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1. Kleff V, Sorg UR, Bury C, Suzuki T, Rattmann I, Jerabek-Willemsen M, Poremba C, Flasshove M, Opalka B, Trapnell B, Dirksen U, Moritz T: Gene Therapy of βc-Deficient Pulmonary Alveolar Proteinosis (βc-PAP): Studies in a Murine in vivo Model. Mol Ther; 2008 Apr;16(4):757-764

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  • Hematopoietic stem cell gene therapy for restoring expression of βc-protein in the hematopoietic system may offer a curative approach.

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  • [Copyright] Copyright © 2008 The American Society of Gene Therapy. Published by Elsevier Inc. All rights reserved.
  • (PMID = 28178466.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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2. Lunzen JV, Glaunsinger T, Stahmer I, Baehr VV, Baum C, Schilz A, Kuehlcke K, Naundorf S, Martinius H, Hermann F, Giroglou T, Newrzela S, Müller I, Brauer F, Brandenburg G, Alexandrov A, von Laer D: Transfer of Autologous Gene-modified T Cells in HIV-infected Patients with Advanced Immunodeficiency and Drug-resistant Virus. Mol Ther; 2007 May;15(5):1024-1033

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  • T-cell infusions were tolerated well, with no severe side effects.
  • Gene-modified cells could be detected in peripheral blood, lymph nodes, and bone marrow throughout the 1-year follow-up, and marking levels correlated with the cell dose.

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  • [Copyright] Copyright © 2007 The American Society of Gene Therapy. Published by Elsevier Inc. All rights reserved.
  • (PMID = 28182893.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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3. Larson Gedman A, Chen Q, Kugel Desmoulin S, Ge Y, LaFiura K, Haska CL, Cherian C, Devidas M, Linda SB, Taub JW, Matherly LH: The impact of NOTCH1, FBW7 and PTEN mutations on prognosis and downstream signaling in pediatric T-cell acute lymphoblastic leukemia: a report from the Children's Oncology Group. Leukemia; 2009 Aug;23(8):1417-25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The impact of NOTCH1, FBW7 and PTEN mutations on prognosis and downstream signaling in pediatric T-cell acute lymphoblastic leukemia: a report from the Children's Oncology Group.
  • We explored the impact of mutations in the NOTCH1, FBW7 and PTEN genes on prognosis and downstream signaling in a well-defined cohort of 47 patients with pediatric T-cell acute lymphoblastic leukemia (T-ALL).
  • Our results suggest that (1) multiple factors should be considered with attempting to identify molecular-based prognostic factors for pediatric T-ALL, and (2) depending on the NOTCH1 signaling status, modifications in the types or dosing of standard chemotherapy drugs for T-ALL, or combinations of agents capable of targeting NOTCH1, AKT and/or mTOR with standard chemotherapy agents may be warranted.

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  • (PMID = 19340001.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA076641-10; United States / NCI NIH HHS / CA / T32-CA009531; United States / NCI NIH HHS / CA / R01 CA076641; United States / NCI NIH HHS / CA / CA76641; United States / NCI NIH HHS / CA / T32 CA009531-22; United States / NCI NIH HHS / CA / T32 CA009531; United States / NCI NIH HHS / CA / T32 CA009531-21
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Cell Cycle Proteins; 0 / DNA, Neoplasm; 0 / F-Box Proteins; 0 / Homeodomain Proteins; 0 / NOTCH1 protein, human; 0 / Neoplasm Proteins; 0 / Receptor, Notch1; 149348-15-2 / HES1 protein, human; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Other-IDs] NLM/ NIHMS98506; NLM/ PMC2726275
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4. Sidhom I, Shaaban K, Soliman S, Ezzat S, El-Anwar W, Hamdy N, Yassin D, Salem S, Hassanein H, Mansour MT: Clinical significance of immunophenotypic markers in pediatric T-cell acute lymphoblastic leukemia. J Egypt Natl Canc Inst; 2008 Jun;20(2):111-20
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  • [Title] Clinical significance of immunophenotypic markers in pediatric T-cell acute lymphoblastic leukemia.
  • BACKGROUND: Cell-marker profiling has led to conflicting conclusions about its prognostic significance in T-ALL.
  • AIM: To investigate the prevalence of the expression of CD34, CD10 and myeloid associated antigens (CD13/ CD33) in childhood T-ALL and to relate their presence to initial clinical and biologic features and early response to therapy.
  • No significant association was encountered between CD34, CD10 or myeloid antigen positivity and the presenting clinical features as age, sex, TLC and CNS leukemia.
  • CD34 and CD13/CD33 expression was significantly associated with T-cell maturation stages (p<0.05).
  • CD34(+), CD13/CD33(+) and early T-cell stage had high MRD levels on day 15 that was statistically highly significant (p<0.01), but CD10(+) had statistically significant lower MRD level on day 15 (p=0.049).
  • CONCLUSIONS: CD34, CD10, CD13/CD33 expression, as well as T-cell maturation stages, may have prognostic significance in pediatric T-ALL as they have a significant impact on early clearance of leukemic cells detected by MRD day 15.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Neoplasm, Residual / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Antigens, CD / metabolism. Antigens, CD13 / metabolism. Antigens, CD34 / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Cell Differentiation. Child. Child, Preschool. Egypt. Female. Flow Cytometry. Humans. Immunophenotyping. Infant. Male. Neprilysin / metabolism. Prognosis. Remission Induction. Sialic Acid Binding Ig-like Lectin 3. Treatment Outcome

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  • (PMID = 20029466.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Biomarkers, Tumor; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13; EC 3.4.24.11 / Neprilysin
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5. Cox CV, Martin HM, Kearns PR, Virgo P, Evely RS, Blair A: Characterization of a progenitor cell population in childhood T-cell acute lymphoblastic leukemia. Blood; 2007 Jan 15;109(2):674-82
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  • [Title] Characterization of a progenitor cell population in childhood T-cell acute lymphoblastic leukemia.
  • A significant proportion of children with T-cell acute lymphoblastic leukemia (T-ALL) continue to fail therapy.
  • Cells from 13 pediatric cases were maintained in vitro for at least 4 weeks and expanded in 8 cases.
  • The immunophenotype and genotype of the original leukemia cells were preserved with serial passage in the NOD/SCID mice.
  • These data demonstrate the long-term repopulating ability of the CD34+/CD4- and CD34+/CD7- subfractions in T-ALL and suggest that a cell with a more primitive phenotype was the target for leukemic transformation in these cases.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Stem Cells / immunology. Stem Cells / pathology
  • [MeSH-minor] Adolescent. Animals. Cell Culture Techniques. Cell Proliferation. Cell Separation. Cells, Cultured. Child. Child, Preschool. Female. Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor / genetics. Genotype. Humans. Immunophenotyping. Infant. Male. Mice. Mice, Inbred NOD. Mice, SCID. Xenograft Model Antitumor Assays


6. Ye QD, Gu LJ, Tang JY, Xue HL, Chen J, Pan C, Chen J, Dong L, Zhou M: [ALL-XH-99 protocol in the treatment of childhood T-cell acute lymphoblastic leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2009 Jan;30(1):26-8
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  • [Title] [ALL-XH-99 protocol in the treatment of childhood T-cell acute lymphoblastic leukemia].
  • OBJECTIVE: To analyze the incidence, clinical characteristics and prognosis of childhood T-cell acute lymphoblastic leukemia (T-ALL).
  • RESULTS: Of 305 childhood ALL patients, 43 were T-ALL.
  • In comparison with that of B cell ALL (B-ALL), the percentages of age older than 10 years, initial WBC count more than 50 x 10(9)/ L, prednisone poor response (PPR), and failed to achieve remission at day 19 of induction chemotherapy in the T-ALLs were all higher.
  • CONCLUSION: There were statistic differences between T-cell and B-cell childhood ALLs in age, initial WBC count, early response to therapy, and eight-year EFS and RFS.
  • Childhood T-ALL was associated with a worse prognosis than other sub-types of childhood ALL.
  • [MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Immunophenotyping. Infant. Karyotyping. Male. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / therapy. Prognosis

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  • (PMID = 19563031.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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7. Savaşan S, Buck S, Ozdemir O, Hamre M, Asselin B, Pullen J, Ravindranath Y: Evaluation of cytotoxicity by flow cytometric drug sensitivity assay in childhood T-cell acute lymphoblastic leukemia. Leuk Lymphoma; 2005 Jun;46(6):833-40
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  • [Title] Evaluation of cytotoxicity by flow cytometric drug sensitivity assay in childhood T-cell acute lymphoblastic leukemia.
  • Risk-based treatment strategies have improved outcome in childhood B-precursor acute lymphoblastic leukemia, and in vitro drug sensitivity assessment using methyl-thiazol-tetrazolium (MTT) assay has been shown to be an independent prognostic marker.
  • To date, such strategies in childhood T-cell acute lymphoblastic leukemia (T-ALL) have proved elusive, and in vitro drug sensitivity testing has had limited success in T-ALL due to poor T-cell lymphoblast survival in vitro.
  • We studied 68 cases of childhood T-ALL for cytarabine (Ara-C) and daunorubicin sensitivity by FCDSA and compared the results with those obtained by MTT assay.
  • Comparison of T-ALL sensitivity with acute myeloid leukemia (AML) cases revealed a unique pattern difference.
  • Although age or white blood cell count at diagnosis was not associated with any particular drug response pattern, CD13 expression on T-lymphoblasts was associated with in vitro resistance.
  • FCDSA is a reliable, practical and reproducible method that can be integrated into studies of drug-target cell interactions in T-ALL.
  • [MeSH-major] Drug Screening Assays, Antitumor. Flow Cytometry / methods. Medical Oncology / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Apoptosis. Bone Marrow Cells / cytology. Bone Marrow Cells / metabolism. Child. Daunorubicin / pharmacology. Humans. Immunophenotyping / methods. Inhibitory Concentration 50. Leukemia, T-Cell / diagnosis. Leukemia, T-Cell / drug therapy. Reproducibility of Results. Sensitivity and Specificity. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology

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  • (PMID = 16019527.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U10-CA29691
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tetrazolium Salts; 0 / Thiazoles; 298-93-1 / thiazolyl blue; ZS7284E0ZP / Daunorubicin
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8. Karrman K, Andersson A, Björgvinsdóttir H, Strömbeck B, Lassen C, Olofsson T, Nguyen-Khac F, Berger R, Bernard O, Fioretos T, Johansson B: Deregulation of cyclin D2 by juxtaposition with T-cell receptor alpha/delta locus in t(12;14)(p13;q11)-positive childhood T-cell acute lymphoblastic leukemia. Eur J Haematol; 2006 Jul;77(1):27-34
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  • [Title] Deregulation of cyclin D2 by juxtaposition with T-cell receptor alpha/delta locus in t(12;14)(p13;q11)-positive childhood T-cell acute lymphoblastic leukemia.
  • OBJECTIVES: The t(12;14)(p13;q11)--a recurrent translocation in childhood T-cell acute lymphoblastic leukemia (T-ALL)--has very recently been molecularly characterized in one case, which displayed overexpression of the cyclin D2 gene (CCND2).
  • PATIENTS AND METHODS: We have characterized two pediatric t(12;14)-positive T-ALLs using fluorescence in situ hybridization (FISH), cDNA microarray, and real-time polymerase chain reaction (PCR).
  • RESULTS: FISH revealed breakpoints (BPs) in the T-cell receptor alpha/delta locus (14q11) and in the vicinity of the CCND2 gene at 12p13.
  • The t(12;14)-positive T-ALL displayed an increased expression of CCND2 compared to the controls, whereas the expression of the other genes was similar in all T-ALLs.
  • Furthermore, it is the first example of a T-cell neoplasm with a targeted deregulation of a member of a cyclin-encoding gene family.
  • [MeSH-major] Cyclins / genetics. Gene Expression Regulation, Neoplastic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell, alpha-beta / genetics. Receptors, Antigen, T-Cell, gamma-delta / genetics. Translocation, Genetic

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  • (PMID = 16548914.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / CCND2 protein, human; 0 / Cyclin D2; 0 / Cyclins; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Antigen, T-Cell, gamma-delta
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9. Jaing TH, Yang CP, Hung IJ, Tsay PK, Tseng CK, Chen SH: Clinical significance of central nervous system involvement at diagnosis of childhood T-cell acute lymphoblastic leukemia. Pediatr Blood Cancer; 2005 Aug;45(2):135-8
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  • [Title] Clinical significance of central nervous system involvement at diagnosis of childhood T-cell acute lymphoblastic leukemia.
  • BACKGROUND: Patients with T-cell acute lymphoblastic leukemia (T-ALL) frequently present with unfavorable features at diagnosis.
  • We sought to correlate initial central nervous system (CNS) disease at diagnosis with shortened survival in childhood T-ALL.
  • The introduction of early and effective CNS-directed therapy might no longer portend a poor prognosis for CNS leukemia.
  • [MeSH-major] Central Nervous System Neoplasms / diagnosis. Leukemia, T-Cell / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 15704218.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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10. Chabay P, De Matteo E, Lorenzetti M, Barón AV, Valva P, Preciado MV: Low frequency of Epstein Barr virus association and high frequency of p53 overexpression in an Argentinean pediatric T-cell lymphoma series. Pediatr Dev Pathol; 2009 Jan-Feb;12(1):28-34
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  • [Title] Low frequency of Epstein Barr virus association and high frequency of p53 overexpression in an Argentinean pediatric T-cell lymphoma series.
  • T-cell non-Hodgkin's lymphomas (NHLs) represent 10% to 15% of all diagnosed lymphomas in Western countries.
  • Various geographic frequencies of T-cell NHL have been documented, in part reflecting increased exposure to pathogenic factors such as Epstein-Barr virus (EBV).
  • Our aims were to assess EBV and p53 expression in Argentine pediatric T-cell lymphoma and to correlate them with patients' survival.
  • Epstein-Barr encoded RNAs (EBERs) in situ hybridization and LMP1 and p53 immunohistochemical staining were performed on formalin-fixed paraffin-embedded lymph node biopsies from 25 pediatric T-lymphoma patients.
  • Epstein-Barr virus expression was found in 8.0% of cases. p53-positive staining was distributed in 92% of pediatric cases.
  • Our data showed a low frequency of EBV association with pediatric T-cell lymphoma.
  • It seems that p53 plays an important role in proliferation in our studied population, since it is overexpressed in 92% of T-cell lymphoma cases.
  • [MeSH-major] Biomarkers, Tumor / analysis. Epstein-Barr Virus Infections / epidemiology. Leukemia, T-Cell / metabolism. Leukemia, T-Cell / virology. Tumor Suppressor Protein p53 / biosynthesis

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  • (PMID = 18540692.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / RNA, Viral; 0 / Tumor Suppressor Protein p53
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11. 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).
  • 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).
  • 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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12. 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.
  • [Title] Pediatric Preclinical Testing Program (PPTP) testing of the CENP-E inhibitor GSK923295A.
  • 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).

