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1. Vergara Domínguez B, Cedré Hernández T, Martínez Cárdenas L, López García C, González Seivane F, Pichs León V, Alegret Martínez M, Pérez García S, Courell Martin G, Castro Martínez ME: [Outcome of acute lymphoblastic leukemia in the pediatric age group over a 29-year period (1972-2000)]. An Pediatr (Barc); 2006 Jan;64(1):52-8
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  • [Title] [Outcome of acute lymphoblastic leukemia in the pediatric age group over a 29-year period (1972-2000)].
  • [Transliterated title] Evolución de la leucemia linfoblástica aguda en la edad pediátrica en 29 años (1972-2000).
  • OBJECTIVE: To evaluate the progress achieved in the treatment of acute lymphoblastic leukemia (ALL) in our hospital.
  • Group 2 was treated with less aggressive classical regimens from the 1970s, and groups 3 and 4 received more aggressive regimens, type Berlin-Frankfurt-Munster (BFM).
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality

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  • (PMID = 16539917.001).
  • [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
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2. Babusíková O, Zelezníková T, Mlcáková A, Kusenda J, Stevulová L: The knowledge on the 3rd type hematogones could contribute to more precise detection of small numbers of precursor B-acute lymphoblastic leukemia. Neoplasma; 2005;52(6):502-9
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  • [Title] The knowledge on the 3rd type hematogones could contribute to more precise detection of small numbers of precursor B-acute lymphoblastic leukemia.
  • Bone marrow hematogones were separately assessed as hematogones 1 population of early stage and hematogones 2 of mid-stage precursor B-cells, respectively.
  • In some (about 30%) of hematogones a third type hematogones could be assessed in bone marrow samples.
  • Quantitative immunophenotyping of this study completed the percent antigen expression data in two main hematogone subtypes and lymphocytes in 16 bone marrow specimens and precursor B-ALL lymphoblasts in some samples.
  • Increased information on benign B-lymphocyte precursors, especially that of existence of the 3rd type hematogones could provide a basis for better discrimination of B-leukemia cells even in a very small amounts.

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  • (PMID = 16284697.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antigens, CD
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3. Patel SR, Ortín M, Cohen BJ, Borrow R, Irving D, Sheldon J, Heath PT: Revaccination of children after completion of standard chemotherapy for acute leukemia. Clin Infect Dis; 2007 Mar 1;44(5):635-42
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  • [Title] Revaccination of children after completion of standard chemotherapy for acute leukemia.
  • BACKGROUND: After the treatment of patients with acute leukemia, there is a decrease in vaccine-specific antibody and an increased susceptibility to certain vaccine-preventable diseases.
  • All children received a single dose of Haemophilus influenzae type b (Hib), tetanus, diphtheria, acellular pertussis, meningococcus C, polio, measles, mumps, and rubella vaccines > or = 6 months after completion of treatment.
  • CONCLUSION: Revaccination of children after standard chemotherapy is important, and protection can be achieved in the majority of these children using a simple schedule of 1 vaccine dose at 6 months after completion of leukemia therapy.
  • [MeSH-major] Leukemia, Myeloid / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Vaccines / immunology
  • [MeSH-minor] Acute Disease. Adolescent. Bacterial Capsules. Child. Child, Preschool. Diphtheria Toxoid / administration & dosage. Diphtheria Toxoid / immunology. Haemophilus Vaccines / administration & dosage. Haemophilus Vaccines / immunology. Humans. Immunization Schedule. Immunosuppressive Agents / therapeutic use. Infant. Measles Vaccine / administration & dosage. Measles Vaccine / immunology. Meningococcal Vaccines / administration & dosage. Meningococcal Vaccines / immunology. Mumps Vaccine / administration & dosage. Mumps Vaccine / immunology. Poliovirus Vaccines / administration & dosage. Poliovirus Vaccines / immunology. Polysaccharides, Bacterial / administration & dosage. Polysaccharides, Bacterial / immunology. Rubella Vaccine / administration & dosage. Rubella Vaccine / immunology. Tetanus Toxoid / administration & dosage. Tetanus Toxoid / immunology. Vaccines, Acellular / administration & dosage. Vaccines, Acellular / immunology

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  • [CommentIn] Clin Infect Dis. 2007 Mar 1;44(5):643-5 [17278053.001]
  • (PMID = 17278052.001).
  • [ISSN] 1537-6591
  • [Journal-full-title] Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
  • [ISO-abbreviation] Clin. Infect. Dis.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Diphtheria Toxoid; 0 / Haemophilus Vaccines; 0 / Haemophilus influenzae type b polysaccharide vaccine; 0 / Immunosuppressive Agents; 0 / Measles Vaccine; 0 / Meningococcal Vaccines; 0 / Mumps Vaccine; 0 / Poliovirus Vaccines; 0 / Polysaccharides, Bacterial; 0 / Rubella Vaccine; 0 / Tetanus Toxoid; 0 / Vaccines; 0 / Vaccines, Acellular
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4. Dokmanovic L, Urosevic J, Janic D, Jovanovic N, Petrucev B, Tosic N, Pavlovic S: Analysis of thiopurine S-methyltransferase polymorphism in the population of Serbia and Montenegro and mercaptopurine therapy tolerance in childhood acute lymphoblastic leukemia. Ther Drug Monit; 2006 Dec;28(6):800-6
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  • [Title] Analysis of thiopurine S-methyltransferase polymorphism in the population of Serbia and Montenegro and mercaptopurine therapy tolerance in childhood acute lymphoblastic leukemia.
  • The aim of this study was to determine the frequency and type of TPMT polymorphisms in the population of Serbia and Montenegro and to assess its relevance in the management of childhood acute lymphoblastic leukemia (ALL).
  • In the study of 50 patients with childhood ALL treated according to the BFM-like protocol, it was found that even TPMT-heterozygous patients are at greater risk of thiopurine drug-related leukopenia (mean duration of period when children missed therapy as a result of leukopenia for TPMT-heterozygous patients was 11.3 weeks vs 3.4 weeks for wild-type genotype patients, P < 0.01).
  • [MeSH-major] 6-Mercaptopurine / therapeutic use. Methyltransferases / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17164697.001).
  • [ISSN] 0163-4356
  • [Journal-full-title] Therapeutic drug monitoring
  • [ISO-abbreviation] Ther Drug Monit
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.- / Methyltransferases; EC 2.1.1.67 / thiopurine methyltransferase
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5. Russo V, Scott IU, Querques G, Stella A, Barone A, Delle Noci N: Orbital and ocular manifestations of acute childhood leukemia: clinical and statistical analysis of 180 patients. Eur J Ophthalmol; 2008 Jul-Aug;18(4):619-23
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  • [Title] Orbital and ocular manifestations of acute childhood leukemia: clinical and statistical analysis of 180 patients.
  • PURPOSE: To investigate the association between presence of orbital or ocular lesions and type and stage of leukemia and to investigate whether orbital and ocular lesions are significant in predicting leukemia prognosis.
  • METHODS: The authors evaluated 180 patients with acute childhood leukemia.
  • Lesions associated with leukemia may be classified as specific (due to leukemic infiltration of various ocular tissues), nonspecific (due to one of the secondary complications), or iatrogenic manifestations caused by chemotherapy.
  • RESULTS: Specific lesions were noted in 66% of patients with acute myeloid leukemia (AML) and 11.5% patients with acute lymphocytic leukemia (ALL) (p<0.05), and were more severe in patients with high risk leukemia than in patients with standard risk leukemia.
  • [MeSH-major] Eye Neoplasms / pathology. Leukemia, Myeloid, Acute / pathology. Leukemic Infiltration / pathology. Orbital Neoplasms / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 18609485.001).
  • [ISSN] 1120-6721
  • [Journal-full-title] European journal of ophthalmology
  • [ISO-abbreviation] Eur J Ophthalmol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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6. Ghosh S, Bandyopadhyay S, Mukherjee K, Mallick A, Pal S, Mandal C, Bhattacharya DK, Mandal C: O-acetylation of sialic acids is required for the survival of lymphoblasts in childhood acute lymphoblastic leukemia (ALL). Glycoconj J; 2007 Jan;24(1):17-24
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  • [Title] O-acetylation of sialic acids is required for the survival of lymphoblasts in childhood acute lymphoblastic leukemia (ALL).
  • Exploiting the selective affinity of Achatinin-H towards 9-O-acetylneuraminic acid(alpha2-6)GalNAc, we have demonstrated the presence of 9-O-acetylated sialoglycoproteins (Neu5,9Ac(2)-GPs) on hematopoietic cells of children suffering from acute lymphoblastic leukemia (ALL), indicative of defective sialylation associated with this disease.
  • [MeSH-major] Lymphocytes / metabolism. Lymphocytes / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Sialic Acids / metabolism
  • [MeSH-minor] Acetylation / drug effects. Annexin A5 / metabolism. Caspase 3 / metabolism. Cell Survival / drug effects. Child. Hematopoietic System / cytology. Humans. Lectins / pharmacology. Models, Immunological. Nitric Oxide / biosynthesis. Nitric Oxide Synthase Type II / metabolism. Sialoglycoproteins / chemistry. Signal Transduction / drug effects

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  • (PMID = 17146715.001).
  • [ISSN] 0282-0080
  • [Journal-full-title] Glycoconjugate journal
  • [ISO-abbreviation] Glycoconj. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Lectins; 0 / Sialic Acids; 0 / Sialoglycoproteins; 0 / achatinin(H); 31C4KY9ESH / Nitric Oxide; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 3.4.22.- / Caspase 3
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7. Li YN, Zou DH, Gu M, Zhao YZ, Qi JY, Mi YC, Wang JX, Qiu LG: [Cytogenetic and prognostic analysis in adult patients with Philadelphia chromosome-positive and bcr-abl positive acute lymphoblastic leukaemia]. Zhonghua Xue Ye Xue Za Zhi; 2009 May;30(5):298-302
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  • [Title] [Cytogenetic and prognostic analysis in adult patients with Philadelphia chromosome-positive and bcr-abl positive acute lymphoblastic leukaemia].
  • OBJECTIVE: To analyze the characteristics of cytogenetic aberration of adults with Philadelphia chromosome-positive (Ph+) and/or bcr-abl positive (bcr-abl+) acute lymphoblastic leukaemia (ALL), and investigate its influence on patients' outcomes.
  • The type, distribution and frequency of chromosome aberration were summarized, and compared among different subgroups. RESULTS:.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19799123.001).
  • [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
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
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8. Laux D, Kratz C, Sauerbrey A: Common acute lymphoblastic leukemia in a girl with genetically confirmed LEOPARD syndrome. J Pediatr Hematol Oncol; 2008 Aug;30(8):602-4
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  • [Title] Common acute lymphoblastic leukemia in a girl with genetically confirmed LEOPARD syndrome.
  • Somatic PTPN11 mutations contribute to leukemogenesis in children with hematologic malignancies including juvenile myelomonocytic leukemia, acute lymphoblastic leukemia, acute myeloid leukemia, and myelodysplasia.
  • Two cases of leukemia (acute myeloid leukemia) have been reported in children with LS.
  • The authors describe for the first time a girl with genetically confirmed LEOPARD syndrome presenting with common acute lymphoblastic leukemia.
  • [MeSH-major] LEOPARD Syndrome / complications. LEOPARD Syndrome / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Child. Female. Humans. Mutation, Missense. Protein Tyrosine Phosphatase, Non-Receptor Type 11 / genetics

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  • (PMID = 18799937.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11
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9. Kim IS, Kim HJ, Yoo KH, Sung KW, Kim SH: A boy with acute lymphoblastic leukemia acquired clonal and nonclonal cytogenetic abnormalities including del(7q) and del(20q) without clinical evidence of disease after sex-mismatched cord blood transplantation. J Pediatr Hematol Oncol; 2006 Aug;28(8):540-3
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  • [Title] A boy with acute lymphoblastic leukemia acquired clonal and nonclonal cytogenetic abnormalities including del(7q) and del(20q) without clinical evidence of disease after sex-mismatched cord blood transplantation.
  • An 8-year-old boy was diagnosed with precursor B-cell acute lymphoblastic leukemia.
  • Postcord blood transplantation cytogenetic studies revealed engraftment failure evidenced by switching into the recipient type (XY), and, notably, various complex chromosomal aberrations in the recipient cells.

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  • (PMID = 16912597.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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10. Brouwer C, Vermunt-de Koning DG, Trueworthy RC, Ter Riet PG, Duley JA, Trijbels FJ, Hoogerbrugge PM, Bökkerink JP, van Wering ER, De Abreu RA: Monitoring of inosine monophosphate dehydrogenase activity in mononuclear cells of children with acute lymphoblastic leukemia: enzymological and clinical aspects. Pediatr Blood Cancer; 2006 Apr;46(4):434-8
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  • [Title] Monitoring of inosine monophosphate dehydrogenase activity in mononuclear cells of children with acute lymphoblastic leukemia: enzymological and clinical aspects.
  • IMPDH activities were determined in children who were diagnosed with and treated for acute lymphoblastic leukemia (ALL), and in a group of control children.
  • CONCLUSION: The decrease of IMPDH activity at remission of ALL seems to be at least partly due to the eradication of lymphoblasts with the type 2 isoform of the enzyme.
  • [MeSH-major] IMP Dehydrogenase / metabolism. Leukocytes, Mononuclear / enzymology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology

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  • (PMID = 16333815.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.1.1.205 / IMP Dehydrogenase
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11. Slone TL, Rai R, Ahmad N, Winick NJ: Risk factors for readmission after initial diagnosis in children with acute lymphoblastic leukemia. Pediatr Blood Cancer; 2008 Sep;51(3):375-9
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  • [Title] Risk factors for readmission after initial diagnosis in children with acute lymphoblastic leukemia.
  • BACKGROUND: Specific hospital discharge criteria following the initial diagnosis of children with acute lymphoblastic leukemia (ALL) have not been reported.
  • PROCEDURE: We reviewed the records of 142 consecutive children with newly diagnosed B-precursor ALL and found 129 eligible patients.
  • Chi square, t-test, and multivariate logistic regression analysis were used to compare differences in absolute neutrophil count (ANC), NCI risk status, age, type of corticosteroid administered, and other potential risk factors for readmission during induction therapy.
  • [MeSH-major] Neutrophils / cytology. Patient Readmission. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Predictive Value of Tests

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • [CommentIn] Pediatr Blood Cancer. 2008 Sep;51(3):318-9 [18506756.001]
  • (PMID = 18393271.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / KL2RR024983
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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12. Thomas DA, Faderl S, O'Brien S, Bueso-Ramos C, Cortes J, Garcia-Manero G, Giles FJ, Verstovsek S, Wierda WG, Pierce SA, Shan J, Brandt M, Hagemeister FB, Keating MJ, Cabanillas F, Kantarjian H: Chemoimmunotherapy with hyper-CVAD plus rituximab for the treatment of adult Burkitt and Burkitt-type lymphoma or acute lymphoblastic leukemia. Cancer; 2006 Apr 1;106(7):1569-80
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  • [Title] Chemoimmunotherapy with hyper-CVAD plus rituximab for the treatment of adult Burkitt and Burkitt-type lymphoma or acute lymphoblastic leukemia.
  • BACKGROUND: Adult Burkitt-type lymphoma (BL) and acute lymphoblastic leukemia (B-ALL) are rare entities composing 1% to 5% of non-Hodgkin lymphomas NHL) or ALL.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Burkitt Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


