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Items 1 to 29 of about 29
1. Lauchle JO, Kim D, Le DT, Akagi K, Crone M, Krisman K, Warner K, Bonifas JM, Li Q, Coakley KM, Diaz-Flores E, Gorman M, Przybranowski S, Tran M, Kogan SC, Roose JP, Copeland NG, Jenkins NA, Parada L, Wolff L, Sebolt-Leopold J, Shannon K: Response and resistance to MEK inhibition in leukaemias initiated by hyperactive Ras. Nature; 2009 Sep 17;461(7262):411-4
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  • [Title] Response and resistance to MEK inhibition in leukaemias initiated by hyperactive Ras.
  • The cascade comprising Raf, mitogen-activated protein kinase kinase (MEK) and extracellular signal-regulated kinase (ERK) is a therapeutic target in human cancers with deregulated Ras signalling, which includes tumours that have inactivated the Nf1 tumour suppressor.
  • We compared the effects of inhibitors of MEK in a myeloproliferative disorder (MPD) initiated by inactivating Nf1 in mouse bone marrow and in acute myeloid leukaemias (AMLs) in which cooperating mutations were induced by retroviral insertional mutagenesis.
  • Drug resistance developed because of outgrowth of AML clones that were present before treatment.
  • We cloned clone-specific retroviral integrations to identify candidate resistance genes including Rasgrp1, Rasgrp4 and Mapk14, which encodes p38alpha.
  • This approach represents a robust strategy for identifying genes and pathways that modulate how primary cancer cells respond to targeted therapeutics and for probing mechanisms of de novo and acquired resistance.

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  • (PMID = 19727076.001).
  • [ISSN] 1476-4687
  • [Journal-full-title] Nature
  • [ISO-abbreviation] Nature
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084221; United States / NCI NIH HHS / CA / K08 CA119105-03; United States / NCI NIH HHS / CA / R37 CA072614-12; United States / NCI NIH HHS / CA / R37 CA72614; United States / NCI NIH HHS / CA / K08 CA119105-01A1; United States / NCI NIH HHS / CA / R37 CA072614-11; United States / NCI NIH HHS / CA / T32 CA009043; United States / NCI NIH HHS / CA / U01 CA084221-06; United States / NICHD NIH HHS / HD / T32HD044331; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / U01 CA084221-07; United States / NCI NIH HHS / CA / K08 CA119105-02; United States / NCI NIH HHS / CA / T32 CA09043; United States / NCI NIH HHS / CA / R37 CA072614; United States / NCI NIH HHS / CA / U01 CA084221-10; United States / NCI NIH HHS / CA / K08 CA119105-04; United States / NCI NIH HHS / CA / U01 CA084221-08; United States / NICHD NIH HHS / HD / T32 HD044331; United States / NCI NIH HHS / CA / R37 CA072614-13; United States / NCI NIH HHS / CA / U01 CA84221; United States / NCI NIH HHS / CA / T32 CA128583; United States / NCI NIH HHS / CA / K08 CA119105; United States / NCI NIH HHS / CA / U01 CA084221-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide; 0 / Benzamides; 0 / Guanine Nucleotide Exchange Factors; 0 / Rasgrp1 protein, mouse; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 14; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS130836; NLM/ PMC4119783
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2. Lin TS, Mahajan S, Frank DA: STAT signaling in the pathogenesis and treatment of leukemias. Oncogene; 2000 May 15;19(21):2496-504
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  • [Title] STAT signaling in the pathogenesis and treatment of leukemias.
  • Leukemias continue to cause significant mortality in adults and children, and the use of standard cytotoxic chemotherapy has reached a therapeutic plateau.
  • Thus, there is great interest in treatments directed against inappropriately activated cell signaling pathways which stimulate the uncontrolled growth of neoplastic cells.
  • Increasing evidence suggests that the STAT signaling cascade may be one target of these therapies.
  • Constitutive STAT activation is present in many malignancies and has been especially well characterized in acute and chronic leukemias.
  • While STAT activation is a common characteristic of leukemias, the specific pattern of activated STATs and the manner by which STAT activation occurs vary with each disease.
  • STAT tyrosine phosphorylation can occur through inappropriate Jak activation or by direct activation of an oncoprotein such as Bcr/Abl, and STAT serine phosphorylation may play an important role in leukemias as well.
  • Thus, the STAT signaling pathway is an attractive target for therapeutic intervention, and strategies designed to inhibit STAT activation and STAT mediated gene transcription may play an important role in the next generation of anti-leukemia therapies.
  • [MeSH-major] DNA-Binding Proteins / metabolism. Leukemia / metabolism. Leukemia / therapy. Milk Proteins. Signal Transduction. Trans-Activators / metabolism
  • [MeSH-minor] Acute Disease. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia-Lymphoma, Adult T-Cell / metabolism. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / therapy. STAT1 Transcription Factor. STAT3 Transcription Factor. STAT5 Transcription Factor

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  • (PMID = 10851048.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA79547
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Milk Proteins; 0 / STAT1 Transcription Factor; 0 / STAT1 protein, human; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / STAT5 Transcription Factor; 0 / Trans-Activators
  • [Number-of-references] 52
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3. Sengul E, Dervisoglu E, Kus E, Ciftci E, Ercin C, Yilmaz A: Acute lymphoblastic leukaemia presenting with acute renal failure: report of two cases. J Pak Med Assoc; 2008 Sep;58(9):512-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute lymphoblastic leukaemia presenting with acute renal failure: report of two cases.
  • Acute renal failure is a well-recognized complication of acute leukaemias.
  • Here we report two patients with acute lymphoblastic leukaemia presenting with acute renal failure due to leukaemic infiltration.
  • The first patient died before the administration of specific therapy for leukaemia, whereas the second case recovered after chemotherapy.
  • She was discharged without necessitating dialysis therapy.
  • [MeSH-major] Acute Kidney Injury / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Fatal Outcome. Humans. Male. Middle Aged. Risk Factors

