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1. 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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2. 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


3. Larson Gedman A, Chen Q, Kugel Desmoulin S, Ge Y, LaFiura K, Haska CL, Cherian C, Devidas M, Linda SB, Taub JW, Matherly LH: The impact of NOTCH1, FBW7 and PTEN mutations on prognosis and downstream signaling in pediatric T-cell acute lymphoblastic leukemia: a report from the Children's Oncology Group. Leukemia; 2009 Aug;23(8):1417-25
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  • [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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  • [Cites] Mol Cell Biol. 2001 Sep;21(17):5925-34 [11486031.001]
  • [Cites] Blood. 2007 Jul 1;110(1):278-86 [17363738.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1825-35 [17646408.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1813-24 [17646409.001]
  • [Cites] Nat Med. 2007 Oct;13(10):1203-10 [17873882.001]
  • [Cites] Leukemia. 2008 Jan;22(1):124-31 [17928886.001]
  • [Cites] J Clin Invest. 2008 Nov;118(11):3762-74 [18830414.001]
  • [Cites] Blood. 2009 Apr 23;113(17):3918-24 [19109228.001]
  • [Cites] J Biol Chem. 2001 Sep 21;276(38):35847-53 [11461910.001]
  • [Cites] J Biol Chem. 2001 Nov 30;276(48):45031-40 [11564735.001]
  • [Cites] Genes Dev. 2002 Feb 1;16(3):295-300 [11825871.001]
  • [Cites] Immunity. 2002 Feb;16(2):231-43 [11869684.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] Nat Rev Mol Cell Biol. 2002 Sep;3(9):673-84 [12209127.001]
  • [Cites] EMBO Rep. 2002 Sep;3(9):840-5 [12223465.001]
  • [Cites] J Cell Physiol. 2003 Mar;194(3):237-55 [12548545.001]
  • [Cites] J Immunol. 2003 Jun 15;170(12):5834-41 [12794108.001]
  • [Cites] J Biol Chem. 2003 Jun 20;278(25):23196-203 [12682059.001]
  • [Cites] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):6854-7 [15466172.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Mol Cell Biol. 2004 Nov;24(21):9265-73 [15485896.001]
  • [Cites] Cell. 1991 Aug 23;66(4):649-61 [1831692.001]
  • [Cites] Cell. 1991 Nov 15;67(4):687-99 [1657403.001]
  • [Cites] Blood. 1997 Dec 1;90(11):4243-51 [9373234.001]
  • [Cites] Blood. 1998 Feb 1;91(3):735-46 [9446631.001]
  • [Cites] J Immunol. 1999 Jan 15;162(2):635-8 [9916679.001]
  • [Cites] Science. 1999 Apr 30;284(5415):770-6 [10221902.001]
  • [Cites] Cell. 2005 Aug 12;122(3):435-47 [16096062.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6306-15 [16155013.001]
  • [Cites] Cancer Res. 2005 Sep 15;65(18):8530-7 [16166334.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] Clin Cancer Res. 2006 Feb 15;12(4):1074-9 [16489059.001]
  • [Cites] Leukemia. 2006 Mar;20(3):537-9 [16424867.001]
  • [Cites] Nat Rev Cancer. 2006 May;6(5):347-59 [16612405.001]
  • [Cites] Clin Cancer Res. 2006 May 15;12(10):3043-9 [16707600.001]
  • [Cites] Mol Cell Biol. 2006 Jun;26(12):4642-51 [16738328.001]
  • [Cites] Genes Dev. 2006 Aug 1;20(15):2096-109 [16847353.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1151-7 [16614245.001]
  • [Cites] Nat Med. 2007 Jan;13(1):70-7 [17173050.001]
  • [Cites] Clin Cancer Res. 2007 Jan 15;13(2 Pt 1):451-7 [17255265.001]
  • [Cites] Cell Cycle. 2007 Jan 1;6(1):80-4 [17245125.001]
  • [Cites] Cancer Res. 2007 Jun 15;67(12):5611-6 [17575125.001]
  • [Cites] Development. 2000 Jul;127(14):3185-95 [10862754.001]
  • [Cites] Mol Cell. 2000 Feb;5(2):197-206 [10882062.001]
  • [Cites] Mol Cell. 2000 Feb;5(2):207-16 [10882063.001]
  • [Cites] Immunity. 2000 Jul;13(1):73-84 [10933396.001]
  • [Cites] EMBO J. 2001 Jul 2;20(13):3427-36 [11432830.001]
  • (PMID = 19340001.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA076641-10; United States / NCI NIH HHS / CA / T32-CA009531; United States / NCI NIH HHS / CA / R01 CA076641; United States / NCI NIH HHS / CA / CA76641; United States / NCI NIH HHS / CA / T32 CA009531-22; United States / NCI NIH HHS / CA / T32 CA009531; United States / NCI NIH HHS / CA / T32 CA009531-21
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Cell Cycle Proteins; 0 / DNA, Neoplasm; 0 / F-Box Proteins; 0 / Homeodomain Proteins; 0 / NOTCH1 protein, human; 0 / Neoplasm Proteins; 0 / Receptor, Notch1; 149348-15-2 / HES1 protein, human; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Other-IDs] NLM/ NIHMS98506; NLM/ PMC2726275
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4. 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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5. 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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  • [Cites] Blood. 2004 Oct 15;104(8):2224-34 [15231578.001]
  • [Cites] Hum Genet. 2003 Aug;113(3):228-37 [12811540.001]
  • [Cites] Eur J Haematol. 1999 Sep;63(3):180-91 [10485273.001]
  • [Cites] Mol Cell Biol. 2004 Dec;24(24):10933-40 [15572694.001]
  • [Cites] Nat Rev Cancer. 2005 Nov;5(11):857-66 [16327764.001]
  • [Cites] BMC Med Genet. 2005;6:39 [16288654.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Jun;7(6):415-25 [16723977.001]
  • [Cites] Cancer Res. 2006 Aug 1;66(15):7615-20 [16885361.001]
  • [Cites] Anal Biochem. 2007 Jan 1;360(1):84-91 [17107651.001]
  • [Cites] J Exp Med. 2007 Jan 22;204(1):7-10 [17190841.001]
  • [Cites] BMC Biol. 2007;5:12 [17376234.001]
  • [Cites] J Appl Physiol (1985). 2005 Feb;98(2):715-21 [15649883.001]
  • [Cites] Science. 2000 Feb 4;287(5454):848-51 [10657297.001]
  • [Cites] Nat Genet. 2000 Aug;25(4):375-6 [10932175.001]
  • [Cites] Am J Hum Genet. 2002 Jan;70(1):38-50 [11727199.001]
  • [Cites] Annu Rev Immunol. 2002;20:165-96 [11861601.001]
  • [Cites] J Med Genet. 2002 Mar;39(3):178-83 [11897817.001]
  • [Cites] Trends Genet. 2003 Apr;19(4):207-16 [12683974.001]
  • [Cites] Annu Rev Genet. 1990;24:305-26 [2088171.001]
  • (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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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. 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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8. Karrman K, Andersson A, Björgvinsdóttir H, Strömbeck B, Lassen C, Olofsson T, Nguyen-Khac F, Berger R, Bernard O, Fioretos T, Johansson B: Deregulation of cyclin D2 by juxtaposition with T-cell receptor alpha/delta locus in t(12;14)(p13;q11)-positive childhood T-cell acute lymphoblastic leukemia. Eur J Haematol; 2006 Jul;77(1):27-34
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  • [Title] Deregulation of cyclin D2 by juxtaposition with T-cell receptor alpha/delta locus in t(12;14)(p13;q11)-positive childhood T-cell acute lymphoblastic leukemia.
  • OBJECTIVES: The t(12;14)(p13;q11)--a recurrent translocation in childhood T-cell acute lymphoblastic leukemia (T-ALL)--has very recently been molecularly characterized in one case, which displayed overexpression of the cyclin D2 gene (CCND2).
  • PATIENTS AND METHODS: We have characterized two pediatric t(12;14)-positive T-ALLs using fluorescence in situ hybridization (FISH), cDNA microarray, and real-time polymerase chain reaction (PCR).
  • RESULTS: FISH revealed breakpoints (BPs) in the T-cell receptor alpha/delta locus (14q11) and in the vicinity of the CCND2 gene at 12p13.
  • Furthermore, it is the first example of a T-cell neoplasm with a targeted deregulation of a member of a cyclin-encoding gene family.
  • [MeSH-major] Cyclins / genetics. Gene Expression Regulation, Neoplastic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell, alpha-beta / genetics. Receptors, Antigen, T-Cell, gamma-delta / genetics. Translocation, Genetic

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

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  • (PMID = 15704218.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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10. 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. Smith MA, Morton CL, Carol H, Gorlick RG, Kang MH, Keir ST, Kolb EA, Lock RB, Maris JM, Houghton PJ: Pediatric Preclinical Testing Program (PPTP) testing of the CENP-E inhibitor GSK923295A. J Clin Oncol; 2009 May 20;27(15_suppl):10015

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  • [Title] Pediatric Preclinical Testing Program (PPTP) testing of the CENP-E inhibitor GSK923295A.
  • METHODS: The PPTP includes a molecularly characterized in vitro panel of cell lines (n = 27) and in vivo panel of xenografts (n = 60) representing most of the common types of childhood solid tumors and childhood acute lymphoblastic leukemia (ALL).
  • RESULTS: GSK923295A demonstrated potent in vitro activity against the PPTP cell line panel with a median IC50 of 27 nM (range 12 nM to > 10 μM).

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  • (PMID = 27962529.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Fauzdar A, Mahajan A, Jain D, Mishra M, Raina V: Amplification of RUNX1 gene in two new cases of childhood B-cell precursor acute lymphoblastic leukemia: A case report. J Clin Oncol; 2009 May 20;27(15_suppl):e21000

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  • [Title] Amplification of RUNX1 gene in two new cases of childhood B-cell precursor acute lymphoblastic leukemia: A case report.
  • : e21000 Background: Chromosome abnormalities of leukemia cells have important prognostic significance in childhood acute lymphoblastic leukemia (ALL).
  • B-cell precursor acute lymphoblastic leukemia (BCP-ALL) ETV6/RUNX1 (alias TEL/AML1) is most frequent i.e.
  • We report two new cases with Pre B- cell ALL without ETV6/RUNX1 rearrangement, showing amplification of AML1 gene detected by FISH analysis.
  • RESULTS: In first case a 3-year girl with four copies of AML (RUNX1) gene were observed in 95% of the cell with normal two copies of TEL (ETV6) gene in both interphase and metaphase FISH.
  • Bone marrow karyotype in combination with molecular cytogenetic techniques like FISH should be done for improvement in sensitivity and accurate cytogenetic analysis in childhood ALL patients for proper identification of prognostic group for optimum treatment.
  • This is one of the few reported studies worldwide for amplification of RUNX1 gene from Indian subcontinent in childhood BCP-ALL.

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  • (PMID = 27960689.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. 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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15. Chinen Y, Taki T, Nishida K, Shimizu D, Okuda T, Yoshida N, Kobayashi C, Koike K, Tsuchida M, Hayashi Y, Taniwaki M: Identification of the novel AML1 fusion partner gene, LAF4, a fusion partner of MLL, in childhood T-cell acute lymphoblastic leukemia with t(2;21)(q11;q22) by bubble PCR method for cDNA. Oncogene; 2008 Apr 3;27(15):2249-56
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  • [Title] Identification of the novel AML1 fusion partner gene, LAF4, a fusion partner of MLL, in childhood T-cell acute lymphoblastic leukemia with t(2;21)(q11;q22) by bubble PCR method for cDNA.
  • The AML1 gene is frequently rearranged by chromosomal translocations in acute leukemia.
  • We identified that the LAF4 gene on 2q11.2-12 was fused to the AML1 gene on 21q22 in a pediatric patient having T-cell acute lymphoblastic leukemia (T-ALL) with t(2;21)(q11;q22) using the bubble PCR method for cDNA.
  • 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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16. 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


17. 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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18. 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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19. 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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20. 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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21. 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


22. 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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  • [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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23. 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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  • [Cites] J Clin Oncol. 2003 Apr 1;21(7):1340-6 [12663724.001]
  • [Cites] Rev Clin Exp Hematol. 2002 Jun;6(2):161-80; discussion 200-2 [12196214.001]
  • [Cites] Blood. 2002 Jul 1;100(1):52-8 [12070008.001]
  • [Cites] Blood. 2002 Jul 1;100(1):43-7 [12070006.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2286-94 [11187920.001]
  • [Cites] Blood. 2000 Jan 15;95(2):416-21 [10627444.001]
  • [Cites] J Clin Oncol. 2003 Oct 1;21(19):3616-22 [14512392.001]
  • [Cites] J Clin Oncol. 2006 Jan 20;24(3):491-9 [16421426.001]
  • [Cites] Leukemia. 1999 Mar;13(3):335-42 [10086723.001]
  • [Cites] Lancet. 1998 Feb 21;351(9102):550-4 [9492773.001]
  • [Cites] Cancer. 1997 Nov 1;80(9):1717-26 [9351539.001]
  • [Cites] N Engl J Med. 1996 May 9;334(19):1238-48 [8606720.001]
  • [Cites] J Clin Oncol. 1995 Jun;13(6):1368-76 [7751881.001]
  • [Cites] J Clin Oncol. 1993 Jun;11(6):1024-32 [8501488.001]
  • [Cites] Med Pediatr Oncol. 1992;20(2):105-13 [1734214.001]
  • [Cites] Med Pediatr Oncol. 1990;18(4):273-9 [2355886.001]
  • [Cites] Blood. 1985 Nov;66(5):1110-4 [3840395.001]
  • [Cites] J Clin Oncol. 1983 Sep;1(9):537-41 [6689428.001]
  • [Cites] Cancer. 1982 May 15;49(10):2112-35 [6896167.001]
  • [Cites] Semin Oncol. 1980 Sep;7(3):332-9 [7414342.001]
  • [Cites] Cancer. 1980 Feb 15;45(4):630-7 [6986967.001]
  • (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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24. Quigley DI, Wolff DJ: Pediatric T-cell acute lymphoblastic leukemia with aberrations of both MLL loci. Cancer Genet Cytogenet; 2006 Jul 1;168(1):77-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric T-cell acute lymphoblastic leukemia with aberrations of both MLL loci.
  • Translocations involving the MLL gene at 11q23 have been implicated in acute lymphoblastic leukemia (ALL), as well as acute myeloid leukemia (AML).
  • Such translocations result in gain of function fusion proteins that drive cell proliferation.
  • Except in cases of T-cell ALL, MLL rearrangement is typically associated with a poor prognosis.
  • We report a case of T-cell ALL with a t(11;19)(q23;p13.3) and deletion of the other chromosome 11 homolog at band q23.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Gene Deletion. Leukemia-Lymphoma, Adult T-Cell / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic / genetics

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  • (PMID = 16772125.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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25. 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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26. 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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27. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A new recurrent 9q34 duplication in pediatric T-cell acute lymphoblastic leukemia.
  • Over the last decade, genetic characterization of T-cell acute lymphoblastic leukemia (T-ALL) has led to the identification of a variety of chromosomal abnormalities.
  • In this study, we used array-comparative genome hybridization (array-CGH) and identified a novel recurrent 9q34 amplification in 33% (12/36) of pediatric T-ALL samples, which is therefore one of the most frequent cytogenetic abnormalities observed in T-ALL thus far.
  • [MeSH-major] Chromosomes, Human, Pair 9. Gene Duplication. Leukemia-Lymphoma, Adult T-Cell / genetics

