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1. Went PT, Zimpfer A, Pehrs AC, Sabattini E, Pileri SA, Maurer R, Terracciano L, Tzankov A, Sauter G, Dirnhofer S: High specificity of combined TRAP and DBA.44 expression for hairy cell leukemia. Am J Surg Pathol; 2005 Apr;29(4):474-8
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  • [Title] High specificity of combined TRAP and DBA.44 expression for hairy cell leukemia.
  • Because of marrow fibrosis, bone marrow aspirations are often nonconclusive in patients with hairy cell leukemia (HCL).
  • DBA.44 reactivity was especially frequent in follicular lymphomas (46%), whereas tartrate-resistant acid phosphatase (TRAP) expression was often seen in mantle cell lymphomas (57%), primary mediastinal large B-cell lymphomas (54%), and chronic lymphocytic leukemia/small lymphocytic lymphoma (41%).
  • A combined DBA.44/TRAP positivity was seen in only 3% of non-HCL non-Hodgkin lymphomas, including cases of diffuse large B-cell lymphomas, follicular lymphomas, chronic lymphatic leukemia/small lymphocytic leukemias, and mantle cell lymphomas.
  • [MeSH-major] Acid Phosphatase / metabolism. Antibodies, Monoclonal / metabolism. Isoenzymes / metabolism. Leukemia, Hairy Cell / metabolism. Lymphoma, Non-Hodgkin / metabolism

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  • (PMID = 15767800.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Isoenzymes; EC 3.1.3.- / tartrate-resistant acid phosphatase; EC 3.1.3.2 / Acid Phosphatase
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2. Schmitt A, Hus I, Schmitt M: Dendritic cell vaccines for leukemia patients. Expert Rev Anticancer Ther; 2007 Mar;7(3):275-83
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  • [Title] Dendritic cell vaccines for leukemia patients.
  • The graft-versus-leukemia effect observed after allogeneic stem cell transplantation strongly suggests that T lymphocytes play a major role in the rejection of leukemic cells.
  • This graft-versus-leukemia effect might be enhanced through dendritic cell vaccination.
  • The characterization of leukemia-specific antigens eliciting immune responses in the autologous host has prompted researchers and clinicians to broaden the spectrum of dendritic cell vaccines to hematological malignancies.
  • Recently, the focus is on acute myeloid leukemia and chronic lymphocytic leukemia.
  • This review summarizes data on the administration of autologous and allogeneic dendritic cells to leukemia patients as an interesting approach in cellular therapy of leukemias.
  • [MeSH-major] Cancer Vaccines / therapeutic use. Dendritic Cells / transplantation. Immunotherapy, Active. Leukemia / therapy
  • [MeSH-minor] Acute Disease. Animals. Antigen Presentation. Bone Marrow Cells / cytology. Bone Marrow Cells / drug effects. Cell Adhesion. Cell Differentiation / drug effects. Cells, Cultured / immunology. Cells, Cultured / transplantation. Clinical Trials as Topic. Cytokines / pharmacology. Humans. Immunophenotyping. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Leukemia, Myeloid / therapy. Lymphocyte Activation. Mice. Models, Immunological. Neoplastic Stem Cells / cytology. Neoplastic Stem Cells / drug effects. T-Lymphocyte Subsets / immunology. Transplantation, Autologous. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 17338648.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Cytokines
  • [Number-of-references] 66
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3. Messmer BT, Messmer D, Allen SL, Kolitz JE, Kudalkar P, Cesar D, Murphy EJ, Koduru P, Ferrarini M, Zupo S, Cutrona G, Damle RN, Wasil T, Rai KR, Hellerstein MK, Chiorazzi N: In vivo measurements document the dynamic cellular kinetics of chronic lymphocytic leukemia B cells. J Clin Invest; 2005 Mar;115(3):755-64
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  • [Title] In vivo measurements document the dynamic cellular kinetics of chronic lymphocytic leukemia B cells.
  • Due to its relatively slow clinical progression, B cell chronic lymphocytic leukemia (B-CLL) is classically described as a disease of accumulation rather than proliferation.
  • We used a nonradioactive, stable isotopic labeling method to measure B-CLL cell kinetics in vivo.
  • Those patients with birth rates greater than 0.35% per day were much more likely to exhibit active or to develop progressive disease than those with lower birth rates Thus, B-CLL is not a static disease that results simply from accumulation of long-lived lymphocytes.
  • A correlation between birth rates and disease activity and progression appears to exist, which may help identify patients at risk for worsening disease in advance of clinical deterioration.

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  • [Cites] Adv Cancer Res. 2000;79:157-73 [10818680.001]
  • [Cites] Blood. 1999 Sep 15;94(6):1848-54 [10477713.001]
  • [Cites] Haematologica. 2000 Dec;85(12):1291-307 [11114137.001]
  • [Cites] Blood. 2001 May 1;97(9):2777-83 [11313271.001]
  • [Cites] Blood. 2002 Feb 1;99(3):1023-9 [11807008.001]
  • [Cites] Br J Haematol. 2001 Dec;115(4):854-61 [11843819.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3854-9 [11891278.001]
  • [Cites] Blood. 2002 Aug 15;100(4):1410-6 [12149225.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4609-14 [12393534.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15345-50 [12424339.001]
  • [Cites] Blood. 2003 Feb 15;101(4):1262-9 [12406914.001]
  • [Cites] N Engl J Med. 2003 May 1;348(18):1764-75 [12724482.001]
  • [Cites] Blood. 2003 Jun 15;101(12):4944-51 [12595313.001]
  • [Cites] Blood. 1967 Apr;29(4):Suppl:566-84 [6022294.001]
  • [Cites] Blood. 1968 Mar;31(3):277-91 [5640626.001]
  • [Cites] Br J Haematol. 1969 Oct;17(4):408 [4899589.001]
  • [Cites] Blood. 1973 Mar;41(3):425-38 [4690140.001]
  • [Cites] Blood. 1973 Oct;42(4):623-36 [4778708.001]
  • [Cites] Clin Haematol. 1977 Feb;6(1):159-67 [334407.001]
  • [Cites] Scand J Haematol. 1978 Jan;20(1):37-51 [580123.001]
  • [Cites] Scand J Haematol. 1978 Nov;21(5):379-89 [310576.001]
  • [Cites] Blood. 1979 Apr;53(4):594-603 [106861.001]
  • [Cites] Scand J Haematol. 1980 Feb;24(2):169-73 [7375818.001]
  • [Cites] Leuk Res. 1983;7(1):1-10 [6834882.001]
  • [Cites] Br J Haematol. 1986 Mar;62(3):567-75 [3954968.001]
  • [Cites] Cancer. 1987 Dec 1;60(11):2712-6 [3677006.001]
  • [Cites] Pharmacol Ther. 1991;49(3):239-68 [1675805.001]
  • [Cites] Blood. 1991 Oct 15;78(8):1901-14 [1912574.001]
  • [Cites] Curr Top Microbiol Immunol. 1992;182:303-11 [1490369.001]
  • [Cites] Histopathology. 1994 May;24(5):445-51 [8088716.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jan 20;95(2):708-13 [9435257.001]
  • [Cites] J Clin Invest. 1998 Oct 15;102(8):1515-25 [9788964.001]
  • [Cites] J Clin Oncol. 1999 Jan;17(1):399-408 [10458259.001]
  • [Cites] Blood. 1999 Sep 15;94(6):1840-7 [10477712.001]
  • [Cites] N Engl J Med. 2000 Dec 28;343(26):1910-6 [11136261.001]
  • (PMID = 15711642.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA087956; United States / NCI NIH HHS / CA / R01 CA81554; United States / NCRR NIH HHS / RR / M01 RR018535; United States / NCI NIH HHS / CA / R01 CA081554; United States / NCI NIH HHS / CA / R01 CA87956
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 059QF0KO0R / Water; 9007-49-2 / DNA; AR09D82C7G / Deuterium
  • [Other-IDs] NLM/ PMC548318
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4. Adams H, Schmid P, Dirnhofer S, Tzankov A: Cytokeratin expression in hematological neoplasms: a tissue microarray study on 866 lymphoma and leukemia cases. Pathol Res Pract; 2008;204(8):569-73
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  • [Title] Cytokeratin expression in hematological neoplasms: a tissue microarray study on 866 lymphoma and leukemia cases.
  • Using tissue microarray technology, we tested 1059 lymphoma and acute leukemia cases, covering the most common disease entities, for aberrant CK expression, using CK22.
  • In total, 866 of the arrayed cases were evaluable (80%), and 13 positive cases (1.5%) were found: 1 out of 230 Hodgkin lymphomas (0.4%), 1 plasma cell myeloma, 2 out of 326 diffuse large B-cell lymphomas (0.6%), 5 out of 18 mantle cell lymphomas (26%), 3 out of 70 small cell lymphomas/chronic lymphocytic leukemias (4%) and 1 out of 27 peripheral T-cell lymphomas, not otherwise specified (4%).
  • All CK22-positive cases, except for one mantle cell lymphoma, expressed the specific simple epithelial CK8 but not the basal/stratified epithelial CK5/6.
  • Aberrant CK expression can be encountered in a small subset of otherwise characteristic B- and T-cell lymphomas, but not in acute leukemias, which should be considered in difficult differential diagnostic settings.
  • [MeSH-major] Keratins / analysis. Leukemia / metabolism. Lymphoma / chemistry. Tissue Array Analysis

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  • (PMID = 18436389.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Germany
  • [Chemical-registry-number] 68238-35-7 / Keratins
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5. Wiemels JL, Kang M, Chang JS, Zheng L, Kouyoumji C, Zhang L, Smith MT, Scelo G, Metayer C, Buffler P, Wiencke JK: Backtracking RAS mutations in high hyperdiploid childhood acute lymphoblastic leukemia. Blood Cells Mol Dis; 2010 Oct 15;45(3):186-91
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  • [Title] Backtracking RAS mutations in high hyperdiploid childhood acute lymphoblastic leukemia.
  • High hyperdiploidy is the single largest subtype of childhood acute lymphoblastic leukemia (ALL) and is defined by the presence of 51-68 chromosomes in a karyotype.
  • We screened for RAS mutations among 517 acute childhood leukemias (including 437 lymphocytic, of which 393 were B-cell subtypes) and found mutations in 30% of high hyperdiploids compared to only 10% of leukemias of other subtypes (P<0.0001).
  • While RAS mutations were previously associated with prior chemical exposures in childhood and adult leukemias, in this study RAS-mutated cases were not significantly associated with parental smoking when compared to study controls.
  • IGH rearrangements were backtracked in three RAS-positive patients (which were negative for KRAS mutation at birth) and found to be evident before birth, confirming a prenatal origin for the leukemia clone.
  • We posit a natural history for hyperdiploid leukemia in which prenatal mitotic catastrophe is followed by a postnatal RAS mutation to produce the leukemic cell phenotype.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • [Cites] N Engl J Med. 2006 Oct 12;355(15):1572-82 [17035650.001]
  • [Cites] Leuk Res. 2006 Sep;30(9):1085-9 [16533526.001]
  • [Cites] Haematologica. 2007 Nov;92(11):1565-8 [18024407.001]
  • [Cites] Cancer Res. 2008 Aug 15;68(16):6803-9 [18701506.001]
  • [Cites] Leukemia. 2008 Sep;22(9):1692-7 [18548099.001]
  • [Cites] Radiat Prot Dosimetry. 2008;132(2):212-9 [18940823.001]
  • [Cites] Leukemia. 2010 May;24(5):924-31 [20237506.001]
  • [Cites] Clin Chem. 2000 May;46(5):620-4 [10794742.001]
  • [Cites] Blood. 2000 Jul 1;96(1):264-8 [10891460.001]
  • [Cites] Blood. 2002 Apr 15;99(8):2992-6 [11929791.001]
  • [Cites] Br J Cancer. 2002 May 6;86(9):1419-24 [11986774.001]
  • [Cites] Blood. 2002 Jul 1;100(1):347-9 [12070048.001]
  • [Cites] Environ Health Perspect. 2002 Sep;110(9):955-60 [12204832.001]
  • [Cites] Genes Chromosomes Cancer. 2004 May;40(1):38-43 [15034866.001]
  • [Cites] Leukemia. 2004 Apr;18(4):685-92 [14990973.001]
  • [Cites] Blood. 2004 May 1;103(9):3544-6 [14670924.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 Jul;13(7):1230-5 [15247135.001]
  • [Cites] Blood. 1992 Jul 1;80(1):203-8 [1351763.001]
  • [Cites] Leukemia. 1993 Mar;7(3):349-60 [8445941.001]
  • [Cites] Leukemia. 1996 Feb;10(2):213-24 [8637229.001]
  • [Cites] Genes Chromosomes Cancer. 1996 May;16(1):40-5 [9162196.001]
  • [Cites] Leukemia. 2005 Mar;19(3):415-9 [15674422.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Oct;44(2):113-22 [15942938.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Mar;15(3):578-81 [16537719.001]
  • [Cites] Am J Epidemiol. 2006 Jun 15;163(12):1091-100 [16597704.001]
  • [Cites] Genes Chromosomes Cancer. 2008 Jan;47(1):26-33 [17910045.001]
  • (PMID = 20688547.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P42-ES04705; United States / NCI NIH HHS / CA / R01 CA089032; United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NCI NIH HHS / CA / R25 CA112355; United States / NCI NIH HHS / CA / R25-CA112355; United States / NIEHS NIH HHS / ES / R01-ES09137; United States / NIEHS NIH HHS / ES / P01 ES018172; United States / NCI NIH HHS / CA / R01-CA089032; United States / NIEHS NIH HHS / ES / P01-ES018172; United States / NIEHS NIH HHS / ES / R01 ES009137
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS224426; NLM/ PMC2943008
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6. Tamura K, Arai H, Ueno E, Saito C, Yagihara H, Isotani M, Ono K, Washizu T, Bonkobara M: Comparison of dendritic cell-mediated immune responses among canine malignant cells. J Vet Med Sci; 2007 Sep;69(9):925-30
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  • [Title] Comparison of dendritic cell-mediated immune responses among canine malignant cells.
  • Dendritic cell (DC) vaccination is one of the most attractive immunotherapies for malignancies in dogs.
  • To examine the differences in DC-mediated immune responses from different types of malignancies in dogs, we vaccinated dogs using autologous DCs pulsed with keyhole limpet hemocyanin (KLH) and cell lysate prepared from squamous cell carcinoma SCC2/88 (SCC-KLH-DC), histiocytic sarcoma CHS-5 (CHS-KLH-DC), or B cell leukemia GL-1 (GL-KLH-DC) in vitro.
  • By contrast, neither CD8 nor CD4 T cell infiltration was found at the DTH challenge site in the dogs vaccinated with CHS-KLH-DC or GL-KLH-DC.
  • These findings may reflect that the efficacy of immune induction by DC vaccination varies among tumor types and that immune responses could be inducible in squamous cell carcinoma.
  • Our results encouraged further investigation of therapeutic vaccination for dogs with advanced squamous cell carcinoma in clinical trials.

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  • (PMID = 17917377.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cancer Vaccines
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7. Chiron D, Bekeredjian-Ding I, Pellat-Deceunynck C, Bataille R, Jego G: Toll-like receptors: lessons to learn from normal and malignant human B cells. Blood; 2008 Sep 15;112(6):2205-13
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  • These encounters promote plasma cell differentiation and antibody production.
  • In hematologic malignancies, cells often retain B cell-specific receptors and associated functions.
  • Among these, TLRs are currently exploited to target different subclasses of B-cell leukemia, and TLR agonists are currently being evaluated in clinical trials.
  • However, accumulating evidence suggests that endogenous TLR ligands or chronic infections promote tumor growth, thus providing a need for further investigations to decipher the exact function of TLRs in the B-cell lineage and in neoplastic B cells.
  • [MeSH-major] B-Lymphocytes / immunology. Toll-Like Receptors / immunology
  • [MeSH-minor] Antibody Formation. Humans. Leukemia, B-Cell / pathology. Ligands. Lymphoma, B-Cell / pathology

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  • [Cites] Blood. 2005 Feb 15;105(4):1614-21 [15507523.001]
  • [Cites] J Leukoc Biol. 2005 Mar;77(3):378-87 [15582984.001]
  • [Cites] Clin Cancer Res. 2005 Feb 15;11(4):1490-9 [15746051.001]
  • [Cites] J Immunol. 2005 Apr 1;174(7):4043-50 [15778362.001]
  • [Cites] Immunol Rev. 2005 Apr;204:27-42 [15790348.001]
  • [Cites] Nat Rev Cancer. 2005 Apr;5(4):263-74 [15776005.001]
  • [Cites] Leukemia. 2006 Jun;20(6):1138-44 [16617319.001]
  • [Cites] Leukemia. 2006 Jun;20(6):1130-7 [16628189.001]
  • [Cites] Immunology. 2006 Aug;118(4):539-48 [16780564.001]
  • [Cites] Blood. 2006 Sep 15;108(6):2020-8 [16728703.001]
  • [Cites] Clin Immunol. 2006 Sep;120(3):272-84 [16766226.001]
  • [Cites] Blood. 2006 Oct 15;108(8):2655-61 [16763205.001]
  • [Cites] Nat Rev Immunol. 2006 Nov;6(11):823-35 [17063184.001]
  • [Cites] Cancer Res. 2006 Nov 1;66(21):10233-7 [17079438.001]
  • [Cites] Haematologica. 2006 Dec;91(12):1697-700 [17145609.001]
  • [Cites] Blood. 2006 Dec 15;108(13):4071-7 [16917008.001]
  • [Cites] Nat Med. 2007 Sep;13(9):1050-9 [17704786.001]
  • [Cites] PLoS One. 2007;2(9):e863 [17848994.001]
  • [Cites] Immunol Rev. 2007 Dec;220:225-36 [17979850.001]
  • [Cites] Immunol Rev. 2007 Dec;220:251-69 [17979852.001]
  • [Cites] J Exp Med. 2007 Dec 24;204(13):3095-101 [18039950.001]
  • [Cites] Oncogene. 2008 Jan 7;27(2):161-7 [18176597.001]
  • [Cites] Mol Ther. 2008 Feb;16(2):269-79 [18071334.001]
  • [Cites] Eur J Immunol. 2008 Feb;38(2):400-9 [18228247.001]
  • [Cites] J Immunol. 2008 Mar 15;180(6):3797-806 [18322186.001]
  • [Cites] Immunobiology. 2008;213(3-4):205-24 [18406368.001]
  • [Cites] Blood. 2005 May 1;105(9):3641-7 [15650062.001]
  • [Cites] Leuk Lymphoma. 2005 Jun;46(6):935-9 [16019542.001]
  • [Cites] Science. 2005 Aug 26;309(5739):1380-4 [16123302.001]
  • [Cites] Cancer Res. 2005 Sep 15;65(18):8479-86 [16166328.001]
  • [Cites] Nature. 2005 Nov 17;438(7066):364-8 [16292312.001]
  • [Cites] Br J Haematol. 2006 Feb;132(4):452-8 [16412017.001]
  • [Cites] Leukemia. 2006 Feb;20(2):286-95 [16341037.001]
  • [Cites] J Exp Med. 2006 Feb 20;203(2):413-24 [16461338.001]
  • [Cites] Cell. 2006 Feb 24;124(4):783-801 [16497588.001]
  • [Cites] Blood. 2006 Mar 15;107(6):2409-14 [16304057.001]
  • [Cites] J Cell Physiol. 2006 May;207(2):480-90 [16419037.001]
  • [Cites] J Immunol. 2006 Mar 15;176(6):3830-9 [16517754.001]
  • [Cites] Eur J Immunol. 2006 Apr;36(4):810-6 [16541472.001]
  • [Cites] Cell Death Differ. 2006 May;13(5):816-25 [16410796.001]
  • [Cites] Blood. 2006 May 1;107(9):3639-46 [16403912.001]
  • [Cites] Nature. 2006 May 18;441(7091):E4; discussion E4 [16710369.001]
  • [Cites] Blood. 2000 Feb 1;95(3):999-1006 [10648415.001]
  • [Cites] Exp Hematol. 2000 May;28(5):558-68 [10812246.001]
  • [Cites] Virology. 2000 Dec 5;278(1):86-94 [11112484.001]
  • [Cites] J Leukoc Biol. 2001 Jan;69(1):81-8 [11200072.001]
  • [Cites] J Immunol. 2002 Jan 15;168(2):554-61 [11777946.001]
  • [Cites] J Immunol. 2002 May 1;168(9):4531-7 [11970999.001]
  • [Cites] J Leukoc Biol. 2002 Jul;72(1):83-92 [12101266.001]
  • [Cites] Science. 2002 Dec 13;298(5601):2199-202 [12481138.001]
  • [Cites] Leukemia. 2007 Jan;21(1):110-20 [17024114.001]
  • [Cites] Leukemia. 2007 Jan;21(1):53-60 [17066089.001]
  • [Cites] Science. 2006 Dec 22;314(5807):1936-8 [17185603.001]
  • [Cites] Cancer Res. 2007 Feb 15;67(4):1823-31 [17308125.001]
  • [Cites] Blood. 2007 Mar 1;109(5):2198-201 [17082317.001]
  • [Cites] J Immunol. 2007 Mar 1;178(5):2803-12 [17312124.001]
  • [Cites] J Immunol. 2007 Mar 15;178(6):3593-601 [17339456.001]
  • [Cites] Nat Immunol. 2007 Apr;8(4):419-29 [17322888.001]
  • [Cites] J Immunol. 2007 Apr 15;178(8):5124-31 [17404295.001]
  • [Cites] Nat Immunol. 2007 May;8(5):487-96 [17417641.001]
  • [Cites] J Immunol. 2007 May 1;178(9):5429-33 [17442923.001]
  • [Cites] J Immunol. 2007 Jun 15;178(12):7779-86 [17548615.001]
  • [Cites] Blood. 2007 Jul 1;110(1):296-304 [17363736.001]
  • [Cites] J Leukoc Biol. 2007 Aug;82(2):265-71 [17470533.001]
  • [Cites] Immunity. 2007 Jul;27(1):64-75 [17658280.001]
  • [Cites] Eur J Immunol. 2007 Aug;37(8):2205-13 [17621369.001]
  • [Cites] J Exp Med. 2003 Feb 17;197(4):403-11 [12591899.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4500-4 [12560217.001]
  • [Cites] Blood. 2003 Aug 1;102(3):956-63 [12689944.001]
  • [Cites] Immunity. 2003 Aug;19(2):225-34 [12932356.001]
  • [Cites] Immunol Rev. 2004 Jun;199:227-50 [15233738.001]
  • [Cites] J Leukoc Biol. 2004 Sep;76(3):514-9 [15178705.001]
  • [Cites] Nat Rev Immunol. 2004 Sep;4(9):665-74 [15343366.001]
  • [Cites] J Immunol. 2004 Oct 1;173(7):4479-91 [15383579.001]
  • [Cites] Blood. 1994 Nov 15;84(10):3457-64 [7949100.001]
  • [Cites] Clin Immunol Immunopathol. 1995 Apr;75(1):26-32 [7882591.001]
  • [Cites] J Exp Med. 1997 Sep 15;186(6):931-40 [9294147.001]
  • [Cites] Leuk Lymphoma. 1999 Mar;33(1-2):147-53 [10194132.001]
  • [Cites] Matrix Biol. 2004 Oct;23(6):341-52 [15533755.001]
  • [Cites] Curr Dir Autoimmun. 2005;8:124-39 [15564719.001]
  • (PMID = 18591383.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ligands; 0 / Toll-Like Receptors
  • [Number-of-references] 80
  • [Other-IDs] NLM/ PMC2532798
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8. Long H, Tang SQ, Zhang XF: [Preliminary study on graft versus leukemia effect of camouflage of mice bone marrow transplantation with methoxy polyethylene glycol modification]. Zhonghua Er Ke Za Zhi; 2005 May;43(5):377-80
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  • [Title] [Preliminary study on graft versus leukemia effect of camouflage of mice bone marrow transplantation with methoxy polyethylene glycol modification].
  • OBJECTIVE: To study if methoxy polyethylene glycol modification (mPEG) affects grafts versus leukemia (GVL) when donor bone marrow mononuclear cells are camouflaged with mPEG in murine bone marrow transplantation (BMT).
  • The bone marrow cells (1 x 10(7)) were mixed with the spleen cells (1 x 10(7)), which were camouflaged or not camouflaged with mPEG, were transplanted into irradiated leukemia mice in C and D groups.
  • The mice in irradiated group (group B) with leukemia cell died of leukemia.
  • The average survival time of group D (with mPEG modification) was 24.2 days, which was longer than that of the other groups (P < 0.05), and the survival rate of group D (27%) was significantly higher than that of the others (P < 0.05), 11 mice (11/15) died of leukemia and the others were still alive.
  • [MeSH-major] Bone Marrow Transplantation. Graft vs Leukemia Effect. Polyethylene Glycols / pharmacology
  • [MeSH-minor] Animals. Female. Graft vs Host Disease / prevention & control. Male. Mice. Mice, Inbred BALB C

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  • (PMID = 15924758.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 30IQX730WE / Polyethylene Glycols; 9004-74-4 / monomethoxypolyethylene glycol
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9. Chiorazzi N: Cell proliferation and death: forgotten features of chronic lymphocytic leukemia B cells. Best Pract Res Clin Haematol; 2007 Sep;20(3):399-413
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  • [Title] Cell proliferation and death: forgotten features of chronic lymphocytic leukemia B cells.
  • Chronic lymphocytic leukemia (CLL) results from an accumulation of abnormal B cells due to an imbalance between birth and death rates such that the former exceeds the latter.
  • CLL has long been considered a disease in which cell accumulation results from decreased death, due to a genetic defect, with minimal birth of the leukemic clone.
  • CLL cells appeared as resting lymphocytes by light microscopy and responded poorly to mitogens (primarily T-cell mitogens)--at a time when T- and B-cell discrimination was not well appreciated.
  • However, recent studies using more sophisticated measures suggest that the initial characterization of CLL biology needs re-evaluation.
  • Using a safe, non-radioactive in-vivo labeling method that permits the determination of CLL-cell birth rates, we have directly documented that a small fraction of the clone (approximately 0.1-1.75%), i.e., between approximately 1x10(9) and 1x10(12) cells are born each day in all patients studied.
  • Thus the dynamic interplay between birth and death that characterizes other leukemias and lymphomas applies to CLL.
  • Therefore, CLL is a disease of both proliferation and accumulation in which a homeostatic balance exists in patients with stable lymphocyte counts or an imbalance exists in patients with rising lymphocyte counts.
  • [MeSH-major] B-Lymphocytes / pathology. Cell Death / physiology. Cell Proliferation. Leukemia, Lymphocytic, Chronic, B-Cell / pathology

