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6. Gros F, Sebti Y, de Guibert S, Branger B, Bernard M, Fauchet R, Amiot L: Soluble HLA-G molecules increase during acute leukemia, especially in subtypes affecting monocytic and lymphoid lineages. Neoplasia; 2006 Mar;8(3):223-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Soluble HLA-G molecules increase during acute leukemia, especially in subtypes affecting monocytic and lymphoid lineages.
  • Assay of these molecules by enzyme-linked immunosorbent assay in patients suffering from another hematologic disorder (acute leukemia) highlights increased sHLA-G secretion.
  • This increased secretion seems more marked in acute leukemia subtypes affecting monocytic and lymphoid lineages such as FABM4 and FABM5, as well as both B and T acute lymphoblastic leukemia (ALL).
  • All these findings suggest that sHLA-G molecules could be a factor in tumoral escape from immune survey during acute leukemia.
  • [MeSH-major] Antigens, Neoplasm / blood. HLA Antigens / blood. Histocompatibility Antigens Class I / blood. Leukemia / blood
  • [MeSH-minor] Acute Disease. Biomarkers, Tumor / blood. Burkitt Lymphoma / blood. Burkitt Lymphoma / genetics. Burkitt Lymphoma / metabolism. Burkitt Lymphoma / pathology. Cell Line, Tumor / chemistry. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Cytokines / blood. Cytokines / pharmacology. Enzyme-Linked Immunosorbent Assay. Gene Expression Regulation, Leukemic / drug effects. HLA-G Antigens. Humans. Leukemia, Myeloid / blood. Leukemia, Myeloid / classification. Leukemia, Myeloid / genetics. Leukemia, Myeloid / metabolism. Leukemia, Myeloid / pathology. Leukemia-Lymphoma, Adult T-Cell / blood. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / metabolism. Leukemia-Lymphoma, Adult T-Cell / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Retrospective Studies. Solubility. Tumor Escape

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  • (PMID = 16611416.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Cytokines; 0 / HLA Antigens; 0 / HLA-G Antigens; 0 / Histocompatibility Antigens Class I
  • [Other-IDs] NLM/ PMC1578523
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7. Wang X, Yuling H, Yanping J, Xinti T, Yaofang Y, Feng Y, Ruijin X, Li W, Lang C, Jingyi L, Zhiqing T, Jingping O, Bing X, Li Q, Chang AE, Sun Z, Youxin J, Jinquan T: CCL19 and CXCL13 synergistically regulate interaction between B cell acute lymphocytic leukemia CD23+CD5+ B Cells and CD8+ T cells. J Immunol; 2007 Sep 1;179(5):2880-8
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  • [Title] CCL19 and CXCL13 synergistically regulate interaction between B cell acute lymphocytic leukemia CD23+CD5+ B Cells and CD8+ T cells.
  • In a previous study, we have reported that ligation of CCL19-CCR7 and CXCL13-CXCR5 activates paternally expressed gene 10 (PEG10), resulting in an enhancement of apoptotic resistance in B-cell acute lymphocytic leukemia (B-ALL) CD23+CD5+ B cells.
  • CCL19/CXCL13-activated B-ALL CD23+CD5+ B cells, in turn, increase IL-10 expression in syngeneic CD8+ T cells in a B cell-derived IL-10-dependent manner and requiring a cell-cell contact.
  • Moreover, using a short hairpin RNA to knockdown PEG10, we provide direct evidence that increased expression of PEG10 in B-ALL CD23+CD5+ B cells is involved in malignant B-T cell interaction, contributing to the up-regulation of IL-10 expression, as well as to the impairment of cytotoxicity of syngeneic CD8+ T cells.
  • [MeSH-major] B-Lymphocytes / immunology. Burkitt Lymphoma / immunology. CD8-Positive T-Lymphocytes / immunology. Chemokine CCL19 / physiology. Chemokine CXCL13 / physiology. Immunologic Surveillance / immunology

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  • [ErratumIn] J Immunol. 2007 Nov 15;179(10):7184
  • (PMID = 17709502.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD5; 0 / CXCL13 protein, human; 0 / Chemokine CCL19; 0 / Chemokine CXCL13; 0 / PEG10 protein, human; 0 / Proteins; 0 / RNA, Small Interfering; 0 / Receptors, IgE; 130068-27-8 / Interleukin-10
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8. Sakamoto Y, Mariya Y, Sasaki S, Teshiromori R, Oshikiri T, Segawa M, Ogura K, Akagi T, Kubo K, Kaimori M, Funato T: WT1 mRNA level in peripheral blood is a sensitive biomarker for monitoring minimal residual disease in acute myeloid leukemia. Tohoku J Exp Med; 2009 Oct;219(2):169-76
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  • [Title] WT1 mRNA level in peripheral blood is a sensitive biomarker for monitoring minimal residual disease in acute myeloid leukemia.
  • The Wilms' tumor gene 1 (WT1) encodes a transcription factor that is involved in normal cellular development and cell survival.
  • WT1 mRNA is overexpressed in the minimal residual disease (MRD) of patients with hematopoietic malignancy patients, particularly acute myeloid leukemia (AML).
  • MRD represents the condition with the low levels of leukemia cells in the bone marrow and is known as a sign of recurrence.
  • The patients included AML (55 patients), acute lymphoblastic leukemia (11), myelodysplastic syndrome (20), malignant lymphoma (5), chronic myeloid leukemia (1), prostatic carcinoma (1), and leukopenia (2).
  • [MeSH-major] Biomarkers, Tumor / blood. Biomarkers, Tumor / genetics. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / genetics. Neoplasm, Residual / genetics. WT1 Proteins / blood. WT1 Proteins / genetics

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  • (PMID = 19776535.001).
  • [ISSN] 1349-3329
  • [Journal-full-title] The Tohoku journal of experimental medicine
  • [ISO-abbreviation] Tohoku J. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / WT1 Proteins
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9. Yu W, Rao Q, Wang M, Tian Z, Lin D, Liu X, Wang J: The Hsp90 inhibitor 17-allylamide-17-demethoxygeldanamycin induces apoptosis and differentiation of Kasumi-1 harboring the Asn822Lys KIT mutation and down-regulates KIT protein level. Leuk Res; 2006 May;30(5):575-82
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  • Heat shock protein 90 (Hsp90) serves as a chaperone for a number of cell signaling proteins, including many tyrosine and serine/threonine kinases, which are involved in proliferation and/or survival.
  • KIT is the receptor for stem cell factor (SCF) and required for normal hematopoiesis.
  • Mutations in c-Kit result in ligand-independent tyrosine kinase activity and uncontrolled cell proliferation.
  • Kasumi-1 is t(8;21) acute myeloid leukemia (AML) cell line harboring mutated KIT with Asn822Lys substitution.
  • [MeSH-major] Apoptosis / drug effects. Benzoquinones / pharmacology. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Lactams, Macrocyclic / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins c-kit / genetics
  • [MeSH-minor] Asparagine / genetics. Cell Cycle / drug effects. Cell Differentiation / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Down-Regulation / drug effects. HL-60 Cells. Humans. Lysine / genetics. Mutation. RNA, Messenger / drug effects. RNA, Messenger / genetics. Time Factors. Tumor Cells, Cultured

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  • (PMID = 16213582.001).
  • [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 / Benzoquinones; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 0 / RNA, Messenger; 4GY0AVT3L4 / tanespimycin; 7006-34-0 / Asparagine; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; K3Z4F929H6 / Lysine
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10. de Witte T, Suciu S, Brand R, Muus P, Kröger N: Autologous stem cell transplantation in myelodysplastic syndromes. Semin Hematol; 2007 Oct;44(4):274-7
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  • [Title] Autologous stem cell transplantation in myelodysplastic syndromes.
  • Allogeneic stem cell transplantation (SCT) is the treatment of choice for the majority of young patients with myelodysplasia (MDS) who have a histocompatible donor (sibling or unrelated donor).
  • For some patients lacking a human leukocyte antigen (HLA)-compatible donor, chemotherapy followed by autologous SCT may be a reasonable alternative, especially for patients with therapy-related MDS/acute myeloid leukemia (AML).
  • Mobilized peripheral blood stem cells are the preferred stem cell source for young patients, especially in view of the more rapid hematopoietic recovery after transplantation with mobilized stem cells, but bone marrow stem cells also may be considered for patients older than 50 years.
  • [MeSH-major] Bone Marrow Transplantation. Hematopoietic Stem Cell Transplantation. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy / methods. Disease-Free Survival. Evidence-Based Medicine. Hematopoietic Stem Cell Mobilization. Humans. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy. Middle Aged. Peripheral Blood Stem Cell Transplantation. Remission Induction. Risk Assessment. Transplantation, Autologous / methods. Transplantation, Homologous / methods


11. Bae SY, Yoon SY, Huh JH, Sung HJ, Choi IK: Hypereosinophilia in biphenotypic (B-cell/T-cell) acute lymphoblastic leukemia. Leuk Lymphoma; 2007 Jul;48(7):1417-9
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  • [Title] Hypereosinophilia in biphenotypic (B-cell/T-cell) acute lymphoblastic leukemia.
  • [MeSH-major] Hypereosinophilic Syndrome / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications


12. Ando T, Mitani N, Matsui K, Yamashita K, Nomiyama J, Tsuru M, Yujiri T, Tanizawa Y: Recurrent extramedullary relapse of acute myelogenous leukemia after allogeneic hematopoietic stem cell transplantation in a patient with the chromosomal abnormality t(8;21) and CD56-positivity. Int J Hematol; 2009 Oct;90(3):374-7
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  • [Title] Recurrent extramedullary relapse of acute myelogenous leukemia after allogeneic hematopoietic stem cell transplantation in a patient with the chromosomal abnormality t(8;21) and CD56-positivity.
  • Isolated extramedullary (EM) relapse of acute myelogenous leukemia (AML) after allogeneic hematopoietic stem cell transplantation (allo-HSCT) is rare.
  • Predisposing factors include CD56 expression and the chromosomal abnormality t(8;21).
  • We describe an AML patient showing the chromosomal abnormality t(8;21) and CD56 expression who experienced a unique EM relapse after allo-HSCT.
  • These findings suggest that the graft-versus-leukemia effect may preferentially maintain marrow remission rather than prevent EM relapse.
  • In addition, our findings show that extended survival is possible after EM relapse following allo-HSCT in patients with marrow hematopoiesis of donor origin, and that augmentation of the graft-versus-leukemia effect may be useful.
  • [MeSH-major] Graft vs Leukemia Effect. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute. Stomach Neoplasms. Translocation, Genetic


13. Cossu F: Genetics of SCID. Ital J Pediatr; 2010;36:76
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  • Human SCID (Severe Combined Immunodeficiency) is a prenatal disorder of T lymphocyte development, that depends on the expression of numerous genes.
  • The knowledge of the genetic basis of SCID is essential for diagnosis (e.g., clinical phenotype, lymphocyte profile) and treatment (e.g., use and type of pre-hematopoietic stem cell transplant conditioning).Over the last years novel genetic defects causing SCID have been discovered, and the molecular and immunological mechanisms of SCID have been better characterized.
  • Distinct forms of SCID show both common and peculiar (e.g., absence or presence of nonimmunological features) aspects, and they are currently classified into six groups according to prevalent pathophysiological mechanisms: impaired cytokine-mediated signaling; pre-T cell receptor defects; increased lymphocyte apoptosis; defects in thymus embryogenesis; impaired calcium flux; other mechanisms.This review is the updated, extended and largely modified translation of the article "Cossu F: Le basi genetiche delle SCID", originally published in Italian language in the journal "Prospettive in Pediatria" 2009, 156:228-238.
  • [MeSH-minor] Genetic Therapy. Genotype. Hematopoietic Stem Cell Transplantation. Humans. Infant, Newborn. Neonatal Screening. T-Lymphocytes / pathology

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  • (PMID = 21078154.001).
  • [ISSN] 1824-7288
  • [Journal-full-title] Italian journal of pediatrics
  • [ISO-abbreviation] Ital J Pediatr
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2999594
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4. Garbe AI, Krueger A, Gounari F, Zúñiga-Pflücker JC, von Boehmer H: Differential synergy of Notch and T cell receptor signaling determines alphabeta versus gammadelta lineage fate. J Exp Med; 2006 Jun 12;203(6):1579-90
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  • [Title] Differential synergy of Notch and T cell receptor signaling determines alphabeta versus gammadelta lineage fate.
  • Thymic precursors expressing the pre-T cell receptor (TCR), the gammadeltaTCR, or the alphabetaTCR can all enter the CD4+ 8+ alphabeta lineage, albeit with different efficacy.
  • In particular, in alphabeta lineage commitment, the pre-TCR synergizes more efficiently with Notch signals than the other two TCRs, whereas gammadeltaTCR-expressing cells can survive and expand in the absence of Notch signals, even though Notch signaling enhances their proliferation.
  • These observations suggest a new model of alphabeta versus gammadelta lineage choice in which lineage fate is determined by the extent of synergy between TCR and Notch signaling and in which the evolutionarily recent advent of the cell-autonomously signaling pre-TCR increased the efficacy of alphabeta T cell generation.

