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1. Chao MM, Todd MA, Kontny U, Neas K, Sullivan MJ, Hunter AG, Picketts DJ, Kratz CP: T-cell acute lymphoblastic leukemia in association with Börjeson-Forssman-Lehmann syndrome due to a mutation in PHF6. Pediatr Blood Cancer; 2010 Oct;55(4):722-4
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  • [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 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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  • [Copyright] Copyright 2010 Wiley-Liss, Inc.
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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
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2. Gutierrez A, Sanda T, Grebliunaite R, Carracedo A, Salmena L, Ahn Y, Dahlberg S, Neuberg D, Moreau LA, Winter SS, Larson R, Zhang J, Protopopov A, Chin L, Pandolfi PP, Silverman LB, Hunger SP, Sallan SE, Look AT: High frequency of PTEN, PI3K, and AKT abnormalities in T-cell acute lymphoblastic leukemia. Blood; 2009 Jul 16;114(3):647-50
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  • [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
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3. Huang X, Chen S, Shen Q, Yang L, Li B, Zhong L, Geng S, Du X, Li Y: Analysis of the expression pattern of the BCL11B gene and its relatives in patients with T-cell acute lymphoblastic leukemia. J Hematol Oncol; 2010;3(1):44
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  • [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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  • (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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4. Riz I, Hawley RG: G1/S transcriptional networks modulated by the HOX11/TLX1 oncogene of T-cell acute lymphoblastic leukemia. Oncogene; 2005 Aug 25;24(36):5561-75
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  • [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
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5. Shamsian BS, Gharib A, Rezaei N, Esfahani SA, Alavi S, Goudarzipour K, Arzanian MT: Development of secondary T-cell acute lymphoblastic leukemia in a child with hemophagocytic lymphohistiocytosis. Pediatr Blood Cancer; 2010 Oct;55(4):725-6
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  • [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
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6. Hoang T: Of mice and men: how an oncogene transgresses the limits and predisposes to T cell acute lymphoblastic leukemia. Sci Transl Med; 2010 Mar 3;2(21):21ps10
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  • [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
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7. Lahortiga I, De Keersmaecker K, Van Vlierberghe P, Graux C, Cauwelier B, Lambert F, Mentens N, Beverloo HB, Pieters R, Speleman F, Odero MD, Bauters M, Froyen G, Marynen P, Vandenberghe P, Wlodarska I, Meijerink JP, Cools J: Duplication of the MYB oncogene in T cell acute lymphoblastic leukemia. Nat Genet; 2007 May;39(5):593-5
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  • [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


8. Cox CV, Martin HM, Kearns PR, Virgo P, Evely RS, Blair A: Characterization of a progenitor cell population in childhood T-cell acute lymphoblastic leukemia. Blood; 2007 Jan 15;109(2):674-82
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  • [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


9. Abla O, Gassas A, Stevens R, Grant R, Abdelhaleem M: bcr-abl-positive T-cell acute lymphoblastic leukemia associated with parvovirus B19 infection. J Pediatr Hematol Oncol; 2006 Feb;28(2):98-9
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  • [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
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10. Kobayashi D, Wofford MM, McLean TW, Lin JJ: Spontaneous tumor lysis syndrome in a child with T-cell acute lymphoblastic leukemia. Pediatr Blood Cancer; 2010 May;54(5):773-5
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  • [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
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11. Janic D, Dokmanovic L, Jovanovic N, Lazic J: T-cell acute lymphoblastic leukemia in a child with ataxia-telangiectasia: case report. J Pediatr Hematol Oncol; 2007 Oct;29(10):713-5
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  • [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


12. Khattab TM, Jastaniah WA, Felimban SK, Elemam N, Abdullah K, Ahmed B: 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. J Clin Oncol; 2009 May 20;27(15_suppl):10048

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  • [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.
  • 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
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13. Kleppe M, Lahortiga I, El Chaar T, De Keersmaecker K, Mentens N, Graux C, Van Roosbroeck K, Ferrando AA, Langerak AW, Meijerink JP, Sigaux F, Haferlach T, Wlodarska I, Vandenberghe P, Soulier J, Cools J: Deletion of the protein tyrosine phosphatase gene PTPN2 in T-cell acute lymphoblastic leukemia. Nat Genet; 2010 Jun;42(6):530-5
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  • [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
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14. Real PJ, Tosello V, Palomero T, Castillo M, Hernando E, de Stanchina E, Sulis ML, Barnes K, Sawai C, Homminga I, Meijerink J, Aifantis I, Basso G, Cordon-Cardo C, Ai W, Ferrando A: Gamma-secretase inhibitors reverse glucocorticoid resistance in T cell acute lymphoblastic leukemia. Nat Med; 2009 Jan;15(1):50-8
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  • [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
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15. Tremblay CS, Hoang T, Hoang T: Early T cell differentiation lessons from T-cell acute lymphoblastic leukemia. Prog Mol Biol Transl Sci; 2010;92:121-56
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  • [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
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16. van Vlierberghe P, Meijerink JP, Lee C, Ferrando AA, Look AT, van Wering ER, Beverloo HB, Aster JC, Pieters R: A new recurrent 9q34 duplication in pediatric T-cell acute lymphoblastic leukemia. Leukemia; 2006 Jul;20(7):1245-53
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  • [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
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17. Wick U, Kirsch M, Rauch A, Chudoba I, Lausen B, Efferth T, Gebhart E: FISH studies on the telomeric regions of the T-cell acute lymphoblastic leukemia cell line CCRF-CEM. Cytogenet Genome Res; 2005;111(1):34-40
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  • [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
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18. Mansour MR, Sulis ML, Duke V, Foroni L, Jenkinson S, Koo K, Allen CG, Gale RE, Buck G, Richards S, Paietta E, Rowe JM, Tallman MS, Goldstone AH, Ferrando AA, Linch DC: Prognostic implications of NOTCH1 and FBXW7 mutations in adults with T-cell acute lymphoblastic leukemia treated on the MRC UKALLXII/ECOG E2993 protocol. J Clin Oncol; 2009 Sep 10;27(26):4352-6
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  • [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 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 / 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 / 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
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19. Bhanushali AA, Babu S, Thangapandi VR, Pillai R, Chheda P, Das BR: Mutations in the HD and PEST domain of Notch-1 receptor in T-cell acute lymphoblastic leukemia: report of novel mutations from Indian population. Oncol Res; 2010;19(2):99-104
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  • [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
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20. Raetz EA, Perkins SL, Bhojwani D, Smock K, Philip M, Carroll WL, Min DJ: Gene expression profiling reveals intrinsic differences between T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma. Pediatr Blood Cancer; 2006 Aug;47(2):130-40
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  • [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
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21. Akahane K, Inukai T, Zhang X, Hirose K, Kuroda I, Goi K, Honna H, Kagami K, Nakazawa S, Endo K, Kubota T, Yagita H, Koyama-Okazaki T, Sugita K: Resistance of T-cell acute lymphoblastic leukemia to tumor necrosis factor--related apoptosis-inducing ligand-mediated apoptosis. Exp Hematol; 2010 Oct;38(10):885-95
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  • [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
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22. Langenau DM, Feng H, Berghmans S, Kanki JP, Kutok JL, Look AT: Cre/lox-regulated transgenic zebrafish model with conditional myc-induced T cell acute lymphoblastic leukemia. Proc Natl Acad Sci U S A; 2005 Apr 26;102(17):6068-73
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  • [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
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23. Marks DI, Paietta EM, Moorman AV, Richards SM, Buck G, DeWald G, Ferrando A, Fielding AK, Goldstone AH, Ketterling RP, Litzow MR, Luger SM, McMillan AK, Mansour MR, Rowe JM, Tallman MS, Lazarus HM: T-cell acute lymphoblastic leukemia in adults: clinical features, immunophenotype, cytogenetics, and outcome from the large randomized prospective trial (UKALL XII/ECOG 2993). Blood; 2009 Dec 10;114(25):5136-45
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  • [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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  • [Cites] J Immunol Methods. 2000 Sep 21;243(1-2):59-75 [10986407.001]
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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 / / G8223452; United Kingdom / Medical Research Council / / MRC/ MC/ U137686856; United States / NCI NIH HHS / CA / R01CA120196; 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; 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
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24. Dohda T, Maljukova A, Liu L, Heyman M, Grandér D, Brodin D, Sangfelt O, Lendahl U: Notch signaling induces SKP2 expression and promotes reduction of p27Kip1 in T-cell acute lymphoblastic leukemia cell lines. Exp Cell Res; 2007 Aug 15;313(14):3141-52
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  • [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
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25. Quentmeier H, Schneider B, Röhrs S, Romani J, Zaborski M, Macleod RA, Drexler HG: SET-NUP214 fusion in acute myeloid leukemia- and T-cell acute lymphoblastic leukemia-derived cell lines. J Hematol Oncol; 2009;2:3
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  • [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


26. Jaing TH, Yang CP, Hung IJ, Tsay PK, Tseng CK, Chen SH: Clinical significance of central nervous system involvement at diagnosis of childhood T-cell acute lymphoblastic leukemia. Pediatr Blood Cancer; 2005 Aug;45(2):135-8
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [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
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27. Riz I, Hawley TS, Luu TV, Lee NH, Hawley RG: TLX1 and NOTCH coregulate transcription in T cell acute lymphoblastic leukemia cells. Mol Cancer; 2010 Jul 09;9:181
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  • [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
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28. Savaşan S, Buck S, Ozdemir O, Hamre M, Asselin B, Pullen J, Ravindranath Y: Evaluation of cytotoxicity by flow cytometric drug sensitivity assay in childhood T-cell acute lymphoblastic leukemia. Leuk Lymphoma; 2005 Jun;46(6):833-40
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  • [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
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29. Chiarini F, Grimaldi C, Ricci F, Tazzari PL, Evangelisti C, Ognibene A, Battistelli M, Falcieri E, Melchionda F, Pession A, Pagliaro P, McCubrey JA, Martelli AM: Activity of the novel dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235 against T-cell acute lymphoblastic leukemia. Cancer Res; 2010 Oct 15;70(20):8097-107
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  • [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


30. Gutierrez A, Dahlberg SE, Neuberg DS, Zhang J, Grebliunaite R, Sanda T, Protopopov A, Tosello V, Kutok J, Larson RS, Borowitz MJ, Loh ML, Ferrando AA, Winter SS, Mullighan CG, Silverman LB, Chin L, Hunger SP, Sallan SE, Look AT: Absence of biallelic TCRgamma deletion predicts early treatment failure in pediatric T-cell acute lymphoblastic leukemia. J Clin Oncol; 2010 Aug 20;28(24):3816-23
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  • [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
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31. Hoelzer D, Gökbuget N: T-cell lymphoblastic lymphoma and T-cell acute lymphoblastic leukemia: a separate entity? Clin Lymphoma Myeloma; 2009;9 Suppl 3:S214-21
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  • [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
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32. Huang L, Lequin M, Pieters R, van den Heuvel-Eibrink MM: The clinical value of follow-up examinations in childhood T-cell acute lymphoblastic leukemia and T-cell non-Hodgkin's lymphoma. Pediatr Blood Cancer; 2007 Apr;48(4):468-72
Genetic Alliance. consumer health - Lymphoblastic lymphoma.