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  • (PMID = 17707829.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR018535; United States / NCI NIH HHS / CA / R01 CA81554; United States / NCI NIH HHS / CA / R01 CA87956
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD
  • [Number-of-references] 83
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10. Chen WC, Completo GC, Sigal DS, Crocker PR, Saven A, Paulson JC: In vivo targeting of B-cell lymphoma with glycan ligands of CD22. Blood; 2010 Jun 10;115(23):4778-86
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  • [Title] In vivo targeting of B-cell lymphoma with glycan ligands of CD22.
  • Antibody-mediated cell depletion therapy has proven to provide significant clinical benefit in treatment of lymphomas and leukemias, driving the development of improved therapies with novel mechanisms of cell killing.
  • A current clinical target for B-cell lymphoma is CD22, a B-cell-specific member of the sialic acid binding Ig-like lectin (siglec) family that recognizes alpha2-6-linked sialylated glycans as ligands.
  • The targeted liposomes are actively bound and endocytosed by CD22 on B cells, and significantly extend life in a xenograft model of human B-cell lymphoma.
  • Moreover, they bind and kill malignant B cells from peripheral blood samples obtained from patients with hairy cell leukemia, marginal zone lymphoma, and chronic lymphocytic leukemia.
  • The results demonstrate the potential for using a carbohydrate recognition-based approach for efficiently targeting B cells in vivo that can offer improved treatment options for patients with B-cell malignancies.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Doxorubicin / pharmacokinetics. Drug Delivery Systems / methods. Lymphoma, B-Cell / drug therapy. Polysaccharides / agonists. Sialic Acid Binding Ig-like Lectin 2

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  • [Cites] Annu Rev Med. 2008;59:237-50 [18186705.001]
  • [Cites] Nat Rev Drug Discov. 2005 Feb;4(2):145-60 [15688077.001]
  • [Cites] J Control Release. 2008 Feb 18;126(1):50-8 [18068849.001]
  • [Cites] Immunology. 2008 Mar;123(3):314-25 [18067554.001]
  • [Cites] PLoS One. 2008;3(4):e1967 [18414664.001]
  • [Cites] J Am Chem Soc. 2008 May 28;130(21):6680-1 [18452295.001]
  • [Cites] Clin Lymphoma Myeloma. 2008 Feb;8(1):21-32 [18501085.001]
  • [Cites] J Am Chem Soc. 2008 Jun 18;130(24):7736-45 [18505252.001]
  • [Cites] Exp Hematol. 2008 Jul;36(7):755-68 [18565392.001]
  • [Cites] Cancer Res. 2008 Aug 1;68(15):6300-5 [18676854.001]
  • [Cites] PLoS One. 2009;4(1):e4171 [19137069.001]
  • [Cites] Curr Pharm Des. 2009;15(2):153-72 [19149610.001]
  • [Cites] Trends Pharmacol Sci. 2009 May;30(5):240-8 [19359050.001]
  • [Cites] Exp Mol Pathol. 2009 Jun;86(3):215-23 [19186176.001]
  • [Cites] Med Res Rev. 2010 Mar;30(2):270-89 [19626595.001]
  • [Cites] Cancer Lett. 2008 Feb 18;260(1-2):137-45 [18077084.001]
  • [Cites] Curr Opin Chem Biol. 2004 Dec;8(6):617-25 [15556405.001]
  • [Cites] Blood. 1994 Aug 1;84(3):702-7 [7519071.001]
  • [Cites] Clin Cancer Res. 2000 Apr;6(4):1476-87 [10778980.001]
  • [Cites] Blood. 2001 Jan 1;97(1):288-96 [11133773.001]
  • [Cites] Blood. 2001 Jan 15;97(2):528-35 [11154233.001]
  • [Cites] Biochemistry. 2001 May 22;40(20):5964-74 [11352731.001]
  • [Cites] N Engl J Med. 2001 Jul 26;345(4):241-7 [11474661.001]
  • [Cites] Med Oncol. 2002;19(1):55-8 [12025891.001]
  • [Cites] Anticancer Res. 2002 May-Jun;22(3):1845-8 [12168880.001]
  • [Cites] J Am Chem Soc. 2002 Dec 18;124(50):14922-33 [12475334.001]
  • [Cites] Structure. 2003 May;11(5):557-67 [12737821.001]
  • [Cites] Lancet. 2003 Jul 12;362(9378):139-46 [12867117.001]
  • [Cites] Methods Enzymol. 2003;373:3-16 [14714393.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 20;101(16):6104-9 [15079087.001]
  • [Cites] J Clin Oncol. 2004 Jul 1;22(13):2662-70 [15226333.001]
  • [Cites] Am J Clin Pathol. 2005 Jun;123(6):826-32 [15899772.001]
  • [Cites] Clin Cancer Res. 2006 Jan 1;12(1):242-9 [16397048.001]
  • [Cites] Mol Cell Biol. 2006 Feb;26(4):1549-57 [16449664.001]
  • [Cites] Mol Cancer Ther. 2006 Apr;5(4):818-24 [16648551.001]
  • [Cites] J Immunol. 2006 Sep 1;177(5):2994-3003 [16920935.001]
  • [Cites] J Immunol. 2006 Sep 1;177(5):3063-73 [16920943.001]
  • [Cites] Cancer Res. 2006 Sep 1;66(17):8740-8 [16951190.001]
  • [Cites] Nat Rev Immunol. 2007 Apr;7(4):255-66 [17380156.001]
  • [Cites] Mol Cell Biol. 2007 Aug;27(16):5699-710 [17562860.001]
  • [Cites] Int J Nanomedicine. 2006;1(3):229-39 [17717964.001]
  • [Cites] Leukemia. 2007 Nov;21(11):2240-5 [17657218.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2007;:233-42 [18024635.001]
  • [Cites] Exp Eye Res. 2008 Jan;86(1):138-49 [18036523.001]
  • [Cites] Int J Cancer. 1990 Mar 15;45(3):481-5 [2307538.001]
  • [Cites] Blood. 1993 Aug 15;82(4):1277-87 [7688993.001]
  • [Cites] Biochim Biophys Acta. 1993 Sep 19;1151(2):201-15 [8373796.001]
  • [CommentIn] Expert Rev Vaccines. 2010 Nov;9(11):1251-6 [21087105.001]
  • [CommentIn] Blood. 2010 Jun 10;115(23):4626-7 [20538811.001]
  • [ErratumIn] Blood. 2011 May 19;117(20):5551
  • (PMID = 20181615.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA138891; United Kingdom / Wellcome Trust / / 081882; United States / NIAID NIH HHS / AI / R01 AI050143; United States / NIAID NIH HHS / AI / R01-AI050143; United States / NIGMS NIH HHS / GM / R01 GM060938; United States / NIGMS NIH HHS / GM / R01-GM060938
  • [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 / Antibiotics, Antineoplastic; 0 / CD22 protein, human; 0 / Ligands; 0 / Liposomes; 0 / Polysaccharides; 0 / Sialic Acid Binding Ig-like Lectin 2; 80168379AG / Doxorubicin
  • [Other-IDs] NLM/ PMC2890185
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11. de Totero D, Meazza R, Zupo S, Cutrona G, Matis S, Colombo M, Balleari E, Pierri I, Fabbi M, Capaia M, Azzarone B, Gobbi M, Ferrarini M, Ferrini S: Interleukin-21 receptor (IL-21R) is up-regulated by CD40 triggering and mediates proapoptotic signals in chronic lymphocytic leukemia B cells. Blood; 2006 May 1;107(9):3708-15
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  • [Title] Interleukin-21 receptor (IL-21R) is up-regulated by CD40 triggering and mediates proapoptotic signals in chronic lymphocytic leukemia B cells.
  • Here we demonstrate that surface IL-21 receptor (R) is expressed at variable levels by chronic lymphocytic leukemia (CLL) B cells freshly isolated from 33 different patients.
  • IL-21R expression was up-regulated following cell stimulation via surface CD40.
  • IL-21 signaling failed to stimulate CLL B-cell proliferation, but induced their apoptosis.
  • The present findings thus provide a set of new mechanisms involved in the balance between cell-survival and apoptotic signals in CLL B cells.
  • [MeSH-major] Antigens, CD40 / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Receptors, Interleukin / genetics

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  • (PMID = 16391014.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / DNA, Neoplasm; 0 / IL21R protein, human; 0 / Il21r protein, mouse; 0 / Interleukin-21 Receptor alpha Subunit; 0 / JAK3 protein, human; 0 / Jak1 protein, mouse; 0 / Receptors, Interleukin; 0 / Receptors, Interleukin-21; 0 / STAT1 Transcription Factor; 0 / STAT1 protein, human; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / STAT5 Transcription Factor; EC 2.7.010.2 / JAK1 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Jak3 protein, mouse; EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / Janus Kinase 3
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12. Malavasi F, Deaglio S, Funaro A, Ferrero E, Horenstein AL, Ortolan E, Vaisitti T, Aydin S: Evolution and function of the ADP ribosyl cyclase/CD38 gene family in physiology and pathology. Physiol Rev; 2008 Jul;88(3):841-86
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  • These reaction products are essential for the regulation of intracellular Ca(2+), the most ancient and universal cell signaling system.
  • The entire family of enzymes controls complex processes, including egg fertilization, cell activation and proliferation, muscle contraction, hormone secretion, and immune responses.
  • CD38 is a powerful disease marker for human leukemias and myelomas, is directly involved in the pathogenesis and outcome of human immunodeficiency virus infection and chronic lymphocytic leukemia, and controls insulin release and the development of diabetes.
  • [MeSH-minor] Animals. Antibodies, Monoclonal / therapeutic use. Disease Models, Animal. GPI-Linked Proteins. Humans. Immunoconjugates / therapeutic use. Immunotherapy / methods. Ligands. Models, Animal. Models, Molecular. Phylogeny. Protein Conformation. Signal Transduction / immunology. Tissue Distribution

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  • (PMID = 18626062.001).
  • [ISSN] 0031-9333
  • [Journal-full-title] Physiological reviews
  • [ISO-abbreviation] Physiol. Rev.
  • [Language] eng
  • [Grant] Italy / Telethon / / GTF06004
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / GPI-Linked Proteins; 0 / Immunoconjugates; 0 / Ligands; EC 3.2.2.5 / ADP-ribosyl Cyclase; EC 3.2.2.5 / ADP-ribosyl cyclase 2; EC 3.2.2.5 / Antigens, CD38
  • [Number-of-references] 367
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13. Calin GA, Liu CG, Ferracin M, Hyslop T, Spizzo R, Sevignani C, Fabbri M, Cimmino A, Lee EJ, Wojcik SE, Shimizu M, Tili E, Rossi S, Taccioli C, Pichiorri F, Liu X, Zupo S, Herlea V, Gramantieri L, Lanza G, Alder H, Rassenti L, Volinia S, Schmittgen TD, Kipps TJ, Negrini M, Croce CM: Ultraconserved regions encoding ncRNAs are altered in human leukemias and carcinomas. Cancer Cell; 2007 Sep;12(3):215-29
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  • [Title] Ultraconserved regions encoding ncRNAs are altered in human leukemias and carcinomas.
  • Genome-wide profiling revealed that UCRs have distinct signatures in human leukemias and carcinomas.
  • We identified certain UCRs whose expression may be regulated by microRNAs abnormally expressed in human chronic lymphocytic leukemia, and we proved that the inhibition of an overexpressed UCR induces apoptosis in colon cancer cells.
  • [MeSH-major] Carcinoma / genetics. Leukemia / genetics. RNA, Untranslated / chemistry

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  • (PMID = 17785203.001).
  • [ISSN] 1535-6108
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ DQ644536/ DQ644537/ DQ644538
  • [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 / MicroRNAs; 0 / RNA, Untranslated
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14. Franco G, Palazzolo R, Liardo E, Tripodo C, Mancuso S: T cell large granular lymphocytic leukemia in association with Sjögren's syndrome. Acta Haematol; 2010;124(1):5-8
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  • [Title] T cell large granular lymphocytic leukemia in association with Sjögren's syndrome.
  • T cell large granular lymphocytic (LGL) leukemia is a rare condition accounting for 2-3% of all mature lymphoid leukemias.
  • Hematological assessment revealed the presence of a T cell LGL leukemia.
  • At the time of T cell LGL leukemia diagnosis, the patient developed xerophthalmia and xerostomia, and a diagnosis of Sjögren's syndrome was made following salivary gland biopsy.
  • The finding of large granular lymphocytes in the context of autoimmune disorders is well-known, though it often occurs with rheumatoid arthritis or in association with a positive autoantibody titer in the absence of an overt clinical picture.
  • The concomitant presentation of T cell LGL leukemia with Sjögren's syndrome is a rare event which is worth reporting.
  • [MeSH-major] Leukemia, Large Granular Lymphocytic / complications. Sjogren's Syndrome / complications

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  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • (PMID = 20501987.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
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15. Romano S, Mallardo M, Chiurazzi F, Bisogni R, D'Angelillo A, Liuzzi R, Compare G, Romano MF: The effect of FK506 on transforming growth factor beta signaling and apoptosis in chronic lymphocytic leukemia B cells. Haematologica; 2008 Jul;93(7):1039-48
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  • [Title] The effect of FK506 on transforming growth factor beta signaling and apoptosis in chronic lymphocytic leukemia B cells.
  • BACKGROUND: Loss of response to transforming growth factor-beta (TGF-beta ) is thought to contribute to the progression of chronic lymphocytic leukemia.
  • Recent findings of over-activation of the TGF-beta signal in FKBP12-knockout mouse prompted us to investigate whether FK506, the canonical ligand of FKBP, can activate the TGF-beta signal in chronic lymphocytic leukemia.
  • DESIGN AND METHODS: We studied 62 chronic lymphocytic leukemia samples from patients with Rai/Binet stage 0 to 4 disease.
  • RESULTS: Twenty-two out of 62 chronic lymphocytic leukemia samples were sensitive to TGF-beta-induced apoptosis.
  • A loss of mitochondrial membrane potential preceded caspase activation and cell death.
  • CONCLUSIONS: Our study shows that most chronic lymphocytic leukemia cells escape the homeostatic control of TGF-beta and that FK506 restores the TGF-beta signal in a proportion of non-responsive samples.
  • We demonstrated that FK506 activates TGF-beta receptor I kinase activity in chronic lymphocytic leukemia, which transduces apoptosis by a mitochondrial-dependent pathway.
  • [MeSH-major] Apoptosis. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Tacrolimus / pharmacology. Transforming Growth Factor beta / metabolism
  • [MeSH-minor] Disease Progression. Humans. Immunosuppressive Agents / pharmacology. Kinetics. Ligands. Mitochondria / metabolism. Mutation. Proto-Oncogene Proteins c-bcl-2 / metabolism. Signal Transduction. Smad Proteins / metabolism. Tacrolimus Binding Proteins / metabolism. bcl-X Protein / metabolism

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  • (PMID = 18492692.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 0 / Ligands; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Smad Proteins; 0 / Transforming Growth Factor beta; 0 / bcl-X Protein; EC 5.2.1.- / Tacrolimus Binding Proteins; WM0HAQ4WNM / Tacrolimus
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16. Chen YH, Tang YM, Shen HQ, Song H, Yang SL, Shi SW, Qian BQ, Xu WQ, Ning BT: [Targeted killing of the Nalm-6 cells with 2E8-Genistein immunotoxin and its mechanism]. Zhonghua Er Ke Za Zhi; 2009 Jan;47(1):57-61
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  • OBJECTIVE: Leukemia is the most common hematopoietic malignancies in children.
  • Chemotherapy is currently the primary modality of treatment for this fatal disease.
  • Although chemotherapy is very effective in terms of cell killing, severe side effects such as severe infections, intracranial hemorrhage etc. are frequently encountered due to its poor selective damage between normal and malignant cells or tissues.
  • The aim of this study was to investigate the targeting efficacy in vitro with a new clone of anti-human CD19 antibody immunotoxin 2E8-Genistein on B lineage leukemia cell line Nalm-6 cells and its mechanisms in order to provide the evidence of target therapy on B lineage leukemia and lymphoma.
  • Nalm-6, a CD19+ B cell leukemia cell line, was used as target cells, while Molt-3, a CD19-T cell leukemia cell line, was taken as the negative control.
  • Two-color flow cytometry was applied to study the mechanism of cell killing.
  • RESULTS: After 24 hours of culture, 2E8-Genistein showed marked target killing on Nalm-6 cells at nine different concentrations from 20 nmol/L through 100 nmol/L with cell survival rates from (71.8 +/- 7.9)% down to (16.6 +/- 12.9)%, respectively (n = 3), which were all significantly lower than that of control group (100 +/- 13.9)% (P < 0.05).
  • Significant difference was observed between the cell growth curve of Nalm-6 cultured with 100 nmol/L of 2E8-Gen and those of Nalm-6 cultured with medium (blank), PBS (negative control) or the same concentration of pure 2E8 antibody (negative control) groups (F = 152.15, P = 2.15 x 10(-7)), but there was no significant difference among the three control groups (F = 1.51, P = 0.29).
  • When Molt-3 cells were used as target cells, the cell growth curves of Molt-3 cultured with 2E8-Gen (100 nmol/L) and with negative control of blank did not show any significant difference (F = 0.34, P = 0.59).
  • [MeSH-minor] Antigens, CD19. Apoptosis / drug effects. Cell Line, Tumor. Flow Cytometry. Humans. Leukemia, B-Cell / immunology

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  • (PMID = 19573385.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD19; 0 / Immunotoxins; DH2M523P0H / Genistein
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17. Hanson CA, Morice WG: The clinical and laboratory approach to the CD5/CD10 negative B-cell chronic lymphoproliferative leukemias. Am J Hematol; 2008 May;83(5):347-8
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  • [Title] The clinical and laboratory approach to the CD5/CD10 negative B-cell chronic lymphoproliferative leukemias.
  • [MeSH-major] Antigens, CD / analysis. Antigens, Neoplasm / analysis. B-Lymphocyte Subsets / chemistry. Disease Management. Immunophenotyping. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Neoplastic Stem Cells / chemistry

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  • [CommentOn] Am J Hematol. 2008 May;83(5):349-54 [18186522.001]
  • (PMID = 18383327.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm
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18. Foss F: Clinical experience with denileukin diftitox (ONTAK). Semin Oncol; 2006 Feb;33(1 Suppl 3):S11-6
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  • The high-affinity form of this receptor is expressed on activated T lymphocytes, activated B lymphocytes, and activated macrophages.
  • A number of leukemias and lymphomas, including cutaneous T-cell lymphoma, chronic lymphocytic leukemia, and B-cell non-Hodgkin's lymphoma, express a component of the receptor.
  • Ex vivo studies have shown that denileukin diftitox interacts with the high- and intermediate-affinity IL-2 receptor on the cell surface and undergoes internalization.
  • Subsequent cleavage in the endosome releases the diphtheria toxin into the cytosol, which then inhibits cellular protein synthesis, resulting in rapid cell death.
  • This article examines the clinical profile and potential benefits of denileukin diftitox in the treatment of cutaneous T-cell lymphoma and other hematologic disorders.
  • [MeSH-minor] Graft vs Host Disease / drug therapy. Humans. Lymphoma, B-Cell / drug therapy. Lymphoma, T-Cell, Cutaneous / drug therapy. Receptors, Interleukin-2 / metabolism. Recombinant Fusion Proteins / therapeutic use

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  • (PMID = 16516670.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diphtheria Toxin; 0 / Interleukin-2; 0 / Receptors, Interleukin-2; 0 / Recombinant Fusion Proteins; 25E79B5CTM / denileukin diftitox
  • [Number-of-references] 15
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19. Kotani A, Ha D, Schotte D, den Boer ML, Armstrong SA, Lodish HF: A novel mutation in the miR-128b gene reduces miRNA processing and leads to glucocorticoid resistance of MLL-AF4 acute lymphocytic leukemia cells. Cell Cycle; 2010 Mar 15;9(6):1037-42
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  • [Title] A novel mutation in the miR-128b gene reduces miRNA processing and leads to glucocorticoid resistance of MLL-AF4 acute lymphocytic leukemia cells.
  • MLL-AF4 acute lymphocytic leukemia has a poor prognosis, and the mechanisms by which these leukemias develop are not understood despite intensive research based on well-known concepts and methods.

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  • [Cites] Cell. 2005 Jan 14;120(1):15-20 [15652477.001]
  • [Cites] Nature. 2004 Sep 16;431(7006):350-5 [15372042.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Jun 17;331(4):1439-44 [15883035.001]
  • [Cites] Nature. 2005 Jun 9;435(7043):828-33 [15944707.001]
  • [Cites] Nature. 2005 Jun 9;435(7043):834-8 [15944708.001]
  • [Cites] Cell. 2005 Aug 26;122(4):553-63 [16122423.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):14028-33 [16169901.001]
  • [Cites] N Engl J Med. 2005 Oct 27;353(17):1793-801 [16251535.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2257-61 [16461460.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 May 2;103(18):7024-9 [16641092.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6097-104 [16778182.001]
  • [Cites] Cell. 2007 Apr 6;129(1):147-61 [17382377.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Apr 24;104(17):7080-5 [17438277.001]
  • [Cites] Oncogene. 2007 May 17;26(23):3352-63 [17130830.001]
  • [Cites] Lancet. 2007 Jul 21;370(9583):240-50 [17658395.001]
  • [Cites] Cell. 2007 Oct 5;131(1):146-59 [17923094.001]
  • [Cites] Cancer Res. 2007 Oct 15;67(20):9852-61 [17942916.001]
  • [Cites] Blood. 2009 Nov 5;114(19):4169-78 [19749093.001]
  • [Cites] Leukemia. 2003 Apr;17(4):700-6 [12682627.001]
  • [Cites] Genes Chromosomes Cancer. 2004 Feb;39(2):167-9 [14695998.001]
  • [Cites] Science. 2004 Jan 2;303(5654):83-6 [14657504.001]
  • [Cites] Cell. 2004 Jan 23;116(2):281-97 [14744438.001]
  • [Cites] Science. 2004 Apr 23;304(5670):594-6 [15105502.001]
  • [Cites] Leukemia. 2004 Jun;18(6):1064-71 [14990976.001]
  • [Cites] Cancer Res. 2004 Jun 1;64(11):3753-6 [15172979.001]
  • [Cites] Oncogene. 2004 Aug 19;23(37):6237-49 [15221006.001]
  • [Cites] Cell. 2005 Mar 11;120(5):635-47 [15766527.001]
  • (PMID = 20237425.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK068348-05; United States / NIDDK NIH HHS / DK / DK068348-06A1; United States / NIDDK NIH HHS / DK / R56 DK068348-06A1; United States / NIDDK NIH HHS / DK / R01 DK068348-05; United States / NIDDK NIH HHS / DK / R56 DK068348; United States / NIDDK NIH HHS / DK / R01 DK068348
  • [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 / Glucocorticoids; 0 / MIRN128 microRNA, human; 0 / MIRN221 microRNA, human; 0 / MicroRNAs
  • [Other-IDs] NLM/ NIHMS277523; NLM/ PMC3096720
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20. Vallera DA, Brechbiel MW, Burns LJ, Panoskaltsis-Mortari A, Dusenbery KE, Clohisy DR, Vitetta ES: Radioimmunotherapy of CD22-expressing Daudi tumors in nude mice with a 90Y-labeled anti-CD22 monoclonal antibody. Clin Cancer Res; 2005 Nov 1;11(21):7920-8
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  • Labeled RFB4 selectively bound to the CD22(+) Burkitt's lymphoma cell line Daudi, but not to CD22(-) control cells in vitro as compared with a control antibody, and was more significantly bound (P = 0.03) to Daudi solid tumors growing in athymic nude mice.
  • These findings indicate that anti-CD22 radioimmunotherapy with Y22 is highly effective in vivo against CD22-expressing malignancies and may be a useful therapy for drug-refractory B cell leukemia patients.
  • [MeSH-minor] Animals. Antigens, CD19 / biosynthesis. Antigens, CD45 / biosynthesis. Antigens, Differentiation, B-Lymphocyte / chemistry. Bone Marrow / metabolism. Bone Marrow / pathology. Bone Marrow Cells / cytology. Cell Line, Tumor. Female. Flow Cytometry. Humans. Hybridomas / pathology. Mice. Mice, Nude. Protein Binding. Time Factors. Tissue Distribution

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  • (PMID = 16278417.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA36725
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD19; 0 / Antigens, Differentiation, B-Lymphocyte; 0 / Sialic Acid Binding Ig-like Lectin 2; 0 / Yttrium Radioisotopes; EC 3.1.3.48 / Antigens, CD45
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21. O'Malley DP: T-cell large granular leukemia and related proliferations. Am J Clin Pathol; 2007 Jun;127(6):850-9
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  • [Title] T-cell large granular leukemia and related proliferations.
  • Session 9 of the 2005 Society for Hematopathology/European Association for Haematopathology Workshop focused on large granular lymphocyte (LGL) leukemias and related disorders.
  • T-cell LGL (T-LGL) leukemias, discussed herein, account for 2% to 3% of cases of small lymphocytic leukemia.
  • T-LGL diseases cover a heterogeneous spectrum of disorders that include reactive conditions, typically associated with autoimmune disease, to outright leukemia.
  • These disorders are found in older people, with an average age at initial examination of approximately 60 years and a median survival of more than 10 years in T-LGL leukemia.
  • Lymphocytosis, composed of small mature lymphocytes with increased cytoplasm, is common.
  • The spleen and bone marrow are involved in T-LGL leukemia, although morphologic findings may be subtle.
  • Some cases may be due to chronic immune stimulation, with subsequent clonal escape and proliferation of a neoplastic population of lymphocytes.
  • [MeSH-major] Leukemia, Lymphoid / pathology. T-Lymphocytes / pathology

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  • (PMID = 17509982.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 57
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22. Hodge DL, Yang J, Buschman MD, Schaughency PM, Dang H, Bere W, Yang Y, Savan R, Subleski JJ, Yin XM, Loughran TP Jr, Young HA: Interleukin-15 enhances proteasomal degradation of bid in normal lymphocytes: implications for large granular lymphocyte leukemias. Cancer Res; 2009 May 1;69(9):3986-94
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  • [Title] Interleukin-15 enhances proteasomal degradation of bid in normal lymphocytes: implications for large granular lymphocyte leukemias.
  • Large granular lymphocyte (LGL) leukemia is a clonal proliferative disease of T and natural killer (NK) cells.
  • Interleukin (IL)-15 is important for the development and progression of LGL leukemia and is a survival factor for normal NK and T memory cells.
  • Overall, these data provide a novel molecular mechanism for IL-15 control of Bid that potentially links this cytokine to leukemogenesis through targeted proteasome degradation of Bid and offers the possibility that proteasome inhibitors may aid in the treatment of LGL leukemia.

