[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 5395
1. Kharfan-Dabaja MA, Fahed R, Hussein M, Santos ES: Evolving role of monoclonal antibodies in the treatment of chronic lymphocytic leukemia. Expert Opin Investig Drugs; 2007 Nov;16(11):1799-815
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evolving role of monoclonal antibodies in the treatment of chronic lymphocytic leukemia.
  • Recognition of cancer-specific antigens resulted in development of monoclonal antibodies as treatments for various neoplasms including chronic lymphocytic leukemia (CLL).
  • Two monoclonal antibodies, alemtuzumab and rituximab, have been extensively studied, as monotherapy or in combination, in patients with various clinical stages of CLL.
  • Alemtuzumab, particularly when combined with fludarabine-based chemotherapy, sequentially or concomitantly, represents a promising therapeutic approach that results in improved efficacy by further reducing levels of residual disease in previously untreated or relapsed/refractory CLL.
  • On the other hand, single-agent rituximab has limited activity by itself, even at very high doses, and seldom induces complete remissions.
  • Newer monoclonal antibodies are already showing activity in relapsed/refractory CLL and will eventually be evaluated in combinations with conventional chemotherapy, or with already established antibodies.
  • Modern definitions for assessment of responses such as minimal residual disease negativity (MRD negativity) are emerging and, consequently, development of assays capable of measuring such responses.
  • MRD negativity should become the primary objective of clinical trials when evaluating treatment interventions in patients with CLL.
  • The future of monoclonal antibodies for treatment of CLL is bright.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antibodies, Monoclonal, Murine-Derived. Antibodies, Neoplasm / therapeutic use. Hematopoietic Stem Cell Transplantation. Humans. Rituximab

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17970639.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 106
  •  go-up   go-down


2. Nickerson P: The impact of immune gene polymorphisms in kidney and liver transplantation. Clin Lab Med; 2008 Sep;28(3):455-68, vii
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This finding raises the possibility that differences in genetic phenotypes may account for the interindividual responses seen in the context of the alloimmune response.
  • [MeSH-minor] Antigens, CD80 / genetics. Antigens, CD80 / immunology. Antigens, CD86 / genetics. Antigens, CD86 / immunology. Cell Adhesion Molecules / genetics. Cell Adhesion Molecules / immunology. Chemokines / genetics. Chemokines / immunology. Cytokines / genetics. Cytokines / immunology. Humans. Intercellular Signaling Peptides and Proteins / genetics. Intercellular Signaling Peptides and Proteins / immunology

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Kidney Transplantation.
  • MedlinePlus Health Information. consumer health - Liver Transplantation.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19028263.001).
  • [ISSN] 1557-9832
  • [Journal-full-title] Clinics in laboratory medicine
  • [ISO-abbreviation] Clin. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / Antigens, CD86; 0 / Cell Adhesion Molecules; 0 / Chemokines; 0 / Cytokines; 0 / Intercellular Signaling Peptides and Proteins
  • [Number-of-references] 71
  •  go-up   go-down


3. Herishanu Y, Polliack A: Chronic lymphocytic leukemia: a review of some new aspects of the biology, factors influencing prognosis and therapeutic options. Transfus Apher Sci; 2005 Feb;32(1):85-97
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic lymphocytic leukemia: a review of some new aspects of the biology, factors influencing prognosis and therapeutic options.
  • This review provides some basic information on chronic lymphocytic leukemia (CLL) and attempts to present some of the newer data which have accumulated in recent years including those relating to familial aggregation of CLL and the detection of monoclonal CD5+ lymphocytosis in the general population and families of CLL patients.
  • Novel data on the pathogenesis and concepts of cell origin in CLL are also reviewed stressing the fact that there is biased IgVH gene usage, and the importance of mutational status of the CLL cell, as reported in recent years by different authors.
  • A brief review of the significance of the microenvironmental interactions between stromal cells and other accessory cells, and the leukemic CLL cells is also provided.
  • Other clinical aspects are discussed including diagnostic criteria, clinical staging, and the newer prognostic factors which influence survival and timing of therapy for CLL patients.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / pathology
  • [MeSH-minor] Age Factors. Aged. Antibodies, Monoclonal / chemistry. Antigens, CD5 / biosynthesis. DNA Mutational Analysis. Female. Humans. Immunoglobulin Heavy Chains / genetics. Male. Middle Aged. Mutation. Prognosis. Remission Induction. Stem Cell Transplantation / methods. Time Factors. Treatment Outcome

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15737877.001).
  • [ISSN] 1473-0502
  • [Journal-full-title] Transfusion and apheresis science : official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis
  • [ISO-abbreviation] Transfus. Apher. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD5; 0 / Immunoglobulin Heavy Chains
  • [Number-of-references] 122
  •  go-up   go-down


Advertisement
4. Hogan M, Claffey J, Fitzpatrick E, Hickey T, Pampillón C, Tacke M: Synthesis and cytotoxicity studies of titanocene C analogues. Met Based Drugs; 2008;2008:754358
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • These three lithiated intermediates underwent a transmetallation reaction with TiCl(4') resulting in N,N-dimethylamino-functionalised titanocenes 5a-c.
  • When these titanocenes were tested against a pig kidney epithelial cell line (LLC-PK), the IC50 values obtained were of 23, and 52 muM for titanocenes 5a and 5b, respectively.
  • The most cytotoxic titanocene in this paper, 5c with an IC50 value of 13 muM, was found to be approximately two times less cytotoxic than its analogue Titanocene C (IC50=5.5 muM) and almost four times less cytotoxic than cisplatin, which showed an IC50 value of 3.3 muM when tested on the LLC-PK cell line.

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Org Chem. 2002 May 17;67(10):3355-9 [12003546.001]
  • [Cites] Crit Rev Oncol Hematol. 2002 Jun;42(3):309-15 [12050022.001]
  • [Cites] Met Ions Biol Syst. 2004;42:353-84 [15206108.001]
  • [Cites] Invest New Drugs. 1996;13(4):327-32 [8824351.001]
  • [Cites] Cancer Chemother Pharmacol. 1998;42(5):415-7 [9771957.001]
  • [Cites] J Inorg Biochem. 2006 Sep;100(9):1479-86 [16764931.001]
  • [Cites] Anticancer Drugs. 2005 Nov;16(10):1071-3 [16222148.001]
  • [Cites] Anticancer Drugs. 2005 Nov;16(10):1091-8 [16222151.001]
  • [Cites] Anticancer Drugs. 2006 Mar;17(3):333-6 [16520662.001]
  • [Cites] Eur J Pharmacol. 2006 Mar 18;534(1-3):264-70 [16513106.001]
  • [Cites] Apoptosis. 2006 Jul;11(7):1205-14 [16699961.001]
  • [Cites] J Inorg Biochem. 2004 Dec;98(12):1987-94 [15541486.001]
  • (PMID = 18274663.001).
  • [ISSN] 0793-0291
  • [Journal-full-title] Metal-based drugs
  • [ISO-abbreviation] Met Based Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2225981
  •  go-up   go-down


5. Stilgenbauer S: Advances in the use of alemtuzumab in CLL. Clin Adv Hematol Oncol; 2008 Jan;6(1):23-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Advances in the use of alemtuzumab in CLL.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18322437.001).
  • [ISSN] 1543-0790
  • [Journal-full-title] Clinical advances in hematology & oncology : H&O
  • [ISO-abbreviation] Clin Adv Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / CD52 antigen; 0 / Glycoproteins; 3A189DH42V / alemtuzumab
  • [Number-of-references] 7
  •  go-up   go-down


6. Lim SM, Jang JW, Kim BW, Choi H, Choi KY, Park SJ, Han CW: [Hepatitis B virus reactivation during chlorambucil and prednisolone treatment in an HBsAg-negative and anti-HBs-positive patient with B-cell chronic lymphocytic leukemia]. Korean J Hepatol; 2008 Jun;14(2):213-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Hepatitis B virus reactivation during chlorambucil and prednisolone treatment in an HBsAg-negative and anti-HBs-positive patient with B-cell chronic lymphocytic leukemia].
  • Here we report a case of severe hepatitis that manifested during chemotherapy in a female patient with chronic lymphocytic leukemia (CLL) who had been initially seronegative for HBsAg and seropositive for anti-HBs.
  • The patient received chlorambucil and prednisolone for the treatment of CLL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chlorambucil / therapeutic use. Hepatitis B / diagnosis. Hepatitis B Antibodies / blood. Hepatitis B Surface Antigens / blood. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Prednisolone / therapeutic use


7. Zubair AC, Kao G, Daley H, Schott D, Freedman A, Ritz J: CD34(+) CD38(-) and CD34(+) HLA-DR(-) cells in BM stem cell grafts correlate with short-term engraftment but have no influence on long-term hematopoietic reconstitution after autologous transplantation. Cytotherapy; 2006;8(4):399-407
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD34(+) CD38(-) and CD34(+) HLA-DR(-) cells in BM stem cell grafts correlate with short-term engraftment but have no influence on long-term hematopoietic reconstitution after autologous transplantation.
  • The aim of this study was to investigate whether these immature CD34(+) subsets also correlate with long-term hematopoietic reconstitution (LHR) in recipients of ABMT.
  • METHODS: We examined stem cell grafts from 58 patients with B-cell lymphoma or CLL who underwent ABMT after myeloablative conditioning.
  • We determined whether total mononuclear cell dose (MNC), colony-forming unit-granulocyte-monocyte (CFU-GM), CD34(+) cell dose and CD34(+) cell subsets (CD34(+) CD38(-) and CD34(+) HLA-DR(-) were associated with SHR and/or LHR.
  • RESULTS AND DISCUSSION: CD34(+) cell dose and CD34(+) cell subsets were significantly associated with SHR.
  • However, at day 100 and 1 year post-transplant only total CD34(+) cell dose was associated with LHR.
  • The association of total CD34(+) cell dose with LHR persisted after adjusting for age, sex and disease.
  • None of the CD34(+) cell subsets analyzed showed evidence of significant association with LHR.

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16923616.001).
  • [ISSN] 1465-3249
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA102824; United States / NHLBI NIH HHS / HL / HL04095
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / HLA-DR Antigens; 0 / Membrane Glycoproteins; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human
  •  go-up   go-down


8. Malarkannan S, Regunathan J, Chu H, Kutlesa S, Chen Y, Zeng H, Wen R, Wang D: Bcl10 plays a divergent role in NK cell-mediated cytotoxicity and cytokine generation. J Immunol; 2007 Sep 15;179(6):3752-62
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bcl10 plays a divergent role in NK cell-mediated cytotoxicity and cytokine generation.
  • [MeSH-minor] Animals. Antigens, Ly / physiology. Antigens, Surface / physiology. CHO Cells. Cell Differentiation / genetics. Cell Differentiation / immunology. Cell Line, Tumor. Chemokines / antagonists & inhibitors. Chemokines / biosynthesis. Cricetinae. Cricetulus. Immunity, Innate / genetics. Interleukin-2 / physiology. Lectins, C-Type / physiology. Mice. Mice, Inbred C57BL. Mice, Knockout. NK Cell Lectin-Like Receptor Subfamily A. NK Cell Lectin-Like Receptor Subfamily B. NK Cell Lectin-Like Receptor Subfamily K. Receptors, Immunologic / physiology. Receptors, NK Cell Lectin-Like. Receptors, Natural Killer Cell. Self Tolerance / genetics. Self Tolerance / immunology

  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17785812.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United States / PHS HHS / / N01-HHSN26600500032C; United States / PHS HHS / / R01 A1064826-01; United States / NIAID NIH HHS / AI / R01 AI52327; United States / NHLBI NIH HHS / HL / R01 HL073284; United States / NIAID NIH HHS / AI / U19 AI062627-01
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antigens, Ly; 0 / Antigens, Surface; 0 / Bcl10 protein, mouse; 0 / Chemokines; 0 / Cytokines; 0 / Interleukin-2; 0 / Klra4 protein, mouse; 0 / Klrk1 protein, mouse; 0 / Lectins, C-Type; 0 / NK Cell Lectin-Like Receptor Subfamily A; 0 / NK Cell Lectin-Like Receptor Subfamily B; 0 / NK Cell Lectin-Like Receptor Subfamily K; 0 / Receptors, Immunologic; 0 / Receptors, NK Cell Lectin-Like; 0 / Receptors, Natural Killer Cell
  •  go-up   go-down


9. Baskar S, Suschak JM, Samija I, Srinivasan R, Childs RW, Pavletic SZ, Bishop MR, Rader C: A human monoclonal antibody drug and target discovery platform for B-cell chronic lymphocytic leukemia based on allogeneic hematopoietic stem cell transplantation and phage display. Blood; 2009 Nov 12;114(20):4494-502
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A human monoclonal antibody drug and target discovery platform for B-cell chronic lymphocytic leukemia based on allogeneic hematopoietic stem cell transplantation and phage display.
  • Allogeneic hematopoietic stem cell transplantation (alloHSCT) is the only potentially curative treatment available for patients with B-cell chronic lymphocytic leukemia (B-CLL).
  • Here, we show that post-alloHSCT antibody repertoires can be mined for the discovery of fully human monoclonal antibodies to B-CLL cell-surface antigens.
  • Sera collected from B-CLL patients at defined times after alloHSCT showed selective binding to primary B-CLL cells.
  • To identify post-alloHSCT serum antibodies and subsequently B-CLL cell-surface antigens they recognize, we generated a human antibody-binding fragment (Fab) library from post-alloHSCT peripheral blood mononuclear cells and selected it on primary B-CLL cells by phage display.
  • A panel of Fab with B-CLL cell-surface reactivity was strongly enriched.
  • One Fab was converted to immunoglobulin G1 and analyzed for reactivity with peripheral blood mononuclear cells from B-CLL patients and healthy volunteers.
  • Cell-surface antigen expression was restricted to primary B cells and up-regulated in primary B-CLL cells.
  • Mining post-alloHSCT antibody repertoires offers a novel route to discover fully human monoclonal antibodies and identify antigens of potential therapeutic relevance to B-CLL and possibly other cancers.
  • Trials described herein were registered at www.clinicaltrials.gov as nos.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antigens, Neoplasm / immunology. Hematopoietic Stem Cell Transplantation. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Peptide Library

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, B-cell, chronic.
  • Genetic Alliance. consumer health - Transplantation.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2004 Jan 15;103(2):656-63 [14563636.001]
  • [Cites] Blood. 2004 Jan 1;103(1):353-9 [14512314.001]
  • [Cites] J Exp Med. 2004 Apr 19;199(8):1133-42 [15096539.001]
  • [Cites] Nat Rev Cancer. 2004 May;4(5):371-80 [15122208.001]
  • [Cites] J Exp Med. 1984 Jan 1;159(1):208-20 [6319530.001]
  • [Cites] Leuk Res. 1990;14(4):381-7 [2159091.001]
  • [Cites] Blood. 1993 Aug 1;82(3):1036-8 [8338937.001]
  • [Cites] Leukemia. 1994 Mar;8(3):476-84 [8127151.001]
  • [Cites] Hum Pathol. 1994 Dec;25(12):1276-82 [8001921.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Dec 5;92(25):11810-3 [8524854.001]
  • [Cites] Bone Marrow Transplant. 1998 Jun;21(12):1223-30 [9674856.001]
  • [Cites] N Engl J Med. 2005 Feb 24;352(8):804-15 [15728813.001]
  • [Cites] Curr Opin Immunol. 2005 Apr;17(2):202-10 [15766682.001]
  • [Cites] Blood. 2005 May 15;105(10):3945-50 [15692072.001]
  • [Cites] Clin Cancer Res. 2005 Jun 15;11(12):4504-11 [15958636.001]
  • [Cites] Br J Haematol. 2005 Aug;130(3):418-21 [16042692.001]
  • [Cites] Nat Biotechnol. 2005 Sep;23(9):1105-16 [16151404.001]
  • [Cites] Cancer Immunol Immunother. 2006 Feb;55(2):188-96 [16187090.001]
  • [Cites] Expert Opin Emerg Drugs. 2006 Mar;11(1):167-89 [16503834.001]
  • [Cites] Nat Rev Immunol. 2006 May;6(5):343-57 [16622479.001]
  • [Cites] Adv Immunol. 2006;90:133-73 [16730263.001]
  • [Cites] Int J Hematol. 2006 May;83(4):351-5 [16757438.001]
  • [Cites] Adv Drug Deliv Rev. 2006 Aug 7;58(5-6):755-65 [16820243.001]
  • [Cites] Nat Rev Immunol. 2006 Oct;6(10):728-40 [16998507.001]
  • [Cites] J Immunol Methods. 2007 Jan 10;318(1-2):75-87 [17140598.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Jan;13(1 Suppl 1):87-97 [17222778.001]
  • [Cites] Bone Marrow Transplant. 2007 Apr;39(8):441-6 [17322931.001]
  • [Cites] Am J Transplant. 2007 Jul;7(7):1808-14 [17524074.001]
  • [Cites] Annu Rev Biochem. 2007;76:1-22 [17328676.001]
  • [Cites] Expert Opin Biol Ther. 2007 Dec;7(12):1789-97 [18034645.001]
  • [Cites] Semin Hematol. 2008 Apr;45(2):95-103 [18381104.001]
  • [Cites] J Immunol. 2008 May 1;180(9):6374-84 [18424761.001]
  • [Cites] Blood. 2008 Jul 15;112(2):394-7 [18434611.001]
  • [Cites] J Mol Biol. 2008 Dec 31;384(5):1143-56 [18809410.001]
  • [Cites] Biol Blood Marrow Transplant. 2009 Jan;15(1 Suppl):53-8 [19147079.001]
  • [Cites] Cancer Immunol Immunother. 2004 Mar;53(3):144-7 [14727084.001]
  • [Cites] Philos Trans R Soc Lond B Biol Sci. 2000 Mar 29;355(1395):357-60 [10794054.001]
  • [Cites] J Clin Invest. 2000 Sep;106(5):705-14 [10974024.001]
  • [Cites] Int J Cancer. 2001 Feb 15;91(4):474-80 [11251968.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jun 19;98(13):7492-7 [11416219.001]
  • [Cites] J Exp Med. 2001 Dec 3;194(11):1625-38 [11733577.001]
  • [Cites] J Exp Med. 2001 Dec 3;194(11):1639-47 [11733578.001]
  • [Cites] Blood. 2002 Jun 1;99(11):4087-93 [12010811.001]
  • [Cites] Cytotherapy. 2001;3(3):211-20 [12171728.001]
  • [Cites] Blood. 2002 Sep 15;100(6):2123-31 [12200376.001]
  • [Cites] Cancer Res. 2002 Oct 1;62(19):5517-22 [12359762.001]
  • [Cites] FASEB J. 2002 Dec;16(14):2000-2 [12397091.001]
  • [Cites] J Mol Biol. 2003 Jan 10;325(2):325-35 [12488098.001]
  • [CommentIn] Blood. 2009 Nov 12;114(20):4324 [19965705.001]
  • (PMID = 19667400.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00003838/ NCT00055744
  • [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 / Antibodies, Monoclonal; 0 / Antibodies, Neoplasm; 0 / Antigens, Neoplasm; 0 / Immunoglobulin Fab Fragments; 0 / Peptide Library
  • [Other-IDs] NLM/ PMC2777128
  •  go-up   go-down


10. Belessi C, Stamatopoulos K, Hadzidimitriou A, Hatzi K, Smilevska T, Stavroyianni N, Marantidou F, Paterakis G, Fassas A, Anagnostopoulos A, Laoutaris N: Analysis of expressed and non-expressed IGK locus rearrangements in chronic lymphocytic leukemia. Mol Med; 2005 Jan-Dec;11(1-12):52-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of expressed and non-expressed IGK locus rearrangements in chronic lymphocytic leukemia.
  • Immunoglobulin kappa (IGK) locus rearrangements were analyzed in parallel on cDNA/genomic DNA in 188 kappa- and 103 lambda-chronic lymphocytic leukemia (CLL) cases.
  • In kappa-CLL, only 3 of 188 cases carried double in-frame IGKV-J transcripts: in such cases, the possibility that leukemic cells expressed more than one kappa chain cannot be excluded.
  • Twenty-eight kappa-CLL cases also carried nonexpressed (nontranscribed and/or out-of-frame) IGKV-J rearrangements.
  • Taking IGKV-J, IGKV-KDE, and IGKJ-C-intron-KDE rearrangements together, 38% of kappa-CLL cases carried biallelic IGK locus rearrangements.
  • In lambda-CLL, 69 IGKV-J rearrangements were detected in 64 of 103 cases (62%); 24 rearrangements (38.2%) were in-frame.
  • In all, taking IGKV-J, IGKV-KDE, and IGKJ-C-intron-KDE rearrangements together, 97% of lambda-CLL cases had at least 1 rearranged IGK allele, in keeping with normal cells.
  • IG repertoire comparisons in kappa- versus lambda-CLL revealed that CLL precursor cells tried many rearrangements on the same IGK allele before they became lambda producers.
  • Thirteen of 28 and 26 of 69 non-expressed sequences in, respectively, kappa- or lambda-CLL had < 100% homology to germline.
  • This finding might be considered as evidence for secondary rearrangements occurring after the onset of somatic hypermutation, at least in some cases.
  • The inactivation of potentially functional IGKV-J joints by secondary rearrangements indicates active receptor editing in CLL and provides further evidence for the role of antigen in CLL immunopathogenesis.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / immunology. Gene Rearrangement, B-Lymphocyte / immunology. Immunoglobulin kappa-Chains / biosynthesis. Immunoglobulin kappa-Chains / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / immunology
  • [MeSH-minor] Adult. Aged. Amino Acid Sequence. Cells, Cultured. Female. Humans. Immunoglobulin Joining Region / biosynthesis. Immunoglobulin Joining Region / genetics. Immunoglobulin Variable Region / biosynthesis. Immunoglobulin Variable Region / genetics. Immunoglobulin lambda-Chains / biosynthesis. Immunoglobulin lambda-Chains / genetics. Immunoglobulin lambda-Chains / metabolism. Male. Middle Aged. Molecular Sequence Data. RNA Editing / immunology. Receptors, Antigen, B-Cell / genetics. Recombination, Genetic / immunology

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Invest. 1996 Oct 15;98(8):1843-50 [8878436.001]
  • [Cites] Immunity. 1997 Jan;6(1):97-105 [9052841.001]
  • [Cites] J Clin Invest. 1997 Apr 1;99(7):1614-27 [9120005.001]
  • [Cites] Immunol Rev. 2004 Feb;197:231-42 [14962199.001]
  • [Cites] J Cell Sci. 2004 Feb 29;117(Pt 6):899-906 [14762111.001]
  • [Cites] Immunology. 2004 Feb;111(2):212-22 [15027907.001]
  • [Cites] J Clin Invest. 2004 Apr;113(7):1008-16 [15057307.001]
  • [Cites] Nucleic Acids Res. 2004;32(11):3304-15 [15210863.001]
  • [Cites] Nucleic Acids Res. 2004 Jul 1;32(Web Server issue):W435-40 [15215425.001]
  • [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] Nature. 1984 Feb 23-29;307(5953):749-52 [6422305.001]
  • [Cites] Nucleic Acids Res. 1986 Jun 11;14(11):4591-603 [3086844.001]
  • [Cites] Nucleic Acids Res. 1987 Mar 25;15(6):2699-705 [3104881.001]
  • [Cites] J Exp Med. 1988 Mar 1;167(3):840-52 [3127527.001]
  • [Cites] J Exp Med. 1997 Apr 21;185(8):1435-45 [9126924.001]
  • [Cites] Clin Exp Immunol. 1997 Jul;109(1):194-203 [9218844.001]
  • [Cites] J Immunol. 1997 Nov 1;159(9):4362-6 [9379033.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Mar 3;95(5):2463-8 [9482908.001]
  • [Cites] Immunol Rev. 1998 Apr;162:261-80 [9602370.001]
  • [Cites] J Clin Invest. 1998 Aug 15;102(4):688-94 [9710436.001]
  • [Cites] J Exp Med. 1998 Oct 5;188(7):1231-8 [9763602.001]
  • [Cites] J Immunol. 2001 Jan 1;166(1):95-102 [11123281.001]
  • [Cites] Blood. 2001 Feb 15;97(4):1001-8 [11159529.001]
  • [Cites] Science. 2001 Feb 23;291(5508):1541-4 [11222858.001]
  • [Cites] Nat Immunol. 2000 Sep;1(3):207-13 [10973277.001]
  • [Cites] Mol Immunol. 2000 Aug-Sep;37(12-13):775-81 [11275262.001]
  • [Cites] J Exp Med. 2001 Sep 3;194(5):645-56 [11535632.001]
  • [Cites] Arthritis Rheum. 2001 Oct;44(10):2275-84 [11665968.001]
  • [Cites] Arthritis Rheum. 2001 Nov;44(11):2620-32 [11710718.001]
  • [Cites] Eur J Immunol. 2001 Dec;31(12):3631-7 [11745383.001]
  • [Cites] Eur J Immunol. 2001 Dec;31(12):3638-48 [11745384.001]
  • [Cites] J Exp Med. 2002 Jan 21;195(2):181-8 [11805145.001]
  • [Cites] Nat Rev Immunol. 2001 Dec;1(3):177-86 [11905826.001]
  • [Cites] Eur J Immunol. 2002 Apr;32(4):957-66 [11920561.001]
  • [Cites] J Biol Chem. 2002 May 24;277(21):18489-93 [11889124.001]
  • [Cites] J Clin Immunol. 2003 Mar;23(2):107-18 [12757263.001]
  • [Cites] Blood. 2003 Jun 15;101(12):4952-7 [12586612.001]
  • [Cites] Immunol Rev. 2003 Aug;194:8-18 [12846803.001]
  • [Cites] Science. 2003 Sep 5;301(5638):1374-7 [12920303.001]
  • [Cites] Mol Pathol. 2003 Oct;56(5):249-55 [14514917.001]
  • [Cites] J Exp Med. 2004 Jan 5;199(1):145-50 [14699083.001]
  • [Cites] J Immunol. 2004 Feb 15;172(4):2092-9 [14764674.001]
  • [Cites] Immunol Rev. 2004 Feb;197:60-74 [14962187.001]
  • [Cites] Science. 1999 Jul 2;285(5424):113-6 [10390361.001]
  • [Cites] J Immunol. 1999 Jul 15;163(2):1027-36 [10395701.001]
  • [Cites] Curr Top Microbiol Immunol. 1999;246:193-8 [10396056.001]
  • [Cites] Hum Mol Genet. 1999;8(10):1893-900 [10469842.001]
  • [Cites] Nucleic Acids Res. 2005 Jan 1;33(Database issue):D593-7 [15608269.001]
  • [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] Annu Rev Immunol. 2005;23:161-96 [15771569.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3575-83 [16076869.001]
  • [Cites] J Exp Med. 2003 Apr 7;197(7):939-45 [12682112.001]
  • [Cites] J Immunol. 2000 Apr 15;164(8):4111-9 [10754305.001]
  • [Cites] Annu Rev Immunol. 2000;18:19-51 [10837051.001]
  • [Cites] J Exp Med. 2000 Oct 16;192(8):1151-64 [11034605.001]
  • [Cites] Blood. 1988 Aug;72(2):422-8 [3261179.001]
  • [Cites] J Exp Med. 1988 Dec 1;168(6):2131-7 [2848920.001]
  • [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] Blood. 1989 Jul;74(1):262-9 [2502202.001]
  • [Cites] Blood. 1990 Aug 1;76(3):562-9 [2378986.001]
  • [Cites] J Exp Med. 1991 Mar 1;173(3):639-45 [1900078.001]
  • [Cites] J Exp Med. 1991 May 1;173(5):1065-72 [1902500.001]
  • [Cites] J Immunol. 1991 Aug 1;147(3):1060-6 [1907304.001]
  • [Cites] J Immunol. 1992 Aug 1;149(3):832-40 [1634771.001]
  • [Cites] J Exp Med. 1993 Apr 1;177(4):1009-20 [8459201.001]
  • [Cites] J Exp Med. 1993 Apr 1;177(4):1165-73 [8459210.001]
  • [Cites] J Immunol. 1993 Sep 1;151(5):2839-51 [8360495.001]
  • [Cites] J Exp Med. 1995 Aug 1;182(2):541-8 [7629511.001]
  • [Cites] Mol Immunol. 1995 Jul;32(10):683-96 [7659095.001]
  • [Cites] Eur J Immunol. 1995 Nov;25(11):3108-14 [7489750.001]
  • [Cites] Immunity. 1995 Dec;3(6):747-55 [8777720.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] Leukemia. 1996 Sep;10(9):1551-6 [8751479.001]
  • (PMID = 16622520.001).
  • [ISSN] 1076-1551
  • [Journal-full-title] Molecular medicine (Cambridge, Mass.)
  • [ISO-abbreviation] Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Joining Region; 0 / Immunoglobulin Variable Region; 0 / Immunoglobulin kappa-Chains; 0 / Immunoglobulin lambda-Chains; 0 / Receptors, Antigen, B-Cell
  • [Other-IDs] NLM/ PMC1449522
  •  go-up   go-down


