[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 9871
6. Hillmen P: Chronic lymphocytic leukemia--aiming at a moving target! Haematologica; 2005 Nov;90(11):1451-2
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] Chronic lymphocytic leukemia--aiming at a moving target!
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / therapy

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Haematologica. 2005 Nov;90(11):1533-40 [16266901.001]
  • (PMID = 16266890.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Genetic Markers
  •  go-up   go-down


7. Frazer R, Irvine AE, McMullin MF: Chronic Myeloid Leukaemia in The 21st Century. Ulster Med J; 2007 Jan;76(1):8-17
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] Chronic Myeloid Leukaemia in The 21st Century.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive
  • [MeSH-minor] Cytogenetic Analysis / methods. Global Health. Humans. Immunosuppression / methods. Incidence. Molecular Diagnostic Techniques / methods. Prognosis. Stem Cell Transplantation / methods. Transplantation, Homologous

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Leukemia. 2003 May;17(5):829-38 [12750693.001]
  • [Cites] Br J Haematol. 2003 Mar;120(6):990-9 [12648069.001]
  • [Cites] N Engl J Med. 2003 Oct 9;349(15):1399-401 [14534331.001]
  • [Cites] N Engl J Med. 2003 Oct 9;349(15):1451-64 [14534339.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2003;:132-52 [14633780.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2003;:279-93 [14633786.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2392-400 [14523462.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2474-86 [14562124.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2318-57 [14562125.001]
  • [Cites] Blood. 2004 Jan 15;103(2):451-5 [14512312.001]
  • [Cites] Leuk Res. 2004 May;28 Suppl 1:S39-45 [15036940.001]
  • [Cites] Leukemia. 2004 Apr;18(4):864-71 [14973502.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1597-600 [15084690.001]
  • [Cites] Oncologist. 2004;9(3):259-70 [15169981.001]
  • [Cites] Oncologist. 2004;9(3):271-81 [15169982.001]
  • [Cites] Science. 2004 Jul 16;305(5682):399-401 [15256671.001]
  • [Cites] Leukemia. 2004 Aug;18(8):1321-31 [15215876.001]
  • [Cites] Hematol Oncol Clin North Am. 2004 Jun;18(3):569-84, viii [15271393.001]
  • [Cites] Hematol Oncol Clin North Am. 2004 Jun;18(3):605-17, viii [15271395.001]
  • [Cites] Hematol Oncol Clin North Am. 2004 Jun;18(3):619-39, ix [15271396.001]
  • [Cites] Hematol Oncol Clin North Am. 2004 Jun;18(3):641-56, ix [15271397.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2926-32 [15256429.001]
  • [Cites] Blood. 1999 Jun 15;93(12):4149-53 [10361112.001]
  • [Cites] N Engl J Med. 1999 Jul 15;341(3):164-72 [10403855.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2004;:146-62 [15561681.001]
  • [Cites] Cancer Cell. 2005 Feb;7(2):117-9 [15710324.001]
  • [Cites] Leukemia. 2005 Nov;19(11):1872-9 [16179913.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2005;:174-82 [16304377.001]
  • [Cites] Biochim Biophys Acta. 2005 Dec 30;1754(1-2):3-13 [16172030.001]
  • [Cites] Curr Opin Genet Dev. 2006 Feb;16(1):92-9 [16343892.001]
  • [Cites] JAMA. 2006 Jan 25;295(4):369-70 [16434621.001]
  • [Cites] Crit Rev Oncol Hematol. 2006 Feb;57(2):145-64 [16213151.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1582-90 [16249384.001]
  • [Cites] Br J Cancer. 2006 Jun 19;94(12):1765-9 [16721371.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2531-41 [16775234.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2542-51 [16775235.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2594-6 [16775240.001]
  • [Cites] Blood. 2006 Jul 1;108(1):28-37 [16522812.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1328-33 [16614241.001]
  • [Cites] Blood. 2000 Jan 1;95(1):62-6 [10607685.001]
  • [Cites] Blood. 2000 Feb 1;95(3):1014-22 [10648417.001]
  • [Cites] J Clin Oncol. 2000 Oct 15;18(20):3513-21 [11032593.001]
  • [Cites] Cell. 2000 Oct 13;103(2):211-25 [11057895.001]
  • [Cites] Blood. 2000 Nov 15;96(10):3343-56 [11071626.001]
  • [Cites] Blood. 2001 Apr 1;97(7):1999-2007 [11264164.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1031-7 [11287972.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1084-6 [11287980.001]
  • [Cites] Science. 2001 Aug 3;293(5531):876-80 [11423618.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1701-7 [11535500.001]
  • [Cites] J Clin Oncol. 2002 Jan 1;20(1):325-34 [11773186.001]
  • [Cites] Leukemia. 2002 Jan;16(1):53-9 [11840263.001]
  • [Cites] N Engl J Med. 2002 Feb 28;346(9):645-52 [11870241.001]
  • [Cites] N Engl J Med. 2002 Feb 28;346(9):683-93 [11870247.001]
  • [Cites] J Clin Oncol. 2002 May 1;20(9):2334-43 [11981005.001]
  • [Cites] Biochim Biophys Acta. 2002 Jun 21;1602(2):114-30 [12020799.001]
  • [Cites] Leukemia. 2002 Sep;16(9):1579-83 [12200666.001]
  • [Cites] Br J Haematol. 2002 Oct;119(1):15-24 [12358949.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2002;:111-35 [12446421.001]
  • [Cites] N Engl J Med. 2003 Mar 13;348(11):994-1004 [12637609.001]
  • [Cites] N Engl J Med. 2003 Mar 13;348(11):1048-50 [12637616.001]
  • [Cites] Blood. 2003 Jul 1;102(1):276-83 [12623848.001]
  • (PMID = 17288299.001).
  • [ISSN] 0041-6193
  • [Journal-full-title] The Ulster medical journal
  • [ISO-abbreviation] Ulster Med J
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Northern Ireland
  • [Number-of-references] 62
  • [Other-IDs] NLM/ PMC1940291
  •  go-up   go-down


8. Davidovich T, Rimbroth S, Chazan B, Colodner R, Markel A: Recurrent septicemia and osteomyelitis caused by Pasteurella multocida in a patient with chronic lymphatic leukemia. Isr Med Assoc J; 2008 Aug-Sep;10(8-9):653-4
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] Recurrent septicemia and osteomyelitis caused by Pasteurella multocida in a patient with chronic lymphatic leukemia.
  • [MeSH-major] Immunocompromised Host. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Osteomyelitis / microbiology. Pasteurella Infections / diagnosis. Pasteurella multocida. Sepsis / microbiology

  • Genetic Alliance. consumer health - Osteomyelitis.
  • MedlinePlus Health Information. consumer health - Sepsis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Isr Med Assoc J. 2008 Aug-Sep;10(8-9):648-9 [18847171.001]
  • (PMID = 18847173.001).
  • [ISSN] 1565-1088
  • [Journal-full-title] The Israel Medical Association journal : IMAJ
  • [ISO-abbreviation] Isr. Med. Assoc. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Israel
  •  go-up   go-down


9. Mato AR, Luger SM: Autologous stem cell transplant in ALL: who should we be transplanting in first remission? Bone Marrow Transplant; 2006 Jun;37(11):989-95
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] Autologous stem cell transplant in ALL: who should we be transplanting in first remission?
  • Long-term disease-free survival (DFS) has been reported after autologous stem cell transplantation for acute lymphoblastic leukemia.
  • Phase II studies have evaluated its role in first and subsequent complete remission (CR) with DFS rates of up to 50%.
  • It has been under-utilized in 1st CR in part, due to a concern that patients who relapse after autologous stem cell transplantation (ASCT) have fewer options for salvage treatment of relapsed disease.
  • Unfortunately, survival rates of <5% are reported in patients who relapse, regardless of initial therapy.
  • Factors such as risk features at diagnosis, and minimal residual disease following induction therapy greatly affect outcome following ASCT.
  • The available data as well as the questions that remain to be answered will be discussed and reviewed.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Stem Cell Transplantation
  • [MeSH-minor] Bone Marrow Purging. Clinical Trials as Topic. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Neoplasm, Residual. Patient Selection. Recurrence. Remission Induction. Transplantation, Autologous. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16633362.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 41
  •  go-up   go-down


10. Deriano L, Guipaud O, Merle-Béral H, Binet JL, Ricoul M, Potocki-Veronese G, Favaudon V, Maciorowski Z, Muller C, Salles B, Sabatier L, Delic J: Human chronic lymphocytic leukemia B cells can escape DNA damage-induced apoptosis through the nonhomologous end-joining DNA repair pathway. Blood; 2005 Jun 15;105(12):4776-83
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] Human chronic lymphocytic leukemia B cells can escape DNA damage-induced apoptosis through the nonhomologous end-joining DNA repair pathway.
  • The B cells of some B-chronic lymphocytic leukemia (B-CLL) patients are resistant to radiation-induced apoptosis in vitro.
  • We found that at 15 minutes after irradiation, the levels of NHEJ (as measured by an in vitro DSB end-ligation assay) and DNA-PK catalytic subunit (DNA-PKcs) activity were, respectively, 2-fold and 4-fold higher in radio-resistant than in radio-sensitive B-CLL cells or Epstein-Barr virus (EBV)-transformed B cells.
  • Ku70/Ku80 heterodimer DNA end-binding activity was also 2- to 3-fold higher in the resistant B-CLL cell subset compared with the sensitive B-CLL cell subset.
  • [MeSH-major] Apoptosis. DNA Repair. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / pathology
  • [MeSH-minor] Androstadienes / pharmacology. Antibiotics, Antineoplastic / pharmacology. Antigens, Nuclear / metabolism. Antineoplastic Agents, Phytogenic / pharmacology. B-Lymphocytes / pathology. Blotting, Western. Cell Line, Transformed. Cell Line, Tumor. Cell-Free System. Chromones / pharmacology. DNA / metabolism. DNA Damage. DNA-Binding Proteins / metabolism. Dimerization. Dose-Response Relationship, Drug. Enzyme Inhibitors / pharmacology. Etoposide / pharmacology. Gamma Rays. Humans. Morpholines / pharmacology. Okadaic Acid / pharmacology. Phosphatidylinositol 3-Kinases / pharmacology. Protein Binding. Telomere / ultrastructure. Time Factors. Zinostatin / pharmacology

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. OKADAIC ACID .
  • 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 = 15718417.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(morpholin-4-yl)benzo(h)chromen-4-one; 0 / Androstadienes; 0 / Antibiotics, Antineoplastic; 0 / Antigens, Nuclear; 0 / Antineoplastic Agents, Phytogenic; 0 / Chromones; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / Ku autoantigen; 0 / Morpholines; 1W21G5Q4N2 / Okadaic Acid; 6PLQ3CP4P3 / Etoposide; 9007-49-2 / DNA; 9014-02-2 / Zinostatin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; XVA4O219QW / wortmannin
  •  go-up   go-down


11. Eun YG, Park DC, Kim SG, Kim MG, Yeo SG: Immunoglobulins and transcription factors in adenoids of children with otitis media with effusion and chronic rhinosinusitis. Int J Pediatr Otorhinolaryngol; 2009 Oct;73(10):1412-6
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] Immunoglobulins and transcription factors in adenoids of children with otitis media with effusion and chronic rhinosinusitis.
  • METHODS: The study population consisted of 30 children with otitis media with effusion (OME), 22 children with chronic rhinosinusitis (CRS) and 27 children with adenoid hyperplasia.
  • We also compared the levels of expression of B lymphocyte inducer of maturation program 1 (BLIMP-1), a promoter of plasmacytosis, and B cell leukemia/lymphoma-6 (BCL-6), a repressor of plasmacytosis, in the adenoids of these children.
  • RESULTS: The expression of antibody to Ig A in the OME and CRS groups each was significantly lower than the score in the adenoid hyperplasia group.
  • The staining scores of antibodies to IgG, IgD and Ig M did not differ significantly among the three groups.
  • Staining scores of Antibody to BCL-6 did not differ significantly among the three groups.
  • [MeSH-minor] Biomarkers / metabolism. Chi-Square Distribution. Child. Child, Preschool. Chronic Disease. Cohort Studies. Female. Follow-Up Studies. Humans. Hyperplasia / immunology. Hyperplasia / pathology. Incidence. Male. Republic of Korea. Risk Assessment. Sensitivity and Specificity. Severity of Illness Index. Statistics, Nonparametric

  • MedlinePlus Health Information. consumer health - Adenoids.
  • MedlinePlus Health Information. consumer health - Sinusitis.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19674797.001).
  • [ISSN] 1872-8464
  • [Journal-full-title] International journal of pediatric otorhinolaryngology
  • [ISO-abbreviation] Int. J. Pediatr. Otorhinolaryngol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Immunoglobulins; 0 / Transcription Factors
  •  go-up   go-down


12. Burger JA, Quiroga MP, Hartmann E, Bürkle A, Wierda WG, Keating MJ, Rosenwald A: High-level expression of the T-cell chemokines CCL3 and CCL4 by chronic lymphocytic leukemia B cells in nurselike cell cocultures and after BCR stimulation. Blood; 2009 Mar 26;113(13):3050-8
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] High-level expression of the T-cell chemokines CCL3 and CCL4 by chronic lymphocytic leukemia B cells in nurselike cell cocultures and after BCR stimulation.
  • In lymphatic tissues, chronic lymphocytic leukemia (CLL) cells are interspersed with CD68(+) nurselike cells (NLCs), T cells, and other stromal cells that constitute the leukemia microenvironment.
  • However, the mechanism regulating colocalization of CLL and these accessory cells are largely unknown.
  • To dissect the molecular cross talk between CLL and NLCs, we profiled the gene expression of CD19-purified CLL cells before and after coculture with NLCs.
  • NLC coculture induced high-level expression of B-cell maturation antigen and 2 chemoattractants (CCL3, CCL4) by CLL cells.
  • CCL3/CCL4 induction in NLC cocultures correlated with ZAP-70 expression by CLL cells.
  • High CCL3/CCL4 protein levels were found in CLL cocultures with NLCs, and CCL3/CCL4 induction was abrogated by R406, a Syk inhibitor, suggesting that NLCs induce these chemokines via B-cell receptor (BCR) activation.
  • BCR triggering also caused robust CCL3/CCL4 protein secretion by CLL cells.
  • High CCL3 and CCL4 plasma levels in CLL patients suggest that this pathway plays a role in vivo.
  • These studies reveal a novel mechanism of cross talk between CLL cells and their microenvironment, namely, the secretion of 2 T-cell chemokines in response to NLC coculture and BCR stimulation.
  • Through these chemokines, CLL cells can recruit accessory cells and thereby actively create a supportive microenvironment.
  • [MeSH-major] B-Lymphocytes / metabolism. Chemokine CCL3 / genetics. Chemokine CCL4 / genetics. Leukemia, Myeloid / genetics. Lymphocyte Activation / physiology
  • [MeSH-minor] Antibodies, Anti-Idiotypic / pharmacology. Coculture Techniques / methods. Culture Media, Conditioned / chemistry. Culture Media, Conditioned / metabolism. Gene Expression Profiling. Gene Expression Regulation, Leukemic / drug effects. Humans. Oligonucleotide Array Sequence Analysis. Proto-Oncogene Proteins c-bcr / metabolism. T-Lymphocytes / metabolism. Tumor Cells, Cultured. Up-Regulation / drug effects. ZAP-70 Protein-Tyrosine Kinase / genetics. ZAP-70 Protein-Tyrosine Kinase / metabolism

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, T-cell, chronic.
  • 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] Blood. 1983 Dec;62(6):1289-96 [6357309.001]
  • [Cites] Blood. 2005 Sep 1;106(5):1824-30 [15905192.001]
  • [Cites] J Exp Med. 1995 May 1;181(5):1661-72 [7722446.001]
  • [Cites] Annu Rev Immunol. 2003;21:231-64 [12427767.001]
  • [Cites] Eur J Immunol. 2002 May;32(5):1403-13 [11981828.001]
  • [Cites] Blood. 2005 Sep 15;106(6):2169-74 [15933054.001]
  • [Cites] Blood. 2008 May 1;111(9):4764-70 [18174380.001]
  • [Cites] J Immunol. 1999 Apr 15;162(8):4455-63 [10201982.001]
  • [Cites] Eur J Immunol. 1995 Jan;25(1):64-8 [7531149.001]
  • [Cites] Nature. 1980 Jan 24;283(5745):402-4 [6965423.001]
  • [Cites] Blood. 2001 May 1;97(9):2777-83 [11313271.001]
  • [Cites] Br J Haematol. 1996 Jan;92(1):97-103 [8562418.001]
  • [Cites] J Histochem Cytochem. 1980 Aug;28(8):746-60 [7003001.001]
  • [Cites] Hum Pathol. 2006 Feb;37(2):152-9 [16426914.001]
  • [Cites] N Engl J Med. 2005 Feb 24;352(8):804-15 [15728813.001]
  • [Cites] Science. 1993 Apr 16;260(5106):355-8 [7682337.001]
  • [Cites] Blood. 2003 Jun 15;101(12):4998-5006 [12623842.001]
  • [Cites] J Immunol. 2006 May 15;176(10 ):5715-9 [16670274.001]
  • [Cites] J Exp Med. 1993 Jun 1;177(6):1821-6 [7684437.001]
  • [Cites] J Immunol. 2007 Dec 1;179(11):7276-86 [18025170.001]
  • [Cites] Leuk Lymphoma. 2004 Dec;45(12):2365-72 [15621749.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2655-63 [11023495.001]
  • [Cites] Blood. 2002 Mar 15;99(6):2277-8 [11902141.001]
  • [Cites] Leukemia. 1999 Dec;13(12):1954-9 [10602415.001]
  • [Cites] N Engl J Med. 2004 Nov 18;351(21):2159-69 [15548776.001]
  • [Cites] Clin Immunol. 2001 Jan;98(1):39-45 [11141325.001]
  • [Cites] Blood. 2005 Apr 15;105(8):3042-50 [15613544.001]
  • [Cites] Nature. 2006 Apr 13;440(7086):890-5 [16612374.001]
  • [Cites] Blood. 2002 Feb 1;99(3):1030-7 [11807009.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jun 8;96(12):6873-8 [10359806.001]
  • [Cites] Blood. 1999 Dec 1;94(11):3658-67 [10572077.001]
  • [Cites] Cytokine Growth Factor Rev. 2002 Dec;13(6):455-81 [12401480.001]
  • [Cites] Br J Haematol. 2003 Nov;123(3):380-8 [14616995.001]
  • [Cites] Blood. 2008 Jan 15;111(2):846-55 [17928528.001]
  • [Cites] Hum Pathol. 1999 Jun;30(6):648-54 [10374772.001]
  • [Cites] Cancer Res. 2006 Jul 15;66(14):7158-66 [16849562.001]
  • [Cites] Nature. 1998 Feb 19;391(6669):799-803 [9486651.001]
  • [Cites] Blood. 2000 Jul 15;96(2):671-5 [10887133.001]
  • [Cites] Blood. 2008 May 15;111(10):5173-81 [18326821.001]
  • [Cites] Blood. 2005 Aug 1;106(3):1012-20 [15860672.001]
  • [Cites] N Engl J Med. 2004 Aug 26;351(9):893-901 [15329427.001]
  • [Cites] Mol Cancer Ther. 2006 Dec;5(12):3113-21 [17172414.001]
  • [Cites] Blood. 2005 Mar 1;105(5):2036-41 [15514014.001]
  • [Cites] Cell. 1999 Jan 8;96(1):5-8 [9989491.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1795-801 [12176902.001]
  • [Cites] Eur J Immunol. 1999 May;29(5):1617-25 [10359116.001]
  • [Cites] Science. 2001 Sep 14;293(5537):2111-4 [11509691.001]
  • [Cites] Blood. 1998 Apr 1;91(7):2387-96 [9516138.001]
  • [Cites] Cell. 1998 May 29;93(5):677-80 [9630212.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2973-9 [12351410.001]
  • [Cites] Nature. 2000 Jul 20;406(6793):309-14 [10917533.001]
  • [Cites] J Clin Invest. 2003 Jul;112(2):286-97 [12865416.001]
  • [Cites] J Pharmacol Exp Ther. 2006 Dec;319(3):998-1008 [16946104.001]
  • [Cites] Blood. 2007 Jan 15;109(2):703-10 [16973958.001]
  • [Cites] Blood. 2004 Apr 15;103(8):3148-57 [15070697.001]
  • [Cites] Blood. 2003 Feb 1;101(3):1087-93 [12393552.001]
  • [Cites] Blood. 2001 Nov 15;98 (10 ):3050-7 [11698290.001]
  • [Cites] Blood. 2007 Nov 1;110(9):3316-25 [17652619.001]
  • [Cites] Blood. 2008 Feb 15;111(4):2230-7 [18006696.001]
  • [Cites] Immunity. 2000 Feb;12(2):121-7 [10714678.001]
  • [Cites] Leukemia. 2001 May;15(5):752-6 [11368435.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4609-14 [12393534.001]
  • [Cites] J Immunol. 2000 Feb 15;164(4):2200-6 [10657675.001]
  • (PMID = 19074730.001).
  • [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 / Antibodies, Anti-Idiotypic; 0 / Chemokine CCL3; 0 / Chemokine CCL4; 0 / Culture Media, Conditioned; 0 / anti-IgM; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
  • [Other-IDs] NLM/ PMC4916945
  •  go-up   go-down


13. Kaufman M, Rai K: The challenge of treating complex autoimmune cytopenias in chronic lymphocytic leukemia. Leuk Lymphoma; 2010 Apr;51(4):574-5
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] The challenge of treating complex autoimmune cytopenias in chronic lymphocytic leukemia.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Purpura, Thrombocytopenic, Idiopathic / therapy

  • 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
  • [CommentOn] Leuk Lymphoma. 2010 Apr;51(4):620-7 [20302386.001]
  • (PMID = 20367181.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antineoplastic Agents, Alkylating
  •  go-up   go-down


1
Advertisement
4. Foon KA, Hallek MJ: Changing paradigms in the treatment of chronic lymphocytic leukemia. Leukemia; 2010 Mar;24(3):500-11
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] Changing paradigms in the treatment of chronic lymphocytic leukemia.
  • Progress in our understanding of chronic lymphocytic leukemia and its treatment has resulted in a more tailored approach to patient management, with different therapeutic regimens for different patient populations.
  • Selection of appropriate initial therapy should be based primarily on patient characteristics such as age, performance status and the expected clinical course of the leukemia based on established risk factors.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. Bendamustine .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • SciCrunch. DrugBank: Data: Chemical .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20033051.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents, Alkylating; 0 / Nitrogen Mustard Compounds; 0 / Purines; 8N3DW7272P / Cyclophosphamide; 981Y8SX18M / Bendamustine Hydrochloride
  • [Number-of-references] 12
  •  go-up   go-down


15. O'Brien SM, Keating MJ, Mocarski ES: Updated guidelines on the management of cytomegalovirus reactivation in patients with chronic lymphocytic leukemia treated with alemtuzumab. Clin Lymphoma Myeloma; 2006 Sep;7(2):125-30
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] Updated guidelines on the management of cytomegalovirus reactivation in patients with chronic lymphocytic leukemia treated with alemtuzumab.
  • The anti-CD52 monoclonal antibody alemtuzumab is highly active in the treatment of chronic lymphocytic leukemia (CLL) in patients with previously treated, relapsed, and/or refractory CLL as well as in patients with previously untreated disease.
  • In particular, cytomegalovirus (CMV) reactivation is now a well-documented complication in patients receiving alemtuzumab.
  • This article discusses several strategies for monitoring and treating CMV reactivation in patients with CLL receiving alemtuzumab-based therapy and provides practical recommendations for CMV management by building upon the guidelines published previously in 2004.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antibodies, Neoplasm / adverse effects. Antineoplastic Agents / adverse effects. Cytomegalovirus Infections / therapy. Guidelines as Topic. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Virus Activation / drug effects

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Cytomegalovirus Infections.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17026823.001).
  • [ISSN] 1557-9190
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [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] 25
  •  go-up   go-down