  • [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


33. Sudhakar N, Nirmala K, Rajalekshmy KR, Rajkumar T: Does TAL-1 deletion contribute to the high incidence of T-cell acute lymphoblastic leukemia in South Indian patients? Asian Pac J Cancer Prev; 2008 Jan-Mar;9(1):127-30
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [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
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34. Yeh C, Ma W, Kantarjian H, Zhang ZJ, Cortes J, Albitar M: BCR-ABL truncation due to premature translation termination as a mechanism of resistance to kinase inhibitors. J Clin Oncol; 2009 May 20;27(15_suppl):7028

  • [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
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35. Medyouf H, Alcalde H, Berthier C, Guillemin MC, dos Santos NR, Janin A, Decaudin D, de Thé H, Ghysdael J: Targeting calcineurin activation as a therapeutic strategy for T-cell acute lymphoblastic leukemia. Nat Med; 2007 Jun;13(6):736-41
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  • [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
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36. Palomero T, Ferrando A: Therapeutic targeting of NOTCH1 signaling in T-cell acute lymphoblastic leukemia. Clin Lymphoma Myeloma; 2009;9 Suppl 3:S205-10
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  • [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
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37. Chiaretti S, Messina M, Tavolaro S, Zardo G, Elia L, Vitale A, Fatica A, Gorello P, Piciocchi A, Scappucci G, Bozzoni I, Fozza C, Candoni A, Guarini A, Foà R: Gene expression profiling identifies a subset of adult T-cell acute lymphoblastic leukemia with myeloid-like gene features and over-expression of miR-223. Haematologica; 2010 Jul;95(7):1114-21
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  • [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


38. Sidhom I, Shaaban K, Soliman S, Ezzat S, El-Anwar W, Hamdy N, Yassin D, Salem S, Hassanein H, Mansour MT: Clinical significance of immunophenotypic markers in pediatric T-cell acute lymphoblastic leukemia. J Egypt Natl Canc Inst; 2008 Jun;20(2):111-20
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  • [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
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39. De Keersmaecker K: ABL1 fusions in T-cell acute lymphoblastic leukemia. Verh K Acad Geneeskd Belg; 2008;70(4):245-55
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  • [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
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40. Abdelouahed K, Laghmari M, Tachfouti S, Cherkaoui W, Khorassani M, M'Seffer FA, Mohcine Z: [T-cell acute lymphoblastic leukemia /orbital lymphoblastic lymphoma in children]. J Fr Ophtalmol; 2005 Feb;28(2):197-200
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  • [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
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41. Ballerini P, Landman-Parker J, Cayuela JM, Asnafi V, Labopin M, Gandemer V, Perel Y, Michel G, Leblanc T, Schmitt C, Fasola S, Hagemejier A, Sigaux F, Auclerc MF, Douay L, Leverger G, Baruchel A: 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. Haematologica; 2008 Nov;93(11):1658-65
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  • [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
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42. Pui CH: T cell acute lymphoblastic leukemia: NOTCHing the way toward a better treatment outcome. Cancer Cell; 2009 Feb 3;15(2):85-7
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  • [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
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43. Scupoli MT, Perbellini O, Krampera M, Vinante F, Cioffi F, Pizzolo G: Interleukin 7 requirement for survival of T-cell acute lymphoblastic leukemia and human thymocytes on bone marrow stroma. Haematologica; 2007 Feb;92(2):264-6
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  • [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
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44. Van Vlierberghe P, van Grotel M, Beverloo HB, Lee C, Helgason T, Buijs-Gladdines J, Passier M, van Wering ER, Veerman AJ, Kamps WA, Meijerink JP, Pieters R: The cryptic chromosomal deletion del(11)(p12p13) as a new activation mechanism of LMO2 in pediatric T-cell acute lymphoblastic leukemia. Blood; 2006 Nov 15;108(10):3520-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The cryptic chromosomal deletion del(11)(p12p13) as a new activation mechanism of LMO2 in pediatric T-cell acute lymphoblastic leukemia.
  • To identify new cytogenetic abnormalities associated with leukemogenesis or disease outcome, T-cell acute lymphoblastic leukemia (T-ALL) patient samples were analyzed by means of the array-comparative genome hybridization technique (array-CGH).
  • LMO2 rearrangements, including this del(11)(p12p13) and t(11;14) (p13;q11) or t(7;11)(q35;p13), were found in the absence of other recurrent cytogenetic abnormalities involving HOX11L2, HOX11, CALM-AF10, TAL1, MLL, or MYC.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 11. DNA-Binding Proteins / metabolism. Metalloproteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16873670.001).
  • [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
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45. Reichard KK, Zhang QY, Sanchez L, Hozier J, Viswanatha D, Foucar K: Acute myeloid leukemia of donor origin after allogeneic bone marrow transplantation for precursor T-cell acute lymphoblastic leukemia: case report and review of the literature. Am J Hematol; 2006 Mar;81(3):178-85
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  • [Title] Acute myeloid leukemia of donor origin after allogeneic bone marrow transplantation for precursor T-cell acute lymphoblastic leukemia: case report and review of the literature.
  • We report a case of donor-derived acute myeloid leukemia (AML) occurring in a 33-year-old man after allogeneic bone marrow transplantation (BMT) for precursor T-cell acute lymphoblastic -leukemia (T-ALL).
  • Fluorescence in-situ hybridization (FISH) analysis showed the AML to be of donor origin (i.e., karyotypically female) with an 11q23 (mixed lineage leukemia (MLL) gene) translocation, while the original T-ALL exhibited a male karyotype with abnormalities of chromosomes 6, 8, and a t(10;14)(q24;q11.2).
  • Donor-cell leukemia (DCL) after allogeneic BMT is a rare, yet well-documented, event.
  • [MeSH-major] Bone Marrow Transplantation. Leukemia, Myeloid, Acute / etiology. Living Donors. Neoplasms, Second Primary / etiology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / therapy. Transplantation Chimera


46. Matsumoto T, Jimi S, Hara S, Takamatsu Y, Suzumiya J, Tamura K: Am80 inhibits stromal cell-derived factor-1-induced chemotaxis in T-cell acute lymphoblastic leukemia cells. Leuk Lymphoma; 2010 Mar;51(3):507-14
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  • [Title] Am80 inhibits stromal cell-derived factor-1-induced chemotaxis in T-cell acute lymphoblastic leukemia cells.
  • C-X-C motif chemokine receptor 4 (CXCR4) and stromal cell-derived factor-1 (SDF-1) play a potent role in metastasis and infiltration of many types of tumors, including T-cell acute lymphoblastic leukemia (T-ALL), into the central nervous system or lymph nodes.
  • Although higher levels of CXCR4 expression have been shown to correlate with shorter survival of patients, effective drugs affecting cell surface CXCR4 expression are still unknown.
  • [MeSH-major] Benzoates / pharmacology. Chemokine CXCL12 / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. T-Lymphocytes / immunology. Tetrahydronaphthalenes / pharmacology
  • [MeSH-minor] Cell Membrane / metabolism. Cell Movement. Chemotaxis. Flow Cytometry / methods. Gene Expression Regulation, Leukemic. Humans. Jurkat Cells. K562 Cells. Protein Kinase C / metabolism. Receptors, CXCR4 / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20141446.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzoates; 0 / CXCR4 protein, human; 0 / Chemokine CXCL12; 0 / Receptors, CXCR4; 0 / Tetrahydronaphthalenes; 08V52GZ3H9 / tamibarotene; EC 2.7.11.13 / Protein Kinase C
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47. Lewis HD, Leveridge M, Strack PR, Haldon CD, O'neil J, Kim H, Madin A, Hannam JC, Look AT, Kohl N, Draetta G, Harrison T, Kerby JA, Shearman MS, Beher D: Apoptosis in T cell acute lymphoblastic leukemia cells after cell cycle arrest induced by pharmacological inhibition of notch signaling. Chem Biol; 2007 Feb;14(2):209-19
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  • [Title] Apoptosis in T cell acute lymphoblastic leukemia cells after cell cycle arrest induced by pharmacological inhibition of notch signaling.
  • In this report, inhibitors of the gamma-secretase enzyme have been exploited to characterize the antiproliferative relationship between target inhibition and cellular responses in Notch-dependent human T cell acute lymphoblastic leukemia (T-ALL) cell lines.
  • Inhibition of gamma-secretase led to decreased Notch signaling, measured by endogenous NOTCH intracellular domain (NICD) formation, and was associated with decreased cell viability.
  • Flow cytometry revealed that decreased cell viability resulted from a G(0)/G(1) cell cycle block, which correlated strongly to the induction of apoptosis.
  • Together, these data strengthen the rationale for using gamma-secretase inhibitors therapeutically and suggest that programmed cell death may contribute to reduction of tumor burden in the clinic.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Apoptosis / drug effects. Enzyme Inhibitors / pharmacology. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / pathology. Receptors, Notch / antagonists & inhibitors
  • [MeSH-minor] Cell Cycle / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Cyclic S-Oxides / pharmacology. Flow Cytometry. Humans. Signal Transduction / drug effects. Thiadiazoles / pharmacology

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  • (PMID = 17317574.001).
  • [ISSN] 1074-5521
  • [Journal-full-title] Chemistry & biology
  • [ISO-abbreviation] Chem. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclic S-Oxides; 0 / Enzyme Inhibitors; 0 / MRK 003; 0 / Receptors, Notch; 0 / Thiadiazoles; EC 3.4.- / Amyloid Precursor Protein Secretases
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48. Larson Gedman A, Chen Q, Kugel Desmoulin S, Ge Y, LaFiura K, Haska CL, Cherian C, Devidas M, Linda SB, Taub JW, Matherly LH: The impact of NOTCH1, FBW7 and PTEN mutations on prognosis and downstream signaling in pediatric T-cell acute lymphoblastic leukemia: a report from the Children's Oncology Group. Leukemia; 2009 Aug;23(8):1417-25
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  • [Title] The impact of NOTCH1, FBW7 and PTEN mutations on prognosis and downstream signaling in pediatric T-cell acute lymphoblastic leukemia: a report from the Children's Oncology Group.
  • We explored the impact of mutations in the NOTCH1, FBW7 and PTEN genes on prognosis and downstream signaling in a well-defined cohort of 47 patients with pediatric T-cell acute lymphoblastic leukemia (T-ALL).

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  • (PMID = 19340001.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA076641-10; United States / NCI NIH HHS / CA / T32-CA009531; United States / NCI NIH HHS / CA / R01 CA076641; United States / NCI NIH HHS / CA / CA76641; United States / NCI NIH HHS / CA / T32 CA009531-22; United States / NCI NIH HHS / CA / T32 CA009531; United States / NCI NIH HHS / CA / T32 CA009531-21
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Cell Cycle Proteins; 0 / DNA, Neoplasm; 0 / F-Box Proteins; 0 / Homeodomain Proteins; 0 / NOTCH1 protein, human; 0 / Neoplasm Proteins; 0 / Receptor, Notch1; 149348-15-2 / HES1 protein, human; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Other-IDs] NLM/ NIHMS98506; NLM/ PMC2726275
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49. Baak U, Gökbuget N, Orawa H, Schwartz S, Hoelzer D, Thiel E, Burmeister T, German Multicenter ALL Study Group: Thymic adult T-cell acute lymphoblastic leukemia stratified in standard- and high-risk group by aberrant HOX11L2 expression: experience of the German multicenter ALL study group. Leukemia; 2008 Jun;22(6):1154-60
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  • [Title] Thymic adult T-cell acute lymphoblastic leukemia stratified in standard- and high-risk group by aberrant HOX11L2 expression: experience of the German multicenter ALL study group.
  • Adult T-cell acute lymphoblastic leukemia (T-ALL) continues to represent an unfavorable disease.
  • [MeSH-major] Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Proto-Oncogene Proteins / genetics. Thymus Gland / pathology

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  • (PMID = 18368072.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / TLX3 protein, human; 143275-75-6 / TLX1 protein, human
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50. Batova A, Cottam H, Yu J, Diccianni MB, Carrera CJ, Yu AL: EFA (9-beta-D-erythrofuranosyladenine) is an effective salvage agent for methylthioadenosine phosphorylase-selective therapy of T-cell acute lymphoblastic leukemia with L-alanosine. Blood; 2006 Feb 1;107(3):898-903
Hazardous Substances Data Bank. (L)-ALANINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] EFA (9-beta-D-erythrofuranosyladenine) is an effective salvage agent for methylthioadenosine phosphorylase-selective therapy of T-cell acute lymphoblastic leukemia with L-alanosine.
  • The deficiency of methylthioadenosine phosphorylase (MTAP) in T-cell acute lymphoblastic leukemia (T-ALL) and other cancers, while constitutively expressed in normal cells, allows for selective therapy using L-alanosine, an inhibitor of de novo AMP synthesis.
  • We demonstrate that MTAP- T-ALL cells obtained at relapse are as sensitive to L-alanosine toxicity as diagnosis samples.