13. Pendino F, Nguyen E, Jonassen I, Dysvik B, Azouz A, Lanotte M, Ségal-Bendirdjian E, Lillehaug JR: Functional involvement of RINF, retinoid-inducible nuclear factor (CXXC5), in normal and tumoral human myelopoiesis. Blood; 2009 Apr 2;113(14):3172-81
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  • Retinoids triggers differentiation of acute promyelocytic leukemia (APL) blasts by transcriptional regulation of myeloid regulatory genes.
  • Using a microarray approach, we have identified a novel retinoid-responsive gene (CXXC5) encoding a nuclear factor, retinoid-inducible nuclear factor (RINF), that contains a CXXC-type zinc-finger motif.
  • Interestingly, RINF localizes to 5q31.3, a small region often deleted in myeloid leukemia (acute myeloid leukemia [AML]/myelodysplasia [MDS]) and suspected to harbor one or several tumor suppressor gene.
  • [MeSH-minor] Amino Acid Sequence. Gene Expression Profiling. Gene Expression Regulation / drug effects. Granulocyte Precursor Cells / drug effects. Granulocyte Precursor Cells / physiology. HL-60 Cells. Humans. K562 Cells. Models, Biological. Molecular Sequence Data. Oligonucleotide Array Sequence Analysis. Sequence Homology, Amino Acid. Tretinoin / pharmacology. Tumor Cells, Cultured


14. Bryant J, Picot J, Levitt G, Sullivan I, Baxter L, Clegg A: Cardioprotection against the toxic effects of anthracyclines given to children with cancer: a systematic review. Health Technol Assess; 2007 Jul;11(27):iii, ix-x, 1-84
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  • RESULTS: Four randomised controlled trials (RCTs) met the inclusion criteria of the review, each considering a different cardioprotective intervention; all trials included children with acute lymphoblastic leukaemia, and one also included children with non-Hodgkin's lymphoma.
  • Two cohort studies considering atrial natriuretic peptide and two considering brain (B-type) natriuretic peptide suggested that these chemicals are elevated in some subgroups of children treated with anthracyclines for cancer.
  • N-terminal B-type natriuretic peptide levels were significantly elevated in children treated with anthracyclines who had cardiac dysfunction.
  • [MeSH-major] Anthracyclines / adverse effects. Anthracyclines / economics. Antibiotics, Antineoplastic / adverse effects. Antibiotics, Antineoplastic / economics. Cardiovascular Agents / therapeutic use. Heart Diseases / prevention & control. Lymphoma, Non-Hodgkin / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 17610809.001).
  • [ISSN] 1366-5278
  • [Journal-full-title] Health technology assessment (Winchester, England)
  • [ISO-abbreviation] Health Technol Assess
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antibiotics, Antineoplastic; 0 / Biomarkers; 0 / Cardiovascular Agents
  • [Number-of-references] 44
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15. Hornakova T, Chiaretti S, Lemaire MM, Foà R, Ben Abdelali R, Asnafi V, Tartaglia M, Renauld JC, Knoops L: ALL-associated JAK1 mutations confer hypersensitivity to the antiproliferative effect of type I interferon. Blood; 2010 Apr 22;115(16):3287-95
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  • [Title] ALL-associated JAK1 mutations confer hypersensitivity to the antiproliferative effect of type I interferon.
  • Activating mutations in JAK1 have been reported in acute lymphoblastic leukemias (ALLs).
  • In this study, we found a type I interferon (IFN) transcriptional signature in JAK1 mutation-positive human ALL samples.
  • Beside the constitutive activation of the type I IFN signaling cascade, JAK1 mutations also strongly potentiated the response to IFN in vitro.
  • Typically, the proliferation of cell lines expressing JAK1(A634D) was abrogated by type I IFNs.
  • Interestingly, we found that different JAK1 mutations differentially potentiate responses to type I IFNs or to interleukin-9, another cytokine using JAK1 to mediate its effects.
  • This suggests that the type of mutation influences the specificity of the effect on distinct cytokine receptor signaling.
  • Finally, we also showed in an in vivo leukemia model that cells expressing JAK1(A634D) are hypersensitive to the antiproliferative and antitumorigenic effect of type I IFN, suggesting that type I IFNs should be considered as a potential therapy for ALL with JAK1-activating mutations.
  • [MeSH-major] Interferon Type I / immunology. Janus Kinase 1 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Signal Transduction / physiology

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  • (PMID = 20167706.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon Type I; EC 2.7.010.2 / JAK1 protein, human; EC 2.7.10.2 / Janus Kinase 1
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16. Kwan ML, Buffler PA, Wiemels JL, Metayer C, Selvin S, Ducore JM, Block G: Breastfeeding patterns and risk of childhood acute lymphoblastic leukaemia. Br J Cancer; 2005 Aug 8;93(3):379-84
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  • [Title] Breastfeeding patterns and risk of childhood acute lymphoblastic leukaemia.
  • The risk of childhood acute lymphoblastic leukaemia (ALL) was investigated in relation to breastfeeding patterns in the Northern California Childhood Leukaemia Study.
  • Data collected by self-administered and in-person questionnaires from biological mothers of leukaemia cases (age 0-14 years) in the period 1995-2002 were matched to birth certificate controls on date of birth, sex, Hispanic ethnic status, and maternal race.
  • Complimentary feeding characteristics such as type of milk/formula used and age started eating solid foods among breastfed children were not associated with ALL risk.

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  • (PMID = 16052219.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NIEHS NIH HHS / ES / R01 ES009137; United States / NCHHSTP CDC HHS / PS / PS42 ES04705; United States / NIEHS NIH HHS / ES / R01 ES09137
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2361562
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17. Schmiegelow K, Al-Modhwahi I, Andersen MK, Behrendtz M, Forestier E, Hasle H, Heyman M, Kristinsson J, Nersting J, Nygaard R, Svendsen AL, Vettenranta K, Weinshilboum R, Nordic Society for Paediatric Haematology and Oncology: Methotrexate/6-mercaptopurine maintenance therapy influences the risk of a second malignant neoplasm after childhood acute lymphoblastic leukemia: results from the NOPHO ALL-92 study. Blood; 2009 Jun 11;113(24):6077-84
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  • [Title] Methotrexate/6-mercaptopurine maintenance therapy influences the risk of a second malignant neoplasm after childhood acute lymphoblastic leukemia: results from the NOPHO ALL-92 study.
  • Among 1614 children with acute lymphoblastic leukemia (ALL) treated with the Nordic Society for Paediatric Haematology and Oncology (NOPHO) ALL-92 protocol, 20 patients developed a second malignant neoplasm (SMN) with a cumulative risk of 1.6% at 12 years from the diagnosis of ALL.
  • Nine of the 16 acute myeloid leukemias or myelodysplastic syndromes had monosomy 7 (n = 7) or 7q deletions (n = 2).
  • Among 427 TPMT wild-type patients for whom the 6MP dose was registered, those who developed SMN received higher average 6MP doses than the remaining patients (69.7 vs 60.4 mg/m2; P = .03).

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  • (PMID = 19224761.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM028157; United States / NIGMS NIH HHS / GM / U01 GM061388; United States / NIGMS NIH HHS / GM / R01-GM28157; United States / NIGMS NIH HHS / GM / U01 GM61388
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.- / Methyltransferases; EC 2.1.1.67 / thiopurine methyltransferase; YL5FZ2Y5U1 / Methotrexate
  • [Other-IDs] NLM/ PMC2699230
  • [Investigator] Schmiegelow K; Hejl M; Østergård M; Schrøder H; Pihkala U; Ilanmaa E; Antila K; Korpela K; Vuorinen O; Perkkiö M; Kojo N; Nyman R; Pere M; Lanning M; Niemi A; Vuoristo A; Niemi S; Isotalo J; Laapas H; Mäkipernaa A; Salmi T; Varsamäki T; Kristinsson J; Zeller B; Danielsen O; Madsen B; Nielsen B; Stensvold K; Lund JH; Danielsen K; Brekke P; Stamnes O; Glomstein A; Widing E; Hapnes C; Stokland T; Kolmannskog S; Halvorsen B; Spangen S; Carlsson G; Bergkvist M; Skanka N; Korlén B; Dimberg A; Adrian BA; Mellander L; Aronson S; Jensen D; Winiarski J; Lagerwall A; Jonsson NO; Cervin T; Samuelsson U; Berg A; Nilsson H; Behrendtz M; Wiebe T; Ljung R; Tessin I; Ljungren CG; Dohlwitz A; Christensen HO; Ronge E; Berglund M; Björk O; Fransson D; Eriksson M; Forestier E; Kreuger A; Blomgren M; Rönnblad B; Eriksson B; Berg T; Hedling L; Forsberg T; Lindquist B; Kriström B; Hjalmars U
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18. Hornakova T, Staerk J, Royer Y, Flex E, Tartaglia M, Constantinescu SN, Knoops L, Renauld JC: Acute lymphoblastic leukemia-associated JAK1 mutants activate the Janus kinase/STAT pathway via interleukin-9 receptor alpha homodimers. J Biol Chem; 2009 Mar 13;284(11):6773-81
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  • [Title] Acute lymphoblastic leukemia-associated JAK1 mutants activate the Janus kinase/STAT pathway via interleukin-9 receptor alpha homodimers.
  • Activating mutations in JAK1 have been reported in acute lymphoblastic leukemias, but little is known about the mechanisms involved in their constitutive activation.
  • IL-9Ralpha variants with mutations of the JAK-interacting BOX1 region not only failed to promote JAK1 activation but also acted as dominant negative forms reverting the effect of wild-type IL-9Ralpha.
  • Co-expression of wild-type JAK3 partially reverted the inhibition by gammac, indicating that JAK3 cooperates with JAK1 mutants within the IL-9 receptor complex.
  • [MeSH-major] Janus Kinase 1 / metabolism. Mutation, Missense. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptors, Interleukin-9 / metabolism. STAT Transcription Factors / metabolism. Signal Transduction

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  • (PMID = 19139102.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IL2RB protein, human; 0 / IL9R protein, human; 0 / Il2rb protein, mouse; 0 / Il9r protein, mouse; 0 / Interleukin-2 Receptor beta Subunit; 0 / JAK3 protein, human; 0 / Jak1 protein, mouse; 0 / Receptors, Interleukin-9; 0 / STAT Transcription Factors; EC 2.7.010.2 / JAK1 protein, human; EC 2.7.10.2 / Jak3 protein, mouse; EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / Janus Kinase 3
  • [Other-IDs] NLM/ PMC2652315
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19. Derwich K, Sedek L, Meyer C, Pieczonka A, Dawidowska M, Gaworczyk A, Wachowiak J, Konatkowska B, Witt M, Marschalek R, Szczepański T: Infant acute bilineal leukemia. Leuk Res; 2009 Jul;33(7):1005-8
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  • [Title] Infant acute bilineal leukemia.
  • Most cases of acute leukemia can be assigned to the myeloid, B or T lineage.
  • There are rare cases of acute leukemia, which cannot be clearly classified, because either blasts express antigens of more than one lineage (acute biphenotypic leukemias) or distinct blast populations of two lineages co-exist (acute bilineal leukemias, aBLL).
  • We present a 10-month-old infant with de novo aBLL, characterized by blasts of monocytic and B-cell precursor lineages.
  • Despite poor initial response, both to acute lymphoblastic leukemia (ALL) induction treatment and acute myeloid leukemia induction blocks, the child reached complete clinical remission with minimal residual disease negative status and was transplanted.
  • This case report illustrates that aBLL is a very aggressive type of acute leukemia that should be individually treated and monitored, particularly in children less than 1 year of age.
  • [MeSH-major] B-Lymphocytes / pathology. Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Neoplasm, Residual / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 19286255.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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20. Pichler H, Möricke A, Mann G, Teigler-Schlegel A, Niggli F, Nebral K, König M, Inthal A, Krehan D, Dworzak MN, Janousek D, Harbott J, Schrappe M, Gadner H, Strehl S, Haas OA, Panzer-Grümayer R, Attarbaschi A, Berlin-Frankfurt-Münster (BFM) Study Group: Prognostic relevance of dic(9;20)(p11;q13) in childhood B-cell precursor acute lymphoblastic leukaemia treated with Berlin-Frankfurt-Münster (BFM) protocols containing an intensive induction and post-induction consolidation therapy. Br J Haematol; 2010 Apr;149(1):93-100
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  • [Title] Prognostic relevance of dic(9;20)(p11;q13) in childhood B-cell precursor acute lymphoblastic leukaemia treated with Berlin-Frankfurt-Münster (BFM) protocols containing an intensive induction and post-induction consolidation therapy.
  • The presence of a dicentric chromosome dic(9;20) has been reported to have an unfavourable prognosis in children with B-cell precursor acute lymphoblastic leukaemia (BCP-ALL).
  • As outcome may be influenced by type and composition of treatment, we analyzed 19 BCP-ALL patients with dic(9;20) who have been treated with ALL-BFM (Berlin-Frankfurt-Münster) protocols that included a 4-drug induction and subsequent consolidation therapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Chromosomes, Human, Pair 20 / genetics. Chromosomes, Human, Pair 9 / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20067563.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; ZS7284E0ZP / Daunorubicin; PVDA protocol
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21. Zeller B, Gustafsson G, Forestier E, Abrahamsson J, Clausen N, Heldrup J, Hovi L, Jonmundsson G, Lie SO, Glomstein A, Hasle H, Nordic Society of Paediatric Haematology and Oncology (NOPHO): Acute leukaemia in children with Down syndrome: a population-based Nordic study. Br J Haematol; 2005 Mar;128(6):797-804
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  • [Title] Acute leukaemia in children with Down syndrome: a population-based Nordic study.
  • To determine the epidemiology and outcome of children with Down syndrome (DS) diagnosed with acute leukaemia in the Nordic countries, data registered in the Nordic Society of Paediatric Haematology and Oncology (NOPHO) population-based leukaemia registry were analysed.
  • Of 3494 children with acute leukaemia diagnosed between July 1984 and December 2001, 136 patients (3.9%) with DS were identified.
  • 2.1% of the children with acute lymphoid leukaemia (ALL) and 14.0% of the children with acute myeloid leukaemia (AML) had DS.
  • None of the DS patients had T cell leukaemia.
  • DS patients with AML had significantly lower platelet and white blood cell counts and two-thirds were type M7 as according to the French-American-British classification.
  • [MeSH-major] Down Syndrome / complications. Leukemia, Myeloid / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications
  • [MeSH-minor] Acute Disease. Age Distribution. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Infant, Newborn. Male. Norway / epidemiology

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  • (PMID = 15755283.001).
  • [ISSN] 0007-1048
  • [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
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22. Gupta L, Jayavanth S, Ramaiah A: Identification of different types of lymphoblasts in acute lymphoblastic leukemia using relevance vector machines. Conf Proc IEEE Eng Med Biol Soc; 2009;2009:6675-8
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  • [Title] Identification of different types of lymphoblasts in acute lymphoblastic leukemia using relevance vector machines.
  • Acute Lymphoblastic Leukemia (ALL) is a blood cancer, which is characterized by an abnormal proliferation of lymphoblasts (a form of white blood cells).
  • The different counts of three different lymphoblasts can affect the type and intensity of the therapy to be used as well as the likely course of the disease.
  • [MeSH-major] Algorithms. Lymphocytes / classification. Lymphocytes / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 19964704.001).
  • [ISSN] 1557-170X
  • [Journal-full-title] Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual Conference
  • [ISO-abbreviation] Conf Proc IEEE Eng Med Biol Soc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Hejmadi RK, Thompson D, Shah F, Naresh KN: Cutaneous presentation of aleukemic monoblastic leukemia cutis - a case report and review of literature with focus on immunohistochemistry. J Cutan Pathol; 2008 Oct;35 Suppl 1:46-9
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  • [Title] Cutaneous presentation of aleukemic monoblastic leukemia cutis - a case report and review of literature with focus on immunohistochemistry.
  • Aleukemic monoblastic leukemia cutis is a rare cutaneous manifestation of a systemic hematological disorder associated with dermal infiltration of monoblasts preceding bone marrow or peripheral blood involvement.
  • Microscopy of the skin biopsy showed features of monoblastic leukemia.
  • We present this case to alert dermatologists of innocuous erythematous skin lesions clinically resembling a viral exanthema, which, in rare instances, may be a presenting feature of an aleukemic monoblastic leukemia cutis.
  • This entity poses problems for dermatopathologists even on immunohistochemistry as monoblasts are negative for hemopoietic precursor cell antigens like CD34, Terminal deoxynncleotidy1 transferase (TdT) and CD117.
  • [MeSH-major] Leukemia, Monocytic, Acute / metabolism. Leukemia, Monocytic, Acute / pathology. Skin Neoplasms / metabolism. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Antigens, CD / metabolism. Diabetes Mellitus, Type 2. Diagnosis, Differential. Exanthema / pathology. Female. Humans. Hypothyroidism / complications. Immunohistochemistry. Myocardial Ischemia / complications. Peripheral Vascular Diseases / complications. Pulmonary Disease, Chronic Obstructive / complications. Sweet Syndrome / pathology

