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[Title] T-cell acute lymphoblastic leukemia in association with Börjeson-Forssman-Lehmann syndrome due to a mutation in PHF6.

We describe a 9-year-old male with BFLS, who developed T-cell acute lymphoblastic leukemia (T-ALL).

Previously, overexpression of Phf6 was observed in murine T-cell lymphomas.

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[CommentIn] Pediatr Blood Cancer. 2010 Oct;55(4):595-6 [20589626.001]

(PMID = 20806366.001).

[ISSN] 1545-5017

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] ENG

[Grant] Canada / Canadian Institutes of Health Research / / ; United States / Intramural NIH HHS / /

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

[Publication-country] United States

[Chemical-registry-number] 0 / Carrier Proteins; 0 / PHF6 protein, human

[Other-IDs] NLM/ NIHMS218607; NLM/ PMC2933084

   

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

[Title] High frequency of PTEN, PI3K, and AKT abnormalities in T-cell acute lymphoblastic leukemia.

To more comprehensively assess the pathogenic contribution of the PTEN-PI3K-AKT pathway to T-cell acute lymphoblastic leukemia (T-ALL), we examined diagnostic DNA samples from children with T-ALL using array comparative genomic hybridization and sequence analysis.

Induction chemotherapy failed to induce remission in 3 of the 4 patients whose lymphoblasts harbored PTEN deletions at the time of diagnosis, compared with none of the 12 patients with mutations of PTEN exon 7 (P = .007), suggesting that PTEN deletion has more adverse therapeutic consequences than mutational disruptions that preserve the phosphatase domain.

[MeSH-major] Mutation. PTEN Phosphohydrolase / genetics. Phosphatidylinositol 3-Kinases / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-akt / genetics

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(PMID = 19458356.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Grant] United States / NCI NIH HHS / CA / K08 CA133103-04; United States / NCI NIH HHS / CA / K08 CA133103-01; United States / NCI NIH HHS / CA / U24 CA114766; United States / NCI NIH HHS / CA / K08 CA133103; United States / NCI NIH HHS / CA / K08 CA133103-03; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / K08 CA133103-02; United States / NCI NIH HHS / CA / P01 CA068484

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 3.1.3.67 / PTEN protein, human

[Other-IDs] NLM/ PMC2713461

   

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

[Title] Analysis of the expression pattern of the BCL11B gene and its relatives in patients with T-cell acute lymphoblastic leukemia.

BACKGROUND: In a human T-cell acute lymphoblastic leukemia (T-ALL) cell line (Molt-4), siRNA-mediated suppression of BCL11B expression was shown to inhibit proliferation and induce apoptosis, functions which may be related to genes involved in apoptosis (such as TNFSF10 and BCL2L1) and TGF-β pathways (such as SPP1and CREBBP).

[MeSH-major] CREB-Binding Protein / biosynthesis. Gene Expression Regulation, Neoplastic / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Repressor Proteins / biosynthesis. Tumor Suppressor Proteins / biosynthesis. bcl-X Protein / biosynthesis

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[Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]

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(PMID = 21080944.001).

[ISSN] 1756-8722

[Journal-full-title] Journal of hematology & oncology

[ISO-abbreviation] J Hematol Oncol

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / BCL11B protein, human; 0 / BCL2L1 protein, human; 0 / CREBBP protein, human; 0 / Repressor Proteins; 0 / Tumor Suppressor Proteins; 0 / bcl-X Protein; EC 2.3.1.48 / CREB-Binding Protein

[Other-IDs] NLM/ PMC2992472

   

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

[Title] Of mice and men: how an oncogene transgresses the limits and predisposes to T cell acute lymphoblastic leukemia.

The gene encoding LIM-only 2 (LMO2), an oncogenic transcription factor, is frequently activated in T cell acute lymphoblastic leukemia (T-ALL), but how LMO2 transforms primary hematopoietic cells to induce T-ALL remains an open question.

McCormack et al. now show that, in mice, Lmo2 confers self-renewal potential on normally nonrenewing thymocyte progenitor cells, and this property is maintained over four serial transplantations when the cells are transplanted into irradiated mice that lack thymocytes.

These leukemia-initiating cells are resistant to irradiation, indicating the need to develop new therapeutic drugs that specifically target the oncogene itself.

[MeSH-major] DNA-Binding Proteins / genetics. Genetic Predisposition to Disease. Metalloproteins / genetics. Oncogenes / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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(PMID = 20374994.001).

[ISSN] 1946-6242

[Journal-full-title] Science translational medicine

[ISO-abbreviation] Sci Transl Med

[Language] eng

[Grant] Canada / Canadian Institutes of Health Research / /

[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 / Lmo2 protein, mouse; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins

   

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

[Title] Duplication of the MYB oncogene in T cell acute lymphoblastic leukemia.

We identified a duplication of the MYB oncogene in 8.4% of individuals with T cell acute lymphoblastic leukemia (T-ALL) and in five T-ALL cell lines.

The duplication is associated with a threefold increase in MYB expression, and knockdown of MYB expression initiates T cell differentiation.

[MeSH-major] Cell Differentiation / genetics. Gene Duplication. Genes, myb / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. T-Lymphocytes / pathology

[MeSH-minor] Cell Line, Tumor. Chromosomes, Artificial / genetics. Flow Cytometry. Gene Dosage. Gene Expression Regulation, Neoplastic / genetics. Genetic Testing. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Mutation / genetics. Nucleic Acid Hybridization / genetics. RNA, Small Interfering / genetics. Statistics, Nonparametric

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(PMID = 17435759.001).

[ISSN] 1061-4036

[Journal-full-title] Nature genetics

[ISO-abbreviation] Nat. Genet.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / RNA, Small Interfering

   

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

[Title] Deletion of the protein tyrosine phosphatase gene PTPN2 in T-cell acute lymphoblastic leukemia.

In this work, we describe the identification of focal deletions of PTPN2 in human T-cell acute lymphoblastic leukemia (T-ALL).

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(PMID = 20473312.001).

[ISSN] 1546-1718

[Journal-full-title] Nature genetics

[ISO-abbreviation] Nat. Genet.

[Language] ENG

[Databank-accession-numbers] RefSeq/ NM/ 002828/ NM/ 008977/ NM/ 080422/ NM/ 080423

[Grant] United States / NCI NIH HHS / CA / R01 CA120196-01A1; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / CA129382; United States / NCI NIH HHS / CA / CA120196; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / CA120196-01A1

[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 / Benzamides; 0 / Chemokine CCL1; 0 / Homeodomain Proteins; 0 / Interleukin-2; 0 / Interleukin-7; 0 / Piperazines; 0 / Proto-Oncogene Proteins; 0 / Pyrimidines; 143275-75-6 / TLX1 protein, human; 8A1O1M485B / Imatinib Mesylate; EC 3.1.3.48 / PTPN2 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 2

[Other-IDs] NLM/ NIHMS239727; NLM/ PMC2957655

   

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

[Title] G1/S transcriptional networks modulated by the HOX11/TLX1 oncogene of T-cell acute lymphoblastic leukemia.

The HOX11/TLX1 homeobox gene is aberrantly expressed in a subset of T-cell acute lymphoblastic leukemia (T-ALL).

Here, we employed oligonucleotide microarrays to compare the expression profiles of the K3P and Sil leukemic cell lines originating from patients with HOX11+ T-ALL to that of Jurkat cells, which originated from a distinct subtype of T-ALL (TAL1+).

