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1. Jevremovic D, Dronca RS, Morice WG, McPhail ED, Kurtin PJ, Zent CS, Hanson CA: CD5+ B-cell lymphoproliferative disorders: Beyond chronic lymphocytic leukemia and mantle cell lymphoma. Leuk Res; 2010 Sep;34(9):1235-8
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  • [Title] CD5+ B-cell lymphoproliferative disorders: Beyond chronic lymphocytic leukemia and mantle cell lymphoma.
  • CD5 positivity in B-cell lymphoproliferative disorders (LPD) is usually considered characteristic of either chronic lymphocytic leukemia (CLL) or mantle cell lymphoma (MCL).
  • Applying strict flow cytometry criteria, using genetic studies, and deferring to a lymph node/tissue diagnosis in non-classical cases are critical for accurate diagnosis and classification of CD5+ B-cell LPD.
  • [MeSH-major] Antigens, CD5 / immunology. B-Lymphocytes / immunology. Lymphoma, Mantle-Cell / immunology. Lymphoproliferative Disorders / immunology


2. Roman E, Simpson J, Ansell P, Kinsey S, Mitchell CD, McKinney PA, Birch JM, Greaves M, Eden T, United Kingdom Childhood Cancer Study Investigators: Childhood acute lymphoblastic leukemia and infections in the first year of life: a report from the United Kingdom Childhood Cancer Study. Am J Epidemiol; 2007 Mar 1;165(5):496-504
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  • [Title] Childhood acute lymphoblastic leukemia and infections in the first year of life: a report from the United Kingdom Childhood Cancer Study.
  • The United Kingdom Childhood Cancer Study was designed to examine the relation between childhood cancer and preceding exposure to infectious diseases.
  • The authors analyzed the relation between diagnosis (1991-1996) of acute lymphoblastic leukemia (ALL) at ages 2-5 years and clinically diagnosed infections in infancy.
  • Almost all study children (96% of both cases and controls) were taken to a general practitioner for a non-immunization-associated visit at least once before their first birthday.
  • Cases who had more than one neonatal infectious episode tended to be diagnosed with ALL at a comparatively young age; the mean age at ALL diagnosis was 37.7 months for cases with two or more episodes versus 45.3 months for cases with only one episode or none (p < 0.01).
  • [MeSH-major] Infection / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology


3. Stachel D, Albert M, Meilbeck R, Kreutzer B, Haas RJ, Schmid I: Bone marrow Th2 cytokine expression as predictor for relapse in childhood acute lymphoblastic leukemia (ALL). Eur J Med Res; 2006 Mar 27;11(3):102-13
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  • [Title] Bone marrow Th2 cytokine expression as predictor for relapse in childhood acute lymphoblastic leukemia (ALL).
  • Samples from 49 consecutive pediatric patients with B cell precursor acute lymphocytic leukemia (BCP ALL) were analyzed by semiquantitative RT-PCR.
  • Taqman RT-PCR of sorted cell populations showed that IL-10 mRNA was synthetized almost exclusively by NK or T cells.
  • [MeSH-major] Bone Marrow Cells / immunology. Burkitt Lymphoma / genetics. Burkitt Lymphoma / immunology. Cytokines / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Th2 Cells / immunology

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  • (PMID = 16751110.001).
  • [ISSN] 0949-2321
  • [Journal-full-title] European journal of medical research
  • [ISO-abbreviation] Eur. J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD86; 0 / CD86 protein, human; 0 / Cytokines; 0 / Interleukin-1; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4
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4. Tsuji A, Sasaki M, Ishii T, Sato S, Kanki H, Suzuki S, Takeuchi S, Fukuda T: Persistent eosinophilic infiltration of the myocardium in a child in complete remission of acute lymphoblastic leukemia and eosinophilia. Potential role in late cardiac disease? Keio J Med; 2010;59(2):64-8
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  • [Title] Persistent eosinophilic infiltration of the myocardium in a child in complete remission of acute lymphoblastic leukemia and eosinophilia. Potential role in late cardiac disease?
  • This report describes the long-term (23 years) follow-up of a pediatric patient with acute lymphoblastic leukemia and eosinophilia who underwent multiple valve replacements.
  • An 8-year-old boy with this complex disease was admitted in January 1984 and treated with 6-week course of vincristine, L-asparaginase, and prednisolone, which induced complete remission.
  • The present study indicates that a subset of patients in complete remission of acute lymphoblastic leukemia and eosinophilia can show persistent myocardial eosinophilic infiltration and are at risk of late cardiac disease.
  • [MeSH-major] Cardiomyopathies / etiology. Cardiomyopathies / pathology. Eosinophilia / complications. Eosinophilia / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications
  • [MeSH-minor] Adolescent. Adult. Child. Heart Valve Diseases / etiology. Heart Valve Diseases / pathology. Humans. Male. Time Factors. Young Adult


5. La Rosée P, Holm-Eriksen S, Konig H, Härtel N, Ernst T, Debatin J, Mueller MC, Erben P, Binckebanck A, Wunderle L, Shou Y, Dugan M, Hehlmann R, Ottmann OG, Hochhaus A: Phospho-CRKL monitoring for the assessment of BCR-ABL activity in imatinib-resistant chronic myeloid leukemia or Ph+ acute lymphoblastic leukemia patients treated with nilotinib. Haematologica; 2008 May;93(5):765-9
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  • [Title] Phospho-CRKL monitoring for the assessment of BCR-ABL activity in imatinib-resistant chronic myeloid leukemia or Ph+ acute lymphoblastic leukemia patients treated with nilotinib.
  • Actual BCR-ABL kinase inhibition in vivo as determined by phospho-CRKL (pCRKL) monitoring has been recognized as a prognostic parameter in patients with chronic myelogenous leukemia treated with imatinib.
  • We report a biomarker sub-study of the international phase I clinical trial of nilotinib (AMN107) using the established pCRKL assay in imatinib-resistant chronic myeloid leukemia or Ph+ acute lymphoblastic leukemia.
  • A minimum dose (200 mg) required for effective BCR-ABL inhibition in imatinib resistant/intolerant leukemia was determined.
  • Substantial differences between peripheral blood baseline pCRKL/CRKL ratios were observed when comparing chronic myeloid leukemia with Ph+ acute lymphoblastic leukemia.
  • Finally, rapid BCR-ABL-reactivation shortly after starting nilotinib treatment was seen in acute lymphoblastic leukemia patients with progressive disease carrying the P-loop mutations Y253H, E255K, or mutation T315I.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / chemistry. Antineoplastic Agents / pharmacology. Fusion Proteins, bcr-abl / metabolism. Gene Expression Regulation, Leukemic. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Nuclear Proteins / chemistry. Piperazines / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / pharmacology


6. Mallouk A, Pham PT, Pham PC: Concurrent FSGS and Hodgkin's lymphoma: case report and literature review on the link between nephrotic glomerulopathies and hematological malignancies. Clin Exp Nephrol; 2006 Dec;10(4):284-9
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  • In solid tumors, the NS is most often due to membranous glomerulonephropathy, whereas in common hematological malignancies, minimal-change disease predominates.
  • METHODS: We report a case of the simultaneous diagnoses of FSGS and Hodgkin's lymphoma, and review the literature on various nephrotic glomerulonephropathies associated with common leukemia and lymphoma.
  • RESULTS: Although nephrotic glomerulonephropathies rarely occur in association with acute leukemia, they have often been described in chronic lymphocytic leukemia (CLL).
  • While minimal-change disease is most commonly found in association with Hodgkin's lymphoma, more diverse and complex renal lesions are associated with non-Hodgkin's lymphoma.
  • [MeSH-major] Glomerulosclerosis, Focal Segmental / complications. Hodgkin Disease / complications
  • [MeSH-minor] Adult. Glomerulonephritis / etiology. Humans. Leukemia / complications. Lymphoma / complications. Male. Nephrotic Syndrome / etiology

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  • [Cites] Clin Nephrol. 1986 Dec;26(6):311-3 [3802598.001]
  • [Cites] Nephrol Dial Transplant. 2003 Aug;18 Suppl 6:vi45-51 [12953042.001]
  • [Cites] Rev Clin Exp Hematol. 2003 Dec;7(4):362-74 [15129648.001]
  • [Cites] Am J Kidney Dis. 1998 Nov;32(5):785-93 [9820448.001]
  • [Cites] Scand J Work Environ Health. 1985;11 Suppl 1:83-90 [3906873.001]
  • [Cites] Lancet. 1974 Sep 7;2(7880):556-60 [4140273.001]
  • [Cites] Leuk Lymphoma. 2002 Nov;43(11):2083-92 [12533032.001]
  • [Cites] Kidney Int. 1999 Jul;56(1):355-77 [10411717.001]
  • [Cites] Mayo Clin Proc. 1983 Sep;58(9):568-77 [6887974.001]
  • [Cites] Am J Kidney Dis. 1994 Jun;23(6):773-83 [8203357.001]
  • [Cites] Postgrad Med J. 1988 May;64(751):395-7 [3200784.001]
  • [Cites] Kidney Int. 1992 Jul;42(1):127-35 [1635342.001]
  • [Cites] AIDS Patient Care STDS. 1998 Aug;12(8):605-9 [15468431.001]
  • [Cites] Br Med J. 1922 Dec 23;2(3234):1201-1208.2 [20770949.001]
  • [Cites] J Pathol. 2002 Aug;197(5):677-83 [12210089.001]
  • [Cites] J Clin Pathol. 1995 Feb;48(2):160-3 [7745117.001]
  • [Cites] South Med J. 1989 Sep;82(9):1187-9 [2772690.001]
  • [Cites] N Engl J Med. 1983 Apr 14;308(15):888-96 [6835286.001]
  • [Cites] Ann Intern Med. 1966 Jan;64(1):41-51 [5900782.001]
  • [Cites] Semin Oncol. 1999 Oct;26(5 Suppl 14):107-14 [10561025.001]
  • [Cites] Rev Clin Exp Hematol. 2000 Mar;4(1):5-21 [11491097.001]
  • [Cites] Nephrology (Carlton). 2004 Dec;9(6):387-91 [15663641.001]
  • [Cites] Am J Kidney Dis. 2003 Oct;42(4):631-57 [14520615.001]
  • [Cites] Am J Kidney Dis. 2005 Aug;46(2):278-82 [16112046.001]
  • [Cites] Am J Nephrol. 1983 Jul-Aug;3(4):228-32 [6688503.001]
  • [Cites] Eur J Haematol. 2001 Sep;67(3):158-64 [11737248.001]
  • [Cites] Am J Kidney Dis. 1994 May;23(5):743-6 [8172220.001]
  • [Cites] Ann Intern Med. 1994 Nov 15;121(10):818 [7944068.001]
  • [Cites] Cancer. 1985 Aug 15;56(4):874-5 [4016678.001]
  • [Cites] Oncogene. 1999 Oct 28;18(44):5982-90 [10557087.001]
  • (PMID = 17186334.001).
  • [ISSN] 1342-1751
  • [Journal-full-title] Clinical and experimental nephrology
  • [ISO-abbreviation] Clin. Exp. Nephrol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 31
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7. Duff K: You can make a difference in the administration of intravenous immunoglobulin therapy. J Infus Nurs; 2006 May-Jun;29(3 Suppl):S5-14
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  • Intravenous immunoglobulin is a preparation of immune globulins containing antibodies given intravenously to patients with both inherited and acquired immunodeficiency disorders, such as primary immune deficiency diseases, idiopathic thrombocytopenia purpura, chronic lymphocytic leukemia, and bone marrow transplantation.
  • [MeSH-minor] Bone Marrow Transplantation. Drug Monitoring / nursing. Humans. Immunologic Deficiency Syndromes / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Nursing Assessment. Patient Education as Topic. Patient Selection. Purpura, Thrombocytopenic / drug therapy

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  • (PMID = 16878850.001).
  • [ISSN] 1533-1458
  • [Journal-full-title] Journal of infusion nursing : the official publication of the Infusion Nurses Society
  • [ISO-abbreviation] J Infus Nurs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulins, Intravenous; 0 / Immunologic Factors
  • [Number-of-references] 35
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8. Smit LA, van Maldegem F, Langerak AW, van der Schoot CE, de Wit MJ, Bea S, Campo E, Bende RJ, van Noesel CJ: Antigen receptors and somatic hypermutation in B-cell chronic lymphocytic leukemia with Richter's transformation. Haematologica; 2006 Jul;91(7):903-11
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  • [Title] Antigen receptors and somatic hypermutation in B-cell chronic lymphocytic leukemia with Richter's transformation.
  • It has been proposed that aberrant targeting of the somatic hypermutation machinery is instrumental in initiation and progression of B-cell non Hodgkin's lymphomas.
  • In this study, we investigated the B-cell receptor and the role of the somatic hypermutation machinery in B-cell chronic lymphocytic leukemias (B-CLL) prior to and after transformation to a lymphoma of a higher malignancy grade (Richter's transformation).
  • DESIGN AND METHODS: We investigated the activity of the somatic hypermutation machinery in nine B-CLL and secondary diffuse large B-cell lymphomas by measuring the expression of activation-induced cytidine deaminase, in combination with mutation analysis of immunoglobulin (Ig) and non-Ig genes.
  • Furthermore, activated-induced cytidine deaminase expression and somatic hypermutation activity of most RS B-CLL were found to be higher than those of control (non-transforming) B-CLL.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Receptors, Antigen / immunology. Somatic Hypermutation, Immunoglobulin

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  • [CommentIn] Haematologica. 2006 Jul;91(7):867 [16818267.001]
  • (PMID = 16818277.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / Receptors, Antigen
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9. Kahwash R, Rugg SS, Smith MD: Relapsing B-cell lymphoblastic leukemia in an adult presenting as an infiltrative cardiac mass with tamponade. J Am Soc Echocardiogr; 2007 Nov;20(11):1319.e1-2
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  • [Title] Relapsing B-cell lymphoblastic leukemia in an adult presenting as an infiltrative cardiac mass with tamponade.
  • We present a case of a 51-year-old man with a history of bone-marrow transplantation for acute lymphoblastic leukemia who returned 4 months later with cardiac tamponade.
  • An echocardiogram showed a solid mass encasing the right ventricle (RV).
  • Surgical biopsy of the mass revealed early relapse with lymphoblasts derived from B-cell precursors.
  • We believe that this is the first description of relapsing B-cell acute lymphoblastic leukemia presenting as an intrathoracic mass with direct invasion of the adjacent cardiac structures causing tamponade physiology.
  • [MeSH-major] Cardiac Tamponade / etiology. Cardiac Tamponade / ultrasonography. Heart Neoplasms / etiology. Heart Neoplasms / ultrasonography. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / ultrasonography

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  • (PMID = 17658241.001).
  • [ISSN] 1097-6795
  • [Journal-full-title] Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography
  • [ISO-abbreviation] J Am Soc Echocardiogr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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10. Eholié SP, Tanon AK, Folquet-Amorissani M, Doukouré B, Adoubryn KD, Yattara A, Bissagnéné E: [Three new cases of visceral leishmaniasis in Côte d'Ivoire]. Bull Soc Pathol Exot; 2008 Feb;101(1):60-1
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  • [Transliterated title] Trois nouveaux cas de leishmaniose viscérale autochtone en Côte d'Ivoire.
  • The objective of this work is to report three cases of visceral leishmaniasis in non-HIV infected native patients in Côte d'Ivoire.
  • Factors associated with visceral leishmaniasis regarding the younger and the older adults were respectively young age, chronic lymphoid leukaemia and Burkitt lymphoma.
  • The diagnosis was confirmed by the existence of Leishmania in bone marrow, ganglionic juice and splenic samples.
  • [MeSH-major] Leishmaniasis, Visceral / diagnosis
  • [MeSH-minor] Adult. Aged. Burkitt Lymphoma / complications. Child, Preschool. Cote d'Ivoire. Fatal Outcome. Female. Fever / parasitology. Humans. Immunocompromised Host. Leukemia, Lymphoid / complications. Male. Malnutrition / complications. Myeloproliferative Disorders / parasitology. Pancytopenia / parasitology. Wasting Syndrome / parasitology

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  • (PMID = 18432012.001).
  • [ISSN] 0037-9085
  • [Journal-full-title] Bulletin de la Société de pathologie exotique (1990)
  • [ISO-abbreviation] Bull Soc Pathol Exot
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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11. Bacher U, Schnittger S, Kern W, Hiddemann W, Haferlach T, Schoch C: The incidence of submicroscopic deletions in reciprocal translocations is similar in acute myeloid leukemia, BCR-ABL positive acute lymphoblastic leukemia, and chronic myeloid leukemia. Haematologica; 2005 Apr;90(4):558-9
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  • [Title] The incidence of submicroscopic deletions in reciprocal translocations is similar in acute myeloid leukemia, BCR-ABL positive acute lymphoblastic leukemia, and chronic myeloid leukemia.
  • We compared the incidence of submicroscopic deletions accompanying balanced translocations using interphase fluorescence in situ hybridization (FISH) in 245 patients with chronic myeloid leukemia (CML), 79 patients with acute lymphoblastic leukemia (ALL) and BCR-ABL (n=70) or MLL rearrangements (n=29), and 412 patients with acute myeloid leukemia (AML) with CBFB-MYH11 (n=122), PML-RARalpha (n=108), AML1-ETO (n=112), or MLL rearrangements (n=98).
  • [MeSH-major] Chromosome Deletion. Fusion Proteins, bcr-abl / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Humans. Reproducibility of Results. Translocation, Genetic


12. Specchia G, Buquicchio C, Pansini N, Di Serio F, Liso V, Pastore D, Greco G, Ciuffreda L, Mestice A, Liso A: Monitoring of cardiac function on the basis of serum troponin I levels in patients with acute leukemia treated with anthracyclines. J Lab Clin Med; 2005 Apr;145(4):212-20
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  • [Title] Monitoring of cardiac function on the basis of serum troponin I levels in patients with acute leukemia treated with anthracyclines.
  • In this study we prospectively evaluated serial measurements of serum cardiac markers and echocardiography in patients with de novo acute myeloid and lymphoid leukemias (AML and ALL, respectively) treated with anthracyclines.
  • [MeSH-major] Anthracyclines / adverse effects. Antibiotics, Antineoplastic / adverse effects. Heart Diseases / blood. Heart Diseases / chemically induced. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Troponin I / blood

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  • (PMID = 15962840.001).
  • [ISSN] 0022-2143
  • [Journal-full-title] The Journal of laboratory and clinical medicine
  • [ISO-abbreviation] J. Lab. Clin. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antibiotics, Antineoplastic; 0 / Biomarkers; 0 / Troponin I
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13. Leung J, Pang A, Yuen WH, Kwong YL, Tse EW: Relationship of expression of aquaglyceroporin 9 with arsenic uptake and sensitivity in leukemia cells. Blood; 2007 Jan 15;109(2):740-6
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  • [Title] Relationship of expression of aquaglyceroporin 9 with arsenic uptake and sensitivity in leukemia cells.
  • Arsenic trioxide (As2O3) is highly efficacious in acute promyelocytic leukemia (APL).
  • In 10 of 11 myeloid and lymphoid leukemia lines, quantitative polymerase chain reaction (Q-PCR) and Western blotting showed that AQP9 expression correlated positively with As2O3-induced cytotoxicity.
  • Similarly, the chronic myeloid leukemia line K562 expressed low levels of AQP9 and was As2O3 insensitive.
  • Pretreatment of the myeloid leukemia line HL-60 with all-trans retinoic acid (ATRA) up-regulated AQP9, leading to a significantly increased arsenic uptake and As2O3-induced cytotoxicity on incubation with As2O3, which might explain the synergism between ATRA and As2O3.
  • Q-PCR showed that primary APL cells expressed AQP9 significantly (2-3 logs) higher than other acute myeloid leukemias (AMLs), which might explain their exquisite As2O3 sensitivity.
  • [MeSH-major] Aquaporins / metabolism. Arsenicals / pharmacology. Leukemia, Myeloid / metabolism. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / metabolism. Oxides / pharmacology
  • [MeSH-minor] Acute Disease. Cell Line, Tumor. Cell Proliferation / drug effects. Gene Expression Profiling. Humans. K562 Cells. Point Mutation. Reverse Transcriptase Polymerase Chain Reaction / methods. Sensitivity and Specificity. Tretinoin / pharmacology. Up-Regulation / drug effects

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  • (PMID = 16968895.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AQP9 protein, human; 0 / Aquaporins; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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14. Blum W, Klisovic RB, Becker H, Yang X, Rozewski DM, Phelps MA, Garzon R, Walker A, Chandler JC, Whitman SP, Curfman J, Liu S, Schaaf L, Mickle J, Kefauver C, Devine SM, Grever MR, Marcucci G, Byrd JC: Dose escalation of lenalidomide in relapsed or refractory acute leukemias. J Clin Oncol; 2010 Nov 20;28(33):4919-25
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  • [Title] Dose escalation of lenalidomide in relapsed or refractory acute leukemias.
  • We report results of a phase I dose-escalation trial of lenalidomide in relapsed or refractory acute leukemia.
  • PATIENTS AND METHODS: Thirty-one adults with acute myeloid leukemia (AML) and four adults with acute lymphoblastic leukemia (ALL) were enrolled.
  • Two of four patients who received lenalidomide as initial therapy for AML relapse after allogeneic transplantation achieved durable CR after development of cutaneous graft-versus-host disease, without donor leukocyte infusion.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Thalidomide / analogs & derivatives

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  • [Cites] Biol Blood Marrow Transplant. 2006 Jan;12(1):61-7 [16399569.001]
  • [Cites] Br J Cancer. 2005 Sep 19;93(6):613-9 [16222306.001]
  • [Cites] Blood. 2006 Jul 15;108(2):618-21 [16569772.001]
  • [Cites] N Engl J Med. 2006 Oct 5;355(14):1456-65 [17021321.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jul 3;104(27):11406-11 [17576924.001]
  • [Cites] J Clin Pharmacol. 2007 Dec;47(12):1466-75 [17954615.001]
  • [Cites] Br J Haematol. 2008 Jan;140(1):36-45 [17995965.001]
  • [Cites] Blood. 2008 Jan 1;111(1):86-93 [17893227.001]
  • [Cites] J Clin Invest. 2008 Jul;118(7):2427-37 [18551193.001]
  • [Cites] Clin Cancer Res. 2008 Jul 15;14(14):4650-7 [18628480.001]
  • [Cites] Cancer Immunol Immunother. 2008 Dec;57(12):1849-59 [18392823.001]
  • [Cites] J Clin Oncol. 2008 Nov 1;26(31):5078-87 [18809607.001]
  • [Cites] Blood. 2009 Jan 29;113(5):1002-5 [18824593.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Apr 14;106(15):6250-5 [19332800.001]
  • [Cites] Blood. 2009 Apr 23;113(17):3947-52 [18987358.001]
  • [Cites] J Clin Pharmacol. 2009 Jun;49(6):650-60 [19451403.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Aug 4;106(31):12974-9 [19470455.001]
  • [Cites] Blood. 2009 Nov 5;114(19):4027-33 [19710500.001]
  • [Cites] Br J Haematol. 2010 Jan;148(2):217-25 [19804455.001]
  • [Cites] J Clin Oncol. 2010 Feb 1;28(4):596-604 [20026798.001]
  • [Cites] J Clin Oncol. 2010 Feb 1;28(4):556-61 [20026803.001]
  • [Cites] J Clin Oncol. 2010 Feb 1;28(4):549-55 [20026805.001]
  • [Cites] Blood. 2010 Feb 11;115(6):1204-13 [19965644.001]
  • [Cites] Blood. 2010 Mar 11;115(10):2077-87 [20053754.001]
  • [Cites] Blood. 2010 Apr 1;115(13):2619-29 [19965642.001]
  • [Cites] Proc Natl Acad Sci U S A. 2010 Apr 20;107(16):7473-8 [20368434.001]
  • [Cites] J Clin Oncol. 2010 May 10;28(14):2389-95 [20385984.001]
  • [Cites] Bone Marrow Transplant. 2000 Dec;26(11):1157-63 [11149725.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4642-9 [14673054.001]
  • [Cites] Blood. 1997 Jun 1;89(11):4226-35 [9166868.001]
  • [Cites] Cancer Chemother Pharmacol. 1997;40 Suppl:S9-12 [9272127.001]
  • [Cites] Blood. 1999 Jun 1;93(11):3983-93 [10339508.001]
  • [Cites] J Clin Oncol. 2005 Mar 20;23(9):1969-78 [15632409.001]
  • [Cites] Bone Marrow Transplant. 2005 May;35(10):965-70 [15806131.001]
  • [Cites] Semin Oncol. 2005 Aug;32(4 Suppl 5):S24-30 [16085014.001]
  • [Cites] Future Oncol. 2005 Oct;1(5):575-83 [16556034.001]
  • (PMID = 20956622.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA140158; United States / NCI NIH HHS / CA / K23 CA120708; United States / NCI NIH HHS / CA / P50-CA140158; United States / NCI NIH HHS / CA / K23CA120708; United States / NCRR NIH HHS / RR / UL1 RR025755; United States / NCI NIH HHS / CA / P30 CA016058
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 4Z8R6ORS6L / Thalidomide; F0P408N6V4 / lenalidomide
  • [Other-IDs] NLM/ PMC3020696
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15. San Juan AF, Fleck SJ, Chamorro-Viña C, Maté-Muñoz JL, Moral S, Pérez M, Cardona C, Del Valle MF, Hernández M, Ramírez M, Madero L, Lucia A: Effects of an intrahospital exercise program intervention for children with leukemia. Med Sci Sports Exerc; 2007 Jan;39(1):13-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of an intrahospital exercise program intervention for children with leukemia.
  • PURPOSE: The purpose was to investigate the effect of a 16-wk intrahospital supervised conditioning program including both resistance and aerobic training and a 20-wk detraining period on measures of aerobic fitness, muscular strength, functional mobility, ankle range of motion, and quality of life (QOL) in children receiving treatment for acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Exercise / physiology. Hospitals, Pediatric. Leukemia. Weight Lifting / physiology