16. Zoppoli G, Cea M, Soncini D, Fruscione F, Rudner J, Moran E, Caffa I, Bedognetti D, Motta G, Ghio R, Ferrando F, Ballestrero A, Parodi S, Belka C, Patrone F, Bruzzone S, Nencioni A: Potent synergistic interaction between the Nampt inhibitor APO866 and the apoptosis activator TRAIL in human leukemia cells. Exp Hematol; 2010 Nov;38(11):979-88
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] Potent synergistic interaction between the Nampt inhibitor APO866 and the apoptosis activator TRAIL in human leukemia cells.
  • Here we have explored the interaction between APO866 and TRAIL in leukemia cell lines and in primary B-cell chronic lymphocytic leukemia cells.
  • Viability and mitochondrial transmembrane potential (ΔΨ(m)) were determined by cell staining with propidium iodide and tetramethylrhodamine ethyl ester, respectively, and flow cytometry.
  • Nampt and γ-tubulin levels, as well as caspase-3 cleavage were detected by immunoblotting.
  • RESULTS: APO866 induced NAD(+) depletion, ΔΨ(m) dissipation, and ATP shortage in leukemia cells, thereby leading to autophagic cell death.
  • TRAIL addition to APO866 synergistically increased its activity in leukemia cells by enhancing NAD(+) depletion, ΔΨ(m) dissipation, and ATP shortage.
  • No DR5 upregulation at the cell surface in response to APO866 was observed.
  • CONCLUSIONS: Activation of the extrinsic apoptotic cascade with TRAIL selectively amplifies the sequelae of Nampt inhibition in leukemia cells, and appears as a promising strategy to enhance APO866 activity in hematological malignancies.
  • [MeSH-minor] Adenosine Triphosphate / metabolism. Aged. Apoptosis / drug effects. Autophagy / drug effects. Caspase 3 / metabolism. Cell Line, Tumor. Cells, Cultured. Cytokines / antagonists & inhibitors. Cytokines / metabolism. Drug Synergism. Female. Humans. Immunoblotting. Jurkat Cells. Leukemia / metabolism. Leukemia / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / blood. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Male. Membrane Potential, Mitochondrial / drug effects. Middle Aged. NAD / metabolism. Nicotinamide Phosphoribosyltransferase / antagonists & inhibitors. Nicotinamide Phosphoribosyltransferase / metabolism. Receptors, TNF-Related Apoptosis-Inducing Ligand / metabolism. Tubulin / metabolism

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20696207.001).
  • [ISSN] 1873-2399
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Acrylamides; 0 / Cytokines; 0 / N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide; 0 / Piperidines; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / Tubulin; 0U46U6E8UK / NAD; 8L70Q75FXE / Adenosine Triphosphate; EC 2.4.2.12 / Nicotinamide Phosphoribosyltransferase; EC 2.4.2.12 / nicotinamide phosphoribosyltransferase, human; EC 3.4.22.- / Caspase 3
  •  go-up   go-down


17. Bocchia M, Ippoliti M, Gozzetti A, Abruzzese E, Calabrese S, Amabile M, Pirrotta MT, Crupi R, Tozzuoli D, Trawinska MM, Defina M, Martinelli G, Lauria F: CD34+/Ph+ cells are still detectable in chronic myeloid leukemia patients with sustained and prolonged complete cytogenetic remission during treatment with imatinib mesylate. Leukemia; 2008 Feb;22(2):426-8
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] CD34+/Ph+ cells are still detectable in chronic myeloid leukemia patients with sustained and prolonged complete cytogenetic remission during treatment with imatinib mesylate.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Aged. Benzamides. Bone Marrow / pathology. Cell Count. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Remission Induction


18. Marincevic M, Tobin G, Rosenquist R: Infrequent occurrence of PIK3CA mutations in chronic lymphocytic leukemia. Leuk Lymphoma; 2009 May;50(5):829-30
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] Infrequent occurrence of PIK3CA mutations in chronic lymphocytic leukemia.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Mutation. Phosphatidylinositol 3-Kinases / genetics

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Leuk Lymphoma. 2009 Sep;50(9):1554
  • (PMID = 19330652.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human
  •  go-up   go-down


19. Wang ZH, Gao L, Li YY, Zhang Z, Yuan JM, Wang HW, Zhang L, Zhu L: Induction of apoptosis by buckwheat trypsin inhibitor in chronic myeloid leukemia K562 cells. Biol Pharm Bull; 2007 Apr;30(4):783-6
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] Induction of apoptosis by buckwheat trypsin inhibitor in chronic myeloid leukemia K562 cells.
  • Here, the possible effects of a recombinant buckwheat trypsin inhibitor (rBTI) on the induction of apoptosis of the human K562 cell line were investigated by MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assays and flow cytometric analysis.
  • MTT assay showed that rBTI could specifically inhibit the growth of K562 cells in a dose-dependent manner, but there were minimal effects on normal human peripheral blood mononuclear cells (PBMCs).
  • [MeSH-major] Apoptosis / drug effects. Fagopyrum / enzymology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Trypsin Inhibitors / pharmacology

  • Genetic Alliance. consumer health - Chronic Myeloid 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
  • (PMID = 17409520.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Recombinant Proteins; 0 / Trypsin Inhibitors
  •  go-up   go-down


20. Herling M, Patel KA, Khalili J, Schlette E, Kobayashi R, Medeiros LJ, Jones D: TCL1 shows a regulated expression pattern in chronic lymphocytic leukemia that correlates with molecular subtypes and proliferative state. Leukemia; 2006 Feb;20(2):280-5
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] TCL1 shows a regulated expression pattern in chronic lymphocytic leukemia that correlates with molecular subtypes and proliferative state.
  • Expression of the human oncogene TCL1 in transgenic mice produces B-cell tumors that resemble chronic lymphocytic leukemia (CLL) suggesting its role in B-cell tumorigenesis.
  • To clarify the expression pattern and regulation of TCL1 in CLL, we assessed 213 primary tumors by immunohistochemistry (IHC), flow-cytometry and/or Western blot, using a new monoclonal antibody.
  • TCL1 protein was detectable in the majority of CLL (90% by IHC) but showed marked variations across cases with virtual absence in approximately 10% of tumors.
  • Higher TCL1 levels correlated with markers of the 'pre-germinal center' CLL subtype including unmutated VH status (P=0.005), ZAP70 expression (P=0.007), and presence of chromosome 11q22-23 deletions (P=0.04).
  • In vitro exposure of CLL cells to interleukin-4 (but not other growth factors) produced progressive and irreversible decrease in TCL1 protein levels in association with the onset of proliferation.
  • TCL1 expression patterns in CLL are complex and highly dynamic and appear to reflect both the histogenetic subtypes of the disease and the growth parameters of individual tumors.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] Animals. Cell Differentiation / drug effects. Cell Proliferation / drug effects. Humans. Immunohistochemistry. In Vitro Techniques. Interleukin-4 / pharmacology. Mice. Mice, Transgenic. Mutation. Oncogenes / genetics. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • COS Scholar Universe. author profiles.
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16341048.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / TCL1A protein, human; 207137-56-2 / Interleukin-4
  •  go-up   go-down


21. Gao H, Le Y, Wu X, Silberstein LE, Giese RW, Zhu Z: VentX, a novel lymphoid-enhancing factor/T-cell factor-associated transcription repressor, is a putative tumor suppressor. Cancer Res; 2010 Jan 1;70(1):202-11
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] VentX, a novel lymphoid-enhancing factor/T-cell factor-associated transcription repressor, is a putative tumor suppressor.
  • Lymphoid-enhancing factor/T-cell factors (LEF1/TCF) are a high-mobility group of transcriptional factors that play essential roles in cell fate determination during early embryogenesis and ontogenesis.
  • Aberrant activations of LEF1/TCF-mediated transcription have been implicated in a variety of malignancies.
  • Here, we report that VentX, a human Xom homologue, is a LEF/TCF-associated inhibitor of canonical Wnt/beta-catenin signaling and a negative regulator of cell proliferation.
  • VentX is predominantly expressed in hematopoietic cells, and its expression is significantly downregulated in chronic lymphocytic leukemia.
  • [MeSH-major] Genes, Tumor Suppressor. Homeodomain Proteins / physiology. Leukemia, Lymphocytic, Chronic, B-Cell / genetics

  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • 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 = 20028861.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK071795
  • [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 / Homeodomain Proteins; 0 / VENTX protein, human
  •  go-up   go-down


22. Middleton D, Diler AS, Meenagh A, Sleator C, Gourraud PA: Killer immunoglobulin-like receptors (KIR2DL2 and/or KIR2DS2) in presence of their ligand (HLA-C1 group) protect against chronic myeloid leukaemia. Tissue Antigens; 2009 Jun;73(6):553-60
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] Killer immunoglobulin-like receptors (KIR2DL2 and/or KIR2DS2) in presence of their ligand (HLA-C1 group) protect against chronic myeloid leukaemia.
  • We have analysed the frequency of killer immunoglobulin-like receptors (KIR) in cohorts of patients from Turkey with acute lymphocyte leukaemia (n = 52), acute myeloid leukaemia (n = 54) and chronic myeloid leukaemia (CML) (n = 52) and compared the results with 154 controls.
  • [MeSH-major] Genetic Predisposition to Disease. HLA-C Antigens / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Receptors, KIR / genetics. Receptors, KIR2DL2 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Cohort Studies. Female. Gene Frequency. Genotype. Humans. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Young Adult

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19493232.001).
  • [ISSN] 1399-0039
  • [Journal-full-title] Tissue antigens
  • [ISO-abbreviation] Tissue Antigens
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / HLA-C Antigens; 0 / KIR2DL2 protein, human; 0 / KIR2DS2 protein, human; 0 / Receptors, KIR; 0 / Receptors, KIR2DL2
  •  go-up   go-down


23. Siebolts U, Thiele J, Zander T, Ditschkowski M, Beelen DW, Kröger N, Fehse B, Wickenhauser C: Differences in proportion and dynamics of recipient hematopoiesis following hematopoietic cell transplantation in CML and IMF. Oncol Rep; 2008 Jan;19(1):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.
  • [Title] Differences in proportion and dynamics of recipient hematopoiesis following hematopoietic cell transplantation in CML and IMF.
  • Since decades myeloablation followed by allogeneic stem cell transplantation offered the only opportunity to cure leukemia patients and only recently the development of STI571 created a further alternative in chronic myeloid leukemia (CML).
  • While among all leukemias this transplantation regimen had the best outcome in CML, trials with reduced intensity conditioning regimens (RIC) were rather humbling and recurrence of the neoplastic clone occurred frequently.
  • However, the same therapy in patients with idiopathic myelofibrosis (IMF) resulted in a more favorable outcome.
  • Therefore, long-term mixed chimerism (mCh) was determined on bone marrow (BM) biopsies derived from five IMF patients and from eight CML patients of the pre STI era following sex-mismatched transplantation.
  • Analysis of late transplant period (day +100) revealed a concentration of host cells within the CD34+ precursor cell compartment in both diseases.
  • Taken into account that in CML up to 10% of the host BM CD34+ precursors bear the BCR-ABL translocation our data suggest that the neoplastic CD34+ progenitor cell population might dispose of better strategies to escape immune surveillance in CML than in IMF.
  • [MeSH-major] Bone Marrow Cells / cytology. Hematopoiesis / physiology. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Primary Myelofibrosis / therapy

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18097609.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD34
  •  go-up   go-down


24. Barrera M, Atenafu E, Andrews GS, Saunders F: Factors related to changes in cognitive, educational and visual motor integration in children who undergo hematopoietic stem cell transplant. J Pediatr Psychol; 2008 Jun;33(5):536-46
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.
  • [Title] Factors related to changes in cognitive, educational and visual motor integration in children who undergo hematopoietic stem cell transplant.
  • OBJECTIVES: Investigate cognitive, educational, and perceptual motor skills up to 2 years posttransplant of pediatric hematopoietic progenitor cell transplantation (HPCT) survivors and their correlates.
  • Low depression scores were associated with high Verbal IQ one and 2 years post-HPCT, and with high visual motor scores 2 years post-HPCT.
  • Poor educational outcomes were related to increased time since diagnosis.
  • Maternal age and depression, child's age, and time since diagnosis are critical factors for these outcomes.
  • [MeSH-major] Achievement. Hematopoietic Stem Cell Transplantation / psychology. Intelligence. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid, Acute / therapy. Neoplasms / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Psychomotor Performance


25. Abe A, Minami Y, Hayakawa F, Kitamura K, Nomura Y, Murata M, Katsumi A, Kiyoi H, Jamieson CH, Wang JY, Naoe T: Retention but significant reduction of BCR-ABL transcript in hematopoietic stem cells in chronic myelogenous leukemia after imatinib therapy. Int J Hematol; 2008 Dec;88(5):471-5
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] Retention but significant reduction of BCR-ABL transcript in hematopoietic stem cells in chronic myelogenous leukemia after imatinib therapy.
  • Chronic myelogenous leukemia (CML) is effectively treated with imatinib mesylate (IM), a small molecule inhibitor of the BCR-ABL tyrosine kinase that is expressed in the entire hematopoietic compartment including stem cells (HSC) and progenitors in CML patients.
  • While IM induces disease remission, it does not appear to eradicate BCR-ABL-positive stem cells.
  • We investigated the residual CML cells in HSC and myeloid progenitors isolated using fluorescence-activated cell sorting after IM-therapy.
  • Our results implicate that the sorted and purified stem cells are useful for more sensitive quantification of BCR-ABL-positive minimal residual disease.

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Tohoku J Exp Med. 2006 Dec;210(4):355-63 [17146202.001]
  • [Cites] Nat Med. 2006 Oct;12(10):1181-4 [17013383.001]
  • [Cites] Leukemia. 2007 Mar;21(3):494-504 [17252012.001]
  • [Cites] Exp Hematol. 2007 Apr;35(4 Suppl 1):144-54 [17379100.001]
  • [Cites] Clin Lymphoma Myeloma. 2007 Mar;7 Suppl 2:S71-80 [17382016.001]
  • [Cites] Blood. 2007 Oct 15;110(8):2828-37 [17626839.001]
  • [Cites] Cancer Biomark. 2007;3(4-5):183-91 [17917148.001]
  • [Cites] Cell Stem Cell. 2007 Dec 13;1(6):635-45 [18371405.001]
  • [Cites] Nat Rev Cancer. 2008 May;8(5):341-50 [18385684.001]
  • [Cites] Br J Haematol. 1999 Dec;107(3):587-99 [10583264.001]
  • [Cites] Stem Cells. 1998;16 Suppl 1:77-83; discussion 89 [11012149.001]
  • [Cites] Blood. 2002 Jan 1;99(1):319-25 [11756187.001]
  • [Cites] Leukemia. 2002 Mar;16(3):393-9 [11896544.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Sep 3;99(18):11872-7 [12193648.001]
  • [Cites] Blood. 2003 Jun 15;101(12):4701-7 [12576334.001]
  • [Cites] N Engl J Med. 2004 Aug 12;351(7):657-67 [15306667.001]
  • [Cites] Blood. 2004 Oct 1;104(7):2204-5 [15377577.001]
  • [Cites] Exp Hematol. 1979;7 Suppl 5:65-75 [299448.001]
  • [Cites] Blood. 1984 Jul;64(1):78-83 [6234038.001]
  • [Cites] Blood. 1985 Aug;66(2):312-8 [2410064.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):294-7 [15549090.001]
  • [Cites] Nature. 2005 Jun 30;435(7046):1267-70 [15988530.001]
  • [Cites] Haematologica. 2005 Jul;90(7):979-81 [15996937.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 18;103(16):6224-9 [16603627.001]
  • [Cites] Int J Hematol. 2006 May;83(4):289-93 [16757426.001]
  • [Cites] Blood. 2006 Jul 1;108(1):28-37 [16522812.001]
  • [Cites] Blood. 2006 Sep 15;108(6):1809-20 [16709930.001]
  • [Cites] N Engl J Med. 2006 Dec 7;355(23):2408-17 [17151364.001]
  • (PMID = 19039626.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA043054-22; United States / NCI NIH HHS / CA / R01 CA043054; United States / NCI NIH HHS / CA / R01 CA043054-22
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ NIHMS86110; NLM/ PMC2626150
  •  go-up   go-down


26. Vardiman JW: Chronic myelogenous leukemia, BCR-ABL1+. Am J Clin Pathol; 2009 Aug;132(2):250-60
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] Chronic myelogenous leukemia, BCR-ABL1+.
  • Session 1 of the 2007 Workshop of the Society for Hematopathology/European Association for Haematopathology focused on chronic myelogenous leukemia, BCR-ABL1+ (CML).
  • CML is a myeloproliferative neoplasm arising at the level of a pluripotent stem cell and consistently associated with the BCR-ABL1 fusion gene.
  • CML most commonly manifests in a chronic phase of the disease with neutrophilic leukocytosis, and the demonstration of the Philadelphia chromosome is the ultimate confirmation of the diagnosis.
  • However, in select cases, the initial diagnosis remains challenging, and a number of issues pertaining to the manifestations and disease evolution remain unresolved.
  • These issues have been illustrated by the cases submitted to our workshop and include unusual manifestations of CML, including manifestation in the accelerated and/or blast phase, and patterns of disease progression and therapy resistance in the era of protein tyrosine kinase inhibitor therapy.
  • [MeSH-major] Fusion Proteins, bcr-abl. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19605820.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 59
  •  go-up   go-down


27. Shanafelt TD, Rabe KG, Kay NE, Zent CS, Call TG, Slager SL, Bowen DA, Schwager SM, Nowakowski GS: Statin and non-steroidal anti-inflammatory drug use in relation to clinical outcome among patients with Rai stage 0 chronic lymphocytic leukemia. Leuk Lymphoma; 2010 Jul;51(7):1233-40
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] Statin and non-steroidal anti-inflammatory drug use in relation to clinical outcome among patients with Rai stage 0 chronic lymphocytic leukemia.
  • In vitro studies suggest that statins and NSAIDs may have potential as anticancer therapies in low-grade non-Hodgkin lymphomas including chronic lymphocytic leukemia (CLL), and a recent observational study found statin use was associated with improved event free survival in patients with follicular lymphoma.
  • We therefore conducted an observational cohort study of 686 patients with newly diagnosed Rai stage 0 CLL to evaluate whether statin or NSAID use was related to their clinical outcome or influenced the efficacy of rituximab therapy.
  • At diagnosis, 136 (20%) patients took statins and 230 (34%) scheduled daily aspirin, ibuprofen, or naproxen.
  • Although previous studies suggested statins may improve event free survival among patients with follicular lymphoma, we find no impact of statins on time to initial therapy in this large study of patients with Rai stage 0 CLL.
  • The in vitro observation that statins reduce rituximab efficacy does not appear to have clinical significance in CLL care.

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Statins.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Haematol. 2007 Nov;139(3):398-404 [17910629.001]
  • [Cites] Leuk Lymphoma. 2007 Dec;48(12):2412-7 [18067017.001]
  • [Cites] Cancer Immunol Immunother. 2008 Mar;57(3):347-58 [17668203.001]
  • [Cites] Leuk Lymphoma. 2008 Jan;49(1):49-56 [18203011.001]
  • [Cites] Invest New Drugs. 2008 Apr;26(2):139-49 [18094935.001]
  • [Cites] PLoS Med. 2008 Mar 25;5(3):e64 [18366248.001]
  • [Cites] Atherosclerosis. 2008 Apr;197(2):829-39 [17826781.001]
  • [Cites] Br J Haematol. 2008 May;141(5):615-21 [18373706.001]
  • [Cites] Br J Haematol. 2008 May;141(5):607-14 [18384436.001]
  • [Cites] Ann Pharmacother. 2008 Sep;42(9):1208-15 [18648016.001]
  • [Cites] J Clin Oncol. 2008 Nov 20;26(33):5486; author reply 5486 [18936467.001]
  • [Cites] Leukemia. 2008 Dec;22(12):2184-92 [18784741.001]
  • [Cites] N Engl J Med. 2009 Jan 8;360(2):192; author reply 193 [19129537.001]
  • [Cites] Lancet. 2009 Apr 11;373(9671):1301-9 [19328542.001]
  • [Cites] J Clin Oncol. 2010 Jan 20;28(3):412-7 [20008638.001]
  • [Cites] JAMA. 2002 Jan 16;287(3):337-44 [11790213.001]
  • [Cites] Br J Haematol. 2001 Dec;115(4):854-61 [11843819.001]
  • [Cites] Cancer Res. 2002 Oct 15;62(20):5711-9 [12384529.001]
  • [Cites] Br J Haematol. 2003 Apr;121(2):287-95 [12694251.001]
  • [Cites] Exp Hematol. 2003 Sep;31(9):779-83 [12962723.001]
  • [Cites] Int J Oncol. 2003 Oct;23(4):1055-69 [12963986.001]
  • [Cites] Exp Cell Res. 1984 Jul;153(1):91-8 [6610562.001]
  • [Cites] Biochem Biophys Res Commun. 1994 Mar 30;199(3):1209-15 [8147861.001]
  • [Cites] Lipids. 1997 Mar;32(3):255-62 [9076662.001]
  • [Cites] Blood. 1998 Aug 15;92(4):1406-14 [9694730.001]
  • [Cites] Atheroscler Suppl. 2004 Oct;5(3):67-80 [15531278.001]
  • [Cites] J Clin Invest. 2005 Apr;115(4):959-68 [15776112.001]
  • [Cites] Blood. 2005 Jul 15;106(2):650-7 [15802535.001]
  • [Cites] Leukemia. 2005 Jul;19(7):1216-23 [15858619.001]
  • [Cites] Clin Immunol. 2006 Jul;120(1):76-90 [16473553.001]
  • [Cites] J Clin Oncol. 2006 Jul 1;24(19):3218-9; author reply 3219-20 [16809747.001]
  • [Cites] Leuk Lymphoma. 2006 Jun;47(6):1053-61 [16840197.001]
  • [Cites] J Clin Oncol. 2006 Oct 1;24(28):4634-41 [17008705.001]
  • [Cites] Leuk Lymphoma. 2006 Dec;47(12):2625-34 [17169808.001]
  • [Cites] Immunology. 2007 Mar;120(3):315-24 [17140403.001]
  • [Cites] Cancer Chemother Pharmacol. 2007 Sep;60(4):545-53 [17186240.001]
  • (PMID = 20496995.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K23 CA113408; United States / NCI NIH HHS / CA / CA113408
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 4F4X42SYQ6 / Rituximab
  • [Other-IDs] NLM/ NIHMS549713; NLM/ PMC3913168
  •  go-up   go-down


28. Power JP, El Chaar M, Temple J, Thomas M, Spillane D, Candotti D, Allain JP: HBV reactivation after fludarabine chemotherapy identified on investigation of suspected transfusion-transmitted Hepatitis B virus. J Hepatol; 2010 Oct;53(4):780-7
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.
  • Acute viral infections may then be attributed either to transfusion-transmitted infection (TTI) or reactivation of a past infection.
  • METHODS: A patient with chronic lymphocytic leukemia (CLL) who had >250 blood donor exposures developed acute Hepatitis B virus (HBV) infection.
  • RESULTS: Review of historical, molecular, and antigenic evidence demonstrated reactivation of a recovered HBV infection dating >30 years and the selection of a rare escape mutant that briefly replicated and caused acute liver disease.
  • Correcting the C139Y substitution by site directed mutagenesis of recombinant surface proteins re-established assay reactivity.
  • CONCLUSIONS: Fludarabine, but not Chlorambucil, appeared sufficiently immunosuppressive to trigger reactivation despite low levels of neutralizing antibodies.
  • [MeSH-minor] Blood Transfusion. Disease Transmission, Infectious. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Male. Middle Aged

  • Genetic Alliance. consumer health - Hepatitis.
  • MedlinePlus Health Information. consumer health - Hepatitis B.
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. VIDARABINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
  • (PMID = 20638744.001).
  • [ISSN] 1600-0641
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  •  go-up   go-down


29. Spaner DE, Shi Y, White D, Shaha S, He L, Masellis A, Wong K, Gorczynski R: A phase I/II trial of TLR-7 agonist immunotherapy in chronic lymphocytic leukemia. Leukemia; 2010 Jan;24(1):222-6
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] A phase I/II trial of TLR-7 agonist immunotherapy in chronic lymphocytic leukemia.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Toll-Like Receptor 7 / agonists

  • 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 = 19759558.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / / MOP-79389
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Toll-Like Receptor 7
  •  go-up   go-down


30. Bilban M, Heintel D, Scharl T, Woelfel T, Auer MM, Porpaczy E, Kainz B, Kröber A, Carey VJ, Shehata M, Zielinski C, Pickl W, Stilgenbauer S, Gaiger A, Wagner O, Jäger U, German CLL Study Group: Deregulated expression of fat and muscle genes in B-cell chronic lymphocytic leukemia with high lipoprotein lipase expression. Leukemia; 2006 Jun;20(6):1080-8
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] Deregulated expression of fat and muscle genes in B-cell chronic lymphocytic leukemia with high lipoprotein lipase expression.
  • Lipoprotein lipase (LPL) is a prognostic marker in B-cell chronic lymphocytic leukemia (B-CLL) related to immunoglobulin V(H) gene (IgV(H))mutational status.
  • We determined gene expression profiles using Affymetrix U133A GeneChips in two groups of B-CLLs selected for either high ('LPL+', n=10) or low ('LPL-', n=10) LPL mRNA expression.
  • A total of 111 genes discriminated LPL+ from LPL- B-CLLs.
  • Of these, the top three genes associated with time to first treatment were Septin10, DMD and Gravin (P</=0.01).
  • The relationship of LPL+ and LPL- B-CLL gene expression signatures to 52 tissues was statistically analyzed.
  • The LPL+ B-CLL expression signature, represented by 64 genes was significantly related to fat, muscle and PB dendritic cells (P<0.001).
  • Exploration of microarray data to define functional alterations related to the biology of LPL+ CLL identified two functional modules, fatty acid degradation and MTA3 signaling, as being altered with higher statistical significance.
  • Our data show that LPL+ B-CLL cells have not only acquired gene expression changes in fat and muscle-associated genes but also in functional pathways related to fatty acid degradation and signaling which may ultimately influence CLL biology and clinical outcome.
  • [MeSH-major] Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Leukemic. Immunoglobulin Heavy Chains / genetics. Immunoglobulin Variable Region / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / enzymology. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Lipoprotein Lipase / genetics