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  • (PMID = 16754723.001).
  • [ISSN] 0022-1007
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI045846; United States / NCI NIH HHS / CA / P01 CA10990; United States / NIAID NIH HHS / AI / R01 AI47281; United States / NIAID NIH HHS / AI / R01 AI047281; United States / NIAID NIH HHS / AI / R01 AI45846
  • [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 / Homeodomain Proteins; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Antigen, T-Cell, gamma-delta; 0 / Receptors, Notch; 128559-51-3 / RAG-1 protein
  • [Other-IDs] NLM/ PMC2118312
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15. Derré L, Bruyninx M, Baumgaertner P, Ferber M, Schmid D, Leimgruber A, Zoete V, Romero P, Michielin O, Speiser DE, Rufer N: Distinct sets of alphabeta TCRs confer similar recognition of tumor antigen NY-ESO-1157-165 by interacting with its central Met/Trp residues. Proc Natl Acad Sci U S A; 2008 Sep 30;105(39):15010-5
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  • Here, we studied T cell receptor (TCR) primary structure and function of 605 HLA-A*0201/NY-ESO-1(157-165)-specific CD8 T cell clones derived from five melanoma patients.
  • All remaining T cell clones belong to two additional sets expressing BV1 or BV13 TCRs, associated with alpha-chains with highly diverse VJ usage, CDR3 amino acid sequence, and length.
  • Yet, all T cell clonotypes recognize tumor antigen with similar functional avidity.
  • Two residues, Met-160 and Trp-161, located in the middle region of the NY-ESO-1(157-165) peptide, are critical for recognition by most of the T cell clonotypes.
  • [MeSH-major] Neoplasm Proteins / immunology. Peptide Fragments / immunology. Receptors, Antigen, T-Cell, alpha-beta / immunology

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  • (PMID = 18809922.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Peptide Fragments; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / peptide NY-ESO-1 157-165; 2ZD004190S / Threonine; AE28F7PNPL / Methionine
  • [Other-IDs] NLM/ PMC2567484
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16. Martínez-Delgado B, Cuadros M, Honrado E, Ruiz de la Parte A, Roncador G, Alves J, Castrillo JM, Rivas C, Benítez J: Differential expression of NF-kappaB pathway genes among peripheral T-cell lymphomas. Leukemia; 2005 Dec;19(12):2254-63
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  • [Title] Differential expression of NF-kappaB pathway genes among peripheral T-cell lymphomas.
  • Nuclear factor kappa B (NF-kappaB) is one important pathway in T-cell proliferation and survival.
  • In a previously reported microarray study, we found NF-kappaB pathway genes differentially expressed between peripheral (PTCL) and lymphoblastic lymphomas.
  • This distinction was found among all T-cell lymphoma categories analyzed (PTCL unspecified, angioimmunoblastic, cutaneous and natural killer/T lymphomas) with the exception of anaplastic lymphomas (ALCL), which were characterized by reduced NF-kappaB expression in anaplastic cells.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma, T-Cell, Peripheral / genetics. NF-kappa B / genetics

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  • (PMID = 16270046.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NF-kappa B
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17. Tedeschi R, Luostarinen T, Marus A, Bzhalava D, Ogmundsdottir HM, Dillner J, De Paoli P, Surcel HM, Pukkala E, Lehtinen M, Lehtinen T: No risk of maternal EBV infection for childhood leukemia. Cancer Epidemiol Biomarkers Prev; 2009 Oct;18(10):2790-2
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  • [Title] No risk of maternal EBV infection for childhood leukemia.
  • We performed a large nested case-control study within the Finnish and Icelandic maternity cohorts to verify/falsify the association of maternal EBV infection with an increased risk of acute lymphoblastic leukemia (ALL) in the offspring found in previous studies.
  • For each index mother of a leukemia case, three matched control mothers with cancer-free offspring were identified.
  • [MeSH-major] Epstein-Barr Virus Infections / epidemiology. Herpesvirus 4, Human / isolation & purification. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / virology. Pregnancy Complications, Infectious / epidemiology. Pregnancy Complications, Infectious / virology

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  • (PMID = 19755652.001).
  • [ISSN] 1538-7755
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Viral; 0 / Capsid Proteins; 0 / Epstein-Barr viral capsid antigen
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18. Fujimoto K, Endo T, Nishio M, Obara M, Yamaguchi K, Takeda Y, Goto H, Kasahara I, Sato N, Koike T: Complete remission of splenic marginal zone lymphoma after an acute flare-up of hepatitis B in a hepatitis B virus carrier. Int J Hematol; 2009 Dec;90(5):601-4
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  • [Title] Complete remission of splenic marginal zone lymphoma after an acute flare-up of hepatitis B in a hepatitis B virus carrier.
  • The diagnosis of splenic marginal zone lymphoma (SMZL) was made by a splenectomy.
  • Two years after the splenectomy, she was admitted for an acute flare-up of hepatitis B.
  • There has been no recurrence of acute hepatitis and she has been in complete remission for SMZL for more than 6 years.
  • The clinical course of this patient suggests that an immune response against HBV also affects the clearance of lymphoma cells.
  • [MeSH-major] Hepatitis B / immunology. Lymphoma, B-Cell, Marginal Zone / virology. Remission, Spontaneous. Splenic Neoplasms / surgery

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  • (PMID = 19802732.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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19. Or R, Hadar E, Bitan M, Resnick IB, Aker M, Ackerstein A, Samuel S, Tsirigotis P, Gesundheit B, Slavin S, Shapira MY: Safety and efficacy of donor lymphocyte infusions following mismatched stem cell transplantation. Biol Blood Marrow Transplant; 2006 Dec;12(12):1295-301
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Safety and efficacy of donor lymphocyte infusions following mismatched stem cell transplantation.
  • The use of a mismatched allograft necessitates T cell depletion for prevention of uncontrolled graft-versus-host disease (GVHD), thus impairing a graft-versus-leukemia effect.
  • Data on donor lymphocyte infusion (DLI) after mismatched stem cell transplantation are lacking.
  • Death was frequent and usually related to the basic disease rather than to DLI complications.
  • Future developments using cell therapy with selective or targeted anticancer activity are warranted, with special attention to prophylactic treatment of T cell depleted mismatched allografts recipients.
  • [MeSH-major] Graft Enhancement, Immunologic. Leukemia, Myeloid / surgery. Lymphocyte Transfusion. Peripheral Blood Stem Cell Transplantation
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Child, Preschool. Feasibility Studies. Female. Graft vs Host Disease / mortality. Graft vs Host Disease / prevention & control. Graft vs Leukemia Effect. HLA Antigens / immunology. Histocompatibility. Humans. Kaplan-Meier Estimate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery. Leukocyte Reduction Procedures. Lymphoma / surgery. Male. Middle Aged. Myelodysplastic Syndromes / surgery. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / surgery. Remission Induction. Survival Analysis. Tissue Donors. Transplantation Conditioning. Tumor Burden

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  • (PMID = 17162211.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA Antigens
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20. Cheng Y, Zhang Z, Slape C, Aplan PD: Cre-loxP-mediated recombination between the SIL and SCL genes leads to a block in T-cell development at the CD4- CD8- to CD4+ CD8+ transition. Neoplasia; 2007 Apr;9(4):315-21
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  • [Title] Cre-loxP-mediated recombination between the SIL and SCL genes leads to a block in T-cell development at the CD4- CD8- to CD4+ CD8+ transition.
  • In the most common form of stem cell leukemia (SCL) gene rearrangement, an interstitial deletion of 82 kb brings SCL under the control of regulatory elements that normally govern expression of the ubiquitously expressed SCL interrupting locus (SIL) gene, which is located directly upstream of SCL.
  • To investigate the effect of this fusion in a mouse model, a bacterial artificial chromosome (BAC) clone containing both human SIL and SCL genes was isolated, and loxP sites were inserted into intron 1 of both the SIL and SCL genes, corresponding to the sites at which recombination occurs in human T-cell acute lymphocytic leukemia patients.
  • These transgenic mice were subsequently bred to Lck-Cre mice that express the Cre recombinase specifically in the thymus.
  • Aberrant SCL gene expression in the thymus was verified by reverse transcription-polymerase chain reaction.
  • These results demonstrate that conditional activation of SCL under control of SIL regulatory elements can impair normal T-cell development.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. CD4-Positive T-Lymphocytes / enzymology. CD8-Positive T-Lymphocytes / enzymology. Cell Differentiation / genetics. Extracellular Matrix Proteins / physiology. Gene Rearrangement, T-Lymphocyte / genetics. Integrases / genetics. Intracellular Signaling Peptides and Proteins / genetics. Protein-Lysine 6-Oxidase / physiology. Proto-Oncogene Proteins / genetics

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  • (PMID = 17460775.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 SC010379-06
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD8; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Extracellular Matrix Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Proto-Oncogene Proteins; 0 / STIL protein, human; 135471-20-4 / TAL1 protein, human; 149137-54-2 / Lox protein, mouse; EC 1.4.3.13 / Protein-Lysine 6-Oxidase; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
  • [Other-IDs] NLM/ PMC1854848
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21. Au WY, Chan LC, Liang R, Kwong YL: Myelodysplastic syndrome and acute myeloid leukemia after treatment with fludarabine, mitoxantrone, and dexamethasone. Am J Hematol; 2006 Jun;81(6):471-3
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  • [Title] Myelodysplastic syndrome and acute myeloid leukemia after treatment with fludarabine, mitoxantrone, and dexamethasone.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Lymphoma, B-Cell / drug therapy. Lymphoma, T-Cell / drug therapy. Myelodysplastic Syndromes / chemically induced. Neoplasms, Second Primary / chemically induced


22. Yonekura K, Utsunomiya A, Takatsuka Y, Takeuchi S, Tashiro Y, Kanzaki T, Kanekura T: Graft-versus-adult T-cell leukemia/lymphoma effect following allogeneic hematopoietic stem cell transplantation. Bone Marrow Transplant; 2008 Jun;41(12):1029-35
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  • [Title] Graft-versus-adult T-cell leukemia/lymphoma effect following allogeneic hematopoietic stem cell transplantation.
  • Allogeneic hematopoietic stem cell transplantation (allo-HSCT) has proven effective in adult T-cell leukemia/lymphoma (ATL) patients.
  • Of these, 18 had acute-, 2 had lymphoma- and 1 had chronic-type ATL; at allo-HSCT, seven patients were in CR, one was in PR, five had stable disease (SD) and eight had progressive disease (PD).
  • Disease state after allo-HSCT was CR in 14, PR in 3, SD in 1 and PD in 3 patients.
  • [MeSH-major] Graft vs Leukemia Effect. Hematopoietic Stem Cell Transplantation / methods. Leukemia-Lymphoma, Adult T-Cell / therapy
  • [MeSH-minor] Adult. Cohort Studies. Disease-Free Survival. Drug Administration Schedule. Female. Graft vs Host Disease / drug therapy. Humans. Immunosuppressive Agents / administration & dosage. Immunosuppressive Agents / adverse effects. Kaplan-Meier Estimate. Male. Middle Aged. Recurrence. Retrospective Studies. Skin Diseases / pathology. Transplantation, Homologous

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  • (PMID = 18332910.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
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23. Advani A, Jin T, Bolwell B, Copelan E, Sekeres M, Sobecks R, Sungren S, Yurch M, Kalaycio M: A prognostic scoring system for adult patients less than 60 years of age with acute lymphoblastic leukemia in first relapse. Leuk Lymphoma; 2009 Jul;50(7):1126-31
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  • [Title] A prognostic scoring system for adult patients less than 60 years of age with acute lymphoblastic leukemia in first relapse.
  • The outcome of patients with acute lymphoblastic leukemia (ALL) in first relapse is poor.
  • For all patients, a scoring system of 0-3 was developed with 1 point for each of the following: age at diagnosis >or=45 years, lactate dehydrogenase (LDH) at the time of relapse >or=1.5 times upper limits of normal (ULN), not proceeding to allogeneic bone marrow transplant (BMT).
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Adult. Female. Humans. L-Lactate Dehydrogenase / metabolism. Male. Medical Oncology / methods. Middle Aged. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / pathology. Neoplasm Staging / methods. Prognosis. Recurrence. Retrospective Studies. Treatment Outcome

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  • (PMID = 19557633.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.1.1.27 / L-Lactate Dehydrogenase
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24. Hoshino T, Tahara K, Miyawaki K, Hatsumi N, Takada S, Miyawaki S, Sakura T: [Clinical profiles of 7 patients with chronic myelogenous leukemia or Philadelphia chromosome-positive acute lymphoblastic leukemia treated with dasatinib]. Rinsho Ketsueki; 2010 Mar;51(3):181-8
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  • [Title] [Clinical profiles of 7 patients with chronic myelogenous leukemia or Philadelphia chromosome-positive acute lymphoblastic leukemia treated with dasatinib].
  • We retrospectively analyzed the clinical outcome of dasatinib in 7 patients with chronic myelogenous leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ALL) resistant or intolerant to imatinib.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / administration & dosage. Thiazoles / administration & dosage


25. Kondo T, Yasumoto A, Arita K, Sugita J, Shigematsu A, Okada K, Takahata M, Onozawa M, Kahata K, Takeda Y, Obara M, Yamamoto S, Endo T, Nishio M, Sato N, Tanaka J, Hashino S, Koike T, Asaka M, Imamura M: Successful treatment of acute myelogenous leukemia with favorable cytogenetics by reduced-intensity stem cell transplantation. Int J Hematol; 2010 Mar;91(2):310-21
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  • [Title] Successful treatment of acute myelogenous leukemia with favorable cytogenetics by reduced-intensity stem cell transplantation.
  • Acute myelogenous leukemia (AML) with favorable cytogenetics responds well to chemotherapy.
  • If the leukemia relapses, allogenic hematopoietic stem transplantation (allo-HSCT) is considered as a treatment option.
  • Since the efficacy of reduced-intensity stem cell transplantation (RIST) for AML with favorable cytogenetics has not been established, we retrospectively analyzed the outcomes of allo-HSCT in AML patients according to cytogenetic risks.
  • Both the 3-year OS and RFS rates were 81% in the conventional stem cell transplantation (CST) group.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Transplantation Conditioning / methods
  • [MeSH-minor] Adult. Aged. Cytogenetics. Disease-Free Survival. Female. Graft vs Host Disease / mortality. Humans. Karyotyping. Male. Middle Aged. Retrospective Studies. Risk Factors. Survival Analysis. Young Adult


26. Akiyama M, Kobayashi N, Fujisawa K, Eto Y: Disseminated Varicella-Zoster virus infection in a girl with T-lineage acute lymphoblastic leukemia. Pediatr Blood Cancer; 2007 Jun 15;48(7):716
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  • [Title] Disseminated Varicella-Zoster virus infection in a girl with T-lineage acute lymphoblastic leukemia.
  • [MeSH-major] Herpes Zoster / complications. Leukemia-Lymphoma, Adult T-Cell / complications

