[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 30 of about 30
1. Mossallam GI, Abdel Hamid TM, Samra MA: Glutathione S-transferase GSTM1 and GSTT1 polymorphisms in adult acute myeloid leukemia; its impact on toxicity and response to chemotherapy. J Egypt Natl Canc Inst; 2006 Sep;18(3):264-73
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glutathione S-transferase GSTM1 and GSTT1 polymorphisms in adult acute myeloid leukemia; its impact on toxicity and response to chemotherapy.
  • BACKGROUND AND PURPOSE: Heterogeneity in patient' s response to chemotherapy is consistently observed across populations.
  • Pharmacogenomics, the study of inherited differences in drug disposition and effects, is emerging as a tool to predict efficacy and toxicity of drugs.
  • It has been associated with altered response and toxicity from cytotoxic chemotherapy.
  • In this study, we investigated the impact of these polymorphisms on response and side effects of chemotherapy in adult acute myeloid leukaemia (AML) patients.
  • Induction therapy included Doxorubicin and Cytosine arabinoside (3+7) regimen.
  • Treatment outcomes were compared in those with or without GSTM1 and GSTT1 genes.
  • On the other hand, the rate of complete remission (CR) in patients with GSTM1 present compared to those with GSTM1 null genotype was 12/27 (48%) versus 23/36 (64%), p=0.21.
  • GSTT1 null genotype was significantly associated with lymphoid marker (mainly CD7) expression (p=0.03), known with its adverse effect on prognosis.
  • No significant associations were encountered between GST genotypes and treatment outcomes.
  • Studies on larger numbers are needed focusing on selection of anticancer agents to avoid adverse reactions and therapeutic failure, with special emphasis on drug toxicity and dose adjustment.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Glutathione Transferase / genetics. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / mortality. Polymorphism, Genetic
  • [MeSH-minor] Acute Disease. Adult. Aged. Female. Humans. Male. Middle Aged. Treatment Failure. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17671537.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase
  •  go-up   go-down


2. Coustan-Smith E, Mullighan CG, Onciu M, Behm FG, Raimondi SC, Pei D, Cheng C, Su X, Rubnitz JE, Basso G, Biondi A, Pui CH, Downing JR, Campana D: Early T-cell precursor leukaemia: a subtype of very high-risk acute lymphoblastic leukaemia. Lancet Oncol; 2009 Feb;10(2):147-56
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Early T-cell precursor leukaemia: a subtype of very high-risk acute lymphoblastic leukaemia.
  • BACKGROUND: About a fifth of children with acute T-lymphoblastic leukaemia (T-ALL) succumb to the disease, suggesting an unrecognised biological heterogeneity that might contribute to drug resistance.
  • We postulated that T-ALL originating from early T-cell precursors (ETPs), a recently defined subset of thymocytes that retain stem-cell-like features, would respond poorly to lymphoid-cell-directed therapy.
  • We studied leukaemic cells, collected at diagnosis, to identify cases with ETP features and determine their clinical outcome.
  • METHODS: Leukaemic cells from 239 patients with T-ALL enrolled at St Jude Children's Research Hospital (n=139) and in the Italian national study Associazione Italiana Ematologia Oncologia Pediatrica (AIEOP) ALL-2000 (n=100) were assessed by gene-expression profiling, flow cytometry, and single nucleotide polymorphism array analysis.
  • Probabilities of survival and treatment failure were calculated for subgroups considered to have ETP-ALL or typical T-ALL.
  • Patients with this form of leukaemia had high risk of remission failure or haematological relapse (72% [95% CI 40-100] at 10 years vs 10% [4-16] at 10 years for patients with typical T-ALL treated at St Jude Children's Research Hospital; and 57% [25-89] at 2 years vs 14% [6-22] at 2 years for patients treated in the AIEOP trial).
  • INTERPRETATION: ETP-ALL is a distinct, previously unrecognised, pathobiological entity that confers a poor prognosis with use of standard intensive chemotherapy.

  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2005 Mar 1;105(5):1930-6 [15522952.001]
  • [Cites] Lancet. 1998 Nov 28;352(9142):1731-8 [9848348.001]
  • [Cites] J Clin Oncol. 2005 Nov 1;23(31):7936-41 [16258093.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] Blood. 2006 Apr 15;107(8):3131-7 [16384926.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1151-7 [16614245.001]
  • [Cites] J Clin Oncol. 2006 Oct 10;24(29):4714-20 [16954520.001]
  • [Cites] J Clin Oncol. 2006 Dec 20;24(36):5742-9 [17179108.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] J Immunol. 2007 Jul 1;179(1):421-38 [17579063.001]
  • [Cites] Nature. 2007 Jun 21;447(7147):966-71 [17515920.001]
  • [Cites] Nat Rev Immunol. 2008 Jan;8(1):9-21 [18097446.001]
  • [Cites] Nature. 2008 Apr 10;452(7188):764-7 [18401411.001]
  • [Cites] Nature. 2008 Apr 10;452(7188):768-72 [18401412.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] Leukemia. 1999 Nov;13(11):1696-707 [10557041.001]
  • [Cites] J Immunol Methods. 2000 Sep 21;243(1-2):59-75 [10986407.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2691-6 [11023499.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6567-72 [12011421.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] J Clin Oncol. 2003 Oct 1;21(19):3616-22 [14512392.001]
  • [Cites] Blood. 2004 Jan 15;103(2):442-50 [14504110.001]
  • [Cites] Lancet. 2004 Feb 14;363(9408):535-6 [14975618.001]
  • [Cites] Nat Immunol. 2004 Mar;5(3):247-53 [14985712.001]
  • [Cites] Blood. 2004 Jul 15;104(2):558-60 [15044257.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2690-6 [15251979.001]
  • [Cites] Blood. 1989 Apr;73(5):1247-58 [2467704.001]
  • [Cites] Blood. 1990 Jan 1;75(1):166-73 [1688495.001]
  • [Cites] Leukemia. 1993 Jan;7(1):35-40 [8418377.001]
  • [Cites] Blood. 1993 Aug 1;82(3):889-94 [7687897.001]
  • [Cites] Cancer. 1995 Apr 1;75(7):1684-93 [8826928.001]
  • [Cites] J Clin Oncol. 1997 Jun;15(6):2214-21 [9196133.001]
  • [Cites] Lancet. 1998 Feb 21;351(9102):550-4 [9492773.001]
  • [Cites] Blood. 1998 Jul 15;92(2):596-9 [9657760.001]
  • [CommentIn] Lancet Oncol. 2009 Feb;10(2):105-6 [19185830.001]
  • (PMID = 19147408.001).
  • [ISSN] 1474-5488
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA060419-12; United States / NCI NIH HHS / CA / R01 CA060419-12; United States / NCI NIH HHS / CA / CA060419-10; United States / NCI NIH HHS / CA / R01 CA060419-13; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / R01 CA060419; United States / NCI NIH HHS / CA / CA60419; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA060419-11; United States / NCI NIH HHS / CA / R01 CA060419-10; None / None / / R01 CA060419-13; United States / NCI NIH HHS / CA / R01 CA060419-11; United States / NCI NIH HHS / CA / U01 CA060419
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS118479; NLM/ PMC2840241
  •  go-up   go-down


3. Apfelbeck U, Hoefler G, Neumeister P, Fonatsch C, Linkesch W, Sill H: Extramedullary T cell lymphoblastic transformation of chronic myeloid leukaemia successfully treated with matched unrelated donor bone marrow transplantation. Bone Marrow Transplant; 2000 Nov;26(10):1111-2
MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extramedullary T cell lymphoblastic transformation of chronic myeloid leukaemia successfully treated with matched unrelated donor bone marrow transplantation.
  • Chronic myeloid leukaemia (CML) inevitably terminates in blast crisis (BC) which is of myeloid phenotype in approximately two-thirds and B-lymphoid in one-third of patients.
  • After treatment with combination chemotherapy she achieved a second chronic phase and underwent an allogeneic BMT from an HLA-matched unrelated donor.
  • At 30 months follow-up she is still in complete molecular remission and in good clinical condition.
  • We conclude that unrelated donor BMT should be considered as a therapeutic option for patients with extramedullary BC.
  • [MeSH-major] Blast Crisis / therapy. Bone Marrow Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. T-Lymphocytes / pathology

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11108312.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] ENGLAND
  •  go-up   go-down


Advertisement
4. Idris M, Farid J, Sarwar J, Ahmed S, Wiqar MA, Badsha S: Response rate of Pakistani children with acute lymphoblastic leukaemia to Medical Research Council acute lymphoblastic leukaemia 97 chemotherapy protocol. J Ayub Med Coll Abbottabad; 2010 Jul-Sep;22(3):8-11
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Response rate of Pakistani children with acute lymphoblastic leukaemia to Medical Research Council acute lymphoblastic leukaemia 97 chemotherapy protocol.
  • BACKGROUND: Acute lymphoblastic leukaemia (ALL), a malignancy of lymphoid lineage cells, has excellent prognosis in children.
  • In Pakistan, a few studies highlighted the response of ALL to chemotherapy.
  • The Present study was planned to see the response rate of Pakistani children with ALL to Medical Research Council ALL 97 (MRCALL97) chemotherapy protocol.
  • Presenting clinical features, blood counts and blood and bone marrow blasts percentage were used to see the response on day 29 post chemotherapy.
  • At the end of induction, complete remission was achieved in 31 out of 33 (94%) patients while two patients did not achieve remission.
  • CONCLUSION: Response rate of Pakistani children with ALL to chemotherapy was superior to the previously reported figures from Pakistan.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Protocols. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Child. Child, Preschool. Female. Humans. Infant. Male. Pakistan / epidemiology. Prognosis. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 22338406.001).
  • [ISSN] 1025-9589
  • [Journal-full-title] Journal of Ayub Medical College, Abbottabad : JAMC
  • [ISO-abbreviation] J Ayub Med Coll Abbottabad
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
  •  go-up   go-down


