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Items 1 to 100 of about 171660
1. Kontny U, Boppana S, Jung A, Goebel H, Strahm B, Peters A, Dormann S, Werner M, Bader P, Fisch P, Niemeyer C: Post-transplantation lymphoproliferative disorder of recipient origin in a boy with acute T-cell leukemia with detection of B-cell clonality 3 months before stem cell transplantation. Haematologica; 2005 Nov;90 Suppl:ECR27
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  • [Title] Post-transplantation lymphoproliferative disorder of recipient origin in a boy with acute T-cell leukemia with detection of B-cell clonality 3 months before stem cell transplantation.
  • Post-transplantation lymphoproliferative disorder is an infrequent complication after hematopoietic stem cell transplantation.
  • It is hypothesized that lack of T-cell surveillance following transplantation permits reactivation of latent EBV leading to polyclonal B-cell expansion and finally outgrowth of a predominant clone.
  • Here, we describe an 8-year old boy with early onset post-transplantation lymphoproliferative disorder following matched-unrelated stem cell transplantation for high-risk T-cell leukemia whose disease was unusual for two reasons.
  • First, his B-cell clone was of host origin and, in contrast to the few PTLD of host origin described so far, not associated with autologous reconstitution.
  • Secondly, using clonal analysis, we could retrospectively show that the B-cell clone emerged during consolidation chemotherapy for T-cell leukemia, 3 months before stem cell transplantation.
  • [MeSH-major] B-Lymphocytes / pathology. Clone Cells / pathology. Epstein-Barr Virus Infections / complications. Leukemia-Lymphoma, Adult T-Cell / surgery. Lymphoproliferative Disorders / etiology. Postoperative Complications / etiology
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Antilymphocyte Serum / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Asparaginase / administration & dosage. Asparaginase / adverse effects. Child. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Cyclosporine / adverse effects. Cyclosporine / therapeutic use. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Daunorubicin / adverse effects. Dexamethasone / administration & dosage. Etoposide / administration & dosage. Etoposide / pharmacology. Fatal Outcome. Glucocorticoids / administration & dosage. Glucocorticoids / adverse effects. Graft vs Host Disease / drug therapy. Herpesvirus 4, Human / isolation & purification. Humans. Immunosuppressive Agents / adverse effects. Immunosuppressive Agents / therapeutic use. Lymphocyte Transfusion. Male. Prednisolone / adverse effects. Prednisolone / therapeutic use. Rituximab. Time Factors. Transplantation Chimera. Transplantation Conditioning. Vincristine / administration & dosage. Vincristine / adverse effects. Virus Activation / drug effects. Whole-Body Irradiation

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  • (PMID = 16266918.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antilymphocyte Serum; 0 / Glucocorticoids; 0 / Immunosuppressive Agents; 04079A1RDZ / Cytarabine; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; 83HN0GTJ6D / Cyclosporine; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; EC 3.5.1.1 / Asparaginase; ZS7284E0ZP / Daunorubicin
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2. Soulier J, Clappier E, Cayuela JM, Regnault A, García-Peydró M, Dombret H, Baruchel A, Toribio ML, Sigaux F: HOXA genes are included in genetic and biologic networks defining human acute T-cell leukemia (T-ALL). Blood; 2005 Jul 1;106(1):274-86
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  • [Title] HOXA genes are included in genetic and biologic networks defining human acute T-cell leukemia (T-ALL).
  • Using a combination of molecular cytogenetic and large-scale expression analysis in human T-cell acute lymphoblastic leukemias (T-ALLs), we identified and characterized a new recurrent chromosomal translocation, targeting the major homeobox gene cluster HOXA and the TCRB locus.
  • Real-time quantitative polymerase chain reaction (RQ-PCR) analysis showed that the expression of the whole HOXA gene cluster was dramatically dysregulated in the HOXA-rearranged cases, and also in MLL and CALM-AF10-related T-ALL cases, strongly suggesting that HOXA genes are oncogenic in these leukemias.
  • Inclusion of HOXA-translocated cases in a general molecular portrait of 92 T-ALLs based on large-scale expression analysis shows that this rearrangement defines a new homogeneous subgroup, which shares common biologic networks with the TLX1- and TLX3-related cases.
  • Because T-ALLs derive from T-cell progenitors, expression profiles of the distinct T-ALL subgroups were analyzed with respect to those of normal human thymic subpopulations.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Differentiation / genetics. Child. Child, Preschool. Female. Gene Expression Profiling. Humans. Infant. Male. Middle Aged. Multigene Family. T-Lymphocytes / cytology. T-Lymphocytes / physiology

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  • (PMID = 15774621.001).
  • [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 / Homeodomain Proteins; 157907-48-7 / HoxA protein
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3. 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

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  • However, leukemia cells studied to date have shown variable susceptibility to TRAIL.
  • Our study demonstrates that cells of acute T-lymphoblastic leukemia MOLT-4 are resistant to TRAIL and that ionizing radiation in the therapeutically achievable dose of 1 Gy sensitizes TRAIL-resistant cells MOLT-4 to the TRAIL-induced apoptosis by increase in death receptors for TRAIL DR5.
  • When TRAIL is applied after the irradiation in the time of increased DR5 positivity more efficient cell killing is achieved.

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  • (PMID = 28550838.001).
  • [ISSN] 1211-4286
  • [Journal-full-title] Acta medica (Hradec Kralove)
  • [ISO-abbreviation] Acta Medica (Hradec Kralove)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Czech Republic
  • [Keywords] NOTNLM ; Apoptosis / DR5 / Ionizing radiation / Leukemia / TRAIL
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4. Bremer E, ten Cate B, Samplonius DF, de Leij LF, Helfrich W: CD7-restricted activation of Fas-mediated apoptosis: a novel therapeutic approach for acute T-cell leukemia. Blood; 2006 Apr 1;107(7):2863-70
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  • [Title] CD7-restricted activation of Fas-mediated apoptosis: a novel therapeutic approach for acute T-cell leukemia.
  • Consequently, new antileukemia strategies based on Fas activation have to meet the criterion of strictly localized action at the tumor-cell surface.
  • We report on a novel fusion protein, designated scFvCD7:sFasL, that is designed to have leukemia-restricted activity.
  • ScFvCD7:sFasL consists of sFasL genetically linked to a high-affinity single-chain fragment of variable regions (scFv) antibody fragment specific for the T-cell leukemia-associated antigen CD7.
  • Soluble homotrimeric scFvCD7:sFasL is inactive and acquires tumoricidal activity only after specific binding to tumor cell-surface-expressed CD7.
  • Treatment of T-cell acute lymphoblastic leukemia (T-ALL) cell lines and patient-derived T-ALL, peripheral T-cell lymphoma (PTCL), and CD7-positive acute myeloid leukemia (AML) cells with homotrimeric scFvCD7:sFasL revealed potent CD7-restricted induction of apoptosis that was augmented by conventional drugs, farnesyl transferase inhibitor L-744832, and the proteasome inhibitor bortezomib (Velcade; Millenium, Cambridge, MA).
  • CD7-restricted activation of Fas in T-cell leukemic cells by scFvCD7:sFasL revitalizes interest in the applicability of Fas signaling in leukemia therapy.
  • [MeSH-major] Antigens, CD7 / immunology. Apoptosis / immunology. Leukemia-Lymphoma, Adult T-Cell / therapy. Membrane Glycoproteins / immunology. Tumor Necrosis Factors / immunology
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Bystander Effect. Cell Line, Tumor. DNA Primers. Fas Ligand Protein. Humans. Jurkat Cells

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  • (PMID = 16332967.001).
  • [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 / Antigens, CD7; 0 / Antineoplastic Agents; 0 / DNA Primers; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Tumor Necrosis Factors
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5. Dos Santos NR, Ghezzo MN, da Silva RC, Fernandes MT: NF-κB in T-cell Acute Lymphoblastic Leukemia: Oncogenic Functions in Leukemic and in Microenvironmental Cells. Cancers (Basel); 2010;2(4):1838-60

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NF-κB in T-cell Acute Lymphoblastic Leukemia: Oncogenic Functions in Leukemic and in Microenvironmental Cells.
  • T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy of thymocytes that despite significant therapeutic advances can still be fatal.
  • Although mutations in NF-κB genes have not been reported in T-ALL, NF-κB constitutive activation in human T-ALL and in acute T-cell leukemia mouse models has been observed.
  • Although these studies revealed activation of members of both canonical and noncanonical NF-κB pathways in acute T-cell leukemia, only inhibition of canonical NF-κB signaling was shown to impair leukemic T cell growth.
  • Besides playing an important pro-oncogenic role in leukemic T cells, NF-κB signaling also appears to modulate T-cell leukemogenesis through its action in microenvironmental stromal cells.

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  • (PMID = 24281204.001).
  • [ISSN] 2072-6694
  • [Journal-full-title] Cancers
  • [ISO-abbreviation] Cancers (Basel)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Other-IDs] NLM/ PMC3840450
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6. Karanikas V, Speletas M, Zamanakou M, Kalala F, Loules G, Kerenidi T, Barda AK, Gourgoulianis KI, Germenis AE: Foxp3 expression in human cancer cells. J Transl Med; 2008;6:19

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  • OBJECTIVE: Transcription factor forkhead box protein 3 (Foxp3) specifically characterizes the thymically derived naturally occurring regulatory T cells (Tregs).
  • Limited evidence indicates that it is also expressed, albeit to a lesser extent, in tissues other than thymus and spleen, while, very recently, it was shown that Foxp3 is expressed by pancreatic carcinoma.
  • MATERIALS AND METHODS: Twenty five tumor cell lines of different tissue origins (lung cancer, colon cancer, breast cancer, melanoma, erythroid leukemia, acute T-cell leukemia) were studied.
  • RESULTS: Foxp3 mRNA as well as Foxp3 protein was detected in all tumor cell lines, albeit in variable levels, not related to the tissue of origin.
  • [MeSH-minor] Cell Line, Tumor. Flow Cytometry. Humans. Immunohistochemistry. Interleukin-10 / biosynthesis. Jurkat Cells. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tissue Distribution. Transcription Factors / metabolism. Transforming Growth Factor beta1 / biosynthesis

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  • (PMID = 18430198.001).
  • [ISSN] 1479-5876
  • [Journal-full-title] Journal of translational medicine
  • [ISO-abbreviation] J Transl Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / RNA, Messenger; 0 / Transcription Factors; 0 / Transforming Growth Factor beta1; 130068-27-8 / Interleukin-10
  • [Other-IDs] NLM/ PMC2386447
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7. Yu C, Friday BB, Lai JP, Yang L, Sarkaria J, Kay NE, Carter CA, Roberts LR, Kaufmann SH, Adjei AA: Cytotoxic synergy between the multikinase inhibitor sorafenib and the proteasome inhibitor bortezomib in vitro: induction of apoptosis through Akt and c-Jun NH2-terminal kinase pathways. Mol Cancer Ther; 2006 Sep;5(9):2378-87
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Multiple tumor cell lines of varying histiotypes, including A549 (lung adenocarcinoma), 786-O (renal cell carcinoma), HeLa (cervical carcinoma), MDA-MB-231 (breast), K562 (chronic myelogenous leukemia), Jurkat (acute T-cell leukemia), MEC-2 (B-chronic lymphocytic leukemia), and U251 and D37 (glioma), as well as cells derived from primary human glioma tumors that are likely a more clinically relevant model were treated with sorafenib or bortezomib alone or in combination.
  • Sorafenib and bortezomib synergistically induced a marked increase in mitochondrial injury and apoptosis, reflected by cytochrome c release, caspase-3 cleavage, and poly(ADP-ribose) polymerase degradation in a broad range of solid tumor and leukemia cell lines.
  • These findings were accompanied by several biochemical changes, including decreased phosphorylation of vascular endothelial growth factor receptor-2, platelet-derived growth factor receptor-beta, and Akt and increased phosphorylation of stress-related c-Jun NH2-terminal kinase (JNK).
  • These findings show that sorafenib interacts synergistically with bortezomib to induce apoptosis in a broad spectrum of neoplastic cell lines and show an important role for the Akt and JNK pathways in mediating synergism.
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Bortezomib. Cell Line, Tumor. Drug Synergism. Humans. Jurkat Cells. K562 Cells. MAP Kinase Signaling System / drug effects. Niacinamide / analogs & derivatives. Phenylurea Compounds. Proteasome Endopeptidase Complex / metabolism

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  • (PMID = 16985072.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Boronic Acids; 0 / Phenylurea Compounds; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 69G8BD63PP / Bortezomib; 9ZOQ3TZI87 / sorafenib; EC 2.7.11.1 / Oncogene Protein v-akt; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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8. Das B, Reddy VS, Krishnaiah M, Sharma AV, Ravi Kumar K, Rao JV, Sridhar V: Acetylated pseudoguaianolides from Parthenium hysterophorus and their cytotoxic activity. Phytochemistry; 2007 Aug;68(15):2029-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The structures of the compounds were derived from detailed studies of their spectral (1D and 2D NMR and FABMS) data and by comparison of the values with those of parthenin, a major known constituent of the plant.
  • The cytotoxic activity of parthenin and the constituents was evaluated using Jurkat (human: T lymphocyte; acute T cell leukemia), HL-60 (human leukemia) and Hela (human cervical carcinoma) cells.
  • [MeSH-minor] Acetylation. Cell Line, Tumor. Cell Survival / drug effects. Crystallography, X-Ray. Flowers / chemistry. Humans. Models, Molecular. Molecular Structure

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  • (PMID = 17570445.001).
  • [ISSN] 0031-9422
  • [Journal-full-title] Phytochemistry
  • [ISO-abbreviation] Phytochemistry
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Parthenium hysterophorus extract; 0 / Plant Extracts; 0 / Sesquiterpenes, Guaiane
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9. Ben-Omran TI, Cerosaletti K, Concannon P, Weitzman S, Nezarati MM: A patient with mutations in DNA Ligase IV: clinical features and overlap with Nijmegen breakage syndrome. Am J Med Genet A; 2005 Sep 1;137A(3):283-7
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  • We report a 4(1/2)-year-old boy who presented with acute T-cell leukemia.
  • The patient died shortly after the onset of treatment for his T-cell leukemia.
  • In this study, we review the clinical features of this rare syndrome and provide suggestions for differential diagnosis.
  • [MeSH-minor] Blotting, Western. Cells, Cultured. Child, Preschool. Chromosome Aberrations / radiation effects. Chromosome Breakage. Developmental Disabilities / pathology. Diagnosis, Differential. Face / abnormalities. Fibroblasts / cytology. Fibroblasts / metabolism. Fibroblasts / radiation effects. Growth Disorders / pathology. Humans. Male. Microcephaly / pathology. Syndrome

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16088910.001).
  • [ISSN] 1552-4825
  • [Journal-full-title] American journal of medical genetics. Part A
  • [ISO-abbreviation] Am. J. Med. Genet. A
  • [Language] eng
  • [Databank-accession-numbers] OMIM/ 251260
  • [Grant] United States / NCI NIH HHS / CA / CA57569
  • [Publication-type] Case Reports; 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] United States
  • [Chemical-registry-number] EC 6.5.1.- / DNA Ligases; EC 6.5.1.1 / DNA ligase (ATP)
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10. Liu YC, Lai WC, Chuang KA, Shen YJ, Hu WS, Ho CH, Chen YB, Hsu MF, Hsu HC, Lieu CH: Blockade of JAK2 activity suppressed accumulation of β-catenin in leukemic cells. J Cell Biochem; 2010 Oct 1;111(2):402-11
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  • We found β-catenin abnormally accumulated in both human acute T cell leukemia Jurkat cells and human erythroleukemia HEL cells.
  • Taken together; these results suggest that β-Trcp plays a key role in the cross-talk between JAK/STAT and Wnt/β-catenin signaling in leukemia cells.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Janus Kinase 2 / metabolism. Leukemia, Erythroblastic, Acute / metabolism. Leukemia, T-Cell / metabolism. beta Catenin / genetics. beta-Transducin Repeat-Containing Proteins / physiology

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  • [Copyright] © 2010 Wiley-Liss, Inc.
  • (PMID = 20503246.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / beta Catenin; 0 / beta-Transducin Repeat-Containing Proteins; EC 2.7.10.2 / Janus Kinase 2; WYQ7N0BPYC / Acetylcysteine
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11. Liao YF, Hung YC, Chang WH, Tsay GJ, Hour TC, Hung HC, Liu GY: The PKC delta inhibitor, rottlerin, induces apoptosis of haematopoietic cell lines through mitochondrial membrane depolarization and caspases' cascade. Life Sci; 2005 Jun 24;77(6):707-19
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  • [Title] The PKC delta inhibitor, rottlerin, induces apoptosis of haematopoietic cell lines through mitochondrial membrane depolarization and caspases' cascade.
  • It shown to be effective against several human tumor cell lines and in potentiating chemotherapy-induced cytotoxcicity.
  • Using the trypan blue exclusion assay, we demonstrated that rottlerin reduced the viability in a dose- and time-dependent manner of human leukemia HL60 cells, human acute T cell leukemia Jurkat cells and mouse macrophage RAW 264.7 cells.
  • Expression of PKCdelta and Bcl-2 protein inhibited Deltapsim change and repressed cell death.
  • [MeSH-minor] Animals. Cell Line, Tumor. DNA Fragmentation / drug effects. DNA Fragmentation / physiology. Enzyme Inhibitors / pharmacology. Humans. Membrane Potentials. Mice. Protein Kinase C-delta. Signal Transduction / drug effects. Signal Transduction / physiology