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  • [Cites] Nat Immunol. 2007 Aug;8(8):856-63 [17618288.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):9472-81 [17909057.001]
  • [Cites] J Clin Oncol. 2007 Oct 20;25(30):4813-20 [17947730.001]
  • [Cites] J Cell Biol. 2007 Dec 31;179(7):1453-66 [18166654.001]
  • [Cites] Apoptosis. 2008 Jan;13(1):53-62 [17955375.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2797-805 [18160669.001]
  • [Cites] Med Oncol. 2009;26(2):193-201 [19016012.001]
  • [Cites] J Clin Invest. 1997 Mar 1;99(5):937-43 [9062351.001]
  • [Cites] Cell. 1998 Aug 21;94(4):491-501 [9727492.001]
  • [Cites] Immunity. 1998 Nov;9(5):669-76 [9846488.001]
  • [Cites] Nature. 1999 Aug 26;400(6747):886-91 [10476969.001]
  • [Cites] Int J Hematol. 2004 Oct;80(3):205-9 [15540893.001]
  • [Cites] Mol Cancer Ther. 2005 Mar;4(3):443-9 [15767553.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6294-304 [16024631.001]
  • [Cites] Cell. 2005 Aug 26;122(4):579-91 [16122425.001]
  • [Cites] Cell. 2005 Aug 26;122(4):593-603 [16122426.001]
  • [Cites] Cell. 2006 Mar 24;124(6):1283-98 [16564017.001]
  • [Cites] J Interferon Cytokine Res. 2006 Oct;26(10):706-18 [17032165.001]
  • [Cites] Oncogene. 2007 Feb 26;26(9):1324-37 [17322918.001]
  • [Cites] J Exp Med. 2000 Mar 6;191(5):771-80 [10704459.001]
  • [Cites] Blood. 2000 May 15;95(10):3219-22 [10807792.001]
  • [Cites] J Biol Chem. 2000 Jul 14;275(28):21648-52 [10801801.001]
  • [Cites] J Exp Med. 2001 Jan 15;193(2):219-31 [11208862.001]
  • [Cites] J Immunol. 2001 Jun 15;166(12):7486-95 [11390502.001]
  • [Cites] Nat Cell Biol. 2001 Nov;3(11):973-82 [11715018.001]
  • [Cites] Blood. 2002 Nov 15;100(10):3633-8 [12393617.001]
  • [Cites] Nat Cell Biol. 2002 Nov;4(11):842-9 [12402042.001]
  • [Cites] Immunity. 2002 Nov;17(5):537-47 [12433361.001]
  • [Cites] Immunity. 2002 Nov;17(5):561-73 [12433363.001]
  • [Cites] Genes Dev. 2003 Jan 15;17(2):229-39 [12533511.001]
  • [Cites] Folia Neuropathol. 2002;40(3):151-3 [12572921.001]
  • [Cites] Blood. 2003 Jun 15;101(12):4887-93 [12586624.001]
  • [Cites] Science. 2004 Feb 6;303(5659):844-8 [14704432.001]
  • [Cites] Nat Cell Biol. 2004 May;6(5):443-50 [15077116.001]
  • [Cites] Immunol Invest. 2004 May;33(2):109-42 [15195693.001]
  • [Cites] Immunity. 2004 Sep;21(3):357-66 [15357947.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Mar 15;90(6):2189-93 [8460122.001]
  • [Cites] Science. 1994 May 13;264(5161):965-8 [8178155.001]
  • [Cites] J Exp Med. 1994 Oct 1;180(4):1395-403 [7523571.001]
  • [Cites] Oncogene. 1995 Jul 6;11(1):199-210 [7624128.001]
  • [Cites] Cell Immunol. 1995 Nov;166(1):158-61 [7585976.001]
  • [Cites] Br J Haematol. 1996 Feb;92(2):308-14 [8602990.001]
  • [Cites] Blood. 1997 Jan 1;89(1):201-11 [8978293.001]
  • [Cites] Blood. 1997 Jan 1;89(1):256-60 [8978299.001]
  • [Cites] Nat Med. 1997 Feb;3(2):189-95 [9018238.001]
  • [Cites] J Exp Med. 1997 Feb 3;185(3):499-505 [9053450.001]
  • [Cites] Cell. 2007 Apr 20;129(2):423-33 [17448999.001]
  • (PMID = 19366803.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / N01CO12400; United States / Intramural NIH HHS / / ZIA BC009283-25
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BH3 Interacting Domain Death Agonist Protein; 0 / Bid protein, mouse; 0 / Interleukin-15; 0 / Interleukin-2; 0 / Proteasome Inhibitors; EC 3.4.25.1 / Proteasome Endopeptidase Complex; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  • [Other-IDs] NLM/ NIHMS161038; NLM/ PMC2786937
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23. Kazemi T, Asgarian-Omran H, Memarian A, Shabani M, Sharifian RA, Vossough P, Ansaripour B, Rabbani H, Shokri F: Low representation of Fc receptor-like 1-5 molecules in leukemic cells from Iranian patients with acute lymphoblastic leukemia. Cancer Immunol Immunother; 2009 Jun;58(6):989-96
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  • [Title] Low representation of Fc receptor-like 1-5 molecules in leukemic cells from Iranian patients with acute lymphoblastic leukemia.
  • Recent studies have demonstrated expression of Fc receptor-like (FCRL) molecules, a newly identified family with preferential B-cell lineage expression, in some chronic B-cell leukemias with possible implication for classification and/or targeted immunotherapy.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Cell Surface / genetics. Receptors, Fc / genetics. Receptors, Immunologic / genetics

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  • (PMID = 18802695.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / FCRL2 protein, human; 0 / FCRL4 protein, human; 0 / FCRL5 protein, human; 0 / FCRLA protein, human; 0 / Receptors, Cell Surface; 0 / Receptors, Fc; 0 / Receptors, Immunologic
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24. Reichardt VL, Brossart P: Current status of vaccination therapy for leukemias. Curr Hematol Rep; 2005 Jan;4(1):73-6
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  • [Title] Current status of vaccination therapy for leukemias.
  • Acute and chronic leukemias are common diseases in the clinical practice but few vaccination protocols have found their way to phase I trials in leukemias.
  • Therapeutic vaccination protocols share the goal of inducing or augmenting leukemia-specific immune responses in the tumor-bearing host in order to potentially achieve therapeutical benefit in these otherwise fatal diseases.
  • Major interest has been drawn to the use of dendritic cell (DC-based immunotherapy protocols relying on the unique properties of these most powerful antigen-presenting cells.
  • With the bcr-abl oncogene a target of specific immunotherapy has been determined in chronic myelogenous leukemia (CML), while there is a limited information on leukemia-specific tumor antigens in acute myelogenous and lymphoblastic leukemias.
  • This review will focus on immunotherapy development in acute and chronic leukemias and will discuss published clinical trials in acute myelogenous leukemia (AML), acute lymphoblastic leukemia (ALL), chronic lymphocytic leukemia (CLL) and CML.
  • [MeSH-major] Cancer Vaccines / therapeutic use. Leukemia / therapy. Vaccination
  • [MeSH-minor] Acute Disease. Clinical Trials as Topic. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Treatment Outcome

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  • (PMID = 15610663.001).
  • [ISSN] 1541-0714
  • [Journal-full-title] Current hematology reports
  • [ISO-abbreviation] Curr. Hematol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cancer Vaccines
  • [Number-of-references] 29
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25. Shi Y, White D, He L, Miller RL, Spaner DE: Toll-like receptor-7 tolerizes malignant B cells and enhances killing by cytotoxic agents. Cancer Res; 2007 Feb 15;67(4):1823-31
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  • Using chronic lymphocytic leukemia B cells as a model to facilitate biochemical analysis, the tolerized state was found to be associated with altered receptor components, including down-regulated expression of TLR7 mRNA and decreased levels of interleukin-1 receptor-associated kinase 1.
  • Tolerized chronic lymphocytic leukemia cells were found to be more sensitive to cytotoxic chemotherapeutic agents, in part through altered stress-activated protein kinase signaling pathways.
  • This property of the TLR7-tolerized state may potentially be exploited in the treatment of B cell cancers.
  • [MeSH-major] B-Lymphocytes / drug effects. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Toll-Like Receptor 7 / physiology

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  • (PMID = 17308125.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Imidazoles; 0 / Quinolines; 0 / RNA, Messenger; 0 / S 28690; 0 / TLR7 protein, human; 0 / Toll-Like Receptor 7; 0 / Tumor Necrosis Factor-alpha; 5J49Q6B70F / Vincristine; EC 2.7.11.1 / IRAK1 protein, human; EC 2.7.11.1 / IRAK4 protein, human; EC 2.7.11.1 / Interleukin-1 Receptor-Associated Kinases
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26. Lazaro E, Caubet O, Menard F, Pellegrin JL, Viallard JF: [Large granular lymphocyte leukemia]. Presse Med; 2007 Nov;36(11 Pt 2):1694-700
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  • [Title] [Large granular lymphocyte leukemia].
  • [Transliterated title] Leucémies à grands lymphocytes granuleux.
  • Large granular lymphocyte (LGL) leukemia is a clonal proliferation of cytotoxic cells, either CD3(+) (T-cell) or CD3(-) (natural killer, or NK).
  • T-LGL leukemia is associated with cytopenias and autoimmune diseases and most often has an indolent course and good prognosis.
  • NK-LGL leukemias can be more aggressive.
  • LGL expansion is currently hypothesized to be a virus (Ebstein Barr or human T-cell leukemia viruses) antigen-driven T-cell response that involves disruption of apoptosis.
  • The diagnosis of T-LGL is suggested by flow cytometry and confirmed by T-cell receptor gene rearrangement studies.
  • Clonality is difficult to determine in NK-LGL but use of monoclonal antibodies specific for killer cell immunoglobulin-like receptor (KIR) has improved this process.
  • Treatment is required when T-LGL leukemia is associated with recurrent infections secondary to chronic neutropenia.
  • NK-LGL leukemias may be more aggressive and refractory to conventional therapy.
  • [MeSH-major] Leukemia, Large Granular Lymphocytic

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  • (PMID = 17596907.001).
  • [ISSN] 0755-4982
  • [Journal-full-title] Presse medicale (Paris, France : 1983)
  • [ISO-abbreviation] Presse Med
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 35
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27. Struski S, Helias C, Gervais C, Audhuy B, Zamfir A, Herbrecht R, Lessard M: 13q deletions in B-cell lymphoproliferative disorders: frequent association with translocation. Cancer Genet Cytogenet; 2007 Apr 15;174(2):151-60
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  • [Title] 13q deletions in B-cell lymphoproliferative disorders: frequent association with translocation.
  • The 13q14 deletion is the most frequent abnormality in chronic lymphocytic leukemias/small lymphocytic lymphomas, and this early rearrangement is observed from the start of the disease.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 13. Leukemia, Lymphocytic, Chronic, B-Cell / genetics

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  • (PMID = 17452258.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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28. Steinherz PG, Meyers PA, Steinherz LJ, Jeha S: Clofarabine induced durable complete remission in heavily pretreated adolescents with relapsed and refractory leukemia. J Pediatr Hematol Oncol; 2007 Sep;29(9):656-8
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  • [Title] Clofarabine induced durable complete remission in heavily pretreated adolescents with relapsed and refractory leukemia.
  • Current treatments for relapsed/refractory leukemias are unable to achieve extended remissions in most patients even with multiagent chemotherapy.
  • Clofarabine is a new nucleoside analog that has demonstrated clinical benefit in phase I-II studies, and is currently being studied in children and adults with leukemias and has been approved for the treatment of children with relapsed or refractory acute lymphocytic leukemia.
  • We report the experience of three adolescents, two with acute lymphocytic leukemia in 3rd relapse and one with relapsed/refractory acute myeloid leukemia, who achieved complete remission with clofarabine.
  • [MeSH-major] Adenine Nucleotides / therapeutic use. Arabinonucleosides / therapeutic use. Leukemia, Myeloid / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Female. Humans. Male. Recurrence. Remission Induction

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  • (PMID = 17805046.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Arabinonucleosides; 762RDY0Y2H / clofarabine
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29. Fasseu M, Aplan PD, Chopin M, Boissel N, Bories JC, Soulier J, von Boehmer H, Sigaux F, Regnault A: p16INK4A tumor suppressor gene expression and CD3epsilon deficiency but not pre-TCR deficiency inhibit TAL1-linked T-lineage leukemogenesis. Blood; 2007 Oct 1;110(7):2610-9
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  • Inactivation of the CDKN2 genes that encode the p16(INK4A) and p14(ARF) proteins occurs in the majority of human T-cell acute lymphoblastic leukemias (T-ALLs).
  • In TAL1xLMO1 mice, leukemia develops in 100% of mice at 5 months.
  • We report here that expression of P16(INK4A) in developing TAL1xLMO1 thymocytes blocks leukemogenesis in the majority of the mice, and the leukemias that eventually develop show P16(INK4A) loss of expression.
  • Events related to the T-cell receptor beta selection process are thought to be important for leukemic transformation.

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  • [Cites] EMBO J. 1995 Oct 2;14(19):4641-53 [7588594.001]
  • [Cites] Blood. 2006 Jan 15;107(2):781-5 [16166587.001]
  • [Cites] Mol Cell Biol. 2000 Jun;20(11):3831-42 [10805726.001]
  • [Cites] Blood. 2000 Sep 1;96(5):1906-13 [10961893.001]
  • [Cites] J Virol. 2000 Oct;74(20):9786-91 [11000255.001]
  • [Cites] Leukemia. 2001 Jan;15(1):141-7 [11243382.001]
  • [Cites] Nat Immunol. 2000 Aug;1(2):138-44 [11248806.001]
  • [Cites] Oncogene. 2001 Jun 28;20(29):3897-905 [11439353.001]
  • [Cites] Cancer Res. 2001 Sep 1;61(17):6382-7 [11522630.001]
  • [Cites] J Immunol. 2002 Mar 1;168(5):2325-31 [11859122.001]
  • [Cites] Biochim Biophys Acta. 2002 Mar 14;1602(1):73-87 [11960696.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):451-61 [14706337.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1909-11 [14604958.001]
  • [Cites] Cancer Cell. 2004 Jun;5(6):587-96 [15193261.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Mar;86(6):2031-5 [2467296.001]
  • [Cites] EMBO J. 1990 Feb;9(2):415-24 [2303035.001]
  • [Cites] Science. 1990 Dec 7;250(4986):1426-9 [2255914.001]
  • [Cites] Genes Chromosomes Cancer. 1990 Jan;1(3):194-208 [1964581.001]
  • [Cites] Cell. 1991 Nov 15;67(4):641-4 [1934065.001]
  • [Cites] Mol Cell Biol. 1992 Sep;12(9):4186-96 [1508213.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Dec 1;90(23):11401-5 [8248261.001]
  • [Cites] Eur J Immunol. 1994 Apr;24(4):934-9 [8149963.001]
  • [Cites] Int Immunol. 1994 Jul;6(7):995-1001 [7947468.001]
  • [Cites] Oncogene. 1994 Dec;9(12):3675-81 [7970726.001]
  • [Cites] Blood. 1994 Dec 15;84(12):4038-44 [7994022.001]
  • [Cites] Blood. 1995 Feb 1;85(3):854 [7833489.001]
  • [Cites] Immunity. 1994 Jul;1(4):261-7 [7889413.001]
  • [Cites] Nature. 1995 Jun 29;375(6534):795-8 [7596413.001]
  • [Cites] Oncogene. 1995 Sep 7;11(5):853-62 [7545805.001]
  • [Cites] EMBO J. 1996 Mar 1;15(5):1021-7 [8605871.001]
  • [Cites] Blood. 1996 Mar 15;87(6):2180-6 [8630377.001]
  • [Cites] EMBO J. 1996 Oct 1;15(19):5160-6 [8895560.001]
  • [Cites] Cancer Res. 1997 Mar 1;57(5):832-6 [9041181.001]
  • [Cites] Cell. 1997 Mar 7;88(5):593-602 [9054499.001]
  • [Cites] J Exp Med. 1997 May 5;185(9):1541-7 [9151891.001]
  • [Cites] EMBO J. 1997 May 1;16(9):2408-19 [9171354.001]
  • [Cites] Immunity. 1997 Jun;6(6):703-14 [9208843.001]
  • [Cites] EMBO J. 1997 Jun 2;16(11):3145-57 [9214632.001]
  • [Cites] Blood. 1997 Nov 1;90(9):3720-6 [9345058.001]
  • [Cites] Blood. 2006 Mar 15;107(6):2540-3 [16282337.001]
  • [Cites] Leukemia. 2006 Jan;20(1):82-6 [16270038.001]
  • [Cites] Nat Rev Cancer. 2006 May;6(5):347-59 [16612405.001]
  • [Cites] Blood. 2006 May 15;107(10):4115-21 [16449526.001]
  • [Cites] Oncogene. 2006 May 18;25(21):3023-31 [16407836.001]
  • [Cites] Blood. 2006 Jul 1;108(1):305-10 [16507772.001]
  • [Cites] Leukemia. 2006 Sep;20(9):1496-510 [16826225.001]
  • [Cites] Blood. 1998 Feb 1;91(3):1016-20 [9446664.001]
  • [Cites] Oncogene. 1998 Jan 29;16(4):517-22 [9484841.001]
  • [Cites] Leukemia. 1998 Jun;12(6):845-59 [9639410.001]
  • [Cites] Genes Dev. 1998 Oct 1;12(19):3008-19 [9765203.001]
  • [Cites] Mol Cell Biol. 1999 Jul;19(7):5025-35 [10373552.001]
  • [Cites] Cell. 2005 Feb 25;120(4):513-22 [15734683.001]
  • [Cites] Int J Biochem Cell Biol. 2005 May;37(5):961-76 [15743671.001]
  • [Cites] Blood. 2005 Jul 1;106(1):274-86 [15774621.001]
  • [Cites] Nat Rev Immunol. 2005 Jul;5(7):571-7 [15999096.001]
  • [Cites] Nature. 2005 Aug 4;436(7051):720-4 [16079850.001]
  • [Cites] Ann Neurol. 2005 Sep;58(3):483-7 [16130103.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6306-15 [16155013.001]
  • [Cites] Genes Dev. 1999 Oct 15;13(20):2691-703 [10541555.001]
  • (PMID = 17507663.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / CCND3 protein, human; 0 / CD3E protein, human; 0 / Ccnd3 protein, mouse; 0 / Cyclin D3; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Cyclins; 0 / LIM Domain Proteins; 0 / Lmo1 protein, mouse; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell; 0 / Tal1 protein, mouse; 0 / Transcription Factors; 135471-20-4 / TAL1 protein, human
  • [Other-IDs] NLM/ PMC1988920
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30. Aleskog A, Larsson R, Höglund M, Kristensen J, Nygren P, Lindhagen E: In vitro drug resistance in B cell chronic lymphocytic leukemia: a comparison with acute myelocytic and acute lymphocytic leukemia. Anticancer Drugs; 2005 Mar;16(3):277-83
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  • [Title] In vitro drug resistance in B cell chronic lymphocytic leukemia: a comparison with acute myelocytic and acute lymphocytic leukemia.
  • The aim of the study was to evaluate cellular drug resistance in B cell chronic lymphocytic leukemia (B-CLL) in vitro, and compare it with that in acute myelocytic leukemia (AML) and acute lymphocytic leukemia (ALL).
  • In vitro drug resistance was analyzed by the fluorometric microculture cytotoxicity assay (FMCA) in all samples from patients with leukemia sent to our laboratory between 1992 and 2001.
  • For all drugs, there was a good agreement between the activity in vitro and the known clinical disease-specific activity.
  • The study also demonstrated an acquired cellular drug resistance in B-CLL, but not in the acute leukemias.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


31. Suljagic M, Longo PG, Bennardo S, Perlas E, Leone G, Laurenti L, Efremov DG: The Syk inhibitor fostamatinib disodium (R788) inhibits tumor growth in the Eμ- TCL1 transgenic mouse model of CLL by blocking antigen-dependent B-cell receptor signaling. Blood; 2010 Dec 2;116(23):4894-905
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  • [Title] The Syk inhibitor fostamatinib disodium (R788) inhibits tumor growth in the Eμ- TCL1 transgenic mouse model of CLL by blocking antigen-dependent B-cell receptor signaling.
  • Inhibition of antigen-dependent B-cell receptor (BCR) signaling is considered a promising therapeutic approach in chronic lymphocytic leukemia (CLL), but experimental in vivo evidence to support this view is still lacking.
  • We have now investigated whether inhibition of BCR signaling with the selective Syk inhibitor fostamatinib disodium (R788) will affect the growth of the leukemias that develop in the Eμ-TCL1 transgenic mouse model of CLL.
  • Similarly to human CLL, these leukemias express stereotyped BCRs that react with autoantigens exposed on the surface of senescent or apoptotic cells, suggesting that they are antigen driven.
  • Importantly, the effect of R788 was found to be selective for the malignant clones, as no disturbance in the production of normal B lymphocytes was observed.
  • Collectively, these data provide further rationale for clinical trials with R788 in CLL and establish the BCR-signaling pathway as an important therapeutic target in this disease.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Intracellular Signaling Peptides and Proteins / antagonists & inhibitors. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Oxazines / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyridines / pharmacology
  • [MeSH-minor] Adoptive Transfer. Animals. Blotting, Western. Cell Separation. Disease Models, Animal. Flow Cytometry. Immunophenotyping. In Situ Nick-End Labeling. Mice. Mice, Transgenic. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins / genetics. Receptors, Antigen, B-Cell / drug effects. Signal Transduction / drug effects

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  • (PMID = 20716772.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Intracellular Signaling Peptides and Proteins; 0 / Oxazines; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Pyridines; 0 / Receptors, Antigen, B-Cell; 0 / Tcl1 protein, mouse; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Syk kinase; SQ8A3S5101 / fostamatinib
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32. Clark BR, Ferketich AK, Fisher JL, Ruymann FB, Harris RE, Wilkins JR 3rd: Evidence of population mixing based on the geographical distribution of childhood leukemia in Ohio. Pediatr Blood Cancer; 2007 Nov;49(6):797-802
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  • [Title] Evidence of population mixing based on the geographical distribution of childhood leukemia in Ohio.
  • BACKGROUND: This ecologic study examined the geographic distribution of childhood leukemias in Ohio, 1996-2000, among children aged 0-19 for evidence that population mixing may be a factor.
  • RESULTS: Of the 585 cases, 73.3% were acute lymphocytic leukemia (ALL), 16.6% acute myelogenous leukemia (AML), 3.2% acute monocytic leukemia (AMoL), and 2.6% chronic myelogenous leukemia (CML).
  • Rates for total leukemia burden were significantly below national levels for all races (P = 0.00001), likely due to poor ascertainment of cases.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / epidemiology. Leukemia, Myeloid, Acute / epidemiology. Population Density. Population Dynamics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Rural Population. Urban Population


33. Calin GA, Croce CM: Chronic lymphocytic leukemia: interplay between noncoding RNAs and protein-coding genes. Blood; 2009 Nov 26;114(23):4761-70
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  • [Title] Chronic lymphocytic leukemia: interplay between noncoding RNAs and protein-coding genes.
  • MicroRNAs (miRNAs), small regulatory ncRNAs, are involved in the pathogenesis of all types of human cancers, including leukemias, mainly via dysregulation of expression of cancer genes.
  • Researchers first identified this new paradigm of molecular oncology in patients with chronic lymphocytic leukemia (CLL).
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Genes, Neoplasm. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Neoplasm Proteins / physiology. RNA, Untranslated / physiology
  • [MeSH-minor] Animals. Apoptosis / genetics. B-Lymphocyte Subsets / metabolism. B-Lymphocyte Subsets / pathology. Cell Hypoxia / genetics. Chromosome Aberrations. Conserved Sequence. Disease Progression. Drug Delivery Systems. Forecasting. Gene Regulatory Networks. Genes, Tumor Suppressor. Humans. Mammals / genetics. MicroRNAs / genetics. MicroRNAs / physiology. Neovascularization, Pathologic / genetics. Oncogenes. Signal Transduction / genetics