5. Rubio MT, Dhedin N, Boucheix C, Bourhis JH, Reman O, Boiron JM, Gallo JH, Lhéritier V, Thomas X, Fière D, Vernant JP: Adult T-biphenotypic acute leukaemia: clinical and biological features and outcome. Br J Haematol; 2003 Dec;123(5):842-9
Hazardous Substances Data Bank. VINCRISTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-biphenotypic acute leukaemia: clinical and biological features and outcome.
  • Biphenotypic acute leukaemia with T-lymphoid and myeloid markers is rare and poorly documented.
  • In the Leucemie Aigue Lymphoblastique de l'Adulte (LALA) prospective trial (LALA 94) of treatment for adult acute lymphoblastic leukaemia (ALL), seven patients (0.86%) had T-biphenotypic forms.
  • At diagnosis, all had a tumoural syndrome and five had a mediastinal mass.
  • In all the cases, leukaemic cells expressed myeloid and lymphoid markers.
  • Two patients (28%) entered complete remission (CR) after induction chemotherapy.
  • Four of the five remaining and assessable patients entered CR after designed salvage chemotherapy with mitoxantrone and high-dose cytosine arabinoside.
  • Three patients died, from treatment toxicity in two cases and progressive disease in one case.
  • Thus, biphenotypic T-acute leukaemia is clinically frequently associated with mediastinal involvement and the response to conventional chemotherapy used in ALL is poor.
  • However, sustained CR can be achieved by salvage chemotherapy combining an intercalating agent with high-dose cytosine arabinoside, as used in acute myeloid leukaemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / immunology. Leukemia, T-Cell / immunology
  • [MeSH-minor] Acute Disease. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers / analysis. Cyclophosphamide / administration & dosage. Cytogenetic Analysis. Daunorubicin / administration & dosage. Humans. Idarubicin / administration & dosage. Immunophenotyping. Male. Prednisone / administration & dosage. Retrospective Studies. Treatment Outcome. Vincristine / administration & dosage

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Br J Haematol. 2004 Apr;125(1):94 [15015979.001]
  • [CommentIn] Br J Haematol. 2004 Jun;125(6):814-5 [15180872.001]
  • (PMID = 14632775.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; ZRP63D75JW / Idarubicin; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


6. Telek B, Rejtó L, Kiss A, Batár P, Reményi G, Rák K, Udvardy M: [Experience with fludarabine treatment and review of the literature]. Orv Hetil; 2002 Jun 16;143(24):1459-65
Hazardous Substances Data Bank. NOVANTRONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Experience with fludarabine treatment and review of the literature].
  • Fludarabine inhibits DNA synthesis, acts on non-dividing (G0 phase) cells influencing apoptosis.
  • PATIENTS, RESULTS, CONCLUSIONS: In our institute 47 patients were treated with fludarabine or fludarabine based combination chemotherapy.
  • Fludarabine was given in 19 patients with chronic lymphocytic leukaemia (CLL), complete remission (CR) was achieved in one case, partial remission (PR) was obtained in 10 patients.
  • Fludarabine was more effective in patients who received less intensive chemotherapy prior to fludarabine therapy and in those patients who had less advanced diseases.
  • Elderly patients (over sixty years of age) also responded to fludarabine therapy.
  • Fludarabine and cyclophosphamide combination (FCy) were used in three lymphocytic lymphoma patients, two of them obtained PR, in the third case the disease progressed.
  • Fludarabine + mitoxantrone (Novantrone) + dexamethasone (FND) regimen was administered in nine patients who were previously heavily treated (one patient with B-CLL, one with T-CLL, one with peripheral T-cell lymphoma and six with indolent B-cell lymphoma).
  • FLAG-IDA (fludarabine, high dose Ara-C, granulocyte colony-stimulating factor, idarubicin) was applied in 16 acute leukaemia patients with poor prognosis including therapy refractory and relapsing cases.
  • Three CR and two PR, one CR and three PR was achieved in nine patients with acute myeloid leukaemia and in seven patients with acute lymphoid leukaemia, respectively.
  • For this reason, despite the short period of remission, this regimen can be recommended to patients who are candidate for stem cell transplantation.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Vidarabine / analogs & derivatives. Vidarabine / therapeutic use
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Dexamethasone / administration & dosage. Female. Filgrastim. Granulocyte Colony-Stimulating Factor / administration & dosage. Humans. Idarubicin / administration & dosage. Immunophenotyping. Male. Middle Aged. Mitoxantrone / administration & dosage. Recombinant Proteins. Remission Induction. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. Filgrastim .
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • 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 = 12138643.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Recombinant Proteins; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 7S5I7G3JQL / Dexamethasone; 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; PVI5M0M1GW / Filgrastim; ZRP63D75JW / Idarubicin; Ida-FLAG protocol
  • [Number-of-references] 43
  •  go-up   go-down


7. Kolb HJ, Simoes B, Schmid C: Stem cell transplants for patients with relapsed/refractory leukaemia. Curr Opin Hematol; 2009 Nov;16(6):444-52
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stem cell transplants for patients with relapsed/refractory leukaemia.
  • PURPOSE OF REVIEW: Today the indication for allogeneic stem cell transplantation for a high-risk leukaemia in first remission is well defined by most centres.
  • In patients with primary refractory leukaemia the indication is controversially discussed.
  • Similarly patients with relapse and advanced disease have a poor prognosis with chemotherapy, but also with transplantation.
  • RECENT FINDINGS: The role of alloimmunity in the control of leukaemia has been defined and pretransplant conditioning treatment could be reduced to less intensive protocols.
  • Graft-versus-leukaemia reactions have been demonstrated with the transfusion of donor lymphocytes.
  • Using nonmyeloablative regimens allogeneic stem cell transplantation could be offered to elderly patients, the majority of patients with acute myeloid leukaemia and myelodysplastic syndromes.
  • The use of antibodies and radio-immuno-therapy has improved the treatment of lymphoid malignancies.
  • The combination of molecular monitoring, targeted therapy and transplantation as a form of immunotherapy may improve the results of leukaemia treatment further.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Stem Cell Transplantation
  • [MeSH-minor] Graft vs Host Disease / therapy. Humans. Recurrence

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19652599.001).
  • [ISSN] 1531-7048
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 94
  •  go-up   go-down


8. Telek B, Rejto L, Kiss A, Méhes L, Batár P, Udvardy M: [New perspectives in the evolution of prognosis and treatment of chronic lymphocytic leukaemia]. Orv Hetil; 2004 Aug 29;145(35):1795-800
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [New perspectives in the evolution of prognosis and treatment of chronic lymphocytic leukaemia].
  • [Transliterated title] Uj perspektívák a krónikus lymphoid leukaemia prognózisának megállapításában és kezelésében.
  • Chronic lymphocytic leukaemia is a disease with a variable clinical course and prognosis.
  • Purin analogues, fludarabine and fludarabine based combinations can achieve complete hematological remission in approximately one third of patients with chronic lymphocytic leukaemia.
  • Chemoimmunotherapy (most experience is obtained by combination of fludarabine + cyclophosphamide + rituximab) can increase not only complete remission rate, but also induce molecular remission in some cases.
  • Stem cell transplantation as well as early and effective chemotherapy are curative choices of treatment in patients with chronic lymphocytic leukaemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Mutation. Vidarabine / analogs & derivatives
  • [MeSH-minor] ADP-ribosyl Cyclase / analysis. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Antigens, CD / analysis. Antigens, CD38. Cyclophosphamide / administration & dosage. Humans. Immunotherapy / methods. Membrane Glycoproteins. Predictive Value of Tests. Prognosis. Protein-Tyrosine Kinases / analysis. Recurrence. Remission Induction. Rituximab. Stem Cell Transplantation. ZAP-70 Protein-Tyrosine Kinase

  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15493222.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / Membrane Glycoproteins; 4F4X42SYQ6 / Rituximab; 8N3DW7272P / Cyclophosphamide; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human; EC 3.2.2.5 / ADP-ribosyl Cyclase; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  • [Number-of-references] 45
  •  go-up   go-down


9. Piccaluga PP, Martinelli G, Rondoni M, Visani G, Baccarani M: Advances and potential treatment for Philadelphia chromosome-positive adult acute lymphoid leukaemia. Expert Opin Biol Ther; 2006 Oct;6(10):1011-22
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Advances and potential treatment for Philadelphia chromosome-positive adult acute lymphoid leukaemia.
  • Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukaemia (ALL) is the most common subtype of ALL in adults.
  • Conventional chemotherapy-based approaches that are effective in other precursor B cell ALL cases have a poor chances of cure in patients with a Ph+ diagnosis.
  • Therefore, allogeneic stem cell transplantation performed during the first remission is the recommended therapy.
  • Recently, the availability of imatinib mesylate and other tyrosine kinase inhibitors and small molecules that affect the BCR/ABL signalling pathways has introduced a new therapeutic opportunity, and could change the treatment paradigm and prognosis for these patients.
  • In this article, the results from clinical trials using imatinib in relapsed/refractory patients and as front-line therapy are described.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Philadelphia Chromosome
  • [MeSH-minor] Adult. Animals. Humans. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Randomized Controlled Trials as Topic / trends. Stem Cell Transplantation / methods. Stem Cell Transplantation / trends