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  • (PMID = 16673019.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / NUP214-ABL1 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Receptor, Notch1
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28. 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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  • [Cites] Leukemia. 1999 Nov;13(11):1696-707 [10557041.001]
  • [Cites] Blood. 2002 Feb 1;99(3):863-71 [11806988.001]
  • [Cites] Stem Cells. 2001;19(3):165-79 [11359942.001]
  • [Cites] J Clin Oncol. 2003 Oct 1;21(19):3616-22 [14512392.001]
  • [Cites] Clin Cancer Res. 2004 Jan 1;10(1 Pt 1):272-84 [14734480.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Oct 13;95(21):12522-7 [9770518.001]
  • [Cites] Blood. 1999 May 1;93(9):3033-43 [10216100.001]
  • [Cites] J Exp Med. 2005 Jun 6;201(11):1715-23 [15928199.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] J Clin Oncol. 2005 Nov 1;23(31):7942-50 [16258094.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] J Immunol. 2007 Jul 1;179(1):421-38 [17579063.001]
  • [Cites] Blood. 2007 Sep 1;110(5):1429-38 [17495134.001]
  • [Cites] Curr Biol. 2008 Jan 8;18(1):30-6 [18158243.001]
  • [Cites] J Clin Oncol. 2008 Mar 20;26(9):1496-503 [18349402.001]
  • [Cites] Haematologica. 2008 Nov;93(11):1658-65 [18835836.001]
  • [Cites] Science. 2008 Nov 28;322(5906):1377-80 [19039135.001]
  • [Cites] Nucleic Acids Res. 2009 Jan;37(Database issue):D1006-12 [18978023.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4386-93 [12036866.001]
  • [Cites] Leukemia. 2008 Dec;22(12):2142-50 [18818707.001]
  • [Cites] Lancet Oncol. 2009 Feb;10(2):147-56 [19147408.001]
  • [Cites] Curr Opin Pediatr. 2009 Feb;21(1):1-8 [19242236.001]
  • [Cites] N Engl J Med. 2009 Jun 25;360(26):2730-41 [19553647.001]
  • [Cites] Blood. 2009 Jul 30;114(5):1038-45 [19494353.001]
  • [Cites] J Clin Oncol. 2009 Nov 1;27(31):5175-81 [19805687.001]
  • [Cites] Blood. 2009 Dec 10;114(25):5136-45 [19828704.001]
  • [Cites] J Clin Oncol. 2010 Feb 1;28(4):648-54 [19841326.001]
  • [Cites] Leukemia. 2010 Feb;24(2):371-82 [20010620.001]
  • [Cites] Blood. 2010 Feb 18;115(7):1351-3 [20007809.001]
  • [Cites] N Engl J Med. 2000 Apr 6;342(14):998-1006 [10749961.001]
  • (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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29. Park MJ, Taki T, Oda M, Watanabe T, Yumura-Yagi K, Kobayashi R, Suzuki N, Hara J, Horibe K, Hayashi Y: FBXW7 and NOTCH1 mutations in childhood T cell acute lymphoblastic leukaemia and T cell non-Hodgkin lymphoma. Br J Haematol; 2009 Apr;145(2):198-206
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FBXW7 and NOTCH1 mutations in childhood T cell acute lymphoblastic leukaemia and T cell non-Hodgkin lymphoma.
  • Mutation analysis of FBXW7 and NOTCH1 genes was performed in 55 T cell acute lymphoblastic leukaemia (T-ALL) and 14 T cell non-Hodgkin lymphoma (T-NHL) patients who were treated on the Japan Association of Childhood Leukaemia Study (JACLS) protocols ALL-97 and NHL-98.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Gene Expression Regulation, Leukemic. Lymphoma, T-Cell / genetics. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics. Ubiquitin-Protein Ligases / genetics


30. 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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31. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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32. 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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33. 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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34. 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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35. 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
HAL archives ouvertes. Full text from .

  • [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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36. Van Vlierberghe P, van Grotel M, Tchinda J, Lee C, Beverloo HB, van der Spek PJ, Stubbs A, Cools J, Nagata K, Fornerod M, Buijs-Gladdines J, Horstmann M, van Wering ER, Soulier J, Pieters R, Meijerink JP: The recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-cell acute lymphoblastic leukemia. Blood; 2008 May 1;111(9):4668-80
Genetic Alliance. consumer health - Pediatric T-cell leukemia.

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

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  • [Cites] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128.001]
  • [Cites] Blood. 2007 Dec 15;110(13):4445-54 [17855633.001]
  • [Cites] Nat Genet. 2004 Oct;36(10):1084-9 [15361874.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Mol Cell Biol. 1990 Aug;10(8):4016-26 [2370860.001]
  • [Cites] Cancer Genet Cytogenet. 1990 Oct 15;49(2):241-8 [2208060.001]
  • [Cites] Stat Med. 1990 Jul;9(7):811-8 [2218183.001]
  • [Cites] Mol Cell Biol. 1992 Apr;12(4):1687-97 [1549122.001]
  • [Cites] Genes Chromosomes Cancer. 1992 Oct;5(3):227-34 [1384675.001]
  • [Cites] Oncogene. 1996 Oct 17;13(8):1801-8 [8895527.001]
  • [Cites] Mol Cell Biol. 1997 Jan;17(1):495-505 [8972230.001]
  • [Cites] EMBO J. 1997 Jun 2;16(11):3145-57 [9214632.001]
  • [Cites] EMBO J. 1998 Jul 1;17(13):3714-25 [9649441.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 21;101(51):17765-70 [15591353.001]
  • [Cites] FEBS Lett. 2005 Jan 31;579(3):757-62 [15670842.001]
  • [Cites] Leukemia. 2005 Mar;19(3):358-66 [15674412.001]
  • [Cites] Cell. 2005 Apr 22;121(2):167-78 [15851025.001]
  • [Cites] Blood. 2005 Jul 1;106(1):274-86 [15774621.001]
  • [Cites] Haematologica. 2005 Aug;90(8):1116-27 [16079112.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6306-15 [16155013.001]
  • [Cites] Leukemia. 2005 Nov;19(11):1948-57 [16107895.001]
  • [Cites] Leukemia. 2006 Jan;20(1):82-6 [16270038.001]
  • [Cites] Nat Rev Cancer. 2006 May;6(5):347-59 [16612405.001]
  • [Cites] Genes Dev. 2006 May 1;20(9):1123-36 [16618801.001]
  • [Cites] Genes Dev. 2006 Aug 1;20(15):2096-109 [16847353.001]
  • [Cites] Leukemia. 2006 Sep;20(9):1496-510 [16826225.001]
  • [Cites] Nat Cell Biol. 2006 Sep;8(9):1017-24 [16921363.001]
  • [Cites] Haematologica. 2006 Sep;91(9):1212-21 [16956820.001]
  • [Cites] Mol Cell Biol. 2006 Nov;26(21):8022-31 [16954387.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3520-9 [16873670.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18261-6 [17114293.001]
  • [Cites] Leukemia. 2007 Jan;21(1):121-8 [17039236.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] Bioinformatics. 2002;18 Suppl 1:S96-104 [12169536.001]
  • [Cites] Leukemia. 2003 Jun;17(6):1157-63 [12764384.001]
  • [Cites] Cell. 2001 Jan 12;104(1):119-30 [11163245.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1197-204 [11830466.001]
  • [Cites] Blood. 2003 Jul 1;102(1):262-8 [12637319.001]
  • [Cites] Leukemia. 2004 Feb;18(2):337-40 [14671643.001]
  • [Cites] Mol Cell Biol. 2004 Mar;24(6):2373-84 [14993277.001]
  • [Cites] Haematologica. 2007 Feb;92(2):232-5 [17296573.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Nat Genet. 2007 May;39(5):593-5 [17435759.001]
  • [Cites] Am J Pathol. 2007 Aug;171(2):654-66 [17569777.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1251-61 [17452517.001]
  • [Cites] J Cell Physiol. 2008 Feb;214(2):322-33 [17620317.001]
  • [Cites] Int J Cancer. 2004 Sep 10;111(4):501-7 [15239126.001]
  • (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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37. van Grotel M, Meijerink JP, Beverloo HB, Langerak AW, Buys-Gladdines JG, Schneider P, Poulsen TS, den Boer ML, Horstmann M, Kamps WA, Veerman AJ, van Wering ER, van Noesel MM, Pieters R: The outcome of molecular-cytogenetic subgroups in pediatric T-cell acute lymphoblastic leukemia: a retrospective study of patients treated according to DCOG or COALL protocols. Haematologica; 2006 Sep;91(9):1212-21
Genetic Alliance. consumer health - Pediatric T-cell leukemia.

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

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  • [CommentIn] Haematologica. 2006 Sep;91(9):1156A [16956809.001]
  • (PMID = 16956820.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / AF10-CALM fusion protein, human; 0 / Oncogene Proteins, Fusion
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38. Cleaver AL, Beesley AH, Firth MJ, Sturges NC, O'Leary RA, Hunger SP, Baker DL, Kees UR: Gene-based outcome prediction in multiple cohorts of pediatric T-cell acute lymphoblastic leukemia: a Children's Oncology Group study. Mol Cancer; 2010 May 12;9:105
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

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

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  • [Cites] Leukemia. 2006 Jul;20(7):1197-205 [16688226.001]
  • [Cites] Oncogene. 2006 May 25;25(22):3113-22 [16407823.001]
  • [Cites] PLoS Med. 2006 Mar;3(3):e47 [16417408.001]
  • [Cites] Br J Cancer. 2006 Dec 4;95(11):1537-44 [17117183.001]
  • [Cites] J Clin Oncol. 2006 Dec 20;24(36):5742-9 [17179108.001]
  • [Cites] Nat Med. 2007 Jan;13(1):70-7 [17173050.001]
  • [Cites] J Immunol. 2007 Apr 15;178(8):5132-43 [17404296.001]
  • [Cites] Br J Haematol. 2007 May;137(4):319-28 [17456054.001]
  • [Cites] Prostate. 2007 Jun 15;67(9):955-67 [17440963.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1198-203 [17410184.001]
  • [Cites] Blood. 2007 Sep 1;110(5):1429-38 [17495134.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2324-30 [17609427.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2548-55 [18039957.001]
  • [Cites] Br J Haematol. 2008 Mar;140(6):656-64 [18302714.001]
  • [Cites] Lancet. 2008 Mar 22;371(9617):1030-43 [18358930.001]
  • [Cites] Blood. 2008 May 1;111(9):4477-89 [18285545.001]
  • [Cites] Clin Cancer Res. 2008 Dec 1;14(23):7924-9 [19047123.001]
  • [Cites] Leukemia. 2008 Dec;22(12):2142-50 [18818707.001]
  • [Cites] Leukemia. 2009 Jan;23(1):43-52 [18987663.001]
  • [Cites] Lancet Oncol. 2009 Feb;10(2):147-56 [19147408.001]
  • [Cites] Br J Cancer. 2009 Jun 16;100(12):1926-36 [19436302.001]
  • [Cites] Nature. 2009 Jun 18;459(7249):1000-4 [19536265.001]
  • [Cites] Blood. 2009 Jul 30;114(5):1053-62 [19406988.001]
  • [Cites] Leukemia. 1999 Nov;13(11):1696-707 [10557041.001]
  • [Cites] Cell. 2000 Jan 7;100(1):57-70 [10647931.001]
  • [Cites] J Cell Sci. 2000 Jul;113 ( Pt 13):2385-97 [10852818.001]
  • [Cites] Blood. 2000 Jul 1;96(1):297-306 [10891465.001]
  • [Cites] J Biol Chem. 2001 Aug 17;276(33):31285-95 [11371555.001]
  • [Cites] Blood. 2002 Jun 1;99(11):4109-15 [12010814.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]
  • [Cites] Blood. 2002 Aug 1;100(3):991-7 [12130513.001]
  • [Cites] Nucleic Acids Res. 2003 Feb 15;31(4):e15 [12582260.001]
  • [Cites] Leukemia. 2003 May;17(5):887-93 [12750702.001]
  • [Cites] J Clin Oncol. 2003 Oct 1;21(19):3616-22 [14512392.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2951-9 [12730115.001]
  • [Cites] Cancer Res. 2004 Apr 15;64(8):2898-903 [15087409.001]
  • [Cites] Cancer Sci. 2004 May;95(5):385-92 [15132764.001]
  • [Cites] Nat Rev Mol Cell Biol. 2004 Oct;5(10):816-26 [15459662.001]
  • [Cites] Oncogene. 1995 Oct 5;11(7):1333-8 [7478554.001]
  • [Cites] BMC Bioinformatics. 2005;6:97 [15826317.001]
  • [Cites] BMC Genomics. 2005;6:59 [15854232.001]
  • [Cites] Leuk Lymphoma. 2005 Apr;46(4):483-95 [16019476.001]
  • [Cites] Cytokine Growth Factor Rev. 2005 Aug-Oct;16(4-5):513-33 [15996891.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] Clin Cancer Res. 2005 Nov 1;11(21):7851-60 [16278408.001]
  • [Cites] Br J Haematol. 2005 Nov;131(4):447-56 [16281934.001]
  • [Cites] BMC Cancer. 2006;6:229 [17002788.001]
  • (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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39. 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
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of childhood T-cell lymphoblastic lymphoma according to the strategy for acute lymphoblastic leukaemia, without radiotherapy: long term results of the EORTC CLG 58881 trial.
  • From June 1989 through to November 1998, 121 children with newly diagnosed T-cell lymphoblastic lymphoma (T-LBL) were included in the EORTC 58881 trial conducted by the Children's Leukaemia Group.
  • An intensive acute lymphoblastic leukaemia type chemotherapy regimen without irradiation leads to a high cure and survival rate in childhood T-LBL without an increased CNS recurrence.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 18342502.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5U10-CA11488-18; United States / NCI NIH HHS / CA / 5U10-CA11488-19; United States / NCI NIH HHS / CA / 5U10-CA11488-20; United States / NCI NIH HHS / CA / 5U10-CA11488-21; United States / NCI NIH HHS / CA / 5U10-CA11488-22; United States / NCI NIH HHS / CA / 5U10-CA11488-23; United States / NCI NIH HHS / CA / 5U10-CA11488-24; United States / NCI NIH HHS / CA / 5U10-CA11488-25; United States / NCI NIH HHS / CA / 5U10-CA11488-26; United States / NCI NIH HHS / CA / 5U10-CA11488-27; United States / NCI NIH HHS / CA / 5U10-CA11488-28; United States / NCI NIH HHS / CA / 5U10-CA11488-29; United States / NCI NIH HHS / CA / 5U10-CA11488-30; United States / NCI NIH HHS / CA / 5U10-CA11488-31; United States / NCI NIH HHS / CA / 5U10-CA11488-32; United States / NCI NIH HHS / CA / 5U10-CA11488-33; United States / NCI NIH HHS / CA / 5U10-CA11488-34; United States / NCI NIH HHS / CA / 5U10-CA11488-35; United States / NCI NIH HHS / CA / 5U10-CA11488-36
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Investigator] Philippet P; Otten J; Plouvier E; Béhar C; Boutard P; Millot F; Waterkeyn C; Velde IV; Solbu G
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40. 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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41. 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
MedlinePlus Health Information. consumer health - Bone Marrow Diseases.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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42. 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
SciCrunch. ArrayExpress: Data: Microarray .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of novel molecular prognostic markers for paediatric T-cell acute lymphoblastic leukaemia.
  • In the last four decades the survival of patients with newly diagnosed childhood T-cell acute lymphoblastic leukaemia (T-ALL) has improved dramatically.
  • [MeSH-major] Gene Expression Profiling. Leukemia-Lymphoma, Adult T-Cell / genetics. Oligonucleotide Array Sequence Analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17456054.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA95475
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BTG3 protein, human; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / CFLAR protein, human; 0 / Genetic Markers; 0 / NOTCH2 protein, human; 0 / Proteins; 0 / Receptor, Notch2
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43. Fischer S, Mann G, Konrad M, Metzler M, Ebetsberger G, Jones N, Nadel B, Bodamer O, Haas OA, Schmitt K, Panzer-Grümayer ER: Screening for leukemia- and clone-specific markers at birth in children with T-cell precursor ALL suggests a predominantly postnatal origin. Blood; 2007 Oct 15;110(8):3036-8

