[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 14 of about 14
1. Clavio M, Gatto S, Beltrami G, Cerri R, Carrara P, Pierri I, Canepa L, Miglino M, Balleari E, Masoudi B, Damasio E, Ghio R, Sessarego M, Gobbi M: First line therapy with fludarabine combinations in 42 patients with either post myelodysplastic syndrome or therapy related acute myeloid leukaemia. Leuk Lymphoma; 2001 Jan;40(3-4):305-13
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] First line therapy with fludarabine combinations in 42 patients with either post myelodysplastic syndrome or therapy related acute myeloid leukaemia.
  • Acute myeloid leukaemias (AML) evolving from a myelodysplastic syndrome (MDS) or secondary to chemoradiotherapy frequently display unfavorable biologic characteristics.
  • This may explain the lower remission rate obtained with conventional chemotherapy.
  • At the time of this analysis, after a mean follow-up of 12 months, the mean duration of CR is 16 months (range 3-66) and the mean survival is 11 months (range 1-67).
  • The median time to granulocyte recovery (neutrophils > 0.5 x 10(9)/l) was 20 days (range 12-39) and 50 x 10(9)/l platelets were reached at a median of 26 days (range 9-56).
  • Taken together, these Fludarabine containing regimens proved to be an effective and tolerable treatment for patients with secondary AML.
  • Patients above 70 years of age may also benefit from this therapy, however the problem of treating patients with adverse chromosomal abnormalities still remains unresolved.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / pathology. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Adult. Aged. Cohort Studies. Cytarabine / administration & dosage. Cytarabine / toxicity. Female. Granulocyte Colony-Stimulating Factor / administration & dosage. Granulocyte Colony-Stimulating Factor / toxicity. Humans. Male. Middle Aged. Neoplasms, Second Primary / complications. Neoplasms, Second Primary / drug therapy. Neoplasms, Second Primary / mortality. Remission Induction. Survival Rate


2. Braun T, Fenaux P: Farnesyltransferase inhibitors and their potential role in therapy for myelodysplastic syndromes and acute myeloid leukaemia. Br J Haematol; 2008 May;141(5):576-86
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Farnesyltransferase inhibitors and their potential role in therapy for myelodysplastic syndromes and acute myeloid leukaemia.
  • Novel strategies are required for treatment of acute myeloid leukaemia (AML) and higher risk myelodysplastic syndrome (MDS) patients who are not eligible for intensive chemotherapy and/or allogenic stem cell transplantation.
  • Clinical phase II studies with the oral FTIs tipifarnib and lonafarnib in previously untreated AML, MDS and chronic myelomonocytic leukaemia yielded rather encouraging results while results in relapsed and/or refractory AML were disappointing.
  • Clinical responses were not related to RAS mutations, suggesting additional actions of FTIs on other molecular targets.
  • The combination of existing FTIs with other treatments, such as chemotherapy (in AML) and hypomethylating agents (in MDS and AML), is under investigation.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Farnesyltranstransferase / antagonists & inhibitors. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


3. Abrahamsen AF: [Acute myelogenous leukemia and myelodysplastic syndrome after treatment with cytostatic agents]. Tidsskr Nor Laegeforen; 2000 Sep 10;120(21):2542-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Acute myelogenous leukemia and myelodysplastic syndrome after treatment with cytostatic agents].
  • INTRODUCTION: The introduction of high dose chemotherapy of cancer has been followed by an increased incidence of therapy-related acute myeloid leukaemia and myelodysplastic syndrome.
  • RESULTS: After standard doses of leukaemogenic drugs the incidence of acute myeloid leukaemia and myelodysplastic syndrome is reported to be 0-4%, increasing to 8-10% after high dose therapy.
  • At diagnosis of acute myeloid leukaemia and myelodysplastic syndrome, most of the patients have chromosomal abnormalities.
  • INTERPRETATION: The prognosis of therapy-related acute myeloid leukaemia and myelodysplastic syndrome is poor compared to that in primary acute myeloid leukaemia and myelodysplastic syndrome.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced
  • [MeSH-minor] Dose-Response Relationship, Drug. Humans