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  • [Copyright] Copyright Blackwell Munksgaard 2008.
  • (PMID = 18544052.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD
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24. Ramanujachar R, Richards S, Hann I, Webb D: Adolescents with acute lymphoblastic leukaemia: emerging from the shadow of paediatric and adult treatment protocols. Pediatr Blood Cancer; 2006 Nov;47(6):748-56
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  • [Title] Adolescents with acute lymphoblastic leukaemia: emerging from the shadow of paediatric and adult treatment protocols.
  • Adolescents and young adults (AYA) with acute lymphoblastic leukaemia (ALL) constitute a distinct population from children and older adults.
  • A systematic review of all published clinical trials, which provide data on treatment and outcome of adolescents with ALL, has been summarised in an effort to determine whether they should be treated on paediatric or adult type protocols.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16470520.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 51
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25. Jarfelt M, Fors H, Lannering B, Bjarnason R: Bone mineral density and bone turnover in young adult survivors of childhood acute lymphoblastic leukaemia. Eur J Endocrinol; 2006 Feb;154(2):303-9
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  • [Title] Bone mineral density and bone turnover in young adult survivors of childhood acute lymphoblastic leukaemia.
  • OBJECTIVE: Treatment for childhood leukaemia induces many risk factors for development of decreased bone mineral density (BMD).
  • The aim was to study BMD and markers of bone turnover in a well-defined group of survivors of acute lymphoblastic leukaemia (ALL) who had all reached final height as well as peak bone mass, taking both previous treatment and physical activity into consideration.

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  • (PMID = 16452545.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Collagen Type I; 0 / Peptide Fragments; 0 / Peptides; 0 / Procollagen; 0 / collagen type I trimeric cross-linked peptide; 0 / procollagen type I carboxy terminal peptide; 104982-03-8 / Osteocalcin; EC 3.1.3.1 / Alkaline Phosphatase
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26. Spinola-Castro AM, Siviero-Miachon AA, Andreoni S, Tosta-Hernandez PD, Macedo CR, Lee ML: Transient hyperglycemia during childhood acute lymphocytic leukemia chemotherapy: an old event revisited. Clin Adv Hematol Oncol; 2009 Jul;7(7):465-72
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  • [Title] Transient hyperglycemia during childhood acute lymphocytic leukemia chemotherapy: an old event revisited.
  • Hyperglycemia has been described as a common event occurring during acute lymphocytic leukemia chemotherapy.
  • Our goal was to compare clinical and laboratory findings between hyperglycemic episodes occurring during childhood acute lymphocytic leukemia induction chemotherapy.
  • There were no differences in clinical or laboratory variables among groups, although the majority of episodes occurred in pubescents, regardless of the type of glucocorticoid employed.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Glucocorticoids / adverse effects. Hyperglycemia / chemically induced. Neoplasm Recurrence, Local. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 19701154.001).
  • [ISSN] 1543-0790
  • [Journal-full-title] Clinical advances in hematology & oncology : H&O
  • [ISO-abbreviation] Clin Adv Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Blood Glucose; 0 / Glucocorticoids; EC 3.2.1.- / Amylases
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27. Teitell MA, Pandolfi PP: Molecular genetics of acute lymphoblastic leukemia. Annu Rev Pathol; 2009;4:175-98
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  • [Title] Molecular genetics of acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is mainly a disease of childhood that arises from recurrent genetic insults that block precursor B and T cell differentiation and drive aberrant cell proliferation and survival.
  • Recent discoveries arising from genome-wide surveys and adoptive transfer of leukemia-initiating cells have uncovered multiple gene copy number aberrations and have yielded new insight into at least one type of ALL-originating cell.
  • Here, we review the spectrum of genetic aberrations that promote acute B and T cell leukemias and the mechanisms of cell transformation and malignant progression that are reinforced by mouse models of human ALL.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Gene Expression Regulation, Leukemic. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18783329.001).
  • [ISSN] 1553-4014
  • [Journal-full-title] Annual review of pathology
  • [ISO-abbreviation] Annu Rev Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 153
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28. Yan X, Deng M, Fung WK, Qian M: Detecting differentially expressed genes by relative entropy. J Theor Biol; 2005 Jun 7;234(3):395-402
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  • For example, some genes may display different expression patterns in the same cell type, say, tumor or normal, to form some subtypes.
  • [MeSH-minor] Acute Disease. Animals. Gene Expression. Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Reproducibility of Results

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  • (PMID = 15784273.001).
  • [ISSN] 0022-5193
  • [Journal-full-title] Journal of theoretical biology
  • [ISO-abbreviation] J. Theor. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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29. Jones D, Luthra R, Cortes J, Thomas D, O'Brien S, Bueso-Ramos C, Hai S, Ravandi F, de Lima M, Kantarjian H, Jorgensen JL: BCR-ABL fusion transcript types and levels and their interaction with secondary genetic changes in determining the phenotype of Philadelphia chromosome-positive leukemias. Blood; 2008 Dec 15;112(13):5190-2
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  • We compared BCR-ABL transcript type and level with kinase domain (KD) mutation status, genotype, and phenotype in 1855 Ph(+) leukemias.
  • Compared with e1a2/p190 BCR-ABL cases, de novo e13-e14a2/p210 Ph(+) lymphoid leukemia more frequently showed CML-type background, had higher blast-normalized BCR-ABL transcript levels, and more frequent persistent BCR-ABL transcript in the absence of detectable lymphoblasts.
  • In contrast, myeloid blast transformation was more frequently accompanied by new acquisition of acute myeloid leukemia-type chromosomal aberrations, particularly involving the EVI1 and RUNX1 loci.
  • [MeSH-minor] Cell Transformation, Neoplastic. Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit / genetics. DNA-Binding Proteins / genetics. Gene Amplification. Genotype. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive. Mutation. Phenotype. Precursor Cell Lymphoblastic Leukemia-Lymphoma. Proto-Oncogenes / genetics. RNA, Messenger / analysis. Transcription Factors / genetics

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  • (PMID = 18809762.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA100632
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / RUNX1 protein, human; 0 / Transcription Factors; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ PMC2597614
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30. Uyttebroeck A, Suciu S, Laureys G, Robert A, Pacquement H, Ferster A, Marguerite G, Mazingue F, Renard M, Lutz P, Rialland X, Mechinaud F, Cavé H, Baila L, Bertrand Y, Children's Leukaemia Group (CLG) of the European Organisation for Research and Treatment of Cancer (EORTC): Treatment of childhood T-cell lymphoblastic lymphoma according to the strategy for acute lymphoblastic leukaemia, without radiotherapy: long term results of the EORTC CLG 58881 trial. Eur J Cancer; 2008 Apr;44(6):840-6
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  • [Title] Treatment of childhood T-cell lymphoblastic lymphoma according to the strategy for acute lymphoblastic leukaemia, without radiotherapy: long term results of the EORTC CLG 58881 trial.
  • From June 1989 through to November 1998, 121 children with newly diagnosed T-cell lymphoblastic lymphoma (T-LBL) were included in the EORTC 58881 trial conducted by the Children's Leukaemia Group.
  • An intensive acute lymphoblastic leukaemia type chemotherapy regimen without irradiation leads to a high cure and survival rate in childhood T-LBL without an increased CNS recurrence.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 18342502.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5U10-CA11488-18; United States / NCI NIH HHS / CA / 5U10-CA11488-19; United States / NCI NIH HHS / CA / 5U10-CA11488-20; United States / NCI NIH HHS / CA / 5U10-CA11488-21; United States / NCI NIH HHS / CA / 5U10-CA11488-22; United States / NCI NIH HHS / CA / 5U10-CA11488-23; United States / NCI NIH HHS / CA / 5U10-CA11488-24; United States / NCI NIH HHS / CA / 5U10-CA11488-25; United States / NCI NIH HHS / CA / 5U10-CA11488-26; United States / NCI NIH HHS / CA / 5U10-CA11488-27; United States / NCI NIH HHS / CA / 5U10-CA11488-28; United States / NCI NIH HHS / CA / 5U10-CA11488-29; United States / NCI NIH HHS / CA / 5U10-CA11488-30; United States / NCI NIH HHS / CA / 5U10-CA11488-31; United States / NCI NIH HHS / CA / 5U10-CA11488-32; United States / NCI NIH HHS / CA / 5U10-CA11488-33; United States / NCI NIH HHS / CA / 5U10-CA11488-34; United States / NCI NIH HHS / CA / 5U10-CA11488-35; United States / NCI NIH HHS / CA / 5U10-CA11488-36
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Investigator] Philippet P; Otten J; Plouvier E; Béhar C; Boutard P; Millot F; Waterkeyn C; Velde IV; Solbu G
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31. Asnafi V, Buzyn A, Le Noir S, Baleydier F, Simon A, Beldjord K, Reman O, Witz F, Fagot T, Tavernier E, Turlure P, Leguay T, Huguet F, Vernant JP, Daniel F, Béné MC, Ifrah N, Thomas X, Dombret H, Macintyre E: NOTCH1/FBXW7 mutation identifies a large subgroup with favorable outcome in adult T-cell acute lymphoblastic leukemia (T-ALL): a Group for Research on Adult Acute Lymphoblastic Leukemia (GRAALL) study. Blood; 2009 Apr 23;113(17):3918-24
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  • [Title] NOTCH1/FBXW7 mutation identifies a large subgroup with favorable outcome in adult T-cell acute lymphoblastic leukemia (T-ALL): a Group for Research on Adult Acute Lymphoblastic Leukemia (GRAALL) study.
  • Many somatic genetic abnormalities have been identified in T-cell acute lymphoblastic leukemia (T-ALL) but each individual abnormality accounts for a small proportion of cases; therapeutic stratification consequently still relies on classical clinical markers.
  • We screened 141 adult diagnostic T-ALL samples from patients treated on either the Lymphoblastic Acute Leukemia in Adults (LALA)-94 (n = 87) or the GRAALL-2003 (n = 54) trials.
  • In 88 cases (62%) there were demonstrated NOTCH1 mutations (42% heterodimerization [HD], 10% HD+proline glutamate serine threonine [PEST], 6% PEST, 2% juxtamembrane mutations, 2% transactivation domain [TAD]) and 34 cases (24%) had FBXW7 mutations (21 cases had both NOTCH1 and FBXW7 mutations); 40 cases (28%) were wild type for both.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics. Ubiquitin-Protein Ligases / genetics

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  • (PMID = 19109228.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Receptor, Notch1; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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32. Husak Z, Printz D, Schumich A, Pötschger U, Dworzak MN: Death induction by CD99 ligation in TEL/AML1-positive acute lymphoblastic leukemia and normal B cell precursors. J Leukoc Biol; 2010 Aug;88(2):405-12
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  • [Title] Death induction by CD99 ligation in TEL/AML1-positive acute lymphoblastic leukemia and normal B cell precursors.
  • Our study was performed to examine the role of CD99 in normal and leukemia BCPs.
  • Type I CD99 mRNA was the main isoform in ALLs and was expressed differentially during BCP maturation.
  • [MeSH-major] Antigens, CD / physiology. Cell Adhesion Molecules / physiology. Core Binding Factor Alpha 2 Subunit. Oncogene Proteins, Fusion. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 20453109.001).
  • [ISSN] 1938-3673
  • [Journal-full-title] Journal of leukocyte biology
  • [ISO-abbreviation] J. Leukoc. Biol.
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / P 18196
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD99; 0 / CD99 protein, human; 0 / Cell Adhesion Molecules; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / TEL-AML1 fusion protein
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33. Pession A, Valsecchi MG, Masera G, Kamps WA, Magyarosy E, Rizzari C, van Wering ER, Lo Nigro L, van der Does A, Locatelli F, Basso G, Aricò M: Long-term results of a randomized trial on extended use of high dose L-asparaginase for standard risk childhood acute lymphoblastic leukemia. J Clin Oncol; 2005 Oct 1;23(28):7161-7
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  • [Title] Long-term results of a randomized trial on extended use of high dose L-asparaginase for standard risk childhood acute lymphoblastic leukemia.
  • PURPOSE: Between September 1991 and May 1997, within the International Berlin-Frankfurt-Muenster Study Group (I-BFM-SG), a randomized study was performed aimed at assessing the efficacy of prolonged use of high-dose l-asparaginase (HD-l-ASP) during continuation therapy in children with standard risk (SR) acute lymphoblastic leukemia (ALL), treated with a reduced BFM-type chemotherapy.
  • Treatment consisted of a BFM-type modified backbone with omission of the IB part in induction and elimination of two doses of anthracyclines during reinduction in both arms at the beginning of continuation therapy.
  • CONCLUSION: In this subset of patients, selected with criteria not including monitoring of minimal residual disease, application of extended HD-l-ASP may improve prognosis, compensating reduced leukemia control that results from adoption of a reduced-intensity BFM-backbone for treatment of children with SR ALL.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Asparaginase / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16192600.001).
  • [ISSN] 0732-183X
  • [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] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 3.5.1.1 / Asparaginase
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34. Samochatova EV, Chupova NV, Rudneva A, Makarova O, Nasedkina TV, Fedorova OE, Glotov AS, Kozhekbaeva Zh, Maiorova OA, Roumyantsev AG, Krynetski EY, Krynetskaia NF, Evans WE, Ribeiro RC: TPMT genetic variations in populations of the Russian Federation. Pediatr Blood Cancer; 2009 Feb;52(2):203-8
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  • We also characterized disease features and outcome according to the presence of TPMT SNPs in children with acute lymphoblastic leukemia (ALL).
  • RESULTS: Fifty-five (5.5%) study participants overall had heterozygous TPMT genotypes (1 variant and 1 wild-type allele): TPMT*1/*3A (n = 45; 4.5%), TPMT*1/*3C (n = 8; 0.8%), and TPMT*1/*2 (n = 2; 0.2%).

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
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  • (PMID = 19034904.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [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] United States
  • [Chemical-registry-number] EC 2.1.1.- / Methyltransferases; EC 2.1.1.67 / thiopurine methyltransferase
  • [Other-IDs] NLM/ NIHMS123733; NLM/ PMC2794198
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35. Zhou PY, Li WJ, Wei CX, Zhou Z: [Expression of PRAME gene in adult acute leukemia and its significance in prognosis]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Dec;15(6):1177-81
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  • [Title] [Expression of PRAME gene in adult acute leukemia and its significance in prognosis].
  • The study was aimed to investigate the expression of preferentially expressed antigen of melanoma (PRAME) gene in adult acute leukemia and its clinical significance.
  • The expression of the PRAME gene of bone marrow was measured by reverse transcriptase polymerase chain reaction (RT-PCR) in 73 adult newly diagnosed acute leukemia patients, 3 relapsed patients, 7 patients with idiopathic thrombocytopenic purpura (ITP) and 8 healthy donors, as well as two AL cell-lines (K562 and U937).
  • The results indicated that PRAME mRNA was expressed in 42.9% AML patients (n=24) and 20% ALL patients (n=4), also in two leukemia cell-lines K562 and U937, but not in eight health donors and seven ITP patients.
  • PRAME expression not correlated to the white blood count, hemoglobin level, platelet count and the percentage of blasts at diagnosis, yet independent of age, sex, and FAB type.
  • PRAME gene was overexpressed in adult acute leukemia patients and leukemia cell-lines.
  • It is concluded that the expression of PRAME is an indicator of favorable prognosis and can be a useful tool for monitoring minimal residual disease (MRD) in adult acute leukemia.
  • Differential expression between adult acute leukemia patients and healthy volunteers suggests that the immunogenic antigens PRAME are potential candidates for immunotherapy in adult acute leukemia.