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  • [ErratumIn] J Pak Med Assoc. 2008 Dec;58(12):719
  • (PMID = 18846803.001).
  • [ISSN] 0030-9982
  • [Journal-full-title] JPMA. The Journal of the Pakistan Medical Association
  • [ISO-abbreviation] J Pak Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Pakistan
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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4. Dilber MS, Gahrton G: Suicide gene therapy: possible applications in haematopoietic disorders. J Intern Med; 2001 Apr;249(4):359-67
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  • [Title] Suicide gene therapy: possible applications in haematopoietic disorders.
  • Although the treatment results for some forms of haematologic malignancies are excellent, especially for the childhood acute leukaemias, there is still a significant fraction of patients that will not benefit from the therapy available today.
  • The identification of new techniques, such as gene therapy, may therefore be of great importance for future therapeutic applications.
  • Suicide gene therapy is one of several gene therapeutic approaches to treat cancer.
  • A suicide gene is a gene encoding a protein, frequently an enzyme, that in itself is nontoxic to the genetically modified cell.
  • However, when a cell is exposed to a specific nontoxic prodrug, this is selectively converted by the gene product into toxic metabolites that kill the cell.
  • Therefore, it is important to develop gap junction independent drug delivery systems.
  • Suicide gene technology may also be used for the ex vivo purging of tumour cells in bone marrow or peripheral blood stem cell autografts or for inactivation of effector cells, such as antitumour T donor lymphocytes in allogeneic transplantation to prevent severe graft versus host reactions.
  • New constructs, e.g. combining suicide genes and immune response enhancing genes or suicide genes and connexin inducing genes may further improve the value of suicide gene therapy.
  • [MeSH-major] Genetic Therapy / methods. Hematologic Neoplasms / therapy

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  • (PMID = 11298856.001).
  • [ISSN] 0954-6820
  • [Journal-full-title] Journal of internal medicine
  • [ISO-abbreviation] J. Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Connexins; 0 / ICP35 protein, Human herpesvirus 1; 0 / Prodrugs; 0 / Viral Proteins; EC 2.7.1.21 / Thymidine Kinase; EC 3.5.4.- / Nucleoside Deaminases; EC 3.5.4.1 / Cytosine Deaminase
  • [Number-of-references] 74
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5. Hamed NA, Sharaki OA, Zeidan MM: Leptin in acute leukaemias: relationship to interleukin-6 and vascular endothelial growth factor. Egypt J Immunol; 2003;10(1):57-66
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  • [Title] Leptin in acute leukaemias: relationship to interleukin-6 and vascular endothelial growth factor.
  • This effect may be due to prevention of apoptosis of progenitor cells or upregulation of specific receptors on leukaemic precursors that make them more responsive to stimuli.
  • The relationship to blood cell counts, haemoglobin and response to chemotherapy was also investigated.
  • The study included 25 acute leukaemic male patients [15 acute myeloid leukaemia (AML) and 10 acute lymphoblastic leukaemia (ALL)] and 15 age and sex matched healthy controls.
  • In addition, patients were subjected to bone marrow aspiration, cytochemistry and immunophenotyping study and serum leptin assay after chemotherapy.
  • This elevation was unrelated to the presence of extramedullary infiltration or response to chemotherapy and correlated only with body mass index (p<0.05).
  • In both AML and ALL, there was no significant difference in serum leptin level before and after treatment.

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  • (PMID = 15719623.001).
  • [ISSN] 1110-4902
  • [Journal-full-title] The Egyptian journal of immunology
  • [ISO-abbreviation] Egypt J Immunol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Leptin; 0 / Vascular Endothelial Growth Factor A
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6. Leone G, Sica S, Voso MT, Rutella S, Pagano L: Treatment of acute leukaemias with monoclonal antibodies: current status and future prospects. Cardiovasc Hematol Agents Med Chem; 2006 Jan;4(1):33-52
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  • [Title] Treatment of acute leukaemias with monoclonal antibodies: current status and future prospects.
  • Monoclonal antibodies are a new class of agents targeted at specific receptors on cancer cells.
  • In ALL, rituximab, a humanized anti CD20 antibody, has been combined to chemotherapy mainly in mature B-ALL and Burkitt's lymphoma and preliminary results are promising.
  • Monoclonal antibodies against myeloid antigens have been prevalently used in acute myeloid leukaemias (AML), where the most utilised immunological target is CD33.
  • Targeted chemotherapy with the anti-CD33-calicheamicin construct gemtuzumab ozogamicin (GO) has produced remissions as a single agent in patients with relapsed AML and appears promising when used in combination with standard chemotherapy.
  • GO has been approved by FDA as second-line therapy in older patients with AML.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia / drug therapy
  • [MeSH-minor] Acute Disease. Cell Proliferation / drug effects. Humans

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  • (PMID = 16529548.001).
  • [ISSN] 1871-5257
  • [Journal-full-title] Cardiovascular & hematological agents in medicinal chemistry
  • [ISO-abbreviation] Cardiovasc Hematol Agents Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents
  • [Number-of-references] 166
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7. Jacobs P, Wood L: Myelodysplasia and the acute myeloid leukaemias. Hematology; 2002 Dec;7(6):325-38
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  • [Title] Myelodysplasia and the acute myeloid leukaemias.
  • The myelodysplastic syndromes are increasingly recognised clinical entities reflecting a stem cell defect that gives rise to ineffective clonal haematopoiesis.
  • The spectrum extends from relatively indolent refractory anaemia through varying combinations of leucopoenia and thrombocytopenia to acute leukaemia.
  • Stratification to risk-related protocols range from occasional blood transfusions or erythropoietin through innovative options including thalidomide or amifostine to haematopoietic stem cell transplantation in selected individuals.
  • Acute myeloid leukaemia, conceptually segregated from preleukaemia, is treated differently although accumulating cellular and molecular data favour a more integrated approach.
  • On this basis chemotherapy alone is sufficient in defined sub-groups whereas others benefit by autologous or allogeneic grafting.
  • Attention to demonstrating minimal residual disease is the basis for more specific intervention exemplified by monoclonal antibodies or maturation-inducing agents as with retinoic acid in acute progranulocytic leukaemia
  • [MeSH-major] Leukemia, Myeloid. Myelodysplastic Syndromes

