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1. Larson Gedman A, Chen Q, Kugel Desmoulin S, Ge Y, LaFiura K, Haska CL, Cherian C, Devidas M, Linda SB, Taub JW, Matherly LH: The impact of NOTCH1, FBW7 and PTEN mutations on prognosis and downstream signaling in pediatric T-cell acute lymphoblastic leukemia: a report from the Children's Oncology Group. Leukemia; 2009 Aug;23(8):1417-25
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  • [Title] The impact of NOTCH1, FBW7 and PTEN mutations on prognosis and downstream signaling in pediatric T-cell acute lymphoblastic leukemia: a report from the Children's Oncology Group.
  • We explored the impact of mutations in the NOTCH1, FBW7 and PTEN genes on prognosis and downstream signaling in a well-defined cohort of 47 patients with pediatric T-cell acute lymphoblastic leukemia (T-ALL).
  • 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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2. 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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3. 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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4. 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


5. 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.
  • 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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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. 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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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. 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.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / diagnosis. Lymphoma, T-Cell / diagnosis


11. 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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  • [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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12. 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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13. 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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  • [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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14. 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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15. 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


16. Liu JY, Li ZG, Gao C, Cui L, Wu MY: [Characteristics of T cell receptor beta gene rearrangements and its role in minimal residual disease detection in childhood T-cell acute lymphoblastic leukemia]. Zhonghua Er Ke Za Zhi; 2008 Jul;46(7):487-92
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  • [Title] [Characteristics of T cell receptor beta gene rearrangements and its role in minimal residual disease detection in childhood T-cell acute lymphoblastic leukemia].
  • OBJECTIVE: To explore the characteristics of T cell receptor beta (TCRbeta) gene rearrangements in children with T-cell acute lymphoblastic leukemia (T-ALL) and establish a system of quantitative detection of MRD with real-time quantitative (RQ-PCR) targeted at TCRbeta gene rearrangement.
  • 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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17. 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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18. Chinen Y, Taki T, Nishida K, Shimizu D, Okuda T, Yoshida N, Kobayashi C, Koike K, Tsuchida M, Hayashi Y, Taniwaki M: Identification of the novel AML1 fusion partner gene, LAF4, a fusion partner of MLL, in childhood T-cell acute lymphoblastic leukemia with t(2;21)(q11;q22) by bubble PCR method for cDNA. Oncogene; 2008 Apr 3;27(15):2249-56
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  • [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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19. 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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20. Borriello A, Locasciulli A, Bianco AM, Criscuolo M, Conti V, Grammatico P, Cappellacci S, Zatterale A, Morgese F, Cucciolla V, Delia D, Della Ragione F, Savoia A: A novel Leu153Ser mutation of the Fanconi anemia FANCD2 gene is associated with severe chemotherapy toxicity in a pediatric T-cell acute lymphoblastic leukemia. Leukemia; 2007 Jan;21(1):72-8
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  • [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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21. Van Vlierberghe P, van Grotel M, Beverloo HB, Lee C, Helgason T, Buijs-Gladdines J, Passier M, van Wering ER, Veerman AJ, Kamps WA, Meijerink JP, Pieters R: The cryptic chromosomal deletion del(11)(p12p13) as a new activation mechanism of LMO2 in pediatric T-cell acute lymphoblastic leukemia. Blood; 2006 Nov 15;108(10):3520-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The cryptic chromosomal deletion del(11)(p12p13) as a new activation mechanism of LMO2 in pediatric T-cell acute lymphoblastic leukemia.
  • To identify new cytogenetic abnormalities associated with leukemogenesis or disease outcome, T-cell acute lymphoblastic leukemia (T-ALL) patient samples were analyzed by means of the array-comparative genome hybridization technique (array-CGH).
  • 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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22. Van Vlierberghe P, van Grotel M, Tchinda J, Lee C, Beverloo HB, van der Spek PJ, Stubbs A, Cools J, Nagata K, Fornerod M, Buijs-Gladdines J, Horstmann M, van Wering ER, Soulier J, Pieters R, Meijerink JP: The recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-cell acute lymphoblastic leukemia. Blood; 2008 May 1;111(9):4668-80
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  • [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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23. van Grotel M, Meijerink JP, Beverloo HB, Langerak AW, Buys-Gladdines JG, Schneider P, Poulsen TS, den Boer ML, Horstmann M, Kamps WA, Veerman AJ, van Wering ER, van Noesel MM, Pieters R: The outcome of molecular-cytogenetic subgroups in pediatric T-cell acute lymphoblastic leukemia: a retrospective study of patients treated according to DCOG or COALL protocols. Haematologica; 2006 Sep;91(9):1212-21
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  • [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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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
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  • [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. 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


