[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 10 of about 10
1. Shaha SP, Tomic J, Shi Y, Pham T, Mero P, White D, He L, Baryza JL, Wender PA, Booth JW, Spaner DE: Prolonging microtubule dysruption enhances the immunogenicity of chronic lymphocytic leukaemia cells. Clin Exp Immunol; 2009 Nov;158(2):186-98
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prolonging microtubule dysruption enhances the immunogenicity of chronic lymphocytic leukaemia cells.
  • Cytotoxic chemotherapies do not usually mediate the expression of an immunogenic gene programme in tumours, despite activating many of the signalling pathways employed by highly immunogenic cells.
  • Concomitant use of agents that modulate and complement stress-signalling pathways activated by chemotherapeutic agents may then enhance the immunogenicity of cancer cells, increase their susceptibility to T cell-mediated controls and lead to higher clinical remission rates.
  • Consistent with this hypothesis, the microtubule inhibitor, vincristine, caused chronic lymphocytic leukaemia (CLL) cells to die rapidly, without increasing their immunogenicity.
  • Protein kinase C (PKC) agonists (such as bryostatin) delayed the death of vincristine-treated CLL cells and made them highly immunogenic, with increased stimulatory abilities in mixed lymphocyte responses, production of proinflammatory cytokines, expression of co-stimulatory molecules and activation of c-Jun N-terminal kinase (JNK), p38 and nuclear factor kappa B (NF-kappaB) signalling pathways.

  • Hazardous Substances Data Bank. VINCRISTINE .
  • 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
  • [Cites] Curr Opin Cell Biol. 2002 Feb;14(1):18-24 [11792540.001]
  • [Cites] Blood. 2001 Nov 1;98(9):2603-14 [11675328.001]
  • [Cites] Immunobiology. 2002 Jul;205(3):231-46 [12182451.001]
  • [Cites] J Immunol Methods. 2002 Jun 1;264(1-2):77-87 [12191512.001]
  • [Cites] Blood. 2002 Nov 15;100(10):3741-8 [12393602.001]
  • [Cites] Nat Rev Cancer. 2003 Jan;3(1):11-22 [12509763.001]
  • [Cites] Cancer Immunol Immunother. 2003 Mar;52(3):185-93 [12649748.001]
  • [Cites] Nat Rev Drug Discov. 2003 Jul;2(7):554-65 [12815381.001]
  • [Cites] Clin Cancer Res. 2003 Dec 1;9(16 Pt 1):5929-35 [14676117.001]
  • [Cites] Blood. 2004 Feb 15;103(4):1202-10 [14576043.001]
  • [Cites] Nat Rev Cancer. 2004 Apr;4(4):253-65 [15057285.001]
  • [Cites] J Leukoc Biol. 2004 Aug;76(2):338-51 [15277580.001]
  • [Cites] Nat Rev Drug Discov. 2004 Oct;3(10):831-44 [15459674.001]
  • [Cites] Leuk Res. 1985;9(7):885-95 [2991669.001]
  • [Cites] J Clin Oncol. 1991 May;9(5):770-6 [2016618.001]
  • [Cites] Science. 1995 Oct 13;270(5234):286-90 [7569976.001]
  • [Cites] FASEB J. 1997 Jul;11(8):649-69 [9240967.001]
  • [Cites] Br J Haematol. 2004 Dec;127(5):531-42 [15566356.001]
  • [Cites] J Med Chem. 2004 Dec 16;47(26):6638-44 [15588099.001]
  • [Cites] J Immunother. 2005 Jan-Feb;28(1):28-39 [15614042.001]
  • [Cites] Curr Opin Immunol. 2005 Aug;17(4):338-44 [15950447.001]
  • [Cites] Leukemia. 2006 Feb;20(2):286-95 [16341037.001]
  • [Cites] J Immunol. 2006 Mar 15;176(6):3830-9 [16517754.001]
  • [Cites] Cancer Immunol Immunother. 2008 Sep;57(9):1381-90 [18297282.001]
  • [Cites] Curr Opin Immunol. 2008 Oct;20(5):504-11 [18573340.001]
  • [Cites] Oncogene. 2008 Oct 20;27(48):6245-51 [18931691.001]
  • [Cites] Eur J Haematol. 2000 Dec;65(6):370-8 [11168494.001]
  • [Cites] Cell Biol Toxicol. 2000;16(5):339-46 [11201057.001]
  • [Cites] Physiol Rev. 2001 Apr;81(2):807-69 [11274345.001]
  • [Cites] Biochem J. 2002 Feb 15;362(Pt 1):1-12 [11829734.001]
  • (PMID = 19737143.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA031845; United States / NCI NIH HHS / CA / R37 CA031845; United States / NCI NIH HHS / CA / CA31845
  • [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, CD; 0 / Antineoplastic Agents, Phytogenic; 0 / Bryostatins; 0 / Enzyme Activators; 0 / Phorbol Esters; 0 / Tubulin Modulators; 0 / Tumor Necrosis Factor-alpha; 37558-16-0 / Phorbol 12,13-Dibutyrate; 5J49Q6B70F / Vincristine; EC 2.7.11.13 / Protein Kinase C
  • [Other-IDs] NLM/ PMC2768808
  •  go-up   go-down