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16989583.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 61
  •  go-up   go-down


10. Russell NH, Byrne JL, Faulkner RD, Gilyead M, Das-Gupta EP, Haynes AP: Donor lymphocyte infusions can result in sustained remissions in patients with residual or relapsed lymphoid malignancy following allogeneic haemopoietic stem cell transplantation. Bone Marrow Transplant; 2005 Sep;36(5):437-41
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Donor lymphocyte infusions can result in sustained remissions in patients with residual or relapsed lymphoid malignancy following allogeneic haemopoietic stem cell transplantation.
  • We treated 17 patients with refractory (n = 7) or relapsed lymphoid malignancy (n = 10) following allogeneic HSCT with donor lymphocyte infusions (DLI).
  • Patients with aggressive disease (n = 9) received prior chemotherapy.
  • In all, 10/17 patients achieved CR including 3/4 patients with chronic lymphatic leukaemia (CLL), 4/4 with mantle cell lymphoma (MCL), 3/4 with follicular NHL but 0/5 with aggressive NHL/Richters.
  • Grade II-IV acute GVHD developed in 45% and chronic GVHD in 8/9 evaluable patients.
  • Of the 11 patients finally achieving CR, one patient with MCL relapsed at 18 months post-DLI but all others remain in remission with a median follow-up of 40 months (range 12-64 months).
  • Aggressive disease responds poorly however, despite pre-DLI chemotherapy.
  • [MeSH-major] Graft vs Host Disease / therapy. Hematopoietic Stem Cell Transplantation. Living Donors. Lymphocyte Transfusion. Lymphoproliferative Disorders / therapy. T-Lymphocytes / transplantation
  • [MeSH-minor] Adult. Female. Humans. Male. Middle Aged. Neoplasm, Residual. Radiotherapy. Recurrence. Remission Induction. Retrospective Studies. Transplantation, Homologous

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Organ Donation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15980879.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


11. Anderson SC, Baquis GD, Jackson A, Monteleone P, Kirkwood JR: Ventral polyradiculopathy with pediatric acute lymphocytic leukemia. Muscle Nerve; 2002 Jan;25(1):106-10
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ventral polyradiculopathy with pediatric acute lymphocytic leukemia.
  • A 3-year-old girl with acute lymphocytic leukemia (ALL) in remission developed lower extremity paraparesis and areflexia 15 days after receiving intrathecal methotrexate, cytarabine, and hydrocortisone.
  • Nerve conduction and EMG abnormalities correlated with MRI root enhancement, facilitated early diagnosis, and distinguished this from a myelopathy or distal polyneuropathy.
  • These findings could represent selective ventral nerve root vulnerability to intrathecal chemotherapy.
  • [MeSH-major] Anti-Inflammatory Agents / administration & dosage. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Cytarabine / administration & dosage. Hydrocortisone / administration & dosage. Methotrexate / administration & dosage. Polyradiculopathy / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2002 John Wiley & Sons, Inc.
  • (PMID = 11754193.001).
  • [ISSN] 0148-639X
  • [Journal-full-title] Muscle & nerve
  • [ISO-abbreviation] Muscle Nerve
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; WI4X0X7BPJ / Hydrocortisone; YL5FZ2Y5U1 / Methotrexate
  •  go-up   go-down


12. Lillington DM, Jaju RJ, Shankar AG, Neat M, Kearney L, Young BD, Saha V: Cytogenetic and molecular evidence of marrow involvement in extramedullary acute myeloid leukaemia. Br J Haematol; 2000 Sep;110(3):547-51
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic and molecular evidence of marrow involvement in extramedullary acute myeloid leukaemia.
  • A diagnosis of granulocytic sarcoma was made in a 2-year-old child based on the detection of myelomonocytic blasts in tissue obtained from a subcutaneous nodule with no evidence of concomitant disease in the bone marrow.
  • The child responded to systemic chemotherapy and is in remission 3 years later.
  • An identical clone with an in frame fusion of the MLL and AF10 genes was identified from both tissue and bone marrow samples.
  • This case illustrates the presence of systemic disease in extramedullary leukaemia, its response to systemic rather than topical therapy and suggests that the events leading to chromosomal translocations in leukaemia may be part of a generalized intracellular event.
  • [MeSH-major] Bone Marrow Cells. Chromosomes, Human, Pair 5. Gene Rearrangement. Leukemia, Myeloid / genetics. Proto-Oncogenes
  • [MeSH-minor] Acute Disease. Artificial Gene Fusion. DNA-Binding Proteins / genetics. Electrophoresis, Agar Gel. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Infant. Karyotyping. Myeloid-Lymphoid Leukemia Protein. Reverse Transcriptase Polymerase Chain Reaction. Transcription Factors / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10997963.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / MLLT10 protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down


13. Isoyama K, Eguchi M, Hibi S, Kinukawa N, Ohkawa H, Kawasaki H, Kosaka Y, Oda T, Oda M, Okamura T, Nishimura S, Hayashi Y, Mori T, Imaizumi M, Mizutani S, Tsukimoto I, Kamada N, Ishii E: Risk-directed treatment of infant acute lymphoblastic leukaemia based on early assessment of MLL gene status: results of the Japan Infant Leukaemia Study (MLL96). Br J Haematol; 2002 Sep;118(4):999-1010

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk-directed treatment of infant acute lymphoblastic leukaemia based on early assessment of MLL gene status: results of the Japan Infant Leukaemia Study (MLL96).
  • We studied the effectiveness of risk-directed therapy for infants younger than 13 months of age with acute lymphoblastic leukaemia (ALL).
  • Fifty-five infants were assigned to different treatment programs (from December 1995 to December 1998) on the basis of their MLL gene status at diagnosis.
  • Forty-two cases (76.3%) had a rearranged MLL gene (MLL+) and were treated with remission induction therapy followed by sequential intensive chemotherapy, including multiple genotoxic agents (MLL9601 protocol).
  • Thirteen infants (23.7%) were classified as MLL- and treated for 2.5 years with intensive chemotherapy for high-risk B-ALL (MLL9602 protocol).
  • Complete remission was induced in 38 of the 42 infants (90.5%) with MLL+ ALL and in all 13 patients (100%) with MLL- disease.
  • In the MLL+ subgroup, the estimated event-free survival (EFS) rate at 3 years post diagnosis was 34.0% +/- 7.5%, compared with 92.3% +/- 7.4% in the MLL- subgroup (overall comparison, P = 0.001 by log-rank analysis).
  • Both age less than 6 months (hazard ratio = 6.87, 95% CI = 0.91-52.3; P = 0.013) and central nervous system (CNS) involvement at diagnosis (hazard ratio = 2.92 95% CI = 1.29-6.63; P = 0.015) were significant independent predictors of an inferior outcome.
  • These findings indicate a strategic advantage in classifying infant ALL as either MLL+ or MLL- early in the clinical course and selecting therapy accordingly.
  • Standard chemotherapy for high-risk B-lineage ALL appeared adequate for MLL- cases.
  • Novel therapeutic initiatives are warranted for infants with MLL+ disease, particularly those with initial CNS leukaemic involvement or age less than 6 months, or both.
  • [MeSH-major] DNA-Binding Proteins / genetics. Gene Rearrangement. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Proto-Oncogenes. Transcription Factors
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytogenetic Analysis. Disease-Free Survival. Follow-Up Studies. Histone-Lysine N-Methyltransferase. Humans. Immunosuppressive Agents / therapeutic use. In Situ Hybridization, Fluorescence. Infant. Infant, Newborn. Japan. Myeloid-Lymphoid Leukemia Protein. Patient Selection. Remission Induction. Risk Assessment. Stem Cell Transplantation

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12199778.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Immunosuppressive Agents; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down


14. Gorelik O, Cohen N, Shpirer I, Almoznino-Sarafian D, Alon I, Koopfer M, Yona R, Modai D: Fatal haemoptysis induced by invasive pulmonary aspergillosis in patients with acute leukaemia during bone marrow and clinical remission: report of two cases and review of the literature. J Infect; 2000 Nov;41(3):277-82
MedlinePlus Health Information. consumer health - Aspergillosis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fatal haemoptysis induced by invasive pulmonary aspergillosis in patients with acute leukaemia during bone marrow and clinical remission: report of two cases and review of the literature.
  • We describe two patients with acute leukaemia who died of massive haemoptysis caused by invasive pulmonary aspergillosis (IPA).
  • The fatal event occurred during the period of bone marrow remission which followed chemotherapy-induced neutropenia.
  • In conclusion, patients with acute non-lymphoid leukaemia are at significant risk for IPA-induced fatal haemoptysis during bone marrow and clinical remission.
  • In view of the potential fatal outcome, aggressive diagnostic and treatment efforts are mandatory.
  • [MeSH-major] Aspergillosis / complications. Hemoptysis / etiology. Leukemia, Myeloid / drug therapy. Lung Diseases, Fungal / complications
  • [MeSH-minor] Acute Disease. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Fatal Outcome. Female. Humans. Middle Aged. Remission Induction