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  • (PMID = 15922001.001).
  • [ISSN] 0024-3205
  • [Journal-full-title] Life sciences
  • [ISO-abbreviation] Life Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Acetophenones; 0 / Benzopyrans; 0 / Enzyme Inhibitors; E29LP3ZMUH / rottlerin; EC 2.7.1.- / Prkcd protein, mouse; EC 2.7.11.13 / PRKCD protein, human; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.13 / Protein Kinase C-delta; EC 3.4.22.- / Caspases
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12. Sampathkumar SG, Jones MB, Yarema KJ: Metabolic expression of thiol-derivatized sialic acids on the cell surface and their quantitative estimation by flow cytometry. Nat Protoc; 2006;1(4):1840-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metabolic expression of thiol-derivatized sialic acids on the cell surface and their quantitative estimation by flow cytometry.
  • The N-acetyl-D-mannosamine (ManNAc) analog Ac5ManNTGc, a non-natural metabolic precursor for the sialic acid biosynthetic pathway, can be used to display thiols on the cell surface.
  • Sugar-expressed cell-surface thiols are readily accessible compared to their protein counterparts, making them ideal for exploitation in cell-adhesion and tissue-engineering applications.
  • This report describes a protocol for the incubation of Jurkat (human acute T-cell leukemia) cells with Ac5ManNTGc and the quantitative estimation of the resulting sialic acid displayed thiols by flow cytometry after a reaction with a water-soluble biotin-conjugated maleimide reagent and fluorescein isothiocyanate-conjugated (FITC) avidin staining.
  • These methods, with minimal optimization, are generally also applicable to other human cell lines.
  • [MeSH-major] Cell Membrane / chemistry. Flow Cytometry / methods. Hexosamines / metabolism. N-Acetylneuraminic Acid / metabolism. Sulfhydryl Compounds / analysis

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  • (PMID = 17487167.001).
  • [ISSN] 1750-2799
  • [Journal-full-title] Nature protocols
  • [ISO-abbreviation] Nat Protoc
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R01CA112314-01A1
  • [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.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 1,3,4,6-tetra-O-acetyl-2-acetylthioacetamido-2-deoxymannopyranose; 0 / Hexosamines; 0 / Oligosaccharides; 0 / Sulfhydryl Compounds; GZP2782OP0 / N-Acetylneuraminic Acid
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13. Vey N, Bourhis J, Dombret H, Bordessoule D, Prebet T, Charbonnier A, Squiban P, Damholt B, Blaise D, Olive D: A phase I study of the anti-natural killer inhibitory receptor (KIR) monoclonal antibody (1-7F9, IPH2101) in elderly patients with acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):3015

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I study of the anti-natural killer inhibitory receptor (KIR) monoclonal antibody (1-7F9, IPH2101) in elderly patients with acute myeloid leukemia (AML).
  • As expected for an IgG4, NK cell numbers were unaffected by the treatment.

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  • (PMID = 27962059.001).
  • [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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14. 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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15. Barret J, Dumontet C, Annereau J, Brel V, Breillout F, Guminski Y, Imbert T, Guilbaud N, Bailly C: A functional procedure using fresh samples to select patients with acute myeloid leukemia prior to treatment with the novel targeted cytotoxic agent F14512. J Clin Oncol; 2009 May 20;27(15_suppl):11087

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A functional procedure using fresh samples to select patients with acute myeloid leukemia prior to treatment with the novel targeted cytotoxic agent F14512.
  • METHODS: The uptake of this probe was first measured by flow cytometry in a panel of human leukemia cell lines.
  • RESULTS: Data showed that high level of fluorescence was detected in F14512 -sensitive cancer cell lines whereas leukemia cells responding poorly to F14512 generally exhibited very low levels of PTS.
  • A panel of 50 fresh human acute myeloid leukemia samples showed a larger inter-individual variation and, interestingly, incorporation of the fluorescent probe was generally higher in leukemia blasts than in lymphocytes.

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  • (PMID = 27963178.001).
  • [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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16. Beltran BE, Morales D, Quiñones P, Salas R, Castillo J: Analysis of prognostic factors in patients with adult T-cell leukemia/lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):8575

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of prognostic factors in patients with adult T-cell leukemia/lymphoma.
  • : 8575 Background: Adult T-cell leukemia/lymphoma (ATLL) is associated with human T-cell lymphotropic virus type-I (HTLV-1) described in Southern Japan, Europe, Caribbean and South America.
  • Diagnosis was based on clinical history and histological findings consistent with ATLL and either positive HTLV-1 serology or evidence of HTLV-1 integration.
  • Clinical types were acute (n=45), lymphomatous (n=43), cutaneous (n=10), smoldering (n=3) and chronic (n=1).
  • Median OS for acute, lymphomatous, smoldering and cutaneous subtype were 2, 11, 17 and 39 months, respectively (log-rank 28.5, p<0.00001).
  • The prognostic index for T-cell lymphoma (PIT) score was determined in 80 patients; 20 (25%), 17 (21%), 33 (41%) and 10 (13%) patients had scores of 0-1, 2, 3 and 4, respectively.
  • CONCLUSIONS: This retrospective series represents the largest Latin-American experience on ATLL, which is a heterogeneous disease with distinct clinical features and outcomes.
  • The IPI ant PIT scores, used for risk-stratification of aggressive B-cell and peripheral T-cell lymphomas, respectively, appear as good prognostic indicators for ATLL as well.
  • Further research is needed to better risk-stratify this unique lymphoma.

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  • (PMID = 27962272.001).
  • [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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17. Tsai DE, Wang W, Reshef R, Vogl D, Stadtmauer E, Andreadis C, Carlson A, Luger S: Effect of bexarotene on platelet counts in patients undergoing cancer treatment: An analysis of clinical trials in lung cancer and leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):e20533

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of bexarotene on platelet counts in patients undergoing cancer treatment: An analysis of clinical trials in lung cancer and leukemia.
  • : e20533 Background: Bexarotene (Bex) is an oral retinoid X receptor agonist with activity against cutaneous T cell lymphoma and currently under investigation for other malignancies.
  • In patients receiving this agent for acute myeloid leukemia (AML), we noted increases in platelet counts.
  • METHODS: We analyzed platelet count data from 3 Bex clinical trials encompassing non-small cell lung cancer (NSCLC) and AML.
  • More patients on Bex than on placebo had an increase in platelet count of at least 50 K/uL (55% vs. 27% for CarP, p<0.0001; 81% vs. 66% for CisV, p<0.0001) over pre-treatment baseline.

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  • (PMID = 27960979.001).
  • [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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18. 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.
  • Total nucleic acids were purified and subjected to two rounds of PCR analysis, with the first PCR designed to eliminate amplification of the wild-type, non-translocated ABL gene.
  • 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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19. Smith MA, Morton CL, Carol H, Gorlick RG, Kang MH, Keir ST, Kolb EA, Lock RB, Maris JM, Houghton PJ: Pediatric Preclinical Testing Program (PPTP) testing of the CENP-E inhibitor GSK923295A. J Clin Oncol; 2009 May 20;27(15_suppl):10015

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: The PPTP includes a molecularly characterized in vitro panel of cell lines (n = 27) and in vivo panel of xenografts (n = 60) representing most of the common types of childhood solid tumors and childhood acute lymphoblastic leukemia (ALL).
  • RESULTS: GSK923295A demonstrated potent in vitro activity against the PPTP cell line panel with a median IC50 of 27 nM (range 12 nM to > 10 μM).
  • Objective responses were noted in 13 of 35 xenografts, including 9 with maintained complete responses (MCR), 3 with complete response (CR), and 1 with partial response (PR).
  • For the neuroblastoma panel, the best response was progressive disease (PD) with growth delay compared to controls (PD2 response), which was observed in 5 of 6 xenografts.

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  • (PMID = 27962529.001).
  • [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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20. Epenetos AA, Kousparou C, Stylianou S: Inhibition of Notch and tumor regression. J Clin Oncol; 2009 May 20;27(15_suppl):e14623

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e14623 Background: Notch signaling is an evolutionary-conserved pathway in vertebrates and invertebrates which is involved many developmental processes, including cell fate decisions, apoptosis, proliferation, and stem-cell self renewal.
  • Increasing evidence suggests that the Notch signaling pathway is frequently up regulated in many forms of cancer including acute T-cell lymphoblastic leukemia, cervical, prostate, lung, breast and others.
  • RESULTS: Our data show that ANTP/DN MAML fusion protein, TR4 contains signals for proper cell targeting, internalization and nuclear transport.

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  • (PMID = 27964214.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Ding W, Knox TR, Smoley SA, Van Dyke DL, Kay NE: Cytogenetic abnormalities in mesenchymal stem cells in chronic lymphocytic leukemia (CLL) patients and normal subjects. J Clin Oncol; 2009 May 20;27(15_suppl):e22002

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic abnormalities in mesenchymal stem cells in chronic lymphocytic leukemia (CLL) patients and normal subjects.
  • : e22002 Background: Mesenchymal stem cells (MSC) residing in the marrow support hematopoiesis and protect cancer cells from undergoing cell death induced by chemotherapy.
  • Recent reports have described clonal cytogenetic abnormalities in the MSC of acute myeloid leukemia and myelodysplastic syndrome patients.
  • After 3-4 non-stimulated cell culture passages, the karyotype was analyzed in 5-40 metaphase cells from each subject Abnormalities were considered clonal using the accepted convention of the same chromosomal gain or rearrangement in 2 or more cells or loss in at least 3 cells.
  • CONCLUSIONS: Marrow MSC derived from CLL patients and normal subjects do show an array of cytogenetic abnormalities including clonal chromosomal abnormalities.

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  • (PMID = 27963169.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Arat N, Bakanay SM, Yildiz E, Tufekcioglu O, Golbasi Z: Complete regression of massive cardiac involvement associated with acute T cell leukemia following chemotheraphy. Eur J Echocardiogr; 2008 May;9(3):388-90

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complete regression of massive cardiac involvement associated with acute T cell leukemia following chemotheraphy.
  • Adult T cell leukemia/lymphomas are aggressive disorders, which infiltrate not only the bone marrow but extensively the visceral organs as well.
  • The dramatic improvement in echocardiographic findings after chemotherapy gave a clue to investigate suspected patients with aggressive leukemia and lymphomas for exclusion of leukemic infiltration of myocardium.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, T-Cell / drug therapy. Leukemia, T-Cell / pathology. Leukemic Infiltration. Myocardium / pathology
  • [MeSH-minor] Acute Disease. Adult. Humans. Male. Remission Induction. Ventricular Dysfunction, Left / etiology

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  • (PMID = 17320483.001).
  • [ISSN] 1532-2114
  • [Journal-full-title] European journal of echocardiography : the journal of the Working Group on Echocardiography of the European Society of Cardiology
  • [ISO-abbreviation] Eur J Echocardiogr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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23. Mukhopadhyay A, Gupta P, Mukhopadhyay S, Dey S, Basak J, Pandey R: Result of adolescent acute lymphoblastic leukemia protocol (MCP 841) from a developing country. J Clin Oncol; 2009 May 20;27(15_suppl):10046

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Result of adolescent acute lymphoblastic leukemia protocol (MCP 841) from a developing country.
  • : 10046 Background: Acute Lymphatic Leukemia is a curable disease in the range of 80 - 90% in developed countries by aggressive protocol like BFM, St. Judes' but result is much less in adolescence age group (60-70%).
  • In a follow-up period of 24 - 88 months (with an average of 54 months) the disease-free survival ( DFS) was 42 (56%) patients with an overall survival of 46 (61.34%) patients.
  • The major cause of the mortality was infection 18% (24.0% patients) followed progressive disease 9 (12.0%) and hemorrhage 2 (2.7%).
  • CONCLUSIONS: The data of acute lymphatic leukemia in adolescent is not satisfactory as compared to other pediatric patients.

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  • (PMID = 27962472.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Andorsky DJ, Yamada R, Steward K, De Vos S, Said J, Timmerman J: Expression of programmed death ligand 1 (PD-L1) by non-Hodgkin's lymphomas (NHL) and effect on tumor-associated T cells. J Clin Oncol; 2009 May 20;27(15_suppl):8526

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: PD-L1 expression was analyzed in 16 NHL cell lines by flow cytometry (FC) and in 111 lymphoma specimens by immunohistochemistry (IHC) (n=92) or FC (n=19).
  • In functional studies, irradiated anaplastic large cell lymphoma (ALCL) cells were co-cultured with allogeneic T cells in the presence of anti-PD-L1 blocking antibody, and IFNγ secretion and thymidine incorporation was used to assess T cell function and proliferation.
  • To further test tumor-T cell interactions, malignant ascites from a patient with ALK+ ALCL and peripheral blood mononuclear cells from a patient with leukemic mantle cell lymphoma, both containing PD-L1-expressing tumor cells and tumor-associated T cells, were stimulated with phytohemagglutinin (a polyclonal T cell activator) and incubated with anti-PD-L1 antibody.
  • Levels of 16 inflammatory cytokines were measured as an assessment of T cell activity.
  • RESULTS: All 9 B cell lymphoma lines were negative for PD-L1, while all 5 ALCL cell lines were strongly positive.
  • One T-cell ALL line was positive, and one peripheral T cell lymphoma was negative.
  • Strong PD-L1 staining was detected by IHC in all 14 ALCL specimens and in 83% of diffuse large B cell lymphomas (DLBCL) analyzed (n=35).
  • In the autologous setting using cultures of ALCL and mantle cell lymphoma specimens containing host T cells, secretion of inflammatory cytokines by tumor-associated T cells, including GMCSF, IFNγ, IL-1, IL-6, IL-8, TNFα, and MIP1α, were increased by incubation with anti-PD-L1 antibody.
  • PD-L1 may play a role in thwarting an effective anti-tumor immune response and represents an attractive target for lymphoma immunotherapy.

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  • (PMID = 27960901.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Cheng PC, Crane J, Hunter T: Combination of bortezomib with a FLT3 inhibitor potentiates inhibition of proliferation and apoptosis of AML in vitro. J Clin Oncol; 2009 May 20;27(15_suppl):e14551

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e14551 Background: FLT3 receptor tyrosine kinase activating mutations contribute to leukemogenesis and poor prognosis in approximately 30% of acute myeloid leukemia (AML).
  • METHODS: In the course of conducting a synthetic lethality screen with a FLT3 inhibitor on the Ba/F3 murine cell line stably expressing human FLT3 or FLT3-ITD, we identified bortezomib, a proteasome inhibitor, as having potent activity against FLT3-ITD cells.
  • The effects of drugs on proliferation, apoptosis, and phosphosignaling were quantified in Ba/F3 cells and in the HL60 (WT FLT3) and MV4-11 (FLT3-ITD) human cell lines, using an MTS- based colorimetric assay, caspase 3 and 7 activity assays, and immunoblotting, respectively.
  • When the FLT3 inhibitor and bortezomib were used at IC25 concentrations, a more pronounced inhibition of cell proliferation was observed when they were used in combination than with either alone.
  • CONCLUSIONS: Bortezomib preferentially kills FLT3- ITD cells, showing a four-fold more potent inhibition of cell proliferation, induces apoptosis, and abrogates activation of FLT3 and its downstream effector pathways.

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  • (PMID = 27963616.001).
  • [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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26. Faderl S, Thomas DA, Gandhi V, Huang X, Borthakur G, O'Brien S, Ravandi F, Plunkett W, Bretz JL, Kantarjian HM: Results of a phase I study of clofarabine (CLO) plus cyclophosphamide (CY) in adult patients (pts) with relapsed and/or refractory acute lymphoblastic leukemia (ALL). J Clin Oncol; 2009 May 20;27(15_suppl):7020

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Results of a phase I study of clofarabine (CLO) plus cyclophosphamide (CY) in adult patients (pts) with relapsed and/or refractory acute lymphoblastic leukemia (ALL).
  • The continual reassessment method (CRM) was used to determine the maximum tolerated dose (MTD) from 4 pre-defined dose levels.
  • Twenty-one pts had pre-B ALL, 5 pts pre-T/T ALL, 1 pt mature B ALL, and 3 pts biphenotypic acute leukemias.
  • All pts had pre-B ALL.