11. Kau CH, Richmond S, Zhurov A, Ovsenik M, Tawfik W, Borbely P, English JD: Use of 3-dimensional surface acquisition to study facial morphology in 5 populations. Am J Orthod Dentofacial Orthop; 2010 Apr;137(4 Suppl):S56.e1-9; discussion S56-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Use of 3-dimensional surface acquisition to study facial morphology in 5 populations.
  • INTRODUCTION: The aim of this study was to assess the use of 3-dimensional facial averages for determining morphologic differences from various population groups.
  • Three-dimensional images of the subjects were obtained in a reproducible and controlled environment with a commercially available stereo-photogrammetric camera capture system.
  • Minolta VI-900 (Konica Minolta, Tokyo, Japan) and 3dMDface (3dMD LLC, Atlanta, Ga) systems were used.
  • Facial morphologic differences were greatest when totally different ethnic variations were compared.
  • Facial morphologic similarities were present in comparable groups, but there were large variations in concentrated areas of the face.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 American Association of Orthodontists. Published by Mosby, Inc. All rights reserved.
  • (PMID = 20381762.001).
  • [ISSN] 1097-6752
  • [Journal-full-title] American journal of orthodontics and dentofacial orthopedics : official publication of the American Association of Orthodontists, its constituent societies, and the American Board of Orthodontics
  • [ISO-abbreviation] Am J Orthod Dentofacial Orthop
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


12. Lee Y, Tchaou WS, Welch KB, Loesche WJ: The transmission of BANA-positive periodontal bacterial species from caregivers to children. J Am Dent Assoc; 2006 Nov;137(11):1539-46
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: The purpose of the authors' study was to use the N-benzoyl-DL-arginine-2-naphthy-lamide (BANA) test (BANAMet LLC, Ann Arbor, Mich.) to obtain information regarding the prevalence of an enzyme unique to certain periodontal pathogens in plaque samples of children, as well as the potential transmission of these pathogens from caregivers to children.
  • Positive results were more frequent in the mixed dentition, as well as in children with gingivitis (P < .001).
  • A logistic regression model showed that if the BANA test results for the care-giver were positive, the odds of the child's also having positive test results were 55 times greater (P < .001; confidence interval [CI] = 14 to 224) than those for a child whose caregiver had negative BANA test results.
  • Other predictors were the presence of a mixed dentition (P < .001; odds ratio [OR] = 11; CI = 3.5 to 33.5) and the children's papillary bleeding scores (P < .001, OR = 3.1, CI = 2.0 to 4.7).
  • A positive reaction was associated with gingivitis, a mixed dentition, a BANA-positive caregiver or a caregiver with a history of periodontal disease in the family.
  • CLINICAL IMPLICATIONS: The authors propose an anaerobic periodontal infection risk model in which children with a mixed dentition who have gingivitis and a caregiver with a history of periodontal disease would undergo the BANA test.
  • [MeSH-major] Caregivers. Clinical Enzyme Tests / methods. Dental Plaque / microbiology. Disease Transmission, Infectious. Endopeptidases / analysis. Periodontal Diseases / microbiology
  • [MeSH-minor] Bacterial Infections / diagnosis. Child. Child, Preschool. Epidemiologic Methods. Humans

  • MedlinePlus Health Information. consumer health - Caregivers.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17082280.001).
  • [ISSN] 0002-8177
  • [Journal-full-title] Journal of the American Dental Association (1939)
  • [ISO-abbreviation] J Am Dent Assoc
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.- / Endopeptidases; EC 3.4.- / N-benzoyl-DL-arginine-4-nitroanilide hydrolyzing enzyme
  •  go-up   go-down


13. Anderson LA, Pfeiffer RM, Rapkin JS, Gridley G, Mellemkjaer L, Hemminki K, Björkholm M, Caporaso NE, Landgren O: Survival patterns among lymphoma patients with a family history of lymphoma. J Clin Oncol; 2008 Oct 20;26(30):4958-65
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Survival patterns among lymphoma patients with a family history of lymphoma.
  • PURPOSE: Genetic factors are important in the etiology and pathogenesis of chronic lymphocytic leukemia (CLL), Hodgkin's lymphoma (HL), and non-Hodgkin's lymphoma (NHL).
  • Only a few small studies have assessed clinical characteristics and prognosis for familial patients, with inconsistent findings.
  • METHODS: Using population-based registries from Sweden and Denmark, 7,749 patients with CLL, 7,476 patients with HL, and 25,801 patients with NHL with linkable first-degree relatives were identified.
  • Kaplan-Meier curves were constructed to compare survival in patients with lymphoma with and without a family history of lymphoma.
  • RESULTS: We found 85 patients with CLL (1.10%), 95 patients with HL (1.28%), and 206 patients with NHL (0.80%) with a family history of any lymphoma.
  • Five-year mortality was similar for patients with CLL (hazard ratio [HR], 1.28; 95% CI, 0.95 to 1.72), HL (HR, 0.78; 95% CI, 0.49 to 1.25), and NHL (HR, 0.91; 95% CI, 0.74 to 1.12) versus without a family history of any lymphoma.
  • Mortality was also similar for patients with versus without a family history of the same lymphoma.
  • T-cell/anaplastic lymphoma patients with a family history of NHL had poorer outcome 5-years after diagnosis (HR, 5.38; 95% CI, 1.65 to 17.52).
  • CONCLUSION: With the exception of T-cell/anaplastic lymphoma, survival patterns for patients with CLL, HL, and NHL with a family history of lymphoma were similar to those for sporadic patients, suggesting that most familial lymphomas do not have an altered clinical course.
  • Our findings provide no evidence to modify therapeutic strategies for patients with CLL, HL, or NHL based solely on family history.

  • MedlinePlus Health Information. consumer health - Hodgkin Disease.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Mar;16(3):365-6 [17372231.001]
  • [Cites] Carcinogenesis. 2007 Mar;28(3):704-12 [17056605.001]
  • [Cites] Br J Haematol. 2007 May;137(4):329-36 [17408400.001]
  • [Cites] Haematologica. 2007 Apr;92(4):478-85 [17488658.001]
  • [Cites] Haematologica. 2007 Jul;92(7):960-9 [17606447.001]
  • [Cites] Int J Cancer. 2007 Nov 15;121(10):2260-6 [17583571.001]
  • [Cites] Cancer Invest. 2000;18(4):303-8 [10808365.001]
  • [Cites] Cancer. 2000 May 15;88(10):2357-66 [10820359.001]
  • [Cites] Hum Genet. 2000 May;106(5):553-6 [10914686.001]
  • [Cites] Br J Haematol. 2000 Jun;109(4):794-9 [10929032.001]
  • [Cites] Eur J Haematol. 2000 Aug;65(2):114-7 [10966171.001]
  • [Cites] Leuk Lymphoma. 2001 Jun;42(1-2):99-108 [11699227.001]
  • [Cites] Lancet. 2001 Nov 17;358(9294):1696-8 [11728548.001]
  • [Cites] Acta Oncol. 2001;40(6):772-7 [11765074.001]
  • [Cites] Annu Rev Med. 2002;53:303-18 [11818476.001]
  • [Cites] Blood. 2002 Oct 15;100(8):3037-40 [12351419.001]
  • [Cites] Clin Cancer Res. 2003 Aug 15;9(9):3435-40 [12960134.001]
  • [Cites] Int J Cancer. 2004 Jan 1;108(1):109-14 [14618624.001]
  • [Cites] Blood. 2004 May 1;103(9):3529-34 [14701701.001]
  • [Cites] Cancer. 2004 May 1;100(9):1902-8 [15112271.001]
  • [Cites] Leuk Lymphoma. 2003;44 Suppl 4:S6-14 [15154738.001]
  • [Cites] Blood. 2004 Sep 15;104(6):1850-4 [15161669.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 Sep;13(9):1415-21 [15342441.001]
  • [Cites] Natl Cancer Inst Monogr. 1971 Dec;34:283-9 [4946580.001]
  • [Cites] N Engl J Med. 1977 Feb 3;296(5):248-50 [831107.001]
  • [Cites] Cancer. 1982 May 15;49(10):2197-200 [7074535.001]
  • [Cites] Br J Cancer. 1983 May;47(5):707-12 [6849804.001]
  • [Cites] Br J Cancer. 1987 Jan;55(1):85-90 [3814482.001]
  • [Cites] Br J Cancer. 1987 Jul;56(1):79-82 [3304389.001]
  • [Cites] Leuk Res. 1988;12(1):81-8 [3357350.001]
  • [Cites] Am J Epidemiol. 1989 Oct;130(4):655-64 [2773914.001]
  • [Cites] Leuk Res. 1991;15(5):305-14 [2046383.001]
  • [Cites] Cancer Invest. 1992;10(2):103-9 [1551021.001]
  • [Cites] Cancer Res. 1994 May 1;54(9):2378-85 [8162584.001]
  • [Cites] J Natl Cancer Inst. 1994 Nov 2;86(21):1600-8 [7932824.001]
  • [Cites] Eur J Epidemiol. 1994 Apr;10(2):211-3 [7813700.001]
  • [Cites] N Engl J Med. 1995 Feb 16;332(7):413-8 [7824015.001]
  • [Cites] Int J Cancer. 1997 Sep 17;72(6):977-81 [9378561.001]
  • [Cites] Dan Med Bull. 1997 Nov;44(5):535-9 [9408738.001]
  • [Cites] Cancer Causes Control. 1998 Jan;9(1):77-82 [9486466.001]
  • [Cites] Blood. 1998 May 15;91(10):3574-81 [9572991.001]
  • [Cites] Cancer. 2005 May 1;103(9):1906-15 [15779016.001]
  • [Cites] Blood. 2005 Jul 15;106(2):668-72 [15811955.001]
  • [Cites] J Med Genet. 2005 Jul;42(7):595-601 [15994882.001]
  • [Cites] J Natl Cancer Inst. 2005 Oct 5;97(19):1466-74 [16204696.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Oct;14(10):2402-6 [16214923.001]
  • [Cites] Bioinformatics. 2006 Feb 15;22(4):466-71 [16339281.001]
  • [Cites] Int J Cancer. 2006 Jun 15;118(12):3095-8 [16395700.001]
  • [Cites] Hum Genet. 2006 Jul;119(6):659-68 [16738949.001]
  • [Cites] Blood. 2006 Jul 15;108(2):638-44 [16574953.001]
  • [Cites] Haematologica. 2006 Aug;91(8):1117-20 [16885053.001]
  • [Cites] Folia Med (Plovdiv). 2006;48(1):11-6 [16918049.001]
  • [Cites] Eur J Cancer. 2006 Oct;42(15):2570-6 [16928444.001]
  • [Cites] Pharmacol Rep. 2006 Sep-Oct;58(5):720-8 [17085864.001]
  • [Cites] Am J Epidemiol. 2007 Jan 15;165(2):126-33 [17071845.001]
  • [Cites] Hum Genet. 2007 Apr;121(2):161-8 [17149600.001]
  • (PMID = 18606984.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2652080
  •  go-up   go-down


14. Gündüz E, Demirel G, Bal C, Gulbas Z: Evaluation of mobilized peripheral stem cells according to CD34 and aldehyde dehydrogenase expression and effect of SSC(lo) ALDH(br) cells on hematopoietic recovery. Cytotherapy; 2010 Dec;12(8):1006-12
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Thirty patients (20 males and 10 females), who were candidates for autologous peripheral blood stem cell transplantation, were included in the study.
  • Primary diagnoses were multiple myeloma (n = 14), Hodgkin's lymphoma (n = 7), non-Hodgkin's lymphoma (n = 2), acute myloid leukemia (n = 2), chronic lymphocytic leukemia (n = 1) and germ cell testis tumor (n = 1).
  • RESULTS: Numbers of SSC(lo) CD45(dim) CD34(hi) cells and SSC(lo) ALDH(br) cells were highly correlated in both peripheral blood and apheresis products (P < 0.001).
  • We could not find a relationship between the transplanted SSC(lo) CD45(dim) CD34(hi) cell dose or SSC(lo) ALDH(br) cell dose and platelet or neutrophil recovery.
  • CONCLUSIONS: According to our data, numbers of SSC(lo) ALDH(br) cells are in very good agreement with numbers of SSC(lo) CD45(dim) CD34(hi) cells and can be a predictor of stem cell mobilization.
  • [MeSH-major] Graft Survival / immunology. Hematopoietic Stem Cell Transplantation. Hematopoietic Stem Cells / metabolism. Leukemia / therapy. Lymphoma / therapy
  • [MeSH-minor] Adult. Aldehyde Dehydrogenase / metabolism. Antigens, CD34 / metabolism. Blood Component Removal. Cells, Cultured. Cyclophosphamide / administration & dosage. Female. Granulocyte Colony-Stimulating Factor / administration & dosage. Hematopoiesis / drug effects. Hematopoietic Stem Cell Mobilization. Humans. Male. Middle Aged

  • MedlinePlus Health Information. consumer health - Leukemia.
  • MedlinePlus Health Information. consumer health - Lymphoma.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20735165.001).
  • [ISSN] 1477-2566
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 8N3DW7272P / Cyclophosphamide; EC 1.2.1.3 / Aldehyde Dehydrogenase
  •  go-up   go-down


15. Nikolova M, Guenova M, Taskov H, Marie-Cardine A, Boumsell L, Bensussan A: SC3 monoclonal antibody defines a novel specific human B-cell surface antigen differentially expressed on B-cell leukaemias and lymphomas and involved in the proliferation of normal and malignant B lymphocytes. Cell Immunol; 2005 Jul-Aug;236(1-2):92-100
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] SC3 monoclonal antibody defines a novel specific human B-cell surface antigen differentially expressed on B-cell leukaemias and lymphomas and involved in the proliferation of normal and malignant B lymphocytes.
  • The monoclonal antibody SC3 was raised against the NK leukaemia cell line YTindi.
  • It detected a 98-kDa surface antigen with weak expression on a restricted number of leukaemia cell lines under reducing conditions.
  • SC3 mAb labelled 5-10% of normal peripheral blood lymphocytes corresponding almost exclusively to B lymphocytes, and 60-70% of tonsillar B cells.
  • Practically, all B-CLL studied expressed SC3 mAb reactive epitope although with variable intensity, while MCL and PLL were negative.
  • Other low grade and high grade B-NHL were variably stained.
  • This effect was much weaker with B-CLL cells but was increased after cross-linking with an anti-IgM antibody.
  • The restricted expression pattern combined with molecular weight and functional data indicate that SC3 mAb may detect a novel B-cell antigen mostly expressed by early and naive B cells.
  • Although its expression in B-cell malignancies was not limited to a single differentiation stage, it might confer specific functional characteristics to the positive malignant cells.
  • [MeSH-major] Antigens, Differentiation, B-Lymphocyte / immunology. Antigens, Surface / immunology. B-Lymphocytes / immunology. Leukemia, B-Cell / immunology. Lymphoma, B-Cell / immunology

  • Genetic Alliance. consumer health - B-Cell Lymphomas.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16197933.001).
  • [ISSN] 0008-8749
  • [Journal-full-title] Cellular immunology
  • [ISO-abbreviation] Cell. Immunol.
  • [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, Differentiation, B-Lymphocyte; 0 / Antigens, Surface; 0 / Epitopes, B-Lymphocyte
  •  go-up   go-down


16. Bacher U, Schnittger S, Kern W, Hiddemann W, Haferlach T, Schoch C: The incidence of submicroscopic deletions in reciprocal translocations is similar in acute myeloid leukemia, BCR-ABL positive acute lymphoblastic leukemia, and chronic myeloid leukemia. Haematologica; 2005 Apr;90(4):558-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The incidence of submicroscopic deletions in reciprocal translocations is similar in acute myeloid leukemia, BCR-ABL positive acute lymphoblastic leukemia, and chronic myeloid leukemia.
  • We compared the incidence of submicroscopic deletions accompanying balanced translocations using interphase fluorescence in situ hybridization (FISH) in 245 patients with chronic myeloid leukemia (CML), 79 patients with acute lymphoblastic leukemia (ALL) and BCR-ABL (n=70) or MLL rearrangements (n=29), and 412 patients with acute myeloid leukemia (AML) with CBFB-MYH11 (n=122), PML-RARalpha (n=108), AML1-ETO (n=112), or MLL rearrangements (n=98).
  • [MeSH-major] Chromosome Deletion. Fusion Proteins, bcr-abl / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Humans. Reproducibility of Results. Translocation, Genetic


17. Aue G, Lindorfer MA, Beum PV, Pawluczkowycz AW, Vire B, Hughes T, Taylor RP, Wiestner A: Fractionated subcutaneous rituximab is well-tolerated and preserves CD20 expression on tumor cells in patients with chronic lymphocytic leukemia. Haematologica; 2010 Feb;95(2):329-32
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fractionated subcutaneous rituximab is well-tolerated and preserves CD20 expression on tumor cells in patients with chronic lymphocytic leukemia.
  • A pilot study previously demonstrated that thrice-weekly, fractionated-dose intravenous rituximab (RTX) limits CD20 loss from chronic lymphocytic leukemia (CLL) B cells, thereby enhancing immunotherapeutic targeting.
  • Here, we investigated the feasibility of giving 20 mg rituximab subcutaneously thrice weekly for up to 12 weeks in 4 previously treated CLL patients.
  • Subcutaneous rituximab was well-tolerated with minimal injection site reactions; a variable degree of efficacy was observed, likely influenced by the size of the patients' B cell/CD20 burden.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, CD20 / genetics. Antineoplastic Agents / therapeutic use. Gene Expression / drug effects. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. RITUXIMAB .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Immunol. 2004 Mar 1;172(5):3280-8 [14978136.001]
  • [Cites] J Immunol Methods. 2004 Jun;289(1-2):97-109 [15251416.001]
  • [Cites] J Clin Invest. 1972 Mar;51(3):583-9 [4622104.001]
  • [Cites] Blood. 1997 Sep 15;90(6):2188-95 [9310469.001]
  • [Cites] J Clin Oncol. 1998 Aug;16(8):2825-33 [9704735.001]
  • [Cites] J Immunol. 2006 Feb 15;176(4):2600-9 [16456022.001]
  • [Cites] Blood. 2001 Sep 1;98(5):1326-31 [11520778.001]
  • [Cites] J Immunol. 2006 Nov 15;177(10):7435-43 [17082663.001]
  • [Cites] Haematologica. 2007 Dec;92(12):1695-8 [18055995.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1456-63 [18024795.001]
  • [Cites] J Immunol. 2008 Aug 15;181(4):2916-24 [18684983.001]
  • [Cites] Curr Opin Immunol. 2008 Aug;20(4):444-9 [18585457.001]
  • [Cites] Clin Cancer Res. 2006 Jul 1;12(13):4027-35 [16818702.001]
  • (PMID = 19679883.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00366418
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  • [Other-IDs] NLM/ PMC2817038
  •  go-up   go-down


18. Numeroso F, Baroni MC, Delsignore R: Association between immune thrombocytopenic purpura and chronic lymphocytic leukemia in a patient carrier of anti-hepatitis C virus antibodies. Ann Ital Med Int; 2005 Jul-Sep;20(3):197-202
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association between immune thrombocytopenic purpura and chronic lymphocytic leukemia in a patient carrier of anti-hepatitis C virus antibodies.
  • Immune thrombocytopenic purpura (ITP) occurs in 2-3% of chronic lymphocytic leukemia (CLL) patients, whereas autoimmune thrombocytopenia is very rare before the diagnosis of lymphoma.
  • Laboratory analysis revealed: marked thrombocytopenia (platelet count 5000/microL); hypogammaglobulinemia (9%, immunoglobulin-IgG 634 mg/dL); presence of HCV antibody (negative HCV-RNA); low-titer anti-nuclear antibody and anti-smooth muscle antibody (1:80); positive cryoglobulin (polycolonal, IgG-IgM, cryocrit 0.5%).
  • Platelet kinetics study showed a markedly reduced platelet half-life (<1 day) with evident splenic uptake.
  • Two years later, the patient underwent a prostatectomy for prostate cancer and within the pelvic nodal screening the histological examination unexpectedly revealed features of B-cell non-Hodgkin's lymphoma, type CCL/small lymphocytic lymphoma; a bone marrow aspirate showed a monotypic CD5+, CD19+, CD23+ B-cell proliferation confirming the diagnosis of CLL.
  • Six months later, a computed tomography scan revealed multiple pathological node enlargements (1.5-3 cm), compatible with a malignant lymphoma.
  • The marked thrombocytopenia may have been an early expression of the lymphoproliferative disease.
  • Otherwise, the association between CLL and ITP might reflect the underlying role of HCV infection causing an immune dysregulation responsible for both pathologies.
  • [MeSH-major] Hepatitis C / complications. Hepatitis C Antibodies / blood. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Purpura, Thrombocytopenic, Idiopathic / complications


19. Vogler M, Butterworth M, Majid A, Walewska RJ, Sun XM, Dyer MJ, Cohen GM: Concurrent up-regulation of BCL-XL and BCL2A1 induces approximately 1000-fold resistance to ABT-737 in chronic lymphocytic leukemia. Blood; 2009 Apr 30;113(18):4403-13
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Concurrent up-regulation of BCL-XL and BCL2A1 induces approximately 1000-fold resistance to ABT-737 in chronic lymphocytic leukemia.
  • ABT-263 shows promising activity in early phase 1 clinical trials in B-cell malignancies, particularly chronic lymphocytic leukemia (CLL).
  • In vitro, peripheral blood CLL cells are extremely sensitive to ABT-737 (EC(50) approximately 7 nM), with rapid induction of apoptosis in all 60 patients tested, independent of parameters associated with disease progression and chemotherapy resistance.
  • In contrast to data from cell lines, ABT-737-induced apoptosis in CLL cells was largely MCL1-independent.
  • Because CLL cells within lymph nodes are more resistant to apoptosis than those in peripheral blood, CLL cells were cultured on CD154-expressing fibroblasts in the presence of interleukin-4 (IL-4) to mimic the lymph node microenvironment.
  • CLL cells thus cultured developed an approximately 1000-fold resistance to ABT-737 within 24 hours.
  • Investigations of the underlying mechanism revealed that this resistance occurred upstream of mitochondrial perturbation and involved de novo synthesis of the antiapoptotic proteins BCL-X(L) and BCL2A1, which were responsible for resistance to low and high ABT-737 concentrations, respectively.
  • Our data indicate that after therapy with ABT-737-related inhibitors, resistant CLL cells might develop in lymph nodes in vivo and that treatment strategies targeting multiple BCL2 antiapoptotic members simultaneously may have synergistic activity.
  • [MeSH-major] Biphenyl Compounds / pharmacology. Drug Resistance, Neoplasm. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Nitrophenols / pharmacology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Sulfonamides / pharmacology. bcl-X Protein / metabolism
  • [MeSH-minor] Apoptosis / drug effects. Blotting, Western. CD40 Ligand / genetics. CD40 Ligand / metabolism. Fibroblasts / cytology. Fibroblasts / drug effects. Fibroblasts / metabolism. Humans. Immunoenzyme Techniques. Immunoprecipitation. Interleukin-4 / genetics. Interleukin-4 / metabolism. Lymph Nodes / drug effects. Lymph Nodes / metabolism. Lymph Nodes / pathology. Lymphocytes / drug effects. Lymphocytes / metabolism. Lymphocytes / pathology. Minor Histocompatibility Antigens. Mitochondria / drug effects. Mitochondria / metabolism. Myeloid Cell Leukemia Sequence 1 Protein. Piperazines / pharmacology. Protein Biosynthesis / drug effects. RNA, Small Interfering / pharmacology. Up-Regulation

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • COS Scholar Universe. author profiles.
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Blood. 2009 Sep 17;114(12):2560-1; author reply 2561-2 [19762501.001]
  • [CommentIn] Blood. 2009 Apr 30;113(18):4132-3 [19406997.001]
  • (PMID = 19008458.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U132615750; United Kingdom / Medical Research Council / / MC/ U132670597; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABT-737; 0 / BCL2-related protein A1; 0 / BCL2L1 protein, human; 0 / Biphenyl Compounds; 0 / Minor Histocompatibility Antigens; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Nitrophenols; 0 / Piperazines; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Small Interfering; 0 / Sulfonamides; 0 / bcl-X Protein; 147205-72-9 / CD40 Ligand; 207137-56-2 / Interleukin-4
  •  go-up   go-down


20. Ruddy KJ, Wu D, Brown JR: Pseudohyperkalemia in chronic lymphocytic leukemia. J Clin Oncol; 2008 Jun 1;26(16):2781-2
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pseudohyperkalemia in chronic lymphocytic leukemia.
  • [MeSH-major] Hyperkalemia / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / blood

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18509189.001).
  • [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] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


21. Seeliger B, Wilop S, Osieka R, Galm O, Jost E: CpG island methylation patterns in chronic lymphocytic leukemia. Leuk Lymphoma; 2009 Mar;50(3):419-26
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CpG island methylation patterns in chronic lymphocytic leukemia.
  • Chronic lymphocytic leukemia (CLL) is the most common leukemia in Western countries.
  • In CLL, a large number of genes affecting cancer-related pathways may be dysregulated by epigenetic silencing.
  • We analysed by methylation-specific polymerase chain reaction the CpG island methylation status of 15 well-characterised cancer-related genes in 32 patients with CLL.
  • Aberrant methylation in the sample of patients with CLL was shown for secreted frizzled-related protein 1 (68.8%), secreted frizzled-related protein 2 (65.6%), death-associated protein kinase 1 (50.0%), E-cadherin (21.9%), secreted frizzled-related protein 4 (15.6%), p15 (9.4%), p16 (6.3%), retinoic acid receptor beta2 (3.1%), secreted frizzled-related protein 5 (3.1%) and tissue inhibitor of matrix metalloproteinases 3 (3.1%).
  • Our results show that aberrant CpG island methylation affecting cancer-related pathways such as Wnt signalling, regulation of apoptosis, cell cycle control and tissue invasion is a common phenomenon in CLL.
  • Epigenetic disturbances may be involved in the pathogenesis of CLL and thus may provide a molecular rationale for therapeutic approaches.
  • [MeSH-major] CpG Islands / genetics. DNA Methylation / genetics. Epigenesis, Genetic / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics
  • [MeSH-minor] Apoptosis / genetics. Cell Cycle / genetics. Genes, Neoplasm / genetics. Humans. Neoplasm Invasiveness / genetics. Polymerase Chain Reaction. Wnt Proteins / genetics


22. Zaballos P, Llambrich A, Cuéllar F, Puig S, Malvehy J: Dermoscopic findings in pyogenic granuloma. Br J Dermatol; 2006 Jun;154(6):1108-11
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: To the best of our knowledge, no specific dermoscopic criteria have been described in the medical literature for the diagnosis of pyogenic granuloma.
  • METHODS: Dermoscopic examination (using the DermLite Foto; 3Gen, LLC, Dana Point, CA, U.S.A.) of 13 patients with pyogenic granulomas was performed to evaluate specific dermoscopic criteria.
  • [MeSH-major] Granuloma, Pyogenic / diagnosis. Skin Neoplasms / diagnosis

  • Genetic Alliance. consumer health - Pyogenic Granuloma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16704641.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  •  go-up   go-down


23. Evens AM, Balasubramanian L, Gordon LI: Motexafin gadolinium induces oxidative stress and apoptosis in hematologic malignancies. Curr Treat Options Oncol; 2005 Jul;6(4):289-96
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Redox mechanisms have been shown to be important in malignant cell survival and are a system that may be modified for the treatment of hematologic malignancies.
  • Motexafin gadolinium (MGd) is a synthetic expanded porphyrin that selectively accumulates in tumor cells and oxidizes various intracellular metabolites, including ascorbate, nicotinamide adenine dinucleotide phosphate, glutathione, and protein thiols, to generate reactive oxygen species in a process known as futile redox cycling.
  • The rationale for its use in hematologic malignancies is that, like naturally occurring porphyrins, it tends to concentrate selectively in cancer cells, and it has a novel mechanism of action of inducing redox stress and triggering apoptosis in a broad range of malignancies.
  • MGd induces apoptosis in B-cell non-Hodgkin's lymphoma, chronic lymphocytic leukemia, and highly resistant myeloma cell lines.
  • Preliminary results from clinical trials with MGd in hematopoietic malignancies have shown that it is well tolerated, with minimal hematologic side effects in both; it has single agent activity in very heavily pretreated chronic lymphocytic leukemia /small lymphocytic lymphoma patients, and it has induced prompt complete remissions in combination with 90Yttrium-ibritumomab (Y-90 Zevalin; Biogen Idec Inc., Cambridge, MA) for relapsed non-Hodgkin's lymphoma in the first two cohorts of patients enrolled.