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  • (PMID = 16234352.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR00827
  • [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 / 9-beta-D-erythrofuranosyladenine; 0 / Antibiotics, Antineoplastic; 0 / Deoxyadenosines; 0 / Enzyme Inhibitors; 0 / Furans; 0 / Thionucleosides; 2CNI71214Y / alanosine; 634Z2VK3UQ / 5'-methylthioadenosine; EC 2.4.2.1 / Purine-Nucleoside Phosphorylase; EC 2.4.2.28 / 5'-methylthioadenosine phosphorylase; JAC85A2161 / Adenine; OF5P57N2ZX / Alanine
  • [Other-IDs] NLM/ PMC1895892
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51. Asnafi V, Buzyn A, Le Noir S, Baleydier F, Simon A, Beldjord K, Reman O, Witz F, Fagot T, Tavernier E, Turlure P, Leguay T, Huguet F, Vernant JP, Daniel F, Béné MC, Ifrah N, Thomas X, Dombret H, Macintyre E: 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. Blood; 2009 Apr 23;113(17):3918-24
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  • [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.
  • [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
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52. Sung ES, Kim A, Park JS, Chung J, Kwon MH, Kim YS: Histone deacetylase inhibitors synergistically potentiate death receptor 4-mediated apoptotic cell death of human T-cell acute lymphoblastic leukemia cells. Apoptosis; 2010 Oct;15(10):1256-69
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Histone deacetylase inhibitors synergistically potentiate death receptor 4-mediated apoptotic cell death of human T-cell acute lymphoblastic leukemia cells.
  • Cell-death signaling through the pro-apoptotic tumor necrosis factor-related apoptosis inducing ligand (TRAIL) receptors, death receptor 4 (DR4) and DR5, has shown tumor-selective apoptotic activity.
  • Here, we examine susceptibility of various leukemia cell lines (HL-60, U937, K562, CCRF-CEM, CEM-CM3, and THP-1) to an anti-DR4 agonistic monoclonal antibody (mAb), AY4, in comparison with TRAIL.
  • While most of the leukemia cell lines were intrinsically resistant to AY4 or TRAIL alone, the two T-cell acute lymphoblastic leukemia (T-ALL) lines, CEM-CM3 and CCRF-CEM cells, underwent synergistic caspase-dependent apoptotic cell death by combination of AY4 or TRAIL with a histone deacetylase inhibitor (HDACI), either suberoylanilide hydroxamic acid (SAHA) or valproic acid (VPA).
  • Our results demonstrate that the HDACIs have synergistic effects on DR4-specific mAb AY4-mediated cell death in the T-ALL cells with comparable competence to those exerted by TRAIL, providing a new strategy for the targeted treatment of human T-ALL cells.
  • [MeSH-major] Apoptosis / drug effects. Histone Deacetylase Inhibitors / pharmacology. Hydroxamic Acids / pharmacology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Receptors, Tumor Necrosis Factor / immunology. Receptors, Tumor Necrosis Factor / metabolism. Valproic Acid / pharmacology
  • [MeSH-minor] Antibodies, Monoclonal / pharmacology. Antineoplastic Agents / pharmacology. Blotting, Western. Caspases / metabolism. Cell Line, Tumor. Down-Regulation. Drug Synergism. Flow Cytometry. Histone Deacetylases / metabolism. Humans. Inhibitor of Apoptosis Proteins / metabolism. Mitochondria / drug effects. Mitochondria / metabolism. RNA, Small Interfering. Receptors, TNF-Related Apoptosis-Inducing Ligand. Signal Transduction / drug effects. TNF-Related Apoptosis-Inducing Ligand / metabolism. TNF-Related Apoptosis-Inducing Ligand / pharmacology

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  • (PMID = 20582477.001).
  • [ISSN] 1573-675X
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Inhibitor of Apoptosis Proteins; 0 / RNA, Small Interfering; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10A protein, human; 58IFB293JI / vorinostat; 614OI1Z5WI / Valproic Acid; EC 3.4.22.- / Caspases; EC 3.5.1.98 / Histone Deacetylases
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53. De Keersmaecker K, Graux C, Odero MD, Mentens N, Somers R, Maertens J, Wlodarska I, Vandenberghe P, Hagemeijer A, Marynen P, Cools J: Fusion of EML1 to ABL1 in T-cell acute lymphoblastic leukemia with cryptic t(9;14)(q34;q32). Blood; 2005 Jun 15;105(12):4849-52
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  • [Title] Fusion of EML1 to ABL1 in T-cell acute lymphoblastic leukemia with cryptic t(9;14)(q34;q32).
  • The BCR-ABL1 fusion kinase is frequently associated with chronic myeloid leukemia and B-cell acute lymphoblastic leukemia but is rare in T-cell acute lymphoblastic leukemia (T-ALL).
  • [MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 9. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Fusion Proteins, bcr-abl / chemistry. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, T-Cell / pathology. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Base Sequence. Benzamides. Blotting, Western. Cell Line. Cell Survival. DNA, Complementary / metabolism. DNA-Binding Proteins / metabolism. Female. Gene Deletion. Genes, abl. Humans. Imatinib Mesylate. In Situ Hybridization, Fluorescence. Karyotyping. Microtubules / metabolism. Milk Proteins / metabolism. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Models, Genetic. Molecular Sequence Data. Open Reading Frames. Phenotype. Phosphorylation. Piperazines / pharmacology. Polymerase Chain Reaction. Protein Kinase Inhibitors / pharmacology. Protein Structure, Tertiary. Protein-Tyrosine Kinases / metabolism. Pyrimidines / pharmacology. Recombinant Fusion Proteins / metabolism. Retroviridae. Reverse Transcriptase Polymerase Chain Reaction. STAT5 Transcription Factor. Signal Transduction. Time Factors. Trans-Activators / metabolism

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  • (PMID = 15713800.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA, Complementary; 0 / DNA-Binding Proteins; 0 / EML1-ABL1 fusion protein, human; 0 / Milk Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Recombinant Fusion Proteins; 0 / STAT5 Transcription Factor; 0 / Trans-Activators; 0 / abl-bcr fusion protein, human; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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54. Cui J, Wang Q, Wang J, Lv M, Zhu N, Li Y, Feng J, Shen B, Zhang J: Basal c-Jun NH2-terminal protein kinase activity is essential for survival and proliferation of T-cell acute lymphoblastic leukemia cells. Mol Cancer Ther; 2009 Dec;8(12):3214-22
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  • [Title] Basal c-Jun NH2-terminal protein kinase activity is essential for survival and proliferation of T-cell acute lymphoblastic leukemia cells.
  • Hyperactivation of c-Jun NH2-terminal protein kinase (JNK) has been found in various malignant lymphocytes and inhibition of JNK activity leads to cell cycle arrest and apoptosis.
  • However, the role of JNK activity in the oncogenic growth of T-cell acute lymphoblastic leukemia (T-ALL) cells remains largely unknown.
  • Here, we report that treatment of T-ALL cells with JNK inhibitors led to cell cycle arrest and apoptosis and increased sensitivity to Fas-mediated apoptosis, whereas weak ectopic expression of MKK7-JNK1 fusion protein, which shows constitutive JNK activity, in T-ALL cells resulted in accelerated cell cycle progression and resistance to Fas-mediated apoptosis.
  • [MeSH-major] Cell Proliferation. JNK Mitogen-Activated Protein Kinases / metabolism. Mitogen-Activated Protein Kinase 8 / metabolism. Mitogen-Activated Protein Kinase 9 / metabolism
  • [MeSH-minor] Acetonitriles / pharmacology. Animals. Anthracenes / pharmacology. Apoptosis / drug effects. Benzothiazoles / pharmacology. Cell Cycle / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Dose-Response Relationship, Drug. Flow Cytometry. Humans. Immunoblotting. Jurkat Cells. MAP Kinase Kinase 7 / genetics. MAP Kinase Kinase 7 / metabolism. Mice. Mice, Inbred C57BL. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Proto-Oncogene Proteins c-myc / metabolism. RNA Interference. Transfection

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  • (PMID = 19996270.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 1,3-benzothiazol-2-yl(2-((2-(3-pyridinyl)ethyl)amino)-4-pyrimidinyl)acetonitrile; 0 / Acetonitriles; 0 / Anthracenes; 0 / Benzothiazoles; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc; 0 / anthra(1,9-cd)pyrazol-6(2H)-one; EC 2.7.1.- / MAP2K7 protein, human; EC 2.7.1.24 / Mitogen-Activated Protein Kinase 9; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 8; EC 2.7.12.2 / MAP Kinase Kinase 7
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55. Zuurbier L, Homminga I, Calvert V, te Winkel ML, Buijs-Gladdines JG, Kooi C, Smits WK, Sonneveld E, Veerman AJ, Kamps WA, Horstmann M, Petricoin EF 3rd, Pieters R, Meijerink JP: NOTCH1 and/or FBXW7 mutations predict for initial good prednisone response but not for improved outcome in pediatric T-cell acute lymphoblastic leukemia patients treated on DCOG or COALL protocols. Leukemia; 2010 Dec;24(12):2014-22
Hazardous Substances Data Bank. PREDNISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NOTCH1 and/or FBXW7 mutations predict for initial good prednisone response but not for improved outcome in pediatric T-cell acute lymphoblastic leukemia patients treated on DCOG or COALL protocols.
  • Aberrant activation of the NOTCH1 pathway by inactivating and activating mutations in NOTCH1 or FBXW7 is a frequent phenomenon in T-cell acute lymphoblastic leukemia (T-ALL).
  • We retrospectively investigated the relevance of NOTCH1/FBXW7 mutations for pediatric T-ALL patients enrolled on Dutch Childhood Oncology Group (DCOG) ALL7/8 or ALL9 or the German Co-Operative Study Group for Childhood Acute Lymphoblastic Leukemia study (COALL-97) protocols.
  • NOTCH1-activating mutations were less frequently associated with mature T-cell developmental stage.
  • [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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  • [CommentIn] Leukemia. 2010 Dec;24(12):2003-4 [21157484.001]
  • (PMID = 20861909.001).
  • [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 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / TLX3 protein, human; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases; VB0R961HZT / Prednisone
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56. Van Vlierberghe P, van Grotel M, Tchinda J, Lee C, Beverloo HB, van der Spek PJ, Stubbs A, Cools J, Nagata K, Fornerod M, Buijs-Gladdines J, Horstmann M, van Wering ER, Soulier J, Pieters R, Meijerink JP: The recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-cell acute lymphoblastic leukemia. Blood; 2008 May 1;111(9):4668-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) is mostly characterized by specific chromosomal abnormalities, some occurring in a mutually exclusive manner that possibly delineate specific T-ALL subgroups.
  • This deletion results in a conserved SET-NUP214 fusion product, which was also identified in the T-ALL cell line LOUCY.
  • We conclude that SET-NUP214 may contribute to the pathogenesis of T-ALL by enforcing T-cell differentiation arrest.

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  • (PMID = 18299449.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA11560
  • [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 / Chromosomal Proteins, Non-Histone; 0 / Histone Chaperones; 0 / Homeodomain Proteins; 0 / NUP214 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / SET protein, human; 0 / Transcription Factors; 157907-48-7 / HoxA protein
  • [Other-IDs] NLM/ PMC2343598
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57. van Grotel M, Meijerink JP, Beverloo HB, Langerak AW, Buys-Gladdines JG, Schneider P, Poulsen TS, den Boer ML, Horstmann M, Kamps WA, Veerman AJ, van Wering ER, van Noesel MM, Pieters R: The outcome of molecular-cytogenetic subgroups in pediatric T-cell acute lymphoblastic leukemia: a retrospective study of patients treated according to DCOG or COALL protocols. Haematologica; 2006 Sep;91(9):1212-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The outcome of molecular-cytogenetic subgroups in pediatric T-cell acute lymphoblastic leukemia: a retrospective study of patients treated according to DCOG or COALL protocols.
  • BACKGROUND AND OBJECTIVES: Subgroups of T-cell acute lymphoblastic leukemia (T-ALL), defined according to recurrent cytogenetic aberrations, may have different prognoses.
  • HOX11L2 was associated with both immunophenotypically immature cases as well as cases committed to the gammadelta-lineage.
  • TAL1 abnormalities were associated with alphabeta-lineage commitment, and tended to be associated with a good outcome.
  • In relation to the expression of early T-cell transcription factors, high TAL1 levels were found in immunophenotypically-advanced cases, whereas high LYL1 levels were found in immature subgroups.
  • Our data on CALM-AF10 rearranged T-ALL, albeit based on only three patients, suggest that this type of leukemia is associated with a poor outcome.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Cytogenetic Analysis. Leukemia-Lymphoma, Adult T-Cell / diagnosis

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  • [CommentIn] Haematologica. 2006 Sep;91(9):1156A [16956809.001]
  • (PMID = 16956820.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / AF10-CALM fusion protein, human; 0 / Oncogene Proteins, Fusion
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58. Řezáčová M, Vávrová J, Vokurková D: Ionizing Radiation Sensitizes Leukemic MOLT-4 Cells to TRAIL-induced Apoptosis. Acta Medica (Hradec Kralove); 2008;51(2):101-105

  • [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
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59. Winter SS, Holdsworth MT, Devidas M, Raisch DW, Chauvenet A, Ravindranath Y, Ducore JM, Amylon MD: Antimetabolite-based therapy in childhood T-cell acute lymphoblastic leukemia: a report of POG study 9296. Pediatr Blood Cancer; 2006 Feb;46(2):179-86
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antimetabolite-based therapy in childhood T-cell acute lymphoblastic leukemia: a report of POG study 9296.
  • PURPOSE: A previous Pediatric Oncology Group (POG) study showed high incidence of secondary acute myelogenous leukemia (AML) in children treated for T-cell acute lymphoblastic leukemia (T-ALL) or higher-stage lymphoblastic lymphoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Anthracyclines / administration & dosage. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Agents, Alkylating / administration & dosage. Asparaginase / administration & dosage. Asparaginase / adverse effects. Child. Child, Preschool. Disease-Free Survival. Drug Hypersensitivity / etiology. Female. Follow-Up Studies. Humans. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / mortality. Male. Pilot Projects. Remission Induction. Sepsis / etiology. Sepsis / mortality