2. Jurado M, Deeg H, Gooley T, Anasetti C, Chauncey T, Flowers M, Myerson D, Storb R, Appelbaum F: Haemopoietic stem cell transplantation for advanced polycythaemia vera or essential thrombocythaemia. Br J Haematol; 2001 Feb;112(2):392-6
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.
  • HSCT was performed because of progression to the spent phase of the disease with myelofibrosis and splenomegaly in 10 patients and evolution into a myelodysplastic syndrome (MDS) or acute myelogenous leukaemia (AML) in nine patients.
  • The interval from diagnosis to HSCT was 77-300 months (median 170).
  • Eleven patients received a transplant from a related, and eight from an unrelated, donor following conditioning with chemotherapy only or chemotherapy plus total body irradiation regimens.
  • Twelve patients are surviving 5-116 months (median 41) after transplant, 10 in continued complete remission, one in haematological remission with residual marrow fibrosis and one with mixed haemopoietic chimaerism currently receiving therapy with interferon.
  • Seven patients (six with AML/MDS and one with myelofibrosis) died of transplant-related complications.
  • These data show that HSCT can provide curative therapy for patients with PV and ET with advanced disease.
  • [MeSH-minor] Adult. Disease-Free Survival. Female. Humans. Male. Middle Aged. Regression Analysis. Remission Induction. Retrospective Studies. Splenectomy. Statistics, Nonparametric

  • Genetic Alliance. consumer health - Transplantation.
  • 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 = 11167837.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA18029; United States / NCI NIH HHS / CA / CA87948; United States / NHLBI NIH HHS / HL / HL36444
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  •  go-up   go-down


3. Pullarkat V, Veliz L, Chang K, Mohrbacher A, Teotico AL, Forman SJ, Slovak ML: Therapy-related, mixed-lineage leukaemia translocation-positive, monoblastic myeloid sarcoma of the uterus. J Clin Pathol; 2007 May;60(5):562-4
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] Therapy-related, mixed-lineage leukaemia translocation-positive, monoblastic myeloid sarcoma of the uterus.
  • These tumours can, on occasion, occur without concurrent or antecedent leukaemia.
  • An unusual case of therapy-related acute myeloid leukaemia (t-AML) presenting as isolated monoblastic myeloid sarcoma of the uterus in a patient who had received adjuvant chemotherapy for breast cancer is presented.
  • Fluorescence in situ hybridisation analysis performed on paraffin-wax-embedded tumour tissue revealed a mixed-lineage leukaemia (MLL) gene rearrangement, supporting the association of this malignancy with prior chemotherapy.
  • This case illustrates that t-AML can rarely present as isolated extramedullary tumours, and the detection of specific chromosomal abnormalities in these myeloid sarcomas can be useful for risk assessment and guiding definitive therapy.