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, B-cell, chronic.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Leukemia. 2008 Jan;22(1):224-6 [17657217.001]
  • (PMID = 16617321.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytoskeletal Proteins; 0 / Dystrophin; 0 / Fatty Acids; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / RNA, Messenger; EC 3.1.1.34 / Lipoprotein Lipase; EC 3.6.1.- / GTP Phosphohydrolases; EC 3.6.1.- / SEPT10 protein, human; EC 3.6.1.- / Septins
  •  go-up   go-down


36. Erdag G, Meck JM, Meloni-Ehrig A, Matyakhina L, Donohue T, Srinivasan R, Mowrey P, Kelly J, Smith A, Childs R: Long-term persistence of nonpathogenic clonal chromosome abnormalities in donor hematopoietic cells after allogeneic stem cell transplantation. Cancer Genet Cytogenet; 2009 Apr 15;190(2):125-30
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] Long-term persistence of nonpathogenic clonal chromosome abnormalities in donor hematopoietic cells after allogeneic stem cell transplantation.
  • We describe the cases of two unrelated patients who exhibited multiple chromosomal abnormalities in donor cells after allogeneic peripheral blood stem cell transplantation (PBSCT).
  • The patients were diagnosed with chronic myeloid leukemia and chronic lymphocytic leukemia, respectively, and both underwent nonmyeloablative conditioning with cyclophosphamide and fludarabine followed by PBSCT from their HLA-matched opposite-sex siblings.
  • In contrast, only rare reports of chromosome abnormalities in donor cells exist, all of which have been associated with post-bone marrow transplant myelodysplastic syndrome or acute leukemias.
  • [MeSH-major] Chromosome Aberrations. Hematopoietic Stem Cell Transplantation
  • [MeSH-minor] Aged. Female. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / immunology. Male. Middle Aged

  • Genetic Alliance. consumer health - Transplantation.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Am J Hematol. 2000 Jan;63(1):46-53 [10602169.001]
  • [Cites] Am J Hematol. 2007 Aug;82(8):758-60 [17301975.001]
  • [Cites] Bone Marrow Transplant. 2002 Mar;29(5):453-6 [11919737.001]
  • [Cites] J Clin Oncol. 2002 Sep 15;20(18):3878-84 [12228208.001]
  • [Cites] Cancer Genet Cytogenet. 2003 Apr 15;142(2):124-8 [12699888.001]
  • [Cites] Semin Cancer Biol. 2003 Jun;13(3):203-9 [12959351.001]
  • [Cites] Bone Marrow Transplant. 2004 Jun;33(12):1253-6 [15146169.001]
  • [Cites] Hematology. 2004 Jun;9(3):179-87 [15204099.001]
  • [Cites] Leuk Lymphoma. 2004 Jul;45(7):1453-8 [15359647.001]
  • [Cites] Leuk Lymphoma. 2004 Nov;45(11):2197-203 [15512807.001]
  • [Cites] Am J Hematol. 1977;2(3):283-90 [339712.001]
  • [Cites] N Engl J Med. 1984 Apr 5;310(14):903-6 [6366558.001]
  • [Cites] Transplantation. 1986 Jul;42(1):61-3 [3727020.001]
  • [Cites] Blood. 1987 Oct;70(4):1099-104 [3307946.001]
  • [Cites] Int J Cancer. 1989 Jan 15;43(1):80-6 [2910833.001]
  • [Cites] N Engl J Med. 1990 Jun 21;322(25):1794-6 [2189070.001]
  • [Cites] N Engl J Med. 1991 Nov 7;325(19):1330-6 [1922234.001]
  • [Cites] N Engl J Med. 1991 Dec 12;325(24):1682-7 [1944468.001]
  • [Cites] Leuk Lymphoma. 1993 Aug;10(6):419-25 [8401178.001]
  • [Cites] Br J Haematol. 1993 Oct;85(2):326-31 [8280605.001]
  • [Cites] Blood. 1994 May 15;83(10):2931-8 [8180388.001]
  • [Cites] Blood. 1998 Aug 1;92(3):810-21 [9680349.001]
  • [Cites] Cell Biol Toxicol. 1999 Feb;15(1):13-7 [10195346.001]
  • [Cites] Cancer Genet Cytogenet. 2005 Feb;157(1):70-3 [15676151.001]
  • [Cites] Lancet Oncol. 2005 Oct;6(10):809-12 [16198987.001]
  • [Cites] Blood. 2006 Jan 15;107(2):480-2 [16195326.001]
  • [Cites] Am J Hematol. 2006 Mar;81(3):178-85 [16493618.001]
  • [Cites] Leukemia. 2001 Jun;15(6):963-70 [11417484.001]
  • (PMID = 19380032.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 HL999999
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS129478; NLM/ PMC2764294
  •  go-up   go-down


37. Ikezoe T, Yang Y, Bandobashi K, Saito T, Takemoto S, Machida H, Togitani K, Koeffler HP, Taguchi H: Oridonin, a diterpenoid purified from Rabdosia rubescens, inhibits the proliferation of cells from lymphoid malignancies in association with blockade of the NF-kappa B signal pathways. Mol Cancer Ther; 2005 Apr;4(4):578-86
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] Oridonin, a diterpenoid purified from Rabdosia rubescens, inhibits the proliferation of cells from lymphoid malignancies in association with blockade of the NF-kappa B signal pathways.
  • This study found that oridonin, a natural diterpenoid purified from Rabdosia rubescens, inhibited growth of multiple myeloma (MM; U266, RPMI8226), acute lymphoblastic T-cell leukemia (Jurkat), and adult T-cell leukemia (MT-1) cells with an effective dose that inhibited 50% of target cells (ED50) ranging from 0.75 to 2.7 microg/mL.
  • Terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling staining showed that oridonin caused apoptosis of MT-1 cells in a time-dependent manner.
  • Oridonin also blocked tumor necrosis factor-alpha- and lipopolysaccharide-stimulated NF-kappa B activity in Jurkat cells as well as RAW264.7 murine macrophages.
  • Of note, oridonin decreased survival of freshly isolated adult T-cell leukemia (three samples), acute lymphoblastic leukemia (one sample), chronic lymphocytic leukemia (one sample), non-Hodgkin's lymphoma (three samples), and MM (four samples) cells from patients in association with inhibition of NF-kappa B DNA-binding activity.
  • On the other hand, oridonin did not affect survival of normal lymphoid cells from healthy volunteers.
  • Taken together, oridonin might be useful as adjunctive therapy for individuals with lymphoid malignancies, including the lethal disease adult T-cell leukemia.
  • [MeSH-major] Cell Proliferation / drug effects. Diterpenes / pharmacology. Isodon / metabolism. NF-kappa B / metabolism. Phytotherapy / methods. Plant Extracts / pharmacology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Apoptosis. Blotting, Western. Cell Line. Cell Line, Tumor. Diterpenes, Kaurane. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Female. Genes, Reporter. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / metabolism. Humans. In Situ Nick-End Labeling. Jurkat Cells. Leukemia / drug therapy. Leukemia / pathology. Lipopolysaccharides / metabolism. Male. Mice. Middle Aged. Models, Chemical. Multiple Myeloma / drug therapy. Multiple Myeloma / pathology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Signal Transduction. T-Lymphocytes / metabolism. T-Lymphocytes / virology. Thymidine / chemistry. Thymidine / metabolism. Time Factors. Transfection. Trypan Blue / pharmacology. bcl-X Protein

  • MedlinePlus Health Information. consumer health - Herbal Medicine.
  • Hazardous Substances Data Bank. Trypan blue .
  • 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 = 15827331.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL2L1 protein, human; 0 / Bcl2l1 protein, mouse; 0 / Diterpenes; 0 / Diterpenes, Kaurane; 0 / Lipopolysaccharides; 0 / NF-kappa B; 0 / Plant Extracts; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-X Protein; 0APJ98UCLQ / oridonin; I2ZWO3LS3M / Trypan Blue; VC2W18DGKR / Thymidine
  •  go-up   go-down


38. Kamohara H, Takahashi M, Ishiko T, Ogawa M, Baba H: Induction of interleukin-8 (CXCL-8) by tumor necrosis factor-alpha and leukemia inhibitory factor in pancreatic carcinoma cells: Impact of CXCL-8 as an autocrine growth factor. Int J Oncol; 2007 Sep;31(3):627-32
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] Induction of interleukin-8 (CXCL-8) by tumor necrosis factor-alpha and leukemia inhibitory factor in pancreatic carcinoma cells: Impact of CXCL-8 as an autocrine growth factor.
  • Chronic inflammation leads to cancer development and progression.
  • In the present study, we analyzed whether various cytokines affect cell proliferation by CXCL-8 expression in pancreas carcinoma cells.
  • In our previous study, LIF promoted cell growth in Hs-700T cells.
  • LIF induced CXCL-8 mRNA in a dose- and time-dependent manner.
  • Addition of recombinant CXCL-8 did not induce cell growth of Hs-700T.
  • Anti-CXCL-8 IgG significantly suppressed cell growth.
  • Curcumin (diferuloylmethane), NF-kappaB inhibitor, suppressed cell proliferation in Hs-700T cells.
  • [MeSH-major] Interleukin-8 / metabolism. Leukemia Inhibitory Factor / metabolism. Pancreatic Neoplasms / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Cycloheximide / pharmacology. Cytokines / metabolism. Dactinomycin / pharmacology. Humans. Immunoglobulin G / chemistry. Inflammation. Intercellular Signaling Peptides and Proteins / metabolism. RNA, Messenger / metabolism. Time Factors

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • Hazardous Substances Data Bank. DACTINOMYCIN .
  • Hazardous Substances Data Bank. CYCLOHEXIMIDE .
  • 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 = 17671691.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Cytokines; 0 / Immunoglobulin G; 0 / Intercellular Signaling Peptides and Proteins; 0 / Interleukin-8; 0 / Leukemia Inhibitory Factor; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 1CC1JFE158 / Dactinomycin; 98600C0908 / Cycloheximide
  •  go-up   go-down


39. Morice WG, Jevremovic D, Olteanu H, Roden A, Nowakowski G, Kroft S, Hanson CA, Kurtin PJ: Chronic lymphoproliferative disorder of natural killer cells: a distinct entity with subtypes correlating with normal natural killer cell subsets. Leukemia; 2010 Apr;24(4):881-4
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 lymphoproliferative disorder of natural killer cells: a distinct entity with subtypes correlating with normal natural killer cell subsets.
  • [MeSH-minor] Antigens, CD56 / metabolism. Cells, Cultured. Female. Flow Cytometry. Humans. Immunophenotyping. Middle Aged. NK Cell Lectin-Like Receptor Subfamily B / metabolism. Receptors, KIR / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20111066.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / KLRB1 protein, human; 0 / NK Cell Lectin-Like Receptor Subfamily B; 0 / Receptors, KIR
  •  go-up   go-down


40. Hess G, Bunjes D, Siegert W, Schwerdtfeger R, Ledderose G, Wassmann B, Kobbe G, Bornhäuser M, Hochhaus A, Ullmann AJ, Kindler T, Haus U, Gschaidmeier H, Huber C, Fischer T: Sustained complete molecular remissions after treatment with imatinib-mesylate in patients with failure after allogeneic stem cell transplantation for chronic myelogenous leukemia: results of a prospective phase II open-label multicenter study. J Clin Oncol; 2005 Oct 20;23(30):7583-93
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] Sustained complete molecular remissions after treatment with imatinib-mesylate in patients with failure after allogeneic stem cell transplantation for chronic myelogenous leukemia: results of a prospective phase II open-label multicenter study.
  • PURPOSE: In the era of molecular therapy of chronic myelogenous leukemia (CML) applying BCR-ABL tyrosine kinase inhibitors, the usefulness of molecular end points, in particular, quantitative polymerase chain reaction (PCR) for BCR-ABL in monitoring responses has been broadly accepted.
  • PATIENTS AND METHODS: As a clinical model, we adopted minimal residual disease (MRD) found in relapse after allogeneic stem cell transplantation (SCT) in CML.
  • This suggests the possibility of long-term tumor control in a subset of patients.
  • CONCLUSION: The treatment strategy showed that IM treatment was well-tolerated and highly efficacious in MRD after allogeneic SCT.
  • Moreover, this study demonstrated that evaluation of a molecular end point within a multicenter trial can be a safe and effective tool for clinical decision making.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Stem Cell Transplantation / adverse effects
  • [MeSH-minor] Adult. Benzamides. Feasibility Studies. Fusion Proteins, bcr-abl / genetics. Fusion Proteins, bcr-abl / metabolism. Graft vs Host Disease / prevention & control. Humans. Imatinib Mesylate. Maximum Tolerated Dose. Polymerase Chain Reaction. Prospective Studies. Protein-Tyrosine Kinases / antagonists & inhibitors. Remission Induction. Time Factors. Transplantation, Homologous. Treatment Outcome

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16234522.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  •  go-up   go-down


41. Sherborne AL, Houlston RS: What are genome-wide association studies telling us about B-cell tumor development? Oncotarget; 2010 Sep;1(5):367-72
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] What are genome-wide association studies telling us about B-cell tumor development?
  • It has long been speculated that common genetic variation influences the development of B-cell malignancy, however until recently evidence for this assertion was lacking.
  • Recent GWAS of chronic lymphocytic leukemia (CLL) and acute lymphoblastic leukemia (ALL) have identified novel disease genes for CLL and ALL and underscore the importance of polymorphic variation in B-cell development genes as determinants of leukemia risk.
  • [MeSH-major] B-Lymphocytes / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Gene Expression Regulation, Leukemic. Genetic Predisposition to Disease. Genome-Wide Association Study. Humans. Phenotype. Risk Assessment. Risk Factors

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2007 Nov 1;110(9):3326-33 [17687107.001]
  • [Cites] Blood. 2010 Mar 4;115(9):1765-7 [20042726.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jan 20;95(2):657-62 [9435248.001]
  • [Cites] Blood. 1999 Sep 15;94(6):1848-54 [10477713.001]
  • [Cites] Nat Rev Immunol. 2005 Mar;5(3):230-42 [15738953.001]
  • [Cites] Leukemia. 2005 Jun;19(6):1025-8 [15800670.001]
  • [Cites] EMBO J. 2005 Oct 19;24(20):3565-75 [16177824.001]
  • [Cites] Nat Rev Cancer. 2006 Mar;6(3):193-203 [16467884.001]
  • [Cites] Semin Oncol. 2006 Apr;33(2):195-201 [16616066.001]
  • [Cites] Leukemia. 2002 Feb;16(2):297-8 [11840299.001]
  • [Cites] Cell Growth Differ. 2002 Mar;13(3):95-106 [11959810.001]
  • [Cites] J Virol. 2002 Nov;76(21):11133-8 [12368356.001]
  • [Cites] Annu Rev Immunol. 2004;22:55-79 [15032574.001]
  • [Cites] Nat Genet. 2006 Jun;38(6):652-8 [16682969.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3451-61 [17170124.001]
  • [Cites] Nat Genet. 2007 May;39(5):645-9 [17401363.001]
  • [Cites] Nat Genet. 2007 May;39(5):631-7 [17401366.001]
  • [Cites] Nature. 2007 Jun 28;447(7148):1087-93 [17529967.001]
  • [Cites] Nat Genet. 2007 Aug;39(8):984-8 [17618284.001]
  • [Cites] Nat Rev Immunol. 2008 Jan;8(1):22-33 [18097447.001]
  • [Cites] Nat Genet. 2008 Oct;40(10):1204-10 [18758461.001]
  • [Cites] Nat Genet. 2008 Nov;40(11):1307-12 [18794855.001]
  • [Cites] Blood. 2008 Nov 15;112(10):4028-38 [18799728.001]
  • [Cites] Cancer Res. 2009 Jul 1;69(13):5568-74 [19549893.001]
  • [Cites] Nat Genet. 2009 Aug;41(8):885-90 [19561604.001]
  • [Cites] Nat Genet. 2009 Sep;41(9):1001-5 [19684603.001]
  • [Cites] Nat Genet. 2009 Sep;41(9):1006-10 [19684604.001]
  • [Cites] Br J Haematol. 2008 Jun;142(2):238-45 [18503587.001]
  • [Cites] Nat Genet. 2010 Feb;42(2):132-6 [20062064.001]
  • [Cites] Cell. 1994 Oct 7;79(1):143-56 [7923373.001]
  • (PMID = 21307401.001).
  • [ISSN] 1949-2553
  • [Journal-full-title] Oncotarget
  • [ISO-abbreviation] Oncotarget
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3157732
  •  go-up   go-down


42. Giafis N, Katsoulidis E, Sassano A, Tallman MS, Higgins LS, Nebreda AR, Davis RJ, Platanias LC: Role of the p38 mitogen-activated protein kinase pathway in the generation of arsenic trioxide-dependent cellular responses. Cancer Res; 2006 Jul 1;66(13):6763-71
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.
  • In the present study, we provide evidence that the kinases MAPK kinase 3 (Mkk3) and Mkk6 are activated during treatment of leukemic cell lines with As(2)O(3) to regulate downstream engagement of the p38 mitogen-activated protein kinase.
  • Pharmacologic inhibition of p38 enhances As(2)O(3)-dependent activation of the c-jun NH(2)-terminal kinase (JNK) and subsequent induction of apoptosis of chronic myelogenous leukemia (CML)- or acute promyelocytic leukemia (APL)-derived cell lines.
  • In addition, in APL blasts, inhibition of p38 enhances myeloid cell differentiation in response to As(2)O(3), as well as suppression of Bcl-2 expression and loss of mitochondrial membrane potential.
  • In other studies, we show that the small-molecule p38 inhibitors SD-282 and SCIO-469 potentiate As(2)O(3)-mediated suppression of myeloid leukemic progenitor growth from CML patients, indicating a critical regulatory role for p38 in the induction of antileukemic responses.
  • Altogether, our data indicate that the Mkk3/6-p38 signaling cascade is activated in a negative regulatory feedback manner to control induction of As(2)O(3)-mediated antileukemic effects.
  • [MeSH-major] Arsenicals / pharmacology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / enzymology. MAP Kinase Signaling System / drug effects. Oxides / pharmacology. p38 Mitogen-Activated Protein Kinases / metabolism
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Cell Line, Tumor. Humans. Mice. Mice, Knockout. Phosphorylation / drug effects


43. Montillo M, Schinkoethe T, Elter T: Eradication of minimal residual disease with alemtuzumab in B-cell chronic lymphocytic leukemia (B-CLL) patients: the need for a standard method of detection and the potential impact of bone marrow clearance on disease outcome. Cancer Invest; 2005;23(6):488-96
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.
  • [Title] Eradication of minimal residual disease with alemtuzumab in B-cell chronic lymphocytic leukemia (B-CLL) patients: the need for a standard method of detection and the potential impact of bone marrow clearance on disease outcome.
  • The introduction of new therapeutic agents, such as fludarabine phosphate (Fludara) and alemtuzumab (MabCampath, Campath), has made it possible to treat B-cell chronic lymphocytic leukemia (B-CLL) more effectively, compared with alkylating agents.
  • However, although an increasing number of patients are able to achieve complete remission (CR), relapse is almost inevitable, because of the re-emergence of the malignant clone from small numbers of residual malignant cells.
  • This phenomenon has introduced a need for a more sensitive assessment of low-level disease which, in turn, has encouraged the development of therapies aimed at the eradication of all residual disease in CR patients.
  • The eradication of residual disease is associated with improved remission durability and has great potential in offering the possibility of cure.
  • Alemtuzumab is the foundation of many eradication-based treatment approaches because of its ability to achieve clinical remissions and to successfully purge minimal residual disease (MRD) from both blood and bone marrow in B-CLL patients.
  • The ability to clear MRD from bone marrow in patients achieving clinical CR using alemtuzumab is a significant step forward in the treatment of B-CLL, and supports treatment strategies in which alemtuzumab is used in combination with other agents.
  • Purging of MRD from both blood and bone marrow also enables patients to proceed to autologous hematopoietic stem cell transplantation, a strategy that is able to achieve long-term remission.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Neoplasm, Residual / diagnosis. Neoplasm, Residual / drug therapy

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, B-cell, chronic.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16203656.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; 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] 55
  •  go-up   go-down


44. Signer RA, Montecino-Rodriguez E, Witte ON, McLaughlin J, Dorshkind K: Age-related defects in B lymphopoiesis underlie the myeloid dominance of adult leukemia. Blood; 2007 Sep 15;110(6):1831-9
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] Age-related defects in B lymphopoiesis underlie the myeloid dominance of adult leukemia.
  • Reduced lymphopoiesis during aging contributes to declines in immunity, but little consideration has been given to its effect on the development of hematologic disease.
  • This report demonstrates that age-related defects in lymphopoiesis underlie the myeloid dominance of adult leukemia.
  • Using a murine model of chronic myeloid leukemia, an adult-onset malignancy that arises from transformation of hematopoietic stem cells by the BCR-ABL(P210) oncogene, we demonstrate that young bone marrow (BM) cells that were transformed with BCR-ABL(P210) initiated both a myeloproliferative disorder (MPD) and B-lymphoid leukemia, whereas BCR-ABL(P210)-transformed old BM cells recapitulated the human disease by inducing an MPD with rare lymphoid involvement.