26. 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
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  • [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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27. 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


28. 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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29. 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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  • [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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30. 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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31. 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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32. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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33. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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34. van Grotel M, Meijerink JP, van Wering ER, Langerak AW, Beverloo HB, Buijs-Gladdines JG, Burger NB, Passier M, van Lieshout EM, Kamps WA, Veerman AJ, van Noesel MM, Pieters R: Prognostic significance of molecular-cytogenetic abnormalities in pediatric T-ALL is not explained by immunophenotypic differences. Leukemia; 2008 Jan;22(1):124-31

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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35. 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


36. 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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37. 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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38. 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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39. 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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40. 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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41. 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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  • [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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42. 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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43. Forsythe A, Breland T, Majumdar S, Elkin TD, Johnson D, Megason G: Gender differences in incidence rates of childhood B-precursor acute lymphocytic leukemia in Mississippi. J Pediatr Oncol Nurs; 2010 May-Jun;27(3):164-7

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  • [Title] Gender differences in incidence rates of childhood B-precursor acute lymphocytic leukemia in Mississippi.
  • The authors studied pediatric patients with B-precursor acute lymphocytic leukemia (ALL) to determine whether Mississippi's gender incidences correlate with national statistics.
  • A retrospective chart review was performed of pediatric B-precursor ALL patients diagnosed at the Children's Cancer Clinic at the University of Mississippi Medical Center from 1995 to 2005.
  • However, the national average includes T-cell ALL, which is known to be significantly more prevalent in boys.
  • Of greater significance, boys were noted to present with high-risk B-precursor ALL 4 times more than girls, suggesting the need for further investigation into possible causes of this phenomenon.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / epidemiology
  • [MeSH-minor] Academic Medical Centers. Bias (Epidemiology). Causality. Chi-Square Distribution. Child. Female. Humans. Incidence. Male. Mississippi / epidemiology. Population Surveillance. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Prevalence. Retrospective Studies. Risk Assessment. Sex Distribution. United States / epidemiology

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  • (PMID = 20164246.001).
  • [ISSN] 1532-8457
  • [Journal-full-title] Journal of pediatric oncology nursing : official journal of the Association of Pediatric Oncology Nurses
  • [ISO-abbreviation] J Pediatr Oncol Nurs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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44. 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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  • [Cites] Blood. 1997 Jun 1;89(11):4161-6 [9166859.001]
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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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45. Wang Z, Hu T, Cao LZ, Kang R, Zhao MY, Yu Y, Xu WQ: [Expression of WAVE1 in childhood acute lymphocytic leukemia and in the apoptosis of Jurkat cells induced by adriamycin]. Zhongguo Dang Dai Er Ke Za Zhi; 2008 Oct;10(5):620-4
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  • [Title] [Expression of WAVE1 in childhood acute lymphocytic leukemia and in the apoptosis of Jurkat cells induced by adriamycin].
  • OBJECTIVE: To investigate whether WASP/Verprolin homologous protein 1 (WAVE1) plays a role in the pathogenesis of childhood acute lymphoblastic leukemia (ALL).
  • The cell proliferation was detected with MTT.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Apoptosis / drug effects. Doxorubicin / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Wiskott-Aldrich Syndrome Protein Family / physiology
  • [MeSH-minor] Adolescent. Blotting, Western. Cell Proliferation / drug effects. Child. Child, Preschool. Female. Humans. Infant. Jurkat Cells. Male. RNA, Messenger / analysis

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  • (PMID = 18947485.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / RNA, Messenger; 0 / WASF1 protein, human; 0 / Wiskott-Aldrich Syndrome Protein Family; 80168379AG / Doxorubicin
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46. 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