Advertisement
4. Nivatpumin PJ, Gore SD: Emerging drugs for the treatment of myelodysplastic syndrome. Expert Opin Emerg Drugs; 2005 Aug;10(3):569-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Emerging drugs for the treatment of myelodysplastic syndrome.
  • Myelodysplastic syndromes (MDS) are a heterogeneous group of clonal haematopoietic stem cell disorders characterised by ineffective haematopoiesis and an increased risk of developing acute myeloid leukaemia.
  • However, the majority of patients are not eligible for this therapy, due to excessive treatment-related morbidity and mortality or lack of a suitable donor.
  • As a result, the need for alternative therapies is great.
  • Our improved understanding of the molecular pathogenesis of MDS has resulted in several new promising therapeutic agents.
  • [MeSH-major] Drug Industry / trends. Drugs, Investigational / therapeutic use. Myelodysplastic Syndromes / drug therapy


5. Karran P, Offman J, Bignami M: Human mismatch repair, drug-induced DNA damage, and secondary cancer. Biochimie; 2003 Nov;85(11):1149-60
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human mismatch repair, drug-induced DNA damage, and secondary cancer.
  • More recently, it has become apparent that MMR defects are common in acute myeloid leukaemia/myelodysplastic syndrome (AML/MDS) that follows successful chemotherapy for a primary malignancy.
  • Therapy-related haematological malignancies are often associated with treatment with alkylating agents.
  • There is also evidence for an association between MMR deficient AML/MDS and immunosuppressive treatment with thiopurine drugs.
  • Here we review how MMR interacts with alkylating agent and thiopurine-induced DNA damage and suggest possible ways in which MMR defects may arise in therapy-related AML/MDS.
  • [MeSH-major] Base Pair Mismatch / genetics. DNA Damage / drug effects. DNA Repair / genetics. DNA Repair / physiology. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced


6. Au WY, Fung A, Man C, Ma SK, Wan TS, Liang R, Kwong YL: Aberrant p15 gene promoter methylation in therapy-related myelodysplastic syndrome and acute myeloid leukaemia: clinicopathological and karyotypic associations. Br J Haematol; 2003 Mar;120(6):1062-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant p15 gene promoter methylation in therapy-related myelodysplastic syndrome and acute myeloid leukaemia: clinicopathological and karyotypic associations.
  • Seventeen patients with therapy-related myelodysplastic syndrome/acute myeloid leukaemia (t-MDS/AML) were examined for aberrant p15 gene methylation by methylation-specific polymerase chain reaction.
  • Ten patients (58%) showed p15 methylation, which was significantly related to monosomy/deletion of chromosome 7q, but not to antecedent chemotherapy, blast count, leukaemic evolution or survival.
  • [MeSH-major] Cell Cycle Proteins. Leukemia, Myeloid / metabolism. Myelodysplastic Syndromes / metabolism. Promoter Regions, Genetic. Transcription Factors / genetics. Tumor Suppressor Proteins
  • [MeSH-minor] Acute Disease. Adult. Aged. Bone Marrow Transplantation. Cyclin-Dependent Kinase Inhibitor p15. DNA Methylation. Female. Humans. Male. Middle Aged. Polymerase Chain Reaction / methods. Time Factors

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12648079.001).
  • [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 / CDKN2B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins
  •  go-up   go-down


7. Bolufer P, Barragan E, Collado M, Cervera J, López JA, Sanz MA: Influence of genetic polymorphisms on the risk of developing leukemia and on disease progression. Leuk Res; 2006 Dec;30(12):1471-91
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The polymorphisms of genes encoding drug-metabolising enzymes (CYP family, NQO1, GSTT1, GSTM1, GSTP1), enzymes involved in folate metabolism (MTHFR, TYMS, SHMT1, MTRR), and DNA repair enzymes (XPD, XPG, RAD51, XRCC1, XRCC3, CHEK2, ATM) were considered in the review.
  • RESULTS: There was a good agreement on the influence of NQO1*2 polymorphism and those of the enzymes involved in DNA repair with the increased risk of therapy-related leukemia/myelodysplastic syndrome.
  • Most studies found a strong association between the polymorphisms MTHFR, C677T or A1298C, and NQO1*2 or *3 and the risk of acute lymphoblastic leukemia (ALL).
  • In addition, most of the studies reported an association between GSTT1 deletions and an increased risk of de novo acute myeloid leukemia.
  • CONCLUSION: The reports reviewed support the hypothesis that several low-penetrance genes with multiplicative effects together with dietary effects, ambient exposition, and individual immune system responses, may account for the risk of leukaemia.