  • Genetic Alliance. consumer health - Myeloid sarcoma.
  • MedlinePlus Health Information. consumer health - Uterine Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Am J Clin Pathol. 2000 Nov;114(5):807-11 [11068557.001]
  • [Cites] Leuk Lymphoma. 2001 Apr;41(3-4):255-76 [11378539.001]
  • [Cites] Am J Pathol. 2002 Jun;160(6):1967-72 [12057901.001]
  • [Cites] Leuk Lymphoma. 2002 Nov;43(11):2151-3 [12533040.001]
  • [Cites] Int J Surg Pathol. 2003 Oct;11(4):271-82 [14615822.001]
  • [Cites] Leukemia. 2005 Feb;19(2):183-90 [15618964.001]
  • [Cites] Urology. 1986 Mar;27(3):268-70 [3082059.001]
  • [Cites] Gynecol Oncol. 1992 Jul;46(1):128-37 [1634133.001]
  • [Cites] Blood. 1993 Dec 15;82(12):3705-11 [8260707.001]
  • [Cites] Am J Clin Pathol. 1995 Oct;104(4):431-43 [7572794.001]
  • [Cites] Am J Surg Pathol. 1997 Oct;21(10):1156-65 [9331287.001]
  • [Cites] Leuk Res. 2004 Nov;28(11):1165-9 [15380340.001]
  • (PMID = 17513515.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA030206; United States / NCI NIH HHS / CA / 2 P01 CA030206-24A1; United States / NCI NIH HHS / CA / 5P30 CA33572
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1994540
  •  go-up   go-down


Advertisement
4. Main C, Pitt M, Moxham T, Stein K: The clinical effectiveness and cost-effectiveness of rituximab for the first-line treatment of chronic lymphocytic leukaemia: an evidence review of the submission from Roche. Health Technol Assess; 2010 Oct;14(Suppl. 2):27-32
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The clinical effectiveness and cost-effectiveness of rituximab for the first-line treatment of chronic lymphocytic leukaemia: an evidence review of the submission from Roche.
  • This paper presents a summary of the evidence review group (ERG) report into the clinical effectiveness and cost-effectiveness of rituximab for the first-line treatment of chronic lymphocytic leukaemia (CLL) based upon a review of the manufacturer's submission to the National Institute for Health and Clinical Excellence (NICE) as part of the single technology appraisal (STA) process.
  • The submission's evidence came from a single, unpublished, well-conducted randomised controlled trial (RCT) comparing rituximab in combination with fludarabine and cyclophosphamide (R-FC) with fludarabine and cyclophosphamide (FC) alone for the first-line treatment of CLL.
  • However, the initial significant treatment benefit for R-FC compared with FC for overall survival was not maintained at a slightly longer follow-up time [median 25.4 months; adjusted HR 0.72 (95% CI 0.48 to 1.09)].
  • Response rates, numbers of patients with event-free survival and duration of response all favoured treatment with R-FC.
  • Additional evidence from a mixed-treatment comparison model indicated R-FC to be significantly superior to chlorambucil alone for both PFS and overall and complete response rates.
  • Dose modifications were also more frequent in this arm, but this did not lead to differences in treatment discontinuation.
  • The model used a cycle length of 1 month and a lifetime time horizon.
  • The base-case analysis produced an incremental cost-effectiveness ratio (ICER) of 13,189 pounds per quality-adjusted life-year (QALY) for R-FC versus FC, and 6422 pounds per QALY for the comparison of R-FC versus chlorambucil, suggesting that R-FC is cost-effective at normal willingness-to-pay thresholds.
  • One-way sensitivity analyses produced a range of ICERs from 10,249 pounds to 22,661 pounds per QALY for R-FC versus FC, and 5612 pounds and 6921 pounds per QALY for R-FC versus chlorambucil.
  • Probabilistic sensitivity analysis results matched the deterministic results very closely.
  • However, the sensitivity analysis did not fully investigate the uncertainty associated with differential values across arms or with the structural assumptions of the model, and utility values were not drawn from an empirical study.
  • The NICE guidance issued as a result of the STA states that: Rituximab in combination with fludarabine and cyclophosphamide (R-FC) is recommended as an option for the first-line treatment of chronic lymphocytic leukaemia in people for whom fludarabine in combination with cyclophosphamide (FC) is considered appropriate.
  • Rituximab in combination with chemotherapy agents other than fludarabine and cyclophosphamide is not recommended for the first-line treatment of chronic lymphocytic leukaemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived / administration & dosage. Antibodies, Monoclonal, Murine-Derived / economics. Cost-Benefit Analysis. Cyclophosphamide / administration & dosage. Cyclophosphamide / economics. Great Britain. Humans. Randomized Controlled Trials as Topic. Rituximab. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Vidarabine / economics

  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. VIDARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21047488.001).
  • [ISSN] 2046-4924
  • [Journal-full-title] Health technology assessment (Winchester, England)
  • [ISO-abbreviation] Health Technol Assess
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  •  go-up   go-down