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  • [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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47. Smith MT, McHale CM, Wiemels JL, Zhang L, Wiencke JK, Zheng S, Gunn L, Skibola CF, Ma X, Buffler PA: Molecular biomarkers for the study of childhood leukemia. Toxicol Appl Pharmacol; 2005 Aug 07;206(2):237-45
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  • [Title] Molecular biomarkers for the study of childhood leukemia.
  • Various specific chromosome rearrangements, including t(8;21), t(15;17), and inv(16), are found in acute myeloid leukemia (AML) and in childhood acute lymphocytic leukemia (ALL), t(12;21) and t(1;19) are common.
  • We sequenced the translocation breakpoints of 56 patients with childhood ALL or AML harboring t(12;21), t(8;21), t(15;17), inv(16), and t(1;19), and demonstrated, with the notable exception of t(1;19), that these rearrangements are commonly detected in the neonatal blood spots (Guthrie cards) of the cases.
  • These findings show that most childhood leukemias begin before birth and that maternal and perinatal exposures such as chemical and infectious agents are likely to be critical.
  • Indeed, we have reported that exposure to indoor pesticides during pregnancy and the first year of life raises leukemia risk, but that later exposures do not.
  • We have also examined aberrant gene methylation in different cytogenetic subgroups and have found striking differences between them, suggesting that epigenetic events are also important in the development of some forms of childhood leukemia.
  • Further, at least two studies now show that the inactivating NAD(P)H:quinone acceptor oxidoreductase (NQO1) C609T polymorphism is positively associated with leukemias arising in the first 1-2 years of life and polymorphisms in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene have been associated with adult and childhood ALL.
  • Thus, low folate intake and compounds that are detoxified by NQO1 may be important in elevating leukemia risk in children.
  • Finally, we are exploring the use of proteomics to subclassify leukemia, because cytogenetic analysis is costly and time-consuming.
  • Several proteins have been identified that may serve as useful biomarkers for rapidly identifying different forms of childhood leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15967214.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NIEHS NIH HHS / ES / P42ES04705; United States / NIEHS NIH HHS / ES / R01 ES0098137
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 935E97BOY8 / Folic Acid; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human
  • [Number-of-references] 55
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48. Wandroo F, Bell A, Darbyshire P, Pratt G, Stankovic T, Gordon J, Lawson S, Moss P: ZAP-70 is highly expressed in most cases of childhood pre-B cell acute lymphoblastic leukemia. Int J Lab Hematol; 2008 Apr;30(2):149-57
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  • [Title] ZAP-70 is highly expressed in most cases of childhood pre-B cell acute lymphoblastic leukemia.
  • ZAP-70 is, however, expressed in adult B cell chronic lymphocytic leukemia where it correlates with a poor prognosis.
  • We wished to determine if ZAP-70 is also expressed in pediatric B cell malignancy.
  • A quantitative PCR assay for ZAP-70 expression was established and ZAP-70 expression in a range of human B cell lines was compared with expression in the Jurkat T cell line.
  • ZAP-70 expression was then determined in bone marrow lymphoblasts obtained from 12 patients with pre-B cell acute lymphoblastic leukemia (ALL).
  • ZAP-70 expression was not detected in mature B cell lines but was detected in pre-B cell lines at a level comparable to that seen in T cells.
  • ZAP-70 expression was strongly expressed in nine of the 12 cases of primary pre-B cell lymphoblastic leukemia.
  • The T cell-associated protein kinase ZAP-70 is highly expressed in pre-B lineage cells and most cases of pre-B acute lymphoblastic leukemia.
  • [MeSH-major] B-Lymphocytes / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cells, B-Lymphoid / metabolism. ZAP-70 Protein-Tyrosine Kinase / metabolism
  • [MeSH-minor] Adolescent. Blotting, Western. Bone Marrow Cells / metabolism. Cell Line, Transformed. Cell Line, Tumor. Child. Child, Preschool. Female. Flow Cytometry. Gene Expression. Humans. Jurkat Cells. Male. Polymerase Chain Reaction