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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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13. Graham DK, Salzberg DB, Kurtzberg J, Sather S, Matsushima GK, Keating AK, Liang X, Lovell MA, Williams SA, Dawson TL, Schell MJ, Anwar AA, Snodgrass HR, Earp HS: Ectopic expression of the proto-oncogene Mer in pediatric T-cell acute lymphoblastic leukemia. Clin Cancer Res; 2006 May 1;12(9):2662-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ectopic expression of the proto-oncogene Mer in pediatric T-cell acute lymphoblastic leukemia.
  • To determine if Mer expression is ectopic in T-cell acute lymphoblastic leukemia (ALL) and potentially important in leukemogenesis, we analyzed Mer expression in normal human thymocytes and lymphocytes and in pediatric ALL patient samples.
  • Mer expression in 34 T-cell ALL (T-ALL) patient samples was evaluated by reverse transcription-PCR, and Mer protein expression in a separate cohort of 16 patient samples was assayed by flow cytometry and Western blot.
  • CONCLUSIONS: Transforming Mer signals may contribute to T-cell leukemogenesis, and abnormal Mer expression may be a novel therapeutic target in pediatric ALL therapy.

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  • (PMID = 16675557.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / T32 CA082086; United States / NCI NIH HHS / CA / CA 68346; United States / NCI NIH HHS / CA / P30 CA46934; United States / NCI NIH HHS / CA / T32CA8608604
  • [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; 0 / RNA, Neoplasm; EC 2.7.10.1 / MERTK protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
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14. Quigley DI, Wolff DJ: Pediatric T-cell acute lymphoblastic leukemia with aberrations of both MLL loci. Cancer Genet Cytogenet; 2006 Jul 1;168(1):77-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric T-cell acute lymphoblastic leukemia with aberrations of both MLL loci.
  • Translocations involving the MLL gene at 11q23 have been implicated in acute lymphoblastic leukemia (ALL), as well as acute myeloid leukemia (AML).
  • Such translocations result in gain of function fusion proteins that drive cell proliferation.
  • Except in cases of T-cell ALL, MLL rearrangement is typically associated with a poor prognosis.
  • We report a case of T-cell ALL with a t(11;19)(q23;p13.3) and deletion of the other chromosome 11 homolog at band q23.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Gene Deletion. Leukemia-Lymphoma, Adult T-Cell / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic / genetics

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  • (PMID = 16772125.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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15. van Grotel M, van den Heuvel-Eibrink MM, van Wering ER, van Noesel MM, Kamps WA, Veerman AJ, Pieters R, Meijerink JP: CD34 expression is associated with poor survival in pediatric T-cell acute lymphoblastic leukemia. Pediatr Blood Cancer; 2008 Dec;51(6):737-40
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  • [Title] CD34 expression is associated with poor survival in pediatric T-cell acute lymphoblastic leukemia.
  • BACKGROUND: Children with T-lineage acute lymphoblastic leukemia (T-ALL) have an inferior outcome with combination chemotherapy compared to B-lineage ALL, and still about 30% of the patients relapse within the first 2 years following diagnosis.
  • As CD34 has been related with poor outcome in ALL in general, we investigated the prognostic significance of the stem cell marker CD34, as well as the association of CD34 positivity with the expression of several multidrug resistance (MDR) genes.
  • PROCEDURE: In this retrospective study, we investigated the prognostic significance of the expression of the early T-cell differentiation marker CD34 and the expression of MDR genes in relation to outcome in a cohort of 72 newly diagnosed pediatric T-ALL patients.
  • [MeSH-major] Antigens, CD34 / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / mortality

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  • (PMID = 18683236.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / Antigens, CD34; 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; 0 / multidrug resistance-associated protein 1
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16. Efferth T, Gillet JP, Sauerbrey A, Zintl F, Bertholet V, de Longueville F, Remacle J, Steinbach D: Expression profiling of ATP-binding cassette transporters in childhood T-cell acute lymphoblastic leukemia. Mol Cancer Ther; 2006 Aug;5(8):1986-94
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  • [Title] Expression profiling of ATP-binding cassette transporters in childhood T-cell acute lymphoblastic leukemia.
  • A major issue in the treatment of T-cell acute lymphoblastic leukemia (T-ALL) is resistance to chemotherapeutic drugs.
  • [MeSH-major] ATP-Binding Cassette Transporters / genetics. Drug Resistance, Neoplasm / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics

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  • (PMID = 16928819.001).
  • [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 / ABCA2 protein, human; 0 / ABCA3 protein, human; 0 / Antineoplastic Agents; 0 / Multidrug Resistance-Associated Proteins
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17. Huang L, Lequin M, Pieters R, van den Heuvel-Eibrink MM: The clinical value of follow-up examinations in childhood T-cell acute lymphoblastic leukemia and T-cell non-Hodgkin's lymphoma. Pediatr Blood Cancer; 2007 Apr;48(4):468-72
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  • [Title] The clinical value of follow-up examinations in childhood T-cell acute lymphoblastic leukemia and T-cell non-Hodgkin's lymphoma.
  • BACKGROUND: The aim of this study was to evaluate the value of follow-up investigations of T-cell acute lymphoblastic leukemia (T-ALL) and T-cell non-Hodgkin's lymphoma (T-NHL), including cerebrospinal fluid (CSF) examination, bone marrow (BM) aspiration, peripheral blood (PB) count, serum lactate dehydrogenase (LDH) and chest X-rays in patients with an initial mediastinal enlargement.
  • PROCEDURE: We reviewed clinical records of all T-ALL patients from 1987 to 2002 and all T-NHL patients from 1977 to 2002, seen at a single institution.
  • All T-ALL and T-NHL patients with a mediastinal relapse were symptomatic.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / diagnosis. Lymphoma, T-Cell / diagnosis


18. Winter SS, Holdsworth MT, Devidas M, Raisch DW, Chauvenet A, Ravindranath Y, Ducore JM, Amylon MD: Antimetabolite-based therapy in childhood T-cell acute lymphoblastic leukemia: a report of POG study 9296. Pediatr Blood Cancer; 2006 Feb;46(2):179-86
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antimetabolite-based therapy in childhood T-cell acute lymphoblastic leukemia: a report of POG study 9296.
  • PURPOSE: A previous Pediatric Oncology Group (POG) study showed high incidence of secondary acute myelogenous leukemia (AML) in children treated for T-cell acute lymphoblastic leukemia (T-ALL) or higher-stage lymphoblastic lymphoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16007607.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5 U10 CA5312; United States / NCI NIH HHS / CA / CA29139
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Alkylating; EC 3.5.1.1 / Asparaginase
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19. van Vlierberghe P, Meijerink JP, Lee C, Ferrando AA, Look AT, van Wering ER, Beverloo HB, Aster JC, Pieters R: A new recurrent 9q34 duplication in pediatric T-cell acute lymphoblastic leukemia. Leukemia; 2006 Jul;20(7):1245-53
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  • [Title] A new recurrent 9q34 duplication in pediatric T-cell acute lymphoblastic leukemia.
  • Over the last decade, genetic characterization of T-cell acute lymphoblastic leukemia (T-ALL) has led to the identification of a variety of chromosomal abnormalities.
  • In this study, we used array-comparative genome hybridization (array-CGH) and identified a novel recurrent 9q34 amplification in 33% (12/36) of pediatric T-ALL samples, which is therefore one of the most frequent cytogenetic abnormalities observed in T-ALL thus far.
  • [MeSH-major] Chromosomes, Human, Pair 9. Gene Duplication. Leukemia-Lymphoma, Adult T-Cell / genetics

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  • (PMID = 16673019.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / NUP214-ABL1 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Receptor, Notch1
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20. Gutierrez A, Dahlberg SE, Neuberg DS, Zhang J, Grebliunaite R, Sanda T, Protopopov A, Tosello V, Kutok J, Larson RS, Borowitz MJ, Loh ML, Ferrando AA, Winter SS, Mullighan CG, Silverman LB, Chin L, Hunger SP, Sallan SE, Look AT: Absence of biallelic TCRgamma deletion predicts early treatment failure in pediatric T-cell acute lymphoblastic leukemia. J Clin Oncol; 2010 Aug 20;28(24):3816-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Absence of biallelic TCRgamma deletion predicts early treatment failure in pediatric T-cell acute lymphoblastic leukemia.
  • PURPOSE: To identify children with T-cell acute lymphoblastic leukemia (T-ALL) at high risk of induction chemotherapy failure by using DNA copy number analysis of leukemic cells collected at diagnosis.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Comparative Genomic Hybridization. Gene Deletion. Genes, T-Cell Receptor gamma. Polymerase Chain Reaction. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20644084.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1K08CA133103; United States / NCI NIH HHS / CA / CA98543; United States / NCI NIH HHS / CA / NCI 5P01CA68484; United States / NCI NIH HHS / CA / R01 CA129382-01A1; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / K08 CA133103-04; United States / NCI NIH HHS / CA / K08 CA133103-01; United States / NCI NIH HHS / CA / CA114766; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U24 CA114766; United States / NCI NIH HHS / CA / L40 CA124083-01; United States / NCI NIH HHS / CA / K08 CA133103; United States / NCI NIH HHS / CA / L40 CA124083; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / K08 CA133103-03; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / R01 CA120196-01A1; United States / NCI NIH HHS / CA / L40 CA124083-02; United States / NCI NIH HHS / CA / CA98413; United States / NCI NIH HHS / CA / K08 CA133103-02; United States / NCI NIH HHS / CA / P01 CA068484
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2940399
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21. Baysal BE: A recurrent stop-codon mutation in succinate dehydrogenase subunit B gene in normal peripheral blood and childhood T-cell acute leukemia. PLoS One; 2007 May 09;2(5):e436
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  • [Title] A recurrent stop-codon mutation in succinate dehydrogenase subunit B gene in normal peripheral blood and childhood T-cell acute leukemia.
  • Here, I describe that succinate dehydrogenase (SDH; mitochondrial complex II) subunit B gene (SDHB) is somatically mutated at a cytidine residue in normal peripheral blood mononuclear cells (PBMCs) and T-cell acute leukemia.
  • Examination of the PBMC cell-type subsets identifies monocytes and natural killer (NK) cells as primary sources of the mutant transcript, although lesser contributions also come from B and T lymphocytes.
  • Transcript sequence analyses in leukemic cell lines derived from monocyte, NK, T and B cells indicate that the mutational mechanism targeting SDHB is operational in T-cell acute leukemia.
  • Accordingly, substantial levels (more than 3%) of the mutant SDHB transcripts are detected in five of 20 primary childhood T-cell acute lymphoblastic leukemia (T-ALL) bone marrow samples, but in none of 20 B-ALL samples.
  • In addition, distinct heterozygous SDHB missense DNA mutations are identified in Jurkat and TALL-104 cell lines which are derived from T-ALLs.

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  • (PMID = 17487275.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA98543; United States / NCI NIH HHS / CA / CA114766; United States / NCI NIH HHS / CA / U24 CA114766; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA11236
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon, Terminator; 0 / DNA Primers; 0 / RNA, Messenger; EC 1.3.99.1 / Succinate Dehydrogenase
  • [Other-IDs] NLM/ PMC1855983
  • [General-notes] NLM/ Original DateCompleted: 20070727
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22. Karrman K, Forestier E, Heyman M, Andersen MK, Autio K, Blennow E, Borgström G, Ehrencrona H, Golovleva I, Heim S, Heinonen K, Hovland R, Johannsson JH, Kerndrup G, Nordgren A, Palmqvist L, Johansson B, Nordic Society of Pediatric Hematology, Oncology (NOPHO), Swedish Cytogenetic Leukemia Study Group (SCLSG), NOPHO Leukemia Cytogenetic Study Group (NLCSG): Clinical and cytogenetic features of a population-based consecutive series of 285 pediatric T-cell acute lymphoblastic leukemias: rare T-cell receptor gene rearrangements are associated with poor outcome. Genes Chromosomes Cancer; 2009 Sep;48(9):795-805
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical and cytogenetic features of a population-based consecutive series of 285 pediatric T-cell acute lymphoblastic leukemias: rare T-cell receptor gene rearrangements are associated with poor outcome.
  • Clinical characteristics and cytogenetic aberrations were ascertained and reviewed in a population-based consecutive series of 285 pediatric T-cell acute lymphoblastic leukemias (T-ALLs) diagnosed between 1992 and 2006 in the Nordic countries.
  • The most frequent abnormalities were T-cell receptor (TCR) gene rearrangements (20%) [TCR;11p13 (10%), TCR;10q24 (3%), TCR;other (8%)], del(9p) (17%), +8 (14%), del(6q) (12%), and 11q23 rearrangements (6%).
  • The clinical characteristics of this Nordic patient cohort agreed well with previous larger series, with a median age of 9.0 years, male predominance (male/female ratio 3.1), median white blood cell (WBC) count of 66.5 x 10(9)/l, and a high incidence of mediastinal mass and central nervous system involvement (59% and 9.5%, respectively).
  • In conclusion, in this large series of childhood T-ALLs from the Nordic countries, the cytogenetic findings were not associated with risk of therapy failure with the exception of the TCR;other group.
  • [MeSH-major] Chromosome Aberrations. Gene Rearrangement, T-Lymphocyte. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell / genetics