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  • (PMID = 27961382.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Tsujimura H, Mimura N, Ise M, Sakai C, Shimada H, Nagata M, Kumagai K: Incidence of therapy-related leukemia following chemoradiotherapy for esophageal cancer. J Clin Oncol; 2009 May 20;27(15_suppl):e15663

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidence of therapy-related leukemia following chemoradiotherapy for esophageal cancer.
  • METHODS: From July 2000 to March 2008, 348 patients with esophageal squamous cell carcinoma underwent CRT.
  • RESULTS: Four patients, who achieved CR after CRT, developed leukemia.
  • Case1, 60-yo-male, developed overt acute myeloid leukemia (AML) from myelodysplastic syndrome 48 months after CRT.
  • Case3, 72-yo-male, developed Burkitt leukemia with t(8;14)(q24;q32) 19 months after CRT.
  • Case4, 65-yo-male, developed myeloid crisis of chronic myelogenous leukemia with complicated abnormalities including t(9;22)(q34;q11) 48 months after CRT.
  • Case 1 and 3 had localized disease and received single course of neoadjuvant CRT.
  • Case 2 and 4 had advance disease and received 2 courses of CRT.
  • All patients eventually died of leukemia.
  • To this end, atypical cytogenetic abnormalities seen in the present cases give a new insight into the biology of therapy-related leukemia.
  • Notably, this is the first report presenting the incidence of secondary leukemia by nedaplatin.

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  • (PMID = 27962759.001).
  • [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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28. Sobol I, Palacios C, Osborne G, Hildes J, MacDonald W, Harty A, Sanguya I, Gilbert M: Initial management of an outbreak of the HTLV-1 virus in Nunavut, Canada. Alaska Med; 2007;49(2 Suppl):204-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The Dept. of Health and Social Services in Nunavut became aware of the presence of this virus in the Nunavut population in early June, 2005 when an individual infected with HTLV-1 died from Acute T-cell leukemia.
  • There has been at least one death from Acute T-cell leukemia in an individual infected.
  • [MeSH-major] Deltaretrovirus Infections / epidemiology. Disease Outbreaks / prevention & control. Human T-lymphotropic virus 1. Program Development. Program Evaluation
  • [MeSH-minor] Acute Disease. Antiviral Agents / therapeutic use. Canada / epidemiology. Health Care Surveys. Humans. Interviews as Topic. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / epidemiology. Nunavut / epidemiology

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  • (PMID = 17929633.001).
  • [ISSN] 0002-4538
  • [Journal-full-title] Alaska medicine
  • [ISO-abbreviation] Alaska Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents
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29. di Carlo E, de Totero D, Piazza T, Fabbi M, Ferrini S: Role of IL-21 in immune-regulation and tumor immunotherapy. Cancer Immunol Immunother; 2007 Sep;56(9):1323-34
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • These include regulation of T, B and NK cell proliferation, survival, differentiation, and effector functions.
  • Besides its activities on normal lymphoid cells, IL-21 is an in vitro growth factor for myeloma and acute-T cell leukemia cells, whereas it induces the apoptosis of B-CLL (chronic lymphocytic leukemia) cells.
  • Since IL-2, but not IL-21, is specifically required for the development of regulatory T (Treg) cell immune-suppressive functions, IL-21 may be a new tool for cancer immunotherapy.

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  • (PMID = 17447063.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interleukins; 0 / interleukin-21
  • [Number-of-references] 92
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30. Fukuyama T, Tajima Y, Ueda H, Hayashi K, Shutoh Y, Harada T, Kosaka T: Apoptosis in immunocytes induced by several types of pesticides. J Immunotoxicol; 2010 Mar;7(1):39-56
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  • Several types of pesticides, such as organophosphates and organochlorines, can induce thymocyte apoptosis, resulting in thymic atrophy and predisposing the highly sensitive fetal immune system to loss of tolerance to self-antigens and subsequent increased risk for autoimmune disease and allergies.
  • In the studies here, mouse primary thymocytes and a human acute T-cell leukemia cell line (J45.01) were employed to examine potential thymocyte apoptosis induced by several types of chemicals, including several commonly-used pesticides.
  • Apoptosis, cell viability, the proportion of Annexin-V+ cells, the activities of caspases 3/7, 8, and 9, and the levels of DNA fragmentation in both the J45.01 cells and thymocytes were then examined.
  • The results here show that with both cell types, there was an increase in the proportion of annexin-V+ cells and levels of DNA fragmentation following exposure to parathion, PNMC, methoxychlor, or dexamethasone (positive control); however, the levels of sensitivity appeared to differ between the cell types.
  • A more precise characterization of these inter-cellular differences is the logical next step in our studies of the effects of these (and other) pesticides on immune cell integrity.
  • [MeSH-major] Apoptosis / drug effects. Pesticides / toxicity. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. T-Lymphocytes / drug effects. Thymus Gland / drug effects
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. DNA Fragmentation. DNA, Neoplasm / analysis. Female. Humans. Mice. Mice, Inbred BALB C

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  • (PMID = 19911945.001).
  • [ISSN] 1547-6901
  • [Journal-full-title] Journal of immunotoxicology
  • [ISO-abbreviation] J Immunotoxicol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Pesticides
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31. Iversen PO, Sørensen DR, Tronstad KJ, Gudbrandsen OA, Rustan AC, Berge RK, Drevon CA: A bioactively modified fatty acid improves survival and impairs metastasis in preclinical models of acute leukemia. Clin Cancer Res; 2006 Jun 1;12(11 Pt 1):3525-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A bioactively modified fatty acid improves survival and impairs metastasis in preclinical models of acute leukemia.
  • PURPOSE: Polyunsaturated fatty acids (PUFA) and the sulfur-substituted fatty acid tetradecylthioacetic acid (TTA) inhibit proliferation and induce apoptosis in lymphoma and leukemic cell lines, but it is unknown if they can modify leukemogenesis in the intact organism.
  • EXPERIMENTAL DESIGN: We now examined the effects of PUFA and TTA in rats transplanted with either acute promyelocytic leukemia or acute T-cell leukemia.
  • RESULTS: Whereas TTA prolonged survival (P < 0.05) in both types of rat leukemia, n-3 PUFA had no significant effect compared with controls.
  • CONCLUSIONS: Dietary intake of TTA, but not of n-3 PUFA, in rats with acute leukemia, prolonged their survival.
  • TTA intake was also associated with reduced leukemic cell burden as well as diminished extramedullar dissemination.
  • TTA represents a modified fatty acid that exerts unique effects on malignant hematopoietic cells, and the present study indicates that TTA may have a therapeutic potential in patients with acute leukemias.
  • [MeSH-major] Fatty Acids, Unsaturated / administration & dosage. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Sulfides / administration & dosage
  • [MeSH-minor] Animals. Apoptosis / drug effects. Diet. Disease Models, Animal. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Enzyme Activation / drug effects. Humans. Leukemic Infiltration / diagnosis. Matrix Metalloproteinases / drug effects. Neoplasm Metastasis. Rats. Structure-Activity Relationship. Survival Rate. Transplantation, Heterologous. Xenograft Model Antitumor Assays

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  • (PMID = 16740779.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fatty Acids, Unsaturated; 0 / Sulfides; 2921-20-2 / 1-(carboxymethylthio)tetradecane; EC 3.4.24.- / Matrix Metalloproteinases
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32. Nieto-Miguel T, Gajate C, Mollinedo F: Differential targets and subcellular localization of antitumor alkyl-lysophospholipid in leukemic versus solid tumor cells. J Biol Chem; 2006 May 26;281(21):14833-40
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  • Edelfosine induced rapid apoptosis in human leukemic cells, including acute T-cell leukemia Jurkat and Peer cells, but promoted a late apoptotic response, preceded by G(2)/M arrest, in human solid tumor cells such as cervix epitheloid carcinoma HeLa cells and lung carcinoma A549 cells. c-Jun amino-terminal kinase (JNK) and caspase-3 were accordingly activated at earlier times in edelfosine-treated Jurkat cells as compared with drug-treated HeLa cells.
  • Both leukemic and solid tumor cells took up this alkyl-lysophospholipid and expressed the two putative edelfosine targets, namely cell surface Fas death receptor (also known as APO-1 or CD95) and endoplasmic reticulum CTP: phosphocholine cytidylyltransferase.
  • These data indicate that edelfosine targets two different subcellular structures in a cell type-dependent manner, namely cell surface lipid rafts in leukemic cells and endoplasmic reticulum in solid tumor cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Leukemia / metabolism. Lysophospholipids / chemistry. Neoplasms / metabolism. Phospholipid Ethers / pharmacology

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  • (PMID = 16540473.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Antineoplastic Agents; 0 / Lysophospholipids; 0 / Phospholipid Ethers; 1Y6SNA8L5S / edelfosine; EC 2.7.12.2 / MAP Kinase Kinase 4; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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33. Lee SK, Jurata LW, Nowak R, Lettieri K, Kenny DA, Pfaff SL, Gill GN: The LIM domain-only protein LMO4 is required for neural tube closure. Mol Cell Neurosci; 2005 Feb;28(2):205-14
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  • LMO2 is necessary for development of the entire hematopoietic system and overexpression of LMO1 or LMO2 results in human acute T cell leukemia.
  • LMO4 mutant mice die embryonically and exhibit exencephaly, which is associated with abnormal patterns of cell proliferation and with high levels of apoptotic cell death within the neuroepithelium.
  • LMO4 is also expressed in Schwann cell progenitors after these contact neurites, a process mediated in part by neuregulin (Nrg).
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Animals. Apoptosis / genetics. Body Patterning / genetics. Cell Communication / physiology. Cell Differentiation / genetics. Cell Proliferation. Epithelial Cells / cytology. Epithelial Cells / metabolism. LIM Domain Proteins. Mice. Mice, Knockout. Neural Crest / cytology. Neural Crest / embryology. Neural Crest / metabolism. Neuregulin-1 / metabolism. Neurons / cytology. Neurons / metabolism. Protein Structure, Tertiary / genetics. Schwann Cells / cytology. Schwann Cells / metabolism. Stem Cells / cytology. Stem Cells / metabolism


34. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia.
  • : 10048 Background: T-cell acute lymphoblastic leukemia (T-ALL) is representing 10-15% of pediatric ALL.
  • Our published data showed that T-ALL phenotype patients fared poorly with 5 year survival of 27% versus 83% for precursor B-ALL (Recent Advances Research Update: 2006, 7; 1, P 51-56).
  • OBJECTIVES: We reviewed all patients diagnosed with T-ALL to assess risk classification according to NCI criteria, type of therapy received, overall survival and causes of mortality.
  • METHODS: Retrospective review of all patients files diagnosed with T-ALL from 1989 until now with data collection including; sex, age, white cell count (WBCs), CNS disease, type of protocol used, length of survival, overall survival, cause of death (toxic, disease).
  • Median WBCs 50,000/Cmm (range: 1.500-619,000/Cmm) and positive CNS at diagnosis 10/52 (20%).
  • Overall survival 27/52 (52%) and 25 pts. died (48%); 15 secondary to disease recurrence (9 on UKALL, 4 BFM, 2 CCG 1961); 4 during induction, 1 fulminant hepatic failure, 1 tumor lysis syndrome, and 4 due to toxicities (mucormycosis, staphylococcal toxic shock syndrome, CMV pneumonia, pseudomonas sepsis).
  • Further risk and response stratification in addition to intensification of therapy for T-cell ALL in our center may prove to be beneficial.

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  • (PMID = 27962474.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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35. Alduaij A, Butera JN, Treaba D, Castillo J: Complete remission in two cases of adult T-cell leukemia/lymphoma treated with hyper-CVAD: a case report and review of the literature. Clin Lymphoma Myeloma Leuk; 2010 Dec;10(6):480-3
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  • [Title] Complete remission in two cases of adult T-cell leukemia/lymphoma treated with hyper-CVAD: a case report and review of the literature.
  • BACKGROUND: Acute T-cell leukemia/lymphoma (ATLL) is a post thymic (peripheral) T-cell neoplasm caused by human T-cell lymphotropic virus type 1 (HTLV-1).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy
  • [MeSH-minor] Combined Modality Therapy. Cyclophosphamide / administration & dosage. Dexamethasone / administration & dosage. Doxorubicin / administration & dosage. Female. Hematopoietic Stem Cell Transplantation / methods. Humans. Male. Middle Aged. Remission Induction. Transplantation, Homologous. Treatment Outcome. Vincristine / administration & dosage

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  • (PMID = 21156467.001).
  • [ISSN] 2152-2669
  • [Journal-full-title] Clinical lymphoma, myeloma & leukemia
  • [ISO-abbreviation] Clin Lymphoma Myeloma Leuk
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide
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36. Yu C, Bruzek LM, Meng XW, Gores GJ, Carter CA, Kaufmann SH, Adjei AA: The role of Mcl-1 downregulation in the proapoptotic activity of the multikinase inhibitor BAY 43-9006. Oncogene; 2005 Oct 20;24(46):6861-9
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  • BAY 43-9006, a multikinase inhibitor that targets Raf, prevents tumor cell proliferation in vitro and inhibits diverse human tumor xenografts in vivo.
  • Similar BAY 43-9006-induced Mcl-1 downregulation was observed in ACHN (renal cell), HT-29 (colon), MDA-MB-231 (breast), KMCH (cholangiocarcinoma), Jurkat (acute T-cell leukemia), K562 (chronic myelogenous leukemia) and MEC-2 (chronic lymphocytic leukemia) cells.
  • [MeSH-minor] Adamantane / analogs & derivatives. Adamantane / pharmacology. Base Sequence. Caspases / metabolism. Cell Line, Tumor. DNA Primers. Enzyme Activation. Humans. Hydroquinones / pharmacology. MAP Kinase Signaling System. Myeloid Cell Leukemia Sequence 1 Protein. Niacinamide / analogs & derivatives. Phenylurea Compounds. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16007148.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA69008; United States / NIDDK NIH HHS / DK / R01 DK59427
  • [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 / Benzenesulfonates; 0 / DNA Primers; 0 / Hydroquinones; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / NSC 680410; 0 / Neoplasm Proteins; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 3.4.22.- / Caspases; PJY633525U / Adamantane
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37. Borthakur G, Faderl S, Ravandi F, Padmanabhan S, Stock W, Wu K, Li J, Curt G, Tallman M, Minden M: Clinical, pharmacokinetic (PK), and pharmacodynamic findings from a phase I trial of an Eg5 inhibitor (AZD4877) in patients with refractory acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):3580

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  • [Title] Clinical, pharmacokinetic (PK), and pharmacodynamic findings from a phase I trial of an Eg5 inhibitor (AZD4877) in patients with refractory acute myeloid leukemia (AML).
  • Eg5 inhibition is thus specific for dividing cells, resulting in monoastral mitotic spindles (monoasters) and apoptotic cell death.
  • Preclinically, hematologic tumor cell lines were generally more sensitive to AZD4877 than those derived from solid tumors.