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  • (PMID = 18088461.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / PRAME protein, human; 0 / RNA, Messenger
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36. Zhen ZJ, Xia Y, Ling JY, Tong GL, Lin L, Cai Y, Sun XF: [Prophylaxis and treatment of modified BFM-90 regimen for lymphoblastic lymphoma in children and adolescents accompanied with infection]. Ai Zheng; 2009 Jul;28(7):718-24
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  • The value of procalcitonin (PCT) in identifying the infection type and the outcome of anti-infection treatment was evaluated.
  • The sensitivity and specificity of PCT in diagnosing sepsis were 83.3% and 70.2%, but it failed to identify the infection type.
  • The positive diagnosis rate of the pathogen is too low to identify most of the infection type.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bacterial Infections / drug therapy. Cross Infection / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Respiratory Tract Infections / drug therapy

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  • (PMID = 19624898.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antifungal Agents; 0 / Cephalosporins; 04079A1RDZ / Cytarabine; 304NUG5GF4 / Itraconazole; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; E7WED276I5 / 6-Mercaptopurine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin; AIEOP acute lymphoblastic leukemia protocol
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37. Rudolph C, Hegazy AN, von Neuhoff N, Steinemann D, Schröck E, Stripecke R, Klein C, Schlegelberger B: Cytogenetic characterization of a BCR-ABL transduced mouse cell line. Cancer Genet Cytogenet; 2005 Aug;161(1):51-6
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  • Most patients with Philadelphia (Ph)-positive acute lymphoblastic leukemia (ALL) show evidence of secondary chromosome aberrations that may influence the course of disease and response to treatment.
  • The human wild-type BCR-ABL gene was expressed at a level comparable with that in human Ph-positive leukemias at diagnosis.
  • [MeSH-major] Chromosome Aberrations. Fusion Proteins, bcr-abl / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Animals. Cell Line, Transformed. DNA, Neoplasm / analysis. Humans. In Situ Hybridization, Fluorescence. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Mice. Mice, Inbred C57BL. Philadelphia Chromosome. Retroviridae / genetics. Reverse Transcriptase Polymerase Chain Reaction. Spectral Karyotyping. Transfection. Tumor Cells, Cultured

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  • (PMID = 16080957.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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38. Alberth M, Majoros L, Kovalecz G, Borbás E, Szegedi I, J Márton I, Kiss C: Significance of oral Candida infections in children with cancer. Pathol Oncol Res; 2006;12(4):237-41
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  • The study group consisted of 30 consecutive children and adolescents, 16 with acute lymphoblastic leukemia and 14 with solid tumors.
  • Four of the nonalbicans Candida strains were resistant to azole-type antifungal agents.
  • [MeSH-major] Antifungal Agents / therapeutic use. Candidiasis, Oral / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • (PMID = 17189988.001).
  • [ISSN] 1219-4956
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antifungal Agents
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39. Wu J, Nihal M, Siddiqui J, Vonderheid EC, Wood GS: Low FAS/CD95 expression by CTCL correlates with reduced sensitivity to apoptosis that can be restored by FAS upregulation. J Invest Dermatol; 2009 May;129(5):1165-73
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  • FAS expression was generally low in 30 of 31 cutaneous T-cell lymphoma (CTCL) cases (mycosis fungoides/Sezary syndrome, SS) as well as in 5 of 6 large plaque parapsoriasis cases (a CTCL precursor).
  • To investigate this phenomenon, we explored FAS transcript levels, cell-surface FAS protein expression and susceptibility to FAS-mediated apoptosis in four CTCL lines (MyLa, HH, SZ4, and SeAx), freshly isolated leukemic cells from a patient with SS, an acute lymphoblastic leukemia T-cell line (Jurkat), and JFL (a FAS-low variant of Jurkat).
  • When the FAS-deficient cell lines were transfected with a wild-type FAS construct, FAS expression and sensitivity to FAS-mediated apoptosis were restored.

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  • [CommentIn] J Invest Dermatol. 2009 May;129(5):1059-61 [19369931.001]
  • (PMID = 18923451.001).
  • [ISSN] 1523-1747
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / FAS protein, human; 0 / FASLG protein, human; 0 / Fas Ligand Protein
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40. 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
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  • [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.
  • All four SNPs showed predominant wild type alleles.
  • [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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41. Venkatraman R, Jayashree M, Singhi S, Marwaha RK: Hyperglycemic hyperosmolar nonketotic syndrome in a child with acute lymphoblastic leukemia undergoing induction chemotherapy: case report. J Pediatr Hematol Oncol; 2005 Apr;27(4):234-5
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  • [Title] Hyperglycemic hyperosmolar nonketotic syndrome in a child with acute lymphoblastic leukemia undergoing induction chemotherapy: case report.
  • Hyperglycemic hyperosmolar nonketotic syndrome, a life-threatening complication commonly associated with uncontrolled type 2 diabetes mellitus in adults, is characterized by severe hyperglycemia, a marked increase in serum osmolality, and clinical evidence of dehydration without the accumulation of beta-hydroxybutyric or acetoacetic ketoacids.
  • The syndrome has been rarely reported in children with leukemia undergoing induction therapy.
  • [MeSH-major] Hyperglycemic Hyperosmolar Nonketotic Coma / etiology. Hyperglycemic Hyperosmolar Nonketotic Coma / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • (PMID = 15838400.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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42. Litzow MR: Evolving paradigms in the therapy of Philadelphia-chromosome-negative acute lymphoblastic leukemia in adults. Hematology Am Soc Hematol Educ Program; 2009;:362-70
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  • [Title] Evolving paradigms in the therapy of Philadelphia-chromosome-negative acute lymphoblastic leukemia in adults.
  • Important studies challenging previous approaches to the treatment of adults with Philadelphia chromosome-negative acute lymphoblastic leukemia (ALL) have emerged in the past decade.
  • Donor versus no donor comparisons of allogeneic transplant highlight a potent graft-versus-leukemia effect in ALL, and the application of reduced-intensity conditioning transplants may exploit this effect while reducing non-relapse mortality.
  • The adoption of the use of pediatric intensity-type regimens in adolescents and young adults shows promise to improve outcomes in this population.

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  • (PMID = 20008222.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins
  • [Number-of-references] 70
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43. Sucak GT, Ozkurt ZN, Aki Z, Yagci M, Cengel A, Haznedar R: Cardiac systolic function in patients receiving hematopoetic stem cell transplantation: risk factors for posttransplantation cardiac toxicity. Transplant Proc; 2008 Jun;40(5):1586-90
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  • Pretransplantation ferritin levels and the type of HSCT did not seem to have an effect on posttransplantation cardiac complications.
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Ferritins / blood. Humans. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / surgery. Male. Middle Aged. Multiple Myeloma / mortality. Multiple Myeloma / surgery. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / surgery. Retrospective Studies. Risk Factors. Survival Rate

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  • (PMID = 18589156.001).
  • [ISSN] 0041-1345
  • [Journal-full-title] Transplantation proceedings
  • [ISO-abbreviation] Transplant. Proc.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-73-2 / Ferritins
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44. Meisel R, Toschke AM, Heiligensetzer C, Dilloo D, Laws HJ, von Kries R: Increased risk for invasive pneumococcal diseases in children with acute lymphoblastic leukaemia. Br J Haematol; 2007 Jun;137(5):457-60
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  • [Title] Increased risk for invasive pneumococcal diseases in children with acute lymphoblastic leukaemia.
  • There are no current data available on the risk of IPD in children with acute lymphoblastic leukaemia (ALL), the most common type of childhood malignancy.
  • [MeSH-major] Pneumococcal Infections / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / microbiology. Streptococcus pneumoniae

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  • (PMID = 17488489.001).
  • [ISSN] 0007-1048
  • [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
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45. Cole PD, Drachtman RA, Masterson M, Smith AK, Glod J, Zebala JA, Lisi S, Drapala DA, Kamen BA: Phase 2B trial of aminopterin in multiagent therapy for children with newly diagnosed acute lymphoblastic leukemia. Cancer Chemother Pharmacol; 2008 Jun;62(1):65-75
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  • [Title] Phase 2B trial of aminopterin in multiagent therapy for children with newly diagnosed acute lymphoblastic leukemia.
  • During weekly AMT therapy, higher mean neutrophil counts were observed among patients who were wild type for polymorphisms in methylene tetrahydrofolate reductase and methionine synthase reductase.

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  • (PMID = 17768625.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI068282-01; United States / NIAID NIH HHS / AI / R43 AI068282; United States / NIAID NIH HHS / AI / R43 AI068282-01
  • [Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antidotes; 0 / Antimetabolites, Antineoplastic; 0 / Folic Acid Antagonists; JYB41CTM2Q / Aminopterin; Q573I9DVLP / Leucovorin; YL5FZ2Y5U1 / Methotrexate
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46. Campana D: Molecular determinants of treatment response in acute lymphoblastic leukemia. Hematology Am Soc Hematol Educ Program; 2008;:366-73
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  • [Title] Molecular determinants of treatment response in acute lymphoblastic leukemia.
  • Treatment response in patients with acute lymphoblastic leukemia (ALL) is best assessed using assays for minimal residual disease (MRD).
  • The degree of leukemia cytoreduction and MRD clearance is determined by the collective influence of multiple factors.
  • Gene profiles depend, in turn, on the cell of origin for leukemic transformation, the type of underlying genetic abnormalities and/or epigenetic regulatory mechanisms.
  • Full knowledge of the molecular features associated with treatment response is required for precise leukemia prognostication and monitoring, and can provide clues to useful targets for novel therapies.

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  • (PMID = 19074112.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA115422; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA60419
  • [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 / AHNAK protein, human; 0 / Homeodomain Proteins; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 143275-75-6 / TLX1 protein, human; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 41
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47. Ru YX, Mi YC, Liu JH, Wang HJ, Zhao SX, Cui W, Li CW, Li QH, Zhu XF, Xiao ZJ, Pang JX, Wang JX: Significance of transmission electron microscopy in subtyping of monocytic leukemia. Ultrastruct Pathol; 2009 Mar-Apr;33(2):67-75
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  • [Title] Significance of transmission electron microscopy in subtyping of monocytic leukemia.
  • The objective of this paper is to produce an ultrastructural classification of acute monocytic leukemia (AML-M5) in relation to clinical behaviors.
  • Monoblast-type patients expressed weaker monocytic enzymograms and specific antigen staining for CD14 and CD64, compared with promonocyte-type patients.
  • [MeSH-major] Immunophenotyping / methods. Leukemia, Monocytic, Acute / classification. Microscopy, Electron, Transmission / methods. Monocyte-Macrophage Precursor Cells / ultrastructure

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  • (PMID = 19274583.001).
  • [ISSN] 1521-0758
  • [Journal-full-title] Ultrastructural pathology
  • [ISO-abbreviation] Ultrastruct Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.11.1.7 / Peroxidase
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48. Molteni CG, Te Kronnie G, Bicciato S, Villa T, Tartaglia M, Basso G, Biondi A, Cazzaniga G: PTPN11 mutations in childhood acute lymphoblastic leukemia occur as a secondary event associated with high hyperdiploidy. Leukemia; 2010 Jan;24(1):232-5
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  • [Title] PTPN11 mutations in childhood acute lymphoblastic leukemia occur as a secondary event associated with high hyperdiploidy.
  • [MeSH-major] Diploidy. Mutation. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Protein Tyrosine Phosphatase, Non-Receptor Type 11 / genetics

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  • (PMID = 19776760.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] Italy / Telethon / / GGP07115
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11
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49. Jakovljević G, Nakić M, Rogosić S, Kardum-Skelin I, Mrsić-Davidović S, Zadro R, Kruslin B: Pre-B-cell acute lymphoblastic leukemia with bulk extramedullary disease and chromosome 22 (EWSR1) rearrangement masquerading as Ewing sarcoma. Pediatr Blood Cancer; 2010 Apr;54(4):606-9
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  • [Title] Pre-B-cell acute lymphoblastic leukemia with bulk extramedullary disease and chromosome 22 (EWSR1) rearrangement masquerading as Ewing sarcoma.
  • After finding lymphoblasts in peripheral blood, the diagnosis of acute lymphoblastic leukemia was established.
  • The tissue was positive for immature B-cell markers and an immunoglobulin heavy chain gene rearrangement, which confirmed the final diagnosis of common type acute lymphoblastic leukemia with bulk extramedullary disease.
  • [MeSH-major] Chromosomes, Human, Pair 22 / genetics. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Sarcoma, Ewing / diagnosis. Soft Tissue Neoplasms / diagnosis. Transcription Factors / genetics

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  • (PMID = 20049929.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / EWS-FLI fusion protein; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Protein c-fli-1; 0 / RNA-Binding Protein EWS; 0 / Transcription Factors
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50. De Milito A, Iessi E, Logozzi M, Lozupone F, Spada M, Marino ML, Federici C, Perdicchio M, Matarrese P, Lugini L, Nilsson A, Fais S: Proton pump inhibitors induce apoptosis of human B-cell tumors through a caspase-independent mechanism involving reactive oxygen species. Cancer Res; 2007 Jun 1;67(11):5408-17
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  • Proton pumps like the vacuolar-type H+ ATPase (V-ATPase) are involved in the control of cellular pH in normal and tumor cells.
  • First, we showed that PPI treatment increased the sensitivity to vinblastine of a pre-B acute lymphoblastic leukemia (ALL) cell line.
  • [MeSH-major] Apoptosis / drug effects. Caspases / metabolism. Enzyme Inhibitors / pharmacology. Lymphoma, B-Cell / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Proton Pump Inhibitors. Reactive Oxygen Species / metabolism

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  • (PMID = 17545622.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Caspase Inhibitors; 0 / Enzyme Inhibitors; 0 / Proton Pump Inhibitors; 0 / Reactive Oxygen Species; 5V9KLZ54CY / Vinblastine; EC 3.4.22.- / Caspases; KG60484QX9 / Omeprazole
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51. Dirnhofer S, Went P, Tichelli A: Diagnostic problems in follow-up bone marrow biopsies of patients treated for acute and chronic leukaemias and MDS. Pathobiology; 2007;74(2):115-20
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  • [Title] Diagnostic problems in follow-up bone marrow biopsies of patients treated for acute and chronic leukaemias and MDS.
  • In the present paper, we suggest a systematic, integrative and interdisciplinary approach that includes knowledge of the original diagnosis and of the type of prior therapy, considers treatment effects and a use of standardized response criteria for AML and MDS.
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myeloid / diagnosis. Myelodysplastic Syndromes / diagnosis. Myeloproliferative Disorders / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Acute Disease. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Biopsy. Bone Marrow Transplantation. Chronic Disease. Humans. Treatment Outcome