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  • [CommentOn] Pediatr Blood Cancer. 2005 Aug;45(2):191-4 [15880424.001]
  • (PMID = 16607647.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / gamma-Globulins
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27. Candoni A, Michelutti A, Simeone E, Damiani D, Baccarani M, Fanin R: Efficacy of liposomal daunorubicin and cytarabine as reinduction chemotherapy in relapsed acute lymphoblastic leukaemia despite expression of multidrug resistance-related proteins. Eur J Haematol; 2006 Oct;77(4):293-9
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  • [Title] Efficacy of liposomal daunorubicin and cytarabine as reinduction chemotherapy in relapsed acute lymphoblastic leukaemia despite expression of multidrug resistance-related proteins.
  • The treatment of relapsed adult acute lymphoblastic leukaemia (ALL) is frequently unsuccessful with current chemotherapy regimens, and often there is an overexpression of multidrug resistance (MDR)-related proteins.
  • Liposomal encapsulation makes daunorubicin (DNR) less sensitive to the efflux effect of P-glycoprotein (PGP), and in vitro data indicate that liposomal-encapsulated DNR (Daunoxome-DNX) is more toxic than DNR against ALL cell lines.
  • Twenty pts (80%) achieved a complete remission (CR) and two (8%) entered a partial remission (PR) for an overall response (OR) rate of 88% (22/25), with a tolerable toxicity and without significant cardiotoxicity.
  • Before the start of DNX therapy, 18/25 (72%) cases overexpressed at least one MDR-related protein compared with 9/25 (36%) cases with MDR overexpression at diagnosis (P = 0.01).
  • Taking into account the small number of cases, the response rate was not affected by MDR expression and the in vitro results also showed a higher uptake and apoptotic cell death by DNX compared with DNR.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Multidrug Resistance-Associated Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16856922.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Liposomes; 0 / Multidrug Resistance-Associated Proteins; 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
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28. Olwill SA, McGlynn H, Gilmore WS, Alexander HD: Annexin II cell surface and mRNA expression in human acute myeloid leukaemia cell lines. Thromb Res; 2005;115(1-2):109-14
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  • [Title] Annexin II cell surface and mRNA expression in human acute myeloid leukaemia cell lines.
  • INTRODUCTION: Acute promyelocytic leukaemia (APL) (M3) is associated with both a characteristic t(15;17) and severe bleeding diathesis caused by disseminated intravascular coagulation (DIC) and/or hyperfibrinolysis.
  • MATERIALS AND METHODS: This study examined the level of annexin II cell surface and mRNA expression in a range of acute myeloid leukaemia (AML) cell lines.
  • The evidence that annexin II levels are higher in APL would lend support to the hypothesis that the bleeding disorder seen in APL is caused by hyperfibrinolysis.
  • RESULTS: Cell surface annexin II was found to be expressed at higher levels on NB4 (promyelocytic) cells than on either KG1a (early myeloid) or HL60 (myelocytic) cells.
  • MM6 cells showed a threefold increase in annexin II mRNA compared to any of the other cell lines.
  • Further investigations are required to identify the significance of annexin II expression and regulation in leukaemia.
  • [MeSH-major] Annexin A2 / genetics. Gene Expression Regulation, Neoplastic. Leukemia, Myeloid / metabolism. Leukemia, Promyelocytic, Acute / complications. RNA, Messenger / analysis
  • [MeSH-minor] Cell Line, Tumor. Fibrinolysis. Hemorrhage / etiology. Humans. Membrane Proteins

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  • (PMID = 15567461.001).
  • [ISSN] 0049-3848
  • [Journal-full-title] Thrombosis research
  • [ISO-abbreviation] Thromb. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ANXA2 protein, human; 0 / Annexin A2; 0 / Membrane Proteins; 0 / RNA, Messenger
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29. Nezu M, Tomonaga T, Sakai C, Ishii A, Itoga S, Nishimura M, Matsuo Y, Tagawa M, Nomura F: Expression of the fetal-oncogenic fibroblast growth factor-8/17/18 subfamily in human hematopoietic tumors. Biochem Biophys Res Commun; 2005 Sep 30;335(3):843-9
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  • To elucidate whether these FGFs (FGF-8, -9, -10, -11, -12, -13, -14, -16, -17, -18, -19, -20, and -21) are expressed in leukemic cells, we performed RT-PCR analyses using 28 cell lines.
  • Realtime quantitative-PCR analysis showed that FGF-8/-17 were aberrantly expressed in patients with acute leukemia.
  • Moreover, cell proliferation assays revealed the proliferation activity of FGF-17 on leukemic cells expressing its receptors.
  • [MeSH-minor] Base Sequence. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Cell Line, Tumor. DNA Primers. Humans. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16095560.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA Primers; 62031-54-3 / Fibroblast Growth Factors
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30. Holler E: Risk assessment in haematopoietic stem cell transplantation: GvHD prevention and treatment. Best Pract Res Clin Haematol; 2007 Jun;20(2):281-94
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  • [Title] Risk assessment in haematopoietic stem cell transplantation: GvHD prevention and treatment.
  • Graft-versus-host disease (GvHD) is the major cause of transplant-related mortality and morbidity.
  • As it is closely related to the major therapeutic principle, graft-versus-leukaemia (GvL) effect, risk assessment has to balance both risks depending on the pre-transplant status.
  • While the majority of approaches aiming at T-cell depletion show efficacy in reducing acute and chronic GvHD and transplant-related mortality, T-cell depletion also affects graft-versus-leukaemia effects and thus results in a higher relapse rate.
  • Thus, standard prophylaxis relying on calcineurin inhibitors frequently results in at least equivalent or even superior long-term disease-free survival, and the risk of relapse has to be considered when selecting regimens for prevention of GvHD.
  • [MeSH-major] Graft vs Host Disease / drug therapy. Graft vs Host Disease / prevention & control. Hematopoietic Stem Cell Transplantation / adverse effects
  • [MeSH-minor] Acute Disease. Adrenal Cortex Hormones / therapeutic use. Calcineurin Inhibitors. Chronic Disease / drug therapy. Cyclosporine / therapeutic use. Graft vs Leukemia Effect / drug effects. Humans. Immunosuppressive Agents / therapeutic use. Methotrexate / therapeutic use. Methylprednisolone / therapeutic use. Mycophenolic Acid / analogs & derivatives. Mycophenolic Acid / therapeutic use. Risk Assessment. T-Lymphocytes / physiology. Tacrolimus / therapeutic use

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  • (PMID = 17448962.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Calcineurin Inhibitors; 0 / Immunosuppressive Agents; 83HN0GTJ6D / Cyclosporine; 9242ECW6R0 / mycophenolate mofetil; HU9DX48N0T / Mycophenolic Acid; WM0HAQ4WNM / Tacrolimus; X4W7ZR7023 / Methylprednisolone; YL5FZ2Y5U1 / Methotrexate
  • [Number-of-references] 95
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36. Advani AS, Lim K, Gibson S, Shadman M, Jin T, Copelan E, Kalaycio M, Sekeres MA, Sobecks R, Hsi E: OCT-2 expression and OCT-2/BOB.1 co-expression predict prognosis in patients with newly diagnosed acute myeloid leukemia. Leuk Lymphoma; 2010 Apr;51(4):606-12
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  • [Title] OCT-2 expression and OCT-2/BOB.1 co-expression predict prognosis in patients with newly diagnosed acute myeloid leukemia.
  • OCT-2 and its co-activator, BOB.1, are B-cell associated transcription factors expressed in a subset of patients with acute myeloid leukemia (AML).
  • OCT-2 may act as a cell survival factor in AML by mediating expression of downstream targets, such as BCL-2.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Octamer Transcription Factor-2 / metabolism. Trans-Activators / metabolism

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  • (PMID = 20141429.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Octamer Transcription Factor-2; 0 / POU2AF1 protein, human; 0 / POU2F2 protein, human; 0 / Trans-Activators
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37. Cines DB, Liebman H, Stasi R: Pathobiology of secondary immune thrombocytopenia. Semin Hematol; 2009 Jan;46(1 Suppl 2):S2-14
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  • Primary immune thrombocytopenic purpura (ITP) remains a diagnosis of exclusion both from nonimmune causes of thrombocytopenia and immune thrombocytopenia that develops in the context of other disorders (secondary immune thrombocytopenia).
  • The pathobiology, natural history, and response to therapy of the diverse causes of secondary ITP differ from each other and from primary ITP, so accurate diagnosis is essential.
  • Immune thrombocytopenia can be secondary to medications or to a concurrent disease, such as an autoimmune condition (eg, systemic lupus erythematosus [SLE], antiphospholipid antibody syndrome [APS], immune thyroid disease, or Evans syndrome), a lymphoproliferative disease (eg, chronic lymphocytic leukemia or large granular T-lymphocyte lymphocytic leukemia), or chronic infection, eg, with Helicobacter pylori, human immunodeficiency virus (HIV), or hepatitis C virus (HCV).
  • This thrombocytopenia may be caused by cross-reacting antibodies and closely mimics acute ITP of childhood.
  • Proper diagnosis and treatment of the underlying disorder, where necessary, play an important role in patient management.

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  • (PMID = 19245930.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL040387-16; United States / NHLBI NIH HHS / HL / P01 HL040387; United States / NHLBI NIH HHS / HL / P01 HL040387-16
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 185
  • [Other-IDs] NLM/ NIHMS99872; NLM/ PMC2682438
  •  go-up   go-down


38. Turano M, Napolitano G, Dulac C, Majello B, Bensaude O, Lania L: Increased HEXIM1 expression during erythroleukemia and neuroblastoma cell differentiation. J Cell Physiol; 2006 Mar;206(3):603-10
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  • [Title] Increased HEXIM1 expression during erythroleukemia and neuroblastoma cell differentiation.
  • To determine the causative role of HEXIM1 during cell differentiation we analyzed the biochemical and functional consequences of HEXIM1 protein levels in several in vitro differentiation systems.
  • These findings highlight a crucial role of HEXIM1 protein during cell differentiation.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Leukemia, Erythroblastic, Acute / genetics. Neuroblastoma / genetics. Positive Transcriptional Elongation Factor B / metabolism. RNA-Binding Proteins / genetics
  • [MeSH-minor] Acetamides / pharmacology. Animals. Cell Differentiation. Cell Line, Tumor. Dimethyl Sulfoxide / pharmacology. Humans. Mice. Transcription, Genetic / drug effects. Tretinoin / pharmacology. U937 Cells

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16222702.001).
  • [ISSN] 0021-9541
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acetamides; 0 / HEXIM1 protein, human; 0 / RNA-Binding Proteins; 5688UTC01R / Tretinoin; EC 2.7.11.- / Positive Transcriptional Elongation Factor B; LA133J59VU / hexamethylene bisacetamide; YOW8V9698H / Dimethyl Sulfoxide
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39. Serwold T, Hochedlinger K, Swindle J, Hedgpeth J, Jaenisch R, Weissman IL: T-cell receptor-driven lymphomagenesis in mice derived from a reprogrammed T cell. Proc Natl Acad Sci U S A; 2010 Nov 2;107(44):18939-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell receptor-driven lymphomagenesis in mice derived from a reprogrammed T cell.
  • Pluripotent stem cell lines can now be generated from an individual's own cells, facilitating the generation of immunologically acceptable stem cell-based therapeutics.
  • Many cell types can undergo nuclear reprogramming, leading to the question of whether the identity of the reprogrammed cell of origin has a biological consequence.
  • Peripheral blood, containing a mixture of T, B, NK, and myeloid cell types, represents one potential source of reprogrammable cells.
  • In this study, we describe the unique case of mice derived from a reprogrammed T cell.
  • These mice have prerearranged T-cell receptor (TCR) genes in all cells.
  • Surprisingly, ≈50% of mice with prerearranged TCR genes develop spontaneous T cell lymphomas, which originate in the thymus.
  • The lymphomas arise from developing T cells, and contain activated Notch1, similar to most human and mouse T-cell acute lymphoblastic lymphomas.
  • Furthermore, inhibitors of multiple branches of TCR signaling suppress lymphoma growth, implicating TCR signaling as an essential component in lymphoma proliferation.
  • The lymphomagenesis in mice derived from a reprogrammed T cell demonstrates the deleterious consequences of misregulation of the TCR rearrangement and signaling pathways and illustrates one case of cellular reprogramming where the identity of the cell of origin has profound consequences.
  • [MeSH-major] Adult Stem Cells / metabolism. Cell Dedifferentiation. Gene Rearrangement, alpha-Chain T-Cell Antigen Receptor. Gene Rearrangement, beta-Chain T-Cell Antigen Receptor. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptors, Antigen, T-Cell, alpha-beta / metabolism. Signal Transduction. T-Lymphocytes / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Female. Humans. Male. Mice. Mice, Knockout. Receptor, Notch1 / genetics. Receptor, Notch1 / immunology. Receptor, Notch1 / metabolism

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  • (PMID = 20956329.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA086065; United States / NICHD NIH HHS / HD / R37 HD045022
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Notch1 protein, mouse; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell, alpha-beta
  • [Other-IDs] NLM/ PMC2973852
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40. Hyde RK, Liu PP: RUNX1 repression-independent mechanisms of leukemogenesis by fusion genes CBFB-MYH11 and AML1-ETO (RUNX1-RUNX1T1). J Cell Biochem; 2010 Aug 1;110(5):1039-45
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  • The core binding factor (CBF) acute myeloid leukemias (AMLs) are a prognostically distinct subgroup that includes patients with the inv(16) and t(8:21) chromosomal rearrangements.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Leukemia / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Acute Disease. Gene Expression Regulation, Leukemic. Humans. Leukemia, Myeloid / genetics. Models, Genetic