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  • (PMID = 16007607.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5 U10 CA5312; United States / NCI NIH HHS / CA / CA29139
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Alkylating; EC 3.5.1.1 / Asparaginase
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60. Basu D, Siddaraju N, Murugan P, Badhe BA, Akkarappatty C, Dutta TK: Cytologic aspects of T-cell acute lymphoblastic leukemia presenting as a massive pericardial effusion: a case report. Acta Cytol; 2009 May-Jun;53(3):337-40
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  • [Title] Cytologic aspects of T-cell acute lymphoblastic leukemia presenting as a massive pericardial effusion: a case report.
  • BACKGROUND: Acute lymphoblastic leukemia (ALL) with a clinical presentation of cardiac tamponade and the presence of blasts in the pericardial fluid is an uncommon event.
  • A cytopathologist needs to adopt a cautious interpretive approach while dealing with a lymphoid-rich pericardial effusion in order to prevent a false negative diagnosis.
  • On detailed clinical examination, a diagnosis of anemia with cardiac tamponade was made.
  • Cytology of pericardial fluid revealed a large number of lymphoid cells in a hemorrhagic background that, under low magnification, closely resembled mature lymphocytes.
  • However, a careful examination of May-Grünwald-Giemsa-stained cytologic smears, under an oil immersion objective (x 1,000), showed atypical lymphoid cells having blastoid morphology.
  • Rare lymphoid cells displayed a "hand mirror" appearance.
  • A hematologic workup was carried out to exclude leukemia/lymphoma.
  • Complete blood count revealed pancytopenia with abnormal lymphoid cells.
  • A diagnosis of T-cell acute lymphoblastic leukemia (FAB L1) was offered, and the patient was started on a remission and induction regimen.
  • The abnormal lymphoid cells found in the pericardial fluid in such situations need to be interpreted cautiously, as their presence is of clinical significance.
  • [MeSH-major] Cardiac Tamponade / pathology. Pericardial Effusion / pathology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 19534280.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Biomarkers, Tumor; EC 2.7.7.31 / DNA Nucleotidylexotransferase
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61. Przybylski GK, Dik WA, Grabarczyk P, Wanzeck J, Chudobska P, Jankowski K, von Bergh A, van Dongen JJ, Schmidt CA, Langerak AW: The effect of a novel recombination between the homeobox gene NKX2-5 and the TRD locus in T-cell acute lymphoblastic leukemia on activation of the NKX2-5 gene. Haematologica; 2006 Mar;91(3):317-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The effect of a novel recombination between the homeobox gene NKX2-5 and the TRD locus in T-cell acute lymphoblastic leukemia on activation of the NKX2-5 gene.
  • Here, we describe for the first time a fusion between NKX2-5 and the T-cell receptor delta locus (TRD) resulting in NKX2-5 activation in a case of T-cell acute lymphoblastic leukemia (T-ALL).
  • Expression of NKX2-5 was analyzed by real-time quantitative PCR in the T-ALL case with the NKX2-5-TRD rearrangement, 18 other cases of T-ALL, three T-ALL derived cell lines, two non-hematopoietic cell lines, peripheral blood mononuclear cells from six healthy individuals and sorted thymocyte subsets.
  • High NKX2-5 expression was also found in the T-cell lines PEER and CCRF-CEM, which harbor an NKX2-5-BCL11B rearrangement, and in the embryonic kidney cell line 293.
  • INTERPRETATION AND CONCLUSIONS: Our finding of overexpression of yet another homeobox gene in T-ALL further supports the hypothesis that homeobox genes play an important role in malignant transformation of particular types of T-ALL.
  • [MeSH-major] Genes, T-Cell Receptor delta / genetics. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Leukemia-Lymphoma, Adult T-Cell / genetics. Recombination, Genetic / genetics. Transcription Factors / genetics. Transcription Factors / metabolism

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  • [CommentIn] Haematologica. 2006 Mar;91(3):290A [16531247.001]
  • (PMID = 16531254.001).
  • [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 / Genetic Markers; 0 / Homeodomain Proteins; 0 / NKX2-5 protein, human; 0 / Transcription Factors
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62. Cleaver AL, Beesley AH, Firth MJ, Sturges NC, O'Leary RA, Hunger SP, Baker DL, Kees UR: Gene-based outcome prediction in multiple cohorts of pediatric T-cell acute lymphoblastic leukemia: a Children's Oncology Group study. Mol Cancer; 2010 May 12;9:105
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene-based outcome prediction in multiple cohorts of pediatric T-cell acute lymphoblastic leukemia: a Children's Oncology Group study.
  • BACKGROUND: Continuous complete clinical remission in T-cell acute lymphoblastic leukemia (T-ALL) is now approaching 80% due to the implementation of aggressive chemotherapy protocols but patients that relapse continue to have a poor prognosis.
  • Such patients could benefit from augmented therapy if their clinical outcome could be more accurately predicted at the time of diagnosis.
  • In T-ALL cell lines, low IL-7R expression was correlated with diminished growth response to IL-7 and enhanced glucocorticoid resistance.
  • Analysis of biological pathways identified the NF-kappaB and Wnt pathways, and the cell adhesion receptor family (particularly integrins) as being predictive of relapse.
  • CONCLUSIONS: We have used two different approaches to identify, for the first time, robust gene signatures that can successfully discriminate relapse and CCR patients at the time of diagnosis across multiple patient cohorts and platforms.

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  • (PMID = 20459861.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA114766; United States / NCI NIH HHS / CA / CA95475; United States / NCI NIH HHS / CA / CA98543
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / NF-kappa B; 0 / Receptors, Interleukin-7; 0 / Wnt Proteins
  • [Other-IDs] NLM/ PMC2879253
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63. Fischer L, Gökbuget N, Schwartz S, Burmeister T, Rieder H, Brüggemann M, Hoelzer D, Thiel E: CD56 expression in T-cell acute lymphoblastic leukemia is associated with non-thymic phenotype and resistance to induction therapy but no inferior survival after risk-adapted therapy. Haematologica; 2009 Feb;94(2):224-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD56 expression in T-cell acute lymphoblastic leukemia is associated with non-thymic phenotype and resistance to induction therapy but no inferior survival after risk-adapted therapy.
  • BACKGROUND: Expression of CD56 has been associated with poor prognosis in acute myeloid leukemia and aggressive lymphoma.
  • DESIGN AND METHODS: We analyzed the impact of CD56 expression in a cohort of 452 newly diagnosed adult T-cell acute lymphoblastic leukemia (T-ALL) patients; clinical data were available for 306 patients.
  • A clonal T-cell receptor rearrangement was detected in 22/23 CD56(+) ALL.
  • Treatment of CD56(+) ALL resulted in a lower rate of complete remissions (70% vs. 88%) (p=0.001) and a higher rate of resistant disease (21% vs. 8%) (p=0.004).
  • CD56 expression had no significant influence on overall (48% vs. 59%) and disease free survival (67% vs. 57%) at three years.
  • [MeSH-major] Antigens, CD56. Drug Resistance, Neoplasm. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis


64. Quigley DI, Wolff DJ: Pediatric T-cell acute lymphoblastic leukemia with aberrations of both MLL loci. Cancer Genet Cytogenet; 2006 Jul 1;168(1):77-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric T-cell acute lymphoblastic leukemia with aberrations of both MLL loci.
  • Translocations involving the MLL gene at 11q23 have been implicated in acute lymphoblastic leukemia (ALL), as well as acute myeloid leukemia (AML).
  • Such translocations result in gain of function fusion proteins that drive cell proliferation.
  • Except in cases of T-cell ALL, MLL rearrangement is typically associated with a poor prognosis.
  • We report a case of T-cell ALL with a t(11;19)(q23;p13.3) and deletion of the other chromosome 11 homolog at band q23.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Gene Deletion. Leukemia-Lymphoma, Adult T-Cell / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic / genetics

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  • (PMID = 16772125.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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65. Taghdisi SM, Abnous K, Mosaffa F, Behravan J: Targeted delivery of daunorubicin to T-cell acute lymphoblastic leukemia by aptamer. J Drug Target; 2010 May;18(4):277-81
Hazardous Substances Data Bank. DAUNORUBICIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted delivery of daunorubicin to T-cell acute lymphoblastic leukemia by aptamer.
  • Application of daunorubicin in treatment of leukemia has been limited for its side effects like cardiotoxicity.
  • In conclusion, sgc8-daunorubicin complex is introduced as a simple and efficient system for targeted delivery of drug to acute lymphoblastic leukemia T cells.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Aptamers, Nucleotide / chemistry. Daunorubicin / administration & dosage. Drug Delivery Systems. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Base Sequence. Cell Line, Tumor. Flow Cytometry. Humans. Nucleic Acid Conformation. Spectrometry, Fluorescence

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  • (PMID = 19943768.001).
  • [ISSN] 1029-2330
  • [Journal-full-title] Journal of drug targeting
  • [ISO-abbreviation] J Drug Target
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Aptamers, Nucleotide; ZS7284E0ZP / Daunorubicin
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66. Weng AP, Millholland JM, Yashiro-Ohtani Y, Arcangeli ML, Lau A, Wai C, Del Bianco C, Rodriguez CG, Sai H, Tobias J, Li Y, Wolfe MS, Shachaf C, Felsher D, Blacklow SC, Pear WS, Aster JC: c-Myc is an important direct target of Notch1 in T-cell acute lymphoblastic leukemia/lymphoma. Genes Dev; 2006 Aug 1;20(15):2096-109
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  • [Title] c-Myc is an important direct target of Notch1 in T-cell acute lymphoblastic leukemia/lymphoma.
  • Human acute T-cell lymphoblastic leukemias and lymphomas (T-ALL) are commonly associated with gain-of-function mutations in Notch1 that contribute to T-ALL induction and maintenance.
  • Starting from an expression-profiling screen, we identified c-myc as a direct target of Notch1 in Notch-dependent T-ALL cell lines, in which Notch accounts for the majority of c-myc expression.
  • In functional assays, inhibitors of c-myc interfere with the progrowth effects of activated Notch1, and enforced expression of c-myc rescues multiple Notch1-dependent T-ALL cell lines from Notch withdrawal.

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  • (PMID = 16847353.001).
  • [ISSN] 0890-9369
  • [Journal-full-title] Genes & development
  • [ISO-abbreviation] Genes Dev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R56 CA092433; United States / NCI NIH HHS / CA / T32 CA 09140-31-35; United States / NCI NIH HHS / CA / R56 CA092433-06A1; United States / NCI NIH HHS / CA / R01 CA092433; United States / NCI NIH HHS / CA / T32 CA009140; None / None / / R01 CA092433-06A2; United States / NCI NIH HHS / CA / CA119130-01; United States / NCI NIH HHS / CA / R01 CA119130; United States / NCI NIH HHS / CA / P01 CA119070-01A19001; United States / NCI NIH HHS / CA / CA119070-01A19001; None / None / / R56 CA092433-06A1; United States / NCI NIH HHS / CA / R01 CA092433-06A2; United States / NCI NIH HHS / CA / R01 CA119130-01; 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 / Notch1 protein, mouse; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptor, Notch1
  • [Other-IDs] NLM/ PMC1536060
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67. Lo TC, Barnhill LM, Kim Y, Nakae EA, Yu AL, Diccianni MB: Inactivation of SHIP1 in T-cell acute lymphoblastic leukemia due to mutation and extensive alternative splicing. Leuk Res; 2009 Nov;33(11):1562-6
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  • [Title] Inactivation of SHIP1 in T-cell acute lymphoblastic leukemia due to mutation and extensive alternative splicing.
  • No cell lines or primary ALLs harbored PIK3CA mutations.
  • PTEN was expressed in just one-third of the cell lines, but in two-thirds of the primary ALLs, though in the inactivated (phosphorylated) form.
  • SHIP1 was undetectable in most primary ALL and in the T-ALL cell line Jurkat, which harbored a bi-allelic null mutation and a frame-shift deletion; primary ALL harbored the frame-shift as well as other translationally-inactivating deletions and insertions.