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  • (PMID = 19530250.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell
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23. Van Vlierberghe P, van Grotel M, Beverloo HB, Lee C, Helgason T, Buijs-Gladdines J, Passier M, van Wering ER, Veerman AJ, Kamps WA, Meijerink JP, Pieters R: The cryptic chromosomal deletion del(11)(p12p13) as a new activation mechanism of LMO2 in pediatric T-cell acute lymphoblastic leukemia. Blood; 2006 Nov 15;108(10):3520-9
Genetic Alliance. consumer health - Pediatric T-cell leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The cryptic chromosomal deletion del(11)(p12p13) as a new activation mechanism of LMO2 in pediatric T-cell acute lymphoblastic leukemia.
  • To identify new cytogenetic abnormalities associated with leukemogenesis or disease outcome, T-cell acute lymphoblastic leukemia (T-ALL) patient samples were analyzed by means of the array-comparative genome hybridization technique (array-CGH).
  • Here, we report the identification of a new recurrent and cryptic deletion on chromosome 11 (del(11)(p12p13)) in about 4% (6/138) of pediatric T-ALL patients.
  • LMO2 abnormalities represent about 9% (13/138) of pediatric T-ALL cases and are more frequent in pediatric T-ALL than appreciated until now.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 11. DNA-Binding Proteins / metabolism. Metalloproteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16873670.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LMO2 protein, human; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins
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24. Zuurbier L, Homminga I, Calvert V, te Winkel ML, Buijs-Gladdines JG, Kooi C, Smits WK, Sonneveld E, Veerman AJ, Kamps WA, Horstmann M, Petricoin EF 3rd, Pieters R, Meijerink JP: NOTCH1 and/or FBXW7 mutations predict for initial good prednisone response but not for improved outcome in pediatric T-cell acute lymphoblastic leukemia patients treated on DCOG or COALL protocols. Leukemia; 2010 Dec;24(12):2014-22
Hazardous Substances Data Bank. PREDNISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NOTCH1 and/or FBXW7 mutations predict for initial good prednisone response but not for improved outcome in pediatric T-cell acute lymphoblastic leukemia patients treated on DCOG or COALL protocols.
  • Aberrant activation of the NOTCH1 pathway by inactivating and activating mutations in NOTCH1 or FBXW7 is a frequent phenomenon in T-cell acute lymphoblastic leukemia (T-ALL).
  • We retrospectively investigated the relevance of NOTCH1/FBXW7 mutations for pediatric T-ALL patients enrolled on Dutch Childhood Oncology Group (DCOG) ALL7/8 or ALL9 or the German Co-Operative Study Group for Childhood Acute Lymphoblastic Leukemia study (COALL-97) protocols.
  • NOTCH1-activating mutations were less frequently associated with mature T-cell developmental stage.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Prednisone / therapeutic use. Receptor, Notch1 / genetics. Ubiquitin-Protein Ligases / genetics

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  • [CommentIn] Leukemia. 2010 Dec;24(12):2003-4 [21157484.001]
  • (PMID = 20861909.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Homeodomain Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / TLX3 protein, human; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases; VB0R961HZT / Prednisone
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25. van Grotel M, Meijerink JP, Beverloo HB, Langerak AW, Buys-Gladdines JG, Schneider P, Poulsen TS, den Boer ML, Horstmann M, Kamps WA, Veerman AJ, van Wering ER, van Noesel MM, Pieters R: The outcome of molecular-cytogenetic subgroups in pediatric T-cell acute lymphoblastic leukemia: a retrospective study of patients treated according to DCOG or COALL protocols. Haematologica; 2006 Sep;91(9):1212-21
Genetic Alliance. consumer health - Pediatric T-cell leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The outcome of molecular-cytogenetic subgroups in pediatric T-cell acute lymphoblastic leukemia: a retrospective study of patients treated according to DCOG or COALL protocols.
  • BACKGROUND AND OBJECTIVES: Subgroups of T-cell acute lymphoblastic leukemia (T-ALL), defined according to recurrent cytogenetic aberrations, may have different prognoses.
  • The aim of this study was to determine the prognostic relevance of molecular-cytogenetic abnormalities in pediatric patients using quantitative real-time polymerase chain reaction and fluorescence in situ hybridization.
  • In relation to the expression of early T-cell transcription factors, high TAL1 levels were found in immunophenotypically-advanced cases, whereas high LYL1 levels were found in immature subgroups.
  • Our data on CALM-AF10 rearranged T-ALL, albeit based on only three patients, suggest that this type of leukemia is associated with a poor outcome.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Cytogenetic Analysis. Leukemia-Lymphoma, Adult T-Cell / diagnosis

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  • [CommentIn] Haematologica. 2006 Sep;91(9):1156A [16956809.001]
  • (PMID = 16956820.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / AF10-CALM fusion protein, human; 0 / Oncogene Proteins, Fusion
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26. Borriello A, Locasciulli A, Bianco AM, Criscuolo M, Conti V, Grammatico P, Cappellacci S, Zatterale A, Morgese F, Cucciolla V, Delia D, Della Ragione F, Savoia A: A novel Leu153Ser mutation of the Fanconi anemia FANCD2 gene is associated with severe chemotherapy toxicity in a pediatric T-cell acute lymphoblastic leukemia. Leukemia; 2007 Jan;21(1):72-8
Genetic Alliance. consumer health - Pediatric T-cell leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel Leu153Ser mutation of the Fanconi anemia FANCD2 gene is associated with severe chemotherapy toxicity in a pediatric T-cell acute lymphoblastic leukemia.
  • We report the clinical and molecular features of a patient initially identified as a potential FA case only because of chemotherapy toxicity during the treatment of a T-lineage acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Fanconi Anemia Complementation Group D2 Protein / genetics. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation

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  • (PMID = 17096012.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] Italy / Telethon / / TGM06S01
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / FANCD2 protein, human; 0 / Fanconi Anemia Complementation Group D2 Protein; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
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27. Van Vlierberghe P, van Grotel M, Tchinda J, Lee C, Beverloo HB, van der Spek PJ, Stubbs A, Cools J, Nagata K, Fornerod M, Buijs-Gladdines J, Horstmann M, van Wering ER, Soulier J, Pieters R, Meijerink JP: The recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-cell acute lymphoblastic leukemia. Blood; 2008 May 1;111(9):4668-80
Genetic Alliance. consumer health - Pediatric T-cell leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) is mostly characterized by specific chromosomal abnormalities, some occurring in a mutually exclusive manner that possibly delineate specific T-ALL subgroups.
  • This deletion results in a conserved SET-NUP214 fusion product, which was also identified in the T-ALL cell line LOUCY.
  • We conclude that SET-NUP214 may contribute to the pathogenesis of T-ALL by enforcing T-cell differentiation arrest.

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  • (PMID = 18299449.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA11560
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / Histone Chaperones; 0 / Homeodomain Proteins; 0 / NUP214 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / SET protein, human; 0 / Transcription Factors; 157907-48-7 / HoxA protein
  • [Other-IDs] NLM/ PMC2343598
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28. Cleaver AL, Beesley AH, Firth MJ, Sturges NC, O'Leary RA, Hunger SP, Baker DL, Kees UR: Gene-based outcome prediction in multiple cohorts of pediatric T-cell acute lymphoblastic leukemia: a Children's Oncology Group study. Mol Cancer; 2010 May 12;9:105
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene-based outcome prediction in multiple cohorts of pediatric T-cell acute lymphoblastic leukemia: a Children's Oncology Group study.
  • BACKGROUND: Continuous complete clinical remission in T-cell acute lymphoblastic leukemia (T-ALL) is now approaching 80% due to the implementation of aggressive chemotherapy protocols but patients that relapse continue to have a poor prognosis.
  • In T-ALL cell lines, low IL-7R expression was correlated with diminished growth response to IL-7 and enhanced glucocorticoid resistance.
  • Analysis of biological pathways identified the NF-kappaB and Wnt pathways, and the cell adhesion receptor family (particularly integrins) as being predictive of relapse.

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  • (PMID = 20459861.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA114766; United States / NCI NIH HHS / CA / CA95475; United States / NCI NIH HHS / CA / CA98543
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / NF-kappa B; 0 / Receptors, Interleukin-7; 0 / Wnt Proteins
  • [Other-IDs] NLM/ PMC2879253
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29. Chinen Y, Taki T, Nishida K, Shimizu D, Okuda T, Yoshida N, Kobayashi C, Koike K, Tsuchida M, Hayashi Y, Taniwaki M: Identification of the novel AML1 fusion partner gene, LAF4, a fusion partner of MLL, in childhood T-cell acute lymphoblastic leukemia with t(2;21)(q11;q22) by bubble PCR method for cDNA. Oncogene; 2008 Apr 3;27(15):2249-56
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of the novel AML1 fusion partner gene, LAF4, a fusion partner of MLL, in childhood T-cell acute lymphoblastic leukemia with t(2;21)(q11;q22) by bubble PCR method for cDNA.
  • The AML1 gene is frequently rearranged by chromosomal translocations in acute leukemia.
  • We identified that the LAF4 gene on 2q11.2-12 was fused to the AML1 gene on 21q22 in a pediatric patient having T-cell acute lymphoblastic leukemia (T-ALL) with t(2;21)(q11;q22) using the bubble PCR method for cDNA.
  • The LAF4 gene is a member of the AF4/FMR2 family and was previously identified as a fusion partner of MLL in B-precursor ALL with t(2;11)(q11;q23), although AML1-LAF4 was in T-ALL.
  • LAF4 is the first gene fused with both AML1 and MLL in acute leukemia.
  • Almost all AML1 translocations except for TEL-AML1 are associated with myeloid leukemia; however, AML1-LAF4 was associated with T-ALL as well as AML1-FGA7 in t(4;21)(q28;q22).
  • [MeSH-major] Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 21. Core Binding Factor Alpha 2 Subunit / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Fusion / genetics. Polymerase Chain Reaction / methods. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Base Sequence. Child. DNA Mutational Analysis / methods. DNA, Complementary / analysis. Humans. Male. Models, Biological. Molecular Sequence Data

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  • (PMID = 17968322.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AFF3 protein, human; 0 / AML1-LAF4 fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA, Complementary; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human
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30. Liu JY, Li ZG, Gao C, Cui L, Wu MY: [Characteristics of T cell receptor beta gene rearrangements and its role in minimal residual disease detection in childhood T-cell acute lymphoblastic leukemia]. Zhonghua Er Ke Za Zhi; 2008 Jul;46(7):487-92
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Characteristics of T cell receptor beta gene rearrangements and its role in minimal residual disease detection in childhood T-cell acute lymphoblastic leukemia].
  • OBJECTIVE: To explore the characteristics of T cell receptor beta (TCRbeta) gene rearrangements in children with T-cell acute lymphoblastic leukemia (T-ALL) and establish a system of quantitative detection of MRD with real-time quantitative (RQ-PCR) targeted at TCRbeta gene rearrangement.
  • RESULTS: Clonal rearrangements were identified in 92.3% childhood T-ALL (Vbeta-Dbeta-Jbeta rearrangements in 84.6%, Dbeta-Jbeta rearrangements in 50%).
  • The segment Jbeta2.7 in childhood T-ALL was preferentially used.
  • [MeSH-major] Gene Rearrangement, beta-Chain T-Cell Antigen Receptor / genetics. Neoplasm, Residual / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19099802.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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31. Ballerini P, Landman-Parker J, Cayuela JM, Asnafi V, Labopin M, Gandemer V, Perel Y, Michel G, Leblanc T, Schmitt C, Fasola S, Hagemejier A, Sigaux F, Auclerc MF, Douay L, Leverger G, Baruchel A: Impact of genotype on survival of children with T-cell acute lymphoblastic leukemia treated according to the French protocol FRALLE-93: the effect of TLX3/HOX11L2 gene expression on outcome. Haematologica; 2008 Nov;93(11):1658-65
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  • [Title] Impact of genotype on survival of children with T-cell acute lymphoblastic leukemia treated according to the French protocol FRALLE-93: the effect of TLX3/HOX11L2 gene expression on outcome.
  • BACKGROUND: The prognostic value of the ectopic activation of TLX3 gene expression, a major oncogenetic event associated with pediatric T-cell acute lymphoblastic leukemia, is controversial.
  • Likewise, the frequency and the prognostic significance in pediatric T-cell acute lymphoblastic leukemia of the newly characterized NUP214-ABL1 fusion transcript is not yet clear.
  • DESIGN AND METHODS: Two hundred children with T-cell acute lymphoblastic leukemia were treated in the French FRALLE-93 study from 1993 to 1999.
  • At 5 years the overall survival (+/- standard deviation, %) was 62 (+/-3%) and leukemia-free survival was 58 (+/-3%).
  • Patients with T-cell acute lymphoblastic leukemia positive for TLX3 had a poorer survival compared to those with T-ALL negative for TLX3 (overall survival: 45+/-11% vs. 57+/-5%, p=0.049).
  • SILTAL expression did not significantly affect the prognosis of patients with T-cell acute lymphoblastic leukemia.
  • CONCLUSIONS: TLX3 gene expression is an independent risk factor predicting poor survival in childhood T-cell acute lymphoblastic leukemia.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Genotype. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18835836.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / TLX3 protein, human
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32. 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

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  • [Title] Prognostic significance of molecular-cytogenetic abnormalities in pediatric T-ALL is not explained by immunophenotypic differences.
  • 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.
  • We extensively studied 72 pediatric T-ALL cases for genetic abnormalities and expression of transcription factors, NOTCH1 mutations and expression of specific CD markers.
  • 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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33. Guastadisegni MC, Lonoce A, Impera L, Albano F, D'Addabbo P, Caruso S, Vasta I, Panagopoulos I, Leszl A, Basso G, Rocchi M, Storlazzi CT: Bone marrow ectopic expression of a non-coding RNA in childhood T-cell acute lymphoblastic leukemia with a novel t(2;11)(q11.2;p15.1) translocation. Mol Cancer; 2008;7:80
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  • [Title] Bone marrow ectopic expression of a non-coding RNA in childhood T-cell acute lymphoblastic leukemia with a novel t(2;11)(q11.2;p15.1) translocation.
  • T-cell acute lymphoblastic leukemia (T-ALL) is associated with a large number of such rearrangements.
  • We report the ectopic expression of the 3' portion of EST DA926692 in the bone marrow of a childhood T-ALL case showing a t(2;11)(q11.2;p15.1) translocation as the sole chromosome abnormality.
  • Bioinformatic analysis excluded that this small non-coding RNA is a precursor of micro-RNA, although it is conceivable that it has a different, yet unknown, functional role.
  • [MeSH-major] Bone Marrow / metabolism. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 2 / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA, Untranslated / genetics. Translocation, Genetic