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Radiat Oncol Biol Phys. 2001 Apr 1;49(5):1381-90 [11286846.001]
  • [Cites] Blood. 2001 Aug 1;98(3):805-13 [11468182.001]
  • [Cites] Chem Commun (Camb). 2002 Nov 21;(22):2730-1 [12510321.001]
  • [Cites] Free Radic Biol Med. 1998 Mar 1;24(4):586-93 [9559871.001]
  • [Cites] EMBO J. 1999 Nov 1;18(21):6027-36 [10545114.001]
  • [Cites] J Clin Oncol. 2003 Jul 1;21(13):2529-36 [12829672.001]
  • [Cites] J Clin Oncol. 2004 Jan 1;22(1):157-65 [14701778.001]
  • [Cites] Invest Radiol. 1994 Mar;29(3):330-8 [8175308.001]
  • [Cites] Science. 1985 Jan 25;227(4685):375-81 [2981433.001]
  • [Cites] Blood. 2002 Feb 1;99(3):1038-43 [11807010.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1999 Nov 1;45(4):981-9 [10571206.001]
  • [Cites] J Clin Oncol. 2001 Apr 1;19(7):2074-83 [11283141.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jun 25;93(13):6610-5 [8692865.001]
  • [Cites] J Biol Chem. 1988 Nov 25;263(33):17205-8 [3053703.001]
  • [Cites] Free Radic Biol Med. 2002 Sep 15;33(6):755-64 [12208364.001]
  • [Cites] Clin Cancer Res. 2001 Oct;7(10):3215-21 [11595717.001]
  • [Cites] J Pharmacol Exp Ther. 2001 Jun;297(3):888-94 [11356908.001]
  • [Cites] Pathol Int. 1999 Feb;49(2):91-102 [10355961.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2002 Oct 1;54(2):536-41 [12243833.001]
  • [Cites] Radiology. 1999 Sep;212(3):755-9 [10478243.001]
  • [Cites] Clin Cancer Res. 2002 Feb;8(2):566-72 [11839678.001]
  • [Cites] Clin Cancer Res. 2002 Dec;8(12):3658-68 [12473574.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Oct;79(20):6246-9 [6959113.001]
  • [Cites] Blood. 2001 Nov 1;98(9):2771-7 [11675350.001]
  • [Cites] Med Res Rev. 2004 Jan;24(1):40-89 [14595672.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 2001;41:261-95 [11264458.001]
  • [Cites] Blood. 1999 Sep 15;94(6):2102-11 [10477740.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2001 Nov 15;51(4):1025-36 [11704327.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2004 Apr 1;58(5):1570-6 [15050338.001]
  • [Cites] Biochem Pharmacol. 2000 Apr 1;59(7):733-9 [10718331.001]
  • [Cites] Clin Cancer Res. 2004 Feb 15;10(4):1481-91 [14977852.001]
  • [Cites] Clin Cancer Res. 1999 Apr;5(4):739-45 [10213207.001]
  • [Cites] Cell Death Differ. 2003 Mar;10(3):323-34 [12700632.001]
  • [Cites] Blood. 2005 Feb 1;105(3):1265-73 [15388578.001]
  • [Cites] J Clin Oncol. 2002 Aug 15;20(16):3445-53 [12177105.001]
  • (PMID = 15967082.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Metalloporphyrins; 0 / Reactive Oxygen Species; 6433A42F4F / motexafin gadolinium
  • [Number-of-references] 37
  •  go-up   go-down


24. Reslan L, Mestas JL, Herveau S, Béra JC, Dumontet C: Transfection of cells in suspension by ultrasound cavitation. J Control Release; 2010 Mar 3;142(2):251-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this study, we evaluated sonoporation as a method to transfect nucleic acids in suspension cells, including the human follicular lymphoma cell line RL and fresh human Chronic Lymphocytic Leukemia (CLL) cells.
  • RL and CLL cells were exposed to continuous ultrasound waves (445 kHz) in the presence of either plasmid DNA coding for green fluorescent protein (GFP) or fluorescent siRNA directed against BCL2L1.
  • Transfection efficiency and cell viability were assessed using fluorescent microscopy and flow cytometry analysis, respectively.
  • Sonoporation allows a highly efficient transfection of nucleic acid in suspension cells with a low rate of mortality, both in a tumor cell line and in fresh human leukemic cells.
  • [MeSH-major] DNA / administration & dosage. RNA, Small Interfering / administration & dosage. Transfection / instrumentation. bcl-X Protein / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Cells, Cultured. Equipment Design. Female. Humans. Leukemia, Lymphoid / genetics. Lymphoma, Follicular / genetics. Mice. Mice, SCID. Plasmids / administration & dosage. Ultrasonics

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2009 Elsevier B.V. All rights reserved.
  • (PMID = 19896995.001).
  • [ISSN] 1873-4995
  • [Journal-full-title] Journal of controlled release : official journal of the Controlled Release Society
  • [ISO-abbreviation] J Control Release
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / BCL2L1 protein, human; 0 / RNA, Small Interfering; 0 / bcl-X Protein; 9007-49-2 / DNA
  •  go-up   go-down


25. Boesch-Saadatmandi C, Wagner AE, Graeser AC, Hundhausen C, Wolffram S, Rimbach G: Ochratoxin A impairs Nrf2-dependent gene expression in porcine kidney tubulus cells. J Anim Physiol Anim Nutr (Berl); 2009 Oct;93(5):547-54
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Therefore, in the present study, the effects of OTA on the nuclear translocation and transactivation of the transcription factor Nrf2 as well as mRNA levels of Nrf2 target genes including glutathione-S-transferase and gamma-glutamylcysteinyl synthetase have been studied in cultured porcine kidney tubulus cells (LLC-PK1).
  • Nrf2 was induced by sulforaphane, a well-known activator of this transcription factor.
  • Ochratoxin A significantly decreased gamma-glutamylcysteinyl synthetase and glutathione-S-transferase mRNA levels in LLC-PK1 cells.
  • [MeSH-minor] Animals. Cell Line. Isothiocyanates. Polymerase Chain Reaction / veterinary. Swine. Thiocyanates / pharmacology

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. OCHRATOXIN A .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18547363.001).
  • [ISSN] 1439-0396
  • [Journal-full-title] Journal of animal physiology and animal nutrition
  • [ISO-abbreviation] J Anim Physiol Anim Nutr (Berl)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Isothiocyanates; 0 / NF-E2-Related Factor 2; 0 / Ochratoxins; 0 / Thiocyanates; 1779SX6LUY / ochratoxin A; 4478-93-7 / sulforafan
  •  go-up   go-down


26. Agirre X, Román-Gómez J, Vázquez I, Jiménez-Velasco A, Garate L, Montiel-Duarte C, Artieda P, Cordeu L, Lahortiga I, Calasanz MJ, Heiniger A, Torres A, Minna JD, Prósper F: Abnormal methylation of the common PARK2 and PACRG promoter is associated with downregulation of gene expression in acute lymphoblastic leukemia and chronic myeloid leukemia. Int J Cancer; 2006 Apr 15;118(8):1945-53
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Abnormal methylation of the common PARK2 and PACRG promoter is associated with downregulation of gene expression in acute lymphoblastic leukemia and chronic myeloid leukemia.
  • We have studied the role of promoter hypermethylation in the regulation of PARK2 and PACRG expression in different tumor cell lines and primary patient samples.
  • Abnormal methylation of the common promoter of PARK2 and PACRG was observed in 26% of patients with acute lymphoblastic leukemia and 20% of patients with chronic myelogenous leukemia (CML) in lymphoid blast crisis, but not in ovarian, breast, lung, neuroblastoma, astrocytoma or colon cancer cells.
  • In conclusion, our results demonstrate for the first time that the candidate tumor suppressor genes PARK2 and PACRG are epigenetically regulated in human leukemia, suggesting that abnormal methylation and regulation of PARK2 and PACRG may play a role in the pathogenesis and development of this hematological neoplasm.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proteins / physiology. Ubiquitin-Protein Ligases / biosynthesis

  • Genetic Alliance. consumer health - Chronic Myeloid Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16287063.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50CA70907; United States / NCI NIH HHS / CA / U01CA7629303
  • [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 / Molecular Chaperones; 0 / PACRG protein, human; 0 / Proteins; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / parkin protein
  •  go-up   go-down


27. Brown JR: Inherited predisposition to chronic lymphocytic leukemia. Expert Rev Hematol; 2008 Oct;1(1):51-61
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inherited predisposition to chronic lymphocytic leukemia.
  • Inherited susceptibility to chronic lymphocytic leukemia (CLL) has been recognized for decades.
  • Approximately 10% of individuals with CLL report a family history of CLL or a related lymphoproliferative disorder, and genetic predisposition is the best understood risk factor for CLL.
  • Studies of familial CLL have suggested that the disease features are largely similar to sporadic CLL, although recent data suggest that familial CLL may more commonly show somatic hypermutation of the immunoglobulin heavy-chain variable region, suggesting a more indolent disease course.
  • Monoclonal B-cell lymphocytosis (MBL) has been identified recently as a likely precursor to CLL; it is found in the general population with increasing age and enriched in unaffected relatives of individuals with familial CLL.
  • Studies of MBL as well as mouse models of CLL may lead to better understanding of early CLL pathogenesis that is relevant to familial predisposition.
  • To date, the identification of genes that predispose to familial CLL has been slow, primarily due to the relatively few families available for study, the small size of those families and disease causation most likely by multiple genes that each confer smaller risks.
  • In the coming years, the application of systematic genomics approaches to familial CLL should, hopefully, lead to the identification of novel loci involved in the disease.

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2002 Jul 15;100(2):635-9 [12091358.001]
  • [Cites] Leukemia. 2002 Jul;16(7):1229-32 [12094247.001]
  • [Cites] Leuk Res. 2002 Sep;26(9):791-4 [12127552.001]
  • [Cites] Blood. 2002 Aug 1;100(3):1100-1 [12150154.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2289-90 [12239136.001]
  • [Cites] Br J Haematol. 1997 Apr;97(1):107-12 [9136948.001]
  • [Cites] Immunity. 1997 Nov;7(5):703-13 [9390693.001]
  • [Cites] Leukemia. 1998 Nov;12(11):1696-8 [9823943.001]
  • [Cites] Am J Hum Genet. 1999 Jul;65(1):265-9 [10364544.001]
  • [Cites] Leukemia. 1999 Oct;13(10):1497-500 [10516748.001]
  • [Cites] Nat Rev Genet. 2005 Oct;6(10):756-65 [16205715.001]
  • [Cites] N Engl J Med. 2005 Oct 27;353(17):1793-801 [16251535.001]
  • [Cites] Lancet Oncol. 2006 Jan;7(1):27-38 [16389181.001]
  • [Cites] Int J Immunogenet. 2006 Feb;33(1):21-4 [16426238.001]
  • [Cites] Leukemia. 2006 Feb;20(2):280-5 [16341048.001]
  • [Cites] Cytometry B Clin Cytom. 2007 Sep;72(5):344-53 [17266153.001]
  • [Cites] Cytogenet Genome Res. 2007;118(1):8-12 [17901694.001]
  • [Cites] Int J Cancer. 2007 Nov 15;121(10):2260-6 [17583571.001]
  • [Cites] Blood. 2007 Nov 1;110(9):3326-33 [17687107.001]
  • [Cites] Nat Genet. 2007 Nov;39(11):1315-7 [17934461.001]
  • [Cites] Br J Haematol. 2007 Dec;139(5):690-700 [18021083.001]
  • [Cites] Br J Haematol. 2007 Dec;139(5):701-8 [18021084.001]
  • [Cites] Br J Haematol. 2007 Dec;139(5):724-9 [18021087.001]
  • [Cites] Br J Haematol. 2007 Dec;139(5):762-71 [18021089.001]
  • [Cites] Br J Haematol. 2007 Dec;139(5):774-9 [18021091.001]
  • [Cites] Br J Haematol. 2007 Dec;139(5):645-57 [17941951.001]
  • [Cites] Br J Haematol. 2007 Dec;139(5):809-19 [17941952.001]
  • [Cites] Br J Haematol. 2007 Dec;139(5):744-52 [17961188.001]
  • [Cites] J Clin Oncol. 2007 Dec 1;25(34):5448-57 [17968022.001]
  • [Cites] Nat Genet. 2008 Mar;40(3):281-3 [18264098.001]
  • [Cites] Nat Genet. 2008 May;40(5):631-7 [18372901.001]
  • [Cites] Nat Genet. 2008 May;40(5):623-30 [18372905.001]
  • [Cites] Nat Genet. 2008 May;40(5):616-22 [18385676.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5446-56 [18216293.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5691-3 [18424666.001]
  • [Cites] N Engl J Med. 2008 Aug 7;359(6):575-83 [18687638.001]
  • [Cites] Leuk Res. 2009 Jan;33(1):162-5 [18556064.001]
  • [Cites] Br J Haematol. 1999 Dec;107(3):616-24 [10583268.001]
  • [Cites] Blood. 2000 Feb 15;95(4):1413-9 [10666219.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3028-33 [10716693.001]
  • [Cites] Eur J Haematol. 2000 Aug;65(2):114-7 [10966171.001]
  • [Cites] Mol Cell. 2000 Aug;6(2):395-407 [10983986.001]
  • [Cites] Blood. 2000 Dec 1;96(12):3982-4 [11090088.001]
  • [Cites] N Engl J Med. 2000 Dec 28;343(26):1910-6 [11136261.001]
  • [Cites] Blood. 2001 Apr 1;97(7):2098-104 [11264177.001]
  • [Cites] Int J Cancer. 2001 Apr 15;92(2):203-7 [11291046.001]
  • [Cites] Cancer. 2001 Sep 1;92(5):1325-30 [11571749.001]
  • [Cites] Leuk Lymphoma. 2001 Jun;42(1-2):99-108 [11699227.001]
  • [Cites] Lancet. 2002 Mar 30;359(9312):1114-9 [11943260.001]
  • [Cites] Blood. 2002 Jun 1;99(11):4216-8 [12010828.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6955-60 [12011454.001]
  • [Cites] Blood. 2002 Jul 15;100(2):603-9 [12091354.001]
  • [Cites] Br J Haematol. 2002 Dec;119(3):713-5 [12437649.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15524-9 [12434020.001]
  • [Cites] Cancer Causes Control. 2002 Nov;13(9):791-5 [12462543.001]
  • [Cites] Leuk Lymphoma. 2002 Oct;43(10):1987-90 [12481897.001]
  • [Cites] Cytometry B Clin Cytom. 2003 Mar;52(1):1-12 [12599176.001]
  • [Cites] Br J Haematol. 2003 Jun;121(6):866-73 [12786797.001]
  • [Cites] Leuk Res. 2003 Oct;27(10):973-5 [12860021.001]
  • [Cites] Blood. 2004 Mar 15;103(6):2337-42 [14630808.001]
  • [Cites] Cancer Res. 2004 Apr 1;64(7):2424-33 [15059895.001]
  • [Cites] J Natl Cancer Inst. 2004 May 5;96(9):673-82 [15126604.001]
  • [Cites] Leukemia. 2004 Jun;18(6):1162-3 [15085160.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 Jun;13(6):1065-7 [15184265.001]
  • [Cites] Semin Hematol. 2004 Jul;41(3):201-6 [15269880.001]
  • [Cites] Blood. 2004 Sep 15;104(6):1850-4 [15161669.001]
  • [Cites] Cancer Cell. 2004 Oct;6(4):399-408 [15488762.001]
  • [Cites] N Engl J Med. 1987 May 21;316(21):1289-94 [3574400.001]
  • [Cites] Leuk Res. 1991;15(5):305-14 [2046383.001]
  • [Cites] Cancer Res. 1992 Jan 15;52(2):437-43 [1370214.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Dec 1;89(23):11376-80 [1454823.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Dec 20;91(26):12530-4 [7809072.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] Am J Hum Genet. 1996 Nov;59(5):990-8 [8900225.001]
  • [Cites] Leuk Res. 2005 Jan;29(1):59-61 [15541476.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Nov 23;101(47):16600-5 [15545599.001]
  • [Cites] N Engl J Med. 2005 Apr 21;352(16):1667-76 [15843669.001]
  • [Cites] Cancer. 2005 May 1;103(9):1906-15 [15779016.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 May;14(5):1245-50 [15894680.001]
  • [Cites] Leukemia. 2005 Jun;19(6):1025-8 [15800670.001]
  • [Cites] J Natl Cancer Inst. 2005 Jul 20;97(14):1088-9; author reply 1093-5 [16030308.001]
  • [Cites] J Natl Cancer Inst. 2005 Jul 20;97(14):1089-90; author reply 1093-5 [16030309.001]
  • [Cites] J Natl Cancer Inst. 2005 Jul 20;97(14):1090-1; author reply 1093-5 [16030310.001]
  • [Cites] J Natl Cancer Inst. 2005 Jul 20;97(14):1091-2; author reply 1093-5 [16030311.001]
  • [Cites] J Natl Cancer Inst. 2005 Jul 20;97(14):1092-3; author reply 1093-5 [16030312.001]
  • [Cites] Br J Haematol. 2005 Aug;130(3):325-32 [16042682.001]
  • [Cites] Am J Hum Genet. 2005 Sep;77(3):420-9 [16080117.001]
  • [Cites] J Immunol. 2005 Oct 1;175(7):4309-19 [16177071.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):13944-9 [16166262.001]
  • [Cites] J Natl Cancer Inst. 2005 Oct 5;97(19):1466-74 [16204696.001]
  • [Cites] Int J Cancer. 2006 Apr 1;118(7):1831-5 [16217763.001]
  • [Cites] J Clin Oncol. 2006 Feb 20;24(6):983-7 [16432079.001]
  • [Cites] Br J Haematol. 2006 Apr;133(1):59-61 [16512829.001]
  • [Cites] Leukemia. 2006 Apr;20(4):728-9 [16437141.001]
  • [Cites] Semin Oncol. 2006 Apr;33(2):195-201 [16616066.001]
  • [Cites] Nat Genet. 2006 Jun;38(6):659-62 [16715099.001]
  • [Cites] Blood. 2006 Jul 15;108(2):638-44 [16574953.001]
  • [Cites] Haematologica. 2006 Aug;91(8):1117-20 [16885053.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1334-8 [16670263.001]
  • [Cites] Leuk Res. 2006 Dec;30(12):1573-6 [16581122.001]
  • [Cites] Blood. 2007 Feb 1;109(3):916-25 [17047154.001]
  • [Cites] Blood. 2007 Feb 1;109(3):1202-10 [17053054.001]
  • [Cites] Int J Cancer. 2007 Mar 1;120(5):1099-102 [17131330.001]
  • [Cites] Br J Haematol. 2007 Apr;137(2):173-5 [17391501.001]
  • [Cites] Nat Genet. 2007 May;39(5):645-9 [17401363.001]
  • [Cites] Nat Genet. 2007 May;39(5):631-7 [17401366.001]
  • [Cites] Cell. 2007 Jun 1;129(5):879-90 [17540169.001]
  • [Cites] Blood. 2007 Jun 15;109(12):5079-86 [17351108.001]
  • [Cites] Leuk Lymphoma. 2007 Jun;48(6):1087-91 [17577771.001]
  • [Cites] Nature. 2007 Jun 28;447(7148):1087-93 [17529967.001]
  • [Cites] Nat Genet. 2007 Aug;39(8):977-83 [17603485.001]
  • [Cites] Nat Genet. 2007 Aug;39(8):984-8 [17618284.001]
  • (PMID = 19802369.001).
  • [ISSN] 1747-4094
  • [Journal-full-title] Expert review of hematology
  • [ISO-abbreviation] Expert Rev Hematol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K23 CA115682-03; United States / NCI NIH HHS / CA / K23 CA115682-04; None / None / / K23 CA115682-03; United States / NCI NIH HHS / CA / CA115682-01; United States / NCI NIH HHS / CA / K23 CA115682; United States / NCI NIH HHS / CA / CA115682-04; United States / NCI NIH HHS / CA / K23 CA115682-01; United States / NCI NIH HHS / CA / CA115682-02; United States / NCI NIH HHS / CA / K23 CA115682-02
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [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 / Atm protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Keywords] NOTNLM ; association / familial chronic lymphocytic leukemia / linkage / lymphocytosis / monoclonal B cell
  •  go-up   go-down


28. Packham G, Stevenson F: The role of the B-cell receptor in the pathogenesis of chronic lymphocytic leukaemia. Semin Cancer Biol; 2010 Dec;20(6):391-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of the B-cell receptor in the pathogenesis of chronic lymphocytic leukaemia.
  • The key molecule for normal B cells is the surface Ig (sIg) of the B-cell receptor, which influences cell behaviour, even after neoplastic transformation.
  • During B-cell maturation, sIg accumulates somatic mutations in the Ig variable region (V) genes and tumours retain these patterns, thereby revealing the point of differentiation of the B cell of origin.
  • The importance of origin is strikingly illustrated in CLL where the two major subsets with distinctive clinical behaviour express either unmutated (U) or mutated (M) V genes.
  • Biased selection of VDJ genes also occurs in CLL, allowing further identification of the normal B-cell counterparts, with U-CLL apparently derived from circulating naïve B cells.
  • Surface IgM of CLL is functional, with evidence for ongoing interaction with antigen in vivo.
  • Signalling connects to cell survival, proliferation and migration, key determinants of tumour cell behaviour.
  • Probing of B-cell receptor-mediated signalling pathways, either constitutively activated or open for activation, reveals dynamic, possibly repetitive, stimulatory events, likely to occur in tissue sites.
  • Subtle differences in signal responsiveness between U-CLL or M-CLL subsets, together with microenvironmental factors, may explain clinical outcome.
  • Knowledge of the critical signalling pathways should reveal the steps vulnerable to inhibition and allow development of a new range of therapeutic drugs, targeted particularly against the more aggressive subset, U-CLL.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Receptors, Antigen, B-Cell / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20816790.001).
  • [ISSN] 1096-3650
  • [Journal-full-title] Seminars in cancer biology
  • [ISO-abbreviation] Semin. Cancer Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulins; 0 / Receptors, Antigen, B-Cell
  •  go-up   go-down


29. Liu CC, Huang CC, Lin WT, Hsieh CC, Huang SY, Lin SJ, Yang SC: Lycopene supplementation attenuated xanthine oxidase and myeloperoxidase activities in skeletal muscle tissues of rats after exhaustive exercise. Br J Nutr; 2005 Oct;94(4):595-601
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The purpose of the present study was to investigate the effects of lycopene, an antioxidant nutrient, at a relatively low dose (2.6 mg/kg per d) and a relatively high dose (7.8 mg/kg per d) on the antioxidant status of blood and skeletal muscle tissues in rats after exhaustive exercise.
  • Rats were divided into six groups: sedentary control (C); sedentary control with low-dose lycopene (CLL); sedentary control with high-dose lycopene (CHL); exhaustive exercise (E); exhaustive exercise with low-dose lycopene (ELL); exhaustive exercise with high-dose lycopene (EHL).
  • There was no significant difference in the GSH concentrations of erythrocytes in each group; however, exhaustive exercise resulted in a significant decrease in the GSH content of muscle.