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

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  • (PMID = 17557895.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LMO2 protein, human; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins; 0 / Receptor, Notch1; 135471-20-4 / TAL1 protein, human
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44. 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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45. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • [Cites] Cancer. 1985 Jan 15;55(2):323-36 [3880656.001]
  • [Cites] Pediatr Blood Cancer. 2008 Oct;51(4):489-94 [18618503.001]
  • [Cites] Blood. 1991 Aug 1;78(3):739-47 [1859886.001]
  • [Cites] Med Pediatr Oncol. 1992;20(2):105-13 [1734214.001]
  • [Cites] Leukemia. 1992;6 Suppl 1:47-59 [1548936.001]
  • [Cites] Blood. 1993 Jun 15;81(12):3449-57 [8507880.001]
  • [Cites] Med Pediatr Oncol. 1994;23(4):350-3 [8058006.001]
  • [Cites] N Engl J Med. 1996 May 9;334(19):1238-48 [8606720.001]
  • [Cites] Leukemia. 1997 Dec;11(12):2192-9 [9447840.001]
  • [Cites] Blood. 2000 Jan 15;95(2):416-21 [10627444.001]
  • [Cites] Leukemia. 2000 May;14(5):816-25 [10803512.001]
  • [Cites] Lancet Oncol. 2001 Oct;2(10):597-607 [11902549.001]
  • [Cites] Lancet Oncol. 2001 Jul;2(7):409-17 [11905735.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2399-402 [12239148.001]
  • [Cites] Br J Haematol. 2003 Jan;120(1):74-9 [12492579.001]
  • [Cites] J Pediatr Hematol Oncol. 2003 Feb;25(2):109-13 [12571460.001]
  • [Cites] Leukemia. 2003 Mar;17(3):585-9 [12646948.001]
  • [Cites] Br J Haematol. 2003 Jun;121(6):823-38 [12786792.001]
  • [Cites] Leukemia. 2004 Apr;18(4):703-8 [14961034.001]
  • [Cites] Leukemia. 2004 May;18(5):934-8 [15029212.001]
  • [Cites] N Engl J Med. 1977 Sep 1;297(9):461-4 [301987.001]
  • [Cites] Am J Med. 1978 May;64(5):788-94 [347933.001]
  • [Cites] Blood. 1979 Apr;53(4):687-94 [581853.001]
  • [Cites] J Natl Cancer Inst. 1980 Jul;65(1):33-42 [6993744.001]
  • [Cites] Semin Oncol. 1980 Sep;7(3):332-9 [7414342.001]
  • [Cites] Leuk Res. 1981;5(4-5):281-99 [6974808.001]
  • [Cites] Leuk Res. 1981;5(4-5):301-9 [7026903.001]
  • [Cites] Am J Clin Pathol. 1983 Nov;80(5):655-9 [6356870.001]
  • [Cites] Lancet. 1998 Feb 21;351(9102):550-4 [9492773.001]
  • [Cites] Leukemia. 2005 Sep;19(9):1643-7 [16049513.001]
  • [Cites] Pediatr Blood Cancer. 2005 Nov;45(6):753-69 [15929129.001]
  • [Cites] J Clin Oncol. 2006 Jan 20;24(3):491-9 [16421426.001]
  • [Cites] Pediatr Blood Cancer. 2006 Aug;47(2):130-40 [16358311.001]
  • [Cites] Leukemia. 2006 Aug;20(8):1422-9 [16738692.001]
  • [Cites] Cancer Genet Cytogenet. 2007 Jan 1;172(1):1-11 [17175373.001]
  • [Cites] Br J Haematol. 2007 Aug;138(4):459-66 [17608768.001]
  • [Cites] Leuk Lymphoma. 2007 Sep;48(9):1745-54 [17786710.001]
  • [Cites] J Clin Oncol. 2007 Nov 20;25(33):5254-61 [18024872.001]
  • [Cites] Leuk Res. 1985;9(7):905-11 [3894804.001]
  • (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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46. 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.
  • [Cites] Transplantation. 1999 Oct 27;68(8):1135-9 [10551642.001]
  • [Cites] Arch Pathol Lab Med. 1999 Dec;123(12):1189-207 [10583924.001]
  • [Cites] Int J Cancer. 2001 Mar 15;91(6):869-75 [11275994.001]
  • [Cites] Pediatr Transplant. 2001 Aug;5(4):250-7 [11472603.001]
  • [Cites] Cytometry B Clin Cytom. 2004 Mar;58(1):47-52 [14994375.001]
  • [Cites] J Pediatr Hematol Oncol. 2004 Apr;26(4):217-26 [15087948.001]
  • [Cites] Am J Surg Pathol. 2004 Mar;28(3):410-5 [15104308.001]
  • [Cites] Am J Surg Pathol. 2004 Jul;28(7):967-73 [15223970.001]
  • [Cites] Am J Transplant. 2004 Sep;4(9):1534-8 [15307843.001]
  • [Cites] Surgery. 1981 Aug;90(2):204-13 [6266059.001]
  • [Cites] Blood. 1993 Jul 1;82(1):247-61 [8100721.001]
  • [Cites] Cancer. 1994 Jun 15;73(12):3064-72 [8200004.001]
  • [Cites] J Clin Oncol. 1995 Apr;13(4):961-8 [7707124.001]
  • [Cites] Blood. 1996 Nov 1;88(9):3626-33 [8896433.001]
  • [Cites] J Clin Oncol. 1997 Jun;15(6):2222-30 [9196134.001]
  • [Cites] Cancer. 1998 Mar 1;82(5):983-92 [9486591.001]
  • [Cites] Transplantation. 1999 Apr 15;67(7):990-8 [10221483.001]
  • [Cites] J Heart Lung Transplant. 1999 May;18(5):492-5 [10363695.001]
  • [Cites] Br J Haematol. 2004 Nov;127(4):429-32 [15521920.001]
  • [Cites] Pediatr Blood Cancer. 2005 Mar;44(3):270-6 [15468305.001]
  • [Cites] Am J Clin Pathol. 2005 Feb;123(2):222-8 [15842046.001]
  • [Cites] Cell Mol Biol Lett. 2005;10(3):479-98 [16217558.001]
  • (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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47. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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48. Han X, Bueso-Ramos CE: Precursor T-cell acute lymphoblastic leukemia/lymphoblastic lymphoma and acute biphenotypic leukemias. Am J Clin Pathol; 2007 Apr;127(4):528-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Precursor T-cell acute lymphoblastic leukemia/lymphoblastic lymphoma and acute biphenotypic leukemias.
  • Session 4 of the 2005 Society of Hematopathology/European Association for Haematopathology Workshop focused on case presentations of precursor T-cell acute lymphoblastic leukemia/lymphoblastic lymphoma (pre-T ALL/LBL) and acute biphenotypic leukemia.
  • Pre-T ALL represents approximately 15% of childhood and 25% of adult ALL cases.
  • Acute biphenotypic leukemias are characterized by a single population of blasts that express myeloid, T- or B-lineage antigens in various combinations and account for fewer than 4% of all acute leukemias.
  • An accurate diagnosis of pre-T ALL/LBL and acute biphenotypic leukemia requires a multiparametric approach, including examination of morphologic features, immunophenotype, clinical characteristics, and cytogenetic and molecular findings.
  • [MeSH-major] Biomarkers, Tumor / analysis. Leukemia, Lymphoid / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis


49. Settin A, Al Haggar M, Al Dosoky T, Al Baz R, Abdelrazik N, Fouda M, Aref S, Al-Tonbary Y: Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia. Indian J Pediatr; 2007 Mar;74(3):255-63
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  • [Title] Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia.
  • OBJECTIVE: To evaluate children with acute lymphoblastic leukemia (ALL) showing resistance to immediate induction chemotherapy in relation to conventional and advanced cytogenetic analysis.
  • CONCLUSION: Some cytogenetic and molecular characterizations of childhood ALL could add prognostic criteria for proper therapy allocation.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17401264.001).
  • [ISSN] 0973-7693
  • [Journal-full-title] Indian journal of pediatrics
  • [ISO-abbreviation] Indian J Pediatr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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50. Dunwell TL, Hesson LB, Pavlova T, Zabarovska V, Kashuba V, Catchpoole D, Chiaramonte R, Brini AT, Griffiths M, Maher ER, Zabarovsky E, Latif F: Epigenetic analysis of childhood acute lymphoblastic leukemia. Epigenetics; 2009 Apr 1;4(3):185-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epigenetic analysis of childhood acute lymphoblastic leukemia.
  • We used a chromosome 3 wide NotI microarray for identification of epigenetically inactivated genes in childhood acute lymphoblastic leukemia (ALL).
  • Three novel genes demonstrated frequent methylation in childhood ALL.
  • In our series of childhood ALL BNC1 was frequently methylated in both T (77%) and B-ALL (79%), whilst MSX1 showed T-ALL (25%) specific methylation.
  • The methylation of the above five genes was cancer specific and expression of the genes could be restored in methylated leukemia cell lines treated with 5-aza-2'-deoxycytidine.
  • This is the first report demonstrating frequent epigenetic inactivation of PPP2R3A, FBLN2, THRB, BNC1 and MSX1 in leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 3 / genetics. DNA Methylation. Epigenesis, Genetic. Gene Expression Regulation, Leukemic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Base Sequence. Cell Line, Tumor. Gene Expression Profiling. Gene Silencing. Humans. Molecular Sequence Data. Oligonucleotide Array Sequence Analysis


51. Kikuchi A, Maeda M, Hanada R, Okimoto Y, Ishimoto K, Kaneko T, Ikuta K, Tsuchida M, Tokyo Children's Cancer Study Group (TCCSG): Moyamoya syndrome following childhood acute lymphoblastic leukemia. Pediatr Blood Cancer; 2007 Mar;48(3):268-72
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  • [Title] Moyamoya syndrome following childhood acute lymphoblastic leukemia.
  • BACKGROUND: Long-term survivors of childhood acute lymphoblastic leukemia (ALL) sometimes suffer from adverse long-term sequelae.
  • We analyzed the incidence, clinical course and prognosis of moyamoya syndrome (MoS) following childhood ALL.
  • None of the patients had central nervous system (CNS) leukemia.
  • [MeSH-major] Cranial Irradiation / adverse effects. Moyamoya Disease / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16615044.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; EC 3.5.1.1 / Asparaginase
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52. Mansur MB, Emerenciano M, Splendore A, Brewer L, Hassan R, Pombo-de-Oliveira MS, Brazilian Collaborative Study Group of Infant Acute Leukemia: T-cell lymphoblastic leukemia in early childhood presents NOTCH1 mutations and MLL rearrangements. Leuk Res; 2010 Apr;34(4):483-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell lymphoblastic leukemia in early childhood presents NOTCH1 mutations and MLL rearrangements.
  • T-cell acute lymphoblastic leukemia (T-ALL) may affect children in very early age.
  • We used standard methods to explore NOTCH1 mutations and other specific molecular markers in 15 early childhood T-ALL cases.
  • Despite being found in a lower frequency than that described for overall pediatric T-ALL, NOTCH1 alterations were the most frequent ones.
  • [MeSH-major] Mutation. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics
  • [MeSH-minor] Cell Transformation, Neoplastic / genetics. Child, Preschool. Chromosome Aberrations. Female. Gene Rearrangement / physiology. Genes, T-Cell Receptor delta. Genes, T-Cell Receptor gamma. Genetic Testing. Histone-Lysine N-Methyltransferase. Humans. Infant. Male

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19631984.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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53. Podgornik H, Debeljak M, Zontar D, Cernelc P, Prestor VV, Jazbec J: RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia. Cancer Genet Cytogenet; 2007 Oct 1;178(1):77-81
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  • [Title] RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia.
  • Amplification of RUNX1 (alias AML1) is a recurrent karyotypic abnormality in childhood acute lymphoblastic leukemia (ALL) that is generally associated with a poor outcome.
  • It does not occur with other primary chromosomal abnormalities in acute ALL.
  • AML1 amplification in acute myelogenous leukemia (AML) is a rare secondary event described mainly in therapy-related cases.
  • AML1 amplification was found in a 13-year-old patient with AML M4/M5 leukemia that occurred 5 years after she had been diagnosed with common B-cell ALL.
  • Conventional cytogenetic, fluorescent in situ hybridization (FISH), and polymerase chain reaction methods revealed no other chromosomal change expected to occur in a disease that we assumed to be a secondary leukemia.
  • While the first course of chemotherapy successfully eradicated the cell line with the t(12;21), the second cell line with AML1 amplification remained latent during the time of complete remission and reappeared with a different immunophenotype.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Neoplastic. Leukemia, B-Cell / genetics. Leukemia, B-Cell / pathology. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology


54. Pérez Martínez A, Alonso Ojembarrena A, Ramírez Orellana M, García Castro J, González-Vicent M, Contra Gómez T, Madero López L, Díaz Pérez MA: [Twenty years of treating childhood acute lymphoblastic leukemia]. An Pediatr (Barc); 2006 Sep;65(3):198-204
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Twenty years of treating childhood acute lymphoblastic leukemia].
  • BACKGROUND: Conventional prognostic factors for relapse in patients with acute lymphoblastic leukemia (ALL) are the main basis of risk-stratified treatments.
  • The only significant prognostic factor for relapse identified by multivariate analysis was leukocyte [white blood cell (WBC)] count higher than 80,000/ml at diagnosis (hazard ratio [HR]: 4.63; 95 % CI: 1.61-13.3; p 5 0,004).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
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  • [CommentIn] An Pediatr (Barc). 2006 Sep;65(3):195-7 [16956496.001]
  • (PMID = 16956497.001).
  • [ISSN] 1695-4033
  • [Journal-full-title] Anales de pediatría (Barcelona, Spain : 2003)
  • [ISO-abbreviation] An Pediatr (Barc)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; E7WED276I5 / 6-Mercaptopurine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin; AIEOP acute lymphoblastic leukemia protocol; ALL-BFM-95 protocol; BFM-86 protocol; DAV regimen
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55. Watanabe A: [Recent advance in treatment of childhood acute lymphoblastic leukemia]. Gan To Kagaku Ryoho; 2007 Feb;34(2):150-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Recent advance in treatment of childhood acute lymphoblastic leukemia].
  • The five-year event-free survival of nearly 80% in childhood acute lymphoblastic leukemia (ALL) achieved in the 1990 s attested to the effectiveness of risk-directed therapy developed through well-designed clinical trials by 4 groups in clinical study, containing CCLSG, TCCSG, KYCCSG and JACLS.
  • Japanese Pediatric Leukemia/Lymphoma Study Group (JPLSG) was organized in 2003 and includes all four clinical study groups in Japan.
  • The 2004 ALL protocol of Childhood Cancer and Leukemia Group in Japan (CCLSG) contained a new 2-step stratification based on initial age/WBC count and minimal residual disease at day 91.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 17301519.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
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56. Teuffel O, Stanulla M, Cario G, Ludwig WD, Rottgers S, Schafer BW, Zimmermann M, Schrappe M, Niggli FK: Anemia and survival in childhood acute lymphoblastic leukemia. Haematologica; 2008 Nov;93(11):1652-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anemia and survival in childhood acute lymphoblastic leukemia.
  • BACKGROUND: Several studies have demonstrated that patients with childhood acute lymphoblastic leukemia presenting with mild anemia at diagnosis have an increased risk of poor outcome compared to patients with more severe anemia.
  • However, it has not been reported whether there is any correlation between degree of anemia and leukemia subtype.
  • DESIGN AND METHODS: In a cohort of 1162 patients with childhood acute lymphoblastic leukemia we analyzed whether there was a correlation between degree of anemia and leukemia subtype.
  • The degree of anemia was significantly different for three distinct groups of patients compared to the remaining patients (mean hemoglobin; T-cell leukemia: 106 g/L versus 76 g/L (precursor B-cell acute lymphoblastic leukemia); within precursor B-cell ALL: TEL-AML1 positive: 68 g/L versus 79 g/L; BCR-ABL positive: 93 g/L versus 76 g/L; each p<0.05).
  • Furthermore, in contrast to the entire study group, patients with T-cell leukemia, TEL-AML1(+), and BCR-ABL(+) precursor B-cell leukemia had a more favorable prognosis if presenting with a higher hemoglobin level (>/=80 g/L).
  • CONCLUSIONS: These observations indicate that the formerly reported direct correlation between severity of anemia and survival in childhood acute lymphoblastic leukemia mainly reflects differences in the degree of anemia between distinct biological subgroups with different treatment outcomes.
  • [MeSH-major] Anemia / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality
  • [MeSH-minor] Burkitt Lymphoma / complications. Burkitt Lymphoma / genetics. Burkitt Lymphoma / mortality. Child. Cohort Studies. Core Binding Factor Alpha 2 Subunit / genetics. Disease-Free Survival. Fusion Proteins, bcr-abl / genetics. Hemoglobins / metabolism. Homeodomain Proteins / genetics. Humans. Leukemia, T-Cell / complications. Leukemia, T-Cell / genetics. Leukemia, T-Cell / mortality. Leukocyte Count. Mutation. Oncogene Proteins, Fusion / genetics. Risk Factors. Survival Analysis. Treatment Outcome