The resulting HOX11 gene expression signature, which was validated for representative signaling pathways by transient transfection of reporter constructs, was characterized by elevated expression of transcriptional programs involved in cell proliferation, including those regulated by E2F, c-Myc and cAMP response element-binding protein.

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(PMID = 15897879.001).

[ISSN] 0950-9232

[Journal-full-title] Oncogene

[ISO-abbreviation] Oncogene

[Language] ENG

[Grant] United States / NHLBI NIH HHS / HL / R01HL65519; United States / NHLBI NIH HHS / HL / R01 HL066305-05; United States / NCRR NIH HHS / RR / R24RR16209; United States / NHLBI NIH HHS / HL / R01 HL065519; United States / NHLBI NIH HHS / HL / R01 HL066305; United States / NHLBI NIH HHS / HL / R01 HL066305-04; United States / NCRR NIH HHS / RR / R24 RR016209; United States / NHLBI NIH HHS / HL / HL066305-05; United States / NHLBI NIH HHS / HL / R01HL66305

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

[Publication-country] England

[Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Proto-Oncogene Proteins; 0 / Retinoblastoma Protein; 143275-75-6 / TLX1 protein, human; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.- / Phosphoric Monoester Hydrolases

[Other-IDs] NLM/ NIHMS51737; NLM/ PMC2408753

   

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

[Title] Characterization of a progenitor cell population in childhood T-cell acute lymphoblastic leukemia.

A significant proportion of children with T-cell acute lymphoblastic leukemia (T-ALL) continue to fail therapy.

Consequently, characterization of the cells that proliferate to maintain the disease should provide valuable information on the most relevant therapeutic targets.

The immunophenotype and genotype of the original leukemia cells were preserved with serial passage in the NOD/SCID mice.

These data demonstrate the long-term repopulating ability of the CD34+/CD4- and CD34+/CD7- subfractions in T-ALL and suggest that a cell with a more primitive phenotype was the target for leukemic transformation in these cases.

[MeSH-major] Leukemia-Lymphoma, Adult T-Cell / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Stem Cells / immunology. Stem Cells / pathology

[MeSH-minor] Adolescent. Animals. Cell Culture Techniques. Cell Proliferation. Cell Separation. Cells, Cultured. Child. Child, Preschool. Female. Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor / genetics. Genotype. Humans. Immunophenotyping. Infant. Male. Mice. Mice, Inbred NOD. Mice, SCID. Xenograft Model Antitumor Assays

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(PMID = 17003368.001).

[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

   

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

[Title] Development of secondary T-cell acute lymphoblastic leukemia in a child with hemophagocytic lymphohistiocytosis.

Hemophagocytic lymphohistiocytosis (HLH) is a severe life-threatening disorder, characterized by hyperactivation of macrophages.

A 12-year-old female was referred to our center; the diagnosis of HLH was made for the patient and immunosuppressive regimen was started.

After a 2-year follow-up, the patient developed secondary T-cell acute lymphoblastic leukemia (T-ALL), confirmed by flow cytometric studies.

[MeSH-major] Lymphohistiocytosis, Hemophagocytic / complications. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / etiology

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[Copyright] Copyright 2010 Wiley-Liss, Inc.

(PMID = 20589661.001).

[ISSN] 1545-5017

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Publication-type] Case Reports; 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] bcr-abl-positive T-cell acute lymphoblastic leukemia associated with parvovirus B19 infection.

The authors report an unusual presentation of a Philadelphia chromosome-positive acute lymphoblastic leukemia with two unusual features: a bcr-abl fusion mRNA coding for p210 protein and a T-cell immunophenotype.

The patient was a 16-year-old boy who presented with septic shock and pancytopenia, likely precipitated by an acute parvovirus B19 infection.

Management consisted of supportive therapy, followed by chemotherapy for T-cell acute lymphoblastic leukemia and stem cell transplantation.

He died 8 months after transplant due to idiopathic pneumonia syndrome, but without evidence of relapsed disease.

[MeSH-major] Leukemia-Lymphoma, Adult T-Cell / etiology. Parvoviridae Infections / complications. Parvovirus B19, Human / pathogenicity. Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Preleukemia / complications

[MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Asparaginase / administration & dosage. Bone Marrow / virology. Cerebral Hemorrhage / etiology. Combined Modality Therapy. Disseminated Intravascular Coagulation / etiology. Fatal Outcome. Fusion Proteins, bcr-abl / blood. Genes, abl. Hematopoietic Stem Cell Transplantation. Humans. Male. Methotrexate / administration & dosage. Multiple Organ Failure / etiology. Neoplasm Proteins / blood. Pancytopenia / etiology. Pneumonia / etiology. Prednisone / administration & dosage. Shock, Septic / etiology. Staphylococcal Infections / complications. Vincristine / administration & dosage

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(PMID = 16462583.001).

[ISSN] 1077-4114

[Journal-full-title] Journal of pediatric hematology/oncology

[ISO-abbreviation] J. Pediatr. Hematol. Oncol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Neoplasm Proteins; 5J49Q6B70F / Vincristine; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate

   

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

[Title] Spontaneous tumor lysis syndrome in a child with T-cell acute lymphoblastic leukemia.

We report a 5-year-old female who presented with unexplained acute renal failure (ARF) and hyperuricemia and who was subsequently diagnosed of T-cell acute lymphoblastic leukemia (ALL).

Two weeks later, peripheral smear showed 40% blasts and bone marrow demonstrated T-cell ALL.

However, in contrast to previous reports in ALL or acute myeloid leukemia, our patient did not have blasts noted on periphereal blood smear and her white blood cell count and serum lactate dehydrogenase level were normal on admission, a time when dialysis-dependent ARF and severe hyperuricemia were present.

[MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / complications. Tumor Lysis Syndrome / etiology

[MeSH-minor] Acute Kidney Injury / etiology. Acute Kidney Injury / therapy. Child, Preschool. Female. Humans. Hyperuricemia / etiology. Renal Dialysis

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(PMID = 19998467.001).

[ISSN] 1545-5017

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Publication-type] Case Reports; 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] T-cell acute lymphoblastic leukemia in a child with ataxia-telangiectasia: case report.

We present a patient with acute lymphoblastic leukemia and ataxia-telangiectasia (A-T).

At the age of 4 she was diagnosed with T-cell acute lymphoblastic leukemia and treated according to Berlin-Frankfurt-Munster strategy.

[MeSH-major] Ataxia Telangiectasia / complications. Leukemia-Lymphoma, Adult T-Cell / etiology

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(PMID = 17921854.001).

[ISSN] 1077-4114

[Journal-full-title] Journal of pediatric hematology/oncology

[ISO-abbreviation] J. Pediatr. Hematol. Oncol.

[Language] eng

[Publication-type] Case Reports; 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] Amplification of RUNX1 gene in two new cases of childhood B-cell precursor acute lymphoblastic leukemia: A case report.

: e21000 Background: Chromosome abnormalities of leukemia cells have important prognostic significance in childhood acute lymphoblastic leukemia (ALL).

B-cell precursor acute lymphoblastic leukemia (BCP-ALL) ETV6/RUNX1 (alias TEL/AML1) is most frequent i.e.

We report two new cases with Pre B- cell ALL without ETV6/RUNX1 rearrangement, showing amplification of AML1 gene detected by FISH analysis.