45. Velasco-Castrejón O, Rivas-Sánchez B, Gutiérrez E, Chávez L, Duarte P, Chavarria S, Rivera-Reyes HH: [Leptospira, does it simulate or cause leukemia?]. Rev Cubana Med Trop; 2005 Jan-Apr;57(1):17-24
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] [Leptospira, does it simulate or cause leukemia?].
  • [Transliterated title] Leptospira simulador o causante de leucemia?
  • Two cases of chronic leptospirosis in bicitopenic and pancitopenic patients, respectively, with mucocutaneous and visceral bleedings were presented.
  • They were diagnosed myeloblastic leukemia M3 and acute lymphoblastic leukemia L2 by bone marrow aspiration and they were treated as such at the hematology department of a general hospital.
  • It was reviewed the possibility that leptospira could cause leukemoid syndromes and/or leukemia.
  • [MeSH-major] Leptospirosis / complications. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology
  • [MeSH-minor] Aged. Aged, 80 and over. Bone Marrow / microbiology. Bone Marrow Examination. Chronic Disease. Fluorescent Antibody Technique. Humans. Kidney / microbiology. Leptospira / isolation & purification. Lung / microbiology. Male. Myelodysplastic Syndromes / diagnosis. Myelodysplastic Syndromes / etiology. Silver Staining

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17966470.001).
  • [ISSN] 0375-0760
  • [Journal-full-title] Revista cubana de medicina tropical
  • [ISO-abbreviation] Rev Cubana Med Trop
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Cuba
  •  go-up   go-down


46. Gozzetti A, Calabrese S, Crupi R, Zaja F, Tozzuoli D, Tassi M, Raspadori D, Lenoci M, Lauria F: Trisomy 8 in chronic lymphocytic leukemia: a report of two cases. Cancer Genet Cytogenet; 2007 Jun;175(2):175-6
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] Trisomy 8 in chronic lymphocytic leukemia: a report of two cases.
  • [MeSH-major] Chromosomes, Human, Pair 8 / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Trisomy / genetics

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Cancer Genet Cytogenet. 2007 Jan 1;172(1):66-9 [17175382.001]
  • (PMID = 17556077.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Comment; Letter
  • [Publication-country] United States
  •  go-up   go-down


47. Boons GJ: Liposomes modified by carbohydrate ligands can target B cells for the treatment of B-cell lymphomas. Expert Rev Vaccines; 2010 Nov;9(11):1251-6
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] Liposomes modified by carbohydrate ligands can target B cells for the treatment of B-cell lymphomas.
  • In vivo targeting of B-cell lymphoma with glycan ligands of CD22.
  • A strategy has been developed to deliver selectively chemotherapeutic drugs to B cells by employing doxorubicin-loaded liposomes modified by a ligand for the B-cell-specific cell-surface protein CD22, also known as Siglec-2.
  • The liposomes bound in a rapid and saturable manner to the human Burkitt lymphoma Daudi B-cell line and exhibited significantly higher cytotoxicity in vitro and in vivo compared with similar untargeted liposomes.
  • The CD22-targeted liposome bound to B cells isolated from lymphoma patients and although binding was proportional to CD22 expression on the cell surface, low levels of expression on chronic lymphocytic leukemia cells were sufficient to effect cell neutralization.
  • The glycan-based strategy for delivery of chemotherapeutic agents may provide a new strategy for the treatment of B-cell lymphomas.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Blood. 2010 Jun 10;115(23):4778-86 [20181615.001]
  • (PMID = 21087105.001).
  • [ISSN] 1744-8395
  • [Journal-full-title] Expert review of vaccines
  • [ISO-abbreviation] Expert Rev Vaccines
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA088986; United States / NCI NIH HHS / CA / R01CA088986
  • [Publication-type] Comment; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS258963; NLM/ PMC3016876
  •  go-up   go-down


48. Wodarz D: Stem cell regulation and the development of blast crisis in chronic myeloid leukemia: Implications for the outcome of Imatinib treatment and discontinuation. Med Hypotheses; 2008;70(1):128-36
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] Stem cell regulation and the development of blast crisis in chronic myeloid leukemia: Implications for the outcome of Imatinib treatment and discontinuation.
  • Chronic myeloid leukemia (CML) is a cancer of the hematopoietic system that is initiated by a single genetic alteration (the BCR-ABL fusion gene or Philadelphia chromosome) and progresses in several phases: during the chronic phase the number of cells grows slowly and the fraction of immature cells is low.
  • The mechanisms that drive the transition from the chronic phase to blast crisis are not understood, and the requirement of genetic instability and further mutations has been suggested.
  • Using mathematical models, I describe a theory that can account for the transition from the chronic phase to blast crisis without the need to invoke further mutations.
  • The transition to blast crisis can be explained solely by feedback mechanisms that regulate the patterns of stem cell division, in particular the occurrence of symmetric versus asymmetric cell division.
  • According to the model, treatment can lead to the low level persistence of CML stem cells without assuming that these cells are less susceptible to drug-mediated activity, and this might explain why disease tends to relapse after treatment discontinuation even in the absence of acquired drug resistance.
  • Further, the model defines conditions when Imatinib treatment might lead to the eradication of CML, which is relevant in the context of recent data that show absence of relapse as long as two years after treatment cessation.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Blast Crisis / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Cell Division / drug effects. Disease Progression. Drug Administration Schedule. Humans. Imatinib Mesylate. Models, Biological. Stem Cells / pathology


49. Wang X, Ren J, Qu X: Targeted RNA interference of cyclin A2 mediated by functionalized single-walled carbon nanotubes induces proliferation arrest and apoptosis in chronic myelogenous leukemia K562 cells. ChemMedChem; 2008 Jun;3(6):940-5
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] Targeted RNA interference of cyclin A2 mediated by functionalized single-walled carbon nanotubes induces proliferation arrest and apoptosis in chronic myelogenous leukemia K562 cells.
  • Cyclin A(2) plays critical role in DNA replication, transcription, and cell cycle regulation.
  • Its overexpression has been detected and related to many types of cancers including leukemia, suggesting that suppression of cyclin A(2) would be an attractive strategy to prevent tumor progression.
  • Herein, we apply functionalized single wall carbon nanotubes (f-SWNTs) to carry small interfering RNA (siRNA) into K562 cells and determine whether inhibition of cyclin A(2) would be a potential therapeutic target for chronic myelogenous leukemia.
  • We demonstrate that depletion of cyclin A(2) in this manner inhibits cell proliferation and promotes apoptosis, and cyclin A(2) can serve as a novel therapeutic target. siRNA against cyclin A(2) delivered by functionalized single wall carbon nanotubes may be a useful therapeutic strategy for chronic myelogenous leukemia cells.
  • This would provide new insights on additional therapeutic options for chronic myelogenous leukemia beyond chemotherapy in light of increasing multidrug resistance.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Cyclin A / antagonists & inhibitors. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Nanotubes, Carbon / chemistry. RNA, Small Interfering / pharmacology
  • [MeSH-minor] Cell Proliferation / drug effects. Cyclin A2. Drug Carriers / chemistry. Drug Screening Assays, Antitumor. Humans. K562 Cells. RNA Interference

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • 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 = 18286553.001).
  • [ISSN] 1860-7187
  • [Journal-full-title] ChemMedChem
  • [ISO-abbreviation] ChemMedChem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CCNA2 protein, human; 0 / Cyclin A; 0 / Cyclin A2; 0 / Drug Carriers; 0 / Nanotubes, Carbon; 0 / RNA, Small Interfering
  •  go-up   go-down


50. Soh BN, Klein F, Feldhahn N, Müschen M: B-lymphoid or myeloid lineage identity of cell lines derived from chronic myeloid leukemia blast crisis. Cancer Genet Cytogenet; 2005 Sep;161(2):187-8
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] B-lymphoid or myeloid lineage identity of cell lines derived from chronic myeloid leukemia blast crisis.
  • [MeSH-major] Blast Crisis. Cell Lineage. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • [MeSH-minor] B-Lymphocytes / pathology. Cell Line, Tumor. Granulocyte Precursor Cells / pathology. Humans


51. Tsimberidou AM, Catovsky D, Schlette E, O'Brien S, Wierda WG, Kantarjian H, Garcia-Manero G, Wen S, Do KA, Lerner S, Keating MJ: Outcomes in patients with splenic marginal zone lymphoma and marginal zone lymphoma treated with rituximab with or without chemotherapy or chemotherapy alone. Cancer; 2006 Jul 1;107(1):125-35
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] Outcomes in patients with splenic marginal zone lymphoma and marginal zone lymphoma treated with rituximab with or without chemotherapy or chemotherapy alone.
  • BACKGROUND: The optimal management of patients with splenic marginal zone lymphoma/marginal zone lymphoma (SMZL) is controversial.
  • METHODS: The Leukemia Service database was searched for patients with splenic lymphoma who were registered between May 1995 and October 2004.
  • The indications for treatment were the same as those used for patients with chronic lymphocytic leukemia.
  • The median number of CD20 molecules per cell was 69 x 10(3).
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma / drug therapy. Splenic Neoplasms / drug therapy

  • MedlinePlus Health Information. consumer health - Lymphoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2006 American Cancer Society.
  • (PMID = 16700034.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  •  go-up   go-down


52. Hejmadi RK, Thompson D, Shah F, Naresh KN: Cutaneous presentation of aleukemic monoblastic leukemia cutis - a case report and review of literature with focus on immunohistochemistry. J Cutan Pathol; 2008 Oct;35 Suppl 1:46-9
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] Cutaneous presentation of aleukemic monoblastic leukemia cutis - a case report and review of literature with focus on immunohistochemistry.
  • Aleukemic monoblastic leukemia cutis is a rare cutaneous manifestation of a systemic hematological disorder associated with dermal infiltration of monoblasts preceding bone marrow or peripheral blood involvement.
  • We report a case of a 75-year-old woman who presented with an erythematous maculopapular rash, which was clinically diagnosed as viral exanthema.
  • Microscopy of the skin biopsy showed features of monoblastic leukemia.
  • We present this case to alert dermatologists of innocuous erythematous skin lesions clinically resembling a viral exanthema, which, in rare instances, may be a presenting feature of an aleukemic monoblastic leukemia cutis.
  • This entity poses problems for dermatopathologists even on immunohistochemistry as monoblasts are negative for hemopoietic precursor cell antigens like CD34, Terminal deoxynncleotidy1 transferase (TdT) and CD117.
  • [MeSH-major] Leukemia, Monocytic, Acute / metabolism. Leukemia, Monocytic, Acute / pathology. Skin Neoplasms / metabolism. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Antigens, CD / metabolism. Diabetes Mellitus, Type 2. Diagnosis, Differential. Exanthema / pathology. Female. Humans. Hypothyroidism / complications. Immunohistochemistry. Myocardial Ischemia / complications. Peripheral Vascular Diseases / complications. Pulmonary Disease, Chronic Obstructive / complications. Sweet Syndrome / pathology

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright Blackwell Munksgaard 2008.
  • (PMID = 18544052.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD
  •  go-up   go-down


53. Milani C, Castillo J: Veltuzumab, an anti-CD20 mAb for the treatment of non-Hodgkin's lymphoma, chronic lymphocytic leukemia and immune thrombocytopenic purpura. Curr Opin Mol Ther; 2009 Apr;11(2):200-7
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] Veltuzumab, an anti-CD20 mAb for the treatment of non-Hodgkin's lymphoma, chronic lymphocytic leukemia and immune thrombocytopenic purpura.
  • Veltuzumab is a humanized, second-generation anti-CD20 mAb currently under development by Immunomedics Inc for the potential treatment of B-cell non-Hodgkin's lymphoma (NHL) and chronic lymphocytic leukemia (CLL).
  • In vitro studies have demonstrated that veltuzumab has enhanced binding avidities and a stronger effect on complement-dependent cytotoxicity compared with rituximab in selected cell lines.
  • In dose-finding phase I/II clinical trials in patients with low-grade NHL, intravenous veltuzumab demonstrated a substantial rate of complete responses in concurrence with shorter and more tolerable infusions compared with rituximab.
  • Veltuzumab is undergoing clinical trials using a low-dose subcutaneous formulation in patients with NHL, CLL and ITP.
  • Prospective, randomized clinical trials are needed to clarify the role veltuzumab will play in a market where the therapy of B-cell lymphoproliferative disorders is dominated by rituximab.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Non-Hodgkin / drug therapy. Purpura, Thrombocytopenic, Idiopathic / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Cell Line. Clinical Trials as Topic. Humans


54. Wu Z, Xu Y: IL-15R alpha-IgG1-Fc enhances IL-2 and IL-15 anti-tumor action through NK and CD8+ T cells proliferation and activation. J Mol Cell Biol; 2010 Aug;2(4):217-22
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.
  • NK cells in combination with monoclonal antibodies to surface antigens of the tumor cell have been proved to be effective in a number of clinical trials.
  • We then measured the cytotoxicity of expanded NK and CD8(+) T cells against tumor cell lines and primary tumor cells.
  • Expanded NK and CD8(+) T cell populations had cytotoxic function against the PC3, LNCaP, K562 and chronic lymphocytic leukemia (CLL) patient primary B cell lymphoma.
  • These data support clinical testing IL-2/IL-15Ralpha-IgG1-Fc expanded NK cells in patients with prostate cancer and CLL.
  • [MeSH-major] Antineoplastic Agents / immunology. CD8-Positive T-Lymphocytes / immunology. Cell Proliferation. Immunoglobulin Fc Fragments / immunology. Interleukin-15 / immunology. Interleukin-15 Receptor alpha Subunit / immunology. Interleukin-2 / immunology. Killer Cells, Natural / immunology
  • [MeSH-minor] Cell Line, Tumor. Cells, Cultured. Humans. Immunoglobulin G / genetics. Immunoglobulin G / immunology. Lymphocyte Activation. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20671116.001).
  • [ISSN] 1759-4685
  • [Journal-full-title] Journal of molecular cell biology
  • [ISO-abbreviation] J Mol Cell Biol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunoglobulin Fc Fragments; 0 / Immunoglobulin G; 0 / Interleukin-15; 0 / Interleukin-15 Receptor alpha Subunit; 0 / Interleukin-2; 0 / Recombinant Fusion Proteins
  •  go-up   go-down


55. Eichhorst B, Hallek M, Dreyling M, ESMO Guidelines Working Group: Chronic lymphocytic leukaemia: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up. Ann Oncol; 2010 May;21 Suppl 5:v162-4
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 leukaemia: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20555070.001).
  • [ISSN] 1569-8041
  • [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; Practice Guideline; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD20; 0 / Antigens, CD5; 0 / Receptors, IgE
  •  go-up   go-down


56. Farina L, Carniti C, Dodero A, Vendramin A, Raganato A, Spina F, Patriarca F, Narni F, Benedetti F, Olivieri A, Corradini P: Qualitative and quantitative polymerase chain reaction monitoring of minimal residual disease in relapsed chronic lymphocytic leukemia: early assessment can predict long-term outcome after reduced intensity allogeneic transplantation. Haematologica; 2009 May;94(5):654-62
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] Qualitative and quantitative polymerase chain reaction monitoring of minimal residual disease in relapsed chronic lymphocytic leukemia: early assessment can predict long-term outcome after reduced intensity allogeneic transplantation.
  • BACKGROUND: The graft-versus-leukemia effect is able to induce clinical responses in patients with chronic lymphocytic leukemia treated with a reduced intensity conditioning regimen, followed by allogeneic stem cell transplantation.
  • We investigated whether molecular remissions could be attained after reduced intensity conditioning and allogeneic stem cell transplantation in patients with relapsed chronic lymphocytic leukemia and whether the assessment of minimal residual disease might be used to predict the clinical outcome.
  • DESIGN AND METHODS: Minimal residual disease was monitored by polymerase chain reaction using the immunoglobulin heavy-chain gene rearrangement as a molecular marker in 29 relapsed patients who achieved complete remission following reduced intensity conditioning and allogeneic stem cell transplantation.
  • RESULTS: Three patterns of minimal residual disease were observed: negative (31%), mixed (24%), and always positive (45%).
  • The cumulative incidence of relapse according to the minimal residual disease status at 6 and 12 months after transplantation was significantly different between polymerase chain reaction-negative and -positive patients (p=0.031 and p=0.04, respectively).
  • Two-year disease-free survival was 93% and 46% for polymerase chain reaction-negative and -positive patients at 6 months after transplantation, respectively (p=0.012).
  • Similarly, 2-year disease-free survival was 100% and 57% for polymerase chain reaction-negative and -positive patients at 12 months, respectively (p=0.037).
  • No clinical or biological factors were predictive of the achievement of polymerase chain reaction negativity after allogeneic stem cell transplantation.
  • Graft-versus-host disease was more frequent in patients who did not relapse (p=0.04).
  • Quantitative monitoring of minimal residual disease was able to identify polymerase chain reaction-positive patients with a higher risk of relapse.
  • CONCLUSIONS: These findings demonstrate that relapsed patients can achieve molecular remission after reduced intensity conditioning and allogeneic stem cell transplantation and suggest a minimal residual disease-driven intervention that might be useful to prevent overt hematologic relapse.
  • [MeSH-major] Immunoglobulin Heavy Chains / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Neoplasm, Residual / genetics. Polymerase Chain Reaction / methods
  • [MeSH-minor] Adult. Aged. Female. Gene Rearrangement. Graft vs Host Disease / diagnosis. Graft vs Host Disease / genetics. Graft vs Leukemia Effect / genetics. Hematopoietic Stem Cell Transplantation / methods. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Outcome Assessment (Health Care) / methods. Predictive Value of Tests. Prognosis. Reproducibility of Results. Survival Analysis. Time Factors. Transplantation Conditioning. Transplantation, Homologous

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Bone Marrow Transplant. 2000 Apr;25(7):717-22 [10745256.001]
  • [Cites] J Clin Oncol. 2008 Nov 1;26(31):5094-100 [18711173.001]
  • [Cites] Bone Marrow Transplant. 2000 Dec;26(12):1305-11 [11223970.001]
  • [Cites] Leukemia. 2001 Mar;15(3):445-51 [11237069.001]
  • [Cites] Blood. 2002 Jan 1;99(1):75-82 [11756155.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Blood. 2002 Mar 1;99(5):1873-4 [11871387.001]
  • [Cites] Bone Marrow Transplant. 2002 May;29(10):817-23 [12058231.001]
  • [Cites] Leukemia. 2003 May;17(5):841-8 [12750695.001]
  • [Cites] Leukemia. 2003 Jun;17(6):1013-34 [12764363.001]
  • [Cites] J Clin Oncol. 2003 Jul 15;21(14):2747-53 [12860954.001]
  • [Cites] Exp Hematol. 2004 Jan;32(1):28-35 [14725898.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2850-8 [14670929.001]
  • [Cites] Blood. 2004 Oct 15;104(8):2600-2 [15205268.001]
  • [Cites] Blood. 1981 Feb;57(2):267-76 [7004534.001]
  • [Cites] J Clin Oncol. 1983 Nov;1(11):710-9 [6668489.001]
  • [Cites] Bone Marrow Transplant. 1995 Jun;15(6):825-8 [7581076.001]
  • [Cites] Bone Marrow Transplant. 1996 Mar;17(3):371-5 [8704689.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] Bone Marrow Transplant. 1996 Sep;18(3):669-72 [8879640.001]
  • [Cites] Leukemia. 1997 Oct;11(10):1793-8 [9324303.001]
  • [Cites] Ann Oncol. 1998 Sep;9(9):1023-6 [9818078.001]
  • [Cites] Blood. 1999 Sep 15;94(6):1848-54 [10477713.001]
  • [Cites] J Clin Oncol. 2005 May 20;23(15):3433-8 [15809449.001]
  • [Cites] J Clin Oncol. 2005 Jun 1;23(16):3819-29 [15809448.001]
  • [Cites] J Clin Oncol. 2005 Nov 1;23(31):8122-3; author reply 8123-4 [16258114.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4389-96 [16131571.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1724-30 [16239425.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4563-9 [16449533.001]
  • [Cites] Leukemia. 2007 Apr;21(4):604-11 [17287850.001]
  • [Cites] Leukemia. 2007 May;21(5):956-64 [17361231.001]
  • [Cites] Leukemia. 2007 Nov;21(11):2316-23 [17597807.001]
  • [Cites] Leukemia. 2008 Jul;22(7):1377-86 [18418404.001]
  • [Cites] J Clin Oncol. 2008 Aug 20;26(24):3913-5 [18711176.001]
  • [Cites] Biol Blood Marrow Transplant. 2000;6(3):241-53 [10871149.001]
  • (PMID = 19377072.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains
  • [Other-IDs] NLM/ PMC2675677
  •  go-up   go-down


57. Chang G, Meadows ME, Orav EJ, Antin JH: Mental status changes after hematopoietic stem cell transplantation. Cancer; 2009 Oct 1;115(19):4625-35
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] Mental status changes after hematopoietic stem cell transplantation.
  • BACKGROUND: The growing numbers of survivors of innovative cancer treatments, such as hematopoietic stem cell transplantation (HSCT), often report subsequent cognitive difficulties.
  • The objective of this study was to evaluate and compare neurocognitive changes in patients with chronic myelogenous leukemia (CML) or primary myelodysplastic syndrome (MDS) after allogeneic HSCT or other therapies.
  • METHODS: In this prospective cohort study, serial evaluations of attention, concentration, memory, mood, and quality of life were used in a consecutive sample of 106 eligible patients who had CML (n = 91) or MDS (n = 15) at enrollment and then 12 months and 18 months after HSCT or other therapy.
  • CONCLUSIONS: The current study indicated that time and diagnosis may be important factors when assessing neurocognitive and other changes.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / psychology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / psychology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Mental Health. Myelodysplastic Syndromes / psychology. Myelodysplastic Syndromes / therapy


58. Carver JD, Calverley D, Shen P: Chronic lymphocytic leukemia/small lymphocytic lymphoma presenting in urinary bladder without peripheral blood lymphocytosis: case report and literature review. Leuk Lymphoma; 2006 Jun;47(6):1163-5
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] Chronic lymphocytic leukemia/small lymphocytic lymphoma presenting in urinary bladder without peripheral blood lymphocytosis: case report and literature review.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Urinary Bladder Neoplasms / diagnosis
  • [MeSH-minor] Aged, 80 and over. Cell Proliferation. Epithelial Cells / metabolism. Humans. Immunohistochemistry. Lymphocytes / metabolism. Male. Treatment Outcome

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16840214.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  •  go-up   go-down


59. Podhorecka M, Halicka D, Klimek P, Kowal M, Chocholska S, Dmoszynska A: Simvastatin and purine analogs have a synergic effect on apoptosis of chronic lymphocytic leukemia cells. Ann Hematol; 2010 Nov;89(11):1115-24
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] Simvastatin and purine analogs have a synergic effect on apoptosis of chronic lymphocytic leukemia cells.
  • Despite many therapeutic regimens introduced recently, chronic lymphocytic leukemia (CLL) is still an incurable disorder.
  • Thus, there is an urgent need to discover novel, less toxic and more effective drugs for CLL patients.
  • In this study, we attempted to assess simvastatin, widely used as a cholesterol-lowering drug, both as a single agent and in combination with purine analogs-fludarabine and cladribine-in terms of its effect on apoptosis and DNA damage of CLL cells.
  • The experiments were done in ex vivo short-term cell cultures of blood and bone marrow cells from newly diagnosed untreated patients.
  • Results of our study revealed that simvastatin induced apoptosis of CLL cells concurrently with lowering of BCL-2/BAX ratio, and its pro-apoptotic effect is tumor-specific, not affecting normal lymphocytes.
  • Interestingly, the rate of apoptosis caused by simvastatin alone and in combination was independent of markers of disease progression like ZAP-70 and CD38 expression or clinical stage according to Rai classification.
  • The results suggest that simvastatin can be used in the treatment of CLL patients as a single agent as well as in combination with purine analogs, being equally effective both in high-risk and good-prognosis patients.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cladribine / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Simvastatin / pharmacology. Tumor Cells, Cultured / drug effects. Vidarabine / analogs & derivatives
  • [MeSH-minor] Anticholesteremic Agents / pharmacology. Antigens, CD38 / metabolism. Apoptosis / drug effects. Ataxia Telangiectasia Mutated Proteins. Caspase 3 / metabolism. Cell Cycle Proteins / metabolism. DNA-Binding Proteins / metabolism. Enzyme Activation. Histones / metabolism. Humans. Prognosis. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Purines / chemistry. Purines / pharmacology. Tumor Suppressor Proteins / metabolism. ZAP-70 Protein-Tyrosine Kinase / metabolism. bcl-2-Associated X Protein / metabolism

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. CLADRIBINE .
  • Hazardous Substances Data Bank. VIDARABINE .
  • Hazardous Substances Data Bank. SIMVASTATIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Ann Med. 2000 Apr;32(3):164-76 [10821323.001]
  • [Cites] J Immunol. 2000 Sep 1;165(5):2712-8 [10946302.001]
  • [Cites] J Investig Med. 2001 Jul;49(4):319-24 [11478407.001]
  • [Cites] Atherosclerosis. 2002 Mar;161(1):17-26 [11882313.001]
  • [Cites] Leukemia. 2002 Apr;16(4):508-19 [11960327.001]
  • [Cites] Br J Cancer. 2002 May 6;86(9):1436-9 [11986777.001]
  • [Cites] Pharmacotherapy. 2002 Jul;22(7):853-63 [12126219.001]
  • [Cites] Curr Opin Lipidol. 2002 Dec;13(6):637-44 [12441888.001]
  • [Cites] Eur Heart J. 2003 Feb;24(3):225-48 [12590901.001]
  • [Cites] N Engl J Med. 2003 May 1;348(18):1764-75 [12724482.001]
  • [Cites] Exp Hematol. 2003 Sep;31(9):779-83 [12962723.001]
  • [Cites] Br J Cancer. 2004 Feb 9;90(3):635-7 [14760377.001]
  • [Cites] Leuk Res. 2004 May;28(5):429-42 [15068894.001]
  • [Cites] Oncol Rep. 2004 May;11(5):1053-8 [15069546.001]
  • [Cites] Circulation. 2004 Jun 15;109(23 Suppl 1):III50-7 [15198967.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 May 1;88(9):3628-32 [1673788.001]
  • [Cites] Leuk Lymphoma. 1997 Feb;24(5-6):533-7 [9086443.001]
  • [Cites] Blood. 1997 Jun 1;89(11):4153-60 [9166858.001]
  • [Cites] Blood Rev. 1997 Sep;11(3):119-28 [9370043.001]
  • [Cites] Blood. 1999 Feb 15;93(4):1308-18 [9949174.001]
  • [Cites] J Clin Oncol. 1999 Jan;17(1):399-408 [10458259.001]
  • [Cites] Blood. 1999 Sep 15;94(6):1848-54 [10477713.001]
  • [Cites] Transfus Apher Sci. 2005 Feb;32(1):33-44 [15737872.001]
  • [Cites] Carcinogenesis. 2005 May;26(5):883-91 [15705602.001]
  • [Cites] Int J Oncol. 2005 Oct;27(4):1113-24 [16142330.001]
  • [Cites] Haematologica. 2006 Apr;91(4):542-5 [16585018.001]
  • [Cites] Methods Mol Biol. 2006;314:81-93 [16673876.001]
  • [Cites] Cancer Biother Radiopharm. 2006 Aug;21(4):364-72 [16999602.001]
  • [Cites] Cell Cycle. 2006 Sep;5(17):1940-5 [16940754.001]
  • [Cites] Oncol Rep. 2006 Dec;16(6):1389-95 [17089066.001]
  • [Cites] Leukemia. 2007 Feb;21(2):248-52 [17122863.001]
  • [Cites] Cancer Invest. 2007 Aug;25(5):279-84 [17661201.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2008;:444-9 [19074124.001]
  • [Cites] Br J Haematol. 2009 Jan;144(1):41-52 [19006566.001]
  • [Cites] Pharmacology. 2009;84(4):191-5 [19729986.001]
  • [Cites] Clin Lymphoma Myeloma. 2009 Oct;9(5):365-70 [19858055.001]
  • [Cites] Cancer Res. 2010 Jan 15;70(2):440-6 [20068163.001]
  • [Cites] Clin Cancer Res. 2003 Jan;9(1):10-9 [12538446.001]
  • (PMID = 20499237.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anticholesteremic Agents; 0 / Antineoplastic Agents; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / H2AFX protein, human; 0 / Histones; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Purines; 0 / Tumor Suppressor Proteins; 0 / bcl-2-Associated X Protein; 47M74X9YT5 / Cladribine; AGG2FN16EV / Simvastatin; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.2.2.5 / Antigens, CD38; EC 3.4.22.- / Caspase 3; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  • [Other-IDs] NLM/ PMC2940031
  •  go-up   go-down