5. Rezk H, el-Shazly AM, Soliman M, el-Nemr HI, Nagaty IM, Fouad MA: Coccidiosis among immuno-competent and -compromised adults. J Egypt Soc Parasitol; 2001 Dec;31(3):823-34
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.
  • There was significant increase in coccidia positive cases among Hodgkin lymphoma receiving chemotherapy as compared to control group (p < 0.05).
  • The increase was highly significant in the group of acute lymphocytic leukaemia receiving chemotherapy as compared to control group (P < 0.01).
  • The total percent of cases with single type of coccidia were 12.2% compared to multiple coccidial infections (4.3%).
  • The most commonly associated parasite was Cryptosporidium.
  • The total cryptosporidial infections (single and mixed with other coccidia) were 12.1% of the total studied cases.
  • Microsporidial infections (single and mixed with other coccidia), being the least detected among the four intestinal spores forming coccidia, were 2.4% in the immunocompromised groups.
  • The total cyclosporal infections (single and mixed with other coccidia) were 6.3% of the total studied cases.
  • In the immunocompromised groups, the prevalence was (8.3%) where in immunocompetent group, was 2.8%.
  • Single cyclospora was 3.0% while mixed Cyclospora represented 3.3% of all studied cases.
  • The Isospora infections (single and mixed) were 3.8% of total patients.
  • The prevalence among immunocompromised group was 5.2% and in immunocompetent patients was 2.8%.
  • [MeSH-minor] Adult. Aged. Animals. Antineoplastic Agents / adverse effects. Egypt / epidemiology. Female. Hodgkin Disease / complications. Hodgkin Disease / drug therapy. Hodgkin Disease / immunology. Humans. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11775108.001).
  • [ISSN] 1110-0583
  • [Journal-full-title] Journal of the Egyptian Society of Parasitology
  • [ISO-abbreviation] J Egypt Soc Parasitol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


6. Gaspar HB, Parsley KL, Howe S, King D, Gilmour KC, Sinclair J, Brouns G, Schmidt M, Von Kalle C, Barington T, Jakobsen MA, Christensen HO, Al Ghonaium A, White HN, Smith JL, Levinsky RJ, Ali RR, Kinnon C, Thrasher AJ: Gene therapy of X-linked severe combined immunodeficiency by use of a pseudotyped gammaretroviral vector. Lancet; 2004 Dec 18-31;364(9452):2181-7
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] Gene therapy of X-linked severe combined immunodeficiency by use of a pseudotyped gammaretroviral vector.
  • BACKGROUND: X-linked severe combined immunodeficiency (SCID-X1) is caused by mutations in the common cytokine-receptor gamma chain (gamma(c)), resulting in disruption of development of T lymphocytes and natural-killer cells.
  • Allogeneic bone-marrow transplantation is successful if HLA-matched family donors are available, but HLA-mismatched procedures are associated with substantial morbidity and mortality.
  • We investigated the application of somatic gene therapy by use of a gibbon-ape-leukaemia-virus pseudotyped gammaretroviral vector.
  • Autologous CD34-positive haemopoietic bone-marrow stem cells were transduced ex vivo and returned to the patients without preceding cytoreductive chemotherapy.
  • FINDINGS: All patients have shown substantial improvements in clinical and immunological features, and prophylactic medication could be withdrawn in two.
  • Where assessable, humoral immunity, in terms of antibody production, was also restored and associated with increasing rates of somatic mutation in immunoglobulin genes.
  • INTERPRETATION: Gene therapy for SCID-X1 is a highly effective strategy for restoration of functional cellular and humoral immunity.
  • [MeSH-major] Genetic Diseases, X-Linked / therapy. Genetic Therapy. Severe Combined Immunodeficiency / therapy
  • [MeSH-minor] Antigens, CD34 / analysis. Bone Marrow Cells / immunology. Bone Marrow Transplantation. Child, Preschool. Gammaretrovirus. Gene Transfer Techniques. Genetic Vectors. Humans. Immunity. Immunoglobulins / blood. Infant. Interleukin Receptor Common gamma Subunit. Lymphocyte Activation. Lymphocyte Culture Test, Mixed. Mutation. Receptors, Interleukin-7 / genetics. T-Lymphocytes / immunology. Transduction, Genetic