8. Buchmann I, Meyer RG, Herr W, Helisch A, Bartenstein P: [Radioimmunotherapy for treatment of acute myeloid leukaemia and myelodysplastic syndrome: conceptual chances]. Nuklearmedizin; 2005;44(3):107-17; quiz N21-2
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Radioimmunotherapy for treatment of acute myeloid leukaemia and myelodysplastic syndrome: conceptual chances].
  • [Transliterated title] Radioimmuntherapien zur Behandlung der akuten myeloischen Leukämie und des myelodysplastischen Syndroms: Konzeptionelle Chancen.
  • The prognosis of patients with acute myeloid leukaemia (AML) has improved considerably by introduction of aggressive consolidation chemotherapy and haematopoietic stem cell transplantation (SCT).
  • The most common cause of treatment failure is relapse.
  • Additionally, mortality rates are significantly increased by therapy-related causes such as toxicity of chemotherapy and complications of SCT.
  • Including radioimmunotherapies in the treatment of AML and myelodyplastic syndrome (MDS) allows for the achievement of a pronounced antileukaemic effect for the reduction of relapse rates on the one hand.
  • On the other hand, no increase of acute toxicity and later complications should be induced.
  • This paper provides a systematic and critical review of the currently used radionuclides and immunoconjugates for the treatment of AML and MDS and summarizes the literature on primary tumour cell reductive radioimmunotherapies on the one hand and conditioning radioimmunotherapies before SCT on the other hand.
  • [MeSH-major] Leukemia, Myeloid, Acute / radiotherapy. Myelodysplastic Syndromes / radiotherapy. Radioimmunotherapy


9. Bolufer P, Collado M, Barragan E, Calasanz MJ, Colomer D, Tormo M, González M, Brunet S, Batlle M, Cervera J, Sanz MA: Profile of polymorphisms of drug-metabolising enzymes and the risk of therapy-related leukaemia. Br J Haematol; 2007 Feb;136(4):590-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Profile of polymorphisms of drug-metabolising enzymes and the risk of therapy-related leukaemia.
  • Therapy-related acute myeloid leukaemia/myelodysplastic syndrome (t-AML/t-MDS) results from an impaired ability to detoxify chemotherapeutic drugs or repair drug-induced genetic damage caused by genetic polymorphisms in enzymes involved in the metabolism of drugs.
  • We analysed the prevalence of genetic polymorphisms of CYP1A1*2A(T6235C), CYP2E1*5B(C-1019T), CYP3A4*1B(A-290G), del{GSTT1}, del{GSTM1}, NQO1*2(C609T), MTHFR(C677T) and TYMS 2R/3R in 78 t-AML/t-MDS and 458 normal individuals (control group, CG) using real-time and conventional polymerase chain reaction (PCR)-based methods.
  • Thus, the profiles of genetic polymorphisms of drug-metabolising enzymes might explain the increased risk to t-AML/t-MDS observed in some patients treated with polychemotherapy.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / genetics. Polymorphism, Genetic
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Cytochrome P-450 CYP1A1 / genetics. Female. Genetic Predisposition to Disease. Genotype. Glutathione Transferase / genetics. Humans. Inactivation, Metabolic / genetics. Infant. Male. Middle Aged. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / enzymology. Myelodysplastic Syndromes / genetics. NAD(P)H Dehydrogenase (Quinone) / genetics. Neoplasm Proteins / genetics. Retrospective Studies

  • Pharmacogenomics Knowledge Base. meta-databases - Pharmacogenomic Annotation 827860313 for PMID:17367411 [PharmGKB] .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17367411.001).
  • [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 / Antineoplastic Agents; 0 / Neoplasm Proteins; EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase
  •  go-up   go-down


10. Anargyrou K, Vaiopoulos G, Terpos E, Tsironi M, Konstantopoulos K, Samarkos M, Meletis J: Low dose melphalan is a treatment option in elderly patients with high risk myelodysplastic syndrome or secondary acute myeloblastic leukaemia. Haematologia (Budap); 2002;32(2):169-73
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low dose melphalan is a treatment option in elderly patients with high risk myelodysplastic syndrome or secondary acute myeloblastic leukaemia.
  • We present the case of a 71 year-old man with secondary acute myeloblastic leukemia, who was successfully treated with low dose melphalan plus Epo plus G-CSF.
  • We treated the patient with 2 mg of melphalan once a day orally, G-CSF 5 mg/kg 3 times a week and Epo 10.000 ui subcutaneously 3 times a week until the maximum response was obtained.
  • Complete remission was achieved after 16 weeks of continuous treatment.
  • Treatment-related toxicity was not significant.
  • We recommend the use of low dose melphalan in elderly patients with high risk MDS as a treatment option.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Melphalan / administration & dosage. Myelodysplastic Syndromes / drug therapy
  • [MeSH-minor] Aged. Anemia, Refractory, with Excess of Blasts / drug therapy. Drug Therapy, Combination. Erythropoietin / administration & dosage. Granulocyte Colony-Stimulating Factor / administration & dosage. Humans. Male. Remission Induction. Risk Assessment