60. Au WY, Fung A, Wong KF, Chan CH, Liang R: Tumor necrosis factor alpha promoter polymorphism and the risk of chronic lymphocytic leukemia and myeloma in the Chinese population. Leuk Lymphoma; 2006 Oct;47(10):2189-93
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] Tumor necrosis factor alpha promoter polymorphism and the risk of chronic lymphocytic leukemia and myeloma in the Chinese population.
  • The -308 GA promoter polymorphism of tumor necrosis factor alpha (TNFalpha) has been reported to be associated with an increased risk of lymphoid malignancies in Caucasians.
  • We studied the incidence and prognostic significance of this polymorphism in Chinese patients with plasma cell myeloma (PCM), chronic lymphocytic leukemia (CLL) and lymphomas.
  • Despite a far lower incidence of PCM and CLL in the Chinese population compared with Caucasians, the rates of TNFalpha-308A were similar to those in Caucasians, both in the study and control populations.
  • Similarly, there was no increased rate of TNFalpha-308A in all the lymphomas studied, irrespective of lineage.
  • However, TNFalpha-308A is significantly associated with female CLL cases and confers a strong negative prognostic impact for Chinese CLL.
  • These argue for a possible biological role for increased TNFalpha production in CLL progression in low-risk individuals.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Multiple Myeloma / genetics. Polymorphism, Genetic. Promoter Regions, Genetic. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Lineage. China. Disease Progression. Female. Humans. Male. Middle Aged. Prognosis

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Multiple Myeloma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17071494.001).
  • [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 / Tumor Necrosis Factor-alpha
  •  go-up   go-down


61. San José-Eneriz E, Agirre X, Jiménez-Velasco A, Cordeu L, Martín V, Arqueros V, Gárate L, Fresquet V, Cervantes F, Martínez-Climent JA, Heiniger A, Torres A, Prósper F, Roman-Gomez J: Epigenetic down-regulation of BIM expression is associated with reduced optimal responses to imatinib treatment in chronic myeloid leukaemia. Eur J Cancer; 2009 Jul;45(10):1877-89
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] Epigenetic down-regulation of BIM expression is associated with reduced optimal responses to imatinib treatment in chronic myeloid leukaemia.
  • DESIGN AND METHODS: We analysed the mRNA expression of BIM in 100 newly diagnosed patients with CML in chronic phase by Q-RT-PCR and the protein levels by Western blot analysis.
  • CML cell lines were treated with imatinib and 5-aza-2'-deoxycytidine, and were transfected with two different siRNAs against BIM and cell proliferation and apoptosis were analysed.
  • RESULTS: We demonstrated that down-regulation of BIM expression was present in 36% of the patients and was significantly associated with a lack of optimal response to imatinib as indicated by the decrease in cytogenetic and molecular responses at 6, 12 and 18 months in comparison with patients with normal BIM expression (p<0.05).
  • Using CML cell lines with low and normal expression of BIM we further demonstrated that the expression of BIM is required for imatinib-induced CML apoptosis.
  • CONCLUSION: Our data indicate that down-regulation of BIM is epigenetically controlled by methylation in a percentage of CML patients and has an unfavourable prognostic impact, and that the combination of imatinib with a de-methylating agent may result in improved responses in patients with decreased expression of BIM.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis Regulatory Proteins / biosynthesis. Down-Regulation / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Membrane Proteins / biosynthesis. Piperazines / pharmacology. Proto-Oncogene Proteins / biosynthesis. Pyrimidines / pharmacology
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Benzamides. Cell Proliferation / drug effects. DNA Methylation. DNA Modification Methylases / antagonists & inhibitors. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical / methods. Drug Resistance, Neoplasm / genetics. Epigenesis, Genetic. Female. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / genetics. Humans. Imatinib Mesylate. Male. Middle Aged. Promoter Regions, Genetic / genetics. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • Hazardous Substances Data Bank. AZACITIDINE .
  • 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 = 19403302.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Benzamides; 0 / Membrane Proteins; 0 / Piperazines; 0 / Proto-Oncogene Proteins; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 776B62CQ27 / decitabine; 8A1O1M485B / Imatinib Mesylate; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
  •  go-up   go-down


62. Jensen M, Engert A, Weissinger F, Knauf W, Kimby E, Poynton C, Oliff IA, Rummel MJ, Osterborg A: Phase I study of a novel pro-apoptotic drug R-etodolac in patients with B-cell chronic lymphocytic leukemia. Invest New Drugs; 2008 Apr;26(2):139-49
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] Phase I study of a novel pro-apoptotic drug R-etodolac in patients with B-cell chronic lymphocytic leukemia.
  • R-etodolac is a novel pro-apoptotic agent with potential antitumor activity against B-cell chronic lymphocytic leukemia (B-CLL).
  • This phase I clinical trial was conducted to determine the tolerability, safety, and maximum tolerated dose (MTD) of R-etodolac, administered orally twice a day (BID), in patients with B-CLL.
  • Secondary objectives included evaluating clinical response, pharmacodynamic activity (reduction of lymphocytes), and pharmacokinetic (PK) profile.
  • Adverse events were generally mild and self-limiting, although in an apparent dose-response relationship, grade 2 and 3 gastrointestinal toxicities and grade 3 skin toxicities were reported with the highest dose regimens (1,800 and 2,400 mg BID).
  • PK results indicated that oral absorption of R-etodolac was rapid (time to maximum concentration ranged from 2 to 4 h), and the half-life ranged from 5 to 7 h.
  • R-etodolac significantly reduced absolute lymphocyte count (ALC) in B-CLL patients in a dose-dependent manner up to 1,800 mg BID and caused partial responses in 2 patients.
  • Further study of R-etodolac as a possible new maintenance therapy or as a part of combination therapy of B-CLL appears warranted.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Etodolac / adverse effects. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Maximum Tolerated Dose
  • [MeSH-minor] Administration, Oral. Adult. Aged. Alanine Transaminase / drug effects. Apoptosis / drug effects. Dose-Response Relationship, Drug. Female. Half-Life. Humans. Lymphocytes / drug effects. Male. Middle Aged

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, B-cell, chronic.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] N Engl J Med. 1992 Sep 10;327(11):749-54 [1501650.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2003;:153-75 [14633781.001]
  • [Cites] N Engl J Med. 2005 Mar 17;352(11):1131-2 [15713947.001]
  • [Cites] Acta Haematol. 2004;111(1-2):107-23 [14646349.001]
  • [Cites] Eur J Haematol. 2005 Sep;75(3):212-20 [16104877.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):3118-23 [14973184.001]
  • [Cites] Blood. 2002 Apr 1;99(7):2625-6 [11926185.001]
  • [Cites] Blood. 1999 Apr 1;93(7):2386-94 [10090950.001]
  • [Cites] Invest New Drugs. 2007 Aug;25(4):297-303 [17440681.001]
  • [Cites] Clin Adv Hematol Oncol. 2004 Feb;2(2):107-13 [16163170.001]
  • [Cites] J Clin Oncol. 2005 Oct 1;23(28):7024-31 [16145065.001]
  • [Cites] N Engl J Med. 2005 Feb 24;352(8):804-15 [15728813.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6325-32 [16155015.001]
  • [Cites] J Exp Med. 1999 Aug 16;190(4):445-50 [10449515.001]
  • [Cites] J Intern Med. 2005 Aug;258(2):115-23 [16018788.001]
  • [Cites] Clin Pharmacokinet. 1994 Apr;26(4):259-74 [8013160.001]
  • [Cites] Aust N Z J Med. 1990 Feb;20(1):44-50 [2322201.001]
  • [Cites] Cancer. 2006 Jan 15;106(2):337-45 [16353201.001]
  • [Cites] Leuk Res. 2006 Feb;30(2):123-35 [16046235.001]
  • [Cites] N Engl J Med. 2000 Dec 14;343(24):1750-7 [11114313.001]
  • [Cites] Curr Treat Options Oncol. 2006 May;7(3):200-12 [16615876.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Feb 15;102(7):2525-30 [15699354.001]
  • [Cites] Cancer Cell. 2004 Jun;5(6):565-74 [15193259.001]
  • [Cites] Blood. 1998 Aug 15;92 (4):1406-14 [9694730.001]
  • [Cites] Cancer Chemother Pharmacol. 2007 Sep;60(4):545-53 [17186240.001]
  • [Cites] J Med Chem. 1983 Dec;26(12):1778-80 [6227748.001]
  • [Cites] Ann Intern Med. 1998 Oct 1;129(7):559-66 [9758577.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] Blood. 2005 Jul 15;106(2):706-12 [15802527.001]
  • [Cites] N Engl J Med. 1995 Oct 19;333(16):1052-7 [7675049.001]
  • [Cites] Blood. 1993 Sep 15;82(6):1695-700 [8400226.001]
  • [Cites] Drug Saf. 2002;25(7):537-44 [12093311.001]
  • [Cites] Drug Metab Dispos. 1990 Jul-Aug;18(4):471-5 [1976070.001]
  • (PMID = 18094935.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 2M36281008 / Etodolac; EC 2.6.1.2 / Alanine Transaminase
  •  go-up   go-down


63. Hiraoka H, Hisasue M, Nagashima N, Miyama T, Tanimoto T, Watanabe M, Itamoto K, Mizuno T, Inokuma H, Okuda M: A dog with myelodysplastic syndrome: chronic myelomonocytic leukemia. J Vet Med Sci; 2007 Jun;69(6):665-8
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] A dog with myelodysplastic syndrome: chronic myelomonocytic leukemia.
  • The bone marrow revealed dysplastic features in all three hematopoietic cell lines, and an increase in the monocytic cell line.
  • Based on the features of the bone marrow and the peripheral blood, this case was confirmed to be myelodysplastic syndrome--Chronic myelomonocytic leukaemia (MDS-CMML).

  • Hazardous Substances Data Bank. CYCLOSPORIN A .
  • 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 = 17611368.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 83HN0GTJ6D / Cyclosporine
  •  go-up   go-down


64. Manu N, Amir P, Pinto M, Rajiv C: Reactivation of hepatitis B in an elderly patient with chronic lymphatic leukemia. J Clin Gastroenterol; 2006 Sep;40(8):762-3
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] Reactivation of hepatitis B in an elderly patient with chronic lymphatic leukemia.
  • [MeSH-major] Hepatitis B / virology. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Leukemia, Lymphocytic, Chronic, B-Cell / virology. Virus Activation

  • Genetic Alliance. consumer health - Hepatitis.
  • MedlinePlus Health Information. consumer health - Hepatitis B.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16940893.001).
  • [ISSN] 0192-0790
  • [Journal-full-title] Journal of clinical gastroenterology
  • [ISO-abbreviation] J. Clin. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  •  go-up   go-down


65. Jønsson V, Bock JE, Hilden J, Houlston RS, Wiik A: The influence of pregnancy on the development of autoimmunity in chronic lymphocytic leukemia. Leuk Lymphoma; 2006 Aug;47(8):1481-7
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 influence of pregnancy on the development of autoimmunity in chronic lymphocytic leukemia.
  • To examine whether pregnancy influences the development of autoimmunity in chronic lymphocytic leukemia (CLL), we studied 591 consecutive CLL patients (202 post-menopausal women and 389 men).
  • Autoimmune manifestations were analyzed in 194 women with known obstetric history and known number of long-term sexual partners, and in the 389 male CLL patients for comparison.
  • One hundred and fifty-nine of the CLL patients exhibited autoimmune manifestations, 38% in females and 21% in men.
  • In female CLL patients, the frequency of autoimmunity and the number of pregnancies and the number of partners were strongly correlated.
  • The impact of pregnancy on expressed autoimmunity increased with each additional sexual partner (the odds of autoimmunity increased 11 times with each long-term sexual partner).
  • The average numbers of pregnancies in female CLL patients with and without autoimmunity were 4.92 and 2.24, respectively (P < 0.001).
  • Coombs' positive autoimmune anemia, a gastric ulcer with parietal cell autoantibodies and idiopathic thrombocytopenic purpura were equally common in women and men, whereas autoimmune thyroiditis, Sjögren's syndrome, rheumatoid arthritis and systemic lupus erythematosus were seen in higher rates in women than in men.
  • The spectrum of autoimmunity suggests that pregnancy-related alloimmunization may be involved in the development of autoimmunity in CLL.
  • [MeSH-major] Autoimmunity. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Pregnancy Complications, Neoplastic / immunology

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Pregnancy.
  • MedlinePlus Health Information. consumer health - Tumors and Pregnancy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Leuk Lymphoma. 2006 Aug;47(8):1443-4 [16966247.001]
  • [CommentIn] Leuk Lymphoma. 2006 Aug;47(8):1445-6 [16966248.001]
  • (PMID = 16966257.001).
  • [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 / Autoantibodies
  •  go-up   go-down


66. Campbell PJ, Pleasance ED, Stephens PJ, Dicks E, Rance R, Goodhead I, Follows GA, Green AR, Futreal PA, Stratton MR: Subclonal phylogenetic structures in cancer revealed by ultra-deep sequencing. Proc Natl Acad Sci U S A; 2008 Sep 02;105(35):13081-6
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.
  • During the clonal expansion of cancer from an ancestral cell with an initiating oncogenic mutation to symptomatic neoplasm, the occurrence of somatic mutations (both driver and passenger) can be used to track the on-going evolution of the neoplasm.
  • We used ultra-deep pyrosequencing to investigate intraclonal diversification at the Ig heavy chain locus in 22 patients with B-cell chronic lymphocytic leukemia.
  • Analysis of a non-polymorphic control locus revealed artifactual insertions and deletions resulting from sequencing errors and base substitutions caused by polymerase misincorporation during PCR amplification.
  • This proved capable of detecting multiple rare subclones with frequencies as low as 1 in 5000 copies and allowed the characterization of phylogenetic interrelationships among subclones within each patient.
  • This study demonstrates the potential for ultra-deep resequencing to recapitulate the dynamics of clonal evolution in cancer cell populations.
  • [MeSH-major] Cell Lineage. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Sequence Analysis, DNA / methods

  • 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
  • [Cites] Methods Enzymol. 2006;409:195-213 [16793403.001]
  • [Cites] Semin Oncol. 2006 Apr;33(2):150-6 [16616061.001]
  • [Cites] Science. 2006 Oct 13;314(5797):268-74 [16959974.001]
  • [Cites] Anal Biochem. 2007 Jan 1;360(1):84-91 [17107651.001]
  • [Cites] Blood. 2007 Feb 15;109(4):1559-67 [17082314.001]
  • [Cites] Nature. 2007 Mar 8;446(7132):153-8 [17344846.001]
  • [Cites] Nucleic Acids Res. 2007;35(13):e91 [17576693.001]
  • [Cites] Genome Res. 2007 Aug;17(8):1195-201 [17600086.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2242-9 [17496200.001]
  • [Cites] Science. 2008 Jan 18;319(5861):336-9 [18202291.001]
  • [Cites] Nat Methods. 2008 Feb;5(2):179-81 [18193056.001]
  • [Cites] J Immunol. 2000 Nov 1;165(9):5122-6 [11046043.001]
  • [Cites] Blood. 2002 Aug 1;100(3):1014-8 [12130516.001]
  • [Cites] J Exp Med. 2002 Sep 2;196(5):629-39 [12208878.001]
  • [Cites] Nat Rev Cancer. 2003 Sep;3(9):639-49 [12951583.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2257-317 [14671650.001]
  • [Cites] Blood. 2004 May 1;103(9):3490-5 [14695232.001]
  • [Cites] Nucleic Acids Res. 1988 Nov 11;16(21):10393 [3194225.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Apr;87(7):2833-7 [2320591.001]
  • [Cites] J Gen Virol. 1998 Dec;79 ( Pt 12):2921-8 [9880005.001]
  • [Cites] N Engl J Med. 2005 Feb 24;352(8):786-92 [15728811.001]
  • [Cites] J Clin Invest. 2005 Mar;115(3):755-64 [15711642.001]
  • [Cites] Cancer Res. 2005 Sep 1;65(17):7591-5 [16140923.001]
  • [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] Br J Haematol. 2006 Apr;133(1):50-8 [16512828.001]
  • [Cites] Nat Med. 2006 Jul;12(7):852-5 [16799556.001]
  • (PMID = 18723673.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / / 088340; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Nucleotides
  • [Other-IDs] NLM/ PMC2529122
  •  go-up   go-down


67. Young FM, Campbell A, Emo KL, Jansson J, Wang PY, Jordan CT, Mullen CA: High-risk acute lymphoblastic leukemia cells with bcr-abl and INK4A/ARF mutations retain susceptibility to alloreactive T cells. Biol Blood Marrow Transplant; 2008 Jun;14(6):622-30
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] High-risk acute lymphoblastic leukemia cells with bcr-abl and INK4A/ARF mutations retain susceptibility to alloreactive T cells.
  • INK4A/ARF mutations are acquired in bcr/abl(+) lymphoid blast phase chronic myelogenous leukemia (CML) and bcr/abl(+) acute lymphoblastic leukemia (ALL).
  • Donor lymphocyte infusion and graft-versus-leukemia (GVL) are generally ineffective in such ALLs, whereas GVL is highly active against bcr/abl(+) CML, which does not have a lesion in the INK4A/ARF locus.
  • The mechanisms for the ineffectiveness of GVL are not fully known, and it is possible that intrinsic resistance of acute lymphoid leukemias to immune effectors associated with allogeneic GVL may contribute to ineffectiveness.
  • These ALL lines were then studied in a murine model of MHC-matched, mHA-mismatched allogeneic BMT.
  • Thus, ALLs with INK4A/ARF or bcr/abl mutations are not intrinsically resistant to allogeneic T cell responses, suggesting that active immunotherapies against mHA have the potential to control such acute lymphoblastic leukemias.

  • Genetic Alliance. consumer health - Acute Lymphoblastic 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
  • [Cites] Blood. 2000 Apr 1;95(7):2426-33 [10733517.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2578-85 [17601986.001]
  • [Cites] Cancer Res. 2000 Oct 15;60(20):5797-802 [11059776.001]
  • [Cites] Curr Opin Hematol. 2001 Nov;8(6):349-54 [11604574.001]
  • [Cites] Leukemia. 2002 Apr;16(4):559-62 [11960332.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 28;99(11):7622-7 [12032333.001]
  • [Cites] Leuk Lymphoma. 2002 Aug;43(8):1637-44 [12400607.001]
  • [Cites] Bone Marrow Transplant. 2003 May;31(10):865-75 [12748663.001]
  • [Cites] Blood. 2004 Feb 1;103(3):767-76 [12958064.001]
  • [Cites] Leukemia. 2004 Apr;18(4):693-702 [15044926.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4010-22 [14982876.001]
  • [Cites] Genes Dev. 1994 May 1;8(9):1043-57 [7926786.001]
  • [Cites] Blood. 1995 Sep 1;86(5):2041-50 [7655033.001]
  • [Cites] Cell. 1996 Apr 5;85(1):27-37 [8620534.001]
  • [Cites] J Clin Oncol. 1997 Feb;15(2):433-44 [9053463.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 16;96(6):2988-93 [10077624.001]
  • [Cites] Cancer Res. 1999 Apr 1;59(7):1525-30 [10197624.001]
  • [Cites] Leukemia. 2005 May;19(5):713-20 [15789066.001]
  • [Cites] Mutat Res. 2005 Aug 25;576(1-2):22-38 [15878778.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 25;103(17):6688-93 [16618932.001]
  • [Cites] Oncogene. 2006 May 18;25(21):3023-31 [16407836.001]
  • [Cites] Oncogene. 2006 Jul 6;25(29):4110-5 [16491120.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Jan;13(1):34-45 [17222751.001]
  • [Cites] Immunity. 2007 Jun;26(6):703-14 [17582343.001]
  • [Cites] Bone Marrow Transplant. 2000 Sep;26(5):511-6 [11019840.001]
  • (PMID = 18489987.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA106289-05; United States / NCI NIH HHS / CA / 1R01CA10628; United States / NCI NIH HHS / CA / R01 CA106289-05
  • [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 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Minor Histocompatibility Antigens; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ NIHMS52879; NLM/ PMC2517424
  •  go-up   go-down


68. Kamat AV, Goldsmith D, O'Donnell P, van der Walt J, Carr R: Renal failure with granulomatous interstitial nephritis and diffuse leukemic renal infiltration in chronic lymphocytic leukemia. Ren Fail; 2007;29(6):763-5
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] Renal failure with granulomatous interstitial nephritis and diffuse leukemic renal infiltration in chronic lymphocytic leukemia.
  • Renal dysfunction is uncommon in patients with leukemic infiltration of the kidney due to Chronic Lymphocytic Leukanemia (CLL).
  • GIN combined with leukemic infiltration by CLL is very uncommon.
  • We present a 72-year-old male with Binet stage A CLL who developed progressive renal failure over a period of four years requiring maintenance dialysis.
  • [MeSH-major] Kidney / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemic Infiltration. Nephritis, Interstitial / etiology. Renal Insufficiency / etiology

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17763176.001).
  • [ISSN] 0886-022X
  • [Journal-full-title] Renal failure
  • [ISO-abbreviation] Ren Fail
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


69. Matthews K, Lim Z, Afzali B, Pearce L, Abdallah A, Kordasti S, Pagliuca A, Lombardi G, Madrigal JA, Mufti GJ, Barber LD: Imbalance of effector and regulatory CD4 T cells is associated with graft-versus-host disease after hematopoietic stem cell transplantation using a reduced intensity conditioning regimen and alemtuzumab. Haematologica; 2009 Jul;94(7):956-66
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] Imbalance of effector and regulatory CD4 T cells is associated with graft-versus-host disease after hematopoietic stem cell transplantation using a reduced intensity conditioning regimen and alemtuzumab.
  • BACKGROUND: A variety of immune pathways can lead to graft-versus-host disease.
  • A better understanding of the type of immune response causing graft-versus-host disease in defined clinical hematopoietic stem cell transplant settings is required to inform development of methods for monitoring patients and providing them tailored care.
  • DESIGN AND METHODS: Twenty-five patients were recruited presenting with myeloid malignancies and treated with a reduced intensity conditioning transplant regimen with graft-versus-host disease prophylaxis comprising in vivo lymphocyte depletion with alemtuzumab and cyclosporin.
  • A prospective study was performed of lymphocyte subset reconstitution in peripheral blood in relation to the incidence of graft-versus-host disease.
  • RESULTS: Acute graft-versus-host disease was associated with significantly higher numbers of natural killer cells and donor-derived effector CD4 T cells (CD45RO(+) CD27(-)) early (day 30) after transplantation (p=0.04 and p=0.02, respectively).
  • Although numbers of regulatory CD4 T cells (CD25(high) Foxp3(+)) were similar at day 30 in all patients, a significant deficit in those who developed acute graft-versus-host disease was apparent relative to effector CD4 T cells (median of 41 effectors per regulatory cell compared to 12 to 1 for patients without graft-versus-host disease) (p=0.03).
  • By day 180, a functional regulatory CD4 T-cell population had expanded significantly in patients who developed chronic graft-versus-host disease, reversing the imbalance (median of 3 effectors per regulatory cell compared to 9.6 to 1 for patients without graft-versus-host disease) (p=0.018) suggesting no overt absence of immune regulation in the late onset form of the disease.
  • CONCLUSIONS: Imbalance of effector and regulatory CD4 T cells is a signature of graft-versus-host disease in this transplantation protocol.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antibodies, Neoplasm / pharmacology. Antineoplastic Agents / pharmacology. CD4-Positive T-Lymphocytes / metabolism. Graft vs Host Disease / metabolism. T-Lymphocytes, Regulatory / metabolism. Transplantation Conditioning / methods
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal, Humanized. Female. Hematopoietic Stem Cell Transplantation / methods. Humans. Male. Middle Aged. Models, Biological. Prospective Studies