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  • (PMID = 12475737.001).
  • [ISSN] 1024-5332
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 50
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8. Maring JG, Groen HJ, Wachters FM, Uges DR, de Vries EG: Genetic factors influencing pyrimidine-antagonist chemotherapy. Pharmacogenomics J; 2005;5(4):226-43
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  • [Title] Genetic factors influencing pyrimidine-antagonist chemotherapy.
  • Pyrimidine antagonists, for example, 5-fluorouracil (5-FU), cytarabine (ara-C) and gemcitabine (dFdC), are widely used in chemotherapy regimes for colorectal, breast, head and neck, non-small-cell lung cancer, pancreatic cancer and leukaemias.
  • Interindividual variation in the activity of metabolising enzymes can affect the extent of prodrug activation and, as a result, act on the efficacy of chemotherapy treatment.
  • In addition, the role of germline polymorphisms, tumour-specific somatic mutations and protein expression levels in the metabolic pathways and clinical pharmacology of these drugs are described.
  • [MeSH-major] Antineoplastic Agents / metabolism. Gene Expression Regulation, Enzymologic. Neoplasms / drug therapy. Pharmacogenetics. Polymorphism, Genetic. Pyrimidines / antagonists & inhibitors

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  • (PMID = 16041392.001).
  • [ISSN] 1470-269X
  • [Journal-full-title] The pharmacogenomics journal
  • [ISO-abbreviation] Pharmacogenomics J.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Pyrimidines
  • [Number-of-references] 196
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9. Gorschlüter M, Mey U, Strehl J, Ziske C, Schepke M, Schmidt-Wolf IG, Sauerbruch T, Glasmacher A: Neutropenic enterocolitis in adults: systematic analysis of evidence quality. Eur J Haematol; 2005 Jul;75(1):1-13

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: Neutropenic enterocolitis is a life-threatening complication occurring most frequently after intensive chemotherapy in acute leukaemias.
  • Are there good quality studies supporting specific interventions: Which empiric antimicrobial therapy is recommendable?
  • There were no prospective trials or case control studies on the therapy of neutropenic enterocolitis.
  • We suggest applying a combination of clinical and radiological criteria: fever, abdominal pain and any bowel wall thickening >4 mm detected by ultrasonography (US) or computed tomography.
  • We calculated a pooled incidence rate from 21 studies of 5.3% (266/5058; 95% CI: 4.7%-5.9%) in patients hospitalised for haematological malignancies, for high-dose chemotherapy in solid tumours or for aplastic anaemia.
  • CONCLUSIONS: This systematic review provides diagnostic criteria for neutropenic enterocolitis, presents a quantitative synthesis on its incidence and discusses its treatment recommendations.
  • [MeSH-major] Enterocolitis, Neutropenic / diagnosis. Enterocolitis, Neutropenic / therapy
  • [MeSH-minor] Adult. Anemia, Aplastic / complications. Anemia, Aplastic / drug therapy. Humans. Neoplasms / classification. Neoplasms / drug therapy

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  • [Copyright] (c) Blackwell Munksgaard 2005.
  • (PMID = 15946304.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Denmark
  • [Number-of-references] 158
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10. Gupta S, Kanodia AK: Biological response modifiers in cancer therapy. Natl Med J India; 2002 Jul-Aug;15(4):202-7
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  • [Title] Biological response modifiers in cancer therapy.
  • Recent advances in tumour immunology have enabled the development of specific agents targeted against cancer cells.
  • Monoclonal antibodies directed against tumour-specific agents have been approved for the treatment of breast cancer (trastuzumab), non-Hodgkin's lymphoma (rituximab) and for the diagnosis of certain cancers (oncoscint).
  • Interferons are indicated for the treatment of certain leukaemias and Kaposi's sarcoma to inhibit tumour proliferation and angiogenesis.
  • Interleukin-2 is the most widely studied interleukin, and is used for immunostimulation in metastatic renal cell carcinoma and malignant melanoma.
  • Haematopoletic growth factors are often combined with chemotherapy and radiotherapy to restore bone marrow function and treat complications such as infection and bleeding.
  • Various anticancer vaccines are being developed using tumour cells, carbohydrates, peptides and heat-shock proteins as antigens.
  • [MeSH-major] Immunologic Factors / therapeutic use. Neoplasms / drug therapy

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  • (PMID = 12296474.001).
  • [ISSN] 0970-258X
  • [Journal-full-title] The National medical journal of India
  • [ISO-abbreviation] Natl Med J India
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Immunologic Factors
  • [Number-of-references] 80
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11. Seymour JF: Ovarian tissue cryopreservation for cancer patients: who is appropriate? Reprod Fertil Dev; 2001;13(1):81-9
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  • [Title] Ovarian tissue cryopreservation for cancer patients: who is appropriate?
  • In recent decades there has been parallel progress in the fields of cancer chemotherapy and reproductive medicine technology, which has led to increasing numbers of women surviving their malignancies, often with significant reproductive impairment, and a range of choices for the potential preservation of fertility, including storage of embryos, mature oocytes, immature oocytes or ovarian tissue.
  • Although each of these procedures has specific relative advantages and disadvantages, there are no clear guidelines for selection of patients for such interventions.
  • (1) the risk of sterility with the proposed treatment program;.
  • (3) the potential risks of delaying chemotherapy;.
  • (5) the impact of any required hormonal manipulation on the tumour itself; and (6) the possibility of tumour contamination of the harvested tissue.
  • Thus the remaining 32% of patients with invasive cancer in this age group (267 per year) are potentially curable, and require initial treatment, including chemotherapy.
  • These tumours comprise predominantly breast cancer (161 cases or 19%), sarcomas of bone and soft-tissue (32 cases or 4%), and the haematologic malignancies (Hodgkin's disease, non-Hodgkin's lymphomas, and the leukaemias, each approximately 25 cases or 3%).
  • Current data relating to the six issues noted earlier using contemporary treatment programmes will be presented and discussed as they apply to each of these categories of patient.
  • [MeSH-major] Cryopreservation. Infertility / prevention & control. Neoplasms / drug therapy. Ovary
  • [MeSH-minor] Drug-Related Side Effects and Adverse Reactions. Female. Humans