RESULTS: In first case a 3-year girl with four copies of AML (RUNX1) gene were observed in 95% of the cell with normal two copies of TEL (ETV6) gene in both interphase and metaphase FISH.

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(PMID = 27960689.001).

[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] Gamma-secretase inhibitors reverse glucocorticoid resistance in T cell acute lymphoblastic leukemia.

Gamma-secretase inhibitors (GSIs) block the activation of the oncogenic protein Notch homolog-1 (NOTCH1) in T cell acute lymphoblastic leukemia (T-ALL).

Inhibition of NOTCH1 signaling in glucocorticoid-resistant T-ALL restored glucocorticoid receptor autoupregulation and induced apoptotic cell death through induction of the gene encoding BCL-2-like apoptosis initiator-11 (BCL2L11).

GSI treatment resulted in cell cycle arrest and accumulation of goblet cells in the gut mediated by upregulation of the gene encoding the transcription factor Krüppel-like factor-4 (Klf4), a negative regulator of the cell cycle required for goblet cell differentiation.

In contrast, glucocorticoid treatment induced transcriptional upregulation of cyclin D2 (Ccnd2) and protected mice from developing the intestinal goblet cell metaplasia typically induced by inhibition of NOTCH signaling with GSIs.

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(PMID = 19098907.001).

[ISSN] 1546-170X

[Journal-full-title] Nature medicine

[ISO-abbreviation] Nat. Med.

[Language] ENG

[Databank-accession-numbers] GEO/ GSE11184/ GSE7067

[Grant] United States / NCI NIH HHS / CA / 1R01 CA105129; United States / NCI NIH HHS / CA / CA133379-01A1; United States / NCI NIH HHS / CA / R01 CA120196-03; United States / NCI NIH HHS / CA / R01 CA133379; United States / NCI NIH HHS / CA / R01 CA105129-04; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / 1R01 CA133379; United States / NCI NIH HHS / CA / R01 CA149655; United States / NCI NIH HHS / CA / R01 CA105129; United States / NCI NIH HHS / CA / R01 CA133379-01A1; United States / NCI NIH HHS / CA / CA120196-03; United States / NIAID NIH HHS / AI / R56 AI070310-01A1; United States / NCI NIH HHS / CA / R01 CA120196; United States / NIAID NIH HHS / AI / AI070310-01A1; United States / NIAID NIH HHS / AI / R56 AI070310; United States / NCI NIH HHS / CA / CA105129-04

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

[Publication-country] United States

[Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Ccnd2 protein, mouse; 0 / Cyclin D2; 0 / Cyclins; 0 / Enzyme Inhibitors; 0 / Glucocorticoids; 0 / Membrane Proteins; 0 / NR3C1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptor, Notch1; 0 / Receptors, Glucocorticoid; 7S5I7G3JQL / Dexamethasone; EC 3.4.- / Amyloid Precursor Protein Secretases

[Other-IDs] NLM/ NIHMS103250; NLM/ PMC2692090

   

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

[Title] Early T cell differentiation lessons from T-cell acute lymphoblastic leukemia.

Upon entering the thymus, these cells undergo progressive commitment and differentiation driven by the thymic stroma and the pre-T cell receptor (pre-TCR).

These processes are disrupted in T-cell acute lymphoblastic leukemia (T-ALL).

This prevalence is indicative of their importance in the T lineage, and their dominant mechanisms of transformation.

Together, these genetic lesions alter key regulatory processes in the cell, favoring self-renewal and subvert the normal control of thymocyte homeostasis.

[MeSH-major] Cell Differentiation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Signal Transduction. T-Lymphocytes / cytology. Thymus Gland / cytology

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

(PMID = 20800819.001).

[ISSN] 1877-1173

[Journal-full-title] Progress in molecular biology and translational science

[ISO-abbreviation] Prog Mol Biol Transl Sci

[Language] eng

[Grant] Canada / Canadian Institutes of Health Research / /

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

[Publication-country] Netherlands

[Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Oncogene Proteins; 0 / Transcription Factors

   

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

[Title] A new recurrent 9q34 duplication in pediatric T-cell acute lymphoblastic leukemia.

Over the last decade, genetic characterization of T-cell acute lymphoblastic leukemia (T-ALL) has led to the identification of a variety of chromosomal abnormalities.

Fluorescence in situ hybridization (FISH) analysis revealed that this 9q34 amplification was in fact a 9q34 duplication on one chromosome and could be identified in 17-39 percent of leukemic cells at diagnosis.

[MeSH-major] Chromosomes, Human, Pair 9. Gene Duplication. Leukemia-Lymphoma, Adult T-Cell / genetics

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(PMID = 16673019.001).

[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 / NOTCH1 protein, human; 0 / NUP214-ABL1 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Receptor, Notch1

   

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

[Title] FISH studies on the telomeric regions of the T-cell acute lymphoblastic leukemia cell line CCRF-CEM.

Therefore, the telomeres of a karyotypically rather well characterized T-cell acute lymphoblastic leukemia (T-ALL) cell line (CCRF-CEM) with several marker chromosomes were examined using peptide nucleic acid (PNA) telomere FISH probes to compare the telomere length of these markers with that of the chromosome arms of their origin.

Two markers could be newly defined and a concise karyotype of the cell line could be obtained by these detailed examinations: 42-47,X,-X,del(5) (q35?

However, it could be shown, that in four different passages of the examined cell line the observed differences between relative telomere lengths of the markers and the chromosomes of their origin, with two exceptions (short arms of del/inv9 and der22), were not significant.

[MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Telomere / genetics

[MeSH-minor] Cell Line, Tumor. Chromosome Aberrations. Chromosome Mapping. Genetic Markers. Humans. In Situ Hybridization, Fluorescence. Karyotyping

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(PMID = 16093718.001).

[ISSN] 1424-859X

[Journal-full-title] Cytogenetic and genome research

[ISO-abbreviation] Cytogenet. Genome Res.

[Language] eng

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

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Genetic Markers

   

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

[Title] Prognostic implications of NOTCH1 and FBXW7 mutations in adults with T-cell acute lymphoblastic leukemia treated on the MRC UKALLXII/ECOG E2993 protocol.

PURPOSE: Notch pathway activation by mutations in either NOTCH1 and/or FBXW7 is one of the most common molecular events in T-cell acute lymphoblastic leukemia (T-ALL) and, in pediatric disease, predicts for favorable outcome.

We sought to evaluate the outcome according to mutation status of patients with adult T-ALL treated on the United Kingdom Acute Lymphoblastic Leukaemia XII (UKALLXII)/Eastern Cooperative Oncology Group (ECOG) E2993 protocol.

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

[MeSH-minor] Adolescent. Adult. Chromatography, High Pressure Liquid / methods. DNA Mutational Analysis. Disease-Free Survival. Female. Follow-Up Studies. Gene Frequency. Genotype. Humans. Male. Middle Aged. Multivariate Analysis. Prognosis. Treatment Outcome. United Kingdom. Young Adult

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(PMID = 19635999.001).

[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

[Databank-accession-numbers] ClinicalTrials.gov/ NCT00002514

[Grant] United Kingdom / Medical Research Council / / MC/ U137686856; United States / NCI NIH HHS / CA / R01 CA129382; United Kingdom / Medical Research Council / / ; United Kingdom / Medical Research Council / / G0500389; 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 / 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 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; EC 2.3.2.27 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / FBXW7 protein, human

[Other-IDs] NLM/ PMC2744275

   

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

[Title] Mutations in the HD and PEST domain of Notch-1 receptor in T-cell acute lymphoblastic leukemia: report of novel mutations from Indian population.