  • Genetic Alliance. consumer health - Aspergillosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2000 The British Infection Society.
  • (PMID = 11120621.001).
  • [ISSN] 0163-4453
  • [Journal-full-title] The Journal of infection
  • [ISO-abbreviation] J. Infect.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] ENGLAND
  • [Number-of-references] 31
  •  go-up   go-down


15. Apostolidou E, Swords R, Alvarado Y, Giles FJ: Treatment of acute lymphoblastic leukaemia : a new era. Drugs; 2007;67(15):2153-71
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of acute lymphoblastic leukaemia : a new era.
  • Acute lymphocytic leukaemia (ALL) is a heterogeneous group of disorders that result from the clonal proliferation and expansion of malignant lymphoid cells in the bone marrow, blood and other organs.
  • Distinct clinicopathological ALL entities have been identified, resulting in the adoption of risk-oriented treatment approaches.
  • Advances in ALL therapy have led to long-term survival rates of >80% in children.
  • Contemporary ALL treatment programmes include induction, intensified consolidation, maintenance phases and CNS prophylaxis.
  • The optimal treatment of Philadelphia chromosome-positive patients requires the addition of BCR-ABL tyrosine kinase inhibitors, such as imatinib, whereas allogeneic stem-cell transplantation remains the preferred approach for high-risk patients in first remission.
  • Since only approximate, approximately 38% of adult ALL patients are free of disease 5 years after diagnosis and the outcome of salvage chemotherapy is very poor (complete remission rates of 20-30%, median survival of 3-6 months), novel agents are desperately required.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Acute Disease. Animals. Chemistry, Pharmaceutical. Folic Acid Antagonists / therapeutic use. Humans. Microtubules / drug effects. Nucleosides / therapeutic use. Oncogene Proteins v-abl / antagonists & inhibitors. Proto-Oncogene Proteins c-bcr / antagonists & inhibitors

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • 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] Cancer Chemother Pharmacol. 2000;46(5):427-32 [11127949.001]
  • [Cites] Leuk Lymphoma. 2000 Jan;36(3-4):263-73 [10674898.001]
  • [Cites] Semin Oncol. 2005 Apr;32(2 Suppl 2):S5-8 [15818537.001]
  • [Cites] Br J Cancer. 2006 Jun 19;94(12):1765-9 [16721371.001]
  • [Cites] Cancer Chemother Pharmacol. 1997;39(6):521-31 [9118464.001]
  • [Cites] J Clin Oncol. 2003 Mar 15;21(6):1167-73 [12637486.001]
  • [Cites] Clin Cancer Res. 2006 Feb 1;12(3 Pt 1):832-8 [16467096.001]
  • [Cites] Am J Pediatr Hematol Oncol. 1986 Summer;8(2):99-104 [3526939.001]
  • [Cites] Leuk Lymphoma. 1993;10 Suppl:147-50 [8481663.001]
  • [Cites] Mol Cancer Ther. 2006 Oct;5(10):2549-55 [17041099.001]
  • [Cites] Blood. 1991 Dec 1;78(11):2814-22 [1835410.001]
  • [Cites] Blood. 2007 Apr 1;109 (7):2744-50 [17132721.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2379-86 [12791647.001]
  • [Cites] Clin Cancer Res. 2005 Sep 15;11(18):6615-24 [16166440.001]
  • [Cites] Ann Oncol. 2000 Jan;11(1):69-72 [10690390.001]
  • [Cites] Br J Cancer. 2004 Apr 5;90(7):1464-8 [15054472.001]
  • [Cites] Curr Med Chem. 1999 Apr;6(4):329-52 [10101216.001]
  • [Cites] Blood. 1995 Apr 15;85(8):2025-37 [7718875.001]
  • [Cites] Cancer Chemother Pharmacol. 1998;42(2):127-34 [9654112.001]
  • [Cites] Curr Opin Investig Drugs. 2005 Jun;6(6):623-30 [15988914.001]
  • [Cites] J Natl Cancer Inst. 1990 Oct 17;82(20):1641-2 [2145440.001]
  • [Cites] Clin Transl Oncol. 2006 Aug;8(8):560-5 [16952844.001]
  • [Cites] Anticancer Drugs. 1993 Feb;4(1):37-48 [8457713.001]
  • [Cites] Rev Pneumol Clin. 2005 Sep;61(4 Pt 2):4S5-7 [16273001.001]
  • [Cites] Pharmacol Ther. 1991 Oct;52(1):35-84 [1687171.001]
  • [Cites] Lung Cancer. 2005 Sep;49(3):401-12 [15923057.001]
  • [Cites] Int J Clin Pharmacol Ther. 2005 Dec;43(12):567-9 [16372519.001]
  • [Cites] Circ Res. 1999 Aug 6;85(3):221-8 [10436164.001]
  • [Cites] Clin Cancer Res. 2004 Aug 15;10 (16):5335-41 [15328169.001]
  • [Cites] Ann Oncol. 2005 Oct;16(10):1639-45 [16087696.001]
  • [Cites] Cancer Res. 1977 Feb;37(2):535-40 [264412.001]
  • [Cites] J Med Chem. 2002 Oct 24;45(22):4913-22 [12383017.001]
  • [Cites] Cancer Res. 1999 Oct 1;59(19):4937-43 [10519407.001]
  • [Cites] Biochem Pharmacol. 2003 Apr 1;65(7):1163-70 [12663051.001]
  • [Cites] Cancer. 2004 Dec 15;101(12):2788-801 [15481055.001]
  • [Cites] J Clin Oncol. 2005 Sep 1;23(25):5929-37 [16135464.001]
  • [Cites] Cancer Res. 1983 Nov;43(11):5601-7 [6352020.001]
  • [Cites] Mol Pharmacol. 1995 Sep;48(3):459-71 [7565626.001]
  • [Cites] J Clin Oncol. 2005 May 20;23(15):3376-82 [15908649.001]
  • [Cites] Blood. 2007 May 15;109 (10 ):4164-7 [17264295.001]
  • [Cites] Nat Rev Cancer. 2004 Apr;4(4):253-65 [15057285.001]
  • [Cites] N Engl J Med. 1986 Sep 11;315(11):657-63 [2943992.001]
  • [Cites] Cancer Chemother Pharmacol. 1994;33(5):359-65 [8306408.001]
  • [Cites] Adv Drug Deliv Rev. 2003 Sep 26;55(10 ):1293-302 [14499708.001]
  • [Cites] Cell Prolif. 1992 Nov;25(6):523-36 [1457603.001]
  • [Cites] Blood. 2002 Feb 1;99(3):863-71 [11806988.001]
  • [Cites] Carbohydr Res. 1985 Feb 28;136:391-6 [4005892.001]
  • [Cites] Invest New Drugs. 1999;17(1):81-7 [10555126.001]
  • [Cites] Lancet. 1987 Apr 4;1(8536):786-9 [2882192.001]
  • [Cites] Cancer Chemother Pharmacol. 1998;42(6):461-70 [9788572.001]
  • [Cites] Leukemia. 1998 May;12(5):660-5 [9593262.001]
  • [Cites] Biochem Pharmacol. 2001 Apr 1;61(7):857-65 [11274972.001]
  • [Cites] Leukemia. 1997 Dec;11(12):2039-44 [9447817.001]
  • [Cites] Lancet Oncol. 2005 Aug;6(8):548 [16094758.001]
  • [Cites] Clin Adv Hematol Oncol. 2006 Nov;4(11):804-5 [17143248.001]
  • [Cites] Br J Cancer. 2001 Sep 1;85(5):649-55 [11531245.001]
  • [Cites] Cancer Res. 1993 Apr 1;53(7):1583-9 [8453627.001]
  • [Cites] Ann Pharmacother. 1997 May;31(5):616-24 [9161659.001]
  • [Cites] Invest New Drugs. 1986;4(1):85-105 [3516918.001]
  • [Cites] Cancer Chemother Pharmacol. 2004 Sep;54(3):273-81 [15173957.001]
  • [Cites] Blood. 2007 Jun 15;109(12):5136-42 [17344466.001]
  • [Cites] J Med Chem. 1994 Jul 8;37(14):2167-74 [8035423.001]
  • [Cites] Bioorg Med Chem Lett. 2001 Jul 9;11(13):1671-3 [11425534.001]
  • [Cites] Blood. 1997 Feb 1;89(3):1013-8 [9028333.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1328-33 [16614241.001]
  • [Cites] J Med Chem. 1993 Mar 19;36(6):758-64 [8459402.001]
  • [Cites] Anticancer Drugs. 2002 Sep;13(8):797-805 [12394263.001]
  • [Cites] Eur J Haematol. 2006 Oct;77(4):293-9 [16856922.001]
  • [Cites] Int J Cancer. 2004 Jul 10;110(5):767-74 [15146568.001]
  • [Cites] Cancer Chemother Pharmacol. 1996;37(4):351-5 [8548881.001]
  • [Cites] J Clin Oncol. 2005 Oct 1;23(28):7161-7 [16192600.001]
  • [Cites] Nat Genet. 2004 May;36(5):453-61 [15098032.001]
  • [Cites] EMBO J. 2002 Nov 1;21(21):5766-74 [12411494.001]
  • [Cites] Bone Marrow Transplant. 1998 Dec;22(12):1137-43 [9894715.001]
  • [Cites] Nature. 1998 Jan 8;391(6663):199-203 [9428769.001]
  • [Cites] Br J Cancer. 1995 Oct;72(4):896-904 [7547237.001]
  • [Cites] J Med Chem. 2001 Dec 6;44(25):4416-30 [11728187.001]
  • [Cites] Mol Pharmacol. 1995 Oct;48(4):758-65 [7476904.001]
  • [Cites] Clin Lung Cancer. 2004 Apr;5 Suppl 2:S75-9 [15117429.001]
  • [Cites] Adv Exp Med Biol. 1984;165 Pt B:309-14 [6609537.001]
  • [Cites] Cancer. 1976 Jan;37(1):220-8 [1061636.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Dec 15;90(24):11598-602 [8265596.001]
  • [Cites] Cancer. 1993 Oct 1;72(7):2155-60 [8374873.001]
  • [Cites] Leukemia. 1999 Mar;13(3):335-42 [10086723.001]
  • [Cites] Anticancer Res. 1999 Mar-Apr;19(2A):1277-83 [10368688.001]
  • [Cites] Cancer. 1999 Oct 1;86(7):1203-9 [10506705.001]
  • [Cites] Annu Rev Med. 1997;48:353-74 [9046968.001]
  • [Cites] Blood. 2007 Feb 1;109(3):944-50 [17032921.001]
  • [Cites] J Med Chem. 1998 Dec 17;41(26):5310-9 [9857098.001]
  • [Cites] Cancer Chemother Pharmacol. 2001;47(2):179-84 [11269745.001]
  • [Cites] Cancer. 2006 Jan 1;106(1):120-7 [16331634.001]
  • [Cites] Cancer Chemother Pharmacol. 2006 Apr;57(4):427-35 [16322992.001]
  • [Cites] Int J Exp Pathol. 2002 Feb;83(1):21-38 [12059907.001]
  • [Cites] Int J Cancer. 1997 Sep 4;72 (5):844-50 [9311603.001]
  • [Cites] J Clin Oncol. 1999 Feb;17(2):697-705 [10080616.001]
  • [Cites] Rev Clin Exp Hematol. 2002 Jun;6(2):114-41; discussion 200-2 [12196212.001]
  • [Cites] Anticancer Res. 1998 Mar-Apr;18(2A):727-37 [9615712.001]
  • [Cites] Adv Exp Med Biol. 1993;338:461-4 [8304158.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3658-61 [11369666.001]
  • [Cites] Cancer. 1994 May 15;73(10):2515-9 [8174048.001]
  • [Cites] Hematol Oncol Clin North Am. 2001 Feb;15(1):163-205 [11253606.001]
  • [Cites] Cancer Res. 1994 Apr 1;54(7):1702-6 [8137285.001]
  • [Cites] Cancer Res. 1994 Mar 15;54(6):1479-84 [8137251.001]
  • [Cites] Cancer. 2005 Dec 1;104(11):2449-56 [16258975.001]
  • [Cites] Leukemia. 1992;6 Suppl 2:148-52 [1578919.001]
  • [Cites] Biochemistry. 1997 Apr 15;36(15):4399-411 [9109647.001]
  • [Cites] J Med Chem. 1991 Feb;34(2):574-9 [1995880.001]
  • [Cites] J Pediatr Hematol Oncol. 2004 Apr;26(4):217-26 [15087948.001]
  • [Cites] Nat Rev Drug Discov. 2006 Jan;5(1):17-8 [16485343.001]
  • [Cites] Clin Cancer Res. 2006 Sep 15;12(18):5329-35 [17000665.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2542-51 [16775235.001]
  • [Cites] Clin Cancer Res. 2005 Feb 1;11(3):982-92 [15709163.001]
  • [Cites] J Pharmacol Exp Ther. 2001 Sep;298(3):1206-12 [11504822.001]
  • [Cites] Biochem Pharmacol. 1996 May 17;51(10):1331-40 [8787549.001]
  • [Cites] Curr Opin Oncol. 2001 Jan;13(1):14-20 [11148680.001]
  • [Cites] J Clin Oncol. 1993 Sep;11(9):1780-6 [8355045.001]
  • [Cites] Mol Cancer Ther. 2002 Feb;1(4):275-86 [12467223.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]
  • [Cites] Eur J Cancer. 1991;27(4):482-7 [1827725.001]
  • [Cites] Expert Opin Investig Drugs. 2003 May;12(5):853-63 [12720495.001]
  • [Cites] Jpn J Cancer Res. 1998 Sep;89(9):954-62 [9818032.001]
  • [Cites] Nat Rev Drug Discov. 2005 May;Suppl:S16-7 [15962527.001]
  • [Cites] Pediatr Nurs. 1995 Sep-Oct;21(5):471-4, 490 [8684851.001]
  • [Cites] Biochemistry. 1964 Jan;3:15-8 [14114497.001]
  • [Cites] Cancer Chemother Pharmacol. 2002 Jul;50(1):6-8 [12111105.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3760-7 [16105981.001]
  • [Cites] Biochem Biophys Res Commun. 1972 May 26;47(4):685-91 [5026289.001]
  • [Cites] Cancer Res. 1998 Jul 15;58(14):3036-50 [9679969.001]
  • [Cites] Cancer Res. 1976 Apr;36(4):1499-502 [1260766.001]
  • [Cites] Blood. 2002 Mar 15;99(6):1986-94 [11877270.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4341-4 [11389057.001]
  • [Cites] Hematol J. 2002;3(1):2-6 [11960387.001]
  • [Cites] Clin Cancer Res. 1996 Nov;2(11):1843-9 [9816139.001]
  • [Cites] Clin Colorectal Cancer. 2005 Nov;5(4):257-62 [16356302.001]
  • [Cites] Leuk Lymphoma. 1993;10 Suppl:153-7 [8481665.001]
  • [Cites] Blood. 2006 Apr 15;107(8):3288-94 [16368880.001]
  • [Cites] J Clin Oncol. 1988 Apr;6(4):583-7 [3282032.001]
  • [Cites] Cancer Res. 1990 Jul 15;50(14):4260-6 [2194651.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1421-3 [16601247.001]
  • [Cites] J Clin Oncol. 2003 Jul 15;21(14):2636-44 [12860938.001]
  • [Cites] Biochem Pharmacol. 1998 Apr 15;55(8):1229-34 [9719477.001]
  • (PMID = 17927282.001).
  • [ISSN] 0012-6667
  • [Journal-full-title] Drugs
  • [ISO-abbreviation] Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Folic Acid Antagonists; 0 / Nucleosides; 0 / Oncogene Proteins v-abl; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
  • [Number-of-references] 159
  •  go-up   go-down