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  • (PMID = 11545168.001).
  • [ISSN] 1031-3613
  • [Journal-full-title] Reproduction, fertility, and development
  • [ISO-abbreviation] Reprod. Fertil. Dev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Australia
  • [Number-of-references] 49
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12. Nikolaropoulos S, Tsavdaridis D, Arsenou E, Papageorgiou A, Karaberis E, Mourelatos D: Synergistic antineoplastic and cytogenetic effects by the combined action of two homo-aza-steroidal esters of nitrogen mustards on P388 and L1210 leukaemias in vivo and in vitro. Anticancer Res; 2000 Jul-Aug;20(4):2745-51

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  • [Title] Synergistic antineoplastic and cytogenetic effects by the combined action of two homo-aza-steroidal esters of nitrogen mustards on P388 and L1210 leukaemias in vivo and in vitro.
  • In order to increase the damaging effects on specific DNA sequences and decrease the subsequent toxicity, the use of homo-aza-steroidal esters of nitrogen mustards is already known.
  • Two specific homo-aza-steroidal esters were mixed at different proportions and the resultant final mixtures were tested in vivo and in vitro.
  • The effects of these on P388 and L1210 leukaemias, on SCE rates and on human lymphocyte proliferation kinetics were studied.
  • A correlation was observed (p < 0.001) between the magnitude of the SCE response and the depression of the cell proliferation index.
  • [MeSH-major] Antineoplastic Agents, Alkylating / administration & dosage. Leukemia L1210 / drug therapy. Leukemia P388 / drug therapy. Nitrogen Mustard Compounds / administration & dosage. Sister Chromatid Exchange / drug effects. Steroids / administration & dosage

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  • (PMID = 10953353.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] GREECE
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Nitrogen Mustard Compounds; 0 / Steroids
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13. Lowdell MW, Craston R, Samuel D, Wood ME, O'Neill E, Saha V, Prentice HG: Evidence that continued remission in patients treated for acute leukaemia is dependent upon autologous natural killer cells. Br J Haematol; 2002 Jun;117(4):821-7
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  • [Title] Evidence that continued remission in patients treated for acute leukaemia is dependent upon autologous natural killer cells.
  • Although it has been known for more than 40 years that allogeneic immune responses cure leukaemias after bone marrow transplantation, autologous leukaemia-specific immunity remains controversial and its impact upon survival has not been established.
  • Here we have tested 25 patients with de novo acute leukaemias, while in remission at completion of their anti-leukaemia therapy, for evidence of autologous cytolytic immunity to their leukaemic cells taken and cryopreserved at disease presentation.
  • We have measured this degree of cell-mediated cytotoxicity in vitro and termed it "leukaemia cytolytic activity" (LCA).
  • We propose that it is this immune response, rather than the chemotherapy per se, which is responsible for continued remission and that measurement of LCA in patients at completion of therapy may be used as an indicator of risk of subsequent relapse.
  • Patients lacking this response will require further treatment, either with an allogeneic donor transplant or an alternative immunotherapeutic strategy.
  • [MeSH-major] Killer Cells, Natural / immunology. Leukemia / drug therapy. Leukemia / immunology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antigens, CD56 / immunology. Bone Marrow Transplantation. CD8-Positive T-Lymphocytes / immunology. Child. Graft vs Leukemia Effect / immunology. Humans. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / immunology. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Prognosis. Recurrence. Remission Induction. Retrospective Studies. Sensitivity and Specificity. Transplantation, Autologous. Transplantation, Homologous

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  • (PMID = 12060116.001).
  • [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, CD56
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14. Benati D, Baldari CT: SRC family kinases as potential therapeutic targets for malignancies and immunological disorders. Curr Med Chem; 2008;15(12):1154-65
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  • [Title] SRC family kinases as potential therapeutic targets for malignancies and immunological disorders.
  • Based on their amino acid sequence, Src family kinases are grouped into two subfamilies, which are also characterised by different tissue specificity.
  • Several pieces of evidence implicate Src family kinases in cancer development, as a consequence of changes in protein expression and/or kinase activity, and have prompted the design of potent specific inhibitors, the most common of which are adenine mimetics, as tools of relevant clinical interest for the treatment of both solid tumours and leukaemias.
  • In addition, the finding that some Src kinases expressed in haematopoietic cells play pivotal roles in lymphocyte maturation and activation has fostered the development of safe and effective inhibitors selective for specific Src family members, which are currently being tested in clinical trials as immunosuppressants for the treatment of immunological disorders.
  • Here we shall review the recent literature on the involvement of Src family kinases in human neoplasias and immunological disorders and the goals reached in the search for selective pharmacological inhibitors.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Immune System Diseases / drug therapy. Neoplasms / drug therapy. src-Family Kinases / drug effects
  • [MeSH-minor] Animals. Catalysis. Enzyme Inhibitors / pharmacology. Enzyme Inhibitors / therapeutic use. Humans. Lymphocyte Specific Protein Tyrosine Kinase p56(lck) / antagonists & inhibitors. Receptors, Cell Surface / drug effects. Signal Transduction / drug effects. Signal Transduction / physiology

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  • (PMID = 18473810.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Receptors, Cell Surface; EC 2.7.10.2 / Lymphocyte Specific Protein Tyrosine Kinase p56(lck); EC 2.7.10.2 / src-Family Kinases
  • [Number-of-references] 79
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15. Li S: Src kinases as targets for B cell acute lymphoblastic leukaemia therapy. Expert Opin Ther Targets; 2005 Apr;9(2):329-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Src kinases as targets for B cell acute lymphoblastic leukaemia therapy.
  • The participation of Src kinases in the induction of BCR-ABL-induced B cell acute lymphoblastic leukaemia (B-ALL), but not chronic myeloid leukaemia (CML), demonstrates cell type-specific signalling in Philadelphia chromosome-positive (Ph+) leukaemias.
  • Different therapeutic strategies are therefore needed for B-ALL and CML.
  • Thus, Src kinases provide a mechanism for resistance to the BCR-ABL kinase inhibitors and potential targets for B-ALL therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Burkitt Lymphoma / drug therapy. Burkitt Lymphoma / enzymology. Drug Delivery Systems / methods. Protein Kinase Inhibitors / therapeutic use. src-Family Kinases / antagonists & inhibitors