Notch-1 is a transmembrane receptor protein that directs T-cell differentiation.

Gain-of-function mutations in Notch-1 have been reported in more than 50% of human T-cell acute lymphoblastic leukemia (T-ALL).

RNA was isolated from peripheral blood/bone marrow of 15 de novo T-ALL subjects; the Notch-1 HD and PEST regions were amplified and sequenced.

[MeSH-major] Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics

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(PMID = 21302811.001).

[ISSN] 0965-0407

[Journal-full-title] Oncology research

[ISO-abbreviation] Oncol. Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

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

   

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

[Title] Gene expression profiling reveals intrinsic differences between T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma.

BACKGROUND: T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LL) and are often thought to represent a spectrum of a single disease.

The malignant cells in T-ALL and T-LL are morphologically indistinguishable, and they share the expression of common cell surface antigens and cytogenetic characteristics.

However, despite these similarities, differences in the clinical behavior of T-ALL and T-LL are observed.

PROCEDURE: We analyzed the gene expression profiles of T-ALL and T-LL samples obtained from Children's Oncology Group (COG) tumor banks using DNA arrays.

RESULTS: Unsupervised hierarchical clustering of all samples showed complete segregation of T-ALL and T-LL into distinct clusters.

Genes representing several functional groups were differentially expressed in T-LL and T-ALL.

Prediction analysis of microarrays (PAM) identified a subset of genes, which accurately classified all 19 T-ALL and T-LL samples with an overall misclassification error rate of 0.

CONCLUSIONS: Despite significant similarities between the malignant T-cell precursors, clear differences in the gene expression profiles were observed between T-ALL and T-LL implying underlying differences in the biology of the two entities.

[MeSH-major] Gene Expression Profiling. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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(PMID = 16358311.001).

[ISSN] 1545-5009

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Grant] United States / NCI NIH HHS / CA / U01 CA88361

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

[Publication-country] United States

   

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

[Title] Resistance of T-cell acute lymphoblastic leukemia to tumor necrosis factor--related apoptosis-inducing ligand-mediated apoptosis.

OBJECTIVE: Cytotoxic ligands are involved in tumor immunity and graft-vs.-leukemia effect after allogeneic stem cell transplantation for leukemia.

To clarify the susceptibility of T-cell acute lymphoblastic leukemia (T-ALL) to tumor immunity, sensitivity to recombinant human soluble Fas ligand (rhsFasL) and tumor necrosis factor-related apoptosis-inducing ligand (rhsTRAIL) was determined.

MATERIALS AND METHODS: Sensitivity to rhsFasL and rhsTRAIL and cell surface expression of their receptors were tested in T-ALL cell lines (n = 7) and patients' samples (n = 17) and compared with those in B-precursor ALL cell lines (n = 30).

Expression of components of the death-inducing signaling complex and the TRAIL receptor genes (DR4/DR5), and the methylation status and promoter activity of the DR4/DR5 gene were tested in T-ALL cell lines.

RESULTS: T-ALL cell lines showed higher level of Fas expression and higher sensitivity to rhsFasL than did B-precursor ALL cell lines.

Despite comparable expression of components of death-inducing signaling complex, cell lines and patients' samples of T-ALL showed TRAIL-resistance associated with low cell surface expression of DR4/DR5.

Gene expression of DR4/DR5 in T-ALL cell lines was significantly lower than that in B-precursor ALL cell lines, and the methylation status of the gene promoter in T-ALL cell lines was associated with the gene expression level at least for DR4.

[MeSH-major] Apoptosis / drug effects. Cell Proliferation / drug effects. Fas Ligand Protein / pharmacology. TNF-Related Apoptosis-Inducing Ligand / pharmacology

[MeSH-minor] Antigens, CD95 / metabolism. Cell Line, Tumor. Cells, Cultured. DNA Methylation / drug effects. Dose-Response Relationship, Drug. Drug Resistance. Flow Cytometry. Gene Expression / drug effects. Humans. Immunoblotting. Jurkat Cells. Luciferases / genetics. Luciferases / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Promoter Regions, Genetic / genetics. Receptors, TNF-Related Apoptosis-Inducing Ligand / genetics. Reverse Transcriptase Polymerase Chain Reaction

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[Copyright] Copyright © 2010 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc. All rights reserved.

(PMID = 20670671.001).

[ISSN] 1873-2399

[Journal-full-title] Experimental hematology

[ISO-abbreviation] Exp. Hematol.

[Language] eng

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

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antigens, CD95; 0 / FAS protein, human; 0 / Fas Ligand Protein; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / TNF-Related Apoptosis-Inducing Ligand; EC 1.13.12.- / Luciferases

   

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

[Title] Cre/lox-regulated transgenic zebrafish model with conditional myc-induced T cell acute lymphoblastic leukemia.

We have created a stable transgenic rag2-EGFP-mMyc zebrafish line that develops GFP-labeled T cell acute lymphoblastic leukemia (T-ALL), allowing visualization of the onset and spread of this disease.

Here, we show that leukemias from this transgenic line are highly penetrant and render animals moribund by 80.7 +/- 17.6 days of life (+/-1 SD, range = 50-158 days).

These T cell leukemias are clonally aneuploid, can be transplanted into irradiated recipient fish, and express the zebrafish orthologues of the human T-ALL oncogenes tal1/scl and lmo2, thus providing an animal model for the most prevalent molecular subgroup of human T-ALL.

Thus, we have created a conditional transgene in which the EGFP-mMyc oncogene is preceded by a loxed dsRED2 gene and have generated stable rag2-loxP-dsRED2-loxP-EGFP-mMyc transgenic zebrafish lines, which have red fluorescent thymocytes and do not develop leukemia.

Transgenic progeny from one of these lines can be induced to develop T-ALL by injecting Cre RNA into one-cell-stage embryos, demonstrating the utility of the Cre/lox system in the zebrafish and providing an essential step in preparing this model for chemical and genetic screens designed to identify modifiers of Myc-induced T-ALL.

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(PMID = 15827121.001).

[ISSN] 0027-8424

[Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America

[ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.

[Language] ENG

[Databank-accession-numbers] PIR/ AF398514

[Grant] United States / NCI NIH HHS / CA / P01 CA068484; United States / NCI NIH HHS / CA / P30 CA006516; United States / NCI NIH HHS / CA / CA-06516; United States / NCI NIH HHS / CA / CA-68484

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

[Publication-country] United States

[Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Extracellular Matrix Proteins; 0 / Genetic Markers; 0 / Nuclear Proteins; 0 / RAG2 protein, human; 0 / Rag2 protein, mouse; 0 / V(D)J recombination activating protein 2; 0 / enhanced green fluorescent protein; 147336-22-9 / Green Fluorescent Proteins; 149137-54-2 / Lox protein, mouse; EC 1.4.3.13 / Protein-Lysine 6-Oxidase; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases

[Other-IDs] NLM/ PMC1087915

   

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

[Title] T-cell acute lymphoblastic leukemia in adults: clinical features, immunophenotype, cytogenetics, and outcome from the large randomized prospective trial (UKALL XII/ECOG 2993).