11. Díaz Beveridge R, Aparicio Urtasun J: [Therapy-related acute leukaemia and myelodysplastic syndrome]. An Med Interna; 2003 May;20(5):257-68
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Therapy-related acute leukaemia and myelodysplastic syndrome].
  • [Transliterated title] Leucemias agudas y síndromes mielodisplásicos secundarios al tratamiento oncológico.
  • Secondary hematological malignancies represent a severe complication of cancer treatment.
  • Their real incidence is unknown because of the heterogeneity of primary tumors, their therapies, and their prognosis.
  • The usual presentation is an acute leukemia or myelodysplastic syndrome.
  • Two different diseases have been described with particular clinical and cytogenetic features, namely the one associated with alkylating drugs and that related to epipodophylotoxins.
  • Conventional chemotherapy is mainly palliative, whereas allogenic transplantation allows the cure of a small percentage of cases.
  • Thus, potential curative therapies for solid tumors should be optimized and patients maintained in long-term surveillance programs.
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Agents, Phytogenic / adverse effects. Leukemia, Myeloid / chemically induced. Myelodysplastic Syndromes / chemically induced. Neoplasms, Second Primary / chemically induced. Podophyllotoxin / adverse effects
  • [MeSH-minor] Acute Disease. Bone Marrow Transplantation. Female. Hematopoietic Stem Cell Transplantation. Humans. Male. Neoplasms / drug therapy. Palliative Care. Prognosis

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • Hazardous Substances Data Bank. PODOFILOX .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12831302.001).
  • [ISSN] 0212-7199
  • [Journal-full-title] Anales de medicina interna (Madrid, Spain : 1984)
  • [ISO-abbreviation] An Med Interna
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; L36H50F353 / Podophyllotoxin
  • [Number-of-references] 83
  •  go-up   go-down


12. Bergh J, Wiklund T, Erikstein B, Lidbrink E, Lindman H, Malmström P, Kellokumpu-Lehtinen P, Bengtsson NO, Söderlund G, Anker G, Wist E, Ottosson S, Salminen E, Ljungman P, Holte H, Nilsson J, Blomqvist C, Wilking N: Tailored fluorouracil, epirubicin, and cyclophosphamide compared with marrow-supported high-dose chemotherapy as adjuvant treatment for high-risk breast cancer: a randomised trial. Scandinavian Breast Group 9401 study. Lancet; 2000 Oct 21;356(9239):1384-91
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tailored fluorouracil, epirubicin, and cyclophosphamide compared with marrow-supported high-dose chemotherapy as adjuvant treatment for high-risk breast cancer: a randomised trial. Scandinavian Breast Group 9401 study.
  • BACKGROUND: Chemotherapy drug distribution varies greatly among individual patients.
  • Therefore, we developed an individualised fluorouracil, epirubicin, cyclophosphamide (FEC) regimen to improve outcomes in patients with high-risk early breast cancer.
  • We then did a randomised trial to compare this individually tailored FEC regimen with conventional adjuvant chemotherapy followed by consolidation with high-dose chemotherapy with stem-cell support.
  • METHODS: 525 women younger than 60 years of age with high-risk primary breast cancer were randomised after surgery to receive nine cycles of tailored FEC to haematological equitoxicity with granulocyte colony-stimulating factor (G-CSF) support (n=251), or three cycles of FEC at standard doses followed by high-dose chemotherapy with cyclophosphamide, thiotepa, and carboplatin (CTCb), and peripheral-blood stem-cell or bone-marrow support (n=274).
  • Both groups received locoregional radiation therapy and tamoxifen for 5 years.
  • Patients in the CTCb group experienced more grade 3 or 4 acute toxicity compared with the tailored FEC group (p<0.0001).
  • Two treatment-related deaths (0.7%) occurred in the CTCb group.
  • Six patients in the tailored FEC group developed acute myeloid leukaemia and three developed myelodysplastic syndrome.
  • INTERPRETATION: Tailored FEC with G-CSF support resulted in a significantly improved relapse-free survival and fewer grade 3 and 4 toxicities compared with marrow-supported high-dose chemotherapy with CTCb as adjuvant therapy of women with high-risk primary breast cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Algorithms. Carboplatin / administration & dosage. Carboplatin / adverse effects. Chemotherapy, Adjuvant. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Disease-Free Survival. Epirubicin / administration & dosage. Epirubicin / adverse effects. Female. Fluorouracil / administration & dosage. Fluorouracil / adverse effects. Granulocyte Colony-Stimulating Factor / therapeutic use. Hematopoietic Stem Cell Transplantation. Humans. Infusions, Intravenous. Leukemia, Myeloid / chemically induced. Lymphatic Metastasis. Mastectomy, Segmental. Middle Aged. Proportional Hazards Models. Sweden. Thiotepa / administration & dosage. Thiotepa / adverse effects