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  • (PMID = 18815194.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Hemoglobins; 0 / Homeodomain Proteins; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human; 146150-85-8 / E2A-Pbx1 fusion protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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57. Jamroziak K, Robak T: Do polymorphisms in ABC transporter genes influence risk of childhood acute lymphoblastic leukemia? Leuk Res; 2008 Aug;32(8):1173-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Do polymorphisms in ABC transporter genes influence risk of childhood acute lymphoblastic leukemia?
  • It is widely accepted that pathogenesis of childhood acute lymphoblastic leukemia (ALL) is related to the interplay between specific environmental exposure and inherited background.
  • Here, we review several recent reports on potential association between single nucleotide polymorphisms (SNPs) in genes encoding for ABC transporters with predisposition to pediatric ALL.
  • [MeSH-major] ATP-Binding Cassette Transporters / genetics. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [CommentOn] Leuk Res. 2008 Aug;32(8):1214-20 [18243305.001]
  • (PMID = 18294687.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / P-Glycoprotein
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58. Abdelhaleem M: Frequent but nonrandom expression of myeloid markers on de novo childhood acute lymphoblastic leukemia. Exp Mol Pathol; 2007 Aug;83(1):138-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequent but nonrandom expression of myeloid markers on de novo childhood acute lymphoblastic leukemia.
  • The expression of the myeloid markers CD13, CD33, and CD15 in two hundred and eighty-three cases of de novo childhood acute lymphoblastic leukemia (ALL) is examined.
  • Certain patterns of myeloid antigen expression can be recognized including: no expression of CD13, CD33, and CD15 in mature B-ALL, significantly higher levels of CD13 and CD33 and significantly lower levels of CD15 in TEL-AML1-positive B cell precursor ALL, no expression of CD13 and CD33 in E2A-PBX1-positive B cell precursor ALL cases and common T-ALL (double positive for CD4 and CD8), and no expression of CD13 in MLL-AF4-positive B cell precursor ALL cases.
  • Although the numbers in some ALL subtypes are small, these patterns are consistent with nonrandom expression of myeloid markers in de novo childhood ALL.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Myeloid Cells / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Antigens, CD / metabolism. Antigens, CD13 / metabolism. Antigens, CD15 / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Burkitt Lymphoma / metabolism. Burkitt Lymphoma / pathology. Cell Differentiation. Child. Core Binding Factor Alpha 2 Subunit / metabolism. Homeodomain Proteins / metabolism. Humans. Oncogene Proteins, Fusion / metabolism. Sialic Acid Binding Ig-like Lectin 3


59. Bhojwani D, Howard SC, Pui CH: High-risk childhood acute lymphoblastic leukemia. Clin Lymphoma Myeloma; 2009;9 Suppl 3:S222-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-risk childhood acute lymphoblastic leukemia.
  • Although most children with acute lymphoblastic leukemia (ALL) are cured, certain subsets have a high risk of relapse.
  • Though early treatment response can be assessed by the peripheral blast cell count after 1 week of single-agent glucocorticoid treatment or percent of bone marrow blasts by morphology after 1 or 2 weeks of multiagent induction treatment, determination of minimal residual disease by polymerase chain reaction (PCR) or flow cytometry after 2 to 6 weeks of induction is the most precise and useful measure.
  • Infants with mixed-lineage leukemia (MLL)-rearranged ALL comprise a very poor-risk group wherein further intensification of chemotherapy causes significant toxicity.
  • Hybrid protocols incorporating drugs effective for acute myeloid leukemia could improve survival, a strategy being tested in international trials.
  • New agents and methods to overcome resistance are under investigation, and allogeneic stem cell transplantation is recommended for certain subsets of patients, for example those with Ph+ and T-cell ALL with poor early response.
  • Genome-wide interrogation of leukemic cell genetic abnormalities and germline genetic variations promise to identify new molecular targets for therapy.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • [Cites] Blood. 2008 Mar 15;111(6):2984-90 [18182569.001]
  • [Cites] Bone Marrow Transplant. 2008 Mar;41(5):447-53 [17968326.001]
  • [Cites] J Clin Oncol. 2008 Mar 20;26(9):1496-503 [18349402.001]
  • [Cites] Lancet. 2008 Mar 22;371(9617):1030-43 [18358930.001]
  • [Cites] Leukemia. 2008 Apr;22(4):771-82 [18239620.001]
  • [Cites] Blood. 2008 May 1;111(9):4477-89 [18285545.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5477-85 [18388178.001]
  • [Cites] Bone Marrow Transplant. 2008 Jun;41 Suppl 2:S71-4 [18545248.001]
  • [Cites] Clin Cancer Res. 2008 Jul 1;14(13):4027-31 [18593977.001]
  • [Cites] J Clin Oncol. 2008 Jul 1;26(19):3204-12 [18541900.001]
  • [Cites] Clin Cancer Res. 2008 Jul 15;14(14):4392-9 [18628453.001]
  • [Cites] Haematologica. 2008 Aug;93(8):1155-60 [18519521.001]
  • [Cites] Blood. 2008 Aug 15;112(4):1005-12 [18477770.001]
  • [Cites] J Clin Oncol. 2008 Sep 20;26(27):4376-84 [18802149.001]
  • [Cites] Blood. 2008 Nov 15;112(10):4318-27 [18723429.001]
  • [Cites] Semin Hematol. 2009 Jan;46(1):39-51 [19100367.001]
  • [Cites] Semin Hematol. 2009 Jan;46(1):100-6 [19100372.001]
  • [Cites] JAMA. 2009 Jan 28;301(4):393-403 [19176441.001]
  • [Cites] N Engl J Med. 2009 Jan 29;360(5):470-80 [19129520.001]
  • [Cites] Lancet Oncol. 2009 Feb;10(2):147-56 [19147408.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Jun 9;106(23):9414-8 [19470474.001]
  • [Cites] J Clin Oncol. 2009 Nov 1;27(31):5175-81 [19805687.001]
  • [Cites] Blood. 2006 Jul 1;108(1):97-102 [16537802.001]
  • [Cites] Blood. 2006 Jul 15;108(2):441-51 [16556894.001]
  • [Cites] Leukemia. 2006 Aug;20(8):1368-76 [16761017.001]
  • [Cites] Blood. 2006 Aug 1;108(3):1050-7 [16627760.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1469-77 [16638934.001]
  • [Cites] Clin Cancer Res. 2006 Sep 15;12(18):5329-35 [17000665.001]
  • [Cites] J Clin Oncol. 2006 Dec 20;24(36):5742-9 [17179108.001]
  • [Cites] J Clin Oncol. 2007 Jan 1;25(1):16-24 [17194902.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Feb;13(2):218-27 [17241927.001]
  • [Cites] Blood. 2007 Feb 1;109(3):896-904 [17003366.001]
  • [Cites] Blood. 2007 Feb 1;109(3):926-35 [17003380.001]
  • [Cites] Nat Rev Drug Discov. 2007 Feb;6(2):149-65 [17268486.001]
  • [Cites] Blood. 2007 Mar 15;109(6):2327-30 [17095619.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Lancet. 2007 Jun 9;369(9577):1947-54 [17560447.001]
  • [Cites] Blood. 2007 Jul 15;110(2):727-34 [17405907.001]
  • [Cites] Lancet. 2007 Jul 21;370(9583):240-50 [17658395.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1112-5 [17473063.001]
  • [Cites] J Clin Oncol. 2007 Oct 20;25(30):4813-20 [17947730.001]
  • [Cites] Leukemia. 2007 Nov;21(11):2258-63 [17690691.001]
  • [Cites] Nat Rev Cancer. 2007 Nov;7(11):823-33 [17957188.001]
  • [Cites] N Engl J Med. 2000 Apr 6;342(14):998-1006 [10749961.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3310-22 [10828010.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2223-33 [11187913.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2257-66 [11187917.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1038-42 [11287973.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]
  • [Cites] Blood. 2002 Jun 1;99(11):3885-91 [12010785.001]
  • [Cites] Lancet. 2002 Jun 1;359(9321):1909-15 [12057554.001]
  • [Cites] Blood. 2002 Jul 1;100(1):43-7 [12070006.001]
  • [Cites] Leukemia. 2002 Sep;16(9):1668-72 [12200679.001]
  • [Cites] Br J Haematol. 2002 Nov;119(2):445-53 [12406084.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):173-83 [12620411.001]
  • [Cites] Bone Marrow Transplant. 2003 May;31(10):909-18 [12748668.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2736-40 [12843002.001]
  • [Cites] Pediatr Blood Cancer. 2004 Jan;42(1):8-23 [14752789.001]
  • [Cites] Leukemia. 2004 Mar;18(3):521-9 [14712291.001]
  • [Cites] Leukemia. 2004 Mar;18(3):499-504 [14981525.001]
  • [Cites] Nat Genet. 2004 May;36(5):453-61 [15098032.001]
  • [Cites] Ann Hematol. 2004;83 Suppl 1:S124-6 [15124703.001]
  • [Cites] Nature. 2004 May 27;429(6990):464-8 [15164072.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2690-6 [15251979.001]
  • [Cites] J Clin Oncol. 1985 Nov;3(11):1513-21 [3863894.001]
  • [Cites] Blood. 1994 Nov 1;84(9):3122-33 [7949185.001]
  • [Cites] Cancer. 1997 Nov 1;80(9):1717-26 [9351539.001]
  • [Cites] J Clin Oncol. 1998 Feb;16(2):527-35 [9469337.001]
  • [Cites] N Engl J Med. 1998 Jun 4;338(23):1663-71 [9614257.001]
  • [Cites] Cancer. 1998 Nov 1;83(9):2030-9 [9806664.001]
  • [Cites] Lancet. 1998 Nov 28;352(9142):1731-8 [9848348.001]
  • [Cites] Leukemia. 1999 Aug;13(8):1221-6 [10450750.001]
  • [Cites] Blood. 2005 Jan 15;105(2):821-6 [15388585.001]
  • [Cites] JAMA. 2005 Mar 23;293(12):1485-9 [15784872.001]
  • [Cites] Blood. 2005 May 1;105(9):3749-56 [15637143.001]
  • [Cites] Lancet. 2005 Aug 20-26;366(9486):635-42 [16112299.001]
  • [Cites] Blood. 2005 Oct 1;106(7):2484-90 [15956279.001]
  • [Cites] Biol Blood Marrow Transplant. 2005 Dec;11(12):999-1005 [16338622.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] J Clin Oncol. 2006 Jan 20;24(3):460-6 [16344315.001]
  • [Cites] Leukemia. 2006 Feb;20(2):264-71 [16357833.001]
  • [Cites] J Clin Oncol. 2008 Jan 10;26(2):283-9 [18182669.001]
  • [Cites] Clin Cancer Res. 2008 Jan 15;14(2):352-9 [18223208.001]
  • [Cites] Curr Probl Pediatr Adolesc Health Care. 2008 Mar;38(3):78-94 [18279790.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2548-55 [18039957.001]
  • [Cites] Lancet Oncol. 2008 Mar;9(3):257-68 [18308251.001]
  • (PMID = 19778845.001).
  • [ISSN] 1938-0712
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / P30 CA021765-31; United States / NCI NIH HHS / CA / CA21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Glucocorticoids
  • [Number-of-references] 92
  • [Other-IDs] NLM/ NIHMS163517; NLM/ PMC2814411
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60. Nurmio M, Keros V, Lähteenmäki P, Salmi T, Kallajoki M, Jahnukainen K: Effect of childhood acute lymphoblastic leukemia therapy on spermatogonia populations and future fertility. J Clin Endocrinol Metab; 2009 Jun;94(6):2119-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of childhood acute lymphoblastic leukemia therapy on spermatogonia populations and future fertility.
  • CONTEXT: Isolation of spermatogonial stem cells before potentially sterilizing cancer therapy, followed by transplantation of these cells into the testis after such treatment, may be an effective approach to prevent infertility among prepubertal boys suffering from acute lymphoblastic leukemia (ALL).
  • A key clinical consideration in this context is the timing of biopsy, if collection of spermatogonia could be delayed from diagnosis to the later phase of leukemia treatment, better patient selection could be offered.
  • OBJECTIVE: The objective of the study was to examine the routine testicular biopsy material collected to detect testicular leukemia to evaluate if treatment for leukemia affects numbers and maturation of the spermatogonia during the prepubertal period.
  • OUTCOME MEASURE: Samples were stained immunohistochemically to evaluate the expression of the spermatogonial markers MAGE 4A, OCT4, CD9, and AP2gamma, and of the Sertoli cell marker WT-1.
  • No significant alteration in spermatogonial numbers was associated with testicular leukemia.
  • CONCLUSION: Treatment for childhood leukemia without high-dose cyclophosphamide seldom depletes the spermatogonial stem cell pool totally.
  • [MeSH-major] Cyclophosphamide / adverse effects. Fertility / drug effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Sperm Count. Spermatogonia / pathology

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  • (PMID = 19318447.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 8N3DW7272P / Cyclophosphamide
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61. Wehrli LA, Braun J, Buetti LN, Hagleitner N, Hengartner H, Kühne T, Lüer S, Ozsahin H, Popovic MB, Niggli FK, Betts DR, Bourquin JP: Non-classical karyotypic features in relapsed childhood B-cell precursor acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2009 Feb;189(1):29-36
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  • [Title] Non-classical karyotypic features in relapsed childhood B-cell precursor acute lymphoblastic leukemia.
  • Karyotype analysis of acute lymphoblastic leukemia (ALL) at diagnosis has provided valuable prognostic markers for treatment stratification.
  • We compared the karyotypes from 436 nonselected B-cell precursor ALL patients at initial diagnosis and of 76 patients at first relapse.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Chromosome Aberrations. Female. Humans. Infant. Karyotyping. Male. Recurrence. Translocation, Genetic. Treatment Outcome


62. Kolmannskog S, Flaegstad T, Helgestad J, Hellebostad M, Zeller B, Glomstein A: [Childhood acute lymphoblastic leukemia in Norway 1992-2000]. Tidsskr Nor Laegeforen; 2007 May 31;127(11):1493-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Childhood acute lymphoblastic leukemia in Norway 1992-2000].
  • BACKGROUND: Acute lymphoblastic leukemia is the most common malignancy in childhood.
  • Four of 6 infants with acute lymphoblastic leukemia and all 4 with mature B-cell leukemia are alive.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Neoplasm Recurrence, Local. Norway / epidemiology. Risk Factors. Stem Cell Transplantation. Treatment Outcome

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  • (PMID = 17551551.001).
  • [ISSN] 0807-7096
  • [Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række
  • [ISO-abbreviation] Tidsskr. Nor. Laegeforen.
  • [Language] nor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Norway
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63. Hosking FJ, Papaemmanuil E, Sheridan E, Kinsey SE, Lightfoot T, Roman E, Irving JA, Allan JM, Taylor M, Tomlinson IP, Greaves M, Houlston RS: Genome-wide homozygosity signatures and childhood acute lymphoblastic leukemia risk. Blood; 2010 Jun 3;115(22):4472-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genome-wide homozygosity signatures and childhood acute lymphoblastic leukemia risk.
  • To examine whether homozygosity is associated with an increased risk of developing childhood B-cell precursor acute lymphoblastic leukemia (BCP-ALL), we analyzed 824 ALL cases and 2398 controls genotyped for 292 200 tagging SNPs.