The biology and outcome of adult T-cell acute lymphoblastic leukemia are poorly understood.

Central nervous system involvement at diagnosis did not affect survival (47% vs 48%, P = not significant).

This study provides a baseline for trials of new drugs, such as nelarabine, and may allow risk-adapted therapy in patients with poor-prognosis T-cell ALL.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Stem Cell Transplantation / methods. T-Lymphocytes / pathology

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(PMID = 19828704.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Grant] United Kingdom / Medical Research Council / / MC/ U137686856; United Kingdom / Medical Research Council / / G8223452; United Kingdom / Medical Research Council / / G0500389; United States / NCI NIH HHS / CA / R01CA120196; 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; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl

[Other-IDs] NLM/ PMC2792210

   

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

[Title] Notch signaling induces SKP2 expression and promotes reduction of p27Kip1 in T-cell acute lymphoblastic leukemia cell lines.

In T-cell acute lymphoblastic leukemia (T-ALL) NOTCH 1 receptors are frequently mutated.

This leads to aberrantly high Notch signaling, but how this translates into deregulated cell cycle control and the transformed cell type is poorly understood.

Notch activity, measured immediately downstream of the NOTCH 1 receptor, is high, but expression of the canonical downstream Notch response genes HES 1 and HEY 2 is low both in primary cells from T-ALL patients and in T-ALL cell lines.

We show that in T-ALL cell lines, recruitment of NOTCH 1 intracellular domain (ICD) to the SKP2 promoter was accompanied by high SKP2 and low p27Kip1 protein levels.

T-ALL cells show a rapid G1-S cell cycle transition, while blocked Notch signaling resulted in G0/G1 cell cycle arrest, also observed by transfection of p27Kip1 or, to a smaller extent, a dominant negative SKP2 allele.

Collectively, our data suggest that the aberrantly high Notch signaling in T-ALL maintains SKP2 at a high level and reduces p27Kip1, leading to more rapid cell cycle progression.

[MeSH-major] Intracellular Signaling Peptides and Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptor, Notch1 / metabolism. S-Phase Kinase-Associated Proteins / metabolism. Signal Transduction / physiology. T-Lymphocytes / metabolism

[MeSH-minor] Basic Helix-Loop-Helix Transcription Factors / genetics. Basic Helix-Loop-Helix Transcription Factors / metabolism. Cell Cycle / physiology. Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Child. Cyclin-Dependent Kinase Inhibitor p27. Gene Expression Profiling. Humans. Oligonucleotide Array Sequence Analysis. Promoter Regions, Genetic. Repressor Proteins / genetics. Repressor Proteins / metabolism

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(PMID = 17560996.001).

[ISSN] 0014-4827

[Journal-full-title] Experimental cell research

[ISO-abbreviation] Exp. Cell Res.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / CDKN1B protein, human; 0 / Cell Cycle Proteins; 0 / HEY1 protein, human; 0 / HEY2 protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / Repressor Proteins; 0 / S-Phase Kinase-Associated Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27

   

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

[Title] SET-NUP214 fusion in acute myeloid leukemia- and T-cell acute lymphoblastic leukemia-derived cell lines.

BACKGROUND: SET-NUP214 fusion resulting from a recurrent cryptic deletion, del(9)(q34.11q34.13) has recently been described in T-cell acute lymphoblastic leukemia (T-ALL) and in one case of acute myeloid leukemia (AML).

The fusion protein appears to promote elevated expression of HOXA cluster genes in T-ALL and may contribute to the pathogenesis of the disease.

We screened a panel of ALL and AML cell lines for SET-NUP214 expression to find model systems that might help to elucidate the cellular function of this fusion gene.

RESULTS: Of 141 human leukemia/lymphoma cell lines tested, only the T-ALL cell line LOUCY and the AML cell line MEGAL expressed the SET(TAF-Ibeta)-NUP214 fusion gene transcript.

RT-PCR analysis specifically recognizing the alternative first exons of the two TAF-I isoforms revealed that the cell lines also expressed TAF-Ialpha-NUP214 mRNA.

Quantitative genomic PCR also confirmed loss of genomic material between SET and NUP214 in both cell lines.

Both cell lines expressed the 140 kDa SET-NUP214 fusion protein.

CONCLUSION: Cell lines LOUCY and MEGAL express the recently described SET-NUP214 fusion gene.

The cell lines are promising model systems for SET-NUP214 studies and should facilitate investigating cellular functions of the the SET-NUP214 protein.

[MeSH-major] Histone Chaperones / genetics. Leukemia, Myeloid, Acute / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics

[MeSH-minor] Base Sequence. Cell Line, Tumor. Cytogenetic Analysis. Gene Expression Regulation, Leukemic. Genetic Testing. Humans. Models, Biological. Molecular Sequence Data. Sequence Analysis, DNA

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(PMID = 19166587.001).

[ISSN] 1756-8722

[Journal-full-title] Journal of hematology & oncology

[ISO-abbreviation] J Hematol Oncol

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Histone Chaperones; 0 / NUP214 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / SET protein, human; 0 / Transcription Factors

[Other-IDs] NLM/ PMC2636835

   

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

[Title] Clinical significance of central nervous system involvement at diagnosis of childhood T-cell acute lymphoblastic leukemia.

BACKGROUND: Patients with T-cell acute lymphoblastic leukemia (T-ALL) frequently present with unfavorable features at diagnosis.

We sought to correlate initial central nervous system (CNS) disease at diagnosis with shortened survival in childhood T-ALL.

For univariate prognostic analyses, we used the log-rank test to determine the influence of patient characteristics (age, sex, lymphomatous presentations, initial leukocyte count, CNS disease, and newer therapeutic strategies) on each point.

Median survival was 37 months, and 5-year overall survival and disease-free survival rates were 49.5% +/- 8.1% and 47.1% +/- 8.2%, respectively.

Disease-free survival was not influenced by age, leukocyte count, or other factors analyzed.

CONCLUSIONS: Patients who present with initial CNS involvement have a prognosis worse than that of patients without CNS disease.

The introduction of early and effective CNS-directed therapy might no longer portend a poor prognosis for CNS leukemia.

[MeSH-major] Central Nervous System Neoplasms / diagnosis. Leukemia, T-Cell / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

[MeSH-minor] Child. Disease-Free Survival. Female. Humans. Male. Prognosis. Recurrence. Retrospective Studies. Statistics, Nonparametric. Survival Rate. Taiwan / epidemiology

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(PMID = 15704218.001).

[ISSN] 1545-5009

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[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] TLX1 and NOTCH coregulate transcription in T cell acute lymphoblastic leukemia cells.

BACKGROUND: The homeobox gene TLX1 (for T-cell leukemia homeobox 1, previously known as HOX11) is inappropriately expressed in a major subgroup of T cell acute lymphoblastic leukemia (T-ALL) where it is strongly associated with activating NOTCH1 mutations.

In addition, the TLX1/NOTCH/MYC transcriptional network coregulates genes involved in T cell development, such as CD1 and RAG family members, and therefore may prescribe the early cortical stage of differentiation arrest characteristic of the TLX1 subgroup of T-ALL.

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(PMID = 20618946.001).