  • MedlinePlus Health Information. consumer health - Antioxidants.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16197586.001).
  • [ISSN] 0007-1145
  • [Journal-full-title] The British journal of nutrition
  • [ISO-abbreviation] Br. J. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antioxidants; 268B43MJ25 / Uric Acid; 36-88-4 / Carotenoids; EC 1.11.1.7 / Peroxidase; EC 1.17.3.2 / Xanthine Oxidase; GAN16C9B8O / Glutathione; SB0N2N0WV6 / lycopene
  •  go-up   go-down


30. Desouki MM, Post GR, Cherry D, Lazarchick J: PAX-5: a valuable immunohistochemical marker in the differential diagnosis of lymphoid neoplasms. Clin Med Res; 2010 Jul;8(2):84-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PAX-5: a valuable immunohistochemical marker in the differential diagnosis of lymphoid neoplasms.
  • OBJECTIVE: Undifferentiated tumors and hematolymphoid neoplasms can be diagnostically challenging due to potential overlap of morphologic features and variant antigen expression.
  • PAX-5, a transcription factor expressed throughout B-cell maturation, is detected in most B-cell neoplasms including those that lack expression of mature B-cell markers, such as classical Hodgkin lymphoma (cHL), B-lymphoblastic leukemia and B-cell lymphomas following rituximab therapy.
  • The lack of PAX-5 expression in most CD30-positive non-hematopoietic malignancies (embryonal carcinoma and seminoma) and T-cell lymphomas, such as anaplastic large cell lymphoma (ALCL), suggests that the absence of PAX-5 may be used to confirm non-B-cell lineage.
  • DESIGN: Diagnostic lymph node, decalcified core bone marrow biopsies and tissue sections from 111 archived paraffin-embedded tissue blocks and a tissue lymphoma microarray were immunostained using a monoclonal antibody to PAX-5.
  • RESULTS: Nuclear PAX-5 immunoreactivity was detected in 88% (36/41) of Hodgkin lymphoma, all cases of diffuse large B-cell lymphoma (n=72), small B-cell lymphomas (n=5), B-lymphoblastic leukemia/lymphoma and mixed phenotype acute leukemia with B-cell lineage (n=5).
  • PAX-5 was not detected in ALCL (n=22), T-cell lymphoblastic leukemia/lymphoma, mixed phenotype acute leukemia with T-cell lineage (n=5), acute myeloid leukemia (n=4), carcinoid tumors with typical morphology (n=5), melanoma (n=3), and undifferentiated/metastatic tumors (n=8).
  • Non-neoplastic bone marrow sections showed scattered nuclear staining in small B-cell lymphocytes/hematogones.
  • CONCLUSION: Overall, our results demonstrate that including PAX-5 in a panel with other immunomarkers helps establish B-cell lineage and increases diagnostic yield.
  • [MeSH-major] B-Cell-Specific Activator Protein / analysis. Biomarkers, Tumor / analysis. Lymphoma / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Hodgkin Disease / diagnosis. Humans. Immunohistochemistry. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large-Cell, Anaplastic / diagnosis

  • MedlinePlus Health Information. consumer health - Lymphoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Haematol. 2001 Sep;114(4):881-3 [11564080.001]
  • [Cites] Immunity. 2001 Jun;14(6):779-90 [11420047.001]
  • [Cites] Leuk Lymphoma. 2002 Dec;43(12):2335-41 [12613521.001]
  • [Cites] Cancer Res. 2003 Aug 1;63(15):4620-5 [12907641.001]
  • [Cites] Am J Clin Pathol. 2003 Nov;120(5):767-77 [14608905.001]
  • [Cites] Carcinogenesis. 2004 Oct;25(10):1839-46 [15155532.001]
  • [Cites] Cancer Res. 2004 Oct 15;64(20):7399-404 [15492262.001]
  • [Cites] Genomics. 1991 Oct;11(2):424-34 [1685142.001]
  • [Cites] Blood. 1992 Jul 15;80(2):470-7 [1378322.001]
  • [Cites] Genes Dev. 1992 Sep;6(9):1589-607 [1516825.001]
  • [Cites] Blood. 1998 Aug 15;92(4):1308-16 [9694719.001]
  • [Cites] Clin Cancer Res. 1999 Mar;5(3):611-5 [10100713.001]
  • [Cites] Arch Pathol Lab Med. 2005 Jan;129(1):32-8 [15628906.001]
  • [Cites] Am J Surg Pathol. 2005 May;29(5):687-92 [15832095.001]
  • [Cites] Mod Pathol. 2005 Dec;18(12):1542-9 [16056244.001]
  • [Cites] Mod Pathol. 2006 Jul;19(7):1010-8 [16648862.001]
  • [Cites] Am J Clin Pathol. 2006 Aug;126(2):235-40 [16891199.001]
  • [Cites] Am J Clin Pathol. 2006 Oct;126(4):534-44 [16938666.001]
  • [Cites] Oncol Rep. 2006 Nov;16(5):1003-8 [17016584.001]
  • [Cites] Am J Clin Pathol. 2006 Nov;126(5):798-804 [17050077.001]
  • [Cites] Leuk Lymphoma. 2007 Jun;48(6):1127-38 [17577776.001]
  • [Cites] Mod Pathol. 2007 Aug;20(8):871-7 [17529924.001]
  • [Cites] Lab Invest. 2009 Mar;89(3):301-14 [19139719.001]
  • [Cites] Am J Surg Pathol. 2009 May;33(5):775-80 [19145202.001]
  • [Cites] J Clin Pathol. 2007 Jun;60(6):709-14 [16837628.001]
  • [Cites] Am J Surg Pathol. 2002 Oct;26(10):1343-50 [12360049.001]
  • (PMID = 20660931.001).
  • [ISSN] 1554-6179
  • [Journal-full-title] Clinical medicine & research
  • [ISO-abbreviation] Clin Med Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / PAX5 protein, human
  • [Other-IDs] NLM/ PMC2910102
  •  go-up   go-down


31. Maddocks-Christianson K, Slager SL, Zent CS, Reinalda M, Call TG, Habermann TM, Bowen DA, Hoyer JD, Schwager S, Jelinek DF, Kay NE, Shanafelt TD: Risk factors for development of a second lymphoid malignancy in patients with chronic lymphocytic leukaemia. Br J Haematol; 2007 Nov;139(3):398-404
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk factors for development of a second lymphoid malignancy in patients with chronic lymphocytic leukaemia.
  • Previous studies suggested that patients with chronic lymphocytic leukaemia (CLL) are at a three- to fivefold increased risk of developing a second lymphoproliferative disorder (LPD).
  • This observational cohort study used the Mayo Clinic CLL Database to identify factors associated with developing a second LPD.
  • A second LPD was identified in 26 (2.7%) of 962 CLL patients during a median follow-up of 3.3 years.
  • Diffuse large B-cell lymphoma was the most common subtype of secondary LPD (12 of 26 cases).
  • Patients previously treated for CLL had a trend toward higher prevalence of second LPD (4%) compared with previously untreated patients (2%; P = 0.053).
  • No statistically significant association was observed between risk of second LPD and other CLL characteristics (ZAP-70, CD38, IgV(H) mutation status or cytogenetic abnormalities).
  • In this series, prior treatments with PNA or anthracyclines were the only significant factors associated with risk of developing a second LPD in patients with CLL.
  • Physicians should strictly adhere to established criteria to initiate treatment for CLL patients who are not participating in clinical trials.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma / etiology. Neoplasms, Second Primary / etiology

  • MedlinePlus Health Information. consumer health - Lymphoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. VIDARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17910629.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 113408; United States / NCI NIH HHS / CA / CA 94919; United States / NCI NIH HHS / CA / CA 97274
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Purine Nucleotides; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  •  go-up   go-down


32. Bles N, Di Pietrantonio L, Boeynaems JM, Communi D: ATP confers tumorigenic properties to dendritic cells by inducing amphiregulin secretion. Blood; 2010 Oct 28;116(17):3219-26
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Supernatants of LPS+ATPγS-stimulated DCs induced smooth muscle cell and Lewis Lung Carcinoma (LLC) cell growth in vitro.
  • The coinjection of LPS+ATPγS-stimulated DCs or their supernatants with LLC cells increased tumor weight in mice compared with LPS-treated DCs.
  • The preincubation of LPS+ATPγS-treated DC supernatants with an anti-AREG blocking antibody inhibited their positive effect on smooth muscle cell density and tumor growth.
  • [MeSH-minor] Amphiregulin. Animals. Bone Marrow Cells / cytology. Cell Line, Tumor. Cell Proliferation. EGF Family of Proteins. Epidermal Growth Factor / genetics. Gene Expression Regulation, Neoplastic. Humans. Lipopolysaccharides / immunology. Male. Mice. Mice, Inbred C57BL. Monocytes / immunology. Myocytes, Smooth Muscle / cytology. Up-Regulation

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20651071.001).
  • [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 / AREG protein, human; 0 / Amphiregulin; 0 / Areg protein, mouse; 0 / EGF Family of Proteins; 0 / Glycoproteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Lipopolysaccharides; 35094-46-3 / adenosine 5'-O-(3-thiotriphosphate); 62229-50-9 / Epidermal Growth Factor; 8L70Q75FXE / Adenosine Triphosphate
  •  go-up   go-down


33. Ouillette P, Erba H, Kujawski L, Kaminski M, Shedden K, Malek SN: Integrated genomic profiling of chronic lymphocytic leukemia identifies subtypes of deletion 13q14. Cancer Res; 2008 Feb 15;68(4):1012-21
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Integrated genomic profiling of chronic lymphocytic leukemia identifies subtypes of deletion 13q14.
  • Chronic lymphocytic leukemia (CLL) is a biologically heterogeneous illness with a variable clinical course.
  • Loss of chromosomal material on chromosome 13 at cytoband 13q14 is the most frequent genetic abnormality in CLL, but the molecular aberrations underlying del13q14 in CLL remain incompletely characterized.
  • We analyzed 171 CLL cases for loss of heterozygosity and subchromosomal copy loss on chromosome 13 in DNA from fluorescence-activated cell sorting-sorted CD19(+) cells and paired buccal cells using the Affymetrix XbaI 50k SNP array platform.
  • The resulting high-resolution genomic maps, together with array-based measurements of expression levels of RNA in CLL cases with and without del13q14 and quantitative PCR-based expression analysis of selected genes, support the following conclusions: (a) del13q14 is heterogeneous and composed of multiple subtypes, with deletion of Rb or the miR15a/miR16 loci serving as anatomic landmarks, respectively;.
  • (b) del13q14 type Ia deletions are relatively uniform in length and extend from breakpoints close to the miR15a/miR16 cluster to a newly identified telomeric breakpoint cluster at the approximately 50.2 to 50.5 Mb physical position;.
  • (c) LATS2 RNA levels are approximately 2.6-fold to 2.8-fold lower in cases with del13q14 type I that do not delete Rb, as opposed to del13q14 type II or all other CLL cases;.
  • (d) PHLPP RNA is absent in approximately 50% of CLL cases with del13q14; and (e) approximately 15% of CLL cases display marked reductions in miR15a/miR16 expression that are often but not invariably associated with bi-allelic miR15a/miR16 loss.
  • These data should aid future investigations into biological differences imparted on CLL by different del13q14 subtypes.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 13. Leukemia, Lymphocytic, Chronic, B-Cell / genetics

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18281475.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R21 CA124420-01A1; United States / NCI NIH HHS / CA / 5 P30 CA46592
  • [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 / Nuclear Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins; EC 2.7.1.11 / LATS2 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.1.3.16 / PHLPP1 protein, human; EC 3.1.3.16 / Phosphoprotein Phosphatases
  •  go-up   go-down


34. Hewamana S, Alghazal S, Lin TT, Clement M, Jenkins C, Guzman ML, Jordan CT, Neelakantan S, Crooks PA, Burnett AK, Pratt G, Fegan C, Rowntree C, Brennan P, Pepper C: The NF-kappaB subunit Rel A is associated with in vitro survival and clinical disease progression in chronic lymphocytic leukemia and represents a promising therapeutic target. Blood; 2008 May 1;111(9):4681-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The NF-kappaB subunit Rel A is associated with in vitro survival and clinical disease progression in chronic lymphocytic leukemia and represents a promising therapeutic target.
  • In this study, we characterized nuclear factor kappaB (NF-kappaB) subunit DNA binding in chronic lymphocytic leukemia (CLL) samples and demonstrated heterogeneity in basal and inducible NF-kappaB.
  • Subunit analysis revealed DNA binding of p50, Rel A, and c-Rel in primary CLL cells, and Rel A DNA binding was associated with in vitro survival (P = .01) with high white cell count (P = .01) and shorter lymphocyte doubling time (P = .01).
  • NF-kappaB induction after in vitro stimulation with anti-IgM was associated with increased in vitro survival (P < .001) and expression of the signaling molecule ZAP-70 (P = .003).
  • Prompted by these data, we evaluated the novel parthenolide analog, LC-1, in 54 CLL patient samples.
  • LC-1 induced apoptosis in all the samples tested with a mean LD(50) of 2.8 microM after 24 hours; normal B and T cells were significantly more resistant to its apoptotic effects (P < .001).
  • Furthermore, Rel A DNA binding was inversely correlated with sensitivity to fludarabine (P = .001, r(2) = 0.3), implicating Rel A in fludarabine resistance.
  • Taken together, these data indicate that Rel A represents an excellent therapeutic target for this incurable disease.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Transcription Factor RelA / metabolism
  • [MeSH-minor] Apoptosis. DNA / metabolism. Disease Progression. Humans. Protein Binding. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Blood. 2008 May 1;111(9):4427 [18441243.001]
  • (PMID = 18227347.001).
  • [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 / Transcription Factor RelA; 9007-49-2 / DNA
  •  go-up   go-down


35. Grönroos M, Chen M, Jahnukainen T, Capitanio A, Aizman RI, Celsi G: Methotrexate induces cell swelling and necrosis in renal tubular cells. Pediatr Blood Cancer; 2006 May 1;46(5):624-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Methotrexate induces cell swelling and necrosis in renal tubular cells.
  • BACKGROUND: The present study was carried out to investigate if methotrexate (MTX) has a direct lethal effect in renal tubular cells, and if so, to further clarify the mechanisms of cell death.
  • MATERIALS AND METHODS: Renal tubular cells (LLC-PK(1) cells) were incubated with MTX (0.01 microM, 0.1 microM, and 1 microM), either alone or in combination with 0.1 microM amiloride (Na(+)/H(+) antiporter inhibitor) or 1 microM carbachol (M-cholinergic agonist).
  • Cell viability was then determined by means of trypan blue (TB) exclusion tests and MTT assays.
  • Cell death induced by MTX was time-dependent and did not show apoptotic features.
  • On the contrary, cell swelling was discovered.
  • This cell death was prevented by co-incubating the cells with amiloride or carbachol.
  • CONCLUSIONS: MTX induces cell swelling and cell death in renal tubular LLC-PK(1) cells.
  • The tubular cell death induced by MTX is time-dependent.
  • Cell death can be prevented by co-incubating with amiloride, thus indicating that the Na(+)/H(+) antiporter and possibly other volume regulatory factors in renal tubular cells are involved in MTX-induced renal failure.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Cell Size / drug effects. Cell Survival / drug effects. Kidney Tubules, Proximal / drug effects. Methotrexate / pharmacology
  • [MeSH-minor] Amiloride / pharmacology. Animals. LLC-PK1 Cells / cytology. LLC-PK1 Cells / drug effects. Necrosis. Sodium Channel Blockers / pharmacology. Swine

  • Hazardous Substances Data Bank. METHOTREXATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Pediatr Blood Cancer. 2007 Aug;49(2):216;author reply 219 [16786587.001]
  • (PMID = 16025437.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Sodium Channel Blockers; 7DZO8EB0Z3 / Amiloride; YL5FZ2Y5U1 / Methotrexate
  •  go-up   go-down


36. Bulian P, Del Poeta G, Gattei V: How would I manage a sample submitted for flow cytometry analysis for suspicious chronic lymphocytic leukaemia. Hematol Oncol; 2009 Dec;27(4):186-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] How would I manage a sample submitted for flow cytometry analysis for suspicious chronic lymphocytic leukaemia.
  • Samples submitted for a suspect of chronic lymphocytic leukemia are the most frequently observed in flow cytometry laboratories.
  • These cases require not only a precise and prompt diagnosis but also an evaluation on the possibility of performing additional prognostic tests.
  • [MeSH-major] Flow Cytometry / methods. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2009 John Wiley & Sons, Ltd.
  • (PMID = 19569256.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 23
  •  go-up   go-down


37. Moraga FA, Pedreros CP, Rodríguez CE: Acute mountain sickness in children and their parents after rapid ascent to 3500 m (Putre, Chile). Wilderness Environ Med; 2008;19(4):287-92
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Acute mountain sickness symptoms were evaluated using the Children's Lake Louise Score (CLLS) in children and the Lake Louise Scoring System in their parents.
  • RESULTS: The mean CLLS was 10.8 +/- 3 at Putre, with 92% of children developing AMS.
  • Low oxygen saturation (80% +/- 2%) and tachycardia (129 +/- 9 beats/min) were observed in children with higher AMS scores.

  • Genetic Alliance. consumer health - Acute Mountain Sickness.
  • MedlinePlus Health Information. consumer health - Traveler's Health.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19099320.001).
  • [ISSN] 1080-6032
  • [Journal-full-title] Wilderness & environmental medicine
  • [ISO-abbreviation] Wilderness Environ Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


38. Alamdari HS, Pinter-Brown L, Cassarino DS, Chiu MW: Severe cutaneous interface drug eruption associated with bendamustine. Dermatol Online J; 2010;16(7):1
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Bendamustine is an anti-neoplastic agent approved by the FDA in 2008 for use as monotherapy or in combination with other agents to treat chronic lymphocytic leukemia (CLL) and progressed indolent B-cell non-Hodgkin lymphoma (NHL).
  • [MeSH-major] Antineoplastic Agents / adverse effects. Drug Eruptions / pathology. Lymphoma, B-Cell / drug therapy. Nitrogen Mustard Compounds / adverse effects

  • Hazardous Substances Data Bank. Bendamustine .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20673529.001).
  • [ISSN] 1087-2108
  • [Journal-full-title] Dermatology online journal
  • [ISO-abbreviation] Dermatol. Online J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Nitrogen Mustard Compounds; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; 981Y8SX18M / Bendamustine Hydrochloride; VB0R961HZT / Prednisone; COP protocol 2
  •  go-up   go-down


39. Haferlach T, Kohlmann A, Schnittger S, Dugas M, Hiddemann W, Kern W, Schoch C: Global approach to the diagnosis of leukemia using gene expression profiling. Blood; 2005 Aug 15;106(4):1189-98
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Global approach to the diagnosis of leukemia using gene expression profiling.
  • Accurate diagnosis and classification of leukemias are the bases for the appropriate management of patients.
  • We analyzed gene expression profiles in 937 bone marrow and peripheral blood samples from 892 patients with all clinically relevant leukemia subtypes and from 45 nonleukemic controls by U133A and U133B GeneChip arrays.
  • Prediction accuracy was estimated by 10-fold cross-validation and was assessed for robustness in a 100-fold resampling approach using randomly chosen test sets consisting of one third of the samples.
  • In particular, acute myeloid leukemia (AML) with t(15;17), AML with t(8;21), AML with inv(16), chronic lymphatic leukemia (CLL), and pro-B-cell acute lymphoblastic leukemia (pro-B-ALL) with t(11q23) were classified with 100% sensitivity and 100% specificity.
  • Gene expression profiling can predict all clinically relevant subentities of leukemia with high accuracy.
  • [MeSH-major] Gene Expression Profiling. Leukemia / diagnosis. Molecular Diagnostic Techniques / standards

  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15878973.001).
  • [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
  •  go-up   go-down


40. Zhang W, Liu JN, Tan XY: Vaccination with xenogeneic tumor endothelial proteins isolated in situ inhibits tumor angiogenesis and spontaneous metastasis. Int J Cancer; 2009 Jul 1;125(1):124-32
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The administration of these tumor EP as a vaccine to mice reduced the microvessel density in subcutaneous primary LLC tumors, delayed spontaneous LLC tumor metastasis and prolonged post-surgery life span.
  • T lymphocytes from tumor EP-vaccinated mice lysed human umbilical vascular endothelial cells, but not tumor cells in vitro, in a dose-dependent manner.
  • Furthermore, adoptive transfer of antitumor EP antibodies in vivo targeted to tumor endothelium and inhibited spontaneous LLC tumor metastasis.
  • [MeSH-minor] Adoptive Transfer. Angiogenesis Inhibitors / therapeutic use. Animals. Biotinylation. Cell Movement. Electrophoresis, Gel, Two-Dimensional. Female. Flow Cytometry. Immunoblotting. Immunoenzyme Techniques. Immunoglobulin G / administration & dosage. Mice. Mice, Inbred C57BL. Rabbits. Rats. Rats, Inbred F344. Vaccination

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19350628.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Immunoglobulin G; 0 / Neoplasm Proteins
  •  go-up   go-down


41. Sampath D, Plunkett W: The role of DNA repair in chronic lymphocytic leukemia pathogenesis and chemotherapy resistance. Curr Oncol Rep; 2007 Sep;9(5):361-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of DNA repair in chronic lymphocytic leukemia pathogenesis and chemotherapy resistance.
  • Front-line therapy for chronic lymphocytic leukemia (CLL) with alkylating agents is associated with low rates of complete remission and no improvement in overall survival.
  • The ability of CLL cells to efficiently repair alkylator-induced damage to DNA might explain this lack of response.
  • Novel strategies that inhibit DNA repair, such as combinations of alkylating agents, purine nucleoside analogues, and immunotherapy, have produced durable clinical and molecular remission in both untreated and relapsed CLL.
  • This review evaluates the contribution of DNA repair processes in the development of resistance to chemotherapy and the impact of therapies that exploit the DNA repair capacity of CLL cells to therapeutic advantage.
  • [MeSH-major] Alkylating Agents / therapeutic use. Antineoplastic Agents / pharmacology. DNA Repair / drug effects. DNA, Neoplasm / genetics. Drug Resistance, Neoplasm / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] N Engl J Med. 1998 May 21;338(21):1506-14 [9593789.001]
  • [Cites] Br J Cancer. 1999 Mar;79(7-8):1215-9 [10098762.001]
  • [Cites] Bioessays. 1994 Sep;16(9):651-5 [7980491.001]
  • [Cites] Blood. 2006 Dec 15;108(13):4187-93 [16954499.001]
  • [Cites] Mol Cell Biol. 1995 Apr;15(4):2173-9 [7891712.001]
  • [Cites] J Clin Oncol. 2007 Mar 20;25(9):1114-20 [17296974.001]
  • [Cites] Leukemia. 2004 Mar;18(3):409-14 [14712290.001]
  • [Cites] Blood. 1982 Nov;60(5):1110-21 [6751436.001]
  • [Cites] Pathol Biol (Paris). 2006 May;54(4):185-93 [16563661.001]
  • [Cites] J Mol Histol. 2006 Sep;37(5-7):261-9 [17120107.001]
  • [Cites] Biochem Pharmacol. 2003 Jul 15;66(2):225-37 [12826265.001]
  • [Cites] Br J Haematol. 2003 Jun;121(5):692-702 [12780783.001]
  • [Cites] Leuk Lymphoma. 2004 Jan;45(1):79-84 [15061201.001]
  • [Cites] Leuk Lymphoma. 1999 Dec;36(1-2):57-65 [10613450.001]
  • [Cites] Cancer Lett. 1995 Apr 14;90(2):139-48 [7736449.001]
  • [Cites] J Pharmacol Exp Ther. 2007 Jun;321(3):848-55 [17351105.001]
  • [Cites] Cancer. 2006 Jan 15;106(2):337-45 [16353201.001]
  • [Cites] EMBO J. 2006 Nov 29;25(23):5539-48 [17093500.001]
  • [Cites] N Engl J Med. 2000 Dec 14;343(24):1750-7 [11114313.001]
  • [Cites] Blood. 2005 Jun 15;105(12 ):4776-83 [15718417.001]
  • [Cites] EMBO J. 2000 Feb 1;19(3):463-71 [10654944.001]
  • [Cites] Clin Cancer Res. 2001 Nov;7(11):3580-9 [11705880.001]
  • [Cites] J Natl Cancer Inst. 1996 Oct 2;88(19):1346-60 [8827012.001]
  • [Cites] Blood. 2007 Jan 15;109(2):405-11 [17008537.001]
  • [Cites] Curr Treat Options Oncol. 2006 May;7(3):200-12 [16615876.001]
  • [Cites] Clin Cancer Res. 2003 Aug 1;9(8):3204-12 [12912974.001]
  • [Cites] Haematologica. 2005 Oct;90(10):1357-64 [16219572.001]
  • [Cites] Am J Clin Oncol. 1986 Aug;9(4):277-80 [3751964.001]
  • [Cites] Cancer. 2006 Jun 1;106(11):2412-20 [16649223.001]
  • [Cites] Trends Biochem Sci. 1993 Nov;18(11):433-7 [8291090.001]
  • [Cites] Leukemia. 2002 Jan;16(1):36-43 [11840261.001]
  • [Cites] J Clin Oncol. 2003 Apr 1;21(7):1278-84 [12663715.001]
  • [Cites] Leuk Lymphoma. 2002 Apr;43(4):767-72 [12153163.001]
  • [Cites] Cancer Res. 1985 Apr;45(4):1737-43 [3919945.001]
  • [Cites] Nat Cell Biol. 2007 Jun;9(6):683-90 [17486112.001]
  • [Cites] Nat Struct Mol Biol. 2006 Aug;13(8):729-33 [16845393.001]
  • [Cites] Curr Opin Genet Dev. 1997 Feb;7(1):99-104 [9024627.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4070-8 [15767647.001]
  • [Cites] Clin Cancer Res. 1996 Oct;2(10):1731-41 [9816124.001]
  • [Cites] Mol Pharmacol. 1996 May;49(5):766-71 [8622624.001]
  • [Cites] J Clin Oncol. 2007 Mar 1;25(7):793-8 [17283364.001]
  • [Cites] Blood. 2006 Feb 1;107(3):885-91 [16219797.001]
  • [Cites] DNA Repair (Amst). 2006 May 10;5(5):534-43 [16531125.001]
  • [Cites] Br J Haematol. 2001 Aug;114(2):342-8 [11529853.001]
  • [Cites] Mol Cell Biol. 2000 Nov;20(21):7980-90 [11027268.001]
  • [Cites] Mol Cell Biol. 2003 Aug;23(16):5706-15 [12897142.001]
  • [Cites] Clin Cancer Res. 1999 Aug;5(8):2178-84 [10473103.001]
  • [Cites] J Clin Oncol. 2001 Mar 1;19(5):1414-20 [11230486.001]
  • [Cites] J Biol Chem. 1993 Apr 5;268(10):7179-85 [7681821.001]
  • [Cites] Semin Oncol. 2006 Apr;33(2):250-6 [16616072.001]
  • [Cites] Cancer Detect Prev. 2004;28(6):433-42 [15582267.001]
  • [Cites] Cancer Chemother Pharmacol. 1995;36(3):181-8 [7781136.001]
  • [Cites] Biochimie. 2003 Nov;85(11):1161-73 [14726021.001]
  • [Cites] Biochem Pharmacol. 2002 May 1;63(9):1585-8 [12007561.001]
  • [Cites] Mol Pharmacol. 2000 Nov;58(5):920-7 [11040038.001]
  • [Cites] Biochemistry. 1996 Aug 6;35(31):10004-13 [8756462.001]
  • [Cites] Semin Oncol. 1998 Apr;25(2 Suppl 5):4-12 [9609103.001]
  • [Cites] Leuk Lymphoma. 2004 Jun;45(6):1159-65 [15359995.001]
  • [Cites] Curr Hematol Rep. 2005 Jan;4(1):31-8 [15610657.001]
  • [Cites] Blood. 2005 Nov 1;106(9):3175-82 [16014569.001]
  • [Cites] EMBO J. 2006 Oct 18;25(20):4921-32 [17036055.001]
  • [Cites] Cancer. 2003 Jan 1;97(1):114-20 [12491512.001]
  • [Cites] Anticancer Drugs. 1997 Oct;8(9):876-85 [9402315.001]
  • [Cites] J Pharmacol Exp Ther. 2005 Aug;314(2):495-505 [15843498.001]
  • [Cites] Blood. 2006 Jul 15;108(2):473-9 [16551966.001]
  • (PMID = 17706164.001).
  • [ISSN] 1523-3790
  • [Journal-full-title] Current oncology reports
  • [ISO-abbreviation] Curr Oncol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Antineoplastic Agents; 0 / DNA, Neoplasm
  • [Number-of-references] 65
  •  go-up   go-down