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  • (PMID = 19473701.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA023100-23; United States / NCI NIH HHS / CA / P30 CA023100; United States / NCI NIH HHS / CA / P30 CA023100-23
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.56 / inositol-polyphosphate 5-phosphatase
  • [Other-IDs] NLM/ NIHMS114983; NLM/ PMC2735879
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68. Graux C, Stevens-Kroef M, Lafage M, Dastugue N, Harrison CJ, Mugneret F, Bahloula K, Struski S, Grégoire MJ, Nadal N, Lippert E, Taviaux S, Simons A, Kuiper RP, Moorman AV, Barber K, Bosly A, Michaux L, Vandenberghe P, Lahortiga I, De Keersmaecker K, Wlodarska I, Cools J, Hagemeijer A, Poirel HA, Groupe Francophone de Cytogénétique Hématologique, Belgian Cytogenetic Group for Hematology and Oncology: Heterogeneous patterns of amplification of the NUP214-ABL1 fusion gene in T-cell acute lymphoblastic leukemia. Leukemia; 2009 Jan;23(1):125-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Heterogeneous patterns of amplification of the NUP214-ABL1 fusion gene in T-cell acute lymphoblastic leukemia.
  • An associated abnormality involving TLX1 or TLX3 was found in all investigated cases.
  • In addition, intrachromosomal amplification (small hsr) was identified either as the only change or in association with episomes in four cases and two T-ALL cell lines (PEER and ALL-SIL).
  • [MeSH-major] Gene Amplification. Leukemia-Lymphoma, Adult T-Cell / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Adolescent. Adult. Cell Line, Tumor. Child. Child, Preschool. Female. Homeodomain Proteins / genetics. Humans. Male. Middle Aged. Plasmids. Proto-Oncogene Proteins / genetics. Sex Factors. Treatment Outcome. Young Adult

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  • (PMID = 18923437.001).
  • [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 / Homeodomain Proteins; 0 / NUP214-ABL1 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / TLX3 protein, human; 143275-75-6 / TLX1 protein, human
  • [Investigator] Barin C; Berger R; Bilhou-Nabera C; Cabrol C; Callet-Bauchu E; Cornillet-Lefebvre P; Laï JL; Lefebvre C; Luquet I; Perot C; Radford-Weiss I; Speleman F; Cauwelier B; Talmant P; Terré C; Tigaud I; Van DenAkker J; Viguié F
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69. van Grotel M, van den Heuvel-Eibrink MM, van Wering ER, van Noesel MM, Kamps WA, Veerman AJ, Pieters R, Meijerink JP: CD34 expression is associated with poor survival in pediatric T-cell acute lymphoblastic leukemia. Pediatr Blood Cancer; 2008 Dec;51(6):737-40
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  • [Title] CD34 expression is associated with poor survival in pediatric T-cell acute lymphoblastic leukemia.
  • BACKGROUND: Children with T-lineage acute lymphoblastic leukemia (T-ALL) have an inferior outcome with combination chemotherapy compared to B-lineage ALL, and still about 30% of the patients relapse within the first 2 years following diagnosis.
  • As CD34 has been related with poor outcome in ALL in general, we investigated the prognostic significance of the stem cell marker CD34, as well as the association of CD34 positivity with the expression of several multidrug resistance (MDR) genes.
  • PROCEDURE: In this retrospective study, we investigated the prognostic significance of the expression of the early T-cell differentiation marker CD34 and the expression of MDR genes in relation to outcome in a cohort of 72 newly diagnosed pediatric T-ALL patients.
  • RESULTS: CD34 expression was related to a poor 5-year disease-free-survival and a poor 5-year overall survival.
  • [MeSH-major] Antigens, CD34 / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / mortality

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  • (PMID = 18683236.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / Antigens, CD34; 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; 0 / multidrug resistance-associated protein 1
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70. Cools J: Identification and characterization of novel oncogenes in chronic eosinophilic leukemia and T-cell acute lymphoblastic leukemia. Verh K Acad Geneeskd Belg; 2010;72(1-2):55-70
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  • [Title] Identification and characterization of novel oncogenes in chronic eosinophilic leukemia and T-cell acute lymphoblastic leukemia.
  • Insights into these mechanisms may help us to design novel strategies to treat leukemia.
  • Sorafenib was originally developed as a BRAF inhibitor, but our work demonstrates that sorafenib can also be used to treat FIP1L1-PDGFRA positive leukemia, demonstrating that new therapies to treat rare leukemias may be simply found by testing drugs that are already in use for the treatment of other diseases.
  • [MeSH-major] Hypereosinophilic Syndrome / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Platelet-Derived Growth Factor alpha / genetics. mRNA Cleavage and Polyadenylation Factors / genetics

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  • (PMID = 20726440.001).
  • [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
  • [Publication-country] Belgium
  • [Chemical-registry-number] 0 / Benzenesulfonates; 0 / FIP1L1-PDGFRA fusion protein, human; 0 / NUP214 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins; 0 / Oncogene Proteins, Fusion; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 0 / mRNA Cleavage and Polyadenylation Factors; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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71. De Keersmaecker K, Lahortiga I, Mentens N, Folens C, Van Neste L, Bekaert S, Vandenberghe P, Odero MD, Marynen P, Cools J: In vitro validation of gamma-secretase inhibitors alone or in combination with other anti-cancer drugs for the treatment of T-cell acute lymphoblastic leukemia. Haematologica; 2008 Apr;93(4):533-42
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  • [Title] In vitro validation of gamma-secretase inhibitors alone or in combination with other anti-cancer drugs for the treatment of T-cell acute lymphoblastic leukemia.
  • BACKGROUND: Activating NOTCH1 mutations are common in T-cell acute lymphoblastic leukemia.
  • Inhibition of NOTCH1 signaling with gamma-secretase inhibitors causes cell cycle block, but only after treatment for several days.
  • We further documented the effects of gamma-secretase inhibitor treatment on T-cell acute lymphoblastic leukemia cell lines and tested whether combining gamma-secretase inhibitors with other anti-cancer drugs offers a therapeutic advantage.
  • DESIGN AND METHODS: The effect of gamma-secretase inhibitor treatment and combinations of gamma-secretase inhibitors with chemotherapy or glucocorticoids was assessed on T-cell acute lymphoblastic leukemia cell lines.
  • We sequenced NOTCH1 in T-cell acute lymphoblastic leukemia cases with ABL1 fusions and tested combinations of gamma-secretase inhibitors and the ABL1 inhibitor imatinib in a T-cell acute lymphoblastic leukemia cell line.
  • RESULTS: gamma-secretase inhibitor treatment for 5-7 days reversibly inhibited cell proliferation, caused cell cycle block in sensitive T-cell acute lymphoblastic leukemia cell lines, and caused differentiation of some T-cell acute lymphoblastic leukemia cell lines.
  • The cytotoxic effects of the chemotherapeutic agent vincristine were not significantly enhanced by addition of gamma-secretase inhibitors to T-cell acute lymphoblastic leukemia cell lines, but gamma-secretase inhibitor treatment sensitized cells to the effect of dexamethasone.
  • NOTCH1 mutations were identified in all T-cell acute lymphoblastic leukemia patients with ABL1 fusions and in a T-cell acute lymphoblastic leukemia cell line expressing NUP214-ABL1.
  • In this cell line, the anti-proliferative effect of imatinib was increased by pre-treatment with gamma-secretase inhibitors.
  • CONCLUSIONS: Short-term treatment of T-cell acute lymphoblastic leukemia cell lines with gamma-secretase inhibitors had limited effects on cell proliferation and survival.
  • Combinations of gamma-secretase inhibitors with other drugs may be required to obtain efficient therapeutic effects in T-cell acute lymphoblastic leukemia, and not all combinations may be useful.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Antineoplastic Agents / pharmacology. Benzodiazepinones / pharmacology. Carbamates / pharmacology. Dipeptides / pharmacology. Enzyme Inhibitors / pharmacology. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Neoplasm Proteins / antagonists & inhibitors. Receptor, Notch1 / antagonists & inhibitors
  • [MeSH-minor] Apoptosis / drug effects. Benzamides. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor / drug effects. Cell Line, Tumor / enzymology. DNA, Neoplasm / genetics. Daunorubicin / administration & dosage. Daunorubicin / pharmacology. Dexamethasone / administration & dosage. Dexamethasone / pharmacology. Drug Screening Assays, Antitumor. Drug Synergism. Humans. Imatinib Mesylate. In Vitro Techniques. Mutation. Oncogene Proteins, Fusion / antagonists & inhibitors. Oncogene Proteins, Fusion / genetics. Piperazines / administration & dosage. Piperazines / pharmacology. Pyrimidines / administration & dosage. Pyrimidines / pharmacology. Sequence Analysis, DNA. Vincristine / administration & dosage. Vincristine / pharmacology

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  • [CommentIn] Haematologica. 2008 Apr;93(4):493-7 [18379008.001]
  • (PMID = 18322257.001).
  • [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 / 2-(((3,5-difluorophenyl)acetyl)amino)-N-(1-methyl-2-oxo-5-phenyl-2,3-dihydro-1H-1,4-benzodiazepin-3-yl)propanamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Benzodiazepinones; 0 / Carbamates; 0 / DNA, Neoplasm; 0 / Dipeptides; 0 / Enzyme Inhibitors; 0 / L 685458; 0 / NOTCH1 protein, human; 0 / NUP214-ABL1 fusion protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / Receptor, Notch1; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 8A1O1M485B / Imatinib Mesylate; EC 3.4.- / Amyloid Precursor Protein Secretases; ZS7284E0ZP / Daunorubicin
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72. Nelarabine (Arranon) for T-cell acute lymphoblastic leukemia. Med Lett Drugs Ther; 2006 Feb 13;48(1228):14-5
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  • [Title] Nelarabine (Arranon) for T-cell acute lymphoblastic leukemia.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Arabinonucleosides / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Lymphoma, T-Cell / drug therapy. Prodrugs / therapeutic use

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  • (PMID = 16467734.001).
  • [ISSN] 0025-732X
  • [Journal-full-title] The Medical letter on drugs and therapeutics
  • [ISO-abbreviation] Med Lett Drugs Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Arabinonucleosides; 0 / Prodrugs; 60158CV180 / nelarabine
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73. Scupoli MT, Donadelli M, Cioffi F, Rossi M, Perbellini O, Malpeli G, Corbioli S, Vinante F, Krampera M, Palmieri M, Scarpa A, Ariola C, Foà R, Pizzolo G: Bone marrow stromal cells and the upregulation of interleukin-8 production in human T-cell acute lymphoblastic leukemia through the CXCL12/CXCR4 axis and the NF-kappaB and JNK/AP-1 pathways. Haematologica; 2008 Apr;93(4):524-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bone marrow stromal cells and the upregulation of interleukin-8 production in human T-cell acute lymphoblastic leukemia through the CXCL12/CXCR4 axis and the NF-kappaB and JNK/AP-1 pathways.
  • BACKGROUND: Cytokines released in the bone marrow and thymic microenvironments play a key role in the growth of T-cell acute lymphoblastic leukemia.
  • Among such cytokines, interleukin-8 is highly expressed in T-cell acute lymphoblastic leukemia cells refractory to chemotherapy.
  • In this study we explored whether bone marrow stromal cells can regulate IL-8 expression in T-cell acute lymphoblastic leukemia and investigated the role of the stromal CXCL12 chemokine in this event.
  • DESIGN AND METHODS: We analyzed the expression of interleukin-8 in primary cells from ten adult patients with T-cell acute lymphoblastic leukemia when these cells were cultured with bone marrow stromal cells or stimulated with exogenous CXCL12.
  • Nuclear factor-kappaB and JNK/AP-1 activation was investigated by using specific inhibitors of these pathways, immunoblotting, electrophoretic mobility-shift assay and cell transfection assays.
  • RESULTS: Bone marrow stromal cells upregulated interleukin-8 mRNA in T-cell acute lymphoblastic leukemia cells through the activity of CXCR4, the CXCL12 receptor, as assessed by the use of neutralizing antibodies.
  • Exogenous CXCL12 induced a significant increase in the production of IL-8 mRNA and protein in all T-cell acute lymphoblastic leukemia cases.
  • CONCLUSIONS: Interleukin-8 is physiologically regulated by the CXCL12/CXCR4 axis and the nuclear factor-kappaB and JNK/AP-1 pathways are required for interleukin-8 expression in T-cell acute lymphoblastic leukemia.
  • We propose that, by upregulating interleukin-8, the bone marrow microenvironment and the CXCL12/CXCR4 axis may play a role in the pathogenesis of T-cell acute lymphoblastic leukemia.
  • [MeSH-major] Bone Marrow Cells / metabolism. Chemokine CXCL12 / physiology. Gene Expression Regulation, Leukemic / physiology. Interleukin-8 / biosynthesis. JNK Mitogen-Activated Protein Kinases / physiology. Leukemia-Lymphoma, Adult T-Cell / metabolism. NF-kappa B / physiology. Neoplasm Proteins / physiology. Receptors, CXCR4 / physiology. Stromal Cells / metabolism. Transcription Factor AP-1 / physiology. Up-Regulation / physiology

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  • [CommentIn] Haematologica. 2008 Apr;93(4):493-7 [18379008.001]
  • (PMID = 18322253.001).
  • [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 / CXCL12 protein, human; 0 / CXCR4 protein, human; 0 / Chemokine CXCL12; 0 / Interleukin-8; 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, CXCR4; 0 / Recombinant Fusion Proteins; 0 / Transcription Factor AP-1; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
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74. Epenetos AA, Kousparou C, Stylianou S: Inhibition of Notch and tumor regression. J Clin Oncol; 2009 May 20;27(15_suppl):e14623

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  • : 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
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75. Fauzdar A, Mahajan A, Jain D, Mishra M, Raina V: Amplification of RUNX1 gene in two new cases of childhood B-cell precursor acute lymphoblastic leukemia: A case report. J Clin Oncol; 2009 May 20;27(15_suppl):e21000