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  • [Copyright] Published 2010 Wiley-Liss, Inc.
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  • (PMID = 20589720.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / ZIA HG000030-16
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human
  • [Other-IDs] NLM/ NIHMS360619; NLM/ PMC3298446
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41. Giebel S, Holowiecki J, Krawczyk-Kulis M, Jagoda K, Stella-Holowiecka B, Sadus-Wojciechowska M, Hellmann A, Dmoszynska A, Paluszewska M, Robak T, Konopka L, Seferynska I, Skotnicki AB, Kyrcz-Krzemien S: Impact of granulocyte colony stimulating factor administered during induction and consolidation of adults with acute lymphoblastic leukemia on survival: long-term follow-up of the Polish adult leukemia group 4-96 study. Leuk Lymphoma; 2009 Jun;50(6):1050-3
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  • [Title] Impact of granulocyte colony stimulating factor administered during induction and consolidation of adults with acute lymphoblastic leukemia on survival: long-term follow-up of the Polish adult leukemia group 4-96 study.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 19455463.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor
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42. Kalra S, Paul MK, Balaram H, Mukhopadhyay AK: Application of HPLC to study the kinetics of a branched bi-enzyme system consisting of hypoxanthine-guanine phosphoribosyltransferase and xanthine oxidase--an important biochemical system to evaluate the efficiency of the anticancer drug 6-mercaptopurine in ALL cell line. J Chromatogr B Analyt Technol Biomed Life Sci; 2007 May 1;850(1-2):7-14
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  • [Title] Application of HPLC to study the kinetics of a branched bi-enzyme system consisting of hypoxanthine-guanine phosphoribosyltransferase and xanthine oxidase--an important biochemical system to evaluate the efficiency of the anticancer drug 6-mercaptopurine in ALL cell line.
  • The thiopurine antimetabolite 6-mercaptopurine (6MP) is an important chemotherapeutic drug in the conventional treatment of childhood acute lymphoblastic leukemia (ALL).
  • This method was further validated using actively growing T-ALL cell line (Jurkat) to study the branched kinetics, wherein it was observed that treatment of 50 microM 6MP led to the generation of 12 microM TIMP and 0.8 microM 6TUA in 6 h at 37 degrees C.
  • [MeSH-major] 6-Mercaptopurine / therapeutic use. Antineoplastic Agents / therapeutic use. Chromatography, High Pressure Liquid / methods. Hypoxanthine Phosphoribosyltransferase / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Xanthine Oxidase / metabolism
  • [MeSH-minor] Adolescent. Cell Line, Tumor. Humans. Male. Reproducibility of Results. Sensitivity and Specificity. Spectrophotometry / methods

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  • (PMID = 17081813.001).
  • [ISSN] 1570-0232
  • [Journal-full-title] Journal of chromatography. B, Analytical technologies in the biomedical and life sciences
  • [ISO-abbreviation] J. Chromatogr. B Analyt. Technol. Biomed. Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; E7WED276I5 / 6-Mercaptopurine; EC 1.17.3.2 / Xanthine Oxidase; EC 2.4.2.8 / Hypoxanthine Phosphoribosyltransferase
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43. Zhang X, Inukai T, Hirose K, Akahane K, Nemoto A, Takahashi K, Sato H, Kagami K, Goi K, Sugita K, Nakazawa S: Induction of impaired membrane phospholipid asymmetry in mature erythrocytes after chemotherapy. Int J Hematol; 2005 Aug;82(2):132-6
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  • Senescent erythrocytes undergo a loss of phospholipid asymmetry in the plasma membrane and are removed from the circulation by phagocytosis.To examine the loss of phospholipid asymmetry in mature erythrocytes after chemotherapy, we monitored phosphatidylserine (PS)-exposing erythrocytes by using flow cytometry to detect annexin V-bound erythrocytes in the circulation of acute lymphoblastic leukemia patients after consolidation chemotherapy.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Cytarabine / administration & dosage. Erythrocyte Membrane / metabolism. Phospholipids / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Annexin A5 / metabolism. Bone Marrow / metabolism. Bone Marrow / pathology. Cell Aging / drug effects. Erythropoiesis / drug effects. Humans

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44. Hagner N, Joerger M: Cancer chemotherapy: targeting folic acid synthesis. Cancer Manag Res; 2010;2:293-301
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  • Methotrexate is one of the earliest anticancer drugs and is extensively used in lymphoma, acute lymphoblastic leukemia, and osteosarcoma, among others.
  • Pemetrexed has been approved in combination with cisplatin as first-line treatment for advanced non-squamous-cell lung cancer, as a single agent for relapsed non-small-cell lung cancer after platinum-containing chemotherapy, and in combination with cisplatin for the treatment of pleural mesothelioma.
  • Pralatrexate has recently been approved in the United States for relapsed or refractory peripheral T-cell lymphoma.

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  • (PMID = 21301589.001).
  • [ISSN] 1179-1322
  • [Journal-full-title] Cancer management and research
  • [ISO-abbreviation] Cancer Manag Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC3033035
  • [Keywords] NOTNLM ; antifolates / cancer / folate metabolism / methotrexate / molecular pharmacology / pemetrexed
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45. Van Vlierberghe P, van Grotel M, Tchinda J, Lee C, Beverloo HB, van der Spek PJ, Stubbs A, Cools J, Nagata K, Fornerod M, Buijs-Gladdines J, Horstmann M, van Wering ER, Soulier J, Pieters R, Meijerink JP: The recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-cell acute lymphoblastic leukemia. Blood; 2008 May 1;111(9):4668-80
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  • [Title] The recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) is mostly characterized by specific chromosomal abnormalities, some occurring in a mutually exclusive manner that possibly delineate specific T-ALL subgroups.
  • This deletion results in a conserved SET-NUP214 fusion product, which was also identified in the T-ALL cell line LOUCY.
  • We conclude that SET-NUP214 may contribute to the pathogenesis of T-ALL by enforcing T-cell differentiation arrest.

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  • (PMID = 18299449.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA11560
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / Histone Chaperones; 0 / Homeodomain Proteins; 0 / NUP214 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / SET protein, human; 0 / Transcription Factors; 157907-48-7 / HoxA protein
  • [Other-IDs] NLM/ PMC2343598
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46. Jia MR, Wei T, Xu WF: The Analgesic Activity of Bestatin as a Potent APN Inhibitor. Front Neurosci; 2010;4:50
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  • (1) an immunomodifier for enhancing the proliferation of normal human bone marrow granulocyte-macrophage progenitor cells to form CFU-GM colonies; Bestatin exerts a direct stimulating effect on lymphocytes via its fixation on the cell surface and an indirect effect on monocytes via aminopeptidase B inhibition of tuftsin catabolism;.
  • (2) an immunorestorator and curative or preventive agent for spontaneous tumor; Bestatin alone or its combination with chemicals can prolongate the disease-free interval and survival period in adult acute or chronic leukemia, therefore, it was primarily marketed in 1987 in Japan as an anticancer drug and servers as the only marketed inhibitor of Aminopeptidase N (APN/CD13) to cure leukemia to date;.

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  • (PMID = 20631848.001).
  • [ISSN] 1662-453X
  • [Journal-full-title] Frontiers in neuroscience
  • [ISO-abbreviation] Front Neurosci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Other-IDs] NLM/ PMC2903224
  • [Keywords] NOTNLM ; Bestatin / analgesic activity / application / mechanism / neuropeptides
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47. Won HJ, Han CH, Kim YH, Kwon HJ, Kim BW, Choi JS, Kim KH: Induction of apoptosis in human acute leukemia Jurkat T cells by Albizzia julibrissin extract is mediated via mitochondria-dependent caspase-3 activation. J Ethnopharmacol; 2006 Jul 19;106(3):383-9
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  • [Title] Induction of apoptosis in human acute leukemia Jurkat T cells by Albizzia julibrissin extract is mediated via mitochondria-dependent caspase-3 activation.
  • To understand antitumor activity of Albizzia julibrissin Durazz (Leguminosae), which has been used as a traditional oriental medicine, the mechanism underlying cytotoxic effect of its extract on human acute leukemia Jurkat T cells were investigated.
  • [MeSH-minor] Caspase 3. Cell Cycle / drug effects. Dose-Response Relationship, Drug. Flow Cytometry. Humans. In Situ Nick-End Labeling. Jurkat Cells / drug effects. Leukemia / drug therapy. Leukocytes, Mononuclear / drug effects. Mitochondria / drug effects. Mitochondria / metabolism

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  • (PMID = 16533581.001).
  • [ISSN] 0378-8741
  • [Journal-full-title] Journal of ethnopharmacology
  • [ISO-abbreviation] J Ethnopharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Plant Extracts; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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48. Zanrosso CW, Hatagima A, Emerenciano M, Ramos F, Figueiredo A, Félix TM, Segal SL, Giugliani R, Muniz MT, Pombo-de-Oliveira MS: The role of methylenetetrahydrofolate reductase in acute lymphoblastic leukemia in a Brazilian mixed population. Leuk Res; 2006 Apr;30(4):477-81
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  • [Title] The role of methylenetetrahydrofolate reductase in acute lymphoblastic leukemia in a Brazilian mixed population.
  • In order to investigate the influence of two polymorphisms in the MTHFR gene, 677C>T and 1298A>C, on the risk of acute lymphoblastic leukemia (ALL) we performed a case-control study in children from different Brazilians' regions.
  • Our investigation provides interesting data concerning the opposite effect of A1298C polymorphisms, particularly in the light of relatively scarce data regarding the MTHFR role in leukemia susceptibility in different populations.
  • [MeSH-major] Methylenetetrahydrofolate Reductase (NADPH2) / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • [ErratumIn] Leuk Res. 2009. doi: 10.1016/j.leukres.2009.01.019. Guigliani, Roberto [corrected to Giugliani, Roberto]
  • [ErratumIn] Leuk Res. 2009 Jul;33(7):1009
  • (PMID = 16182363.001).
  • [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] EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
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49. Fukumoto T, Kubota Y, Kitanaka A, Yamaoka G, Ohara-Waki F, Imataki O, Ohnishi H, Ishida T, Tanaka T: Gab1 transduces PI3K-mediated erythropoietin signals to the Erk pathway and regulates erythropoietin-dependent proliferation and survival of erythroid cells. Cell Signal; 2009 Dec;21(12):1775-83
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  • Knockdown of Gab1 by the introduction of the Gab1 siRNA expression vector into F-36P human erythroleukemia (F-36P-Gab1-siRNA) cells resulted in a reduction of cell proliferation and survival in response to EPO.
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. Cell Proliferation. Chromones / pharmacology. Enzyme Inhibitors / pharmacology. GRB2 Adaptor Protein / metabolism. Gene Knockdown Techniques. Humans. Janus Kinase 2 / antagonists & inhibitors. Janus Kinase 2 / metabolism. Leukemia, Erythroblastic, Acute / metabolism. Morpholines / pharmacology. Protein Tyrosine Phosphatase, Non-Receptor Type 11 / metabolism. Receptors, Erythropoietin / metabolism. SOS1 Protein / metabolism

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  • (PMID = 19665053.001).
  • [ISSN] 1873-3913
  • [Journal-full-title] Cellular signalling
  • [ISO-abbreviation] Cell. Signal.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Chromones; 0 / Enzyme Inhibitors; 0 / GAB1 protein, human; 0 / GRB2 Adaptor Protein; 0 / GRB2 protein, human; 0 / Morpholines; 0 / Receptors, Erythropoietin; 0 / SOS1 Protein; 11096-26-7 / Erythropoietin; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11
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50. Hirabayashi K, Shiohara M, Saito S, Tanaka M, Yanagisawa R, Tsuruta G, Fukuyama T, Hidaka Y, Nakazawa Y, Shimizu T, Sakashita K, Koike K: Polymyxin-direct hemoperfusion for sepsis-induced multiple organ failure. Pediatr Blood Cancer; 2010 Jul 15;55(1):202-5
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  • We report a case of multiple organ failure caused by the Bacillus cereus infection during acute lymphoblastic leukemia therapy, who was treated successfully.
  • [MeSH-major] Hemodiafiltration / methods. Multiple Organ Failure / etiology. Multiple Organ Failure / therapy. Polymyxins / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Sepsis / complications. Sepsis / therapy

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  • (PMID = 20486188.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Plasminogen Activator Inhibitor 1; 0 / Polymyxins
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51. Savani BN, Mielke S, Rezvani K, Montero A, Yong AS, Wish L, Superata J, Kurlander R, Singh A, Childs R, Barrett AJ: Absolute lymphocyte count on day 30 is a surrogate for robust hematopoietic recovery and strongly predicts outcome after T cell-depleted allogeneic stem cell transplantation. Biol Blood Marrow Transplant; 2007 Oct;13(10):1216-23
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  • [Title] Absolute lymphocyte count on day 30 is a surrogate for robust hematopoietic recovery and strongly predicts outcome after T cell-depleted allogeneic stem cell transplantation.
  • Several studies have shown that a higher lymphocyte count 3-4 weeks after allogeneic stem cell transplantation (SCT) is associated with better transplant outcome.
  • To further explore the relationship between lymphocyte recovery and outcome we analyzed lymphocyte counts and other engraftment parameters in 157 patients with leukemia (48 acute myelogenous leukemia, 80 chronic myelogenous leukemia, and 29 acute lymphoblastic leukemia [ALL]) receiving T cell-depleted myeloablative SCT from an HLA-identical sibling.
  • In multivariate analysis the day 30 absolute lymphocyte count (LC30) above the median of 450/muL was associated with improved survival (71% +/- 5% versus 38% +/- 6%, P < .0001), less relapse (21% +/- 5% versus 44% +/- 7%, P = .009), less nonrelapse mortality (NRM; 9 +/- 3 versus 36% +/- 6%, P < .0001) and less acute graft-versus-host disease (aGVHD) (34% +/- 5% versus 51% +/- 6%, P = .025).
  • The beneficial effect of a higher LC30 influenced outcome in patients with both standard and high-risk disease but did not affect survival and relapse in ALL.
  • These results indicate that LC30 is a surrogate for robust engraftment and identifies an "at-risk" population of patients after T cell-depleted SCT.
  • [MeSH-major] Graft Survival / physiology. Hematopoietic Stem Cell Transplantation / methods. Lymphocyte Count
  • [MeSH-minor] Adolescent. Adult. Biomarkers. Child. Cohort Studies. Female. Humans. Kaplan-Meier Estimate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid, Acute / therapy. Male. Neoplasm Recurrence, Local. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Predictive Value of Tests. Transplantation, Homologous / methods

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  • (PMID = 17889359.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / ZIA HL006105-01
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers
  • [Other-IDs] NLM/ NIHMS31874; NLM/ PMC3426353
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52. van Anders SM, Hamilton LD, Schmidt N, Watson NV: Associations between testosterone secretion and sexual activity in women. Horm Behav; 2007 Apr;51(4):477-82
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  • On three separate nights, they provided pre-activity, post-activity, and next-morning saliva samples and completed brief questionnaires at the last two timepoints.
  • Women's T was higher pre-intercourse than pre-control activity.
  • Women's T was also higher post-intercourse than post-control activity, though the percent change in T from pre- to post-activity was highest for cuddling, then intercourse, then exercise.