42. Levin M, Libster D: Allergic reaction to chlorambucil in chronic lymphocytic leukemia presenting with fever and lymphadenopathy. Leuk Lymphoma; 2005 Aug;46(8):1195-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allergic reaction to chlorambucil in chronic lymphocytic leukemia presenting with fever and lymphadenopathy.
  • Chronic lymphocytic leukemia (CLL) is commonly treated with the alkylating agent chlorambucil.
  • Neither of the patients were treated for infection or disease progression.
  • This type of reaction to chlorambucil has not been described previously.
  • These reactions could be confused with the onset of infection, progression of disease or even a Richter's transformation.
  • [MeSH-major] Chlorambucil / adverse effects. Drug Hypersensitivity / diagnosis. Fever / etiology. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Lymphatic Diseases / etiology
  • [MeSH-minor] Aged. Disease Progression. Female. Humans. Male. Middle Aged


43. Sellick GS, Webb EL, Allinson R, Matutes E, Dyer MJ, Jonsson V, Langerak AW, Mauro FR, Fuller S, Wiley J, Lyttelton M, Callea V, Yuille M, Catovsky D, Houlston RS: A high-density SNP genomewide linkage scan for chronic lymphocytic leukemia-susceptibility loci. Am J Hum Genet; 2005 Sep;77(3):420-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A high-density SNP genomewide linkage scan for chronic lymphocytic leukemia-susceptibility loci.
  • Chronic lymphocytic leukemia (CLL) and other B-cell lymphoproliferative disorders (LPDs) show clear evidence of familial aggregation, but the inherited basis is largely unknown.
  • To identify a susceptibility gene for CLL, we conducted a genomewide linkage analysis of 115 pedigrees, using a high-density single-nucleotide polymorphism (SNP) array containing 11,560 markers.
  • In addition, four other chromosomal positions (5q22-23, 6p22, 10q25, and 14q32) displayed HLOD scores >1.15 (which corresponds to a nominal P value <.01).
  • None of the regions coincided with areas of common chromosomal abnormalities frequently observed for CLL.
  • These findings strengthen the argument for an inherited predisposition to CLL and related B-cell LPDs.
  • [MeSH-major] Genetic Linkage. Genetic Predisposition to Disease / genetics. Genome, Human / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Genet. 2000 May;25(1):12-3 [10802644.001]
  • [Cites] Bioinformatics. 2005 Jul 1;21(13):3060-1 [15840706.001]
  • [Cites] Folia Med (Plovdiv). 2000;42(3):5-10 [11347338.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):97-101 [11731797.001]
  • [Cites] Blood. 2002 Jul 15;100(2):603-9 [12091354.001]
  • [Cites] Blood. 2002 Jul 15;100(2):635-9 [12091358.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2289-90 [12239136.001]
  • [Cites] Br J Haematol. 2003 Jun;121(6):866-73 [12786797.001]
  • [Cites] Leuk Res. 2003 Oct;27(10):871-6 [12860003.001]
  • [Cites] Genome Res. 2004 Mar;14(3):414-25 [14993208.001]
  • [Cites] Am J Hum Genet. 2004 Jul;75(1):54-64 [15154113.001]
  • [Cites] Am J Hum Genet. 2004 Oct;75(4):687-92 [15311375.001]
  • [Cites] Blood. 2004 Sep 15;104(6):1850-4 [15161669.001]
  • [Cites] Am J Hum Genet. 2004 Dec;75(6):1106-12 [15492927.001]
  • [Cites] Am J Hum Genet. 2004 Dec;75(6):948-65 [15514889.001]
  • [Cites] Scand J Haematol. 1973;11(2):97-105 [4272677.001]
  • [Cites] Scand J Haematol. 1975 Sep;15(2):117-31 [1188315.001]
  • [Cites] N Engl J Med. 1987 May 21;316(21):1289-94 [3574400.001]
  • [Cites] Br J Cancer. 1987 Jul;56(1):79-82 [3304389.001]
  • [Cites] Genetics. 1987 Oct;117(2):331-41 [3666445.001]
  • [Cites] Am J Epidemiol. 1989 Oct;130(4):655-64 [2773914.001]
  • [Cites] Leuk Res. 1991;15(5):305-14 [2046383.001]
  • [Cites] Genet Epidemiol. 1993;10(1):75-83 [8472936.001]
  • [Cites] Am J Hum Genet. 1994 Mar;54(3):497-505 [8116619.001]
  • [Cites] Biometrics. 1994 Mar;50(1):118-27 [8086596.001]
  • [Cites] Eur J Epidemiol. 1994 Apr;10(2):211-3 [7813700.001]
  • [Cites] Nat Genet. 1995 Nov;11(3):241-7 [7581446.001]
  • [Cites] Genomics. 1995 Sep 20;29(2):311-22 [8666377.001]
  • [Cites] Am J Hum Genet. 1996 Jun;58(6):1347-63 [8651312.001]
  • [Cites] Lancet. 1999 Jan 2;353(9146):26-9 [10023947.001]
  • [Cites] Leukemia. 1999 Oct;13(10):1497-500 [10516748.001]
  • [Cites] Nucleic Acids Res. 2004;32(20):e164 [15561999.001]
  • [Cites] Hematology. 2004 Oct-Dec;9(5-6):383-5 [15763978.001]
  • [Cites] Int J Cancer. 2001 Apr 15;92(2):203-7 [11291046.001]
  • (PMID = 16080117.001).
  • [ISSN] 0002-9297
  • [Journal-full-title] American journal of human genetics
  • [ISO-abbreviation] Am. J. Hum. Genet.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1226207
  •  go-up   go-down


44. Amexis G, Young NS: Multiple antigenic peptides as vaccine platform for the induction of humoral responses against dengue-2 virus. Viral Immunol; 2007 Dec;20(4):657-63
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Dengue is an important agent of human disease for which no licensed vaccine is available to the public.
  • Commercially available software (MacVector 7.0) was used to identify potential antigenic B-cell epitopes of E-glycoprotein.
  • Anti-DEN-2 ELISA showed high levels of anti-DEN-2 antibodies and post-immune sera reduced viral infectivity and prevented infection of monkey kidney cells (LLC-MK2) with live DEN-2 virus.

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18158738.001).
  • [ISSN] 0882-8245
  • [Journal-full-title] Viral immunology
  • [ISO-abbreviation] Viral Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Viral; 0 / Antigens, Viral; 0 / Dengue Vaccines; 0 / Glycoproteins; 0 / Vaccines, Subunit; 0 / Vaccines, Synthetic
  •  go-up   go-down


45. Fujii T, Ohira Y, Itomi Y, Takahashi Y, Asano S, Morii M, Takeguchi N, Sakai H: Inhibition of P-type ATPases by [(dihydroindenyl)oxy]acetic acid (DIOA), a K+ -Cl- cotransporter inhibitor. Eur J Pharmacol; 2007 Apr 10;560(2-3):123-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of P-type ATPases by [(dihydroindenyl)oxy]acetic acid (DIOA), a K+ -Cl- cotransporter inhibitor.
  • [(Dihydroindenyl)oxy]acetic acid (DIOA) has been used as a potent inhibitor of K+ -Cl- cotransporter (IC(50)=10 microM).
  • Here we found that DIOA inhibited activities of P-type ATPases such as dog kidney Na+,K+-ATPase (IC(50)=53 microM), hog gastric H+,K+-ATPase (IC(50)=97 microM) and rabbit muscle Ca(2+)-ATPase (IC(50)=127 microM).
  • In the membrane preparation of the LLC-PK1 cells stably expressing rabbit gastric H+,K+-ATPase, DIOA inhibited activities of the endogenous Na+,K+-ATPase (IC(50)=95 microM) and the exogenous H+,K+-ATPase (IC(50)=75 microM).
  • 5-Nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), a Cl- channel blocker, had no effects on the DIOA-elicited inhibition of the P-type ATPases.
  • These findings suggest that lower concentration of DIOA (< 20-30 microM) should be used for evaluation of the activity of K+ -Cl- cotransporter without affecting the activities of coexisting Na+,K+ -ATPase and/or H+,K+-ATPase in cells.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17303113.001).
  • [ISSN] 0014-2999
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Acetates; 0 / Enzyme Inhibitors; 0 / Indenes; 0 / Proton Pump Inhibitors; 0 / Symporters; 0 / potassium-chloride symporters; 106105-17-3 / ((2-n-butyl-6,7-dichloro-2-cyclopentyl-2,3-dihydro-1-oxo-1H-inden-5-yl)oxy)acetic acid; EC 3.6.3.9 / Sodium-Potassium-Exchanging ATPase
  •  go-up   go-down


46. Billaud G, Morfin F, Vabret A, Boucher A, Gillet Y, Crassard N, Galambrun C, Ferraris O, Legrand L, Aymard M, Lina B, Freymuth F, Thouvenot D: Human parainfluenza virus type 4 infections: a report of 20 cases from 1998 to 2002. J Clin Virol; 2005 Sep;34(1):48-51
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human parainfluenza virus type 4 infections: a report of 20 cases from 1998 to 2002.
  • BACKGROUND: Human Parainfluenza Viruses (HPIV) type 4 are responsible for respiratory infections.
  • STUDY DESIGN: From 1998 to 2002, in 20 respiratory samples of hospitalised patient, we isolated viruses presenting a large syncytial cytopathic effect when inoculated on LLC-MK2 cells.
  • [MeSH-minor] Adult. Base Sequence. Cell Line. Child. DNA Primers. Humans. Nasopharynx / virology. Pharynx / virology. Respiratory System / virology. Reverse Transcriptase Polymerase Chain Reaction. Specimen Handling / methods

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16087124.001).
  • [ISSN] 1386-6532
  • [Journal-full-title] Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology
  • [ISO-abbreviation] J. Clin. Virol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA Primers
  •  go-up   go-down


47. Kalnina I, Zvagule T, Gabruseva N, Kirilova J, Kurjane N, Bruvere R, Kesters A, Kizane G, Kirilovs G, Meirovics I: Structural changes in lymphocytes membrane of Chernobyl clean-up workers from Latvia. J Fluoresc; 2007 Nov;17(6):633-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Structural changes in lymphocytes membrane of Chernobyl clean-up workers from Latvia.
  • It is necessary to note that all investigated parameters significantly differ in observed groups of patients.
  • These findings reinforce our understanding that that the cell membrane is a significant biological target of radiation.
  • The role of the membrane in the expression and course of cell damage after radiation exposure must be considered.
  • So ten years dynamic of PBMC membrane characteristics by ABM (spectral shift and anisotropy indexes) in Chernobyl clean-up workers reveal progressive trend toward certain resemblance with those of chronic B-cell lymphoid leukemia.
  • [MeSH-major] Chernobyl Nuclear Accident. Lymphocytes / chemistry. Lymphocytes / radiation effects. Occupational Diseases / blood. Radiation Injuries / blood
  • [MeSH-minor] Benz(a)Anthracenes. Case-Control Studies. Cell Membrane / chemistry. Cell Membrane / radiation effects. Fluorescence Polarization. Fluorescent Dyes. Follow-Up Studies. Humans. Latvia. Male. Membrane Fluidity / radiation effects. Occupational Exposure. Serum Albumin / metabolism

  • MedlinePlus Health Information. consumer health - Occupational Health.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Radiat Biol. 1991 Jan;59(1):59-69 [1671076.001]
  • [Cites] Radiat Environ Biophys. 1996 Nov;35(4):289-95 [9008006.001]
  • [Cites] Radiat Res. 1991 Apr;126(1):27-35 [2020736.001]
  • [Cites] Radiat Res. 2003 Apr;159(4):471-83 [12643792.001]
  • [Cites] Proc Natl Acad Sci U S A. 1970 Oct;67(2):579-89 [5289011.001]
  • [Cites] Radiat Res. 1978 Jul;75(1):31-45 [684166.001]
  • (PMID = 17924176.001).
  • [ISSN] 1053-0509
  • [Journal-full-title] Journal of fluorescence
  • [ISO-abbreviation] J Fluoresc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Benz(a)Anthracenes; 0 / Fluorescent Dyes; 0 / Serum Albumin
  •  go-up   go-down


48. Bäckman E, Bergh AC, Lagerdahl I, Rydberg B, Sundström C, Tobin G, Rosenquist R, Linderholm M, Rosén A: Thioredoxin, produced by stromal cells retrieved from the lymph node microenvironment, rescues chronic lymphocytic leukemia cells from apoptosis in vitro. Haematologica; 2007 Nov;92(11):1495-504
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Thioredoxin, produced by stromal cells retrieved from the lymph node microenvironment, rescues chronic lymphocytic leukemia cells from apoptosis in vitro.
  • We have previously shown that extracellular thioredoxin protects B-cell chronic lymphocytic leukemia (CLL) cells from apoptosis in vitro.
  • In this study we were interested to determine whether thioredoxin is produced by cells surrounding the CLL cells in the in vivo microenvironment and whether this cell-derived thioredoxin has any leukemia growth-promoting effect in vitro.
  • DESIGN AND METHODS: Lymph nodes from CLL patients (n=25) were analyzed for thioredoxin expression by immunohistology.
  • Stromal cells purified from the lymph nodes were analyzed for thioredoxin secretion at the single cell level using an ELIspot assay.
  • The survival effect of the stromal-derived thioredoxin was tested by co-culturing stromal- and CLL cells with and without Fab-fragments of an anti-thioredoxin antibody.
  • RESULTS: The results indicated that the thioredoxin production correlated with the amount of proliferating cells and was mainly localized to the proliferation centers (pseudofollicles) in the CLL lymph nodes.
  • The leukemia cells per se showed minimal thioredoxin levels; in contrast, stromal cells strongly expressed thioredoxin.
  • Purified primary stromal cells, which secreted extracellular thioredoxin, significantly protected the CLL cells from undergoing apoptosis in 72 h co-cultures.
  • INTERPRETATION AND CONCLUSIONS: In conclusion, we have shown that stromal cells in the lymph node microenvironment produce thioredoxin and that the thioredoxin production is localized to the proliferation centers of the CLL lymph nodes.
  • In addition, thioredoxin produced by purified stromal cells rescued CLL cells from apoptosis in vitro.
  • [MeSH-major] Apoptosis. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Lymph Nodes / pathology. Stromal Cells / chemistry. Thioredoxins / analysis

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18024398.001).
  • [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] 52500-60-4 / Thioredoxins
  •  go-up   go-down


49. Shinohara ET, Geng L, Tan J, Chen H, Shir Y, Edwards E, Halbrook J, Kesicki EA, Kashishian A, Hallahan DE: DNA-dependent protein kinase is a molecular target for the development of noncytotoxic radiation-sensitizing drugs. Cancer Res; 2005 Jun 15;65(12):4987-92
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • DNA-dependent protein kinase (DNA-PK)-defective severe combined immunodeficient (SCID) mice have a greater sensitivity to ionizing radiation compared with wild-type mice due to deficient repair of DNA double-strand break.
  • IC87361 enhanced radiation sensitivity in wild-type C57BL6 endothelial cells but not in SCID cells.
  • The tumor vascular window model was used to assess IC87361-induced radiosensitization of SCID and wild-type tumor microvasculature.
  • Vascular density was 5% in irradiated SCID host compared with 50% in C57BL6 mice (P < 0.05).
  • IC87361 induced radiosensitization of tumor microvasculature in wild-type mice that resembled the radiosensitive phenotype of tumor vessels in SCID mice.
  • Irradiated LLC and B16F0 tumors implanted into SCID mice showed greater tumor growth delay compared with tumors implanted into either wild-type C57BL6 or nude mice.
  • Furthermore, LLC tumors treated with radiation and IC87361 showed tumor growth delay that was significantly greater than tumors treated with radiation alone (P < 0.01 for 3 Gy alone versus 3 Gy + IC87361).
  • [MeSH-minor] Animals. Carcinoma, Lewis Lung / blood supply. Carcinoma, Lewis Lung / drug therapy. Carcinoma, Lewis Lung / enzymology. Carcinoma, Lewis Lung / radiotherapy. Cell Growth Processes / drug effects. Cell Growth Processes / radiation effects. Cell Line, Tumor. Combined Modality Therapy. DNA-Activated Protein Kinase. Endothelial Cells / cytology. Endothelial Cells / drug effects. Endothelial Cells / radiation effects. Melanoma, Experimental / blood supply. Melanoma, Experimental / drug therapy. Melanoma, Experimental / enzymology. Melanoma, Experimental / radiotherapy. Mice. Mice, Nude. Mice, SCID. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / enzymology. Neovascularization, Pathologic / pathology. Neovascularization, Pathologic / radiotherapy

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15958537.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30-CA68485; United States / NCI NIH HHS / CA / P50-CA90949; United States / NCI NIH HHS / CA / R01-CA112385; United States / NCI NIH HHS / CA / R01-CA58508; United States / NCI NIH HHS / CA / R01-CA70937; United States / NCI NIH HHS / CA / R01-CA88076; United States / NCI NIH HHS / CA / R01-CA89888; United States / NCI NIH HHS / CA / R21-CA89674; United States / NCI NIH HHS / CA / T-32CA93240
  • [Publication-type] 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 / DNA-Binding Proteins; 0 / Protein Kinase Inhibitors; 0 / Radiation-Sensitizing Agents; EC 2.7.11.1 / DNA-Activated Protein Kinase; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  •  go-up   go-down


50. Salerno E, Scaglione BJ, Coffman FD, Brown BD, Baccarini A, Fernandes H, Marti G, Raveche ES: Correcting miR-15a/16 genetic defect in New Zealand Black mouse model of CLL enhances drug sensitivity. Mol Cancer Ther; 2009 Sep;8(9):2684-92
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Correcting miR-15a/16 genetic defect in New Zealand Black mouse model of CLL enhances drug sensitivity.
  • Alterations in the human 13q14 genomic region containing microRNAs mir-15a and mir-16-1 are present in most human chronic lymphocytic leukemia (CLL).
  • We have previously found the development of CLL in the New Zealand Black murine model to be associated with a point mutation in the primary mir-15a/16-1 region, which correlated with a decrease in mature miR-16 and miR-15a levels.
  • In this study, addition of exogenous miR-15a and miR-16 led to an accumulation of cells in G(1) in non-New Zealand Black B cell and New Zealand Black-derived malignant B-1 cell lines.
  • However, the New Zealand Black line had significantly greater G(1) accumulation, suggesting a restoration of cell cycle control upon exogenous miR-15a/16 addition.
  • Our experiments showed a reduction in protein levels of cyclin D1, a miR-15a/16 target and cell cycle regulator of G(1)/S transition, in the New Zealand Black cell line following miR-15a/16 addition.
  • These microRNAs were shown to directly target the cyclin D1 3' untranslated region using a green fluorescent protein lentiviral expression system. miR-16 was also shown to augment apoptosis induction by nutlin, a mouse double minute 2 (MDM2) antagonist, and genistein, a tyrosine kinase inhibitor, when added to a B-1 cell line derived from multiple in vivo passages of malignant B-1 cells from New Zealand Black mice with CLL. miR-16 synergized with nutlin and genistein to induce apoptosis.
  • Our data support a role for the mir-15a/16-1 cluster in cell cycle regulation and suggest that these mature microRNAs in both the New Zealand Black model and human CLL may be targets for therapeutic efficacy in this disease.
  • [MeSH-major] Disease Models, Animal. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. MicroRNAs / genetics

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. GENISTEIN .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19723889.001).
  • [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 / Antineoplastic Agents; 0 / DNA Primers; 0 / Imidazoles; 0 / MicroRNAs; 0 / Piperazines; 0 / RNA, Messenger; 0 / nutlin 3; 136601-57-5 / Cyclin D1; DH2M523P0H / Genistein
  •  go-up   go-down


51. Cai L, Zeng T, Zeng Q, Li B, Lin X, Gong Y, Liu W, Zhang Z, Zhang S: Schistosoma japonicum: protective immunity induced by schistosomulum-derived cells in a mouse model. J Parasitol; 2008 Apr;94(2):395-403
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Schistosoma japonicum: protective immunity induced by schistosomulum-derived cells in a mouse model.
  • In the present work, 2 immune protective experiments were designed to further validate the protective effect induced by this type of vaccine and to optimize the immunization protocol, including the number of inoculations and parasite stages from which immunogenic cells were derived.
  • Three antigens derived from 18-day-old postinfection live (LLC) and dead (DLC) larval worm cells and from dead 42-day-old postinfection adult worm cells (DAC) were used as immunogens.
  • A 38-kDa polypeptide was recognized by sera from LLC immunized animals.
  • [MeSH-minor] Animals. Blotting, Western. Disease Models, Animal. Enzyme-Linked Immunosorbent Assay. Female. Granuloma / parasitology. Granuloma / pathology. Image Processing, Computer-Assisted. Immune Sera / chemistry. Immune Sera / immunology. Immunization, Secondary / methods. Immunization, Secondary / standards. Immunoglobulin G / biosynthesis. Immunoglobulin G / blood. Larva / cytology. Larva / immunology. Liver / parasitology. Liver / pathology. Mice. Rabbits

  • MedlinePlus Health Information. consumer health - Immunization.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18564740.001).
  • [ISSN] 0022-3395
  • [Journal-full-title] The Journal of parasitology
  • [ISO-abbreviation] J. Parasitol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Helminth; 0 / Antigens, Helminth; 0 / Immune Sera; 0 / Immunoglobulin G
  •  go-up   go-down


52. Sutton LA, Kostareli E, Hadzidimitriou A, Darzentas N, Tsaftaris A, Anagnostopoulos A, Rosenquist R, Stamatopoulos K: Extensive intraclonal diversification in a subgroup of chronic lymphocytic leukemia patients with stereotyped IGHV4-34 receptors: implications for ongoing interactions with antigen. Blood; 2009 Nov 12;114(20):4460-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extensive intraclonal diversification in a subgroup of chronic lymphocytic leukemia patients with stereotyped IGHV4-34 receptors: implications for ongoing interactions with antigen.
  • Several studies indicate that the development of chronic lymphocytic leukemia (CLL) may be influenced by antigen recognition through the clonotypic B-cell receptors (BCRs).
  • However, it is still unclear whether antigen involvement is restricted to the malignant transformation phase or whether the putative antigen(s) may continuously trigger the CLL clone and affect not only the progenitor cell but also the leukemic cells themselves.
  • To address this issue, we conducted a large-scale subcloning study of rearranged immunoglobulin heavy variable (IGHV) genes of diverse mutational status from 71 CLL cases (total, 1496 subcloned sequences), belonging to both the common IgM/IgD variant and the rare IgG-positive variant.
  • Although most cases showed no or low levels of intraclonal diversification (ID), we report intense ID in the IGHV genes of selected cases, especially a subgroup of 13 IgG-switched cases expressing stereotyped, mutated IGHV4-34 rearrangements (subset 4).
  • We demonstrate that the ID evident in subset 4 cases cannot be attributed to IGHV4-34 usage, IGHV gene-mutated status, class-switch recombination, or BCR stereotypy in general; rather, it represents a unique phenomenon strongly correlated with the distinctive BCR of subset 4.
  • In such cases, the observed ID patterns may imply a stereotyped response to an active, ongoing interaction with antigen(s).
  • [MeSH-major] Antigens / immunology. Genes, Immunoglobulin Heavy Chain / genetics. Genes, Immunoglobulin Heavy Chain / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19713457.001).
  • [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 / Antigens
  •  go-up   go-down


53. Casal RF, Adachi R, Jimenez CA, Sarkiss M, Morice RC, Eapen GA: Diagnosis of invasive aspergillus tracheobronchitis facilitated by endobronchial ultrasound-guided transbronchial needle aspiration: a case report. J Med Case Rep; 2009;3:9290
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis of invasive aspergillus tracheobronchitis facilitated by endobronchial ultrasound-guided transbronchial needle aspiration: a case report.
  • Although this infection frequently involves the lung parenchyma, it is unusual to find it limited to the tracheobronchial tree, a condition known as invasive aspergillus tracheobronchitis.
  • CASE PRESENTATION: A 65 year-old Hispanic man from Bolivia with a history of chronic lymphocytic leukemia developed cough and malaise eight months after having an allogenic stem cell transplant.
  • A computed tomography of the chest revealed an area of diffuse soft tissue thickening around the left main stem bronchus, which was intensely fluorodeoxyglucose-avid on positron emission tomography scanning.
  • CONCLUSION: We describe the first case of invasive aspergillus tracheobronchitis in which the diagnosis was facilitated by the use of endobronchial ultrasound guided trans-bronchial needle aspiration.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Ann Hematol. 2007 Jan;86(1):9-15 [17021839.001]
  • [Cites] Infect Dis Clin North Am. 2006 Sep;20(3):545-61, vi [16984868.001]
  • [Cites] Nephrol Dial Transplant. 1999 Jul;14(7):1784-5 [10435898.001]
  • [Cites] Thorax. 1995 Jul;50(7):812-3 [7570425.001]
  • [Cites] Bone Marrow Transplant. 1999 Nov;24(10):1145-9 [10578166.001]
  • [Cites] Am Rev Respir Dis. 1991 Sep;144(3 Pt 1):552-6 [1654038.001]
  • [Cites] Am J Med. 1973 Jan;54(1):6-15 [4345262.001]
  • [Cites] Medicine (Baltimore). 1970 Mar;49(2):147-73 [4913991.001]
  • [Cites] Clin Nucl Med. 2003 Mar;28(3):234-5 [12592137.001]
  • [Cites] Chest. 1994 Oct;106(4):1265-7 [7924508.001]
  • (PMID = 19946509.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2783092
  •  go-up   go-down