  • [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
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76. Nagel S, Scherr M, Kel A, Hornischer K, Crawford GE, Kaufmann M, Meyer C, Drexler HG, MacLeod RA: Activation of TLX3 and NKX2-5 in t(5;14)(q35;q32) T-cell acute lymphoblastic leukemia by remote 3'-BCL11B enhancers and coregulation by PU.1 and HMGA1. Cancer Res; 2007 Feb 15;67(4):1461-71
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  • [Title] Activation of TLX3 and NKX2-5 in t(5;14)(q35;q32) T-cell acute lymphoblastic leukemia by remote 3'-BCL11B enhancers and coregulation by PU.1 and HMGA1.
  • In T-cell acute lymphoblastic leukemia, alternative t(5;14)(q35;q32.2) forms effect dysregulation of either TLX3 or NKX2-5 homeobox genes at 5q35 by juxtaposition with 14q32.2 breakpoints dispersed across the BCL11B downstream genomic desert.
  • Leukemic gene dysregulation by t(5;14) was investigated by DNA inhibitory treatments with 26-mer double-stranded DNA oligonucleotides directed against candidate enhancers at, or near, orphan T-cell DNase I hypersensitive sites located between 3'-BCL11B and VRK1.
  • We suggest that HMGA1 and PU.1 coregulate ectopic homeobox gene expression in t(5;14) T-cell acute lymphoblastic leukemia by interactions mediated at the nuclear matrix.
  • [MeSH-major] DNA-Binding Proteins / genetics. Gene Expression Regulation, Leukemic. HMGA Proteins / genetics. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Oncogene Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins / genetics. Repressor Proteins / genetics. Trans-Activators / genetics. Transcription Factors / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 17308084.001).
  • [ISSN] 0008-5472
  • [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 / BCL11B protein, human; 0 / DNA-Binding Proteins; 0 / HMGA Proteins; 0 / Histones; 0 / Homeodomain Proteins; 0 / NKX2-5 protein, human; 0 / Oligonucleotides; 0 / Oncogene Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 0 / Repressor Proteins; 0 / TLX3 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / proto-oncogene protein Spi-1; EC 3.1.21.1 / Deoxyribonuclease I
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77. Nishimoto N, Imai Y, Ueda K, Nakagawa M, Shinohara A, Ichikawa M, Nannya Y, Kurokawa M: T cell acute lymphoblastic leukemia arising from familial platelet disorder. Int J Hematol; 2010 Jul;92(1):194-7
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  • [Title] T cell acute lymphoblastic leukemia arising from familial platelet disorder.
  • Familial platelet disorder (FPD) is a rare autosomal dominant disorder which causes moderate thrombocytopenia with or without impaired platelet function.
  • Patients have a propensity to develop acute myeloid leukemia (AML), and various types of second hits have been postulated in the evolution to AML.
  • However, only a few cases of acute lymphoblastic leukemia (ALL) have been reported thus far.
  • The proband of the family developed AML and her son had ALL of the T cell lineage.
  • Taken together, t(1;7)(p34.1;q22) is thought to be one of the somatic second hits that predisposes FPD to acute leukemia with T cell phenotype.
  • [MeSH-major] Blood Platelet Disorders / complications. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / etiology

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  • (PMID = 20549580.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit
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78. Cooper TM: Role of nelarabine in the treatment of T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma. Ther Clin Risk Manag; 2007 Dec;3(6):1135-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of nelarabine in the treatment of T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma.
  • T-cell malignancies have distinct biochemical, immunologic, and clinical features which set them apart from non-T-cell malignancies.
  • In the past, T-cell leukemia portended a worse prognosis than leukemia of B-cell origin.
  • Cure rates have improved with intensification of therapy and advanced understanding of the molecular genetics of T-cell malignancies.
  • Further advances in the treatment of T-cell leukemia will require the development of novel agents that can target specific malignancies without a significant increase in toxicity.
  • Food and Drug Administration (FDA) for the treatment of relapsed/refractory T-ALL and T-LBL in adults and children.
  • Nelarabine is water soluble and rapidly converted to ara-G, which is specifically cytotoxic to T-lymphocytes and T-lymphoblastoid cells.
  • Clinical and pharmacokinetic investigations have established that nelarabine is active as a single agent which has led to exploration of an expanded role in the treatment of T-cell hematologic malignances.

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  • (PMID = 18516261.001).
  • [ISSN] 1176-6336
  • [Journal-full-title] Therapeutics and clinical risk management
  • [ISO-abbreviation] Ther Clin Risk Manag
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2387290
  • [Keywords] NOTNLM ; 9-β-D-arabinofuranosylguanine / T-cell acute lymphoblastic leukemia / nelarabine
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79. Schrauder A, Reiter A, Gadner H, Niethammer D, Klingebiel T, Kremens B, Peters C, Ebell W, Zimmermann M, Niggli F, Ludwig WD, Riehm H, Welte K, Schrappe M: Superiority of allogeneic hematopoietic stem-cell transplantation compared with chemotherapy alone in high-risk childhood T-cell acute lymphoblastic leukemia: results from ALL-BFM 90 and 95. J Clin Oncol; 2006 Dec 20;24(36):5742-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Superiority of allogeneic hematopoietic stem-cell transplantation compared with chemotherapy alone in high-risk childhood T-cell acute lymphoblastic leukemia: results from ALL-BFM 90 and 95.
  • PURPOSE: The role of hematopoietic stem-cell transplantation (SCT) in first complete remission (CR1) for children with very high-risk (VHR) acute lymphoblastic leukemia (ALL) is still under critical discussion.
  • T-cell ALL (T-ALL) patients with poor in vivo response to initial treatment represented the largest homogeneous subgroup within VHR patients.
  • The median time to SCT was 5 months (range, 2.4 to 10.8 months) from diagnosis.
  • The 5-year disease-free survival (DFS) was 67% +/- 8% for 36 patients who received an SCT in CR1 and 42% +/- 5% for the 120 patients treated with chemotherapy alone having an event-free survival time of at least the median time to transplantation (Mantel-Byar, P = .01).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Histocompatibility Testing. Humans. Infant. Infant, Newborn. Male. Risk Factors. Transplantation, Homologous


80. Smith AC, Raimondi AR, Salthouse CD, Ignatius MS, Blackburn JS, Mizgirev IV, Storer NY, de Jong JL, Chen AT, Zhou Y, Revskoy S, Zon LI, Langenau DM: High-throughput cell transplantation establishes that tumor-initiating cells are abundant in zebrafish T-cell acute lymphoblastic leukemia. Blood; 2010 Apr 22;115(16):3296-303
ZFIN. ZFIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-throughput cell transplantation establishes that tumor-initiating cells are abundant in zebrafish T-cell acute lymphoblastic leukemia.
  • Self-renewal is a feature of cancer and can be assessed by cell transplantation into immune-compromised or immune-matched animals.
  • Here, Myc-induced T-cell acute lymphoblastic leukemias (T-ALLs) have been made in syngeneic, clonal zebrafish and can be transplanted into sibling animals without the need for immune suppression.
  • Large-scale single-cell transplantation experiments established that T-ALLs can be initiated from a single cell and that leukemias exhibit wide differences in tumor-initiating potential.
  • T-ALLs also can be introduced into clonal-outcrossed animals, and T-ALLs arising in mixed genetic backgrounds can be transplanted into clonal recipients without the need for major histocompatibility complex matching.
  • Our experiments highlight the large numbers of zebrafish that can be experimentally assessed by cell transplantation and establish new high-throughput methods to functionally interrogate gene pathways involved in cancer self-renewal.

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  • (PMID = 20056790.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 5 R01 CA103846-04; United States / NIGMS NIH HHS / GM / T32 GM007753; United States / NCI NIH HHS / CA / R01 CA103846; United States / NIAMS NIH HHS / AR / 3 K01 AR055619-03S1; United States / NIAMS NIH HHS / AR / K01 AR055619-01A1; United States / NIAMS NIH HHS / AR / K01 AR055619
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2858492
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81. Malyukova A, Dohda T, von der Lehr N, Akhoondi S, Corcoran M, Heyman M, Spruck C, Grandér D, Lendahl U, Sangfelt O: The tumor suppressor gene hCDC4 is frequently mutated in human T-cell acute lymphoblastic leukemia with functional consequences for Notch signaling. Cancer Res; 2007 Jun 15;67(12):5611-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The tumor suppressor gene hCDC4 is frequently mutated in human T-cell acute lymphoblastic leukemia with functional consequences for Notch signaling.
  • Notch signaling is of crucial importance in normal T-cell development and Notch 1 is frequently mutated in T-cell acute lymphoblastic leukemias (T-ALL), leading to aberrantly high Notch signaling.
  • We show that the hCDC4 gene is mutated in leukemic cells from more than 30% of patients with pediatric T-ALL and derived cell lines.
  • Cells inactivated for hCdc4 and T-ALL cells containing hCDC4 mutations exhibited an increased Notch1 protein half-life, consistent with the proposed role of hCdc4 in ubiquitin-dependent proteolysis of Notch1.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Receptor, Notch1 / metabolism. Signal Transduction / physiology. Ubiquitin-Protein Ligases / genetics

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  • [ErratumIn] Cancer Res. 2008 Mar 15;68(6):2051. Akhondi, Shahab [corrected to Akhoondi, Shahab]
  • (PMID = 17575125.001).
  • [ISSN] 0008-5472
  • [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 / 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
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82. Sudhakar N, Nancy NK, Rajalekshmy KR, Ramanan G, Rajkumar T: T-cell receptor gamma and delta gene rearrangements and junctional region characteristics in south Indian patients with T-cell acute lymphoblastic leukemia. Am J Hematol; 2007 Mar;82(3):215-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell receptor gamma and delta gene rearrangements and junctional region characteristics in south Indian patients with T-cell acute lymphoblastic leukemia.
  • Clonal T-cell receptor (TCR) gamma and delta gene rearrangements were studied in 40 T-ALL cases (pediatrics, 29; adults, 11) using PCR with homo-heteroduplex analysis.
  • The junctional region of TCRD is more diverse than TCRG; nevertheless, the frequency of TCRG was more than that of TCRD and hence we rely more on TCRG clonal markers to quantitate the minimal residual disease in T-ALL.
  • [MeSH-major] Aging / genetics. Gene Rearrangement, delta-Chain T-Cell Antigen Receptor / genetics. Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor / genetics. Genes, T-Cell Receptor delta / genetics. Genes, T-Cell Receptor gamma / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics

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  • [Copyright] Copyright (c) 2006 Wiley-Liss, Inc.
  • (PMID = 17133429.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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83. Masuda S, Kumano K, Suzuki T, Tomita T, Iwatsubo T, Natsugari H, Tojo A, Shibutani M, Mitsumori K, Hanazono Y, Ogawa S, Kurokawa M, Chiba S: Dual antitumor mechanisms of Notch signaling inhibitor in a T-cell acute lymphoblastic leukemia xenograft model. Cancer Sci; 2009 Dec;100(12):2444-50
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  • [Title] Dual antitumor mechanisms of Notch signaling inhibitor in a T-cell acute lymphoblastic leukemia xenograft model.
  • Constitutive activation of Notch signaling is required for the proliferation of a subgroup of human T-cell acute lymphoblastic leukemias (T-ALL).
  • Treatment of established subcutaneous tumors with GSI resulted in partial or complete regression of tumors arising from four T-ALL cell lines that were also sensitive to GSI in vitro.
  • These findings indicate that the remarkable efficacy of GSI might be attributable to dual mechanisms, directly via apoptosis of DND-41 cells through the inhibition of cell-autonomous Notch signaling, and indirectly via disturbance of tumor angiogenesis through the inhibition of non-cell-autonomous Notch signaling.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Antineoplastic Agents / pharmacology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Receptors, Notch / antagonists & inhibitors. Signal Transduction / drug effects
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Mice. Mice, SCID. Xenograft Model Antitumor Assays