7. Eiden C, Peyrière H, Tichit R, Cociglio M, Amedro P, Blayac JP, Margueritte G, Hillaire-Buys D: Inherited long QT syndrome revealed by antifungals drug-drug interaction. J Clin Pharm Ther; 2007 Jun;32(3):321-4
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] Inherited long QT syndrome revealed by antifungals drug-drug interaction.
  • A 14-year-old Tahitian girl with acute myeloid leukaemia and a suspected mucormucosis infection was treated with intravenous voriconazole and caspofungin.
  • During the switch, the patient presented with QT interval prolongation with 'torsades de pointes' and reversible cardiac arrest.
  • The association of antifungal agents with pro-arrhythmogenic drugs and other risk factors led to torsades de pointes and the revealing of inherited QT syndrome.
  • [MeSH-major] Antifungal Agents / adverse effects. Long QT Syndrome / chemically induced. Torsades de Pointes / chemically induced
  • [MeSH-minor] Acute Disease. Adolescent. Aryl Hydrocarbon Hydroxylases / genetics. Cytochrome P-450 CYP2C19. Cytochrome P-450 CYP2C9. Female. Genotype. Humans. Injections, Intravenous. Leukemia, Myeloid / complications. Mixed Function Oxygenases / genetics. Mucormycosis / complications. Mucormycosis / drug therapy. Pyrimidines / administration & dosage. Pyrimidines / adverse effects. Pyrimidines / therapeutic use. Triazoles / administration & dosage. Triazoles / adverse effects. Triazoles / therapeutic use. Voriconazole

  • Genetic Alliance. consumer health - Long QT Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17489884.001).
  • [ISSN] 0269-4727
  • [Journal-full-title] Journal of clinical pharmacy and therapeutics
  • [ISO-abbreviation] J Clin Pharm Ther
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Pyrimidines; 0 / Triazoles; 6TK1G07BHZ / posaconazole; EC 1.- / Mixed Function Oxygenases; EC 1.14.13.- / CYP2C9 protein, human; EC 1.14.13.- / Cytochrome P-450 CYP2C19; EC 1.14.13.- / Cytochrome P-450 CYP2C9; EC 1.14.14.1 / Aryl Hydrocarbon Hydroxylases; EC 1.14.14.1 / CYP2C19 protein, human; JFU09I87TR / Voriconazole
  •  go-up   go-down


8. Pieters R, Schrappe M, De Lorenzo P, Hann I, De Rossi G, Felice M, Hovi L, LeBlanc T, Szczepanski T, Ferster A, Janka G, Rubnitz J, Silverman L, Stary J, Campbell M, Li CK, Mann G, Suppiah R, Biondi A, Vora A, Valsecchi MG: A treatment protocol for infants younger than 1 year with acute lymphoblastic leukaemia (Interfant-99): an observational study and a multicentre randomised trial. Lancet; 2007 Jul 21;370(9583):240-50
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 treatment protocol for infants younger than 1 year with acute lymphoblastic leukaemia (Interfant-99): an observational study and a multicentre randomised trial.
  • BACKGROUND: Acute lymphoblastic leukaemia in infants younger than 1 year is rare, and infants with the disease have worse outcomes than do older children.
  • We initiated an international study to investigate the effects of a new hybrid treatment protocol with elements designed to treat both acute lymphoblastic leukaemia and acute myeloid leukaemia, and to identify any prognostic factors for outcome in infants.
  • We also did a randomised trial to establish the value of a late intensification course.
  • Eligible patients were stratified for risk according to their peripheral blood response to a 7-day prednisone prophase, and then given a hybrid regimen based on the standard protocol for acute lymphoblastic leukaemia, with some elements designed for treatment of acute myeloid leukaemia.
  • Before the maintenance phase, a subset of patients in complete remission were randomly assigned to receive either standard treatment or a more intensive chemotherapy course with high-dose cytarabine and methotrexate.
  • The primary outcomes were event-free survival (EFS) for the initial cohort of patients and disease-free survival (DFS) for the patients randomly assigned to a treatment group.
  • FINDINGS: In the 482 enrolled patients who underwent hybrid treatment, 260 (58%) were in complete remission at a median follow-up of 38 (range 1-78) months, and EFS at 4 years was 47.0% (SE 2.6, 95% CI 41.9-52.1).
  • Of 445 patients in complete remission after 5 weeks of induction treatment, 191 were randomised: 95 patients to receive a late intensification course, and 96 to a control group.
  • At a median follow-up of 42 (range 1-73) months, 60 patients in the treatment group and 57 controls were disease-free.
  • DFS at 4 years did not differ between the two groups (60.9% [SE 5.2] for treatment group vs 57.0% [5.5] for controls; p=0.81).
  • During the intensification phase, of 71 patients randomly assigned to the treatment group, and for whom toxicity data were available, 35 (49%) had infections, 21 (30%) patients had mucositis, 22 (31%) patients had toxic effects on the liver, and 2 (3%) had neurotoxicity.
  • All types of rearrangements in the (mixed lineage leukaemia) MLL gene, very high white blood cell count, age of younger than 6 months, and a poor response to the prednisone prophase were independently associated with inferior outcomes.
  • INTERPRETATION: Patients treated with our hybrid protocol, and especially those who responded poorly to prednisone, had higher EFS than most reported outcomes for treatment of infant ALL.
  • Delayed intensification of chemotherapy did not benefit patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. METHOTREXATE .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Lancet. 2007 Jul 21;370(9583):198-200 [17658376.001]
  • (PMID = 17658395.001).
  • [ISSN] 1474-547X
  • [Journal-full-title] Lancet (London, England)
  • [ISO-abbreviation] Lancet
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00015873; ISRCTN/ ISRCTN24251487
  • [Grant] United Kingdom / Medical Research Council / / G0300130
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate
  •  go-up   go-down