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  • (PMID = 17218878.001).
  • [ISSN] 0195-9131
  • [Journal-full-title] Medicine and science in sports and exercise
  • [ISO-abbreviation] Med Sci Sports Exerc
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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16. Erduran E, Tekelioglu Y, Karakas T, Gedik Y, Mert FM: Comparision of the apoptotic effects on lymphoblasts and on increase of myeloid lineage cells of a short-time, high-dose methylprednisolone and the conventional-dose prednisolone treatments in children with acute lymphoblastic leukemia. Pediatr Hematol Oncol; 2006 Oct-Nov;23(7):587-98
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  • [Title] Comparision of the apoptotic effects on lymphoblasts and on increase of myeloid lineage cells of a short-time, high-dose methylprednisolone and the conventional-dose prednisolone treatments in children with acute lymphoblastic leukemia.
  • The authors compare the apoptotic effect on the lymphoblasts and the proliferative effect on the myeloid lineage cells of a short-course high-dose methylprednisolone (HDMP) and the conventional-dose prednisolone treatments in children with acute lymphoblastic leukemia (ALL).
  • The apoptotic percentages of lymphpblasts and the percentages of blasts and myeloid lineage cells were determined after performing the bone marrow aspiration (BMA) at diagnosis on the 0th, 3rd, and 7th days of the treatments in all patients.
  • [MeSH-major] Apoptosis / drug effects. Lymphocytes / drug effects. Methylprednisolone / administration & dosage. Myeloid Cells / drug effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Prednisolone / administration & dosage
  • [MeSH-minor] Adolescent. Antigens, CD / analysis. Antigens, CD13 / analysis. Antigens, Differentiation, Myelomonocytic / analysis. Cell Lineage. Child. Child, Preschool. Female. Humans. Infant. Male. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 16928654.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 9PHQ9Y1OLM / Prednisolone; EC 3.4.11.2 / Antigens, CD13; X4W7ZR7023 / Methylprednisolone
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17. 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.
  • After a median follow-up of 9 years, the probability of disease-free survival at 10 years was 87.5% (SE, 2.5) for YES-ASP arm versus 78.7% (SE, 3.3) for NO-ASP arm (P = .03).
  • 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
  • [MeSH-minor] Adolescent. Age Factors. Child. Child, Preschool. Disease-Free Survival. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Infant. Male. Treatment Outcome

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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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18. Matsuzaki A, Nagatoshi Y, Inada H, Nakayama H, Yanai F, Ayukawa H, Kawakami K, Moritake H, Suminoe A, Okamura J: Prognostic factors for relapsed childhood acute lymphoblastic leukemia: impact of allogeneic stem cell transplantation--a report from the Kyushu-Yamaguchi Children's Cancer Study Group. Pediatr Blood Cancer; 2005 Aug;45(2):111-20
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  • [Title] Prognostic factors for relapsed childhood acute lymphoblastic leukemia: impact of allogeneic stem cell transplantation--a report from the Kyushu-Yamaguchi Children's Cancer Study Group.
  • BACKGROUND: The treatment results of childhood acute lymphoblastic leukemia (ALL) with a first relapse were retrospectively analyzed to determine prognostic factors.
  • In particular, an attempt was made to clarify whether stem cell transplantation (SCT) had any advantages over chemotherapy.
  • The potential prognostic factors examined were: the time of initial diagnosis, gender, immunophenotype of leukemic blasts and the NCI-risk classification at initial diagnosis, the site of relapse, the time of relapse (early: within 18 months after diagnosis, intermediate: other than either early or late relapse, late: later than 6 months after the discontinuation of front-line chemotherapy), and the treatment after relapse (chemotherapy alone and SCT).
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Stem Cell Transplantation
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Japan / epidemiology. Male. Multivariate Analysis. Prognosis. Proportional Hazards Models. Recurrence. Retrospective Studies. Risk


19. Baillargeon J, Langevin AM, Lewis M, Grady JJ, Thomas PJ, Mullins J, Estrada J, Pitney A, Sacks N, Pollock BH: Therapy-related changes in body size in Hispanic children with acute lymphoblastic leukemia. Cancer; 2005 Apr 15;103(8):1725-9
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  • [Title] Therapy-related changes in body size in Hispanic children with acute lymphoblastic leukemia.
  • BACKGROUND: The objective of this study was to examine changes over time in body mass index (BMI) from diagnosis through chemotherapy for pediatric patients with B-precursor acute lymphoblastic leukemia (ALL).
  • METHODS: The study cohort consisted of 141 white Hispanic pediatric patients who were diagnosed with ALL and were treated at 2 South Texas pediatric oncology centers between 1993 and 2002.
  • CONCLUSIONS: Although it is known that leukemia therapy is associated with prevalent obesity in survivorship, its pattern of development during therapy has not been elucidated.
  • In the current cohort of Hispanic children with ALL, BMI scores were elevated at diagnosis (mean +/- standard deviation standardized BMI Z score, 0.33 +/- 1.4), then increased, and remained elevated for the entire duration of chemotherapy.
  • Patients who were classified as normal weight exhibited an increase in BMI over time; patients who were classified as overweight at diagnosis exhibited BMI patterns that were relatively stable; and patients who were classified as obese exhibited a very slight decline over time.
  • [MeSH-major] Body Mass Index. Obesity / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • [Copyright] (c) 2005 American Cancer Society.
  • (PMID = 15754333.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA11078
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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20. 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
  • [MeSH-minor] Disease-Free Survival. Female. Histone-Lysine N-Methyltransferase. Humans. Infant. Japan. Male. Remission Induction. Retrospective Studies. Survival Rate

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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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21. Zenz T, Döhner K, Denzel T, Döhner H, Stilgenbauer S, Bullinger L: Chronic lymphocytic leukaemia and acute myeloid leukaemia are not associated with AKT1 pleckstrin homology domain (E17K) mutations. Br J Haematol; 2008 May;141(5):742-3
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  • [Title] Chronic lymphocytic leukaemia and acute myeloid leukaemia are not associated with AKT1 pleckstrin homology domain (E17K) mutations.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Myeloid, Acute / genetics. Mutation. Proto-Oncogene Proteins c-akt / genetics

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  • (PMID = 18410456.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Blood Proteins; 0 / Neoplasm Proteins; 0 / Phosphoproteins; 0 / platelet protein P47; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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22. Védrine PO, Coffinet L, Temam S, Montagne K, Lapeyre M, Oberlin O, Orbach D, Simon C, Sommelet D: Mucoepidermoid carcinoma of salivary glands in the pediatric age group: 18 clinical cases, including 11 second malignant neoplasms. Head Neck; 2006 Sep;28(9):827-33
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  • [Title] Mucoepidermoid carcinoma of salivary glands in the pediatric age group: 18 clinical cases, including 11 second malignant neoplasms.
  • METHODS: This survey was conducted among 34 French pediatric oncology departments.
  • Eleven patients had been previously treated by radiotherapy and/or chemotherapy for a first malignant tumor, specifically, lymphoid leukemia (n = 4), lymphoma (n = 3), brain tumor (n = 2), sarcoma (n = 1), and retinoblastoma (n = 1).
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Humans. Lymphoma / pathology. Male. Neoplasms, Neuroepithelial / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Rhabdomyosarcoma / pathology

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  • [Copyright] (c) 2006 Wiley Periodicals, Inc.
  • (PMID = 16783829.001).
  • [ISSN] 1043-3074
  • [Journal-full-title] Head & neck
  • [ISO-abbreviation] Head Neck
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 39
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23. Liang DC, Yang CP, Lin DT, Hung IJ, Lin KH, Chen JS, Hsiao CC, Chang TT, Peng CT, Lin MT, Chang TK, Jaing TH, Liu HC, Wang LY, Yeh TC, Jou ST, Lu MY, Cheng CN, Sheen JM, Chiou SS, Wu KH, Hung GY, Chen RL, Chen SH, Cheng SN, Chang YH, Chen BW, Ho WL, Wang JL, Lin ST, Hsieh YL, Wang SC, Chang HH, Yang YL, Huang FL, Chang CY, Chang WH, Lin KS: Long-term results of Taiwan Pediatric Oncology Group studies 1997 and 2002 for childhood acute lymphoblastic leukemia. Leukemia; 2010 Feb;24(2):397-405
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  • [Title] Long-term results of Taiwan Pediatric Oncology Group studies 1997 and 2002 for childhood acute lymphoblastic leukemia.
  • The long-term outcome of 1390 children with acute lymphoblastic leukemia (ALL), treated in two successive clinical trials (Taiwan Pediatric Oncology Group (TPOG)-ALL-97 and TPOG-ALL-2002) between 1997 and 2007, is reported.
  • High-risk B-lineage ALL, T-cell, CD10 negativity, t(9;22), infant, and higher leukocyte count were consistently adverse factors, whereas hyperdiploidy >50 was a consistently favorable factor.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoplasm Recurrence, Local / therapy. Neoplasms, Second Primary / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy


24. Fraser CK, Lousberg EL, Kumar R, Hughes TP, Diener KR, Hayball JD: Dasatinib inhibits the secretion of TNF-alpha following TLR stimulation in vitro and in vivo. Exp Hematol; 2009 Dec;37(12):1435-44
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  • OBJECTIVE: Dasatinib (SPRYCEL, BMS-354825) is a small molecule Src/Abl tyrosine kinase inhibitor approved for the treatment of chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia.
  • The production of TNF-alpha was also impaired in vitro in response to TLR3, TLR4, and TLR9 stimulation of the mouse macrophage cell line RAW264.7, as well as TLR4 and TLR9 stimulation of BMDM; IL-6 production was also impaired in dasatinib-treated BMDM.
  • [MeSH-minor] Animals. Bone Marrow Cells / cytology. Bone Marrow Cells / drug effects. Bone Marrow Cells / metabolism. Cell Line. Cells, Cultured. Dasatinib. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Injections, Intraperitoneal. Interleukin-10 / blood. Interleukin-10 / metabolism. Interleukin-6 / blood. Interleukin-6 / metabolism. Lipopolysaccharides / administration & dosage. Lung / drug effects. Lung / metabolism. Mice. Mice, Inbred C57BL. Mice, Inbred Strains. Neutrophils / cytology. Neutrophils / drug effects. Toll-Like Receptor 3 / metabolism. Toll-Like Receptor 4 / metabolism. Toll-Like Receptor 9 / metabolism

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  • (PMID = 19786067.001).
  • [ISSN] 1873-2399
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Lipopolysaccharides; 0 / Pyrimidines; 0 / TLR3 protein, mouse; 0 / Thiazoles; 0 / Tlr4 protein, mouse; 0 / Tlr9 protein, mouse; 0 / Toll-Like Receptor 3; 0 / Toll-Like Receptor 4; 0 / Toll-Like Receptor 9; 0 / Toll-Like Receptors; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; RBZ1571X5H / Dasatinib
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25. Cen D, Lü JX, Pei RZ, Tu ZG, Yu XL, Wen YA: [The clinical significance of real-time fluorescence PCR quantification of hepatocyte growth factor mRNA expression in acute leukemia]. Zhonghua Nei Ke Za Zhi; 2008 May;47(5):401-4
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  • [Title] [The clinical significance of real-time fluorescence PCR quantification of hepatocyte growth factor mRNA expression in acute leukemia].
  • OBJECTIVE: To detect quantitatively hepatocyte growth factor (HGF) mRNA expressions of bone marrow mononuclear cells (MNCs) in acute leukemia (AL) and investigate its clinical significance.
  • METHODS: Total mRNA of quantitated bone marrow MNCs isolated from 67 de novo AL cases was extracted and then cDNA was synthesized.
  • RESULTS: Expressions of HGF mRNA in a group of AL were higher significantly than these in a control group (6.936 +/- 1.613, 0.407 +/- 0.170, P < 0.001), but there was similarity between a group of acute myeloid leukemia (AML) and group of acute lymphoblastic leukemia (ALL) (7.127 +/- 1.911, 6.635 +/- 0.934, P > 0.05).
  • In addition, expressions of HGF mRNA in the remission group were lower than these in the non-remission group (6.393 +/- 1.165, 8.041 +/- 1.848, P < 0.005).
  • It is suggested that HGF mRNA is a suitable index for AL diagnosis and treatment.
  • [MeSH-major] Hepatocyte Growth Factor / genetics. Leukemia / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Child. Child, Preschool. Female. Fluorescence. Gene Expression Regulation, Leukemic. Humans. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Young Adult

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  • (PMID = 18953951.001).
  • [ISSN] 0578-1426
  • [Journal-full-title] Zhonghua nei ke za zhi
  • [ISO-abbreviation] Zhonghua Nei Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / RNA, Messenger; 67256-21-7 / Hepatocyte Growth Factor
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26. Zhang W, Fu R, Liu WH, Cheng YQ, Song WX, DU LJ, Ruan EB, Zhang LT, Wang XM, Liang Y, Wang GJ, Qu W, Song J, Zhang RL, Guan J, Li LJ, Zou P, Shao ZH: [Prognosis and related factors of acute lymphoblastic leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Oct;15(5):1102-6
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  • [Title] [Prognosis and related factors of acute lymphoblastic leukemia].
  • In order to analyze the prognosis and related factors of acute lymphoblastic leukemia (ALL), 53 newly diagnosed ALL patients were enrolled in this study.
  • White blood cell count and hemoglobin level of newly diagnosed patients were significantly correlated with OS and EFS.
  • In order to decrease the relapse rate and prolong the EFS, individual therapeutical regimens and prophylaxis of complicating diseases should be applied to ALL patients.

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  • (PMID = 17956700.001).
  • [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
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27. Kourti M, Vavatsi N, Gombakis N, Sidi V, Tzimagiorgis G, Papageorgiou T, Koliouskas D, Athanassiadou F: Expression of multidrug resistance 1 (MDR1), multidrug resistance-related protein 1 (MRP1), lung resistance protein (LRP), and breast cancer resistance protein (BCRP) genes and clinical outcome in childhood acute lymphoblastic leukemia. Int J Hematol; 2007 Aug;86(2):166-73
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  • [Title] Expression of multidrug resistance 1 (MDR1), multidrug resistance-related protein 1 (MRP1), lung resistance protein (LRP), and breast cancer resistance protein (BCRP) genes and clinical outcome in childhood acute lymphoblastic leukemia.
  • We prospectively studied 49 children (26 boys and 23 girls) with acute lymphoblastic leukemia (ALL) (median age, 5.5 years; range, 15 months to 12.5 years) who were treated with the BFM95 chemotherapy protocol.
  • Expression of each of the MDR genes was independent of the initial white blood cell count, immunophenotype, National Cancer Institute risk classification, and prednisone response.
  • Interestingly, MDR1 expression was significantly higher at relapse than at diagnosis for 4 sample pairs.
  • Evaluation of MDR1 expression at diagnosis of childhood ALL may contribute to the early identification of patients at risk of treatment failure.
  • [MeSH-major] ATP-Binding Cassette Transporters / genetics. Drug Resistance, Multiple / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Vault Ribonucleoprotein Particles / genetics


28. Khalilzadeh A, Wangoo KT, Morris DL, Pourgholami MH: Epothilone-paclitaxel resistant leukemic cells CEM/dEpoB300 are sensitive to albendazole: Involvement of apoptotic pathways. Biochem Pharmacol; 2007 Aug 1;74(3):407-14
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  • Here, we assess the role of apoptotic mediators in eliciting an anti-proliferative response to paclitaxel (PTX) in a T cell acute lymphoblastic leukemia (ALL) cell line CEM and its epothilone-paclitaxel resistant sub-line CEM/dEpoB300.
  • In cell proliferation studies, CEM cells were sensitive to both PTX and ABZ, while the CEM/dEpoB300 cells were highly resistant to PTX (IC(50) 2.86 nM versus 30.26 nM, respectively).
  • These results reveal for the first time, the changes in apoptotic mediators following development of resistance to PTX in an ALL cell and the significantly increased sensitivity of these PTX resistant cells to ABZ.
  • [MeSH-major] Albendazole / pharmacology. Apoptosis / drug effects. Epothilones / pharmacology. Paclitaxel / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Base Sequence. Caspase 3 / metabolism. Cell Line, Tumor. Cell Proliferation. Cytochromes c / metabolism. DNA Primers. Humans. Myeloid Cell Leukemia Sequence 1 Protein. Neoplasm Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Tumor Suppressor Protein p53 / metabolism. bcl-2-Associated X Protein / metabolism

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  • (PMID = 17560963.001).
  • [ISSN] 0006-2952
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Epothilones; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; 9007-43-6 / Cytochromes c; EC 3.4.22.- / Caspase 3; F4216019LN / Albendazole; P88XT4IS4D / Paclitaxel
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29. Ma X, Buffler PA, Wiemels JL, Selvin S, Metayer C, Loh M, Does MB, Wiencke JK: Ethnic difference in daycare attendance, early infections, and risk of childhood acute lymphoblastic leukemia. Cancer Epidemiol Biomarkers Prev; 2005 Aug;14(8):1928-34
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  • [Title] Ethnic difference in daycare attendance, early infections, and risk of childhood acute lymphoblastic leukemia.
  • A role for infectious agents has been proposed in the etiology of childhood acute lymphoblastic leukemia (ALL), particularly for common ALL (c-ALL; ALL diagnosed in children ages 2-5 years and expressing CD10 and CD19 surface antigens).
  • We evaluated the possible etiologic role of daycare attendance (a proxy measure for exposure to infectious agents) and infections during infancy in the Northern California Childhood Leukemia Study.
  • In non-Hispanic White children, daycare attendance measured by child-hours was associated with a significantly reduced risk of ALL.
  • The magnitude of effect associated with the same number of child-hours was stronger for daycare attendance during infancy than for daycare attendance before diagnosis.
  • In addition, self-reported ear infection during infancy was associated with a significantly reduced risk of c-ALL (OR, 0.32; 95% CI, 0.14-0.74) in non-Hispanic White children.
  • These results offer indirect yet strong support for the infectious disease hypothesis in the etiology of ALL in non-Hispanic White children and highlight an important ethnic difference.
  • [MeSH-major] Child Day Care Centers. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology

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  • (PMID = 16103439.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / 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, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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30. Luo CY, Li BS, Jiang H, Gu LJ: [Study of the correlation between the expression level of asparagine synthetase and the outcome of children with acute lymphocytic leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2008 Jul;29(7):446-9
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  • [Title] [Study of the correlation between the expression level of asparagine synthetase and the outcome of children with acute lymphocytic leukemia].
  • OBJECTIVE: To determine whether the high level of asparagine synthetase (AS) expression in childhood acute lymphocytic leukemia (ALL) is associated with an inferior prognosis.
  • The two-year estimated disease free survival was much lower in children with high AS expression (53.8%) than in those with low AS expression (84.6%) (P<0.05).
  • [MeSH-major] Aspartate-Ammonia Ligase / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology

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  • (PMID = 19035175.001).
  • [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 6.3.1.1 / Aspartate-Ammonia Ligase
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31. Zwick D, Cooley L, Hetherington M: Minimal residual disease testing of acute leukemia by flow cytometry immunophenotyping: a retrospective comparison of detection rates with flow cytometry DNA ploidy or FISH-based methods. Lab Hematol; 2006;12(2):75-81
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  • [Title] Minimal residual disease testing of acute leukemia by flow cytometry immunophenotyping: a retrospective comparison of detection rates with flow cytometry DNA ploidy or FISH-based methods.
  • The detection and quantification of minimal residual leukemia (MRD) has importance for monitoring continued disease response and detection of early relapse.
  • We retrospectively compared MRD detection rates and percentages of residual leukemia by flow cytometry immunophenotyping (FCIP) with results obtained by either flow cytometry DNA (FCDNA) ploidy (n = 14) and/or fluorescent in situ hybridization (FISH) (n = 33) testing for cases with 1.5% or less residual leukemia.
  • A total of 42 paired results were obtained from 20 pediatric patients, including 16 with B lineage acute lymphocytic leukemia and 4 patients with acute myeloid leukemia during the course of induction and/or relapse.
  • There was reasonable correlation coefficients for quantity of residual disease by FCIP and FCDNA ploidy, and poor correlation coefficients for levels of residual disease between FCIP- and FISH-based results.
  • [MeSH-major] Flow Cytometry / methods. Leukemia / diagnosis. Neoplasm, Residual / diagnosis
  • [MeSH-minor] Acute Disease. Diagnostic Techniques and Procedures / standards. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Ploidies. Retrospective Studies

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  • (PMID = 16751134.001).
  • [ISSN] 1080-2924
  • [Journal-full-title] Laboratory hematology : official publication of the International Society for Laboratory Hematology
  • [ISO-abbreviation] Lab Hematol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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32. Figueroa ME, Reimers M, Thompson RF, Ye K, Li Y, Selzer RR, Fridriksson J, Paietta E, Wiernik P, Green RD, Greally JM, Melnick A: An integrative genomic and epigenomic approach for the study of transcriptional regulation. PLoS One; 2008 Mar 26;3(3):e1882
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  • The molecular heterogeneity of acute leukemias and other tumors constitutes a major obstacle towards understanding disease pathogenesis and developing new targeted-therapies.
  • We predicted that integration of different genome-wide epigenetic regulatory marks along with gene expression levels would provide greater power in capturing biological differences between leukemia subtypes.
  • Gene expression, cytosine methylation and histone H3 lysine 9 (H3K9) acetylation were measured using high-density oligonucleotide microarrays in primary human acute myeloid leukemia (AML) and acute lymphocytic leukemia (ALL) specimens.
  • We found that DNA methylation and H3K9 acetylation distinguished these leukemias of distinct cell lineage, as expected, but that an integrative analysis combining the information from each platform revealed hundreds of additional differentially expressed genes that were missed by gene expression arrays alone.