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  • (PMID = 18333847.001).
  • [ISSN] 1751-5521
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
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49. 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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  • [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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50. Isoda T, Ito S, Kajiwara M, Nagasawa M: Successful high-dose methotrexate chemotherapy in a patient with acute lymphocytic leukemia who developed acute renal failure during the initial treatment. Pediatr Int; 2007 Dec;49(6):1018-9
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  • [Title] Successful high-dose methotrexate chemotherapy in a patient with acute lymphocytic leukemia who developed acute renal failure during the initial treatment.
  • Methotrexate (MTX) is a key drug in the chemotherapy for childhood acute lymphocytic leukemia (ALL).
  • [MeSH-major] Acute Kidney Injury / chemically induced. Antimetabolites, Antineoplastic / adverse effects. Methotrexate / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 18045317.001).
  • [ISSN] 1328-8067
  • [Journal-full-title] Pediatrics international : official journal of the Japan Pediatric Society
  • [ISO-abbreviation] Pediatr Int
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; YL5FZ2Y5U1 / Methotrexate
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51. 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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52. 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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53. Hou Y, Hu Q, Liu AG, Zhang LQ, Liu SY: [Expression of survivin and its location in bone marrow cells of childhood acute leukemia: relationship to therapeutic efficacy]. Zhongguo Dang Dai Er Ke Za Zhi; 2006 Apr;8(2):101-4
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  • [Title] [Expression of survivin and its location in bone marrow cells of childhood acute leukemia: relationship to therapeutic efficacy].
  • OBJECTIVE: Survivin, a unique member of the inhibitor of apoptosis protein (IAP) family, plays an important role in regulating both apoptosis and cell division.
  • METHODS: The expression of survivin protein was detected by immunohistochemical assay in bone marrow cells from 62 children with acute leukemia and 40 hospitalized children who did not have leukemia (Control group), and in a human acute T lymphocytic leukemia cell line (Molt-4 cells) treated in vitro with daunorubicin (DNR).
  • Cell apoptosis was detected using flow cytometry.
  • RESULTS: Survivin protein was expressed in 41.9% of the 62 children with acute leukemia but in only 5.0% of the Control group (chi(2)=16.66; P < 0.01).
  • The expression rate of survivin was 46.2% in cytoplasm and 53.9% in nucleus in the children with acute leukemia (chi(2)0.3077; P> 0.05).
  • DNR treatment also induced survivin transllocation from cytoplasm to nucleus and cell apoptosis in a time and dosage-dependent manner.
  • CONCLUSIONS: Survivin may play an important role in the development and prognosis of childhood acute leukemia.
  • The different expression pattern of survivin in the cytoplasm and the nucleus may be associated with therapeutic efficacy and prognosis in acute leukemia.
  • DNR may reduce the survivin expression in leukemic cells and induce cell apoptosis.
  • [MeSH-major] Bone Marrow Cells / chemistry. Daunorubicin / therapeutic use. Leukemia, Myeloid, Acute / metabolism. Microtubule-Associated Proteins / analysis. Neoplasm Proteins / analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 16613699.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; ZS7284E0ZP / Daunorubicin
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54. Stachel D, Albert M, Meilbeck R, Kreutzer B, Haas RJ, Schmid I: Bone marrow Th2 cytokine expression as predictor for relapse in childhood acute lymphoblastic leukemia (ALL). Eur J Med Res; 2006 Mar 27;11(3):102-13
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  • [Title] Bone marrow Th2 cytokine expression as predictor for relapse in childhood acute lymphoblastic leukemia (ALL).
  • Samples from 49 consecutive pediatric patients with B cell precursor acute lymphocytic leukemia (BCP ALL) were analyzed by semiquantitative RT-PCR.
  • We identified interleukin (IL)-10 expression as a significant adverse prognostic indicator in childhood BCP-ALL.
  • Taqman RT-PCR of sorted cell populations showed that IL-10 mRNA was synthetized almost exclusively by NK or T cells.
  • These findings emphasize the role of the immune system for the outcome of childhood ALL.
  • [MeSH-major] Bone Marrow Cells / immunology. Burkitt Lymphoma / genetics. Burkitt Lymphoma / immunology. Cytokines / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Th2 Cells / immunology

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  • (PMID = 16751110.001).
  • [ISSN] 0949-2321
  • [Journal-full-title] European journal of medical research
  • [ISO-abbreviation] Eur. J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD86; 0 / CD86 protein, human; 0 / Cytokines; 0 / Interleukin-1; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4
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55. Eby GA: Treatment of acute lymphocytic leukemia using zinc adjuvant with chemotherapy and radiation--a case history and hypothesis. Med Hypotheses; 2005;64(6):1124-6
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  • [Title] Treatment of acute lymphocytic leukemia using zinc adjuvant with chemotherapy and radiation--a case history and hypothesis.
  • Low blood levels of zinc are often noted in acute lymphocytic leukemia (ALL), but zinc is not administered as part of any modern chemotherapy program in the treatment of ALL.
  • The result was a bone marrow remission from 95+% blast cells to an observed zero blast cell count in both hips within the first 14 days of treatment which never relapsed.
  • In addition to the reduction of blast cells to an observed count of zero (not a single leukemic or normal blast), red blood cell production and other hemopoietic functions returned to normal at a clinically remarkable rate.
  • The extremely broad role of zinc in pre-leukemic adverse health conditions, viral, fungal and tumoral immunity, hemopoietics, cell growth, division and differentiation, genetics and chemotherapy interactions are considered.
  • Since treatment with zinc and other identified deficient nutrients, particularly magnesium, did not appear injurious in ALL and they appear to be highly beneficial, controlled clinical studies of zinc (3.18 mg/kg body weight/day) with magnesium (8.0 mg/kg body weight/day) as adjuvants to chemotherapy in the treatment of childhood ALL are suggested.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Gluconates / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Zinc / physiology