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  • (PMID = 20231427.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / / 10417; United Kingdom / Cancer Research UK / / C1298/A8362
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Erythropoietin
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64. Sherborne AL, Hosking FJ, Prasad RB, Kumar R, Koehler R, Vijayakrishnan J, Papaemmanuil E, Bartram CR, Stanulla M, Schrappe M, Gast A, Dobbins SE, Ma Y, Sheridan E, Taylor M, Kinsey SE, Lightfoot T, Roman E, Irving JA, Allan JM, Moorman AV, Harrison CJ, Tomlinson IP, Richards S, Zimmermann M, Szalai C, Semsei AF, Erdelyi DJ, Krajinovic M, Sinnett D, Healy J, Gonzalez Neira A, Kawamata N, Ogawa S, Koeffler HP, Hemminki K, Greaves M, Houlston RS: Variation in CDKN2A at 9p21.3 influences childhood acute lymphoblastic leukemia risk. Nat Genet; 2010 Jun;42(6):492-4
SciCrunch. OMIM: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Variation in CDKN2A at 9p21.3 influences childhood acute lymphoblastic leukemia risk.
  • Using data from a genome-wide association study of 907 individuals with childhood acute lymphoblastic leukemia (cases) and 2,398 controls and with validation in samples totaling 2,386 cases and 2,419 controls, we have shown that common variation at 9p21.3 (rs3731217, intron 1 of CDKN2A) influences acute lymphoblastic leukemia risk (odds ratio = 0.71, P = 3.01 x 10(-11)), irrespective of cell lineage.

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  • [Cites] J Biol Chem. 2002 Nov 29;277(48):46289-97 [12228235.001]
  • [Cites] PLoS Genet. 2005 Dec;1(6):e78 [16362079.001]
  • [Cites] Haematologica. 2006 Jul;91(7):881-5 [16818274.001]
  • [Cites] Science. 2007 Jun 1;316(5829):1341-5 [17463248.001]
  • [Cites] Blood. 2009 Jan 1;113(1):100-7 [18838613.001]
  • [Cites] Leukemia. 2009 Jul;23(7):1209-18 [19242497.001]
  • [Cites] Science. 2007 Jun 8;316(5830):1488-91 [17478681.001]
  • [Cites] Nat Genet. 2009 Aug;41(8):920-5 [19578364.001]
  • [Cites] Nat Genet. 2009 Aug;41(8):915-9 [19578365.001]
  • [Cites] Nat Genet. 2009 Aug;41(8):899-904 [19578367.001]
  • [Cites] Nat Genet. 2009 Sep;41(9):1001-5 [19684603.001]
  • [Cites] Nat Genet. 2009 Sep;41(9):1006-10 [19684604.001]
  • [Cites] Leukemia. 2010 Jan;24(1):66-73 [19759560.001]
  • [Cites] Nat Genet. 2009 Aug;41(8):909-14 [19578363.001]
  • (PMID = 20453839.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] ENG
  • [Grant] United Kingdom / Medical Research Council / / MC/ U137686856; United States / NCI NIH HHS / CA / R01 CA026038-31; United Kingdom / Medical Research Council / / MC/ U137686861; United Kingdom / Cancer Research UK / / C1298/A8362; United States / NIGMS NIH HHS / GM / T32 GM008243; United States / NCI NIH HHS / CA / R01 CA026038-32; United States / NCI NIH HHS / CA / CA026038-30A2; United States / NCI NIH HHS / CA / R01 CA026038; United States / NCI NIH HHS / CA / R01 CA026038-30A2; United Kingdom / Cancer Research UK / / 10417
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS400186; NLM/ PMC3434228
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65. Athanassiadou F, Tragiannidis A, Rousso I, Katsos G, Sidi V, Papageorgiou T, Papastergiou C, Tsituridis I, Koliouskas D: Bone mineral density in survivors of childhood acute lymphoblastic leukemia. Turk J Pediatr; 2006 Apr-Jun;48(2):101-4
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] Bone mineral density in survivors of childhood acute lymphoblastic leukemia.
  • The aim of our study was to evaluate bone metabolism with measurement of bone mineral density (BMD) after management (chemo-, radiotherapy) for childhood acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Antineoplastic Agents / adverse effects. Bone Diseases, Metabolic / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • (PMID = 16848106.001).
  • [ISSN] 0041-4301
  • [Journal-full-title] The Turkish journal of pediatrics
  • [ISO-abbreviation] Turk. J. Pediatr.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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66. Liu Y, Chen J, Tang J, Ni S, Xue H, Pan C: Cost of childhood acute lymphoblastic leukemia care in Shanghai, China. Pediatr Blood Cancer; 2009 Oct;53(4):557-62
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] Cost of childhood acute lymphoblastic leukemia care in Shanghai, China.
  • BACKGROUND: Acute lymphoblastic leukemia (ALL) is the most common and curable malignant pediatric disease in children.
  • Here, we analyzed the overall costs for pediatric ALL therapies and their constitutive elements.
  • Average overall costs for childhood ALL in this study were less than US $11,000, with reasonable clinical results.
  • [MeSH-major] Health Care Costs. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 19526524.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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67. Zhu YM, Zhao WL, Fu JF, Shi JY, Pan Q, Hu J, Gao XD, Chen B, Li JM, Xiong SM, Gu LJ, Tang JY, Liang H, Jiang H, Xue YQ, Shen ZX, Chen Z, Chen SJ: NOTCH1 mutations in T-cell acute lymphoblastic leukemia: prognostic significance and implication in multifactorial leukemogenesis. Clin Cancer Res; 2006 May 15;12(10):3043-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NOTCH1 mutations in T-cell acute lymphoblastic leukemia: prognostic significance and implication in multifactorial leukemogenesis.
  • PURPOSE: NOTCH signaling pathway is essential in T-cell development and NOTCH1 mutations are frequently present in T-cell acute lymphoblastic leukemia (T-ALL).
  • Interestingly, the statistically significant difference of survival according to NOTCH1 mutations was only observed in adult patients (>18 years) but not in pediatric patients (< or = 18 years), possibly due to the relatively good overall response of childhood T-ALL to the current chemotherapy.
  • CONCLUSION: NOTCH1 mutation is an important prognostic marker in T-ALL and its predictive value could be even further increased if coevaluated with other T-cell-related regulatory genes.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Receptor, Notch1 / genetics

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  • [ErratumIn] Clin Cancer Res. 2009 Feb 15;15(4):1506
  • (PMID = 16707600.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
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68. Settin A, Al Haggar M, Al Dosoky T, Al Baz R, Abdelrazik N, Fouda M, Aref S, Al-Tonbary Y: Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia: cases from Mansoura, Egypt. Hematology; 2006 Oct;11(5):341-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia: cases from Mansoura, Egypt.
  • OBJECTIVE: To evaluate children with acute lymphoblastic leukemia (ALL) showing resistance to immediate induction chemotherapy in relation to conventional and advanced cytogenetic analysis.
  • CONCLUSIONS: Cytogenetic and molecular characterizations of childhood ALL may add prognostic criteria for optimal therapy allocation.
  • [MeSH-major] Cytogenetic Analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 17607584.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers
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69. Pakakasama S, Sirirat T, Kanchanachumpol S, Udomsubpayakul U, Mahasirimongkol S, Kitpoka P, Thithapandha A, Hongeng S: Genetic polymorphisms and haplotypes of DNA repair genes in childhood acute lymphoblastic leukemia. Pediatr Blood Cancer; 2007 Jan;48(1):16-20
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] Genetic polymorphisms and haplotypes of DNA repair genes in childhood acute lymphoblastic leukemia.
  • This study was performed to evaluate the effect of the polymorphisms of DNA repair genes on risk of childhood acute lymphoblastic leukemia (ALL).
  • CONCLUSION: The XRCC1 194Trp allele and haplotype B showed a protective effect against development of childhood ALL.
  • [MeSH-major] Alleles. DNA Repair. DNA-Binding Proteins / genetics. Genetic Predisposition to Disease. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16435384.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / X-ray repair cross complementing protein 1
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70. Settin A, Al Haggar M, Al Dosoky T, Al Baz R, Abdelrazik N, Fouda M, Aref S, Al-Tonbary Y: Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia: cases from Mansoura Egypt. Hematology; 2007 Apr;12(2):103-11
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] Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia: cases from Mansoura Egypt.
  • The objective of the work was to evaluate children with acute lymphoblastic leukemia (ALL) showing resistance to immediate induction chemotherapy in relation to conventional and advanced cytogenetic analysis.
  • Our conclusions were that cytogenetic and molecular characterizations of childhood ALL could add prognostic criteria for proper therapy allocation.
  • [MeSH-major] Aneuploidy. Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17454190.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Genetic Markers
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71. Udayakumar AM, Bashir WA, Pathare AV, Wali YA, Zacharia M, Khan AA, Soliman H, Al-Lamki Z, Raeburn JA: Cytogenetic profile of childhood acute lymphoblastic leukemia in Oman. Arch Med Res; 2007 Apr;38(3):305-12
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] Cytogenetic profile of childhood acute lymphoblastic leukemia in Oman.
  • BACKGROUND: Chromosomal abnormalities have important diagnostic and prognostic significance in acute lymphoblastic leukemia (ALL).
  • METHODS: Bone marrow chromosomal studies with GTG banding were performed in untreated ALL pediatric patients aged from 7 days to 14 years.
  • To our knowledge, this is the first report from the Middle East of a cytogenetic study on childhood ALL.
  • [MeSH-major] Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17350480.001).
  • [ISSN] 0188-4409
  • [Journal-full-title] Archives of medical research
  • [ISO-abbreviation] Arch. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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72. Banklau C, Jindadamrongwech S, Sawangpanich R, Apibal S, Hongeng S, Paisooksantivatana K, Pakakasama S: Effect of genetic alterations of cytarabine- metabolizing enzymes in childhood acute lymphoblastic leukemia. Hematol Oncol Stem Cell Ther; 2010;3(3):103-8
Hazardous Substances Data Bank. CYTARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of genetic alterations of cytarabine- metabolizing enzymes in childhood acute lymphoblastic leukemia.
  • Currently, treatment of childhood acute lymphoblastic leukemia (ALL) includes cytarabine, especially in high-risk patients.
  • PATIENTS AND METHODS: We included children diagnosed with ALL and lymphoblastic lymphoma (LL) stage III and IV.
  • CONCLUSION: The dCK-360G allele was found to increase the risk of mucositis after exposure to low-dose cytarabine in childhood ALL therapy.
  • [MeSH-major] Cytarabine / therapeutic use. Cytidine Deaminase / genetics. Deoxycytidine Kinase / genetics. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20890066.001).
  • [ISSN] 1658-3876
  • [Journal-full-title] Hematology/oncology and stem cell therapy
  • [ISO-abbreviation] Hematol Oncol Stem Cell Ther
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Saudi Arabia
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; EC 2.7.1.74 / Deoxycytidine Kinase; EC 3.1.3.48 / Antigens, CD45; EC 3.5.4.5 / Cytidine Deaminase
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73. Chang JS, Wiemels JL, Chokkalingam AP, Metayer C, Barcellos LF, Hansen HM, Aldrich MC, Guha N, Urayama KY, Scélo G, Green J, May SL, Kiley VA, Wiencke JK, Buffler PA: Genetic polymorphisms in adaptive immunity genes and childhood acute lymphoblastic leukemia. Cancer Epidemiol Biomarkers Prev; 2010 Sep;19(9):2152-63
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic polymorphisms in adaptive immunity genes and childhood acute lymphoblastic leukemia.
  • BACKGROUND: Childhood acute lymphoblastic leukemia (ALL) has been hypothesized to have an infection- and immune-related etiology.
  • The lack of immune priming in early childhood may result in abnormal immune responses to infections later in life and increase ALL risk.
  • METHODS: The current analyses examined the association between childhood ALL and 208 single-nucleotide polymorphisms (SNP) of 29 adaptive immune function genes among 377 ALL cases and 448 healthy controls.
  • RESULTS: Of the 208 SNPs, only rs583911 of IL12A, which encodes a critical modulator of T-cell development, remained significant after accounting for multiple testing (odds ratio for each copy of the variant G allele, 1.52; 95% confidence interval, 1.25-1.85; P = 2.9 x 10(-5)).
  • This increased risk was stronger among firstborn children of all ethnicities and among non-Hispanic children with less day care attendance, consistent with the hypothesis about the role of early immune modulation in the development of childhood ALL.
  • Haplotype analyses identified additional regions of CD28, FCGR2, GATA3, IL2RA, STAT4, and STAT6 associated with childhood ALL.
  • CONCLUSION: Polymorphisms of genes on the adaptive immunity pathway are associated with childhood ALL risk.
  • IMPACT: Results of this study support an immune-related etiology of childhood ALL.