34. 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.
  • 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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35. Schrauder A, Reiter A, Gadner H, Niethammer D, Klingebiel T, Kremens B, Peters C, Ebell W, Zimmermann M, Niggli F, Ludwig WD, Riehm H, Welte K, Schrappe M: Superiority of allogeneic hematopoietic stem-cell transplantation compared with chemotherapy alone in high-risk childhood T-cell acute lymphoblastic leukemia: results from ALL-BFM 90 and 95. J Clin Oncol; 2006 Dec 20;24(36):5742-9
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  • [Title] Superiority of allogeneic hematopoietic stem-cell transplantation compared with chemotherapy alone in high-risk childhood T-cell acute lymphoblastic leukemia: results from ALL-BFM 90 and 95.
  • PURPOSE: The role of hematopoietic stem-cell transplantation (SCT) in first complete remission (CR1) for children with very high-risk (VHR) acute lymphoblastic leukemia (ALL) is still under critical discussion.
  • T-cell ALL (T-ALL) patients with poor in vivo response to initial treatment represented the largest homogeneous subgroup within VHR patients.
  • CONCLUSION: SCT in CR1 is superior to treatment with chemotherapy alone for childhood HR-T-ALL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


36. Attarbaschi A, Pisecker M, Inthal A, Mann G, Janousek D, Dworzak M, Pötschger U, Ullmann R, Schrappe M, Gadner H, Haas OA, Panzer-Grümayer R, Strehl S, Austrian Berlin-Frankfurt-Münster (BFM) Study Group: Prognostic relevance of TLX3 (HOX11L2) expression in childhood T-cell acute lymphoblastic leukaemia treated with Berlin-Frankfurt-Münster (BFM) protocols containing early and late re-intensification elements. Br J Haematol; 2010 Jan;148(2):293-300
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  • [Title] Prognostic relevance of TLX3 (HOX11L2) expression in childhood T-cell acute lymphoblastic leukaemia treated with Berlin-Frankfurt-Münster (BFM) protocols containing early and late re-intensification elements.
  • TLX3 expression (TLX3+) in childhood T-cell acute lymphoblastic leukaemia (T-ALL) seems to be associated with a poor prognosis when treated with regimens that lack early and/or late re-intensification therapy elements.
  • Thirty-one/131 childhood T-ALL cases (24%) enrolled into four population-based Austrian ALL-BFM therapy studies were TLX3+.
  • After a median observation time of 4.9 years (range 0.4-16.1 years) 28/31 TLX3+ cases remained in first complete remission after chemotherapy with one after additional stem cell transplantation.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols. Homeodomain Proteins / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 19821827.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Homeodomain Proteins; 0 / NUP214-ABL1 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / TLX3 protein, human; 5J49Q6B70F / Vincristine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; ZS7284E0ZP / Daunorubicin; PVDA protocol
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37. Berman JN, Look AT: Targeting transcription factors in acute leukemia in children. Curr Drug Targets; 2007 Jun;8(6):727-37
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  • [Title] Targeting transcription factors in acute leukemia in children.
  • Transcription factors play essential roles in controlling normal blood development and their alteration leads to abnormalities in cell proliferation, differentiation and survival.
  • In many childhood acute leukemias, transcription factors are altered through chromosomal translocations that change their functional properties resulting in repressed activity or inappropriate activation.
  • The development of therapies that specifically target these molecular abnormalities holds promise for improving the outcome in diseases that remain challenging to treat, such as childhood T-cell acute lymphoblastic leukemia and acute myeloid leukemia, with improved toxicity profiles.
  • All trans-retinoic acid and arsenic trioxide have already demonstrated efficacy in acute promyelocytic leukemia in both adults and children.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Delivery Systems. Leukemia / drug therapy. Transcription Factors / drug effects
  • [MeSH-minor] Acute Disease. Arsenicals / pharmacology. Arsenicals / therapeutic use. Child. DNA Methylation / drug effects. Histone Deacetylase Inhibitors. Humans. Oxides / pharmacology. Oxides / therapeutic use. Tretinoin / pharmacology. Tretinoin / therapeutic use

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  • (PMID = 17584028.001).
  • [ISSN] 1873-5592
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Histone Deacetylase Inhibitors; 0 / Oxides; 0 / Transcription Factors; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 113
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38. Sandlund JT, Pui CH, Zhou Y, Behm FG, Onciu M, Razzouk BI, Hijiya N, Campana D, Hudson MM, Ribeiro RC: Effective treatment of advanced-stage childhood lymphoblastic lymphoma without prophylactic cranial irradiation: results of St Jude NHL13 study. Leukemia; 2009 Jun;23(6):1127-30
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  • [Title] Effective treatment of advanced-stage childhood lymphoblastic lymphoma without prophylactic cranial irradiation: results of St Jude NHL13 study.
  • There has been a steady improvement in cure rates for children with advanced-stage lymphoblastic non-Hodgkin's lymphoma.
  • To further improve cure rates whereas minimizing long-term toxicity, we designed a protocol (NHL13) based on a regimen for childhood T-cell acute lymphoblastic leukemia, which features intensive intrathecal chemotherapy for central -nervous system-directed therapy and excludes prophylactic cranial irradiation.
  • From 1992 to 2002, 41 patients with advanced-stage lymphoblastic lymphoma were enrolled on the protocol.
  • Thirty-three cases had a precursor T-cell immunophenotype, five had precursor B-cell immunophenotype and in three immunophenotype was not determined.
  • Adverse events included two induction failures, one death from typhlitis during remission, three relapses and one secondary acute myeloid leukemia.
  • The treatment described here produces high cure rates in children with lymphoblastic lymphoma without the use of prophylactic cranial irradiation.

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  • (PMID = 19194463.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; None / None / / P30 CA021765-31; United States / NCI NIH HHS / CA / CA 21765; United States / NCI NIH HHS / CA / P30 CA021765-31
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; 8N3DW7272P / Cyclophosphamide; E7WED276I5 / 6-Mercaptopurine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ NIHMS161582; NLM/ PMC2843413
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39. Stark B, Avigad S, Luria D, Manor S, Reshef-Ronen T, Avrahami G, Yaniv I: Bone marrow minimal disseminated disease (MDD) and minimal residual disease (MRD) in childhood T-cell lymphoblastic lymphoma stage III, detected by flow cytometry (FC) and real-time quantitative polymerase chain reaction (RQ-PCR). Pediatr Blood Cancer; 2009 Jan;52(1):20-5
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  • [Title] Bone marrow minimal disseminated disease (MDD) and minimal residual disease (MRD) in childhood T-cell lymphoblastic lymphoma stage III, detected by flow cytometry (FC) and real-time quantitative polymerase chain reaction (RQ-PCR).
  • BACKGROUND: Despite overlapping features of T-cell lymphoblastic lymphoma (T-LLy) and T-cell acute lymphoblastic leukemia (T-ALL), which respond favorably to T-ALL treatment, clinical and biological differences exist.
  • PROCEDURE: Four-color flow cytometry (FC) was used for lymphoma associated immunophenotype and real-time quantitative polymerase chain reaction (RQ-PCR) for T-cell receptor (TCR beta/delta/gamma) gene rearrangements with at least 0.01% sensitivity.
  • [MeSH-major] Bone Marrow Diseases / diagnosis. Neoplasm, Residual / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 19006253.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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40. Su XY, Della-Valle V, Andre-Schmutz I, Lemercier C, Radford-Weiss I, Ballerini P, Lessard M, Lafage-Pochitaloff M, Mugneret F, Berger R, Romana SP, Bernard OA, Penard-Lacronique V: HOX11L2/TLX3 is transcriptionally activated through T-cell regulatory elements downstream of BCL11B as a result of the t(5;14)(q35;q32). Blood; 2006 Dec 15;108(13):4198-201
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  • [Title] HOX11L2/TLX3 is transcriptionally activated through T-cell regulatory elements downstream of BCL11B as a result of the t(5;14)(q35;q32).
  • The t(5;14)(q35;q32) chromosomal translocation is specifically observed in up to 20% of childhood T-cell acute lymphoblastic leukemia (T-ALL).
  • Our data indicate that the basis of the specific association between t(5;14) and T-ALL lies on the juxtaposition of TLX3 to long-range cis-activating regions active during T-cell differentiation.
  • [MeSH-major] Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, Pair 5 / genetics. DNA-Binding Proteins / genetics. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Oncogene Proteins / genetics. Oncogene Proteins, Fusion / genetics. Repressor Proteins / genetics. Translocation, Genetic. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Cell Differentiation / genetics. Humans. Jurkat Cells. Promoter Regions, Genetic / genetics. T-Lymphocytes / metabolism. T-Lymphocytes / pathology. Transcription, Genetic

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  • (PMID = 16926283.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL11B protein, human; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / Oncogene Proteins; 0 / Oncogene Proteins, Fusion; 0 / Repressor Proteins; 0 / TLX3 protein, human; 0 / Tumor Suppressor Proteins
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41. 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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  • [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).
  • Frequencies of LOH were compared in 113 pediatric T-LBL and 125 T-ALL who were treated uniformly according to ALL-BFM strategies.
  • [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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42. 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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  • [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


43. 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
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  • [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 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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44. Coustan-Smith E, Sandlund JT, Perkins SL, Chen H, Chang M, Abromowitch M, Campana D: Minimal disseminated disease in childhood T-cell lymphoblastic lymphoma: a report from the children's oncology group. J Clin Oncol; 2009 Jul 20;27(21):3533-9
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  • [Title] Minimal disseminated disease in childhood T-cell lymphoblastic lymphoma: a report from the children's oncology group.
  • PURPOSE Disease dissemination to the bone marrow is detected at diagnosis in approximately 15% of children with T-cell lymphoblastic lymphoma (T-LL).
  • PATIENTS AND METHODS Using a flow cytometric method that can detect one T-LL cell among 10,000 normal cells, we examined bone marrow and peripheral-blood samples collected from 99 children with T-LL at diagnosis, as well as blood samples collected from 42 patients during treatment.
  • [MeSH-major] Disease Transmission, Infectious. Lymphoma, T-Cell / chemistry. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma. Transplantation Conditioning
  • [MeSH-minor] Bone Marrow Cells. Bone Marrow Diseases / microbiology. Child. Flow Cytometry. Humans. Lymphoma, B-Cell / blood. Lymphoma, Non-Hodgkin. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19546402.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U10-CA98543; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / R01 CA060419; United States / NCI NIH HHS / CA / CA60419; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / U10 CA098413-07; United States / NCI NIH HHS / CA / U01 CA060419
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2717759
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45. Yang F, Li Y, Braylan R, Hunger SP, Yang LJ: Pediatric T-cell post-transplant lymphoproliferative disorder after solid organ transplantation. Pediatr Blood Cancer; 2008 Feb;50(2):415-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric T-cell post-transplant lymphoproliferative disorder after solid organ transplantation.
  • PTLD has extended from its initial description as an Epstein-Barr virus (EBV)-driven B-cell proliferation to include EBV-negative and non B-lineage cases.
  • T-cell PTLD (T-PTLD) is rare in both adults and children.
  • We report two cases of pediatric T-PTLD after SOT (liver and lungs) and review cases reported in the literature.
  • Both patients had a bimodal response to therapy with initial eradication of bulky nodal disease with regimens typically used to treat leukemia, but persistence of low-level clonal T-cells in marrow, CSF and lung in one case.

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
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  • (PMID = 17051534.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK064054
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS397340; NLM/ PMC3419753
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46. Haltrich I, Kost-Alimova M, Kovács G, Dobos M, Klein G, Fekete G, Imreh S: Multipoint interphase FISH in childhood T-acute lymphoblastic leukemia detects subpopulations that carry different chromosome 3 aberrations. Cancer Genet Cytogenet; 2007 Jan 1;172(1):54-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multipoint interphase FISH in childhood T-acute lymphoblastic leukemia detects subpopulations that carry different chromosome 3 aberrations.
  • We examined chromosome 3 in 32 childhood acute lymphoblastic leukemia (ALL) bone marrow samples.
  • Using interphase multipoint FISH (mp-FISH), which was developed by our group, with 42 chromosome 3-specific probes, we detected clonal chromosome 3 aberrations in 4 T-cell ALL (T-ALL) cases.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 3 / genetics. DNA, Neoplasm / genetics. Interphase / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics

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  • (PMID = 17175380.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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47. Uyttebroeck A, Suciu S, Laureys G, Robert A, Pacquement H, Ferster A, Marguerite G, Mazingue F, Renard M, Lutz P, Rialland X, Mechinaud F, Cavé H, Baila L, Bertrand Y, Children's Leukaemia Group (CLG) of the European Organisation for Research and Treatment of Cancer (EORTC): Treatment of childhood T-cell lymphoblastic lymphoma according to the strategy for acute lymphoblastic leukaemia, without radiotherapy: long term results of the EORTC CLG 58881 trial. Eur J Cancer; 2008 Apr;44(6):840-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of childhood T-cell lymphoblastic lymphoma according to the strategy for acute lymphoblastic leukaemia, without radiotherapy: long term results of the EORTC CLG 58881 trial.
  • From June 1989 through to November 1998, 121 children with newly diagnosed T-cell lymphoblastic lymphoma (T-LBL) were included in the EORTC 58881 trial conducted by the Children's Leukaemia Group.
  • An intensive acute lymphoblastic leukaemia type chemotherapy regimen without irradiation leads to a high cure and survival rate in childhood T-LBL without an increased CNS recurrence.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 18342502.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5U10-CA11488-18; United States / NCI NIH HHS / CA / 5U10-CA11488-19; United States / NCI NIH HHS / CA / 5U10-CA11488-20; United States / NCI NIH HHS / CA / 5U10-CA11488-21; United States / NCI NIH HHS / CA / 5U10-CA11488-22; United States / NCI NIH HHS / CA / 5U10-CA11488-23; United States / NCI NIH HHS / CA / 5U10-CA11488-24; United States / NCI NIH HHS / CA / 5U10-CA11488-25; United States / NCI NIH HHS / CA / 5U10-CA11488-26; United States / NCI NIH HHS / CA / 5U10-CA11488-27; United States / NCI NIH HHS / CA / 5U10-CA11488-28; United States / NCI NIH HHS / CA / 5U10-CA11488-29; United States / NCI NIH HHS / CA / 5U10-CA11488-30; United States / NCI NIH HHS / CA / 5U10-CA11488-31; United States / NCI NIH HHS / CA / 5U10-CA11488-32; United States / NCI NIH HHS / CA / 5U10-CA11488-33; United States / NCI NIH HHS / CA / 5U10-CA11488-34; United States / NCI NIH HHS / CA / 5U10-CA11488-35; United States / NCI NIH HHS / CA / 5U10-CA11488-36
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Investigator] Philippet P; Otten J; Plouvier E; Béhar C; Boutard P; Millot F; Waterkeyn C; Velde IV; Solbu G
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48. 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
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cooperative genetic defects in TLX3 rearranged pediatric T-ALL.
  • T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive neoplastic disorder, in which multiple genetic abnormalities cooperate in the malignant transformation of thymocytes.
  • About 20% of pediatric T-ALL cases are characterized by TLX3 expression due to a cryptic translocation t(5;14)(q35;q32).
  • [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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49. Erbilgin Y, Sayitoglu M, Hatirnaz O, Dogru O, Akcay A, Tuysuz G, Celkan T, Aydogan G, Salcioglu Z, Timur C, Yuksel-Soycan L, Ure U, Anak S, Agaoglu L, Devecioglu O, Yildiz I, Ozbek U: Prognostic significance of NOTCH1 and FBXW7 mutations in pediatric T-ALL. Dis Markers; 2010;28(6):353-60