16. Lundin J, Porwit-MacDonald A, Rossmann ED, Karlsson C, Edman P, Rezvany MR, Kimby E, Osterborg A, Mellstedt H: Cellular immune reconstitution after subcutaneous alemtuzumab (anti-CD52 monoclonal antibody, CAMPATH-1H) treatment as first-line therapy for B-cell chronic lymphocytic leukaemia. Leukemia; 2004 Mar;18(3):484-90
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cellular immune reconstitution after subcutaneous alemtuzumab (anti-CD52 monoclonal antibody, CAMPATH-1H) treatment as first-line therapy for B-cell chronic lymphocytic leukaemia.
  • Little information is available on long-term immune reconstitution after therapy with alemtuzumab in B-CLL patients.
  • We present long-term follow-up data for blood lymphocyte subsets analysed by flow cytometry in previously untreated B-CLL patients who received alemtuzumab subcutaneously as first-line therapy.
  • All lymphoid subsets were significantly (P<0.001) and profoundly reduced; the median end-of-treatment counts for CD4(+), CD8(+), CD3(-)56(+) (natural killer (NK)), CD3(+)56(+) (NK-T) and CD19(+)5(-) (normal B) cells were 43, 20, 4, 1 and 8 cells/microl, respectively.
  • The median cell count of all subsets remained at <25% of the baseline values for >9 months post-treatment.
  • CD4(+) and CD8(+) levels in blood had reached >100 cells/microl in >50% of the patients at 4 months after the end of treatment.
  • One patient had a cytomegalovirus reactivation and one patient developed Pneumocystis carinii pneumonia during therapy.
  • CD52(-) T-cell subsets occurred during the treatment and comprised >80% of all CD4(+) and CD8(+) cells in the blood at the end of therapy.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Antibodies, Neoplasm / administration & dosage. Antineoplastic Agents / administration & dosage. Killer Cells, Natural / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. T-Lymphocytes / immunology
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal, Humanized. Antigens, CD / immunology. Case-Control Studies. Follow-Up Studies. Humans. Immunity, Cellular. Immunophenotyping. Injections, Subcutaneous. Middle Aged. Remission Induction. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Leukemia. 2005 Jan;19(1):153-4 [15496971.001]
  • (PMID = 14749699.001).
  • [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 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  •  go-up   go-down