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  • (PMID = 15934919.001).
  • [ISSN] 1744-7631
  • [Journal-full-title] Expert opinion on therapeutic targets
  • [ISO-abbreviation] Expert Opin. Ther. Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; EC 2.7.10.2 / src-Family Kinases
  • [Number-of-references] 114
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16. Reske SN, Bunjes D, Buchmann I, Seitz U, Glatting G, Neumaier B, Kotzerke J, Buck A, Martin H, Döhner H, Bergmann L: Targeted bone marrow irradiation in the conditioning of high-risk leukaemia prior to stem cell transplantation. Eur J Nucl Med; 2001 Jul;28(7):807-15
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  • [Title] Targeted bone marrow irradiation in the conditioning of high-risk leukaemia prior to stem cell transplantation.
  • Disease recurrence following stem cell transplantation (SCT) remains a major problem.
  • Despite the sensitivity of leukaemias to chemotherapy and irradiation, conventional conditioning before SCT is limited by significant organ toxicity.
  • In this study, 27 patients with high-risk or relapsing leukaemia were treated with rhenium-188-labelled CD66a,b,c,e radioimmunoconjugates (188Re-mAb) specific for normal bone marrow in addition to conventional conditioning with high-dose chemotherapy and 12 Gy total body irradiation prior to SCT.
  • Mean radiation doses (Gy; range in parentheses) to relevant organs and whole body were as follows: 13.1 (6.5-22) to bone marrow, 11.6 (1.7-31.1) to spleen, 5.0 (2.0-11.7) to liver, 7.0 (2.3-11.6) to kidneys, 0.7 (0.3-1.3) to lungs and 1.4 (0.8-2.1) to the whole body.
  • Radioimmunotherapy with the bone marrow-seeking 188Re-labelled CD66 mAb can double the dose to bone marrow and spleen without undue extramedullary acute organ toxicity, when given in addition to high-dose chemotherapy and 12 Gy TBI before allogeneic SCT.
  • This intensified conditioning regimen may reduce the relapse rate of high-risk leukaemia.
  • [MeSH-major] Bone Marrow / radiation effects. Hematopoietic Stem Cell Transplantation. Leukemia / therapy. Radioimmunotherapy. Transplantation Conditioning
  • [MeSH-minor] Adolescent. Adult. Antibodies, Monoclonal / therapeutic use. Antigens, CD / immunology. Disease-Free Survival. Female. Humans. Male. Middle Aged. Radiation Dosage. Radioisotopes / therapeutic use. Recurrence. Rhenium / therapeutic use. Survival Rate. Whole-Body Irradiation

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  • (PMID = 11504076.001).
  • [ISSN] 0340-6997
  • [Journal-full-title] European journal of nuclear medicine
  • [ISO-abbreviation] Eur J Nucl Med
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Radioisotopes; 7440-15-5 / Rhenium
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17. Hamada A, Kawaguchi T, Nakano M: Clinical pharmacokinetics of cytarabine formulations. Clin Pharmacokinet; 2002;41(10):705-18
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  • Cytarabine (cytosine arabinoside, Ara-C) is an effective chemotherapeutic agent for the treatment of acute myelogenous leukaemia and lymphocytic leukaemias.
  • As cytarabine is an S-phase-specific drug, prolonged exposure of cells to cytotoxic concentrations is critical to achieve maximum cytotoxic activity.
  • Protection of cytarabine from fast degradation and elimination has been investigated by encapsulating the drug into pharmaceutically acceptable carriers.
  • Cytarabine encapsulated into multivesicular liposomes has been approved in several countries for the intrathecal treatment of lymphomatous meningitis.
  • [MeSH-minor] Animals. Area Under Curve. Chemistry, Pharmaceutical. Delayed-Action Preparations. Emulsions. Half-Life. Humans. Liposomes. Metabolic Clearance Rate. Neoplasms / drug therapy

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  • (PMID = 12162758.001).
  • [ISSN] 0312-5963
  • [Journal-full-title] Clinical pharmacokinetics
  • [ISO-abbreviation] Clin Pharmacokinet
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Delayed-Action Preparations; 0 / Emulsions; 0 / Liposomes; 04079A1RDZ / Cytarabine
  • [Number-of-references] 91
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18. Ng A, Taylor GM, Eden OB: Treatment-related leukaemia--a clinical and scientific challenge. Cancer Treat Rev; 2000 Oct;26(5):377-91
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  • [Title] Treatment-related leukaemia--a clinical and scientific challenge.
  • The development of a second tumour, including treatment-related leukaemia (TRL), is the most devastating complication of intensive cancer chemotherapy.
  • Most TRLs are myeloid leukaemias and carry an overall poor prognosis when compared with their de novo counterparts.
  • Despite the well known association with specific cytotoxic agents, improved understanding of the pathogenesis and risk factors of TRL is ultimately essential if we are to develop successful strategies for prevention and treatment.
  • Here we review these aspects, together with the clinical and diverse biological features of this complication and the efficacy of current therapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia / chemically induced. Leukemia, Radiation-Induced / physiopathology. Neoplasms, Second Primary / chemically induced