  • Genetic Alliance. consumer health - Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2004 May 15;103(10):3986-8 [14764530.001]
  • [Cites] Blood. 2004 Mar 15;103(6):2410-6 [14604970.001]
  • [Cites] Blood. 2004 Sep 15;104(6):1616-23 [15059843.001]
  • [Cites] Blood. 2004 Oct 1;104(7):2187-93 [15172973.001]
  • [Cites] Blood. 2004 Oct 15;104(8):2403-9 [15231569.001]
  • [Cites] Blood. 1990 Jul 15;76(2):418-23 [2142440.001]
  • [Cites] Semin Hematol. 1991 Jul;28(3):250-9 [1887253.001]
  • [Cites] J Exp Med. 1994 Apr 1;179(4):1155-61 [7511682.001]
  • [Cites] Immunology. 1996 May;88(1):13-9 [8707338.001]
  • [Cites] Bone Marrow Transplant. 1997 Dec;20(11):945-52 [9422473.001]
  • [Cites] Blood. 1998 Feb 1;91(3):756-63 [9446633.001]
  • [Cites] Bone Marrow Transplant. 2005 Jan;35(2):183-90 [15531897.001]
  • [Cites] Blood. 2005 Feb 1;105(3):1362-4 [15459005.001]
  • [Cites] Am J Transplant. 2005 Mar;5(3):465-74 [15707400.001]
  • [Cites] Blood. 2005 Mar 15;105(6):2594-600 [15536148.001]
  • [Cites] Blood. 2005 Apr 1;105(7):2973-8 [15613541.001]
  • [Cites] J Exp Med. 2005 Jun 6;201(11):1793-803 [15939793.001]
  • [Cites] Exp Hematol. 2005 Aug;33(8):894-900 [16038781.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2903-11 [15972448.001]
  • [Cites] J Immunol. 2005 Nov 15;175(10):6489-97 [16272303.001]
  • [Cites] Eur J Immunol. 2005 Nov;35(11):3332-42 [16231285.001]
  • [Cites] Biol Blood Marrow Transplant. 2006 Jan;12(1 Suppl 2):22-30 [16399598.001]
  • [Cites] Blood. 2006 Feb 1;107(3):1018-23 [16210336.001]
  • [Cites] Biol Blood Marrow Transplant. 2006 Mar;12(3):267-74 [16503495.001]
  • [Cites] Blood. 2006 Apr 1;107(7):2993-3001 [16352808.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 25;103(17):6659-64 [16617117.001]
  • [Cites] Blood. 2006 Jul 15;108(2):756-62 [16551963.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1291-7 [16627754.001]
  • [Cites] Leukemia. 2006 Sep;20(9):1557-65 [16826221.001]
  • [Cites] J Clin Invest. 2006 Sep;116(9):2423-33 [16955142.001]
  • [Cites] Br J Haematol. 2006 Oct;135(2):201-9 [16939494.001]
  • [Cites] Transplantation. 2006 Nov 27;82(10):1342-51 [17130784.001]
  • [Cites] Eur J Immunol. 2007 Jan;37(1):129-38 [17154262.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Jan;13(1 Suppl 1):2-10 [17222762.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Feb;13(2):197-205 [17241925.001]
  • [Cites] Leukemia. 2007 Mar;21(3):472-9 [17215853.001]
  • [Cites] Int J Hematol. 2007 Feb;85(2):154-62 [17321995.001]
  • [Cites] Blood. 2007 Mar 15;109(6):2649-56 [17095616.001]
  • [Cites] Blood. 2007 Jun 1;109(11):5058-61 [17317850.001]
  • [Cites] Br J Haematol. 2007 Aug;138(4):517-26 [17608767.001]
  • [Cites] Leukemia. 2007 Oct;21(10):2145-52 [17673900.001]
  • [Cites] Blood. 2007 Oct 15;110(8):2983-90 [17644734.001]
  • [Cites] Blood. 2008 Sep 1;112(5):2129-38 [18550852.001]
  • [Cites] J Exp Med. 2002 Mar 18;195(6):789-94 [11901204.001]
  • [Cites] Nat Med. 2002 Apr;8(4):379-85 [11927944.001]
  • [Cites] Blood. 2002 May 15;99(10):3493-9 [11986199.001]
  • [Cites] Blood. 2002 May 15;99(10):3844-7 [11986245.001]
  • [Cites] J Exp Med. 2002 Aug 5;196(3):389-99 [12163567.001]
  • [Cites] J Exp Med. 2002 Aug 5;196(3):401-6 [12163568.001]
  • [Cites] Biol Blood Marrow Transplant. 2003 Apr;9(4):243-56 [12720217.001]
  • [Cites] Blood. 2003 Aug 1;102(3):814-9 [12689936.001]
  • [Cites] Blood Rev. 2003 Dec;17(4):187-94 [14556773.001]
  • [Cites] Br J Haematol. 2004 Sep;126(5):697-703 [15327522.001]
  • (PMID = 19491336.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0500429
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  • [Other-IDs] NLM/ PMC2704306
  •  go-up   go-down


70. Heim D, Friess D, Christen S, Stüssi G, Meyer-Monard S, Tichelli A, Passweg JR, Gratwohl A: Intensive chemotherapy and autologous hematopoietic stem cell mobilization, collection and transplantation with simultaneous Imatinib therapy in patients with blast crisis chronic myeloid leukaemia. Leukemia; 2006 May;20(5):898-900
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] Intensive chemotherapy and autologous hematopoietic stem cell mobilization, collection and transplantation with simultaneous Imatinib therapy in patients with blast crisis chronic myeloid leukaemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Blast Crisis / therapy. Hematopoietic Stem Cell Mobilization / methods. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16525490.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  •  go-up   go-down


71. 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


72. Lin TS, Ruppert AS, Johnson AJ, Fischer B, Heerema NA, Andritsos LA, Blum KA, Flynn JM, Jones JA, Hu W, Moran ME, Mitchell SM, Smith LL, Wagner AJ, Raymond CA, Schaaf LJ, Phelps MA, Villalona-Calero MA, Grever MR, Byrd JC: Phase II study of flavopiridol in relapsed chronic lymphocytic leukemia demonstrating high response rates in genetically high-risk disease. J Clin Oncol; 2009 Dec 10;27(35):6012-8
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] Phase II study of flavopiridol in relapsed chronic lymphocytic leukemia demonstrating high response rates in genetically high-risk disease.
  • PURPOSE: Patients with chronic lymphocytic leukemia (CLL) with high-risk genomic features achieve poor outcomes with traditional therapies.
  • A phase I study of a pharmacokinetically derived schedule of flavopiridol suggested promising activity in CLL, irrespective of high-risk features.
  • Given the relevance of these findings to treating genetically high-risk CLL, a prospective confirmatory study was initiated.
  • PATIENTS AND METHODS: Patients with relapsed CLL were treated with single-agent flavopiridol, with subsequent addition of dexamethasone to suppress cytokine release syndrome (CRS).
  • Reducing the number of weekly treatments per cycle from four to three and adding prophylactic dexamethasone, which abrogated interleukin-6 release and CRS (P < or = .01), resulted in improved tolerability and treatment delivery.
  • CONCLUSION: Flavopiridol achieves significant clinical activity in patients with relapsed CLL, including those with high-risk genomic features and bulky lymphadenopathy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Flavonoids / administration & dosage. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Piperidines / administration & dosage. Protein Kinase Inhibitors / administration & dosage
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosome Deletion. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 17. Dexamethasone / administration & dosage. Disease-Free Survival. Female. Gene Expression Regulation, Leukemic. Genetic Predisposition to Disease. Humans. Kaplan-Meier Estimate. Logistic Models. Male. Middle Aged. Prospective Studies. Recurrence. Risk Assessment. Risk Factors. Time Factors. Treatment Outcome. Tumor Lysis Syndrome / etiology. Tumor Lysis Syndrome / prevention & control

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • 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
  • [Cites] J Clin Oncol. 2000 Jan;18(2):371-5 [10637252.001]
  • [Cites] Blood. 2009 Mar 19;113(12):2637-45 [18981292.001]
  • [Cites] Blood. 2000 Jul 15;96(2):393-7 [10887097.001]
  • [Cites] Ann N Y Acad Sci. 2000 Jun;910:207-21; discussion 221-2 [10911915.001]
  • [Cites] J Clin Oncol. 2001 Apr 1;19(7):1985-92 [11283131.001]
  • [Cites] J Clin Oncol. 2001 Apr 15;19(8):2153-64 [11304767.001]
  • [Cites] Clin Cancer Res. 2001 Jun;7(6):1590-9 [11410495.001]
  • [Cites] J Clin Oncol. 2002 Apr 15;20(8):2157-70 [11956278.001]
  • [Cites] Blood. 2002 May 15;99(10):3554-61 [11986207.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3804-16 [9808574.001]
  • [Cites] J Clin Oncol. 2005 Jun 1;23(16):3819-29 [15809448.001]
  • [Cites] Clin Cancer Res. 2005 Jun 1;11(11):4176-81 [15930354.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4079-88 [15767648.001]
  • [Cites] Leuk Res. 2005 Nov;29(11):1253-7 [15916806.001]
  • [Cites] Haematologica. 2005 Oct;90(10):1435-6 [16219582.001]
  • [Cites] Blood. 2007 Jan 15;109(2):399-404 [17003373.001]
  • [Cites] J Clin Oncol. 2007 Mar 1;25(7):799-804 [17283363.001]
  • [Cites] Lancet. 2007 Jul 21;370(9583):230-9 [17658394.001]
  • [Cites] Leuk Lymphoma. 2002 Apr;43(4):793-7 [12153166.001]
  • [Cites] N Engl J Med. 2002 Aug 8;347(6):452-3 [12167696.001]
  • [Cites] J Clin Oncol. 2002 Sep 15;20(18):3891-7 [12228210.001]
  • [Cites] Cancer Res. 2003 Jan 1;63(1):36-8 [12517774.001]
  • [Cites] Clin Cancer Res. 2003 Feb;9(2):562-70 [12576419.001]
  • [Cites] Ann Hematol. 2003 Dec;82(12):759-65 [14551737.001]
  • [Cites] Blood. 2004 May 1;103(9):3278-81 [14726385.001]
  • [Cites] J Natl Cancer Inst. 1992 Nov 18;84(22):1736-40 [1279187.001]
  • [Cites] Blood. 1995 Mar 15;85(6):1580-9 [7888675.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] Cancer Res. 1996 Jul 1;56(13):2973-8 [8674031.001]
  • [Cites] Blood. 1998 Jan 15;91(2):458-65 [9427698.001]
  • [Cites] Best Pract Res Clin Haematol. 2007 Sep;20(3):545-56 [17707839.001]
  • [Cites] J Natl Cancer Inst. 2000 Mar 1;92(5):376-87 [10699068.001]
  • (PMID = 19826119.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K23 CA102276-05; United States / NCI NIH HHS / CA / 2 P01 CA81534; United States / NCI NIH HHS / CA / P01 CA081534; United States / NCI NIH HHS / CA / U01 CA076576; United States / NCI NIH HHS / CA / P30 CA 16058; United States / NCRR NIH HHS / RR / UL1 RR025755; United States / NCI NIH HHS / CM / N01 CM62207; United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / N01CM62207; United States / NCI NIH HHS / CA / K23 CA102276; United States / NCI NIH HHS / CA / U01 CA76576
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Piperidines; 0 / Protein Kinase Inhibitors; 45AD6X575G / alvocidib; 7S5I7G3JQL / Dexamethasone
  • [Other-IDs] NLM/ PMC2793044
  •  go-up   go-down


73. Wang DM, Xu W, Dong HJ, Fang C, Zhu DX, Cao X, Zhu HY, Zhuang Y, Qiu HR, Yang H, Li JY: [Cytogenetics of chronic lymphocytic leukemia stimulated by CpG-oligodeoxynucleotides and IL-2]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Oct;18(5):1114-8
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] [Cytogenetics of chronic lymphocytic leukemia stimulated by CpG-oligodeoxynucleotides and IL-2].
  • This study was to explore the stimulating effect of CpG-oligodeoxynucleotides (CpG-ODN) in combination with interleukin-2 (IL-2) on cytogenetic features of chronic lymphocytic leukemia (CLL) cells.
  • Peripheral blood or bone marrow cells of 115 patients with CLL were cultured for 72 hours with CpG-ODN plus interleukin-2 (IL-2), and routine karyotype analysis was performed with R-banding technique.
  • The results showed that among the 115 CLL patients, successful stimulation rate was 74.8%.
  • It is concluded that most of CLL patients have chromosome abnormality, and the number abnormality are more frequent than the structural aberrations.
  • CpG-ODN plus IL-2 can effectively raise the number of cells at metaphase and the detection rate of chromosome aberrations in CLL patients.

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21129242.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CPG-oligonucleotide; 0 / Interleukin-2; 0 / Oligodeoxyribonucleotides
  •  go-up   go-down


74. Yeramilli VA, Knight KL: Requirement for BAFF and APRIL during B cell development in GALT. J Immunol; 2010 May 15;184(10):5527-36
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.
  • [Title] Requirement for BAFF and APRIL during B cell development in GALT.
  • The effects of B cell-activating factor belonging to the TNF family (BAFF) on B cell maturation and survival in the mouse are relatively well understood.
  • In contrast, little is known about the role of BAFF in B cell development in other mammals, such as rabbits, that use GALT to develop and maintain the B cell compartment.
  • We examined the expression and requirement of BAFF and a proliferation-inducing ligand (APRIL) during peripheral B cell development in young rabbits.
  • In the appendix, the size and number of proliferating B cell follicles were greatly reduced, demonstrating that although BAFF/APRIL is dispensable for B cell development in BM, it is required for B cell development in GALT.
  • Additionally, we propose that this chronic occupancy of BBRs on B cells may provide a tonic and/or survival signal for the maintenance of peripheral B cells in adults after B lymphopoiesis is arrested in BM.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cell Biol. 2004 Feb;24(3):997-1006 [14729948.001]
  • [Cites] Dev Comp Immunol. 2007;31(12):1211-9 [17499850.001]
  • [Cites] J Exp Med. 2008 Jan 21;205(1):155-68 [18180309.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2744-54 [18172003.001]
  • [Cites] Dev Comp Immunol. 2008;32(8):980-91 [18329710.001]
  • [Cites] Dev Comp Immunol. 2008;32(9):1076-87 [18395254.001]
  • [Cites] J Immunol. 2008 Jul 15;181(2):976-90 [18606649.001]
  • [Cites] J Immunol. 2008 Jul 15;181(2):1012-8 [18606652.001]
  • [Cites] Dev Comp Immunol. 2009 May;33(5):697-708 [19124039.001]
  • [Cites] Blood. 2009 Feb 26;113(9):1967-76 [18981294.001]
  • [Cites] Vet Immunol Immunopathol. 2009 Jul 15;130(1-2):125-30 [19269694.001]
  • [Cites] Nat Rev Immunol. 2009 Jul;9(7):491-502 [19521398.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Aug 18;106(33):13945-50 [19666484.001]
  • [Cites] J Immunol. 2009 Sep 15;183(6):3561-7 [19726767.001]
  • [Cites] J Exp Med. 1999 Dec 6;190(11):1697-710 [10587360.001]
  • [Cites] Nature. 2000 Apr 27;404(6781):995-9 [10801128.001]
  • [Cites] Immunology. 2000 May;100(1):119-30 [10809967.001]
  • [Cites] J Exp Med. 2000 Jul 3;192(1):129-35 [10880534.001]
  • [Cites] Immunol Rev. 2000 Jun;175:214-28 [10933605.001]
  • [Cites] J Biol Chem. 2000 Nov 10;275(45):35478-85 [10956646.001]
  • [Cites] J Exp Med. 2000 Nov 20;192(10):1453-66 [11085747.001]
  • [Cites] J Immunol. 2001 Jan 1;166(1):6-10 [11123269.001]
  • [Cites] Blood. 2001 Jan 1;97(1):198-204 [11133761.001]
  • [Cites] Nat Immunol. 2000 Sep;1(3):252-6 [10973284.001]
  • [Cites] Arthritis Rheum. 2001 Jun;44(6):1313-9 [11407690.001]
  • [Cites] Nat Immunol. 2001 Jul;2(7):638-43 [11429549.001]
  • [Cites] Immunity. 2001 Aug;15(2):289-302 [11520463.001]
  • [Cites] Science. 2001 Sep 14;293(5537):2111-4 [11509691.001]
  • [Cites] Science. 2001 Sep 14;293(5537):2108-11 [11509692.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] J Immunol. 2002 Jun 1;168(11):5605-11 [12023357.001]
  • [Cites] Ann Rheum Dis. 2003 Feb;62(2):168-71 [12525388.001]
  • [Cites] J Clin Invest. 2003 Jul;112(2):286-97 [12865416.001]
  • [Cites] J Immunol. 2003 Dec 15;171(12):6372-80 [14662835.001]
  • [Cites] Int Immunol. 2004 Jan;16(1):139-48 [14688069.001]
  • [Cites] J Exp Med. 2004 Jan 5;199(1):91-8 [14707116.001]
  • [Cites] J Immunol. 2004 Jan 15;172(2):1118-24 [14707086.001]
  • [Cites] Leukemia. 1994 Dec;8(12):2144-55 [7808003.001]
  • [Cites] Adv Exp Med Biol. 1994;355:249-53 [7709830.001]
  • [Cites] Immunity. 1994 Nov;1(8):647-59 [7600292.001]
  • [Cites] J Exp Med. 1996 May 1;183(5):2119-21 [8642322.001]
  • [Cites] J Immunol. 1996 Dec 15;157(12):5478-86 [8955197.001]
  • [Cites] Int Rev Immunol. 1997;15(3-4):165-83 [9222818.001]
  • [Cites] J Immunol. 1998 Mar 15;160(6):2725-9 [9510172.001]
  • [Cites] J Exp Med. 1998 Sep 21;188(6):1185-90 [9743536.001]
  • [Cites] J Exp Med. 1999 Jun 7;189(11):1747-56 [10359578.001]
  • [Cites] Nat Genet. 2005 Aug;37(8):820-8 [16007087.001]
  • [Cites] Arthritis Rheum. 2005 Dec;52(12):3943-54 [16320342.001]
  • [Cites] Mol Immunol. 2007 Feb;44(6):1471-6 [16828163.001]
  • [Cites] J Clin Invest. 2006 Dec;116(12):3266-76 [17111048.001]
  • [Cites] Int Immunol. 2007 Feb;19(2):203-15 [17220480.001]
  • [Cites] J Immunol. 2007 May 1;178(9):5612-22 [17442944.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 16;101(11):3903-8 [14988498.001]
  • [Cites] Int Arch Allergy Appl Immunol. 1968;33(1):65-88 [4171257.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 May;85(9):3130-4 [2834733.001]
  • [Cites] Cell. 1991 Mar 8;64(5):995-1005 [1900459.001]
  • [Cites] Res Immunol. 1993 Jul-Sep;144(6-7):486-91; discussion 491-4 [8303070.001]
  • [Cites] Adv Immunol. 1994;56:179-218 [8073947.001]
  • [Cites] J Immunol. 2007 Nov 1;179(9):5947-57 [17947668.001]
  • [Cites] Cytokine. 2007 Sep;39(3):192-200 [17822916.001]
  • [Cites] J Immunol. 2004 Mar 1;172(5):3268-79 [14978135.001]
  • (PMID = 20400696.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI050260; United States / NIAID NIH HHS / AI / R01 AI068390; United States / NIAID NIH HHS / AI / AI050260; United States / NIAID NIH HHS / AI / AI068390
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell Activating Factor; 0 / B-Cell Activation Factor Receptor; 0 / Ligands; 0 / Tumor Necrosis Factor Ligand Superfamily Member 13
  • [Other-IDs] NLM/ NIHMS394519; NLM/ PMC3410555
  •  go-up   go-down


75. Bund D, Mayr C, Kofler DM, Hallek M, Wendtner CM: CD23 is recognized as tumor-associated antigen (TAA) in B-CLL by CD8+ autologous T lymphocytes. Exp Hematol; 2007 Jun;35(6):920-30
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] CD23 is recognized as tumor-associated antigen (TAA) in B-CLL by CD8+ autologous T lymphocytes.
  • OBJECTIVE: CD23 is constitutively and atypically expressed on malignant B cells in patients with chronic lymphocytic leukemia (B-CLL).
  • Here, we investigated whether CD23-derived peptides might function as B-CLL-specific tumor-associated antigen (TAA).
  • RESULTS: We were able to expand autologous T cells from 8/11 B-CLL patients by using native and CD40L-activated B-CLL cells as antigen-presenting cells (APCs) in 5 cases whereas for 3 samples an autologous T cell response could only be evoked by use of CD40L-stimulated B-CLL cells as APCs.
  • The number of CD8(+) T cells could be expanded during 4 weeks of in vitro culture with native or CD40L-activated B-CLL cells.
  • Furthermore, these T cells not only recognized HLA-A0201-binding CD23-derived peptides presented by T2 cells, but also CD23-overexpressing autologous B-CLL cells in an MHC-I-restricted manner.
  • CONCLUSION: In sum, CD23-derived peptides were shown to be naturally processed and presented as TAA in primary B-CLL, enabling the expansion of autologous tumor-specific T cells.
  • [MeSH-major] Antigens, Neoplasm / immunology. CD8-Positive T-Lymphocytes / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Lymphocyte Activation / immunology. Peptides / immunology. Receptors, IgE / immunology

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17533046.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; 0 / Peptides; 0 / Receptors, IgE; 147205-72-9 / CD40 Ligand; 82115-62-6 / Interferon-gamma
  •  go-up   go-down


76. Dzietczenia J, Wróbel T, Jaźwiec B, Mazur G, Butrym A, Poręba R, Kuliczkowski K: Expression of bone morphogenetic proteins (BMPs) receptors in patients with B-cell chronic lymphocytic leukemia (B-CLL). Int J Lab Hematol; 2010 Dec;32(6 Pt 1):e217-21
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] Expression of bone morphogenetic proteins (BMPs) receptors in patients with B-cell chronic lymphocytic leukemia (B-CLL).
  • They regulate proliferation, differentiation, and apoptosis in a variety of cells including hematopoietic cells.
  • BMPs act because of binding to two types of serine/threonine kinase receptors: BMP type I receptors (IA and IB) and BMP type II receptor.
  • The aim of our study was to examine the percentage of expression of BMPs receptors on lymphocytes of patients with B-cell chronic lymphocytic leukemia (B-CLL).
  • A total of 46 patients with B-CLL (27 men and 19 women) and 10 healthy persons were evaluated.
  • On cells of patients with B-CLL, the percentage of expression of BMP RIA, BMP RIB, and BMP RII was significantly higher than in normal cells of the control group.
  • The percentage of the expression of BMP RIA and BMP RIB was higher in patients with advanced stage of disease.
  • [MeSH-major] Bone Morphogenetic Protein Receptors, Type I / biosynthesis. Bone Morphogenetic Protein Receptors, Type II / biosynthesis. Leukemia, Lymphocytic, Chronic, B-Cell / physiopathology

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, B-cell, chronic.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] © 2010 Blackwell Publishing Ltd.
  • (PMID = 20491995.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.11.30 / Bone Morphogenetic Protein Receptors; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors, Type I; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors, Type II
  •  go-up   go-down


77. Nikitin EA, Malakho SG, Biderman BV, Baranova AV, Lorie YY, Shevelev AY, Peklo MM, Vlasik TN, Moskalev EA, Zingerman BV, Vorob'ev IA, Poltaraus AB, Sudarikov AB, Vorobjev AI: Expression level of lipoprotein lipase and dystrophin genes predict survival in B-cell chronic lymphocytic leukemia. Leuk Lymphoma; 2007 May;48(5):912-22
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] Expression level of lipoprotein lipase and dystrophin genes predict survival in B-cell chronic lymphocytic leukemia.
  • Mutational status of immunoglobulin variable region genes (VH-genes) is known as the strongest predictor of long term prognosis in B-CLL.
  • In this study, we have compared prognostic values of real time PCR quantification of the expression levels of four genes previously shown to be differentially expressed in V(H)-unmutated and mutated B-CLL subtypes: ZAP-70, ZBTB20, DMD and LPL.
  • The study included 134 B-CLL patients.
  • Prognostic values of LPL gene expression levels were significant even for CLL patients with stage A.
  • [MeSH-major] Dystrophin / biosynthesis. Gene Expression Regulation, Neoplastic. Leukemia, B-Cell / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Lipoprotein Lipase / biosynthesis

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, B-cell, chronic.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17487735.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R15CA113331-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dystrophin; EC 3.1.1.34 / Lipoprotein Lipase
  •  go-up   go-down


78. Komarova NL, Katouli AA, Wodarz D: Combination of two but not three current targeted drugs can improve therapy of chronic myeloid leukemia. PLoS One; 2009;4(2):e4423
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] Combination of two but not three current targeted drugs can improve therapy of chronic myeloid leukemia.
  • Chronic myeloid leukemia (CML) is a cancer of the hematopoietic system and has been treated with the drug Imatinib relatively successfully.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • [MeSH-minor] Humans. Models, Biological. Treatment Outcome. Tumor Stem Cell Assay