17. Stam RW, den Boer ML, Pieters R: Towards targeted therapy for infant acute lymphoblastic leukaemia. Br J Haematol; 2006 Mar;132(5):539-51
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Towards targeted therapy for infant acute lymphoblastic leukaemia.
  • Despite the greatly improved treatment regimes for childhood acute lymphoblastic leukaemia (ALL) in general, resulting in long-term survival in approximately 80% of cases, current therapies still fail in >50% of ALL cases diagnosed within the first year of life (i.e. in infants).
  • Therefore, more adequate treatment strategies are urgently needed to also improve the prognosis for these very young patients with ALL.
  • Here we review the current acquaintance with the biology of infant ALL and describe how this knowledge may lead to innovative therapeutic approaches.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Age of Onset. Forecasting. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Infant. Mutation. Myeloid-Lymphoid Leukemia Protein / genetics. Prognosis. Remission Induction. Translocation, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16445826.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 139
  •  go-up   go-down


18. Telek B, Batár P, Uvardy M: [Successful combined treatment with rituximab and high dose immunoglobulin in a patient with chronic lymphocytic leukemia with fludarabine-induced severe immune thrombocytopenia]. Orv Hetil; 2005 Aug 21;146(34):1791-3
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Successful combined treatment with rituximab and high dose immunoglobulin in a patient with chronic lymphocytic leukemia with fludarabine-induced severe immune thrombocytopenia].
  • [Transliterated title] Krónikus lymphoid leukaemia fludarabin kezeléséhez társuló súlyos immun-thrombocytopenia sikeres, rituximab es nagy adag immunglobulinnal történt kombinált kezelése.
  • Chronic lymphocytic leukemia is rarely associated with immune thrombocytopenia.
  • Although fludarabine treatment is widely used in the treatment of chronic lymphocytic leukemia, it can also increase the incidence and severity of immune thrombocytopenia.
  • The authors present a case of chronic lymphocytic leucaemia after relapse of the disease.
  • Fludarabine + cyclophosphamide treatment was administered which resulted in a nearly complete hematological remission but severe immune thrombocytopenia has occurred (platelet count < 5 x 10(9)/l).
  • Conventional steroid and immunosuppressive treatment have failed and, in addition, autoimmune hemolysis has developed after six weeks.
  • Rituximab (375 mg/m2) and high dose intavenous immunglobuline treatment was started and platelet count has increased (40 x 10(9)/l).
  • Prolonged (> 1.5 year) remission and subsided hemolysis have been observed due to the rituximab treatment.
  • Successful treatment of choice can be rituximab in those cases of chronic lymphocytic leukemia which previously have been treated with fludarabine and associated with severe immune thrombocytopenia.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Immunoglobulins / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Myeloablative Agonists / adverse effects. Thrombocytopenia / drug therapy. Thrombocytopenia / etiology. Vidarabine / analogs & derivatives
  • [MeSH-minor] Aged. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Cyclophosphamide / administration & dosage. Drug Therapy, Combination. Humans. Immunologic Factors / therapeutic use. Male. Rituximab. Severity of Illness Index. Treatment Outcome

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Immune thrombocytopenia.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16184881.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Immunoglobulins; 0 / Immunologic Factors; 0 / Myeloablative Agonists; 4F4X42SYQ6 / Rituximab; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  •  go-up   go-down


19. Nagatoshi Y, Kawano Y, Nagayama J, Okamura J: Treatment of isolated central nervous system relapse in high-risk lymphoid malignancy with allogeneic bone marrow transplantation and extended intrathecal therapy. Br J Haematol; 2004 Jun;125(6):766-8
Hazardous Substances Data Bank. HYDROCORTISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of isolated central nervous system relapse in high-risk lymphoid malignancy with allogeneic bone marrow transplantation and extended intrathecal therapy.
  • We performed allogeneic bone marrow transplantation (BMT) with an extended period of post-transplant intrathecal (IT) chemotherapy for five patients with acute lymphoblastic leukaemia and non-Hodgkin's lymphoma who had relapsed in the central nervous system either in the very early phase or more than twice.
  • Disease relapse occurred in one patient and the other patients remained in complete remission for 39-196 months post-BMT.
  • [MeSH-major] Bone Marrow Transplantation. Central Nervous System Diseases / therapy. Lymphoma, Non-Hodgkin / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Chemotherapy, Adjuvant. Child. Child, Preschool. Cytarabine / therapeutic use. Disease-Free Survival. Female. Humans. Hydrocortisone / therapeutic use. Injections, Spinal. Male. Recurrence. Remission Induction. Transplantation Conditioning. Transplantation, Homologous

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.
  • Hazardous Substances Data Bank. CYTARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15180866.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 04079A1RDZ / Cytarabine; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


20. Khanim FL, Bradbury CA, Arrazi J, Hayden RE, Rye A, Basu S, MacWhannell A, Sawers A, Griffiths M, Cook M, Freeman S, Nightingale KP, Grimwade D, Falciani F, Turner BM, Bunce CM, Craddock C: Elevated FOSB-expression; a potential marker of valproate sensitivity in AML. Br J Haematol; 2009 Feb;144(3):332-41
Hazardous Substances Data Bank. VALPROIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Histone deacetylase inhibitors (HDIs) are emerging as valuable new agents in the treatment of acute myeloid leukaemia (AML).
  • In a trial of 20 patients treated with the HDI sodium valproate (VPA) in combination with all trans retinoic acid and theophylline, three patients responded clinically with one complete remission (CR) and two partial remissions.
  • Microarray analysis of the primary AMLs and a panel of haemato-lymphoid cell lines, with a similar range of VPA sensitivities as the primary leukaemic blasts, identified elevated FOSB-expression as a potential marker of VPA sensitivity.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Gene Expression Regulation, Leukemic. Histone Deacetylases / adverse effects. Leukemia, Myeloid, Acute / drug therapy. Proto-Oncogene Proteins c-fos / genetics. Valproic Acid / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Blotting, Western. Cell Line, Tumor. Female. Gene Expression. Gene Expression Profiling / methods. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19036090.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / FOSB protein, human; 0 / Proto-Oncogene Proteins c-fos; 614OI1Z5WI / Valproic Acid; EC 3.5.1.98 / Histone Deacetylases
  •  go-up   go-down