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  • (PMID = 15823699.001).
  • [ISSN] 0306-9877
  • [Journal-full-title] Medical hypotheses
  • [ISO-abbreviation] Med. Hypotheses
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Chickenpox Vaccine; 0 / Gluconates; 5J49Q6B70F / Vincristine; E7WED276I5 / 6-Mercaptopurine; J41CSQ7QDS / Zinc; R4R8J0Q44B / gluconic acid; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate
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56. 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
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  • [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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57. Ebeid E, Kamel M, Moussa H, Galal U: ZAP-70 as a possible prognostic factor in childhood acute lymphoblastic leukemia. J Egypt Natl Canc Inst; 2008 Jun;20(2):121-6
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  • [Title] ZAP-70 as a possible prognostic factor in childhood acute lymphoblastic leukemia.
  • BACKGROUND: Zeta-chain-associated protein (ZAP- 70) is a 70kD adaptor protein that acts quickly after T cell activation to propagate signal.
  • The role of ZAP-70 in Tcell function is well established, and in the previous years, this molecule was considered to be T-cell specific.
  • Interest in ZAP-70 has grown since it has been shown, through gene expression profiling, that it is expressed in a subset of cases of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL).
  • PURPOSE: The aim of this study was to investigate the expression of ZAP-70 in leukemic blasts of 50 newly diagnosed patients of B-lineage acute lymphoblastic leukemia (ALL), and to assess the correlation between ZAP-70 expression and various prognostic factors and outcome.
  • PATIENTS AND METHODS: This study included 50 pediatric patients with newly diagnosed B-lineage ALL.
  • They were 28 males (56% ) and 22 females (44% ) presented to the Pediatric Oncology Department, National Cancer Institute, Cairo University, during the period from 2005 to 2007.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Neoplasm Recurrence, Local / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. ZAP-70 Protein-Tyrosine Kinase / metabolism

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  • (PMID = 20029467.001).
  • [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 / Biomarkers, Tumor; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
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58. Abadie C, Bernard F, Netchine I, Sanlaville D, Roque A, Rossignol S, Coupier I: Acute lymphocytic leukaemia in a child with Beckwith-Wiedemann syndrome harbouring a CDKN1C mutation. Eur J Med Genet; 2010 Nov-Dec;53(6):400-3
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  • [Title] Acute lymphocytic leukaemia in a child with Beckwith-Wiedemann syndrome harbouring a CDKN1C mutation.
  • Beckwith-Wiedemann syndrome (BWS) is a rare overgrowth syndrome associated with an increased risk in childhood tumours.
  • We report the case of a 10-year-old patient diagnosed with BWS, harbouring a CDKN1C (p57(KIP2)) mutation, who developed a T-type acute lymphoblastic leukaemia.
  • To our knowledge it is the first report of an acute lymphoblastic leukaemia of T-type in a child with BWS.
  • [MeSH-major] Beckwith-Wiedemann Syndrome / genetics. Cyclin-Dependent Kinase Inhibitor p57 / genetics. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] Copyright © 2010 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20826236.001).
  • [ISSN] 1878-0849
  • [Journal-full-title] European journal of medical genetics
  • [ISO-abbreviation] Eur J Med Genet
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / CDKN1C protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p57
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59. Dubowy R, Graham M, Hakami N, Kletzel M, Mahoney D, Newman E, Ravindranath Y, Camitta B: Sequential oral hydroxyurea and intravenous cytosine arabinoside in refractory childhood acute leukemia: a pediatric oncology group phase 1 study. J Pediatr Hematol Oncol; 2008 May;30(5):353-7
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  • [Title] Sequential oral hydroxyurea and intravenous cytosine arabinoside in refractory childhood acute leukemia: a pediatric oncology group phase 1 study.
  • At concentrations >0.1 mM, hydroxyurea (HU) enhances the accumulation of cytosine arabinoside (ara-C) in leukemia cells in vitro.
  • This study of children with refractory acute leukemia was designed to take advantage of this biochemical modulation.
  • Thirty-three children [26 acute lymphocytic leukemia (ALL), 7 acute nonlymphocytic leukemia] were treated; 29 received at least 1 full course.
  • [MeSH-major] Cytarabine / toxicity. Hydroxyurea / toxicity. Leukemia / drug therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Humans. Infection / epidemiology. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / mortality. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / mortality. Liver / drug effects. Liver / pathology. Skin / drug effects. Skin / pathology. Survival Analysis

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  • (PMID = 18458568.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U10 CA098543
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; X6Q56QN5QC / Hydroxyurea
  • [Other-IDs] NLM/ NIHMS721202; NLM/ PMC4601800
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60. Borgmann A, Zinn C, Hartmann R, Herold R, Kaatsch P, Escherich G, Möricke A, Henze G, von Stackelberg A, ALL-REZ BFM Study Group: Secondary malignant neoplasms after intensive treatment of relapsed acute lymphoblastic leukaemia in childhood. Eur J Cancer; 2008 Jan;44(2):257-68