9. Hawwa AF, Collier PS, Millership JS, McCarthy A, Dempsey S, Cairns C, McElnay JC: Population pharmacokinetic and pharmacogenetic analysis of 6-mercaptopurine in paediatric patients with acute lymphoblastic leukaemia. Br J Clin Pharmacol; 2008 Dec;66(6):826-37
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] Population pharmacokinetic and pharmacogenetic analysis of 6-mercaptopurine in paediatric patients with acute lymphoblastic leukaemia.
  • AIMS: To investigate the population pharmacokinetics of 6-mercaptopurine (6-MP) active metabolites in paediatric patients with acute lymphoblastic leukaemia (ALL) and examine the effects of various genetic polymorphisms on the disposition of these metabolites.
  • METHODS: Data were collected prospectively from 19 paediatric patients with ALL (n = 75 samples, 150 concentrations) who received 6-MP maintenance chemotherapy (titrated to a target dose of 75 mg m(-2) day(-1)).
  • Population pharmacokinetic analysis was performed with the nonlinear mixed effects modelling program (nonmem) to determine the population mean parameter estimate of clearance for the active metabolites.
  • RESULTS: The developed model revealed considerable interindividual variability (IIV) in the clearance of 6-MP active metabolites [6-thioguanine nucleotides (6-TGNs) and 6-methylmercaptopurine nucleotides (6-mMPNs)].
  • Body surface area explained a significant part of 6-TGNs clearance IIV when incorporated in the model (IIV reduced from 69.9 to 29.3%).
  • The other genetic covariates tested were not statistically significant and therefore were not included in the final model.
  • CONCLUSIONS: The developed pharmacokinetic model (if successful at external validation) would offer a more rational dosing approach for 6-MP than the traditional empirical method since it combines the current practice of using body surface area in 6-MP dosing with a pharmacogenetically guided dosing based on TPMT genotype.
  • [MeSH-major] 6-Mercaptopurine / analogs & derivatives. Antimetabolites, Antineoplastic / pharmacokinetics. Antineoplastic Combined Chemotherapy Protocols / pharmacokinetics. Methyltransferases / pharmacokinetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Genotype. Humans. Male. Metabolic Clearance Rate / genetics. Models, Biological. Pharmacogenetics. Prospective Studies