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  • (PMID = 27961757.001).
  • [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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38. Xicoy B, Ribera JM, Oriol A, Sanz MA, Abella E, Tormo M, del Potro E, Bueno J, Grande C, Fernández-Calvo J, Orts M, Novo A, Rivas C, Hernández-Rivas JM, Feliu E, Ortega JJ: [Prognostic influence of immunological subtypes of T-cell acute lymphoblastic leukemia. Study of 81 patients]. Med Clin (Barc); 2006 Jan 21;126(2):41-6
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  • [Title] [Prognostic influence of immunological subtypes of T-cell acute lymphoblastic leukemia. Study of 81 patients].
  • [Transliterated title] Significado pronóstico de los subtipos inmunológicos de la leucemia aguda linfoblástica T del adulto. Estudio de 81 pacientes.
  • BACKGROUND AND OBJECTIVE: T-cell acute lymphoblastic leukemia (ALL) includes 4 immunological subtypes: pro-T, pre-T, thymic or cortical and mature.
  • In some studies, pro-T and mature subtypes have a poor prognosis.
  • The objective of this study was to describe the clinical characteristics, the result of treatment and the prognosis of the immunological subtypes of T-cell ALL in 81 adult patients included in 2 protocols of the Spanish PETHEMA group (ALL-96 and ALL-93).
  • The main clinical and biological parameters as well as the rate of response to treatment, the frequency of complete remission , disease free survival and overall survival were compared in each T-cell ALL subtype.
  • RESULTS: Of the 64 evaluable patients the distribution of the immunological subtypes was: 3 pro-T, 17 pre-T, 22 thymic or cortical and 22 mature.
  • Patients with mature T-cell ALL had a slow rate of response to treatment in comparison with patients wit pre-T and mature T-cell ALL but this did not translate to significant differences in frequency of complete remission (77% vs 94%), disease free survival (42% vs 46%) and overall survival (29% vs 47%).
  • CONCLUSIONS: Although patients with mature T-cell ALL had a slow rate of response to treatment and their survival tended to be shorter, in the present study there were no statistically significant differences in the prognosis of the different subtypes of T-cell ALL.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / mortality

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  • (PMID = 16426542.001).
  • [ISSN] 0025-7753
  • [Journal-full-title] Medicina clínica
  • [ISO-abbreviation] Med Clin (Barc)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
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39. Demarest RM, Ratti F, Capobianco AJ: It's T-ALL about Notch. Oncogene; 2008 Sep 1;27(38):5082-91
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  • T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive subset of ALL with poor clinical outcome compared to B-ALL.
  • Therefore, to improve treatment, it is imperative to delineate the molecular blueprint of this disease.
  • In addition to the activating mutations of Notch previously described, this review will outline combinations of mutations in pathways that contribute to Notch signaling and appear to drive T-ALL development by 'mimicking' Notch effects on cell cycle and apoptosis.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Neoplasm Proteins / physiology. Receptors, Notch / physiology. T-Lymphocytes / pathology
  • [MeSH-minor] Animals. Apoptosis / physiology. Cell Cycle / physiology. F-Box Proteins / physiology. Gene Expression Regulation, Leukemic. Genes, Tumor Suppressor. Humans. Ikaros Transcription Factor / genetics. Ikaros Transcription Factor / physiology. Ligands. Mice. Mice, Transgenic. Oncogenes. PTEN Phosphohydrolase / deficiency. PTEN Phosphohydrolase / genetics. PTEN Phosphohydrolase / physiology. Signal Transduction / physiology. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / physiology. Tumor Suppressor Proteins / physiology. Ubiquitin-Protein Ligases / physiology

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  • (PMID = 18758476.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA09171
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / F-Box Proteins; 0 / Fbxw7 protein, mouse; 0 / IKZF1 protein, human; 0 / Ligands; 0 / Neoplasm Proteins; 0 / Receptors, Notch; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 148971-36-2 / Ikaros Transcription Factor; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Number-of-references] 84
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40. Tosello V, Mansour MR, Barnes K, Paganin M, Sulis ML, Jenkinson S, Allen CG, Gale RE, Linch DC, Palomero T, Real P, Murty V, Yao X, Richards SM, Goldstone A, Rowe J, Basso G, Wiernik PH, Paietta E, Pieters R, Horstmann M, Meijerink JP, Ferrando AA: WT1 mutations in T-ALL. Blood; 2009 Jul 30;114(5):1038-45
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  • The molecular mechanisms involved in disease progression and relapse in T-cell acute lymphoblastic leukemia (T-ALL) are poorly understood.
  • This analysis showed that diagnosis and relapsed cases have common genetic alterations, but also that relapsed samples frequently lose chromosomal markers present at diagnosis, suggesting that relapsed T-ALL emerges from an ancestral clone different from the major leukemic population at diagnosis.

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  • (PMID = 19494353.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE15931
  • [Grant] United States / NCI NIH HHS / CA / R01 CA120196-03; United States / NCI NIH HHS / CA / CA114737; United Kingdom / Medical Research Council / / MC/ U137686856; United States / NCI NIH HHS / CA / R01 CA129382; United Kingdom / Medical Research Council / / ; United Kingdom / Medical Research Council / / MC/ U137686861; United States / NCI NIH HHS / CA / CA02111; United Kingdom / Medical Research Council / / G0500389; 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 / U24 CA114737
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / WT1 Proteins
  • [Other-IDs] NLM/ PMC2721784
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41. Gu L, Zhou C, Liu H, Gao J, Li Q, Mu D, Ma Z: Rapamycin sensitizes T-ALL cells to dexamethasone-induced apoptosis. J Exp Clin Cancer Res; 2010;29:150
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • BACKGROUND: Glucocorticoid (GC) resistance is frequently seen in acute lymphoblastic leukemia of T-cell lineage (T-ALL).
  • METHODS: Cell proliferation was detected by 3-(4,5-dimethylthiazol-2-yl)- 2,5-diphenyltetrazolium bromide (MTT) assay.
  • Fluorescence-activated cell sorting (FACS) analysis was used to analyze apoptosis and cell cycles.
  • Western blot analysis was performed to test the expression of the downstream effector proteins of mammalian target of rapamycin (mTOR), the cell cycle regulatory proteins, and apoptosis associated proteins.
  • Cell cycle arrest was associated with modulation of G1-S phase regulators.
  • Rapamycin enhanced GC-induced apoptosis and this was not achieved by modulation of glucocorticoid receptor (GR) expression, but synergistically up-regulation of pro-apoptotic proteins like caspase-3, Bax, and Bim, and down-regulation of anti-apoptotic protein of Mcl-1.
  • CONCLUSION: Our data suggests that rapamycin can effectively reverse GC resistance in T-ALL and this effect is achieved by inducing cell cycles arrested at G0/G1 phase and activating the intrinsic apoptotic program.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Dexamethasone / pharmacology. Drug Resistance, Neoplasm / drug effects. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Sirolimus / pharmacology
  • [MeSH-minor] Blotting, Western. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Separation. Drug Synergism. Flow Cytometry. Humans

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  • (PMID = 21083937.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 7S5I7G3JQL / Dexamethasone; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC2998469
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42. Ferrando AA: The role of NOTCH1 signaling in T-ALL. Hematology Am Soc Hematol Educ Program; 2009;:353-61
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The identification of activating mutations in NOTCH1 in over 50% of T-cell acute lymphoblastic leukemias (T-ALL) has generated major interest in the elucidation of the mechanisms of transformation downstream of oncogenic NOTCH and in the targeting of the NOTCH signaling pathway in this disease.

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  • (PMID = 20008221.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA120196-03; United States / NCI NIH HHS / CA / CA129382-02; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / CA120196-03; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / R01 CA129382-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / NOTCH1 protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptor, Notch1; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Number-of-references] 40
  • [Other-IDs] NLM/ NIHMS168983; NLM/ PMC2847371
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43. Chadwick N, Zeef L, Portillo V, Boros J, Hoyle S, van Doesburg JC, Buckle AM: Notch protection against apoptosis in T-ALL cells mediated by GIMAP5. Blood Cells Mol Dis; 2010 Oct 15;45(3):201-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent studies have highlighted the role of Notch signalling in the development of T cell acute lymphoblasic leukaemia (T-ALL).
  • The aims of this study were to determine the effect of Notch signalling on apoptosis in human T-ALL cell lines and to identify targets of Notch signalling that may mediate this effect.
  • Microarray analysis revealed that GIMAP5, a gene coding for an anti-apoptotic intracellular protein, is upregulated by Notch in T-ALL cell lines.
  • [MeSH-major] Apoptosis. GTP-Binding Proteins / biosynthesis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptor, Notch1 / metabolism. Receptors, Notch / metabolism. Signal Transduction

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20817506.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GIMAP5 protein, human; 0 / Glucocorticoids; 0 / NOTCH1 protein, human; 0 / NOTCH3 protein, human; 0 / Protease Inhibitors; 0 / Receptor, Notch1; 0 / Receptors, Notch; EC 3.6.1.- / GTP-Binding Proteins
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44. Van Vlierberghe P, Homminga I, Zuurbier L, Gladdines-Buijs J, van Wering ER, Horstmann M, Beverloo HB, Pieters R, Meijerink JP: Cooperative genetic defects in TLX3 rearranged pediatric T-ALL. Leukemia; 2008 Apr;22(4):762-70
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive neoplastic disorder, in which multiple genetic abnormalities cooperate in the malignant transformation of thymocytes.
  • [MeSH-major] Chromosome Aberrations. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Sequence Deletion
  • [MeSH-minor] Cell Cycle Proteins / genetics. Child. DNA Mutational Analysis. F-Box Proteins / genetics. Gene Dosage. Gene Rearrangement. Genome, Human. Humans. In Situ Hybridization, Fluorescence. Ubiquitin-Protein Ligases / genetics. WT1 Proteins / genetics

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  • (PMID = 18185524.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Homeodomain Proteins; 0 / TLX3 protein, human; 0 / WT1 Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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45. Dik WA, Brahim W, Braun C, Asnafi V, Dastugue N, Bernard OA, van Dongen JJ, Langerak AW, Macintyre EA, Delabesse E: CALM-AF10+ T-ALL expression profiles are characterized by overexpression of HOXA and BMI1 oncogenes. Leukemia; 2005 Nov;19(11):1948-57
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The t(10;11)(p13;q14-21) is found in T-ALL and acute myeloid leukemia and fuses CALM (Clathrin-Assembly protein-like Lymphoid-Myeloid leukaemia gene) to AF10.
  • Microarray results were validated by quantitative RT-PCR on an independent group of T-ALL and compared to mixed lineage leukemia-translocated acute leukemias (MLL-t AL).
  • We propose to define a HOXA+ leukemia group composed of at least MLL-t, CALM-AF10 and HOXA-t AL, which may benefit from adapted management.
  • [MeSH-major] Homeodomain Proteins / biosynthesis. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Nuclear Proteins / biosynthesis. Oncogene Proteins, Fusion / biosynthesis. Proto-Oncogene Proteins / biosynthesis. Repressor Proteins / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Cell Proliferation. Cell Transformation, Neoplastic. Child. Gene Expression Profiling. Humans. Oligonucleotide Array Sequence Analysis. Polycomb Repressive Complex 1. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic. Up-Regulation

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  • (PMID = 16107895.001).
  • [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 / AF10-CALM fusion protein, human; 0 / BMI1 protein, human; 0 / Homeodomain Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 157907-48-7 / HoxA protein; EC 6.3.2.19 / Polycomb Repressive Complex 1
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46. Clappier E, Cuccuini W, Kalota A, Crinquette A, Cayuela JM, Dik WA, Langerak AW, Montpellier B, Nadel B, Walrafen P, Delattre O, Aurias A, Leblanc T, Dombret H, Gewirtz AM, Baruchel A, Sigaux F, Soulier J: The C-MYB locus is involved in chromosomal translocation and genomic duplications in human T-cell acute leukemia (T-ALL), the translocation defining a new T-ALL subtype in very young children. Blood; 2007 Aug 15;110(4):1251-61
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] The C-MYB locus is involved in chromosomal translocation and genomic duplications in human T-cell acute leukemia (T-ALL), the translocation defining a new T-ALL subtype in very young children.
  • The C-Myb transcription factor is essential for hematopoiesis, including in the T-cell lineage.
  • Here, we identified 2 types of genomic alterations involving the C-MYB locus at 6q23 in human T-cell acute leukemia (T-ALL).
  • Expression analysis, including allele-specific approaches, showed stronger C-MYB expression in the MYB-rearranged cases compared with other T-ALLs, and a dramatically skewed C-MYB allele expression in the TCRB-MYB cases, which suggests that a translocation-driven deregulated expression may overcome a cellular attempt to down-regulate C-MYB.
  • Strikingly, profiling of the T-ALLs by clinical, genomic, and large-scale gene expression analyses shows that the TCRB-MYB translocation defines a new T-ALL subtype associated with a very young age for T-cell leukemia (median, 2.2 years) and with a proliferation/mitosis expression signature.
  • [MeSH-major] Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 7 / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Proto-Oncogene Proteins c-myb / genetics. Translocation, Genetic

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  • (PMID = 17452517.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA101859
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myb
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47. O'Neil J, Calvo J, McKenna K, Krishnamoorthy V, Aster JC, Bassing CH, Alt FW, Kelliher M, Look AT: Activating Notch1 mutations in mouse models of T-ALL. Blood; 2006 Jan 15;107(2):781-5
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent studies have demonstrated that most patients with T-cell acute lymphocytic leukemia (T-ALL) have activating mutations in NOTCH1.
  • We sequenced the heterodimerization domain and the PEST domain of Notch1 in our mouse model of TAL1-induced leukemia and found that 74% of the tumors harbor activating mutations in Notch1.
  • Cell lines derived from these tumors undergo G(0)/G(1) arrest and apoptosis when treated with a gamma-secretase inhibitor.
  • Thus, Notch1 mutations are often acquired as a part of the molecular pathogenesis of T-ALLs that develop in mice with known predisposing genetic alterations.
  • [MeSH-major] Disease Models, Animal. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma / genetics. Mutation / genetics. Receptor, Notch1 / genetics. Thymus Neoplasms / genetics
  • [MeSH-minor] Amyloid Precursor Protein Secretases. Animals. Apoptosis. Aspartic Acid Endopeptidases. Basic Helix-Loop-Helix Transcription Factors / genetics. Basic Helix-Loop-Helix Transcription Factors / physiology. DNA-Binding Proteins / genetics. DNA-Binding Proteins / physiology. Endopeptidases / chemistry. Enzyme Inhibitors / pharmacology. Female. G0 Phase. G1 Phase. Histones / genetics. Histones / physiology. Humans. Male. Mice. Mice, Transgenic. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / physiology. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / physiology

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  • (PMID = 16166587.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096899
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / H2AX protein, mouse; 0 / Histones; 0 / NOTCH1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Rag2 protein, mouse; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse; 0 / Tumor Suppressor Protein p53; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.- / Endopeptidases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / BACE1 protein, human; EC 3.4.23.46 / Bace1 protein, mouse
  • [Other-IDs] NLM/ PMC1895623
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48. Liu S, Breit S, Danckwardt S, Muckenthaler MU, Kulozik AE: Downregulation of Notch signaling by gamma-secretase inhibition can abrogate chemotherapy-induced apoptosis in T-ALL cell lines. Ann Hematol; 2009 Jul;88(7):613-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Downregulation of Notch signaling by gamma-secretase inhibition can abrogate chemotherapy-induced apoptosis in T-ALL cell lines.
  • Activation of Notch1 signaling plays an important role in the pathogenesis of precursor T-cell lymphoblastic leukemia (T-ALL).
  • In this study, we analyzed the response of four T-ALL cell lines to compound E, a potent gamma-secretase inhibitor, and to the combination of compound E with vincristine, daunorubicin, L-asparaginase (L-ASP), and dexamethasone (DEX).
  • We identified two distinct types of responses: In type 1 cell lines, represented by TALL1 and HSB2, GSI-induced apoptosis followed cell cycle arrest and enhanced the induction of apoptosis caused by DEX and L-ASP.
  • In type 2 cell lines, represented by CEM and Jurkat J6, GSI caused neither cell cycle block nor cell death.
  • In type 2 cells, GSI induced the upregulation of Bcl-xl mRNA and protein, which was thus identified as a candidate mechanism for the inhibition of apoptosis.
  • [MeSH-major] Amyloid Precursor Protein Secretases / physiology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Receptor, Notch1 / antagonists & inhibitors
  • [MeSH-minor] Asparaginase / pharmacology. Benzodiazepinones / pharmacology. Cell Line, Tumor. Daunorubicin / pharmacology. Dexamethasone / pharmacology. Down-Regulation. Humans. Signal Transduction. Vincristine / pharmacology

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  • (PMID = 19057901.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 2-(((3,5-difluorophenyl)acetyl)amino)-N-(1-methyl-2-oxo-5-phenyl-2,3-dihydro-1H-1,4-benzodiazepin-3-yl)propanamide; 0 / Benzodiazepinones; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.5.1.1 / Asparaginase; ZS7284E0ZP / Daunorubicin
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49. Imataki O, Koike A, Iwabu M, Shintani T, Waki F, Ohue Y, Ohnishi H, Ishida T: [Limited but potential efficacy by graft-versus-leukemia (GVL) for Pro T-ALL]. Gan To Kagaku Ryoho; 2008 Nov;35(11):1911-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Limited but potential efficacy by graft-versus-leukemia (GVL) for Pro T-ALL].
  • We present a 22-year-old male diagnosed with pro T-acute lymphoblastic leukemia (ALL).
  • Flow cytometry analysis of the leukemic cells showed cCD3+, CD7+, CD2+, CD1a-, CD3-, CD5-, CD4-, CD8-, CD34+, and HLA-DR+ as a pro T-cell phenotype.
  • He underwent up-front stem cell transplantation (SCT) from an HLA-full matched sibling, with early relapse just before transplantation.
  • Based on the immature T cell phenotype frequently with myeloid markers, a graft-versus- leukemic effect might be expected after allogeneic SCT for Pro T-ALL and a positive indication of SCT for this disease should be considered.
  • [MeSH-major] Graft vs Leukemia Effect / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 19011341.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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50. Indraccolo S, Minuzzo S, Masiero M, Amadori A: Ligand-driven activation of the notch pathway in T-ALL and solid tumors: why Not(ch)? Cell Cycle; 2010 Jan 1;9(1):80-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ligand-driven activation of the notch pathway in T-ALL and solid tumors: why Not(ch)?
  • The Notch pathway is an evolutionally conserved cell-cell interaction signalling system involved in several key aspects of cell life, ranging from differentiation and proliferation to apoptosis.
  • The clearest example of oncogenic Notch signalling is observed in T acute lymphoblastic leukemia (T-ALL), an aggressive neoplasm of immature T-cells, due to genetic alterations leading to ligand-independent increased Notch1 receptor signalling.
  • In solid tumors, however, extrinsic regulation through canonical cell-cell interactions appears to drive activation of the pathway.
  • [MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptors, Notch / metabolism
  • [MeSH-minor] Animals. Humans. Intracellular Signaling Peptides and Proteins. Leukemia / metabolism. Membrane Proteins / metabolism. Models, Biological. Neovascularization, Pathologic / metabolism. Signal Transduction / genetics. Signal Transduction / physiology

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  • (PMID = 20016278.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / Receptors, Notch; 0 / delta protein
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51. Dik WA, Nadel B, Przybylski GK, Asnafi V, Grabarczyk P, Navarro JM, Verhaaf B, Schmidt CA, Macintyre EA, van Dongen JJ, Langerak AW: Different chromosomal breakpoints impact the level of LMO2 expression in T-ALL. Blood; 2007 Jul 1;110(1):388-92

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The t(11;14)(p13;q11) is presumed to arise from an erroneous T-cell receptor delta TCRD V(D)J recombination and to result in LMO2 activation.
  • We performed combined in vivo, ex vivo, and in silico analyses on 9 new t(11;14)(p13;q11)-positive T-cell acute lymphoblastic leukemia (T-ALL) as well as normal thymocytes.
  • [MeSH-major] Chromosome Breakage. DNA-Binding Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Metalloproteins / genetics
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 14. Genes, T-Cell Receptor delta. Humans. LIM Domain Proteins. Proto-Oncogene Proteins / genetics. Translocation, Genetic

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  • (PMID = 17360939.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LMO2 protein, human; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins
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52. Cullion K, Draheim KM, Hermance N, Tammam J, Sharma VM, Ware C, Nikov G, Krishnamoorthy V, Majumder PK, Kelliher MA: Targeting the Notch1 and mTOR pathways in a mouse T-ALL model. Blood; 2009 Jun 11;113(24):6172-81
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  • Mutations in NOTCH1 are frequently detected in patients with T-cell acute lymphoblastic leukemia (T-ALL) and in mouse T-ALL models.
  • Treatment of mouse or human T-ALL cell lines in vitro with gamma-secretase inhibitors (GSIs) results in growth arrest and/or apoptosis.
  • T-ALL cell lines also exhibit PI3K/mTOR pathway activation, indicating that rapamycin may also have therapeutic benefit.