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  • (PMID = 19775286.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Notch; EC 3.4.- / Amyloid Precursor Protein Secretases
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84. Bacher U, Haferlach T, Kern W, Harich HD, Schnittger S, Haferlach C: A case of chronic myeloproliferative syndrome followed by precursor T-cell acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2007 May;175(1):52-6
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  • [Title] A case of chronic myeloproliferative syndrome followed by precursor T-cell acute lymphoblastic leukemia.
  • Interlineage switch from myeloid to lymphatic malignancies is a rare phenomenon.
  • Progression from a BCR-ABL negative chronic myeloproliferative disorder (CMPD) to acute lymphoblastic leukemia (ALL) has been reported in very few cases.
  • We describe the case of a 62-year-old man who developed precursor T-cell (pre-T) ALL 18 months after the diagnosis of an unclassifiable chronic myeloproliferative syndrome (CMPD, U), which had been treated with hydroxyurea (HU) over 12 months.
  • Diverse pathways should be considered in this transformation process: although therapeutic induction of ALL is extremely rare and no MLL/11q23 rearrangement was detected by chromosome banding analyses and interphase fluorescence in situ hybridization (FISH), T-lineage ALL might have been caused by HU therapy for the CMPD.
  • Chance coincidence of both disorders seems improbable, given the short interval from the diagnosis of the CMPD to the development of the pre-T-ALL, but nonetheless must be considered.
  • A third explanation might be provided by a spontaneous interlineage switch, which would give further support to the theory that the CMPDs are disorders of a pluripotent stem cell.
  • Interlineage switch might result from an aberrant differentiation of the malignant clone or from selection within a mixed population.
  • [MeSH-major] Myeloproliferative Disorders / pathology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Cell Transformation, Neoplastic / genetics. Chromosome Aberrations. Chromosome Banding. Chromosome Painting. Disease Progression. Humans. Hydroxyurea / therapeutic use. Karyotyping. Male. Middle Aged. Nucleic Acid Synthesis Inhibitors / therapeutic use. Syndrome

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  • (PMID = 17498558.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nucleic Acid Synthesis Inhibitors; X6Q56QN5QC / Hydroxyurea
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85. Leung KT, Li KK, Sun SS, Chan PK, Ooi VE, Chiu LC: Activation of the JNK pathway promotes phosphorylation and degradation of BimEL--a novel mechanism of chemoresistance in T-cell acute lymphoblastic leukemia. Carcinogenesis; 2008 Mar;29(3):544-51
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  • [Title] Activation of the JNK pathway promotes phosphorylation and degradation of BimEL--a novel mechanism of chemoresistance in T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemias (T-ALLs) are highly malignant tumors with 20% of patients continues to fail therapy, in part due to chemoresistance of T-ALL cells via largely unknown mechanisms.
  • Here, we showed that lack of Bcl-2-interacting mediator of cell death (Bim)(EL) protein expression, a BH3-only member of the Bcl-2 family proteins, conferred resistance of a T-ALL cell line, Sup-T1, to etoposide-induced apoptosis.
  • [MeSH-major] Apoptosis Regulatory Proteins / metabolism. Drug Resistance, Neoplasm. Leukemia-Lymphoma, Adult T-Cell / metabolism. MAP Kinase Kinase 4 / metabolism. Membrane Proteins / metabolism. Proto-Oncogene Proteins / metabolism


86. Chiarini F, Falà F, Tazzari PL, Ricci F, Astolfi A, Pession A, Pagliaro P, McCubrey JA, Martelli AM: Dual inhibition of class IA phosphatidylinositol 3-kinase and mammalian target of rapamycin as a new therapeutic option for T-cell acute lymphoblastic leukemia. Cancer Res; 2009 Apr 15;69(8):3520-8
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  • [Title] Dual inhibition of class IA phosphatidylinositol 3-kinase and mammalian target of rapamycin as a new therapeutic option for T-cell acute lymphoblastic leukemia.
  • Recent investigations have documented that constitutively activated 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 strongly influences growth and survival.
  • Here, we have analyzed the therapeutic potential of the dual PI3K/mTOR inhibitor PI-103, a small synthetic molecule of the pyridofuropyrimidine class, on both T-ALL cell lines and patient samples, which displayed constitutive activation of PI3K/Akt/mTOR signaling.
  • PI-103 induced G(0)-G(1) phase cell cycle arrest and apoptosis, which was characterized by activation of caspase-3 and caspase-9.


87. Chinen Y, Taki T, Nishida K, Shimizu D, Okuda T, Yoshida N, Kobayashi C, Koike K, Tsuchida M, Hayashi Y, Taniwaki M: Identification of the novel AML1 fusion partner gene, LAF4, a fusion partner of MLL, in childhood T-cell acute lymphoblastic leukemia with t(2;21)(q11;q22) by bubble PCR method for cDNA. Oncogene; 2008 Apr 3;27(15):2249-56
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  • [Title] Identification of the novel AML1 fusion partner gene, LAF4, a fusion partner of MLL, in childhood T-cell acute lymphoblastic leukemia with t(2;21)(q11;q22) by bubble PCR method for cDNA.
  • The AML1 gene is frequently rearranged by chromosomal translocations in acute leukemia.
  • We identified that the LAF4 gene on 2q11.2-12 was fused to the AML1 gene on 21q22 in a pediatric patient having T-cell acute lymphoblastic leukemia (T-ALL) with t(2;21)(q11;q22) using the bubble PCR method for cDNA.
  • LAF4 is the first gene fused with both AML1 and MLL in acute leukemia.
  • Almost all AML1 translocations except for TEL-AML1 are associated with myeloid leukemia; however, AML1-LAF4 was associated with T-ALL as well as AML1-FGA7 in t(4;21)(q28;q22).
  • [MeSH-major] Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 21. Core Binding Factor Alpha 2 Subunit / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Fusion / genetics. Polymerase Chain Reaction / methods. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Base Sequence. Child. DNA Mutational Analysis / methods. DNA, Complementary / analysis. Humans. Male. Models, Biological. Molecular Sequence Data

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  • (PMID = 17968322.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AFF3 protein, human; 0 / AML1-LAF4 fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA, Complementary; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human
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88. Falà F, Blalock WL, Tazzari PL, Cappellini A, Chiarini F, Martinelli G, Tafuri A, McCubrey JA, Cocco L, Martelli AM: Proapoptotic activity and chemosensitizing effect of the novel Akt inhibitor (2S)-1-(1H-Indol-3-yl)-3-[5-(3-methyl-2H-indazol-5-yl)pyridin-3-yl]oxypropan2-amine (A443654) in T-cell acute lymphoblastic leukemia. Mol Pharmacol; 2008 Sep;74(3):884-95
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  • [Title] Proapoptotic activity and chemosensitizing effect of the novel Akt inhibitor (2S)-1-(1H-Indol-3-yl)-3-[5-(3-methyl-2H-indazol-5-yl)pyridin-3-yl]oxypropan2-amine (A443654) in T-cell acute lymphoblastic leukemia.
  • Constitutively activated AKT kinase is a common feature of T-cell acute lymphoblastic leukemia (T-ALL).
  • Here, we report that the novel AKT inhibitor (2S)-1-(1H-indol-3-yl)-3-[5-(3-methyl-2H-indazol-5-yl)pyridin-3-yl]oxypropan2-amine (A443654) leads to rapid cell death of T-ALL lines and patient samples.
  • Effects were time- and dose-dependent, resulting in apoptotic cell death.
  • Apoptotic cell death was mostly dependent on caspase-2 activation, as demonstrated by preincubation with a selective pharmacological inhibitor.
  • It is remarkable that A443654 was highly effective against the drug-resistant cell line CEM-VBL100, which expresses 170-kDa P-glycoprotein.
  • Moreover, A443654 synergized with the DNA-damaging agent etoposide in both drug-sensitive and drug-resistant cell lines when coadministered [combination index (CI) = 0.39] or when pretreated with etoposide followed by A443654 (CI = 0.689).
  • At 1 microM, the inhibitor was able to induce apoptotic cell death of T-ALL blast cells, as indicated by flow cytometric analysis of samples immunostained for active (cleaved) caspase-3.

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  • (PMID = 18577685.001).
  • [ISSN] 1521-0111
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA098195-05; United States / NCI NIH HHS / CA / R01 CA098195-05; United States / NCI NIH HHS / CA / R01-CA091025
  • [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 / A 443654; 0 / Indazoles; 0 / Indoles; 1114-81-4 / Phosphothreonine; 17885-08-4 / Phosphoserine; 6PLQ3CP4P3 / Etoposide; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ NIHMS79780; NLM/ PMC2659779
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89. Karrman K, Andersson A, Björgvinsdóttir H, Strömbeck B, Lassen C, Olofsson T, Nguyen-Khac F, Berger R, Bernard O, Fioretos T, Johansson B: Deregulation of cyclin D2 by juxtaposition with T-cell receptor alpha/delta locus in t(12;14)(p13;q11)-positive childhood T-cell acute lymphoblastic leukemia. Eur J Haematol; 2006 Jul;77(1):27-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Deregulation of cyclin D2 by juxtaposition with T-cell receptor alpha/delta locus in t(12;14)(p13;q11)-positive childhood T-cell acute lymphoblastic leukemia.
  • OBJECTIVES: The t(12;14)(p13;q11)--a recurrent translocation in childhood T-cell acute lymphoblastic leukemia (T-ALL)--has very recently been molecularly characterized in one case, which displayed overexpression of the cyclin D2 gene (CCND2).
  • RESULTS: FISH revealed breakpoints (BPs) in the T-cell receptor alpha/delta locus (14q11) and in the vicinity of the CCND2 gene at 12p13.
  • Furthermore, it is the first example of a T-cell neoplasm with a targeted deregulation of a member of a cyclin-encoding gene family.
  • [MeSH-major] Cyclins / genetics. Gene Expression Regulation, Neoplastic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell, alpha-beta / genetics. Receptors, Antigen, T-Cell, gamma-delta / genetics. Translocation, Genetic

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  • (PMID = 16548914.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / CCND2 protein, human; 0 / Cyclin D2; 0 / Cyclins; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Antigen, T-Cell, gamma-delta
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90. Liu JY, Li ZG, Gao C, Cui L, Wu MY: [Characteristics of T cell receptor beta gene rearrangements and its role in minimal residual disease detection in childhood T-cell acute lymphoblastic leukemia]. Zhonghua Er Ke Za Zhi; 2008 Jul;46(7):487-92
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  • [Title] [Characteristics of T cell receptor beta gene rearrangements and its role in minimal residual disease detection in childhood T-cell acute lymphoblastic leukemia].
  • OBJECTIVE: To explore the characteristics of T cell receptor beta (TCRbeta) gene rearrangements in children with T-cell acute lymphoblastic leukemia (T-ALL) and establish a system of quantitative detection of MRD with real-time quantitative (RQ-PCR) targeted at TCRbeta gene rearrangement.
  • Samples at diagnosis were serially diluted in DNA obtained from mononuclear cells (MNC) from a pool of 20 healthy donors to generate the patient specific standard curves.
  • [MeSH-major] Gene Rearrangement, beta-Chain T-Cell Antigen Receptor / genetics. Neoplasm, Residual / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19099802.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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91. Kovac L, Bilić M, Bumber B, Topić I: Primary laryngeal manifestation in precursor T-cell acute lymphoblastic leukemia. Otolaryngol Head Neck Surg; 2008 Sep;139(3):474-5
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  • [Title] Primary laryngeal manifestation in precursor T-cell acute lymphoblastic leukemia.
  • [MeSH-major] Airway Obstruction / etiology. Glottis. Laryngeal Neoplasms / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Precursor Cells, T-Lymphoid. Tracheal Stenosis / etiology

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  • (PMID = 18722237.001).
  • [ISSN] 0194-5998
  • [Journal-full-title] Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery
  • [ISO-abbreviation] Otolaryngol Head Neck Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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92. Guastadisegni MC, Lonoce A, Impera L, Albano F, D'Addabbo P, Caruso S, Vasta I, Panagopoulos I, Leszl A, Basso G, Rocchi M, Storlazzi CT: Bone marrow ectopic expression of a non-coding RNA in childhood T-cell acute lymphoblastic leukemia with a novel t(2;11)(q11.2;p15.1) translocation. Mol Cancer; 2008;7:80
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  • [Title] Bone marrow ectopic expression of a non-coding RNA in childhood T-cell acute lymphoblastic leukemia with a novel t(2;11)(q11.2;p15.1) translocation.
  • T-cell acute lymphoblastic leukemia (T-ALL) is associated with a large number of such rearrangements.
  • We report the ectopic expression of the 3' portion of EST DA926692 in the bone marrow of a childhood T-ALL case showing a t(2;11)(q11.2;p15.1) translocation as the sole chromosome abnormality.
  • [MeSH-major] Bone Marrow / metabolism. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 2 / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA, Untranslated / genetics. Translocation, Genetic


93. Asnafi V, Buzyn A, Thomas X, Huguet F, Vey N, Boiron JM, Reman O, Cayuela JM, Lheritier V, Vernant JP, Fiere D, Macintyre E, Dombret H: Impact of TCR status and genotype on outcome in adult T-cell acute lymphoblastic leukemia: a LALA-94 study. Blood; 2005 Apr 15;105(8):3072-8
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  • [Title] Impact of TCR status and genotype on outcome in adult T-cell acute lymphoblastic leukemia: a LALA-94 study.
  • Patients with T-cell acute lymphoblastic leukemias (T-ALLs) within the Leucemies Aigues Lymphoblastiques de l'Adulte-94 (LALA-94) prospective trial were treated with a 4-drug per 4-week induction, with intermediate-dose cytarabine and mitoxantrone salvage treatment for patients not achieving complete remission (CR) in 1 course.
  • Representative patients with T-ALL (91 patients) were classified into surface T-cell receptor (TCR)-expressing T-ALL patients (TCRalphabeta+ or TCRgammadelta+), pre-alphabeta T-ALL patients (cTCRbeta+, TCR-), and immature (IM) cTCRbeta-, TCR- T-ALL patients; 81 patients underwent genotyping for SIL-TAL1, CALM-AF10, HOX11, and HOX11L2.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell / genetics