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  • [Cites] Proc Natl Acad Sci U S A. 2008 Feb 5;105(5):1608-13 [18227514.001]
  • [Cites] Leukemia. 2008 Feb;22(2):330-8 [17989717.001]
  • [Cites] Cancer Res. 2008 Feb 15;68(4):1012-21 [18281475.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5446-56 [18216293.001]
  • [Cites] Oncogene. 2008 Sep 4;27(39):5204-13 [18504438.001]
  • [Cites] Br J Haematol. 2008 Sep;142(5):732-44 [18537969.001]
  • [Cites] Nat Genet. 2008 Oct;40(10):1204-10 [18758461.001]
  • [Cites] Cancer Res. 2008 Oct 15;68(20):8535-40 [18922928.001]
  • [Cites] Trends Cell Biol. 2008 Oct;18(10):505-16 [18774294.001]
  • [Cites] Nature. 2008 Oct 23;455(7216):1124-8 [18806776.001]
  • [Cites] Nat Med. 2008 Nov;14(11):1271-7 [18931683.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3207-12 [19202062.001]
  • [Cites] Leukemia. 2009 Mar;23(3):625-7 [18818704.001]
  • [Cites] Nat Rev Cancer. 2009 Apr;9(4):293-302 [19262572.001]
  • [Cites] Blood. 2009 Apr 16;113(16):3801-8 [18941118.001]
  • [Cites] Blood. 2009 Apr 16;113(16):3744-53 [19096009.001]
  • [Cites] PLoS Genet. 2009 Apr;5(4):e1000459 [19390609.001]
  • [Cites] Cell. 2009 May 1;137(3):586-586.e1 [19410551.001]
  • [Cites] Blood. 2009 May 21;113(21):5237-45 [19144983.001]
  • [Cites] Blood. 2009 May 28;113(22):5568-74 [19336759.001]
  • [Cites] Curr Opin Cell Biol. 2009 Jun;21(3):470-9 [19411171.001]
  • [Cites] Blood. 2009 Jun 18;113(25):6411-8 [19211935.001]
  • [Cites] Blood. 2009 Jun 18;113(25):6498-9; author reply 6499-500 [19541840.001]
  • [Cites] Leukemia. 2009 Nov;23(11):2174-7 [19536169.001]
  • [Cites] N Engl J Med. 2000 Dec 28;343(26):1910-6 [11136261.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6955-60 [12011454.001]
  • [Cites] Nat Rev Cancer. 2002 Sep;2(9):647-56 [12209154.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15524-9 [12434020.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Mar 11;105(10):3945-50 [18308931.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Mar 11;105(10):3903-8 [18308936.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Apr 1;105(13):5166-71 [18362358.001]
  • [Cites] J Pathol. 2008 May;215(1):13-20 [18348159.001]
  • [Cites] Br J Haematol. 2008 May;141(5):742-3 [18410456.001]
  • [Cites] Int J Cancer. 2008 Jul 15;123(2):372-9 [18449891.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2003;:153-75 [14633781.001]
  • [Cites] Science. 2004 Jan 2;303(5654):83-6 [14657504.001]
  • [Cites] Science. 2004 May 28;304(5675):1321-5 [15131266.001]
  • [Cites] Bioinformatics. 2004 Aug 4;20 Suppl 1:i40-8 [15262779.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 10;101(32):11755-60 [15284443.001]
  • [Cites] Hematol Oncol Clin North Am. 2004 Aug;18(4):783-94, vii [15325698.001]
  • [Cites] Nature. 2004 Sep 16;431(7006):350-5 [15372042.001]
  • [Cites] Science. 1984 Nov 30;226(4678):1097-9 [6093263.001]
  • [Cites] J Exp Med. 1990 Feb 1;171(2):559-64 [2106002.001]
  • [Cites] Cancer Res. 1997 Jul 1;57(13):2765-80 [9205089.001]
  • [Cites] Blood. 1998 May 1;91(9):3379-89 [9558396.001]
  • [Cites] Oncogene. 2005 Jan 20;24(4):697-705 [15580306.001]
  • [Cites] N Engl J Med. 2005 Feb 24;352(8):804-15 [15728813.001]
  • [Cites] Cell. 2005 Mar 11;120(5):635-47 [15766527.001]
  • [Cites] N Engl J Med. 2005 Apr 21;352(16):1667-76 [15843669.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):13944-9 [16166262.001]
  • [Cites] N Engl J Med. 2005 Oct 27;353(17):1793-801 [16251535.001]
  • [Cites] Nature. 2005 Dec 1;438(7068):685-9 [16258535.001]
  • [Cites] Leukemia. 2006 Feb;20(2):280-5 [16341048.001]
  • [Cites] N Engl J Med. 2006 Feb 2;354(5):524-5; author reply 524-5 [16452567.001]
  • [Cites] Nature. 2006 May 4;441(7089):87-90 [16625209.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Aug 1;103(31):11713-8 [16864779.001]
  • [Cites] Cancer Res. 2006 Aug 1;66(15):7390-4 [16885332.001]
  • [Cites] Nat Rev Cancer. 2006 Nov;6(11):857-66 [17060945.001]
  • [Cites] Biomed Pharmacother. 2006 Nov;60(9):633-8 [16962735.001]
  • [Cites] Cancer Res. 2006 Dec 15;66(24):11590-3 [17178851.001]
  • [Cites] Science. 2007 Jan 5;315(5808):97-100 [17204650.001]
  • [Cites] Mol Cell Biol. 2007 Mar;27(5):1859-67 [17194750.001]
  • [Cites] Mol Cell Biol. 2007 Mar;27(6):2240-52 [17242205.001]
  • [Cites] J Clin Oncol. 2007 Apr 10;25(11):1341-9 [17312329.001]
  • [Cites] Development. 2007 May;134(9):1635-41 [17409118.001]
  • [Cites] Blood. 2007 Apr 1;109(7):3015-23 [17148583.001]
  • [Cites] Br J Haematol. 2007 Jun;137(5):443-53 [17488487.001]
  • [Cites] Blood. 2007 Jun 1;109(11):4944-51 [17327404.001]
  • [Cites] Blood. 2007 Jun 15;109(12):5079-86 [17351108.001]
  • [Cites] Nature. 2007 Jun 28;447(7148):1130-4 [17554337.001]
  • [Cites] Oncogene. 2007 Jul 26;26(34):5017-22 [17297439.001]
  • [Cites] J Clin Invest. 2007 Aug;117(8):2059-66 [17671640.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1330-3 [17496199.001]
  • [Cites] Gastroenterology. 2007 Aug;133(2):647-58 [17681183.001]
  • [Cites] Curr Biol. 2007 Aug 7;17(15):1298-307 [17656095.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Aug 14;104(33):13513-8 [17686970.001]
  • [Cites] Cancer Cell. 2007 Sep;12(3):215-29 [17785203.001]
  • [Cites] Genes Chromosomes Cancer. 2007 Nov;46(11):1039-50 [17696194.001]
  • [Cites] Oncogene. 2007 Sep 13;26(42):6133-40 [17404574.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15805-10 [17890317.001]
  • [Cites] Nat Rev Cancer. 2007 Nov;7(11):819-22 [17914404.001]
  • [Cites] Cancer Sci. 2007 Dec;98(12):1914-20 [17892514.001]
  • [Cites] J Biol Chem. 2007 Nov 9;282(45):32582-90 [17827156.001]
  • [Cites] PLoS One. 2007;2(11):e1133 [17989771.001]
  • [Cites] J Clin Oncol. 2007 Dec 1;25(34):5448-57 [17968022.001]
  • [Cites] Science. 2007 Dec 21;318(5858):1931-4 [18048652.001]
  • [Cites] Methods. 2008 Jan;44(1):55-60 [18158133.001]
  • [Cites] Cell Res. 2008 Jan;18(1):198-213 [18166978.001]
  • [Cites] J Biol Chem. 2008 Jan 11;283(2):1026-33 [17991735.001]
  • (PMID = 19745066.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / Neoplasm Proteins; 0 / RNA, Untranslated
  • [Number-of-references] 92
  • [Other-IDs] NLM/ PMC2786287
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34. Chiaretti S, Ritz J, Foa R: Genomic analysis in lymphoid leukemias. Rev Clin Exp Hematol; 2005 Jun;9(1):E3
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  • [Title] Genomic analysis in lymphoid leukemias.
  • Important biological insights have been revealed by this technique in several tumors: in acute lymphoblastic leukemia (ALL), these studies have allowed to identify specific patterns associated with known molecular abnormalities, as well as with phenotypic characteristics and with different prognostic features.
  • In chronic lymphocytic leukemia (CLL), this approach has helped to dissect that this disease is a single entity with distinct variants that are characterized by a diverse IgVH mutational status, that can be discriminated by a small set of genes, has allowed to define a similarity between this disease and memory B cells and has also led to hypothesize that CLL cells from IgVH unmutated patients may be continuously stimulated in vivo, thus showing a gene profile that is reminiscent of the B cell receptor.
  • In multiple myeloma (MM), gene expression profiles has provided insights into the disease and has offered the opportunity of stratifying patients according to the degree of aggressiveness of the disease.
  • [MeSH-major] Genomics / methods. Leukemia, Lymphoid / genetics

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  • (PMID = 16027105.001).
  • [ISSN] 1825-151X
  • [Journal-full-title] Reviews in clinical and experimental hematology
  • [ISO-abbreviation] Rev Clin Exp Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Number-of-references] 140
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35. Meyers JA, Su DW, Lerner A: Chronic lymphocytic leukemia and B and T cells differ in their response to cyclic nucleotide phosphodiesterase inhibitors. J Immunol; 2009 May 1;182(9):5400-11
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  • [Title] Chronic lymphocytic leukemia and B and T cells differ in their response to cyclic nucleotide phosphodiesterase inhibitors.
  • Phosphodiesterase (PDE)4 inhibitors, which activate cAMP signaling by reducing cAMP catabolism, are known to induce apoptosis in B lineage chronic lymphocytic leukemia (CLL) cells but not normal human T cells.
  • Affymetrix gene chip analysis in the three cell populations following treatment with the PDE4 inhibitor rolipram identified a set of up-regulated transcripts with unusually high fold changes in the CLL samples, several of which are likely part of compensatory negative feedback loops.
  • The high fold changes were due to low basal transcript levels in CLL cells, suggesting that cAMP-mediated signaling may be unusually tightly regulated in this cell type.
  • Rolipram treatment augmented cAMP levels and induced ATF-1/CREB serine 63/133 phosphorylation in both B lineage cell types but not T cells.
  • As treatment with the broad-spectrum PDE inhibitor 3-isobutyl-1-methylxanthine induced T cell CREB phosphorylation, we tested a series of family-specific PDE inhibitors for their ability to mimic 3-isobutyl-1-methylxanthine-induced ATF-1/CREB phosphorylation.
  • Combined PDE3/4 inhibition did not induce T cell apoptosis, suggesting that cAMP-mediated signal transduction that leads to robust ATF-1/CREB serine 63/133 phosphorylation is not sufficient to induce apoptosis in this lymphoid lineage.

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  • [Cites] Mol Reprod Dev. 2000 Jun;56(2 Suppl):228-9 [10824972.001]
  • [Cites] Biochem Pharmacol. 2005 Feb 1;69(3):473-83 [15652238.001]
  • [Cites] Br J Pharmacol. 2000 Dec;131(8):1607-18 [11139438.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 May 22;98(11):6319-24 [11371644.001]
  • [Cites] Bioinformatics. 2001 Jun;17(6):509-19 [11395427.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2001 Oct;281(4):L832-43 [11557587.001]
  • [Cites] Clin Cancer Res. 2002 Feb;8(2):589-95 [11839681.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 28;99(11):7728-33 [12032351.001]
  • [Cites] Biochem J. 2003 Feb 15;370(Pt 1):1-18 [12444918.001]
  • [Cites] Mol Cell. 2003 Apr;11(4):1101-8 [12718894.001]
  • [Cites] Blood. 2003 May 15;101(10):4122-30 [12531792.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2661-7 [14615375.001]
  • [Cites] J Biol Chem. 2004 May 14;279(20):20858-65 [14996839.001]
  • [Cites] Mol Cell Endocrinol. 2004 Aug 31;223(1-2):55-62 [15279911.001]
  • [Cites] J Biol Chem. 2004 Oct 8;279(41):42438-44 [15299028.001]
  • [Cites] J Immunol. 2004 Oct 15;173(8):4847-58 [15470025.001]
  • [Cites] Endocrinology. 2004 Nov;145(11):5177-84 [15284208.001]
  • [Cites] Biochem J. 1987 Apr 15;243(2):533-9 [2820385.001]
  • [Cites] Biochem Pharmacol. 1991 Jul 25;42(4):869-77 [1651080.001]
  • [Cites] Nucleic Acids Res. 1993 Jun 11;21(11):2715-21 [7687344.001]
  • [Cites] Cell. 1993 Dec 3;75(5):875-86 [8252624.001]
  • [Cites] J Immunol. 1995 Feb 15;154(4):1634-43 [7836748.001]
  • [Cites] Cell Signal. 1996 Feb;8(2):97-110 [8730511.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 1;93(20):11236-41 [8855339.001]
  • [Cites] Br J Pharmacol. 1996 Aug;118(8):1945-58 [8864528.001]
  • [Cites] Br J Pharmacol. 1997 May;121(2):221-31 [9154331.001]
  • [Cites] Oncogene. 1997 Aug 14;15(7):827-36 [9266969.001]
  • [Cites] Br J Haematol. 1997 Dec;99(4):784-9 [9432022.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2484-94 [9746789.001]
  • [Cites] Science. 1999 Feb 5;283(5403):848-51 [9933169.001]
  • [Cites] Biochem Pharmacol. 1999 Sep 15;58(6):935-50 [10509746.001]
  • [Cites] Nucleic Acids Res. 2005 Jan 1;33(Database issue):D562-6 [15608262.001]
  • [Cites] Biostatistics. 2005 Jan;6(1):59-75 [15618528.001]
  • [Cites] Cell. 2004 Dec 29;119(7):1041-54 [15620361.001]
  • [Cites] Genome Biol. 2005;6(2):R16 [15693945.001]
  • [Cites] Curr Opin Pharmacol. 2005 Jun;5(3):238-44 [15907909.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8561-6 [15939874.001]
  • [Cites] J Immunol. 2005 Aug 15;175(4):2357-65 [16081806.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 11;102(41):14771-6 [16186489.001]
  • [Cites] Biochem J. 2006 Jan 1;393(Pt 1):21-41 [16336197.001]
  • [Cites] Nat Genet. 2006 May;38(5):500-1 [16642009.001]
  • [Cites] Mol Cell Biol. 2006 Sep;26(17):6333-46 [16914720.001]
  • [Cites] J Clin Invest. 2007 Jan;117(1):112-21 [17200714.001]
  • [Cites] Nature. 2007 Feb 15;445(7129):771-5 [17220874.001]
  • [Cites] Clin Cancer Res. 2007 Aug 15;13(16):4920-7 [17699872.001]
  • [Cites] Expert Opin Investig Drugs. 2007 Sep;16(9):1489-506 [17714033.001]
  • [Cites] Expert Opin Investig Drugs. 2007 Oct;16(10):1585-99 [17922623.001]
  • [Cites] Methods Mol Biol. 2000;132:365-86 [10547847.001]
  • [Cites] Curr Biol. 2000 Oct 19;10(20):1291-4 [11069111.001]
  • (PMID = 19380787.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106705-04; United States / NCI NIH HHS / CA / R01 CA106705; United States / NCI NIH HHS / CA / CA106705; United States / NCI NIH HHS / CA / CA106705-04; United States / NHLBI NIH HHS / HL / T32 HL007501-27; United States / NHLBI NIH HHS / HL / HL007501-27; United States / NHLBI NIH HHS / HL / T32 HL007501; United States / NHLBI NIH HHS / HL / HL007501
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Phosphodiesterase 3 Inhibitors; 0 / Phosphodiesterase 4 Inhibitors; E0399OZS9N / Cyclic AMP
  • [Other-IDs] NLM/ NIHMS108934; NLM/ PMC2676892
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36. Josef K, Heidi M, Robert P, Pavel K, Marek T: Expression of CD66 in non-Hodgkin lymphomas and multiple myeloma. Eur J Haematol; 2010 Dec;85(6):496-501
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  • PATIENTS AND METHODS: Bone marrow samples from 260 patients were examined for the expression of CD66 on tumor cells in 104 B-chronic lymphocytic leukemias (B-CLL), 28 mantle cell lymphomas (MCL), 22 follicular lymphomas (FCL), 15 marginal zone lymphomas (MZL), 12 lymphoplasmacytic lymphomas (LPL), 13 diffuse large B cell lymphomas (DLBCL), 4 T-non-Hodgkin lymphomas (T-NHL), 3 B-NHL not otherwise specified (B-NHL NOS), 3 B acute lymphoblastic leukemias (B-ALL), and in 56 multiple myelomas (MM) by flow cytometry.
  • [MeSH-major] Antigens, CD / biosynthesis. Bone Marrow / metabolism. Cell Adhesion Molecules / biosynthesis. Gene Expression Regulation, Neoplastic. Lymphoma, Non-Hodgkin / metabolism. Multiple Myeloma / metabolism

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  • [Copyright] © 2010 John Wiley & Sons A/S.
  • [CommentIn] Eur J Haematol. 2011 Dec;87(6):554-5 [21883478.001]
  • (PMID = 20887387.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / CD66 antigens; 0 / Cell Adhesion Molecules
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37. Yang I, Weiss L, Abdul-Hai A, Kasir J, Reich S, Slavin S: Induction of early post-transplant graft-versus-leukemia effects using intentionally mismatched donor lymphocytes and elimination of alloantigen-primed donor lymphocytes for prevention of graft-versus-host disease. Cancer Res; 2005 Nov 1;65(21):9735-40
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  • [Title] Induction of early post-transplant graft-versus-leukemia effects using intentionally mismatched donor lymphocytes and elimination of alloantigen-primed donor lymphocytes for prevention of graft-versus-host disease.
  • Graft-versus-leukemia (GVL) effects can be induced in tolerant mixed chimeras prepared with nonmyeloablative conditioning.
  • Unfortunately, DLI is frequently associated with graft-versus-host disease (GVHD).
  • We investigated the feasibility of induction of potent GVL effects by DLI using intentionally mismatched lymphocytes followed by elimination of alloreactive donor T cells by cyclophosphamide for prevention of lethal GVHD following induction of very short yet most potent GVL effects.
  • Mice inoculated with B-cell leukemia (BCL1) and mismatched donor lymphocytes were treated 2 weeks later with low-dose or high-dose cyclophosphamide.
  • All mice receiving cyclophosphamide 2 weeks after DLI survived GVHD, and no residual disease was detected by PCR; all control mice receiving DLI alone died of GVHD.
  • Our working hypothesis suggests that short-term yet effective and safe adoptive immunotherapy of leukemia may be accomplished early post-transplantation using alloreactive donor lymphocytes, with prevention of GVHD by elimination of GVL effector cells.
  • [MeSH-major] Graft vs Host Disease / prevention & control. Isoantigens / immunology. Leukemia, B-Cell / immunology. Leukemia, B-Cell / therapy. Lymphocytes / immunology
  • [MeSH-minor] Animals. Bone Marrow Transplantation / immunology. Cyclophosphamide / pharmacology. Graft vs Leukemia Effect. Immunosuppressive Agents / pharmacology. Lymphocyte Transfusion. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Neoplasm, Residual. Transplantation Chimera

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  • [ErratumIn] Cancer Res. 2006 Jul 1;66(13):6894. Yung, Iris [corrected to Yang, Iris]
  • (PMID = 16266994.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 0 / Isoantigens; 8N3DW7272P / Cyclophosphamide
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38. Bende RJ, Aarts WM, Riedl RG, de Jong D, Pals ST, van Noesel CJ: Among B cell non-Hodgkin's lymphomas, MALT lymphomas express a unique antibody repertoire with frequent rheumatoid factor reactivity. J Exp Med; 2005 Apr 18;201(8):1229-41
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  • [Title] Among B cell non-Hodgkin's lymphomas, MALT lymphomas express a unique antibody repertoire with frequent rheumatoid factor reactivity.
  • Follicular lymphomas, diffuse large B cell lymphomas, Burkitt's lymphomas, and myelomas expressed a CDR3 repertoire comparable to that of normal B cells.
  • Mantle cell lymphomas and B cell chronic lymphocytic leukemias (B-CLLs) expressed clearly restricted albeit different CDR3 repertoires.
  • Lymphomas of mucosa-associated lymphoid tissues (MALTs) were unique as 8 out of 45 (18%) of gastric- and 13 out of 32 (41%) of salivary gland-MALT lymphomas expressed B cell antigen receptors with strong CDR3 homology to rheumatoid factors (RFs).
  • [MeSH-major] Antibodies, Neoplasm / biosynthesis. Lymphoma, B-Cell / immunology. Lymphoma, B-Cell, Marginal Zone / immunology. Rheumatoid Factor / immunology

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  • [Cites] Leukemia. 1996 Jul;10(7):1190-7 [8684001.001]
  • [Cites] Eur J Immunol. 1996 Oct;26(10):2480-6 [8898963.001]
  • [Cites] Blood. 1996 Dec 15;88(12):4445-51 [8977236.001]
  • [Cites] Am J Pathol. 1997 Mar;150(3):919-27 [9060830.001]
  • [Cites] Blood. 1997 May 1;89(9):3335-44 [9129040.001]
  • [Cites] Br J Haematol. 1997 Jun;97(4):830-6 [9217184.001]
  • [Cites] Blood. 1997 Jul 15;90(2):776-82 [9226178.001]
  • [Cites] Nucleic Acids Res. 1997 Sep 1;25(17):3389-402 [9254694.001]
  • [Cites] Am J Surg Pathol. 1997 Nov;21(11):1307-15 [9351568.001]
  • [Cites] N Engl J Med. 1998 Mar 19;338(12):804-10 [9504941.001]
  • [Cites] Blood. 2003 Oct 15;102(8):3003-9 [12842981.001]
  • [Cites] N Engl J Med. 2004 Jan 15;350(3):239-48 [14724303.001]
  • [Cites] J Clin Invest. 2004 Apr;113(7):1008-16 [15057307.001]
  • [Cites] Blood. 1998 Mar 15;91(6):1864-72 [9490668.001]
  • [Cites] Lab Invest. 1998 Mar;78(3):277-87 [9520941.001]
  • [Cites] Blood. 1998 Jun 1;91(11):4292-9 [9596678.001]
  • [Cites] Immunol Rev. 1998 Apr;162:261-80 [9602370.001]
  • [Cites] J Clin Invest. 1998 Oct 15;102(8):1515-25 [9788964.001]
  • [Cites] Dev Immunol. 1998;6(3-4):187-95 [9814592.001]
  • [Cites] Electrophoresis. 1999 Apr-May;20(4-5):1092-7 [10344290.001]
  • [Cites] Curr Top Microbiol Immunol. 1999;246:217-22; discussion 223-4 [10396059.001]
  • [Cites] Blood. 1999 Sep 15;94(6):1848-54 [10477713.001]
  • [Cites] Clin Immunol. 1999 Nov;93(2):132-42 [10527689.001]
  • [Cites] Hum Pathol. 1988 Jul;19(7):766-76 [3136072.001]
  • [Cites] Hum Pathol. 1988 Nov;19(11):1315-26 [3141260.001]
  • [Cites] J Exp Med. 1989 Jan 1;169(1):255-68 [2462608.001]
  • [Cites] J Autoimmun. 1988 Oct;1(5):469-81 [2473761.001]
  • [Cites] Exp Cell Res. 1989 Aug;183(2):463-72 [2767160.001]
  • [Cites] Int J Hematol. 1999 Oct;70(3):200-6 [10561915.001]
  • [Cites] Blood. 2000 Jan 15;95(2):627-32 [10627472.001]
  • [Cites] Blood. 2000 Feb 15;95(4):1393-9 [10666216.001]
  • [Cites] Blood. 2000 Mar 1;95(5):1797-803 [10688840.001]
  • [Cites] Blood. 2000 May 1;95(9):2922-9 [10779440.001]
  • [Cites] Blood. 2000 Jun 15;95(12):3878-84 [10845923.001]
  • [Cites] Eur J Immunol. 2000 Oct;30(10):2918-23 [11069074.001]
  • [Cites] Blood. 2000 Nov 15;96(10):3578-84 [11071657.001]
  • [Cites] J Biol Chem. 2001 Jun 1;276(22):19012-9 [11262391.001]
  • [Cites] Gastroenterology. 2001 Jun;120(7):1884-5 [11398794.001]
  • [Cites] Blood. 2001 Dec 15;98(13):3745-9 [11739181.001]
  • [Cites] Blood. 2002 Mar 15;99(6):2259-61 [11877309.001]
  • [Cites] Nature. 2002 Apr 11;416(6881):603-7 [11948342.001]
  • [Cites] Leukemia. 2002 Apr;16(4):636-44 [11960344.001]
  • [Cites] Gastroenterology. 2002 May;122(5):1286-94 [11984515.001]
  • [Cites] N Engl J Med. 2002 Jul 11;347(2):89-94 [12110736.001]
  • [Cites] J Immunol. 2002 Aug 1;169(3):1349-56 [12133958.001]
  • [Cites] Science. 2002 Dec 13;298(5601):2199-202 [12481138.001]
  • [Cites] Am J Pathol. 2003 Apr;162(4):1113-22 [12651604.001]
  • [Cites] Cancer Res. 2003 May 1;63(9):2067-71 [12727821.001]
  • [Cites] Blood. 2003 May 15;101(10):4047-54 [12637326.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4500-4 [12560217.001]
  • [Cites] Blood. 2003 Aug 1;102(3):1012-8 [12676782.001]
  • [Cites] Science. 2003 Sep 5;301(5638):1374-7 [12920303.001]
  • [Cites] J Natl Cancer Inst. 2004 Apr 21;96(8):586-94 [15100336.001]
  • [Cites] J Exp Med. 2004 Aug 16;200(4):519-25 [15314077.001]
  • [Cites] Leukemia. 2004 Oct;18(10):1722-6 [15356642.001]
  • [Cites] Blood. 2004 Oct 15;104(8):2499-504 [15217828.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2879-85 [15217826.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Jun;78(6):3799-803 [6167990.001]
  • [Cites] J Immunol Methods. 1984 May 11;70(1):83-90 [6201562.001]
  • [Cites] Science. 1987 May 29;236(4805):1103-6 [2883731.001]
  • [Cites] Blood. 1990 Aug 1;76(3):562-9 [2378986.001]
  • [Cites] J Clin Invest. 1990 Oct;86(4):1320-8 [2170450.001]
  • [Cites] J Am Acad Dermatol. 1991 Apr;24(4):584-90 [2033136.001]
  • [Cites] Lancet. 1991 Nov 9;338(8776):1175-6 [1682595.001]
  • [Cites] J Exp Med. 1992 Apr 1;175(4):983-91 [1552291.001]
  • [Cites] Cell Immunol. 1992 Sep;143(2):310-23 [1324802.001]
  • [Cites] Am J Pathol. 1993 Jan;142(1):285-92 [8424461.001]
  • [Cites] Blood. 1993 Nov 15;82(10):3103-12 [7693035.001]
  • [Cites] Arthritis Rheum. 1994 Jun;37(6):860-8 [8003058.001]
  • [Cites] Immunol Today. 1995 May;16(5):237-42 [7779254.001]
  • [Cites] J Immunol. 1995 Oct 1;155(7):3630-7 [7561062.001]
  • [Cites] Blood. 1995 Nov 1;86(9):3528-34 [7579460.001]
  • [Cites] Blood. 1996 May 15;87(10):4296-301 [8639788.001]
  • [Cites] J Pathol. 1996 Feb;178(2):122-7 [8683376.001]
  • (PMID = 15837810.001).
  • [ISSN] 0022-1007
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AY281324/ AY281325/ AY281326/ AY281327/ AY281328/ AY281329/ AY281330/ AY281331/ AY281332/ AY281333/ AY281334/ AY281335/ AY281336/ AY281337/ AY281338/ AY281339/ AY281340/ AY281341/ AY281342/ AY281343/ AY466502/ AY466503/ AY561708/ AY927657/ AY927658/ AY927659/ AY927660/ AY927661/ AY927662/ AY927663/ AY927664/ AY927665/ AY927666/ AY927667/ AY927668
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Complementarity Determining Regions; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Light Chains; 9009-79-4 / Rheumatoid Factor
  • [Other-IDs] NLM/ PMC2213160
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39. Fenaux P: Inhibitors of DNA methylation: beyond myelodysplastic syndromes. Nat Clin Pract Oncol; 2005 Dec;2 Suppl 1:S36-44
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  • DNA methyltransferase (DNMT) inhibitors, azacitidine (Vidaza, Pharmion, Boulder, CO, USA) and decitabine (Dacogen; SuperGen Inc, Dublin, CA, USA, and MGI Pharma Inc, Bloomington, MN, USA), have had a significant impact on the treatment paradigm of myelodysplastic syndromes (MDSs), previously managed mainly by supportive care and hematopoietic-stem-cell transplantation.
  • In that respect, the majority of data for these agents are in the setting of acute myelogenous leukemia (AML).
  • Some use has also been described in chronic myelogenous leukemia and acute lymphocytic leukemia.
  • Further studies are needed to clarify the appropriate dose and the number and duration of cycles in the treatment of leukemias, and to identify ideal candidates for therapy, explore the role of DNMT inhibitors in combination with other agents, especially histone deacetylase inhibitors, delineate differences between the commercially available agents, and establish the long-term safety of these agents.
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Leukemia / drug therapy. Leukemia / genetics

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  • (PMID = 16341239.001).
  • [ISSN] 1743-4254
  • [Journal-full-title] Nature clinical practice. Oncology
  • [ISO-abbreviation] Nat Clin Pract Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
  • [Number-of-references] 73
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40. Terzakis JA, Santagada E, Hernandez A, Taskin M: Scanning electron microscopy of peripheral blood smears: comparison of normal blood with some common leukemias. Ultrastruct Pathol; 2005 Jan-Feb;29(1):19-28
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  • [Title] Scanning electron microscopy of peripheral blood smears: comparison of normal blood with some common leukemias.
  • Peripheral blood smears prepared routinely from nonneoplastic and leukemia cases were studied using the scanning electron microscope (SEM).
  • Certain cell features are measured as well with the use of the measuring software resident in the SEM.
  • The problem of cell constituent loss and overall shrinkage in the routinely processed and sectioned material is noted.
  • The monoblast resembles the normal monocyte but both cell size and nuclear size are greater; the moderately reticulated nuclear chromatin distinguishes the monoblast.
  • The neoplastic lymphoid cell shows coarse clumping of nuclear chromatin and in some instances coarse chromatin anastomoses to distinguish it from the normal lymphocyte.
  • Lymphoid cells of acute lymphoblastic leukemia are 33% larger than those of chronic lymphocytic leukemia and normal lymphocytes.
  • A candidate for such a cell is recognized morphologically as well.
  • [MeSH-major] Blood Cells / pathology. Blood Cells / ultrastructure. Cytodiagnosis. Leukemia / diagnosis. Microscopy, Electron, Scanning
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Size. Female. Flow Cytometry. Humans. Male. Middle Aged. Reproducibility of Results

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  • (PMID = 15931777.001).
  • [ISSN] 0191-3123
  • [Journal-full-title] Ultrastructural pathology
  • [ISO-abbreviation] Ultrastruct Pathol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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41. Liang X, Moseman EA, Farrar MA, Bachanova V, Weisdorf DJ, Blazar BR, Chen W: Toll-like receptor 9 signaling by CpG-B oligodeoxynucleotides induces an apoptotic pathway in human chronic lymphocytic leukemia B cells. Blood; 2010 Jun 17;115(24):5041-52
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  • [Title] Toll-like receptor 9 signaling by CpG-B oligodeoxynucleotides induces an apoptotic pathway in human chronic lymphocytic leukemia B cells.
  • Chronic lymphocytic leukemia (CLL) is the most prevalent human leukemia and is characterized by the progressive accumulation of long-lived malignant B cells.
  • TLR9-CpG ODN ligation-induced apoptosis of B-CLL cells is confirmed by viable cell counts, annexin V/propidium iodide and tetramethyl-rhodamine ethylester staining, Western blots of the activation, and cleaved caspases and poly (ADP-ribose) polymerase.
  • Treating B-CLL cells in vitro or in vivo with CpG-B ODN reduces the number of leukemia cells that engraft in NOD-scid mice.