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  • (PMID = 19246562.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096899; United States / NCI NIH HHS / CA / CA096899; United States / NIDDK NIH HHS / DK / P30DK32529
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Carrier Proteins; 0 / Cyclic S-Oxides; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / MRK 003; 0 / Proto-Oncogene Proteins; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse; 0 / Thiadiazoles; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ PMC2699237
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53. 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.
  • Four percent of cases were pro-T, 47% pre-T, 39% cortical T, and 10% mature T-ALL.
  • Fifty-six percent of patients with pro-T + pre-T-ALL achieved complete remission (CR) compared with 91% for cortical + mature cases (P = .002).
  • 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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54. Dohnal AM, Inthal A, Felzmann T, Glatt S, Sommergruber W, Mann G, Gadner H, Panzer-Grümayer ER: Leukemia-associated antigenic isoforms induce a specific immune response in children with T-ALL. Int J Cancer; 2006 Dec 15;119(12):2870-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukemia-associated antigenic isoforms induce a specific immune response in children with T-ALL.
  • The potential immunogenicity of acute lymphoblastic leukemia of the T cell (T-ALL), a small subgroup of childhood leukemia with increased risk for treatment failure and early relapse, was addressed by serological identification of leukemia-derived antigens by recombinant expression cloning (SEREX).
  • Further characterization of the 4 novel isoforms revealed that 3 (HECTD1Delta, CX-ORF-15Delta and hCAP-EDelta) had restricted mRNA expression in more than 70% of T-ALLs (n = 22) and that specific antibodies against these isoforms were detected in up to 30% of patients (n = 16), with the highest frequency for HECTD1Delta.
  • The latter protein was present at high abundance in T-ALLs but not in normal hematopoietic tissues.
  • Given that the leukemia-associated antigens detected in this study have an intracellular localization, the generation of immune effector responses most likely requires antigen presentation.
  • To test this assumption, dendritic cells were loaded with HECTD1Delta protein and used for T cell stimulation.
  • A specific T cell response was induced in vitro in all 3 healthy donors studied, including a former T-ALL patient.
  • [MeSH-major] Antigens, Neoplasm / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 17016825.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, Neoplasm; 0 / DNA, Complementary; 0 / Protein Isoforms; 0 / RNA, Messenger; 82115-62-6 / Interferon-gamma
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55. O'Neil J, Tchinda J, Gutierrez A, Moreau L, Maser RS, Wong KK, Li W, McKenna K, Liu XS, Feng B, Neuberg D, Silverman L, DeAngelo DJ, Kutok JL, Rothstein R, DePinho RA, Chin L, Lee C, Look AT: Alu elements mediate MYB gene tandem duplication in human T-ALL. J Exp Med; 2007 Dec 24;204(13):3059-66
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  • Recent studies have demonstrated that the MYB oncogene is frequently duplicated in human T cell acute lymphoblastic leukemia (T-ALL).

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  • (PMID = 18070937.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE7615
  • [Grant] United States / NCI NIH HHS / CA / P01 CA109901; United States / NIGMS NIH HHS / GM / R37 GM050237; United States / NCI NIH HHS / CA / CA11560; United States / NIGMS NIH HHS / GM / GM067055; United States / NIGMS NIH HHS / GM / R01 GM067055; United States / NIGMS NIH HHS / GM / R01 GM050237; United States / NCI NIH HHS / CA / R01 CA111560; United States / NCI NIH HHS / CA / R21 CA115853; United States / NIGMS NIH HHS / GM / GM050237; United States / NCI NIH HHS / CA / CA115853; United States / NCI NIH HHS / CA / CA68484-11; United States / NCI NIH HHS / CA / P01 CA068484; United States / NCI NIH HHS / CA / CA109901
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myb
  • [Other-IDs] NLM/ PMC2150982
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56. Calzavara E, Chiaramonte R, Cesana D, Basile A, Sherbet GV, Comi P: Reciprocal regulation of Notch and PI3K/Akt signalling in T-ALL cells in vitro. J Cell Biochem; 2008 Apr 1;103(5):1405-12
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Our analyses indicate that the PI3K/Akt pathway is constitutively active in the four T-ALL cell lines tested.
  • PTEN expression was not detected in 3/4 cell lines tested, suggesting the loss of PTEN-mediated Akt activation.
  • We analysed the relationship between Notch-1 and the PI3K/Akt signalling and show that inhibition of the Akt pathway changes Notch expression; Notch-1 protein decreased in all the cell lines upon treatment with the inhibitor.
  • [MeSH-major] Phosphatidylinositol 3-Kinases / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptor, Notch1 / metabolism. Signal Transduction

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  • [Copyright] 2007 Wiley-Liss, Inc.
  • (PMID = 17849443.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / bcl-2-Associated X Protein; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 3.6.5.2 / ras Proteins
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57. Krieger D, Moericke A, Oschlies I, Zimmermann M, Schrappe M, Reiter A, Burkhardt B: Frequency and clinical relevance of DNA microsatellite alterations of the CDKN2A/B, ATM and p53 gene loci: a comparison between pediatric precursor T-cell lymphoblastic lymphoma and T-cell lymphoblastic leukemia. Haematologica; 2010 Jan;95(1):158-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequency and clinical relevance of DNA microsatellite alterations of the CDKN2A/B, ATM and p53 gene loci: a comparison between pediatric precursor T-cell lymphoblastic lymphoma and T-cell lymphoblastic leukemia.
  • Although deletions of cell cycle regulatory gene loci have long been reported in various malignancies, little is known regarding their relevance in pediatric T-cell lymphoblastic lymphoma (T-LBL) and T-cell lymphoblastic leukemia (TALL).
  • [MeSH-major] Cell Cycle Proteins / genetics. Cyclin-Dependent Kinase Inhibitor p15 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. DNA-Binding Proteins / genetics. Genetic Loci / genetics. Leukemia, T-Cell / genetics. Microsatellite Repeats / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Protein-Serine-Threonine Kinases / genetics. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 19586936.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / CDKN2B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / Genetic Markers; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ PMC2805736
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58. Guo D, Ye J, Dai J, Li L, Chen F, Ma D, Ji C: Notch-1 regulates Akt signaling pathway and the expression of cell cycle regulatory proteins cyclin D1, CDK2 and p21 in T-ALL cell lines. Leuk Res; 2009 May;33(5):678-85
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  • [Title] Notch-1 regulates Akt signaling pathway and the expression of cell cycle regulatory proteins cyclin D1, CDK2 and p21 in T-ALL cell lines.
  • Gain-of-function mutations in Notch-1 are common in T-cell lymphoblastic leukemia (T-ALL), making this receptor a promising target for drugs such as gamma-secretase inhibitors (GSIs).
  • However, GSIs seem to be active in only a small fraction of T-ALL cell lines with constitutive Notch-1 activity and the downstream response of Notch signaling is only partially understood.
  • To further investigate the molecular mechanisms underlying proliferation suppression and apoptosis and explore effective downstream target genes, we used RNA interference (RNAi) technology to down-regulate the expression of Notch-1 in GSIs-resistant T-ALL cell lines.
  • Results showed that down-regulation of Notch-1 by transfection of a small interfering RNA (siRNA) could cause SupT1 cells proliferation inhibition by inducing G(0)/G(1) cell cycle arrest and apoptosis.
  • The proliferation inhibitory and apoptotic effects resulting from down-regulation of Notch-1 may be mediated through regulating the expression of cell cycle regulatory proteins cyclin D1, CDK2 and p21 and the activity of Akt signaling.
  • Taken together, cell cycle regulatory proteins and Akt signaling may be attractive targets in T-ALL.
  • [MeSH-major] CDC2 Protein Kinase / genetics. Cyclin D1 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-akt / metabolism. Receptor, Notch1 / physiology. Signal Transduction / physiology
  • [MeSH-minor] Apoptosis. Base Sequence. Cell Cycle. Cell Line, Tumor. Cell Proliferation. Down-Regulation / physiology. Humans. Mutation. RNA Interference. RNA, Small Interfering. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19091404.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / NOTCH1 protein, human; 0 / RNA, Small Interfering; 0 / Receptor, Notch1; 136601-57-5 / Cyclin D1; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.22 / CDC2 Protein Kinase
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59. Balgobind BV, Van Vlierberghe P, van den Ouweland AM, Beverloo HB, Terlouw-Kromosoeto JN, van Wering ER, Reinhardt D, Horstmann M, Kaspers GJ, Pieters R, Zwaan CM, Van den Heuvel-Eibrink MM, Meijerink JP: Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis. Blood; 2008 Apr 15;111(8):4322-8
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  • [Title] Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis.
  • Neurofibromatosis type 1 (NF1) is an autosomal dominant genetic disorder caused by mutations in the NF1 gene.
  • Patients with NF1 have a higher risk to develop juvenile myelomonocytic leukemia (JMML) with a possible progression toward acute myeloid leukemia (AML).
  • In an oligo array comparative genomic hybridization-based screening of 103 patients with pediatric T-cell acute lymphoblastic leukemia (T-ALL) and 71 patients with MLL-rearranged AML, a recurrent cryptic deletion, del(17)(q11.2), was identified in 3 patients with T-ALL and 2 patients with MLL-rearranged AML.
  • Since the NF1 protein is a negative regulator of the RAS pathway (RAS-GTPase activating protein), homozygous NF1 inactivation represent a novel type I mutation in pediatric MLL-rearranged AML and T-ALL with a predicted frequency that is less than 10%.
  • NF1 inactivation may provide an additional proliferative signal toward the development of leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation / genetics. Neurofibromatoses / genetics. Neurofibromin 1 / genetics

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  • (PMID = 18172006.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neurofibromin 1; 0 / RNA, Messenger
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60. Marçais A, Jeannet R, Hernandez L, Soulier J, Sigaux F, Chan S, Kastner P: Genetic inactivation of Ikaros is a rare event in human T-ALL. Leuk Res; 2010 Apr;34(4):426-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The Ikaros (Ikzf1) gene, encoding a transcription regulator, is a major tumor suppressor in B-cell acute lymphoblastic leukemia (B-ALL).
  • [MeSH-major] Gene Silencing. Ikaros Transcription Factor / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • [CommentIn] Leuk Res. 2010 Apr;34(4):416-7 [19892402.001]
  • (PMID = 19796813.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / IKZF1 protein, human; 0 / Protein Isoforms; 148971-36-2 / Ikaros Transcription Factor
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61. Hernandez CP, Morrow K, Lopez-Barcons LA, Zabaleta J, Sierra R, Velasco C, Cole J, Rodriguez PC: Pegylated arginase I: a potential therapeutic approach in T-ALL. Blood; 2010 Jun 24;115(25):5214-21
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  • Adult patients with acute lymphoblastic T cell leukemia (T-ALL) have a very poor prognosis and few effective therapeutic options.
  • In addition, treatment of malignant T-cell lines with peg-Arg I significantly impaired their proliferation, which correlated with a decreased progression into the cell cycle, followed by the induction of apoptosis.
  • The results suggest the potential benefit of L-Arginine depletion by peg-Arg I in the treatment of T-cell malignancies.

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  • (PMID = 20407034.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / P20RR021970; United States / NCRR NIH HHS / RR / P20 RR021970; United States / NCI NIH HHS / CA / R01 CA082689; United States / NIGMS NIH HHS / GM / P20 GM103501; United States / NCI NIH HHS / CA / R01 CA107974
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CCND3 protein, human; 0 / Cyclin D3; 04079A1RDZ / Cytarabine; 30IQX730WE / Polyethylene Glycols; 94ZLA3W45F / Arginine; EC 3.5.3.1 / Arginase
  • [Other-IDs] NLM/ PMC2892956
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62. Eguchi-Ishimae M, Eguchi M, Kempski H, Greaves M: NOTCH1 mutation can be an early, prenatal genetic event in T-ALL. Blood; 2008 Jan 1;111(1):376-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • NOTCH1 mutations are common in T-lineage acute lymphoblastic leukemia (T-ALL).
  • Twin studies and retrospective screening of neonatal blood spots provide evidence that fusion genes and other chromosomal abnormalities associated with pediatric leukemias can originate prenatally.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics

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  • (PMID = 17901244.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
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63. Estes DA, Lovato DM, Khawaja HM, Winter SS, Larson RS: Genetic alterations determine chemotherapy resistance in childhood T-ALL: modelling in stage-specific cell lines and correlation with diagnostic patient samples. Br J Haematol; 2007 Oct;139(1):20-30
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] Genetic alterations determine chemotherapy resistance in childhood T-ALL: modelling in stage-specific cell lines and correlation with diagnostic patient samples.
  • Acquired drug resistance eventually leads to treatment failure in T-cell acute lymphoblastic leukaemia (T-ALL).
  • Immunophenotypic and cytogenetic heterogeneities within T-ALL influence susceptibility to cytotoxic therapy, and little is known about the mechanisms of drug resistance at specific stages of T-cell ontogeny.
  • We developed tolerance to therapeutic concentrations of daunorubicin (DNR) and L-asparaginase (L-asp) in Jurkat (CD1a(-), sCD3(+)) and Sup T1 (CD1a(+), sCD3(-)) cell lines, having respective 'mature' and 'cortical' stages of developmental arrest.
  • Microarray analysis identified upregulation of asparagine synthetase (ASNS) and argininosuccinate synthase 1 (ASS1) to cell lines with acquired resistance to L-asp, and in the case of DNR, upregulation of ATP-binding cassette B1 (ABCB1).
  • This study expands the pool of available drug resistant cell lines having cortical and mature stages of developmental arrest, introduces three new drug resistant T-ALL cell lines, and identifies gene interactions leading to L-asp and DNR resistance.
  • [MeSH-major] Cell Line, Tumor. Drug Resistance, Neoplasm / genetics. Gene Expression Regulation, Leukemic. Genes, MDR. Leukemia-Lymphoma, Adult T-Cell / genetics

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  • (PMID = 17854304.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1 R01 CA114589; United States / NCI NIH HHS / CA / U10 CA98543-03-14305
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / P-Glycoprotein; 0 / RNA, Small Interfering; 5J49Q6B70F / Vincristine; 9PHQ9Y1OLM / Prednisolone; EC 3.5.1.1 / Asparaginase; EC 6.3.1.1 / Aspartate-Ammonia Ligase; EC 6.3.4.5 / Argininosuccinate Synthase; ZS7284E0ZP / Daunorubicin
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64. van Grotel M, Meijerink JP, van Wering ER, Langerak AW, Beverloo HB, Buijs-Gladdines JG, Burger NB, Passier M, van Lieshout EM, Kamps WA, Veerman AJ, van Noesel MM, Pieters R: Prognostic significance of molecular-cytogenetic abnormalities in pediatric T-ALL is not explained by immunophenotypic differences. Leukemia; 2008 Jan;22(1):124-31