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of NOTCH1 and FBXW7 mutations in pediatric T-ALL.
  • The NOTCH signaling pathway plays important role in the development of multicellular organisms, as it regulates cell proliferation, survival, and differentiation.
  • In this study, the mutation analysis of NOTCH1 and FBXW7 genes was performed in 87 pediatric T-ALLs who were treated on the ALL-BFM protocols.
  • NOTCH1 and FBXW7, NOTCH1 alone were found correlated with lower initial leucocyte counts which was independent from the sex and T- cell immunophenotype.
  • However, NOTCH1 and FBXW7 mutations were not predictive of outcome in the overall cohort of pediatric T-ALLs.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Mutation / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics. Ubiquitin-Protein Ligases / genetics

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  • (PMID = 20683149.001).
  • [ISSN] 1875-8630
  • [Journal-full-title] Disease markers
  • [ISO-abbreviation] Dis. Markers
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / NOTCH1 protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptor, Notch1; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Other-IDs] NLM/ PMC3833232
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50. Fischer S, Mann G, Konrad M, Metzler M, Ebetsberger G, Jones N, Nadel B, Bodamer O, Haas OA, Schmitt K, Panzer-Grümayer ER: Screening for leukemia- and clone-specific markers at birth in children with T-cell precursor ALL suggests a predominantly postnatal origin. Blood; 2007 Oct 15;110(8):3036-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Screening for leukemia- and clone-specific markers at birth in children with T-cell precursor ALL suggests a predominantly postnatal origin.
  • Childhood T-cell precursor acute lymphoblastic leukemia (TCP ALL) is an aggressive disease with a presumably short latency that differs in many biologic respects from B-cell precursor (BCP) ALL.
  • We therefore addressed the issue of in utero origin of this particular type of leukemia by tracing oncogenic mutations and clone-specific molecular markers back to birth.
  • These markers included various first- and second-hit genetic alterations (TCRD-LMO2 breakpoint regions, n = 2; TAL1 deletions, n = 3; Notch1 mutations, n = 1) and nononcogenic T-cell receptor rearrangements (n = 13) that were derived from leukemias of 16 children who were 1.5 to 11.2 years old at diagnosis of leukemia.
  • Despite highly sensitive polymerase chain reaction (PCR) approaches (1 cell with a specific marker among 100,000 normal cells), we identified the leukemic clone in the neonatal blood spots in only 1 young child.
  • [MeSH-major] Biomarkers, Tumor / genetics. Gene Rearrangement, T-Lymphocyte / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17557895.001).
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LMO2 protein, human; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins; 0 / Receptor, Notch1; 135471-20-4 / TAL1 protein, human
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51. Gottardo NG, Hoffmann K, Beesley AH, Freitas JR, Firth MJ, Perera KU, de Klerk NH, Baker DL, Kees UR: Identification of novel molecular prognostic markers for paediatric T-cell acute lymphoblastic leukaemia. Br J Haematol; 2007 May;137(4):319-28
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of novel molecular prognostic markers for paediatric T-cell acute lymphoblastic leukaemia.
  • In the last four decades the survival of patients with newly diagnosed childhood T-cell acute lymphoblastic leukaemia (T-ALL) has improved dramatically.
  • [MeSH-major] Gene Expression Profiling. Leukemia-Lymphoma, Adult T-Cell / genetics. Oligonucleotide Array Sequence Analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17456054.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA95475
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BTG3 protein, human; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / CFLAR protein, human; 0 / Genetic Markers; 0 / NOTCH2 protein, human; 0 / Proteins; 0 / Receptor, Notch2
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52. Friedrich C, Schrum J, Chott A, Janka-Schaub G, Kabisch H: Ongoing remission after intensive ALL-type chemotherapy in pediatric intestinal T-cell lymphoma. Pediatr Blood Cancer; 2010 Apr;54(4):610-2
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  • [Title] Ongoing remission after intensive ALL-type chemotherapy in pediatric intestinal T-cell lymphoma.
  • A rare case of primary intestinal T-cell lymphoma (ITL) of an 8-year-old boy is reported.
  • They showed monoclonal rearrangement of the T-cell receptor gamma-chain and no evidence of EBV infection.
  • Our patient remains in first remission 30 months after finishing the acute lymphoblastic leukemia protocol COALL-07-03 high risk standard.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Intestinal Neoplasms / drug therapy. Intestinal Neoplasms / pathology. Lymphoma, T-Cell / drug therapy. Lymphoma, T-Cell / pathology
  • [MeSH-minor] 6-Mercaptopurine / administration & dosage. Child. Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Dexamethasone / administration & dosage. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Humans. Male. Methotrexate / administration & dosage. Methylprednisolone / administration & dosage. Neoplasm Staging. Receptors, Antigen, T-Cell, gamma-delta / genetics. Remission Induction. Thioguanine / administration & dosage. Vincristine / administration & dosage

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  • (PMID = 20049930.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, gamma-delta; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; E7WED276I5 / 6-Mercaptopurine; FTK8U1GZNX / Thioguanine; X4W7ZR7023 / Methylprednisolone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin
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53. Goemans BF, Zwaan CM, Harlow A, Loonen AH, Gibson BE, Hählen K, Reinhardt D, Creutzig U, Heinrich MC, Kaspers GJ: In vitro profiling of the sensitivity of pediatric leukemia cells to tipifarnib: identification of T-cell ALL and FAB M5 AML as the most sensitive subsets. Blood; 2005 Nov 15;106(10):3532-7
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  • [Title] In vitro profiling of the sensitivity of pediatric leukemia cells to tipifarnib: identification of T-cell ALL and FAB M5 AML as the most sensitive subsets.
  • Although the prognosis of pediatric leukemias has improved considerably, many patients still have relapses.
  • Tipifarnib, a farnesyl transferase inhibitor (FTI), was developed to target malignancies with activated RAS, including leukemia.
  • We tested 52 pediatric acute myeloid leukemia (AML) and 36 pediatric acute lymphoblastic leukemia (ALL) samples for in vitro sensitivity to tipifarnib using a total cell-kill assay and compared these results to those obtained with normal bone marrow (N BM) samples (n = 25).
  • AML samples were significantly more sensitive to tipifarnib compared to B-cell precursor ALL (BCP ALL) or N BM samples.
  • T-cell ALL samples were significantly more sensitive than BCP ALL and N BM samples.
  • In addition, clinical studies, especially in T-cell ALL, seem warranted.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Biomarkers, Tumor / metabolism. Drug Resistance, Neoplasm. Leukemia, Monocytic, Acute / enzymology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology. Quinolones / pharmacology

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  • (PMID = 16051737.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Quinolones; 192185-72-1 / tipifarnib; EC 2.5.1.29 / Farnesyltranstransferase; EC 3.6.5.2 / Oncogene Protein p21(ras)
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54. Buysse K, Crepel A, Menten B, Pattyn F, Antonacci F, Veltman JA, Larsen LA, Tümer Z, de Klein A, van de Laar I, Devriendt K, Mortier G, Speleman F: Mapping of 5q35 chromosomal rearrangements within a genomically unstable region. J Med Genet; 2008 Oct;45(10):672-8
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  • This region is also targeted by the recurrent cryptic t(5;14)(q35;q32) translocation, which occurs in approximately 20% of childhood T cell acute lymphoblastic leukaemia (T-ALL).

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  • [ErratumIn] J Med Genet. 2009 Dec;46(12):861
  • (PMID = 18628311.001).
  • [ISSN] 1468-6244
  • [Journal-full-title] Journal of medical genetics
  • [ISO-abbreviation] J. Med. Genet.
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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55. Jiang G, Freywald T, Webster J, Kozan D, Geyer R, DeCoteau J, Narendran A, Freywald A: In human leukemia cells ephrin-B-induced invasive activity is supported by Lck and is associated with reassembling of lipid raft signaling complexes. Mol Cancer Res; 2008 Feb;6(2):291-305
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  • [Title] In human leukemia cells ephrin-B-induced invasive activity is supported by Lck and is associated with reassembling of lipid raft signaling complexes.
  • We show here that ephrin-B1, a member of the ephrin-B group, is expressed in pediatric T-cell leukemias, including leukemia cell line Jurkat.
  • [MeSH-major] Ephrin-B1 / metabolism. Leukemia-Lymphoma, Adult T-Cell / enzymology. Leukemia-Lymphoma, Adult T-Cell / pathology. Lymphocyte Specific Protein Tyrosine Kinase p56(lck) / metabolism. Membrane Microdomains / enzymology. Signal Transduction
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / metabolism. Cell Adhesion. Child. Ephrin-B3 / metabolism. Fibronectins / metabolism. Humans. Jurkat Cells. Neoplasm Invasiveness. Nuclear Proteins / metabolism. Protein Structure, Tertiary. Protein Transport. rac1 GTP-Binding Protein / metabolism

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  • (PMID = 18314490.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / CRKL protein; 0 / Ephrin-B1; 0 / Ephrin-B3; 0 / Fibronectins; 0 / Nuclear Proteins; EC 2.7.10.2 / Lymphocyte Specific Protein Tyrosine Kinase p56(lck); EC 3.6.5.2 / rac1 GTP-Binding Protein
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56. Hundsdoerfer P, Dietrich I, Schmelz K, Eckert C, Henze G: XIAP expression is post-transcriptionally upregulated in childhood ALL and is associated with glucocorticoid response in T-cell ALL. Pediatr Blood Cancer; 2010 Aug;55(2):260-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] XIAP expression is post-transcriptionally upregulated in childhood ALL and is associated with glucocorticoid response in T-cell ALL.
  • BACKGROUND: Resistance to glucocorticoid induced apoptosis is one of the major risk factors for relapse and poor outcome in childhood acute lymphoblastic leukemia (ALL).
  • PROCEDURE: XIAP protein and mRNA expression were determined in leukemic blasts of 51 childhood ALL patients and normal bone marrow mononuclear cells.
  • RESULTS: XIAP protein but not mRNA expression was found to be highly increased in childhood ALL compared to control bone marrow mononuclear cells (MNC) (median: 3.5 vs. 0.14 ng/10(5) MNC, P < 0.0001) indicating a post-transcriptional regulation of XIAP expression.
  • In patients with T-cell ALL, poor prednisone response was associated with increased XIAP expression (median: 2.8 in good vs. 5.8 in poor responders; P = 0.005).
  • Similarly, T-cell ALL patients suffering adverse events showed higher initial XIAP levels than patients in continuous complete remission (CCR) (median: 2.7 in patients in CCR vs. 5.6 in patients suffering adverse events; P = 0.007).
  • CONCLUSION: In childhood ALL compared to control bone marrow, the expression of the apoptosis inhibitor XIAP is highly increased by post-transcriptional regulation.
  • The association with poor in vivo glucocorticoid response and outcome in T-cell ALL suggests XIAP inhibition as a promising novel approach for the treatment of resistant ALL.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Glucocorticoids / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. X-Linked Inhibitor of Apoptosis Protein / genetics
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Bone Marrow Cells / pathology. Bone Marrow Examination. Child. Drug Resistance. Female. Humans. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Male. Monocytes / pathology. Pharmacogenetics. Prognosis. RNA, Messenger / analysis. Treatment Outcome. Up-Regulation

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  • [Copyright] (c) 2010 Wiley-Liss, Inc.
  • (PMID = 20582956.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / RNA, Messenger; 0 / X-Linked Inhibitor of Apoptosis Protein
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57. Al-Khabori M, Minden MD, Yee KW, Gupta V, Schimmer AD, Schuh AC, Xu W, Brandwein JM: Improved survival using an intensive, pediatric-based chemotherapy regimen in adults with T-cell acute lymphoblastic leukemia. Leuk Lymphoma; 2010 Jan;51(1):61-5
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  • [Title] Improved survival using an intensive, pediatric-based chemotherapy regimen in adults with T-cell acute lymphoblastic leukemia.
  • All patients with newly diagnosed T-cell acute lymphoblastic leukemia (T-ALL) and treated over a 17-year period at a single institution were retrospectively analyzed.
  • From 2000 to 2007, a pediatric-based protocol, DFCI (Dana Farber Cancer Institute), was used as the standard regimen for all patients (n = 32).
  • The results provide evidence supporting the superior efficacy of asparaginase-intensive pediatric-based regimens for adults with T-ALL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / mortality


58. 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.
  • Subsequent analysis showed WT1 mutations in 28 of 211 (13.2%) of pediatric and 10 of 85 (11.7%) of adult T-ALL cases.
  • Survival analysis demonstrated that WT1 mutations do not confer adverse prognosis in pediatric and adult T-ALL.