52. Jansen MW, Corral L, van der Velden VH, Panzer-Grümayer R, Schrappe M, Schrauder A, Marschalek R, Meyer C, den Boer ML, Hop WJ, Valsecchi MG, Basso G, Biondi A, Pieters R, van Dongen JJ: Immunobiological diversity in infant acute lymphoblastic leukemia is related to the occurrence and type of MLL gene rearrangement. Leukemia; 2007 Apr;21(4):633-41
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  • [Title] Immunobiological diversity in infant acute lymphoblastic leukemia is related to the occurrence and type of MLL gene rearrangement.
  • The aim of this study was to identify immunobiological subgroups in 133 infant acute lymphoblastic leukemia (ALL) cases as assessed by their immunophenotype, immunoglobulin (Ig) and T-cell receptor (TCR) gene rearrangement pattern, and the presence of mixed lineage leukemia (MLL) rearrangements.
  • As compared to childhood precursor-B-ALL, Ig/TCR rearrangements in infant ALL were less frequent and more oligoclonal.
  • The immature Ig/TCR pattern in infant ALL correlated with young age at diagnosis, CD10 negativity and predominantly with the presence and the type of MLL translocation.
  • [MeSH-major] Gene Rearrangement. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17268512.001).
  • [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 / MLL protein, human; 0 / Receptors, Antigen, T-Cell; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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53. Faure C, Mollié A, Bellec S, Guyot-Goubin A, Clavel J, Hémon D: Geographical variations in the incidence of childhood acute leukaemia in France over the period 1990-2004. Eur J Cancer Prev; 2009 Aug;18(4):267-79
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  • [Title] Geographical variations in the incidence of childhood acute leukaemia in France over the period 1990-2004.
  • Spatial variations in childhood acute leukaemia (AL) incidence rates were investigated by département, in mainland France, over the period 1990-2004.
  • French National Registry of Childhood Haematological Malignancies data and population counts by type of leukaemia (AL, acute lymphoblastic leukaemia, acute myeloblastic leukaemia), time period (1990-2004, 1990-1994, 1995-1999 and 2000-2004), sex, and age group (0-14, 0-4, 5-9 and 10-14 years of age) were considered.
  • The overall homogeneity of the relative risks of leukaemia was tested, as well as comparison to 1 of each relative risk by the exact Poisson test.
  • The associated maps were slightly heterogeneous; the smoothed SIRs of overall acute lymphoblastic leukaemia of the south-west départements were slightly higher than those of the north-east.
  • The results, however, did not remain stable when investigated by leukaemia type, time period, sex or age group.
  • [MeSH-major] Demography. Leukemia, Myeloid, Acute / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

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  • (PMID = 19444126.001).
  • [ISSN] 1473-5709
  • [Journal-full-title] European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)
  • [ISO-abbreviation] Eur. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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54. Sung L, Klaassen RJ, Dix D, Pritchard S, Yanofsky R, Dzolganovski B, Almeida R, Klassen A: Identification of paediatric cancer patients with poor quality of life. Br J Cancer; 2009 Jan 13;100(1):82-8
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  • This Canadian multi-institutional cross-sectional study included children with cancer receiving any type of active treatment.
  • In multiple regression, children with acute lymphoblastic leukemia had better physical health (OR: 0.37, 95% CI 0.23, 0.60; P<0.0001) while intensive chemotherapy treatment (OR: 2.34, 95% CI: 1.42, 3.85; P=0.0008) and having a sibling with a chronic condition (OR: 2.53, 95% CI: 1.54, 4.15; P=0.0002) were associated with poor physical QoL.
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Cross-Sectional Studies. Emotions. Female. Humans. Logistic Models. Male. Precursor Cell Lymphoblastic Leukemia-Lymphoma / psychology. Regression Analysis

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  • (PMID = 19066605.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2634672
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55. Hertzberg L, Vendramini E, Ganmore I, Cazzaniga G, Schmitz M, Chalker J, Shiloh R, Iacobucci I, Shochat C, Zeligson S, Cario G, Stanulla M, Strehl S, Russell LJ, Harrison CJ, Bornhauser B, Yoda A, Rechavi G, Bercovich D, Borkhardt A, Kempski H, te Kronnie G, Bourquin JP, Domany E, Izraeli S: Down syndrome acute lymphoblastic leukemia, a highly heterogeneous disease in which aberrant expression of CRLF2 is associated with mutated JAK2: a report from the International BFM Study Group. Blood; 2010 Feb 4;115(5):1006-17
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  • [Title] Down syndrome acute lymphoblastic leukemia, a highly heterogeneous disease in which aberrant expression of CRLF2 is associated with mutated JAK2: a report from the International BFM Study Group.
  • We report gene expression and other analyses to elucidate the molecular characteristics of acute lymphoblastic leukemia (ALL) in children with Down syndrome (DS).
  • Nevertheless, 62% (33/53) of the DS-ALL samples analyzed were characterized by high expression of the type I cytokine receptor CRLF2 caused by either immunoglobulin heavy locus (IgH@) translocations or by interstitial deletions creating chimeric transcripts P2RY8-CRLF2.
  • [MeSH-major] Down Syndrome / genetics. Janus Kinase 2 / genetics. Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Cytokine / genetics


56. Rubnitz JE, Onciu M, Pounds S, Shurtleff S, Cao X, Raimondi SC, Behm FG, Campana D, Razzouk BI, Ribeiro RC, Downing JR, Pui CH: Acute mixed lineage leukemia in children: the experience of St Jude Children's Research Hospital. Blood; 2009 May 21;113(21):5083-9
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  • [Title] Acute mixed lineage leukemia in children: the experience of St Jude Children's Research Hospital.
  • To characterize the biology and optimal therapy of acute mixed-lineage leukemia in children, we reviewed the pathologic and clinical features, including response to therapy, of 35 patients with mixed-lineage leukemia.
  • Overall survival rates for the B/myeloid and T/myeloid subgroups were not significantly different from each other or from the rate for acute myeloid leukemia (AML) but were inferior to the outcome in children with acute lymphoblastic leukemia (ALL).
  • We propose that treatment for biphenotypic leukemia begin with one course of AML-type induction therapy, with a provision for a switch to lymphoid-type induction therapy with a glucocorticoid, vincristine, and L-asparaginase if the patient responds poorly.

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  • (PMID = 19131545.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / P30 CA-21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2686179
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57. Pieters R: [Acute lymphoblastic leukaemia in children and adolescents: chance of cure now higher than 80%]. Ned Tijdschr Geneeskd; 2010;154:A1577
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  • [Title] [Acute lymphoblastic leukaemia in children and adolescents: chance of cure now higher than 80%].
  • [Transliterated title] Behandeling van acute lymfatische leukemie bij kinderen en adolescenten. Zijn we er bijna?
  • Acute lymphoblastic leukaemia (ALL) is the most prevalent type of cancer in patients under the age of 18 years.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality

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  • (PMID = 20858304.001).
  • [ISSN] 1876-8784
  • [Journal-full-title] Nederlands tijdschrift voor geneeskunde
  • [ISO-abbreviation] Ned Tijdschr Geneeskd
  • [Language] dut
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Netherlands
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58. Li ZG, Zhao W, Wu MY, Hu YM: [Variant fusion transcript in ALL children with E2A-PBX1 fusion gene positive]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Jun;14(3):516-20
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  • The study was aimed to investigate the expression of E2A-PBX1 fusion gene in children with acute lymphoblastic leukemia (ALL).
  • Furthermore, all the positive cases expressed a variant type of fusion transcript.
  • Analyses with BLASTn indicated that the variant type of transcript retained the open reading frame.

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  • (PMID = 16800933.001).
  • [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 / Homeodomain Proteins; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 146150-85-8 / E2A-Pbx1 fusion protein
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59. Ek T, Mellander L, Hahn-Zoric M, Abrahamsson J: Avidity of tetanus and Hib antibodies after childhood acute lymphoblastic leukaemia - implications for vaccination strategies. Acta Paediatr; 2006 Jun;95(6):701-6
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  • [Title] Avidity of tetanus and Hib antibodies after childhood acute lymphoblastic leukaemia - implications for vaccination strategies.
  • AIM: To investigate the possible relationship between serum levels and avidities of antibodies against tetanus toxoid (TT) and Haemophilus influenzae type b (Hib) in children that were vaccinated after treatment for childhood acute lymphoblastic leukaemia (ALL).
  • [MeSH-major] Antibodies, Bacterial / immunology. Antibody Affinity. Haemophilus Vaccines / immunology. Haemophilus influenzae / immunology. Polysaccharides, Bacterial / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Tetanus Toxoid / immunology

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  • (PMID = 16754551.001).
  • [ISSN] 0803-5253
  • [Journal-full-title] Acta paediatrica (Oslo, Norway : 1992)
  • [ISO-abbreviation] Acta Paediatr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Antibodies, Bacterial; 0 / Haemophilus Vaccines; 0 / Haemophilus influenzae type b polysaccharide vaccine; 0 / Polysaccharides, Bacterial; 0 / Tetanus Toxoid
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60. Childhood Acute Lymphoblastic Leukaemia Collaborative Group (CALLCG): Beneficial and harmful effects of anthracyclines in the treatment of childhood acute lymphoblastic leukaemia: a systematic review and meta-analysis. Br J Haematol; 2009 May;145(3):376-88
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  • [Title] Beneficial and harmful effects of anthracyclines in the treatment of childhood acute lymphoblastic leukaemia: a systematic review and meta-analysis.
  • Anthracyclines are used to treat childhood acute lymphoblastic leukaemia (ALL) but non-randomized studies suggest that cardiotoxicity may be a problem.
  • Results were grouped and combined according to: addition of an anthracycline to standard therapy, type of anthracycline, mode of administration, and the use of a cardioprotectant.
  • The evidence on type of anthracycline, method of administration or use of cardioprotectant was insufficient to be able to rule out important differences.
  • [MeSH-major] Anthracyclines / therapeutic use. Antibiotics, Antineoplastic / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 19236609.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U137686856; United States / NCI NIH HHS / CA / U10 CA029139-22; United Kingdom / Medical Research Council / / ; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antibiotics, Antineoplastic; 0 / Cardiotonic Agents
  • [Number-of-references] 29
  • [Other-IDs] NLM/ NIHMS163765; NLM/ PMC2812732
  • [Investigator] Yetgin S; Obek NY; Masera G; Valsecchi MG; Dacou-Voutetakis; Loening L; Schrappe M; Zimmermann M; Henze G; von Stackelberg A; Gadner H; Mann G; Attarbaschi A; Brandalise SR; Carroll WL; Gaynon P; Boyett JM; Nachman J; Devidas M; Sather HN; Escherich G; Janka G; Gelber RD; Sallan SE; Pieters R; Bierings M; Kamps WA; Otten J; Suciu S; Viana MB; Baruchel A; Auclerc M; Perez C; Solidaro A; Stark B; Steinberg D; Koizumi S; Tsurusawa M; Zintl F; Schiller I; Matsuzaki A; Eden TO; Lilleyman JS; Richards S; Steinherz PG; Steinherz L; Kochupillai V; Bakhshi S; Ortega JJ; Nachman J; Appelbaum FR; Cheng C; Pei D; Pui CH; Kukure P; Nakazawa S; Tsuchida M; Elphinstone T; Evans V; Gettins L; Hicks C; MacKinnon L; Morris P; Richards S; Wade R
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61. van Tilburg CM, Sanders EA, Rovers MM, Wolfs TF, Bierings MB: Loss of antibodies and response to (re-)vaccination in children after treatment for acute lymphocytic leukemia: a systematic review. Leukemia; 2006 Oct;20(10):1717-22
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  • [Title] Loss of antibodies and response to (re-)vaccination in children after treatment for acute lymphocytic leukemia: a systematic review.
  • Intensified chemotherapy regimens resulting in improved survival of children with acute lymphocytic leukemia (ALL) lead to concerns about therapy-induced immune damage reflected by the loss of protection of previous immunizations and the efficacy of (re-)vaccination.
  • Regarding antibody titers after treatment, the number of children who had preserved the defined protection level for antibodies differed widely, ranging from 17 to 98% for diphtheria, 27 to 82% for Bordetella pertussis, 20 to 98% for tetanus, 62 to 100% for poliomyelitis, 35 to 100% for Haemophilus influenzae type B (HiB), 29 to 92% for mumps, 29 to 60% for measles and 72 to 92% for rubella.
  • [MeSH-major] Antibodies / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Vaccination. Vaccines / immunology

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  • (PMID = 16888619.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / Vaccines
  • [Number-of-references] 48
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62. Krajinovic M, Robaey P, Chiasson S, Lemieux-Blanchard E, Rouillard M, Primeau M, Bournissen FG, Moghrabi A: Polymorphisms of genes controlling homocysteine levels and IQ score following the treatment for childhood ALL. Pharmacogenomics; 2005 Apr;6(3):293-302
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  • INTRODUCTION: One of the causes of long-term morbidity associated with the treatment of acute lymphoblastic leukemia (ALL) is late neurotoxicity manifesting as impairment of higher cognitive functions.
  • [MeSH-major] Homocysteine / genetics. Intelligence Tests. Nitric Oxide Synthase Type III / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy

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  • (PMID = 16013960.001).
  • [ISSN] 1462-2416
  • [Journal-full-title] Pharmacogenomics
  • [ISO-abbreviation] Pharmacogenomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0LVT1QZ0BA / Homocysteine; EC 1.14.13.39 / Nitric Oxide Synthase Type III; EC 1.18.1.- / methionine synthase reductase; EC 1.18.1.2 / Ferredoxin-NADP Reductase; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2); EC 2.1.1.13 / 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase; EC 4.2.1.22 / Cystathionine beta-Synthase
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63. Roti G, La Starza R, Ballanti S, Crescenzi B, Romoli S, Foá R, Tartaglia M, Aversa F, Fabrizio Martelli M, Mecucci C: Acute lymphoblastic leukaemia in Noonan syndrome. Br J Haematol; 2006 May;133(4):448-50
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  • [Title] Acute lymphoblastic leukaemia in Noonan syndrome.
  • [MeSH-major] Noonan Syndrome / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Germ-Line Mutation. Humans. Intracellular Signaling Peptides and Proteins / genetics. Male. Protein Tyrosine Phosphatase, Non-Receptor Type 11. Protein Tyrosine Phosphatases / genetics

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  • (PMID = 16643459.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 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
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64. Dohda T, Maljukova A, Liu L, Heyman M, Grandér D, Brodin D, Sangfelt O, Lendahl U: Notch signaling induces SKP2 expression and promotes reduction of p27Kip1 in T-cell acute lymphoblastic leukemia cell lines. Exp Cell Res; 2007 Aug 15;313(14):3141-52
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  • [Title] Notch signaling induces SKP2 expression and promotes reduction of p27Kip1 in T-cell acute lymphoblastic leukemia cell lines.
  • In T-cell acute lymphoblastic leukemia (T-ALL) NOTCH 1 receptors are frequently mutated.
  • This leads to aberrantly high Notch signaling, but how this translates into deregulated cell cycle control and the transformed cell type is poorly understood.
  • [MeSH-major] Intracellular Signaling Peptides and Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptor, Notch1 / metabolism. S-Phase Kinase-Associated Proteins / metabolism. Signal Transduction / physiology. T-Lymphocytes / metabolism

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  • (PMID = 17560996.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / CDKN1B protein, human; 0 / Cell Cycle Proteins; 0 / HEY1 protein, human; 0 / HEY2 protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / Repressor Proteins; 0 / S-Phase Kinase-Associated Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
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65. Kundu M, Compton S, Garrett-Beal L, Stacy T, Starost MF, Eckhaus M, Speck NA, Liu PP: Runx1 deficiency predisposes mice to T-lymphoblastic lymphoma. Blood; 2005 Nov 15;106(10):3621-4
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  • Chromosomal rearrangements affecting RUNX1 and CBFB are common in acute leukemias.
  • In addition, loss-of-function mutations in Runt-related transcription factor 1 (RUNX1) have been identified in sporadic cases of acute myeloid leukemia (AML) and in association with the familial platelet disorder with propensity to develop AML (FPD/AML).
  • In order to examine the hypothesis that decreased gene dosage of RUNX1 may be a critical event in the development of leukemia, we treated chimeric mice generated from Runx1(lacZ/lacZ) embryonic stem (ES) cells that have homozygous disruption of the Runx1 gene with N-ethyl-N-nitrosourea (ENU).
  • We observed an increased incidence of T-lymphoblastic lymphoma in Runx1(lacZ/lacZ) compared with wild-type chimeras and confirmed that the tumors were of ES-cell origin.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / deficiency. Genetic Predisposition to Disease / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Animals. Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Mice. Mice, Mutant Strains. Oncogene Proteins, Fusion / genetics

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  • (PMID = 16051740.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA058343
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Runx1 protein, mouse
  • [Other-IDs] NLM/ PMC1459843
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66. Navid F, Billups C, Liu T, Krasin MJ, Rodriguez-Galindo C: Second cancers in patients with the Ewing sarcoma family of tumours. Eur J Cancer; 2008 May;44(7):983-91
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  • Cumulative incidence (CI) of SM by the type of malignancy and treatment was estimated.
  • Secondary leukaemia (SL) developed in 8 patients (2 ALL, 6 MDS/AML), a median 2.6 years (range 1.4-19.6 years) after diagnosis of ESFT.