[ISSN] 1476-4598

[Journal-full-title] Molecular cancer

[ISO-abbreviation] Mol. Cancer

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01CA120316; United States / NHLBI NIH HHS / HL / R01HL65519; United States / NHLBI NIH HHS / HL / R01HL66305

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

[Publication-country] England

[Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Proto-Oncogene Proteins; 0 / Receptors, Notch; 143275-75-6 / TLX1 protein, human

[Other-IDs] NLM/ PMC2913983

   

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

[Title] Evaluation of cytotoxicity by flow cytometric drug sensitivity assay in childhood T-cell acute lymphoblastic leukemia.

Risk-based treatment strategies have improved outcome in childhood B-precursor acute lymphoblastic leukemia, and in vitro drug sensitivity assessment using methyl-thiazol-tetrazolium (MTT) assay has been shown to be an independent prognostic marker.

To date, such strategies in childhood T-cell acute lymphoblastic leukemia (T-ALL) have proved elusive, and in vitro drug sensitivity testing has had limited success in T-ALL due to poor T-cell lymphoblast survival in vitro.

Comparison of T-ALL sensitivity with acute myeloid leukemia (AML) cases revealed a unique pattern difference.

Although age or white blood cell count at diagnosis was not associated with any particular drug response pattern, CD13 expression on T-lymphoblasts was associated with in vitro resistance.

FCDSA is a reliable, practical and reproducible method that can be integrated into studies of drug-target cell interactions in T-ALL.

[MeSH-major] Drug Screening Assays, Antitumor. Flow Cytometry / methods. Medical Oncology / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

[MeSH-minor] Apoptosis. Bone Marrow Cells / cytology. Bone Marrow Cells / metabolism. Child. Daunorubicin / pharmacology. Humans. Immunophenotyping / methods. Inhibitory Concentration 50. Leukemia, T-Cell / diagnosis. Leukemia, T-Cell / drug therapy. Reproducibility of Results. Sensitivity and Specificity. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology

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(PMID = 16019527.001).

[ISSN] 1029-2403

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Grant] United States / NCI NIH HHS / CA / U10-CA29691

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

[Publication-country] England

[Chemical-registry-number] 0 / Tetrazolium Salts; 0 / Thiazoles; 298-93-1 / thiazolyl blue; ZS7284E0ZP / Daunorubicin

   

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

[Title] Activity of the novel dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235 against T-cell acute lymphoblastic leukemia.

Recent findings have highlighted that constitutively active phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling is a common feature of T-cell acute lymphoblastic leukemia (T-ALL), where it upregulates cell proliferation, survival, and drug resistance.

Here, we have analyzed the therapeutic potential of the novel dual PI3K/mTOR inhibitor NVP-BEZ235, an orally bioavailable imidazoquinoline derivative, which has entered clinical trials for solid tumors, on both T-ALL cell lines and patient samples.

NVP-BEZ235 was cytotoxic to a panel of T-ALL cell lines as determined by MTT assays.

NVP-BEZ235 treatment resulted in cell cycle arrest and apoptosis.

Remarkably, NVP-BEZ235 targeted the side population of both T-ALL cell lines and patient lymphoblasts, which might correspond to leukemia-initiating cells, and synergized with chemotherapeutic agents (cyclophosphamide, cytarabine, dexamethasone) currently used for treating T-ALL patients.

[MeSH-major] Imidazoles / therapeutic use. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Quinolines / therapeutic use

[MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Autophagy / drug effects. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Coculture Techniques. Flow Cytometry. Humans. Jurkat Cells / drug effects. Mice. Stromal Cells / drug effects

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[Copyright] ©2010 AACR.

(PMID = 20876803.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Imidazoles; 0 / Quinolines; RUJ6Z9Y0DT / dactolisib

   

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

[Title] Absence of biallelic TCRgamma deletion predicts early treatment failure in pediatric T-cell acute lymphoblastic leukemia.

PURPOSE: To identify children with T-cell acute lymphoblastic leukemia (T-ALL) at high risk of induction chemotherapy failure by using DNA copy number analysis of leukemic cells collected at diagnosis.

CONCLUSION: Lymphoblasts from children with T-ALL should be evaluated at diagnosis for deletion within the TCRgamma locus.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Comparative Genomic Hybridization. Gene Deletion. Genes, T-Cell Receptor gamma. Polymerase Chain Reaction. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

[MeSH-minor] Adolescent. Alleles. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Kaplan-Meier Estimate. Male. Predictive Value of Tests. Prognosis. Remission Induction. Risk Assessment. Risk Factors. Time Factors. Treatment Failure

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(PMID = 20644084.001).

[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

[Grant] United States / NCI NIH HHS / CA / 1K08CA133103; United States / NCI NIH HHS / CA / CA98543; United States / NCI NIH HHS / CA / NCI 5P01CA68484; United States / NCI NIH HHS / CA / R01 CA129382-01A1; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / K08 CA133103-04; United States / NCI NIH HHS / CA / K08 CA133103-01; United States / NCI NIH HHS / CA / CA114766; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U24 CA114766; United States / NCI NIH HHS / CA / L40 CA124083-01; United States / NCI NIH HHS / CA / K08 CA133103; United States / NCI NIH HHS / CA / L40 CA124083; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / K08 CA133103-03; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / R01 CA120196-01A1; United States / NCI NIH HHS / CA / L40 CA124083-02; United States / NCI NIH HHS / CA / CA98413; United States / NCI NIH HHS / CA / K08 CA133103-02; United States / NCI NIH HHS / CA / P01 CA068484

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

[Publication-country] United States

[Other-IDs] NLM/ PMC2940399

   

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

[Title] T-cell lymphoblastic lymphoma and T-cell acute lymphoblastic leukemia: a separate entity?

T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LBL) are considered the same disease, differing by the extent of bone marrow infiltration.

According to recent gene expression profiling data, T-ALL and T-LBL can be separated by prediction analysis of microarrays showing an overexpression of MML1 in T-LBL and CD47 in T-ALL.

Immunophenotypes of T-LBL and T-ALL are identical but differ in frequency, with a higher rate of cortical or mature immunophenotypes in T-LBL, which is probably related to the higher rate (> 90%) of mediastinal tumors.

Strategies for stem cell transplantation (SCT) in T-LBL and T-ALL differ.

MRD may guide further treatment strategies in T-ALL and probably also in T-LBL as indications for a SCT or for the evaluation of novel, particularly T-cell-specific, drugs.

[MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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(PMID = 19778844.001).

[ISSN] 1938-0712

[Journal-full-title] Clinical lymphoma & myeloma

[ISO-abbreviation] Clin Lymphoma Myeloma

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Number-of-references] 39

   

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

[Title] The clinical value of follow-up examinations in childhood T-cell acute lymphoblastic leukemia and T-cell non-Hodgkin's lymphoma.

BACKGROUND: The aim of this study was to evaluate the value of follow-up investigations of T-cell acute lymphoblastic leukemia (T-ALL) and T-cell non-Hodgkin's lymphoma (T-NHL), including cerebrospinal fluid (CSF) examination, bone marrow (BM) aspiration, peripheral blood (PB) count, serum lactate dehydrogenase (LDH) and chest X-rays in patients with an initial mediastinal enlargement.

T-ALL (13/30) with mediastinal enlargement at first diagnosis relapsed versus 2/16 of those without mediastinal enlargement.

All T-ALL and T-NHL patients with a mediastinal relapse were symptomatic.

CONCLUSIONS: This study suggests that routine CSF examinations during treatment can detect relapses of T-ALL and T-NHL before onset of symptoms, which might be of clinical value.