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  • (PMID = 17320881.001).
  • [ISSN] 0018-506X
  • [Journal-full-title] Hormones and behavior
  • [ISO-abbreviation] Horm Behav
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 3XMK78S47O / Testosterone
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53. Valmary S, Danjoux M, Delsol G, Brousset P: [Diagnostic value of anti-terminal deoxynucleotidyl transferase antibody (TdT) in hematologic pathology]. Ann Pathol; 2005 Feb;25(1):25-32
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  • [Transliterated title] Intérêt diagnostique de l'anticorps anti-terminal désoxynucleotidyl transférase (TdT) en pathologie hématologique.
  • AIMS: The diagnosis of primitive hematologic malignancies depends on a panel of monoclonal antibodies which is growing over time.
  • The distinction between immature (lymphoblastic lymphoma/acute lymphoblastic leukaemia) and mature lymphoma is sometimes difficult.
  • In this study, we evaluated anti-TdT antibody in the diagnosis and classification of these proliferations.
  • MATERIALS AND METHODS: 13 lesions were examined by immunohistochemistry: 4 B and T lymphoblastic lymphomas, 2 Burkitt's lymphomas, 5 B and T acute lymphoblastic leukemias and 2 acute monoblastic leukemias.
  • TdT is not expressed by mature B or T cell lymphomas such as Burkitt's lymphomas.
  • Significant numbers of cases of acute myeloblastic leukemias are TdT positive but could be easily distinguished from lymphoblastic proliferations.
  • CONCLUSION: Anti-TdT antibody represents a useful marker for differentiating lymphoma/acute lymphoblastic leukemia from other lymphomas.
  • This marker, available in routine diagnosis should be systematically included in the panel of antibodies used for immunophenotyping hematologic malignancies.
  • [MeSH-major] Antibodies. DNA Nucleotidylexotransferase / analysis. DNA Nucleotidylexotransferase / immunology. Hematologic Neoplasms / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Burkitt Lymphoma / diagnosis. Child. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Immunophenotyping. Leukemia, Monocytic, Acute / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Lymphoma, B-Cell / diagnosis. Lymphoma, T-Cell / diagnosis. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 15981929.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antibodies; EC 2.7.7.31 / DNA Nucleotidylexotransferase
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54. Fukushima-Nakase Y, Naoe Y, Taniuchi I, Hosoi H, Sugimoto T, Okuda T: Shared and distinct roles mediated through C-terminal subdomains of acute myeloid leukemia/Runt-related transcription factor molecules in murine development. Blood; 2005 Jun 1;105(11):4298-307
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  • [Title] Shared and distinct roles mediated through C-terminal subdomains of acute myeloid leukemia/Runt-related transcription factor molecules in murine development.
  • AML1/Runx1 is a frequent target of human leukemia-associated gene aberration and encodes a transcription factor with nonredundant biologic functions in initial development of definitive hematopoiesis, T-cell development, and steady-state platelet production.
  • To directly determine the presence of functional overlap among runt-related transcription factor (Runx) family molecules, we replaced the C-terminal portion of acute myeloid leukemia 1 (AML1) with that derived from its family members, which are variable in contrast to conserved Runt domain, using the gene knock-in method.
  • However, while AML2 substituted for AML1 could effectively rescue lymphoid lineages, AML3 could not, resulting in a smaller thymus and lymphoid deficiency in peripheral blood.
  • [MeSH-minor] Animals. Blood Cells. Cell Lineage. Cells, Cultured. Chimera / growth & development. Core Binding Factor Alpha 1 Subunit. Core Binding Factor Alpha 2 Subunit. Core Binding Factor Alpha 3 Subunit. DNA-Binding Proteins. Growth and Development. Lymphocytes / cytology. Mice. Myeloid Cells / cytology. Protein Engineering. Protein Structure, Tertiary. Proto-Oncogene Proteins. Thymus Gland / growth & development. Transcription Factor AP-2

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  • (PMID = 15713794.001).
  • [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 / Core Binding Factor Alpha 1 Subunit; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor Alpha 3 Subunit; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / Runx1 protein, mouse; 0 / Runx2 protein, mouse; 0 / Runx3 protein, mouse; 0 / Transcription Factor AP-2; 0 / Transcription Factors
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55. Sun K, Li M, Sayers TJ, Welniak LA, Murphy WJ: Differential effects of donor T-cell cytokines on outcome with continuous bortezomib administration after allogeneic bone marrow transplantation. Blood; 2008 Aug 15;112(4):1522-9
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  • [Title] Differential effects of donor T-cell cytokines on outcome with continuous bortezomib administration after allogeneic bone marrow transplantation.
  • Dissociating graft-versus-tumor (GVT) effect from acute graft-versus-host disease (GVHD) still remains a great challenge in allogeneic bone marrow transplantation (allo-BMT).
  • In the current study, the effects of T-cell subsets and their associated cytokines on the efficacy of bortezomib in murine allogeneic BMT were investigated.
  • Importantly, prolonged administration of bortezomib after transplantation of purified CD8(+) T cells resulted in enhanced GVT response, which was dependent on donor CD8(+) T cell-derived IFNgamma.

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  • (PMID = 18539902.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102282-05; None / None / / R01 CA102282-05; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / R01 CA102282; United States / NCI NIH HHS / CA / N01CO12400
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / Cytokines; 0 / Pyrazines; 0 / Tumor Necrosis Factor-alpha; 69G8BD63PP / Bortezomib; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC2515132
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56. Takeshita A, Shinjo K, Naito K, Matsui H, Sahara N, Shigeno K, Horii T, Shirai N, Maekawa M, Ohnishi K, Naoe T, Ohno R: Efficacy of gemtuzumab ozogamicin on ATRA- and arsenic-resistant acute promyelocytic leukemia (APL) cells. Leukemia; 2005 Aug;19(8):1306-11
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  • [Title] Efficacy of gemtuzumab ozogamicin on ATRA- and arsenic-resistant acute promyelocytic leukemia (APL) cells.
  • Acute promyelocytic leukemia (APL) cells express a considerable level of CD33, which is a target of gemtuzumab ozogamicin (GO), and a significantly lower level of P-glycoprotein (P-gp).
  • Cells used were an APL cell line in which P-gp was undetectable (NB4), ATRA-resistant NB4 (NB4/RA), NB4 and NB4/RA that had been transfected with MDR-1 cDNA (NB4/MDR and NB4/RA/MDR, respectively), ATO-resistant NB4 (NB4/As) and blast cells from eight patients with clinically ATRA-resistant APL including two patients with ATRA- and ATO-resistant APL.
  • The efficacy of GO was analyzed by (3)H-thymidine incorporation, the dye exclusion test and cell cycle distribution.
  • Leukemia (2005) 19, 1306-1311. doi:10.1038/sj.leu.2403807; published online 26 May 2005.
  • [MeSH-major] Aminoglycosides / pharmacology. Antibodies, Monoclonal / pharmacology. Drug Resistance, Neoplasm. Leukemia, Promyelocytic, Acute / pathology
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Arsenicals / pharmacology. Cell Cycle. Cell Proliferation / drug effects. Humans. Oxides / pharmacology. P-Glycoprotein / analysis. Treatment Outcome. Tretinoin / pharmacology. Tumor Cells, Cultured

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  • (PMID = 15920495.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Arsenicals; 0 / Oxides; 0 / P-Glycoprotein; 0 / gemtuzumab; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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57. Wenandy L, Kollgaard T, Letsch A, Andersen RS, Stather D, Seremet T, Svane IM, Vindeløv L, Andersen MH, thor Straten P: The 1170 A-P single-nucleotide polymorphism (SNP) in the Her-2/neu protein (HER2) as a minor histocompatibility antigen (mHag). Leukemia; 2009 Oct;23(10):1926-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Breast Neoplasms / genetics. Leukemia, Myeloid, Acute / genetics. Minor Histocompatibility Antigens / metabolism. Polymorphism, Single Nucleotide / genetics. Receptor, ErbB-2 / genetics
  • [MeSH-minor] Cell Proliferation. Cell Survival. Female. Flow Cytometry. Humans. Polymerase Chain Reaction. T-Lymphocytes, Cytotoxic / immunology. Tumor Cells, Cultured

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  • (PMID = 19458631.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Minor Histocompatibility Antigens; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2
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58. Stewart AK, Bergsagel PL, Greipp PR, Dispenzieri A, Gertz MA, Hayman SR, Kumar S, Lacy MQ, Lust JA, Russell SJ, Witzig TE, Zeldenrust SR, Dingli D, Reeder CB, Roy V, Kyle RA, Rajkumar SV, Fonseca R: A practical guide to defining high-risk myeloma for clinical trials, patient counseling and choice of therapy. Leukemia; 2007 Mar;21(3):529-34
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  • Indeed, as in acute leukemias and non-hodgkins lymphoma, we believe it is no longer acceptable to consider MM a single disease entity.
  • As such, the accurate diagnosis of MM subtypes and the adoption of common criteria for the identification and stratification of MM patients has become critical.
  • Although acknowledging that more refined classifications will continue to be developed, we propose that the definition of high-risk disease (any of the t(4;14), t(14;16), t(14;20), deletion 17q13, aneuploidy or deletion chromosome 13 by metaphase cytogenetics, or plasma cell labeling index >3.0) be adopted.

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  • (PMID = 17230230.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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59. Dunwell TL, Hesson LB, Pavlova T, Zabarovska V, Kashuba V, Catchpoole D, Chiaramonte R, Brini AT, Griffiths M, Maher ER, Zabarovsky E, Latif F: Epigenetic analysis of childhood acute lymphoblastic leukemia. Epigenetics; 2009 Apr 1;4(3):185-93
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  • [Title] Epigenetic analysis of childhood acute lymphoblastic leukemia.
  • We used a chromosome 3 wide NotI microarray for identification of epigenetically inactivated genes in childhood acute lymphoblastic leukemia (ALL).
  • The methylation of the above five genes was cancer specific and expression of the genes could be restored in methylated leukemia cell lines treated with 5-aza-2'-deoxycytidine.
  • This is the first report demonstrating frequent epigenetic inactivation of PPP2R3A, FBLN2, THRB, BNC1 and MSX1 in leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 3 / genetics. DNA Methylation. Epigenesis, Genetic. Gene Expression Regulation, Leukemic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Base Sequence. Cell Line, Tumor. Gene Expression Profiling. Gene Silencing. Humans. Molecular Sequence Data. Oligonucleotide Array Sequence Analysis


60. Shalapour S, Eckert C, Seeger K, Pfau M, Prada J, Henze G, Blankenstein T, Kammertoens T: Leukemia-associated genetic aberrations in mesenchymal stem cells of children with acute lymphoblastic leukemia. J Mol Med (Berl); 2010 Mar;88(3):249-65
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  • [Title] Leukemia-associated genetic aberrations in mesenchymal stem cells of children with acute lymphoblastic leukemia.
  • Childhood acute lymphoblastic leukemia (ALL) is caused by malignant immature lymphocytes.
  • Given the high plasticity of cells, we searched for leukemia-associated genetic aberrations and immunoglobulin (IG) gene rearrangements in mesenchymal stem cells (MSC) from childhood B-cell precursor ALL patients.
  • MSC from all ten ALL patients analyzed presented the chromosomal translocations that had been detected in leukemia cells (TEL-AML1, E2A-PBX1, or MLL rearrangement).
  • Leukemia-specific IG gene rearrangements were detected in the MSC from three ALL patients.
  • The detection of leukemia-associated genetic aberrations in MSC indicates a clonal relationship between MSC and leukemia cells and suggests their involvement in the pathogenesis and/or pathophysiology of childhood ALL.
  • [MeSH-major] Mesenchymal Stromal Cells / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • (PMID = 20155409.001).
  • [ISSN] 1432-1440
  • [Journal-full-title] Journal of molecular medicine (Berlin, Germany)
  • [ISO-abbreviation] J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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61. Advani AS, Gibson SE, Douglas E, Jin T, Zhao X, Kalaycio M, Copelan E, Sobecks R, Sekeres M, Sungren S, Hsi ED: Histone H4 acetylation by immunohistochemistry and prognosis in newly diagnosed adult acute lymphoblastic leukemia (ALL) patients. BMC Cancer; 2010;10:387
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  • [Title] Histone H4 acetylation by immunohistochemistry and prognosis in newly diagnosed adult acute lymphoblastic leukemia (ALL) patients.
  • To determine whether HDAC inhibitors may be useful in the treatment of adult acute lymphoblastic leukemia (ALL), we examined the acetylation of histone H4 by immunohistochemistry in newly diagnosed ALL patients and evaluated the impact of acetylation on complete remission (CR) rate, relapse-free survival (RFS), and overall survival (OS).
  • [MeSH-major] Histones / metabolism. Neoplasm Recurrence, Local / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 20663136.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Butyrates; 0 / Histones
  • [Other-IDs] NLM/ PMC2921396
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62. Foss FM: The role of purine analogues in low-intensity regimens with allogeneic hematopoietic stem cell transplantation. Semin Hematol; 2006 Apr;43(2 Suppl 2):S35-43
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  • [Title] The role of purine analogues in low-intensity regimens with allogeneic hematopoietic stem cell transplantation.
  • High-dose chemoradiation conditioning regimens have been associated with a significant incidence of organ toxicity and acute and chronic graft-versus-host disease (GVHD).
  • Recent efforts to diminish the acute transplant-associated toxicities have focused on the development of relatively nontoxic, nonmyeloablative, or less myeloablative conditioning regimens, with the emphasis being predominantly on induction of immunosuppression to enable engraftment.
  • Without ablative chemotherapy, disease control in these regimens is largely relegated to the graft-versus-leukemia/lymphoma (GVL) effect.
  • While the evolution these regimens has resulted in successful engraftment of allogeneic stem cells with minimal toxicity, acute and chronic GVHD occurs in 20% to 50% of patients and remains a major cause of transplant-associated morbidity.
  • Strategies to lower the incidence of acute GVHD have primarily focused on more precise molecular donor/recipient matching, alternative stem cell sources, and T-cell depletion of the graft.
  • While successful in lowering the frequency and severity of GVHD, T-cell-depleted grafts have been associated with compromised the graft-versus-disease effect.
  • While fludarabine and cladribine have been shown to be effective, these agents have been associated with an increased incidence of serious infection and severe acute GVHD.
  • Regimens using pentostatin/extracorporeal photopheresis (ECP)/total body irradiation (TBI) have been shown to be well tolerated and associated with early full donor engraftment with a predominance of donor dendritic cell (DC)2 cells and a low incidence of acute GVHD.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Purine Nucleosides / therapeutic use. Transplantation Conditioning / methods
  • [MeSH-minor] Dendritic Cells / immunology. Dendritic Cells / physiology. Graft vs Host Disease / prevention & control. Hematologic Neoplasms / mortality. Hematologic Neoplasms / therapy. Humans. Transplantation, Homologous