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  • (PMID = 18353632.001).
  • [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 / CA23099; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / P01 CA023099; United States / NCI NIH HHS / CA / P30 CA021765-29; United States / NCI NIH HHS / CA / P30 CA021765
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor
  • [Other-IDs] NLM/ NIHMS51653; NLM/ PMC2423466
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67. De Braekeleer M, Morel F, Le Bris MJ, Herry A, Douet-Guilbert N: The MLL gene and translocations involving chromosomal band 11q23 in acute leukemia. Anticancer Res; 2005 May-Jun;25(3B):1931-44
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  • [Title] The MLL gene and translocations involving chromosomal band 11q23 in acute leukemia.
  • The cloning of the genes located at the breakpoints of chromosomal translocations in leukemia and lymphoma has led to the identification of new genes involved in carcinogenesis.
  • Based on 7969 cases of acute myeloblastic leukemia (AML) and 1252 cases of acute lymphoblastic leukemia (ALL) taken from the literature, band 11q23 and/or the MLL gene was involved in 5.2% of AML and 22% of ALL.
  • Differences in the frequency and the distribution of translocations were noted according to the type of acute leukemia and age of the patients.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Chromosome Banding. Histone-Lysine N-Methyltransferase. Humans. Myeloid-Lymphoid Leukemia Protein. Translocation, Genetic

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  • (PMID = 16158928.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 55
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68. Furuichi Y, Goi K, Inukai T, Sato H, Nemoto A, Takahashi K, Akahane K, Hirose K, Honna H, Kuroda I, Zhang X, Kagami K, Hayashi Y, Harigaya K, Nakazawa S, Sugita K: Fms-like tyrosine kinase 3 ligand stimulation induces MLL-rearranged leukemia cells into quiescence resistant to antileukemic agents. Cancer Res; 2007 Oct 15;67(20):9852-61
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  • [Title] Fms-like tyrosine kinase 3 ligand stimulation induces MLL-rearranged leukemia cells into quiescence resistant to antileukemic agents.
  • Fms-like tyrosine kinase 3 (FLT3) is highly expressed in acute lymphoblastic leukemia with the mixed-lineage leukemia (MLL) gene rearrangement refractory to chemotherapy.
  • We examined the biological effect of FLT3-ligand (FL) on 18 B-precursor leukemic cell lines with variable karyotypic abnormalities, and found that nine of nine MLL-rearranged cell lines with wild-type FLT3, in contrast to other leukemic cell lines, are significantly inhibited in their proliferation in a dose-dependent manner by FL.
  • A marked up-regulation of p27 by suppression of its protein degradation and an abrogation of constitutive signal transducers and activators of transcription 5 phosphorylation were revealed in arrested leukemia cells after FL stimulation.
  • Importantly, FL treatment rendered not only cell lines but also primary leukemia cells with MLL rearrangement resistant to chemotherapeutic agents.
  • MLL-rearranged leukemia cells adhering to the bone marrow stromal cell line, which expresses FL as the membrane-bound form, were induced to quiescent state resistant to chemotherapeutic agents, but their chemosensitivity was significantly restored in the presence of neutralizing anti-FL antibody.
  • The FL/FLT3 interaction between leukemia cells and bone marrow stromal cells expressing FL at high levels should contribute, at least in part, to persistent minimal-residual disease of MLL-rearranged leukemia in bone marrow.
  • [MeSH-major] Membrane Proteins / pharmacology. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 17942916.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / MLL protein, human; 0 / Membrane Proteins; 0 / STAT5 Transcription Factor; 0 / flt3 ligand protein; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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69. Corthals SL, Wynne K, She K, Shimizu H, Curman D, Garbutt K, Reid GS: Differential immune effects mediated by Toll-like receptors stimulation in precursor B-cell acute lymphoblastic leukaemia. Br J Haematol; 2006 Feb;132(4):452-8
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  • [Title] Differential immune effects mediated by Toll-like receptors stimulation in precursor B-cell acute lymphoblastic leukaemia.
  • Acute lymphoblastic leukaemia (ALL) is the most common paediatric malignancy and, although current therapy is widely effective, relapse remains a significant clinical problem for which new treatment strategies are required.
  • The ligation of Toll-like receptors (TLR) on antigen-presenting cells stimulates the generation of strong T-cell helper type 1 (Th1) adaptive immune responses.
  • Although TLR9 ligation has been shown to enhance immunogenicity of a number of leukaemia cell types, there have been few reports of the effects mediated through other TLR.
  • In this study we analysed both the expression of TLR by B-cell precursor ALL cell lines and the effects of individual TLR ligation on the ability of ALL cells to stimulate allogeneic T cells.
  • [MeSH-major] Immunotherapy / methods. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / therapy. Toll-Like Receptors / metabolism

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  • (PMID = 16412017.001).
  • [ISSN] 0007-1048
  • [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 / Antigens, CD40; 0 / Ligands; 0 / Peptidoglycan; 0 / RNA, Messenger; 0 / Toll-Like Receptor 1; 0 / Toll-Like Receptor 2; 0 / Toll-Like Receptor 3; 0 / Toll-Like Receptor 4; 0 / Toll-Like Receptor 5; 0 / Toll-Like Receptor 7; 0 / Toll-Like Receptor 9; 0 / Toll-Like Receptors; 12133JR80S / Guanosine; 82115-62-6 / Interferon-gamma; 9CAS0V66OI / loxoribine
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70. Abdelhameed A, Pond GR, Mitsakakis N, Brandwein J, Chun K, Gupta V, Kamel-Reid S, Lipton JH, Minden MD, Schimmer A, Schuh A, Yee K, Messner HA: Outcome of patients who develop acute leukemia or myelodysplasia as a second malignancy after solid tumors treated surgically or with strategies that include chemotherapy and/or radiation. Cancer; 2008 Apr 1;112(7):1513-21
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  • [Title] Outcome of patients who develop acute leukemia or myelodysplasia as a second malignancy after solid tumors treated surgically or with strategies that include chemotherapy and/or radiation.
  • BACKGROUND: Evaluation of therapeutic outcomes and risk factors was undertaken for patients with primary solid tumors (PST) developing acute leukemia or myelodysplasia (MDS) as a second malignancy.
  • METHODS: In all, 131 consecutive patients presenting to a single institution with leukemia or MDS after treatment for PST with surgery or chemotherapy/radiotherapy were examined.
  • Management of the secondary acute leukemia and MDS consisted either of intensive therapy including allogeneic blood and marrow transplants or supportive measures.
  • RESULTS: The time from diagnosis of PST to development of acute leukemia or MDS, the cytogenetic profile of patients, and their survival were similar irrespective of PST therapy with surgery alone or strategies involving chemotherapy and/or radiation.
  • CONCLUSIONS: Patients developing acute leukemia or MDS after PST demonstrated similar cytogenetic profiles and clinical outcomes independent of the type of treatment.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / etiology. Neoplasms / therapy. Neoplasms, Second Primary / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology


71. Desire S, Balasubramanian P, Bajel A, George B, Viswabandya A, Mathews V, Srivastava A, Chandy M: Frequency of TPMT alleles in Indian patients with acute lymphatic leukemia and effect on the dose of 6-mercaptopurine. Med Oncol; 2010 Dec;27(4):1046-9
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  • [Title] Frequency of TPMT alleles in Indian patients with acute lymphatic leukemia and effect on the dose of 6-mercaptopurine.
  • A total of 98 patients (66 pediatric and 32 adults) with precursor B acute lymphoblastic leukemia (Pre-B ALL) were evaluated for TPMT gene polymorphisms.
  • Three of the 5 patients (60%) heterozygous for TPMT*2 or TPMT*3C polymorphisms and 12/61 patients (20%) with wild type TPMT genotype had more than 10% of reduction of 6-MP dose (P=0.07).
  • [MeSH-major] 6-Mercaptopurine / therapeutic use. Antimetabolites, Antineoplastic / therapeutic use. Methyltransferases / genetics. Polymorphism, Genetic / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19830600.001).
  • [ISSN] 1559-131X
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.- / Methyltransferases; EC 2.1.1.67 / thiopurine methyltransferase
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72. Keam SJ: Dasatinib: in chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia. BioDrugs; 2008;22(1):59-69
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  • [Title] Dasatinib: in chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia.
  • In vitro, dasatinib is 325-fold more potent than imatinib against cells expressing wild-type BCR-ABL.
  • The efficacy and tolerability of oral dasatinib has been established in the START phase II trials in adults with chronic myeloid leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph-positive ALL) who were intolerant or resistant to imatinib, and optimal dasatinib dosage regimens were identified in phase III randomized trials.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Thiazoles / administration & dosage
  • [MeSH-minor] Animals. Controlled Clinical Trials as Topic. Dasatinib. Humans. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


73. Aste-Amézaga M, Zhang N, Lineberger JE, Arnold BA, Toner TJ, Gu M, Huang L, Vitelli S, Vo KT, Haytko P, Zhao JZ, Baleydier F, L'Heureux S, Wang H, Gordon WR, Thoryk E, Andrawes MB, Tiyanont K, Stegmaier K, Roti G, Ross KN, Franlin LL, Wang H, Wang F, Chastain M, Bett AJ, Audoly LP, Aster JC, Blacklow SC, Huber HE: Characterization of Notch1 antibodies that inhibit signaling of both normal and mutated Notch1 receptors. PLoS One; 2010 Feb 08;5(2):e9094
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  • NRR antibodies also strongly inhibit ligand-independent signaling in heterologous cells transiently expressing Notch1 receptors with diverse NRR "class I" point mutations, the most common type of mutation found in human T-cell acute lymphoblastic leukemia (T-ALL).
  • These antibodies may have clinical utility for conditions in which inhibition of signaling by wild-type Notch1 is desired, but are likely to be of limited value for treatment of T-ALLs associated with aberrant Notch1 activation.

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  • (PMID = 20161710.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R56 CA092433; United States / NCI NIH HHS / CA / P01 CA119070-040003; United States / NCI NIH HHS / CA / R56 CA092433-06A1; United States / NCI NIH HHS / CA / CA119070-049001; United States / NCI NIH HHS / CA / R01 CA092433; None / None / / R01 CA092433-06A2; United States / NCI NIH HHS / CA / CA119070-040003; United States / PHS HHS / / P01 119070; None / None / / R56 CA092433-06A1; United States / NCI NIH HHS / CA / R01 CA092433-06A2; United States / NCI NIH HHS / CA / P01 CA119070-049001; United States / NCI NIH HHS / CA / P01 CA119070
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Intercellular Signaling Peptides and Proteins; 0 / JAG2 protein, human; 0 / Ligands; 0 / Membrane Proteins; 0 / Receptor, Notch1
  • [Other-IDs] NLM/ PMC2817004
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74. Chang HH, Lu MY, Jou ST, Lin KH, Tien HF, Lin DT: Cytogenetics in childhood acute lymphoblastic leukemia in Taiwan: a single-institutional experience. Pediatr Hematol Oncol; 2006 Sep;23(6):495-506
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  • [Title] Cytogenetics in childhood acute lymphoblastic leukemia in Taiwan: a single-institutional experience.
  • In conclusion, the frequency and type of acquired chromosomal aberrations found in these Taiwanese children with ALL are similar to those reported in the literature.
  • [MeSH-major] Chromosome Aberrations / statistics & numerical data. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


75. Smith AR, Baker KS, Defor TE, Verneris MR, Wagner JE, Macmillan ML: Hematopoietic cell transplantation for children with acute lymphoblastic leukemia in second complete remission: similar outcomes in recipients of unrelated marrow and umbilical cord blood versus marrow from HLA matched sibling donors. Biol Blood Marrow Transplant; 2009 Sep;15(9):1086-93
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  • [Title] Hematopoietic cell transplantation for children with acute lymphoblastic leukemia in second complete remission: similar outcomes in recipients of unrelated marrow and umbilical cord blood versus marrow from HLA matched sibling donors.
  • Transplant decisions for children with acute lymphoblastic leukemia (ALL) in second complete remission (CR2) are often based on the type of available donor.
  • Although the incidence of neutrophil recovery was similar in all groups, the overall incidence of grades II-IV acute graft-versus-host disease (aGVHD) and chronic GVHD (cGVHD) was 37% and 9%, respectively, with a higher incidence of aGVHD in recipients of URD grafts.
  • Leukemia-free survival (LFS) at 5 years was lower in recipients of MM-URD grafts, but was comparable in all other groups.
  • Together, these results support the continued investigation of URD HCT for ALL in CR2, and suggest the timing of HCT in these children should be based primarily on the risk of relapse with conventional chemotherapy and not on the type of donor available.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 19660721.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA065493; United States / NCI NIH HHS / CA / P01-CA65493
  • [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 / HLA Antigens
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76. Sharma P, Singh T, Mishra D, Gaiha M: Parvovirus B-19 induced acute pure red cell aplasia in patients with chronic lymphocytic leukemia and neurofibromatosis type-1. Hematology; 2006 Aug;11(4):257-9
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  • [Title] Parvovirus B-19 induced acute pure red cell aplasia in patients with chronic lymphocytic leukemia and neurofibromatosis type-1.
  • We present two cases, an adult patient with chronic lymphocytic leukemia (CLL) and a child with neurofibromatosis type-1 (NF-1), where the abrupt appearance of severe anemia raised ominous clinical suspicions.
  • Evidence of recent parvovirus B19 infection in association with the selective erythroid precursor deficiency in marrow helped exclude other etiologies.
  • An association of NF-1 with acute PRCA has not been described in indexed English literature in the past.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / complications. Neurofibromatosis 1 / complications. Parvoviridae Infections / complications. Parvovirus B19, Human / pathogenicity. Red-Cell Aplasia, Pure / etiology
  • [MeSH-minor] Acute Disease. Bone Marrow / pathology. Bone Marrow / virology. Child. Diagnosis, Differential. Erythroid Precursor Cells / pathology. Hematologic Diseases / diagnosis. Humans. Infection / diagnosis. Male. Middle Aged


77. McQueen FM, Dalbeth N: Will Jill come tumbling after? The case for a JAK2-type mutation as a prequel to the connective tissue disorders. Med Hypotheses; 2009 Nov;73(5):651-4
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  • [Title] Will Jill come tumbling after? The case for a JAK2-type mutation as a prequel to the connective tissue disorders.
  • Thus, a common mutation affecting a haematopoietic precursor stem cell is capable of giving rise to diverse clinical phenotypes.
  • In this hypothesis paper, we propose that a similar mutation affecting a stem cell precursor, most likely of the B cell lineage, could underlie the development of the connective tissue disorders which could be regarded as "lymphoproliferative" disorders.
  • Diseases within each family can transform into each other and sometimes into haematological malignancies (most often B cell origin non-Hodgkins lymphoma for the connective tissue disorders and acute myeloid leukemia for the myeloproliferative disorders).