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  • [Copyright] Copyright 2000 Harcourt Publishers Ltd.
  • (PMID = 11006138.001).
  • [ISSN] 0305-7372
  • [Journal-full-title] Cancer treatment reviews
  • [ISO-abbreviation] Cancer Treat. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Enzyme Inhibitors
  • [Number-of-references] 148
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19. Saglio G, Cilloni D, Rancati F, Boano L: Glivec and CML: a lucky date. J Biol Regul Homeost Agents; 2004 Apr-Jun;18(2):246-51
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  • Chronic Myeloid Leukemia (CML) has always been an ideal model to understand the molecular pathogenesis of human leukaemias and the way to cure them.
  • This can be ascribed to the fact that CML was the first human cancer demonstrated to be strongly associated to the presence of a recurrent chromosomal translocation (the t(9;22)(q34;q11) that creates the Philadelphia (Ph)-chromosome) and to a specific molecular defect, the formation of a hybrid BCR-ABL gene that generates new fusion proteins endowed with a constitutive tyrosine-kinase (TK) activity, strongly implicated in the pathogenesis of the disease.
  • The introduction into clinical practice of imatinib, (Glivec, Gleevec, Novartis), a potent tyrosine kinase inhibitor of the Bcr-Abl protein as well as of a restricted number of other TKs, has not only produced a substantial improvement in the treatment of CML, but represents a major break-through in the perspective of opening a new era, that of molecularly targeted therapy, in the management of other types of leukemia, lymphoma and cancer in general.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / pharmacokinetics. Antineoplastic Agents / therapeutic use. Benzamides. Bone Marrow Transplantation. Clinical Trials as Topic. Drug Monitoring. Drug Resistance, Neoplasm / physiology. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / genetics. Fusion Proteins, bcr-abl / metabolism. Humans. Imatinib Mesylate. Interferon-alpha / therapeutic use. Leukemia / drug therapy. Leukemia / genetics. Leukemia / therapy. Philadelphia Chromosome. Protein Kinase Inhibitors / administration & dosage. Protein Kinase Inhibitors / pharmacokinetics. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / genetics. Protein-Tyrosine Kinases / metabolism. Treatment Outcome

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  • (PMID = 15739279.001).
  • [ISSN] 0393-974X
  • [Journal-full-title] Journal of biological regulators and homeostatic agents
  • [ISO-abbreviation] J. Biol. Regul. Homeost. Agents
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Interferon-alpha; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 48
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20. Storm HH, Klint A, Tryggvadóttir L, Gislum M, Engholm G, Bray F, Hakulinen T: Trends in the survival of patients diagnosed with malignant neoplasms of lymphoid, haematopoietic, and related tissue in the Nordic countries 1964-2003 followed up to the end of 2006. Acta Oncol; 2010 Jun;49(5):694-712
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  • [Title] Trends in the survival of patients diagnosed with malignant neoplasms of lymphoid, haematopoietic, and related tissue in the Nordic countries 1964-2003 followed up to the end of 2006.
  • BACKGROUND: Hodgkin lymphoma, Non-Hodgkin lymphoma, multiple myeloma, and acute and other leukaemias constitute about 7% of the overall cancer incidence and 8% of cancer mortality in the Nordic countries.
  • MATERIAL AND METHODS: Using the NORDCAN database 1964-2003, we estimated age-standardised incidence and mortality rates, 5-year relative survival, and excess mortality rates for varying follow-up periods, and age-specific 5-year relative survival by country, sex, and 5-year diagnostic period.
  • High 5-year relative survival ratios of over 80% were seen in the most recent period 1999-2003 for Hodgkin lymphoma, between 50 and 60% for Non-Hodgkin lymphoma, 38-49% for acute leukaemia and 60-73% for other leukaemia.
  • CONCLUSION: Although the recent trends and absolute levels of incidence, mortality and survival for the lympho-haematopoietic malignancies are similar, the consistently lower survival of Danish patients--irrespective of type of malignancy--points to an impact of co-morbidity related lifestyle factors, which may negatively affect the chemotherapy and radiation offered as standard treatments for these diseases.
  • [MeSH-major] Hematologic Neoplasms / mortality. Leukemia / mortality. Lymphoma / mortality

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  • (PMID = 20491526.001).
  • [ISSN] 1651-226X
  • [Journal-full-title] Acta oncologica (Stockholm, Sweden)
  • [ISO-abbreviation] Acta Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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21. Schmidmaier R, Baumann P: ANTI-ADHESION evolves to a promising therapeutic concept in oncology. Curr Med Chem; 2008;15(10):978-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ANTI-ADHESION evolves to a promising therapeutic concept in oncology.
  • All five classes of cell adhesion molecules (CAM) - integrins, cadherins, immunoglobulin-like CAMs, selectins and CD44s - are characteristically dysregulated in human cancer.
  • Furthermore, cell adhesion mediates drug resistance (CAM-DR) in multiple myeloma, malignant lymphoma, acute and chronic leukaemias, as well as in pancreatic cancer, neuroblastoma, small cell and non-small cell lung cancer, mesothelioma, colorectal carcinoma, and breast cancer.
  • Cell adhesion protects from death by radiation, genotoxic chemotherapy, or targeted pathway inhibitors.
  • Adhesion molecules are overexpressed on drug resistant cells (e.g. multiple myeloma or prostate cancer).
  • Very recently, several cell adhesion mediated survival pathways have been elucidated, with key mediators being LFA-1, VLA-4, FAK, ILK, Src, PI3K, Akt, Ras, MEK, Erk, HMG-CoA reductase, Rho, Rho kinase, PKC, and NFkB.
  • Because the surface and the intracellular targets are now known and because specific compounds are becoming increasingly available, first clinical trials regarding ANTI-ADHESION therapies are ongoing.
  • However, in comparison to the comprehensive preclinical and clinical knowledge about CAMs, the number of drugs developed thusfar is quite low.
  • ANTI-ADHESION strategies include targeting of surface antigens, inhibition of cell adhesion associated pathways, inhibition of CAM-DR, and targeted drug delivery.
  • As ANTI-ADHESION is based on general characteristics of cancer cells independent of specific disease entities or treatment modalities, it may become a successful, low-toxic and broadly applicable concept in cancer treatment.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cell Adhesion / drug effects. Cell Adhesion Molecules / antagonists & inhibitors. Neoplasms / drug therapy. Signal Transduction / drug effects