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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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59. 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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  • 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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60. 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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61. Gualco G, Klumb CE, Barber GN, Weiss LM, Bacchi CE: Pediatric lymphomas in Brazil. Clinics (Sao Paulo); 2010;65(12):1267-77
MedlinePlus Health Information. consumer health - Lymphoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric lymphomas in Brazil.
  • OBJECTIVE: This study provides the clinical pathological characteristics of 1301 cases of pediatric/adolescent lymphomas in patients from different geographic regions of Brazil.
  • METHODS: A retrospective analyses of diagnosed pediatric lymphoma cases in a 10-year period was performed.
  • We believe that it represents the largest series of pediatric lymphomas presented from Brazil.
  • RESULTS: Non-Hodgkin lymphomas represented 68% of the cases, including those of precursor (36%) and mature (64%) cell origin.
  • Mature cell lymphomas comprised 81% of the B-cell phenotype and 19% of the T-cell phenotype.
  • Among mature B-cell lymphomas, most of the cases were Burkitt lymphomas (65%), followed by diffuse large B-cell lymphomas (24%).
  • In the mature T-cell group, anaplastic large cell lymphoma, ALK-positive was the most prevalent (57%), followed by peripheral T-cell lymphoma, then not otherwise specified (25%).

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  • (PMID = 21340214.001).
  • [ISSN] 1980-5322
  • [Journal-full-title] Clinics (São Paulo, Brazil)
  • [ISO-abbreviation] Clinics (Sao Paulo)
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / P30 AI073961
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Other-IDs] NLM/ PMC3020336
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62. Zweidler-McKay PA: Notch signaling in pediatric malignancies. Curr Oncol Rep; 2008 Nov;10(6):459-68
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] Notch signaling in pediatric malignancies.
  • Because many pediatric malignancies arise from dysregulated development, roles for Notch signaling in these cancers are to be expected.
  • Evidence to support this is now emerging as the Notch pathway is being explored in more pediatric cancers.
  • As examples, although activating mutations of Notch1 are found in the majority of T-cell acute lymphoblastic leukemia (ALL) cases, Notch/HES1 signaling appears to play a tumor suppressor role in precursor B-cell ALL; although Notch/HES1 signaling appears to contribute to osteosarcoma metastasis, Notch signaling also promotes medulloblastoma "stem cell" survival and contributes to angiogenesis in neuroblastoma.
  • Further understanding of the roles of Notch signaling in specific pediatric cancers will provide a rationale for Notch-based therapeutic strategies.
  • [MeSH-minor] Animals. Cell Lineage. Cell Survival. Child. Genes, Tumor Suppressor. Humans. Mutation. Neoplasm Metastasis. Osteosarcoma / therapy. Signal Transduction. Stem Cells / cytology

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  • (PMID = 18928660.001).
  • [ISSN] 1534-6269
  • [Journal-full-title] Current oncology reports
  • [ISO-abbreviation] Curr Oncol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Notch
  • [Number-of-references] 50
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63. 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.
  • [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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64. 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
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] 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.
  • [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

  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
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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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65. Komatsu H, Inui A, Sogo T, Fujisawa T, Nagasaka H, Nonoyama S, Sierro S, Northfield J, Lucas M, Vargas A, Klenerman P: Large scale analysis of pediatric antiviral CD8+ T cell populations reveals sustained, functional and mature responses. Immun Ageing; 2006;3:11
HIV InSite. treatment guidelines - Malaria and HIV .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Large scale analysis of pediatric antiviral CD8+ T cell populations reveals sustained, functional and mature responses.
  • However, although CMV infection occurs during childhood, relatively little is know about the typical quantity and quality of T cell responses in pediatric populations.
  • We analyzed the CD8+ T cell responses to CMV, comparing these to responses in children and young.
  • RESULTS: We observed consistently high frequency and phenotypically "mature" (CD27 low, CD28 low, CD45RA+) CMV-specific CD8+ T cell responses in children, including those studied in the first year of life.
  • CONCLUSION: CMV consistently elicits a very strong CD8+ T cell response in infants and large pools of CMV specific CD8+ T cells are maintained throughout childhood.
  • The presence of CMV may considerably mould the CD8+ T cell compartment over time, but the relative frequencies of CMV-specific cells do not show the evidence of a population-level increase during childhood and adulthood.
  • This study indicates that large scale analysis of peptide specific T cell responses in infants is readily possible.

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  • (PMID = 17156440.001).
  • [ISSN] 1742-4933
  • [Journal-full-title] Immunity & ageing : I & A
  • [ISO-abbreviation] Immun Ageing
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1784110
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66. Dawidowska M, Jółkowska J, Szczepański T, Derwich K, Wachowiak J, Witt M: Implementation of the standard strategy for identification of Ig/TCR targets for minimal residual disease diagnostics in B-cell precursor ALL pediatric patients: Polish experience. Arch Immunol Ther Exp (Warsz); 2008 Nov-Dec;56(6):409-18

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Implementation of the standard strategy for identification of Ig/TCR targets for minimal residual disease diagnostics in B-cell precursor ALL pediatric patients: Polish experience.
  • INTRODUCTION: Minimal residual disease (MRD), detected based on immunoglobulin and T-cell receptor (Ig/TCR) gene rearrangements as markers of residual leukemic cells, is currently the most reliable prognostic factor in acute lymphoblastic leukemia (ALL).
  • MATERIALS AND METHODS: The PCR-heteroduplex approach based on BIOMED-1 and BIOMED-2 protocols (recommended as the European standard) was used to detect IGH, IGK-Kde, TCRD, TCRG, and TCRB rearrangements in 58 Polish B-cell precursor ALL patients.
  • [MeSH-minor] Adolescent. Cell Line, Tumor. Child. Child, Preschool. Europe. Female. Gene Rearrangement. Humans. Immunoglobulin Heavy Chains / genetics. Infant. Male. Poland. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Prognosis. Receptors, Antigen, T-Cell / metabolism

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  • (PMID = 19043668.001).
  • [ISSN] 1661-4917
  • [Journal-full-title] Archivum immunologiae et therapiae experimentalis
  • [ISO-abbreviation] Arch. Immunol. Ther. Exp. (Warsz.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Receptors, Antigen, T-Cell
  • [Other-IDs] NLM/ PMC2805919
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67. Bassuk AG, Mohile NA, Stack C: T-cell lymphoma presenting with neurologic features in immunocompetent children. Pediatr Neurol; 2006 Nov;35(5):314-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell lymphoma presenting with neurologic features in immunocompetent children.
  • Systemic T-cell lymphoma presenting with neurologic symptoms is infrequently reported in immunocompetent children.
  • We investigated the presenting features in all 20 immunocompetent children diagnosed with T-cell lymphoma at our institution from 1992-2004.
  • These findings suggest that early neurologic involvement of T-cell lymphoma in immunocompetent children is underrecognized and that central nervous system involvement in these patients should be more thoroughly investigated.
  • [MeSH-major] Central Nervous System Diseases / etiology. Immunocompetence. Lymphoma, T-Cell / complications

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  • (PMID = 17074600.001).
  • [ISSN] 0887-8994
  • [Journal-full-title] Pediatric neurology
  • [ISO-abbreviation] Pediatr. Neurol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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68. Lovisa F, Mussolin L, Corral L, Pillon M, Cazzaniga G, Biondi A, Rosolen A: IGH and IGK gene rearrangements as PCR targets for pediatric Burkitt's lymphoma and mature B-ALL MRD analysis. Lab Invest; 2009 Oct;89(10):1182-6
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] IGH and IGK gene rearrangements as PCR targets for pediatric Burkitt's lymphoma and mature B-ALL MRD analysis.
  • We recently reported that minimal residual disease (MRD) and minimal disseminated disease (MDD), assessed by long-distance PCR (LD-PCR) for t(8;14), are negative prognostic factors in mature B-cell acute lymphoblastic leukemia (B-ALL) and in Burkitt's lymphoma (BL).
  • [MeSH-major] Burkitt Lymphoma / genetics. Gene Rearrangement, B-Lymphocyte, Heavy Chain. Gene Rearrangement, B-Lymphocyte, Light Chain. Immunoglobulin Heavy Chains / genetics. Immunoglobulin kappa-Chains / genetics. Leukemia, B-Cell / genetics

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  • (PMID = 19668242.001).
  • [ISSN] 1530-0307
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin kappa-Chains
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69. Starkova J, Zamostna B, Mejstrikova E, Krejci R, Drabkin HA, Trka J: HOX gene expression in phenotypic and genotypic subgroups and low HOXA gene expression as an adverse prognostic factor in pediatric ALL. Pediatr Blood Cancer; 2010 Dec 1;55(6):1072-82

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HOX gene expression in phenotypic and genotypic subgroups and low HOXA gene expression as an adverse prognostic factor in pediatric ALL.
  • However, HOX expression patterns in leukemia cells compared to normal lymphoid progenitors have not been systematically studied in acute lymphoblastic leukemia (ALL) subtypes.
  • PROCEDURE: The RNA expression levels of HOXA, HOXB, and CDX1/2 genes were analyzed by qRT-PCR in a cohort of 61 diagnostic pediatric ALL samples and FACS-sorted subpopulations of normal lymphoid progenitors.
  • HOXA7 gene was low expressed at the RNA level in patients with hyperdiploid leukemia, whereas HOXB7 and CDX2 genes were low expressed in TEL/AML1-positive and BCR/ABL-positive cases, respectively.
  • In contrast to previous findings in acute myeloid leukemia, high HOXA RNA expression was associated with an excellent prognosis in Cox's regression model (P = 0.03).
  • CONCLUSIONS: HOX gene RNA expression cannot discriminate leukemia subgroups or relative maturity of leukemic cells.
  • [MeSH-major] Gene Expression Regulation, Leukemic / physiology. Homeodomain Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics

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  • (PMID = 20672366.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDX1 protein, human; 0 / CDX2 protein, human; 0 / HOXB2 protein, human; 0 / HOXB4 protein, human; 0 / Homeodomain Proteins; 0 / HoxB3 protein, human; 0 / Transcription Factors; 157907-48-7 / HoxA protein
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70. Roecker AM, Stockert A, Kisor DF: Nelarabine in the treatment of refractory T-cell malignancies. Clin Med Insights Oncol; 2010 Dec 01;4:133-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nelarabine in the treatment of refractory T-cell malignancies.
  • Nelarabine is a nucleoside analog indicated for the treatment of adult and pediatric patients with T-cell acute lymphoblastic leukemia (T-ALL) or T-cell lymphoblastic lymphoma (T-LBL) that is refractory or has relapsed after treatment with at least two chemotherapy regimens.

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  • (PMID = 21151585.001).
  • [ISSN] 1179-5549
  • [Journal-full-title] Clinical Medicine Insights. Oncology
  • [ISO-abbreviation] Clin Med Insights Oncol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2999959
  • [Keywords] NOTNLM ; Arranon / Atriance / T-cell / leukemia / lymphoma / nelarabine
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71. 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
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  • [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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72. Rakheja D, Kapur P, Tomlinson GE, Margraf LR: Pediatric renal cell carcinomas with Xp11.2 rearrangements are immunoreactive for hMLH1 and hMSH2 proteins. Pediatr Dev Pathol; 2005 Nov-Dec;8(6):615-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric renal cell carcinomas with Xp11.2 rearrangements are immunoreactive for hMLH1 and hMSH2 proteins.
  • Alveolar soft part sarcoma and pediatric renal cell carcinoma share a similar chromosomal abnormality, t(X;17)(p11.2;q25).
  • We performed immunohistochemistry for hMLH1 and hMSH2 in 4 cases of pediatric renal cell carcinomas with Xp11.2 rearrangements.
  • Our study demonstrates that inactivation of the DNA mismatch repair genes hMLH1 and hMSH2 does not appear to play a role in the tumorigenesis of pediatric renal cell carcinomas with Xp11.2 rearrangements.
  • [MeSH-major] Carcinoma, Renal Cell / genetics. Carcinoma, Renal Cell / metabolism. Carrier Proteins / biosynthesis. Kidney Neoplasms / genetics. Kidney Neoplasms / metabolism. Neoplasm Proteins / biosynthesis. Nuclear Proteins / biosynthesis

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  • (PMID = 16328670.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Biomarkers, Tumor; 0 / Carrier Proteins; 0 / MLH1 protein, human; 0 / MLH2 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins
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73. Park JA, Ghim T, Bae KW, Koh KN, Im HJ, Seo JJ: Improved outcome in childhood ALL with intensive consolidation and hematopoietic stem cell transplant. Korean J Hematol; 2010 Jun;45(2):109-14

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Improved outcome in childhood ALL with intensive consolidation and hematopoietic stem cell transplant.
  • BACKGROUND: Despite advances in chemotherapy, the prognosis of relapsed acute lymphoblastic leukemia (ALL) remains poor.
  • Few studies on relapsed ALL have reported the importance of intensive consolidation followed with or without allogeneic hematopoietic stem cell transplantation (HSCT).
  • We found that second remission, consolidation of pediatric oncology group chemotherapy regimen (POG 9411), and HSCT significantly affected the outcome of the disease after relapse (P<0.001; P=0.004; P=0.05).