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  • [Cites] Blood. 2002 May 15;99(10):3554-61 [11986207.001]
  • [Cites] J Immunol. 2002 May 1;168(9):4531-7 [11970999.001]
  • [Cites] Blood. 2003 Apr 15;101(8):2940-54 [12480704.001]
  • [Cites] Blood. 2003 May 1;101(9):3413-5 [12522009.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4500-4 [12560217.001]
  • [Cites] Clin Cancer Res. 2003 Jun;9(6):2166-72 [12796382.001]
  • [Cites] Blood. 2003 Aug 1;102(3):956-63 [12689944.001]
  • [Cites] Cancer Res. 2003 Aug 1;63(15):4497-506 [12907623.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1763-9 [14615377.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):3118-23 [14973184.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2547-53 [14670916.001]
  • [Cites] N Engl J Med. 2004 Aug 26;351(9):893-901 [15329427.001]
  • [Cites] J Exp Med. 1993 Apr 1;177(4):925-35 [7681471.001]
  • [Cites] Blood. 1993 Sep 15;82(6):1820-8 [8104532.001]
  • [Cites] Blood. 1995 Jan 15;85(2):307-18 [7811987.001]
  • [Cites] Science. 1997 Nov 28;278(5343):1630-2 [9374464.001]
  • [Cites] J Clin Invest. 1997 Dec 15;100(12):3140-8 [9399961.001]
  • [Cites] J Clin Invest. 1998 Oct 1;102(7):1385-92 [9769331.001]
  • [Cites] Blood. 1999 Mar 15;93(6):1992-2002 [10068672.001]
  • [Cites] Biol Blood Marrow Transplant. 2005 Jan;11(1):23-34 [15625541.001]
  • [Cites] J Leukoc Biol. 2005 Mar;77(3):378-87 [15582984.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4070-8 [15767647.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4079-88 [15767648.001]
  • [Cites] J Clin Invest. 2005 Jul;115(7):1797-805 [15965501.001]
  • [Cites] Bone Marrow Transplant. 2005 Sep;36(5):437-41 [15980879.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6325-32 [16155015.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1276-83 [16204307.001]
  • [Cites] Lancet Oncol. 2006 Jun;7(6):480-8 [16750498.001]
  • [Cites] Nat Rev Drug Discov. 2006 Jun;5(6):471-84 [16763660.001]
  • [Cites] Blood. 2007 Jan 15;109(2):405-11 [17008537.001]
  • [Cites] J Clin Invest. 2007 May;117(5):1184-94 [17476348.001]
  • [Cites] Nat Med. 2007 May;13(5):552-9 [17479101.001]
  • [Cites] Blood. 2007 Oct 15;110(8):2811-8 [17638850.001]
  • [Cites] J Immunother. 2007 Nov-Dec;30(8):789-97 [18049330.001]
  • [Cites] Blood. 2008 Jun 1;111(11):5291-7 [18334676.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5446-56 [18216293.001]
  • [Cites] J Leukoc Biol. 2008 Jul;84(1):319-25 [18426971.001]
  • [Cites] J Clin Invest. 2008 Jul;118(7):2427-37 [18551193.001]
  • [Cites] Blood. 2008 Aug 1;112(3):711-20 [18497318.001]
  • [Cites] Blood. 2000 Feb 1;95(3):999-1006 [10648415.001]
  • [Cites] Oncogene. 2000 May 15;19(21):2496-504 [10851048.001]
  • [Cites] N Engl J Med. 2000 Dec 28;343(26):1910-6 [11136261.001]
  • [Cites] J Leukoc Biol. 2001 Jan;69(1):81-8 [11200072.001]
  • [Cites] Blood. 2001 May 1;97(9):2777-83 [11313271.001]
  • [Cites] J Biol Chem. 2001 Jul 27;276(30):28340-7 [11309387.001]
  • [Cites] Blood. 2001 Aug 1;98(3):814-22 [11468183.001]
  • [Cites] Nat Immunol. 2001 Aug;2(8):675-80 [11477402.001]
  • [Cites] Blood. 2001 Aug 15;98(4):1217-25 [11493473.001]
  • [Cites] J Exp Med. 2001 Sep 17;194(6):863-9 [11561001.001]
  • [Cites] J Clin Oncol. 2002 Sep 15;20(18):3891-7 [12228210.001]
  • (PMID = 20339095.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R21 AI050737; United States / NIAID NIH HHS / AI / R01 AI050737; United States / NIAID NIH HHS / AI / AI050737; United States / NCI NIH HHS / CA / R01 CA72669; United States / NCI NIH HHS / CA / R01 CA072669
  • [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 / Adjuvants, Immunologic; 0 / CPG-oligonucleotide; 0 / IL10 protein, human; 0 / NF-kappa B; 0 / Oligodeoxyribonucleotides; 0 / Receptors, Interleukin-2; 0 / STAT1 Transcription Factor; 0 / STAT1 protein, human; 0 / TLR9 protein, human; 0 / Toll-Like Receptor 9; 130068-27-8 / Interleukin-10; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC2890142
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42. Zhang X, Wang M, Zhou C, Chen S, Wang J: The expression of iASPP in acute leukemias. Leuk Res; 2005 Feb;29(2):179-83
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  • [Title] The expression of iASPP in acute leukemias.
  • To examine the role of iASPP in acute leukemia (AL), we analyzed iASPP mRNA expression in AL by semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR).
  • There was no significant difference between acute lymphocytic leukemia (ALL) cells and acute myeloid leukemia (AML) cells (P = 0.593).
  • However, iASPP gene expression in AL cells was not associated with gender, age, initial white blood cell count or p53 type, but was associated with CD34 expression.
  • The results of the present study suggest that iASPP gene overexpression may play an important role in the leukemogenesis and/or disease progression of AL.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Intracellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid, Acute / genetics. RNA, Messenger / genetics
  • [MeSH-minor] Adolescent. Adult. Cell Line, Tumor. Female. Humans. Male. Mutation. Repressor Proteins. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Suppressor Protein p53 / antagonists & inhibitors. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Up-Regulation

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  • (PMID = 15607367.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / PPP1R13L protein, human; 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / Tumor Suppressor Protein p53
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43. Ma W, Kantarjian H, Zhang K, Zhang X, Wang X, Chen C, Donahue AC, Zhang Z, Yeh CH, O'Brien S, Garcia-Manero G, Caporaso N, Landgren O, Albitar M: Significant association between polymorphism of the erythropoietin gene promoter and myelodysplastic syndrome. BMC Med Genet; 2010 Nov 16;11:163
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  • METHODS: We genotyped the EPO rS1617640 SNP in 189 patients with MDS, 257 with acute myeloid leukemia (AML), 106 with acute lymphoblastic leukemia, 97 with chronic lymphocytic leukemia, 353 with chronic myeloid leukemia, and 95 healthy controls.
  • RESULTS: The G/G genotype was significantly more common in MDS patients (47/187; 25.1%) than in controls (6/95; 6.3%) or in patients with other leukemias (101/813; 12.4%) (all P < 0.001).
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Case-Control Studies. Genotype. Humans. Leukemia, Lymphocytic, Chronic, B-Cell. Leukemia, Myelogenous, Chronic, BCR-ABL Positive. Leukemia, Myeloid, Acute. Middle Aged. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma. Treatment Outcome. Young Adult


44. Gertz MA, Geyer SM, Badros A, Kahl BS, Erlichman C: Early results of a phase I trial of oblimersen sodium for relapsed or refractory Waldenstrom's macroglobulinemia. Clin Lymphoma; 2005 Mar;5(4):282-4
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  • Oblimersen sodium is an antisense oligonucleotide to the first 6 codons of the B-cell leukemia gene 2 (bcl-2) open reading frame.
  • It prevents the expression of the bcl-2 gene product and leads to apoptosis in cells that express Bcl-2. bcl-2 is one of the major apoptosis regulatory gene families and is found in a variety of low-grade B-cell non-Hodgkin's lymphomas.
  • The in vitro use of oblimersen in Waldenstrom's macroglobulinemia (WM) cell line results in enhanced toxicity when exposed to fludarabine, dexamethasone, or rituximab.

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  • (PMID = 15794866.001).
  • [ISSN] 1526-9655
  • [Journal-full-title] Clinical lymphoma
  • [ISO-abbreviation] Clin Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CM / N01 CM 17104
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligonucleotides, Antisense; 0 / Thionucleotides; 85J5ZP6YSL / oblimersen
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45. Pérez-Campos-Mayoral L, Ruiz-Argüelles A, Pérez-Romano B, Zenteno E, Hernández-Cruz P, Martínez-Cruz R, Martínez-Cruz M, Pina-Canseco S, Pérez-Campos E: Potential use of the Macrobrachium rosenbergii lectin for diagnosis of T-cell acute lymphoblastic leukemia. Tohoku J Exp Med; 2008 Jan;214(1):11-6
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  • [Title] Potential use of the Macrobrachium rosenbergii lectin for diagnosis of T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia is the most common form of cancer in children.
  • Lectins are proteins or glycoproteins from plants or animals that recognize oligossacharides on the cell surface and have been used to characterize the structural changes of oligosaccharides in leukemias.
  • In this study, we used the lectin from the freshwater prawn Macrobrachium (M. rosenbergii), specific for acetyl groups in sialylated glycans, because increased sialylation of glycoproteins and glycolipids has been identified in lymphoblastic leukemias.
  • We compared the specificity of the M. rosenbergii lectin for lymphoblastic leukemias with the specificities of the lectins from Triticum vulgaris, Solanum tuberosum, Arachis hipogaea, and Phytolacca americana.
  • By morphologic and phenotype characterization with a panel of monoclonal antibodies, we identified four types of leukemias from 106 leukemia patients: 11 cases of T-cell acute lymphoblastic leukemia, 61 cases of B-cell acute lymphoblastic leukemia, 24 cases of acute myeloblastic leukemia, and 10 cases of acute biphenotypic leukemia.
  • As determined by cytofluorometric assays, nine of the eleven cases with T-cell acute lymphoblastic leukemia (8 +/- 3 years old) were specifically identified with the lectin from M. rosenbergii.
  • In contrast, only six cases of B-cell leukemia, one case of myeloblastic leukemia, and 2 cases of biphenotypic leukemia were identified with this M. rosenbergii lectin.
  • The other lectins tested showed no capacity to differentiate, in a significant manner, any of the four types of leukemias tested.
  • Thus, the lectin from M. rosenbergii could be considered a useful tool for the diagnosis and study of T-cell acute lymphoblastic leukemia.
  • [MeSH-major] Lectins. Leukemia, Biphenotypic, Acute / diagnosis. Palaemonidae / chemistry
  • [MeSH-minor] Animals. Antibodies, Monoclonal. Antigens, CD45 / analysis. Antigens, Neoplasm / immunology. Child. Diagnosis, Differential. Flow Cytometry. Humans. Lymphocytes / drug effects. Lymphocytes / metabolism. Phenotype

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  • (PMID = 18212483.001).
  • [ISSN] 0040-8727
  • [Journal-full-title] The Tohoku journal of experimental medicine
  • [ISO-abbreviation] Tohoku J. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Lectins; EC 3.1.3.48 / Antigens, CD45
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46. Horny HP, Sotlar K, Valent P: Differential diagnoses of systemic mastocytosis in routinely processed bone marrow biopsy specimens: a review. Pathobiology; 2010;77(4):169-80
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  • Diagnosis of systemic mastocytosis (SM) is mainly based on the morphological demonstration of compact mast cell infiltrates in various tissue sites.
  • Reliable immunohistochemical markers for the diagnosis and grading of SM have been established, but various differential diagnoses including myeloproliferative neoplasms, basophilic and eosinophilic leukemias may be very difficult to delineate.
  • Even more challenging is the recognition of hematological neoplasms with signs of mast cell differentiation but not fulfilling diagnostic criteria for SM, especially the rare myelomastocytic leukemia.
  • It is also important to separate the reactive state of mast cell hyperplasia from indolent variants of SM, especially those with a very low degree of bone marrow infiltration and absence of compact mast cell infiltrates.
  • When the lymphocytic component of the SM infiltrate is very prominent, SM may be confused with an indolent lymphoma, especially lymphoplasmacytic lymphoma which almost always shows a marked reactive increase in mast cells.
  • This hypogranulation can be regarded as cellular atypia and may lead to the misdiagnosis aspect of monocytic leukemia or histiocytic neoplasm.
  • Thus, anaplastic large cell lymphoma or Hodgkin's disease may first be considered rather than SM.

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  • (PMID = 20616612.001).
  • [ISSN] 1423-0291
  • [Journal-full-title] Pathobiology : journal of immunopathology, molecular and cellular biology
  • [ISO-abbreviation] Pathobiology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
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47. Swerdlow SH: T-cell and NK-cell posttransplantation lymphoproliferative disorders. Am J Clin Pathol; 2007 Jun;127(6):887-95
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  • [Title] T-cell and NK-cell posttransplantation lymphoproliferative disorders.
  • Posttransplantation lymphoproliferative disorders (PTLDs) of T-cell or natural killer (NK)-cell origin are an uncommon heterogeneous group of lymphoid proliferations that fulfill the criteria for one of the T- or NK-cell lymphomas/leukemias.
  • This report summarizes 130 T/NK-cell PTLDs reported in the literature or presented at the Society for Hematopathology/European Association for Haematopathology Workshop on T/NK-cell malignancies.
  • The T/NK-cell PTLDs occur at a median of 66 months following transplantation and are usually extranodal.
  • The most common types reported are peripheral T-cell lymphoma, unspecified, and hepatosplenic T-cell lymphoma.
  • EBV+ cases have a significantly longer survival than EBV- cases, even when indolent T-cell large granular lymphocytic leukemias are included among the EBV- cases.
  • Many T/NK-cell PTLDs have been treated with chemotherapy, often together with decreased immunosuppression, but there are infrequent patients who have done well without chemotherapy or radiation.
  • [MeSH-major] Killer Cells, Natural / pathology. Lymphoproliferative Disorders / pathology. Organ Transplantation / adverse effects. T-Lymphocytes / pathology
  • [MeSH-minor] Epstein-Barr Virus Infections / complications. Humans. Lymphoma, T-Cell, Peripheral / etiology. Lymphoma, T-Cell, Peripheral / mortality. Lymphoma, T-Cell, Peripheral / pathology. Postoperative Complications. Survival Rate

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  • (PMID = 17509986.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Congresses
  • [Publication-country] United States
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48. Garcia-Manero G, Yang H, Bueso-Ramos C, Ferrajoli A, Cortes J, Wierda WG, Faderl S, Koller C, Morris G, Rosner G, Loboda A, Fantin VR, Randolph SS, Hardwick JS, Reilly JF, Chen C, Ricker JL, Secrist JP, Richon VM, Frankel SR, Kantarjian HM: Phase 1 study of the histone deacetylase inhibitor vorinostat (suberoylanilide hydroxamic acid [SAHA]) in patients with advanced leukemias and myelodysplastic syndromes. Blood; 2008 Feb 1;111(3):1060-6
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  • [Title] Phase 1 study of the histone deacetylase inhibitor vorinostat (suberoylanilide hydroxamic acid [SAHA]) in patients with advanced leukemias and myelodysplastic syndromes.
  • Vorinostat (suberoylanilide hydroxamic acid, SAHA) is a histone deacetylase inhibitor active clinically in cutaneous T-cell lymphoma and preclinically in leukemia.
  • Patients with relapsed or refractory leukemias or myelodysplastic syndromes (MDS) and untreated patients who were not candidates for chemotherapy were eligible.
  • Of 41 patients, 31 had acute myeloid leukemia (AML), 4 chronic lymphocytic leukemia, 3 MDS, 2 acute lymphoblastic leukemia, and 1 chronic myelocytic leukemia.
  • [MeSH-major] Enzyme Inhibitors / therapeutic use. Histone Deacetylase Inhibitors. Hydroxamic Acids / therapeutic use. Leukemia / drug therapy. Leukemia / pathology. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / pathology


49. Merimi M, Ozkan Y, Cleuter Y, Griebel P, Burny A, Martiat P, Van den Broeke A: Epigenetics and leukemia: unraveling oncogenic processes in the BLV ovine model. Front Biosci (Schol Ed); 2009;1:154-63
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  • [Title] Epigenetics and leukemia: unraveling oncogenic processes in the BLV ovine model.
  • Bovine Leukemia Virus (BLV)-induced B-cell leukemia in sheep is a valuable large animal model for investigating oncogenic mechanisms, particularly those associated with human T-cell leukemia virus 1 (HTLV-1).
  • Multiple factors including viral genes, genetic and epigenetic alterations, and the host immune system are likely to contribute and cooperate in the leukemogenesis of adult T-cell leukemia (ATL) in human and B-cell leukemia in sheep.
  • Future studies in sheep will increase the number of genes identified that are aberrantly regulated by epigenetic processes and identify potential biomarkers which may be used as therapeutic targets in leukemia.
  • [MeSH-major] Epigenesis, Genetic. Leukemia / virology. Leukemia Virus, Bovine / pathogenicity. Oncogenes

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  • (PMID = 19482691.001).
  • [ISSN] 1945-0524
  • [Journal-full-title] Frontiers in bioscience (Scholar edition)
  • [ISO-abbreviation] Front Biosci (Schol Ed)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 93
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50. Vargo MA, Voss OH, Poustka F, Cardounel AJ, Grotewold E, Doseff AI: Apigenin-induced-apoptosis is mediated by the activation of PKCdelta and caspases in leukemia cells. Biochem Pharmacol; 2006 Sep 14;72(6):681-92
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  • [Title] Apigenin-induced-apoptosis is mediated by the activation of PKCdelta and caspases in leukemia cells.
  • In the present study, the treatment of different cell lines with apigenin resulted in selective antiproliferative and apoptotic effect in monocytic and lymphocytic leukemias.
  • Pharmacological inhibition of PKCdelta, the expression of dominant-negative PKCdelta and silencing of PKCdelta in leukemia cells showed that apigenin-induced-apoptosis requires PKCdelta activity.
  • Together, these results indicate that this flavonoid provides selective activity to promote caspase-dependent-apoptosis of leukemia cells and uncover an essential role of PKCdelta during the induction of apoptosis by apigenin.
  • [MeSH-minor] 3T3 Cells. Animals. Caspase 3. Caspase 9. Enzyme Activation / drug effects. HL-60 Cells. Humans. Jurkat Cells. K562 Cells. Leukemia / pathology. Mice. Mitochondria / metabolism. Reactive Oxygen Species / metabolism. Tumor Cells, Cultured. U937 Cells

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  • (PMID = 16844095.001).
  • [ISSN] 0006-2952
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R01HL075040-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; 7V515PI7F6 / Apigenin; EC 2.7.11.13 / Protein Kinase C-delta; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Casp9 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9; EC 3.4.22.- / Caspases
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51. Krämer A, Neben K, Ho AD: Centrosome aberrations in hematological malignancies. Cell Biol Int; 2005 May;29(5):375-83
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  • Normally, the single centrosome of a G1 cell duplicates precisely once prior to mitosis in a process that is intimately linked to the cell division cycle via cyclin-dependent kinase (cdk) 2 activity that couples centrosome duplication to the onset of DNA replication at the G1/S transition.
  • In addition to solid neoplasias, centrosome aberrations have recently been described in several different hematological malignancies like acute myeloid leukemias, myelodysplastic syndromes, Hodgkin's as well as non-Hodgkin's lymphomas, chronic lymphocytic leukemias and multiple myelomas.
  • In analogy to many solid tumors a correlation between centrosome abnormalities on the one hand and karyotype aberrations as well as clinical aggressiveness on the other hand seems to exist in myeloid malignancies, chronic lymphocytic leukemias and at least some types of non-Hodgkin's lymphomas.
  • [MeSH-minor] Cell Cycle

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  • (PMID = 15996491.001).
  • [ISSN] 1065-6995
  • [Journal-full-title] Cell biology international
  • [ISO-abbreviation] Cell Biol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 90
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52. Staratschek-Jox A, Classen S, Gaarz A, Debey-Pascher S, Schultze JL: Blood-based transcriptomics: leukemias and beyond. Expert Rev Mol Diagn; 2009 Apr;9(3):271-80
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  • [Title] Blood-based transcriptomics: leukemias and beyond.
  • In 1999, Golub et al. proposed for the first time microarray-based transcriptional profiling to be used as a new technology for the differential diagnosis of acute myeloid leukemias and acute lymphocytic leukemias.
  • This very preliminary study sparked great enthusiasm beyond the leukemias.
  • Here we highlight the advances in the field of blood transcriptomics during the last 10 years and also critically discuss the issues that need to be resolved before blood transcriptomics will become part of daily diagnostics in the leukemias, as well as in other diseases showing involvement of peripheral blood.
  • [MeSH-major] Blood. Gene Expression Profiling / methods. Leukemia / diagnosis. Leukemia / genetics. Oligonucleotide Array Sequence Analysis / methods

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  • (PMID = 19379085.001).
  • [ISSN] 1744-8352
  • [Journal-full-title] Expert review of molecular diagnostics
  • [ISO-abbreviation] Expert Rev. Mol. Diagn.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 57
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53. Burger M, Hartmann T, Krome M, Rawluk J, Tamamura H, Fujii N, Kipps TJ, Burger JA: Small peptide inhibitors of the CXCR4 chemokine receptor (CD184) antagonize the activation, migration, and antiapoptotic responses of CXCL12 in chronic lymphocytic leukemia B cells. Blood; 2005 Sep 1;106(5):1824-30
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  • [Title] Small peptide inhibitors of the CXCR4 chemokine receptor (CD184) antagonize the activation, migration, and antiapoptotic responses of CXCL12 in chronic lymphocytic leukemia B cells.
  • Growth and survival of chronic lymphocytic leukemia (CLL) B cells are favored by interactions between CLL and nontumoral accessory cells.
  • CLL cells express CXCR4 chemokine receptors that direct leukemia cell chemotaxis.
  • TC14012 and TN14003 antagonized the antiapoptotic effect of synthetic CXCL12 and stromal cell-mediated protection of CLL cells from spontaneous apoptosis.
  • As such, small molecular CXCR4 antagonists may have activity in the treatment of patients with this disease.
  • [MeSH-major] Apoptosis / drug effects. Chemokines, CXC / antagonists & inhibitors. Chemokines, CXC / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Oligopeptides / pharmacology. Receptors, CXCR4 / antagonists & inhibitors
  • [MeSH-minor] Actins / drug effects. Actins / metabolism. Cell Line, Tumor. Cell Movement / drug effects. Cell Movement / physiology. Chemokine CXCL12. Chemotaxis / drug effects. Dose-Response Relationship, Drug. Humans. Mitogen-Activated Protein Kinases / drug effects. Mitogen-Activated Protein Kinases / metabolism. Molecular Weight. Peptides / pharmacology. Stromal Cells / drug effects. Stromal Cells / physiology. Structure-Activity Relationship. Time Factors. Vidarabine / analogs & derivatives. Vidarabine / pharmacology

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  • (PMID = 15905192.001).
  • [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 / Actins; 0 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Oligopeptides; 0 / Peptides; 0 / Receptors, CXCR4; 0 / T140 peptide; 0 / TC14012; 0 / TN14003; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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54. Ohnishi N, Yuasa H, Tanaka S, Sawa H, Miura M, Matsui A, Higashi H, Musashi M, Iwabuchi K, Suzuki M, Yamada G, Azuma T, Hatakeyama M: Transgenic expression of Helicobacter pylori CagA induces gastrointestinal and hematopoietic neoplasms in mouse. Proc Natl Acad Sci U S A; 2008 Jan 22;105(3):1003-8
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  • Infection with cagA-positive Helicobacter pylori is associated with gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma of B cell origin.
  • Systemic expression of wild-type CagA further induced leukocytosis with IL-3/GM-CSF hypersensitivity and some mice developed myeloid leukemias and B cell lymphomas, the hematological malignancies also caused by gain-of-function SHP-2 mutations.
  • [MeSH-major] Antigens, Bacterial / metabolism. Bacterial Proteins / metabolism. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Gastrointestinal Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Helicobacter pylori / metabolism. Hematologic Neoplasms / metabolism