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

[MeSH-minor] Adolescent. Biomarkers, Tumor / blood. Bone Marrow Examination. Child. Child, Preschool. Diagnostic Tests, Routine. Disease Management. Follow-Up Studies. Humans. Incidence. Infant. L-Lactate Dehydrogenase / blood. Leukemic Infiltration / diagnosis. Leukemic Infiltration / epidemiology. Mediastinum / pathology. Prognosis. Recurrence. Remission Induction. Retrospective Studies

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(PMID = 16514610.001).

[ISSN] 1545-5009

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Publication-type] Evaluation Studies; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; EC 1.1.1.27 / L-Lactate Dehydrogenase

   

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

[Title] Does TAL-1 deletion contribute to the high incidence of T-cell acute lymphoblastic leukemia in South Indian patients?

BACKGROUND: The incidence of T-cell acute lymphoblastic leukemia (T-ALL) in South India is very high (43.1%) when compared to the Western countries (10-20%).

TAL-1 deletion is the most common genetic abnormality in T-ALL.

[MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins / genetics

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(PMID = 18439091.001).

[ISSN] 2476-762X

[Journal-full-title] Asian Pacific journal of cancer prevention : APJCP

[ISO-abbreviation] Asian Pac. J. Cancer Prev.

[Language] eng

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

[Publication-country] Thailand

[Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Proto-Oncogene Proteins; 135471-20-4 / TAL1 protein, human

   

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

: 7028 Background: The major mechanism underlying imatinib resistance in patients with chronic myeloid leukemia (CML) is clonal expansion of leukemic cells with point mutations in the BCR-ABL tyrosine kinase.

We describe three novel ABL premature termination mutations leading to BCR-ABL truncation in leukemia patients with multidrug (imatinib/nilotinib/dasatinib) resistance.

HL60 cells (a Ph-negative myeloid leukemia cell line) and peripheral blood of healthy subjects were used as negative controls; a human CML cell line (K562) was used as a positive control.

RESULTS: We identified an exon 7 deletion in three CML patients, a 4-nt insertion (908insCAGG) near the exon 5/6 junction in one CML case, and an exon 6 point mutation (997C>T) in one patient with acute lymphoblastic leukemia (ALL).

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(PMID = 27961401.001).

[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] Targeting calcineurin activation as a therapeutic strategy for T-cell acute lymphoblastic leukemia.

In the T-cell lineage, calcineurin activation is important for pre-T-cell receptor (TCR) signaling, TCR-mediated positive selection of thymocytes into mature T cells, and many aspects of the immune response.

We observed sustained calcineurin activation in human B- and T-cell lymphomas and in all mouse models of lymphoid malignancies analyzed.

In intracellular NOTCH1 (ICN1)- and TEL-JAK2-induced T-cell lymphoblastic leukemia, two mouse models relevant to human malignancies, in vivo inhibition of calcineurin activity by CsA or FK506 induced apoptosis of leukemic cells and rapid tumor clearance, and substantially prolonged mouse survival.

In contrast, ectopic expression of a constitutively activated mutant of calcineurin favored leukemia progression.

Moreover, CsA treatment induced apoptosis in human lymphoma and leukemia cell lines.

Thus, calcineurin activation is critical for the maintenance of the leukemic phenotype in vivo, identifying this pathway as a relevant therapeutic target in lymphoid malignancies.

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

[MeSH-minor] Animals. Calcineurin Inhibitors. Cell Line, Tumor. Cyclosporine / pharmacology. Disease Models, Animal. Enzyme Activation / drug effects. Humans. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / enzymology. Lymphoma, B-Cell / pathology. Mice. Mice, Inbred C57BL. Mice, Knockout. Mice, Transgenic. Oncogene Proteins, Fusion / deficiency. Oncogene Proteins, Fusion / genetics. Receptor, Notch1 / physiology. Tacrolimus / pharmacology

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[CommentIn] Nat Med. 2007 Jun;13(6):669-71 [17554330.001]

(PMID = 17515895.001).

[ISSN] 1078-8956

[Journal-full-title] Nature medicine

[ISO-abbreviation] Nat. Med.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Calcineurin Inhibitors; 0 / NOTCH1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Receptor, Notch1; 0 / TEL-JAK2 fusion protein, mouse; 83HN0GTJ6D / Cyclosporine; EC 3.1.3.16 / Calcineurin; WM0HAQ4WNM / Tacrolimus

   

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

[Title] Therapeutic targeting of NOTCH1 signaling in T-cell acute lymphoblastic leukemia.

The recent identification of activating mutations in NOTCH1 in the majority of T-cell acute lymphoblastic leukemias (T-ALLs) has brought major interest toward targeting the NOTCH signaling pathway in this disease.

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(PMID = 19778842.001).

[ISSN] 1938-0712

[Journal-full-title] Clinical lymphoma & myeloma

[ISO-abbreviation] Clin Lymphoma Myeloma

[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 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Ligands; 0 / NOTCH1 protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptor, Notch1; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases

[Number-of-references] 85

[Other-IDs] NLM/ NIHMS153170; NLM/ PMC2814179

   

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

[Title] Gene expression profiling identifies a subset of adult T-cell acute lymphoblastic leukemia with myeloid-like gene features and over-expression of miR-223.

BACKGROUND: Until recently, few molecular aberrations were recognized in acute lymphoblastic leukemia of T-cell origin; novel lesions have recently been identified and a certain degree of overlap between acute myeloid leukemia and T-cell acute lymphoblastic leukemia has been suggested.

To identify novel T-cell acute lymphoblastic leukemia entities, gene expression profiling was performed and clinico-biological features were studied.

DESIGN AND METHODS: Sixty-nine untreated adults with T-cell acute lymphoblastic leukemia were evaluated by oligonucleotide arrays: unsupervised and supervised analyses were performed.

The up-regulation of myeloid genes and miR-223 expression were validated by quantitative polymerase chain reaction analysis.

Of these, one branch included seven patients whose gene expression profile resembled that of acute myeloid leukemia.

These cases were characterized by over-expression of a large set of myeloid-related genes for surface antigens, transcription factors and granule proteins.

We, therefore, evaluated the expression levels of miR-223, involved in myeloid differentiation: these cases had significantly higher levels of miR-223 than had the other cases of T-cell acute lymphoblastic leukemia, with values comparable to those observed in acute myeloid leukemia.

CONCLUSIONS: Using gene profiling we identified a subset of adult T-cell acute lymphoblastic leukemia, accounting for 10% of the cases analyzed, which displays myeloid features.

These cases were not recognized by standard approaches, underlining the importance of gene profiling in identifying novel acute leukemia subsets.

[MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Leukemia, Myeloid, Acute / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. MicroRNAs / genetics

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(PMID = 20418243.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

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

[Publication-country] Italy

[Chemical-registry-number] 0 / MIRN223 microRNA, human; 0 / MicroRNAs

[Other-IDs] NLM/ PMC2895035

   

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

[Title] Clinical significance of immunophenotypic markers in pediatric T-cell acute lymphoblastic leukemia.

BACKGROUND: Cell-marker profiling has led to conflicting conclusions about its prognostic significance in T-ALL.

AIM: To investigate the prevalence of the expression of CD34, CD10 and myeloid associated antigens (CD13/ CD33) in childhood T-ALL and to relate their presence to initial clinical and biologic features and early response to therapy.