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  • (PMID = 16549113.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Purine Nucleosides
  • [Number-of-references] 62
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63. Jabbour EJ, Faderl S, Kantarjian HM: Adult acute lymphoblastic leukemia. Mayo Clin Proc; 2005 Nov;80(11):1517-27
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  • [Title] Adult acute lymphoblastic leukemia.
  • Much progress has been made in understanding the biology of and therapy for acute lymphoblastic leukemia (ALL).
  • Prognosis has Improved especially in mature B-cell ALL and T-cell lineage ALL.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 16295033.001).
  • [ISSN] 0025-6196
  • [Journal-full-title] Mayo Clinic proceedings
  • [ISO-abbreviation] Mayo Clin. Proc.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 148
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64. McReynolds LJ, Gupta S, Figueroa ME, Mullins MC, Evans T: Smad1 and Smad5 differentially regulate embryonic hematopoiesis. Blood; 2007 Dec 1;110(12):3881-90
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  • [Title] Smad1 and Smad5 differentially regulate embryonic hematopoiesis.
  • The bone morphogenetic protein (BMP) signaling pathway regulates multiple steps of hematopoiesis, mediated through receptor-regulated Smads, including Smad1 and Smad5.
  • Here, we use loss-of-function approaches in zebrafish to compare the roles of Smad1 and Smad5 during embryonic hematopoiesis.
  • We show that knockdown of Smad1 or Smad5 generates distinct and even opposite hematopoietic phenotypes.
  • Embryos depleted for Smad1 have an increased number of primitive erythrocytes, but fail to produce mature embryonic macrophages.
  • In contrast, Smad5-depleted embryos are defective in primitive erythropoiesis, yet have normal numbers of macrophages.
  • Loss of either Smad1 or Smad5 causes a failure in the generation of definitive hematopoietic progenitors.
  • To investigate the mechanism behind these phenotypes, we used rescue experiments and found that Smad5 is unable to rescue the Smad1 loss-of-function phenotype, indicating that the 2 highly related proteins have inherently distinct activities.
  • Microarray experiments revealed that the 2 proteins redundantly regulate the key initiators of the hemato-vascular program, including scl, lmo2, and gfi1.
  • However, each also regulates a remarkably distinct genetic program, with Smad5 uniquely regulating the BMP signaling pathway itself.
  • Our results suggest that specificity of BMP signaling output, with respect to hematopoiesis, can be explained by differential functions of Smad1 and Smad5.

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  • (PMID = 17761518.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM056326; United States / NHLBI NIH HHS / HL / R01 HL056182; United States / NIGMS NIH HHS / GM / GM56326; United States / NHLBI NIH HHS / HL / HL056182; United States / NHLBI NIH HHS / HL / R37 HL056182; United States / NIGMS NIH HHS / GM / T32 GM007288; United States / NIGMS NIH HHS / GM / R56 GM056326
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Bone Morphogenetic Proteins; 0 / DNA-Binding Proteins; 0 / Gfi1 protein, zebrafish; 0 / LIM Domain Proteins; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins; 0 / Smad1 Protein; 0 / Smad5 Protein; 0 / Transcription Factors; 0 / Zebrafish Proteins; 0 / lmo2 protein, zebrafish; 0 / smad5 protein, zebrafish; 0 / tal1 protein, zebrafish
  • [Other-IDs] NLM/ PMC2200801
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65. Lightfoot TJ, Johnston WT, Painter D, Simpson J, Roman E, Skibola CF, Smith MT, Allan JM, Taylor GM, United Kingdom Childhood Cancer Study: Genetic variation in the folate metabolic pathway and risk of childhood leukemia. Blood; 2010 May 13;115(19):3923-9
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  • [Title] Genetic variation in the folate metabolic pathway and risk of childhood leukemia.
  • Studies of childhood leukemia and the potential etiologic role of genetic variation in folate metabolism have produced conflicting findings and have often been based on small numbers.
  • We investigated the association between polymorphisms in key folate metabolism enzymes (MTHFR 677 C>T, MTHFR 1298 A>C, SHMT1 1420 C>T, MTR 2756 A>G, TS 1494del6, and TS 28bp repeat) in 939 cases of childhood acute lymphoblastic leukemia (ALL) and 89 cases of acute myeloid leukemia (AML) recruited into the United Kingdom Childhood Cancer Study.
  • These data suggest that genetic variation in methionine synthase could mediate risk of childhood leukemia, either via effects on DNA methylation or via effects on fetal growth and development.
  • [MeSH-major] Folic Acid / metabolism. Genetic Variation / genetics. Glycine Hydroxymethyltransferase / genetics. Leukemia, Myeloid, Acute / genetics. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Phosphotransferases (Alcohol Group Acceptor) / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20101025.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NCI NIH HHS / CA / CA104862; United Kingdom / Cancer Research UK / / ; United Kingdom / Department of Health / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 935E97BOY8 / Folic Acid; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2); EC 2.1.2.1 / Glycine Hydroxymethyltransferase; EC 2.1.2.1 / SHMT protein, human; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.100 / 5-methylthioribose kinase
  • [Other-IDs] NLM/ PMC2869556
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66. Parovichnikova EN, Savchenko VG, Verniuk MA, Vinogradova OA, Misiurin AV, Vorob'ev IA, Domracheva EV, Tikhonova LIu, Rukavitsyn OA, Rossiev VA, Kliasova GA, Turkina AG, Liubimova LS, Mendeleeva LP, Isaev VG: [Acute lymphoblastic leukemias with aberrations of BCR-ABL genes]. Ter Arkh; 2005;77(7):11-6
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  • [Title] [Acute lymphoblastic leukemias with aberrations of BCR-ABL genes].
  • AIM: To develop an original therapeutic strategy in Ph-positive acute lymphoblastic leukemia (ALL).
  • The diagnosis of Ph-positive ALL was established in detection of translocation t(9;22) by standard cytogenetic test or fluorescent hibridization in situ with double signal (D-FISH), or by polymerase chain reaction with reverse transcription (RT-PCR).
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16116902.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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67. Owatari S, Otsuka M, Uozumi K, Takeshita T, Hanada S: Two cases of secondary acute myeloid leukemia accompanying adult T-cell leukemia/lymphoma. Int J Hematol; 2007 Jan;85(1):32-5
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  • [Title] Two cases of secondary acute myeloid leukemia accompanying adult T-cell leukemia/lymphoma.
  • We identified 2 cases of secondary acute myeloid leukemia (AML) following adult T-cell leukemia/lymphoma (ATL) in patients who had previously received chemotherapy.
  • In our hospital, only these 2 cases of secondary AML accompanying ATL were identified among 90 cases of acute- or lymphoma-type ATL diagnosed from October 1999 to July 2006.
  • The frequency of coexisting AML and ATL is lower than that reported for acute leukemia coexisting with other lymphoid malignancies.
  • The low frequency of secondary leukemia with ATL may be associated with the short survival times of ATL patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid / chemically induced. Leukemia-Lymphoma, Adult T-Cell / complications. Neoplasms, Second Primary / chemically induced
  • [MeSH-minor] Acute Disease. Alkylating Agents / therapeutic use. Anthracyclines / therapeutic use. Chromosome Aberrations. Female. Humans. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myelomonocytic, Acute / chemically induced. Male. Middle Aged. Podophyllotoxin / therapeutic use

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  • (PMID = 17261499.001).
  • [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 / Alkylating Agents; 0 / Anthracyclines; L36H50F353 / Podophyllotoxin
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68. Kretz-Rommel A, Qin F, Dakappagari N, Cofiell R, Faas SJ, Bowdish KS: Blockade of CD200 in the presence or absence of antibody effector function: implications for anti-CD200 therapy. J Immunol; 2008 Jan 15;180(2):699-705
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  • CD200 is an immunosuppressive molecule overexpressed in multiple hematologic malignancies such as B cell chronic lymphocytic leukemia, multiple myeloma, and acute myeloid leukemia.
  • In this report, we seek to select the best candidate to move forward into the clinic and begin to decipher the mechanisms of tumor cell killing by comparing anti-CD200-G1 vs anti-CD200-G2G4 in two related animal models.
  • Separately, in a model that evaluates the effect of the Abs on the immune cell component of the xenograft NOD/SCID hu-mouse model distinctly from the effects of binding to CD200 on tumor cells, we find that the administration of anti-CD200-G1 Abs completely abolished human PBMC-mediated tumor growth inhibition.

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  • (PMID = 18178807.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / antigens, CD200
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69. Kerst G, Bergold N, Gieseke F, Coustan-Smith E, Lang P, Kalinova M, Handgretinger R, Trka J, Müller I: WT1 protein expression in childhood acute leukemia. Am J Hematol; 2008 May;83(5):382-6
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  • [Title] WT1 protein expression in childhood acute leukemia.
  • In patients with acute leukemia, Wilms' tumor gene 1 (WT1) has been used as a target for the detection of minimal residual disease (MRD) by PCR techniques.
  • To determine the relation between expression of WT1 transcripts and of the encoded protein, we examined leukemic cell lines and primary childhood leukemia samples using both real-time quantitative PCR (RQ-PCR) and flow cytometry.
  • WT1 protein was highly expressed in the leukemic cell lines K562, HL-60, PLB 985, KG-1a and CEM.
  • By contrast, 40 primary samples of acute lymphoblastic leukemia (ALL; B-ALL, n = 15 and T-ALL, n = 10) and acute myeloid leukemia (n = 15) expressed low levels of WT1 protein.
  • RQ-PCR detected WT1 transcript levels in the same range as reported in earlier studies in childhood acute leukemia.
  • (ii) WT1 is not a suitable marker for flow cytometric MRD detection in childhood acute leukemia.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Neoplasm Proteins / analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. WT1 Proteins / analysis
  • [MeSH-minor] Adolescent. Adult. Biomarkers, Tumor. Blood Cells / metabolism. Bone Marrow Cells / metabolism. Burkitt Lymphoma / genetics. Burkitt Lymphoma / metabolism. Burkitt Lymphoma / pathology. Cell Line, Tumor / metabolism. Child. Child, Preschool. Female. Flow Cytometry. Genes, Wilms Tumor. Humans. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / metabolism. Leukemia-Lymphoma, Adult T-Cell / pathology. Male. RNA, Messenger / biosynthesis. RNA, Neoplasm / biosynthesis. Sensitivity and Specificity

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  • [Copyright] Copyright 2008 Wiley-Liss, Inc.
  • (PMID = 18161786.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / WT1 Proteins
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70. Lu J, Quearry B, Harada H: p38-MAP kinase activation followed by BIM induction is essential for glucocorticoid-induced apoptosis in lymphoblastic leukemia cells. FEBS Lett; 2006 Jun 12;580(14):3539-44
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  • [Title] p38-MAP kinase activation followed by BIM induction is essential for glucocorticoid-induced apoptosis in lymphoblastic leukemia cells.
  • Treatment of CCRF-CEM (T cell acute lymphoblastic leukemia) cells with the GC, dexamethasone (Dex), activates p38-mitogen activated protein kinase (p38-MAPK) and then induces mRNA transcription and synthesis levels of BIM, a BH3-only pro-apoptotic BCL-2 family member.
  • These findings indicate that BIM induction through p38-MAPK activation is a critical pathway in GC-induced cell death.
  • [MeSH-major] Apoptosis / drug effects. Apoptosis Regulatory Proteins / biosynthesis. Dexamethasone / pharmacology. Leukemia-Lymphoma, Adult T-Cell / pathology. Membrane Proteins / biosynthesis. Proto-Oncogene Proteins / biosynthesis. p38 Mitogen-Activated Protein Kinases / metabolism
  • [MeSH-minor] Base Sequence. Blotting, Western. Cell Line, Tumor. DNA Primers. Enzyme Activation. Humans