54. Oliere S, Arguello M, Mesplede T, Tumilasci V, Nakhaei P, Stojdl D, Sonenberg N, Bell J, Hiscott J: Vesicular stomatitis virus oncolysis of T lymphocytes requires cell cycle entry and translation initiation. J Virol; 2008 Jun;82(12):5735-49
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vesicular stomatitis virus oncolysis of T lymphocytes requires cell cycle entry and translation initiation.
  • Vesicular stomatitis virus (VSV) is a candidate oncolytic virus that replicates and induces cell death in cancer cells while sparing normal cells.
  • We previously demonstrated that VSV infection induces apoptosis in proliferating CD4(+) T lymphocytes from adult T-cell leukemia samples but not in resting T lymphocytes or primary chronic lymphocytic leukemia cells that remain arrested in G(0).
  • Activation of primary CD4(+) T lymphocytes with anti-CD3/CD28 is sufficient to induce VSV replication and cell death in a manner dependent on activation of the MEK1/2, c-Jun NH(2)-terminal kinase, or phosphatidylinositol 3-kinase pathway but not p38.
  • VSV replication is specifically impaired by the cell cycle inhibitor olomoucine or rapamycin, which induces early G(1) arrest, but not by aphidicolin or Taxol, which blocks at the G(1)1S or G(2)1M phase, respectively; this result suggests a requirement for cell cycle entry for efficient VSV replication.
  • Furthermore, VSV protein production in activated T cells is diminished by small interfering RNA-mediated eIF4E knockdown.
  • These results demonstrate that VSV replication in primary T lymphocytes relies on cell cycle transition from the G(0) phase to the G(1) phase, which is characterized by a sharp increase in ribogenesis and protein synthesis.
  • [MeSH-major] CD4-Positive T-Lymphocytes / virology. Cell Cycle. Protein Biosynthesis. Vesicular stomatitis Indiana virus / physiology
  • [MeSH-minor] B-Lymphocytes / virology. Cell Death. Cell Line. Flow Cytometry. Humans. Lymphocyte Activation. RNA, Small Interfering / metabolism. RNA, Small Interfering / pharmacology. Transfection. Viral Plaque Assay. Virus Replication


55. Osterborg A, Karlsson C, Lundin J, Kimby E, Mellstedt H: Strategies in the management of alemtuzumab-related side effects. Semin Oncol; 2006 Apr;33(2 Suppl 5):S29-35
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • B-cell chronic lymphocytic leukemia has traditionally been treated with alkylating agents and purine analogues.
  • The introduction of alemtuzumab, a CD52 monoclonal antibody with significant clinical activity in chemotherapy refractory B-cell chronic lymphocytic leukemia, is accompanied by a side effect profile different from that resulting from chemotherapy.
  • Alternatively, administration of alemtuzumab subcutaneously may markedly reduce the occurrence of general side effects but results in limited transient local skin reactions in most patients.
  • Neutropenia (grade 4) may occur in approximately 20% of patients, but is usually transient and/or responds promptly to colony stimulating factor therapy; episodes of febrile neutropenia are infrequent.
  • The major side effect of alemtuzumab is T-cell depletion, leading to an increased risk of infection, in particular reactivation of cytomegalovirus.
  • This event typically occurs 3 to 8 weeks after initiation of therapy, coinciding with the T-cell nadir.
  • The overall safety profile of alemtuzumab appears to be beneficial in relation to disease severity and prognosis in patients with fludarabine-refractory B-cell chronic lymphocytic leukemia.
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Bacterial Infections / prevention & control. Drug Eruptions / prevention & control. Humans. Immunosuppression / adverse effects. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Neutropenia / prevention & control. T-Lymphocytes / drug effects. Virus Diseases / prevention & control

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16720201.001).
  • [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 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  • [Number-of-references] 35
  •  go-up   go-down


56. Montes-Ares O, Moya-Quiles MR, Montes-Casado M, Guerra-Pérez N, Campillo JA, González C, López-Bermejo A, Tamayo M, Majado MJ, Parrado A, Muro M, Marín L, Alvarez-López MR: Human leucocyte antigen-C in B chronic lymphocytic leukaemia. Br J Haematol; 2006 Nov;135(4):517-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human leucocyte antigen-C in B chronic lymphocytic leukaemia.
  • This study aimed at characterising the distribution of human leucocyte antigen (HLA)-C alleles in a large group of patients with B chronic lymphocytic leukaemia from Southeastern Spain.
  • [MeSH-major] HLA-C Antigens / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Case-Control Studies. Female. Gene Frequency. Genetic Predisposition to Disease. Histocompatibility Testing / methods. Humans. Male. Middle Aged. Polymerase Chain Reaction / methods

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17054674.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA-C Antigens
  •  go-up   go-down


57. Domingo-Domènech E, Benavente Y, Alvaro T, Hernández M, de Sevilla AF, de Sanjosé S: Family clustering of blood cancers as a risk factor for lymphoid neoplasms. Haematologica; 2005 Mar;90(3):416-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Family clustering of blood cancers as a risk factor for lymphoid neoplasms.
  • Family aggregation of cancer was significantly more common among 588 incident cases with lymphoid neoplasms than among 631 controls (OR: 1.4; 95%CI= 1.1-1.8, p value=0.004).
  • This association was of particular relevance among cases of multiple myeloma and chronic lymphocytic leukemia, with a 2-fold increased risk, the latter also showing an almost 4-fold increased risk of family aggregation of hematologic cancers.
  • [MeSH-major] Family Health. Leukemia, Lymphoid / etiology. Lymphoma / etiology


58. Ochoa Undargarain O, Hermida Pérez JA, Ochoa Montes de Oca J, Félix León JM: [Well-differentiated lymphocytic lymphoma of the prostate. Case report and bibliographic review]. Arch Esp Urol; 2006 Jun;59(5):538-41
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Well-differentiated lymphocytic lymphoma of the prostate. Case report and bibliographic review].
  • [Transliterated title] Linfoma linfocítico, bien diferenciado de la próstata, presentación de un caso y breve revisión de la literatura.
  • OBJECTIVE: To report a case of prostate lymphoma and a brief review of the literature.
  • Surgery with retropubic prostatectomy was performed, and pathology revealed a primary prostate lymphoma.
  • The case study is followed by a brief bibliographic review, where we analyse clinical menifestations of this entity, complementary studies useful for diagnosis (laboratory test, trasrectal prostate biopsy, transuretral resection, ultrasound and computerised axial tomography), treatment options (surgery, polychemotherapy, radiotherapy) as well as survival in these patients.
  • CONCLUSIONS: Of the cases reviewed, mean age at diagnosis was 57 years.
  • Clinical debut was with prostate symptoms, with or without AUR and sometimes manifestations of renal failure due to obstructive uropathy, as well as general symptoms (astenia, anorexia, weight loss).
  • PSA values remain unaltered in prostate lymphoma patients.
  • Histologic diagnosis may be made by transrectal prostate biopsy, although transurethral resection (TUR) may be necessary for confirmation.
  • Ultrasound and CT scan are of great utility for diagnosis of both local and distant tumors.
  • From a therapeutic point of view, surgery for the obstruction of the lower urinary tract (TURP or retropubic prostatectomy) may be necessary, as well as the cyclophosphamide based polychemotherapy with corticosteroids and other cytostatic agents, and radiotherapy; intratecal chemotherapy has also been used adjuvant bone marrow transplantation.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Prostatic Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16903560.001).
  • [ISSN] 0004-0614
  • [Journal-full-title] Archivos españoles de urología
  • [ISO-abbreviation] Arch. Esp. Urol.
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Number-of-references] 26
  •  go-up   go-down


59. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • The systematic use of a panel of interphase fluorescence in situ hybridization (FISH) may not reveal some probes (targeting chromosomes 11q, 13q, 17p, and chromosome 12) structural abnormalities.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 13. Leukemia, Lymphocytic, Chronic, B-Cell / genetics

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


60. Mainiero A, Schnatz PF: Chronic lymphocytic leukemia presenting with localized gynecologic symptoms. J Low Genit Tract Dis; 2010 Jan;14(1):63-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic lymphocytic leukemia presenting with localized gynecologic symptoms.
  • BACKGROUND: Although no cure exists for chronic lymphocytic leukemia (CLL), treatment can reduce morbidity and/or improve survival in advanced disease.
  • Identification of patients in an early disease state allows monitoring and treatment as soon as appropriate.
  • We were unable to find previous reports of early CLL disease presenting with gynecologic symptoms.
  • This report seeks to alert gynecologists of their potential role in identifying CLL patients.
  • Peripheral blood flow cytometry confirmed a diagnosis of early-stage CLL.
  • The patient remains asymptomatic and is currently monitored for disease progression.
  • CONCLUSION: Early CLL can present with localized gynecologic symptoms or cervical lesions.
  • The recognition of early disease can assure optimal treatment.
  • [MeSH-major] Genital Diseases, Female / etiology. Genital Diseases, Female / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20040839.001).
  • [ISSN] 1526-0976
  • [Journal-full-title] Journal of lower genital tract disease
  • [ISO-abbreviation] J Low Genit Tract Dis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


61. Filip B, Milczarek M, Wietrzyk J, Chodyński M, Kutner A: Antitumor properties of (5E,7E) analogs of vitamin D3. J Steroid Biochem Mol Biol; 2010 Jul;121(1-2):399-402
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Removal of the triene protecting group, in a key synthetic step, yielded the title compounds PRI-2208 and PRI-2209, respectively.
  • The analogs were examined for their antiproliferative activity in vitro against human breast cancer cells (MCF-7) and promyelocytic leukemia (HL-60) cells.
  • The antitumor activity of these analogs in the LLC mice tumor model was studied.
  • Analog PRI-2208 was found to be more active in inhibiting LLC tumor growth than 1alpha,25(OH)2D3, as well as than PRI-2191 and PRI-2209.
  • [MeSH-minor] Animals. Calcium / metabolism. Cell Proliferation. Chemistry, Pharmaceutical / methods. Drug Design. Drug Screening Assays, Antitumor. Female. HL-60 Cells. Humans. Mice. Mice, Inbred C57BL. Neoplasm Transplantation. Stereoisomerism

  • Hazardous Substances Data Bank. CHOLECALCIFEROL .
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20227499.001).
  • [ISSN] 1879-1220
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 1C6V77QF41 / Cholecalciferol; SY7Q814VUP / Calcium
  •  go-up   go-down


62. Xin H, Sun R, Kanehira M, Takahata T, Itoh J, Mizuguchi H, Saijo Y: Intratracheal delivery of CX3CL1-expressing mesenchymal stem cells to multiple lung tumors. Mol Med; 2009 Sep-Oct;15(9-10):321-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Mesenchymal stem cells (MSCs), nonhematopoietic stem cells capable of differentiating into various mesoderm-type cells, have a propensity to migrate to and proliferate in tumor tissues after systemic administration.
  • We intratracheally injected MSCs expressing CX3CL1 (MSC/RGDFKN) into the lung of lung tumor-bearing mice with multiple metastases of C26 or Lewis lung carcinoma (LLC).
  • Intratracheal injection of MSC/RGDFKN strongly inhibited growth of lung metastases of C26 or LLC, and thus prolonged survival.
  • [MeSH-major] Carcinoma, Lewis Lung / secondary. Carcinoma, Lewis Lung / therapy. Chemokine CX3CL1 / biosynthesis. Mesenchymal Stem Cell Transplantation / methods. Mesenchymal Stromal Cells / physiology
  • [MeSH-minor] Adenoviridae / genetics. Animals. BALB 3T3 Cells. Bronchoalveolar Lavage Fluid / chemistry. Cell Line, Tumor. Cell Movement / physiology. Data Interpretation, Statistical. Drug Administration Routes. Histocytochemistry. Kaplan-Meier Estimate. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Trachea

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2003 Apr 15;101(8):2999-3001 [12480709.001]
  • [Cites] Am J Respir Crit Care Med. 2007 Dec 15;176(12):1261-8 [17641155.001]
  • [Cites] Gene Ther. 2004 Jul;11(14):1155-64 [15141157.001]
  • [Cites] Cancer. 1981 Jun 1;47(11):2595-602 [7260854.001]
  • [Cites] Nat Genet. 1994 Sep;8(1):42-51 [7527271.001]
  • [Cites] J Virol. 1995 Apr;69(4):2004-15 [7884845.001]
  • [Cites] Hum Gene Ther. 1995 May;6(5):667-703 [7578402.001]
  • [Cites] Hum Gene Ther. 1995 Jul;6(7):895-903 [7578408.001]
  • [Cites] N Engl J Med. 1999 Jun 24;340(25):1948-53 [10379018.001]
  • [Cites] J Natl Cancer Inst. 2004 Nov 3;96(21):1593-603 [15523088.001]
  • [Cites] Cancer Sci. 2005 Mar;96(3):149-56 [15771617.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3307-18 [15833864.001]
  • [Cites] Eur J Immunol. 2005 May;35(5):1371-80 [15789339.001]
  • [Cites] JAMA. 2001 May 23-30;285(20):2594-603 [11368733.001]
  • [Cites] Gene Ther. 2001 May;8(9):730-5 [11406768.001]
  • [Cites] J Exp Med. 2002 Jun 17;195(12):1549-63 [12070283.001]
  • [Cites] Exp Cell Res. 2005 Jun 10;306(2):330-5 [15925588.001]
  • [Cites] Am J Respir Cell Mol Biol. 2005 Oct;33(4):371-7 [16037486.001]
  • [Cites] Brain. 2006 Oct;129(Pt 10):2734-45 [16901914.001]
  • [Cites] Mol Ther. 2006 Dec;14(6):840-50 [16965940.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2007 Feb;292(2):H1120-8 [16980338.001]
  • [Cites] Stem Cells. 2007 Jul;25(7):1618-26 [17412895.001]
  • [Cites] Cancer Res. 2007 Jul 1;67(13):6304-13 [17616689.001]
  • [Cites] Gene Ther. 2007 Aug;14(16):1226-34 [17597794.001]
  • [Cites] Cancer Res. 2003 Aug 1;63(15):4420-5 [12907614.001]
  • (PMID = 19603106.001).
  • [ISSN] 1528-3658
  • [Journal-full-title] Molecular medicine (Cambridge, Mass.)
  • [ISO-abbreviation] Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokine CX3CL1; 0 / Cx3cl1 protein, mouse
  •  go-up   go-down


63. Bilan F, Nacfer M, Fresquet F, Norez C, Melin P, Martin-Berge A, Costa de Beauregard MA, Becq F, Kitzis A, Thoreau V: Endosomal SNARE proteins regulate CFTR activity and trafficking in epithelial cells. Exp Cell Res; 2008 Jul 1;314(11-12):2199-211
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In LLC-PK1 cells transfected with CFTR and in Caco-2 cells endogenously expressing CFTR, we demonstrated that endosomal SNARE protein overexpression inhibits CFTR activity but not swelling- or calcium-activated iodide efflux, indicating a specific effect upon CFTR activity.
  • Moreover, co-immunoprecipitation experiments in LLC-PK1-CFTR cells showed that CFTR and SNARE proteins belong to a same complex and pull-down assays showed that VAMP8 and vti1b preferentially interact with CFTR N-terminus tail.
  • By cell surface biotinylation and immunofluorescence experiments, we evidenced that endosomal SNARE overexpression disturbs CFTR apical targeting.
  • [MeSH-minor] Animals. Cell Line. Endosomes / metabolism. Humans. Iodides / metabolism. Protein Transport / physiology. RNA Interference. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. rab GTP-Binding Proteins / genetics. rab GTP-Binding Proteins / metabolism

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18570918.001).
  • [ISSN] 1090-2422
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Iodides; 0 / Qa-SNARE Proteins; 0 / Qb-SNARE Proteins; 0 / R-SNARE Proteins; 0 / Recombinant Fusion Proteins; 0 / SNARE Proteins; 0 / VAMP8 protein, human; 0 / VTI1B protein, human; 126880-72-6 / Cystic Fibrosis Transmembrane Conductance Regulator; EC 3.6.1.- / rab GTP-Binding Proteins; EC 3.6.1.- / rab11 protein
  •  go-up   go-down


64. Palma M, Adamson L, Hansson L, Kokhaei P, Rezvany R, Mellstedt H, Osterborg A, Choudhury A: Development of a dendritic cell-based vaccine for chronic lymphocytic leukemia. Cancer Immunol Immunother; 2008 Nov;57(11):1705-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of a dendritic cell-based vaccine for chronic lymphocytic leukemia.
  • Evidence for the existence of CLL-specific antigens recognized by the immune system can be gathered from the observation that many patients display monoclonal or oligoclonal expansions and skewed repertoire of T cells.
  • Antileukemic cellular immunity may be boosted in vivo using dendritic cell-based immunotherapy.
  • Our preclinical studies provide evidence that DC that had endocytosed apoptotic CLL cells (Apo-DC) were superior to fusion hybrids, tumor lysate or RNA in eliciting antileukemic T-cell responses in vitro.
  • We have validated a method for enriching the small number of monocyte precursors present in the peripheral blood of CLL patients and utilize them for generating individualized, Apo-DC cellular vaccines.
  • Cryopreservation and thawing did not affect the phenotype or the T cell stimulatory function of Apo-DC.
  • CLL patients receive 10(7) Apo-DC for at least five immunizations and monitored clinically and immunologically for 52 weeks.
  • Cohort I receives Apo-DC alone; Cohort II: Apo-DC+ repeated doses of low-dose GM-CSF; Cohort III: low-dose cyclophosphamide followed by Apo-DC + GM-CSF.
  • [MeSH-major] Cancer Vaccines / immunology. Dendritic Cells / immunology. Immunotherapy. Leukemia, Lymphocytic, Chronic, B-Cell / therapy

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18663443.001).
  • [ISSN] 0340-7004
  • [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; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cancer Vaccines
  • [Number-of-references] 44
  •  go-up   go-down


65. Amiel A, Goldzak G, Gaber E, Yosef G, Fejgin MD, Yukla M, Lishner M: Random aneuploidy and telomere capture in chronic lymphocytic leukemia and chronic myeloid leukemia patients. Cancer Genet Cytogenet; 2005 Nov;163(1):12-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Random aneuploidy and telomere capture in chronic lymphocytic leukemia and chronic myeloid leukemia patients.
  • We investigated telomere capture and aneuploidy rates in chronic lymphocytic leukemia (CLL) and chronic myeloid leukemia (CML) patients, as well as in healthy control subsets.
  • Higher aneuploidy rates were found in the leukocytes of CLL and CML patients, compared with the control group, for the 21q22 and SNRPN loci.
  • There was no difference in the aneuploidy rate between the CML and CLL groups.
  • Telomere capture was found in the two groups (CLL and CML), but not in the control group.
  • [MeSH-major] Aneuploidy. Chromosomes, Human, Pair 21. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Telomere / genetics. Trisomy


66. Jindra P, Koza V, Lysák D, Vozobulová V, Steinerová K: Inefficiency of high-dose G-CSF alone as second mobilization regimen in fludarabin-cyclophosphamide-treated CLL patients who failed to mobilize after chemotherapy and G-CSF. Bone Marrow Transplant; 2005 Apr;35(7):729-30
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inefficiency of high-dose G-CSF alone as second mobilization regimen in fludarabin-cyclophosphamide-treated CLL patients who failed to mobilize after chemotherapy and G-CSF.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / administration & dosage. Hematopoietic Stem Cell Mobilization / methods. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Vidarabine / analogs & derivatives
  • [MeSH-minor] Cyclophosphamide / therapeutic use. Peripheral Blood Stem Cell Transplantation / methods. Treatment Failure

  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. VIDARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15785772.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  •  go-up   go-down


67. Palamarchuk A, Efanov A, Nazaryan N, Santanam U, Alder H, Rassenti L, Kipps T, Croce CM, Pekarsky Y: 13q14 deletions in CLL involve cooperating tumor suppressors. Blood; 2010 May 13;115(19):3916-22
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 13q14 deletions in CLL involve cooperating tumor suppressors.
  • B-cell chronic lymphocytic leukemia (CLL) is the most common human leukemia.
  • 13q14 deletions are most common chromosomal alterations in CLL.
  • Recent studies of transgenic mouse models demonstrated the importance of the nuclear factor-kappaB (NF-kappaB) pathway in CLL.
  • To examine the possible role of DLEU7 in CLL, we investigated the effect of DLEU7 expression on NF-kappaB and nuclear factor of activated T cells (NFAT) activity.
  • We found that DLEU7 functions as a potent NF-kappaB and NFAT inhibitor by physically interacting and inhibiting TACI and BCMA, members of the tumor necrosis factor (TNF) receptor family involved in B-CLL.
  • In addition, DLEU7 expression in A549 lung cancer cells resulted in a decrease in S phase and increased apoptosis.
  • The results suggest that loss of DLEU7 may cooperate with the loss of miR-15/16 in the pathogenesis of CLL.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3028-33 [10716693.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 16;105(50):19643-8 [19064921.001]
  • [Cites] N Engl J Med. 2000 Dec 28;343(26):1910-6 [11136261.001]
  • [Cites] J Cell Sci. 2002 Feb 15;115(Pt 4):679-88 [11865024.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6955-60 [12011454.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15524-9 [12434020.001]
  • [Cites] Annu Rev Immunol. 2003;21:231-64 [12427767.001]
  • [Cites] FEBS Lett. 2004 Jan 2;556(1-3):75-80 [14706829.001]
  • [Cites] Cancer Cell. 2004 Oct;6(4):399-408 [15488762.001]
  • [Cites] J Biol Chem. 1989 May 15;264(14):8222-9 [2722778.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Dec 1;89(23):11376-80 [1454823.001]
  • [Cites] Leuk Lymphoma. 1996 Nov;23(5-6):583-92 [9031090.001]
  • [Cites] Immunity. 1997 Nov;7(5):703-13 [9390693.001]
  • [Cites] J Immunol. 1998 Jul 1;161(1):277-85 [9647234.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Nov 23;101(47):16600-5 [15545599.001]
  • [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] Cancer Res. 2005 Dec 15;65(24):11282-6 [16357133.001]
  • [Cites] Immunology. 2006 Jul;118(3):281-92 [16827889.001]
  • [Cites] J Biol Chem. 2006 Nov 3;281(44):33761-72 [16950787.001]
  • [Cites] J Cell Biochem. 2007 Apr 1;100(5):1109-18 [17131382.001]
  • [Cites] Blood. 2007 Sep 15;110(6):2121-7 [17567982.001]
  • [Cites] Cancer Res. 2008 Feb 15;68(4):1012-21 [18281475.001]
  • [Cites] Biochem Pharmacol. 2008 Sep 1;76(5):662-71 [18644347.001]
  • [CommentIn] Blood. 2010 May 13;115(19):3858-9 [20466868.001]
  • (PMID = 20071661.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA081534; United States / NCI NIH HHS / CA / P01-CA81534
  • [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 / B-Cell Maturation Antigen; 0 / DLEU7 protein, human; 0 / MIRN16 microRNA, human; 0 / MicroRNAs; 0 / NF-kappa B; 0 / NFATC Transcription Factors; 0 / TNFRSF13B protein, human; 0 / TNFRSF17 protein, human; 0 / Transmembrane Activator and CAML Interactor Protein; 0 / Tumor Suppressor Proteins; EC 1.13.12.- / Luciferases
  • [Other-IDs] NLM/ PMC2869560
  •  go-up   go-down


68. Trinidad EM, Ballesteros M, Zuloaga J, Zapata A, Alonso-Colmenar LM: An impaired transendothelial migration potential of chronic lymphocytic leukemia (CLL) cells can be linked to ephrin-A4 expression. Blood; 2009 Dec 3;114(24):5081-90
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An impaired transendothelial migration potential of chronic lymphocytic leukemia (CLL) cells can be linked to ephrin-A4 expression.
  • Chronic lymphocytic leukemia (CLL) cell migration into lymphoid tissues is an important aspect of the pathobiology of this disease.
  • Here, we investigated the role of ephrin-A4 (EFNA4) in the transendothelial migration (TEM) capacity of CLL and normal B cells through interacting with endothelial EphA2 (erythropoietin-producing hepatocellular carcinoma).
  • CLL cells showed a remarkable impairment in the adhesion to and transmigration through human umbilical vein endothelial cell (HUVEC) monolayers, correlating with their higher EFNA4 expression.
  • In vitro, TEM was mediated by EFNA4 binding to endothelial EphA2 receptor, which is highly expressed in tumor necrosis factor-alpha-activated HUVECs as well as in the CD31(+) endothelial cells of human lymph nodes.
  • The pretreatment of CLL cells with EphA2 homodimers further impaired their adhesion to and transmigration through HUVEC monolayers, whereas pretreatment of HUVECs with EFNA4 homodimers improved those phenomena in both CLL and normal B cells, suggesting that EFNA4 signaling negatively contributed to TEM.
  • In fact, EFNA4 signaling into CLL cells significantly reduced their adhesion to intercellular adhesion molecule 1, vascular cell adhesion molecule 1, and several extracellular matrix molecules and impaired CCL-19-mediated TEM and chemotaxis.
  • Our results suggest that EFNA4-EphA2 interactions are involved in CLL cell trafficking between blood and the tissues and therefore may become a therapeutic target in the future.
  • [MeSH-major] Chemotaxis, Leukocyte / physiology. Endothelium / metabolism. Ephrin-A4 / biosynthesis. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism
  • [MeSH-minor] Cell Adhesion / physiology. Chemokine CCL19 / metabolism. Flow Cytometry. Fluorescent Antibody Technique. Humans. Intercellular Adhesion Molecule-1 / metabolism. Microscopy, Confocal. Receptor, EphA2 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Vascular Cell Adhesion Molecule-1 / metabolism

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19828693.001).
  • [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 / Chemokine CCL19; 0 / Ephrin-A4; 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1; EC 2.7.10.1 / Receptor, EphA2
  •  go-up   go-down


69. Burton BJ, Cunningham ET Jr, Cree IA, Pavesio CE: Eye involvement mimicking scleritis in a patient with chronic lymphocytic leukaemia. Br J Ophthalmol; 2005 Jun;89(6):775-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Eye involvement mimicking scleritis in a patient with chronic lymphocytic leukaemia.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemic Infiltration / diagnosis. Sclera / pathology. Scleritis / diagnosis
  • [MeSH-minor] Aged. Aged, 80 and over. Diagnosis, Differential. Humans. Male

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Eye (Lond). 2003 Jan;17(1):27-30 [12579166.001]
  • [Cites] Arch Ophthalmol. 1961 Oct;66:490-508 [13860566.001]
  • [Cites] Surv Ophthalmol. 1983 Jan-Feb;27(4):211-32 [6342189.001]
  • [Cites] Br J Ophthalmol. 1968 Oct;52(10):781-5 [5686969.001]
  • (PMID = 15923522.001).
  • [ISSN] 0007-1161
  • [Journal-full-title] The British journal of ophthalmology
  • [ISO-abbreviation] Br J Ophthalmol
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1772664
  •  go-up   go-down


70. Zhou HJ, Zhang JL, Li A, Wang Z, Lou XE: Dihydroartemisinin improves the efficiency of chemotherapeutics in lung carcinomas in vivo and inhibits murine Lewis lung carcinoma cell line growth in vitro. Cancer Chemother Pharmacol; 2010 May;66(1):21-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dihydroartemisinin improves the efficiency of chemotherapeutics in lung carcinomas in vivo and inhibits murine Lewis lung carcinoma cell line growth in vitro.
  • Our purpose was to evaluate in vitro antitumoral properties of DHA in the murine Lewis lung carcinoma (LLC) cell line.
  • At the same time, we observed the therapeutic effect of DHA combined with cyclophosphamide (CTX) in the LLC and combined with cisplatin (CDDP) in the human non-small cell lung cancer A549 xenotransplanted carcinoma in vivo.
  • RESULTS: Dihydroartemisinin exhibited high anti-cancer activity in LLC cell line.
  • DHA also induced apoptosis of LLC cells and influenced the expression of VEGF receptor KDR/flk-1.
  • The affection by DHA combined CTX on LLC tumor metastasis was significant.
  • CONCLUSIONS: Dihydroartemisinin is a potent compound against LLC cell line in vitro.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Proliferation / drug effects. Cell Survival / drug effects. Drug Screening Assays, Antitumor. Female. Humans. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Neoplasm Metastasis / drug therapy. Neoplasms / drug therapy. Neoplasms / metabolism. Random Allocation. Tumor Burden / drug effects. Vascular Endothelial Growth Factor Receptor-2 / metabolism. Xenograft Model Antitumor Assays