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. MERCAPTOPURINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Natl Cancer Inst. 1999 Dec 1;91(23):1983-5 [10580012.001]
  • [Cites] Clin Oncol (R Coll Radiol). 2007 Feb;19(1):23-37 [17305252.001]
  • [Cites] J Pharmacokinet Biopharm. 1981 Aug;9(4):503-12 [7310648.001]
  • [Cites] N Engl J Med. 1983 Apr 28;308(17):1005-9 [6572786.001]
  • [Cites] Clin Pharmacol Ther. 1986 Sep;40(3):287-92 [3461899.001]
  • [Cites] Biochem Pharmacol. 1986 Oct 15;35(20):3533-41 [3533081.001]
  • [Cites] Science. 1989 Apr 7;244(4900):41-7 [2649979.001]
  • [Cites] Clin Pharmacokinet. 1989 Jun;16(6):327-36 [2661101.001]
  • [Cites] J Clin Oncol. 1989 Dec;7(12):1816-23 [2585022.001]
  • [Cites] J Pediatr. 1991 Dec;119(6):985-9 [1960624.001]
  • [Cites] Nutrition. 1989 Sep-Oct;5(5):303-11; discussion 312-3 [2520314.001]
  • [Cites] Br J Cancer Suppl. 1992 Aug;18:S23-9 [1503923.001]
  • [Cites] Eur J Clin Pharmacol. 1992;43(4):329-39 [1451710.001]
  • [Cites] Cancer Chemother Pharmacol. 1993;32(6):411-8 [8258188.001]
  • [Cites] Clin Pharmacokinet. 1996 May;30(5):329-32 [8743333.001]
  • [Cites] Eur J Pharm Sci. 1999 Aug;8(4):329-34 [10425383.001]
  • [Cites] Cancer Res. 1958 Aug;18(7):853-6 [13573353.001]
  • [Cites] Med Sci Monit. 2004 Nov;10(11):RA247-54 [15507865.001]
  • [Cites] Oncogene. 2006 Mar 13;25(11):1629-38 [16550163.001]
  • [Cites] Aliment Pharmacol Ther. 2006 Sep 1;24(5):715-29 [16918876.001]
  • [Cites] Pediatr Int. 2001 Dec;43(6):673-7 [11737747.001]
  • (PMID = 18823306.001).
  • [ISSN] 1365-2125
  • [Journal-full-title] British journal of clinical pharmacology
  • [ISO-abbreviation] Br J Clin Pharmacol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 6V404DV25O / 6-methylthiopurine; E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.- / Methyltransferases; EC 2.1.1.67 / thiopurine methyltransferase
  • [Other-IDs] NLM/ PMC2675766
  •  go-up   go-down


10. Rubnitz JE, Inaba H, Dahl G, Ribeiro RC, Bowman WP, Taub J, Pounds S, Razzouk BI, Lacayo NJ, Cao X, Meshinchi S, Degar B, Airewele G, Raimondi SC, Onciu M, Coustan-Smith E, Downing JR, Leung W, Pui CH, Campana D: Minimal residual disease-directed therapy for childhood acute myeloid leukaemia: results of the AML02 multicentre trial. Lancet Oncol; 2010 Jun;11(6):543-52
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] Minimal residual disease-directed therapy for childhood acute myeloid leukaemia: results of the AML02 multicentre trial.
  • BACKGROUND: We sought to improve outcome in patients with childhood acute myeloid leukaemia (AML) by applying risk-directed therapy that was based on genetic abnormalities of the leukaemic cells and measurements of minimal residual disease (MRD) done by flow cytometry during treatment.
  • METHODS: From Oct 13, 2002, to June 19, 2008, 232 patients with de-novo AML (n=206), therapy-related or myelodysplasia-related AML (n=12), or mixed-lineage leukaemia (n=14) were enrolled at eight centres.
  • The primary aim of the study was to compare the incidence of MRD positivity of the high-dose group and the low-dose group at day 22 of induction 1.
  • Induction 2 consisted of ADE with or without gemtuzumab ozogamicin (GO anti-CD33 monoclonal antibody); consolidation therapy included three additional courses of chemotherapy or haematopoietic stem-cell transplantation (HSCT).
  • Both MRD and genetic abnormalities at diagnosis were used to determine the final risk classification.
  • Low-risk patients (n=68) received five courses of chemotherapy, whereas high-risk patients (n=79), and standard-risk patients (n=69) with matched sibling donors, were eligible for HSCT (done for 48 high-risk and eight standard-risk patients).
  • All 230 randomised patients were analysed for the primary endpoint.
  • Other analyses were limited to the 216 patients with AML, excluding those with mixed-lineage leukaemia.
  • Induction failures included two deaths from toxic effects and ten cases of resistant leukaemia.
  • The introduction of high-dose versus low-dose cytarabine did not significantly lower the rate of MRD-positivity after induction 1 (34%vs 42%, p=0.17).
  • The 6-month cumulative incidence of grade 3 or higher infection was 79.3% (SE 4.0) for patients in the high-dose group and 75.5% (4.2) for the low-dose group.
  • 3-year event-free survival and overall survival were 63.0% (SE 4.1) and 71.1% (3.8), respectively.
  • 80% (155 of 193) of patients achieved MRD of less than 0.1% after induction 2, and the cumulative incidence of relapse for this group was 17% (SE 3).
  • INTERPRETATION: Our findings suggest that the use of targeted chemotherapy and HSCT, in the context of a comprehensive risk-stratification strategy based on genetic features and MRD findings, can improve outcome in patients with childhood AML.
  • FUNDING: National Institutes of Health and American Lebanese Syrian Associated Charities (ALSAC).
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Adolescent. Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Cytarabine / administration & dosage. Cytogenetic Analysis. Daunorubicin / administration & dosage. Disease-Free Survival. Etoposide / administration & dosage. Female. Flow Cytometry. Humans. Infant. Infant, Newborn. Male. Neoplasm, Residual. Remission Induction. Survival Rate. Young Adult