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  • (PMID = 16730715.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / DNA Primers; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 7S5I7G3JQL / Dexamethasone; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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76. Baessler T, Krusch M, Schmiedel BJ, Kloss M, Baltz KM, Wacker A, Schmetzer HM, Salih HR: Glucocorticoid-induced tumor necrosis factor receptor-related protein ligand subverts immunosurveillance of acute myeloid leukemia in humans. Cancer Res; 2009 Feb 1;69(3):1037-45
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  • [Title] Glucocorticoid-induced tumor necrosis factor receptor-related protein ligand subverts immunosurveillance of acute myeloid leukemia in humans.
  • Here, we studied the role of GITR and its ligand (GITRL) in human acute myeloid leukemia (AML).
  • Surface expression of GITRL was observed on AML cells in six of seven investigated cell lines, and 34 of 60 investigated AML patients whereas healthy CD34(+) cells did not express GITRL.
  • Furthermore, triggering GITR by surface-expressed and sGITRL impaired NK cell cytotoxicity and IFN-gamma production in cocultures with leukemia cells, and NK cell reactivity could be restored by blocking GITR and neutralization of sGITRL and IL-10.
  • Thus, whereas a stimulatory role of the GITR-GITRL system in mouse antitumor immunity has been reported, our data show that in humans GITRL expression subverts NK cell immunosurveillance of AML.
  • Our results provide useful information for therapeutic approaches in AML, which, like haploidentical stem cell transplantation, rely on a sufficient NK cell response.
  • [MeSH-major] Leukemia, Myeloid / immunology. Tumor Necrosis Factors / immunology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Cell Differentiation / immunology. Cell Line, Tumor. Cytokines / immunology. Female. Humans. Immunologic Surveillance / immunology. Interferon-gamma / biosynthesis. Killer Cells, Natural / immunology. Male. Middle Aged. Monocytes / immunology. Young Adult

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  • (PMID = 19155305.001).
  • [ISSN] 1538-7445
  • [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 / Cytokines; 0 / TNFSF18 protein, human; 0 / Tumor Necrosis Factors; 82115-62-6 / Interferon-gamma
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77. Steiner M, Attarbaschi A, König M, Gadner H, Haas OA, Mann G: Equal frequency of TEL/AML1+ acute lymphoblastic leukemia in children with and without Down syndrome. Pediatr Hematol Oncol; 2005 Jan-Feb;22(1):11-6
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  • [Title] Equal frequency of TEL/AML1+ acute lymphoblastic leukemia in children with and without Down syndrome.
  • Constitutional trisomy 21 is the most prominent predisposing factor to childhood leukemia, whereas the t(12;21)(p13;q22) with its molecular genetic counterpart, the TEL/AML1 fusion gene, is the most common acquired chromosomal rearrangement in childhood B-cell precursor (BCP) acute lymphoblastic leukemia (ALL).
  • Accordingly, they were able to analyze 8 of 10 individuals with DS and a BCP ALL, including 2 who suffered from a TEL/AML1+ leukemia.
  • Based on this observation we concluded that individuals with a constitutional trisomy 21 may have the similar likelihood to develop a TEL/AML1+ leukemia as BCP ALL patients without this specific predisposingfactor.
  • [MeSH-major] Down Syndrome / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [RepublishedIn] Pediatr Hematol Oncol. 2005 Apr-May;22(3):229-34 [16020107.001]
  • (PMID = 15770827.001).
  • [ISSN] 0888-0018
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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78. Mishra P, Kumar R, Mahapatra M, Sharma S, Dixit A, Chaterjee T, Choudhry DR, Saxena R, Choudhry VP: Tuberculosis in acute leukemia: a clinico-hematological profile. Hematology; 2006 Oct;11(5):335-40
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  • [Title] Tuberculosis in acute leukemia: a clinico-hematological profile.
  • We studied 130 consecutive cases of acute leukemia over a 2-year period and identified 9 cases (6.9%) with active tuberculosis (TB).
  • Eight patients with TB had acute myeloid leukemia (AML).
  • Patients with AML were more likely to develop TB as compared to patients with acute lymphoblastic leukemia (ALL) despite the wider use of steroids and radiotherapy in ALL protocols {OR 4.41 (CI 0.53-36.44)}.
  • However it is not a commonly described infection in acute leukemia and a high index of suspicion is warranted especially in areas endemic for TB.
  • [MeSH-major] Leukemia / complications. Tuberculosis / etiology
  • [MeSH-minor] Acute Disease. Adult. Antitubercular Agents / therapeutic use. Female. Humans. Incidence. Leukemia, Myeloid. Male. Neutropenia. Precursor Cell Lymphoblastic Leukemia-Lymphoma

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  • (PMID = 17607583.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antitubercular Agents
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79. Vago L, Perna SK, Zanussi M, Mazzi B, Barlassina C, Stanghellini MT, Perrelli NF, Cosentino C, Torri F, Angius A, Forno B, Casucci M, Bernardi M, Peccatori J, Corti C, Bondanza A, Ferrari M, Rossini S, Roncarolo MG, Bordignon C, Bonini C, Ciceri F, Fleischhauer K: Loss of mismatched HLA in leukemia after stem-cell transplantation. N Engl J Med; 2009 Jul 30;361(5):478-88
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  • [Title] Loss of mismatched HLA in leukemia after stem-cell transplantation.
  • The donor T-cell infusions associated with such transplantation can promote post-transplantation immune reconstitution and control residual disease.
  • METHODS: We identified 43 patients who underwent haploidentical transplantation and infusion of donor T cells for acute myeloid leukemia or myelodysplastic syndrome and conducted post-transplantation studies that included morphologic examination of bone marrow, assessment of hematopoietic chimerism with the use of short-tandem-repeat amplification, and HLA typing.
  • The genomic rearrangements in mutant variants of leukemia were studied with the use of genomic HLA typing, microsatellite mapping, and single-nucleotide-polymorphism arrays.
  • RESULTS: In 5 of 17 patients with leukemia relapse after haploidentical transplantation and infusion of donor T cells, we identified mutant variants of the original leukemic cells.
  • T cells from the donor and the patient after transplantation did not recognize the mutant leukemic cells, whereas the original leukemic cells taken at the time of diagnosis were efficiently recognized and killed.
  • [MeSH-major] Graft vs Leukemia Effect / genetics. HLA Antigens / genetics. Hematopoietic Stem Cell Transplantation. Histocompatibility Testing. Leukemia, Myeloid, Acute / therapy. T-Lymphocytes / immunology

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  • [Copyright] 2009 Massachusetts Medical Society
  • [CommentIn] N Engl J Med. 2009 Jul 30;361(5):524-5 [19641211.001]
  • (PMID = 19641204.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Grant] Italy / Telethon / / GGP08201
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA Antigens
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80. Hao CL, Tang KJ, Chen S, Xing HY, Wang M, Wang JX: [5-Aza-2'-deoxycytidine enhances differentiation and apoptosis induced by phenylbutyrate in Kasumi-1 cells]. Zhonghua Zhong Liu Za Zhi; 2005 Mar;27(3):148-51
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  • OBJECTIVE: To investigate whether phenylbutyrate (PB) combined with 5-aza-2'-deoxycytidine (5-Aza-CdR)could inhibit transcription repression and induce t(8;21) acute myelogenous leukemia (AML) Kasumi-1 cells to differentiate and undergo apoptosis.
  • Cellular proliferation was determined by the MTT assay, expression of myeloid-specific differentiation antigen and cell cycles were analyzed by flow cytometry.
  • Cell apoptosis were assessed using AnnexinV/PI staining and flow cytometry.
  • Treatment of Kasumi-1 cells with PB resulted in cell cycle arrest at G(0)/G(1), while combined treatment with PB and 5-Aza-CdR led to cell cycle arrest at G(2)/M.
  • Expression of myeloid cell differentiation antigens CD11b and CD13 induced by PB was enhanced when Kasumi-1 cells were pretreated with low dose of 5-Aza-CdR.
  • CONCLUSION: Phenylbuty rate, when combined with 5-Aza-CdR, inhibits AML cell in vitro proliferation and increases apoptosis in a synergistic fashion.
  • [MeSH-major] Apoptosis / drug effects. Azacitidine / analogs & derivatives. Leukemia, Myeloid / pathology. Phenylbutyrates / pharmacology
  • [MeSH-minor] Acute Disease. Antigens, CD11b / metabolism. Antigens, CD13 / metabolism. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Drug Synergism. Humans

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  • (PMID = 15946563.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Phenylbutyrates; 776B62CQ27 / decitabine; EC 3.4.11.2 / Antigens, CD13; M801H13NRU / Azacitidine
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81. Ando T, Mitani N, Matsunaga K, Nakazora T, Gondo T, Yujiri T, Tanizawa Y: Gemtuzumab ozogamicin therapy for isolated extramedullary AML relapse after allogeneic hematopoietic stem-cell transplantation. Tohoku J Exp Med; 2010 Feb;220(2):121-6
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  • [Title] Gemtuzumab ozogamicin therapy for isolated extramedullary AML relapse after allogeneic hematopoietic stem-cell transplantation.
  • The treatment of isolated extramedullary relapse (IEMR) after allogeneic hematopoietic stem-cell transplantation (allo-HSCT) poses a challenge for which no standard approach exists.
  • Gemtuzumab ozogamicin (GO) is a recombinant humanized monoclonal antibody, conjugated to calicheamicin, which targets the CD33 antigen that is expressed in acute myelogenous leukemia (AML) blasts.
  • The selectivity of GO for CD33-positive leukemic cells makes it an attractive agent for use in patients with multiple sites of IEMR after allo-HSCT, because GO does not suppress cells responsible for the putative graft-versus-leukemia (GVL) effect.
  • Herein, we describe a 54-year-old male patient who developed AML with multiple sites of extramedullary (EM) relapse after allo-HSCT, and who exhibited apparent donor-derived hematopoiesis in the bone marrow.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Sarcoma, Myeloid / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antineoplastic Agents / therapeutic use. Bone and Bones / radionuclide imaging. CD8-Positive T-Lymphocytes / pathology. Graft vs Leukemia Effect / immunology. Humans. Leukocytes / metabolism. Leukocytes / pathology. Lumbosacral Region / pathology. Lumbosacral Region / radionuclide imaging. Male. Middle Aged. Peroxidase / metabolism. Recurrence. Transplantation, Homologous

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  • (PMID = 20139663.001).
  • [ISSN] 1349-3329
  • [Journal-full-title] The Tohoku journal of experimental medicine
  • [ISO-abbreviation] Tohoku J. Exp. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / gemtuzumab; EC 1.11.1.7 / Peroxidase
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82. Groninger E, Meeuwsen-de Boer T, Koopmans P, Uges D, Sluiter W, Veerman A, Kamps W, de Graaf S: Vincristine pharmacokinetics and response to vincristine monotherapy in an up-front window study of the Dutch Childhood Leukaemia Study Group (DCLSG). Eur J Cancer; 2005 Jan;41(1):98-103
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  • [Title] Vincristine pharmacokinetics and response to vincristine monotherapy in an up-front window study of the Dutch Childhood Leukaemia Study Group (DCLSG).
  • Since vincristine plays a key role in the treatment of childhood acute lymphoblastic leukaemia (ALL), it is worthwhile to explore if efficacy can be improved by individual dose adjustment.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacokinetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Vincristine / pharmacokinetics

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  • (PMID = 15617994.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 5J49Q6B70F / Vincristine
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83. Joshita S, Kitano K, Nagaya T, Kamijo A, Nakazawa K, Ishida F: Zygomycosis presenting as acute myocardial infarction during hematological malignancies. Intern Med; 2008;47(9):839-42
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  • [Title] Zygomycosis presenting as acute myocardial infarction during hematological malignancies.
  • The second case, a 52-year-old woman with acute lymphoblastic leukemia, developed febrile neutropenia and skin eruptions with induration on the face and extremities during the first induction chemotherapy.
  • She experienced sudden bradycardia with unstable hemodynamics and died of acute myocardial infarction.
  • In light of the above, it should be kept in mind that cardiac zygomycosis might occur in hematologically compromised patients presenting with acute myocardial infarction.
  • [MeSH-major] Coronary Vessels / microbiology. Myelodysplastic Syndromes / microbiology. Myocardial Infarction / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / microbiology. Zygomycosis / complications


84. Ohnuki K, Watanabe Y, Takahashi Y, Kobayashi S, Watanabe S, Ogawa S, Kotani M, Kozono H, Tanabe K, Abe R: Antigen-specific CD4+ effector T cells: analysis of factors regulating clonal expansion and cytokine production: clonal expansion and cytokine production by CD4+ effector T cells. Biochem Biophys Res Commun; 2009 Mar 20;380(4):742-7
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  • In order to fully understand T cell-mediated immunity, the mechanisms that regulate clonal expansion and cytokine production by CD4(+) antigen-specific effector T cells in response to a wide range of antigenic stimulation needs clarification.
  • For this purpose, panels of antigen-specific CD4(+) T cell clones with different thresholds for antigen-induced proliferation were generated by repeated stimulation with high- or low-dose antigen.
  • There was no significant difference in antigen-dependent cytokine production by TG40 cells transfected with TCR obtained from either high- or low-dose-responding T cell clones, suggesting that the affinity of TCRs for their ligands is not primary determinant of T cell antigen reactivity.
  • The proliferative responses of all T cell clones to both peptide stimulation and to TCRbeta crosslinking revealed parallel dose-response curves.
  • Finally, the antigen responses of high- and low-peptide-responding T cell clones reveal that clonal expansion and cytokine production of effector T cells occur independently of antigen concentration.
  • [MeSH-minor] Animals. Cell Adhesion Molecules / metabolism. Clone Cells. Flow Cytometry. Mice. Mice, Inbred BALB C. Ovalbumin / immunology. Peptide Fragments / immunology. Receptors, Antigen, T-Cell / metabolism