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  • [Copyright] (c) 2010 AACR.
  • [Cites] Br J Cancer. 2000 Jan;82(1):234-40 [10638995.001]
  • [Cites] Int J Epidemiol. 2010 Jun;39(3):718-32 [20110276.001]
  • [Cites] Am J Epidemiol. 2000 Dec 15;152(12):1136-44 [11130619.001]
  • [Cites] Am J Hum Genet. 2001 Jul;69(1):138-47 [11404819.001]
  • [Cites] Eur J Immunol. 2001 Nov;31(11):3394-402 [11745358.001]
  • [Cites] Int J Epidemiol. 2001 Dec;30(6):1428-37 [11821358.001]
  • [Cites] Br J Cancer. 2002 Apr 8;86(7):1064-9 [11953850.001]
  • [Cites] Br J Cancer. 2002 May 6;86(9):1419-24 [11986774.001]
  • [Cites] Med Pediatr Oncol. 2002 Jun;38(6):391-7 [11984799.001]
  • [Cites] Science. 2002 Jun 21;296(5576):2225-9 [12029063.001]
  • [Cites] Nat Rev Immunol. 2003 Feb;3(2):133-46 [12563297.001]
  • [Cites] Int J Cancer. 2003 Jun 10;105(2):255-60 [12673688.001]
  • [Cites] Nature. 2003 Dec 18;426(6968):789-96 [14685227.001]
  • [Cites] Br J Cancer. 2004 Jan 12;90(1):139-45 [14710221.001]
  • [Cites] Am J Epidemiol. 2004 May 15;159(10):915-21 [15128601.001]
  • [Cites] Immunology. 2004 Jul;112(3):352-63 [15196202.001]
  • [Cites] Am J Phys Anthropol. 1986 Aug;70(4):433-41 [3766713.001]
  • [Cites] Am J Phys Anthropol. 1986 Aug;70(4):489-503 [3766715.001]
  • [Cites] BMJ. 1989 Nov 18;299(6710):1259-60 [2513902.001]
  • [Cites] J Epidemiol Community Health. 1989 Dec;43(4):352-5 [2614325.001]
  • [Cites] Br J Cancer. 1995 Jan;71(1):1-5 [7819022.001]
  • [Cites] J Natl Cancer Inst. 1997 Jul 2;89(13):939-47 [9214673.001]
  • [Cites] Br J Cancer. 1997;76(9):1241-7 [9365177.001]
  • [Cites] J Immunol. 1998 May 15;160(10):4730-7 [9590218.001]
  • [Cites] Vaccine. 1998 Aug-Sep;16(14-15):1415-9 [9711781.001]
  • [Cites] Clin Exp Allergy. 1998 Nov;28 Suppl 5:39-44; discussion 50-1 [9988446.001]
  • [Cites] Br J Cancer. 1999 May;80(3-4):585-90 [10408870.001]
  • [Cites] Br J Cancer. 1999 Aug;80(11):1844-51 [10468308.001]
  • [Cites] Bioinformatics. 2005 Jan 15;21(2):263-5 [15297300.001]
  • [Cites] Paediatr Perinat Epidemiol. 2005 Mar;19(2):152-64 [15787890.001]
  • [Cites] BMJ. 2005 Jun 4;330(7503):1294 [15849205.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Aug;14(8):1928-34 [16103439.001]
  • [Cites] Nucleic Acids Res. 2006 Jan 1;34(Database issue):D617-21 [16381944.001]
  • [Cites] Nat Rev Cancer. 2006 Mar;6(3):193-203 [16467884.001]
  • [Cites] BMC Genet. 2006;7:38 [16774684.001]
  • [Cites] Clin Exp Allergy. 2006 Nov;36(11):1357-66 [17083345.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Dec;15(12):2533-6 [17164381.001]
  • [Cites] Am J Hum Genet. 2007 Feb;80(2):273-90 [17236132.001]
  • [Cites] Am J Epidemiol. 2007 Mar 1;165(5):496-504 [17182983.001]
  • [Cites] Int J Cancer. 2007 Aug 15;121(4):819-24 [17390373.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Aug;16(8):1686-90 [17684147.001]
  • [Cites] Am J Epidemiol. 2008 Mar 1;167(5):598-606 [18079130.001]
  • [Cites] Adv Genet. 2008;60:335-405 [18358327.001]
  • [Cites] Br J Cancer. 2008 Nov 4;99(9):1529-33 [18827817.001]
  • [Cites] Cancer Causes Control. 2000 Apr;11(4):303-7 [10843442.001]
  • (PMID = 20716621.001).
  • [ISSN] 1538-7755
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / R01 ES009137-08; United States / NIEHS NIH HHS / ES / ES009137-10; United States / NIEHS NIH HHS / ES / P42 ES004705-22S10023; United States / NIEHS NIH HHS / ES / R01 ES009137-01A1; United States / NIEHS NIH HHS / ES / P42 ES004705-22S20023; United States / NIEHS NIH HHS / ES / ES009137-05S1; United States / NIEHS NIH HHS / ES / P42 ES004705-200023; United States / NIEHS NIH HHS / ES / P42 ES004705-220023; United States / NIEHS NIH HHS / ES / ES009137-02; United States / NIEHS NIH HHS / ES / ES009137-05; United States / NIEHS NIH HHS / ES / ES009137-04; United States / NIEHS NIH HHS / ES / ES009137-01A1; United States / NIEHS NIH HHS / ES / R01 ES009137-02; United States / NIEHS NIH HHS / ES / R01 ES009137-03; United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NCI NIH HHS / CA / R25 CA112355; United States / NIEHS NIH HHS / ES / ES004705-22S30023; United States / NIEHS NIH HHS / ES / R01 ES009137-10S1; United States / NIEHS NIH HHS / ES / ES009137-03S1; United States / NIEHS NIH HHS / ES / R01 ES009137-07; United States / NIEHS NIH HHS / ES / ES004705-190023; United States / NIEHS NIH HHS / ES / ES004705-200023; United States / NIEHS NIH HHS / ES / R01 ES009137-05S1; United States / NIEHS NIH HHS / ES / R01 ES009137-10; United States / NIEHS NIH HHS / ES / ES004705-230023; United States / NIEHS NIH HHS / ES / PS42ES04705; United States / NIEHS NIH HHS / ES / ES004705-210023; United States / NIEHS NIH HHS / ES / ES009137-06A1; United States / NIEHS NIH HHS / ES / P42 ES004705-22S30023; United States / NIEHS NIH HHS / ES / P42 ES004705-210023; United States / NIEHS NIH HHS / ES / R01 ES009137-03S1; United States / NIEHS NIH HHS / ES / P42 ES004705-230023; United States / NIEHS NIH HHS / ES / ES009137-07; United States / NIEHS NIH HHS / ES / R01 ES009137-04; United States / NIEHS NIH HHS / ES / ES009137-09; United States / NIEHS NIH HHS / ES / ES004705-220023; United States / NIEHS NIH HHS / ES / R01ES09137; United States / NIEHS NIH HHS / ES / ES004705-22S10023; United States / NIEHS NIH HHS / ES / R01 ES009137-06A1; United States / NIEHS NIH HHS / ES / ES004705-22S20023; United States / NIEHS NIH HHS / ES / R01 ES009137; United States / NIEHS NIH HHS / ES / ES009137-10S1; United States / NIEHS NIH HHS / ES / R01 ES009137-05; United States / NIEHS NIH HHS / ES / ES009137-03; United States / NIEHS NIH HHS / ES / P42 ES004705-190023; United States / NIEHS NIH HHS / ES / R01 ES009137-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS220398; NLM/ PMC3257312
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74. Schmiegelow K, Vestergaard T, Nielsen SM, Hjalgrim H: Etiology of common childhood acute lymphoblastic leukemia: the adrenal hypothesis. Leukemia; 2008 Dec;22(12):2137-41
Hazardous Substances Data Bank. HYDROCORTISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Etiology of common childhood acute lymphoblastic leukemia: the adrenal hypothesis.
  • The pattern of infections in the first years of life modulates our immune system, and a low incidence of infections has been linked to an increased risk of common childhood acute lymphoblastic leukemia (ALL).
  • We here present a new interpretation of these observations--the adrenal hypothesis--that proposes that the risk of childhood ALL is reduced when early childhood infections induce qualitative and quantitative changes in the hypothalamus-pituitary-adrenal axis that increase plasma cortisol levels.
  • [MeSH-major] Hypothalamo-Hypophyseal System / immunology. Infection / immunology. Pituitary-Adrenal System / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • (PMID = 18719616.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 50
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75. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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76. Lazić J, Dokmanović L, Krstovski N, Predojević J, Tosić N, Pavlović S, Janić D: [Immunoglobulin genes and T-cell receptors as molecular markers in children with acute lymphoblastic leukaemia]. Srp Arh Celok Lek; 2009 Jul-Aug;137(7-8):384-90

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Immunoglobulin genes and T-cell receptors as molecular markers in children with acute lymphoblastic leukaemia].
  • INTRODUCTION: Acute lymphoblastic leukaemia (ALL) is a malignant clonal disease, one of the most common malignancies in childhood.
  • [MeSH-major] Gene Rearrangement. Immunoglobulin Heavy Chains / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell / genetics

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  • (PMID = 19764592.001).
  • [ISSN] 0370-8179
  • [Journal-full-title] Srpski arhiv za celokupno lekarstvo
  • [ISO-abbreviation] Srp Arh Celok Lek
  • [Language] srp
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Serbia
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Receptors, Antigen, T-Cell
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77. Aricó M, Baruchel A, Bertrand Y, Biondi A, Conter V, Eden T, Gadner H, Gaynon P, Horibe K, Hunger SP, Janka-Schaub G, Masera G, Nachman J, Pieters R, Schrappe M, Schmiegelow K, Valsecchi MG, Pui CH: The seventh international childhood acute lymphoblastic leukemia workshop report: Palermo, Italy, January 29--30, 2005. Leukemia; 2005 Jul;19(7):1145-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The seventh international childhood acute lymphoblastic leukemia workshop report: Palermo, Italy, January 29--30, 2005.
  • Between 1995 and 2004, six International Childhood Acute Lymphoblastic Leukemia (ALL) Workshop have been held, and the completion of several collaborative projects has established the clinical relevance and treatment options for several specific genetic subtypes of ALL.
  • [MeSH-major] Neoplasm, Residual / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15902295.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-29139; United States / NCI NIH HHS / CA / CA-31566; United States / NCI NIH HHS / CA / CA-37379; United States / NCI NIH HHS / CA / CA-51001; United States / NCI NIH HHS / CA / CA-78824; United States / NIGMS NIH HHS / GM / GM-61393; United States / NIGMS NIH HHS / GM / GM61374
  • [Publication-type] Congresses; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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78. Trehan A, Cheetham T, Bailey S: Hypercalcemia in acute lymphoblastic leukemia: an overview. J Pediatr Hematol Oncol; 2009 Jun;31(6):424-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypercalcemia in acute lymphoblastic leukemia: an overview.
  • It is an uncommon albeit well recognized biochemical feature of childhood malignancies including acute leukemia.
  • Most of the children presenting with acute lymphoblastic leukemia and hypercalcemia tend to be in older age groups and have an absence of blasts in the peripheral blood film.
  • [MeSH-major] Hypercalcemia / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • (PMID = 19648791.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 29
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79. Joseph T, Kusumakumary P, Chacko P, Abraham A, Pillai MR: DNA repair gene XRCC1 polymorphisms in childhood acute lymphoblastic leukemia. Cancer Lett; 2005 Jan 10;217(1):17-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA repair gene XRCC1 polymorphisms in childhood acute lymphoblastic leukemia.
  • Genetic polymorphisms in XRCC1 gene could, through alteration of protein structure, lead to defective functioning of DNA Polbeta, PARP and LIG3 enzymes resulting in defective DNA repair and increased risk of childhood acute lymphoblastic leukemia (ALL).
  • The role of DNA repair gene XRCC1 in susceptibility to childhood ALL has, however, not been widely studied and no data exists from Indian children.
  • [MeSH-major] DNA-Binding Proteins / genetics. Genetic Predisposition to Disease. Polymorphism, Restriction Fragment Length. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15596292.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / X-ray repair cross complementing protein 1
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80. Novara F, Beri S, Bernardo ME, Bellazzi R, Malovini A, Ciccone R, Cometa AM, Locatelli F, Giorda R, Zuffardi O: Different molecular mechanisms causing 9p21 deletions in acute lymphoblastic leukemia of childhood. Hum Genet; 2009 Oct;126(4):511-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Different molecular mechanisms causing 9p21 deletions in acute lymphoblastic leukemia of childhood.
  • Deletion of chromosome 9p21 is a crucial event for the development of several cancers including acute lymphoblastic leukemia (ALL).
  • We have cloned 23 breakpoint junctions for a total of 46 breakpoints in 17 childhood ALL (9 B- and 8 T-lineages) showing different size deletions at one or both homologous chromosomes 9 to investigate which particular sequences make the region susceptible to interstitial deletion.
  • [MeSH-major] Chromosomes, Human, Pair 9 / genetics. Cyclin-Dependent Kinase Inhibitor p15 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Sequence Deletion / genetics

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  • [Cites] Oncogene. 2003 Jun 12;22(24):3792-8 [12802286.001]
  • [Cites] Nat Genet. 2009 Apr;41(4):385-6 [19338077.001]
  • [Cites] Proc Natl Acad Sci U S A. 1971 Apr;68(4):820-3 [5279523.001]
  • [Cites] Genes Dev. 1989 Jul;3(7):1053-61 [2777075.001]
  • [Cites] Mol Cell Biol. 1989 Jul;9(7):3049-57 [2550794.001]
  • [Cites] Med Pediatr Oncol. 1992;20(6):497-505 [1435520.001]
  • [Cites] Mol Cell Biol. 1993 Feb;13(2):1078-92 [8380891.001]
  • [Cites] J Immunol. 1994 Nov 15;153(10):4520-9 [7963524.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jun 11;93(12):6203-8 [8650244.001]
  • [Cites] Blood. 1997 Nov 1;90(9):3720-6 [9345058.001]
  • [Cites] Leukemia. 1998 Jun;12(6):845-59 [9639410.001]
  • [Cites] Biochim Biophys Acta. 1998 Oct 14;1378(2):F115-77 [9823374.001]
  • [Cites] Am J Pathol. 1999 Jul;155(1):105-13 [10393843.001]
  • [Cites] Carcinogenesis. 1999 Aug;20(8):1403-10 [10426784.001]
  • [Cites] J Biol Chem. 2004 Nov 12;279(46):47411-4 [15326170.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3053-8 [15833833.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Sep;7(9):667-77 [16921403.001]
  • [Cites] DNA Repair (Amst). 2006 Sep 8;5(9-10):1273-81 [16931177.001]
  • [Cites] Br J Dermatol. 2006 Nov;155(5):999-1005 [17034532.001]
  • [Cites] Trends Biochem Sci. 2007 Jun;32(6):271-8 [17493823.001]
  • [Cites] Oncogene. 2007 Jun 21;26(29):4306-18 [17237825.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jun 26;104(26):10950-5 [17573529.001]
  • [Cites] Lancet. 2007 Jul 21;370(9583):240-50 [17658395.001]
  • [Cites] Genome Res. 2007 Sep;17(9):1296-303 [17675364.001]
  • [Cites] Hum Mol Genet. 2007 Dec 1;16(23):2783-94 [17666407.001]
  • [Cites] Nat Genet. 2008 Jan;40(1):90-5 [18059269.001]
  • [Cites] Leukemia. 1999 Dec;13(12):1901-28 [10602411.001]
  • [Cites] Nat Rev Cancer. 2001 Nov;1(2):157-62 [11905807.001]
  • [Cites] J Biol Chem. 2002 Nov 29;277(48):46289-97 [12228235.001]
  • [Cites] Genes Chromosomes Cancer. 2003 May;37(1):44-57 [12661005.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Jun;37(2):141-8 [12696062.001]
  • [Cites] Am J Hum Genet. 2008 Mar;82(3):763-71 [18304490.001]
  • [Cites] Leuk Res. 2008 Aug;32(8):1228-35 [18328560.001]
  • [Cites] Nat Genet. 2008 Oct;40(10):1199-203 [18776910.001]
  • [Cites] Genes Chromosomes Cancer. 2009 Jan;48(1):22-38 [18803328.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Nov 11;105(45):17453-6 [18988746.001]
  • [Cites] PLoS Biol. 2009 Feb 17;7(2):e36 [19226189.001]
  • [Cites] Nat Genet. 2009 Apr;41(4):446-9 [19287382.001]
  • [Cites] Nat Genet. 2009 Apr;41(4):455-9 [19287384.001]
  • [Cites] Nat Genet. 2009 Apr;41(4):450-4 [19287385.001]
  • [Cites] Nat Genet. 2004 Sep;36(9):949-51 [15286789.001]
  • (PMID = 19484265.001).
  • [ISSN] 1432-1203
  • [Journal-full-title] Human genetics
  • [ISO-abbreviation] Hum. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / CDKN2B protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA Primers
  • [Other-IDs] NLM/ PMC2762534
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81. Pui CH, Campana D, Pei D, Bowman WP, Sandlund JT, Kaste SC, Ribeiro RC, Rubnitz JE, Raimondi SC, Onciu M, Coustan-Smith E, Kun LE, Jeha S, Cheng C, Howard SC, Simmons V, Bayles A, Metzger ML, Boyett JM, Leung W, Handgretinger R, Downing JR, Evans WE, Relling MV: Treating childhood acute lymphoblastic leukemia without cranial irradiation. N Engl J Med; 2009 Jun 25;360(26):2730-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treating childhood acute lymphoblastic leukemia without cranial irradiation.
  • BACKGROUND: Prophylactic cranial irradiation has been a standard treatment in children with acute lymphoblastic leukemia (ALL) who are at high risk for central nervous system (CNS) relapse.
  • CNS leukemia (CNS-3 status) or a traumatic lumbar puncture with blast cells at diagnosis and a high level of minimal residual disease (> or = 1%) after 6 weeks of remission induction were significantly associated with poorer event-free survival.
  • Risk factors for CNS relapse included the genetic abnormality t(1;19)(TCF3-PBX1), any CNS involvement at diagnosis, and T-cell immunophenotype.
  • CONCLUSIONS: With effective risk-adjusted chemotherapy, prophylactic cranial irradiation can be safely omitted from the treatment of childhood ALL. (ClinicalTrials.gov number, NCT00137111. )
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] 6-Mercaptopurine / administration & dosage. Adolescent. Asparaginase / administration & dosage. Asparaginase / adverse effects. Central Nervous System Neoplasms / drug therapy. Child. Child, Preschool. Combined Modality Therapy. Cranial Irradiation. Cyclophosphamide / administration & dosage. Daunorubicin / administration & dosage. Dexamethasone / administration & dosage. Hematopoietic Stem Cell Transplantation. Humans. Infant. Methotrexate / adverse effects. Remission Induction / methods. Risk Factors. Secondary Prevention. Survival Analysis. Treatment Outcome. Vincristine / administration & dosage