78. Hijiya N, Hudson MM, Lensing S, Zacher M, Onciu M, Behm FG, Razzouk BI, Ribeiro RC, Rubnitz JE, Sandlund JT, Rivera GK, Evans WE, Relling MV, Pui CH: Cumulative incidence of secondary neoplasms as a first event after childhood acute lymphoblastic leukemia. JAMA; 2007 Mar 21;297(11):1207-15
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  • [Title] Cumulative incidence of secondary neoplasms as a first event after childhood acute lymphoblastic leukemia.
  • CONTEXT: Little is known about the incidence of secondary neoplasms after 15 to 20 years in children and adolescents who were treated for acute lymphoblastic leukemia.
  • OBJECTIVES: To investigate the cumulative incidence of secondary neoplasms in pediatric patients treated for acute lymphoblastic leukemia over 30 years and to characterize late-occurring tumors.
  • DESIGN, SETTING, AND PATIENTS: Retrospective study of 2169 patients with acute lymphoblastic leukemia treated between 1962 and 1998 at St Jude Children's Research Hospital, Memphis, Tenn, who achieved complete remission and had a median follow-up time of 18.7 years (range, 2.4-41.3 years).
  • The cumulative incidence of each tumor type at 30 years was 2.19% (SE, 0.32%) for myeloid malignancy, 0.17% (SE, 0.10%) for lymphoma, 3.00% (SE, 0.59%) for brain tumor, 4.91% (SE, 1.04%) for carcinoma, and 0.57% (SE, 0.37%) for sarcoma.
  • CONCLUSIONS: The cumulative incidence of secondary neoplasms increases steadily over 30 years after treatment of acute lymphoblastic leukemia.
  • These results suggest that lifelong follow-up of acute lymphoblastic leukemia survivors is needed to ascertain the full impact of treatment and other leukemia-related factors on secondary neoplasm development.

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  • (PMID = 17374815.001).
  • [ISSN] 1538-3598
  • [Journal-full-title] JAMA
  • [ISO-abbreviation] JAMA
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-36401; United States / NCI NIH HHS / CA / CA-51001; United States / NCI NIH HHS / CA / CA-60419; United States / NCI NIH HHS / CA / CA-71907; United States / NCI NIH HHS / CA / CA-78224; United States / NIGMS NIH HHS / GM / GM-61393
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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79. Zuo YX, Zhang LP, Lu AD, Wang B, Liu GL: [Clinical characteristics of children with B cell type acute lymphoblastic leukemia carrying different fusion gene]. Zhongguo Dang Dai Er Ke Za Zhi; 2010 Mar;12(3):172-6
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  • [Title] [Clinical characteristics of children with B cell type acute lymphoblastic leukemia carrying different fusion gene].
  • OBJECTIVE: To investigate whether there were differences in the clinical characteristics, cytogenetic characteristics, immunophenotype and prognosis in children with B cell type acute lymphoblastic leukemia (B-ALL) carrying different fusion genes.
  • In the 11 children with BCR/ABL+B-ALL, 10 children showed common B type immunophenotype.
  • [MeSH-major] Gene Fusion. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit / genetics. Female. Homeodomain Proteins / genetics. Humans. Immunophenotyping. Infant. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 20350423.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Homeodomain Proteins; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 146150-85-8 / E2A-Pbx1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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80. van Scherpenzeel Thim V, Remacle S, Picard J, Cornu G, Gofflot F, Rezsohazy R, Verellen-Dumoulin C: Mutation analysis of the HOX paralogous 4-13 genes in children with acute lymphoid malignancies: identification of a novel germline mutation of HOXD4 leading to a partial loss-of-function. Hum Mutat; 2005 Apr;25(4):384-95
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  • [Title] Mutation analysis of the HOX paralogous 4-13 genes in children with acute lymphoid malignancies: identification of a novel germline mutation of HOXD4 leading to a partial loss-of-function.
  • We aimed to explore the possibility that germline alterations of HOX genes might be involved in childhood acute lymphoid malignancies.
  • A cohort of 86 children diagnosed with acute lymphoid malignancy was studied, 20 of them concurrently presenting a congenital anomaly of the skeleton.
  • While 13 changes were also observed in healthy controls, three variants were exclusively found in acute lymphoid malignancy cases.
  • These comprised the germline c.242A>T (p.Glu81Val) missense mutation of HOXD4, detected in two children diagnosed with acute lymphoblastic leukemia (ALL).
  • Functional analysis of the murine Hoxd4 homolog revealed that mutant Hoxd4 protein had lower transcriptional activity than wild-type protein in vitro.
  • [MeSH-major] Germ-Line Mutation. Homeodomain Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics

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  • (PMID = 15776434.001).
  • [ISSN] 1098-1004
  • [Journal-full-title] Human mutation
  • [ISO-abbreviation] Hum. Mutat.
  • [Language] eng
  • [Databank-accession-numbers] OMIM/ 142981; RefSeq/ NM/ 014621
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HOXD1 protein, human; 0 / Homeodomain Proteins; 0 / Hoxd4 protein, mouse; 0 / Transcription Factors
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81. Thomas DA, O'Brien S, Kantarjian HM: Monoclonal antibody therapy with rituximab for acute lymphoblastic leukemia. Hematol Oncol Clin North Am; 2009 Oct;23(5):949-71, v
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  • [Title] Monoclonal antibody therapy with rituximab for acute lymphoblastic leukemia.
  • Significant advances have been achieved in the treatment of acute lymphoblastic leukemia (ALL) with the incorporation of targeted therapy agents.
  • Targeting leukemia surface antigens with monoclonal antibodies is another promising strategy.
  • This article comprehensively reviews available data regarding the use of rituximab for the treatment of Burkitt-type leukemia/lymphoma and CD20-positive precursor B-cell ALL.
  • The incorporation of rituximab into frontline chemotherapy regimens for Burkitt-type leukemia/lymphoma appears to improve outcome.
  • Preliminary data regarding the use of rituximab in frontline therapy for CD20- positive precursor B-cell ALL suggest its use may also be beneficial, particularly for the younger subsets.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 19825447.001).
  • [ISSN] 1558-1977
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. Clin. North Am.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 95
  • [Other-IDs] NLM/ NIHMS675208; NLM/ PMC4458386
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82. Baldus CD, Thibaut J, Goekbuget N, Stroux A, Schlee C, Mossner M, Burmeister T, Schwartz S, Bloomfield CD, Hoelzer D, Thiel E, Hofmann WK: Prognostic implications of NOTCH1 and FBXW7 mutations in adult acute T-lymphoblastic leukemia. Haematologica; 2009 Oct;94(10):1383-90
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  • [Title] Prognostic implications of NOTCH1 and FBXW7 mutations in adult acute T-lymphoblastic leukemia.
  • BACKGROUND: NOTCH1 mutations have been associated with a favorable outcome in pediatric acute T-lymphoblastic leukemia.
  • However, the results of studies on the prognostic significance of NOTCH1 mutations in adult T-lymphoblastic leukemia remain controversial.
  • DESIGN AND METHODS: Here we have investigated the prognostic impact of mutations in the NOTCH1 pathway, in particular, the NOTCH1 and FBXW7 genes, in a large cohort of adult patients with T-lymphoblastic leukemia (n=126).
  • The characteristics of patients carrying NOTCH1 and/or FBXW7 (NOTCH1-FBXW7) mutations were similar to those with wild-type genes.
  • In the overall cohort, no significant differences were seen in the complete remission or event-free survival rates between patients with mutated or wild-type NOTCH1-FBXW7 (p=0.39).
  • CONCLUSIONS: NOTCH1 and FBXW7 mutations were not predictive of outcome in the overall cohort of adult patients with T-lymphoblastic leukemia, but there was a trend towards a favorable prognostic impact of NOTCH1-FBXW7 mutations in the small subgroup of patients with low-risk ERG/BAALC expression status.
  • Our findings further confirm the high frequency of NOTCH1 mutations in adult T-lymphoblastic leukemia.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Mutation / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics. Ubiquitin-Protein Ligases / genetics

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  • (PMID = 19794083.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Receptor, Notch1; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Other-IDs] NLM/ PMC2754954
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83. Dai L, Gast A, Horska A, Schrappe M, Bartram CR, Hemminki K, Kumar R, Bermejo JL: A case-control study of childhood acute lymphoblastic leukaemia and polymorphisms in the TGF-beta and receptor genes. Pediatr Blood Cancer; 2009 Jul;52(7):819-23
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  • [Title] A case-control study of childhood acute lymphoblastic leukaemia and polymorphisms in the TGF-beta and receptor genes.
  • BACKGROUND: Inherited genetic variants in critical genes can putatively modulate susceptibility to childhood acute lymphoblastic leukemia (ALL).
  • METHODS: We used allelic discrimination method to genotype 19 polymorphisms in the transforming growth factor-beta1 (TGF-beta1), transforming growth factor-beta receptor 1 (TGF-betaR1) and transforming growth factor-beta receptor 2 (TGF-betaR2) genes in 460 cases of childhood acute ALL and 552 ethnically matched controls.
  • [MeSH-major] Polymorphism, Single Nucleotide / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Protein-Serine-Threonine Kinases / genetics. Receptors, Transforming Growth Factor beta / genetics. Transforming Growth Factor beta / genetics

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19229971.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; EC 2.7.1.11 / TGF-beta type I receptor; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor
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84. Beesley AH, Firth MJ, Ford J, Weller RE, Freitas JR, Perera KU, Kees UR: Glucocorticoid resistance in T-lineage acute lymphoblastic leukaemia is associated with a proliferative metabolism. Br J Cancer; 2009 Jun 16;100(12):1926-36
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  • [Title] Glucocorticoid resistance in T-lineage acute lymphoblastic leukaemia is associated with a proliferative metabolism.
  • Glucocorticoids (GCs) are among the most important drugs for acute lymphoblastic leukaemia (ALL), yet despite their clinical importance, the exact mechanisms involved in GC cytotoxicity and the development of resistance remain uncertain.
  • The data also provide the first evidence that altered expression of wild-type MLL may contribute to GC-resistant phenotypes.
  • [MeSH-major] Cell Proliferation / drug effects. Dexamethasone / pharmacology. Drug Resistance, Neoplasm. Methylprednisolone / pharmacology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Signal Transduction / drug effects


85. Handrup MM, Møller JK, Frydenberg M, Schrøder H: Placing of tunneled central venous catheters prior to induction chemotherapy in children with acute lymphoblastic leukemia. Pediatr Blood Cancer; 2010 Aug;55(2):309-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Placing of tunneled central venous catheters prior to induction chemotherapy in children with acute lymphoblastic leukemia.
  • BACKGROUND: Tunneled central venous catheters (CVCs) are inevitable in children with acute lymphoid leukemia (ALL).
  • The aim of this study was to evaluate the risk of CVC-related complications in children with ALL in relation to timing of catheter placement and type of catheter.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Catheter-Related Infections / etiology. Catheterization, Central Venous / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • [Copyright] (c) 2010 Wiley-Liss, Inc.
  • (PMID = 20582964.001).
  • [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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86. Bercovich D, Ganmore I, Scott LM, Wainreb G, Birger Y, Elimelech A, Shochat C, Cazzaniga G, Biondi A, Basso G, Cario G, Schrappe M, Stanulla M, Strehl S, Haas OA, Mann G, Binder V, Borkhardt A, Kempski H, Trka J, Bielorei B, Avigad S, Stark B, Smith O, Dastugue N, Bourquin JP, Tal NB, Green AR, Izraeli S: Mutations of JAK2 in acute lymphoblastic leukaemias associated with Down's syndrome. Lancet; 2008 Oct 25;372(9648):1484-92
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  • [Title] Mutations of JAK2 in acute lymphoblastic leukaemias associated with Down's syndrome.
  • BACKGROUND: Children with Down's syndrome have a greatly increased risk of acute megakaryoblastic and acute lymphoblastic leukaemias.
  • Acute megakaryoblastic leukaemia in Down's syndrome is characterised by a somatic mutation in GATA1.
  • We tested the hypothesis that mutations in JAK2 might be a common molecular event in acute lymphoblastic leukaemia associated with Down's syndrome.
  • METHODS: JAK2 DNA mutational analysis was done on diagnostic bone marrow samples obtained from 88 patients with Down's syndrome-associated acute lymphoblastic leukaemia; and 216 patients with sporadic acute lymphoblastic leukaemia, Down's syndrome-associated acute megakaryoblastic leukaemia, and essential thrombocythaemia.
  • FINDINGS: Somatically acquired JAK2 mutations were identified in 16 (18%) patients with Down's syndrome-associated acute lymphoblastic leukaemia.
  • The only patient with non-Down's syndrome-associated leukaemia but with a JAK2 mutation had an isochromosome 21q.
  • INTERPRETATION: A specific genotype-phenotype association exists between the type of somatic mutation within the JAK2 pseudokinase domain and the development of B-lymphoid or myeloid neoplasms.
  • Somatically acquired R683 JAK2 mutations define a distinct acute lymphoblastic leukaemia subgroup that is uniquely associated with trisomy 21.
  • JAK2 inhibitors could be useful for treatment of this leukaemia.
  • [MeSH-major] Down Syndrome / complications. Down Syndrome / genetics. GATA1 Transcription Factor / genetics. Janus Kinase 2 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


87. Lowas S, Malempati S, Marks D: Body mass index predicts insulin resistance in survivors of pediatric acute lymphoblastic leukemia. Pediatr Blood Cancer; 2009 Jul;53(1):58-63
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  • [Title] Body mass index predicts insulin resistance in survivors of pediatric acute lymphoblastic leukemia.
  • BACKGROUND: Pediatric acute lymphoblastic leukemia (ALL) therapies have been associated with many late effects, including obesity, hyperglycemia, and insulin resistance.
  • Insulin resistance was not predicted by glucose levels during treatment, cumulative steroid or asparaginase dose, or type of steroid received.
  • [MeSH-major] Body Mass Index. Hyperglycemia / epidemiology. Insulin Resistance. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Survivors / statistics & numerical data

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  • [Copyright] Copyright 2009 Wiley-Liss, Inc.
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  • (PMID = 19340854.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / UL1 RR024140; United States / NCRR NIH HHS / RR / UL1 RR024140; United States / NCRR NIH HHS / RR / UL1 RR024140-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS123017; NLM/ PMC3804011
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88. Klingebiel T, Cornish J, Labopin M, Locatelli F, Darbyshire P, Handgretinger R, Balduzzi A, Owoc-Lempach J, Fagioli F, Or R, Peters C, Aversa F, Polge E, Dini G, Rocha V, Pediatric Diseases and Acute Leukemia Working Parties of the European Group for Blood and Marrow Transplantation (EBMT): Results and factors influencing outcome after fully haploidentical hematopoietic stem cell transplantation in children with very high-risk acute lymphoblastic leukemia: impact of center size: an analysis on behalf of the Acute Leukemia and Pediatric Disease Working Parties of the European Blood and Marrow Transplant group. Blood; 2010 Apr 29;115(17):3437-46
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  • [Title] Results and factors influencing outcome after fully haploidentical hematopoietic stem cell transplantation in children with very high-risk acute lymphoblastic leukemia: impact of center size: an analysis on behalf of the Acute Leukemia and Pediatric Disease Working Parties of the European Blood and Marrow Transplant group.
  • T cell-depleted haploidentical hematopoietic stem cell transplantation (haploHSCT) is an option to treat children with very high-risk acute lymphoblastic leukemia (ALL) lacking an HLA-identical donor.
  • The 5-year leukemia-free survival (LFS) was 30%, 34%, 22%, and 0%, respectively.
  • In a multivariate analysis, haploHSCT performed in larger centers (performing > or = 231 allotransplantations in the studied period) was associated with improved LFS rate and decreased RI (adjusted P = .01 and P = .04, respectively), adjusting for different patient-, disease-, and transplant-related factors such as number of previous autotransplantations, cytomegalovirus serology status, type of T-cell depletion, and use of total body irradiation and antithymocyte globulin.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Hospitals, Pediatric. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy