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  • (PMID = 15637138.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Receptors, Antigen, T-Cell; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone
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94. Fiorentino S, Chopin M, Dastot H, Boissel N, Reboul M, Legrès L, Janin A, Aplan P, Sigaux F, Regnault A: Disruption of T cell regulatory pathways is necessary for immunotherapeutic cure of T cell acute lymphoblastic leukemia in mice. Eur Cytokine Netw; 2005 Dec;16(4):300-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Disruption of T cell regulatory pathways is necessary for immunotherapeutic cure of T cell acute lymphoblastic leukemia in mice.
  • Acute lymphoblastic leukemia (ALL) is the most common cancer in children.
  • In recent years, the outcome has been globally improved by current therapies, but it remains poor in patients with high, persistent residual disease following the first course of chemotherapy, prompting evaluation of the possible beneficial effects of immunotherapy protocols.
  • In this study, we hypothesized that the disruption of two immunoregulatory pathways controlling the auto-reactive T cell response might synergize with dendritic cell-based immunotherapy of the disease, which is considered to be poorly immunogenic.
  • In this study, we used TAL1xLMO1 leukemia cells adoptively transferred in mice, to generate murine leukemia with poorly immunogenic cells as a model for human T-ALL.
  • We compared the efficiency of a classical, dendritic cell-based immunotherapy (injection of dendritic cells loaded with tumor-derived antigenic products), to a combined treatment associating injection of antigen-loaded dendritic cells and disruption of the two immunoregulatory pathways: CD25+ suppressive T cells and cytotoxic T lymphocyte-associated antigens (CTLA-4).
  • [MeSH-major] Immunotherapy, Adoptive. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / therapy. Signal Transduction / immunology. T-Lymphocytes / immunology
  • [MeSH-minor] Animals. Antigens, CD / metabolism. Antigens, Neoplasm / administration & dosage. CTLA-4 Antigen. Cell Line, Tumor. Dendritic Cells / immunology. Dendritic Cells / metabolism. Dendritic Cells / transplantation. Disease Models, Animal. Immunologic Memory. Interleukin-2 Receptor alpha Subunit / biosynthesis. Lymphocyte Depletion. Mice. Mice, Inbred C3H. Mice, Inbred C57BL. T-Lymphocytes, Regulatory / immunology. T-Lymphocytes, Regulatory / metabolism. Tumor Necrosis Factor-alpha / secretion

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  • (PMID = 16464745.001).
  • [ISSN] 1148-5493
  • [Journal-full-title] European cytokine network
  • [ISO-abbreviation] Eur. Cytokine Netw.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CTLA-4 Antigen; 0 / CTLA4 protein, human; 0 / Ctla4 protein, mouse; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Tumor Necrosis Factor-alpha
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95. Borriello A, Locasciulli A, Bianco AM, Criscuolo M, Conti V, Grammatico P, Cappellacci S, Zatterale A, Morgese F, Cucciolla V, Delia D, Della Ragione F, Savoia A: A novel Leu153Ser mutation of the Fanconi anemia FANCD2 gene is associated with severe chemotherapy toxicity in a pediatric T-cell acute lymphoblastic leukemia. Leukemia; 2007 Jan;21(1):72-8
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  • [Title] A novel Leu153Ser mutation of the Fanconi anemia FANCD2 gene is associated with severe chemotherapy toxicity in a pediatric T-cell acute lymphoblastic leukemia.
  • Fanconi anemia (FA) is an autosomal recessive disease characterized by pancitopenia, congenital malformations, predisposition to cancers and chromosomal instability.
  • We report the clinical and molecular features of a patient initially identified as a potential FA case only because of chemotherapy toxicity during the treatment of a T-lineage acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Fanconi Anemia Complementation Group D2 Protein / genetics. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation
  • [MeSH-minor] Amino Acid Substitution. Antigens, CD. Antigens, CD13. Antigens, Differentiation, Myelomonocytic. Child. Chromosomal Instability. Disease Progression. Fanconi Anemia / genetics. Humans. Infection / etiology. Infection / genetics. Male. Pancytopenia / chemically induced. Pancytopenia / genetics. Remission Induction. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 17096012.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] Italy / Telethon / / TI/ TGM06S01
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / FANCD2 protein, human; 0 / Fanconi Anemia Complementation Group D2 Protein; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
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96. Roman-Gomez J, Jimenez-Velasco A, Agirre X, Prosper F, Heiniger A, Torres A: Lack of CpG island methylator phenotype defines a clinical subtype of T-cell acute lymphoblastic leukemia associated with good prognosis. J Clin Oncol; 2005 Oct 1;23(28):7043-9
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  • [Title] Lack of CpG island methylator phenotype defines a clinical subtype of T-cell acute lymphoblastic leukemia associated with good prognosis.
  • PURPOSE: To examine cancer genes undergoing epigenetic inactivation in a set of T-cell acute lymphoblastic leukemias (T-ALLs) to obtain the CpG island methylator phenotype (CIMP) in the disease and its possible correlation with clinical features and outcome of the patients.
  • Results were compared with results obtained in 286 B-cell acute lymphoblastic leukemias (B-ALLs).
  • Estimated disease-free survival (DFS) rate at 12 years and overall survival (OS) rate at 13 years were 100% and 91% for the CIMP- group and 20% and 17% for the CIMP+ group, respectively (P = .0006 and P = .003, respectively).
  • [MeSH-major] CpG Islands / genetics. DNA Methylation. Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


97. Arima K, Hasegawa D, Ogawa C, Kato I, Imamura T, Takusagawa A, Takahashi H, Kitagawa Y, Hori T, Tsurusawa M, Manabe A, Hosoya R: Detection of submicroscopic disease in the bone marrow and unaffected testis of a child with T-cell acute lymphoblastic leukemia who experienced "isolated" testicular relapse. Int J Hematol; 2009 Oct;90(3):370-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of submicroscopic disease in the bone marrow and unaffected testis of a child with T-cell acute lymphoblastic leukemia who experienced "isolated" testicular relapse.
  • Testicular relapse has an impact on the prognosis of boys with acute lymphoblastic leukemia (ALL).
  • A 12-year-old boy with T-ALL suffered from isolated testicular relapse at 27 months after diagnosis.
  • We retrospectively estimated the minimal residual disease in the bone marrow (BM) and the testis by detection of clone-specific T-cell receptor rearrangement of leukemic cells.
  • We detected leukemic cells in the affected testis at relapse, as well as in the BM at initial diagnosis.
  • In addition, we confirmed submicroscopic disease in the unaffected testis and the BM at relapse.
  • We conclude that molecular analysis could reveal the submicroscopic disease in the patient with apparently isolated testicular relapse.
  • This finding may provide a rationale for intensified systemic treatment of patients with isolated testicular relapse.
  • [MeSH-major] Bone Marrow / pathology. Neoplasm Recurrence, Local / pathology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Testicular Neoplasms / pathology. Testis / pathology

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  • (PMID = 19688235.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; ZS7284E0ZP / Daunorubicin; PVDA protocol
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98. Jabbour E, Koscielny S, Sebban C, Peslin N, Patte C, Gargi T, Biron P, Fermé C, Bourhis JH, Vantelon JM, Arnaud P, Ribrag V: High survival rate with the LMT-89 regimen in lymphoblastic lymphoma (LL), but not in T-cell acute lymphoblastic leukemia (T-ALL). Leukemia; 2006 May;20(5):814-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High survival rate with the LMT-89 regimen in lymphoblastic lymphoma (LL), but not in T-cell acute lymphoblastic leukemia (T-ALL).
  • The most appropriate treatment for lymphoblastic lymphomas (LL) remains uncertain.
  • Four patients had central nervous system involvement and 12 had bone marrow involvement and 24/27 (89%) had advanced Ann Arbor stage III-IV disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Bone Marrow / pathology. Disease Progression. Disease-Free Survival. Dose-Response Relationship, Drug. Female. Follow-Up Studies. Humans. Male. Middle Aged. Predictive Value of Tests. Prognosis. Remission Induction. Survival Rate. Treatment Outcome

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  • (PMID = 16511514.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] England
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99. Vitale A, Guarini A, Ariola C, Mancini M, Mecucci C, Cuneo A, Pane F, Saglio G, Cimino G, Tafuri A, Meloni G, Fabbiano F, Recchia A, Kropp MG, Krampera M, Cascavilla N, Ferrara F, Romano A, Mazza P, Fozza C, Paoloni F, Vignetti M, Foà R: Adult T-cell acute lymphoblastic leukemia: biologic profile at presentation and correlation with response to induction treatment in patients enrolled in the GIMEMA LAL 0496 protocol. Blood; 2006 Jan 15;107(2):473-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell acute lymphoblastic leukemia: biologic profile at presentation and correlation with response to induction treatment in patients enrolled in the GIMEMA LAL 0496 protocol.
  • Between 1996 and 2000, 90 newly diagnosed adult patients with T-acute lymphoblastic leukemia (T-ALL) were registered in the Gruppo Italiano Malattie Ematologiche dell'Adulto (GIMEMA) Leucemia Acuta Limfoide (LAL) 0496 protocol.
  • Thirty-one (36.5%) of 85 patients had an abnormal karyotype, the most common abnormality (15%) being a partial del(6q).
  • [MeSH-major] Chromosome Aberrations. Leukemia-Lymphoma, Adult T-Cell. Oncogene Proteins, Fusion / metabolism. P-Glycoprotein / metabolism
  • [MeSH-minor] Adolescent. Adult. Cytogenetic Analysis. Drug Resistance, Multiple. Female. Humans. Immunophenotyping. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Prognosis. Remission Induction. Treatment Outcome

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  • (PMID = 16179376.001).
  • [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 / Oncogene Proteins, Fusion; 0 / P-Glycoprotein
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100. Rao SS, O'Neil J, Liberator CD, Hardwick JS, Dai X, Zhang T, Tyminski E, Yuan J, Kohl NE, Richon VM, Van der Ploeg LH, Carroll PM, Draetta GF, Look AT, Strack PR, Winter CG: Inhibition of NOTCH signaling by gamma secretase inhibitor engages the RB pathway and elicits cell cycle exit in T-cell acute lymphoblastic leukemia cells. Cancer Res; 2009 Apr 1;69(7):3060-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of NOTCH signaling by gamma secretase inhibitor engages the RB pathway and elicits cell cycle exit in T-cell acute lymphoblastic leukemia cells.
  • NOTCH signaling is deregulated in the majority of T-cell acute lymphoblastic leukemias (T-ALL) as a result of activating mutations in NOTCH1.
  • We have investigated the mechanisms of GSI sensitivity across a panel of T-ALL cell lines, yielding an approach for patient stratification based on pathway activity and also providing a rational combination strategy for enhanced response to GSI.
  • Furthermore, inhibition of the NOTCH pathway activity signature correlates with the induction of the cyclin-dependent kinase inhibitors CDKN2D (p19(INK4d)) and CDKN1B (p27(Kip1)), leading to derepression of RB and subsequent exit from the cell cycle.
  • Consistent with this evidence of cell cycle exit, short-term exposure of GSI resulted in sustained molecular and phenotypic effects after withdrawal of the compound.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Cyclic S-Oxides / pharmacology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Protease Inhibitors / pharmacology. Receptor, Notch1 / antagonists & inhibitors. Retinoblastoma Protein / metabolism. Thiadiazoles / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Cyclin-Dependent Kinase 4 / antagonists & inhibitors. Cyclin-Dependent Kinase Inhibitor p19 / biosynthesis. Cyclin-Dependent Kinase Inhibitor p27. G1 Phase / drug effects. G1 Phase / genetics. Gene Expression Profiling. Humans. Intracellular Signaling Peptides and Proteins / metabolism. Phosphorylation. S Phase / drug effects. S Phase / genetics. Signal Transduction / drug effects. Transcription, Genetic. Transfection

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  • (PMID = 19318552.001).
  • [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 / CDKN1B protein, human; 0 / CDKN2D protein, human; 0 / Cyclic S-Oxides; 0 / Cyclin-Dependent Kinase Inhibitor p19; 0 / Intracellular Signaling Peptides and Proteins; 0 / MRK 003; 0 / NOTCH1 protein, human; 0 / Protease Inhibitors; 0 / Receptor, Notch1; 0 / Retinoblastoma Protein; 0 / Thiadiazoles; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 3.4.- / Amyloid Precursor Protein Secretases
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