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary malignant neoplasms after intensive treatment of relapsed acute lymphoblastic leukaemia in childhood.
  • PURPOSE: To investigate the cumulative incidence of and the risk factors for developing second malignant neoplasms (SMN) in children and adolescents following treatment for relapse of acute lymphocytic leukaemia (ALL).
  • METHODS: Patients (1376) up to 18 years of age with first relapse of non-B-cell ALL were treated and achieved a 2nd complete remission (CR).
  • RESULTS: Out of the 1376 patients 21 were diagnosed with SMN including non-lymphoblastic leukaemia/myelodysplastic syndrome (n=6), osteo-/Ewing's-/fibroblastic sarcoma (n=4), B-cell ALL/lymphoma (n=2), thyroid carcinoma (n=2), basal cell carcinoma, adeno carcinoma, squamous cell carcinoma, meningioma, malignant histiocytosis, glioblastoma and anaplastic astrocytoma (n=1 each).
  • SMN was found to be significantly associated with stem cell transplantation (SCT), and high cumulative doses of cranial irradiation, etoposide and cyclophosphamide.
  • CONCLUSIONS: Despite repeated exposure to intense frontline and relapse treatment (including multiagent chemotherapy, cranial irradiation and stem cell transplantation in some patients) the cumulative incidence of SMN was unexpectedly low, though significantly higher than in the general age-matched population.
  • [MeSH-major] Neoplasms, Second Primary / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 17981026.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Investigator] Mertens R; Imbach P; Pongratz E; Rupprecht T; Henze G; Wickmann L; Otte J; Bode U; Eberl W; Pekrun A; Kirschstein M; Hofmann K; Frank R; Möbius D; Andler W; Niekrens C; Breu H; Suttorp M; Göbel U; Weinmann G; Sauerbrey A; Beck JF; Janka-Schaub G; Welte K; Kulozik A; Tautz C; Graf N; Fink FM; Zintl F; Hermann J; Rupprath G; Dupuis W; Rodehüser M; Schrappe M; Berthold F; Sternschulte W; Körholz D; Schmitt K; Selle B; Gutjahr P; Dürken M; Christiansen H; Rose M; Borkhardt A; Burdach S; Jürgens H; Scheurlen W; Eggers G; Geib R; Dickerhoff R; Bielack S; Rauh W; Niethammer D; Debatin KM; Gadner H; Dohrn B; Schlegel PG; Niggli F
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61. Yamamoto JF, Goodman MT: Patterns of leukemia incidence in the United States by subtype and demographic characteristics, 1997-2002. Cancer Causes Control; 2008 May;19(4):379-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patterns of leukemia incidence in the United States by subtype and demographic characteristics, 1997-2002.
  • OBJECTIVE: Efforts to prevent leukemia have been hampered by an inability to identify significant risk factors.
  • Exploring incidence patterns of leukemia subtypes by sex and race/ethnic group may generate new etiologic hypotheses and identify high-risk groups for further study.
  • METHODS: Data from the North American Association of Central Cancer Registries for 1997-2002 were used to assess patterns of leukemia incidence by subtype, sex, age, race and ethnicity.
  • RESULTS: A total of 144,559 leukemia cases were identified, including 66,067 (46%) acute and 71,860 (50%) chronic leukemias.
  • The highest rates of acute myeloid leukemia with and without maturation were observed in Asian-Pacific Islanders (API).
  • Hispanics had a higher incidence of acute lymphocytic leukemia, particularly in childhood, and promyelocytic leukemia than did non-Hispanics.
  • African-Americans had the highest rates of HTLV-1 positive adult T-cell leukemia/lymphoma.
  • A sharp increase in the incidence of chronic myeloid leukemia was observed for both APIs and Hispanics, 85 years and older.
  • CONCLUSION: Known risk factors are unlikely to explain the observed disparities in leukemia incidence.
  • Further studies of differences in environmental and genetic risk factors in these populations by specific leukemia subtype may provide clues to the etiologies of these malignancies.
  • [MeSH-major] Leukemia / ethnology