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  • [Cites] Science. 1999 Oct 15;286(5439):531-7 [10521349.001]
  • [Cites] Cancer Res. 1999 Aug 1;59(15):3730-40 [10446989.001]
  • [Cites] Bioinformatics. 2005 Jun 1;21(11):2789-90 [15797915.001]
  • [Cites] Clin Cancer Res. 2005 Jul 15;11(14):5167-74 [16033832.001]
  • [Cites] BMC Bioinformatics. 2005;6:166 [15992406.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):305-19 [16075461.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Nov 1;102(44):15785-90 [16243968.001]
  • [Cites] Nat Rev Cancer. 2006 Feb;6(2):107-16 [16491070.001]
  • [Cites] Cancer Res. 2006 Apr 1;66(7):3541-9 [16585178.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6118-28 [16778185.001]
  • [Cites] Genome Res. 2006 Aug;16(8):1046-55 [16809668.001]
  • [Cites] Cancer Res. 2007 Jan 1;67(1):194-201 [17210699.001]
  • [Cites] Nucleic Acids Res. 2007;35(3):801-11 [17202157.001]
  • [Cites] J Biol Chem. 2002 Apr 12;277(15):13286-93 [11825903.001]
  • [Cites] Nat Rev Genet. 2002 Jun;3(6):415-28 [12042769.001]
  • [Cites] Genome Res. 2002 Jun;12(6):996-1006 [12045153.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 25;99(13):8695-700 [12060701.001]
  • [Cites] Genome Res. 2002 Jul;12(7):1112-20 [12097349.001]
  • [Cites] Semin Cancer Biol. 2002 Oct;12(5):347-57 [12191634.001]
  • [Cites] Cancer Res. 2003 May 1;63(9):2164-71 [12727835.001]
  • [Cites] Leukemia. 2003 May;17(5):910-8 [12750705.001]
  • [Cites] N Engl J Med. 2003 Nov 20;349(21):2042-54 [14627790.001]
  • [Cites] Methods Enzymol. 2004;376:315-34 [14975315.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1617-28 [15084694.001]
  • [Cites] Cell. 2004 Jun 11;117(6):721-33 [15186774.001]
  • [Cites] Clin Cancer Res. 2004 Aug 1;10(15):4933-8 [15297393.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jun 9;95(12):6870-5 [9618505.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14863-8 [9843981.001]
  • [Cites] Cancer Res. 2007 Mar 15;67(6):2617-25 [17363581.001]
  • [Cites] BMC Genomics. 2007;8:131 [17524140.001]
  • [Cites] Science. 2001 Aug 10;293(5532):1074-80 [11498575.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10781-6 [11535808.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]
  • [Cites] Genes Dev. 2002 Jan 1;16(1):6-21 [11782440.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Nat Genet. 1999 Jan;21(1):103-7 [9916800.001]
  • [Cites] Cancer Res. 1999 Feb 15;59(4):793-7 [10029064.001]
  • [Cites] Cell. 2005 Jan 28;120(2):169-81 [15680324.001]
  • (PMID = 18365023.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA104348; United States / NICHD NIH HHS / HD / R01 HD044078; United States / NIGMS NIH HHS / GM / T32 GM007288; United States / NIGMS NIH HHS / GM / GM007288
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Histones
  • [Other-IDs] NLM/ PMC2266992
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33. Ulusoy G, Adali O, Tumer TB, Sahin G, Gozdasoglu S, Arinç E: Significance of genetic polymorphisms at multiple loci of CYP2E1 in the risk of development of childhood acute lymphoblastic leukemia. Oncology; 2007;72(1-2):125-31
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  • [Title] Significance of genetic polymorphisms at multiple loci of CYP2E1 in the risk of development of childhood acute lymphoblastic leukemia.
  • BACKGROUND/AIMS: The molecular etiology of childhood acute lymphoblastic leukemia (ALL) is likely to involve interactions between environmental factors and genetic make up.
  • Understanding these interactions between various predisposing genes for the risk of developing childhood leukemia is of considerable importance.
  • The CYP2E1 gene possesses several polymorphisms in humans, and among them, CYP2E1*5B and *6 have been shown to be associated with increased risks of several chemical-induced diseases.
  • [MeSH-major] Cytochrome P-450 CYP2E1 / genetics. Genetic Predisposition to Disease. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] Copyright 2007 S. Karger AG, Basel.
  • (PMID = 18025800.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] EC 1.14.13.- / Cytochrome P-450 CYP2E1
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34. Sun J, Huang H, Zhu YY, Lan JP, Li JY, Lai XY, Yu J: Study on the expression and mutation of human telomeric repeat binding factor (hTRF1) in 10 malignant hematopoietic cell lines. J Zhejiang Univ Sci B; 2005 Dec;6(12):1141-7
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  • [Title] Study on the expression and mutation of human telomeric repeat binding factor (hTRF1) in 10 malignant hematopoietic cell lines.
  • OBJECTIVE: Detecting the expression and mutation of human telomeric repeat binding factor (hTRF1) in 10 malignant hematopoietic cell line cells on the base of determining its genomic structure and its four pseudogenes to clarify if hTRF1 mutation is one of the factors of the activation of telomerase.
  • Real-time RT-PCR was used to detect the expression of hTRF1mRNA in 10 cell line cells, including myelogenous leukemia cell lines K562, HL-60, U-937, NB4, THP-1, HEL and Dami; lymphoblastic leukemia cell lines 6T-CEM, Jurkat and Raji.
  • PCR and sequencing were used to detect mutation of each exon of hTRF1 in 10 cell line cells.
  • All cell line cells showed positive telomerase activity.
  • The expression of hTRF1 was significantly lower in malignant hematopoietic cell lines cells (0.0338, 0.0108-0.0749) than in normal mononuclear cells (0.0493, 0.0369-0.128) (P=0.004).
  • But no significant mutation was found in all exons of hTRF1 in 10 cell line cells.
  • CONCLUSION: hTRF1 mutation is probably not one of the main factors for telomerase activation in malignant hematopoietic disease.
  • [MeSH-minor] Base Sequence. Cell Line, Tumor / metabolism. Gene Expression Regulation, Neoplastic. Genetic Predisposition to Disease / genetics. Humans. Molecular Sequence Data

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  • [Cites] Nucleic Acids Res. 2000 Feb 1;28(3):669-77 [10637317.001]
  • [Cites] Oncol Rep. 2000 Sep-Oct;7(5):987-90 [10948327.001]
  • [Cites] Int J Oncol. 2001 Mar;18(3):593-8 [11179492.001]
  • [Cites] Oncogene. 2001 Mar 22;20(12):1497-508 [11313893.001]
  • [Cites] Cell. 2001 Nov 2;107(3):347-59 [11701125.001]
  • [Cites] Science. 1998 Nov 20;282(5393):1484-7 [9822378.001]
  • [Cites] Exp Neurol. 2004 Aug;188(2):238-45 [15246823.001]
  • [Cites] Annu Rev Genet. 1985;19:253-72 [3909943.001]
  • [Cites] Science. 1995 Dec 8;270(5242):1663-7 [7502076.001]
  • [Cites] Nature. 1997 Feb 20;385(6618):740-3 [9034193.001]
  • [Cites] Somat Cell Mol Genet. 1997 Jul;23(4):275-86 [9542529.001]
  • [Cites] Anticancer Res. 2002 Mar-Apr;22(2B):1315-20 [12168944.001]
  • (PMID = 16358369.001).
  • [ISSN] 1673-1581
  • [Journal-full-title] Journal of Zhejiang University. Science. B
  • [ISO-abbreviation] J Zhejiang Univ Sci B
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / TERF1 protein, human; 0 / Telomere-Binding Proteins
  • [Other-IDs] NLM/ PMC1390634
  •  go-up   go-down


35. Haarman EG, Kaspers GJ, Pieters R, Rottier MM, Veerman AJ: Circumvention of glucocorticoid resistance in childhood leukemia. Leuk Res; 2008 Sep;32(9):1417-23
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  • [Title] Circumvention of glucocorticoid resistance in childhood leukemia.
  • In this study, we determined if in vitro resistance to prednisolone and dexamethasone could be circumvented by cortivazol or methylprednisolone, or reversed by meta-iodobenzylguanidine in pediatric lymphoblastic and myeloid leukemia.
  • As there were strong correlations between the LC50 values (drug concentration inducing 50% leukemic cell kill, LCK) of the different glucocorticoids and median prednisolone/methylprednisolone, prednisolone/dexamethasone and prednisolone/cortivazol LC50 ratios did not differ between the leukemia subtypes, we conclude that none of the glucocorticoids had preferential anti-leukemic activity.
  • Meta-iodobenzylguanidine however, partially reversed glucocorticoid resistance in 19% of the lymphoblastic leukemia samples.
  • [MeSH-major] Drug Resistance, Neoplasm. Glucocorticoids / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Methylprednisolone / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pregnatrienes / therapeutic use
  • [MeSH-minor] Cell Proliferation. Child. Dexamethasone / therapeutic use. Drug Screening Assays, Antitumor. Humans. Prednisolone / therapeutic use. Tumor Cells, Cultured

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  • (PMID = 18395253.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Pregnatrienes; 7S5I7G3JQL / Dexamethasone; 9PHQ9Y1OLM / Prednisolone; X4W7ZR7023 / Methylprednisolone; YM183K0H63 / cortivazol
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36. Campana D: Role of minimal residual disease monitoring in adult and pediatric acute lymphoblastic leukemia. Hematol Oncol Clin North Am; 2009 Oct;23(5):1083-98, vii
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  • [Title] Role of minimal residual disease monitoring in adult and pediatric acute lymphoblastic leukemia.
  • Assays that measure minimal residual disease (MRD) can determine the response to treatment in patients with acute lymphoblastic leukemia (ALL) much more precisely than morphologic screening of bone marrow smears.

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  • [Cites] Blood. 2008 Jun 15;111(12):5477-85 [18388178.001]
  • [Cites] J Clin Oncol. 2008 Jun 20;26(18):3046-50 [18565891.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2008;:366-73 [19074112.001]
  • [Cites] Leukemia. 2008 Dec;22(12):2193-200 [18754029.001]
  • [Cites] Semin Hematol. 2009 Jan;46(1):100-6 [19100372.001]
  • [Cites] JAMA. 2009 Jan 28;301(4):393-403 [19176441.001]
  • [Cites] N Engl J Med. 2009 Jan 29;360(5):470-80 [19129520.001]
  • [Cites] Lancet Oncol. 2009 Feb;10(2):147-56 [19147408.001]
  • [Cites] Blood. 2009 Apr 30;113(18):4153-62 [19141862.001]
  • [Cites] Leukemia. 2009 Jun;23(6):1073-9 [19212338.001]
  • [Cites] J Clin Oncol. 2009 Jul 20;27(21):3533-9 [19546402.001]
  • [Cites] Br J Haematol. 2008 Jun;142(2):227-37 [18492099.001]
  • [Cites] Leukemia. 1999 Dec;13(12):1901-28 [10602411.001]
  • [Cites] Blood. 2000 Feb 1;95(3):790-4 [10648387.001]
  • [Cites] Leukemia. 2000 Jun;14(6):1143-52 [10865981.001]
  • [Cites] Leukemia. 2000 Jul;14(7):1208-14 [10914544.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2691-6 [11023499.001]
  • [Cites] Leukemia. 2000 Nov;14(11):1939-43 [11069029.001]
  • [Cites] Br J Haematol. 2001 Feb;112(2):275-81 [11167819.001]
  • [Cites] Leukemia. 2001 Sep;15(9):1485-7 [11516112.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1982-4 [11535539.001]
  • [Cites] Lancet. 2001 Oct 13;358(9289):1239-41 [11675066.001]
  • [Cites] J Clin Oncol. 2002 Feb 15;20(4):1094-104 [11844835.001]
  • [Cites] Br J Haematol. 2002 Mar;116(3):686-94 [11849234.001]
  • [Cites] Blood. 2002 Mar 15;99(6):1952-8 [11877265.001]
  • [Cites] Blood. 2002 Apr 1;99(7):2315-23 [11895762.001]
  • [Cites] Lancet Oncol. 2001 Oct;2(10):597-607 [11902549.001]
  • [Cites] Lancet Oncol. 2001 Jul;2(7):409-17 [11905735.001]
  • [Cites] Blood. 2002 Jul 1;100(1):43-7 [12070006.001]
  • [Cites] Leukemia. 2004 Dec;18(12):1971-80 [15470492.001]
  • [Cites] Leukemia. 2005 Jan;19(1):49-56 [15538405.001]
  • [Cites] Blood. 2005 Jan 15;105(2):821-6 [15388585.001]
  • [Cites] Br J Haematol. 2005 Mar;128(6):774-82 [15755280.001]
  • [Cites] Leukemia. 2005 Apr;19(4):628-35 [15744351.001]
  • [Cites] Blood. 2005 Jun 15;105(12):4752-8 [15713801.001]
  • [Cites] Blood. 2005 Jul 15;106(2):458-63 [15817679.001]
  • [Cites] Blood. 2002 Jul 1;100(1):52-8 [12070008.001]
  • [Cites] Leukemia. 2002 Aug;16(8):1432-6 [12145681.001]
  • [Cites] Leukemia. 2002 Sep;16(9):1668-72 [12200679.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2399-402 [12239148.001]
  • [Cites] Leukemia. 2003 Jun;17(6):1013-34 [12764363.001]
  • [Cites] Br J Haematol. 2003 Jun;121(6):823-38 [12786792.001]
  • [Cites] Br J Haematol. 2003 Jul;122(1):24-9 [12823342.001]
  • [Cites] Leukemia. 2003 Aug;17(8):1566-72 [12886244.001]
  • [Cites] Bone Marrow Transplant. 2003 Oct;32(8):849-51 [14520434.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2318-57 [14562125.001]
  • [Cites] Leukemia. 2004 Mar;18(3):499-504 [14981525.001]
  • [Cites] Leukemia. 2004 May;18(5):934-8 [15029212.001]
  • [Cites] Br Med J. 1966 Mar 12;1(5488):640-2 [5218168.001]
  • [Cites] Blood. 1980 Sep;56(3):430-41 [6996767.001]
  • [Cites] Leuk Res. 1981;5(4-5):301-9 [7026903.001]
  • [Cites] Blood. 1987 Oct;70(4):1073-8 [3477296.001]
  • [Cites] Blood. 1988 Jul;72(1):299-307 [3291983.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Aug;85(15):5698-702 [3165197.001]
  • [Cites] Leukemia. 1988 Oct;2(10):628-33 [3172839.001]
  • [Cites] Leukemia. 1989 Feb;3(2):155-8 [2536129.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Jul;86(13):5123-7 [2500663.001]
  • [Cites] Blood. 1989 Oct;74(5):1762-7 [2676018.001]
  • [Cites] Blood. 1990 Jul 1;76(1):163-71 [1973061.001]
  • [Cites] Anal Cell Pathol. 1990 Jul;2(4):229-40 [1703434.001]
  • [Cites] Clin Chim Acta. 1991 Apr;198(1-2):93-174 [1863986.001]
  • [Cites] Leukemia. 1991 Aug;5(8):657-67 [1909409.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Jul 1;90(13):6061-5 [8327485.001]
  • [Cites] Blood. 1993 Nov 15;82(10):3063-74 [8219197.001]
  • [Cites] Leukemia. 1993 Dec;7(12):2045-53 [7902888.001]
  • [Cites] Lancet. 1994 Jan 22;343(8891):196-200 [7904666.001]
  • [Cites] Blood. 1995 Nov 15;86(10):3930-7 [7579363.001]
  • [Cites] Blood. 1997 Apr 1;89(7):2602-9 [9116308.001]
  • [Cites] Br J Haematol. 1997 Nov;99(2):314-9 [9375747.001]
  • [Cites] Lancet. 1998 Feb 21;351(9102):550-4 [9492773.001]
  • [Cites] N Engl J Med. 1998 Aug 27;339(9):591-8 [9718378.001]
  • [Cites] Blood. 1998 Dec 1;92(11):4072-9 [9834212.001]
  • [Cites] Lancet. 1998 Nov 28;352(9142):1731-8 [9848348.001]
  • [Cites] J Clin Oncol. 1998 Dec;16(12):3774-81 [9850021.001]
  • [Cites] Leukemia. 1999 Jan;13(1):110-8 [10049045.001]
  • [Cites] Leukemia. 1999 Feb;13(2):196-205 [10025893.001]
  • [Cites] Leukemia. 1999 Mar;13(3):419-27 [10086733.001]
  • [Cites] Curr Top Microbiol Immunol. 1999;246:205-13; discussion 214-5 [10396058.001]
  • [Cites] Cytometry. 1999 Aug 15;38(4):139-52 [10440852.001]
  • [Cites] Leukemia. 1999 Aug;13(8):1221-6 [10450750.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6306-15 [16155013.001]
  • [Cites] Blood. 2006 Feb 1;107(3):1116-23 [16195338.001]
  • [Cites] Blood. 2006 Jul 1;108(1):97-102 [16537802.001]
  • [Cites] Blood. 2006 Aug 1;108(3):1050-7 [16627760.001]
  • [Cites] Blood. 2007 Feb 1;109(3):910-5 [17023577.001]
  • [Cites] Leukemia. 2007 Apr;21(4):604-11 [17287850.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Haematologica. 2007 May;92(5):612-8 [17488684.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1271-7 [17456722.001]
  • [Cites] Blood. 2007 Sep 1;110(5):1607-11 [17485550.001]
  • [Cites] Blood. 2007 Dec 1;110(12):4022-9 [17720883.001]
  • [Cites] Science. 2008 Jan 18;319(5861):336-9 [18202291.001]
  • [Cites] Leukemia. 2008 Apr;22(4):771-82 [18239620.001]
  • (PMID = 19825454.001).
  • [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 / R01 CA060419-13; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / R01 CA060419; United States / NCI NIH HHS / CA / CA60419; United States / NCI NIH HHS / CA / P30 CA021765; None / None / / R01 CA060419-13; United States / NCI NIH HHS / CA / U01 CA060419
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 95
  • [Other-IDs] NLM/ NIHMS132490; NLM/ PMC2762949
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37. Kodama Y, Okamoto Y, Ijichi O, Shinkoda Y, Nishikawa T, Tanabe T, Yoshioka T, Tashiro Y, Mougi H, Kawano Y: Continued complete remission without systemic therapy for isolated testicular relapse after bone marrow transplantation in a boy with acute lymphoblastic leukemia. Pediatr Transplant; 2009 Sep;13(6):769-72
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  • [Title] Continued complete remission without systemic therapy for isolated testicular relapse after bone marrow transplantation in a boy with acute lymphoblastic leukemia.
  • ITR after BMT in cases of acute lymphoblastic leukemia is relatively rare.
  • Treatment for ITR after BMT generally consists of a combination of local irradiation, orchiectomy, and systemic chemotherapy.
  • [MeSH-major] Bone Marrow Transplantation / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Testicular Neoplasms / diagnosis


38. Poyer F, Coquerel B, Pegahi R, Cazin L, Norris V, Vannier JP, Lamacz M: Secretion of MMP-2 and MMP-9 induced by VEGF autocrine loop correlates with clinical features in childhood acute lymphoblastic leukemia. Leuk Res; 2009 Mar;33(3):407-17
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  • [Title] Secretion of MMP-2 and MMP-9 induced by VEGF autocrine loop correlates with clinical features in childhood acute lymphoblastic leukemia.
  • In children with acute lymphoblastic leukemia (ALL), leukemic cells express several members of the VEGF family and the three VEGF receptors which, via an autocrine loop are responsible for secretion of MMP-2/-9.
  • [MeSH-major] Autocrine Communication. Matrix Metalloproteinase 2 / secretion. Matrix Metalloproteinase 9 / secretion. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Vascular Endothelial Growth Factor A / physiology. Vascular Endothelial Growth Factor Receptor-1 / analysis. Vascular Endothelial Growth Factor Receptor-3 / analysis

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  • (PMID = 18829111.001).
  • [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 / Biomarkers; 0 / Hemoglobins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-3; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
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39. Goto H, Yanagimachi M, Kajiwara R, Kuroki F, Yokota S: Lack of mitochondrial depolarization by oxidative stress is associated with resistance to buthionine sulfoximine in acute lymphoblastic leukemia cells. Leuk Res; 2007 Sep;31(9):1293-301
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  • [Title] Lack of mitochondrial depolarization by oxidative stress is associated with resistance to buthionine sulfoximine in acute lymphoblastic leukemia cells.
  • Raised intracellular glutathione is one characteristics of high-risk childhood acute lymphoblastic leukemia (ALL).
  • To assess the role of glutathione in ALL, the toxicity of BSO was studied in B-precursor ALL cell lines.
  • BSO increased oxidative stress equally in all cell lines; however mitochondrial depolarization was observed only in BSO-sensitive cells.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Buthionine Sulfoximine / therapeutic use. Drug Resistance, Neoplasm. Membrane Potentials / drug effects. Mitochondria / metabolism. Oxidative Stress. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Anti-Inflammatory Agents / pharmacology. Cell Proliferation / drug effects. Glutathione / metabolism. Humans. Hydrogen Peroxide / pharmacology. Oxidants / pharmacology. Prednisolone / pharmacology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Tumor Cells, Cultured / drug effects

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  • (PMID = 17306873.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antimetabolites, Antineoplastic; 0 / Oxidants; 0 / Proto-Oncogene Proteins c-bcl-2; 5072-26-4 / Buthionine Sulfoximine; 9PHQ9Y1OLM / Prednisolone; BBX060AN9V / Hydrogen Peroxide; GAN16C9B8O / Glutathione
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40. Abramenko I, Bilous N, Kryachok I, Filonenko I, Pilipenko G, Chumak A, Bazyka D, Bebeshko V: IGHV3-21 gene expression in patients with B-cell chronic lymphocytic leukemia in Ukraine. Exp Oncol; 2007 Sep;29(3):226-30
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  • [Title] IGHV3-21 gene expression in patients with B-cell chronic lymphocytic leukemia in Ukraine.
  • THE AIM of the study was to evaluate the frequency of IGHV3-21 gene usage and its clinical significance for patients with B-cell chronic lymphocytic leukemia (CLL) in Ukraine.
  • [MeSH-major] Gene Expression. Genes, Immunoglobulin Heavy Chain. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Neoplasms, Second Primary / genetics

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  • (PMID = 18004251.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Immunoglobulin Variable Region
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41. Rihani R, Bazzeh F, Faqih N, Sultan I: Secondary hematopoietic malignancies in survivors of childhood cancer: an analysis of 111 cases from the Surveillance, Epidemiology, and End Result-9 registry. Cancer; 2010 Sep 15;116(18):4385-94
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  • Primary cancer and histological subtype, incidence, risk factors, outcomes, and changes in risk patterns of secondary hematological malignancies were analyzed for 1973 to 1985, 1986 to 1995, and 1996 to 2005.
  • The main histological subtype of secondary hematological malignancy was acute myeloid leukemia (AML) (49%), which had the shortest median latency time and the worst 5-year survival (18% ± 5.3%; P = .044).
  • The risk of secondary AML steadily increased from 1986 to 2005, whereas SIRs for acute lymphoblastic leukemia did not change over time.
  • Non-Hodgkin lymphoma, the second most common secondary hematological malignancy, occurred at a median of 112 months, and its risk steadily increased over time periods.

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  • [Copyright] © 2010 American Cancer Society.
  • (PMID = 20549819.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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42. El-Gohary GM, Azzam HM, Ahmed OI, El-Shokry MH: Pro-inflammatory cytokines and depression in patients with acute leukemia. Egypt J Immunol; 2008;15(1):13-24
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  • [Title] Pro-inflammatory cytokines and depression in patients with acute leukemia.
  • The aim of present study was to investigate the relation between pro-infammatory cytokines [Interleukin-6 (IL-6) and Tumor Necrosis Factor-alpha (TNF-alpha)], depression and stressful life events in patients with acute leukemia.
  • Twenty eight patients (18 males and 10 females) suffering from acute leukemia participated in this study.
  • Although, TNF-a gene expression was not associated with depression or stressful life events, it was associated with acute myeloblastic leukemia (AML).
  • IL-6 gene expression was much higher among patients with AML than acute lymphoblastic leukemia (ALL), but the difference did not reach statistical significance.


43. Vezmar S, Schüsseler P, Becker A, Bode U, Jaehde U: Methotrexate-associated alterations of the folate and methyl-transfer pathway in the CSF of ALL patients with and without symptoms of neurotoxicity. Pediatr Blood Cancer; 2009 Jan;52(1):26-32
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  • PROCEDURE: MTX, 5-methyltetrahydrofolate, calcium folinate, S-adenosylmethionine, and S-adenosylhomocysteine were measured in the cerebrospinal fluid (CSF) of 29 patients with acute lymphoblastic leukemia (ALL) who were treated with high-dose MTX (5 g/m(2)) followed by calcium folinate rescue (3 x 15 mg/m(2)) and/or intrathecal (8-12 mg) MTX.
  • RESULTS: In non-toxic patients, CSF concentrations of 5-methyltetrahydrofolate and S-adenosylmethionine were in the normal range 2 weeks after administration of high-dose and intrathecal MTX followed by rescue.
  • S-adenosylhomocysteine was determined in all samples of neurotoxic patients but was below the limit of quantification in most samples of non-toxic patients.
  • [MeSH-major] Cerebrospinal Fluid / metabolism. Folic Acid / metabolism. Metabolic Networks and Pathways / drug effects. Methotrexate / pharmacology. Neurotoxicity Syndromes. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • [CommentIn] Pediatr Blood Cancer. 2009 Jul;53(1):127; author reply 127-8 [19340855.001]
  • (PMID = 19006245.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 935E97BOY8 / Folic Acid; YL5FZ2Y5U1 / Methotrexate
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44. Högler W, Wehl G, van Staa T, Meister B, Klein-Franke A, Kropshofer G: Incidence of skeletal complications during treatment of childhood acute lymphoblastic leukemia: comparison of fracture risk with the General Practice Research Database. Pediatr Blood Cancer; 2007 Jan;48(1):21-7
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  • [Title] Incidence of skeletal complications during treatment of childhood acute lymphoblastic leukemia: comparison of fracture risk with the General Practice Research Database.
  • BACKGROUND: Skeletal complications during or after treatment of acute lymphoblastic leukemia (ALL) have been frequently reported and can cause substantial morbidity, yet their incidence is not well established.
  • PROCEDURE: Medical records of 122 ALL patients diagnosed at our institution from 1992 to 2004 were reviewed for information on fractures, ON, bone pain, and their anatomical location, risk group, phase of antileukemic therapy, and time since diagnosis.
  • Thirteen children were excluded as they were transferred to other institutions shortly after diagnosis.
  • Nearly all skeletal complications occurred during maintenance therapy at a median of 14.92 months (range 0.0-53.8) after diagnosis and in weight-bearing bones.
  • CONCLUSIONS: The doubled fracture rate and the high incidence of skeletal complications during the first years after diagnosis suggest the developing skeleton is very vulnerable in this period.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Fractures, Bone / chemically induced. Fractures, Bone / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality


45. Wojcik I, Szybka M, Golanska E, Rieske P, Blonski JZ, Robak T, Bartkowiak J: Abnormalities of the P53, MDM2, BCL2 and BAX genes in acute leukemias. Neoplasma; 2005;52(4):318-24
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  • [Title] Abnormalities of the P53, MDM2, BCL2 and BAX genes in acute leukemias.
  • Abnormalities of the P53 network have been implicated in the pathogenesis of acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML).
  • To gain further insight into the role of P53 network in the evolution of acute leukemias, the P53, MDM2, BCL2 and BAX mRNAexpressions in portion samples from patients with ALL and AML were analyzed using multiplex RT-PCR.
  • A high frequency of BCL2 mRNA overexpression and a relatively low frequency of BAX mRNA overexpression detected in both analyzed leukemias in this study, indicate that altered transcription of these genes may be involved in leukemogenesis.
  • [MeSH-major] Gene Amplification. Gene Expression Profiling. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16059649.001).
  • [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 / BAX protein, human; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / bcl-2-Associated X Protein; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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46. Spector LG, Xie Y, Robison LL, Heerema NA, Hilden JM, Lange B, Felix CA, Davies SM, Slavin J, Potter JD, Blair CK, Reaman GH, Ross JA: Maternal diet and infant leukemia: the DNA topoisomerase II inhibitor hypothesis: a report from the children's oncology group. Cancer Epidemiol Biomarkers Prev; 2005 Mar;14(3):651-5
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  • [Title] Maternal diet and infant leukemia: the DNA topoisomerase II inhibitor hypothesis: a report from the children's oncology group.
  • BACKGROUND: The MLL 11q23 translocation arises in utero and is present in 75% of infant leukemias.
  • That MLL+ acute myeloid leukemia (AML) can arise following chemotherapy with DNA topoisomerase II (DNAt2) inhibitors suggests that these substances, which also occur naturally in foods, may contribute toward infant leukemia.
  • We hypothesized that maternal consumption of dietary DNAt2 inhibitors during pregnancy would increase the risk of infant leukemia, particularly AML(MLL+).
  • METHODS: This Children's Oncology Group case-control study consisted of 240 incident cases of infant acute leukemia [AML and acute lymphoblastic leukemia (ALL)] diagnosed during 1996 to 2002 and 255 random digit dialed controls.
  • RESULTS: There was little evidence of an association between the specific DNAt2 index and leukemia overall and by subtype.
  • For the vegetable and fruit index, there were significant or near-significant inverse linear trends for all leukemias combined, ALL(MLL+), and AML(MLL-).
  • CONCLUSION: Overall, maternal consumption of fresh vegetables and fruits during pregnancy was associated with a decreased risk of infant leukemia, particularly MLL+.
  • Although based on small numbers, these data provide some support for distinct etiologic pathways in infant leukemia.