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • [Cites] Blood. 2001 Jan 1;97(1):56-62 [11133742.001]
  • [Cites] J Clin Oncol. 2010 Feb 20;28(6):955-9 [20085940.001]
  • [Cites] Blood. 2001 Jun 15;97(12):3727-32 [11389009.001]
  • [Cites] J Clin Oncol. 2002 May 1;20(9):2302-9 [11981001.001]
  • [Cites] Lancet. 2002 May 11;359(9318):1686-9 [12020548.001]
  • [Cites] Blood. 2003 May 1;101(9):3398-406 [12506020.001]
  • [Cites] Br J Haematol. 2003 Jun;121(6):823-38 [12786792.001]
  • [Cites] Br J Haematol. 2003 Oct;123(2):243-52 [14531905.001]
  • [Cites] Cancer. 2003 Dec 15;98(12):2715-22 [14669294.001]
  • [Cites] J Chronic Dis. 1974 Sep;27(7-8):365-75 [4612056.001]
  • [Cites] Br J Cancer. 1977 Jan;35(1):1-39 [831755.001]
  • [Cites] Biometrics. 1979 Sep;35(3):549-56 [497341.001]
  • [Cites] Blood. 1996 Mar 1;87(5):1710-7 [8634416.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4979-89 [8652810.001]
  • [Cites] Blood. 1996 Oct 15;88(8):2841-51 [8874180.001]
  • [Cites] Br J Haematol. 1998 Apr;101(1):130-40 [9576193.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2090-100 [16304571.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2130-8 [16304572.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1315-24 [16254147.001]
  • [Cites] Cancer. 2006 Jun 1;106(11):2495-502 [16639734.001]
  • [Cites] Blood. 2006 Jul 1;108(1):74-80 [16537811.001]
  • [Cites] Cancer. 2006 Jul 1;107(1):116-24 [16721819.001]
  • [Cites] J Clin Oncol. 2006 Aug 1;24(22):3686-92 [16877738.001]
  • [Cites] J Clin Oncol. 2006 Sep 20;24(27):4499-506 [16983120.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]
  • [Cites] Cancer. 2008 Jul 15;113(2):376-82 [18459178.001]
  • [Cites] J Clin Oncol. 2008 Oct 20;26(30):4944-51 [18606980.001]
  • [Cites] Blood. 2009 May 21;113(21):5083-9 [19131545.001]
  • [Cites] N Engl J Med. 2009 Jun 25;360(26):2730-41 [19553647.001]
  • [Cites] Blood. 2009 Jul 30;114(5):937-51 [19357394.001]
  • [Cites] Leukemia. 2009 Aug;23(8):1410-6 [19242495.001]
  • [Cites] J Clin Oncol. 2009 Aug 20;27(24):4007-13 [19620491.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2009;:385-95 [20008224.001]
  • [CommentIn] Lancet Oncol. 2010 Jun;11(6):502-3 [20522371.001]
  • (PMID = 20451454.001).
  • [ISSN] 1474-5488
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00136084
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01 CA115422; United States / NCI NIH HHS / CA / R01 CA115422-02
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 93NS566KF7 / gemtuzumab; ZS7284E0ZP / Daunorubicin; DAV regimen
  • [Other-IDs] NLM/ NIHMS319127; NLM/ PMC3171799
  •  go-up   go-down






Advertisement