89. Okuno K, Horie Y, Kanai K, Kato M, Kuwamoto S, Okazaki T, Hayashi K: Epstein-Barr virus associated post-transplant Hodgkin lymphoma in an adult patient after cord blood stem cell transplantation for acute lymphoblastic leukemia. J Clin Exp Hematop; 2009 May;49(1):45-51
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  • [Title] Epstein-Barr virus associated post-transplant Hodgkin lymphoma in an adult patient after cord blood stem cell transplantation for acute lymphoblastic leukemia.
  • We report a 26-year-old woman case of post-transplant HL, which occurred after CBSCT for relapsed acute lymphoblastic leukemia.
  • Three years and eight months after CBSCT, the enlarged cervical lymph node was histologically diagnosed as EBV associated post-transplant HL, which showed immunophenotypes of classical HL and latency type II EBV infection.
  • [MeSH-major] Cord Blood Stem Cell Transplantation / adverse effects. Hodgkin Disease / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology


90. Oh SH, Park TS, Choi JR, Lee S, Cho SY, Kim SY, Kim J, Park JK, Song SA, Lee JY, Shin JH, Kim HR, Lee JN: Two childhood cases of acute leukemia with t(16;21)(p11.2;q22): second case report of infantile acute lymphoblastic leukemia with unusual type of FUS-ERG chimeric transcript. Cancer Genet Cytogenet; 2010 Jul 15;200(2):180-3
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  • [Title] Two childhood cases of acute leukemia with t(16;21)(p11.2;q22): second case report of infantile acute lymphoblastic leukemia with unusual type of FUS-ERG chimeric transcript.
  • We report two childhood cases of acute leukemia with t(16;21)(p11.2;q22) and FUS-ERG rearrangements.
  • Patient 1 (14 years old) was initially diagnosed with acute myeloid leukemia.
  • Chromosome study showed a t(16;21)(p11.2;q22) clone in more than one third of the cells analyzed, and further investigation with reverse-transcriptase polymerase chain reaction, cloning, and sequencing confirmed FUS-ERG rearrangement (type B).
  • Patient 2 (8 months old) was diagnosed with acute lymphoblastic leukemia (ALL) on the basis of bone marrow morphology and immunophenotyping.
  • Further studies for the detection of a FUS-ERG chimeric transcript were conducted, and an unusual type of FUS-ERG rearrangement was discovered, which has been reported in only three patients including a 1-year-old infant with ALL.
  • Although more clinical studies are necessary, we believe that a possible association between ALL and a specific type of FUS-ERG fusion transcript might be considered, especially in childhood cases with t(16;21).
  • [MeSH-major] Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA, Messenger / analysis. RNA-Binding Protein FUS / genetics. Translocation, Genetic


91. Dekel B, Metsuyanim S, Garcia AM, Quintero C, Sanchez MJ, Izraeli S: Organ-injury-induced reactivation of hemangioblastic precursor cells. Leukemia; 2008 Jan;22(1):103-13
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  • [Title] Organ-injury-induced reactivation of hemangioblastic precursor cells.
  • Early in mammalian development, the stem cell leukemia (SCL/TAL1) gene and its distinct 3' enhancer (SCL 3'En) specify bipotential progenitor cells that give rise to blood and endothelium, thus termed hemangioblasts.
  • Creation of bone marrow chimeras of SCL 3'En transgenic mice into wild-type hosts shows that all three types of SCL 3'En-expressing cells in the adult kidney can originate from the bone marrow.

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  • (PMID = 17898790.001).
  • [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 / Antigens, CD31; 0 / Antigens, CD34; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Tal1 protein, mouse; EC 2.7.10.1 / Flt1 protein, mouse; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 3.1.3.48 / Antigens, CD45
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92. Erdilyi DJ, Kámory E, Csókay B, Andrikovics H, Tordai A, Kiss C, Filni-Semsei A, Janszky I, Zalka A, Fekete G, Falus A, Kovács GT, Szalai C: Synergistic interaction of ABCB1 and ABCG2 polymorphisms predicts the prevalence of toxic encephalopathy during anticancer chemotherapy. Pharmacogenomics J; 2008 Oct;8(5):321-7
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  • Data from 291 children with acute lymphoblastic leukaemia were analysed in this retrospective study.
  • Patients with the ABCG2 421A allele tended to have more complications than wild type homozygotes (OR=2.0; P=0.25).
  • [MeSH-major] ATP-Binding Cassette Transporters / genetics. ATP-Binding Cassette, Sub-Family B, Member 1 / genetics. Antineoplastic Agents / adverse effects. Epistasis, Genetic. Neoplasm Proteins / genetics. Neurotoxicity Syndromes / etiology. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 17938643.001).
  • [ISSN] 1473-1150
  • [Journal-full-title] The pharmacogenomics journal
  • [ISO-abbreviation] Pharmacogenomics J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family B; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins
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93. Xu LP, Huang XJ, Liu KY, Chen H, Liu DH, Zhang YC, Chen YH, Han W, Gao ZY, Lu DP: [Allogeneic hematopoietic stem cell transplantation for treatment of Philadelphia chromosome positive acute lymphoblastic leukemia]. Beijing Da Xue Xue Bao; 2005 Jun 18;37(3):231-5
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  • [Title] [Allogeneic hematopoietic stem cell transplantation for treatment of Philadelphia chromosome positive acute lymphoblastic leukemia].
  • OBJECTIVE: To explore the optimal time of allogeneic hematopoietic stem cell transplantation (allo-HSCT) applied in patients with Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL), and the optimum order of donor selection.
  • The Kaplan-Meier method was used to estimate the probabilities of leukemia-free survival (LFS), overall survival (OS) and relapse incidence (RI), and the factors were compared by means of the Log-rank test.
  • In multiple covariate analysis model, the BCR/ABL type was the risk factor of LFS [P=0.005, Exp(B)=9.971] and RI (P=0.006, Exp(B)=9.488), the status of disease pre-HSCT and BCR/ABL subtype was the risk factor of OS [P was 0.010 and 0.038, Exp(B) was 4.532 and 37.537 respectively].
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy


94. Altucci L, Clarke N, Nebbioso A, Scognamiglio A, Gronemeyer H: Acute myeloid leukemia: therapeutic impact of epigenetic drugs. Int J Biochem Cell Biol; 2005 Sep;37(9):1752-62
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  • [Title] Acute myeloid leukemia: therapeutic impact of epigenetic drugs.
  • Acute myeloid leukemia (AML) is not a single disease but a group of malignancies in which the clonal expansion of various types of hematopoietic precursor cells in the bone marrow leads to perturbation of the delicate balance between self-renewal and differentiation that is characteristic of normal hematopoiesis.
  • While the genetic aberrations occurring in acute myeloid leukemia are fairly well understood, we have only recently become aware of the epigenetic deregulation associated with leukemia, in particular with myeloid leukemias.
  • Indeed, recent results indicate that epi-drugs may constitute an entirely novel type of anti-cancer drugs with unanticipated potential.
  • In this review we focus on the epigenetic mechanisms associated with acute myeloid leukemogenesis and discuss the therapeutic potential of epigenetic modulators such as histone deacetylase and DNA methyltransferase inhibitors.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Epigenesis, Genetic. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics. Mutation / genetics
  • [MeSH-minor] Acetylation. Acute Disease. Amino Acid Sequence. Animals. DNA Methylation. Gene Expression Regulation, Neoplastic. Gene Silencing. Histone Deacetylase Inhibitors. Humans. Molecular Sequence Data

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  • (PMID = 15964234.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Histone Deacetylase Inhibitors
  • [Number-of-references] 54
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95. Nagayama J, Tomizawa D, Koh K, Nagatoshi Y, Hotta N, Kishimoto T, Takahashi Y, Kuno T, Sugita K, Sato T, Kato K, Ogawa A, Nakahata T, Mizutani S, Horibe K, Ishii E, Japan Infant Leukemia Study Group: Infants with acute lymphoblastic leukemia and a germline MLL gene are highly curable with use of chemotherapy alone: results from the Japan Infant Leukemia Study Group. Blood; 2006 Jun 15;107(12):4663-5
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  • [Title] Infants with acute lymphoblastic leukemia and a germline MLL gene are highly curable with use of chemotherapy alone: results from the Japan Infant Leukemia Study Group.
  • Although infants with acute lymphoblastic leukemia (ALL) and a germline MLL gene have a better prognosis than comparable infants with a rearranged MLL gene, their optimal therapy is controversial.
  • All 21 infants with precursor B-cell ALL have been in first complete remission for 3.5 to 8.8 years.
  • These results indicate that chemotherapy of the type described here is both safe and highly effective against infant precursor B-cell ALL with MLL in the germline configuration.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Burkitt Lymphoma / drug therapy. Myeloid-Lymphoid Leukemia Protein

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  • (PMID = 16478880.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [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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96. Schmiegelow K, Forestier E, Kristinsson J, Söderhäll S, Vettenranta K, Weinshilboum R, Wesenberg F, Nordic Society of Paediatric Haematology and Oncology: Thiopurine methyltransferase activity is related to the risk of relapse of childhood acute lymphoblastic leukemia: results from the NOPHO ALL-92 study. Leukemia; 2009 Mar;23(3):557-64
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  • [Title] Thiopurine methyltransferase activity is related to the risk of relapse of childhood acute lymphoblastic leukemia: results from the NOPHO ALL-92 study.
  • Of 601 children with acute lymphoblastic leukemia (ALL) who were treated by the NOPHO ALL-92 protocol, 117 had TPMT genotype determined, whereas for 484 patients only erythrocyte TPMT activity was available.
  • 526 patients had TPMT wild type, 73 were presumed heterozygous, and two were TPMT deficient.
  • Risk of relapse was higher for the 526 TPMT wild type patients than for the remaining 75 patients (18 vs 7%, P=0.03).
  • In Cox multivariate regression analysis, sex (male worse; P=0.06), age (higher age worse, P=0.02), and TPMT activity (wild type worse; P=0.02) were related to risk of relapse.
  • These data suggest that children with ALL and TPMT wild type might have their cure rate improved, if the pharmacokinetics/-dynamics of TPMT low-activity patients could be mimicked without a concurrent excessive risk of second cancers.

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  • (PMID = 18987654.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM028157; United States / NIGMS NIH HHS / GM / U01 GM061388; United States / NIGMS NIH HHS / GM / R01-GM28157; United States / NIGMS NIH HHS / GM / U01 GM61388
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Neoplasm Proteins; E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.- / Methyltransferases; EC 2.1.1.67 / thiopurine methyltransferase; FTK8U1GZNX / Thioguanine
  • [Other-IDs] NLM/ NIHMS546648; NLM/ PMC3898327
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97. Ikawa Y, Sugimoto N, Koizumi S, Yachie A, Saikawa Y: Dense methylation of types 1 and 2 regulatory regions of the CD10 gene promoter in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene. J Pediatr Hematol Oncol; 2010 Jan;32(1):4-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dense methylation of types 1 and 2 regulatory regions of the CD10 gene promoter in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene.
  • SUMMARY: Infant acute lymphoblastic leukemia (ALL) displays distinct biologic and clinical features with a poor prognosis.
  • The CD10-negative immunophenotype of infant ALL is a hallmark and provides a predictable signature of mixed-lineage leukemia (MLL) rearrangement.
  • In this study, CD10-negative infant ALL with MLL/AF4, CD10-positive infant ALL with germline MLL, CD10-positive pre-B ALL cell line, infant acute myeloid leukemia (AML;.
  • Bisulfite sequencing of CD10 type 1 and 2 promoters showed that more than 84% of the cytosine-phosphate-guanine (CpG) dinucleotides identified were methylated in all 3 CD10-negative infant ALL samples with MLL/AF4.
  • [MeSH-major] DNA Methylation. Myeloid-Lymphoid Leukemia Protein. Neprilysin / genetics. Oncogene Proteins, Fusion. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Regulatory Sequences, Nucleic Acid / genetics

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  • (PMID = 20051780.001).
  • [ISSN] 1536-3678
  • [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
  • [Chemical-registry-number] 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Sp1 Transcription Factor; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.4.24.11 / Neprilysin
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98. Best A, Matheson E, Minto L, Hall AG, Irving JA: Mismatch repair and the downstream target genes, PAX5 and Ikaros, in childhood acute lymphoblastic leukemia. Leuk Res; 2010 Aug;34(8):1098-102
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mismatch repair and the downstream target genes, PAX5 and Ikaros, in childhood acute lymphoblastic leukemia.
  • Coding MS in candidate target genes including PAX5, IKZF1, BAX and TGFBRII were all wild type in this patient but the MMR-deficient cell line REH, was confirmed to have a coding MS in both PAX5 and TGFBRII.
  • [MeSH-major] B-Cell-Specific Activator Protein / genetics. DNA Mismatch Repair / genetics. Ikaros Transcription Factor / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Zebrafish Proteins / genetics

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  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20233627.001).
  • [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 / B-Cell-Specific Activator Protein; 0 / BAX protein, human; 0 / IKZF1 protein, human; 0 / RNA, Messenger; 0 / Receptors, Transforming Growth Factor beta; 0 / Zebrafish Proteins; 0 / bcl-2-Associated X Protein; 0 / pax5 protein, zebrafish; 148971-36-2 / Ikaros Transcription Factor; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor
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99. Li Q, Chen Z, You Y, Zou P: Transient pancytopenia preceding acute lymphoblastic leukemia with positive Philadelphia chromosome. Leuk Res; 2008 Aug;32(8):1317-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transient pancytopenia preceding acute lymphoblastic leukemia with positive Philadelphia chromosome.
  • Transient pancytopenia preceding acute lymphoblastic leukemia (pre-ALL) is a rare but well-known occurrence usually affecting children and adolescents.
  • To the best of our knowledge, this is the first report of adult B-cell type pre-ALL with positive Philadelphia chromosome and P190(BCR-ABL) published in the literature.
  • We report the case of a 49-year-old woman who was diagnosed with B-cell type ALL associated positive Philadelphia chromosome and P190(BCR-ABL) preceded by transient pancytopenia.
  • [MeSH-minor] Female. Fusion Proteins, bcr-abl / analysis. Humans. Immunophenotyping. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma. Preleukemia / diagnosis

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  • (PMID = 18291524.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
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100. Ruvolo VR, Kurinna SM, Karanjeet KB, Schuster TF, Martelli AM, McCubrey JA, Ruvolo PP: PKR regulates B56(alpha)-mediated BCL2 phosphatase activity in acute lymphoblastic leukemia-derived REH cells. J Biol Chem; 2008 Dec 19;283(51):35474-85
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PKR regulates B56(alpha)-mediated BCL2 phosphatase activity in acute lymphoblastic leukemia-derived REH cells.
  • Phosphorylation of serine 28 by PKR promotes mitochondrial localization of B56alpha, because wild-type but not mutant S28A B56alpha promoted mitochondrial PP2A activity.
  • Cells expressing wild-type B56alpha but not S28A B56alpha were sensitized to etoposide.






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