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  • (PMID = 15767345.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA079940; United States / NCI NIH HHS / CA / CA79940
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Topoisomerase II Inhibitors
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47. Campana D: Role of minimal residual disease evaluation in leukemia therapy. Curr Hematol Malig Rep; 2008 Jul;3(3):155-60
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  • [Title] Role of minimal residual disease evaluation in leukemia therapy.
  • In patients with acute leukemia, measurements of minimal residual disease (MRD) provide unique information on response to treatment.
  • Many studies in children and adults with acute lymphoblastic leukemia and acute myeloid leukemia have demonstrated a strong association between the presence of MRD and risk of relapse.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Flow Cytometry. Genes, T-Cell Receptor. Humans. Immunophenotyping. Neoplasm, Residual. Polymerase Chain Reaction. Prognosis. Recurrence

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  • [Cites] Lancet Oncol. 2001 Oct;2(10):597-607 [11902549.001]
  • [Cites] Blood. 2000 Feb 1;95(3):815-9 [10648391.001]
  • [Cites] Leukemia. 2002 Mar;16(3):368-75 [11896540.001]
  • [Cites] Leukemia. 1999 Dec;13(12):1901-28 [10602411.001]
  • [Cites] Blood. 2003 Jul 15;102(2):773-4; author reply 774 [12835231.001]
  • [Cites] Leukemia. 1999 Jan;13(1):110-8 [10049045.001]
  • [Cites] Blood. 2007 Sep 1;110(5):1607-11 [17485550.001]
  • [Cites] Lancet. 1998 Feb 21;351(9102):550-4 [9492773.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2387-92 [12239146.001]
  • [Cites] Blood. 2003 Mar 1;101(5):1698-704 [12406915.001]
  • [Cites] Lancet Oncol. 2001 Jul;2(7):409-17 [11905735.001]
  • [Cites] Lancet. 1994 Jan 22;343(8891):196-200 [7904666.001]
  • [Cites] Blood. 2006 Aug 1;108(3):1050-7 [16627760.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5477-85 [18388178.001]
  • [Cites] Leukemia. 2000 Nov;14(11):1939-43 [11069029.001]
  • [Cites] Br J Haematol. 2003 Jun;121(6):823-38 [12786792.001]
  • [Cites] Nat Rev Cancer. 2006 Feb;6(2):146-55 [16491074.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2691-6 [11023499.001]
  • [Cites] Blood. 2002 Jul 1;100(1):52-8 [12070008.001]
  • [Cites] Curr Top Microbiol Immunol. 2007;313:145-56 [17217043.001]
  • [Cites] Leukemia. 2001 Jul;15(7):1072-80 [11455976.001]
  • [Cites] Lancet. 2001 Oct 13;358(9289):1239-41 [11675066.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2399-402 [12239148.001]
  • [Cites] Blood. 2001 Apr 1;97(7):2115-20 [11264179.001]
  • [Cites] Leukemia. 2003 Jun;17(6):1013-34 [12764363.001]
  • [Cites] J Clin Invest. 2007 Apr;117(4):1049-57 [17380207.001]
  • [Cites] Leukemia. 2008 Apr;22(4):771-82 [18239620.001]
  • [Cites] N Engl J Med. 2005 May 26;352(21):2158-60 [15917380.001]
  • [Cites] N Engl J Med. 1998 Aug 27;339(9):591-8 [9718378.001]
  • [Cites] Br J Haematol. 2005 Mar;128(6):774-82 [15755280.001]
  • [Cites] Br J Haematol. 2003 Oct;123(2):243-52 [14531905.001]
  • [Cites] Leukemia. 2004 Mar;18(3):499-504 [14981525.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1746-51 [11535507.001]
  • [Cites] Leukemia. 2004 May;18(5):934-8 [15029212.001]
  • [Cites] Lancet. 1998 Nov 28;352(9142):1731-8 [9848348.001]
  • [Cites] Blood. 2002 Jul 1;100(1):43-7 [12070006.001]
  • [Cites] Leukemia. 2006 Oct;20(10):1783-9 [16838027.001]
  • [Cites] Leukemia. 2003 Nov;17(11):2178-82 [14576731.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2393-8 [12239147.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6306-15 [16155013.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2318-57 [14562125.001]
  • [Cites] Nature. 2004 May 27;429(6990):464-8 [15164072.001]
  • [Cites] Blood. 2003 Jan 1;101(1):64-70 [12393605.001]
  • [Cites] Bone Marrow Transplant. 2003 Oct;32(8):849-51 [14520434.001]
  • [Cites] Blood. 2003 May 1;101(9):3398-406 [12506020.001]
  • [Cites] Leukemia. 2002 Aug;16(8):1432-6 [12145681.001]
  • [Cites] Blood. 2006 Jul 1;108(1):97-102 [16537802.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1271-7 [17456722.001]
  • [Cites] Blood. 2000 Feb 1;95(3):790-4 [10648387.001]
  • (PMID = 20425460.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA115422; 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
  • [Publication-country] United States
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48. Pei SN, Kuo CY, Ma MC, Wang MC: Mediastinal mass and malignant pleural effusion in an aleukemic case with pre-B acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2009 Feb;31(2):139-41
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  • [Title] Mediastinal mass and malignant pleural effusion in an aleukemic case with pre-B acute lymphoblastic leukemia.
  • After a bone marrow examination, we diagnosed the patient with pre-B acute lymphoblastic leukemia (ALL).
  • This is the first reported case of a malignant pleural effusion and a mediastinal mass that preceded pre-B ALL.
  • After standard therapy for ALL, the patient has been disease-free for 7 years.
  • [MeSH-major] Mediastinal Neoplasms / diagnosis. Pleural Effusion, Malignant / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Examination. Disease-Free Survival. Humans. Immunophenotyping. Male. Young Adult

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  • (PMID = 19194202.001).
  • [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
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49. Enzler T, Kater AP, Zhang W, Widhopf GF 2nd, Chuang HY, Lee J, Avery E, Croce CM, Karin M, Kipps TJ: Chronic lymphocytic leukemia of Emu-TCL1 transgenic mice undergoes rapid cell turnover that can be offset by extrinsic CD257 to accelerate disease progression. Blood; 2009 Nov 12;114(20):4469-76
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  • [Title] Chronic lymphocytic leukemia of Emu-TCL1 transgenic mice undergoes rapid cell turnover that can be offset by extrinsic CD257 to accelerate disease progression.
  • Results of heavy-water labeling studies have challenged the notion that chronic lymphocytic leukemia (CLL) represents an accumulation of noncycling B cells.
  • We examined leukemia cell turnover in Emu-TCL1 transgenic (TCL1-Tg) mice, which develop a CLL-like disease at 8 to 12 months of age.
  • We found that leukemia cells in these mice not only had higher proportions of proliferating cells but also apoptotic cells than did nonleukemic lymphocytes.
  • TCL1 x BAFF-Tg mice developed CLL-like disease at a significantly younger age and had more rapid disease progression and shorter survival than TCL1-Tg mice.
  • Leukemia cells of TCL1 x BAFF-Tg mice had similar proportions of proliferating cells, but fewer proportions of dying cells, than did the CLL cells of TCL1-Tg mice.
  • Moreover, leukemia cells from either TCL1 x BAFF-Tg or TCL1-Tg mice produced more aggressive disease when transferred into BAFF-Tg mice than into wild-type (WT) mice.
  • Neutralization of CD257 resulted in rapid reduction in circulating leukemia cells.
  • These results indicate that the leukemia cells of TCL1-Tg mice undergo high levels of spontaneous apoptosis that is offset by relatively high rates of leukemia cell proliferation, which might allow for acquisition of mutations that contribute to disease evolution.
  • [MeSH-major] Apoptosis / physiology. B-Cell Activating Factor / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / pathology
  • [MeSH-minor] Adoptive Transfer. Animals. Blotting, Southern. Blotting, Western. Cell Proliferation. Disease Progression. Flow Cytometry. In Situ Nick-End Labeling. Mice. Mice, Transgenic. Proto-Oncogene Proteins / genetics

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  • [ErratumIn] Blood. 2010 Jul 29;116(4):671
  • (PMID = 19755673.001).
  • [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 / B-Cell Activating Factor; 0 / Proto-Oncogene Proteins; 0 / Tcl1 protein, mouse
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50. Papadhimitriou SI, Polychronopoulou S, Tsakiridou AA, Androutsos G, Paterakis GS, Athanassiadou F: p16 inactivation associated with aggressive clinical course and fatal outcome in TEL/AML1-positive acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2005 Dec;27(12):675-7
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  • [Title] p16 inactivation associated with aggressive clinical course and fatal outcome in TEL/AML1-positive acute lymphoblastic leukemia.
  • The authors describe a 7-year-old boy with TEL/AML1-positive pre-B acute lymphoblastic leukemia, with hemizygous 9p21 deletion at presentation and no p16(INK4A) protein expression.
  • Despite an initial response to a standard chemotherapy regimen, the patient suffered two hematologic relapses and died 34 months after diagnosis.
  • The authors discuss the possibility that complete p16(INK4A) gene inactivation may adversely modify the prognostic significance of TEL/AML1 fusion in childhood acute lymphoblastic leukemia, and present evidence from clinical and in vitro observations in favor of this assumption.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Deletion. Genes, p16. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • Hazardous Substances Data Bank. CYTARABINE .
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  • (PMID = 16344676.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 04079A1RDZ / Cytarabine; 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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51. Oestreicher N, Friedman GD, Jiang SF, Chan J, Quesenberry C Jr, Habel LA: Methylphenidate use in children and risk of cancer at 18 sites: results of surveillance analyses. Pharmacoepidemiol Drug Saf; 2007 Dec;16(12):1268-72
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  • Only one SMR was statistically significant at the p < 0.05 level, which given the number of comparisons is consistent with the absence of a true association at any site.
  • MPH use was associated with increased risk of lymphocytic leukemia (SMR = 2.64 (1.14, 5.20)), based on eight observed cases).
  • The medical records of these exposed cases did not reveal any lymphocytic leukemia risk factors (prior cancer, radiotherapy or chemotherapy, or Down syndrome).
  • Further study of MPH use and lymphocytic leukemia risk is needed to determine whether our results are due to chance alone.

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  • [Copyright] Copyright 2007 John Wiley & Sons, Ltd.
  • [CommentIn] Pharmacoepidemiol Drug Saf. 2007 Dec;16(12):1273-4 [18041105.001]
  • (PMID = 18041106.001).
  • [ISSN] 1053-8569
  • [Journal-full-title] Pharmacoepidemiology and drug safety
  • [ISO-abbreviation] Pharmacoepidemiol Drug Saf
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA098838-04; United States / NCI NIH HHS / CA / R01 CA098838; United States / NCI NIH HHS / CA / R01 CA098838-04; United States / NCI NIH HHS / CA / R01 CA98838
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amphetamines; 0 / Central Nervous System Stimulants; 207ZZ9QZ49 / Methylphenidate; 7GAQ2332NK / Pemoline
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52. Fischer L, Gökbuget N, Schwartz S, Burmeister T, Rieder H, Brüggemann M, Hoelzer D, Thiel E: CD56 expression in T-cell acute lymphoblastic leukemia is associated with non-thymic phenotype and resistance to induction therapy but no inferior survival after risk-adapted therapy. Haematologica; 2009 Feb;94(2):224-9
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  • [Title] CD56 expression in T-cell acute lymphoblastic leukemia is associated with non-thymic phenotype and resistance to induction therapy but no inferior survival after risk-adapted therapy.
  • BACKGROUND: Expression of CD56 has been associated with poor prognosis in acute myeloid leukemia and aggressive lymphoma.
  • DESIGN AND METHODS: We analyzed the impact of CD56 expression in a cohort of 452 newly diagnosed adult T-cell acute lymphoblastic leukemia (T-ALL) patients; clinical data were available for 306 patients.
  • CD56(+) T-ALL were predominantly of non-thymic (pre-T 35%, mature 41%) immunophenotypic subtypes, whereas 53% of the CD56(-) cases were thymic T-ALL (p=0.00002).
  • A clonal T-cell receptor rearrangement was detected in 22/23 CD56(+) ALL.
  • Treatment of CD56(+) ALL resulted in a lower rate of complete remissions (70% vs. 88%) (p=0.001) and a higher rate of resistant disease (21% vs. 8%) (p=0.004).
  • CD56 expression had no significant influence on overall (48% vs. 59%) and disease free survival (67% vs. 57%) at three years.
  • Most CD56(+) ALL were treated in the high-risk arm of the GMALL study protocols owing to their non-thymic phenotype.
  • [MeSH-major] Antigens, CD56. Drug Resistance, Neoplasm. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis


53. Dornbusch HJ, Sovinz P, Lackner H, Schwinger W, Benesch M, Strenger V, Urban C: Effective management of pulmonary aspergillosis invading the thoracic spine in a child with high risk ALL requiring allogeneic bone marrow transplantation. Med Mycol; 2008 Aug;46(5):487-90
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  • Due to unacceptably high mortality, invasive fungal infections (IFI) have long been considered a contraindication against allogeneic stem cell transplantation.
  • Despite severe immunosuppression an 11-year-old girl requiring allogeneic bone marrow transplant (BMT) for relapsed acute lymphoblastic leukemia was cured of a concurrent invasive pulmonary aspergillosis.
  • In hematological remission the child later developed fatal chronic graft-versus-host disease.
  • Combined antifungal treatment and granulocyte support allow for effective management of IFI even in allogeneic stem cell transplant recipients.
  • [MeSH-major] Aspergillosis, Allergic Bronchopulmonary / therapy. Bone Marrow Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications
  • [MeSH-minor] Adoptive Transfer. Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Child. Echinocandins / therapeutic use. Female. Graft vs Host Disease. Granulocytes / immunology. Humans. Pyrimidines / therapeutic use. Radiography, Thoracic. Spine / microbiology. Spine / pathology. Triazoles / therapeutic use. Voriconazole

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  • (PMID = 18608932.001).
  • [ISSN] 1369-3786
  • [Journal-full-title] Medical mycology
  • [ISO-abbreviation] Med. Mycol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Echinocandins; 0 / Pyrimidines; 0 / Triazoles; 0 / liposomal amphotericin B; 7XU7A7DROE / Amphotericin B; F0XDI6ZL63 / caspofungin; JFU09I87TR / Voriconazole
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54. Ambati S, Chamyan G, Restrepo R, Escalon E, Fort J, Pefkarou A, Khatib ZA, Dehner LP: Rosai-Dorfman disease following bone marrow transplantation for pre-B cell acute lymphoblastic leukemia. Pediatr Blood Cancer; 2008 Sep;51(3):433-5
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  • [Title] Rosai-Dorfman disease following bone marrow transplantation for pre-B cell acute lymphoblastic leukemia.
  • A child with acute pre-B cell lymphoblastic leukemia underwent haploidentical bone marrow transplantation (BMT) after first relapse.
  • A biopsy of the presenting lesion demonstrated a polymorphous infiltrate composed predominantly of S-100 protein and CD68 immunoreactive histiocytic cells.
  • Together with the presence of emperipolesis, the process was interpreted as Rosai-Dorfman (R-D) disease.
  • Only one previous example of acute lymphoblastic leukemia in childhood has been reported with R-D disease.
  • [MeSH-major] Bone Marrow Transplantation / adverse effects. Graft vs Host Disease / etiology. Histiocytosis, Sinus / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications


55. Dawidowska M, Wachowiak J, Witt M: [Molecular methods for diagnostics and assessment of treatment effectiveness in modern pediatric hematooncology]. Postepy Biochem; 2006;52(4):408-16
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  • This paper is a review of current diagnostic applications of molecular methods in pediatric hematooncology, including analyses performed at disease presentation, evaluation of prognosis as well as those for assessment of treatment effectiveness.
  • Here we present the examples of important fields of application of molecular methods in pediatric hematooncology, i.e. identification of clinically significant fusion genes in acute lymphoblastic leukemia and monitoring of minimal residual disease in this most frequent childhood malignancy.
  • Moreover, we present the methodology and clinical significance of quantitative analysis of hematopoietic chimerism after allogeneic stem cell transplantation.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / standards. Neoplasm, Residual / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Transplantation Chimera / genetics

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  • (PMID = 17536510.001).
  • [ISSN] 0032-5422
  • [Journal-full-title] Postepy biochemii
  • [ISO-abbreviation] Postepy Biochem.
  • [Language] pol
  • [Publication-type] English Abstract; Evaluation Studies; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Genetic Markers
  • [Number-of-references] 41
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56. Shaheen SP 2nd, Talwalkar SS, Simons R, Yam L: Acute lymphoblastic leukemic transformation in a patient with chronic idiopathic myelofibrosis and paroxysmal nocturnal hemoglobinuria: a case report and review of the literature. Arch Pathol Lab Med; 2005 Jan;129(1):96-9
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  • [Title] Acute lymphoblastic leukemic transformation in a patient with chronic idiopathic myelofibrosis and paroxysmal nocturnal hemoglobinuria: a case report and review of the literature.
  • Leukemic transformation of chronic idiopathic myelofibrosis (CIMF) to acute lymphoblastic leukemia (ALL) is rare.
  • We report a case of a patient with CIMF who developed paroxysmal nocturnal hemoglobinuria (PNH) 2 years after initial presentation.
  • His disease eventually transformed to ALL of precursor B-cell type.
  • In that CIMF and PNH are clonal stem cell disorders with different pathogeneses, there may be an association between them.
  • The simultaneous presentation of CIMF and PNH, complicated by the rare sequela of leukemic transformation, raises important issues with regard to diagnosis and treatment.
  • [MeSH-major] Hemoglobinuria, Paroxysmal / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Primary Myelofibrosis / complications
  • [MeSH-minor] Chronic Disease. Humans. Male. Middle Aged


57. Thomson KJ, Mackinnon S: Role of allogeneic transplantation in low-grade lymphoma and chronic lymphocytic leukemia. Curr Opin Hematol; 2006 Jul;13(4):273-9
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  • [Title] Role of allogeneic transplantation in low-grade lymphoma and chronic lymphocytic leukemia.
  • Exploring the potential of allogeneic transplantation to eradicate disease has therefore been of interest for some time.
  • This review reports on recent developments in this field to evaluate the current status of stem cell transplantation in the management of these conditions.
  • RECENT FINDINGS: Most recent studies examine the application of reduced intensity regimens in follicular non-Hodgkin's lymphoma and chronic lymphocytic leukemia.
  • Furthermore, the discovery of molecular/genetic factors that permit identification of patients with poor prognosis chronic lymphocytic leukemia has led to interest in identifying whether the allogeneic effect can overcome the impact of these factors.
  • [MeSH-major] Biomarkers, Tumor / genetics. Graft vs Leukemia Effect. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Lymphocyte Transfusion. Lymphoma, Non-Hodgkin / therapy. Stem Cell Transplantation

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  • (PMID = 16755225.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 36
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58. Yadav KS, Sawant KK: Formulation optimization of etoposide loaded PLGA nanoparticles by double factorial design and their evaluation. Curr Drug Deliv; 2010 Jan;7(1):51-64
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  • Etoposide is one of the most commonly used drugs in chemotherapy of acute lymphocytic leukemia and acute myelogenous leukaemia.

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  • (PMID = 20044908.001).
  • [ISSN] 1875-5704
  • [Journal-full-title] Current drug delivery
  • [ISO-abbreviation] Curr Drug Deliv
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / polylactic acid-polyglycolic acid copolymer; 26009-03-0 / Polyglycolic Acid; 33X04XA5AT / Lactic Acid; 6PLQ3CP4P3 / Etoposide
  • [Number-of-references] 28
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59. Vormoor HJ: Malignant stem cells in childhood acute lymphoblastic leukemia: the stem cell concept revisited. Cell Cycle; 2009 Apr 1;8(7):996-9
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  • [Title] Malignant stem cells in childhood acute lymphoblastic leukemia: the stem cell concept revisited.
  • We have recently shown that in childhood acute lymphoblastic leukemia (ALL) blasts at different stages of immunophenotypic maturation possess stem cell properties.
  • Leukemia-propagating stem cells in ALL may be more frequent than previously thought!
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Neoplastic Stem Cells / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 19270513.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD20; 0 / Antigens, CD34
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60. Nagel S, Scherr M, Kel A, Hornischer K, Crawford GE, Kaufmann M, Meyer C, Drexler HG, MacLeod RA: Activation of TLX3 and NKX2-5 in t(5;14)(q35;q32) T-cell acute lymphoblastic leukemia by remote 3'-BCL11B enhancers and coregulation by PU.1 and HMGA1. Cancer Res; 2007 Feb 15;67(4):1461-71
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  • [Title] Activation of TLX3 and NKX2-5 in t(5;14)(q35;q32) T-cell acute lymphoblastic leukemia by remote 3'-BCL11B enhancers and coregulation by PU.1 and HMGA1.
  • In T-cell acute lymphoblastic leukemia, alternative t(5;14)(q35;q32.2) forms effect dysregulation of either TLX3 or NKX2-5 homeobox genes at 5q35 by juxtaposition with 14q32.2 breakpoints dispersed across the BCL11B downstream genomic desert.
  • Leukemic gene dysregulation by t(5;14) was investigated by DNA inhibitory treatments with 26-mer double-stranded DNA oligonucleotides directed against candidate enhancers at, or near, orphan T-cell DNase I hypersensitive sites located between 3'-BCL11B and VRK1.
  • We suggest that HMGA1 and PU.1 coregulate ectopic homeobox gene expression in t(5;14) T-cell acute lymphoblastic leukemia by interactions mediated at the nuclear matrix.
  • [MeSH-major] DNA-Binding Proteins / genetics. Gene Expression Regulation, Leukemic. HMGA Proteins / genetics. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Oncogene Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins / genetics. Repressor Proteins / genetics. Trans-Activators / genetics. Transcription Factors / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 17308084.001).
  • [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 / BCL11B protein, human; 0 / DNA-Binding Proteins; 0 / HMGA Proteins; 0 / Histones; 0 / Homeodomain Proteins; 0 / NKX2-5 protein, human; 0 / Oligonucleotides; 0 / Oncogene Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 0 / Repressor Proteins; 0 / TLX3 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / proto-oncogene protein Spi-1; EC 3.1.21.1 / Deoxyribonuclease I
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61. Fulcher JW, Allred TJ, Kulharya A, Satya-Prakash KL, Seigler M, Neibarger D, Mazzella FM: Granular acute lymphoblastic leukemia in adults: report of a case and review of the literature. South Med J; 2006 Aug;99(8):894-7
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  • [Title] Granular acute lymphoblastic leukemia in adults: report of a case and review of the literature.
  • The diagnosis of granular acute lymphoblastic leukemia (ALL) can be problematic as the cytoplasmic granules found in many blast cells may mimic those seen in acute myelogenous leukemia (AML).
  • This rare variant of B-cell ALL is more commonly diagnosed in children, but may occur in adults.
  • [MeSH-major] Bone Marrow Cells / pathology. Cytoplasmic Granules / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Female. Flow Cytometry. Humans. Middle Aged