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Pediatric T-cell acute lymphoblastic leukemia (T-ALL) is characterized by chromosomal rearrangements possibly enforcing arrest at specific development stages.
  • We studied the relationship between molecular-cytogenetic abnormalities and T-cell development stage to investigate whether arrest at specific stages can explain the prognostic significance of specific abnormalities.
  • HOX11 cases were CD1 positive consistent with a cortical stage, but as 4/5 cases lacked cytoplasmatic-beta expression, developmental arrest may precede beta-selection.
  • HOX11L2 was especially confined to immature and pre-AB developmental stages, but 3/17 HOX11L2 mature cases were restricted to the gammadelta-lineage.
  • Classification into T-cell developmental subgroups was not predictive for outcome.
  • [MeSH-major] Gene Rearrangement / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Neoplasm Recurrence, Local / genetics. Receptor, Notch1 / genetics
  • [MeSH-minor] Basic Helix-Loop-Helix Transcription Factors / genetics. Cell Lineage. Child. Female. Homeodomain Proteins / genetics. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Mutation / genetics. Oncogene Proteins, Fusion / genetics. Prognosis. Proto-Oncogene Proteins / genetics. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Receptors, Antigen, T-Cell, alpha-beta / genetics. Receptors, Antigen, T-Cell, gamma-delta / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17928886.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AF10-CALM fusion protein, human; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Homeodomain Proteins; 0 / NOTCH1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Antigen, T-Cell, gamma-delta; 0 / TLX3 protein, human; 135471-20-4 / TAL1 protein, human
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65. Burmeister T, Gökbuget N, Reinhardt R, Rieder H, Hoelzer D, Schwartz S: NUP214-ABL1 in adult T-ALL: the GMALL study group experience. Blood; 2006 Nov 15;108(10):3556-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The NUP214-ABL1 fusion gene in T-cell acute lymphoblastic leukemia (T-ALL) has recently been identified as a possible target for imatinib and related tyrosine kinase inhibitors, but exact data regarding the prognostic impact and frequency of the several putative NUP214-ABL1 mRNA transcripts are still missing.
  • Eleven (3.9%) patients were NUP214-ABL1 positive, and 5 different transcripts were observed; 8 patients had a thymic immunophenotype, 1 had an early T-cell immunophenotype, and 2 had a mature T-cell immunophenotype.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-abl / genetics

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  • (PMID = 16873673.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / NUP214 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
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66. Cauwelier B, Dastugue N, Cools J, Poppe B, Herens C, De Paepe A, Hagemeijer A, Speleman F: Molecular cytogenetic study of 126 unselected T-ALL cases reveals high incidence of TCRbeta locus rearrangements and putative new T-cell oncogenes. Leukemia; 2006 Jul;20(7):1238-44

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  • [Title] Molecular cytogenetic study of 126 unselected T-ALL cases reveals high incidence of TCRbeta locus rearrangements and putative new T-cell oncogenes.
  • Chromosomal aberrations of T-cell receptor (TCR) gene loci often involve the TCRalphadelta (14q11) locus and affect various known T-cell oncogenes.
  • Therefore, we initiated a screening of 126 T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma cases and 19 T-ALL cell lines using FISH break-apart assays for the different TCR loci.
  • Some of these chromosome aberrations target new putative T-cell oncogenes at chromosome 11q24, 20p12 and 6q22.
  • Five patients and one cell line carried chromosomal rearrangements affecting both TCRbeta and TCRalphadelta loci.
  • In conclusion, this study presents the first inventory of chromosomal rearrangements of TCR loci in T-ALL, revealing an unexpected high number of cryptic chromosomal rearrangements of the TCRbeta locus and further broadening the spectrum of genes putatively implicated in T-cell oncogenesis.
  • [MeSH-major] Gene Rearrangement, T-Lymphocyte / genetics. Genes, T-Cell Receptor beta / genetics. Leukemia-Lymphoma, Adult T-Cell / epidemiology. Leukemia-Lymphoma, Adult T-Cell / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Genes, T-Cell Receptor alpha / genetics. Genes, T-Cell Receptor delta / genetics. Humans. In Situ Hybridization, Fluorescence. Incidence. Male. Middle Aged. Retrospective Studies. Translocation, Genetic

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  • (PMID = 16673021.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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67. Gordon WR, Roy M, Vardar-Ulu D, Garfinkel M, Mansour MR, Aster JC, Blacklow SC: Structure of the Notch1-negative regulatory region: implications for normal activation and pathogenic signaling in T-ALL. Blood; 2009 Apr 30;113(18):4381-90
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  • The NRR includes the 3 Lin12/Notch repeats and the juxtamembrane heterodimerization domain, the region of Notch1 most frequently mutated in T-cell acute lymphoblastic leukemia lymphoma (T-ALL).

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  • (PMID = 19075186.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R56 CA092433; United States / NCI NIH HHS / CA / R56 CA092433-06A1; United States / NCI NIH HHS / CA / CA092433; None / None / / R01 CA092433-05; United States / NCI NIH HHS / CA / P01 CA119070-03; United States / NCI NIH HHS / CA / R01 CA092433; United States / NCI NIH HHS / CA / CA119070-030003; United Kingdom / Medical Research Council / / G0500389; United States / NCI NIH HHS / CA / P01 CA119070-029001; None / None / / P01 CA119070-03; United States / NCI NIH HHS / CA / R01 CA092433-04; United States / NCI NIH HHS / CA / P01 CA119070-020003; United States / NCI NIH HHS / CA / R01 CA092433-05S1; United States / NCI NIH HHS / CA / CA119070-029001; United States / NCI NIH HHS / CA / P01 CA119070-039001; United States / NCI NIH HHS / CA / P01 CA119070-030003; None / None / / R01 CA092433-05S1; United States / NCI NIH HHS / CA / R01 CA092433-05; None / None / / R56 CA092433-06A1; United States / NCI NIH HHS / CA / CA119070-039001; United States / NCI NIH HHS / CA / CA119070-020003; United States / NCI NIH HHS / CA / CA092433-04; United States / NCI NIH HHS / CA / P01 CA119070
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / NOTCH2 protein, human; 0 / Receptor, Notch1; 0 / Receptor, Notch2; EC 1.13.12.- / Luciferases
  • [Other-IDs] NLM/ PMC2676092
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68. Xu SN, Chen JP: [Research advance on the pathogenesis of T-ALL induced by notch 1 activating mutations]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Feb;18(1):242-5
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  • T-cell acute lymphoblastic leukemia (T-ALL) is the hematological malignancy of bone marrow characterized by the rapid proliferation and subsequent accumulation of immature T lymphocyte and mainly occurs in children and adolescents.
  • This review briefly discusses the four main subtypes of Notch 1 activating mutations, also focuses on how these mutations change the normal signaling pathways and genes expression during their participation in the pathogenesis of T-ALL, and how these insights will promote the development of newly targeting therapies for patients with this aggressive form of leukemia.

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  • (PMID = 20137156.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Receptor, Notch1
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69. 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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  • [Title] NOTCH1/FBXW7 mutation identifies a large subgroup with favorable outcome in adult T-cell acute lymphoblastic leukemia (T-ALL): a Group for Research on Adult Acute Lymphoblastic Leukemia (GRAALL) study.
  • Many somatic genetic abnormalities have been identified in T-cell acute lymphoblastic leukemia (T-ALL) but each individual abnormality accounts for a small proportion of cases; therapeutic stratification consequently still relies on classical clinical markers.
  • We screened 141 adult diagnostic T-ALL samples from patients treated on either the Lymphoblastic Acute Leukemia in Adults (LALA)-94 (n = 87) or the GRAALL-2003 (n = 54) trials.
  • In 88 cases (62%) there were demonstrated NOTCH1 mutations (42% heterodimerization [HD], 10% HD+proline glutamate serine threonine [PEST], 6% PEST, 2% juxtamembrane mutations, 2% transactivation domain [TAD]) and 34 cases (24%) had FBXW7 mutations (21 cases had both NOTCH1 and FBXW7 mutations); 40 cases (28%) were wild type for both.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics. Ubiquitin-Protein Ligases / genetics

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  • (PMID = 19109228.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Receptor, Notch1; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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70. Jeannet R, Mastio J, Macias-Garcia A, Oravecz A, Ashworth T, Geimer Le Lay AS, Jost B, Le Gras S, Ghysdael J, Gridley T, Honjo T, Radtke F, Aster JC, Chan S, Kastner P: Oncogenic activation of the Notch1 gene by deletion of its promoter in Ikaros-deficient T-ALL. Blood; 2010 Dec 16;116(25):5443-54
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  • The Notch pathway is frequently activated in T-cell acute lymphoblastic leukemias (T-ALLs).
  • Of the Notch receptors, Notch1 is a recurrent target of gain-of-function mutations and Notch3 is expressed in all T-ALLs, but it is currently unclear how these receptors contribute to T-cell transformation in vivo.
  • While deletion of Notch3 has little effect, T cell-specific deletion of floxed Notch1 promoter/exon 1 sequences significantly accelerates leukemogenesis.
  • Further, spontaneous deletion of 5' Notch1 sequences occurs in approximately 75% of Ikaros-deficient T-ALLs.
  • [MeSH-major] Ikaros Transcription Factor / physiology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic / genetics. Receptor, Notch1 / genetics. Transcriptional Activation / physiology
  • [MeSH-minor] Animals. Blotting, Northern. Blotting, Western. Cell Transformation, Neoplastic. DNA Primers / chemistry. DNA Primers / genetics. Flow Cytometry. Gene Expression Regulation, Neoplastic. Immunoglobulin J Recombination Signal Sequence-Binding Protein / physiology. Mice. Mice, Knockout. Mutation / genetics. RNA, Messenger / genetics. Receptors, Notch / physiology. Reverse Transcriptase Polymerase Chain Reaction. Sequence Deletion. Survival Rate

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  • (PMID = 20829372.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / R01 HD034883
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Immunoglobulin J Recombination Signal Sequence-Binding Protein; 0 / Notch1 protein, mouse; 0 / Notch3 protein, mouse; 0 / RNA, Messenger; 0 / Rbpj protein, mouse; 0 / Receptor, Notch1; 0 / Receptors, Notch; 0 / Zfpn1a1 protein, mouse; 148971-36-2 / Ikaros Transcription Factor
  • [Other-IDs] NLM/ PMC3100247
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71. 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.
  • T cells develop from bone marrow-derived self-renewing hematopoietic stem cells (HSC).
  • 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).
  • For example, bHLH oncoproteins inhibit E2A and HEB, revealing their tumor suppressor function in the thymus.
  • The induction of T-ALL, nonetheless, requires collaboration with constitutive NOTCH1 signaling and the pre-TCR, as well as loss-of-function mutations for CDKN2A and PTEN.
  • Significantly, NOTCH1, the pre-TCR pathway, and E2A/HEB proteins control critical checkpoints and branchpoints in early thymocyte development whereas several oncogenic transcription factors, HOXA9, c-MYB, SCL, and LYL-1 control HSC self-renewal.
  • 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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72. Ashworth TD, Pear WS, Chiang MY, Blacklow SC, Mastio J, Xu L, Kelliher M, Kastner P, Chan S, Aster JC: Deletion-based mechanisms of Notch1 activation in T-ALL: key roles for RAG recombinase and a conserved internal translational start site in Notch1. Blood; 2010 Dec 16;116(25):5455-64
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  • Point mutations that trigger ligand-independent proteolysis of the Notch1 ectodomain occur frequently in human T-cell acute lymphoblastic leukemia (T-ALL) but are rare in murine T-ALL, suggesting that other mechanisms account for Notch1 activation in murine tumors.
  • Here we show that most murine T-ALLs harbor Notch1 deletions that fall into 2 types, both leading to ligand-independent Notch1 activation.
  • Type 1 deletions remove exon 1 and the proximal promoter, appear to be RAG-mediated, and are associated with mRNA transcripts that initiate from 3' regions of Notch1.
  • Type 2 deletions remove sequences between exon 1 and exons 26 to 28 of Notch1, appear to be RAG-independent, and are associated with transcripts in which exon 1 is spliced out of frame to 3' Notch1 exons.
  • [MeSH-major] Homeodomain Proteins / physiology. Peptide Chain Initiation, Translational / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic / genetics. Receptor, Notch1 / genetics. Transcriptional Activation / physiology

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  • (PMID = 20852131.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096899
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Notch1 protein, mouse; 0 / RNA, Messenger; 0 / Receptor, Notch1; 0 / Zfpn1a1 protein, mouse; 128559-51-3 / RAG-1 protein; 148971-36-2 / Ikaros Transcription Factor
  • [Other-IDs] NLM/ PMC3031398
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73. Przybylski GK, Dik WA, Wanzeck J, Grabarczyk P, Majunke S, Martin-Subero JI, Siebert R, Dölken G, Ludwig WD, Verhaaf B, van Dongen JJ, Schmidt CA, Langerak AW: Disruption of the BCL11B gene through inv(14)(q11.2q32.31) results in the expression of BCL11B-TRDC fusion transcripts and is associated with the absence of wild-type BCL11B transcripts in T-ALL. Leukemia; 2005 Feb;19(2):201-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Disruption of the BCL11B gene through inv(14)(q11.2q32.31) results in the expression of BCL11B-TRDC fusion transcripts and is associated with the absence of wild-type BCL11B transcripts in T-ALL.
  • T-cell acute lymphoblastic leukemia (T-ALL) is associated with chromosomal aberrations characterized by juxtaposition of proto-oncogenes to T-cell receptor gene loci (TCR), resulting in the deregulated transcription of these proto-oncogenes.
  • The TRDV1-BCL11B joining region was 1344 bp long and contained fragments derived from 20q11.22, 3p21.33 and from 11p12, indicating the complex character of this aberration.
  • A strong expression of in-frame transcripts with truncated BCL11B and TCRD constant region (TRDC) were observed, but in contrast to normal T cells and other T-ALL samples, no wild-type BCL11B transcripts were detected in the T-ALL sample.
  • Screening of 37 other T-ALLs revealed one additional case with expression of the BCL11B-TRDC fusion transcript.
  • As BCL11B appears to play a key role in T-cell differentiation, BCL11B disruption and disturbed expression may contribute to the development of T-cell malignancies in man.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 14. Leukemia-Lymphoma, Adult T-Cell / genetics. Translocation, Genetic

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  • (PMID = 15668700.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BCL11B protein, human; 0 / DNA-Binding Proteins; 0 / Repressor Proteins; 0 / Tumor Suppressor Proteins
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74. Chen LJ, Li JY, Wu YJ, Yang H, Qian SX, Wu HX, Lu H, Xu W, Sheng RL: [Immunophenotyping characteristics of T-cell acute lymphoblastic leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Aug;15(4):692-5
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  • [Title] [Immunophenotyping characteristics of T-cell acute lymphoblastic leukemia].
  • The objective of this study was to investigate the immunophenotypic characteristics of T-cell acute lymphoblastic leukemia (T-ALL).
  • It is concluded that immunophenotyping is an important tool for diagnosis of T-ALL.