22. Hofmann WK, Baldus C, Uharek L, Thiel E: Therapeutic spectrum in the treatment of myelodysplastic syndromes. Expert Opin Pharmacother; 2004 Dec;5(12):2451-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapeutic spectrum in the treatment of myelodysplastic syndromes.
  • It is a clonal disorder, characterised by ineffective haematopoiesis, which can lead to either fatal cytopenias or acute myelogenous leukaemias.
  • Risk-adapted treatment strategies were established, due to the high median age (60 - 75 years) of the MDS patients and the individual history of the disease (i.e. number of cytopenias, cytogenetic changes, transfusion requirements).
  • Allogeneic bone marrow transplantation currently offers the only potentially curative treatment, but this form of therapy is not available for the 'typical' MDS patient, who is > 60 years of age.
  • Therapy with erythropoietin and granulocyte colony-stimulating factor has improved the quality of life of selected patients.
  • The development of target-specific therapies, including antibodies and small molecules directed against specific molecular alterations in MDS, with minimal adverse effects, is the hope for the future.
  • Furthermore, the innovative use of immunomodulatory agents and the optimising of cytotoxic treatment should continue to help in the treatment of MDS.
  • [MeSH-major] Erythropoietin / therapeutic use. Granulocyte Colony-Stimulating Factor / therapeutic use. Myelodysplastic Syndromes / drug therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Forecasting. Humans. Immunosuppressive Agents / therapeutic use. Oxides / therapeutic use. Transplantation, Autologous. Transplantation, Homologous

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  • (PMID = 15571463.001).
  • [ISSN] 1744-7666
  • [Journal-full-title] Expert opinion on pharmacotherapy
  • [ISO-abbreviation] Expert Opin Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Immunosuppressive Agents; 0 / Oxides; 11096-26-7 / Erythropoietin; 143011-72-7 / Granulocyte Colony-Stimulating Factor; S7V92P67HO / arsenic trioxide
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23. Treviño M, Prieto E, Peñalver D, Aguilera A, García-Zabarte A, García-Riestra C, Regueiro BJ: [Diarrhea caused by adenovirus and astrovirus in hospitalized immunodeficient patients]. Enferm Infecc Microbiol Clin; 2001 Jan;19(1):7-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Acute or chronic diarrheal illness are common complications in immunosuppressed patients such as human immunodeficiency virus (HIV)-infected, bone marrow or solid organ transplanted patients and those with leukaemias or other immune deficiency disorders.
  • Due to the importance of recognizing the feasible etiologies of diarrhea in order to give the proper antimicrobial chemotherapy or to avoid a misdiagnosis of rejection in the case of transplanted patients, we have investigated adenovirus and astrovirus antigen in faeces from different immunosuppressed patients.
  • The majority of the cases were related with intestinal bacterial diseases or other circumstances, such as Clostridium difficile infection, both associated with prolonged antimicrobial therapy.
  • An accurate diagnosis about diarrhea etiology is advisable in order to give a specific antimicrobial therapy, when it be necessary, or to avoid a misdiagnosis of rejection, in transplanted patients.

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  • (PMID = 11256256.001).
  • [ISSN] 0213-005X
  • [Journal-full-title] Enfermedades infecciosas y microbiología clínica
  • [ISO-abbreviation] Enferm. Infecc. Microbiol. Clin.
  • [Language] spa
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antibodies, Viral
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24. Ramshaw H, Lopez A, Bardy P: The development of cytokine receptor antagonists as potential therapeutic agents for the myeloproliferative disorders. Curr Pharm Des; 2002;8(5):357-68

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The development of cytokine receptor antagonists as potential therapeutic agents for the myeloproliferative disorders.
  • The aetiology of the myeloproliferative disorders and, in particular, of the myeloid leukaemias is unknown.
  • Chemotherapeutic agents are regularly used to treat patients with leukaemia but they are non-discriminatory treatments that kill both healthy and cancer cells.
  • Consequently patients receiving chemotherapy suffer unwanted toxicities in both the haematological and other systems.
  • Therapies that specifically target malignant cells sparing normal cells are being investigated in a number of contexts.
  • In this review we will discuss the myeloproliferative disorders in particular the leukaemias, the cytokines involved in leukaemogenesis, and the therapeutic potential of new agents that block specific cytokines.
  • [MeSH-minor] Animals. Cytokines / antagonists & inhibitors. Cytokines / physiology. Granulocyte-Macrophage Colony-Stimulating Factor / therapeutic use. Hematopoiesis. Humans. Recombinant Proteins / therapeutic use

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  • (PMID = 12069374.001).
  • [ISSN] 1381-6128
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cytokines; 0 / Receptors, Cytokine; 0 / Recombinant Proteins; 0 / granulocyte-macrophage colony-stimulating factor, Arg(21)-; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Number-of-references] 94
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25. Mauro MJ, Deininger MW: Management of drug toxicities in chronic myeloid leukaemia. Best Pract Res Clin Haematol; 2009 Sep;22(3):409-29
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Management of drug toxicities in chronic myeloid leukaemia.
  • Therapy for patients with chronic myeloid leukaemia has grown in complexity, first with the advent of the prototype ABL kinase inhibitor, imatinib, and subsequently with the availability of alternate (currently second-line) inhibitors.
  • Imatinib, dasatinib and nilotinib each have specific considerations regarding safety and toxicity, in addition to a limited number common to the class of ABL kinase inhibitors.
  • Optimal management of patients on therapy requires intimate knowledge not only of response criteria and of timing but also of potential toxicities and their basis, best approaches to avoid them, strategies to manage them when identified and how they may affect response to therapy and patient outcome.
  • With the availability of several approved kinase inhibitors and the ongoing development of additional therapies for Philadelphia chromosome positive (Ph+) leukaemias, there is increasing incorporation of toxicity considerations into decision making between agents.
  • [MeSH-major] Drug-Related Side Effects and Adverse Reactions / therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Protein Kinase Inhibitors / toxicity
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease Management. Drug Monitoring / methods. Drug Resistance, Neoplasm. Humans. Treatment Failure

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  • (PMID = 19959091.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors
  • [Number-of-references] 74
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26. Trotman J, Presgrave P, Kwan Y, Tiley C, Estell J, Watson AM, O'Brien TA, Peters D: Consensus guidelines for 'rainy day' autologous stem cell harvests in New South Wales. Intern Med J; 2008 Apr;38(4):229-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Consensus guidelines for 'rainy day' autologous stem cell harvests in New South Wales.
  • Autologous stem cell transplantation (ASCT) has a well-established role in the treatment of haematological malignancies.
  • Stem cells are commonly collected following salvage chemotherapy although there may be advantages in collecting earlier in the disease course.
  • Although there are few data to support RDH, there is increasing evidence that such harvests are being carried out, creating storage pressures in stem cell laboratories across New South Wales.
  • Using available evidence, guidelines were developed supporting RDH for specific patients with acute and chronic myeloid leukaemias, follicular and other lymphomas, and multiple myeloma.
  • Physician agreement with these disease-specific guidelines ranged between 58 and 100%.
  • [MeSH-major] Stem Cell Transplantation. Stem Cells. Tissue and Organ Harvesting