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  • (PMID = 16929890.001).
  • [ISSN] 0038-4348
  • [Journal-full-title] Southern medical journal
  • [ISO-abbreviation] South. Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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62. Wen C, Ma FT, Wan WQ: [Expression of CREB/Bcl-2 in bone marrow mononuclear cells of children with acute leukemia]. Zhongguo Dang Dai Er Ke Za Zhi; 2010 Mar;12(3):177-80
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  • [Title] [Expression of CREB/Bcl-2 in bone marrow mononuclear cells of children with acute leukemia].
  • OBJECTIVE: To study the expression and role of cyclic-AMP response binding protein (CREB) and Bcl-2 in children with acute leukemia.
  • METHODS: Ninety-two children with acute leukemia (leukemia group) and 30 children with non-hematologic malignancies (control group) were enrolled.
  • RESULTS: The mRNA and protein expression of CREB and Bcl-2 in the leukemia group was significantly higher than that in the control group (p<0.01).
  • There were no significant differences in the expression of CREB and Bcl-2 between acute lymphoblastic leukemia and acute myeloid leukemia subgroups.
  • At the initial diagnosis, the mRNA and protein expression of CREB and Bcl-2 in children with extramedullary infiltration was higher than that in children without (p<0.05).
  • In the leukemia group, the mRNA and protein expression of CREB and Bcl-2 in the complete remission subgroup was significantly lower than that in the non-complete remission subgroup (p<0.01).
  • High mRNA expression of CREB and Bcl-2 in the leukemia group was positively correlated with peripheral blood leucocyte counts (r=0.62, 0.71 respectively, p<0.05).
  • CONCLUSIONS: The expression of CREB and Bcl-2 may be correlated with the pathogenesis and clinical prognosis of childhood leukemia, however, their expression may not be associated with the classification of acute leukemia.
  • [MeSH-major] Bone Marrow Cells / metabolism. Cyclic AMP Response Element-Binding Protein / genetics. Leukemia / metabolism. Proto-Oncogene Proteins c-bcl-2 / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Female. Humans. Infant. Male. RNA, Messenger / analysis

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  • (PMID = 20350424.001).
  • [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 / CREB1 protein, human; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger
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63. Mussa A, Bertorello N, Porta F, Galletto C, Nicolosi MG, Manicone R, Corrias A, Fagioli F: Prospective bone ultrasound patterns during childhood acute lymphoblastic leukemia treatment. Bone; 2010 Apr;46(4):1016-20
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  • [Title] Prospective bone ultrasound patterns during childhood acute lymphoblastic leukemia treatment.
  • OBJECTIVE: Bone impairment is a well-known complication in childhood acute lymphoblastic leukemia (ALL) survivors but less is known about bone dynamics during ALL therapy.
  • Measurements were performed at diagnosis, and 6, 12, and 24 months thereafter.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone and Bones / ultrasonography. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / ultrasonography

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  • [Copyright] Copyright 2009 Elsevier Inc. All rights reserved.
  • [CommentIn] Bone. 2010 Oct;47(4):835-6; author reply 837-8 [20624504.001]
  • (PMID = 20044045.001).
  • [ISSN] 1873-2763
  • [Journal-full-title] Bone
  • [ISO-abbreviation] Bone
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 8J337D1HZY / Cytosine; 8N3DW7272P / Cyclophosphamide; E7WED276I5 / 6-Mercaptopurine; YL5FZ2Y5U1 / Methotrexate
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64. Geng CD, Schwartz JR, Vedeckis WV: A conserved molecular mechanism is responsible for the auto-up-regulation of glucocorticoid receptor gene promoters. Mol Endocrinol; 2008 Dec;22(12):2624-42
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  • Glucocorticoid (GC) hormones are widely used in the treatment of acute lymphoblastic leukemia (ALL).
  • Whereas a high level of GC receptor (GR) protein is associated with the sensitivity of ALL cells to steroid-mediated apoptosis, the auto-up-regulation of human (h)GR mRNA and protein is also found in hormone-sensitive ALL cell lines.
  • Thus, the hGR 1A GRU (described previously), the -4559/-4525 GRU, and the -2956/-2916 GRU have a similar structure and can mediate cell type-specific hormonal auto-up-regulation of hGR promoter activity in steroid-sensitive ALL cells.
  • The architecture of the GRU and the spectrum of specific transcription factors present in different types of ALL might allow the development of a tailored therapy to enhance steroid sensitivity in ALL patients.

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  • [Cites] Mol Endocrinol. 1988 Dec;2(12):1256-64 [3216865.001]
  • [Cites] J Endocrinol. 2004 Nov;183(2):365-74 [15531724.001]
  • [Cites] J Steroid Biochem. 1989 May;32(5):737-47 [2661921.001]
  • [Cites] J Biol Chem. 1989 Aug 25;264(24):14396-402 [2668288.001]
  • [Cites] Cancer Res. 1990 Mar 15;50(6):1873-8 [2106390.001]
  • [Cites] J Biol Chem. 1990 May 5;265(13):7284-91 [1692020.001]
  • [Cites] Mol Cell Endocrinol. 1999 Nov 25;157(1-2):95-104 [10619401.001]
  • [Cites] Mol Endocrinol. 2000 Mar;14(3):329-47 [10707952.001]
  • [Cites] Biochemistry. 2000 Oct 10;39(40):12234-42 [11015202.001]
  • [Cites] J Biol Chem. 2000 Dec 15;275(50):39296-301 [11005817.001]
  • [Cites] Mol Endocrinol. 2001 Mar;15(3):458-66 [11222746.001]
  • [Cites] J Biol Chem. 2001 May 25;276(21):18007-17 [11279115.001]
  • [Cites] Mol Endocrinol. 2001 Aug;15(8):1381-95 [11463861.001]
  • [Cites] Mol Cell Endocrinol. 2002 Mar 28;189(1-2):191-9 [12039077.001]
  • [Cites] Gene. 2003 Jan 16;303:11-34 [12559563.001]
  • [Cites] Biochemistry. 2003 Sep 23;42(37):10978-90 [12974633.001]
  • [Cites] Mol Endocrinol. 2004 Apr;18(4):912-24 [15044598.001]
  • [Cites] Biochemistry. 2004 Aug 31;43(34):10851-8 [15323545.001]
  • [Cites] Science. 1971 Jan 15;171(3967):189-91 [4395230.001]
  • [Cites] Cancer Res. 1977 Oct;37(10):3785-91 [269011.001]
  • [Cites] J Pathol. 1978 Nov;126(3):181-7 [745025.001]
  • [Cites] Nature. 1980 Apr 10;284(5756):555-6 [6245367.001]
  • [Cites] Lancet. 1980 May 3;1(8175):952-6 [6103302.001]
  • [Cites] Cancer Res. 1981 Nov;41(11 Pt 2):4861-2 [6975165.001]
  • [Cites] Cancer. 1982 Feb 15;49(4):623-32 [6948600.001]
  • [Cites] J Biol Chem. 1987 Aug 5;262(22):10441-4 [2440867.001]
  • [Cites] J Biol Chem. 1988 Feb 25;263(6):2581-4 [3343225.001]
  • [Cites] J Biol Chem. 1988 Aug 25;263(24):12044-8 [3261297.001]
  • [Cites] Mol Cell Biol. 1990 Oct;10(10):5580-5 [2398904.001]
  • [Cites] J Biol Chem. 1991 Apr 15;266(11):7182-8 [1707881.001]
  • [Cites] Steroids. 1991 Feb;56(2):52-8 [2020978.001]
  • [Cites] J Biol Chem. 1991 Jun 5;266(16):10078-85 [2037566.001]
  • [Cites] J Steroid Biochem Mol Biol. 1991;40(1-3):317-23 [1958537.001]
  • [Cites] Mol Cell Biol. 1992 Oct;12(10):4297-304 [1406622.001]
  • [Cites] Mol Endocrinol. 1992 Aug;6(8):1299-309 [1406707.001]
  • [Cites] Proc Natl Acad Sci U S A. 1986 Aug;83(16):5899-903 [3016728.001]
  • [Cites] Prog Nucleic Acid Res Mol Biol. 1992;43:1-36 [1329151.001]
  • [Cites] Blood. 1993 Oct 15;82(8):2304-9 [8400283.001]
  • [Cites] Endocr Rev. 1993 Aug;14(4):459-79 [8223341.001]
  • [Cites] EMBO J. 1993 Dec 15;12(13):5089-96 [8262052.001]
  • [Cites] Nucleic Acids Res. 1996 Feb 15;24(4):766-74 [8604322.001]
  • [Cites] J Biol Chem. 1996 Aug 2;271(31):18662-71 [8702520.001]
  • [Cites] J Steroid Biochem Mol Biol. 2005 Feb;93(2-5):153-60 [15860257.001]
  • [Cites] Biochemistry. 2005 May 24;44(20):7395-405 [15895983.001]
  • [Cites] J Mol Endocrinol. 2005 Oct;35(2):283-92 [16216909.001]
  • [Cites] J Biol Chem. 2005 Dec 30;280(52):43264-71 [16263717.001]
  • [Cites] Blood. 2006 Mar 1;107(5):2061-9 [16293608.001]
  • [Cites] Biochem Pharmacol. 2006 Nov 30;72(11):1529-37 [16930562.001]
  • [Cites] FASEB J. 2006 Dec;20(14):2600-2 [17077285.001]
  • [Cites] J Mol Endocrinol. 2007 Feb;38(1-2):79-90 [17242171.001]
  • [Cites] Mol Endocrinol. 1998 Sep;12(9):1322-33 [9731701.001]
  • [Cites] J Steroid Biochem Mol Biol. 1998 Dec;67(5-6):369-81 [10030686.001]
  • [Cites] Cancer Res. 1999 Mar 15;59(6):1378-85 [10096574.001]
  • [Cites] Mol Endocrinol. 1999 Apr;13(4):604-18 [10194766.001]
  • [Cites] J Steroid Biochem Mol Biol. 1999 Apr-Jun;69(1-6):3-12 [10418975.001]
  • [Cites] Adv Exp Med Biol. 1999;457:593-605 [10500839.001]
  • [Cites] Adv Exp Med Biol. 1999;457:607-14 [10500840.001]
  • [Cites] Cancer. 1949 Nov;2(6):943-5 [15395192.001]
  • [Cites] Cancer Res. 1989 Apr 15;49(8 Suppl):2295s-2302s [2702670.001]
  • (PMID = 18945813.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA116042; United States / NCI NIH HHS / CA / CA116042
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myb; 0 / Receptors, Glucocorticoid; 7S5I7G3JQL / Dexamethasone
  • [Other-IDs] NLM/ PMC2626199
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65. Gil L, Styczynski J, Komarnicki M: Infectious complication in 314 patients after high-dose therapy and autologous hematopoietic stem cell transplantation: risk factors analysis and outcome. Infection; 2007 Dec;35(6):421-7
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  • [Title] Infectious complication in 314 patients after high-dose therapy and autologous hematopoietic stem cell transplantation: risk factors analysis and outcome.
  • BACKGROUND: Infectious complications occur in most of the patients receiving high-dose therapy (HDT) and autologous hematopoietic stem cell transplantation (HSCT).
  • The objective of the study was to analyze of the type and incidence of infectious complications during neutropenia after HDT and autologous HSCT with respect to risk factors related to stem cell transplant setting in patients treated for hematological malignancies in a single center.
  • PATIENTS AND METHODS: A total number of 314 patients diagnosed for Hodgkin's disease (HD), non-Hodgkin's lymphoma (NHL), acute myeloid leukemia (AML), multiple myeloma (MM) or acute lymphoblastic leukemia (ALL) were included in the study.
  • CONCLUSION: Patients at high risk of infection after autologous HSCT were identified as those with acute leukemia and those after conditioning with TBI, all with prolonged neutropenia.
  • [MeSH-major] Bacterial Infections / etiology. Hematopoietic Stem Cell Transplantation / adverse effects. Postoperative Complications / etiology. Transplantation Conditioning / adverse effects. Whole-Body Irradiation / adverse effects
  • [MeSH-minor] Adolescent. Adult. Aged. Bacteria / drug effects. Bacteria / isolation & purification. Female. Fever of Unknown Origin. Humans. Leukemia / complications. Leukemia / therapy. Lymphoma / complications. Lymphoma / therapy. Male. Middle Aged. Neutropenia / complications. Neutropenia / diagnosis. Neutropenia / mortality. Prospective Studies. Risk Factors. Transplantation, Autologous / adverse effects. Treatment Outcome


66. Yanada M, Takeuchi J, Sugiura I, Akiyama H, Usui N, Yagasaki F, Kobayashi T, Ueda Y, Takeuchi M, Miyawaki S, Maruta A, Emi N, Miyazaki Y, Ohtake S, Jinnai I, Matsuo K, Naoe T, Ohno R, Japan Adult Leukemia Study Group: High complete remission rate and promising outcome by combination of imatinib and chemotherapy for newly diagnosed BCR-ABL-positive acute lymphoblastic leukemia: a phase II study by the Japan Adult Leukemia Study Group. J Clin Oncol; 2006 Jan 20;24(3):460-6
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  • [Title] High complete remission rate and promising outcome by combination of imatinib and chemotherapy for newly diagnosed BCR-ABL-positive acute lymphoblastic leukemia: a phase II study by the Japan Adult Leukemia Study Group.
  • PURPOSE: A novel therapeutic approach is urgently needed for BCR-ABL-positive acute lymphoblastic leukemia (ALL).
  • RESULTS: Remission induction therapy resulted in complete remission (CR) in 77 patients (96.2%), resistant disease in one patient, and early death in two patients, as well as polymerase chain reaction negativity of bone marrow in 71.3%.
  • Allogeneic hematopoietic stem-cell transplantation (HSCT) was performed for 49 patients, 39 of whom underwent transplantation during their first CR.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Fusion Proteins, bcr-abl / metabolism. Piperazines / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / administration & dosage

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  • (PMID = 16344315.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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67. Agueli C, Cammarata G, Salemi D, Dagnino L, Nicoletti R, La Rosa M, Messana F, Marfia A, Bica MG, Coniglio ML, Pagano M, Fabbiano F, Santoro A: 14q32/miRNA clusters loss of heterozygosity in acute lymphoblastic leukemia is associated with up-regulation of BCL11a. Am J Hematol; 2010 Aug;85(8):575-8
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  • [Title] 14q32/miRNA clusters loss of heterozygosity in acute lymphoblastic leukemia is associated with up-regulation of BCL11a.
  • This study evaluated the loss and expression level of miRNAs 14q32 clusters in acute lymphoblastic leukemia (ALL) patients with cryptic deletions at 14q32 chromosomal band to investigate their involvement in this disease.
  • As a consequence of miRNAs deregulation we reported an inverse correlation with the expression of their target BCL11a, a transcription factor involved in lymphoid differentiation.
  • These results suggest that 14q32/miRNA clusters LOH may be another mechanism involved in lymphoid B cell transformation and differentiation and therefore, could be used as a diagnostic marker and therapeutic target in subsets of ALL.
  • [MeSH-major] Carrier Proteins / biosynthesis. Chromosomes, Human, Pair 14 / genetics. Gene Expression Regulation, Leukemic / genetics. Loss of Heterozygosity. MicroRNAs / genetics. Neoplasm Proteins / biosynthesis. Nuclear Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA, Neoplasm / genetics. Sequence Deletion
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Differentiation / genetics. Cell Transformation, Neoplastic / genetics. Child. Female. Humans. Male. Middle Aged. Up-Regulation. Young Adult

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  • [Copyright] (c) 2010 Wiley-Liss, Inc.
  • (PMID = 20578197.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL11A protein, human; 0 / Carrier Proteins; 0 / MicroRNAs; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / RNA, Neoplasm
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68. Organista-Nava J, Gómez-Gómez Y, Saavedra-Herrera MV, Rivera-Ramírez AB, Terán-Porcayo MA, Alarcón-Romero Ldel C, Illades-Aguiar B, Leyva-Vázquez MA: Polymorphisms of the gamma-glutamyl hydrolase gene and risk of relapse to acute lymphoblastic leukemia in Mexico. Leuk Res; 2010 Jun;34(6):728-32
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  • [Title] Polymorphisms of the gamma-glutamyl hydrolase gene and risk of relapse to acute lymphoblastic leukemia in Mexico.
  • This study evaluated the association of -401C/T and +452C/T polymorphisms of gamma-glutamyl hydrolase and the risk of relapse to acute lymphoblastic leukemia.
  • Genotyping was performed in 70 children with acute lymphoblastic leukemia and 140 healthy children.
  • An association between the -401C/T polymorphism and the risk of relapse was found (p=0.028), patients with the -401T/T genotype have 10.83 (95% CI 1.30-90.14) more chance of a relapse of leukemia.
  • Therefore, our investigation suggests that the -401C/T polymorphism in the gamma-glutamyl hydrolase may be a factor involved in the generation of relapse to disease in patients with ALL.
  • [MeSH-major] Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. gamma-Glutamyl Hydrolase / genetics

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 20197200.001).
  • [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 / Antimetabolites, Antineoplastic; EC 3.4.19.9 / gamma-Glutamyl Hydrolase; YL5FZ2Y5U1 / Methotrexate
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69. Faderl S, O'Brien S, Pui CH, Stock W, Wetzler M, Hoelzer D, Kantarjian HM: Adult acute lymphoblastic leukemia: concepts and strategies. Cancer; 2010 Mar 01;116(5):1165-76
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  • [Title] Adult acute lymphoblastic leukemia: concepts and strategies.
  • Acute lymphoblastic leukemia (ALL), a clonal expansion of hematopoietic blasts, is a highly heterogeneous disease comprising many entities for which distinct treatment strategies are pursued.
  • Although ALL is a success story in pediatric oncology, results in adults lag behind those in children.
  • An expansion of new drugs, more reliable immunologic and molecular techniques for the assessment of minimal residual disease, and efforts at more precise risk stratification are generating new aspects of adult ALL therapy.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma
  • [MeSH-minor] Adult. Chromosome Aberrations. Hematopoietic Stem Cell Transplantation. Humans. Philadelphia Chromosome. Prognosis. Recurrence

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  • [Cites] Haematologica. 2007 May;92(5):612-8 [17488684.001]
  • [Cites] Curr Opin Pediatr. 2008 Feb;20(1):17-22 [18197034.001]
  • [Cites] J Clin Oncol. 2004 Oct 15;22(20):4075-86 [15353542.001]
  • [Cites] Blood. 2007 May 1;109(9):3676-8 [17213285.001]
  • [Cites] Blood. 2007 Apr 1;109 (7):2744-50 [17132721.001]
  • [Cites] Blood. 1995 Apr 15;85(8):2025-37 [7718875.001]
  • [Cites] Clin Cancer Res. 2007 Mar 15;13(6):1634-7 [17363514.001]
  • [Cites] Blood. 2005 May 1;105(9):3434-41 [15650057.001]
  • [Cites] Blood. 1999 Mar 1;93(5):1643-50 [10029593.001]
  • [Cites] Biol Blood Marrow Transplant. 2009 Jan;15(1 Suppl):7-10 [19147069.001]
  • [Cites] Bone Marrow Transplant. 2008 Apr;41(7):635-42 [18084335.001]
  • [Cites] Hematol Oncol Clin North Am. 2000 Dec;14(6):1267-88 [11147223.001]
  • [Cites] Blood. 2006 Jul 15;108(2):465-72 [16556888.001]
  • [Cites] J Clin Oncol. 2007 Aug 20;25(24):3739-45 [17646667.001]
  • [Cites] Cancer. 2004 Dec 15;101(12):2788-801 [15481055.001]
  • [Cites] Bone Marrow Transplant. 2005 Oct;36(8):683-9 [16113673.001]
  • [Cites] Blood. 1999 Jun 1;93(11):3931-9 [10339502.001]
  • [Cites] J Clin Oncol. 1998 Dec;16(12):3768-73 [9850020.001]
  • [Cites] J Clin Oncol. 2005 May 20;23(15):3376-82 [15908649.001]
  • [Cites] Blood. 2007 May 15;109 (10 ):4164-7 [17264295.001]
  • [Cites] Nat Rev Drug Discov. 2007 Feb;6(2):149-65 [17268486.001]
  • [Cites] J Clin Oncol. 1994 Dec;12(12):2580-7 [7989932.001]
  • [Cites] Oncogene. 2004 Aug 23;23(38):6341-8 [15322509.001]
  • [Cites] J Clin Oncol. 2009 Feb 20;27(6):911-8 [19124805.001]
  • [Cites] Cancer. 2008 Oct 15;113(8):2097-101 [18720356.001]
  • [Cites] Bone Marrow Transplant. 1994 Sep;14(3):383-8 [7994259.001]
  • [Cites] Bone Marrow Transplant. 2008 Mar;41(5):447-53 [17968326.001]
  • [Cites] Adv Drug Deliv Rev. 2003 Sep 26;55(10 ):1293-302 [14499708.001]
  • [Cites] Biol Blood Marrow Transplant. 2009 Jan;15(1 Suppl):11-6 [19147070.001]
  • [Cites] CA Cancer J Clin. 2006 Mar-Apr;56(2):106-30 [16514137.001]
  • [Cites] Blood. 2002 Feb 1;99(3):863-71 [11806988.001]
  • [Cites] J Clin Invest. 2007 Apr;117(4):1049-57 [17380207.001]
  • [Cites] Semin Hematol. 2009 Jan;46(1):100-6 [19100372.001]
  • [Cites] J Clin Oncol. 2006 Apr 20;24(12):1917-23 [16622268.001]
  • [Cites] Blood. 2007 Jan 15;109(2):683-92 [17008550.001]
  • [Cites] Blood. 2003 Feb 15;101(4):1270-6 [12406912.001]
  • [Cites] Blood. 2007 Jun 15;109(12):5136-42 [17344466.001]
  • [Cites] Hematol Oncol Clin North Am. 2000 Dec;14 (6):1327-52 [11147226.001]
  • [Cites] N Engl J Med. 2004 Aug 5;351(6):533-42 [15295046.001]
  • [Cites] Best Pract Res Clin Haematol. 2002 Dec;15(4):741-56 [12617874.001]
  • [Cites] Blood. 2009 Feb 19;113(8):1615-6 [19228927.001]
  • [Cites] Blood. 2009 Feb 19;113(8):1689-98 [19001083.001]
  • [Cites] Blood. 2006 Feb 1;107(3):1116-23 [16195338.001]
  • [Cites] J Clin Oncol. 2005 Oct 1;23(28):7161-7 [16192600.001]
  • [Cites] Cancer. 2003 Oct 1;98(7):1337-54 [14508819.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2309-15 [17496201.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1469-77 [16638934.001]
  • [Cites] Pediatr Blood Cancer. 2007 Mar;48(3):254-61 [16421910.001]
  • [Cites] Blood. 2005 Jun 15;105(12):4752-8 [15713801.001]
  • [Cites] Cancer. 2006 Apr 1;106(7):1569-80 [16502413.001]
  • [Cites] Blood. 1988 Jan;71(1):123-31 [3422030.001]
  • [Cites] N Engl J Med. 2004 Aug 5;351(6):552-9 [15295048.001]
  • [Cites] Nat Rev Cancer. 2006 Mar;6(3):193-203 [16467884.001]
  • [Cites] J Clin Oncol. 2009 Mar 10;27(8):1316-22 [19164206.001]
  • [Cites] Blood. 2007 Feb 1;109(3):944-50 [17032921.001]
  • [Cites] Blood. 2004 Feb 1;103(3):1043-9 [14525776.001]
  • [Cites] Blood. 2008 Feb 15;111(4):1827-33 [18048644.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] Semin Hematol. 2009 Jan;46(1):24-32 [19100365.001]
  • [Cites] Blood. 2000 Aug 1;96(3):1094-9 [10910927.001]
  • [Cites] Nat Rev Cancer. 2001 Nov;1(2):99-108 [11905809.001]
  • [Cites] Br J Haematol. 2002 Sep;118(3):748-54 [12181041.001]
  • [Cites] J Clin Oncol. 2006 Jan 20;24(3):460-6 [16344315.001]
  • [Cites] Blood. 2009 Mar 5;113(10):2284-9 [19020309.001]
  • [Cites] Blood. 2009 Apr 30;113(18):4153-62 [19141862.001]
  • [Cites] Bone Marrow Transplant. 2006 Oct;38(7):467-75 [16892073.001]
  • [Cites] Ann Intern Med. 1991 Jul 1;115(1):13-8 [2048858.001]
  • [Cites] N Engl J Med. 2009 Jan 29;360(5):470-80 [19129520.001]
  • [Cites] Blood. 2005 Apr 15;105(8):3072-8 [15637138.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6306-15 [16155013.001]
  • [Cites] Eur J Haematol. 2006 Dec;77(6):471-9 [16978239.001]
  • [Cites] Blood. 2009 Mar 26;113(13):2902-5 [19179301.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2542-51 [16775235.001]
  • [Cites] Blood. 1998 Jun 1;91(11):3995-4019 [9596644.001]
  • [Cites] J Clin Oncol. 2002 May 15;20(10):2464-71 [12011123.001]
  • [Cites] Blood. 2007 Feb 15;109(4):1408-13 [17062730.001]
  • [Cites] Blood. 2008 Sep 1;112(5):1646-54 [18502832.001]
  • [Cites] Blood. 2004 Aug 15;104(4):923-32 [15155462.001]
  • [Cites] J Clin Oncol. 2003 Mar 1;21(5):774-80 [12610173.001]
  • [Cites] Nature. 2004 May 27;429(6990):464-8 [15164072.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3760-7 [16105981.001]
  • [Cites] Leukemia. 2002 Jul;16(7):1259-66 [12094249.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Sep;13(9):1083-94 [17697971.001]
  • [Cites] Leuk Lymphoma. 2007 Jul;48(7):1269-82 [17613754.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3189-97 [17170120.001]
  • [Cites] Semin Hematol. 2009 Jan;46(1):64-75 [19100369.001]
  • (PMID = 20101737.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 103
  •  go-up   go-down


70. Zunino SJ, Storms DH, Ducore JM: Novel in vivo model of inducible multi-drug resistance in acute lymphoblastic leukemia with chromosomal translocation t(4;11). Cancer Lett; 2010 Oct 1;296(1):49-54
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  • [Title] Novel in vivo model of inducible multi-drug resistance in acute lymphoblastic leukemia with chromosomal translocation t(4;11).
  • Acute lymphoblastic leukemia (ALL) with translocation t(4;11) is found in 60-85% of infants with ALL and is often refractory to conventional chemotherapeutics after relapse.
  • Survival curves showed that leukemia cell growth was initially delayed by vincristine treatment, but the mice eventually succumbed to disease.