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  • (PMID = 17708784.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD3; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3
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75. Cecchinato V, Erba E, Basile A, Scarpati B, Fazi C, Brando B, Comi P, Chiaramonte R: Hexamethylene bisacetamide inhibits malignant phenotype in T-ALL cell lines. Leuk Res; 2008 May;32(5):791-7
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  • [Title] Hexamethylene bisacetamide inhibits malignant phenotype in T-ALL cell lines.
  • T acute lymphoblastic leukemia cell lines treated with hexamethylene bisacetamide (HMBA) undergo a delay in cell cycle progression and increase susceptibility to apoptosis, although they never overcome the differentiation block.
  • In accordance with changes in cell cycle and apoptosis, transitory p53 pathway activation commonly occurs.
  • Bcl-2 inhibition further favours the pro-apoptotic effect of HMBA.
  • Even if HMBA generally reduces Notch1 level in T acute lymphoblastic leukemia (T-ALL) cell lines, this does not commonly influence the biological response; in fact all the analysed cell lines, except CEM cells, display no biological effect following DAPT-induced Notch inhibition.
  • [MeSH-major] Acetamides / pharmacology. Antineoplastic Agents / pharmacology. Leukemia-Lymphoma, Adult T-Cell / drug therapy
  • [MeSH-minor] Cell Line, Tumor. Cyclin-Dependent Kinase 4 / analysis. Humans. Proto-Oncogene Proteins c-bcl-2 / physiology. Receptor, Notch1 / physiology. Signal Transduction. Triglycerides / pharmacology. Tumor Suppressor Protein p53 / physiology. gamma-Aminobutyric Acid / analogs & derivatives. gamma-Aminobutyric Acid / pharmacology

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  • [CommentIn] Leuk Res. 2008 May;32(5):689-90 [18164760.001]
  • (PMID = 17964649.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Acetamides; 0 / Antineoplastic Agents; 0 / NOTCH1 protein, human; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptor, Notch1; 0 / Triglycerides; 0 / Tumor Suppressor Protein p53; 56-12-2 / gamma-Aminobutyric Acid; 93349-26-9 / 1,2-dilinolenoyl-3-(4-aminobutyryl)propane-1,2,3-triol; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; LA133J59VU / hexamethylene bisacetamide
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76. Rodig SJ, Payne EG, Degar BA, Rollins B, Feldman AL, Jaffe ES, Androkites A, Silverman LB, Longtine JA, Kutok JL, Fleming MD, Aster JC: Aggressive Langerhans cell histiocytosis following T-ALL: clonally related neoplasms with persistent expression of constitutively active NOTCH1. Am J Hematol; 2008 Feb;83(2):116-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aggressive Langerhans cell histiocytosis following T-ALL: clonally related neoplasms with persistent expression of constitutively active NOTCH1.
  • Langerhans cell histiocytosis (LCH) and related entities are neoplasms of unknown pathogenesis.
  • Here, we describe studies assessing the role of NOTCH1 mutations in LCH, which were based on a case of fatal Langerhans cell tumor after T-cell acute lymphoblastic leukemia (T-ALL).
  • Although the two types of neoplasm in this patient were temporally and pathologically distinct, molecular analyses showed that they harbored the same T-cell receptor gene rearrangements and two activating NOTCH1 mutations involving exons 27 and 34.
  • Analysis of cDNA prepared from the aggressive Langerhans cell tumor showed that the NOTCH1 mutations were aligned in cis, a configuration that caused synergistic increases in NOTCH1 signal strength in reporter gene assays.
  • Immunohistochemistry confirmed that the Langerhans cell tumor also expressed NOTCH1 protein.
  • Although these data suggested that NOTCH1 mutations might contribute to the pathogenesis of typical sporadic LCH and related neoplasms occurring in the absence of T-ALL, an analysis of 24 cases of LCH and Rosai-Dorfman Disease occurring in patients without an antecedent history of T-ALL revealed no mutations.
  • Thus, activating NOTCH1 mutations appear to be unique to aggressive Langerhans cell tumors occurring after T-ALL.

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  • (PMID = 17874453.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI050225; United States / NCI NIH HHS / CA / CA082308; United States / NCI NIH HHS / CA / CA119070-02; United States / NCI NIH HHS / CA / P01 CA119070-02; United States / NCI NIH HHS / CA / P01 CA119070
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
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77. Cauwelier B, Cavé H, Gervais C, Lessard M, Barin C, Perot C, Van den Akker J, Mugneret F, Charrin C, Pagès MP, Grégoire MJ, Jonveaux P, Lafage-Pochitaloff M, Mozzicconacci MJ, Terré C, Luquet I, Cornillet-Lefebvre P, Laurence B, Plessis G, Lefebvre C, Leroux D, Antoine-Poirel H, Graux C, Mauvieux L, Heimann P, Chalas C, Clappier E, Verhasselt B, Benoit Y, Moerloose BD, Poppe B, Van Roy N, Keersmaecker KD, Cools J, Sigaux F, Soulier J, Hagemeijer A, Paepe AD, Dastugue N, Berger R, Speleman F: Clinical, cytogenetic and molecular characteristics of 14 T-ALL patients carrying the TCRbeta-HOXA rearrangement: a study of the Groupe Francophone de Cytogénétique Hématologique. Leukemia; 2007 Jan;21(1):121-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical, cytogenetic and molecular characteristics of 14 T-ALL patients carrying the TCRbeta-HOXA rearrangement: a study of the Groupe Francophone de Cytogénétique Hématologique.
  • Recently, we and others described a new chromosomal rearrangement, that is, inv(7)(p15q34) and t(7;7)(p15;q34) involving the T-cell receptor beta (TCRbeta) (7q34) and the HOXA gene locus (7p15) in 5% of T-cell acute lymphoblastic leukemia (T-ALL) patients leading to transcriptional activation of especially HOXA10.
  • To further address the clinical, immunophenotypical and molecular genetic findings of this chromosomal aberration, we studied 330 additional T-ALLs.
  • In conclusion, this study defines TCRbeta-HOXA rearranged T-ALLs as a distinct cytogenetic subgroup by clinical, immunophenotypical and molecular genetic characteristics.
  • [MeSH-major] Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Receptors, Antigen, T-Cell, alpha-beta / genetics

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  • (PMID = 17039236.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell, alpha-beta; 140441-81-2 / HOXA10 protein, human
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78. Remke M, Pfister S, Kox C, Toedt G, Becker N, Benner A, Werft W, Breit S, Liu S, Engel F, Wittmann A, Zimmermann M, Stanulla M, Schrappe M, Ludwig WD, Bartram CR, Radlwimmer B, Muckenthaler MU, Lichter P, Kulozik AE: High-resolution genomic profiling of childhood T-ALL reveals frequent copy-number alterations affecting the TGF-beta and PI3K-AKT pathways and deletions at 6q15-16.1 as a genomic marker for unfavorable early treatment response. Blood; 2009 Jul 30;114(5):1053-62
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  • Precursor T-cell acute lymphoblastic leukemia (T-ALL) in children represents a clinical challenge, because relapses are usually fatal.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Deletion. Chromosomes, Human, Pair 6 / genetics. Neoplasm Proteins / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Signal Transduction / genetics

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  • (PMID = 19406988.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GPL5713/ GSE8738
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / NOTCH1 protein, human; 0 / Neoplasm Proteins; 0 / Receptor, Notch1; 0 / Transforming Growth Factor beta; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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79. Matsuoka S, Oike Y, Onoyama I, Iwama A, Arai F, Takubo K, Mashimo Y, Oguro H, Nitta E, Ito K, Miyamoto K, Yoshiwara H, Hosokawa K, Nakamura Y, Gomei Y, Iwasaki H, Hayashi Y, Matsuzaki Y, Nakayama K, Ikeda Y, Hata A, Chiba S, Nakayama KI, Suda T: Fbxw7 acts as a critical fail-safe against premature loss of hematopoietic stem cells and development of T-ALL. Genes Dev; 2008 Apr 15;22(8):986-91
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  • Common molecular machineries between hematopoietic stem cell (HSC) maintenance and leukemia prevention have been highlighted.
  • The tumor suppressor Fbxw7 (F-box and WD-40 domain protein 7), a subunit of an SCF-type ubiquitin ligase complex, induces the degradation of positive regulators of the cell cycle.
  • We demonstrate that inactivation of Fbxw7 in hematopoietic cells causes premature depletion of HSCs due to active cell cycling and p53-dependent apoptosis.
  • Interestingly, Fbxw7 deletion also confers a selective advantage to cells with suppressed p53 function, eventually leading to development of T-cell acute lymphoblastic leukemia (T-ALL).
  • [MeSH-major] F-Box Proteins / metabolism. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / enzymology. Leukemia-Lymphoma, Adult T-Cell / etiology. Ubiquitin-Protein Ligases / metabolism
  • [MeSH-minor] Animals. Cell Cycle. Cells, Cultured. Mice. Mice, Transgenic. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 18367647.001).
  • [ISSN] 0890-9369
  • [Journal-full-title] Genes & development
  • [ISO-abbreviation] Genes Dev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / F-Box Proteins; 0 / Fbxw7 protein, mouse; 0 / Tumor Suppressor Protein p53; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Other-IDs] NLM/ PMC2335330
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80. 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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  • [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.
  • However, the clinical development of GSIs has been hampered by their low cytotoxicity against human T-ALL and the development of significant gastrointestinal toxicity derived from the inhibition of NOTCH signaling in the gut.

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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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81. Gutierrez A, Sanda T, Ma W, Zhang J, Grebliunaite R, Dahlberg S, Neuberg D, Protopopov A, Winter SS, Larson RS, Borowitz MJ, Silverman LB, Chin L, Hunger SP, Jamieson C, Sallan SE, Look AT: Inactivation of LEF1 in T-cell acute lymphoblastic leukemia. Blood; 2010 Apr 08;115(14):2845-51
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inactivation of LEF1 in T-cell acute lymphoblastic leukemia.
  • To further unravel the molecular pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL), we performed high-resolution array comparative genomic hybridization on diagnostic specimens from 47 children with T-ALL and identified monoallelic or biallelic LEF1 microdeletions in 11% (5 of 47) of these primary samples.
  • Gene expression microarrays showed increased expression of MYC and MYC targets in cases with LEF1 inactivation, as well as differentiation arrest at an early cortical stage of thymocyte development characterized by expression of CD1B, CD1E, and CD8, with absent CD34 expression.
  • LEF1 inactivation was associated with a younger age at the time of T-ALL diagnosis, as well as activating NOTCH1 mutations, biallelic INK4a/ARF deletions, and PTEN loss-of-function mutations or activating mutations of PI3K or AKT genes.
  • [MeSH-major] Codon, Terminator. Lymphoid Enhancer-Binding Factor 1 / genetics. Neoplasm Proteins / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Sequence Deletion

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  • (PMID = 20124220.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1K08CA133103; United States / NCI NIH HHS / CA / CA98543; 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 / 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 / CA98413; United States / NCI NIH HHS / CA / K08 CA133103-02; United States / NCI NIH HHS / CA / P01 CA068484; United States / NCI NIH HHS / CA / 5P01CA68484
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Codon, Terminator; 0 / LEF1 protein, human; 0 / Lymphoid Enhancer-Binding Factor 1; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ PMC2854430
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82. Stasiak-Barmuta A, Łuczyński W, Iłendo E, Krawczuk-Rybak M, Szymański M: [Regulatory T cells in children with acute lymphoblastic leukaemia]. Med Wieku Rozwoj; 2009 Jan-Mar;13(1):53-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Regulatory T cells in children with acute lymphoblastic leukaemia].
  • [Transliterated title] Limfocyty t regulatorowe u dzieci z ostra bialaczka limfoblastyczna.
  • One of the methods is to prevent the immunosuppression accompanying neoplastic diseases including acute lymphoblastic leukaemia (ALL) in children.
  • CONCLUSIONS: The finding of smaller number and lower percentage of regulatory T cells with coexpression of CD62L or lack expression of CD103 in children with ALL as compared to the control group, may be interpreted as activation of Treg cells and one of the mechanisms of immunosuppression in cancer of children.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. T-Lymphocytes, Regulatory / immunology

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  • (PMID = 19648661.001).
  • [Journal-full-title] Medycyna wieku rozwojowego
  • [ISO-abbreviation] Med Wieku Rozwoj
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Integrin alpha Chains; 0 / alpha E integrins; 126880-86-2 / L-Selectin
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83. Li X, Gounari F, Protopopov A, Khazaie K, von Boehmer H: Oncogenesis of T-ALL and nonmalignant consequences of overexpressing intracellular NOTCH1. J Exp Med; 2008 Nov 24;205(12):2851-61
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  • Mutations resulting in overexpression of intracellular Notch1 (ICN1) are frequently observed in human T cell acute lymphoblastic leukemia (T-ALL).
  • Early consequences are the generation of polyclonal nontumorigenic CD4(+)8(+) T cell receptor (TCR)-alphabeta(+) cells that do not qualify as tumor precursors despite the observation that they overexpress Notch 1 and c-Myc and degrade the tumor suppressor E2A by posttranslational modification.
  • The first tumorigenic cells are detected among more immature CD4(-)8(+)TCR-alphabeta(-) cells that give rise to monoclonal tumors with a single, unique TCR-beta chain and diverse TCR-alpha chains, pinpointing malignant transformation to a stage after pre-TCR signaling and before completion of TCR-alpha rearrangement.

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  • (PMID = 18981238.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE12948
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI045846; United States / NCI NIH HHS / CA / P01 CA109901; United States / NCI NIH HHS / CA / T32 CA070083; United States / NCI NIH HHS / CA / T32-CA70083; United States / NIAID NIH HHS / AI / R01 AI45846; United States / NCI NIH HHS / CA / CA109901
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Notch1 protein, mouse; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC2585834
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84. Van Vlierberghe P, Palomero T, Khiabanian H, Van der Meulen J, Castillo M, Van Roy N, De Moerloose B, Philippé J, González-García S, Toribio ML, Taghon T, Zuurbier L, Cauwelier B, Harrison CJ, Schwab C, Pisecker M, Strehl S, Langerak AW, Gecz J, Sonneveld E, Pieters R, Paietta E, Rowe JM, Wiernik PH, Benoit Y, Soulier J, Poppe B, Yao X, Cordon-Cardo C, Meijerink J, Rabadan R, Speleman F, Ferrando A: PHF6 mutations in T-cell acute lymphoblastic leukemia. Nat Genet; 2010 Apr;42(4):338-42
SciCrunch. OMIM: Data: Gene Annotation .

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  • [Title] PHF6 mutations in T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy with an increased incidence in males.
  • Mutational loss of PHF6 is importantly associated with leukemias driven by aberrant expression of the homeobox transcription factor oncogenes TLX1 and TLX3.
  • Overall, these results identify PHF6 as a new X-linked tumor suppressor in T-ALL and point to a strong genetic interaction between PHF6 loss and aberrant expression of TLX transcription factors in the pathogenesis of this disease.

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  • (PMID = 20228800.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA120196-03; United States / NIAID NIH HHS / AI / U54-AI057158; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / R01 CA129382-03; United States / NCI NIH HHS / CA / CA129382-03; United States / NCI NIH HHS / CA / CA120196-03; United States / NCI NIH HHS / CA / R01CA120196; United States / NIAID NIH HHS / AI / U54 AI057158; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NLM NIH HHS / LM / 1R01LM010140-01; United States / NCI NIH HHS / CA / U24 CA114737; United States / NLM NIH HHS / LM / R01 LM010140; United States / NCI NIH HHS / CA / R01 CA155743
  • [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 / Carrier Proteins; 0 / Homeodomain Proteins; 0 / PHF6 protein, human; 0 / Proto-Oncogene Proteins; 0 / TLX3 protein, human; 143275-75-6 / TLX1 protein, human
  • [Other-IDs] NLM/ NIHMS176587; NLM/ PMC2847364
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85. Kox C, Zimmermann M, Stanulla M, Leible S, Schrappe M, Ludwig WD, Koehler R, Tolle G, Bandapalli OR, Breit S, Muckenthaler MU, Kulozik AE: The favorable effect of activating NOTCH1 receptor mutations on long-term outcome in T-ALL patients treated on the ALL-BFM 2000 protocol can be separated from FBXW7 loss of function. Leukemia; 2010 Dec;24(12):2005-13
Hazardous Substances Data Bank. PREDNISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Precursor T-cell acute lymphoblastic leukemia (T-ALL) remains an important challenge in pediatric oncology.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Prednisone / therapeutic use. Receptor, Notch1 / genetics. Ubiquitin-Protein Ligases / genetics

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  • (PMID = 20944675.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Receptor, Notch1; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases; VB0R961HZT / Prednisone
  • [Other-IDs] NLM/ PMC3035973
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86. Weng AP, Lau A: Notch signaling in T-cell acute lymphoblastic leukemia. Future Oncol; 2005 Aug;1(4):511-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Notch signaling in T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) is a form of pediatric leukemia that is thought to be caused by approximately 12 distinct chromosomal translocations that lead to aberrant expression of as many different cellular genes.
  • Recent studies, however, have identified a large fraction of T-ALL cases carrying mutations in one of these genes, Notch1, suggesting for the first time that many cases may share a common pathogenic etiology, and perhaps may allow the development of targeted therapies that benefit the majority of patients with this disease.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Receptors, Notch / physiology

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  • (PMID = 16556027.001).
  • [ISSN] 1479-6694
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Notch
  • [Number-of-references] 118
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87. Park MJ, Taki T, Oda M, Watanabe T, Yumura-Yagi K, Kobayashi R, Suzuki N, Hara J, Horibe K, Hayashi Y: FBXW7 and NOTCH1 mutations in childhood T cell acute lymphoblastic leukaemia and T cell non-Hodgkin lymphoma. Br J Haematol; 2009 Apr;145(2):198-206
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FBXW7 and NOTCH1 mutations in childhood T cell acute lymphoblastic leukaemia and T cell non-Hodgkin lymphoma.
  • Mutation analysis of FBXW7 and NOTCH1 genes was performed in 55 T cell acute lymphoblastic leukaemia (T-ALL) and 14 T cell non-Hodgkin lymphoma (T-NHL) patients who were treated on the Japan Association of Childhood Leukaemia Study (JACLS) protocols ALL-97 and NHL-98.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Gene Expression Regulation, Leukemic. Lymphoma, T-Cell / genetics. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics. Ubiquitin-Protein Ligases / genetics
  • [MeSH-minor] Chi-Square Distribution. Child. Chromatography, High Pressure Liquid. DNA Mutational Analysis. Disease-Free Survival. Female. Humans. Kaplan-Meier Estimate. Male. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate


88. Hotfilder M, Röttgers S, Rosemann A, Schrauder A, Schrappe M, Pieters R, Jürgens H, Harbott J, Vormoor J: Leukemic stem cells in childhood high-risk ALL/t(9;22) and t(4;11) are present in primitive lymphoid-restricted CD34+CD19- cells. Cancer Res; 2005 Feb 15;65(4):1442-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Open questions in the pathogenesis of childhood acute lymphoblastic leukemia (ALL) are which hematopoietic cell is target of the malignant transformation and whether primitive stem cells contribute to the leukemic clone.
  • Interestingly, in some patients with ALL/t(4;11), alternative splicing was seen in myeloid progenitors compared with the bulk leukemic population, suggesting that these myeloid colonies might be part of the leukemic cell clone.
  • Fluorescence in situ hybridization analysis, however, shows that none of these myeloid colonies (0 of 41 RT-PCR-positive colonies) originated from a progenitor cell that carries the leukemia-specific translocation.
  • Thus, leukemic, translocation-positive CD34(+)CD19(-) progenitor/stem cells that were copurified by cell sorting were able to survive in these colony assays for up to 28 days allowing amplification of the respective fusion transcripts by sensitive RT-PCR.
  • In conclusion, we show that childhood high-risk ALL/t(9;22) and t(4;11) originate in a primitive CD34(+)CD19(-) progenitor/stem cell without a myeloerythroid developmental potential.
  • [MeSH-major] Antigens, CD19 / biosynthesis. Antigens, CD34 / biosynthesis. Neoplastic Stem Cells / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Translocation, Genetic / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 4 / genetics. Chromosomes, Human, Pair 9 / genetics. Flow Cytometry. Genes, abl / genetics. Humans. In Situ Hybridization, Fluorescence. Myeloid-Lymphoid Leukemia Protein. Oncogene Proteins, Fusion / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15735032.001).
  • [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 / Antigens, CD19; 0 / Antigens, CD34; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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89. Youns M, Fu YJ, Zu YG, Kramer A, Konkimalla VB, Radlwimmer B, Sültmann H, Efferth T: Sensitivity and resistance towards isoliquiritigenin, doxorubicin and methotrexate in T cell acute lymphoblastic leukaemia cell lines by pharmacogenomics. Naunyn Schmiedebergs Arch Pharmacol; 2010 Sep;382(3):221-34
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sensitivity and resistance towards isoliquiritigenin, doxorubicin and methotrexate in T cell acute lymphoblastic leukaemia cell lines by pharmacogenomics.
  • In the present investigation, we compared the cytotoxicity of the chalcone flavonoide, isoliquiritigenin (ISL), with that of doxorubicin (DOX) and methotrexate (MTX) in five T cell acute lymphoblastic leukaemia (T-ALL) cell lines (Jurkat, J-Jhan, J16, HUT78 and Karpas 45).
  • To gain insight into the molecular mechanisms which determine the response of T-ALL cells towards ISL, DOX and MTX, we applied array-based matrix comparative genomic hybridisation and microarray-based mRNA expression profiling and compared the genomic and transcriptomic profiles of the cell lines with their 50% inhibition (IC(50)) values for these three drugs.
  • The IC(50) values for ISL did not correlate with those for DOX or MTX, indicating that ISL was still active in DOX- or MTX-unresponsive cell lines.
  • In conclusion, ISL represents a cytotoxic natural product with activity towards T-ALL cell lines.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm / genetics. Leukemia, T-Cell / drug therapy. Pharmacogenetics / methods
  • [MeSH-minor] Antimetabolites, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / pharmacology. Cell Line, Tumor. Chalcones / administration & dosage. Chalcones / pharmacology. Doxorubicin / administration & dosage. Doxorubicin / pharmacology. Gene Expression Profiling. Humans. Inhibitory Concentration 50. Jurkat Cells. Methotrexate / administration & dosage. Methotrexate / pharmacology. Microarray Analysis. RNA, Messenger / metabolism

  • Hazardous Substances Data Bank. DOXORUBICIN .
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  • (PMID = 20668838.001).
  • [ISSN] 1432-1912
  • [Journal-full-title] Naunyn-Schmiedeberg's archives of pharmacology
  • [ISO-abbreviation] Naunyn Schmiedebergs Arch. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Chalcones; 0 / RNA, Messenger; 80168379AG / Doxorubicin; B9CTI9GB8F / isoliquiritigenin; YL5FZ2Y5U1 / Methotrexate
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90. Staal FJ, van Dongen JJ, Langerak AW: Novel insights into the development of T-cell acute lymphoblastic leukemia. Curr Hematol Malig Rep; 2007 Jul;2(3):176-82
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] Novel insights into the development of T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) results from malignant transformation of immature cells of the T-cell lineage.
  • T-ALL is a heterogeneous disease both clinically and genetically.
  • It is generally accepted that T-ALL cells are the malignant counterpart of normally developing T cells in the thymus (thymocytes).
  • Recent data using genome-wide gene expression profiling and assessment of the rearrangement status of the T-cell receptor loci confirm this notion.
  • [MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / etiology
  • [MeSH-minor] Adult. Animals. Antigens, Differentiation, T-Lymphocyte / analysis. Antigens, Neoplasm / analysis. Antineoplastic Agents / pharmacology. Cell Transformation, Neoplastic. Child. Drug Delivery Systems. Gene Expression Profiling. Gene Expression Regulation, Developmental. Gene Expression Regulation, Leukemic. Humans. Lymphopoiesis / physiology. Mice. Oncogene Proteins, Fusion / antagonists & inhibitors. Oncogene Proteins, Fusion / biosynthesis. Oncogene Proteins, Fusion / genetics. Oncogenes. Receptors, Antigen, T-Cell / genetics. Receptors, Notch / physiology. T-Lymphocytes / immunology. T-Lymphocytes / pathology. Thymus Gland / pathology. Translocation, Genetic. Wnt Proteins / physiology

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  • (PMID = 20425367.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Notch; 0 / Wnt Proteins
  • [Number-of-references] 50
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91. Real PJ, Ferrando AA: NOTCH inhibition and glucocorticoid therapy in T-cell acute lymphoblastic leukemia. Leukemia; 2009 Aug;23(8):1374-7
The Lens. Cited by Patents in .

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  • [Title] NOTCH inhibition and glucocorticoid therapy in T-cell acute lymphoblastic leukemia.
  • Inhibition of NOTCH1 signaling with gamma-secretase inhibitors (GSIs) has been proposed as a molecularly targeted therapy in T-cell acute lymphoblastic leukemia (T-ALL).

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  • (PMID = 19357700.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA120196-03; 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
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Enzyme Inhibitors; 0 / GKLF protein; 0 / Glucocorticoids; 0 / Hes1 protein, mouse; 0 / Homeodomain Proteins; 0 / Kruppel-Like Transcription Factors; 0 / NOTCH1 protein, human; 0 / Neoplasm Proteins; 0 / Notch1 protein, mouse; 0 / Receptor, Notch1; 149348-15-2 / HES1 protein, human; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Number-of-references] 58
  • [Other-IDs] NLM/ NIHMS153167; NLM/ PMC2814171
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92. 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
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] 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


93. Uyttebroeck A, Vanhentenrijk V, Hagemeijer A, Boeckx N, Renard M, Wlodarska I, Vandenberghe P, Depaepe P, De Wolf-Peeters C: Is there a difference in childhood T-cell acute lymphoblastic leukaemia and T-cell lymphoblastic lymphoma? Leuk Lymphoma; 2007 Sep;48(9):1745-54
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Is there a difference in childhood T-cell acute lymphoblastic leukaemia and T-cell lymphoblastic lymphoma?
  • To distinguish the similarities or differences between T-cell acute lymphoblastic leukaemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LBL), we retrospectively analyzed the clinical, immunophenotypic, cytogenetic, and molecular characteristics in 37 children diagnosed between December 1990 and December 2003.
  • The clinical presentation and cytogenetic characteristics are largely similar for T-ALL and T-LBL supporting the concept that both represent a spectrum of one single disease.
  • The differences that were found between both neoplasms, in particular in their phenotype and in their expression profile may suggest that most T-ALL derive from a T-cell progenitor of the bone marrow, while thymocytes represent the normal counterpart of T-LBL.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17786710.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
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94. Nagel S, Venturini L, Przybylski GK, Grabarczyk P, Schmidt CA, Meyer C, Drexler HG, Macleod RA, Scherr M: Activation of miR-17-92 by NK-like homeodomain proteins suppresses apoptosis via reduction of E2F1 in T-cell acute lymphoblastic leukemia. Leuk Lymphoma; 2009 Jan;50(1):101-8
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] Activation of miR-17-92 by NK-like homeodomain proteins suppresses apoptosis via reduction of E2F1 in T-cell acute lymphoblastic leukemia.
  • The NK-like family of homeobox genes includes TLX1, TLX3 and NKX2-5, which are ectopically activated in distinct subsets of T-cell acute lymphoblastic leukemia (T-ALL) cells.
  • Quantification of pri-miR-17-92 in T-ALL cell lines suggested an implication of the NK-like homeodomain proteins in transcriptional regulation.
  • Lentiviral-mediated overexpression of NKX2-5 in the T-ALL cell line MOLT-4 consistently resulted in increased miR-17-92 pri-miRNA levels and decreased amounts of E2F1 protein.
  • Induction of apoptosis by treating miR17-92 or E2F1 transduced T-ALL cells with etoposide led to reduced or enhanced cell viability, respectively.
  • [MeSH-major] Apoptosis / genetics. E2F1 Transcription Factor / metabolism. Homeodomain Proteins / metabolism. Killer Cells, Natural / immunology. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / pathology. MicroRNAs / genetics
  • [MeSH-minor] Cell Line. Gene Expression Regulation, Neoplastic / genetics

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  • (PMID = 19148830.001).
  • [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 / E2F1 Transcription Factor; 0 / Homeodomain Proteins; 0 / MicroRNAs
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95. 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
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Of mice and men: how an oncogene transgresses the limits and predisposes to T cell acute lymphoblastic leukemia.
  • The gene encoding LIM-only 2 (LMO2), an oncogenic transcription factor, is frequently activated in T cell acute lymphoblastic leukemia (T-ALL), but how LMO2 transforms primary hematopoietic cells to induce T-ALL remains an open question.
  • 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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96. Zhu YM, Zhao WL, Fu JF, Shi JY, Pan Q, Hu J, Gao XD, Chen B, Li JM, Xiong SM, Gu LJ, Tang JY, Liang H, Jiang H, Xue YQ, Shen ZX, Chen Z, Chen SJ: NOTCH1 mutations in T-cell acute lymphoblastic leukemia: prognostic significance and implication in multifactorial leukemogenesis. Clin Cancer Res; 2006 May 15;12(10):3043-9
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] NOTCH1 mutations in T-cell acute lymphoblastic leukemia: prognostic significance and implication in multifactorial leukemogenesis.
  • PURPOSE: NOTCH signaling pathway is essential in T-cell development and NOTCH1 mutations are frequently present in T-cell acute lymphoblastic leukemia (T-ALL).
  • These mutations were significantly associated with elevated WBC count at diagnosis and independently linked to short survival time.
  • CONCLUSION: NOTCH1 mutation is an important prognostic marker in T-ALL and its predictive value could be even further increased if coevaluated with other T-cell-related regulatory genes.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Receptor, Notch1 / genetics

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  • [ErratumIn] Clin Cancer Res. 2009 Feb 15;15(4):1506
  • (PMID = 16707600.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
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97. Barata JT, Cardoso AA, Boussiotis VA: Interleukin-7 in T-cell acute lymphoblastic leukemia: an extrinsic factor supporting leukemogenesis? Leuk Lymphoma; 2005 Apr;46(4):483-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interleukin-7 in T-cell acute lymphoblastic leukemia: an extrinsic factor supporting leukemogenesis?
  • The malignant transformation and expansion of tumor cells involve both cell-autonomous mechanisms and microenvironment signals that regulate viability, nutrient utilization, metabolic activity and cell growth.
  • In T-cell acute lymphoblastic leukemia (T-ALL), the co-culture of leukemic cells with stroma or the addition of particular cytokines prevents ex vivo spontaneous apoptosis.
  • PI3K signaling is required for the induction of Bcl-2, the down-regulation of p27(kip1) and cell cycle progression.
  • PI3K signaling is also required for the expression of the glucose transporter Glut1, uptake of glucose, activation of the metabolic machinery, increase in cell size, and maintenance of mitochondrial integrity.
  • [MeSH-major] Interleukin-7 / metabolism. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / metabolism
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Humans. Mitogen-Activated Protein Kinases / drug effects. Mitogen-Activated Protein Kinases / metabolism. Phosphatidylinositol 3-Kinases / drug effects. Phosphatidylinositol 3-Kinases / metabolism. Protein-Serine-Threonine Kinases / drug effects. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / drug effects. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Signal Transduction / drug effects. Signal Transduction / physiology. Trans-Activators / drug effects. Trans-Activators / metabolism

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  • (PMID = 16019476.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI 46548; United States / NCI NIH HHS / CA / P01-CA68484
  • [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.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-7; 0 / Proto-Oncogene Proteins; 0 / Trans-Activators; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; 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 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Number-of-references] 125
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98. Sulis ML, Williams O, Palomero T, Tosello V, Pallikuppam S, Real PJ, Barnes K, Zuurbier L, Meijerink JP, Ferrando AA: NOTCH1 extracellular juxtamembrane expansion mutations in T-ALL. Blood; 2008 Aug 1;112(3):733-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Heterodimerization domain (HD) mutations in NOTCH1 induce ligand-independent activation of the receptor and contribute to the pathogenesis of one-third of human T-cell lymphoblastic leukemias (T-ALLs).
  • Here we report a novel class of activating mutations in NOTCH1 leading to aberrant activation of NOTCH1 signaling in T-cell lymphoblasts.
  • Notably, structure-function analysis of leukemia-derived and synthetic JME mutants demonstrated that the aberrant activation of NOTCH1 signaling is dependent on the number of residues introduced in the extracellular juxtamembrane region of the receptor and not on the specific amino acid sequence of these insertions.

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  • (PMID = 18411416.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA120196-03; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / CA120196; 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 / Receptor, Notch1; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ PMC2481531
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99. 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.
  • 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.
  • Treatment approaches in T-LBL changed from conventional non-Hodgkin lymphoma (NHL) protocols to intensive NHL protocols but recently to ALL-designed protocols.
  • 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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100. Sanda T, Li X, Gutierrez A, Ahn Y, Neuberg DS, O'Neil J, Strack PR, Winter CG, Winter SS, Larson RS, von Boehmer H, Look AT: Interconnecting molecular pathways in the pathogenesis and drug sensitivity of T-cell acute lymphoblastic leukemia. Blood; 2010 Mar 4;115(9):1735-45
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interconnecting molecular pathways in the pathogenesis and drug sensitivity of T-cell acute lymphoblastic leukemia.
  • To identify dysregulated pathways in distinct phases of NOTCH1-mediated T-cell leukemogenesis, as well as small-molecule inhibitors that could synergize with or substitute for gamma-secretase inhibitors (GSIs) in T-cell acute lymphoblastic leukemia (T-ALL) therapy, we compared gene expression profiles in a Notch1-induced mouse model of T-ALL with those in human T-ALL.
  • The overall patterns of NOTCH1-mediated gene expression in human and mouse T-ALLs were remarkably similar, as defined early in transformation in the mouse by the regulation of MYC and its target genes and activation of nuclear factor-kappaB and PI3K/AKT pathways.
  • Later events in murine Notch1-mediated leukemogenesis included down-regulation of genes encoding tumor suppressors and negative cell cycle regulators.
  • When tested in vitro, histone deacetylase, PI3K and proteasome inhibitors synergized with GSI in suppressing T-ALL cell growth in GSI-sensitive cells.

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  • (PMID = 20007543.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA109901; United States / NCI NIH HHS / CA / CA98543; United States / NCI NIH HHS / CA / 5P01CA109901-040001; None / None / / K08 CA133103-03; United States / NCI NIH HHS / CA / K08 CA133103-04; United States / NCI NIH HHS / CA / CA114766; United States / NCI NIH HHS / CA / K08 CA133103-03; United States / NCI NIH HHS / CA / U24 CA114766; None / None / / K08 CA133103-01; None / None / / K08 CA133103-04; United States / NCI NIH HHS / CA / K08 CA133103; United States / NCI NIH HHS / CA / K08 CA133103-02; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / K08 CA133103-01; None / None / / K08 CA133103-02
  • [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 / Enzyme Inhibitors; 0 / NOTCH1 protein, human; 0 / Notch1 protein, mouse; 0 / Receptor, Notch1; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ PMC2832805
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