cell lines treated with hexamethylene bisacetamide (HMBA) undergo a delay in cell cycle progression and increase susceptibility to apoptosis, although they never overcome the differentiation block.

In accordance with changes in cell cycle and apoptosis, transitory p53 pathway activation commonly occurs.

Bcl-2 inhibition further favours the pro-apoptotic effect of HMBA.

Even if HMBA generally reduces Notch1 level in T acute lymphoblastic leukemia (T-ALL) cell lines, this does not commonly influence the biological response; in fact all the analysed cell lines, except CEM cells, display no biological effect following DAPT-induced Notch inhibition.

[MeSH-major] Acetamides / pharmacology. Antineoplastic Agents / pharmacology. Leukemia-Lymphoma, Adult T-Cell / drug therapy

[MeSH-minor] Cell Line, Tumor. Cyclin-Dependent Kinase 4 / analysis. Humans. Proto-Oncogene Proteins c-bcl-2 / physiology. Receptor, Notch1 / physiology. Signal Transduction. Triglycerides / pharmacology. Tumor Suppressor Protein p53 / physiology. gamma-Aminobutyric Acid / analogs & derivatives. gamma-Aminobutyric Acid / pharmacology

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[CommentIn] Leuk Res. 2008 May;32(5):689-90 [18164760.001]

(PMID = 17964649.001).

[ISSN] 0145-2126

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Acetamides; 0 / Antineoplastic Agents; 0 / NOTCH1 protein, human; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptor, Notch1; 0 / Triglycerides; 0 / Tumor Suppressor Protein p53; 56-12-2 / gamma-Aminobutyric Acid; 93349-26-9 / 1,2-dilinolenoyl-3-(4-aminobutyryl)propane-1,2,3-triol; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; LA133J59VU / hexamethylene bisacetamide

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Common molecular machineries between hematopoietic stem cell (HSC) maintenance and leukemia prevention have been highlighted.

The tumor suppressor Fbxw7 (F-box and WD-40 domain protein 7), a subunit of an SCF-type ubiquitin ligase complex, induces the degradation of positive regulators of the cell cycle.

We demonstrate that inactivation of Fbxw7 in hematopoietic cells causes premature depletion of HSCs due to active cell cycling and p53-dependent apoptosis.

Interestingly, Fbxw7 deletion also confers a selective advantage to cells with suppressed p53 function, eventually leading to development of T-cell acute lymphoblastic leukemia (T-ALL).

[MeSH-major] F-Box Proteins / metabolism. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / enzymology. Leukemia-Lymphoma, Adult T-Cell / etiology. Ubiquitin-Protein Ligases / metabolism

[MeSH-minor] Animals. Cell Cycle. Cells, Cultured. Mice. Mice, Transgenic. Tumor Suppressor Protein p53 / metabolism

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(PMID = 18367647.001).

[ISSN] 0890-9369

[Journal-full-title] Genes & development

[ISO-abbreviation] Genes Dev.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / F-Box Proteins; 0 / Fbxw7 protein, mouse; 0 / Tumor Suppressor Protein p53; EC 6.3.2.19 / Ubiquitin-Protein Ligases

[Other-IDs] NLM/ PMC2335330

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Mutations resulting in overexpression of intracellular Notch1 (ICN1) are frequently observed in human T cell acute lymphoblastic leukemia (T-ALL).

Early consequences are the generation of polyclonal nontumorigenic CD4(+)8(+) T cell receptor (TCR)-alphabeta(+) cells that do not qualify as tumor precursors despite the observation that they overexpress Notch 1 and c-Myc and degrade the tumor suppressor E2A by posttranslational modification.

The first tumorigenic cells are detected among more immature CD4(-)8(+)TCR-alphabeta(-) cells that give rise to monoclonal tumors with a single, unique TCR-beta chain and diverse TCR-alpha chains, pinpointing malignant transformation to a stage after pre-TCR signaling and before completion of TCR-alpha rearrangement.

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(PMID = 18981238.001).

[ISSN] 1540-9538

[Journal-full-title] The Journal of experimental medicine

[ISO-abbreviation] J. Exp. Med.

[Language] ENG

[Databank-accession-numbers] GEO/ GSE12948

[Grant] United States / NIAID NIH HHS / AI / R01 AI045846; United States / NCI NIH HHS / CA / P01 CA109901; United States / NCI NIH HHS / CA / T32 CA070083; United States / NCI NIH HHS / CA / T32-CA70083; United States / NIAID NIH HHS / AI / R01 AI45846; United States / NCI NIH HHS / CA / CA109901

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Notch1 protein, mouse; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Tumor Suppressor Protein p53

[Other-IDs] NLM/ PMC2585834

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Precursor T-cell acute lymphoblastic leukemia (T-ALL) remains an important challenge in pediatric oncology.

[MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Prednisone / therapeutic use. Receptor, Notch1 / genetics. Ubiquitin-Protein Ligases / genetics

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(PMID = 20944675.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Receptor, Notch1; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases; VB0R961HZT / Prednisone

[Other-IDs] NLM/ PMC3035973