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  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 7;96(25):14559-64 [10588744.001]
  • [Cites] Gastroenterology. 2005 May;128(5):1229-42 [15887107.001]
  • [Cites] Science. 2002 Jan 25;295(5555):683-6 [11743164.001]
  • [Cites] J Biol Chem. 2002 Mar 1;277(9):6775-8 [11788577.001]
  • [Cites] Nat Rev Cancer. 2002 Jan;2(1):28-37 [11902583.001]
  • [Cites] Lancet Oncol. 2001 Sep;2(9):533-43 [11905707.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14428-33 [12391297.001]
  • [Cites] Mol Cell. 2002 Oct;10(4):745-55 [12419219.001]
  • [Cites] J Cell Biol. 2003 Apr 28;161(2):249-55 [12719469.001]
  • [Cites] Bioessays. 2003 Jun;25(6):542-53 [12766944.001]
  • [Cites] Nat Genet. 2003 Jun;34(2):148-50 [12717436.001]
  • [Cites] J Biol Chem. 2004 Apr 23;279(17):17205-16 [14963045.001]
  • [Cites] Nat Med. 2004 Aug;10(8):849-57 [15273746.001]
  • [Cites] Blood. 2005 Jul 1;106(1):311-7 [15761018.001]
  • [Cites] Eur J Med Genet. 2005 Apr-Jun;48(2):81-96 [16053901.001]
  • [Cites] J Exp Med. 2005 Nov 7;202(9):1235-47 [16275761.001]
  • [Cites] Mol Cell Biol. 2006 Jan;26(1):261-76 [16354697.001]
  • [Cites] Gastroenterology. 2006 Apr;130(4):1181-90 [16618412.001]
  • [Cites] Annu Rev Biochem. 2006;75:137-63 [16756488.001]
  • [Cites] Nature. 2007 May 17;447(7142):330-3 [17507984.001]
  • [Cites] Oncogene. 2007 May 24;26(24):3462-72 [17160020.001]
  • [Cites] Oncogene. 2007 Jul 12;26(32):4617-26 [17237808.001]
  • [Cites] Genes Dev. 2004 Aug 15;18(16):1909-25 [15314019.001]
  • [Cites] Nat Rev Cancer. 2004 Sep;4(9):688-94 [15343275.001]
  • [Cites] Cancer Res. 1992 Dec 15;52(24):6735-40 [1458460.001]
  • [Cites] J Biol Chem. 1993 Dec 15;268(35):26559-70 [8253786.001]
  • [Cites] N Engl J Med. 1994 May 5;330(18):1267-71 [8145781.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Jan 3;92(1):160-4 [7816809.001]
  • [Cites] Cancer Res. 1995 May 15;55(10):2111-5 [7743510.001]
  • [Cites] J Natl Cancer Inst. 1995 Dec 6;87(23):1777-80 [7473834.001]
  • [Cites] Am J Clin Pathol. 1996 Nov;106(5):670-5 [8929480.001]
  • [Cites] Trends Genet. 1996 May;12(5):171-5 [8984731.001]
  • [Cites] J Pharmacol Exp Ther. 1997 Jan;280(1):225-31 [8996200.001]
  • [Cites] Gut. 1997 Mar;40(3):297-301 [9135515.001]
  • [Cites] Mol Cell Biol. 1997 Sep;17(9):5499-507 [9271425.001]
  • [Cites] Am J Gastroenterol. 1998 Mar;93(3):375-9 [9517643.001]
  • [Cites] Gastroenterology. 1998 Sep;115(3):642-8 [9721161.001]
  • [Cites] Cancer Res. 1998 Oct 1;58(19):4255-9 [9766647.001]
  • [Cites] Cancer Res. 2004 Dec 15;64(24):8816-20 [15604238.001]
  • [Cites] Blood. 2001 Feb 15;97(4):911-4 [11159516.001]
  • (PMID = 18192401.001).
  • [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 / Antigens, Bacterial; 0 / Bacterial Proteins; 0 / cagA protein, Helicobacter pylori; 21820-51-9 / Phosphotyrosine
  • [Other-IDs] NLM/ PMC2242726
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55. Erlacher M, Michalak EM, Kelly PN, Labi V, Niederegger H, Coultas L, Adams JM, Strasser A, Villunger A: BH3-only proteins Puma and Bim are rate-limiting for gamma-radiation- and glucocorticoid-induced apoptosis of lymphoid cells in vivo. Blood; 2005 Dec 15;106(13):4131-8
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  • Numerous p53 target genes have been implicated in DNA damage-induced apoptosis signaling, but proapoptotic Bcl-2 (B-cell leukemia 2) family members of the BH3 (Bcl-2 homolog region [BH] 3)-only subgroup appear to play the critical initiating role.
  • In various types of cultured cells, 3 BH3-only proteins, namely Puma (p53 up-regulated modulator of apoptosis), Noxa, and Bim (Bcl-2 interacting mediator of cell death), have been shown to initiate p53-dependent as well as p53-independent apoptosis in response to DNA damage and treatment with anticancer drugs or glucocorticoids.
  • In particular, the absence of Puma or Bim renders thymocytes and mature lymphocytes refractory to varying degrees to death induced in vitro by growth factor withdrawal, DNA damage, or glucocorticoids.
  • Absence of Puma or Bcl-2 overexpression efficiently protected diverse types of lymphocytes from the effects of gamma-radiation in vivo, and loss of Bim provided lower but significant protection in most lymphocytes, whereas Noxa deficiency had no impact.
  • [MeSH-major] Apoptosis / drug effects. Apoptosis / radiation effects. Apoptosis Regulatory Proteins / metabolism. Glucocorticoids / pharmacology. Lymphocytes / drug effects. Lymphocytes / radiation effects. Membrane Proteins / metabolism. Proto-Oncogene Proteins / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Animals. Cell Differentiation. Dexamethasone / pharmacology. Gamma Rays. Mice. Mice, Knockout. Spleen / cytology. Spleen / drug effects. Spleen / metabolism. Spleen / radiation effects. Thymus Gland / cytology. Thymus Gland / drug effects. Thymus Gland / metabolism. Thymus Gland / radiation effects

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  • [Cites] Science. 1999 Nov 26;286(5445):1735-8 [10576740.001]
  • [Cites] Cancer Cell. 2003 Oct;4(4):321-8 [14585359.001]
  • [Cites] J Exp Med. 2000 Jan 3;191(1):195-200 [10620618.001]
  • [Cites] Science. 2000 May 12;288(5468):1053-8 [10807576.001]
  • [Cites] Annu Rev Biochem. 2000;69:217-45 [10966458.001]
  • [Cites] Nature. 2000 Oct 12;407(6805):777-83 [11048728.001]
  • [Cites] Cell. 2000 Dec 8;103(6):839-42 [11136969.001]
  • [Cites] Mol Cell. 2000 Dec;6(6):1389-99 [11163212.001]
  • [Cites] FASEB J. 2001 Mar;15(3):693-9 [11259387.001]
  • [Cites] Mol Cell. 2001 Mar;7(3):673-82 [11463391.001]
  • [Cites] Mol Cell. 2001 Mar;7(3):683-94 [11463392.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):11318-23 [11572983.001]
  • [Cites] Cell Death Differ. 2002 Jan;9(1):6-19 [11803370.001]
  • [Cites] Science. 2003 Nov 7;302(5647):1036-8 [14500851.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):14175-80 [14623954.001]
  • [Cites] Cell. 2004 Jan 23;116(2):205-19 [14744432.001]
  • [Cites] Mol Cell Biol. 2004 Feb;24(4):1570-81 [14749373.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 20;101(16):6164-9 [15079075.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 May 4;101(18):7052-7 [15118096.001]
  • [Cites] Cell Death Differ. 2004 Jul;11 Suppl 1:S45-55 [15243581.001]
  • [Cites] Cell. 1991 Nov 29;67(5):879-88 [1835668.001]
  • [Cites] Cell. 1991 Nov 29;67(5):889-99 [1959134.001]
  • [Cites] Nature. 1993 Apr 29;362(6423):847-9 [8479522.001]
  • [Cites] Nature. 1993 Apr 29;362(6423):849-52 [8479523.001]
  • [Cites] Cell. 1993 Nov 19;75(4):817-25 [8242752.001]
  • [Cites] Cell. 1994 Oct 21;79(2):329-39 [7954799.001]
  • [Cites] EMBO J. 1995 Dec 15;14(24):6136-47 [8557033.001]
  • [Cites] Science. 1998 Mar 20;279(5358):1954-8 [9506948.001]
  • [Cites] Mol Cell. 1997 Dec;1(1):3-11 [9659898.001]
  • [Cites] Immunity. 1998 Aug;9(2):267-76 [9729047.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3706-11 [10097101.001]
  • [Cites] Nature. 1999 Aug 26;400(6747):886-91 [10476969.001]
  • [Cites] Nature. 1999 Oct 7;401(6753):616-20 [10524633.001]
  • [Cites] Mol Cell. 2005 Feb 4;17(3):393-403 [15694340.001]
  • [Cites] Nat Rev Immunol. 2005 Mar;5(3):189-200 [15719025.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Jun 10;331(3):843-50 [15865940.001]
  • [Cites] Cell. 2002 Jan 25;108(2):153-64 [11832206.001]
  • [Cites] Nature. 2002 Feb 21;415(6874):922-6 [11859372.001]
  • [Cites] Cell Death Differ. 2002 May;9(5):505-12 [11973609.001]
  • [Cites] Immunity. 2002 Jun;16(6):759-67 [12121658.001]
  • [Cites] Nat Rev Cancer. 2002 Aug;2(8):594-604 [12154352.001]
  • [Cites] Nat Rev Cancer. 2002 Sep;2(9):647-56 [12209154.001]
  • [Cites] J Exp Med. 2002 Oct 7;196(7):947-55 [12370256.001]
  • [Cites] Blood. 2003 Mar 15;101(6):2393-400 [12433687.001]
  • [Cites] Mol Cell. 2003 Mar;11(3):577-90 [12667443.001]
  • [Cites] J Biol Chem. 2003 Jun 27;278(26):23861-7 [12676946.001]
  • [Cites] Genes Dev. 2003 Sep 15;17(18):2233-8 [12952892.001]
  • [Cites] J Exp Med. 2003 Oct 6;198(7):1119-26 [14517273.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):14943-8 [10611317.001]
  • (PMID = 16118324.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [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 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Glucocorticoids; 0 / Membrane Proteins; 0 / PUMA protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Proteins; 7S5I7G3JQL / Dexamethasone
  • [Other-IDs] NLM/ PMC1895232
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56. Gluzman D, Imamura N, Sklyarenko L, Nadgornaya V, Zavelevich M, Machilo V: Patterns of hematological malignancies in Chernobyl clean-up workers (1996-2005). Exp Oncol; 2006 Mar;28(1):60-3
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  • AIM: The question as to whether the incidence of leukemias and malignant lymphomas among the Chernobyl clean-up workers increased in 20 years after the catastrophe is still a point of much controversy.
  • RESULTS: Various types of oncohematological diseases developing 10-20 years after Chernobyl accident were registered in a group of clean-up workers under study including myelodysplastic syndromes (MDS), acute leukemias (ALL and AML), chronic myelogenous leukemia (CML) and other chronic myeloproliferative diseases, chronic lymphocytic leukemia (B-CLL) and other chronic lymphoproliferative diseases of B and T cell origin.
  • Among 34 AML cases, leukemia was preceded by MDS in seven patients.
  • The relative contribution of CML to the total number of clean-up workers with leukemia was higher than the corresponding percentage value in general population examined at the same period (9.17 vs. 6.59%).
  • CONCLUSION: The verified diagnosis of tumors of hematopoietic and lymphoid tissue according to modern classification (EGIL, WHO) could be the prerequisite for further molecular genetic and analytical epidemiology study of leukemias that may be related to Chernobyl NPP accident consequences.
  • [MeSH-minor] Antigens, CD / analysis. Bone Marrow Cells / pathology. Humans. Immunohistochemistry. Leukemia / epidemiology. Ukraine / epidemiology

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  • (PMID = 16614710.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Radioactive Fallout
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57. Stachel D, Albert M, Meilbeck R, Paulides M, Schmid I: Expression of angiogenic factors in childhood B-cell precursor acute lymphoblastic leukemia. Oncol Rep; 2007 Jan;17(1):147-52
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  • [Title] Expression of angiogenic factors in childhood B-cell precursor acute lymphoblastic leukemia.
  • Pathological angiogenesis is increasingly recognized to be an important feature of pathogenesis in solid tumors and also in leukemias.
  • Vascular endothelial growth factor (VEGF) seems to play a central role in tumor angiogenesis and is associated with a poor prognosis in both solid tumors and adult leukemias.
  • In pediatric acute lymphocytic leukemia however, the expression of angiogenic molecules and its relation to prognosis and relapse are unknown.
  • Therefore, we prospectively analyzed 46 pediatric patients with precursor B cell acute lymphocytic leukemia by semi-quantitative RT-PCR for expression of the angiogenic molecules VEGF, VEGF-C, iNOS and TGF-beta and correlated relapse and survival data with the expression of these factors.
  • Angiogenic factors are expressed in the bone marrow of patients with pediatric B cell precursor ALL and VEGF is a potential candidate for therapeutic intervention as it is significantly higher expressed in children with late relapses.
  • The mRNA expression of iNOS in the surviving children possibly reflects an increased activity of the immune system against the leukemia which leads to a superior survival.
  • [MeSH-major] Angiogenic Proteins / biosynthesis. Burkitt Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 17143492.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Angiogenic Proteins; 0 / RNA, Messenger; 0 / Transforming Growth Factor beta; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C; 103107-01-3 / Fibroblast Growth Factor 2; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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58. Yan XJ, Albesiano E, Zanesi N, Yancopoulos S, Sawyer A, Romano E, Petlickovski A, Efremov DG, Croce CM, Chiorazzi N: B cell receptors in TCL1 transgenic mice resemble those of aggressive, treatment-resistant human chronic lymphocytic leukemia. Proc Natl Acad Sci U S A; 2006 Aug 1;103(31):11713-8
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  • [Title] B cell receptors in TCL1 transgenic mice resemble those of aggressive, treatment-resistant human chronic lymphocytic leukemia.
  • B cell chronic lymphocytic leukemia (B-CLL) is a clonal overgrowth of CD5(+) B lymphocytes.
  • In this disease, the B cell antigen receptor (BCR) is intimately linked to disease severity, because patients with BCRs, comprised of unmutated V(H) genes, follow a much more aggressive course.
  • This and related observations suggest that B-CLL derives from a B cell subset comprised of restricted BCR structural diversity and that antigen-selection and drive are major factors promoting the disease.
  • Nevertheless, the initiating event(s) that lead to the development of B-CLL are still unclear, in part because of the lack of an animal model that spontaneously evolves the molecular abnormalities that occur in the human disease.
  • Because overexpression of the TCL1 gene in murine B cells leads to a CD5(+) B cell lymphoproliferative disorder with many of the features of human B-CLL, we studied leukemias emerging in these mice to examine the extent to which their BCRs resemble those in B-CLL.
  • Our data indicate that the immunoglobulin heavy and light chain rearrangements in TCL1 mice display minimal levels of somatic mutations and exhibit several molecular features found in the human disease.

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  • [Cites] EMBO J. 1990 Jul;9(7):2133-40 [2113468.001]
  • [Cites] J Exp Med. 1989 Jan 1;169(1):255-68 [2462608.001]
  • [Cites] Blood. 1990 Aug 1;76(3):562-9 [2378986.001]
  • [Cites] Eur J Immunol. 1990 Aug;20(8):1855-63 [1976522.001]
  • [Cites] Eur J Immunol. 1991 Feb;21(2):351-9 [1705511.001]
  • [Cites] Cancer Res. 1992 Jan 15;52(2):437-43 [1370214.001]
  • [Cites] Eur J Immunol. 1993 Nov;23(11):2868-75 [8223863.001]
  • [Cites] Int Immunol. 1993 Nov;5(11):1365-73 [8260450.001]
  • [Cites] Immunol Today. 1994 Jun;15(6):288-94 [7520700.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Dec 20;91(26):12530-4 [7809072.001]
  • [Cites] J Exp Med. 1995 Apr 1;181(4):1507-17 [7535340.001]
  • [Cites] J Immunol. 1996 Feb 1;156(3):1038-46 [8557977.001]
  • [Cites] J Mol Biol. 1996 Nov 29;264(2):220-32 [8951372.001]
  • [Cites] J Immunol. 1997 Jan 1;158(1):235-46 [8977195.001]
  • [Cites] Int Immunol. 1997 Jan;9(1):27-41 [9043945.001]
  • [Cites] Int Immunol. 1997 May;9(5):689-702 [9184914.001]
  • [Cites] Oncogene. 1997 Aug 18;15(8):919-26 [9285687.001]
  • [Cites] J Clin Invest. 1998 Oct 15;102(8):1515-25 [9788964.001]
  • [Cites] J Exp Med. 1998 Dec 7;188(11):2151-62 [9841928.001]
  • [Cites] Eur J Immunol. 1999 Jul;29(7):2057-64 [10427967.001]
  • [Cites] Eur J Immunol. 1999 Jul;29(7):2065-71 [10427968.001]
  • [Cites] Eur J Immunol. 1999 Jul;29(7):2072-81 [10427969.001]
  • [Cites] Blood. 1999 Sep 15;94(6):1840-7 [10477712.001]
  • [Cites] Blood. 1999 Sep 15;94(6):1848-54 [10477713.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Nov 23;101(47):16600-5 [15545599.001]
  • [Cites] Blood. 2005 Feb 15;105(4):1678-85 [15466924.001]
  • [Cites] N Engl J Med. 2005 Feb 24;352(8):804-15 [15728813.001]
  • [Cites] J Clin Invest. 2005 Jun;115(6):1636-43 [15902303.001]
  • [Cites] Blood. 2005 Jun 15;105(12):4820-7 [15728130.001]
  • [Cites] Genes Dev. 1999 Nov 15;13(22):2905-27 [10579998.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3028-33 [10716693.001]
  • [Cites] Immunol Rev. 2000 Jun;175:70-9 [10933592.001]
  • [Cites] J Immunol. 2001 Jan 1;166(1):95-102 [11123281.001]
  • [Cites] N Engl J Med. 2000 Dec 28;343(26):1910-6 [11136261.001]
  • [Cites] Immunity. 2001 May;14(5):617-29 [11371363.001]
  • [Cites] J Exp Med. 2002 Jan 21;195(2):181-8 [11805145.001]
  • [Cites] Blood. 2002 Mar 15;99(6):2262-4 [11877310.001]
  • [Cites] Nat Rev Immunol. 2001 Dec;1(3):177-86 [11905826.001]
  • [Cites] J Immunol. 1989 May 15;142(10):3643-51 [2497178.001]
  • [Cites] J Autoimmun. 1988 Oct;1(5):469-81 [2473761.001]
  • [Cites] Adv Immunol. 1989;47:117-85 [2479233.001]
  • [Cites] Mol Immunol. 2005 Jul;42(11):1293-301 [15950725.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3575-83 [16076869.001]
  • [Cites] Curr Top Microbiol Immunol. 2005;294:51-70 [16323427.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):915-20 [16424025.001]
  • [Cites] Leukemia. 2006 Feb;20(2):280-5 [16341048.001]
  • [Cites] J Immunol. 2006 Apr 1;176(7):4221-34 [16547259.001]
  • [Cites] J Immunol. 2005 Jun 15;174(12):7773-80 [15944280.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6955-60 [12011454.001]
  • [Cites] Am J Pharmacogenomics. 2003;3(1):31-6 [12562214.001]
  • [Cites] Annu Rev Immunol. 2003;21:841-94 [12615894.001]
  • [Cites] Blood. 2003 Jun 15;101(12):4952-7 [12586612.001]
  • [Cites] J Mol Biol. 2003 Dec 5;334(4):733-49 [14636599.001]
  • [Cites] Immunol Rev. 2004 Feb;197:60-74 [14962187.001]
  • [Cites] Curr Opin Immunol. 2004 Apr;16(2):246-50 [15023420.001]
  • [Cites] J Clin Invest. 2004 Apr;113(7):1008-16 [15057307.001]
  • [Cites] Blood. 2004 Jun 15;103(12):4389-95 [14962897.001]
  • [Cites] Toxicol Sci. 2004 Sep;81(1):139-47 [15166399.001]
  • [Cites] J Exp Med. 2004 Aug 16;200(4):519-25 [15314077.001]
  • [Cites] Blood. 2004 Oct 15;104(8):2499-504 [15217828.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2879-85 [15217826.001]
  • [Cites] J Exp Med. 1983 Jan 1;157(1):202-18 [6600267.001]
  • [Cites] Blood Cells. 1987;12(2):485-502 [3304473.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 1989;54 Pt 1:209-17 [2639754.001]
  • (PMID = 16864779.001).
  • [ISSN] 0027-8424
  • [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
  • [Databank-accession-numbers] GENBANK/ DQ093183/ DQ093184/ DQ093185
  • [Grant] United States / NIGMS NIH HHS / GM / U54 GM062116; United States / NIGMS NIH HHS / GM / GM62116
  • [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 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Light Chains; 0 / Proto-Oncogene Proteins; 0 / Receptors, Antigen, B-Cell; 0 / Tcl1 protein, mouse
  • [Other-IDs] NLM/ PMC1518806
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59. Vannucchi AM, Masala G, Antonioli E, Chiara Susini M, Guglielmelli P, Pieri L, Maggi L, Caini S, Palli D, Bogani C, Ponziani V, Pancrazzi A, Annunziato F, Bosi A: Increased risk of lymphoid neoplasms in patients with Philadelphia chromosome-negative myeloproliferative neoplasms. Cancer Epidemiol Biomarkers Prev; 2009 Jul;18(7):2068-73
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  • With 4,421 person-years, we found 11 patients developing LPN, including four chronic lymphocytic leukemias, five non-Hodgkin's lymphomas, and two plasma cell disorders, after a median interval time of 68 months from MPN diagnosis.
  • There was a 3.44-fold increased risk of LPN compared with the general population, ranging from 2.86 for plasma cell disorder to 12.42 for chronic lymphocytic leukemia; the risk was significantly increased in JAK2V617F mutated patients (5.46-fold) and in males (4.52-fold).
  • The JAK2V617F mutation was found in lymphoid tumor cells in two of three cases evaluated, indicating that, in some patients, LPN originated in a JAK2V617F mutated common lymphoid-myeloid hematopoietic progenitor cell.

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  • (PMID = 19531676.001).
  • [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] EC 2.7.10.2 / Janus Kinase 2
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60. Dillman RO: Immunophenotyping of chronic lymphoid leukemias. J Clin Oncol; 2008 Mar 10;26(8):1193-4
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  • [Title] Immunophenotyping of chronic lymphoid leukemias.
  • [MeSH-major] Immunophenotyping. Leukemia, Lymphocytic, Chronic, B-Cell / immunology

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  • (PMID = 18323542.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD
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61. Ravandi F, O'Brien S: Chronic lymphoid leukemias other than chronic lymphocytic leukemia: diagnosis and treatment. Mayo Clin Proc; 2005 Dec;80(12):1660-74
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  • [Title] Chronic lymphoid leukemias other than chronic lymphocytic leukemia: diagnosis and treatment.
  • The World Health Organization classification divides lymphoid malignancies into precursor B-cell and T-cell neoplasms as well as mature B-cell and T-cell neoplasms.
  • Mature B-cell neoplasms comprise more than 85% of non-Hodgkin lymphomas worldwide and can be further subclassified according to the postulated cell of origin by using specific morphologic, immunophenotypic, and molecular characteristics.
  • Similarly, the more uncommon mature T-cell neoplasms have been better characterized to include numerous distinct entities with widely varying natural histories.
  • The distinction between lymphoma and leukemia is somewhat arbitrary and is based on variable involvement of the bone marrow, peripheral blood, and lymphatic system.
  • In this article, we review the diagnostic and clinical features of mature B-cell and T-cell lymphoproliferative disorders that commonly have a leukemic presentation.
  • [MeSH-major] Leukemia, Hairy Cell / diagnosis. Leukemia, Hairy Cell / therapy. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Leukemia, T-Cell / diagnosis. Leukemia, T-Cell / therapy

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  • (PMID = 16342661.001).
  • [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] 21
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62. Hernández Sánchez MC, García Quiroga H, Ulibarrena Redondo C, Méndez Sánchez JA: [Concurrent lymphoproliferative and myeloproliferative disorders in three patients]. An Med Interna; 2008 Feb;25(2):78-80
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  • [Transliterated title] Coexistencia de Síndrome Lifoproliferativo Crónico y Síndrome Mieloproliferativo Crónico en tres pacientes.
  • We present two patients with a diagnosis of chronic lymphoproliferative syndrome, chronic lymphocytic leukemia B (CLL B) and lymphoplasmacytic non-Hodgkin's lymphoma (NHL), who developed chronic myeloproliferative syndrome: polycythemia vera (PV) and Philadelphia-positive chronic myeloid leukemia (CML) respectively, and a third patient with chronic myeloproliferative syndrome, polycythemia vera (PV), who developed an undefined immunophenotype cyclin D1-positive chronic lymphoproliferative syndrome.

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  • (PMID = 18432364.001).
  • [ISSN] 0212-7199
  • [Journal-full-title] Anales de medicina interna (Madrid, Spain : 1984)
  • [ISO-abbreviation] An Med Interna
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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63. Mankaï A, Bordron A, Renaudineau Y, Martins-Carvalho C, Takahashi S, Ghedira I, Berthou C, Youinou P: Purine-rich box-1-mediated reduced expression of CD20 alters rituximab-induced lysis of chronic lymphocytic leukemia B cells. Cancer Res; 2008 Sep 15;68(18):7512-9
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  • [Title] Purine-rich box-1-mediated reduced expression of CD20 alters rituximab-induced lysis of chronic lymphocytic leukemia B cells.
  • The anti-CD20 monoclonal antibody rituximab has been less successful in treating chronic lymphocytic leukemia (CLL) than lymphoma, possibly due to the lower density of CD20 on B lymphocytes from CLL patients than on those from lymphoma patients.
  • This abnormality is consistent with our finding of elevated levels of Flt3 ligand (FL) in 20 of 23 CLL sera tested.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antigens, CD20 / biosynthesis. Antineoplastic Agents / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Proto-Oncogene Proteins / genetics. Trans-Activators / genetics
  • [MeSH-minor] Aged. Aged, 80 and over. Antibodies, Monoclonal, Murine-Derived. B-Lymphocytes / immunology. DNA Methylation. Female. Genetic Therapy / methods. Humans. Male. Middle Aged. Organic Cation Transport Proteins / biosynthesis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Rituximab. Transfection. fms-Like Tyrosine Kinase 3 / biosynthesis. fms-Like Tyrosine Kinase 3 / metabolism

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  • (PMID = 18794139.001).
  • [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 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antineoplastic Agents; 0 / Organic Cation Transport Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / SLC22A2 protein, human; 0 / Trans-Activators; 0 / proto-oncogene protein Spi-1; 4F4X42SYQ6 / Rituximab; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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64. Walsh SH, Grabowski P, Berglund M, Thunberg U, Thorsélius M, Tobin G, Aleskog A, Karlsson K, Sundström C, Laurell A, Enblad G, Rosenquist R, Roos G: Telomere length and correlation with histopathogenesis in B-cell leukemias/lymphomas. Eur J Haematol; 2007 Apr;78(4):283-9
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  • [Title] Telomere length and correlation with histopathogenesis in B-cell leukemias/lymphomas.
  • Telomere length was recently reported to correlate with cellular origin of B-cell malignancies in relation to the germinal center (GC).
  • In this report, we measured telomere length by quantitative-PCR in 223 B-cell lymphomas/leukemias and correlated results with immunoglobulin (Ig) mutation status and immunostainings for GC/non-GC subtypes of diffuse large B-cell lymphoma (DLBCL).
  • Shortest telomeres were found in Ig-unmutated chronic lymphocytic leukemia (CLL) [median telomere to single copy gene value (T/S) 0.33], differing significantly to Ig-mutated CLL (0.63).
  • Contrary to this, mantle cell lymphomas (MCLs) exhibited similar telomere lengths regardless of Ig mutation status (0.47).
  • Hairy cell leukemias, which display Ig gene intraclonal heterogeneity, had longer telomeres (0.62) than FLs and non-GC-DLBCL, but shorter than GC-DLBCL.
  • [MeSH-major] Germinal Center / pathology. Immunoglobulins / genetics. Leukemia, B-Cell / genetics. Lymphoma, B-Cell / genetics. Mutation. Telomere / genetics

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  • (PMID = 17286609.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Immunoglobulins
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65. Wiederschain D, Kawai H, Shilatifard A, Yuan ZM: Multiple mixed lineage leukemia (MLL) fusion proteins suppress p53-mediated response to DNA damage. J Biol Chem; 2005 Jul 1;280(26):24315-21
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  • [Title] Multiple mixed lineage leukemia (MLL) fusion proteins suppress p53-mediated response to DNA damage.
  • Chromosomal translocations involving the mixed lineage leukemia (MLL) gene are often observed in acute leukemias of both myeloid and lymphocytic origin.
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. DNA Primers / chemistry. Humans. Immunoprecipitation. Luciferases / metabolism. Models, Genetic. Myeloid-Lymphoid Leukemia Protein. Plasmids / metabolism. Protein Structure, Tertiary. RNA / chemistry. Radiation, Ionizing. Recombinant Fusion Proteins / chemistry. Retroviridae / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic. Transcriptional Activation. Transfection. Translocation, Genetic

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  • (PMID = 15851483.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / ES11627; United States / NCI NIH HHS / CA / R01 CA85679-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / MLL-AF10 fusion protein, human; 0 / MLL-AF9 fusion protein, human; 0 / MLL-ELL fusion protein, human; 0 / MLL-ENL oncoprotein, human; 0 / Oncogene Proteins, Fusion; 0 / Recombinant Fusion Proteins; 0 / Tumor Suppressor Protein p53; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 63231-63-0 / RNA; EC 1.13.12.- / Luciferases
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66. Tasca S, Carli E, Caldin M, Menegazzo L, Furlanello T, Gallego LS: Hematologic abnormalities and flow cytometric immunophenotyping results in dogs with hematopoietic neoplasia: 210 cases (2002-2006). Vet Clin Pathol; 2009 Mar;38(1):2-12
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  • RESULTS: Based on cell morphology and phenotype, cases were classified as: acute lymphoblastic leukemia (ALL, n=51), acute myeloid leukemia (AML, n=33), chronic lymphocytic leukemia (CLL, n=61), and leukemic high-grade lymphoma (L-HGL, n=65).
  • Most cases of ALL (47/51) and L-HGL (41/65) had a B-cell phenotype, while most cases of CLL (54/61) had a T-cell phenotype, with a high prevalence of the large granular lymphocyte subtype (49/61).
  • Neutropenia was seen in 64-78% of acute leukemias (AML and ALL) in contrast to no cases of CLL and 11% of L-HGL.
  • Thrombocytopenia was seen in 88-90% of acute leukemias in contrast to 15% of CLL and 40% of L-HGL.
  • Thrombocytopenia was more prevalent (71% vs 22%) and significantly more severe in T-cell vs B-cell L-HGL.