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  • [Copyright] 2009 Massachusetts Medical Society
  • [Cites] Leukemia. 2002 Jun;16(6):1099-111 [12040440.001]
  • [Cites] JAMA. 2002 Oct 23-30;288(16):2001-7 [12387652.001]
  • [Cites] J Natl Cancer Inst. 2008 Sep 17;100(18):1301-9 [18780868.001]
  • [Cites] J Clin Oncol. 2003 Jan 15;21(2):184-8 [12525508.001]
  • [Cites] Blood. 2003 May 15;101(10):3809-17 [12531809.001]
  • [Cites] N Engl J Med. 2003 Aug 14;349(7):640-9 [12917300.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2736-40 [12843002.001]
  • [Cites] JAMA. 2003 Oct 15;290(15):2001-7 [14559953.001]
  • [Cites] Br J Haematol. 2004 Jan;124(1):33-46 [14675406.001]
  • [Cites] Leukemia. 2004 May;18(5):934-8 [15029212.001]
  • [Cites] Nature. 2004 May 27;429(6990):464-8 [15164072.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2690-6 [15251979.001]
  • [Cites] N Engl J Med. 1993 Jul 29;329(5):314-9 [8321259.001]
  • [Cites] J Clin Oncol. 1995 Jan;13(1):177-9 [7799017.001]
  • [Cites] J Clin Oncol. 1997 Aug;15(8):2786-91 [9256120.001]
  • [Cites] N Engl J Med. 1998 Feb 19;338(8):499-505 [9468466.001]
  • [Cites] Blood. 1998 Jul 15;92(2):411-5 [9657739.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3310-22 [10828010.001]
  • [Cites] Leukemia. 2000 Aug;14(8):1354-61 [10942229.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2691-6 [11023499.001]
  • [Cites] Blood. 2000 Nov 15;96(10):3381-4 [11071631.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2196-204 [11187911.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2223-33 [11187913.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2257-66 [11187917.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2267-75 [11187918.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2286-94 [11187920.001]
  • [Cites] Cancer Chemother Pharmacol. 2001 Sep;48(3):235-40 [11592346.001]
  • [Cites] Blood. 2002 Feb 1;99(3):825-33 [11806983.001]
  • [Cites] Blood. 2002 Apr 15;99(8):2734-9 [11929760.001]
  • [Cites] N Engl J Med. 1998 Aug 27;339(9):605-15 [9718381.001]
  • [Cites] Blood. 1999 May 1;93(9):2817-23 [10216075.001]
  • [Cites] J Clin Invest. 2005 Jan;115(1):110-7 [15630450.001]
  • [Cites] Br J Haematol. 2005 Jun;129(6):734-45 [15952999.001]
  • [Cites] J Clin Oncol. 2005 Oct 1;23(28):7161-7 [16192600.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] J Clin Oncol. 2006 May 20;24(15):2332-6 [16710032.001]
  • [Cites] J Clin Oncol. 2006 Jul 1;24(19):3142-9 [16809737.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1165-73 [16609069.001]
  • [Cites] N Engl J Med. 2006 Oct 12;355(15):1572-82 [17035650.001]
  • [Cites] Blood. 2007 Feb 1;109(3):896-904 [17003366.001]
  • [Cites] JAMA. 2007 Mar 21;297(11):1207-15 [17374815.001]
  • [Cites] Blood. 2007 May 15;109(10):4151-7 [17264302.001]
  • [Cites] JAMA. 2007 Jun 27;297(24):2705-15 [17595271.001]
  • [Cites] J Clin Oncol. 2007 Nov 1;25(31):4914-21 [17971588.001]
  • [Cites] Blood. 2007 Dec 1;110(12):4022-9 [17720883.001]
  • [Cites] Lancet Oncol. 2008 Mar;9(3):257-68 [18308251.001]
  • [Cites] J Clin Oncol. 2008 Apr 20;26(12):1932-9 [18421047.001]
  • [Cites] Blood. 2008 May 1;111(9):4477-89 [18285545.001]
  • [CommentIn] N Engl J Med. 2009 Sep 24;361(13):1310; author reply 1311-2 [19776415.001]
  • [CommentIn] N Engl J Med. 2009 Sep 24;361(13):1310-1; author reply 1311-2 [19780213.001]
  • (PMID = 19553647.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00137111
  • [Grant] United States / NIGMS NIH HHS / GM / U01 GM061393; United States / NCI NIH HHS / CA / R01 CA078224; United States / NCI NIH HHS / CA / R37 CA036401; United States / NCI NIH HHS / CA / CA36401; United States / NCI NIH HHS / CA / R01 CA051001-13; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA78224; United States / NCI NIH HHS / CA / R01 CA060419; United States / NCI NIH HHS / CA / CA60419; United States / NIGMS NIH HHS / GM / GM61393; United States / NCI NIH HHS / CA / P30 CA021765; United States / NIGMS NIH HHS / GM / U01 GM061393-090007; United States / NCI NIH HHS / CA / R01 CA051001; United States / NCI NIH HHS / CA / R01 CA036401; United States / NCI NIH HHS / CA / CA51001; United States / NCI NIH HHS / CA / U01 CA060419
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 8N3DW7272P / Cyclophosphamide; E7WED276I5 / 6-Mercaptopurine; EC 3.5.1.1 / Asparaginase; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ NIHMS118392; NLM/ PMC2754320
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82. Kawahara I, Masui K, Horie N, Matsuo T, Kitagawa N, Tsutsumi K, Nagata I, Morikawa M, Hayashi T: Radiation-induced meningioma following prophylactic radiotherapy for acute lymphoblastic leukemia in childhood. Pediatr Neurosurg; 2007;43(1):36-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radiation-induced meningioma following prophylactic radiotherapy for acute lymphoblastic leukemia in childhood.
  • BACKGROUND: Acute lymphoblastic leukemia (ALL) is the most common childhood malignancy.
  • CONCLUSION: Long-term survivors who received radiotherapy for ALL in childhood are at risk for late complications, including radiation-induced meningioma.
  • [MeSH-major] Meningeal Neoplasms / diagnosis. Meningeal Neoplasms / etiology. Meningioma / diagnosis. Meningioma / etiology. Neoplasms, Radiation-Induced / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy


83. Schotte D, Chau JC, Sylvester G, Liu G, Chen C, van der Velden VH, Broekhuis MJ, Peters TC, Pieters R, den Boer ML: Identification of new microRNA genes and aberrant microRNA profiles in childhood acute lymphoblastic leukemia. Leukemia; 2009 Feb;23(2):313-22
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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 new microRNA genes and aberrant microRNA profiles in childhood acute lymphoblastic leukemia.
  • To identify miRNAs relevant to pediatric acute lymphoblastic leukemia (ALL), we cloned 105 known and 8 new miRNA genes expressed in patients' leukemia cells.
  • Eight miRNAs were differentially expressed between MLL and non-MLL precursor B-ALL cases (P<0.05).
  • Most remarkably, miR-708 was 250- up to 6500-fold higher expressed in 57 TEL-AML1, BCR-ABL, E2A-PBX1, hyperdiploid and B-other cases than in 20 MLL-rearranged and 15 T-ALL cases (0.0001<P<0.01), whereas the expression of miR-196b was 500-fold higher in MLL-rearranged and 800-fold higher in 5 of 15 T-ALL cases as compared with the expression level in the remaining precursor B-ALL cases (P<0.001).
  • The expression did not correlate with the maturation status of leukemia cells based on immunoglobulin and T-cell receptor rearrangements, immunophenotype or MLL-fusion partner.
  • [MeSH-major] MicroRNAs / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA, Neoplasm / genetics
  • [MeSH-minor] Cloning, Molecular. Gene Expression Regulation, Neoplastic. Humans. Infant. Infant, Newborn. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 18923441.001).
  • [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 / MicroRNAs; 0 / RNA, Neoplasm; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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84. Goshen Y, Stark B, Kornreich L, Michowiz S, Feinmesser M, Yaniv I: High incidence of meningioma in cranial irradiated survivors of childhood acute lymphoblastic leukemia. Pediatr Blood Cancer; 2007 Sep;49(3):294-7
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  • [Title] High incidence of meningioma in cranial irradiated survivors of childhood acute lymphoblastic leukemia.
  • BACKGROUND: Most survivors of childhood acute lymphoblastic leukemia (ALL) and T-cell lymphoma (T-NHL) treated before 1990 received cranial radiation.
  • Only one low-grade glioma and two basal-cell carcinomas were found.
  • CONCLUSIONS: Survivors of childhood ALL treated with cranial radiation require prolonged surveillance because of a high incidence of late meningiomas.
  • [MeSH-major] Cranial Irradiation / adverse effects. Meningeal Neoplasms / epidemiology. Meningioma / epidemiology. Neoplasms, Radiation-Induced / epidemiology. Neoplasms, Second Primary / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy


85. Xue TY, Xu W, An Q, Wu Y, Xu CP, Zhang XY: [Expression of nuclear transcription factor kappaB in childhood acute lymphoblastic leukemia and its significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Aug;15(4):767-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of nuclear transcription factor kappaB in childhood acute lymphoblastic leukemia and its significance].
  • To investigate the expression of nuclear transcription factor kappaB (NF-kappaB) in childhood acute lymphoblastic leukemia (ALL) and its significance, the biotin-streptavidin method and microscopy were used to detect NF-kappaB P65 protein in cells from 32 childhood ALL patients and 40 children without hematologic malignancies as control.
  • The results showed that the positive expression rate of NF-kappaB P65 protein in cells from 32 childhood ALL patients was 87.50%, obviously higher than that in control group (12.50%) (chi(2) = 40.56, p < 0.01).
  • In 28 childhood ALL patients with positive expression, the ratio of weakly positive (+) cases to all positive cases was 10.71% (3/28); the ratio of generally positive (++) case was 42.86% (12/28), and the ratio of strongly positive (+++) cases was 46.43% (13/28).
  • It is concluded that NF-kappaB P65 protein expresses in cells of childhood ALL, the inhibition of NF-kappaB transduction pathway may have significant value in childhood ALL treatment.

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  • (PMID = 17708800.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Transcription Factor RelA
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86. Hu RH, Lu Y, Li QH, Ma L, Li B, Zhu XF, Wang JX, Pang TX: [Relationship between midkine expression and drug efflux in childhood acute lymphoblastic leukemia cells]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Dec;17(6):1502-6
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  • [Title] [Relationship between midkine expression and drug efflux in childhood acute lymphoblastic leukemia cells].
  • This study was aimed to investigate the expression of midkine gene in childhood acute lymphoblastic leukemia patients (ALL) and to explore the possible effects of midkine gene on the chemotherapeutic drug efflux.
  • The rhodamine 123 efflux test revealed that MFI in the leukemia cells was obviously lower than that in normal cells (p < 0.01), furthermore, there was an evident negative correlation between the MFI and MK mRNA expression (r = -0.869, p < 0.001).
  • It is concluded that there is powerful drug efflux ability in lymphoblastic leukemia cells with high midkine gene expression.

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  • (PMID = 20030935.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / MDK protein, human; 0 / Nerve Growth Factors; 0 / RNA, Messenger
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87. Yamamoto T, Isomura M, Xu Y, Liang J, Yagasaki H, Kamachi Y, Kudo K, Kiyoi H, Naoe T, Kojma S: PTPN11, RAS and FLT3 mutations in childhood acute lymphoblastic leukemia. Leuk Res; 2006 Sep;30(9):1085-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PTPN11, RAS and FLT3 mutations in childhood acute lymphoblastic leukemia.
  • Recently, PTPN11 mutations have been reported in children with acute lymphoblastic leukemia (ALL).
  • We observed exon 3 and 8 missense mutations of PTPN11 in 6 children with B precursor ALL.
  • These data suggest that PTPN11 mutation may play an important role for leukemogenesis in a proportion of children with ALL, particularly B precursor ALL.
  • [MeSH-major] Burkitt Lymphoma / genetics. Intracellular Signaling Peptides and Proteins / genetics. Mutation, Missense. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Protein Tyrosine Phosphatases / genetics. fms-Like Tyrosine Kinase 3 / genetics. ras Proteins / genetics

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  • (PMID = 16533526.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.6.5.2 / ras Proteins
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88. Schmiegelow K, Forestier E, Hellebostad M, Heyman M, Kristinsson J, Söderhäll S, Taskinen M, Nordic Society of Paediatric Haematology and Oncology: Long-term results of NOPHO ALL-92 and ALL-2000 studies of childhood acute lymphoblastic leukemia. Leukemia; 2010 Feb;24(2):345-54
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  • [Title] Long-term results of NOPHO ALL-92 and ALL-2000 studies of childhood acute lymphoblastic leukemia.
  • Analysis of 2668 children with acute lymphoblastic leukemia (ALL) treated in two successive Nordic clinical trials (Nordic Society of Paediatric Haematology and Oncology (NOPHO) ALL-92 and ALL-2000) showed that 75% of all patients are cured by first-line therapy, and 83% are long-term survivors.
  • Improved risk stratification and chemotherapy have eliminated the previous independent prognostic significance of gender, CNS leukemia and translocation t(1;19)(q23;p13), whereas the post-induction level of minimal residual disease (MRD) has emerged as a new risk grouping feature.
  • Infant leukemia, high leukocyte count, T-lineage immunophenotype, translocation t(4;11)(q21;q23) and hypodiploidy persist to be associated with lower cure rates.
  • To reduce the overall toxicity of the treatment, including the risk of therapy-related second malignant neoplasms, the current NOPHO ALL-2008 protocol does not include CNS irradiation in first remission, the dose of 6-mercaptopurine is reduced for patients with low thiopurine methyltransferase activity, and the protocol restricts the use of hematopoietic stem cell transplantation in first remission to patients without morphological remission after induction therapy or with high levels of MRD after 3 months of therapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Chromosome Aberrations. Combined Modality Therapy. Cranial Irradiation. Female. Follow-Up Studies. Hematopoietic Stem Cell Transplantation. Humans. Immunophenotyping. Infant. Infant, Newborn. Male. Prognosis. Remission Induction. Risk Factors. Survival Rate. Time Factors. Treatment Outcome


89. Bandyopadhyay S, Bhattacharyya A, Mallick A, Sen AK, Tripathi G, Das T, Sa G, Bhattacharya DK, Mandal C: Over-expressed IgG2 antibodies against O-acetylated sialoglycoconjugates incapable of proper effector functioning in childhood acute lymphoblastic leukemia. Int Immunol; 2005 Feb;17(2):177-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Over-expressed IgG2 antibodies against O-acetylated sialoglycoconjugates incapable of proper effector functioning in childhood acute lymphoblastic leukemia.
  • Earlier studies have demonstrated an over-expression of 9-O-acetylated sialoglycoconjugates (9-OAcSGs) on lymphoblasts, concomitant with high titers of anti-9-OAcSGs in childhood acute lymphoblastic leukemia (ALL).
  • Enhanced amount of 9-OAcSA-specific IgG2 induced in ALL was unable to trigger activation of FcgammaR, the complement cascade and cell-mediated cytotoxicity, although its glycotope-binding ability remains unaffected.
  • Interestingly, only IgG1N emerged as the potent mediator of cell-mediated cytotoxicity, complement fixation and activator of effector cells through FcgammaR.
  • [MeSH-major] Glycoconjugates / immunology. Immunoglobulin G / blood. Immunoglobulin G / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Sialic Acids / immunology