  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19756601.001).
  • [ISSN] 1432-0843
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Artemisinins; 6A9O50735X / dihydroartemisinin; 8N3DW7272P / Cyclophosphamide; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


71. Wadhwa PD, Morrison VA: Infectious complications of chronic lymphocytic leukemia. Semin Oncol; 2006 Apr;33(2):240-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Infectious complications of chronic lymphocytic leukemia.
  • Infectious complications continue to be one of the major causes of morbidity and mortality in patients with chronic lymphocytic leukemia (CLL).
  • Hypogammaglobulinemia is an important predisposing factor for infection in patients with early-stage disease and for those treated with conventional alkylating agents.
  • As a result of this therapy, these patients often experience profound and sustained T-cell immunodeficiency.
  • This review focuses on the pathogenesis and risk factors for infections in patients with CLL, the spectrum of infectious organisms associated with the newer agents, and the management of these infections with an emphasis on prophylaxis and vaccination strategies.
  • [MeSH-major] Communicable Diseases / etiology. Communicable Diseases / therapy. Leukemia, Lymphocytic, Chronic, B-Cell / complications

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Infectious Diseases.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16616071.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 85
  •  go-up   go-down


72. Papageorgiou KI, Kaniorou-Larai MG: A case report of Merkel cell carcinoma on chronic lymphocytic leukemia: differential diagnosis of coexisting lymphadenopathy and indications for early aggressive treatment. BMC Cancer; 2005;5:106
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case report of Merkel cell carcinoma on chronic lymphocytic leukemia: differential diagnosis of coexisting lymphadenopathy and indications for early aggressive treatment.
  • BACKGROUND: Chronic lymphocytic leukemia (CLL) is a monoclonal disorder, characterized by a progressive proliferation of functionally incompetent B lymphocytes.
  • There is increased evidence of association between CLL and skin cancers, including the uncommon Merkel cell carcinoma (MCC).
  • CASE PRESENTATION: A case report of an 84-year old male, who presented with an aggressively recurrent form of MCC on the lower lip, on the background of an 8-year history of untreated CLL.
  • During the recurrences of MCC, coexisting regional lymphadenopathy, posed a problem in the differential diagnosis and treatment of lymph node involvement.
  • Histopathology and immunoistochemistry showed that submandibular lymphadenopathy coexisting with the second recurrence of MCC, was due to B-cell small lymphocytic lymphoma.
  • CONCLUSION: MCC has a high incidence of regional lymphadenopathy at presentation (12-45%) and even when it arises on the background of chronic leukemia, lymphadenopathy at presentation should be managed agressively with elective lymph node dissection.
  • We overview the postulated correlation between Merkel tumor and CCL, the differential diagnosis of regional lymphadenopathy during the recurrences of the skin tumor and the strategies of treatment.
  • [MeSH-major] Carcinoma, Merkel Cell / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Lymphatic Diseases / diagnosis
  • [MeSH-minor] Aged, 80 and over. Diagnosis, Differential. Humans. Immunohistochemistry. Lip Neoplasms / metabolism. Lip Neoplasms / pathology. Lymphatic Metastasis. Male. Neoplasm Metastasis. Recurrence. Skin Neoplasms / complications. Skin Neoplasms / diagnosis

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Lymphatic Diseases.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer. 1978 Nov;42(5):2311-21 [719609.001]
  • [Cites] J Clin Oncol. 2002 Jan 15;20(2):588-98 [11786590.001]
  • [Cites] Differentiation. 1984;28(2):136-54 [6084624.001]
  • [Cites] Am J Surg Pathol. 1985 Feb;9(2):95-108 [2579594.001]
  • [Cites] Cancer. 1986 Jan 1;57(1):178-82 [3940617.001]
  • [Cites] J Invest Dermatol. 1986 Jan;86(1):74-7 [2427595.001]
  • [Cites] Cancer. 1987 Dec 15;60(12):2958-64 [3499971.001]
  • [Cites] Am J Ophthalmol. 1992 Jun 15;113(6):674-80 [1598958.001]
  • [Cites] Arch Surg. 1991 Dec;126(12):1514-9 [1842182.001]
  • [Cites] J Am Acad Dermatol. 1993 Aug;29(2 Pt 1):143-56 [8335732.001]
  • [Cites] J Clin Oncol. 1994 Sep;12(9):1974-90 [8083719.001]
  • [Cites] BMJ. 1995 Jun 10;310(6993):1491-5 [7787593.001]
  • [Cites] Br J Cancer. 1996 Dec;74(11):1847-50 [8956805.001]
  • [Cites] Ann Surg Oncol. 1997 Jul-Aug;4(5):389-95 [9259965.001]
  • [Cites] Cancer. 1997 Sep 1;80(5):881-5 [9307187.001]
  • [Cites] Dermatol Surg. 1997 Oct;23(10):929-33 [9357504.001]
  • [Cites] Dermatol Surg. 1999 Jan;25(1):23-5 [9935088.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1999 Feb;8(2):153-8 [10067813.001]
  • [Cites] Arch Surg. 1999 Apr;134(4):388-92; discussion 392-3 [10199311.001]
  • [Cites] Semin Oncol. 1999 Oct;26(5 Suppl 14):107-14 [10561025.001]
  • [Cites] Curr Opin Oncol. 2000 Jan;12(1):22-9 [10687725.001]
  • [Cites] Br J Dermatol. 2000 Mar;142(3):525-8 [10735964.001]
  • [Cites] Cancer. 2000 Apr 15;88(8):1842-51 [10760761.001]
  • [Cites] Arch Otolaryngol Head Neck Surg. 2001 Feb;127(2):149-54 [11177031.001]
  • [Cites] Cancer. 2001 Apr 1;91(7):1358-62 [11283937.001]
  • [Cites] Arch Otolaryngol. 1984 Nov;110(11):707-12 [6487123.001]
  • (PMID = 16111484.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1208865
  •  go-up   go-down


73. Branagan NM, Higgins SP, Halim SA, Le TH: Systemic polyarteritis nodosa mimicking pyoderma gangrenosum in a rare association with small lymphocytic leukaemia/chronic lymphocytic leukaemia. Clin Exp Dermatol; 2009 Jul;34(5):e127-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Systemic polyarteritis nodosa mimicking pyoderma gangrenosum in a rare association with small lymphocytic leukaemia/chronic lymphocytic leukaemia.
  • A 48-year-old patient presented with a nonhealing leg ulcer and a raised white blood cell count.
  • He was diagnosed with pyoderma gangrenosum (PG) and small lymphocytic leukaemia/chronic lymphocytic leukaemia (SLL/CLL).
  • Eight months later, after undergoing treatment with chlorambucil for the SLL/CLL, and prednisone, ciclosporin and intravenous immunoglobulin for the PG, the patient developed livedo reticularis and palpable purpura, and was diagnosed with systemic polyarteritis nodosa (PAN).
  • The case highlights the difficulty in establishing a diagnosis of PAN by biopsy of cutaneous ulcers alone, and that a diagnosis of PG should raise suspicion of another aetiology.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / complications. Polyarteritis Nodosa / diagnosis. Pyoderma Gangrenosum / diagnosis
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Humans. Male. Middle Aged. Skin / pathology

  • Genetic Alliance. consumer health - Polyarteritis nodosa.
  • Genetic Alliance. consumer health - Pyoderma gangrenosum.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19438540.001).
  • [ISSN] 1365-2230
  • [Journal-full-title] Clinical and experimental dermatology
  • [ISO-abbreviation] Clin. Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  •  go-up   go-down


74. Hammami B, Mnejja M, Achour I, Chakroun A, Khabir A, Chakroun A, Boudawara T, Charfeddine I, Ghorbel A: Association of squamous cell carcinoma of the larynx and chronic lymphoid leukemia. Eur Ann Otorhinolaryngol Head Neck Dis; 2010 Sep;127(4):153-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of squamous cell carcinoma of the larynx and chronic lymphoid leukemia.
  • INTRODUCTION: The association of squamous cell carcinoma of the larynx and chronic lymphocytic leukemia (CLL) is exceptional.
  • We report an observation of this association and present the therapeutic problems as well as the effects on prognosis.
  • OBSERVATION: Direct laryngoscopy showed a tumor of the right hemilarynx, with the biopsy concluding in moderately differentiated keratinizing squamous cell carcinoma.
  • The anatomopathological examination of the operative specimen demonstrated infiltration of the larynx and squamous cell carcinoma adenopathies and CLL.
  • It was decided to monitor the chronic lymphoid leukemia, classified as Binet stage B.
  • The synchronous or metachronous onset of a second cancer in a patient with CLL is more frequent than in the general population.
  • The synchronous association of squamous cell carcinoma of the larynx and CLL has been described only rarely.
  • The prognosis is more negative in an association of cervicofacial squamous cell carcinoma and leukemia than in a single cervicofacial cancer.
  • [MeSH-major] Carcinoma, Squamous Cell. Laryngeal Neoplasms. Leukemia, Lymphoid. Neoplasms, Multiple Primary
  • [MeSH-minor] Aged. Chronic Disease. Humans. Male


75. Velasco-Velázquez MA, Maldonado PD, Barrera D, Torres V, Zentella-Dehesa A, Pedraza-Chaverrí J: Aged garlic extract induces proliferation and ameliorates gentamicin-induced toxicity in LLC-PK1 cells. Phytother Res; 2006 Jan;20(1):76-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aged garlic extract induces proliferation and ameliorates gentamicin-induced toxicity in LLC-PK1 cells.
  • The present communication evaluated the effect of AGE and SAC on proliferation and on GM-induced toxicity and genotoxicity of porcine kidney epithelial cell line (LLC-PK1 cells).
  • At the end of this time, cell viability, genotoxicity and proliferation were evaluated.
  • AGE stimulated cell proliferation and protected LLC-PK1 cells from GM-mediated toxicity and genotoxicity.
  • These results suggest that the stimulation of cell proliferation could possibly be one of the mechanisms involved in the in vitro protective effect of AGE in GM-induced toxicity of LLC-PK1 cells.
  • [MeSH-minor] Analysis of Variance. Animals. Bromodeoxyuridine / metabolism. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Drug Interactions. Enzyme-Linked Immunosorbent Assay. LLC-PK1 Cells. Mutagenicity Tests. Phytotherapy. Toxicity Tests

  • MedlinePlus Health Information. consumer health - Antibiotics.
  • Hazardous Substances Data Bank. CYSTEINE .
  • Hazardous Substances Data Bank. BROMODEOXYURIDINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2006 John Wiley & Sons, Ltd.
  • (PMID = 16397848.001).
  • [ISSN] 0951-418X
  • [Journal-full-title] Phytotherapy research : PTR
  • [ISO-abbreviation] Phytother Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Gentamicins; 0 / Plant Extracts; 0 / Protective Agents; 81R3X99M15 / S-allylcysteine; G34N38R2N1 / Bromodeoxyuridine; K848JZ4886 / Cysteine
  •  go-up   go-down


76. Hu X, Mendoza FJ, Sun J, Banerji V, Johnston JB, Gibson SB: Lysophosphatidic acid (LPA) induces the expression of VEGF leading to protection against apoptosis in B-cell derived malignancies. Cell Signal; 2008 Jun;20(6):1198-208
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lysophosphatidic acid (LPA) induces the expression of VEGF leading to protection against apoptosis in B-cell derived malignancies.
  • Vascular endothelial growth factor (VEGF) is a survival and angiogenesis factor that is a target for therapy in a variety of cancers.
  • In many hematological malignancies, VEGF production is increased leading to cell survival responses.
  • Herein, we demonstrate that lysophosphatidic acid (LPA) induces mRNA expression of VEGF in the multiple myeloma cell line, U266, the Burkitt's lymphoma cell line, BJAB, and the chronic lymphocytic leukemia (CLL)-like cell line, I-83.
  • The increase in VEGF expression by LPA is mediated by the activation of c-Jun N-terminal Kinase (JNK) and transcription factor NFkappaB since blocking JNK or NFkappaB activation inhibited LPA induced VEGF expression.
  • Taken together, this indicates that LPA contributes to VEGF production in B cell malignancies leading to cell survival.
  • [MeSH-minor] Burkitt Lymphoma / genetics. Burkitt Lymphoma / metabolism. Cell Line, Tumor. Gene Expression / drug effects. Humans. JNK Mitogen-Activated Protein Kinases / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Multiple Myeloma / genetics. Multiple Myeloma / metabolism. Mutagens / toxicity. NF-kappa B / metabolism. RNA, Messenger / metabolism. Vidarabine / analogs & derivatives. Vidarabine / toxicity

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. VIDARABINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18396013.001).
  • [ISSN] 0898-6568
  • [Journal-full-title] Cellular signalling
  • [ISO-abbreviation] Cell. Signal.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Lysophospholipids; 0 / Mutagens; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; 22002-87-5 / lysophosphatidic acid; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  •  go-up   go-down


77. Guzman ML, Li X, Corbett CA, Rossi RM, Bushnell T, Liesveld JL, Hébert J, Young F, Jordan CT: Rapid and selective death of leukemia stem and progenitor cells induced by the compound 4-benzyl, 2-methyl, 1,2,4-thiadiazolidine, 3,5 dione (TDZD-8). Blood; 2007 Dec 15;110(13):4436-44
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rapid and selective death of leukemia stem and progenitor cells induced by the compound 4-benzyl, 2-methyl, 1,2,4-thiadiazolidine, 3,5 dione (TDZD-8).
  • Leukemia is thought to arise from malignant stem cells, which have been described for acute and chronic myeloid leukemia (AML and CML) and for acute lymphoblastic leukemia (ALL).
  • Leukemia stem cells (LSCs) are relatively resistant to current chemotherapy and likely contribute to disease relapse and progression.
  • Analysis of primary AML, blast crisis CML (bcCML), ALL, and chronic lymphoblastic leukemia (CLL) specimens showed rapid induction of cell death upon treatment with TDZD-8.
  • In addition, for myeloid leukemias, cytotoxicity was observed for phenotypically primitive cells, in vitro colony-forming progenitors, and LSCs as defined by xenotransplantation assays.
  • Notably, cell death was frequently evident within 2 hours or less of TDZD-8 exposure.
  • Cellular and molecular studies indicate that the mechanism by which TDZD-8 induces cell death involves rapid loss of membrane integrity, depletion of free thiols, and inhibition of both the PKC and FLT3 signaling pathways.
  • We conclude that TDZD-8 uses a unique and previously unknown mechanism to rapidly target leukemia cells, including malignant stem and progenitor populations.

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Oncogene. 2000 Aug 10;19(34):3941-7 [10951587.001]
  • [Cites] Int J Hematol. 2005 Aug;82(2):100-7 [16146839.001]
  • [Cites] Hematol Oncol. 2001 Sep;19(3):89-106 [11574931.001]
  • [Cites] Blood. 2001 Oct 15;98(8):2301-7 [11588023.001]
  • [Cites] Blood. 2002 Jan 1;99(1):319-25 [11756187.001]
  • [Cites] J Med Chem. 2002 Mar 14;45(6):1292-9 [11881998.001]
  • [Cites] Leukemia. 2002 Apr;16(4):559-62 [11960332.001]
  • [Cites] Cell. 2002 Apr;109 Suppl:S81-96 [11983155.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1532-42 [12176867.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4594-601 [12393637.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Dec 10;99(25):16220-5 [12451177.001]
  • [Cites] Blood. 2003 Apr 15;101(8):3142-9 [12468427.001]
  • [Cites] Leuk Lymphoma. 2002 Sep;43(9):1715-27 [12685823.001]
  • [Cites] Leukemia. 2004 Mar;18(3):505-12 [14737078.001]
  • [Cites] Cancer Lett. 2004 May 28;208(2):143-53 [15142672.001]
  • [Cites] Oncogene. 2004 Sep 20;23(43):7178-87 [15378078.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2919-25 [15242869.001]
  • [Cites] Am J Med. 1977 Jul;63(1):125-30 [267431.001]
  • [Cites] Baillieres Clin Haematol. 1991 Jul;4(3):577-98 [1958881.001]
  • [Cites] Cell Growth Differ. 1991 Nov;2(11):541-8 [1814434.001]
  • [Cites] J Exp Med. 1992 Jun 1;175(6):1501-9 [1375263.001]
  • [Cites] Leuk Lymphoma. 1992 Oct;8(3):201-11 [1337006.001]
  • [Cites] Nature. 1994 Feb 17;367(6464):645-8 [7509044.001]
  • [Cites] Blood. 1996 Jun 1;87(11):4754-61 [8639846.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] J Biol Chem. 1997 Oct 31;272(44):27521-4 [9346882.001]
  • [Cites] Leukemia. 1997 Nov;11(11):1850-7 [9369417.001]
  • [Cites] Curr Opin Oncol. 1998 Jan;10(1):31-5 [9466482.001]
  • [Cites] Ann Hematol. 1998 Mar-Apr;76(3-4):145-51 [9619732.001]
  • [Cites] Blood. 1999 Sep 15;94(6):2056-64 [10477735.001]
  • [Cites] Clin Cancer Res. 2005 Mar 15;11(6):2436-44 [15788695.001]
  • [Cites] Nat Rev Cancer. 2005 Apr;5(4):297-309 [15803156.001]
  • [Cites] Blood. 2005 Jun 1;105(11):4163-9 [15687234.001]
  • [Cites] Brain Res Mol Brain Res. 2005 Jun 13;137(1-2):193-201 [15950778.001]
  • [Cites] Ann N Y Acad Sci. 2005 Jun;1044:1-5 [15958691.001]
  • [Cites] Clin Cancer Res. 2005 Sep 15;11(18):6520-7 [16166428.001]
  • [Cites] J Med Chem. 2005 Nov 17;48(23):7103-12 [16279768.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4261-8 [16150937.001]
  • [Cites] Br J Pharmacol. 2006 Mar;147(5):575-82 [16314851.001]
  • [Cites] Cancer Lett. 2006 Apr 8;235(1):1-10 [15907369.001]
  • [Cites] Crit Care Med. 2006 May;34(5):1489-96 [16557150.001]
  • [Cites] Shock. 2006 May;25(5):485-91 [16680013.001]
  • [Cites] Clin Immunol. 2006 Jul;120(1):57-67 [16631408.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1316-9 [16642043.001]
  • [Cites] J Pharmacol Exp Ther. 2006 Jul;318(1):79-89 [16601144.001]
  • [Cites] Nat Rev Cancer. 2006 Oct;6(10):813-23 [16990858.001]
  • [Cites] Shock. 2007 Jan;27(1):97-107 [17172987.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):281-94 [17384583.001]
  • [Cites] Leukemia. 2007 May;21(5):926-35 [17330101.001]
  • [Cites] Blood. 1996 Feb 1;87(3):1089-96 [8562934.001]
  • [Cites] Blood. 2005 Jul 15;106(2):673-80 [15797998.001]
  • [Cites] Int J Biochem Cell Biol. 2005 Oct;37(10):2226-38 [16051512.001]
  • [Cites] Crit Care Med. 2005 Sep;33(9):1903-12 [16148458.001]
  • [Cites] Leukemia. 2000 Oct;14(10):1777-84 [11021753.001]
  • (PMID = 17785584.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090446; United States / NCI NIH HHS / CA / R01 CA90446
  • [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 / 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione; 0 / Sulfhydryl Compounds; 0 / Thiadiazoles; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.13 / Protein Kinase C
  • [Other-IDs] NLM/ PMC2234782
  •  go-up   go-down


78. Cesana C, Barbarano L, Miqueleiz S, Lucchesini C, Ricci F, Varettoni M, Filippini D, Lazzarino M, Morra E: Clinical characteristics and outcome of immunoglobulin M-related disorders. Clin Lymphoma; 2005 Mar;5(4):261-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We analyzed the clinical features and prognostic factors for transformation of immunoglobulin Mrelated disorders (IgM-RDs) to malignant lymphoproliferative disease (MLD) in 83 patients with IgM-RDs.
  • We studied 19 patients with type I cryoglobulinemias, 56 patients with type II cryoglobulinemias, 5 patients with peripheral neuropathies (PNs), and 3 patients with idiopathic thrombocytopenic purpuras.
  • Fourteen patients with type II cryoglobulinemias had arthralgias and/or vascular purpura (12 receiving corticosteroids), and 7 presented with PN.
  • At a median of 62 months (12-195 months), 8 cases of IgM-RDs (8.4%) evolved to overt Waldenstrom's macroglobulinemia (n = 6), 1 case to non-Hodgkin's lymphoma, and 1 case to B-cell chronic lymphocytic leukemia.
  • At univariate analysis, male sex (P = 0.02), IgM level > or = 3 g/dL (P < 0.0001), detectable Bence Jones proteinuria (P = 0.0005), lymphocytosis (P = 0.049), and high erythrocyte sedimentation rate (P = 0.003) significantly correlated with the evolution risk.
  • Age, blood cell counts, b2-microglobulin level, degree of marrow lymphoplasmacytic infiltration, type of cryoglobulinemia, and hepatitis C virus positivity did not correlate with transformation.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Blood Sedimentation. Cell Transformation, Neoplastic. Female. Follow-Up Studies. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / etiology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Lymphoma, Non-Hodgkin / etiology. Lymphoma, Non-Hodgkin / pathology. Male. Middle Aged. Prognosis. Risk Factors. Sex Factors. Treatment Outcome. Waldenstrom Macroglobulinemia / etiology. Waldenstrom Macroglobulinemia / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15794861.001).
  • [ISSN] 1526-9655
  • [Journal-full-title] Clinical lymphoma
  • [ISO-abbreviation] Clin Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin M
  •  go-up   go-down


79. Schillaci R, Galeano A, Becu-Villalobos D, Spinelli O, Sapia S, Bezares RF: Autocrine/paracrine involvement of insulin-like growth factor-I and its receptor in chronic lymphocytic leukaemia. Br J Haematol; 2005 Jul;130(1):58-66
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Autocrine/paracrine involvement of insulin-like growth factor-I and its receptor in chronic lymphocytic leukaemia.
  • Chronic lymphocytic leukaemia (CLL) is characterized by the accumulation of long-lived B lymphocytes blocked in G(0/1) by impaired apoptosis.
  • As insulin-like growth factor-I (IGF-I) is known for its antiapoptotic effects in different cell types, we investigated whether IGF-I and its receptor (IGF-IR) participate in autocrine/paracrine loops affecting the survival of CLL cells.
  • IGF-IR protein and mRNA was present in CLL cells in 44% and 59% of patients respectively.
  • IGF-IR expression in CLL patients was positively correlated with the expression of the antiapoptotic protein Bcl-2 and was involved in CLL cell survival in vitro.
  • Serum IGF-I was elevated in CLL patients, but growth hormone (GH) was normal.
  • CLL cells expressed IGF-I mRNA and secreted the growth factor in vitro.
  • This is the first demonstration of IGF-IR expression in a subgroup of CLL patients and of its antiapoptotic effects in vitro, highlighting the importance of this growth factor receptor as a possible therapeutic target in CLL.
  • [MeSH-major] B-Lymphocytes / metabolism. Insulin-Like Growth Factor I / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Receptor, IGF Type 1 / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15982345.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / RNA, Messenger; 67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone; EC 2.7.10.1 / Receptor, IGF Type 1
  •  go-up   go-down


80. Kokhaei P, Palma M, Mellstedt H, Choudhury A: Biology and treatment of chronic lymphocytic leukemia. Ann Oncol; 2005;16 Suppl 2:ii113-23
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biology and treatment of chronic lymphocytic leukemia.