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  • [Copyright] Published by Elsevier Ireland Ltd.
  • [Cites] Leuk Lymphoma. 2005 May;46(5):681-91 [16019505.001]
  • [Cites] N Engl J Med. 1998 Jun 4;338(23):1663-71 [9614257.001]
  • [Cites] Cancer Chemother Pharmacol. 2009 Apr;63(5):761-7 [19034447.001]
  • [Cites] Int J Clin Pharmacol Ther. 2000 Mar;38(3):94-110 [10739113.001]
  • [Cites] Pediatr Hematol Oncol. 2000 Dec;17(8):635-50 [11127395.001]
  • [Cites] Blood. 2002 Jun 1;99(11):4100-8 [12010813.001]
  • [Cites] Leuk Lymphoma. 2003 Jan;44(1):85-95 [12691146.001]
  • [Cites] Blood. 2004 May 15;103(10):3905-14 [14764536.001]
  • [Cites] Biochem Biophys Res Commun. 1986 Dec 30;141(3):956-62 [2880583.001]
  • [Cites] Cancer Res. 1988 Jan 15;48(2):393-8 [2891436.001]
  • [Cites] Science. 1989 Dec 22;246(4937):1597-600 [2595371.001]
  • [Cites] J Immunol Methods. 1991 Jun 3;139(2):271-9 [1710634.001]
  • [Cites] Cancer Res. 1993 Aug 15;53(16):3658-61 [8101765.001]
  • [Cites] Annu Rev Biochem. 1993;62:385-427 [8102521.001]
  • [Cites] Br J Haematol. 1994 Feb;86(2):275-83 [8199015.001]
  • [Cites] Blood. 1996 May 1;87(9):3892-8 [8611717.001]
  • [Cites] Leukemia. 1996 Mar;10(3):558-63 [8642875.001]
  • [Cites] Blood. 1996 Aug 15;88(4):1135-46 [8695830.001]
  • [Cites] Cancer Res. 1996 Oct 1;56(19):4332-7 [8813118.001]
  • [Cites] Blood. 1997 Sep 1;90(5):2015-9 [9292537.001]
  • [Cites] Klin Padiatr. 1997 Jul-Aug;209(4):178-85 [9293448.001]
  • [Cites] Blood. 1998 Mar 15;91(6):2092-8 [9490695.001]
  • [Cites] Crit Rev Clin Lab Sci. 1998 Feb;35(1):1-57 [9532418.001]
  • [Cites] Blood. 1998 Jun 1;91(11):3995-4019 [9596644.001]
  • [Cites] J Cancer Res Clin Oncol. 2007 Nov;133(11):875-93 [17671794.001]
  • (PMID = 20381955.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA122117; United States / NCI NIH HHS / CA / 1R21CA122117-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Ireland
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; EC 3.1.2.15 / UCHL1 protein, human; EC 3.1.2.15 / Ubiquitin Thiolesterase
  • [Other-IDs] NLM/ NIHMS195255; NLM/ PMC2906616
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71. Xicoy B, Ribera JM, Oriol A, Sanz MA, Abella E, Tormo M, del Potro E, Bueno J, Grande C, Fernández-Calvo J, Orts M, Novo A, Rivas C, Hernández-Rivas JM, Feliu E, Ortega JJ: [Prognostic influence of immunological subtypes of T-cell acute lymphoblastic leukemia. Study of 81 patients]. Med Clin (Barc); 2006 Jan 21;126(2):41-6
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  • [Title] [Prognostic influence of immunological subtypes of T-cell acute lymphoblastic leukemia. Study of 81 patients].
  • [Transliterated title] Significado pronóstico de los subtipos inmunológicos de la leucemia aguda linfoblástica T del adulto. Estudio de 81 pacientes.
  • BACKGROUND AND OBJECTIVE: T-cell acute lymphoblastic leukemia (ALL) includes 4 immunological subtypes: pro-T, pre-T, thymic or cortical and mature.
  • The objective of this study was to describe the clinical characteristics, the result of treatment and the prognosis of the immunological subtypes of T-cell ALL in 81 adult patients included in 2 protocols of the Spanish PETHEMA group (ALL-96 and ALL-93).
  • The main clinical and biological parameters as well as the rate of response to treatment, the frequency of complete remission , disease free survival and overall survival were compared in each T-cell ALL subtype.
  • Patients with mature T-cell ALL had a slow rate of response to treatment in comparison with patients wit pre-T and mature T-cell ALL but this did not translate to significant differences in frequency of complete remission (77% vs 94%), disease free survival (42% vs 46%) and overall survival (29% vs 47%).
  • CONCLUSIONS: Although patients with mature T-cell ALL had a slow rate of response to treatment and their survival tended to be shorter, in the present study there were no statistically significant differences in the prognosis of the different subtypes of T-cell ALL.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / mortality

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  • (PMID = 16426542.001).
  • [ISSN] 0025-7753
  • [Journal-full-title] Medicina clínica
  • [ISO-abbreviation] Med Clin (Barc)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
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72. Bandyopadhyay S, Bhattacharyya A, Mallick A, Sen AK, Tripathi G, Das T, Sa G, Bhattacharya DK, Mandal C: Over-expressed IgG2 antibodies against O-acetylated sialoglycoconjugates incapable of proper effector functioning in childhood acute lymphoblastic leukemia. Int Immunol; 2005 Feb;17(2):177-91
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  • [Title] Over-expressed IgG2 antibodies against O-acetylated sialoglycoconjugates incapable of proper effector functioning in childhood acute lymphoblastic leukemia.
  • Earlier studies have demonstrated an over-expression of 9-O-acetylated sialoglycoconjugates (9-OAcSGs) on lymphoblasts, concomitant with high titers of anti-9-OAcSGs in childhood acute lymphoblastic leukemia (ALL).
  • The present study was aimed to evaluate whether this high induction of anti-9-OAcSGs at disease presentation contributes toward immune surveillance.
  • Analysis of glycosylation of anti-9-OAcSGs purified from sera of ALL patients (IgG(ALL)) and normal individuals (IgG(N)) by digoxigenin glycan enzyme assay, fluorimetric estimation, gas-liquid chromatography and lectin-binding assays demonstrated that disease-specific antibodies differ in content and nature as compared with normal controls.
  • Enhanced amount of 9-OAcSA-specific IgG2 induced in ALL was unable to trigger activation of FcgammaR, the complement cascade and cell-mediated cytotoxicity, although its glycotope-binding ability remains unaffected.
  • Interestingly, only IgG1N emerged as the potent mediator of cell-mediated cytotoxicity, complement fixation and activator of effector cells through FcgammaR.
  • In ALL, the observed subclass switching of anti-9-OAcSGs to IgG2, alteration in their glycosylation profile along with impairment of a few Fc-glycosylation-sensitive effector functions hints toward a disbalanced homeostasis, thereby evading the host defense.
  • [MeSH-major] Glycoconjugates / immunology. Immunoglobulin G / blood. Immunoglobulin G / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Sialic Acids / immunology

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  • (PMID = 15629900.001).
  • [ISSN] 0953-8178
  • [Journal-full-title] International immunology
  • [ISO-abbreviation] Int. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glycoconjugates; 0 / Immunoglobulin G; 0 / Receptors, Fc; 0 / Sialic Acids
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73. Ye Q, Wang ZH, Qin SK: [Preparation of heat shock protein 70 (Hsp70) and idiotypic determinant single-chain antibody (Id-ScFv) in a patient with B-cell chronic lymphatic leukemia (B-CLL) and antitumor effect of peptide complex Hsp70-Id]. Ai Zheng; 2008 Feb;27(2):133-8
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  • [Title] [Preparation of heat shock protein 70 (Hsp70) and idiotypic determinant single-chain antibody (Id-ScFv) in a patient with B-cell chronic lymphatic leukemia (B-CLL) and antitumor effect of peptide complex Hsp70-Id].
  • BACKGROUND & OBJECTIVE: Idiotypic determinant (Id) of malignant B lymphocyte surface membrane immunoglobulin (SmIg) is not only a specific marker for chronic B-cell lymphatic leukemia (B-CLL) but also a specific antigen as an attractive target for active immunotherapy.
  • Killing efficiency of activated PBMCs to chronic B-cell leukemia cell line Daudi, chronic myelogenous leukemia cell line K562 and hepatoma carcinoma cell line HepG2 were tested by cell counting.
  • [MeSH-major] Antineoplastic Agents / pharmacology. HSP70 Heat-Shock Proteins / pharmacology. Immunoglobulin Idiotypes / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Single-Chain Antibodies / pharmacology
  • [MeSH-minor] Cell Proliferation / drug effects. Escherichia coli / genetics. Humans. Interleukin-12 / biosynthesis. Leukocytes, Mononuclear / drug effects. Leukocytes, Mononuclear / immunology. Recombinant Proteins / biosynthesis. Recombinant Proteins / isolation & purification. Recombinant Proteins / pharmacology. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 18279608.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / HSP70 Heat-Shock Proteins; 0 / Immunoglobulin Idiotypes; 0 / Recombinant Proteins; 0 / Single-Chain Antibodies; 0 / Tumor Necrosis Factor-alpha; 187348-17-0 / Interleukin-12
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74. Hourani R, Abboud M, Hourani M, Khalifeh H, Muwakkit S: L-asparaginase-induced posterior reversible encephalopathy syndrome during acute lymphoblastic leukemia treatment in children. Neuropediatrics; 2008 Feb;39(1):46-50
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  • [Title] L-asparaginase-induced posterior reversible encephalopathy syndrome during acute lymphoblastic leukemia treatment in children.
  • L-asparaginase is a critical component in the treatment of acute lymphoblastic leukemia in children.
  • We report 3 cases of children with acute lymphoblastic leukemia who developed seizures and altered sensorium after L-asparaginase therapy.
  • [MeSH-major] Asparaginase / adverse effects. Posterior Leukoencephalopathy Syndrome / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 18504683.001).
  • [ISSN] 0174-304X
  • [Journal-full-title] Neuropediatrics
  • [ISO-abbreviation] Neuropediatrics
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 3.5.1.1 / Asparaginase
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75. Ortuño FJ, Castilla C, Moreno MJ, del Mar Osma M, Gonzalez M, Vicente V: Erythrophagocytosis in de novo-philadelphia-positive acute leukemia of ambiguous lineage. Haematologica; 2006 Aug;91(8 Suppl):ECR43
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  • [Title] Erythrophagocytosis in de novo-philadelphia-positive acute leukemia of ambiguous lineage.
  • Erythrophagocytosis by neoplastic cells in acute leukemia has been most frequently associated with FAB M4 and M5 subtypes, with the t(8;16) and with C-MOZ rearrangements, however it is exceptional in acute lymphoblastic leukemia and has not been previously reported in Philadelphia-positive (Ph+) acute leukemia.
  • We herein present a case of Ph+ acute leukemia of ambiguous lineage in which erythrophagocytosis is an outstanding feature.
  • [MeSH-major] Erythrocytes / pathology. Leukemia / pathology. Philadelphia Chromosome

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  • (PMID = 16923527.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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76. Rezvani K, Yong AS, Savani BN, Mielke S, Keyvanfar K, Gostick E, Price DA, Douek DC, Barrett AJ: Graft-versus-leukemia effects associated with detectable Wilms tumor-1 specific T lymphocytes after allogeneic stem-cell transplantation for acute lymphoblastic leukemia. Blood; 2007 Sep 15;110(6):1924-32
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  • [Title] Graft-versus-leukemia effects associated with detectable Wilms tumor-1 specific T lymphocytes after allogeneic stem-cell transplantation for acute lymphoblastic leukemia.
  • To determine whether the leukemia-associated Wilms tumor antigen (WT1) contributes to a graft-versus-leukemia (GVL) effect after allogeneic stem-cell transplantation (SCT) for acute lymphoblastic leukemia (ALL), we studied CD8(+) T-cell responses to WT1 in 10 human lymphocyte antigen (HLA)-A*0201-positive ALL patients during the early phase of immune recovery after SCT (days 30-120).
  • Using WT1/HLA-A*0201 tetramers and intracellular interferon-gamma (IFN-gamma) staining, WT1(+) CD8(+) T-cell responses after SCT were found only in patients with detectable WT1 expression before SCT (5 of 7 vs. 0 of 3; P < .05).
  • To monitor the kinetics of WT1(+) CD8(+) T-cell responses and disease regression after SCT, absolute WT1(+) CD8(+) T-cell numbers and WT1 expression were studied for each time point.
  • Loss of WT1(+) CD8(+) T-cell responses was associated with reappearance of WT1 transcripts, consistent with a molecular relapse (P < .001).
  • [MeSH-major] Burkitt Lymphoma / therapy. Graft vs Leukemia Effect. Immunologic Memory. Stem Cell Transplantation. T-Lymphocytes / metabolism. WT1 Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. CD8-Positive T-Lymphocytes. Child. Cytomegalovirus / pathogenicity. Cytomegalovirus Infections / immunology. Cytomegalovirus Infections / therapy. Cytomegalovirus Infections / virology. Female. Graft vs Host Disease. HLA-A Antigens / metabolism. HLA-A2 Antigen. Humans. Male. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tissue Donors. Transplantation, Homologous

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  • [Cites] J Immunol. 2005 May 15;174(10):6088-94 [15879103.001]
  • [Cites] Immunity. 1999 Aug;11(2):183-90 [10485653.001]
  • [Cites] J Immunol. 2000 Mar 1;164(5):2807-14 [10679124.001]
  • [Cites] Blood. 2000 Apr 1;95(7):2198-203 [10733485.001]
  • [Cites] J Clin Immunol. 2000 May;20(3):195-202 [10941827.001]
  • [Cites] Blood. 2000 Aug 15;96(4):1480-9 [10942395.001]
  • [Cites] J Immunol. 2000 Sep 1;165(5):2458-64 [10946271.001]
  • [Cites] Bone Marrow Transplant. 2000 Sep;26(5):511-6 [11019840.001]
  • [Cites] Blood. 2000 Nov 1;96(9):3126-32 [11049993.001]
  • [Cites] J Exp Med. 2000 Aug 21;192(4):549-56 [10952724.001]
  • [Cites] Leukemia. 2001 Feb;15(2):293-302 [11236950.001]
  • [Cites] Clin Cancer Res. 2001 Mar;7(3 Suppl):761s-765s [11300470.001]
  • [Cites] Methods Mol Med. 2002;68:223-37 [11901505.001]
  • [Cites] Cytotherapy. 2002;4(1):29-40 [11953039.001]
  • [Cites] J Immunol. 2002 Jun 1;168(11):5455-64 [12023339.001]
  • [Cites] Blood. 2002 Sep 15;100(6):2132-7 [12200377.001]
  • [Cites] Blood. 2003 Mar 1;101(5):1698-704 [12406915.001]
  • [Cites] J Clin Invest. 2005 Jun;115(6):1616-26 [15931392.001]
  • [Cites] J Immunol. 2005 Jun 15;174(12):8210-8 [15944330.001]
  • [Cites] Nat Med. 2005 Nov;11(11):1238-43 [16227988.001]
  • [Cites] Biol Blood Marrow Transplant. 2005 Dec;11(12):1014-21 [16338624.001]
  • [Cites] Clin Cancer Res. 2005 Dec 15;11(24 Pt 1):8799-807 [16361568.001]
  • [Cites] Br J Haematol. 2006 Jan;132(1):56-65 [16371020.001]
  • [Cites] Blood. 2006 Jan 1;107(1):205-12 [16144796.001]
  • [Cites] Leukemia. 2006 Feb;20(2):254-63 [16341043.001]
  • [Cites] Clin Immunol. 2006 Aug;120(2):121-8 [16766227.001]
  • [Cites] Cytotherapy. 2007;9(3):245-51 [17464756.001]
  • [Cites] Acta Haematol. 1999;102(2):72-6 [10529509.001]
  • [Cites] Nature. 1999 Oct 14;401(6754):708-12 [10537110.001]
  • [Cites] Blood. 2000 Jan 1;95(1):286-93 [10607714.001]
  • [Cites] J Immunol. 2000 Feb 15;164(4):1873-80 [10657636.001]
  • [Cites] Blood. 2003 Apr 1;101(7):2711-20 [12433688.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Mar 4;100(5):2742-7 [12601144.001]
  • [Cites] Immunogenetics. 2000 Feb;51(2):99-107 [10663572.001]
  • [Cites] Bone Marrow Transplant. 2003 May;31(9):783-8 [12732885.001]
  • [Cites] J Clin Oncol. 2003 May 15;21(10):1988-95 [12743153.001]
  • [Cites] Int J Hematol. 2003 Jul;78(1):56-61 [12894852.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2892-900 [12829610.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2474-86 [14562124.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2318-57 [14562125.001]
  • [Cites] Leukemia. 2004 Jan;18(1):165-6 [14603333.001]
  • [Cites] Biol Blood Marrow Transplant. 2004 Feb;10(2):91-105 [14750075.001]
  • [Cites] Biol Blood Marrow Transplant. 2004 Jan;10(1):49-57 [14752779.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Feb 17;101(7):1969-74 [14762166.001]
  • [Cites] Bone Marrow Transplant. 2004 Apr;33(8):839-46 [14767500.001]
  • [Cites] Br J Haematol. 2004 Jun;125(5):590-600 [15147374.001]
  • [Cites] Leuk Lymphoma. 2004 Mar;45(3):481-8 [15160909.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 21;101(38):13885-90 [15365188.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2794-800 [15226184.001]
  • [Cites] Blood. 1990 Feb 1;75(3):555-62 [2297567.001]
  • [Cites] Leukemia. 1995 Jun;9(6):1060-7 [7596170.001]
  • [Cites] Blood. 1995 Sep 1;86(5):2041-50 [7655033.001]
  • [Cites] Blood. 1996 Mar 15;87(6):2195-204 [8630379.001]
  • [Cites] Blood. 2005 Jan 15;105(2):865-73 [15280205.001]
  • [Cites] Leukemia. 2005 Feb;19(2):268-74 [15538407.001]
  • [Cites] Cancer Res. 1996 Aug 15;56(16):3771-81 [8706023.001]
  • [Cites] Science. 1996 Oct 4;274(5284):94-6 [8810254.001]
  • [Cites] J Immunol. 1997 Jan 15;158(2):560-5 [8992968.001]
  • [Cites] J Clin Oncol. 1997 Feb;15(2):433-44 [9053463.001]
  • [Cites] Blood. 1997 Sep 1;90(5):1751-67 [9292508.001]
  • [Cites] J Exp Med. 1997 Nov 3;186(9):1407-18 [9348298.001]
  • [Cites] Blood. 1998 Mar 15;91(6):2197-207 [9490709.001]
  • [Cites] Nat Med. 1999 Jul;5(7):839-42 [10395333.001]
  • [Cites] J Immunol. 2005 Jun 1;174(11):6571-6 [15905493.001]
  • (PMID = 17505014.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0501963
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / WT1 Proteins
  • [Other-IDs] NLM/ PMC1976363
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77. Yang H, Zhang C, Zhao X, Wu Q, Fu X, Yu B, Shao Y, Guan M, Zhang W, Wan J, Huang X: Analysis of copy number variations of BS69 in multiple types of hematological malignancies. Ann Hematol; 2010 Oct;89(10):959-64
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  • A recent array-based study implicated the presence of copy number variations (CNVs) of BS69 in the genomes of acute myelogenous leukemia.
  • CNVs are present in the general population at varying degrees and have been found to associate with various types of diseases including hematological malignancies.
  • We found significant association between the CNVs of BS69 and these hematological malignancies including acute lymphoblastic leukemia (ALL), acute myelogenous leukemia (AML), chronic lymphocytic leukemia (CLL), chronic myelogenous leukemia (CML), multiple myeloma (MM), and myelodysplastic syndrome (MDS).

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  • (PMID = 20425112.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / RNA, Messenger; 0 / ZMYND11 protein, human
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78. Shivarov V, Stoimenov A, Galabova I, Balatzenko G, Guenova M: Very early onset of an acute myeloid leukemia in an adult patient with B-cell lymphoblastic leukemia. Int J Lab Hematol; 2009 Feb;31(1):106-13
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  • [Title] Very early onset of an acute myeloid leukemia in an adult patient with B-cell lymphoblastic leukemia.
  • We report on a case of a 30-year-old male with acute B-lymphoblastic leukemia (B-ALL) with immunophenotype CD19(+), CD22(+), CD20(+), CD10(+), with aberrant expression of CD13 and CD117, and IgH gene rearrangements.
  • The case is the first report of a very early emergence of myeloid leukemia during the induction treatment for B-ALL in an adult patient.
  • Different pathogenetic mechanisms are discussed - clonal evolution or selection, lineage switch or development of a de novo or therapy-induced leukemia.
  • [MeSH-major] Leukemia, B-Cell / complications. Leukemia, Myeloid, Acute / complications


79. Stachel D, Albert M, Meilbeck R, Paulides M, Schmid I: Expression of angiogenic factors in childhood B-cell precursor acute lymphoblastic leukemia. Oncol Rep; 2007 Jan;17(1):147-52
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  • [Title] Expression of angiogenic factors in childhood B-cell precursor acute lymphoblastic leukemia.
  • Pathological angiogenesis is increasingly recognized to be an important feature of pathogenesis in solid tumors and also in leukemias.
  • Vascular endothelial growth factor (VEGF) seems to play a central role in tumor angiogenesis and is associated with a poor prognosis in both solid tumors and adult leukemias.
  • In pediatric acute lymphocytic leukemia however, the expression of angiogenic molecules and its relation to prognosis and relapse are unknown.
  • Therefore, we prospectively analyzed 46 pediatric patients with precursor B cell acute lymphocytic leukemia by semi-quantitative RT-PCR for expression of the angiogenic molecules VEGF, VEGF-C, iNOS and TGF-beta and correlated relapse and survival data with the expression of these factors.
  • A significantly higher mRNA expression of iNOS was found in surviving patients compared with non-surviving patients (p=0.023).
  • Angiogenic factors are expressed in the bone marrow of patients with pediatric B cell precursor ALL and VEGF is a potential candidate for therapeutic intervention as it is significantly higher expressed in children with late relapses.
  • The mRNA expression of iNOS in the surviving children possibly reflects an increased activity of the immune system against the leukemia which leads to a superior survival.
  • [MeSH-major] Angiogenic Proteins / biosynthesis. Burkitt Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 17143492.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Angiogenic Proteins; 0 / RNA, Messenger; 0 / Transforming Growth Factor beta; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C; 103107-01-3 / Fibroblast Growth Factor 2; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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80. Terwey TH, Hemmati PG, Martus P, Dietz E, Vuong LG, Massenkeil G, Dörken B, Arnold R: A modified EBMT risk score and the hematopoietic cell transplantation-specific comorbidity index for pre-transplant risk assessment in adult acute lymphoblastic leukemia. Haematologica; 2010 May;95(5):810-8
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  • [Title] A modified EBMT risk score and the hematopoietic cell transplantation-specific comorbidity index for pre-transplant risk assessment in adult acute lymphoblastic leukemia.
  • BACKGROUND: Disease stage is the most important prognostic parameter in allogeneic hematopoietic cell transplantation (HCT) for acute lymphoblastic leukemia, but other factors such as donor/host histocompatibility and gender combination, recipient age, performance status and comorbidities need to be considered.
  • Several scoring systems are available to predict outcome in HCT recipients; however, their prognostic relevance in acute lymphoblastic leukemia is not well defined.
  • DESIGN AND METHODS: In the present study we evaluated a modified EBMT risk score (mEBMT) and the HCT-specific comorbidity index (HCT-CI) in 151 adult acute lymphoblastic leukemia patients who received allogeneic HCT from 1995 until 2007 at our center.
  • RESULTS: Disease status was first complete remission (CR1) (47%), CR>1 (21%) or no CR (32%).
  • Overall survival (OS) at one, two and five years was 62%, 51% and 40% and non-relapse mortality (NRM) was 21%, 24% and 32%.
  • Disease stage was the predominant prognostic factor in this score.
  • Comorbidities were present in 71% of patients with mild hepatic disease (29%), moderate pulmonary disease (28%) and infections (23%) being the most common.
  • However, KPS was associated with disease stage and significance was lost in multivariate analysis.
  • CONCLUSIONS: The mEBMT was prognostic in our patient cohort with predominant influence of disease stage, whereas a trend but no significant prognostic value was observed for the HCT-CI.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / standards. Karnofsky Performance Status / standards. Precursor Cell Lymphoblastic Leukemia-Lymphoma / surgery. Preoperative Care / standards. Transplantation Conditioning / standards