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  • (PMID = 15629900.001).
  • [ISSN] 0953-8178
  • [Journal-full-title] International immunology
  • [ISO-abbreviation] Int. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glycoconjugates; 0 / Immunoglobulin G; 0 / Receptors, Fc; 0 / Sialic Acids
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90. Hegedus CM, Gunn L, Skibola CF, Zhang L, Shiao R, Fu S, Dalmasso EA, Metayer C, Dahl GV, Buffler PA, Smith MT: Proteomic analysis of childhood leukemia. Leukemia; 2005 Oct;19(10):1713-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Proteomic analysis of childhood leukemia.
  • Childhood acute lymphoblastic and myeloid leukemias are stratified into molecular and cytogenetic subgroups important for prognosis and therapy.
  • Studies have shown that gene expression profiles can discriminate between leukemia subtypes.
  • Thus, proteome analysis similarly holds the potential for characterizing different subtypes of childhood leukemia.
  • We used surface-enhanced laser desorption/ionization time-of-flight mass spectrometry to analyze cell lysates from childhood leukemia cell lines as well as pretreatment leukemic bone marrow derived from childhood leukemia cases.
  • Comparison of the acute myeloid leukemia (AML) cell line, Kasumi, and the biphenotypic myelomonocytic cell line, MV4;11, with the acute lymphoblastic leukemia (ALL) cell lines, 697 and REH, revealed many differentially expressed proteins.
  • Analysis of childhood leukemia bone marrow showed differentially expressed proteins between AML and ALL, including a similar peak at 8.3 kDa, as well as several proteins that differentiate between the ALL t(12;21) and hyperdiploid subtypes.
  • These results demonstrate the potential for proteome analysis to distinguish between various forms of childhood leukemia.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Leukemia, Myeloid / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proteomics
  • [MeSH-minor] Acute Disease. Adolescent. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Child. Humans. Peptide Mapping. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

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  • (PMID = 16136170.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NIEHS NIH HHS / ES / P30 ES01896; United States / NIEHS NIH HHS / ES / P42ES04705; United States / NIEHS NIH HHS / ES / R01 ES09137
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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91. Wang YR, Jin RM, Xu JW, Xiao Y, Zhou DF, Zhang ZQ: Therapeutic effectiveness of the ALL-XH-99 protocol for childhood acute lymphoblastic leukemia. Zhongguo Dang Dai Er Ke Za Zhi; 2008 Feb;10(1):1-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapeutic effectiveness of the ALL-XH-99 protocol for childhood acute lymphoblastic leukemia.
  • OBJECTIVE: The ALL-XH-99 protocol for the treatment of childhood acute lymphoblastic leukemia (ALL) has been performed in the Union Hospital for 10 years.
  • This study aimed to evaluate the therapeutic effectiveness of the protocol for childhood ALL and to investigate the prognostic factors for childhood ALL.
  • Prognostic factors for childhood ALL were investigated by the stepwise Cox proportional hazard model.
  • Without administering cranial irradiation to all of the patients, the incidence of CNS leukemia relapse (2/115, 1.7%) was not higher than that previously reported.
  • Multivariate analysis showed that the risk degree of leukemia, the presence of t (9; 22)/bcr/abl fusion gene and leukocyte count were independent adverse prognostic factors for ALL and their hazard ratio was 1.867, 3.397 and 2.236 respectively.
  • CONCLUSIONS: The therapeutic effectiveness of the ALL-XH-99 protocol for childhood ALL is satisfactory, with an EFS rate comparable to that of the developed countries. t (9; 22)/bcr/abl is the most important adverse independent prognostic factor for childhood ALL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 18289459.001).
  • [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] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
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92. He J, Chen ZX, Xue YQ, Li JQ, He HL, Huang YP, He YX, Chai YH, Zhu LL: [Detection of fusion genes resulting from chromosome abnormalities in childhood acute lymphoblastic leukemia]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2005 Oct;22(5):551-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Detection of fusion genes resulting from chromosome abnormalities in childhood acute lymphoblastic leukemia].
  • OBJECTIVE: To detect the expression of the fusion genes resulting from chromosome abnormalities in childhood acute lymphoblastic leukemia(ALL) and its conformity to WHO classification.
  • The multiplex RT-PCR in combination with chromosome analysis revealed genetic abnormalities in 69.4%(43/62) of childhood ALL.
  • CONCLUSION: Multiplex RT-PCR combined with chromosome analysis and immunophenotyping can provide reliable and helpful information for the diagnosis, therapy evaluation and prognosis prediction in childhood ALL, which may also serve as a basis on which to implement the criteria of WHO classification.
  • [MeSH-major] Chromosome Aberrations. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit / genetics. Core Binding Factor Alpha 2 Subunit / metabolism. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Flow Cytometry. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Immunophenotyping. Infant. Karyotyping. Myeloid-Lymphoid Leukemia Protein / genetics. Myeloid-Lymphoid Leukemia Protein / metabolism. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. RNA-Binding Protein FUS / genetics. RNA-Binding Protein FUS / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transcription Factors / genetics. Transcription Factors / metabolism

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  • (PMID = 16215946.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / E2a-Hlf fusion protein, human; 0 / Homeodomain Proteins; 0 / MLL-AF10 fusion protein, human; 0 / MLL-AF4 fusion protein, human; 0 / MLL-AF9 fusion protein, human; 0 / MLL-ELL fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RNA-Binding Protein FUS; 0 / TEL-AML1 fusion protein; 0 / TLS-ERG fusion protein, human; 0 / Transcription Factors; 143275-75-6 / TLX1 protein, human; 146150-85-8 / E2A-Pbx1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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93. Badell I, Muñoz A, Estella J, Fernández-Delgado R, Javier G, Verdeguer A, Cubells J, SHOP Leukemia and Lymphoma Studies Committee (Spanish Societies of Pediatric Hematology and Pediatric Oncology): Long-term results of two consecutive trials in childhood acute lymphoblastic leukaemia performed by the Spanish Cooperative Group for Childhood Acute Lymphoblastic Leukemia Group (SHOP) from 1989 to 1998. Clin Transl Oncol; 2008 Feb;10(2):117-24
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  • [Title] Long-term results of two consecutive trials in childhood acute lymphoblastic leukaemia performed by the Spanish Cooperative Group for Childhood Acute Lymphoblastic Leukemia Group (SHOP) from 1989 to 1998.
  • INTRODUCTION: The first multi-centric protocol for childhood acute lymphoblastic leukaemia (ALL) treatment in Spain started in 1989 and was conducted by the Spanish Pediatric Hematology and Oncology Societies.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Combined Modality Therapy. Cranial Irradiation. Disease-Free Survival. Hematopoietic Stem Cell Transplantation. Humans. Infant. Kaplan-Meier Estimate. Time. Transplantation, Autologous. Treatment Outcome

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  • (PMID = 18258511.001).
  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] Spain
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94. Bernaldez-Rios R, Ortega-Alvarez MC, Perez-Saldivar ML, Alatoma-Medina NE, Del Campo-Martinez Mde L, Rodriguez-Zepeda Mdel C, Montero-Ponce I, Franco-Ornelas S, Fernandez-Castillo G, Nuñez-Villegas NN, Taboada-Flores MA, Flores-Lujano J, Argüelles-Sanchez ME, Juarez-Ocaña S, Fajardo-Gutierrez A, Mejia-Arangure JM: The age incidence of childhood B-cell precursor acute lymphoblastic leukemia in Mexico City. J Pediatr Hematol Oncol; 2008 Mar;30(3):199-203
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The age incidence of childhood B-cell precursor acute lymphoblastic leukemia in Mexico City.
  • The objective of this population-based survey was to assess the peak age of incidence of B-cell precursor acute lymphoblastic leukemia (ALL) in children in Mexico City (MC).
  • All patients were classified according to their immunophenotype, and only B-cell precursor and T-lineage were analyzed.
  • The frequency of B-cell precursor ALL was 76.1%, whereas T lineage ALL showed a frequency of 23.6%.
  • B-cell precursor ALL was the major contributor to peak age; T lineage ALL showed a peak among 1 and 3 years of age.
  • We conclude that the age peak for children with ALL in MC is within the ranges reported for developed countries and that B-cell precursor ALL is the main contributor to these peak.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

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  • (PMID = 18376281.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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95. Urayama KY, Wiencke JK, Buffler PA, Chokkalingam AP, Metayer C, Wiemels JL: MDR1 gene variants, indoor insecticide exposure, and the risk of childhood acute lymphoblastic leukemia. Cancer Epidemiol Biomarkers Prev; 2007 Jun;16(6):1172-7
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  • [Title] MDR1 gene variants, indoor insecticide exposure, and the risk of childhood acute lymphoblastic leukemia.
  • Among children enrolled in the Northern California Childhood Leukemia Study, we examined the susceptibility conferred by MDR1 single nucleotide polymorphisms (SNP) and predicted haplotypes and whether they modify the association between indoor insecticide exposure and risk of childhood acute lymphoblastic leukemia (ALL).
  • METHODS: Buccal cell DNA from ALL cases (n = 294) and controls (n = 369) individually matched on gender, date of birth, Hispanic status, and maternal race were whole genome amplified and genotyped for four MDR1 SNPs, T-129C (rs3213619), C1236T (rs1128503), G2677T/A (rs2032582), and C3435T (rs1045642).
  • Overall, the SNPs considered individually or within haplotypes (C1236T-G2677T/A-C3435T) were not significantly associated with childhood ALL.
  • [MeSH-major] Air Pollution, Indoor / adverse effects. Genes, MDR. Insecticides / adverse effects. P-Glycoprotein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17548681.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P42 ES04705; United States / NIEHS NIH HHS / ES / R01 ES09137
  • [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 / Insecticides; 0 / P-Glycoprotein
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96. Ariffin H, Chen SP, Kwok CS, Quah TC, Lin HP, Yeoh AE: Ethnic differences in the frequency of subtypes of childhood acute lymphoblastic leukemia: results of the Malaysia-Singapore Leukemia Study Group. J Pediatr Hematol Oncol; 2007 Jan;29(1):27-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ethnic differences in the frequency of subtypes of childhood acute lymphoblastic leukemia: results of the Malaysia-Singapore Leukemia Study Group.
  • Childhood acute lymphoblastic leukemia (ALL) is clinically heterogeneous with prognostically and biologically distinct subtypes.
  • Although racial differences in frequency of different types of childhood ALL have been reported, many are confounded by selected or limited population samples.
  • The Malaysia-Singapore (MA-SPORE) Leukemia Study Group provided a unique platform for the study of the frequency of major subgroups of childhood ALL in a large cohort of unselected multiethnic Asian children.
  • Our study suggests that there are indeed significant and important racial differences in the frequency of subtypes of childhood ALL.
  • Comprehensive subgrouping of childhood ALL may reveal interesting population frequency differences of the various subtypes, their risk factors and hopefully, its etiology.
  • [MeSH-major] Asian Continental Ancestry Group. Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / ethnology

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  • [CommentIn] J Pediatr Hematol Oncol. 2007 Aug;29(8):585 [17762503.001]
  • (PMID = 17230064.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins
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97. Noble SL, Sherer E, Hannemann RE, Ramkrishna D, Vik T, Rundell AE: Using adaptive model predictive control to customize maintenance therapy chemotherapeutic dosing for childhood acute lymphoblastic leukemia. J Theor Biol; 2010 Jun 7;264(3):990-1002
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Using adaptive model predictive control to customize maintenance therapy chemotherapeutic dosing for childhood acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is a common childhood cancer in which nearly one-quarter of patients experience a disease relapse.
  • However, it has been shown that individualizing therapy for childhood ALL patients by adjusting doses based on the blood concentration of active drug metabolite could significantly improve treatment outcome.
  • An adaptive model predictive control (MPC) strategy is presented in which maintenance therapy for childhood ALL is personalized using routine patient measurements of red blood cell mean corpuscular volume as a surrogate for the active drug metabolite concentration.
  • [MeSH-major] 6-Mercaptopurine / therapeutic use. Dose-Response Relationship, Drug. Models, Biological. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20138060.001).
  • [ISSN] 1095-8541
  • [Journal-full-title] Journal of theoretical biology
  • [ISO-abbreviation] J. Theor. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, American Recovery and Reinvestment Act; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; E7WED276I5 / 6-Mercaptopurine
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98. Hill A, Short MA, Varghese C, Kusumakumary P, Kumari P, Morgan GJ: The t(12:21) is underrepresented in childhood B-lineage acute lymphoblastic leukemia in Kerala, Southern India. Haematologica; 2005 Mar;90(3):414-6
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] The t(12:21) is underrepresented in childhood B-lineage acute lymphoblastic leukemia in Kerala, Southern India.
  • t(12;21) (TEL/AML1) is the most common genetic event in childhood B-cell acute lymphoblastic leukemia (B-ALL) in Western countries.
  • [MeSH-major] Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 21. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Child. Humans. Incidence. India / epidemiology. Leukemia, B-Cell. Molecular Epidemiology

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  • (PMID = 15749681.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] Italy
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99. Lemez P, Attarbaschi A, Béné MC, Bertrand Y, Castoldi G, Forestier E, Garand R, Haas OA, Kagialis-Girard S, Ludwig WD, Matutes E, Mejstríková E, Pages MP, Pickl W, Porwit A, Orfao A, Schabath R, Starý J, Strobl H, Talmant P, van't Veer MB, Zemanová Z, European Group for the Immunological Characterization of Leukemias (EGIL): Childhood near-tetraploid acute lymphoblastic leukemia: an EGIL study on 36 cases. Eur J Haematol; 2010 Oct;85(4):300-8
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Childhood near-tetraploid acute lymphoblastic leukemia: an EGIL study on 36 cases.
  • OBJECTIVES: Patients with near-tetraploid (karyotype: 81 - 103 chromosomes) acute lymphoblastic leukemia (NT-ALL) constitute about 1% of childhood ALL and data reported on them are limited and controversial.
  • Ten children were diagnosed as T-cell ALL (T-ALL) EGIL categories (T-I n=2, T-II n=2, T-III n=3, T-IV n=3) and four displayed various structural chromosomal abnormalities.
  • B-cell precursor (BCP) ALL was diagnosed in 26 children.
  • One girl with hypodiploid and NT metaphases and ETV6-RUNX1-negative BCP-ALL and one of two boys with NT-BCP-ALL not examined for ETV6-RUNX1 died of infection after stem cell transplantation in 2nd/3rd CR.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma

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  • [Copyright] © 2010 John Wiley & Sons A/S.
  • (PMID = 20561032.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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100. Ceppi F, Brown A, Betts DR, Niggli F, Popovic MB: Cytogenetic characterization of childhood acute lymphoblastic leukemia in Nicaragua. Pediatr Blood Cancer; 2009 Dec 15;53(7):1238-41
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] Cytogenetic characterization of childhood acute lymphoblastic leukemia in Nicaragua.
  • BACKGROUND: Within the frame of a twinning programme with Nicaragua, The La Mascota project, we evaluated in our study the contribution of cytogenetic characterization of acute lymphoblastic leukemia (ALL) as prognostic factor compared to clinical, morphological, and immunohistochemical parameters.
  • METHODS: All patients with ALL treated at the only cancer pediatric hospital in Nicaragua during 2006 were studied prospectively.
  • Immunophenotypically 63/66 patients (95%) had a B-precursor, 2 (3%) a T- and 1 (1.5%) a B-mature ALL.
  • [MeSH-major] Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Aneuploidy. Child. Child, Preschool. Chromosome Banding. Core Binding Factor Alpha 2 Subunit / genetics. Female. Fusion Proteins, bcr-abl / genetics. Hepatomegaly / epidemiology. Hepatomegaly / etiology. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Nicaragua / epidemiology. Oncogene Proteins, Fusion / genetics. Prognosis. Prospective Studies. Risk. Splenomegaly / epidemiology. Splenomegaly / etiology

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19672974.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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