79. Zaher M, Akrout I, Mirshahi M, Kolb JP, Billard C: Noxa upregulation is associated with apoptosis of chronic lymphocytic leukemia cells induced by hyperforin but not flavopiridol. Leukemia; 2009 Mar;23(3):594-6
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] Noxa upregulation is associated with apoptosis of chronic lymphocytic leukemia cells induced by hyperforin but not flavopiridol.
  • [MeSH-major] Apoptosis / drug effects. Flavonoids / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Neoplasm Proteins / biosynthesis. Phloroglucinol / analogs & derivatives. Piperidines / pharmacology. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. Terpenes / pharmacology
  • [MeSH-minor] Antibodies, Monoclonal / immunology. Bicyclo Compounds / pharmacology. Humans. Myeloid Cell Leukemia Sequence 1 Protein. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / pathology. Up-Regulation / drug effects

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Hazardous Substances Data Bank. HYPERFORIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18784742.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Bicyclo Compounds; 0 / Flavonoids; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / PMAIP1 protein, human; 0 / Piperidines; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Terpenes; 45AD6X575G / alvocidib; DHD7FFG6YS / Phloroglucinol; RM741E34FP / hyperforin
  •  go-up   go-down


80. Sercan Z, Pehlivan M, Gokturk D, Sercan HO: Beta-catenin mutations are not observed in chronic myeloid leukemia. Tumori; 2009 Nov-Dec;95(6):836-9
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] Beta-catenin mutations are not observed in chronic myeloid leukemia.
  • AIMS AND BACKGROUND: Studies reporting activated Wnt signaling in all stages of chronic myeloid leukemia (CML) have demonstrated that deregulation of the pathway plays a role in the pathogenesis of this disease.
  • MATERIAL AND METHODS: We screened bone marrow specimens from 33 patients with CML in the chronic phase and also examined the K562 cell line for beta-catenin mutations.
  • RESULTS: None of the patients nor the K562 cell line were found to carry mutations.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Mutation. Wnt Proteins / metabolism. beta Catenin / genetics


81. Loskog A, Giandomenico V, Rossig C, Pule M, Dotti G, Brenner MK: Addition of the CD28 signaling domain to chimeric T-cell receptors enhances chimeric T-cell resistance to T regulatory cells. Leukemia; 2006 Oct;20(10):1819-28
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] Addition of the CD28 signaling domain to chimeric T-cell receptors enhances chimeric T-cell resistance to T regulatory cells.
  • We have investigated the effects of T regulatory cells on chimeric T cells specific for the B-cell antigen CD19, as B-cell malignancies are attractive targets for chimeric T-cell therapy.
  • By contrast, expression in T cells of a chimeric receptor consisting of the intracellular portion of the CD28 molecule fused to the zeta-chain and CD19 single-chain Fv not only produced a higher proliferative response and an increased nuclear factor kappaB activation but also sustained these activities in the presence of T regulatory cells.
  • These effects are seen whether the chimeric T cells are derived from normal donors or from patients with B-cell chronic lymphocytic leukemia, indicating the potential for clinical application in B cell malignancies.
  • [MeSH-major] Antigens, CD28 / genetics. Immunotherapy, Adoptive / methods. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Receptors, Antigen, T-Cell / genetics. T-Lymphocytes, Cytotoxic / physiology. T-Lymphocytes, Regulatory / physiology
  • [MeSH-minor] Antigens, CD19 / genetics. Antigens, CD3 / genetics. Cell Division / immunology. Cytokines / metabolism. Flow Cytometry. Humans. K562 Cells. Mutant Chimeric Proteins / chemistry. Mutant Chimeric Proteins / genetics. NF-kappa B / metabolism. Protein Structure, Tertiary. Signal Transduction / physiology. Transduction, Genetic

  • 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] Leukemia. 2007 Jan;21(1):175; author reply 175 [17109027.001]
  • (PMID = 16932339.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA94237
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD28; 0 / Antigens, CD3; 0 / CD3 antigen, zeta chain; 0 / Cytokines; 0 / Mutant Chimeric Proteins; 0 / NF-kappa B; 0 / Receptors, Antigen, T-Cell
  •  go-up   go-down


82. Yu C, Friday BB, Lai JP, Yang L, Sarkaria J, Kay NE, Carter CA, Roberts LR, Kaufmann SH, Adjei AA: Cytotoxic synergy between the multikinase inhibitor sorafenib and the proteasome inhibitor bortezomib in vitro: induction of apoptosis through Akt and c-Jun NH2-terminal kinase pathways. Mol Cancer Ther; 2006 Sep;5(9):2378-87
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.
  • Multiple tumor cell lines of varying histiotypes, including A549 (lung adenocarcinoma), 786-O (renal cell carcinoma), HeLa (cervical carcinoma), MDA-MB-231 (breast), K562 (chronic myelogenous leukemia), Jurkat (acute T-cell leukemia), MEC-2 (B-chronic lymphocytic leukemia), and U251 and D37 (glioma), as well as cells derived from primary human glioma tumors that are likely a more clinically relevant model were treated with sorafenib or bortezomib alone or in combination.
  • Sorafenib and bortezomib synergistically induced a marked increase in mitochondrial injury and apoptosis, reflected by cytochrome c release, caspase-3 cleavage, and poly(ADP-ribose) polymerase degradation in a broad range of solid tumor and leukemia cell lines.
  • These findings show that sorafenib interacts synergistically with bortezomib to induce apoptosis in a broad spectrum of neoplastic cell lines and show an important role for the Akt and JNK pathways in mediating synergism.
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Bortezomib. Cell Line, Tumor. Drug Synergism. Humans. Jurkat Cells. K562 Cells. MAP Kinase Signaling System / drug effects. Niacinamide / analogs & derivatives. Phenylurea Compounds. Proteasome Endopeptidase Complex / metabolism

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • Hazardous Substances Data Bank. NICOTINAMIDE .
  • 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 = 16985072.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Boronic Acids; 0 / Phenylurea Compounds; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 69G8BD63PP / Bortezomib; 9ZOQ3TZI87 / sorafenib; EC 2.7.11.1 / Oncogene Protein v-akt; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  •  go-up   go-down


83. Helbig G, Stella-Hołowiecka B, Hołowiecki J: [Oncogene Fip1-likeL/PDGFRalpha as a target for imatinib in patients with hypereosinophilic syndrome and chronic eosinophilic leukemia. A novel look at pathogenesis and therapy]. Pol Arch Med Wewn; 2005 May;113(5):490-7
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] [Oncogene Fip1-likeL/PDGFRalpha as a target for imatinib in patients with hypereosinophilic syndrome and chronic eosinophilic leukemia. A novel look at pathogenesis and therapy].
  • [Transliterated title] Onkogen Fip1-like1/PDGFRalpha jako cel działania imatinibu u pacjentów z zespołem hipereozynofilowym i przewlekła białaczka eozynofilowa--nowe spojrzenie na patogeneze i leczenie.
  • [MeSH-minor] Algorithms. Benzamides. Cell Transformation, Neoplastic / drug effects. Chronic Disease. Dose-Response Relationship, Drug. Humans. Imatinib Mesylate

  • Genetic Alliance. consumer health - Hypereosinophilic syndromes.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16479834.001).
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] pol
  • [Publication-type] Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / FIP1L1-PDGFRA fusion protein, human; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Number-of-references] 18
  •  go-up   go-down


84. Al-Anazi KA, Eltayeb KI, Bakr M, Al-Mohareb FI: Methotrexate-induced acute leukemia: report of three cases and review of the literature. Clin Med Case Rep; 2009;2:43-9
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] Methotrexate-induced acute leukemia: report of three cases and review of the literature.
  • For many years, methotrexate has been used in the treatment of certain chronic medical disorders e.g. rheumatoid arthritis and psoriasis as well as a number of malignant disorders e.g. acute lymphoblastic leukemia, certain types of lymphoma and breast carcinoma.
  • The association between methotrexate therapy and the development of lymphoma and pseudolymphoma is well established.
  • In patients treated with methotrexate, the development of leukemia has been attributed to either the primary disorder e.g. rheumatoid arthritis or to other drugs used concomitantly e.g. cyclophosphamide.
  • Reported here are two patients with rheumatoid arthritis and one patient with psoriasis treated with low dose methotrexate for variable periods of time.
  • Two of these patients developed acute myeloid leukemia on myelodysplastic syndrome background, while the third patient developed pre-B acute lymphoblastic leukemia that expressed few myeloid markers and had a positive philadelphia chromosome.
  • To our knowledge, these are the first reported cases of methotrexate-induced acute leukemia.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 24179373.001).
  • [ISSN] 1178-6450
  • [Journal-full-title] Clinical medicine. Case reports
  • [ISO-abbreviation] Clin Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC3785348
  • [Keywords] NOTNLM ; acute lymphoblastic leukemia / acute myeloid leukemia / methotrexate / myelodysplastic syndrome / rheumatoid arthritis
  •  go-up   go-down


85. Arana-Yi C, Quintás-Cardama A, Giles F, Thomas D, Carrasco-Yalan A, Cortes J, Kantarjian H, Verstovsek S: Advances in the therapy of chronic idiopathic myelofibrosis. Oncologist; 2006 Sep;11(8):929-43
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] Advances in the therapy of chronic idiopathic myelofibrosis.
  • The molecular basis of chronic idiopathic myelofibrosis (CIMF) has remained elusive, thus hampering the development of effective targeted therapies.
  • However, significant progress regarding the molecular mechanisms involved in the pathogenes is of this disease has been made in recent years that will likely provide ample opportunity for the investigation of novel therapeutic approaches.
  • In addition, the use of reduced-intensity conditioning allogeneic stem cell transplantation has resulted in prolonged survival and lower transplant-related mortality.
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Chronic Disease / therapy. Combined Modality Therapy. Humans. Stem Cell Transplantation

  • Genetic Alliance. consumer health - Myelofibrosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16951397.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 163
  •  go-up   go-down


86. Uzunhan Y, Cadranel J, Boissel N, Gardin C, Arnulf B, Bergeron A: [Lung involvement in lymphoid and lympho-plasmocytic proliferations (except lymphomas)]. Rev Mal Respir; 2010 Jun;27(6):599-610
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] [Lung involvement in lymphoid and lympho-plasmocytic proliferations (except lymphomas)].
  • INTRODUCTION - BACKGROUND: The non infectious pulmonary manifestations occurring in lymphoplasmocytic proliferations others than lymphomas are poorly understood and have rarely been the object of dedicated publications.
  • We will also consider acute lymphoblastic leukaemia, chronic lymphocytic leukaemia and hairy cell leukaemia, as well as malignant plasmocytic disorders such as myeloma, POEMS syndrome and Waldenström's macroglobulinaemia.
  • CONCLUSION: During the course of lymphoplasmocytic diseases, lung manifestations are variable and sometimes require invasive techniques for definitive diagnosis.
  • [MeSH-minor] Humans. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Multiple Myeloma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Waldenstrom Macroglobulinemia / complications

  • MedlinePlus Health Information. consumer health - Lung Diseases.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 SPLF. Published by Elsevier Masson SAS. All rights reserved.
  • (PMID = 20610075.001).
  • [ISSN] 1776-2588
  • [Journal-full-title] Revue des maladies respiratoires
  • [ISO-abbreviation] Rev Mal Respir
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  •  go-up   go-down


87. Kohno T, Yamada Y, Tawara M, Takasaki Y, Kamihira S, Tomonaga M, Matsuyama T: Inactivation of p14ARF as a key event for the progression of adult T cell leukemia/lymphoma. Leuk Res; 2007 Dec;31(12):1625-32
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] Inactivation of p14ARF as a key event for the progression of adult T cell leukemia/lymphoma.
  • [MeSH-major] Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Leukemia-Lymphoma, Adult T-Cell / etiology. Tumor Suppressor Protein p14ARF / metabolism
  • [MeSH-minor] Acute Disease. Adult. Chronic Disease. Disease Progression. Genes, p53 / genetics. Humans. Mutation. Polymerase Chain Reaction. Prognosis. RNA, Messenger / analysis. Survival Rate

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18246599.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p14ARF
  •  go-up   go-down


88. Batlle A, Papadopoulou V, Gomes AR, Willimott S, Melo JV, Naresh K, Lam EW, Wagner SD: CD40 and B-cell receptor signalling induce MAPK family members that can either induce or repress Bcl-6 expression. Mol Immunol; 2009 May;46(8-9):1727-35
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.
  • [Title] CD40 and B-cell receptor signalling induce MAPK family members that can either induce or repress Bcl-6 expression.
  • Bcl-6 is essential for germinal centre development and normal antibody responses, and has major roles in controlling B-cell proliferation and differentiation.
  • Bcl-6 expression is induced in Bcr-Abl expressing lymphoid cell lines by the tyrosine kinase inhibitor, imatinib.
  • Next we analyze p38 function in a germinal centre B-cell line, Ramos. p38 is phosphorylated under basal conditions, and studies with p38 inhibitors show that it induces Bcl-6 expression.
  • Immunocytochemistry of tonsil sections show phosphorylated p38 in a minor population of germinal centre B-cells.
  • [MeSH-major] Antigens, CD40 / physiology. Extracellular Signal-Regulated MAP Kinases / metabolism. Proto-Oncogene Proteins c-bcl-6 / genetics. Receptors, Antigen, B-Cell / physiology
  • [MeSH-minor] Antibodies, Anti-Idiotypic / pharmacology. Blast Crisis / genetics. Blast Crisis / metabolism. Cell Line, Tumor. Cells, Cultured. Enzyme Activation / drug effects. Fusion Proteins, bcr-abl / genetics. Fusion Proteins, bcr-abl / metabolism. Gene Expression Regulation / drug effects. Humans. K562 Cells. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Models, Biological. Palatine Tonsil / drug effects. Palatine Tonsil / metabolism. Palatine Tonsil / pathology. Phosphorylation / drug effects. Signal Transduction / physiology

  • COS Scholar Universe. author profiles.
  • 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 = 19268365.001).
  • [ISSN] 1872-9142
  • [Journal-full-title] Molecular immunology
  • [ISO-abbreviation] Mol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Anti-Idiotypic; 0 / Antigens, CD40; 0 / Proto-Oncogene Proteins c-bcl-6; 0 / Receptors, Antigen, B-Cell; 0 / anti-IgM; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  •  go-up   go-down


89. Stilgenbauer S: ZAP-70 methylation and expression status in chronic lymphocytic leukemia. Haematologica; 2005 Aug;90(8):1012
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] ZAP-70 methylation and expression status in chronic lymphocytic leukemia.
  • [MeSH-major] DNA Methylation. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. ZAP-70 Protein-Tyrosine Kinase / genetics
  • [MeSH-minor] Biomarkers. Chromosome Aberrations. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 17. Dinucleoside Phosphates. Disease Progression. Exons. Humans. Introns. Sequence Deletion. Survival Analysis

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Haematologica. 2005 Aug;90(8):1078-88 [16079107.001]
  • (PMID = 16079094.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Dinucleoside Phosphates; 2382-65-2 / cytidylyl-3'-5'-guanosine; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase
  •  go-up   go-down


90. Altieri A, Bermejo JL, Hemminki K: Familial risk for non-Hodgkin lymphoma and other lymphoproliferative malignancies by histopathologic subtype: the Swedish Family-Cancer Database. Blood; 2005 Jul 15;106(2):668-72
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] Familial risk for non-Hodgkin lymphoma and other lymphoproliferative malignancies by histopathologic subtype: the Swedish Family-Cancer Database.
  • Non-Hodgkin lymphoma (NHL) consists of a heterogeneous group of tumors.
  • A familial history of NHL significantly increased the risk for NHL (SIRparent = 1.8; SIRsibling = 1.9) and for diffuse large B-cell lymphoma (SIRparent = 2.3), follicular lymphoma (SIRsibling = 2.3), and B-cell lymphoma not otherwise specified (NOS) (SIRsibling = 3.4).
  • For a parental history of histopathology-specific concordant cancer, the risks were significantly increased for diffuse large B-cell lymphoma (SIR = 11.8), follicular NHL (SIR = 6.1), plasma cell myeloma (SIR = 2.5), and chronic lymphocytic leukemia (SIR = 5.9).
  • The patterns of risks in parents and siblings support the hypothesis of an autosomal-dominant component for diffuse large B-cell NHL and a recessive one for follicular NHL.
  • [MeSH-major] Lymphoma, Non-Hodgkin / genetics. Lymphoproliferative Disorders / genetics
  • [MeSH-minor] Adult. Aged. Databases, Factual. Female. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / classification. Leukemia, Lymphocytic, Chronic, B-Cell / epidemiology. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Male. Middle Aged. Multiple Myeloma / classification. Multiple Myeloma / epidemiology. Multiple Myeloma / genetics. Multiple Myeloma / pathology. Risk Factors. Sweden / epidemiology


91. Dorfman DM, Shahsafaei A: CD200 (OX-2 membrane glycoprotein) expression in b cell-derived neoplasms. Am J Clin Pathol; 2010 Nov;134(5):726-33
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] CD200 (OX-2 membrane glycoprotein) expression in b cell-derived neoplasms.
  • We studied the expression of CD200, an immunoglobulin superfamily membrane glycoprotein, in a wide range of B cell-derived neoplasms by immunohistochemical staining of paraffin-embedded tissue sections.
  • In addition to chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL), CD200 is expressed in other B-cell lymphoproliferative disorders, including hairy cell leukemia.
  • In addition, neoplastic cells in classical Hodgkin lymphoma are immunoreactive for CD200.
  • CD200 was previously reported to be expressed in acute myeloid leukemia, and we find that it is also expressed in B-lymphoblastic leukemia/lymphoma.
  • We conclude that CD200 may be a useful immunophenotypic marker in the evaluation of B cell-derived neoplasms.
  • Furthermore, since an anti-CD200 immunotherapeutic agent is in clinical trials, a number of B cell-derived neoplasms in addition to CLL/SLL may be suitable therapeutic targets.
  • [MeSH-major] Antigens, CD / metabolism. Leukemia, B-Cell / metabolism. Leukemia, Hairy Cell / metabolism. Lymphoma, B-Cell / metabolism
  • [MeSH-minor] B-Lymphocytes / immunology. B-Lymphocytes / metabolism. B-Lymphocytes / pathology. Humans. Immunohistochemistry

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20959655.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / antigens, CD200
  •  go-up   go-down


92. Robak T: Therapy of chronic lymphocytic leukaemia with purine nucleoside analogues: facts and controversies. Drugs Aging; 2005;22(12):983-1012
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] Therapy of chronic lymphocytic leukaemia with purine nucleoside analogues: facts and controversies.
  • Chronic lymphocytic leukaemia (CLL) is a neoplastic disease of unknown aetiology characterised by an absolute lymphocytosis in peripheral blood and bone marrow.
  • The disease is diagnosed most commonly in the elderly with the median age at diagnosis being about 65 years.
  • The purine nucleoside analogues (PNAs) fludarabine, cladribine (2-chlorodeoxyadenosine) and pentostatin (2'-deoxycoformycin) are highly active in CLL, both in previously treated and in refractory or relapsed patients.
  • Recent randomised studies suggest that fludarabine and cladribine have similar activity in CLL.
  • Patients who received PNAs as their initial therapy and achieved long-lasting response can be successfully retreated with the same agent.
  • PNAs administered in combination with other chemotherapeutic agents and/or monoclonal antibodies may produce higher response rates, including complete response (CR) or molecular CR, compared with PNAs alone or other treatment regimens.
  • Myelosuppression and infections, including opportunistic varieties, are the most frequent adverse effects in patients with CLL treated with PNAs.
  • This review presents current results and treatment strategies with the use of PNAs in CLL, especially in elderly patients.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Purine Nucleosides / therapeutic use
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Administration Routes. Drug Interactions. Drug Resistance, Neoplasm / physiology. Humans. Infection Control. Randomized Controlled Trials as Topic. Recurrence. Stem Cell Transplantation