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  • (PMID = 18064533.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
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62. Hallböök H, Gustafsson G, Smedmyr B, Söderhäll S, Heyman M, Swedish Adult Acute Lymphocytic Leukemia Group, Swedish Childhood Leukemia Group: Treatment outcome in young adults and children &gt;10 years of age with acute lymphoblastic leukemia in Sweden: a comparison between a pediatric protocol and an adult protocol. Cancer; 2006 Oct 1;107(7):1551-61
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  • [Title] Treatment outcome in young adults and children >10 years of age with acute lymphoblastic leukemia in Sweden: a comparison between a pediatric protocol and an adult protocol.
  • BACKGROUND: Several studies have reported a more favorable outcome for teenagers and young adults with acute lymphoblastic leukemia (ALL) when they were treated in pediatric oncology departments compared with adult hematology departments.
  • METHODS: In Sweden during the 1990s, adolescents with ALL were treated in a pediatric oncology unit or in an adult hematologic unit, depending on the initial referral.
  • In the current national, comparative, retrospective study, patients with ALL aged 10 years to 40 years who were treated either according to the Nordic Society of Pediatric Hematology and Oncology (NOPHO) ALL protocol (1992-2000) (NOPHO-92 protocol) or according to the Swedish Adult ALL Group protocol (1994-2000) (Adult protocol) were included.
  • RESULTS: In total, 243 patients with B-precursor and T-cell ALL were treated according to the protocols.
  • CONCLUSIONS: The NOPHO-92 protocol resulted in a better outcome than the Adult protocol; therefore, adolescents may benefit from the pediatric protocol treatment strategy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols. Burkitt Lymphoma / drug therapy. Burkitt Lymphoma / mortality. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / mortality

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  • [Copyright] (c) 2006 American Cancer Society.
  • (PMID = 16955505.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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63. Hesson LB, Dunwell TL, Cooper WN, Catchpoole D, Brini AT, Chiaramonte R, Griffiths M, Chalmers AD, Maher ER, Latif F: The novel RASSF6 and RASSF10 candidate tumour suppressor genes are frequently epigenetically inactivated in childhood leukaemias. Mol Cancer; 2009 Jul 01;8:42
Archivio Istituzionale della Ricerca Unimi. Full text from AIR - Univ. Milan .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The novel RASSF6 and RASSF10 candidate tumour suppressor genes are frequently epigenetically inactivated in childhood leukaemias.
  • We also determined the methylation status of CpG islands associated with RASSF1-10 in a series of childhood acute lymphocytic leukaemias (ALL) and normal blood and bone marrow samples.
  • These data show epigenetic inactivation of the candidate TSGs RASSF6 and RASSF10 is an extremely frequent event in the pathogenesis of childhood leukaemia.
  • [MeSH-major] Genes, Tumor Suppressor. Monomeric GTP-Binding Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Amino Acid Sequence. Cell Line, Tumor. CpG Islands. DNA Methylation. Gene Expression Regulation, Neoplastic. Gene Silencing. Humans. Molecular Sequence Data. Polymerase Chain Reaction. Sequence Alignment

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  • (PMID = 19570220.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G120/844
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RASSF6 protein, human; EC 3.6.5.2 / Monomeric GTP-Binding Proteins
  • [Other-IDs] NLM/ PMC2711046
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64. Lawce H, Olson S: FISH testing for deletions of chromosome 6q21 and 6q23 in hematologic neoplastic disorders. J Assoc Genet Technol; 2009;35(4):167-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Chromosome 6q deletions are also commonly found in lymphoid malignancies such as acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), non-Hodgkins lymphoma (NHL), multiple myeloma (MM), mantle zone lymphoma (MZL), and Waldenström's macroglobulinemia (WM).
  • In childhood B- and T-cell ALL a deletion of 6q is the hallmark of a neutral prognosis; however, it may be cytogenetically obscure or cryptic, requiring interphase FISH analysis.
  • In adult ALL it indicates a favorable prognosis, but in CLL, B-cell small lymphocytic lymphoma (SLL), WM, and MM it has a poor prognosis.

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  • (PMID = 19952391.001).
  • [ISSN] 1523-7834
  • [Journal-full-title] Journal of the Association of Genetic Technologists
  • [ISO-abbreviation] J Assoc Genet Technol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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65. Cines DB, Liebman H, Stasi R: Pathobiology of secondary immune thrombocytopenia. Semin Hematol; 2009 Jan;46(1 Suppl 2):S2-14
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Immune thrombocytopenia can be secondary to medications or to a concurrent disease, such as an autoimmune condition (eg, systemic lupus erythematosus [SLE], antiphospholipid antibody syndrome [APS], immune thyroid disease, or Evans syndrome), a lymphoproliferative disease (eg, chronic lymphocytic leukemia or large granular T-lymphocyte lymphocytic leukemia), or chronic infection, eg, with Helicobacter pylori, human immunodeficiency virus (HIV), or hepatitis C virus (HCV).
  • This thrombocytopenia may be caused by cross-reacting antibodies and closely mimics acute ITP of childhood.