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15958440.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Genetic Markers
  • [Number-of-references] 90
  •  go-up   go-down


81. Booth-Genthe CL, Louie SW, Carlini EJ, Li B, Leake BF, Eisenhandler R, Hochman JH, Mei Q, Kim RB, Rushmore TH, Yamazaki M: Development and characterization of LLC-PK1 cells containing Sprague-Dawley rat Abcb1a (Mdr1a): comparison of rat P-glycoprotein transport to human and mouse. J Pharmacol Toxicol Methods; 2006 Jul-Aug;54(1):78-89
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development and characterization of LLC-PK1 cells containing Sprague-Dawley rat Abcb1a (Mdr1a): comparison of rat P-glycoprotein transport to human and mouse.
  • The contribution of P-glycoprotein-mediated drug transport is being evaluated in early drug discovery stages, particularly for compounds targeted to the central nervous system, using in vitro tools including cell lines expressing P-glycoprotein.
  • The rat Abcb1a form of P-glycoprotein (formerly known as Mdr1a), the predominate isoform in the brain, has not been described in a functional cell system.
  • Here, we describe the development and characterization of LLC-PK1 cells expressing rat Abcb1.
  • METHODS: We cloned rat Abcb1a and generated a stable LLC-PK1 cell line.
  • RESULTS: Two forms of rat Abcb1a were cloned from Sprague-Dawley cDNA that differ by six amino acids and a base pair deletion.
  • The intact form was stably transfected in LLC-PK1 cells.
  • The cells demonstrated P-glycoprotein-mediated function by directional transport of dexamethasone, ritonavir, and vinblastine in a transwell assay that was inhibited in the presence of cyclosporin A, verapamil, or quinidine.
  • [MeSH-major] ATP Binding Cassette Transporter, Sub-Family B / genetics. ATP Binding Cassette Transporter, Sub-Family B / metabolism. ATP-Binding Cassette Transporters / genetics. ATP-Binding Cassette Transporters / metabolism. LLC-PK1 Cells / metabolism

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16545584.001).
  • [ISSN] 1056-8719
  • [Journal-full-title] Journal of pharmacological and toxicological methods
  • [ISO-abbreviation] J Pharmacol Toxicol Methods
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATP Binding Cassette Transporter, Sub-Family B; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / multidrug resistance protein 3
  •  go-up   go-down


82. Haugh M, Stewart R: Optimizing the operation of a high resolution vertical Johann spectrometer using a high energy fluorescer x-ray source. Rev Sci Instrum; 2010 Oct;81(10):10E537
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Optimizing the operation of a high resolution vertical Johann spectrometer using a high energy fluorescer x-ray source.
  • The VJS must have a resolution of E/ΔE=3000 or better to measure the Doppler broadening of highly ionized krypton and operate at a small x-ray angle in order to be used as a diagnostic in a laser plasma target chamber.
  • The VJS was aligned, tested, and optimized using a fluorescer type high energy x-ray (HEX) source located at National Security Technologies (NSTec), LLC, in Livermore, CA.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21034064.001).
  • [ISSN] 1089-7623
  • [Journal-full-title] The Review of scientific instruments
  • [ISO-abbreviation] Rev Sci Instrum
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


83. Tsitsikas DA, Vinicombe S, Sheaff M, Ellis S, Rizvi H, Manuel R, Agrawal SG: A patient with CLL and a dry cough. BMJ; 2010;340:c3051
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A patient with CLL and a dry cough.
  • [MeSH-major] Cough / microbiology. Histoplasmosis / radiography. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Lung Diseases, Fungal / radiography. Multiple Pulmonary Nodules / radiography. Opportunistic Infections / radiography

  • MedlinePlus Health Information. consumer health - Cough.
  • MedlinePlus Health Information. consumer health - Histoplasmosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20591962.001).
  • [ISSN] 1756-1833
  • [Journal-full-title] BMJ (Clinical research ed.)
  • [ISO-abbreviation] BMJ
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  •  go-up   go-down


84. Park HJ, Kim HJ, Park HK, Chung JH: Protective effect of histamine H2 receptor antagonist ranitidine against rotenone-induced apoptosis. Neurotoxicology; 2009 Nov;30(6):1114-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Histamine H(2) receptor antagonists have been reported to improve the motor symptoms of Parkinson's disease (PD) patients and to exert neuroprotective effects.
  • Ranitidine blocked the rotenone-induced phosphorylation of c-Jun NH(2)-terminal protein kinase (JNK) and P38 MAPK (P38), and promoted the phosphorylation of extracellular signal-regulated protein kinase (ERK).
  • Ranitidine also prevented the down-regulation of B-cell CLL/lymphoma 2 (BCL2) and the up-regulation of BCL2-associated X protein (BAX) by rotenone.
  • [MeSH-minor] Analysis of Variance. Caspase 3 / metabolism. Caspase 9 / metabolism. Cell Survival / drug effects. Dose-Response Relationship, Drug. Humans. In Situ Nick-End Labeling. Indoles. JNK Mitogen-Activated Protein Kinases / metabolism. Mitogen-Activated Protein Kinases / metabolism. Neuroblastoma / pathology. Phosphorylation / drug effects. Poly(ADP-ribose) Polymerases / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Up-Regulation / drug effects. bcl-2-Associated X Protein / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism

  • Hazardous Substances Data Bank. RANITIDINE .
  • Hazardous Substances Data Bank. ROTENONE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19723537.001).
  • [ISSN] 1872-9711
  • [Journal-full-title] Neurotoxicology
  • [ISO-abbreviation] Neurotoxicology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Histamine H2 Antagonists; 0 / Indoles; 0 / Insecticides; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; 03L9OT429T / Rotenone; 47165-04-8 / DAPI; 884KT10YB7 / Ranitidine; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9
  •  go-up   go-down


85. Giannopoulos K, Schmitt M, Własiuk P, Chen J, Bojarska-Junak A, Kowal M, Roliñski J, Dmoszyñska A: The high frequency of T regulatory cells in patients with B-cell chronic lymphocytic leukemia is diminished through treatment with thalidomide. Leukemia; 2008 Jan;22(1):222-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The high frequency of T regulatory cells in patients with B-cell chronic lymphocytic leukemia is diminished through treatment with thalidomide.
  • [MeSH-major] Immunosuppressive Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. T-Lymphocytes, Regulatory / immunology. Thalidomide / therapeutic use
  • [MeSH-minor] Adult. Aged. CD4-Positive T-Lymphocytes / metabolism. Female. Forkhead Transcription Factors / metabolism. Humans. Interleukin-2 Receptor alpha Subunit / metabolism. Male. Middle Aged

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, B-cell, chronic.
  • Hazardous Substances Data Bank. THALIDOMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17657216.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Immunosuppressive Agents; 0 / Interleukin-2 Receptor alpha Subunit; 4Z8R6ORS6L / Thalidomide
  •  go-up   go-down


86. Vasilj A, Kojić-Katović S, Maricević I, Zokvić E, Kelcec IB, Tomas D, Curić-Jurić S: Hodgkin's lymphoma variant of Richter's syndrome. Coll Antropol; 2010 Mar;34(1):295-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hodgkin's lymphoma variant of Richter's syndrome.
  • Chronic lymphocytic leukemia/small lymphocitic lymphoma (CLL/SLL) is low-grade malignant lymphoprolipheration, that has tendency to convert to a higher-grade neoplasm over time.
  • More common is the development of a diffuse large cell lymphoma or transformation into prolymphocytic cell population.
  • In rare cases, 0.1-0.5% of patients develop multiple myeloma or Hodgkin's disease.
  • On the basis of clinical simptoms, cytological, hystological and immunohistological finding in April 2008 CLL/SLL were diagnosed.
  • The patient was treated with 8 courses of R-CHOP.
  • The diagnosis was Hodgkin's disease.
  • Immuno-hystological studies of the lymph node was consistent with type I Hodgkin's type of Richter's syndrome.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Hodgkin Disease / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy. Reed-Sternberg Cells / pathology

  • MedlinePlus Health Information. consumer health - Hodgkin Disease.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20437646.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Croatia
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
  •  go-up   go-down


87. Sleep 2009. Abstracts of the 23rd Annual Meeting of the Associated Professional Sleep Societies, LLC. June 6-11, 2009. Seattle, Washington, USA. Sleep; 2009;32 Suppl:A1-427
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sleep 2009. Abstracts of the 23rd Annual Meeting of the Associated Professional Sleep Societies, LLC. June 6-11, 2009. Seattle, Washington, USA.

  • MedlinePlus Health Information. consumer health - Sleep Disorders.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19760817.001).
  • [ISSN] 0161-8105
  • [Journal-full-title] Sleep
  • [ISO-abbreviation] Sleep
  • [Language] eng
  • [Publication-type] Congresses; Overall
  • [Publication-country] United States
  •  go-up   go-down


88. Szmigielska-Kapłon A, Jesionek-Kupnicka D, Góra-Tybor J, Błonski JZ, Lech-Marańda E, Kordek R, Kasznicki M, Robak T: Influence of cladribine alone and in combination with cyclophosphamide or cyclophosphamide and mitoxantrone on bone marrow angiogenesis in chronic lymphocytic leukemia. Leuk Lymphoma; 2007 May;48(5):1042-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Influence of cladribine alone and in combination with cyclophosphamide or cyclophosphamide and mitoxantrone on bone marrow angiogenesis in chronic lymphocytic leukemia.
  • [MeSH-major] Bone Marrow Cells / drug effects. Cladribine / administration & dosage. Cladribine / therapeutic use. Cyclophosphamide / administration & dosage. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Mitoxantrone / administration & dosage. Neovascularization, Pathologic

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Hazardous Substances Data Bank. CLADRIBINE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17487753.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 47M74X9YT5 / Cladribine; 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone
  •  go-up   go-down


89. Steele AJ, Prentice AG, Hoffbrand AV, Yogashangary BC, Hart SM, Lowdell MW, Samuel ER, North JM, Nacheva EP, Chanalaris A, Kottaridis P, Cwynarski K, Wickremasinghe RG: 2-Phenylacetylenesulfonamide (PAS) induces p53-independent apoptotic killing of B-chronic lymphocytic leukemia (CLL) cells. Blood; 2009 Aug 6;114(6):1217-25
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 2-Phenylacetylenesulfonamide (PAS) induces p53-independent apoptotic killing of B-chronic lymphocytic leukemia (CLL) cells.
  • We studied the actions of 2-phenylacetylenesulfonamide (PAS) on B-chronic lymphocytic leukemia (CLL) cells.
  • PAS (5-20 microM) initiated apoptosis within 24 hours, with maximal death at 48 hours asassessed by morphology, cleavage of poly(ADP-ribose) polymerase (PARP), caspase 3 activation, and annexin V staining.
  • PAS treatment of CLL cells failed to up-regulate p53, suggesting that PAS induced apoptosis independently of p53.
  • Furthermore, PAS induced apoptosis in CLL isolates with p53 gene deletion in more than 97% of cells.
  • Normal B lymphocytes were as sensitive to PAS-induced Noxa up-regulation and apoptosis as were CLL cells.
  • However, both T lymphocytes and bone marrow hematopoietic progenitor cells were relatively resistant to PAS.
  • Our data suggest that PAS may represent a novel class of drug that induces apoptosis in CLL cells independently of p53 status by a mechanism involving Noxa up-regulation.
  • [MeSH-major] Antineoplastic Agents / pharmacokinetics. Apoptosis / drug effects. Gene Expression Regulation, Leukemic / drug effects. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. Sulfonamides / pharmacology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Aged. Aged, 80 and over. Annexin A5 / metabolism. Caspase 3 / metabolism. Cytochromes c / metabolism. Cytosol / metabolism. Cytosol / pathology. Dose-Response Relationship, Drug. Drug Resistance / drug effects. Drug Screening Assays, Antitumor. Female. Hematopoietic Stem Cells / metabolism. Hematopoietic Stem Cells / pathology. Humans. Male. Middle Aged. Mitochondria / metabolism. Mitochondria / pathology. Poly(ADP-ribose) Polymerases / metabolism. Protein Transport / drug effects. T-Lymphocytes / metabolism. T-Lymphocytes / pathology. Time Factors. Tumor Cells, Cultured. Up-Regulation / drug effects. bcl-2-Associated X Protein / metabolism

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19515722.001).
  • [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 / Annexin A5; 0 / Antineoplastic Agents; 0 / BAX protein, human; 0 / PMAIP1 protein, human; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Sulfonamides; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; 9007-43-6 / Cytochromes c; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3
  •  go-up   go-down


90. White DH, Chapman PT, O'Donnell JL, James J, Frampton C, Stamp LK: Lack of association between elevated mean red cell volume and haematological toxicity in patients receiving long-term methotrexate for rheumatoid arthritis. Intern Med J; 2010 Aug;40(8):561-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lack of association between elevated mean red cell volume and haematological toxicity in patients receiving long-term methotrexate for rheumatoid arthritis.
  • AIMS: It has been suggested that elevated mean red cell volume (MCV) may be a predictor of haematological toxicity in rheumatoid arthritis (RA) patients receiving methotrexate (MTX).
  • We wished to identify whether there was an association between MCV, red cell folate and haematological toxicity in patients on MTX monotherapy for the long-term management of RA.
  • METHODS: Evidence of haematological toxicity was sought by note review of patients recruited in a cross-sectional study of MTX monotherapy in RA.
  • Any record of cytopenia or the development of haematological malignancy was recorded from commencement of MTX until the present day.
  • Red cell folate concentrations were tested on enrolment to the study.
  • RESULTS: A total of 165 patients was included, 74.5% female, median disease duration 7 years (range 3 months-57 years).
  • Evidence of haematological abnormality was found in six patients (3.6%); chronic lymphocytic leukaemia (1), persistent lymphocytosis (1), persistent monocytosis (1) and neutropenia (3).
  • There was no association between red cell folate or MCV and haematological toxicity.
  • Elevated MCV or low mean red cell folate does not appear to be associated with haematological malignancy or toxicity in this cohort of patients on long-term MTX therapy.


91. Kretz-Rommel A, Qin F, Dakappagari N, Cofiell R, Faas SJ, Bowdish KS: Blockade of CD200 in the presence or absence of antibody effector function: implications for anti-CD200 therapy. J Immunol; 2008 Jan 15;180(2):699-705
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CD200 is an immunosuppressive molecule overexpressed in multiple hematologic malignancies such as B cell chronic lymphocytic leukemia, multiple myeloma, and acute myeloid leukemia.
  • Ab variants with effector function (IgG1 constant region (G1)) or without effector function (IgG2/G4 fusion constant region (G2G4)) exhibited high antitumor activity in a human tumor xenograft model in which CD200 was expressed.
  • In this report, we seek to select the best candidate to move forward into the clinic and begin to decipher the mechanisms of tumor cell killing by comparing anti-CD200-G1 vs anti-CD200-G2G4 in two related animal models.
  • In a CD200-expressing xenograft NOD/SCID hu-mouse model where CD200 ligand/receptor interactions are already established before initiating treatment, we find that anti-CD200-G1 is a less effective Ab compared with anti-CD200-G2G4.
  • Separately, in a model that evaluates the effect of the Abs on the immune cell component of the xenograft NOD/SCID hu-mouse model distinctly from the effects of binding to CD200 on tumor cells, we find that the administration of anti-CD200-G1 Abs completely abolished human PBMC-mediated tumor growth inhibition.
  • [MeSH-minor] Animals. Humans. Mice. Mice, Inbred Strains. T-Lymphocytes / immunology. Xenograft Model Antitumor Assays

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18178807.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / antigens, CD200
  •  go-up   go-down


92. Takhampunya R, Ubol S, Houng HS, Cameron CE, Padmanabhan R: Inhibition of dengue virus replication by mycophenolic acid and ribavirin. J Gen Virol; 2006 Jul;87(Pt 7):1947-52
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The effects of mycophenolic acid (MPA) and ribavirin (RBV) on DEN replication in monkey kidney (LLC-MK2) cells were examined.
  • [MeSH-minor] Animals. Cell Line. Haplorhini. Humans. RNA Replicase / metabolism. RNA, Viral / biosynthesis. RNA, Viral / genetics

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. MYCOPHENOLATE MOFETIL .
  • Hazardous Substances Data Bank. RIBAVIRIN .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16760396.001).
  • [ISSN] 0022-1317
  • [Journal-full-title] The Journal of general virology
  • [ISO-abbreviation] J. Gen. Virol.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI-32078; United States / NIAID NIH HHS / AI / U01 AI 54776
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / RNA, Viral; 49717AWG6K / Ribavirin; EC 2.7.7.48 / RNA Replicase; HU9DX48N0T / Mycophenolic Acid
  •  go-up   go-down


93. Ulmer A, Metzler G, Schanz S, Fierlbeck G: Dapsone in the management of "insect bite-like reaction" in a patient with chronic lymphocytic leukaemia. Br J Dermatol; 2007 Jan;156(1):172-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dapsone in the management of "insect bite-like reaction" in a patient with chronic lymphocytic leukaemia.
  • [MeSH-major] Dapsone / therapeutic use. Dermatologic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Skin Neoplasms / drug therapy

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • Hazardous Substances Data Bank. DAPSONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17199590.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dermatologic Agents; 8W5C518302 / Dapsone
  •  go-up   go-down


94. Dong XP, Xiao TH, Meng LB, Yun CH, Tian H: [Effects of endostatin on the growth and lymphangiogenesis of Lewis lung carcinoma xenograft in mice]. Zhonghua Yi Xue Za Zhi; 2010 Nov 23;90(43):3091-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: to investigate the effects of endostar, a recombined humanized endostatin, on the growth, lymphangiogenesis and lymphatic metastasis of Lewis lung carcinoma xenograft in mice.
  • METHODS: lewis lung carcinoma (LLC) xenograft were established in C57 mice by intravenous transplantation of 1 × 10(6) cells.
  • Six weeks after LLC cell injection mice were sacrificed, and then tumor numbers and size were recorded.
  • Lymphatic metastases were more frequent in control group than in treatment group.
  • Expression of VEGF-C in control group was significantly higher than that in treatment group.
  • CONCLUSION: endostar significantly inhibits the growth, lymphangiogenesis and lymphatic metastasis of Lewis lung carcinoma xenografts, and the inhibitory effect is due to its ability to regulate the expression of VEGF-C of tumors in part.
  • [MeSH-major] Carcinoma, Lewis Lung / pathology. Endostatins / pharmacology. Lymphangiogenesis / drug effects. Lymphatic Metastasis / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21211334.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Endostatins; 0 / Vascular Endothelial Growth Factor C; 0 / vascular endothelial growth factor C, mouse
  •  go-up   go-down


95. Wei C, Farkas T, Sestak K, Jiang X: Recovery of infectious virus by transfection of in vitro-generated RNA from tulane calicivirus cDNA. J Virol; 2008 Nov;82(22):11429-36
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The virus has been cultivated successfully in LLC-MK2 rhesus monkey kidney cells.
  • In this study, we demonstrated that RNA transcripts made in vitro from the full-length genomic cDNA of TV were infectious upon transfection into permissive LLC-MK2 cells.
  • The recombinant virus exhibited plaque morphologies and growth kinetics similar to those of the wild-type virus in this cell line.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Infect Dis. 2000 May;181 Suppl 2:S322-30 [10804145.001]
  • [Cites] J Virol. 2006 Jul;80(13):6597-602 [16775346.001]
  • [Cites] J Virol. 2002 Oct;76(20):10089-98 [12239283.001]
  • [Cites] J Virol. 2003 Feb;77(4):2789-98 [12552024.001]
  • [Cites] Infect Immun. 2003 Jul;71(7):4079-86 [12819098.001]
  • [Cites] J Virol. 2003 Nov;77(21):11790-7 [14557663.001]
  • [Cites] Arch Virol. 2006 Jul;151(7):1291-308 [16502284.001]
  • [Cites] Virology. 2006 Sep 30;353(2):463-73 [16843517.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jun 26;104(26):11050-5 [17581883.001]
  • [Cites] J Gen Virol. 2007 Aug;88(Pt 8):2091-100 [17622609.001]
  • [Cites] Emerg Infect Dis. 2007 Jul;13(7):1071-3 [18214183.001]
  • [Cites] J Virol. 2008 Jun;82(11):5408-16 [18385231.001]
  • [Cites] J Virol. 2003 Dec;77(23):12562-71 [14610179.001]
  • [Cites] J Med Primatol. 2004 Feb;33(1):30-3 [15061730.001]
  • [Cites] J Virol. 2004 May;78(9):4827-37 [15078964.001]
  • [Cites] Virology. 1993 Jul;195(1):51-61 [8391187.001]
  • [Cites] Virology. 1995 Jul 10;210(2):383-90 [7618275.001]
  • [Cites] Arch Virol. 1998;143(6):1215-21 [9687878.001]
  • [Cites] J Virol. 1999 Jan;73(1):819-25 [9847396.001]
  • [Cites] Virology. 1999 Feb 1;254(1):1-5 [9927568.001]
  • [Cites] J Virol. 2005 Feb;79(3):1409-16 [15650167.001]
  • [Cites] J Virol. 2005 Apr;79(7):4012-24 [15767403.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jul 19;102(29):10327-32 [16002473.001]
  • [Cites] Virology. 2006 Mar 15;346(2):312-23 [16343580.001]
  • [Cites] Virology. 2006 Jun 20;350(1):240-50 [16574184.001]
  • [Cites] J Virol. 2002 Jun;76(12):6398-407 [12021375.001]
  • (PMID = 18787011.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI55649; United States / NCRR NIH HHS / RR / R21 RR024871-01; United States / NCRR NIH HHS / RR / RR024871-01; United States / NIAID NIH HHS / AI / R01 AI055649; United States / NICHD NIH HHS / HD / P01 HD013021; United States / NIAID NIH HHS / AI / R01 AI37093; United States / NIAID NIH HHS / AI / R01 AI037093; United States / NCRR NIH HHS / RR / R21 RR024871
  • [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] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / RNA Caps; 0 / RNA, Viral
  • [Other-IDs] NLM/ PMC2573278
  •  go-up   go-down


96. Yegin ZA, Ozkurt ZN, Yağci M: Free light chain: a novel predictor of adverse outcome in chronic lymphocytic leukemia. Eur J Haematol; 2010 May;84(5):406-11
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Free light chain: a novel predictor of adverse outcome in chronic lymphocytic leukemia.
  • OBJECTIVES: Chronic lymphocytic leukemia (CLL) is characterized by a highly variable clinical course.
  • This retrospective study is planned to assess the prognostic value of serum free light chain (sFLC) levels and FLC ratio (FLCR) in CLL.
  • METHODS: Quantitative levels of sFLC were measured nephelometrically in sera collected at diagnosis.
  • RESULTS: In a cohort of 101 patients with a median follow-up of 29 (1-234) months, sFLC levels were found to be high in 55 patients (54.5%).
  • FISH-based genetic risk groups did not differ significantly with respect to sFLC and FLCR (P > 0.05).
  • Median overall survival (OS) was shorter in patients with high sFLC levels (P = 0.01) and abnormal FLCR (P = 0.05).
  • In patients with early stage disease, median OS was shorter in high sFLC (P = 0.03) and abnormal FLCR groups (P = 0.048).
  • CONCLUSIONS: This study highlighted the adverse prognostic impact of high sFLC levels and abnormal FLCR with regard to survival in CLL, even in early stage patients.
  • [MeSH-major] Immunoglobulin Light Chains / blood. Leukemia, Lymphocytic, Chronic, B-Cell / immunology

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20059535.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Light Chains
  •  go-up   go-down


97. Omoti AE, Omoti CE, Momoh RO: Ocular disorders in adult leukemia patients in Nigeria. Middle East Afr J Ophthalmol; 2010 Apr;17(2):165-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ocular disorders in adult leukemia patients in Nigeria.
  • CONTEXT: Leukemias may present with, or be associated with ocular disorders.
  • AIMS: To determine the rates of ophthalmic disorders in adult patients with leukemia.
  • SETTINGS AND DESIGN: A prospective study of ocular disorders in adult patients with leukemia at the University of Benin Teaching Hospital, Benin City, Nigeria, between July 2004 and June 2008 was conducted.
  • RESULTS: Forty-seven patients with leukemias were seen.
  • Nineteen patients (40.4%) had CLL, 14(29.8%) had CML, 9(19.1%) had AML and 5(10.6%) had ALL.
  • Seven patients (14.9%) had ocular disorders due to leukemia.
  • The ocular disorders due to the leukemia were proptosis in two patients (4.3%), retinopathy in one patient (2.1%), conjunctival infiltration in one patient (2.1%), periorbital edema in one patient (2.1%), retinal detachment in one patient (2.1%), and subconjunctival hemorrhage in one patient (2.1%).
  • There was no significant difference in rate of the ocular disorders in the various types of leukemia (Kruskal-Wallis KW= 4.019; corrected for ties. P=0.2595).
  • CONCLUSIONS: Ophthalmic disorders that are potentially blinding occur in leukemias.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Eye (Lond). 2004 Jul;18(7):663-72 [15002029.001]
  • [Cites] Med J Malaysia. 2003 Oct;58(4):546-55 [15190631.001]
  • [Cites] Clin Lab Haematol. 2005 Oct;27(5):302-6 [16178909.001]
  • [Cites] Int J Lab Hematol. 2007 Dec;29(6):426-32 [17988297.001]
  • [Cites] Eur J Ophthalmol. 2008 Jul-Aug;18(4):619-23 [18609485.001]
  • [Cites] Trans Am Ophthalmol Soc. 1978;76:90-101 [289224.001]
  • [Cites] Ophthalmologica. 2003 Nov-Dec;217(6):441-5 [14573980.001]
  • [Cites] Ethiop Med J. 1996 Oct;34(4):217-24 [9164037.001]
  • [Cites] Klin Monbl Augenheilkd. 1998 Jun;212(6):419-27 [9715461.001]
  • [Cites] J Fr Ophtalmol. 2002 Jan;25(1):62-6 [11965121.001]
  • [Cites] Eye (Lond). 2003 Jan;17(1):27-30 [12579166.001]
  • [Cites] Leuk Res. 2003 Jun;27(6):557-9 [12648516.001]
  • [Cites] Clin Lab Haematol. 1991;13(2):217-20 [1934932.001]
  • (PMID = 20616925.001).
  • [ISSN] 0975-1599
  • [Journal-full-title] Middle East African journal of ophthalmology
  • [ISO-abbreviation] Middle East Afr J Ophthalmol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2892134
  • [Keywords] NOTNLM ; Leukemia / Ocular Disorders / Proptosis / Retinal Detachment
  •  go-up   go-down


98. Pratt G, Fenton JA, Allsup D, Fegan C, Morgan GJ, Jackson G, Sunter NJ, Hall AG, Irving JA, Allan JM: A polymorphism in the 3' UTR of IRF4 linked to susceptibility and pathogenesis in chronic lymphocytic leukaemia and Hodgkin lymphoma has limited impact in multiple myeloma. Br J Haematol; 2010 Aug;150(3):371-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A polymorphism in the 3' UTR of IRF4 linked to susceptibility and pathogenesis in chronic lymphocytic leukaemia and Hodgkin lymphoma has limited impact in multiple myeloma.
  • [MeSH-minor] Aged. Female. Genetic Predisposition to Disease. Hodgkin Disease / genetics. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Male. Middle Aged. Polymorphism, Single Nucleotide

  • Genetic Alliance. consumer health - Hodgkin lymphoma.
  • Genetic Alliance. consumer health - Multiple myeloma.
  • MedlinePlus Health Information. consumer health - Multiple Myeloma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20408839.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interferon Regulatory Factors; 0 / Neoplasm Proteins; 0 / interferon regulatory factor-4
  •  go-up   go-down


99. Catovsky D: The changing face of chronic lymphocytic leukemia. Leuk Lymphoma; 2007 Dec;48(12):2283-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The changing face of chronic lymphocytic leukemia.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18066986.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region
  •  go-up   go-down


100. Robak P, Linke A, Cebula B, Robak T, Smolewski P: Cytotoxic effect of R-etodolac (SDX-101) in combination with purine analogs or monoclonal antibodies on ex vivo B-cell chronic lymphocytic leukemia cells. Leuk Lymphoma; 2006 Dec;47(12):2625-34
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytotoxic effect of R-etodolac (SDX-101) in combination with purine analogs or monoclonal antibodies on ex vivo B-cell chronic lymphocytic leukemia cells.
  • R-etodolac (SDX-101) is an isoform of the non-steroidal anti-inflammatory drug, etodolac, and is currently being tested in phase II clinical trials for the treatment of refractory B-cell chronic lymphocytic leukemia (B-CLL).
  • The aim of this study was to evaluate the cytotoxicity of SDX-101 combined with agents proven to be effective as first-line treatment of B-CLL: the purine nucleoside analogs, fludarabine (FA) and cladribine (2-CdA), and the monoclonal antibodies, anti-CD52 (alemtuzumab;.
  • The cytotoxicity and specific pro-apoptotic effects of the study drugs on B-CLL cells were assessed in vitro in samples from overall 37 untreated patients.
  • The combinations of SDX-101 with 2-CdA, FA or RIT exerted additive effects in B-CLL cells, with the following combination indices (CI): 0.89 for SDX-101 + 2-CdA, 0.95 for SDX-101 + RIT, and 1.17 for SDX-101 + FA.
  • In conclusion, these data obtained in vitro indicate that addition of 2-CdA, FA or RIT to SDX-101 significantly enhance cytotoxicity in B-CLL cells.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / administration & dosage. Antibodies, Monoclonal / administration & dosage. Etodolac / administration & dosage. Leukemia, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukocytes, Mononuclear / drug effects. Purines / chemistry
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antibodies, Monoclonal, Murine-Derived. Antibodies, Neoplasm / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Line, Tumor. Cladribine / administration & dosage. Humans. Rituximab. Spectrometry, Fluorescence / methods. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, B-cell, chronic.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. CLADRIBINE .
  • Hazardous Substances Data Bank. VIDARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Leuk Lymphoma. 2006 Dec;47(12):2445-6 [17169789.001]
  • (PMID = 17169808.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 0 / Purines; 2M36281008 / Etodolac; 3A189DH42V / alemtuzumab; 47M74X9YT5 / Cladribine; 4F4X42SYQ6 / Rituximab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  •  go-up   go-down






Advertisement