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Ann Hematol. 2002 May;81(5):258-66 [12029535.001]
  • [Cites] Blood. 2002 Mar 15;99(6):2245-7 [11877305.001]
  • [Cites] Hematol J. 2001;2(5):316-21 [11920267.001]
  • [Cites] J Mol Med (Berl). 1999 Feb;77(2):259-65 [10023779.001]
  • [Cites] Haematologica. 1996 May-Jun;81(3):224-31 [8767527.001]
  • [Cites] N Engl J Med. 1998 May 21;338(21):1506-14 [9593789.001]
  • [Cites] J Clin Oncol. 1999 May;17(5):1574-9 [10334546.001]
  • [Cites] Br J Haematol. 1997 Jun;97(3):669-72 [9207420.001]
  • [Cites] Drugs. 1997 Jun;53(6):1005-37 [9179529.001]
  • [Cites] Cancer. 1997 Jun 1;79(11):2107-14 [9179056.001]
  • [Cites] Br J Cancer. 1990 Jul;62(1):4-5 [2390480.001]
  • [Cites] Cancer. 2005 Jan 15;103(2):216-28 [15578683.001]
  • [Cites] Transfus Apher Sci. 2005 Feb;32(1):33-44 [15737872.001]
  • [Cites] Leuk Lymphoma. 2003 Mar;44(3):477-81 [12688318.001]
  • [Cites] Hematology. 2004 Oct-Dec;9(5-6):387-400 [15763979.001]
  • [Cites] J Clin Oncol. 2001 Nov 15;19(22):4252-8 [11709569.001]
  • [Cites] Br J Haematol. 2001 Mar;112(4):1083-5 [11324637.001]
  • [Cites] Blood. 1993 Jun 1;81(11):2878-84 [8499626.001]
  • [Cites] BMC Pharmacol. 2005 Mar 09;5:4 [15757511.001]
  • [Cites] Br J Haematol. 2001 Sep;114(4):800-9 [11564066.001]
  • [Cites] Hematol J. 2004;5 Suppl 1:S31-7 [15079151.001]
  • [Cites] Anticancer Res. 2000 Sep-Oct;20(5A):2961-6 [11062708.001]
  • [Cites] Leuk Res. 1999 Mar;23(3):277-9 [10071081.001]
  • [Cites] Hematology. 2001;6(5):291-314 [27405524.001]
  • [Cites] Eur J Haematol. 1993 May;50(5):292-6 [7686506.001]
  • [Cites] Blood. 1992 Jul 1;80(1):29-36 [1377051.001]
  • [Cites] Leuk Lymphoma. 1994 Mar;13(1-2):75-80 [8025525.001]
  • [Cites] Leukemia. 1997 Apr;11 Suppl 2:S38-41 [9178837.001]
  • [Cites] Blood. 2002 May 15;99(10):3554-61 [11986207.001]
  • [Cites] Leukemia. 1997 Oct;11(10):1631-5 [9324281.001]
  • [Cites] Leuk Lymphoma. 2003 Nov;44(11):1947-50 [14738148.001]
  • [Cites] Blood. 1994 May 15;83(10):2906-11 [7910051.001]
  • [Cites] Br J Haematol. 2003 Jun;121(5):692-702 [12780783.001]
  • [Cites] Eur J Haematol. 1996 Apr;56(4):235-40 [8641392.001]
  • [Cites] Ann Oncol. 2000 Feb;11(2):231-3 [10761763.001]
  • [Cites] Blood. 1988 Sep;72(3):1069-73 [2901280.001]
  • [Cites] Semin Hematol. 2004 Jul;41(3):246-53 [15269884.001]
  • [Cites] Br J Haematol. 2005 Jan;128(2):145-52 [15638848.001]
  • [Cites] Leukemia. 2005 Jan;19(1):64-8 [15510196.001]
  • [Cites] Blood. 1998 Nov 1;92 (9):3368-75 [9787175.001]
  • [Cites] Ann Oncol. 1998 Jul;9(7):721-6 [9739437.001]
  • [Cites] Ann Hematol. 2002 Sep;81(9):508-13 [12373351.001]
  • [Cites] Eur J Cancer Care (Engl). 2004 Jul;13(3):279-87 [15196232.001]
  • [Cites] Blood. 2003 Jan 1;101(1):6-14 [12393429.001]
  • [Cites] J Clin Oncol. 2002 Sep 15;20(18):3891-7 [12228210.001]
  • [Cites] Blood. 2005 Jan 1;105(1):49-53 [15138165.001]
  • [Cites] Blood. 2002 Nov 1;100(9):3115-20 [12384407.001]
  • [Cites] Ann Oncol. 1993 May;4(5):371-5 [8353071.001]
  • [Cites] Leuk Res. 2004 May;28(5):429-42 [15068894.001]
  • [Cites] Leuk Lymphoma. 1999 Jun;34(1-2):151-7 [10350343.001]
  • [Cites] Leukemia. 2002 Jun;16(6):985-92 [12040430.001]
  • [Cites] Clin Cancer Res. 2004 Jan 15;10(2):508-20 [14760072.001]
  • [Cites] Am J Hematol. 1995 Jun;49(2):135-42 [7771465.001]
  • [Cites] J Clin Oncol. 1993 Oct;11(10):1985-9 [8410123.001]
  • [Cites] N Engl J Med. 2000 Dec 14;343(24):1750-7 [11114313.001]
  • [Cites] Eur J Haematol. 2002 Jul;69(1):27-36 [12270059.001]
  • [Cites] Hematol J. 2004;5 Suppl 1:S20-30 [15079150.001]
  • [Cites] Blood. 1995 Oct 1;86(7):2463-74 [7670093.001]
  • [Cites] Haematologica. 2002 Jul;87(7):695-700; discussion 700 [12091119.001]
  • [Cites] Leukemia. 1997 Jan;11(1):170 [9001435.001]
  • [Cites] BioDrugs. 2005;19(1):9-22 [15691213.001]
  • [Cites] Leukemia. 2000 Jun;14(6):1136-42 [10865980.001]
  • [Cites] Haematologica. 2000 Dec;85(12):1268-70 [11114133.001]
  • [Cites] Best Pract Res Clin Haematol. 2002 Sep;15(3):505-16 [12468402.001]
  • [Cites] Br J Haematol. 2000 Mar;108(3):595-601 [10759719.001]
  • [Cites] Haematologica. 2005 Jul;90(7):994-6 [15996945.001]
  • [Cites] Neoplasma. 2000;47(3):168-71 [11043840.001]
  • [Cites] Blood. 1991 Aug 15;78(4):895-9 [1868250.001]
  • [Cites] Oncogene. 2004 Dec 16;23(58):9408-18 [15516989.001]
  • [Cites] Leuk Lymphoma. 2003 Mar;44(3):391-409 [12688309.001]
  • [Cites] Br J Haematol. 2000 Feb;108(2):357-68 [10691866.001]
  • [Cites] J Clin Oncol. 1995 Sep;13(9):2431-48 [7666104.001]
  • [Cites] Blood. 2004 Sep 1;104(5):1428-34 [15138159.001]
  • [Cites] Acta Haematol. 2004;111(4):185-8 [15153709.001]
  • [Cites] Leukemia. 2004 Mar;18(3):385-93 [14737075.001]
  • [Cites] J Clin Oncol. 2003 Apr 1;21(7):1278-84 [12663715.001]
  • [Cites] Curr Treat Options Oncol. 2004 Aug;5(4):289-303 [15233906.001]
  • [Cites] Blood. 2000 May 1;95(9):2786-92 [10779422.001]
  • [Cites] Pharmacol Ther. 1991;49(3):239-68 [1675805.001]
  • [Cites] Lancet. 1992 Oct 17;340(8825):952-6 [1357355.001]
  • [Cites] J Clin Oncol. 1989 Apr;7(4):433-8 [2784491.001]
  • [Cites] Blood. 1999 Oct 15;94(8):2836-43 [10515887.001]
  • [Cites] Ann Intern Med. 1998 Oct 1;129(7):559-66 [9758577.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4070-8 [15767647.001]
  • [Cites] Curr Opin Infect Dis. 2001 Aug;14(4):409-13 [11964857.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4079-88 [15767648.001]
  • [Cites] J Clin Oncol. 2005 May 1;23(13):2971-9 [15738539.001]
  • [Cites] Br J Haematol. 2002 Mar;116(3):538-48 [11849209.001]
  • [Cites] Cancer. 2002 Apr 1;94(7):2033-9 [11932906.001]
  • [Cites] J Clin Oncol. 1992 Oct;10(10):1514-8 [1357107.001]
  • [Cites] Eur J Haematol. 2002 Jun;68(6):370-5 [12225395.001]
  • [Cites] J Clin Oncol. 1996 Mar;14(3):978-83 [8622049.001]
  • [Cites] Leukemia. 1995 Nov;9(11):1875-81 [7475278.001]
  • [Cites] Eur J Cancer. 1997 Dec;33(14):2347-51 [9616280.001]
  • [Cites] Acta Haematol Pol. 1993;24(2):177-82 [8103959.001]
  • [Cites] J Clin Oncol. 1999 Aug;17(8):2454-60 [10561309.001]
  • [Cites] Cytotherapy. 2002;4(3):217-21 [12194718.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] N Engl J Med. 1992 Oct 8;327(15):1056-61 [1355853.001]
  • [Cites] Leukemia. 2002 Jun;16(6):1015-27 [12040433.001]
  • [Cites] Br J Haematol. 1990 Sep;76(1):45-57 [2223648.001]
  • [Cites] Br J Haematol. 2001 Aug;114(2):342-8 [11529853.001]
  • [Cites] Biochem J. 2001 Nov 1;359(Pt 3):537-46 [11672427.001]
  • [Cites] Cancer Res. 1991 Oct 15;51(20):5570-2 [1680554.001]
  • [Cites] Blood. 2001 Oct 15;98(8):2319-25 [11588025.001]
  • [Cites] Expert Opin Pharmacother. 2004 Jul;5(7):1523-33 [15212603.001]
  • [Cites] J Clin Oncol. 1996 Jul;14(7):2160-6 [8683250.001]
  • [Cites] J Clin Oncol. 2001 Mar 1;19(5):1414-20 [11230486.001]
  • [Cites] Drugs Aging. 2000 Jan;16(1):9-27 [10733261.001]
  • [Cites] Eur J Haematol. 1999 Jan;62(1):49-56 [9918312.001]
  • [Cites] Leuk Lymphoma. 2004 May;45(5):937-44 [15291352.001]
  • [Cites] Lancet. 1993 Aug 28;342(8870):555 [8102691.001]
  • [Cites] Blood Rev. 2002 Sep;16(3):175-84 [12163003.001]
  • [Cites] Ann Hematol. 2005 Jul;84(7):456-61 [15770494.001]
  • [Cites] Leuk Res. 2004 Feb;28(2):139-47 [14654078.001]
  • [Cites] Leukemia. 1998 Nov;12(11):1699-707 [9823944.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2723-9 [11023504.001]
  • [Cites] Expert Rev Anticancer Ther. 2004 Feb;4(1):27-36 [14748654.001]
  • [Cites] Eur J Cancer. 2004 Feb;40(3):383-9 [14746857.001]
  • [Cites] Hematol J. 2002;3(5):244-50 [12391542.001]
  • [Cites] Leuk Lymphoma. 2001 Feb;40(5-6):541-50 [11426527.001]
  • [Cites] Blood. 2000 Nov 15;96(10):3537-43 [11071652.001]
  • [Cites] Br J Haematol. 1999 Apr;105(1):268-70 [10233391.001]
  • [Cites] Eur J Haematol. 2001 Mar;66(3):188-94 [11350487.001]
  • [Cites] Br J Haematol. 2002 Dec;119(4):976-84 [12472576.001]
  • [Cites] Leukemia. 1996 Dec;10(12):1959-65 [8946937.001]
  • [Cites] Blood. 2004 Jan 1;103(1):363-5 [12969985.001]
  • [Cites] Exp Hematol. 2004 Jan;32(1):28-35 [14725898.001]
  • [Cites] Leuk Lymphoma. 2001 Feb;40(5-6):551-64 [11426528.001]
  • [Cites] Clin Pharmacokinet. 2002;41(2):93-103 [11888330.001]
  • [Cites] J Clin Oncol. 2003 Jul 15;21(14):2747-53 [12860954.001]
  • [Cites] J Clin Oncol. 2004 Apr 1;22(7):1260-7 [15051774.001]
  • [Cites] J Biol Chem. 2000 Jan 7;275(1):29-34 [10617581.001]
  • [Cites] Leukemia. 2004 Jun;18(6):1093-101 [15071604.001]
  • [Cites] Semin Oncol. 1998 Feb;25(1):117-25 [9482533.001]
  • [Cites] Leukemia. 2003 Feb;17(2):323-7 [12592330.001]
  • [Cites] Leukemia. 1999 Jun;13(6):918-25 [10360381.001]
  • [Cites] Leukemia. 2005 Jun;19(6):1029-33 [15830011.001]
  • [Cites] Blood. 1995 Mar 15;85(6):1580-9 [7888675.001]
  • [Cites] Ann Intern Med. 1988 May;108(5):733-43 [3282467.001]
  • [Cites] Leuk Lymphoma. 2005 Jan;46(1):87-100 [15621786.001]
  • [Cites] J Clin Oncol. 2005 Jun 1;23(16):3819-29 [15809448.001]
  • [Cites] Blood. 1993 Sep 15;82(6):1695-700 [8400226.001]
  • [Cites] N Engl J Med. 2000 Dec 14;343(24):1799-801 [11114321.001]
  • [Cites] Ann Oncol. 1998 Feb;9(2):167-72 [9553661.001]
  • [Cites] Blood. 1994 Nov 1;84(9):3148-57 [7949187.001]
  • [Cites] Leuk Lymphoma. 1997 Aug;26(5-6):435-49 [9389352.001]
  • [Cites] Lancet. 1996 May 25;347(9013):1432-8 [8676625.001]
  • [Cites] Cancer. 2003 Jan 1;97(1):114-20 [12491512.001]
  • [Cites] Leukemia. 2000 Jan;14(1):40-6 [10637475.001]
  • [Cites] Leukemia. 2001 Oct;15(10):1510-6 [11587207.001]
  • [Cites] Eur J Haematol. 1998 Sep;61(3):197-203 [9753416.001]
  • [Cites] N Engl J Med. 1994 Feb 3;330(5):319-22 [7904047.001]
  • [Cites] Blood. 1998 Aug 15;92(4):1165-71 [9694704.001]
  • [Cites] Hematol Cell Ther. 1999 Feb;41(1):13-8 [10193641.001]
  • [Cites] Hematol Oncol Clin North Am. 2004 Aug;18(4):915-26, x [15325706.001]
  • [Cites] Med Sci Monit. 2005 Oct;11(10):PI71-9 [16192912.001]
  • (PMID = 16363884.001).
  • [ISSN] 1170-229X
  • [Journal-full-title] Drugs & aging
  • [ISO-abbreviation] Drugs Aging
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Purine Nucleosides
  • [Number-of-references] 180
  •  go-up   go-down


93. Tromp JM, Tonino SH, Elias JA, Jaspers A, Luijks DM, Kater AP, van Lier RA, van Oers MH, Eldering E: Dichotomy in NF-kappaB signaling and chemoresistance in immunoglobulin variable heavy-chain-mutated versus unmutated CLL cells upon CD40/TLR9 triggering. Oncogene; 2010 Sep 9;29(36):5071-82
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] Dichotomy in NF-kappaB signaling and chemoresistance in immunoglobulin variable heavy-chain-mutated versus unmutated CLL cells upon CD40/TLR9 triggering.
  • Chronic lymphocytic leukemia (CLL) cells circulating in peripheral blood (PB) differ from the leukemic fraction in lymph nodes (LNs) with respect to cell division and drug sensitivity.
  • CD40 stimulation of PB CLL cells in vitro results in chemoresistance and provides a partial model for the LN microenvironment.
  • The TLR9 ligand CpG induces proliferation in immunoglobulin variable heavy-chain-unmutated CLL, but apoptosis in immunoglobulin variable heavy-chain-mutated CLL.
  • To juxtapose proliferative with antiapoptotic signals, we investigated the effects of CpG in the context of CD40 ligation in mutated versus unmutated CLL cells in this study.
  • Thus, a distinction in NF-kappaB activation and drug susceptibility in mutated versus unmutated (LN-like) CLL cells was uncovered, which was causally linked to Bcl-X(L) levels.
  • [MeSH-major] Antigens, CD40 / agonists. Drug Resistance, Neoplasm. Immunoglobulin Heavy Chains / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. NF-kappa B / physiology. Toll-Like Receptor 9 / agonists
  • [MeSH-minor] Animals. Biphenyl Compounds / pharmacology. CD40 Ligand / metabolism. CD40 Ligand / pharmacology. Cell Proliferation / drug effects. Cells, Cultured. Humans. Immunoglobulin Variable Region / genetics. Lymphocyte Activation / drug effects. Mice. Mutation / physiology. NIH 3T3 Cells. Nitrophenols / pharmacology. Oligodeoxyribonucleotides / pharmacology. Piperazines / pharmacology. Signal Transduction / drug effects. Signal Transduction / physiology. Sulfonamides / pharmacology. bcl-X Protein / metabolism. bcl-X Protein / physiology

  • 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 = 20581863.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABT-737; 0 / Antigens, CD40; 0 / Biphenyl Compounds; 0 / CpG ODN 2006; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / NF-kappa B; 0 / Nitrophenols; 0 / Oligodeoxyribonucleotides; 0 / Piperazines; 0 / Sulfonamides; 0 / Toll-Like Receptor 9; 0 / bcl-X Protein; 147205-72-9 / CD40 Ligand
  •  go-up   go-down


94. O'Donghaile D, Hayden PJ, McCarron SL, Doyle EM, Lawler M, Browne PV, Conneally E, Vandenberghe E, McCann SR: Marrow aplasia developing 13 years after HLA-identical sibling allogeneic transplantation for chronic myeloid leukaemia: successful treatment with antithymocyte globulin and peripheral blood stem cell infusion from the original donor. Eur J Haematol; 2006 Mar;76(3):258-60
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] Marrow aplasia developing 13 years after HLA-identical sibling allogeneic transplantation for chronic myeloid leukaemia: successful treatment with antithymocyte globulin and peripheral blood stem cell infusion from the original donor.
  • We describe a case of profound marrow aplasia occurring 13 years after sibling allogeneic bone marrow transplantation for chronic myeloid leukaemia (CML) in first chronic phase.
  • [MeSH-major] Bone Marrow Diseases / etiology. Bone Marrow Transplantation / adverse effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications
  • [MeSH-minor] Antilymphocyte Serum / therapeutic use. Female. Histocompatibility Testing. Humans. Middle Aged. Peripheral Blood Stem Cell Transplantation. Siblings. Transplantation, Homologous. Treatment Outcome


95. Lu G, Kong Y, Yue C: Genetic and immunophenotypic profile of IGH@ rearrangement detected by fluorescence in situ hybridization in 149 cases of B-cell chronic lymphocytic leukemia. Cancer Genet Cytogenet; 2010 Jan 1;196(1):56-63
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.
  • [Title] Genetic and immunophenotypic profile of IGH@ rearrangement detected by fluorescence in situ hybridization in 149 cases of B-cell chronic lymphocytic leukemia.
  • Recent studies have shown a higher frequency of immunoglobulin heavy (IGH@) locus rearrangement in B-cell chronic lymphocytic leukemia (B-CLL) than previously reported.
  • However, association of the IGH@ rearrangement with specific chromosomal abnormalities and immunophenotypic markers in B-CLL is still under further investigation.
  • In this study, we analyzed 149 bone marrow aspirate or peripheral blood specimens from patients diagnosed with B-CLL, evaluated by four different laboratory studies: morphology examination, three- or four-color flow cytometry analysis, conventional cytogenetics, and fluorescence in situ hybridization (FISH) with a dual-color, break-apart IGH@ probe in addition to a B-CLL FISH probe panel for del(11)(q22) ATM, del(13)(q14.3), del(17)(p13) TP53, and +12.
  • The present results further confirm that IGH@ rearrangement is not a rare genomic abnormality in B-CLL, and also show both that t(14;19)(q32;q13.2) is the most common cytogenetic change involving IGH@ rearrangement detected by FISH in B-CLL and that IGH@ rearrangement is correlated with CD38 expression.
  • It is appropriate to include an IGH@ probe in the FISH panel for B-CLL diagnosis.
  • [MeSH-major] Immunoglobulin Heavy Chains / genetics. Immunophenotyping. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / immunology


96. Bojarska-Junak A, Hus I, Chocholska S, Wasik-Szczepanek E, Sieklucka M, Dmoszyńska A, Roliński J: BAFF and APRIL expression in B-cell chronic lymphocytic leukemia: correlation with biological and clinical features. Leuk Res; 2009 Oct;33(10):1319-27
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] BAFF and APRIL expression in B-cell chronic lymphocytic leukemia: correlation with biological and clinical features.
  • B-cell activating factor (BAFF) and a proliferation-inducing ligand (APRIL) are involved in normal B cell survival and differentiation.
  • We analyzed BAFF and APRIL plasma levels in patients with B-cell chronic lymphocytic leukemia (B-CLL).
  • We also tested intracellular BAFF and APRIL expression in B-CLL and evaluated their prognostic relevance.
  • Moreover, we found a close relationship between LPL protein expression or LPL/ADAM29 MFI ratio and proportion of B-CLL cells with intracellular BAFF or APRIL expression.
  • Furthermore, patients with a low percentage of leukemic cells with intracellular BAFF or APRIL expression had a significantly longer overall survival than those with a high proportion of APRIL or BAFF positive leukemic cells.
  • [MeSH-major] B-Cell Activating Factor / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Tumor Necrosis Factor Ligand Superfamily Member 13 / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. B-Lymphocytes / pathology. Female. Humans. Male. Middle Aged. Neoplasm Staging. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Survivors

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, B-cell, chronic.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Leuk Res. 2009 Oct;33(10):1306-7 [19464058.001]
  • (PMID = 19395025.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / B-Cell Activating Factor; 0 / RNA, Neoplasm; 0 / TNFSF13 protein, human; 0 / TNFSF13B protein, human; 0 / Tumor Necrosis Factor Ligand Superfamily Member 13
  •  go-up   go-down


97. Maki G, Hayes GM, Naji A, Tyler T, Carosella ED, Rouas-Freiss N, Gregory SA: NK resistance of tumor cells from multiple myeloma and chronic lymphocytic leukemia patients: implication of HLA-G. Leukemia; 2008 May;22(5):998-1006
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] NK resistance of tumor cells from multiple myeloma and chronic lymphocytic leukemia patients: implication of HLA-G.
  • Multiple myeloma (MM) and chronic lymphocytic leukemia (CLL) represent the two most prevalent adult hematological malignancies in the western hemisphere.
  • To evaluate the role of NK cells in the immune surveillance and their therapeutic potential for CLL and MM, tumor cell susceptibility to NK-mediated killing was investigated.
  • Results show relative resistance of tumor cells from CLL as well as MM (73 and 70% of the patients, respectively) to NK-mediated killing.
  • To gain insight into molecular mechanisms of this resistance, the expression of the tolerogenic HLA-G molecule in CLL and MM and its relevance to susceptibility to NK-mediated killing were investigated.
  • HLA-G transcript was found in tumor cells from 89% (n=19) of CLL and 100% (n=9) of MM patients examined.
  • HLA-G1 surface expression was observed in CLL and was very low or undetectable in MM.
  • Notably, blocking of HLA-G1 with specific antibody on CLL samples increased their susceptibility to NK-mediated killing, demonstrating that HLA-G participates in protecting CLL cells from NK-mediated killing and may thus contribute to their immune escape in vivo.
  • [MeSH-major] HLA Antigens / immunology. Histocompatibility Antigens Class I / immunology. Killer Cells, Natural / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Multiple Myeloma / immunology. Tumor Escape

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • 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 = 18288133.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / HLA Antigens; 0 / HLA-G Antigens; 0 / Histocompatibility Antigens Class I; 0 / RNA, Neoplasm
  •  go-up   go-down


98. Ghia P, Scielzo C, Frenquelli M, Muzio M, Caligaris-Cappio F: From normal to clonal B cells: Chronic lymphocytic leukemia (CLL) at the crossroad between neoplasia and autoimmunity. Autoimmun Rev; 2007 Dec;7(2):127-31
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] From normal to clonal B cells: Chronic lymphocytic leukemia (CLL) at the crossroad between neoplasia and autoimmunity.
  • Chronic lymphocytic leukemia (CLL) is a B-cell malignancy endowed with a number of features that recall autoimmune disorders, including the CD5 expression and the development of autoimmune manifestations restricted to self antigens expressed by hematopoietic cells.
  • Several evidences strongly support the possibility that an antigenic stimulation through the B-cell receptor (BCR) is involved in the selection and possibly also the expansion of the malignant clone.
  • It appears likely that CLL cells derive from a pool of auto/polyreactive CD5(+) B cells.
  • Hence CLL appears to be a B-cell malignancy triggered or facilitated in its development and evolution by an auto-Ag.
  • The crucial issues have become to what extent this deleterious binding capacity is central to the natural history of the disease and how it relates to the malignant transformation of the cell.
  • [MeSH-major] Autoimmunity. B-Lymphocytes / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Receptors, Antigen, B-Cell / metabolism

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18035322.001).
  • [ISSN] 1568-9972
  • [Journal-full-title] Autoimmunity reviews
  • [ISO-abbreviation] Autoimmun Rev
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD5; 0 / Autoantigens; 0 / Receptors, Antigen, B-Cell
  • [Number-of-references] 40
  •  go-up   go-down


99. Liu YJ, Wu DP, Li CX, He J, Qiu QC, Zhang XG: [The role of CD4+ CD25+ T cell and FOXP3 in hsot acute graft rejection]. Zhonghua Nei Ke Za Zhi; 2006 Oct;45(10):835-8
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] [The role of CD4+ CD25+ T cell and FOXP3 in hsot acute graft rejection].
  • OBJECTIVE: To explore the relationship among CD4+ CD25+ regulatory T cell, the expression of FOXP(3) mRNA levels of donor bone marrow (BM) and graft versus host disease (GVHD) in allogeneic hematopoietic stem cell transplantation (allo-HSCT). METHODS:.
  • The levels of donor CD4+CD25+ regulatory T cell were compared in the patients with GVHD and those without GVHD with immunofluorescence and flow cytometry. (2) The donor BM expressions of FOXP(3) mRNA levels were analyzed by using reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS:.
  • With a median follow-up of 12.8 (8-16) months, acute GVHD (aGVHD) occurred in 15 of the 30 patients (50.0%) with grade II-IV aGVHD (40.0%).
  • Chronic GVHD developed in 6 (extensive 2, limited 4) out of the 30 patients (20.0%). (2) The levels of donor CD4+CD25+ regulatory T cell pre-and post-mobilization were (2.67 +/- 0.38)% and (5.01 +/- 1.33)% respectively; no difference was observed (P > 0.05). (3) Patients with I-II aGVHD demonstrated higher donor-type CD4+CD25+ immune regulatory T cell level than those with III-IV aGVHD.
  • Patients with III-IV aGVHD showed much lower donor-type CD4+CD25+ immune regulatory T cell level than those without GVHD.
  • (1) Donor-type CD4+CD25+ immune regulatory T cell level was related to recipient II-IV aGVHD.
  • Up-grade donor-type CD4+CD25+ immune regulatory T cell level could reduce the incidence of aGVHD. (2) Donor BM FOXP(3) transcripts were detected in patients without serious aGVHD after transplantation.
  • [MeSH-major] CD4-Positive T-Lymphocytes / physiology. Forkhead Transcription Factors / biosynthesis. Graft vs Host Disease / immunology. Interleukin-2 Receptor alpha Subunit / physiology
  • [MeSH-minor] Adolescent. Adult. CD4 Lymphocyte Count. Female. Hematopoietic Stem Cell Transplantation / adverse effects. Humans. Leukemia / surgery. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction. T-Lymphocyte Subsets. Tissue Donors. Transplantation, Homologous

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17217750.001).
  • [ISSN] 0578-1426
  • [Journal-full-title] Zhonghua nei ke za zhi
  • [ISO-abbreviation] Zhonghua Nei Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Interleukin-2 Receptor alpha Subunit
  •  go-up   go-down


100. Rakshit S, Mandal L, Pal BC, Bagchi J, Biswas N, Chaudhuri J, Chowdhury AA, Manna A, Chaudhuri U, Konar A, Mukherjee T, Jaisankar P, Bandyopadhyay S: Involvement of ROS in chlorogenic acid-induced apoptosis of Bcr-Abl+ CML cells. Biochem Pharmacol; 2010 Dec 1;80(11):1662-75
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.
  • Chlorogenic acid (Chl) has been reported to possess a wide range of biological and pharmacological properties including induction of apoptosis of Bcr-Abl(+) chronic myeloid leukemia (CML) cell lines and clinical leukemia samples via inhibition of Bcr-Abl phosphorylation.
  • Antioxidant NAC attenuated Chl-induced oxidative stress-mediated inhibition of Bcr-Abl phosphorylation, DR5 upregulation, caspase activation and CML cell death.
  • The role of ROS in Chl-induced death was confirmed with primary leukemia cells from CML patients in vitro as well as in vivo in nude mice bearing K562 xenografts.
  • [MeSH-major] Apoptosis / physiology. Chlorogenic Acid / pharmacology. Fusion Proteins, bcr-abl / biosynthesis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Reactive Oxygen Species / metabolism

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20832390.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; 318ADP12RI / Chlorogenic Acid; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  •  go-up   go-down






Advertisement