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  • [Cites] Biol Blood Marrow Transplant. 2003 Jul;9(7):472-81 [12869961.001]
  • [Cites] Blood. 2001 Mar 15;97(6):1572-7 [11238093.001]
  • [Cites] Bone Marrow Transplant. 1996 Jan;17(1):13-8 [8673048.001]
  • [Cites] Lancet. 1998 Oct 3;352(9134):1087-92 [9798583.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2912-9 [15994282.001]
  • [Cites] Ann Intern Med. 2006 Mar 21;144(6):407-14 [16549853.001]
  • [Cites] Biol Blood Marrow Transplant. 2006 Sep;12(9):954-64 [16920562.001]
  • [Cites] J Clin Oncol. 2006 Sep 1;24(25):4150-7 [16896000.001]
  • [Cites] Br J Haematol. 2006 Oct;135(2):201-9 [16939494.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Aug;13(8):932-41 [17640597.001]
  • [Cites] Bone Marrow Transplant. 2007 Aug;40(4):381-7 [17563735.001]
  • [Cites] J Clin Oncol. 2007 Sep 20;25(27):4246-54 [17724349.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Dec;13(12):1499-507 [18022580.001]
  • [Cites] Blood. 2007 Dec 15;110(13):4606-13 [17873123.001]
  • [Cites] Blood. 2008 Jan 1;111(1):446-52 [17916744.001]
  • [Cites] Biol Blood Marrow Transplant. 2008 Jan;14(1):28-35 [18158958.001]
  • [Cites] Bone Marrow Transplant. 2008 Apr;41(8):721-7 [18176613.001]
  • [Cites] Cancer. 2008 May 1;112(9):1992-2001 [18311781.001]
  • [Cites] Bone Marrow Transplant. 2008 May;41(9):805-12 [18195682.001]
  • [Cites] Biol Blood Marrow Transplant. 2008 Sep;14(9):985-92 [18721761.001]
  • [Cites] Clin Cancer Res. 2008 Sep 1;14(17):5585-93 [18765552.001]
  • [Cites] J Clin Oncol. 2008 Oct 20;26(30):4912-20 [18794548.001]
  • [Cites] Biol Blood Marrow Transplant. 2008 Nov;14(11):1217-25 [18940675.001]
  • [Cites] Br J Haematol. 2008 Nov;143(3):395-403 [18759762.001]
  • [Cites] Leukemia. 2008 Nov;22(11):2062-9 [18685612.001]
  • [Cites] Eur J Clin Invest. 2008 Dec;38(12):945-52 [19021720.001]
  • [Cites] Biol Blood Marrow Transplant. 2009 Jan;15(1 Suppl):149-53 [19147097.001]
  • [Cites] Biol Blood Marrow Transplant. 2009 Feb;15(2):223-30 [19167682.001]
  • [Cites] Bone Marrow Transplant. 2009 Jan;43(2):133-9 [18762762.001]
  • [Cites] Blood. 2009 Mar 26;113(13):2902-5 [19179301.001]
  • [Cites] Leukemia. 2009 Jun;23(6):1131-8 [19194465.001]
  • [Cites] Curr Hematol Malig Rep. 2009 Jul;4(3):139-47 [20425427.001]
  • [Cites] Hematol Oncol Clin North Am. 2000 Dec;14(6):1307-25, ix [11147225.001]
  • [Cites] Leukemia. 2003 Aug;17(8):1596-9 [12886248.001]
  • (PMID = 20007143.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2864388
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81. Awan FT, Lapalombella R, Trotta R, Butchar JP, Yu B, Benson DM Jr, Roda JM, Cheney C, Mo X, Lehman A, Jones J, Flynn J, Jarjoura D, Desjarlais JR, Tridandapani S, Caligiuri MA, Muthusamy N, Byrd JC: CD19 targeting of chronic lymphocytic leukemia with a novel Fc-domain-engineered monoclonal antibody. Blood; 2010 Feb 11;115(6):1204-13
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  • [Title] CD19 targeting of chronic lymphocytic leukemia with a novel Fc-domain-engineered monoclonal antibody.
  • CD19 is a B cell-specific antigen expressed on chronic lymphocytic leukemia (CLL) cells but to date has not been effectively targeted with therapeutic monoclonal antibodies.
  • The NK cell-mediated cytolytic and secretory function with XmAb5574 compared with the nonengineered antibody is associated with enhanced NK-cell activation, interferon production, extracellular signal-regulated kinase phosphorylation downstream of Fcgamma receptor, and no increased NK-cell apoptosis.
  • Notably, enhanced NK cell-mediated ADCC with XmAb5574 was enhanced further by lenalidomide.
  • These findings provide strong support for further clinical development of XmAb5574 as both a monotherapy and in combination with lenalidomide for the therapy of CLL and related CD19(+) B-cell malignancies.

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  • [Cites] Blood. 2007 Oct 1;110(7):2569-77 [17440052.001]
  • [Cites] Clin Cancer Res. 2007 Aug 1;13(15 Pt 1):4448-55 [17671129.001]
  • [Cites] J Clin Oncol. 2007 Dec 10;25(35):5616-23 [17984186.001]
  • [Cites] Br J Haematol. 2008 Jan;140(1):46-58 [17991300.001]
  • [Cites] Blood. 2008 Apr 15;111(8):4173-83 [18174382.001]
  • [Cites] Nat Immunol. 2008 May;9(5):503-10 [18425107.001]
  • [Cites] Clin Cancer Res. 2008 Jul 15;14(14):4650-7 [18628480.001]
  • [Cites] Cancer Res. 2008 Oct 1;68(19):8049-57 [18829563.001]
  • [Cites] Blood. 2008 Dec 15;112(13):5180-9 [18772452.001]
  • [Cites] Blood. 2009 Apr 16;113(16):3735-43 [19109559.001]
  • [Cites] Blood. 2009 Apr 30;113(18):4352-61 [19147785.001]
  • [Cites] Blood. 2011 Apr 28;117(17):4530-41 [21228331.001]
  • [Cites] Immunol Res. 2000;22(2-3):281-98 [11339363.001]
  • [Cites] Leuk Lymphoma. 2001 Aug;42(4):649-54 [11697493.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1314-9 [11830481.001]
  • [Cites] J Clin Invest. 2002 Oct;110(7):983-92 [12370276.001]
  • [Cites] J Cell Biochem. 2003 May 15;89(2):279-88 [12704791.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1846-54 [14630799.001]
  • [Cites] Ann Hematol. 2004 Oct;83(10):634-45 [15309525.001]
  • [Cites] J Exp Med. 1988 Feb 1;167(2):408-20 [2964496.001]
  • [Cites] Clin Immunol Immunopathol. 1988 May;47(2):219-29 [3258212.001]
  • [Cites] J Exp Med. 1990 Apr 1;171(4):1333-45 [2139103.001]
  • [Cites] Cancer Immunol Immunother. 1991;32(6):364-72 [1706642.001]
  • [Cites] Blood. 1994 Mar 1;83(5):1390-7 [8118040.001]
  • [Cites] Cancer Res. 1995 Feb 15;55(4):840-6 [7531616.001]
  • [Cites] Immunity. 1995 Jul;3(1):39-50 [7542548.001]
  • [Cites] Nature. 1995 Jul 27;376(6538):352-5 [7543183.001]
  • [Cites] Clin Lymphoma Myeloma. 2007 Aug;7 Suppl 5:S192-8 [17877844.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Dec 5;92(25):11558-62 [8524803.001]
  • [Cites] Blood. 1995 Dec 15;86(12):4389-99 [8541526.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] J Immunol. 1996 Jul 1;157(1):48-56 [8683154.001]
  • [Cites] J Exp Med. 1996 Sep 1;184(3):1027-35 [9064320.001]
  • [Cites] J Immunol. 1997 Apr 1;158(7):3062-9 [9120258.001]
  • [Cites] J Immunol. 1997 Apr 1;158(7):3148-54 [9120268.001]
  • [Cites] J Immunol. 1997 May 15;158(10):4662-9 [9144478.001]
  • [Cites] J Immunol. 1997 Oct 1;159(7):3278-87 [9317126.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3804-16 [9808574.001]
  • [Cites] J Immunol. 1998 Dec 15;161(12):6648-56 [9862693.001]
  • [Cites] Leuk Lymphoma. 2005 Jan;46(1):87-100 [15621786.001]
  • [Cites] Leukemia. 2005 May;19(5):835-40 [15744340.001]
  • [Cites] Leukemia. 2006 Feb;20(2):272-9 [16341049.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Mar 14;103(11):4005-10 [16537476.001]
  • [Cites] J Clin Invest. 2006 Sep;116(9):2484-92 [16917543.001]
  • [Cites] Crit Rev Oncol Hematol. 2007 Apr;62(1):26-33 [17240158.001]
  • [Cites] Nat Med. 2007 May;13(5):587-96 [17435771.001]
  • [Cites] Adv Immunol. 2007;96:41-101 [17981204.001]
  • (PMID = 19965644.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA95426; United States / NCI NIH HHS / CA / P50 CA140158; United States / NCI NIH HHS / CA / P01 CA081534; United States / NCI NIH HHS / CA / P01 CA81534; United States / NCRR NIH HHS / RR / UL1 RR025755; United States / NCI NIH HHS / CA / P01 CA095426
  • [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 / Antigens, CD19; 0 / Immunoglobulin Fc Fragments; 0 / RNA, Messenger; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.21.- / Granzymes
  • [Other-IDs] NLM/ PMC2826232
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82. Tedeschi A, Vismara E, Ricci F, Morra E, Montillo M: The spectrum of use of rituximab in chronic lymphocytic leukemia. Onco Targets Ther; 2010;3:227-46
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  • [Title] The spectrum of use of rituximab in chronic lymphocytic leukemia.
  • The monoclonal chimeric anti-CD20 antibody, rituximab, has considerably improved therapeutic outcome in B-cell chronic lymphocytic leukemia.
  • Furthermore the addition of rituximab enabled the eradication of minimal residual disease, which is correlated with the prognosis in a high proportion of patients.
  • Although the role of rituximab as maintenance therapy in low grade non-Hodgkin's lymphomas has been determined, the benefit and optimal schedule in chronic lymphocytic leukemia are still under investigation.
  • This review brings together knowledge of the pharmacokinetics, mechanism of action and clinical use of rituximab in chronic lymphocytic leukemia.

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  • [Cites] N Engl J Med. 2000 Dec 14;343(24):1750-7 [11114313.001]
  • [Cites] Clin Cancer Res. 2001 Mar;7(3):709-23 [11297268.001]
  • [Cites] J Clin Oncol. 2001 Apr 15;19(8):2153-64 [11304767.001]
  • [Cites] J Clin Oncol. 2001 Apr 15;19(8):2165-70 [11304768.001]
  • [Cites] Blood. 1975 Aug;46(2):219-34 [1139039.001]
  • [Cites] Br J Haematol. 2001 Aug;114(2):342-8 [11529853.001]
  • [Cites] Haematologica. 2002 Jan;87(1):33-43 [11801463.001]
  • [Cites] Blood. 2002 Feb 1;99(3):754-8 [11806974.001]
  • [Cites] Leuk Lymphoma. 2002 Jan;43(1):149-51 [11908720.001]
  • [Cites] Hematol J. 2001;2(5):300-6 [11920265.001]
  • [Cites] Hematol J. 2002;3(1):7-9 [11960388.001]
  • [Cites] Blood. 2002 May 15;99(10):3554-61 [11986207.001]
  • [Cites] J Clin Immunol. 2002 May;22(3):124-30 [12078853.001]
  • [Cites] Leuk Lymphoma. 2002 Apr;43(4):767-72 [12153163.001]
  • [Cites] Haematologica. 2002 Sep;87(9):918-25 [12217803.001]
  • [Cites] Blood. 2003 Jan 1;101(1):6-14 [12393429.001]
  • [Cites] Br J Haematol. 2002 Dec;119(4):976-84 [12472576.001]
  • [Cites] Semin Oncol. 2003 Feb;30(1 Suppl 2):34-9 [12652463.001]
  • [Cites] Int J Clin Oncol. 2003 Aug;8(4):212-23 [12955576.001]
  • [Cites] Ann Hematol. 2003 Dec;82(12):759-65 [14551737.001]
  • [Cites] Blood. 2004 Jun 15;103(12):4416-23 [14976046.001]
  • [Cites] Clin Lymphoma. 2004 Mar;4(4):220-7 [15072613.001]
  • [Cites] Leuk Lymphoma. 2004 Nov;45(11):2269-73 [15512816.001]
  • [Cites] Curr Dir Autoimmun. 2005;8:140-74 [15564720.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2965-72 [12351409.001]
  • [Cites] Blood. 2002 Nov 1;100(9):3115-20 [12384407.001]
  • [Cites] Blood. 2003 Feb 1;101(3):949-54 [12393572.001]
  • [Cites] Eur J Haematol. 2002 Sep;69(3):129-34 [12406005.001]
  • [Cites] Blood. 2003 Apr 1;101(7):2507-13 [12446458.001]
  • [Cites] Blood. 2003 May 1;101(9):3413-5 [12522009.001]
  • [Cites] J Clin Oncol. 2003 Apr 1;21(7):1278-84 [12663715.001]
  • [Cites] J Clin Oncol. 2003 May 1;21(9):1746-51 [12721250.001]
  • [Cites] N Engl J Med. 2003 May 1;348(18):1764-75 [12724482.001]
  • [Cites] Blood. 2004 Feb 15;103(4):1472-4 [14563637.001]
  • [Cites] Oncogene. 2003 Oct 20;22(47):7359-68 [14576843.001]
  • [Cites] Blood. 2005 Jan 1;105(1):49-53 [15138165.001]
  • [Cites] Leuk Lymphoma. 2004 May;45(5):945-50 [15291353.001]
  • [Cites] J Clin Oncol. 2005 May 1;23(13):2971-9 [15738539.001]
  • [Cites] Haematologica. 2005 Mar;90(3):391-9 [15749671.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4070-8 [15767647.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4079-88 [15767648.001]
  • [Cites] Cancer. 2006 Jan 15;106(2):337-45 [16353201.001]
  • [Cites] J Clin Oncol. 2006 Apr 1;24(10):1575-81 [16520464.001]
  • [Cites] Cancer Treat Rev. 2006 Aug;32(5):377-89 [16793209.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3295-301 [16873669.001]
  • [Cites] Blood. 2007 Jan 15;109(2):405-11 [17008537.001]
  • [Cites] J Clin Oncol. 2006 Dec 1;24(34):5343-9 [17088571.001]
  • [Cites] Leukemia. 2007 Jan;21(1):12-7 [17109028.001]
  • [Cites] Leuk Lymphoma. 2007 May;48(5):905-11 [17487734.001]
  • [Cites] Cancer. 2007 Jun 1;109(11):2291-8 [17514743.001]
  • [Cites] Leuk Lymphoma. 2007 Jul;48(7):1299-306 [17613757.001]
  • [Cites] Eur J Haematol. 2007 Aug;79(2):107-13 [17635235.001]
  • [Cites] Lancet. 2007 Jul 21;370(9583):230-9 [17658394.001]
  • [Cites] Mol Immunol. 2007 Sep;44(16):3823-37 [17768100.001]
  • [Cites] Cancer. 2008 Jan 1;112(1):119-28 [17999417.001]
  • [Cites] Leuk Lymphoma. 2007 Dec;48(12):2412-7 [18067017.001]
  • [Cites] Clin Cancer Res. 2008 Jan 1;14(1):155-61 [18172266.001]
  • [Cites] J Clin Oncol. 2008 Jan 10;26(2):196-203 [18182662.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5446-56 [18216293.001]
  • [Cites] Blood. 2008 May 15;111(10):4916-21 [18309034.001]
  • [Cites] Haematologica. 2008 Mar;93(3):475-6 [18310545.001]
  • [Cites] Blood. 2008 Jun 1;111(11):5291-7 [18334676.001]
  • [Cites] Lancet. 2008 Mar 22;371(9617):1017-29 [18358929.001]
  • [Cites] Blood. 2008 Aug 15;112(4):975-80 [18411418.001]
  • [Cites] Clin Cancer Res. 2008 Jul 15;14(14):4650-7 [18628480.001]
  • [Cites] Leukemia. 2008 Nov;22(11):2048-53 [18754025.001]
  • [Cites] Cancer. 2008 Oct 15;113(8):2110-8 [18759253.001]
  • [Cites] Leuk Lymphoma. 2008 Oct;49(10):1995-8 [18949622.001]
  • [Cites] J Clin Oncol. 2009 Feb 1;27(4):498-503 [19075274.001]
  • [Cites] Cancer. 2010 May 15;116(10):2360-5 [20225334.001]
  • [Cites] Leuk Lymphoma. 2010 Aug;51(8):1485-93 [20578816.001]
  • [Cites] Expert Rev Hematol. 2010 Apr;3(2):131-48 [21083456.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] Lancet. 1996 May 25;347(9013):1432-8 [8676625.001]
  • [Cites] Blood. 1998 Aug 15;92(4):1165-71 [9694704.001]
  • [Cites] J Clin Oncol. 1998 Aug;16(8):2825-33 [9704735.001]
  • [Cites] J Clin Pathol. 1998 May;51(5):364-9 [9708202.001]
  • [Cites] Blood. 1999 Oct 1;94(7):2217-24 [10498591.001]
  • [Cites] Leuk Lymphoma. 1999 Dec;36(1-2):57-65 [10613450.001]
  • [Cites] J Clin Oncol. 2000 Jan;18(2):317-24 [10637245.001]
  • [Cites] Leuk Res. 2000 May;24(5):411-5 [10785263.001]
  • [Cites] Blood. 2000 Jun 15;95(12):3900-8 [10845926.001]
  • [Cites] Scand J Immunol. 2000 Jun;51(6):634-41 [10849376.001]
  • [Cites] Cancer Biother Radiopharm. 1997 Jun;12(3):177-86 [10851464.001]
  • [Cites] Blood. 2000 Jul 1;96(1):71-5 [10891432.001]
  • [Cites] Acta Haematol. 1989;81(4):181-5 [2502891.001]
  • [Cites] Cancer. 1981 Jul 1;48(1):198-206 [7237385.001]
  • [Cites] Blood. 1993 Jun 1;81(11):2878-84 [8499626.001]
  • [Cites] J Clin Oncol. 1997 Oct;15(10):3266-74 [9336364.001]
  • [Cites] Eur J Haematol. 1999 Feb;62(2):76-82 [10052709.001]
  • [Cites] J Natl Cancer Inst. 1999 May 19;91(10):861-8 [10340906.001]
  • [Cites] Leuk Lymphoma. 1999 Jun;34(1-2):167-70 [10350345.001]
  • [Cites] Blood. 1999 Sep 15;94(6):1840-7 [10477712.001]
  • [Cites] Blood. 1999 Sep 15;94(6):1848-54 [10477713.001]
  • [Cites] N Engl J Med. 2000 Dec 28;343(26):1910-6 [11136261.001]
  • [Cites] J Clin Oncol. 2001 Mar 1;19(5):1414-20 [11230486.001]
  • [Cites] Blood. 2001 Sep 1;98(5):1326-31 [11520778.001]
  • [Cites] Br J Haematol. 2001 Sep;114(4):800-9 [11564066.001]
  • [Cites] Leukemia. 2001 Oct;15(10):1619-26 [11587221.001]
  • [Cites] Blood. 2001 Oct 15;98(8):2319-25 [11588025.001]
  • [Cites] J Clin Oncol. 2002 Sep 15;20(18):3891-7 [12228210.001]
  • [Cites] J Clin Oncol. 2009 Feb 1;27(4):491-7 [19075280.001]
  • [Cites] Cancer. 2009 Jan 15;115(2):373-80 [19117034.001]
  • [Cites] Leuk Lymphoma. 2009 Mar;50(3):514-6 [19347738.001]
  • [Cites] Blood. 2009 Sep 3;114(10):2044-50 [19553638.001]
  • [Cites] Leuk Res. 2010 Mar;34(3):284-8 [19646755.001]
  • [Cites] Leukemia. 2009 Oct;23(10):1779-89 [19693094.001]
  • [Cites] J Clin Oncol. 2009 Sep 20;27(27):4578-84 [19704063.001]
  • [Cites] Blood. 2010 Jan 21;115(3):489-95 [19843887.001]
  • [Cites] Leuk Lymphoma. 2010 Jan;51(1):107-13 [20001234.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2009;:440-9 [20008230.001]
  • [Cites] Cancer. 2010 May 1;116(9):2180-7 [20187101.001]
  • [Cites] J Clin Oncol. 2010 Apr 1;28(10):1756-65 [20194844.001]
  • (PMID = 21289858.001).
  • [ISSN] 1178-6930
  • [Journal-full-title] OncoTargets and therapy
  • [ISO-abbreviation] Onco Targets Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC3024887
  • [Keywords] NOTNLM ; B-cell chronic lymphocytic leukemia / first-line treatment / refractory/relapsed / rituximab
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83. Yang Y, Tian Y, Yan C, Jin X, Tang J, Shen X: Determinants of urinary 8-hydroxy-2'-deoxyguanosine in Chinese children with acute leukemia. Environ Toxicol; 2009 Oct;24(5):446-52
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  • [Title] Determinants of urinary 8-hydroxy-2'-deoxyguanosine in Chinese children with acute leukemia.
  • The 8-hydroxy-2'-deoxyguanosine (8-OHdG), an oxidized nucleoside of DNA, not only is a widely used biomarker for the measurement of endogenous oxidative DNA damage, but might also be a risk factor for many diseases including cancer.
  • In the present study, the level of urinary 8-OHdG was examined in 116 Chinese children with acute leukemia (94 acute lymphoid leukemia, ALL, 22 acute myeloid leukemia, AML), and its correlation with urinary metal elements was investigated.
  • Our result showed that the level of urinary 8-OHdG in children with acute leukemia before treatment was significantly elevated compared with that in normal controls (11.92 +/- 15.42 vs. 4.03 +/- 4.70 ng/mg creatinine, P < 0.05).
  • In particular, urinary 8-OHdG was higher in children with acute leukemia aged under 3 years (20.86 +/- 21.75 ng/mg creatinine) than in those aged 3-15 years (8.09 +/- 9.65 ng/mg creatinine), whereas no differences were shown in terms of gender, parental smoking and education, household income, place of residence, and use of paracetamol.
  • In addition, urinary 8-OHdG levels were similar among different subtypes of acute lymphoid leukemia (ALL) patients.
  • Furthermore, linear regression analysis revealed a significant correlation between urinary 8-OHdG and urinary Cr, but not Fe or As, in group aged <3 years compared with group aged 3-15 years (P = 0.041), indicating that the metal elements may be involved in increasing urinary 8-OHdG level in younger children with acute leukemia.
  • Our results suggest that children with acute leukemia undergo an increased risk of oxidative DNA damage, which may be correlated with high level of Cr exposure in Chinese children with acute leukemia.
  • [MeSH-major] Carcinogens / metabolism. Deoxyguanosine / analogs & derivatives. Leukemia, Myeloid, Acute / urine. Precursor Cell Lymphoblastic Leukemia-Lymphoma / urine

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  • (PMID = 18979530.001).
  • [ISSN] 1522-7278
  • [Journal-full-title] Environmental toxicology
  • [ISO-abbreviation] Environ. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Metals; 88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; G9481N71RO / Deoxyguanosine
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84. Gelfand MS, Cleveland KO, Brewer SC: Rhodococcus equi pneumonia in a patient with fludarabine-treated chronic lymphocytic leukemia and CD4-lymphopenia. Am J Med Sci; 2010 Jul;340(1):80-1
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  • [Title] Rhodococcus equi pneumonia in a patient with fludarabine-treated chronic lymphocytic leukemia and CD4-lymphopenia.
  • Cavitary pneumonia caused by Rhodococcus equi may occur in patients with defective cell-mediated immunity.
  • Prolonged CD4 lymphopenia may develop in patients with chronic lymphocytic leukemia who receive fludarabine.
  • The authors report the first case of a patient with chronic lymphocytic leukemia who developed R equi pneumonia after fludarabine therapy.
  • [MeSH-major] Actinomycetales Infections / microbiology. Leukemia, Lymphoid / drug therapy. Lymphopenia / drug therapy. Pneumonia, Bacterial / microbiology. Rhodococcus equi / isolation & purification
  • [MeSH-minor] Aged, 80 and over. Anti-Bacterial Agents / therapeutic use. Antineoplastic Agents / therapeutic use. Bronchoalveolar Lavage Fluid / microbiology. CD4 Lymphocyte Count. Chronic Disease. Female. Humans. Opportunistic Infections / microbiology. Vidarabine / analogs & derivatives. Vidarabine / therapeutic use