21. Pituch-Noworolska A: [Biological properties and sensitivity to induction therapy of differentiated cells expressing atypical immunophenotype in acute leukemia of children]. Folia Med Cracov; 2001;42(3):5-80
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Biological properties and sensitivity to induction therapy of differentiated cells expressing atypical immunophenotype in acute leukemia of children].
  • [Transliterated title] Właściwości biologiczne i wrazliwość na leczenie indukcyjne komórek rozrostowych o nietypowym immunofenotypie w ostrych białaczkach u dzieci.
  • The atypical immunophenotype (expression of determinant from the another cell lines than line of origin) of acute leukaemia blast cells are noted in a part of cases.
  • The purpose of the study was: precise description of atypical immunophenotypes and analysis of their frequency in different types of acute leukaemia, analysis of association between expression of atypical immunophenotypes and the level of initial leukocytosis, percentage of blast cells in peripheral blood, expression of CD34, analysis of frequency of multidrug resistance molecule (MDR) expression and association between MDR and immunophenotypes of leukaemia cells, analysis of association between atypical immunophenotypes and proliferation, secretion of cytokines (IL-6, TNF) and spontaneous apoptosis of leukaemia cells, analysis of association between atypical immunophenotypes and sensitivity to induction therapy.
  • The bone marrow samples used for routine diagnosis were the basic source of leukaemia cells for the study.
  • The morphological examination and the immunophenotypes of leukaemia cells were done for classification of leukaemia.
  • The spontaneous proliferation of leukaemia cells was studied with 3H-Thymidine uptake after 3-days culture in vitro.
  • The type of proliferation (autocrine, paracrine) was defined based on comparison of shorter (3-days) and longer (6-days) culture of leukaemia cells.
  • The percentage of apoptotic leukaemia cells was analysed with flow cytometry after staining of leukaemia cells with propidium iodide in subdiploidal region of DNA profile.
  • The secretion of cytokines (IL-6 and TNF) was determined by ELISA technique in supernatants of leukaemia cells cultured for 24 hr in vitro.
  • The effect of induction therapy was estimated base on time of cytoreduction in peripheral blood and time of reaching the haematological remission in bone marrow.
  • The study included 230 children with acute leukaemia: lymphoblastic (ALL)--189 children (ALL-proB--19, common ALL--139, ALL-B--5 and ALL-T--26) and myeloid (AML)--34 children.
  • Moreover, into the study 2 cases of acute undifferentiated leukaemia (AUL) and 3--acute mixed lineage leukaemia (AMLL) and 2--biphenotypic leukaemia were included.
  • The all studies of leukaemia cells had been done before the therapy was installed.
  • Basing on the assay of immunophenotypes the following forms of atypical immunophenotypes were distinguished: immunophenotype incomplete, hyperexpression of determinants, asynchronic immunophenotype, coexpression of determinants from the other line than origin of leukaemia cells, balanced expression of determinants from two cells lines (biphenotypic leukaemia) and three cells lines (mixed lineage leukaemia).
  • The expression of CD34, recognised as the one of markers of poorer prognosis, was analysed regarding the leukaemia type and immunophenotype of leukaemia cells.
  • Moreover, in common ALL the expression of CD34 was significantly higher when myeloid determinants were present on common ALL cells (common ALL + My) in comparison to coexpression of lymphoid determinants (common ALL + Ly).
  • The common ALL + My leukaemia cells showed higher ability to proliferation in vitro compare with common ALL without atypical immunophenotype.
  • AML leukaemia cells with coexpression of lymphoid determinants (AML + Ly) showed lower proliferation in vitro than AML without atypical immunophenotype.
  • The autocrine type of proliferation was observed frequently in AML (35.3% of cases) than in ALL (14.2%).
  • This type of spontaneous proliferation was observed only when the leukaemia cells without changes in immunophenotype had been cultured.
  • AML leukaemia cells without changes in immunophenotype released significantly higher amount of these cytokines than AML cells with atypical immunophenotypes (AML + Ly).
  • The above observations suggested that coexpression of myeloid determinants in ALL and lymphoid determinants in AML were leading to changes of some biological properties of these cells.
  • The ALL + My leukaemia cells behaved similarly to myeloid leukaemia cells, while AML + Ly cells showed features of lymphoid leukaemia cells.
  • The common ALL and AML leukaemia cells with atypical immunophenotype showed higher percentage of apoptotic cells (16.1% and 16.9% respectively) comparing to common ALL and AML without changes in immunophenotype (9.0% and 9.2% respectively).
  • In common ALL and AML with typical immunophenotype of leukaemia cells and ALL-T the level of apoptosis was associated positively with the spontaneous proliferation, whereas this relation was negative in AML with atypical immunophenotype.
  • There were no differences of the time of cytoreduction of leukaemia cells in peripheral blood in B cell origin ALL and AML with or without changes in immunophenotype of blastic cells.
  • In ALL-T + My the time of cytoreduction was significantly longer.
  • However, the expression of CD10 in ALL-T had no effect on cytoreduction time.
  • The expression of MDR in ALL-T with typical immunophenotype was independent marker associated with elongation of cytoreduction time.
  • The time of reaching the complete haematological remission was analysed in 186 children with ALL (ALL-proB--18 children, common ALL--137 children, ALL-T--26) and only 19 children with AML.
  • The longest period of time for reaching the remission was observed in AML, shortest--in ALL-T.
  • In common ALL and ALL-T the expression of myeloid determinants was associated with significant elongation of time of reaching the remission.
  • In the majority of AML cases with coexpression lymphoid determinants, the complete remission was reached.
  • The time needed for the reaching of remission was similar in AML with or without coexpression of lymphoid determinants.
  • The results of this study suggest that coexpression of determinants from the other cell line modify the biological properties of leukaemia cells into the cells from the line of origin of these additional determinants.
  • In ALL the combined expression of MDR and atypical immunophenotype of leukaemia cells were associated with poorer response to induction therapy.
  • In AML the combined expression of CD34 and atypical immunophenotype were associated with response to induction therapy by reaching the complete remission, but without any influence on the time of reaching this remission.
  • The results of analysis of cytoreduction time and time of reaching the remission improved the usefulness of these parameters for the estimation of response to the induction therapy.
  • The clinical importance of these observations consist in characterisation of leukaemia cells potentially resistant to the induction therapy what may suggest the modification and individualization of the induction therapy.
  • [MeSH-major] Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Animals. Antigens, CD34 / immunology. Apoptosis. Child. Child, Preschool. Cytokines / secretion. Drug Resistance, Multiple / immunology. Humans. Immunophenotyping. Infant. Mice. Multidrug Resistance-Associated Proteins / immunology. Remission Induction

  • MedlinePlus Health Information. consumer health - Acute 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 = 12353422.001).
  • [ISSN] 0015-5616
  • [Journal-full-title] Folia medica Cracoviensia
  • [ISO-abbreviation] Folia Med Cracov
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Cytokines; 0 / Multidrug Resistance-Associated Proteins
  • [Number-of-references] 160
  •  go-up   go-down


22. Valnet-Rabier MB, Challier B, Thiebault S, Angonin R, Margueritte G, Mougin C, Kantelip B, Deconinck E, Cahn JY, Fest T: c-Flip protein expression in Burkitt's lymphomas is associated with a poor clinical outcome. Br J Haematol; 2005 Mar;128(6):767-73
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The World Health Organization Classification of Lymphoid Neoplasms identifies Burkitt's lymphoma/leukaemia (BL) as a single entity, characterized by unique clinical and genetic features that require specific high intensity chemotherapy regimens.
  • Although remarkable successes in the treatment of the disease have been observed, when compared with paediatric patients, adults are less likely to reach stable complete remission.
  • We investigated 32 BL cases, composed in equal part by adults and children that were treated with the French LMB regimen, for factors that may be implicated in chemoresistance.
  • Immunohistochemical detection of procaspase-8, caspase-3a, survivin, p53, CD95, c-Flip and Phospho-RelA (Ser536) was investigated on paraffin-embedded tissues.
  • The expression of c-Flip was found highly related to a poor prognosis, mostly characterized by adults with a chemoresistant disease, resulting in a high death rate within the first year of diagnosis.
  • All c-Flip-positive BL cases presented a nuclear Phospho-RelA (Ser536) localization, suggesting the presence of an active nuclear factor (NF)-kappa B transcription pathway.
  • These findings show that c-Flip could be a reliable prognostic factor in BL, suggesting new therapeutic approaches that target the NF-kappa B pathway.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15755279.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / CFLAR protein, human; 0 / Intracellular Signaling Peptides and Proteins
  •  go-up   go-down


23. Sazawal S, Gurbuxani S, Bhatia K, Khattar A, Raina V, Arya LS, Vats T, Magrath I, Bhargava M: Incidence, clinical characteristics and early treatment outcome in Indian patients of childhood acute lymphoblastic leukemia with ALL-1 gene rearrangement. Leuk Res; 2001 Aug;25(8):693-8
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidence, clinical characteristics and early treatment outcome in Indian patients of childhood acute lymphoblastic leukemia with ALL-1 gene rearrangement.
  • In a series of 185 patients (median age 7 years) of acute lymphoblastic leukaemia (ALL) from India, the overall incidence of ALL-1 gene rearrangement using the Southern blot technique was 11.4% (21/185).
  • Complete remission (CR) and relapse rates in 98 patients evaluable for response to therapy on a uniform therapy protocol was independent of ALL-1 gene status.
  • [MeSH-major] DNA-Binding Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes. Transcription Factors
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Incidence. India / epidemiology. Infant. Male. Myeloid-Lymphoid Leukemia Protein. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11397475.001).
  • [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 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down


24. Goteri G, Olivieri A, Ranaldi R, Lucesole M, Filosa A, Capretti R, Pieramici T, Leoni P, Rubini C, Fabris G, Lo Muzio L: Bone marrow histopathological and molecular changes of small B-cell lymphomas after rituximab therapy: comparison with clinical response and patients outcome. Int J Immunopathol Pharmacol; 2006 Apr-Jun;19(2):421-31
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bone marrow histopathological and molecular changes of small B-cell lymphomas after rituximab therapy: comparison with clinical response and patients outcome.
  • This study correlates bone marrow changes after Rituximab (RTX) treatment with the clinical characteristics and outcome of 26 patients with small B-cell lymphomas.
  • The percentage, phenotypic profile and clonality pattern of bone marrow lymphoid infiltrate were analysed before and after RTX treatment.
  • Sixteen out of twenty-six patients obtained a complete clinical remission (CR).
  • A favourable histology--follicular lymphoma (FL), hairy cell leukaemia (HCL) and marginal zone lymphoma (MZL)--was associated with a higher frequency of clinical CR and histological remission (HR), in comparison with mantle cell lymphoma (MCL), chronic lymphocytic leukaemia (CLL) and lymphoplasmacytic lymphoma (LPL).
  • 1) complete lymphoid cell disappearance (9 patients); or 2) nodular/interstitial T-cell infiltration (10 patients).
  • 1) persistence of CD20+ small lymphoid cells in 1 patient with MCL;.
  • Molecular response showed no correlations with the further clinical course in 12 patients achieving a complete clinical remission.
  • Persistence of monoclonality after RTX might have a role in evaluating the molecular pattern of CD20-negative clones that can emerge after RTX as a tumoral escape to therapy.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Bone Marrow / metabolism. Bone Marrow / pathology. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / pathology
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal, Murine-Derived. Cloning, Molecular. Female. Follow-Up Studies. Humans. Lymphocytes / immunology. Male. Middle Aged. Phenotype. Reverse Transcriptase Polymerase Chain Reaction. Rituximab. Treatment Outcome

  • Genetic Alliance. consumer health - B-Cell Lymphomas.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16831308.001).
  • [ISSN] 0394-6320
  • [Journal-full-title] International journal of immunopathology and pharmacology
  • [ISO-abbreviation] Int J Immunopathol Pharmacol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  •  go-up   go-down