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  • (PMID = 19171020.001).
  • [ISSN] 0275-6382
  • [Journal-full-title] Veterinary clinical pathology
  • [ISO-abbreviation] Vet Clin Pathol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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67. Winrow CJ, Pankratz DG, Vibat CR, Bowen TJ, Callahan MA, Warren AJ, Hilbush BS, Wynshaw-Boris A, Hasel KW, Weaver Z, Lockhart DJ, Barlow C: Aberrant recombination involving the granzyme locus occurs in Atm-/- T-cell lymphomas. Hum Mol Genet; 2005 Sep 15;14(18):2671-84
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  • [Title] Aberrant recombination involving the granzyme locus occurs in Atm-/- T-cell lymphomas.
  • Ataxia telangiectasia (A-T) is an autosomal recessive disease caused by loss of function of the serine/threonine protein kinase ATM (ataxia telangiectasia mutated).
  • A-T patients have a 250-700-fold increased risk of developing lymphomas and leukemias which are typically highly invasive and proliferative.
  • In addition, a subset of adult acute lymphoblastic leukemias and aggressive B-cell chronic lymphocytic leukemias that occur in the general population show loss of heterozygosity for ATM.
  • To define the specific role of ATM in lymphomagenesis, we studied T-cell lymphomas isolated from mice with mutations in ATM and/or p53 using cytogenetic analysis and mRNA transcriptional profiling.
  • [MeSH-major] Cell Cycle Proteins / genetics. DNA-Binding Proteins / genetics. Gene Expression Regulation, Neoplastic. Lymphoma, T-Cell / genetics. Models, Biological. Protein-Serine-Threonine Kinases / genetics. Recombination, Genetic / genetics. Serine Endopeptidases / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Animals. Ataxia Telangiectasia Mutated Proteins. Blotting, Northern. Cell Line, Tumor. Computational Biology. Cytogenetic Analysis. DNA Primers. Gene Expression Profiling. Granzymes. In Situ Hybridization, Fluorescence. Mice. Mice, Knockout. Microarray Analysis. Mutation / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16087685.001).
  • [ISSN] 0964-6906
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS039601-04
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Atm protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.4.21.- / Granzymes; EC 3.4.21.- / Gzmb protein, mouse; EC 3.4.21.- / Gzmc protein, mouse; EC 3.4.21.- / Serine Endopeptidases
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68. Rainis L, Toki T, Pimanda JE, Rosenthal E, Machol K, Strehl S, Göttgens B, Ito E, Izraeli S: The proto-oncogene ERG in megakaryoblastic leukemias. Cancer Res; 2005 Sep 1;65(17):7596-602
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  • [Title] The proto-oncogene ERG in megakaryoblastic leukemias.
  • Acquired additions of chromosome 21 are a common finding in leukemias, suggesting a contributory role to leukemogenesis.
  • About 10% of patients with a germ line trisomy 21 (Down syndrome) are born with transient megakaryoblastic leukemia.
  • We show that ERG is expressed in hematopoietic stem cells, megakaryoblastic cell lines, and in primary leukemic cells from Down syndrome patients.
  • ERG expression is induced upon megakaryocytic differentiation of the erythroleukemia cell lines K562 and UT-7, and forced expression of ERG in K562 cells induces erythroid to megakaryoblastic phenotypic switch.
  • Furthermore, both ERG and ETS2 bind in vivo the hematopoietic enhancer of SCL/TAL1, a key regulator of hematopoietic stem cell and megakaryocytic development.
  • We propose that trisomy 21 facilitates the occurrence of megakaryoblastic leukemias through a shift toward the megakaryoblastic lineage caused by the excess expression of ERG, and possibly by other chromosome 21 genes, such as RUNX1 and ETS2, in hematopoietic progenitor cells, coupled with a differentiation arrest caused by the acquisition of mutations in GATA1.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Oncogene Proteins / genetics. Trans-Activators / genetics
  • [MeSH-minor] Base Sequence. Basic Helix-Loop-Helix Transcription Factors. Cell Lineage. Chromosomes, Human, Pair 21 / genetics. Erythroid-Specific DNA-Binding Factors. GATA1 Transcription Factor. HeLa Cells. Hematopoietic Stem Cells / metabolism. Humans. K562 Cells. Leukemia, Erythroblastic, Acute / genetics. Leukemia, Erythroblastic, Acute / pathology. Molecular Sequence Data. Promoter Regions, Genetic. Proto-Oncogene Proteins / metabolism. Transcription Factors / genetics. Transcription Factors / metabolism

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  • (PMID = 16140924.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / ERG protein, human; 0 / Erythroid-Specific DNA-Binding Factors; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Oncogene Proteins; 0 / Proto-Oncogene Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 135471-20-4 / TAL1 protein, human
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69. Lucas DM, Edwards RB, Lozanski G, West DA, Shin JD, Vargo MA, Davis ME, Rozewski DM, Johnson AJ, Su BN, Goettl VM, Heerema NA, Lin TS, Lehman A, Zhang X, Jarjoura D, Newman DJ, Byrd JC, Kinghorn AD, Grever MR: The novel plant-derived agent silvestrol has B-cell selective activity in chronic lymphocytic leukemia and acute lymphoblastic leukemia in vitro and in vivo. Blood; 2009 May 7;113(19):4656-66
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  • [Title] The novel plant-derived agent silvestrol has B-cell selective activity in chronic lymphocytic leukemia and acute lymphoblastic leukemia in vitro and in vivo.
  • Therapeutic options for advanced B-cell acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL) are limited.
  • Available treatments can also deplete T lymphocytes, leaving patients at risk of life-threatening infections.
  • In the National Cancer Institute cell line screen, the structurally unique natural product silvestrol produces an unusual pattern of cytotoxicity that suggests activity in leukemia and selectivity for B cells.
  • We investigated silvestrol efficacy using primary human B-leukemia cells, established B-leukemia cell lines, and animal models.
  • In vivo, silvestrol causes significant B-cell reduction in Emu-Tcl-1 transgenic mice and significantly extends survival of 697 xenograft severe combined immunodeficient (SCID) mice without discernible toxicity.
  • These data indicate silvestrol has efficacy against B cells in vitro and in vivo and identify translational inhibition as a potential therapeutic target in B-cell leukemias.

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  • [Cites] Leukemia. 2003 Oct;17(10):1981-9 [14513048.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6955-60 [12011454.001]
  • [Cites] J Org Chem. 2004 May 14;69(10):3350-8 [15132542.001]
  • [Cites] Blood. 2002 Aug 15;100(4):1177-84 [12149195.001]
  • [Cites] J Biol Chem. 2002 Nov 22;277(47):44791-800 [12237314.001]
  • [Cites] J Clin Oncol. 2003 Apr 15;21(8):1466-71 [12697868.001]
  • [Cites] Blood. 2003 Jul 15;102(2):652-8 [12649137.001]
  • [Cites] Am J Respir Cell Mol Biol. 2003 Sep;29(3 Pt 1):367-74 [12663328.001]
  • [Cites] Arch Biochem Biophys. 2003 Sep 15;417(2):141-52 [12941295.001]
  • [Cites] Crit Rev Oncol Hematol. 2004 Jun;50(3):223-61 [15182827.001]
  • [Cites] J Biol Chem. 2004 Jun 25;279(26):26915-21 [15078892.001]
  • [Cites] Leukemia. 2004 Jul;18(7):1207-14 [15116122.001]
  • [Cites] Anticancer Res. 1988 May-Jun;8(3):355-67 [3389740.001]
  • [Cites] J Natl Cancer Inst. 1991 Jun 5;83(11):757-66 [2041050.001]
  • [Cites] J Cell Physiol. 1996 Mar;166(3):523-36 [8600156.001]
  • [Cites] Antiviral Res. 1995 Nov;28(3):265-79 [8629818.001]
  • [Cites] J Nat Prod. 1997 Jun;60(6):606-8 [9214732.001]
  • [Cites] Z Naturforsch C. 1999 Jan-Feb;54(1-2):55-60 [10223787.001]
  • [Cites] J Immunol Methods. 2004 Nov;294(1-2):15-22 [15604012.001]
  • [Cites] Cell Cycle. 2004 Oct;3(10):1259-62 [15467463.001]
  • [Cites] Immunology. 2005 Apr;114(4):441-9 [15804279.001]
  • [Cites] J Immunol. 2005 Jun 1;174(11):7075-84 [15905551.001]
  • [Cites] Blood. 2005 Jul 15;106(2):408-18 [15797997.001]
  • [Cites] Blood. 2005 Oct 1;106(7):2513-9 [15972445.001]
  • [Cites] Semin Oncol. 2006 Apr;33(2):240-9 [16616071.001]
  • [Cites] Cancer Res. 2006 Apr 15;66(8):3978-80 [16618714.001]
  • [Cites] Cell Death Differ. 2006 Aug;13(8):1419-21 [16645636.001]
  • [Cites] Anticancer Agents Med Chem. 2006 Jul;6(4):319-45 [16842234.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Aug 1;103(31):11713-8 [16864779.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1334-8 [16670263.001]
  • [Cites] Anticancer Res. 2006 Sep-Oct;26(5A):3349-56 [17094452.001]
  • [Cites] Blood. 2007 Jan 15;109(2):399-404 [17003373.001]
  • [Cites] Blood. 2007 Mar 1;109(5):2008-13 [17068155.001]
  • [Cites] J Clin Oncol. 2007 Mar 1;25(7):799-804 [17283363.001]
  • [Cites] Expert Opin Emerg Drugs. 2007 Mar;12(1):165-79 [17355221.001]
  • [Cites] Clin Cancer Res. 2007 Apr 1;13(7):2144-50 [17404098.001]
  • [Cites] J Biol Chem. 2007 Aug 3;282(31):22551-62 [17553788.001]
  • [Cites] Anticancer Res. 2007 Jul-Aug;27(4B):2175-83 [17695501.001]
  • [Cites] Cell Death Differ. 2007 Sep;14(9):1576-82 [17612585.001]
  • [Cites] Int J Cancer. 2007 Oct 15;121(8):1839-46 [17565740.001]
  • [Cites] Angew Chem Int Ed Engl. 2007;46(41):7831-4 [17806093.001]
  • [Cites] Angew Chem Int Ed Engl. 2007;46(41):7835-8 [17823902.001]
  • [Cites] Blood. 2008 Mar 15;111(6):3190-9 [18192508.001]
  • [Cites] J Clin Invest. 2008 Jul;118(7):2651-60 [18551192.001]
  • [Cites] Blood. 2008 Nov 1;112(9):3807-17 [18599795.001]
  • [Cites] J Am Chem Soc. 2009 Feb 4;131(4):1607-16 [19140688.001]
  • [Cites] Z Naturforsch C. 1999 Dec;54(12):1075-83 [10685499.001]
  • [Cites] Blood. 2000 Jul 15;96(2):393-7 [10887097.001]
  • [Cites] Biotechniques. 2001 Sep;31(3):464, 466 [11570486.001]
  • [Cites] EMBO J. 2001 Dec 3;20(23):6627-36 [11726499.001]
  • [Cites] Blood. 2002 Mar 15;99(6):1885-93 [11877256.001]
  • [Cites] Leukemia. 2002 Apr;16(4):444-54 [11960321.001]
  • [Cites] Blood. 2004 May 1;103(9):3278-81 [14726385.001]
  • (PMID = 19190247.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U19 CA052956; United States / NCI NIH HHS / CA / P01CA125066; United States / NCI NIH HHS / CA / P01 CA125066; United States / NCI NIH HHS / CA / P01 CA081534; United States / NCI NIH HHS / CA / CA52956
  • [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 / Mcl1 protein, mouse; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / Tcl1 protein, mouse; 0 / Triterpenes; 0 / silvestrol
  • [Other-IDs] NLM/ PMC2680369
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70. Figueroa ME, Reimers M, Thompson RF, Ye K, Li Y, Selzer RR, Fridriksson J, Paietta E, Wiernik P, Green RD, Greally JM, Melnick A: An integrative genomic and epigenomic approach for the study of transcriptional regulation. PLoS One; 2008 Mar 26;3(3):e1882
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  • The molecular heterogeneity of acute leukemias and other tumors constitutes a major obstacle towards understanding disease pathogenesis and developing new targeted-therapies.
  • We predicted that integration of different genome-wide epigenetic regulatory marks along with gene expression levels would provide greater power in capturing biological differences between leukemia subtypes.
  • Gene expression, cytosine methylation and histone H3 lysine 9 (H3K9) acetylation were measured using high-density oligonucleotide microarrays in primary human acute myeloid leukemia (AML) and acute lymphocytic leukemia (ALL) specimens.
  • We found that DNA methylation and H3K9 acetylation distinguished these leukemias of distinct cell lineage, as expected, but that an integrative analysis combining the information from each platform revealed hundreds of additional differentially expressed genes that were missed by gene expression arrays alone.

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  • [Cites] Science. 1999 Oct 15;286(5439):531-7 [10521349.001]
  • [Cites] Cancer Res. 1999 Aug 1;59(15):3730-40 [10446989.001]
  • [Cites] Bioinformatics. 2005 Jun 1;21(11):2789-90 [15797915.001]
  • [Cites] Clin Cancer Res. 2005 Jul 15;11(14):5167-74 [16033832.001]
  • [Cites] BMC Bioinformatics. 2005;6:166 [15992406.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):305-19 [16075461.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Nov 1;102(44):15785-90 [16243968.001]
  • [Cites] Nat Rev Cancer. 2006 Feb;6(2):107-16 [16491070.001]
  • [Cites] Cancer Res. 2006 Apr 1;66(7):3541-9 [16585178.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6118-28 [16778185.001]
  • [Cites] Genome Res. 2006 Aug;16(8):1046-55 [16809668.001]
  • [Cites] Cancer Res. 2007 Jan 1;67(1):194-201 [17210699.001]
  • [Cites] Nucleic Acids Res. 2007;35(3):801-11 [17202157.001]
  • [Cites] J Biol Chem. 2002 Apr 12;277(15):13286-93 [11825903.001]
  • [Cites] Nat Rev Genet. 2002 Jun;3(6):415-28 [12042769.001]
  • [Cites] Genome Res. 2002 Jun;12(6):996-1006 [12045153.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 25;99(13):8695-700 [12060701.001]
  • [Cites] Genome Res. 2002 Jul;12(7):1112-20 [12097349.001]
  • [Cites] Semin Cancer Biol. 2002 Oct;12(5):347-57 [12191634.001]
  • [Cites] Cancer Res. 2003 May 1;63(9):2164-71 [12727835.001]
  • [Cites] Leukemia. 2003 May;17(5):910-8 [12750705.001]
  • [Cites] N Engl J Med. 2003 Nov 20;349(21):2042-54 [14627790.001]
  • [Cites] Methods Enzymol. 2004;376:315-34 [14975315.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1617-28 [15084694.001]
  • [Cites] Cell. 2004 Jun 11;117(6):721-33 [15186774.001]
  • [Cites] Clin Cancer Res. 2004 Aug 1;10(15):4933-8 [15297393.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jun 9;95(12):6870-5 [9618505.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14863-8 [9843981.001]
  • [Cites] Cancer Res. 2007 Mar 15;67(6):2617-25 [17363581.001]
  • [Cites] BMC Genomics. 2007;8:131 [17524140.001]
  • [Cites] Science. 2001 Aug 10;293(5532):1074-80 [11498575.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10781-6 [11535808.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]
  • [Cites] Genes Dev. 2002 Jan 1;16(1):6-21 [11782440.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Nat Genet. 1999 Jan;21(1):103-7 [9916800.001]
  • [Cites] Cancer Res. 1999 Feb 15;59(4):793-7 [10029064.001]
  • [Cites] Cell. 2005 Jan 28;120(2):169-81 [15680324.001]
  • (PMID = 18365023.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA104348; United States / NICHD NIH HHS / HD / R01 HD044078; United States / NIGMS NIH HHS / GM / T32 GM007288; United States / NIGMS NIH HHS / GM / GM007288
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Histones
  • [Other-IDs] NLM/ PMC2266992
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71. Willenbrock K, Jungnickel B, Hansmann ML, Küppers R: Human splenic marginal zone B cells lack expression of activation-induced cytidine deaminase. Eur J Immunol; 2005 Oct;35(10):3002-7
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  • Moreover, the lack of AID-positive MZ B cells questions the recent speculation that B cell chronic lymphocytic leukemias with mutated V genes are derived from mutating MZ B cells.
  • [MeSH-major] B-Lymphocytes / immunology. Cytosine Deaminase / biosynthesis. Spleen / cytology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Lineage / immunology. Cytidine Deaminase. Female. Humans. Immunohistochemistry. Male. Middle Aged. Somatic Hypermutation, Immunoglobulin / immunology

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  • [CommentIn] Eur J Immunol. 2005 Oct;35(10):2789-92 [16180256.001]
  • (PMID = 16180254.001).
  • [ISSN] 0014-2980
  • [Journal-full-title] European journal of immunology
  • [ISO-abbreviation] Eur. J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 3.5.4.- / AICDA (activation-induced cytidine deaminase); EC 3.5.4.1 / Cytosine Deaminase; EC 3.5.4.5 / Cytidine Deaminase
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72. 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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73. Robak T, Robak P: Current treatment options in prolymphocytic leukemia. Med Sci Monit; 2007 Apr;13(4):RA69-80
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  • [Title] Current treatment options in prolymphocytic leukemia.
  • Prolymphocytic leukemia (PLL) is a rare lymphoproliferative disorder characterized by marked leukocytosis and splenomegaly.
  • PLL accounts for approximately 2% of chronic lymphoid leukemias.
  • The clinical course is progressive in the majority of cases due to the resistance of the disease to conventional chemotherapy.
  • The disease is divided according to the cell of origin into the B- (B-PLL) and T-cell (T-PLL) types.
  • Approximately 80% of cases are of B-cell phenotype.
  • PLL has poorer prognosis than chronic lymphocytic leukemia (CLL), and the patients with static disease for a longer period of time are rare.
  • PLL is still considered an incurable disease.
  • Finally, high-dose chemotherapy followed by allogenic or autologous stem cell transplantation seems to be an effective, probably curative, strategy for the treatment of selected patients with PLL.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Leukemia, Prolymphocytic / diagnosis. Leukemia, Prolymphocytic / drug therapy. Leukemia, Prolymphocytic / genetics. Purine Nucleosides / therapeutic use
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antibodies, Monoclonal, Murine-Derived. Antibodies, Neoplasm / therapeutic use. Cladribine / therapeutic use. Drug Therapy / methods. Humans. Pentostatin / therapeutic use. Rituximab. Splenectomy / methods. Stem Cell Transplantation / methods. Vidarabine / analogs & derivatives. Vidarabine / therapeutic use

  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. CLADRIBINE .
  • Hazardous Substances Data Bank. PENTOSTATIN .
  • Hazardous Substances Data Bank. VIDARABINE .
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  • (PMID = 17392661.001).
  • [ISSN] 1234-1010
  • [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; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 0 / Purine Nucleosides; 395575MZO7 / Pentostatin; 3A189DH42V / alemtuzumab; 47M74X9YT5 / Cladribine; 4F4X42SYQ6 / Rituximab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  • [Number-of-references] 118
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74. Song JH, Schnittke N, Zaat A, Walsh CS, Miller CW: FBXW7 mutation in adult T-cell and B-cell acute lymphocytic leukemias. Leuk Res; 2008 Nov;32(11):1751-5
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  • [Title] FBXW7 mutation in adult T-cell and B-cell acute lymphocytic leukemias.
  • Engineered FBXW7 null cells display cell cycle and chromosome stability defects.
  • Mutations of FBXW7 have been found in human colorectal, ovarian, endometrial tumors and T-cell acute lymphocytic leukemias.
  • Prompted by these findings we have examined acute myeloid leukemia, non-Hodgkin's lymphoma, T-cell acute lymphocytic leukemia, B-cell acute lymphocytic leukemia and adult T-cell leukemia DNA for mutations of the FBXW7 gene.
  • As expected, mutations were found in T-cell acute lymphocytic leukemias.
  • However mutations of FBXW7 were also found in four of 118 B-cell acute lymphocytic leukemias and one of 24 adult T-cell leukemia samples.
  • These observations suggest that disruption of FBXW7 has a role in several forms of lymphocytic leukemias and not exclusively T-cell acute lymphocytic leukemia.
  • [MeSH-major] Burkitt Lymphoma / genetics. Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, Non-Hodgkin / genetics. Mutation / genetics. Ubiquitin-Protein Ligases / genetics

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  • (PMID = 18485478.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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75. Lü SQ, Yang JM, Wang JM: [Effects of proteasome inhibitors on leukemias]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Aug;15(4):896-900
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  • [Title] [Effects of proteasome inhibitors on leukemias].
  • A lot of studies on effects of proteasome inhibitors on leukemias, including plasma cell leukemia; chronic lymphocytic leukemia, adult T cell lymphoma/leukemia, chronic myeloid leukemia and acute myeloid leukemia, were reviewed in this article.