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  • (PMID = 19338745.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Cytokines; 0 / OVA 323-339; 0 / Peptide Fragments; 0 / Receptors, Antigen, T-Cell; 9006-59-1 / Ovalbumin
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85. Helbig G, Krzemień S, Francuz T, Wojnar J, Hołowiecki J: Elastin metabolism is disrupted in patients after allogeneic hematopoietic stem cell transplantation (alloHSCT) for acute and chronic myeloid leukemia. Med Sci Monit; 2008 Nov;14(11):CR584-8
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  • [Title] Elastin metabolism is disrupted in patients after allogeneic hematopoietic stem cell transplantation (alloHSCT) for acute and chronic myeloid leukemia.
  • BACKGROUND: The potential role of elastin in patients with myeloid leukemia treated with hematopoietic stem cell transplantation (HSCT) has not been investigated so far.
  • The diagnoses were acute myeloid leukemia (AML, n=25) and chronic myeloid leukemia (CML, n=15).
  • Graft-versus-host disease (GVHD) prophylaxis consisted of cyclosporine and methotrexate.
  • Twenty-three patients experienced acute GVHD and 17 developed chronic GVHD.
  • Plasma elastase activity (EA) and plasma elastin-derived peptide concentration (EDPc) were measured.
  • [MeSH-major] Elastin / metabolism. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / metabolism
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Chronic Disease. Female. Humans. Male. Middle Aged. Pancreatic Elastase / metabolism. Peptide Fragments / biosynthesis. Transplantation, Homologous. Young Adult

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  • (PMID = 18971876.001).
  • [ISSN] 1643-3750
  • [Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research
  • [ISO-abbreviation] Med. Sci. Monit.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Peptide Fragments; 9007-58-3 / Elastin; EC 3.4.21.36 / Pancreatic Elastase
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86. Imanishi H, Okamura N, Yagi M, Noro Y, Moriya Y, Nakamura T, Hayakawa A, Takeshima Y, Sakaeda T, Matsuo M, Okumura K: Genetic polymorphisms associated with adverse events and elimination of methotrexate in childhood acute lymphoblastic leukemia and malignant lymphoma. J Hum Genet; 2007;52(2):166-71
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  • [Title] Genetic polymorphisms associated with adverse events and elimination of methotrexate in childhood acute lymphoblastic leukemia and malignant lymphoma.
  • Methotrexate is administered in high doses to treat childhood acute lymphoblastic leukemia and malignant lymphoma.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Liver Diseases / genetics. Lymphoma / genetics. Methotrexate / therapeutic use. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Genetic Predisposition to Disease. Genotype. Glutathione S-Transferase pi / genetics. Glutathione Transferase / genetics. Humans. Infant. Male. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Risk Factors


87. Tabe Y, Jin L, Tsutsumi-Ishii Y, Xu Y, McQueen T, Priebe W, Mills GB, Ohsaka A, Nagaoka I, Andreeff M, Konopleva M: Activation of integrin-linked kinase is a critical prosurvival pathway induced in leukemic cells by bone marrow-derived stromal cells. Cancer Res; 2007 Jan 15;67(2):684-94
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  • [Title] Activation of integrin-linked kinase is a critical prosurvival pathway induced in leukemic cells by bone marrow-derived stromal cells.
  • Coculture of leukemic NB4 cells with bone marrow-derived stromal mesenchymal stem cells (MSC) resulted in robust activation of multiple signaling pathways, including ILK/Akt, extracellular signal-regulated kinase 1/2 (ERK1/2), signal transducers and activators of transcription 3 (STAT3), and Notch1/Hes.
  • This resulted in induction of apoptosis in both leukemic cell lines and in primary acute myelogenous leukemia samples that was not abrogated by MSC coculture.
  • Hence, disruption of these interactions by ILK inhibitors represents a potential novel therapeutic strategy to eradicate leukemia in the bone marrow microenvironment by simultaneous targeting of both leukemic cells and activated bone marrow stromal cells.
  • [MeSH-major] Cell Communication / physiology. Leukemia, Promyelocytic, Acute / enzymology. Mesenchymal Stromal Cells / enzymology. Protein-Serine-Threonine Kinases / metabolism
  • [MeSH-minor] Basic Helix-Loop-Helix Transcription Factors / metabolism. Bone Marrow Cells / cytology. Bone Marrow Cells / enzymology. Cell Survival / physiology. Chromones / pharmacology. Coculture Techniques. Enzyme Activation / drug effects. Homeodomain Proteins / metabolism. Humans. Janus Kinases / metabolism. Mitogen-Activated Protein Kinase Kinases / metabolism. Morpholines / pharmacology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / metabolism. Phosphorylation / drug effects. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Proto-Oncogene Proteins c-akt / metabolism. Receptors, Notch / metabolism. STAT3 Transcription Factor / metabolism. Signal Transduction / drug effects. Stromal Cells / cytology. Stromal Cells / enzymology

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  • (PMID = 17234779.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P01 CA49639; United States / NCI NIH HHS / CA / P01 CA55164; United States / NCI NIH HHS / CA / R01 CA89346
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Chromones; 0 / Homeodomain Proteins; 0 / Morpholines; 0 / Receptors, Notch; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 149348-15-2 / HES1 protein, human; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.- / integrin-linked kinase; EC 2.7.10.2 / Janus Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
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88. Tomonari A, Takahashi S, Shimohakamada Y, Ooi J, Takasugi K, Ohno N, Konuma T, Uchimaru K, Tojo A, Odawara T, Nakamura T, Iwamoto A, Asano S: Unrelated cord blood transplantation for a human immunodeficiency virus-1-seropositive patient with acute lymphoblastic leukemia. Bone Marrow Transplant; 2005 Aug;36(3):261-2
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  • [Title] Unrelated cord blood transplantation for a human immunodeficiency virus-1-seropositive patient with acute lymphoblastic leukemia.
  • [MeSH-major] Cord Blood Stem Cell Transplantation / methods. Fetal Blood / transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adult. Antiretroviral Therapy, Highly Active. CD4 Lymphocyte Count. CD4-Positive T-Lymphocytes / cytology. Disease-Free Survival. Female. Fusion Proteins, bcr-abl / metabolism. HIV Infections / complications. HIV Infections / drug therapy. HIV Seropositivity. Humans. Reverse Transcriptase Polymerase Chain Reaction


89. Fotoohi K, Skärby T, Söderhäll S, Peterson C, Albertioni F: Interference of 7-hydroxymethotrexate with the determination of methotrexate in plasma samples from children with acute lymphoblastic leukemia employing routine clinical assays. J Chromatogr B Analyt Technol Biomed Life Sci; 2005 Mar 25;817(2):139-44
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  • [Title] Interference of 7-hydroxymethotrexate with the determination of methotrexate in plasma samples from children with acute lymphoblastic leukemia employing routine clinical assays.
  • The accuracy of two clinical assays, the enzyme-multiplied immunoassay (EMIT) and fluorescence polarization immunoassay (FPIA2), universally employed for measurement of plasma levels of methotrexate (MTX) in children administered a high dose of this drug for treatment of acute lymphoblastic leukemia was evaluated here.
  • [MeSH-major] Methotrexate / analogs & derivatives. Methotrexate / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood

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  • (PMID = 15686977.001).
  • [ISSN] 1570-0232
  • [Journal-full-title] Journal of chromatography. B, Analytical technologies in the biomedical and life sciences
  • [ISO-abbreviation] J. Chromatogr. B Analyt. Technol. Biomed. Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] X019Z9S1DL / 7-hydroxymethotrexate; YL5FZ2Y5U1 / Methotrexate
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90. Maggio R, Peragine N, Calabrese E, De Propris MS, Intoppa S, Della Starza I, Ariola C, Vitale A, Foà R, Guarini A: Generation of functional dendritic cells (DC) in adult acute lymphoblastic leukemia: rationale for a DC-based vaccination program for patients in complete hematological remission. Leuk Lymphoma; 2007 Feb;48(2):302-10
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  • [Title] Generation of functional dendritic cells (DC) in adult acute lymphoblastic leukemia: rationale for a DC-based vaccination program for patients in complete hematological remission.
  • The capacity to generate effective dendritic cells (DC) from adult acute lymphoblastic leukemia (ALL) patients in complete remission (CR) and off-therapy was investigated.
  • Monocyte-derived DC cultured in the presence of granulocyte-macrophage colony-stimulating factor, interleukin (IL)-4 and tumor necrosis factor (TNF)-alpha expressed maturation markers, produced IL-12 and loaded apoptotic bodies to a similar extent to normal DC.
  • DC loaded with leukemia-derived apoptotic bodies increased their ability to stimulate both allogeneic and autologous lymphocytes, and to generate specific anti-leukemic CD3 + cells.
  • These findings offer a rationale for the design of DC-based vaccine programs for adult ALL patients in CR with the aim of controlling/eradicating the disease.
  • [MeSH-major] Apoptosis. Dendritic Cells / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / prevention & control. Vaccination
  • [MeSH-minor] Adult. Aged. Cancer Vaccines / therapeutic use. Cell Proliferation. Female. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Humans. Immunophenotyping. Interferon-gamma / metabolism. Interleukin-12 / metabolism. Interleukin-4 / pharmacology. Killer Cells, Natural / immunology. Male. Middle Aged. Phagocytosis. Remission Induction. T-Lymphocytes / immunology. T-Lymphocytes / metabolism. T-Lymphocytes / pathology. T-Lymphocytes, Cytotoxic / immunology. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / pharmacology

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  • [CommentIn] Leuk Lymphoma. 2007 Feb;48(2):217-8 [17325876.001]
  • (PMID = 17325890.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Tumor Necrosis Factor-alpha; 187348-17-0 / Interleukin-12; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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91. Wasik M, Górska E, Popko K, Pawelec K, Matysiak M, Demkow U: The Gln223Arg polymorphism of the leptin receptor gene and peripheral blood/bone marrow leptin level in leukemic children. J Physiol Pharmacol; 2006 Sep;57 Suppl 4:375-83
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  • Leptin is an adipocyte-derived hormone regulating energy homeostasis and body weight.
  • Leptin also plays a role in hematopoiesis, cell cycle regulation, and in oncogenesis.
  • The aim of the study was to evaluate bone marrow and peripheral blood leptin level and frequency of distribution of leptin receptor gene polymorphism Gln223Arg in children with acute leukemia.
  • The examined group included 92 children with acute leukemia (83 ALL and 9 AML) and 39 non-leukemic control children.
  • Leptin level was measured by ELISA method at the day of leukemia diagnosis.
  • The results indicate a possible relation between the leptin level and leukemia development in children.
  • [MeSH-major] Bone Marrow / metabolism. Leptin / metabolism. Leukemia / genetics. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Leptin / genetics

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  • (PMID = 17072067.001).
  • [ISSN] 1899-1505
  • [Journal-full-title] Journal of physiology and pharmacology : an official journal of the Polish Physiological Society
  • [ISO-abbreviation] J. Physiol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Leptin; 0 / Receptors, Leptin; 0 / leptin receptor, human
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92. Fischer G S, Neira L L, Ferreiro M M, Torres C MT, Giadrosich R V, Milinarsky T A, Arriagada M M, Arinoviche S R: [Bone mineral density in leukemic children after completing one month of chemotherapy]. Rev Med Chil; 2005 Jan;133(1):71-6
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  • [Transliterated title] Densitometría ósea en niños leucémicos al completar el primer mes de quimioterapia.
  • BACKGROUND: An important loss of bone mineral density, associated to pain and fractures, has been reported in children with acute lymphoblastic leukemia (ALL).
  • AIM: To measure bone mineral density among children with acute lymphoblastic leukemia (ALL) that completed the remission induction phase with chemotherapy, that lasts 30 days.
  • [MeSH-major] Bone Density. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 15768152.001).
  • [ISSN] 0034-9887
  • [Journal-full-title] Revista médica de Chile
  • [ISO-abbreviation] Rev Med Chil
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Chile
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93. Hackanson B, Bennett KL, Brena RM, Jiang J, Claus R, Chen SS, Blagitko-Dorfs N, Maharry K, Whitman SP, Schmittgen TD, Lübbert M, Marcucci G, Bloomfield CD, Plass C: Epigenetic modification of CCAAT/enhancer binding protein alpha expression in acute myeloid leukemia. Cancer Res; 2008 May 01;68(9):3142-51
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  • [Title] Epigenetic modification of CCAAT/enhancer binding protein alpha expression in acute myeloid leukemia.
  • Here, we show the effect of epigenetic aberrations in regulating C/EBP alpha expression in acute myeloid leukemia (AML).
  • This miRNA is frequently silenced by epigenetic mechanisms in leukemia cell lines, becomes up-regulated after epigenetic treatment, and targets the C/EBP alpha 3' untranslated region.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / genetics. Epigenesis, Genetic. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 18451139.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / U10 CA077658; United States / NCI NIH HHS / CA / P30CA16058; United States / NCI NIH HHS / CA / U10 CA101140; United States / NCI NIH HHS / CA / CA77658
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / MIRN124 microRNA, human; 0 / MicroRNAs; 0 / RNA, Messenger
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94. Barry EV, Silverman LB: Acute lymphoblastic leukemia in adolescents and young adults. Curr Hematol Malig Rep; 2008 Jul;3(3):161-6
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  • [Title] Acute lymphoblastic leukemia in adolescents and young adults.
  • Age at diagnosis remains one of the strongest prognostic factors in acute lymphoblastic leukemia (ALL), with older patients having inferior outcomes compared with younger patients.
  • Compared with younger children with ALL, AYAs are more likely to present with unfavorable presenting characteristics (such as high presenting leukocyte counts, T-cell phenotype, and the Philadelphia chromosome).
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Adult. Age Factors. Antineoplastic Agents / toxicity. Fusion Proteins, bcr-abl / genetics. Humans. Immunophenotyping. Leukocyte Count. Prospective Studies. Stem Cell Transplantation. Survival Rate. Translocation, Genetic. Young Adult

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  • (PMID = 20425461.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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95. Rizzuto GA, Wolchok JD: Persistence makes perfect: the benefits of IL-2 in adoptive immunotherapy. Cytotherapy; 2005;7(5):391-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Acute Disease. Animals. Cell Line, Tumor. Leukemia, Myeloid / immunology. Leukemia, Myeloid / therapy. Mice. Mice, Transgenic. Neoplasms, Experimental / immunology. Neoplasms, Experimental / therapy. T-Lymphocytes / immunology. T-Lymphocytes / transplantation

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  • [CommentOn] Cytotherapy. 2005;7(5):396-407 [16236629.001]
  • (PMID = 16236627.001).
  • [ISSN] 1465-3249
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Publication-type] Comment; Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD28; 0 / Antigens, CD3; 0 / Interleukin-2
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