25. Weide R, Heymanns J, Gores A, Köppler H: Bendamustine mitoxantrone and rituximab (BMR): a new effective regimen for refractory or relapsed indolent lymphomas. Leuk Lymphoma; 2002 Feb;43(2):327-31
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Bendamustine (B) and mitoxantrone (M) have been shown to be potent cytotoxic drugs for the treatment of relapsed or refractory indolent lymphomas.
  • This study was an open label, single center pilot study for patients with relapsed or refractory, CD20-positive (indolent) lymphoma or chronic lymphocytic leukaemia.
  • The therapy consisted of bendamustine (80 mg/m2, day 1-3), mitoxantrone (10 mg/m2, day 1), rituximab (375 mg/m2, week 2-5).
  • The maximum therapy consisted of one BMR-cycle, followed by five BM courses.
  • Treatment was stopped when the disease responded with PR/CR.
  • Median number of previous treatment regimens was two (1-6).
  • Overall response rate was 95% (19/20) with seven patients achieving a CR (35%) and 12 patients achieving a PR (60%).
  • Median time to progression is 7 months (1-21) with a median observation time of 7 months (1-21).
  • Response is still durable in 15/20 patients (75%) (1+ to 21+ months after therapy).
  • Non-symptomatic grade three or four haematotoxicity was seen in 9/20 patients (45%).
  • No major non-haematological toxicity was observed.
  • In conclusion, BMR is a well tolerated, very effective outpatient regimen of treatment for relapsed and refractory indolent lymphoid malignancies.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Lymphoma, B-Cell / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Bendamustine Hydrochloride. Disease-Free Survival. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Middle Aged. Mitoxantrone / administration & dosage. Nitrogen Mustard Compounds / administration & dosage. Remission Induction. Rituximab. Salvage Therapy

  • Hazardous Substances Data Bank. Bendamustine .
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11999564.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Nitrogen Mustard Compounds; 4F4X42SYQ6 / Rituximab; 981Y8SX18M / Bendamustine Hydrochloride; BZ114NVM5P / Mitoxantrone
  •  go-up   go-down


26. Rókusz L, Liptay L, Kádár K: Successful treatment of chronic disseminated candidiasis with fluconazole and a granulocyte-macrophage colony-stimulating factor combination. Scand J Infect Dis; 2001;33(10):784-6
Hazardous Substances Data Bank. FLUCONAZOLE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment of chronic disseminated candidiasis with fluconazole and a granulocyte-macrophage colony-stimulating factor combination.
  • We report a case of chronic disseminated candidiasis in a patient with acute non-lymphoid leukaemia.
  • After 12 months of combined therapy with fluconazole and granulocyte-macrophage colony-stimulating factor, lesions in the liver and spleen resolved completely.
  • The patient has given birth to a healthy baby and has been in complete hematological remission for 3 years.
  • [MeSH-major] Antifungal Agents / therapeutic use. Candidiasis / drug therapy. Fluconazole / therapeutic use. Granulocyte-Macrophage Colony-Stimulating Factor / therapeutic use. Leukemia, Myeloid, Acute / complications
  • [MeSH-minor] Adult. Drug Therapy, Combination. Female. Humans. Liver Diseases / drug therapy. Splenic Diseases / drug therapy

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Yeast Infections.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11728053.001).
  • [ISSN] 0036-5548
  • [Journal-full-title] Scandinavian journal of infectious diseases
  • [ISO-abbreviation] Scand. J. Infect. Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Antifungal Agents; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; 8VZV102JFY / Fluconazole
  •  go-up   go-down


27. Zhang J, Mi YC, Wang Y, Lin D, Li W, Sun XM, Zhou K, Bian SG, Wang JX: [Study on the clinical characteristics of adult biphenotypic acute leukaemia]. Zhonghua Xue Ye Xue Za Zhi; 2009 Jan;30(1):18-21
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Study on the clinical characteristics of adult biphenotypic acute leukaemia].
  • OBJECTIVE: To analyze the clinical and biological characteristics and prognosis of adult biphenotypic acute leukaemia (BAL).
  • The chemotherapy regimens were accordingly for acute lymphoblastic leukaemia (ALL), acute myeloid leukaemia (AML) or for both ALL and AML.
  • (1) The incidence of BAL in acute leukaemias was 6.7%, with a male predominance and 52.3% of BAL patients had WBC > or = 30 x 10(9)/L and 16.9% WBC > or = 100 x 10(9)/L. (2) Percentages of coexpression of myeloid and B lymphoid antigens were 81.5%, of myeloid and T lymphoid antigens 10.8%, of myeloid, B- and T lymphoid antigens 4.6%, and of B and T lymphoid antigens 3.1%. (3) Normal and abnormal karyotypes accounted for 41.5% and 58.5%, respectively in 53 BAL patients with karyotype analysis.
  • The rate of Ph (+) or bcr-abl (+) was 32.1%. (4) 31 (56.4%) of 65 patients achieved complete remission (CR), but CR rate was only 35.3% for Ph (+) or bcr-abl (+) cases. CONCLUSION:.
  • (1) High white blood cell count and coexpression of myeloid/B lymphoid antigens are common in BAL. (2) Abnormal karyotypes and Ph (+) or bcr-abl( +) often happen. (3) The treatment outcome of BAL is poor.
  • [MeSH-major] Leukemia, Biphenotypic, Acute

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19563029.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  •  go-up   go-down


28. Prabhash K, Vikram GS, Nair R, Sengar M, Gujral S, Bakshi A, Gupta S, Parikh PM: Fludarabine in lymphoproliferative malignancies: a single-centre experience. Natl Med J India; 2008 Jul-Aug;21(4):171-4
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Fludarabine has been reported to be an effective drug for the treatment of chronic lymphocytic leukaemia (CLL) and indolent lymphomas.
  • Response evaluation was done as per the National Cancer Institute-Working Group guidelines for CLL and International Workshop criteria for non-Hodgkin lymphomas, respectively, in those patients who received at least 3 cycles of fludarabine.
  • Sixteen patients had a treatment delay, 14 due to myelosuppression.
  • The overall response rate for low grade lymphoma was 88% (63% complete remission) in untreated patients and 79% (43% complete remission) in those with relapsed disease.
  • Two patients died of sepsis and 4 due to disease progression on treatment.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Lymphoid / drug therapy. Lymphoma / drug therapy. Vidarabine / analogs & derivatives


29. Ma SY, Au WY, Chim CS, Lie AK, Lam CC, Tse E, Leung AY, Liang R, Kwong YL: Fludarabine, mitoxantrone and dexamethasone in the treatment of indolent B- and T-cell lymphoid malignancies in Chinese patients. Br J Haematol; 2004 Mar;124(6):754-61
Hazardous Substances Data Bank. NOVANTRONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fludarabine, mitoxantrone and dexamethasone in the treatment of indolent B- and T-cell lymphoid malignancies in Chinese patients.
  • The treatment results of indolent lymphoid malignancies in Chinese are poorly reported.
  • The efficacy of FND (fludarabine 25 mg/m2/d, x3; mitoxantrone 10 mg/m2/d, x1; dexamethasone 20 mg/d, x5; monthly cycles, x6) in 95 Chinese patients with indolent B-cell malignancies (at diagnosis: 55, relapse/refractory disease: 40) and nine Chinese patients with T-cell large granular lymphocyte leukaemia (T-LGL leukaemia) (at diagnosis: two, refractory disease: seven) was evaluated.
  • For B-cell malignancies, the complete response (CR), partial response (PR) and overall response (OR) rates were 50.5%, 18% and 68.5% respectively.
  • Responsive patients (CR/PR) had a better median PFS (44 months vs. 5 months, P < 0.001) and OS (67 months vs. 13 months, P < 0.001) than unresponsive patients.
  • For T-LGL leukaemia, the CR and molecular-remission rates were 56% and 67% (median follow-up: 23 months).
  • FND is an active regimen for the treatment of indolent B- and T-cell malignancies in Chinese patients, with results comparable with Western patients with similar indolent lymphomas.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Prolymphocytic, T-Cell / drug therapy. Lymphoma, B-Cell / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Asian Continental Ancestry Group. Dexamethasone / administration & dosage. Dexamethasone / adverse effects. Disease-Free Survival. Female. Humans. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / ethnology. Male. Middle Aged. Mitoxantrone / administration & dosage. Mitoxantrone / adverse effects. Prospective Studies. Rituximab. Survival Analysis. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / adverse effects. Vidarabine / analogs & derivatives

  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. VIDARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15009063.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 7S5I7G3JQL / Dexamethasone; BZ114NVM5P / Mitoxantrone; FA2DM6879K / Vidarabine; FND protocol
  •  go-up   go-down


30. Piccaluga PP, Malagola M, Rondoni M, Amabile M, Paolini S, Soverini S, Gaitani S, Visani G, Baccarani M, Martinelli G: Dose increase of imatinib mesylate may overcome acquired resistance in bcr/abl-positive acute lymphoid leukaemia. Eur J Haematol; 2004 Apr;72(4):302-3
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dose increase of imatinib mesylate may overcome acquired resistance in bcr/abl-positive acute lymphoid leukaemia.
  • [MeSH-major] Drug Resistance, Neoplasm. Piperazines / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / administration & dosage
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Asparaginase / administration & dosage. Benzamides. Doxorubicin / administration & dosage. Fusion Proteins, bcr-abl / antagonists & inhibitors. Humans. Imatinib Mesylate. Male. Neoplasm Proteins / antagonists & inhibitors. Neoplasm Recurrence, Local. Prednisone / administration & dosage. Remission Induction. Stem Cell Transplantation. Transplantation, Homologous. Vincristine / administration & dosage

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15089772.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Benzamides; 0 / Neoplasm Proteins; 0 / Piperazines; 0 / Pyrimidines; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone
  •  go-up   go-down






Advertisement