Immunophenotypic markers and minimal residual disease (MRD) were studied by five-color flow cytometry.

No significant association was encountered between CD34, CD10 or myeloid antigen positivity and the presenting clinical features as age, sex, TLC and CNS leukemia.

CD34 and CD13/CD33 expression was significantly associated with T-cell maturation stages (p<0.05).

CD34(+), CD13/CD33(+) and early T-cell stage had high MRD levels on day 15 that was statistically highly significant (p<0.01), but CD10(+) had statistically significant lower MRD level on day 15 (p=0.049).

CONCLUSIONS: CD34, CD10, CD13/CD33 expression, as well as T-cell maturation stages, may have prognostic significance in pediatric T-ALL as they have a significant impact on early clearance of leukemic cells detected by MRD day 15.

[MeSH-major] Biomarkers, Tumor / metabolism. Neoplasm, Residual / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / therapy

[MeSH-minor] Adolescent. Antigens, CD / metabolism. Antigens, CD13 / metabolism. Antigens, CD34 / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Cell Differentiation. Child. Child, Preschool. Egypt. Female. Flow Cytometry. Humans. Immunophenotyping. Infant. Male. Neprilysin / metabolism. Prognosis. Remission Induction. Sialic Acid Binding Ig-like Lectin 3. Treatment Outcome

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(PMID = 20029466.001).

[ISSN] 1110-0362

[Journal-full-title] Journal of the Egyptian National Cancer Institute

[ISO-abbreviation] J Egypt Natl Canc Inst

[Language] eng

[Publication-type] Journal Article

[Publication-country] Egypt

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Biomarkers, Tumor; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13; EC 3.4.24.11 / Neprilysin

   

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

[Title] ABL1 fusions in T-cell acute lymphoblastic leukemia.

To obtain insight in the contribution of activated kinases to the pathogenesis ofT-cell acute lymphoblastic leukemia (T-ALL), we studied the NUP214-ABL1 fusion gene that is found in 6% of T-ALL and EML1-ABL1 that we identified in one T-ALL patient.

[MeSH-major] Leukemia, T-Cell / genetics. Leukemia, T-Cell / metabolism. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / antagonists & inhibitors

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(PMID = 19166098.001).

[ISSN] 0302-6469

[Journal-full-title] Verhandelingen - Koninklijke Academie voor Geneeskunde van België

[ISO-abbreviation] Verh. K. Acad. Geneeskd. Belg.

[Language] eng

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

[Publication-country] Belgium

[Chemical-registry-number] 0 / Benzamides; 0 / EML1-ABL1 fusion protein, human; 0 / NUP214 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases

[Number-of-references] 17

   

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

[Title] [T-cell acute lymphoblastic leukemia /orbital lymphoblastic lymphoma in children].

[Transliterated title] Leucémie aiguë lymphoblastique T/Lymphome lymphoblastique orbitaire chez l'enfant.

CASE: The authors report a case of an 6-year-old pediatric patient with a history of acute onset of proptosis of his right eye.

RESULTS: Incisional biopsy of the mass revealed after of histopathologic and immuno-histochemical evaluation a T-cell lymphoblastic lymphoma.

Systemic examination and bone marrow aspirate show a acute lymphoblastic leukemia.

CONCLUSION: Primary T-cell lymphoblastic lymphoma of the orbit is a rare entity in any age group, but it is very rare in children.

When tumors occurs in the orbit, it presents a challenging diagnosis problem, especially in pediatric patients.

[MeSH-major] Leukemia-Lymphoma, Adult T-Cell. Neoplasms, Multiple Primary. Orbital Neoplasms. Precursor Cell Lymphoblastic Leukemia-Lymphoma

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(PMID = 15851954.001).

[ISSN] 0181-5512

[Journal-full-title] Journal français d'ophtalmologie

[ISO-abbreviation] J Fr Ophtalmol

[Language] fre

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

[Publication-country] France

   

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

[Title] Impact of genotype on survival of children with T-cell acute lymphoblastic leukemia treated according to the French protocol FRALLE-93: the effect of TLX3/HOX11L2 gene expression on outcome.

BACKGROUND: The prognostic value of the ectopic activation of TLX3 gene expression, a major oncogenetic event associated with pediatric T-cell acute lymphoblastic leukemia, is controversial.

Likewise, the frequency and the prognostic significance in pediatric T-cell acute lymphoblastic leukemia of the newly characterized NUP214-ABL1 fusion transcript is not yet clear.

DESIGN AND METHODS: Two hundred children with T-cell acute lymphoblastic leukemia were treated in the French FRALLE-93 study from 1993 to 1999.

At 5 years the overall survival (+/- standard deviation, %) was 62 (+/-3%) and leukemia-free survival was 58 (+/-3%).

Patients with T-cell acute lymphoblastic leukemia positive for TLX3 had a poorer survival compared to those with T-ALL negative for TLX3 (overall survival: 45+/-11% vs. 57+/-5%, p=0.049).

SILTAL expression did not significantly affect the prognosis of patients with T-cell acute lymphoblastic leukemia.

CONCLUSIONS: TLX3 gene expression is an independent risk factor predicting poor survival in childhood T-cell acute lymphoblastic leukemia.

[MeSH-major] Gene Expression Regulation, Neoplastic. Genotype. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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(PMID = 18835836.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

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

[Publication-country] Italy

[Chemical-registry-number] 0 / Homeodomain Proteins; 0 / TLX3 protein, human

   

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

[Title] T cell acute lymphoblastic leukemia: NOTCHing the way toward a better treatment outcome.

Gamma-secretase inhibitors block the activation of NOTCH1 but have limited activity against T cell acute lymphoblastic leukemia (T-ALL) and cause severe gastrointestinal toxicity.

In a recent study, Real et al. show that a potent gamma-secretase inhibitor potentiates the cytotoxicity of dexamethasone against glucocorticoid-resistant T-ALL cells, while dexamethasone abrogates the gastrointestinal toxicity induced by the gamma-secretase inhibitor.

[MeSH-major] Dexamethasone / therapeutic use. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma. Receptor, Notch1 / metabolism

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[CommentOn] Nat Med. 2009 Jan;15(1):50-8 [19098907.001]

(PMID = 19185842.001).

[ISSN] 1878-3686

[Journal-full-title] Cancer cell

[ISO-abbreviation] Cancer Cell

[Language] eng

[Publication-type] Comment; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Receptor, Notch1; 7S5I7G3JQL / Dexamethasone; EC 3.4.- / Amyloid Precursor Protein Secretases

   

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

[Title] Interleukin 7 requirement for survival of T-cell acute lymphoblastic leukemia and human thymocytes on bone marrow stroma.

We explored the role of interleukin-7 (IL-7) in the bone marrow (BM) stroma-mediated survival of primary T-cell acute lymphoblastic leukemia (T-ALL) cells and normal thymocytes.

[MeSH-major] Bone Marrow Cells / cytology. Interleukin-7 / physiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Thymus Gland / cytology

[MeSH-minor] Animals. Cell Proliferation. Cell Survival. Child. Child, Preschool. Coculture Techniques. Flow Cytometry. Humans. Infant. Lymphopoiesis. Mice

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(PMID = 17296584.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

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

[Publication-country] Italy

[Chemical-registry-number] 0 / Interleukin-7

   

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

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