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  • (PMID = 21120189.001).
  • [ISSN] 2092-9129
  • [Journal-full-title] The Korean journal of hematology
  • [ISO-abbreviation] Korean J Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2983016
  • [Keywords] NOTNLM ; Acute lymphoblastic leukemia / Hematopoietic stem cell transplantation / Intensive consolidation / Relapse
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74. Isgrò A, Marziali M, Sodani P, Gaziev J, Erer B, Polchi P, Paciaroni K, Roveda A, De Angelis G, Gallucci C, Alfieri C, Simone MD, Zinno F, Isacchi G, Adorno G, Lanti A, Leti W, Aiuti F, Fraboni D, Andreani M, Lucarelli G: Immunohematologic reconstitution in pediatric patients after T cell-depleted HLA-haploidentical stem cell transplantation for thalassemia. Biol Blood Marrow Transplant; 2010 Nov;16(11):1557-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohematologic reconstitution in pediatric patients after T cell-depleted HLA-haploidentical stem cell transplantation for thalassemia.
  • To analyze immunohematologic reconstitution, particularly of natural killer (NK) cells, we evaluated 13 β-thalassemia patients after 20 and 60 days and 1 year posttransplantation with T cell-depleted HLA-haploidentical stem cells.
  • We assessed lymphocyte and bone marrow (BM) progenitor cell phenotype and differentiation capacity, spontaneous BM cytokine production, stromal cells, and stromal cell interleukin (IL)-7 production.
  • Patients initially manifested impaired stem/progenitor cell growth and differentiation capacity in parallel with altered T cell homeostasis and a reduced T cell naïve compartment.
  • We hypothesize that T cell compartment damage partly arises from altered new T cell production from the hematopoietic stem/progenitor cells under stromal cytokine influence.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Histocompatibility, Maternal-Fetal. Lymphocyte Depletion. Lymphocytes / cytology. T-Lymphocytes / cytology. beta-Thalassemia / therapy
  • [MeSH-minor] B-Lymphocytes / cytology. Blood Cells / cytology. Bone Marrow Cells / cytology. Bone Marrow Cells / metabolism. CD4-Positive T-Lymphocytes / cytology. CD8-Positive T-Lymphocytes / cytology. Cell Count. Child. Child, Preschool. Chimera / blood. Colony-Forming Units Assay. Graft Rejection / immunology. Graft Survival / immunology. HLA Antigens / genetics. HLA Antigens / immunology. Humans. Interleukin-2 / metabolism. Interleukin-7 / metabolism. Killer Cells, Natural / cytology. Living Donors. Lymphocyte Count. Mothers. Stromal Cells / cytology. Stromal Cells / metabolism. T-Lymphocyte Subsets / cytology. Transplants. Treatment Outcome. Tumor Necrosis Factor-alpha / metabolism

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  • [Copyright] Copyright © 2010 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20546907.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA Antigens; 0 / IL7 protein, human; 0 / Interleukin-2; 0 / Interleukin-7; 0 / Tumor Necrosis Factor-alpha
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75. 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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76. Mantadakis E, Danilatou V, Stiakaki E, Paterakis G, Papadhimitriou S, Kalmanti M: T-cell acute lymphoblastic leukemia relapsing as acute myelogenous leukemia. Pediatr Blood Cancer; 2007 Mar;48(3):354-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell acute lymphoblastic leukemia relapsing as acute myelogenous leukemia.
  • We present the unusual case of a 16-year-old girl with T-cell acute lymphoblastic leukemia (ALL) with an early thymocyte immunophenotype without myeloid markers, who after 13 months of complete hematological remission relapsed as acute myelogenous leukemia (AML) with minimal differentiation and died of her disease.
  • Whether the AML represented a relapse with lineage switch of the original immature T-cell clone or a new secondary malignancy, could not be proven due to the absence of molecular or clonal markers.
  • This report suggests that a subset of CD7+ T-cell leukemias without mature T-cell antigens (CD4-, CD8-) are minimally differentiated and can relapse as AML.
  • [MeSH-major] Antigens, Differentiation, T-Lymphocyte / analysis. Antigens, Neoplasm / analysis. Leukemia, Myeloid / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology. Neoplastic Stem Cells / pathology. T-Lymphocyte Subsets / pathology
  • [MeSH-minor] 6-Mercaptopurine / administration & dosage. Acute Disease. Adolescent. Antigens, CD7 / analysis. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Asparaginase / administration & dosage. Bone Marrow / pathology. Cell Differentiation. Cell Lineage. Core Binding Factor Alpha 2 Subunit / genetics. Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Dexamethasone / administration & dosage. Diagnosis, Differential. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Etoposide / adverse effects. Fatal Outcome. Female. Gene Dosage. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping. Karyotyping. Methotrexate / administration & dosage. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasms, Second Primary / diagnosis. Proto-Oncogenes. Recurrence. Vincristine / administration & dosage

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  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. MERCAPTOPURINE .
  • Hazardous Substances Data Bank. VINCRISTINE .
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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16206214.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD7; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Antigens, Neoplasm; 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / RUNX1 protein, human; 04079A1RDZ / Cytarabine; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.5.1.1 / Asparaginase; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin
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77. Kolenova A, Hikkel I, Ilencikova D, Hikkelova M, Sejnova D, Kaiserova E, Cizmar A, Puskacova J, Bubanska E, Oravkinova I, Gencik M: Minimal residual disease detection using real-time quantitative PCR analysis of immunoglobulin and T-cell receptor gene rearrangements in the non-MRD-based ALL IC-BFM 2002 protocol for childhood ALL: Slovak experience. Neoplasma; 2010;57(6):552-61

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Minimal residual disease detection using real-time quantitative PCR analysis of immunoglobulin and T-cell receptor gene rearrangements in the non-MRD-based ALL IC-BFM 2002 protocol for childhood ALL: Slovak experience.
  • Acute lymphoblastic leukemia is the most common form of cancer in children.
  • An intense effort has been made to develop methods to determine the degree of minimal residual leukemia cells present in patients considered to be in morphological remission.
  • The MRD monitoring based on real-time quantitative PCR detection of patient-specific immunoglobulin and T-cell receptor (Ig/TCR) gene rearrangements is currently considered to be the most reliable tool for MRD-based diagnosis in ALL.
  • A total of 40 patients with BCP-ALL ( B cell precursor ALL) and 4 patients with T ALL were analyzed for Ig/TCR rearrangement.
  • [MeSH-major] Gene Rearrangement. Gene Rearrangement, T-Lymphocyte. Genes, Immunoglobulin. Polymerase Chain Reaction / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 20845994.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
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78. Olcay L, Koç A: Autoimmune hemolytic anemia preceding T-ALL in a five-year-old girl. Pediatr Hematol Oncol; 2005 Apr-May;22(3):207-13
Genetic Alliance. consumer health - Autoimmune Hemolytic Anemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A 5-year-old girl developed acute lymphoblastic leukemia (T-ALL) 15 months after being diagnosed with autoimmune hemolytic anemia (AHA), while AHA was in partial remission.
  • However, anemia requiring blood transfusion, positive direct Coombs' test, and splenomegaly dissappeared in the 13th month of the leukemia treatment; reticulocytosis and decreased haptoglobin level persisted.
  • This case presents some features that were not reported before, such that ALL was preceded by AHA and involved T-cell lineage, AHA was mediated by warm antibodies, and the two disorders took place in childhood.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • (PMID = 16020103.001).
  • [ISSN] 0888-0018
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Immunoglobulin G
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79. 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.
  • [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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80. Hwang IG, Yoo KH, Lee SH, Park YH, Lim TK, Lee SC, Park S, Park BB, Ko YH, Kim K, Koo HH, Kim WS: Clinicopathologic features and treatment outcomes in malignant lymphoma of pediatric and young adult patients in Korea: comparison of korean all-ages group and Western younger age group. Clin Lymphoma Myeloma; 2007 Nov;7(9):580-6
MedlinePlus Health Information. consumer health - Lymphoma.

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  • [Title] Clinicopathologic features and treatment outcomes in malignant lymphoma of pediatric and young adult patients in Korea: comparison of korean all-ages group and Western younger age group.
  • PURPOSE: The aim of this study is to define distinctive clinicopathologic features of malignant lymphoma in pediatric and young adult patients, particularly in Korea.
  • PATIENTS AND METHODS: From May 1993 to November 2005, 294 pediatric and young adult patients (age range, 0-31 years) with malignant lymphoma were analyzed in this study at Samsung Medical Center.
  • Among patients with non-Hodgkin lymphoma (NHL), T/natural killer cell immunophenotype is more common in the present younger age group than the all-ages group (45.5% vs. 25%; P = .001) and Western younger age group (45.5% vs. 13.3%; P = .001).
  • Lymphoblastic lymphoma and T-anaplastic large-cell lymphoma included relatively higher proportions in the younger age group.
  • CONCLUSION: The incidence of Hodgkin disease and T-cell NHL is relatively higher in pediatric and young-adult population group than the all-ages group.
  • However, treatment outcome of the younger age group, excluding lymphoblastic lymphoma, seems to be similar to those in any age group.

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  • (PMID = 18186966.001).
  • [ISSN] 1557-9190
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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81. Hori T, Suzuki N, Mizue N, Hatakeyama N, Takamuro M, Tsutsumi H: Relapse of T-cell all after stem cell transplant presenting as hypertrophic cardiomyopathy: the value of non-invasive diagnostic imaging in detecting cardiac leukemia. Pediatr Blood Cancer; 2006 Jan;46(1):108-11
MedlinePlus Health Information. consumer health - Diagnostic Imaging.

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  • [Title] Relapse of T-cell all after stem cell transplant presenting as hypertrophic cardiomyopathy: the value of non-invasive diagnostic imaging in detecting cardiac leukemia.
  • We describe a 14-year-old female with acute lymphoblastic leukemia (ALL) with a mediastinal mass at diagnosis who developed hypertrophic cardiomyopathy (HC) after stem cell transplantation (SCT).
  • [MeSH-major] Cardiomyopathy, Hypertrophic / etiology. Diagnostic Imaging. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemic Infiltration. Myocardium / pathology
  • [MeSH-minor] Adolescent. Female. Humans. Magnetic Resonance Imaging. Recurrence. Stem Cell Transplantation. Tomography, X-Ray Computed

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  • (PMID = 16078227.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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82. Burkhardt B, Moericke A, Klapper W, Greene F, Salzburg J, Damm-Welk C, Zimmermann M, Strauch K, Ludwig WD, Schrappe M, Reiter A: Pediatric precursor T lymphoblastic leukemia and lymphoblastic lymphoma: Differences in the common regions with loss of heterozygosity at chromosome 6q and their prognostic impact. Leuk Lymphoma; 2008 Mar;49(3):451-61
Genetic Alliance. consumer health - Lymphoblastic lymphoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric precursor T lymphoblastic leukemia and lymphoblastic lymphoma: Differences in the common regions with loss of heterozygosity at chromosome 6q and their prognostic impact.
  • This study analyzed loss of heterozygosity (LOH) at chromosome 6q and compared the LOH findings in pediatric precursor T lymphoblastic lymphoma (T-LBL) with the LOH findings in precursor-T lymphoblastic leukemia (T-ALL).
  • [MeSH-major] Chromosomes, Human, Pair 6. Loss of Heterozygosity. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18297521.001).
  • [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
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83. 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
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  • [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.
  • [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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84. Troeger A, Siepermann M, Escherich G, Meisel R, Willers R, Gudowius S, Moritz T, Laws HJ, Hanenberg H, Goebel U, Janka-Schaub GE, Mahotka C, Dilloo D: Survivin and its prognostic significance in pediatric acute B-cell precursor lymphoblastic leukemia. Haematologica; 2007 Aug;92(8):1043-50
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] Survivin and its prognostic significance in pediatric acute B-cell precursor lymphoblastic leukemia.
  • BACKGROUND AND OBJECTIVES: Impaired apoptosis, mediated by members of the inhibitor of apoptosis proteins (IAP) family such as survivin, is thought to contribute to leukemic cell survival.
  • To date, however, there is no information available on the prognostic role of survivin in pediatric precursor B-cell acute lymphocytic leukemia (BCP-ALL), the most frequent malignancy in childhood.
  • DESIGN AND METHODS: In a retrospective study including 66 pediatric patients we analyzed the impact of survivin protein levels on outcome in BCP-ALL.
  • [MeSH-major] Inhibitor of Apoptosis Proteins / analysis. Microtubule-Associated Proteins / analysis. Neoplasm Proteins / analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 17640858.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
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85. 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 .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • In this study, we report the identification of inactivating mutations and deletions in the X-linked plant homeodomain finger 6 (PHF6) gene in 16% of pediatric and 38% of adult primary T-ALL samples.

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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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86. Nakamura M, Shimada K, Ishida E, Higuchi T, Nakase H, Sakaki T, Konishi N: Molecular pathogenesis of pediatric astrocytic tumors. Neuro Oncol; 2007 Apr;9(2):113-23
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  • [Title] Molecular pathogenesis of pediatric astrocytic tumors.
  • Astrocytomas are the most common pediatric brain tumors, accounting for 7%-8% of all childhood cancers.
  • Relatively few studies have been performed on their molecular properties; therefore, classification of pediatric astrocytic tumors into genetic subtypes similar to that of adult tumors remains to be defined.
  • Here, we report an extensive characterization of 44 pediatric astrocytomas--16 diffuse astrocytomas (WHO grade II), 10 anaplastic astrocytomas (WHO grade III), and 18 glioblastomas (WHO grade IV)--in terms of genetic alterations frequently observed in adult astrocytomas.
  • Loss of heterozygosity (LOH) on 1p/19q and 10p/10q was less common in pediatric astrocytic tumors than in those seen in adults, but the frequency of LOH on 22q was comparable, occurring in 44% of diffuse astrocytomas, 40% of anaplastic astrocytomas, and 61% of glioblastomas.