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  • (PMID = 17708829.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
  • [Number-of-references] 27
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76. Klener P, Szynal M, Cleuter Y, Merimi M, Duvillier H, Lallemand F, Bagnis C, Griebel P, Sotiriou C, Burny A, Martiat P, Van den Broeke A: Insights into gene expression changes impacting B-cell transformation: cross-species microarray analysis of bovine leukemia virus tax-responsive genes in ovine B cells. J Virol; 2006 Feb;80(4):1922-38
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  • [Title] Insights into gene expression changes impacting B-cell transformation: cross-species microarray analysis of bovine leukemia virus tax-responsive genes in ovine B cells.
  • Large-animal models for leukemia have the potential to aid in the understanding of networks that contribute to oncogenesis.
  • Infection of cattle and sheep with bovine leukemia virus (BLV), a complex retrovirus related to human T-cell leukemia virus type 1 (HTLV-1), is associated with the development of B-cell leukemia.
  • Whereas the natural disease in cattle is characterized by a low tumor incidence, experimental infection of sheep leads to overt leukemia in the majority of infected animals, providing a model for studying the pathogenesis associated with BLV and HTLV-1.
  • Using cDNA-spotted microarrays comprising 10,336 human genes/expressed sequence tags, we identified a cohort of differentially expressed genes, including genes related to apoptosis, DNA transcription, and repair; proto-oncogenes; cell cycle regulators; transcription factors; small Rho GTPases/GTPase-binding proteins; and previously reported Tax(HTLV-1)-responsive genes.
  • Interestingly, genes known to be associated with human neoplasia, especially B-cell malignancies, were extensively represented.
  • Although cross-species approaches do not permit a comprehensive analysis of gene expression patterns, they can provide initial clues for the functional roles of genes that participate in B-cell transformation and pinpoint molecular targets not identified using other methods in animal models.
  • [MeSH-major] B-Lymphocytes / physiology. B-Lymphocytes / virology. Cell Transformation, Viral / genetics. Gene Expression Profiling. Gene Expression Regulation. Gene Products, tax / physiology. Leukemia Virus, Bovine / physiology

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  • [Cites] Annu Rev Immunol. 2001;19:475-96 [11244044.001]
  • [Cites] J Biol Chem. 2001 Apr 20;276(16):13395-401 [11278855.001]
  • [Cites] EMBO J. 2001 May 1;20(9):2273-85 [11331592.001]
  • [Cites] Blood. 2001 Jun 15;97(12):3902-9 [11389033.001]
  • [Cites] Nature. 2001 Jul 19;412(6844):341-6 [11460166.001]
  • [Cites] Oncogene. 2001 Jul 27;20(33):4484-96 [11494144.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Dec 4;98(25):14452-7 [11734645.001]
  • [Cites] Breast Cancer Res Treat. 2001 Sep;69(1):29-38 [11759826.001]
  • [Cites] Dis Markers. 2001;17(3):129-37 [11790876.001]
  • [Cites] Clin Cancer Res. 2002 Feb;8(2):589-95 [11839681.001]
  • [Cites] Blood. 2002 May 1;99(9):3367-75 [11964305.001]
  • [Cites] J Biol Chem. 2002 Apr 26;277(17):14877-83 [11836256.001]
  • [Cites] Vet Immunol Immunopathol. 2002 Jul;86(3-4):229-44 [12007889.001]
  • [Cites] Nat Genet. 2002 Jun;31(2):210-5 [12021785.001]
  • [Cites] Am J Pathol. 2002 Jun;160(6):2309-10 [12057933.001]
  • [Cites] Lab Invest. 2002 Jul;82(7):893-901 [12118091.001]
  • [Cites] Cancer Lett. 2002 Nov 28;185(2):219-23 [12169396.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1795-801 [12176902.001]
  • [Cites] Biotechniques. 2002 Sep;33(3):516-8, 520, 522 passim [12238761.001]
  • [Cites] J Virol. 1987 Aug;61(8):2462-71 [3037109.001]
  • [Cites] EMBO J. 1987 Nov;6(11):3385-9 [2828028.001]
  • [Cites] Leukemia. 1988 Feb;2(2):103-7 [2830439.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Dec;85(23):9263-7 [2848258.001]
  • [Cites] Mol Cell Biol. 1990 Jan;10(1):413-7 [2403646.001]
  • [Cites] EMBO J. 1990 May;9(5):1577-81 [2158445.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 May 1;88(9):3720-4 [1827203.001]
  • [Cites] J Virol. 1992 Jul;66(7):4570-5 [1351105.001]
  • [Cites] J Virol. 1993 Jul;67(7):4078-85 [8389918.001]
  • [Cites] Blood. 1995 Nov 15;86(10):3619-39 [7579327.001]
  • [Cites] J Virol. 1995 Dec;69(12):7541-7 [7494260.001]
  • [Cites] Biotechniques. 1996 Apr;20(4):584-91 [8800675.001]
  • [Cites] Oncogene. 1997 Sep;15(11):1289-94 [9315096.001]
  • [Cites] Int J Cancer. 1998 Sep 25;78(1):27-32 [9724090.001]
  • [Cites] J Virol. 1999 Feb;73(2):1054-65 [9882306.001]
  • [Cites] Int Immunol. 1999 Jul;11(7):1139-47 [10383947.001]
  • [Cites] Biol Chem. 1999 Jun;380(6):653-60 [10430029.001]
  • [Cites] Int J Oncol. 2000 Apr;16(4):757-62 [10717245.001]
  • [Cites] Leuk Lymphoma. 2000 Mar;37(1-2):39-51 [10721768.001]
  • [Cites] Oncogene. 2003 May 1;22(17):2680-8 [12730682.001]
  • [Cites] Mol Cell Biol. 2003 Jun;23(11):3837-46 [12748286.001]
  • [Cites] Hum Mol Genet. 2003 Jun 1;12(11):1261-72 [12761041.001]
  • [Cites] Toxicol Sci. 2003 Aug;74(2):470-84 [12773757.001]
  • [Cites] Cancer Lett. 2003 Jul 18;197(1-2):87-92 [12880965.001]
  • [Cites] Oncogene. 2003 Jul 17;22(29):4531-42 [12881710.001]
  • [Cites] Blood. 2003 Aug 15;102(4):1443-8 [12738680.001]
  • [Cites] Oncogene. 2003 Aug 11;22(33):5131-40 [12910250.001]
  • [Cites] Oncogene. 2003 Aug 11;22(33):5141-9 [12910251.001]
  • [Cites] J Bone Miner Res. 2003 Aug;18(8):1419-29 [12929931.001]
  • [Cites] Cancer Genet Cytogenet. 2003 Sep;145(2):152-60 [12935928.001]
  • [Cites] Arch Virol. 2003 Sep;148(9):1787-804 [14505090.001]
  • [Cites] Cancer Cell. 2003 Sep;4(3):197-207 [14522254.001]
  • [Cites] Oncogene. 2003 Sep 29;22(42):6497-507 [14528274.001]
  • [Cites] J Biochem. 2003 Sep;134(3):327-31 [14561717.001]
  • [Cites] Hepatology. 2003 Nov;38(5):1242-9 [14578863.001]
  • [Cites] Cancer Res. 2002 Oct 1;62(19):5408-12 [12359745.001]
  • [Cites] EMBO J. 2002 Oct 15;21(20):5487-97 [12374749.001]
  • [Cites] Genes Cells. 2002 Nov;7(11):1135-47 [12390248.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4622-8 [12453880.001]
  • [Cites] J Pathol. 2003 Jan;199(1):90-7 [12474231.001]
  • [Cites] Curr Opin Oncol. 2003 Jan;15(1):44-9 [12490760.001]
  • [Cites] Oncogene. 2003 Jan 9;22(1):157-60 [12527918.001]
  • [Cites] Oncogene. 2003 Jan 30;22(4):507-16 [12555064.001]
  • [Cites] Nat Rev Cancer. 2002 Feb;2(2):133-42 [12635176.001]
  • [Cites] Cancer Invest. 2003;21(1):105-36 [12643014.001]
  • [Cites] Nucleic Acids Res. 2003 Apr 15;31(8):2168-77 [12682367.001]
  • [Cites] J Biol Chem. 2003 May 2;278(18):15601-7 [12571245.001]
  • [Cites] Oncol Res. 2003;13(6-10):323-31 [12725521.001]
  • [Cites] Nucleic Acids Res. 2004;32(11):e93 [15247326.001]
  • [Cites] Vet Immunol Immunopathol. 2004 Sep;101(1-2):1-17 [15261689.001]
  • [Cites] Blood. 2004 Aug 15;104(4):1127-36 [15100157.001]
  • [Cites] N Engl J Med. 2004 Aug 5;351(6):533-42 [15295046.001]
  • [Cites] J Immunol Methods. 2000 Apr 3;237(1-2):19-28 [10725448.001]
  • [Cites] J Virol. 2000 Jul;74(13):5872-9 [10846067.001]
  • [Cites] Cancer Lett. 2000 Aug 11;156(2):191-8 [10880769.001]
  • [Cites] Genes Dev. 2000 Jul 1;14(13):1553-77 [10887150.001]
  • [Cites] Am J Pathol. 2000 Aug;157(2):377-84 [10934142.001]
  • [Cites] Adv Cancer Res. 2001;80:189-216 [11034544.001]
  • [Cites] AIDS Res Hum Retroviruses. 2000 Nov 1;16(16):1787-95 [11080828.001]
  • [Cites] J Virol. 2001 Feb;75(3):1095-103 [11152482.001]
  • [Cites] Oncogene. 2004 Aug 5;23(35):5912-22 [15195138.001]
  • [Cites] J Virol. 1987 Jul;61(7):2175-81 [3035218.001]
  • [Cites] Blood. 2004 Jan 1;103(1):229-35 [12946992.001]
  • [Cites] J Biol Chem. 2004 Jan 2;279(1):495-508 [14530271.001]
  • (PMID = 16439548.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax
  • [Other-IDs] NLM/ PMC1367148
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77. Tomomatsu J, Isobe Y, Oshimi K, Tabe Y, Ishii K, Noguchi M, Hirano T, Komatsu N, Sugimoto K: Chronic lymphocytic leukemia in a Japanese population: varied immunophenotypic profile, distinctive usage of frequently mutated IGH gene, and indolent clinical behavior. Leuk Lymphoma; 2010 Dec;51(12):2230-9
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  • [Title] Chronic lymphocytic leukemia in a Japanese population: varied immunophenotypic profile, distinctive usage of frequently mutated IGH gene, and indolent clinical behavior.
  • Chronic lymphocytic leukemia (CLL) is relatively rare in Japan.
  • Among 46 cases of mature B-cell leukemia, we identified 28 Japanese patients with CLL, including prolymphocytoid and lymphoplasmacytoid morphological variants.
  • [MeSH-major] Immunophenotyping. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Asian Continental Ancestry Group. Disease Progression. Female. Gene Frequency. Genes, Immunoglobulin Heavy Chain / genetics. Genes, bcl-2 / genetics. Humans. Immunoglobulin Variable Region / genetics. Male. Middle Aged. Mutation. Population. Prognosis

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  • (PMID = 21067444.001).
  • [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 / IGH-CCND1 fusion protein, human; 0 / Immunoglobulin Variable Region; 0 / Oncogene Proteins, Fusion
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78. Cooper TM: Role of nelarabine in the treatment of T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma. Ther Clin Risk Manag; 2007 Dec;3(6):1135-41
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  • [Title] Role of nelarabine in the treatment of T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma.
  • T-cell malignancies have distinct biochemical, immunologic, and clinical features which set them apart from non-T-cell malignancies.
  • In the past, T-cell leukemia portended a worse prognosis than leukemia of B-cell origin.
  • Cure rates have improved with intensification of therapy and advanced understanding of the molecular genetics of T-cell malignancies.
  • Further advances in the treatment of T-cell leukemia will require the development of novel agents that can target specific malignancies without a significant increase in toxicity.
  • Nelarabine is water soluble and rapidly converted to ara-G, which is specifically cytotoxic to T-lymphocytes and T-lymphoblastoid cells.
  • Clinical and pharmacokinetic investigations have established that nelarabine is active as a single agent which has led to exploration of an expanded role in the treatment of T-cell hematologic malignances.

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  • [Cites] J Clin Oncol. 2005 May 20;23(15):3376-82 [15908649.001]
  • [Cites] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128.001]
  • [Cites] Clin Cancer Res. 2006 Sep 15;12(18):5329-35 [17000665.001]
  • [Cites] J Immunol. 1990 Jan 15;144(2):485-91 [2104895.001]
  • [Cites] Leukemia. 1990 Nov;4(11):739-44 [2232884.001]
  • [Cites] Cancer Res. 1990 Mar 15;50(6):1817-21 [2306735.001]
  • [Cites] Blood. 1988 Dec;72(6):1891-7 [3058229.001]
  • [Cites] Proc Natl Acad Sci U S A. 1978 Oct;75(10):5011-4 [311004.001]
  • [Cites] Lancet. 1975 May 3;1(7914):1010-3 [48676.001]
  • [Cites] J Biol Chem. 1968 Aug 25;243(16):4298-304 [5684726.001]
  • [Cites] Biochem J. 1983 Sep 15;214(3):711-8 [6312962.001]
  • [Cites] Blood. 1983 Apr;61(4):660-6 [6600944.001]
  • [Cites] Cancer Res. 1995 Apr 1;55(7):1517-24 [7533664.001]
  • [Cites] Cancer Res. 1995 Aug 1;55(15):3352-6 [7614470.001]
  • [Cites] Blood. 1994 Nov 1;84(9):3122-33 [7949185.001]
  • [Cites] J Clin Oncol. 1994 Apr;12(4):740-7 [8151317.001]
  • [Cites] Leukemia. 1993 Aug;7(8):1261-7 [8350627.001]
  • [Cites] Blood. 1993 Apr 15;81(8):2110-7 [8471769.001]
  • [Cites] J Clin Oncol. 1996 Jan;14(1):18-24 [8558195.001]
  • [Cites] Blood. 1998 Feb 1;91(3):735-46 [9446631.001]
  • [Cites] J Clin Invest. 1978 May;61(5):1405-9 [96138.001]
  • [Cites] N Engl J Med. 1998 Aug 27;339(9):605-15 [9718381.001]
  • [Cites] Clin Cancer Res. 1997 Nov;3(11):2107-13 [9815603.001]
  • [Cites] J Clin Oncol. 1998 Nov;16(11):3607-15 [9817282.001]
  • [Cites] Cancer Res. 1999 Oct 1;59(19):4937-43 [10519407.001]
  • [Cites] J Clin Oncol. 2000 Mar;18(5):995-1003 [10694549.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2196-204 [11187911.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2223-33 [11187913.001]
  • [Cites] J Clin Oncol. 2001 Apr 15;19(8):2142-52 [11304766.001]
  • [Cites] Leuk Lymphoma. 2001 Apr;41(3-4):321-31 [11378544.001]
  • [Cites] Cancer Res. 2002 Jun 1;62(11):3100-5 [12036920.001]
  • [Cites] Best Pract Res Clin Haematol. 2002 Dec;15(4):741-56 [12617874.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1842-8 [12750168.001]
  • [Cites] N Engl J Med. 2003 Aug 14;349(7):640-9 [12917300.001]
  • [Cites] Br J Haematol. 2003 Nov;123(3):396-405 [14616997.001]
  • [Cites] J Clin Oncol. 2005 May 20;23(15):3396-403 [15908652.001]
  • (PMID = 18516261.001).
  • [ISSN] 1176-6336
  • [Journal-full-title] Therapeutics and clinical risk management
  • [ISO-abbreviation] Ther Clin Risk Manag
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2387290
  • [Keywords] NOTNLM ; 9-β-D-arabinofuranosylguanine / T-cell acute lymphoblastic leukemia / nelarabine
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79. Colussi G: Pseudohyperkalemia in leukemias. Am J Kidney Dis; 2006 Feb;47(2):373
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  • [Title] Pseudohyperkalemia in leukemias.
  • [MeSH-major] Hyperkalemia / etiology. Leukemia, Lymphocytic, Chronic, B-Cell / complications

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  • [CommentOn] Am J Kidney Dis. 2005 Oct;46(4):746-8 [16183430.001]
  • (PMID = 16431273.001).
  • [ISSN] 1523-6838
  • [Journal-full-title] American journal of kidney diseases : the official journal of the National Kidney Foundation
  • [ISO-abbreviation] Am. J. Kidney Dis.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
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80. Reid A, Naresh K, Wagner S, MacDonald D: Interphase FISH using a BCL3 probe to diagnose the t(14;19)(q32;q13)-positive small B-cell leukemia. Leuk Lymphoma; 2008 Feb;49(2):356-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interphase FISH using a BCL3 probe to diagnose the t(14;19)(q32;q13)-positive small B-cell leukemia.
  • [MeSH-major] Leukemia, B-Cell / diagnosis. Leukemia, B-Cell / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics

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  • (PMID = 18231927.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; 0 / proto-oncogene protein bcl-3
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81. Chai YH, Lü H, Li JQ, Lu J, Xiao PF, He YX, Shao XJ: [Classical and molecular cytogenetic abnormalities in 124 pediatric patients with acute lymphoblastic leukemia]. Zhonghua Er Ke Za Zhi; 2007 Sep;45(9):684-6
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  • [Title] [Classical and molecular cytogenetic abnormalities in 124 pediatric patients with acute lymphoblastic leukemia].
  • OBJECTIVE: In childhood acute lymphoblastic leukemia (ALL), cytogenetics plays an important role in diagnosis, allocation of treatment and prognosis.
  • Multiplex polymerase chain reaction (Multiplex PCR) analysis was performed to detect the 29 most common leukemia translocations for routine molecular diagnostic hematopathology practice, and complement the information gained from conventional cytogenetic analysis.
  • Thirteen cases of TEL-AML1, 10 cases of rearrangement in the MLL gene, 4 cases of E2A-PBX1, 4 cases of E2A-HLF, 3 cases of BCR-ABL, 2 cases of TLS-ERG, 32 cases of HOX11 were detected by Multiplex PCR in B-lineage leukemias.
  • SIL-TAL1 had been found in 4 of 7 of T-lineage leukemias.
  • [MeSH-major] Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit / genetics. Cytogenetic Analysis. Karyotyping. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Basic Helix-Loop-Helix Transcription Factors / genetics. Child. Child, Preschool. DNA-Binding Proteins / genetics. Female. Fusion Proteins, bcr-abl / genetics. Gene Fusion / genetics. Homeodomain Proteins. Humans. Immunophenotyping / methods. Infant. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Polymerase Chain Reaction. Proto-Oncogene Proteins / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 18021563.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / TEL-AML1 fusion protein; 0 / pbx1 protein, human; 135471-20-4 / TAL1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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82. Akao Y, Nakagawa Y, Kitade Y, Kinoshita T, Naoe T: Downregulation of microRNAs-143 and -145 in B-cell malignancies. Cancer Sci; 2007 Dec;98(12):1914-20
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  • [Title] Downregulation of microRNAs-143 and -145 in B-cell malignancies.
  • In this study, we demonstrated that the expression of miRNAs (miRs) -143 and -145, the levels of which were previously shown to be reduced in colon cancers and various kinds of established cancer cell lines, was also decreased in most of the B-cell malignancies examined, including chronic lymphocytic leukemias (CLL), B-cell lymphomas, Epstein-Barr virus (EBV)-transformed B-cell lines, and Burkitt lymphoma cell lines.
  • All samples from 13 CLL patients and eight of nine B-cell lymphoma ones tested exhibited an extremely low expression of miRs-143 and -145.
  • The expression levels of miRs-143 and -145 were consistently low in human Burkitt lymphoma cell lines and were inversely associated with the cell proliferation observed in the EBV-transformed B-cell lines.
  • Taken together, these findings suggest that miRs-143 and -145 may be useful as biomarkers that differentiate B-cell malignant cells from normal cells and contribute to carcinogenesis in B-cell malignancies by a newly defined mechanism.
  • [MeSH-major] Down-Regulation. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Lymphoma, B-Cell / genetics. MicroRNAs / genetics. RNA, Neoplasm / genetics
  • [MeSH-minor] Antimetabolites, Antineoplastic / pharmacology. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Burkitt Lymphoma / genetics. Burkitt Lymphoma / pathology. Cell Line, Tumor. Cell Survival. Gene Expression Regulation, Neoplastic. Humans. Hydroxamic Acids / pharmacology. Lymph Nodes / pathology. Tumor Cells, Cultured

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  • (PMID = 17892514.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Hydroxamic Acids; 0 / MicroRNAs; 0 / RNA, Neoplasm; 3X2S926L3Z / trichostatin A; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
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83. Volinia S, Galasso M, Costinean S, Tagliavini L, Gamberoni G, Drusco A, Marchesini J, Mascellani N, Sana ME, Abu Jarour R, Desponts C, Teitell M, Baffa R, Aqeilan R, Iorio MV, Taccioli C, Garzon R, Di Leva G, Fabbri M, Catozzi M, Previati M, Ambs S, Palumbo T, Garofalo M, Veronese A, Bottoni A, Gasparini P, Harris CC, Visone R, Pekarsky Y, de la Chapelle A, Bloomston M, Dillhoff M, Rassenti LZ, Kipps TJ, Huebner K, Pichiorri F, Lenze D, Cairo S, Buendia MA, Pineau P, Dejean A, Zanesi N, Rossi S, Calin GA, Liu CG, Palatini J, Negrini M, Vecchione A, Rosenberg A, Croce CM: Reprogramming of miRNA networks in cancer and leukemia. Genome Res; 2010 May;20(5):589-99
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  • [Title] Reprogramming of miRNA networks in cancer and leukemia.
  • We also built, for the first time, specialized miRNA networks for solid tumors and leukemias.
  • Finally, we experimentally validated the miRNA network with acute lymphocytic leukemia originated in Mir155 transgenic mice.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Leukemia. MicroRNAs / genetics. Neoplasms
  • [MeSH-minor] Adenocarcinoma / metabolism. Animals. Cell Line, Tumor. Gene Dosage. Humans. Lung / metabolism. Lung Neoplasms / metabolism. Mice. Oligonucleotide Array Sequence Analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


84. Casnici C, Volpe G, Lattuada D, Crotta K, Kuka M, Panuzzo C, Mastrotto C, Tonon G, Fazio VM, Saglio G, Marelli O: Out of frame peptides from BCR/ABL alternative splicing are immunogenic in HLA A2.1 transgenic mice. Cancer Lett; 2009 Apr 8;276(1):61-7
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  • New, potentially tumor-specific antigens have been described in Bcr/Abl positive leukemias.
  • These variants are expressed in chronic myelogenous leukemia and acute lymphocytic leukemia patients.
  • Peptides A and B, but not C, induced the production of specific antisera, while A and C induced the generation of specific cytotoxic T lymphocytes.
  • [MeSH-major] Alternative Splicing. Cancer Vaccines / immunology. Frameshift Mutation / immunology. Fusion Proteins, bcr-abl / immunology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • [MeSH-minor] Amino Acid Sequence. Animals. Antigens, Neoplasm / genetics. Antigens, Neoplasm / immunology. Cell Line, Tumor. Enzyme-Linked Immunosorbent Assay. HLA-A2 Antigen / genetics. Humans. Interferon-gamma / biosynthesis. Interferon-gamma / immunology. Mice. Mice, Inbred C57BL. Mice, Transgenic. Molecular Sequence Data. Peptides / genetics. Peptides / immunology. Proto-Oncogene Proteins c-bcr / genetics. Proto-Oncogene Proteins c-bcr / immunology. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 19062160.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / HLA-A2 Antigen; 0 / Peptides; 82115-62-6 / Interferon-gamma; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
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85. Ishdorj G, Johnston JB, Gibson SB: Inhibition of constitutive activation of STAT3 by curcurbitacin-I (JSI-124) sensitized human B-leukemia cells to apoptosis. Mol Cancer Ther; 2010 Dec;9(12):3302-14
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  • [Title] Inhibition of constitutive activation of STAT3 by curcurbitacin-I (JSI-124) sensitized human B-leukemia cells to apoptosis.
  • Phosphorylation of STAT3 on serine 727 regulates gene expression and is found to be elevated in many B-leukemia cells including chronic lymphocytic leukemia (CLL).
  • JSI-124 potently induces apoptosis in 3 B-leukemia cell lines (BJAB, I-83, and NALM-6) and in primary CLL cells and was associated with a reduction in serine 727 phosphorylation of STAT3.
  • Similarly, knockdown of STAT3 expression induced apoptosis in these leukemia cells.
  • Besides apoptosis, we found that JSI-124 also induced cell-cycle arrest prior to apoptosis in B-leukemia cells.
  • This corresponded with reduced expression of the cell-cycle regulatory gene, cdc-2.
  • Thus, we present here for the first time that JSI-124 induced suppression of serine 727 phosphorylation of STAT3, leading to apoptosis and cell-cycle arrest through alterations in gene transcription in B-leukemia cells.
  • [MeSH-major] Apoptosis / drug effects. Leukemia, B-Cell / pathology. STAT3 Transcription Factor / metabolism. Triterpenes / pharmacology
  • [MeSH-minor] Cell Cycle / drug effects. Cell Line, Tumor. Down-Regulation / drug effects. Drug Screening Assays, Antitumor. Gene Knockdown Techniques. Histone Deacetylase 1 / metabolism. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Phosphoserine / metabolism. RNA, Small Interfering / metabolism. Receptors, TNF-Related Apoptosis-Inducing Ligand / metabolism. TNF-Related Apoptosis-Inducing Ligand / pharmacology. Up-Regulation / drug effects. X-Linked Inhibitor of Apoptosis Protein / metabolism

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  • [Copyright] ©2010 AACR.
  • (PMID = 21159613.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / Triterpenes; 0 / X-Linked Inhibitor of Apoptosis Protein; 17885-08-4 / Phosphoserine; 2222-07-3 / cucurbitacin I; EC 3.5.1.98 / HDAC1 protein, human; EC 3.5.1.98 / Histone Deacetylase 1
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86. Joshi AD, Dickinson JD, Hegde GV, Sanger WG, Armitage JO, Bierman PJ, Bociek RG, Devetten MP, Vose JM, Joshi SS: Bulky lymphadenopathy with poor clinical outcome is associated with ATM downregulation in B-cell chronic lymphocytic leukemia patients irrespective of 11q23 deletion. Cancer Genet Cytogenet; 2007 Jan 15;172(2):120-6
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  • [Title] Bulky lymphadenopathy with poor clinical outcome is associated with ATM downregulation in B-cell chronic lymphocytic leukemia patients irrespective of 11q23 deletion.
  • B-cell chronic lymphocytic leukemia (B-CLL) is the most common B-cell leukemia among older populations in Western countries.
  • The clinical course of B-CLL is heterogeneous: in some patients the disease course is indolent, in others it is aggressive.
  • The B-CLL subgroups with chromosome 11q23 deletion have been associated with aggressive disease course involving ATM deletion, extensive bulky lymphadenopathy (BLA), and inferior clinical outcome.
  • Moreover, gene expression analysis in B-CLL patients with and without BLA revealed differences in expression for genes involved in apoptosis, cell cycle, and cell adhesion.
  • These results indicate an association between BLA and reduced expression of ATM, suggesting a role for ATM in disease progression in B-CLL.
  • [MeSH-major] Cell Cycle Proteins / biosynthesis. Cell Cycle Proteins / genetics. Chromosome Deletion. Chromosomes, Human, Pair 11 / genetics. DNA-Binding Proteins / biosynthesis. DNA-Binding Proteins / genetics. Down-Regulation / genetics. Gene Expression Regulation, Leukemic. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Lymphatic Diseases / genetics. Protein-Serine-Threonine Kinases / biosynthesis. Protein-Serine-Threonine Kinases / genetics. Tumor Suppressor Proteins / biosynthesis. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Ataxia Telangiectasia Mutated Proteins. Cell Adhesion / genetics. Cell Cycle / genetics. Female. Humans. Male. Middle Aged. Prognosis

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  • (PMID = 17213020.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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87. Austen B, Powell JE, Alvi A, Edwards I, Hooper L, Starczynski J, Taylor AM, Fegan C, Moss P, Stankovic T: Mutations in the ATM gene lead to impaired overall and treatment-free survival that is independent of IGVH mutation status in patients with B-CLL. Blood; 2005 Nov 1;106(9):3175-82
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  • Mutations in the ATM gene have been previously found in B-cell chronic lymphocytic leukemias (B-CLLs) but their clinical significance is unknown.
  • [MeSH-major] Cell Cycle Proteins / genetics. DNA-Binding Proteins / genetics. Immunoglobulin Heavy Chains / genetics. Immunoglobulin Variable Region / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Mutation / genetics. Protein-Serine-Threonine Kinases / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 16014569.001).
  • [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 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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88. Klinger MB, Guilbault B, Goulding RE, Kay RJ: Deregulated expression of RasGRP1 initiates thymic lymphomagenesis independently of T-cell receptors. Oncogene; 2005 Apr 14;24(16):2695-704
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  • [Title] Deregulated expression of RasGRP1 initiates thymic lymphomagenesis independently of T-cell receptors.
  • RasGRP1 is a Ras-specific exchange factor, which is activated by T-cell receptor (TCR) and promotes TCR-dependent positive selection of thymocytes.
  • RasGRP1 is highly expressed on most T lymphocytic leukemias and is a common site of proviral insertion in retrovirus-induced murine T-cell lymphomas.
  • We used RasGRP1 transgenic mice to determine if deregulated expression of RasGRP1 has a causative role in the development of T-cell malignancies.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Guanine Nucleotide Exchange Factors / metabolism. Lymphoma, T-Cell / genetics. Receptors, Antigen, T-Cell / genetics
  • [MeSH-minor] Animals. Female. Flow Cytometry. Humans. Leukemia / genetics. Male. Mice. Mice, Transgenic. Phenotype. Transgenes

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  • (PMID = 15829980.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Guanine Nucleotide Exchange Factors; 0 / Rasgrp1 protein, mouse; 0 / Receptors, Antigen, T-Cell
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89. Büchau AS, MacLeod DT, Morizane S, Kotol PF, Hata T, Gallo RL: Bcl-3 acts as an innate immune modulator by controlling antimicrobial responses in keratinocytes. J Invest Dermatol; 2009 Sep;129(9):2148-55
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  • We report here the identification of B-cell leukemia (Bcl)-3 as a modulator of innate immune signaling in keratinocytes.

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  • [Cites] Mol Cell Biol. 2000 May;20(10):3407-16 [10779330.001]
  • [Cites] J Biol Chem. 2001 Aug 24;276(34):32080-93 [11387332.001]
  • [Cites] Oncogene. 2001 Oct 11;20(46):6660-8 [11709700.001]
  • [Cites] Mol Cell Biol. 2001 Dec;21(24):8428-36 [11713278.001]
  • [Cites]</