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  • [CommentIn] Intern Med J. 2008 Aug;38(8):680-1; author reply 681 [18808569.001]
  • [CommentIn] Intern Med J. 2008 Apr;38(4):227-8 [18380699.001]
  • (PMID = 18380700.001).
  • [ISSN] 1445-5994
  • [Journal-full-title] Internal medicine journal
  • [ISO-abbreviation] Intern Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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27. Sonneveld P, Pieters R: Immunophenotyping as a guide for targeted therapy. Best Pract Res Clin Haematol; 2003 Dec;16(4):629-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunophenotyping as a guide for targeted therapy.
  • Immunophenotyping of acute and chronic leukaemias has revealed many lineage- and differentiation-specific antigens.
  • It has now become possible to classify leukaemias according to their unique antigenic expression pattern.
  • Among many lineage- and differentiation-specific antigens, disease-specific antigens are increasingly recognized because of their specific prognostic or therapeutic relevance.
  • Expression of the multidrug resistance proteins of the ABC transporter family is associated with a poor response to treatment and a grave clinical prognosis.
  • Recently, attempts to reverse refractory disease by using P-glycoprotein inhibitors have been performed in acute myeloid leukaemia, so far without evidence of clinical benefit.
  • Other new leads to use antigen expression as a way of designing tumour-specific therapy have resulted in imatinib and Flt3 inhibitors which target tyrosine kinases in the leukaemic cell.
  • The development of an antibody-calicheamycin complex directed against the myeloid-specific antigen CD33 has shown clinical activity in patients with relapsed acute myeloid leukaemia.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Drug Delivery Systems. Immunophenotyping. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. P-Glycoproteins / antagonists & inhibitors. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Drug Resistance, Multiple / genetics. Drug Resistance, Neoplasm / genetics. Humans. Proto-Oncogene Proteins / antagonists & inhibitors. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Receptor Protein-Tyrosine Kinases / genetics. Sialic Acid Binding Ig-like Lectin 3. fms-Like Tyrosine Kinase 3

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  • (PMID = 14592647.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / P-Glycoproteins; 0 / Proto-Oncogene Proteins; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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28. Raida L, Papajík T, Pikalová Z, Zapletalová J, Indrák K: [Therapeutic effectiveness of cladribine and cellular immunodeficiency--related effects in hairy-cell leukemia?]. Vnitr Lek; 2002 May;48(5):384-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Therapeutic effectiveness of cladribine and cellular immunodeficiency--related effects in hairy-cell leukemia?].
  • The high therapeutic efficiency of lymphotoxic purine analogues, pentostatin and cladribine in hairy cell leukaemia which express the antigen CD25 (alpha chain interleukin-2 receptor) suggests the hypothesis whether protracted cellular immunodeficiency after treatment does not represent an important mechanism of control of this specific lymphoproliferation.
  • The authors analyzed a group of 45 patients with CD25-positive hairy cell leukaemia treated with cladribine.
  • In addition to the therapeutic response they evaluated also the state of cellular immunity during the subsequent months and years following cladribine administration.
  • Although this retrospective analysis provides only limited information we can deduce from it a long-term decline of CD4 lymphocytes correlating with the relatively low incidence of clinical progression of hairy cell leukaemias.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cladribine / therapeutic use. Immunosuppressive Agents / therapeutic use. Leukemia, Hairy Cell / drug therapy. Lymphocytes / immunology

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  • (PMID = 12061204.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents; 47M74X9YT5 / Cladribine
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29. Gandhi V, Plunkett W: Cellular and clinical pharmacology of fludarabine. Clin Pharmacokinet; 2002;41(2):93-103
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In the past decade, fludarabine has had a major impact in increasing the effectiveness of treatment of patients with indolent B-cell malignancies.
  • Other strategies have used fludarabine to reduce immunological function, thus facilitating non-myeloablative stem cell transplants.
  • Although F-ara-A is not a good substrate for this enzyme, the high specific activity of this protein results in efficient phosphorylation of F-ara-A in certain tissues.
  • Secondarily, incorporation into RNA and inhibition of transcription has been shown in cell lines.
  • Serial sampling of leukaemia cells from patients receiving these standard doses of fludarabine has demonstrated that the peak concentrations of F-ara-ATP are achieved 4 hours after start of fludarabine infusion.
  • Although there is heterogeneity among individuals with respect to rate of F-ara-ATP accumulation, the peak concentrations are generally proportional to the dose of the drug.
  • As a single agent fludarabine has been effective for the indolent leukaemias.
  • Biochemical modulation strategies resulted in enhanced accumulation of cytarabine triphosphate and led to the use of fludarabine for the treatment of acute leukaemias.
  • Combination of fludarabine with DNA damaging agents to inhibit DNA repair processes has been highly effective for indolent leukaemias and lymphomas.
  • This may be useful in the design of future therapeutic approaches.
  • [MeSH-major] Antineoplastic Agents / pharmacokinetics. Leukemia / drug therapy. Lymphoma / drug therapy. Vidarabine / pharmacokinetics
  • [MeSH-minor] Biological Availability. DNA (Cytosine-5-)-Methyltransferase / antagonists & inhibitors. Deoxycytidine Kinase / metabolism. Drug Evaluation, Preclinical. Humans. Phosphorylation. Vidarabine Phosphate / analogs & derivatives. Vidarabine Phosphate / metabolism

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  • (PMID = 11888330.001).
  • [ISSN] 0312-5963
  • [Journal-full-title] Clinical pharmacokinetics
  • [ISO-abbreviation] Clin Pharmacokinet
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA32839; United States / NCI NIH HHS / CA / CA55164; United States / NCI NIH HHS / CA / CA57629
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 106XV160TZ / Vidarabine Phosphate; 1X9VK9O1SC / fludarabine phosphate; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.7.1.74 / Deoxycytidine Kinase; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  • [Number-of-references] 68
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