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  • (PMID = 17327574.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC1871665
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87. Rocha V, Locatelli F: Searching for alternative hematopoietic stem cell donors for pediatric patients. Bone Marrow Transplant; 2008 Jan;41(2):207-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Searching for alternative hematopoietic stem cell donors for pediatric patients.
  • The use of alternative hematopoietic stem cell (HSC) donors has been witnessing important progress, mainly due to: (i) better HLA matching at the allelic level between donor and recipient in unrelated HSC transplantation (HSCT) translating into better patient outcome;.
  • (ii) better donor choice and patient selection in unrelated, often HLA-mismatched, cord blood transplantation and (iii) new strategies of adoptive cell therapy aimed at improving the results of T-cell-depleted haploidentical HSCT from a relative.
  • Therefore, any physician has to carefully evaluate, for each single pediatric patient in need of an allograft, all the possible alternatives to choose the best HSC donor, taking into account type of disease to be treated, urgency of transplantation, donor characteristics and center's experience.
  • This review will analyze in detail the advantages and limitations of each of the three options of alternative donor HSCT and the main criteria to be used for choosing the most suitable donor for pediatric patients lacking an HLA-identical sibling.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Histocompatibility Testing. Tissue Donors
  • [MeSH-minor] Child, Preschool. Cord Blood Stem Cell Transplantation. Graft vs Host Disease. Humans. Lymphocyte Depletion. Survival Analysis. Transplantation, Homologous / adverse effects. Transplantation, Homologous / methods

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  • (PMID = 18084331.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 52
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88. Gaiser T, Haedicke W, Becker MR: A rare pediatric case of a thymic cytotoxic and lymphoblastic T/NK cell lymphoma. Int J Clin Exp Pathol; 2010;3(4):437-42
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  • [Title] A rare pediatric case of a thymic cytotoxic and lymphoblastic T/NK cell lymphoma.
  • Attempts to establish a concise classification of lymphoblastic lymphomas (LBLs) have gained momentum in recent years, mainly due to the expanding possibilities of immunohistochemical and genetic characterization of different disease entities.
  • To further characterize and demonstrate the extended spectrum of LBL, we present an unusual pediatric case of LBL that could not be categorized into one of the subgroups and exhibited a benign course after surgical treatment and subsequent chemotherapy.
  • Further T- aand NK-cell markers CD1a, CD4, CD8, CD10, and CD56 reacted positively, but CD57, CD16 and CD 30 (Ber H2) were all negative.
  • B cell markers (CD20, CD22, Cd79a and IgM) were all negative.
  • No clonal B cell Ig or T cell gamma chain rearrangements were detectable.
  • However, our case represents a rare pediatric lymphoma derived from a thymic precursor committed to T/NK-cell differentiation and a favourable outcome after chemotherapy.
  • [MeSH-major] Biomarkers, Tumor / analysis. Natural Killer T-Cells / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Antigens, CD / biosynthesis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Lineage. Child. Humans. Immunohistochemistry. Immunophenotyping. Male. Polymerase Chain Reaction. Thymus Gland / cytology

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  • (PMID = 20490334.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [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 / Antigens, CD; 0 / Biomarkers, Tumor
  • [Other-IDs] NLM/ PMC2872750
  • [Keywords] NOTNLM ; T/NK cell lymphoma / lymphoblastic lymphomas / pediatric lymphoma
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89. Marston E, Weston V, Jesson J, Maina E, McConville C, Agathanggelou A, Skowronska A, Mapp K, Sameith K, Powell JE, Lawson S, Kearns P, Falciani F, Taylor M, Stankovic T: Stratification of pediatric ALL by in vitro cellular responses to DNA double-strand breaks provides insight into the molecular mechanisms underlying clinical response. Blood; 2009 Jan 1;113(1):117-26
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stratification of pediatric ALL by in vitro cellular responses to DNA double-strand breaks provides insight into the molecular mechanisms underlying clinical response.
  • The molecular basis of different outcomes in pediatric acute lymphoblastic leukemia (ALL) remains poorly understood.
  • We addressed the clinical significance and mechanisms behind in vitro cellular responses to ionizing radiation (IR)-induced DNA double-strand breaks in 74 pediatric patients with ALL.
  • [MeSH-major] DNA Breaks, Double-Stranded. Gene Expression Regulation, Leukemic. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 18941120.001).
  • [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] EC 2.4.2.30 / PARP1 protein, human; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 7; EC 3.4.22.- / Caspase 9
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90. Turin I, Pedrazzoli P, Tullio C, Montini E, La Grotteria MC, Schiavo R, Perotti C, Locatelli F, Carretto E, Maccario R, Siena S, Montagna D: GMP production of anti-tumor cytotoxic T-cell lines for adoptive T-cell therapy in patients with solid neoplasia. Cytotherapy; 2007;9(5):499-507
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  • [Title] GMP production of anti-tumor cytotoxic T-cell lines for adoptive T-cell therapy in patients with solid neoplasia.
  • BACKGROUND: The adoptive transfer of ex vivo-induced tumor-specific T-cell lines provides a promising approach for cancer immunotherapy.
  • We have demonstrated previously the feasibility of inducing in vitro long-term anti-tumor cytotoxic T-cell (CTL) lines directed against different types of solid tumors derived from both autologous and allogeneic PBMC.
  • METHODS: Four patients with advanced solid tumors (two sarcoma, one renal cell cancer and one ovarian cancer), who had received several lines of anticancer therapy, were enrolled.
  • [MeSH-minor] Adult. Antigens, CD8 / immunology. Cell Culture Techniques / methods. Cell Culture Techniques / standards. Cell Line. Cell Proliferation. Cytotoxicity Tests, Immunologic. HLA Antigens / immunology. Humans. Immunophenotyping. Treatment Outcome

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  • (PMID = 17786611.001).
  • [ISSN] 1465-3249
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD8; 0 / HLA Antigens
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91. Ching N, Nielsen-Saines KA, Deville JG, Wei LS, Garratty E, Bryson YJ: Autologous neutralizing antibody to human immunodeficiency virus-1 and replication-competent virus recovered from CD4+ T-cell reservoirs in pediatric HIV-1-infected patients on HAART. AIDS Res Hum Retroviruses; 2010 May;26(5):585-91
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  • [Title] Autologous neutralizing antibody to human immunodeficiency virus-1 and replication-competent virus recovered from CD4+ T-cell reservoirs in pediatric HIV-1-infected patients on HAART.
  • Little is known about the effects of prolonged viral suppression on the ANAB response in pediatric HIV-infected patients receiving HAART because the virus is hard to isolate, except by special methods.
  • We therefore assessed ANAB to pre-HAART PBMC virus isolates and post-HAART replication-competent virus (RCV) isolates recovered from latent CD4(+) T-cell reservoirs in perinatally HIV-infected children by using a PBMC-based assay and 90% neutralization titers.

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  • (PMID = 20455762.001).
  • [ISSN] 1931-8405
  • [Journal-full-title] AIDS research and human retroviruses
  • [ISO-abbreviation] AIDS Res. Hum. Retroviruses
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / 5K23HD051456; United States / NCRR NIH HHS / RR / 5M01RR000865-36; United States / NICHD NIH HHS / HD / R01HD37356; United States / NIAID NIH HHS / AI / U01AI069401
  • [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 / Anti-HIV Agents; 0 / Antibodies, Neutralizing; 0 / HIV Antibodies; 0 / Reverse Transcriptase Inhibitors
  • [Other-IDs] NLM/ PMC2933168
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92. Raetz EA, Perkins SL, Bhojwani D, Smock K, Philip M, Carroll WL, Min DJ: Gene expression profiling reveals intrinsic differences between T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma. Pediatr Blood Cancer; 2006 Aug;47(2):130-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression profiling reveals intrinsic differences between T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma.
  • BACKGROUND: T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LL) and are often thought to represent a spectrum of a single disease.
  • The malignant cells in T-ALL and T-LL are morphologically indistinguishable, and they share the expression of common cell surface antigens and cytogenetic characteristics.
  • CONCLUSIONS: Despite significant similarities between the malignant T-cell precursors, clear differences in the gene expression profiles were observed between T-ALL and T-LL implying underlying differences in the biology of the two entities.
  • [MeSH-major] Gene Expression Profiling. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 16358311.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01 CA88361
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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93. Goldstone AH, Rowe JM: Transplantation in adult ALL. Hematology Am Soc Hematol Educ Program; 2009;:593-601
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  • The value of the allogeneic graft-versus-leukemia effect in adult acute lymphoblastic leukemia (ALL) has now been conclusively demonstrated and confirmed.
  • While this is true for adults in all age groups, it may not be the best clinical option for young adults for whom increasingly intensive pediatric protocols are clearly of benefit.
  • As in childhood ALL minimal residual disease studies may be extremely useful in predicting outcome and, therefore, strategy, but at present there are less definite data in adults.
  • Clinical indications to harness the allogeneic effect will mature as the true value of pediatric protocols in adult patients and the safety and efficacy of a sibling, unrelated and reduced intensity transplant emerge in this disease.

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  • (PMID = 20008244.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins
  • [Number-of-references] 44
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94. Kawamura M, Kaku H, Ito T, Funata N, Taki T, Shimada A, Hayashi Y: FLT3-internal tandem duplication in a pediatric patient with t(8;21) acute myeloid leukemia. Cancer Genet Cytogenet; 2010 Dec;203(2):292-6
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  • [Title] FLT3-internal tandem duplication in a pediatric patient with t(8;21) acute myeloid leukemia.
  • Patients diagnosed with t(8;21)-acute myeloid leukemia (AML) are currently considered to have good prognoses, but about half of these patients relapse.
  • Expression of the neural cell-adhesion molecule (CD56) is also associated with a significantly shorter complete remission duration and survival in patients with t(8;21)-AML.
  • Even though t(8;21)-AML is less likely to co-occur with FLT3-ITD in pediatric patients, this report suggests that prognostic factors, including FLT3 and KIT genes and the surface marker CD56, should be analyzed in these patients.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Gene Duplication. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 21156247.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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95. Keates-Baleeiro J, Moore P, Koyama T, Manes B, Calder C, Frangoul H: Incidence and outcome of idiopathic pneumonia syndrome in pediatric stem cell transplant recipients. Bone Marrow Transplant; 2006 Aug;38(4):285-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidence and outcome of idiopathic pneumonia syndrome in pediatric stem cell transplant recipients.
  • Idiopathic pneumonia syndrome (IPS) is a rare complication following stem cell transplant (SCT) and its incidence among pediatric SCT recipients is not known.
  • There was a significant association between acute or hyperacute graft-versus-host disease (GVHD) and IPS (P=0.035).
  • IPS is a relatively common complication in pediatric SCT recipients and acute GVHD is an important associated factor.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / adverse effects. Pneumonia / etiology

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  • (PMID = 16819436.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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96. Harting MT, Cox CS, Day MC, Walker P, Gee A, Brenneman MM, Grotta JC, Savitz SI: Bone marrow-derived mononuclear cell populations in pediatric and adult patients. Cytotherapy; 2009;11(4):480-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bone marrow-derived mononuclear cell populations in pediatric and adult patients.
  • METHODS: We compared the MNC yield, viability, phenotypic markers and in vitro functionality in pediatric patients compared with adult patients enrolled in clinical trials evaluating autologous BM MNC transplantation.
  • Thirty-six patients (n=10 pediatric and n=26 adult) were included in this analysis.
  • RESULTS: The average total MNC recovered from the BM in pediatric patients was 2.1 x 10(6)/mL and in older patients was 3.2 x 10(6)/mL.
  • There were no differences in cell viability (>97%) or phenotypic markers identifying T cells, natural killer (NK) cells and neutrophils between the two groups.
  • Of note, the Lin(-)CD34(+) cell population was not different between the groups.
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Count. Cell Proliferation. Child. Colony-Forming Units Assay. Humans. Middle Aged

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  • (PMID = 19462318.001).
  • [ISSN] 1477-2566
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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97. Stams WA, Beverloo HB, den Boer ML, de Menezes RX, Stigter RL, van Drunen E, Ramakers-van-Woerden NL, Loonen AH, van Wering ER, Janka-Schaub GE, Pieters R: Incidence of additional genetic changes in the TEL and AML1 genes in DCOG and COALL-treated t(12;21)-positive pediatric ALL, and their relation with drug sensitivity and clinical outcome. Leukemia; 2006 Mar;20(3):410-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidence of additional genetic changes in the TEL and AML1 genes in DCOG and COALL-treated t(12;21)-positive pediatric ALL, and their relation with drug sensitivity and clinical outcome.
  • Clinical heterogeneity within t(12;21) or TEL/AML1-positive ALL (25% of childhood common/preB ALL) indicates that additional genetic changes might contribute to outcome.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 21. Core Binding Factor Alpha 2 Subunit / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • (PMID = 16424874.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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98. Calaminus G, Hense B, Laws HJ, Groeger M, MacKenzie CR, Göbel U: Diphtheria (D) and tetanus (T) antibody values in children with acute lymphoblastic leukaemia (ALL) after treatment according to Co-ALL 05/92. Klin Padiatr; 2007 Nov-Dec;219(6):355-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diphtheria (D) and tetanus (T) antibody values in children with acute lymphoblastic leukaemia (ALL) after treatment according to Co-ALL 05/92.
  • BACKGROUND: Children and adolescents after acute lymphoblastic leukemia are at risk for a prolonged period of immunodeficiency.
  • [MeSH-major] Antibodies, Bacterial / blood. Diphtheria Toxoid / immunology. Immunologic Memory. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Tetanus Toxoid / immunology

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  • (PMID = 18050047.001).
  • [ISSN] 0300-8630
  • [Journal-full-title] Klinische Pädiatrie
  • [ISO-abbreviation] Klin Padiatr
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Bacterial; 0 / Diphtheria Toxoid; 0 / Tetanus Toxoid
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99. Rhodes M, Lautz T, Kavanaugh-Mchugh A, Manes B, Calder C, Koyama T, Liske M, Parra D, Frangoul H: Pericardial effusion and cardiac tamponade in pediatric stem cell transplant recipients. Bone Marrow Transplant; 2005 Jul;36(2):139-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pericardial effusion and cardiac tamponade in pediatric stem cell transplant recipients.
  • Pericardial effusion and cardiac tamponade is a rarely reported complication following stem cell transplant (SCT).
  • The incidence among pediatric SCT recipients is not well defined.
  • All allogeneic recipients had acute or clinically extensive graft-versus-host disease (GVHD) at the time the effusion was diagnosed.
  • Clinically significant pericardial effusions are more common than previously reported in pediatric SCT recipients.
  • Acute and chronic GVHD is an associated factor.
  • [MeSH-major] Cardiac Tamponade. Hematopoietic Stem Cell Transplantation. Pericardial Effusion

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  • (PMID = 15908968.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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100. Cooper TM: Role of nelarabine in the treatment of T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma. Ther Clin Risk Manag; 2007 Dec;3(6):1135-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of nelarabine in the treatment of T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma.
  • T-cell malignancies have distinct biochemical, immunologic, and clinical features which set them apart from non-T-cell malignancies.
  • In the past, T-cell leukemia portended a worse prognosis than leukemia of B-cell origin.
  • Cure rates have improved with intensification of therapy and advanced understanding of the molecular genetics of T-cell malignancies.
  • Further advances in the treatment of T-cell leukemia will require the development of novel agents that can target specific malignancies without a significant increase in toxicity.
  • Clinical and pharmacokinetic investigations have established that nelarabine is active as a single agent which has led to exploration of an expanded role in the treatment of T-cell hematologic malignances.

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  • (PMID = 18516261.001).
  • [ISSN] 1176-6336
  • [Journal-full-title] Therapeutics and clinical risk management
  • [ISO-abbreviation] Ther Clin Risk Manag
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2387290
  • [Keywords] NOTNLM ; 9-β-D-arabinofuranosylguanine / T-cell acute lymphoblastic leukemia / nelarabine
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