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  • (PMID = 19245930.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL040387-16; United States / NHLBI NIH HHS / HL / P01 HL040387; United States / NHLBI NIH HHS / HL / P01 HL040387-16
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 185
  • [Other-IDs] NLM/ NIHMS99872; NLM/ PMC2682438
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66. Strehl S: Searching for prognostic markers in childhood T-cell acute lymphoblastic leukemia. Haematologica; 2006 Sep;91(9):1156A
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] Searching for prognostic markers in childhood T-cell acute lymphoblastic leukemia.
  • [MeSH-major] Neoplasm Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • [CommentOn] Haematologica. 2006 Sep;91(9):1212-21 [16956820.001]
  • (PMID = 16956809.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Transcription Factors
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67. Jotta PY, Ganazza MA, Silva A, Viana MB, da Silva MJ, Zambaldi LJ, Barata JT, Brandalise SR, Yunes JA: Negative prognostic impact of PTEN mutation in pediatric T-cell acute lymphoblastic leukemia. Leukemia; 2010 Jan;24(1):239-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Negative prognostic impact of PTEN mutation in pediatric T-cell acute lymphoblastic leukemia.
  • [MeSH-major] Mutation. PTEN Phosphohydrolase / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19829307.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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68. Van Vlierberghe P, Beverloo HB, Buijs-Gladdines J, van Wering ER, Horstmann M, Pieters R, Meijerink JP: Monoallelic or biallelic LMO2 expression in relation to the LMO2 rearrangement status in pediatric T-cell acute lymphoblastic leukemia. Leukemia; 2008 Jul;22(7):1434-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Monoallelic or biallelic LMO2 expression in relation to the LMO2 rearrangement status in pediatric T-cell acute lymphoblastic leukemia.
  • [MeSH-major] Alleles. DNA-Binding Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Metalloproteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • (PMID = 18079736.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [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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69. Van Vlierberghe P, Meijerink JP, Stam RW, van der Smissen W, van Wering ER, Beverloo HB, Pieters R: Activating FLT3 mutations in CD4+/CD8- pediatric T-cell acute lymphoblastic leukemias. Blood; 2005 Dec 15;106(13):4414-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activating FLT3 mutations in CD4+/CD8- pediatric T-cell acute lymphoblastic leukemias.
  • [MeSH-major] CD4-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / metabolism. Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • [CommentOn] Blood. 2004 Jul 15;104(2):558-60 [15044257.001]
  • (PMID = 16326981.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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70. Davidsson J, Lilljebjörn H, Panagopoulos I, Fioretos T, Johansson B: BRAF mutations are very rare in B- and T-cell pediatric acute lymphoblastic leukemias. Leukemia; 2008 Aug;22(8):1619-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] BRAF mutations are very rare in B- and T-cell pediatric acute lymphoblastic leukemias.
  • [MeSH-major] B-Lymphocytes / immunology. Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins B-raf / genetics. T-Lymphocytes / immunology

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  • [CommentOn] Leukemia. 2005 Feb;19(2):310-2 [15538400.001]
  • (PMID = 18273045.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comment; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
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71. Renneville A, Kaltenbach S, Clappier E, Collette S, Micol JB, Nelken B, Lepelley P, Dastugue N, Benoît Y, Bertrand Y, Preudhomme C, Cavé H: Wilms tumor 1 (WT1) gene mutations in pediatric T-cell malignancies. Leukemia; 2010 Feb;24(2):476-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Wilms tumor 1 (WT1) gene mutations in pediatric T-cell malignancies.
  • [MeSH-major] Mutation / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. WT1 Proteins / genetics

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  • (PMID = 19847202.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / WT1 Proteins
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72. Kratz CP, Niemeyer CM, Jüttner E, Kartal M, Weninger A, Schmitt-Graeff A, Kontny U, Lauten M, Utzolino S, Rädecke J, Fonatsch C, Wimmer K: Childhood T-cell non-Hodgkin's lymphoma, colorectal carcinoma and brain tumor in association with café-au-lait spots caused by a novel homozygous PMS2 mutation. Leukemia; 2008 May;22(5):1078-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Childhood T-cell non-Hodgkin's lymphoma, colorectal carcinoma and brain tumor in association with café-au-lait spots caused by a novel homozygous PMS2 mutation.
  • [MeSH-minor] Brain Neoplasms / etiology. Brain Neoplasms / genetics. Child. Family Health. Female. Homozygote. Humans. Lymphoma, T-Cell / etiology. Lymphoma, T-Cell / genetics

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  • (PMID = 18007577.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.1.- / PMS2 protein, human; EC 6.5.1.- / DNA Repair Enzymes
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