85. Saygili EI, Aksoy N, Pehlivan M, Sever T, Yilmaz M, Cimenci IG, Pehlivan S: Enzyme levels and G-463A polymorphism of myeloperoxidase in chronic lymphocytic leukemia and multiple myeloma. Leuk Lymphoma; 2009 Dec;50(12):2030-7
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  • [Title] Enzyme levels and G-463A polymorphism of myeloperoxidase in chronic lymphocytic leukemia and multiple myeloma.
  • The aim of this study was to investigate how myeloperoxidase (MPO) G-463A gene polymorphism and enzyme levels varied among patients with chronic lymphocytic leukemia (CLL) and multiple myeloma (MM) and to find the relationship between the MPO gene, enzyme levels, and clinical parameters.
  • In accordance with the results of the study, we assess that the increase in the MPO enzyme level in the patient groups with CLL and MM generated bactericidal effects as well as the increased formation of ROP, thus setting off a pro-cell death pathway and playing a role on the pathogenesis of lymphoproliferative malignancies through this mechanism.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Multiple Myeloma / genetics. Peroxidase / genetics


86. Kalac M, Suvic-Krizanic V, Ostojic S, Kardum-Skelin I, Barsic B, Jaksica B: Central nervous system involvement of previously undiagnosed chronic lymphocytic leukemia in a patient with neuroborreliosis. Int J Hematol; 2007 May;85(4):323-5
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  • [Title] Central nervous system involvement of previously undiagnosed chronic lymphocytic leukemia in a patient with neuroborreliosis.
  • Leukemic involvement of the central nervous system (CNS) in previously undiagnosed chronic lymphocytic leukemia (CLL) is very rare.
  • We report the case of a 62-year-old man with neuroborreliosis in which cytologic, immunocytochemical, and flow cytometry analyses revealed the presence of clonal B-lymphocytes in the cerebrospinal fluid (CSF).
  • The application of intrathecal dexamethasone therapy led to the disappearance of B-cell CLL (B-CLL) cells in the CSF.
  • [MeSH-major] Central Nervous System / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemic Infiltration / drug therapy. Leukemic Infiltration / pathology. Lyme Neuroborreliosis / drug therapy. Lyme Neuroborreliosis / pathology

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  • [Cites] Cancer Chemother Pharmacol. 1990;25(5):311-9 [2306790.001]
  • [Cites] Postgrad Med J. 2005 Mar;81(953):194-5 [15749798.001]
  • [Cites] Expert Opin Pharmacother. 2001 Jun;2(6):929-43 [11585009.001]
  • [Cites] Eur J Intern Med. 2003 Feb;14(1):49-52 [12554011.001]
  • [Cites] J Neuroimmunol. 2000 Oct 2;110(1-2):244-51 [11024556.001]
  • [Cites] Leuk Lymphoma. 2002 Jan;43(1):199-201 [11908730.001]
  • [Cites] Infect Immun. 2005 Feb;73(2):1014-22 [15664945.001]
  • [Cites] Br J Haematol. 1999 Mar;104(4):689-94 [10192427.001]
  • [Cites] Blood. 2000 Jul 15;96(2):776-7 [10950515.001]
  • [Cites] Ann Neurol. 1998 Oct;44(4):592-600 [9778257.001]
  • [Cites] Cancer Chemother Pharmacol. 1988;21(1):1-8 [3342460.001]
  • [Cites] J Infect Dis. 1998 Feb;177(2):401-8 [9466528.001]
  • [Cites] Leukemia. 1996 May;10(5):877-95 [8656686.001]
  • [Cites] Leuk Lymphoma. 2005 Apr;46(4):619-21 [16019494.001]
  • [Cites] Leuk Lymphoma. 1998 Feb;28(5-6):603-5 [9613992.001]
  • [Cites] J Clin Pathol. 1996 Aug;49(8):672-5 [8881921.001]
  • [Cites] Ann Hematol. 2002 Jul;81(7):402-4 [12185514.001]
  • [Cites] J Neuroophthalmol. 2005 Jun;25(2):113-5 [15937434.001]
  • [Cites] Leuk Lymphoma. 2003 Jul;44(7):1235-7 [12916878.001]
  • (PMID = 17483076.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Hormonal; 18D0SL7309 / Chlorambucil; 7S5I7G3JQL / Dexamethasone; EC 3.4.24.35 / Matrix Metalloproteinase 9
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87. Schöttker B, Feuchtinger T, Schumm M, Klinker E, Handgretinger R, Einsele H, Stuhler G: Five donors-one recipient: modeling a mosaic of granulocytes, natural killer and T cells from cord-blood and third-party donors. Nat Clin Pract Oncol; 2008 May;5(5):291-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • INVESTIGATIONS: Laboratory tests, immunophenotyping, cytogenetic analyses, bone-marrow biopsy, minimal residual disease analysis using quantitative real-time polymerase chain reaction, differential chimerism analysis using flow cytometry, mixed chimerism analysis, CT scans, electro-encephalography, cerebral magnetic resonance tomography.
  • DIAGNOSIS: Bcr-abl-positive and Philadelphia-chromosome-positive acute lymphoblastic leukemia, and primary graft failure complicated by invasive fungal infection and cytomegalovirus encephalitis.
  • MANAGEMENT: Double cord-blood rescue transplantation, third-party CD34-positive stem-cell rescue transplantation, third-party cytomegalovirus-specific T lymphocyte transplantation.
  • [MeSH-major] Cell Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adult. Cord Blood Stem Cell Transplantation. Granulocytes / transplantation. Humans. Killer Cells, Natural / transplantation. Male. Mosaicism. T-Lymphocytes / transplantation

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  • (PMID = 18364724.001).
  • [ISSN] 1743-4262
  • [Journal-full-title] Nature clinical practice. Oncology
  • [ISO-abbreviation] Nat Clin Pract Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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88. Pichiorri F, Trapasso F, Palumbo T, Aqeilan RI, Drusco A, Blaser BW, Iliopoulos D, Caligiuri MA, Huebner K, Croce CM: Preclinical assessment of FHIT gene replacement therapy in human leukemia using a chimeric adenovirus, Ad5/F35. Clin Cancer Res; 2006 Jun 01;12(11 Pt 1):3494-501
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preclinical assessment of FHIT gene replacement therapy in human leukemia using a chimeric adenovirus, Ad5/F35.
  • Adenovirus 5 (Ad5) virus or adeno-associated viral vectors have been used to study the tumor suppressor function of FHIT in solid tumors, but these tools have not been effective in leukemias.
  • EXPERIMENTAL DESIGN: Infection efficiency of Ad5/F35-FHIT and Ad5/F35-GFP viruses was tested in leukemia cell lines that lacked FHIT expression, and biological effects of successful infection were assessed.
  • An acute myelogenous leukemia, a chronic myelogenous leukemia, and four acute lymphoblastic leukemia human cell lines were examined as well as two EBV-transformed B lymphoblastoid cell lines that expressed endogenous FHIT.
  • RESULTS: Two of four acute lymphoblastic leukemia cell lines, Jurkat and MV4;11, which were efficiently infected with Ad5/F35-FHIT, underwent growth suppression and massive induction of apoptosis without apparent activation of caspase-8 or caspase-2 and late activation of caspase-3.
  • The two remaining infected acute lymphoblastic leukemia cell lines, Molt-3 and RS4;11, were apparently unaffected.
  • Restoration of FHIT expression in the chronic myelogenous leukemia K562 cell line and the acute myelogenous leukemia KG1a cell line also induced apoptosis but at later time points than seen in the acute lymphoblastic leukemia Jurkat and MV4;11 cell lines. I.v. injection of Ad5/F35-FHIT-infected Jurkat cells resulted in abrogation of tumorigenicity in the NOD/SCID xenogeneic engraftment model.
  • CONCLUSION: FHIT restoration in some FHIT-deficient leukemia cells induces both antiproliferative and proapoptotic effects involving the intrinsic caspase apoptotic pathway.
  • [MeSH-major] Acid Anhydride Hydrolases / genetics. Adenoviruses, Human / genetics. Gene Expression Regulation, Neoplastic / genetics. Genetic Therapy / methods. Leukemia / genetics. Neoplasm Proteins / genetics
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / genetics. Cell Cycle. Cell Line, Tumor. Cell Proliferation / drug effects. Disease Models, Animal. Drug Screening Assays, Antitumor. Enzyme Inhibitors / pharmacology. Gene Transfer Techniques. Genetic Vectors / genetics. Green Fluorescent Proteins / genetics. Humans. Kinetics. Mice. Mice, Inbred NOD. Mice, SCID. Structure-Activity Relationship. Transplantation, Heterologous. Xenograft Model Antitumor Assays

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  • [ErratumIn] Clin Cancer Res. 2016 Dec 15;22(24):6304 [27856602.001]
  • (PMID = 16740775.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA56036; United States / NCI NIH HHS / CA / CA77738; United States / NCI NIH HHS / CA / CA78890; United States / NCI NIH HHS / CA / CA89341
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Neoplasm Proteins; 0 / fragile histidine triad protein; 147336-22-9 / Green Fluorescent Proteins; EC 3.6.- / Acid Anhydride Hydrolases
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89. Pettit GR, Thornhill AJ, Moser BR, Hogan F: Antineoplastic agents. 552. Oxidation of combretastatin A-1: trapping the o-quinone intermediate considered the metabolic product of the corresponding phosphate prodrug. J Nat Prod; 2008 Sep;71(9):1561-3
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  • Both phenazines 7 and 11 significantly inhibited (ED50 approximately 0.2 microg/mL) growth of the murine P388 lymphocytic leukemia cell line and provided a new SAR insight in the combretastatin series of naturally occurring anticancer drugs.

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  • [Cites] Anticancer Drug Des. 2000 Jun;15(3):203-16 [11049088.001]
  • [Cites] Chem Res Toxicol. 2007 Dec;20(12):1885-94 [17941699.001]
  • [Cites] Bioorg Med Chem. 2003 Jul 17;11(14):3179-91 [12818681.001]
  • [Cites] Int J Cancer. 2004 Sep 10;111(4):604-10 [15239140.001]
  • [Cites] J Nat Prod. 1987 Jan-Feb;50(1):119-31 [3598594.001]
  • [Cites] Experientia. 1989 Feb 15;45(2):209-11 [2920809.001]
  • [Cites] J Pharm Biomed Anal. 1990;8(3):307-12 [2094431.001]
  • [Cites] Pharmacol Ther. 1993 Aug;59(2):163-228 [8278462.001]
  • [Cites] J Med Chem. 1995 May 12;38(10):1666-72 [7752190.001]
  • [Cites] Anticancer Drug Des. 1995 Jun;10(4):299-309 [7786396.001]
  • [Cites] Anticancer Drug Des. 1998 Apr;13(3):183-91 [9595032.001]
  • [Cites] J Clin Invest. 2005 Nov;115(11):2992-3006 [16224539.001]
  • [Cites] Clin Cancer Res. 2006 Jul 1;12(13):4090-4 [16818709.001]
  • [Cites] Bioorg Med Chem. 2007 Jan 15;15(2):605-15 [17070061.001]
  • [Cites] Expert Opin Investig Drugs. 2007 Apr;16(4):451-65 [17371194.001]
  • [Cites] Curr Opin Oncol. 2008 Jan;20(1):19-24 [18043252.001]
  • [Cites] Biosci Biotechnol Biochem. 2001 Dec;65(12):2613-21 [11826955.001]
  • (PMID = 18729517.001).
  • [ISSN] 1520-6025
  • [Journal-full-title] Journal of natural products
  • [ISO-abbreviation] J. Nat. Prod.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090441-05; United States / NCI NIH HHS / CA / R01 CA090441; United States / NCI NIH HHS / CA / R01 CA090441-01; United States / NCI NIH HHS / CA / R56 CA090441-06A1; United States / NCI NIH HHS / CA / R01 CA090441-02; United States / NCI NIH HHS / CA / 2R56 CA090441-06A1; United States / NCI NIH HHS / CA / R01 CA090441-04; United States / NCI NIH HHS / CA / R01 CA090441-03; United States / NCI NIH HHS / CA / R01 CA90441-01-05; United States / NCI NIH HHS / CA / R56 CA090441
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Biological Products; 0 / Prodrugs; 0 / Quinones; 0 / Stilbenes; 109971-63-3 / combretastatin A-1; I5590ES2QZ / fosbretabulin
  • [Other-IDs] NLM/ NIHMS86312; NLM/ PMC2756244
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90. Uckun FM, Dibirdik I, Qazi S, Yiv S: Therapeutic nanoparticle constructs of a JAK3 tyrosine kinase inhibitor against human B-lineage ALL cells. Arzneimittelforschung; 2010;60(4):210-7
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  • [Title] Therapeutic nanoparticle constructs of a JAK3 tyrosine kinase inhibitor against human B-lineage ALL cells.
  • Notably, WHI-P131-NP was capable of causing apoptotic death in primary leukemia cells from chemotherapy-resistant acute lymphoblastic leukemia (ALL) as well as chronic lymphocytic leukemia (CLL) patients.
  • These experimental results demonstrate that the nanotechnology-enabled delivery of WHI-P131 shows therapeutic potential against leukemias with constitutive activation of the JAK3-STAT3/STAT5 molecular target.
  • [MeSH-major] Antineoplastic Agents. Janus Kinase 3 / antagonists & inhibitors. Leukemia, B-Cell / drug therapy. Leukemia, Biphenotypic, Acute / drug therapy. Protein Kinase Inhibitors / administration & dosage. Protein Kinase Inhibitors / pharmacology. Quinazolines / administration & dosage. Quinazolines / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Calibration. Cell Lineage. Chemistry, Pharmaceutical. Chromatography, High Pressure Liquid. Female. Humans. Liposomes. Mice. Mice, SCID. Nanoparticles. Osmolar Concentration. Particle Size

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  • [ErratumIn] Arzneimittelforschung. 2010;60(5):286
  • (PMID = 20486472.001).
  • [ISSN] 0004-4172
  • [Journal-full-title] Arzneimittel-Forschung
  • [ISO-abbreviation] Arzneimittelforschung
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Liposomes; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / WHI P131; EC 2.7.10.2 / Janus Kinase 3
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91. Tedeschi A, Montillo M, Strocchi E, Cafro AM, Tresoldi E, Intropido L, Nichelatti M, Marbello L, Baratè C, Camaggi CM, Morra E: High-dose idarubicin in combination with Ara-C in patients with relapsed or refractory acute lymphoblastic leukemia: a pharmacokinetic and clinical study. Cancer Chemother Pharmacol; 2007 May;59(6):771-9
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  • [Title] High-dose idarubicin in combination with Ara-C in patients with relapsed or refractory acute lymphoblastic leukemia: a pharmacokinetic and clinical study.
  • OBJECTIVE: High dose (HD) Ara-C combined with a single HD idarubicin dose (IDA) is an efficient and safe salvage regimen for patients with refractory or relapsed acute lymphoblastic leukemia as indicated by phase II studies.
  • PATIENTS AND METHODS: Twenty-five patients with refractory or relapsed acute lymphoblastic leukemia received Ara-C 3 g/m2 from days 1-5, idarubicin (HD-IDA) 40 mg/m2 as rapid intravenous (i.v.) infusion on day 3 and subcutaneous G-CSF 5 microg/kg from day 7 until PMN recovery.
  • RESULTS: Eleven patients (44%, 95% CI: 23-65%) achieved complete remission with median disease free survival for 6 months.
  • Our data do not allow us to clearly attribute this behavior to a pharmacokinetic non-linearity since the baseline creatinine clearance, even within normal values, and patient age are significantly different in the two groups.
  • [MeSH-minor] Adolescent. Adult. Disease-Free Survival. Female. Humans. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Recurrence. Remission Induction. Survival Analysis

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  • (PMID = 17256136.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
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92. Sazawal S, Bakhshi S, Raina V, Swaroop C, Saxena R: Detection and clinical relevance of BCR-ABL fusion gene in childhood T-lineage acute lymphoblastic leukemia: a report on 4 cases. J Pediatr Hematol Oncol; 2009 Nov;31(11):850-2
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  • [Title] Detection and clinical relevance of BCR-ABL fusion gene in childhood T-lineage acute lymphoblastic leukemia: a report on 4 cases.
  • The bcr-abl rearrangement has rarely been reported in T-lineage acute lymphoblastic leukemia and the clinical significance of this translocation is currently unknown.
  • We screened 28 children with T-lineage acute lymphoblastic leukemia at diagnosis by reverse transcription polymerase chain reaction for major and minor break point regions of bcr-abl fusion gene.
  • [MeSH-major] Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 9 / genetics. Genes, abl / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic


93. Murati A, Gervais C, Carbuccia N, Finetti P, Cervera N, Adélaïde J, Struski S, Lippert E, Mugneret F, Tigaud I, Penther D, Bastard C, Poppe B, Speleman F, Baranger L, Luquet I, Cornillet-Lefebvre P, Nadal N, Nguyen-Khac F, Pérot C, Olschwang S, Bertucci F, Chaffanet M, Lessard M, Mozziconacci MJ, Birnbaum D, Groupe Francophone de Cytogénétique Hématologique: Genome profiling of acute myelomonocytic leukemia: alteration of the MYB locus in MYST3-linked cases. Leukemia; 2009 Jan;23(1):85-94
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  • [Title] Genome profiling of acute myelomonocytic leukemia: alteration of the MYB locus in MYST3-linked cases.
  • The t(8;16)(p11;p13) is a rare translocation involved in de novo and therapy-related myelomonocytic and monocytic acute leukemia.
  • MYST3-linked acute myeloid leukemias (AMLs) share specific clinical and biological features and a poor prognosis.
  • We have established the genome and gene expression profiles of a multicentric series of 61 M4/M5 AMLs including 18 MYST3-linked AMLs by using array comparative genome hybridization (aCGH) (n=52) and DNA microarrays (n=44), respectively.
  • These features, reminiscent of T-cell acute lymphoid leukemia (ALL), suggest the targeting of a common T-myeloid progenitor.
  • [MeSH-major] Gene Expression Profiling / methods. Genes, myb / genetics. Histone Acetyltransferases / genetics. Leukemia, Myelomonocytic, Acute / genetics

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  • (PMID = 18818702.001).
  • [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, CD4; 0 / Homeodomain Proteins; 0 / Proto-Oncogene Proteins c-myb; 157907-48-7 / HoxA protein; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human
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94. Beyan C, Kaptan K, Ifran A: Coexistence of chronic lymphocytic leukemia and Hashimoto's thyroiditis. Ann Hematol; 2006 Nov;85(11):811-2
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  • [Title] Coexistence of chronic lymphocytic leukemia and Hashimoto's thyroiditis.
  • [MeSH-major] Hashimoto Disease / etiology. Leukemia, Lymphocytic, Chronic, B-Cell / complications

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  • (PMID = 16845514.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Germany
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95. Dasanu CA: Intrinsic and treatment-related immune alterations in chronic lymphocytic leukaemia and their impact for clinical practice. Expert Opin Pharmacother; 2008 Jun;9(9):1481-94
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  • [Title] Intrinsic and treatment-related immune alterations in chronic lymphocytic leukaemia and their impact for clinical practice.
  • BACKGROUND: Chronic lymphocytic leukaemia patients harbour important impairments in both their cellular- and humoral-mediated immunity, which accounts for their notorious susceptibility to a multitude of infections and various autoimmune cytopenias.
  • It has also been shown that the rate of second cancers is increased in chronic lymphocytic leukaemia.
  • OBJECTIVE: The aim of this study was to review the immune alterations in untreated and treated chronic lymphocytic leukaemia and define their impact for clinical practice.
  • METHODS: The author gives a comprehensive review of the most relevant preclinical and clinical studies pertaining to various immune abnormalities and infectious complications in both untreated and treated chronic lymphocytic leukaemia.
  • Landmark clinical trials involving the contemporary chronic lymphocytic leukaemia chemo- and immunotherapies, alone or in combination, as well as the main epidemiological studies establishing the increased rate of second cancers in chronic lymphocytic leukaemia are also discussed.
  • RESULTS/CONCLUSIONS: Iatrogenic immunosuppression in chronic lymphocytic leukaemia alters the pattern of opportunistic infections, can cause autoimmune cytopenias and might further increase the rate of second malignancies in patients whose disease already places them at a greater risk.
  • Careful consideration of existing risk factors in chronic lymphocytic leukaemia could establish the optimal screening and follow-up schedule for chronic lymphocytic leukaemia patients as its therapeutics evolves.
  • [MeSH-major] Antineoplastic Agents. Immune System Diseases / chemically induced. Immune Tolerance / drug effects. Leukemia, Lymphocytic, Chronic, B-Cell. Neoplasms, Second Primary. Opportunistic Infections

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  • (PMID = 18518779.001).
  • [ISSN] 1744-7666
  • [Journal-full-title] Expert opinion on pharmacotherapy
  • [ISO-abbreviation] Expert Opin Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 69
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96. Qu L, Li Q, Jiang H, Gu L, Zhang Q, Wang C, Li J: Effect of anti-mouse CD52 monoclonal antibody on mouse intestinal intraepithelial lymphocytes. Transplantation; 2009 Sep 27;88(6):766-72
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  • BACKGROUND: CD52 monoclonal antibody (mAb) has been used therapeutically in lymphocytic leukemia, autoimmune disease, and organ transplantation.
  • [MeSH-minor] Animals. Antigens, CD. Antigens, Neoplasm. Apoptosis / immunology. Cell Survival / immunology. Epithelium / immunology. Epithelium / metabolism. Epithelium / pathology. Immunity, Mucosal. Injections, Subcutaneous. Lymphocyte Count. Lymphocyte Depletion / adverse effects. Male. Mice. Mice, Inbred C57BL. Permeability. Transplantation Immunology

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  • (PMID = 19920775.001).
  • [ISSN] 1534-6080
  • [Journal-full-title] Transplantation
  • [ISO-abbreviation] Transplantation
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CD52 antigen; 0 / Glycoproteins
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97. Milne E, Laurvick CL, de Klerk N, Robertson L, Thompson JR, Bower C: Trends in childhood acute lymphoblastic leukemia in Western Australia, 1960-2006. Int J Cancer; 2008 Mar 1;122(5):1130-4
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  • [Title] Trends in childhood acute lymphoblastic leukemia in Western Australia, 1960-2006.
  • Increases in the incidence of childhood acute lymphoblastic leukemia (ALL) have been reported in some countries, while other reports from similar geographical regions have indicated stable rates.
  • The reasons for the discrepancies have been debated in the literature, with the focus on whether the observed increases are "real" or an artifact resulting from improvements in diagnosis, case ascertainment and population coverage over time.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology


98. Nabhan C: Frontline therapy for chronic lymphocytic leukemia: the dilemma continues. Clin Cancer Res; 2008 Jul 1;14(13):4353
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  • [Title] Frontline therapy for chronic lymphocytic leukemia: the dilemma continues.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy

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  • [CommentOn] Clin Cancer Res. 2008 Jan 1;14(1):155-61 [18172266.001]
  • (PMID = 18594019.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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99. Al'-Radi LS, Samoĭlova RS, Tikhonova LIu, Diagileva OA, Obukhova TN, Kaplanskaia IB, Gretsov EM, Vorob'ev IA, Kremenetskaia AM, Kravchenko SK: [Combination of chronic lymphoid leukemia and hairy cell leukemia]. Ter Arkh; 2006;78(7):84-7
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  • [Title] [Combination of chronic lymphoid leukemia and hairy cell leukemia].
  • [MeSH-major] Leukemia, Hairy Cell / complications. Leukemia, Lymphocytic, Chronic, B-Cell / complications

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  • (PMID = 16944757.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Russia (Federation)
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100. Sweetenham JW: Lymphoblastic lymphoma in adults. Curr Hematol Malig Rep; 2006 Dec;1(4):241-7
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  • [Title] Lymphoblastic lymphoma in adults.
  • Understanding of the pathogenesis and biology of precursor T-cell and B-cell neoplasms has advanced significantly with the description of gene expression profiling studies, especially in T-cell disease.
  • Optimal treatment strategies for adult lymphoblastic lymphoma are uncertain, although current evidence supports the use of regimens similar to those used in acute lymphoblastic leukemia, with intensive induction therapy, central nervous system prophylaxis, and prolonged consolidation maintenance therapy.
  • Current studies do not demonstrate a benefit from stem cell transplantation in first remission, although this approach is probably beneficial in relapsed disease.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. B-Lymphocytes / pathology. Child. Combined Modality Therapy. Gene Expression Regulation, Neoplastic. Gene Rearrangement. Hematopoietic Stem Cell Transplantation. Humans. Mediastinal Neoplasms / drug therapy. Mediastinal Neoplasms / pathology. Mediastinal Neoplasms / radiotherapy. Multicenter Studies as Topic / statistics & numerical data. Prognosis. Randomized Controlled Trials as Topic / statistics & numerical data. Remission Induction. Salvage Therapy. T-Lymphocytes / pathology. Treatment Outcome. Young Adult