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. CARBOPLATIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • Hazardous Substances Data Bank. THIO-TEPA .
  • Hazardous Substances Data Bank. EPIRUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Lancet 2000 Dec 23-30;356(9248):2196
  • (PMID = 11052580.001).
  • [ISSN] 0140-6736
  • [Journal-full-title] Lancet (London, England)
  • [ISO-abbreviation] Lancet
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor; 3Z8479ZZ5X / Epirubicin; 8N3DW7272P / Cyclophosphamide; 905Z5W3GKH / Thiotepa; BG3F62OND5 / Carboplatin; U3P01618RT / Fluorouracil; CTCb regimen; FEC protocol
  •  go-up   go-down


13. Kropff MH, Lang N, Bisping G, Dominé N, Innig G, Hentrich M, Mitterer M, Südhoff T, Fenk R, Straka C, Heinecke A, Koch OM, Ostermann H, Berdel WE, Kienast J: Hyperfractionated cyclophosphamide in combination with pulsed dexamethasone and thalidomide (HyperCDT) in primary refractory or relapsed multiple myeloma. Br J Haematol; 2003 Aug;122(4):607-16
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Sixty patients with advanced multiple myeloma received 2-6 monthly treatment courses combining hyperfractionated cyclophosphamide (300 mg/m2 i.v. over 3 h q 12 h x 6, d 1-3) with pulsed dexamethasone (20 mg/m2/d p.o., d 1-4, 9-12, 17-20) and once daily thalidomide at individually escalating doses (100-400 mg/d) depending on tolerability (HyperCDT).
  • During at least one treatment cycle, 67% of patients experienced grade 4 neutropenia resulting in 17% grade 3 and 9% grade 4 infections.
  • Side-effects, presumably related to thalidomide, included neuropathy (40% grade 2, 16% grade 3), constipation (17%), oedema (5%), bradycardia (5%), skin reactions (3%), cerebrovascular events (5%) and deep vein thromboses (8%).
  • Thromboses were not related to known thrombophilic risk factors.
  • Four patients with prior myeloma therapy > 50 months developed myelodysplastic syndrome or secondary acute myeloid leukaemia 2-4 months after study entry.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Multiple Myeloma / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Brain Ischemia / chemically induced. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Dexamethasone / administration & dosage. Dexamethasone / adverse effects. Disease-Free Survival. Drug Administration Schedule. Female. Follow-Up Studies. Hematologic Diseases / chemically induced. Humans. Leukemia, Myeloid / chemically induced. Male. Middle Aged. Myelodysplastic Syndromes / chemically induced. Neoplasms, Second Primary / chemically induced. Opportunistic Infections / chemically induced. Recurrence. Survival Analysis. Survival Rate. Thalidomide / administration & dosage. Thalidomide / adverse effects. Treatment Outcome. Venous Thrombosis / chemically induced

  • Genetic Alliance. consumer health - Multiple myeloma.
  • MedlinePlus Health Information. consumer health - Multiple Myeloma.
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. THALIDOMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12899716.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 4Z8R6ORS6L / Thalidomide; 7S5I7G3JQL / Dexamethasone; 8N3DW7272P / Cyclophosphamide; hyperCDT protocol
  •  go-up   go-down


14. Fern L, Pallis M, Ian Carter G, Seedhouse C, Russell N, Byrne J: Clonal haemopoiesis may occur after conventional chemotherapy and is associated with accelerated telomere shortening and defects in the NQO1 pathway; possible mechanisms leading to an increased risk of t-AML/MDS. Br J Haematol; 2004 Jul;126(1):63-71
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clonal haemopoiesis may occur after conventional chemotherapy and is associated with accelerated telomere shortening and defects in the NQO1 pathway; possible mechanisms leading to an increased risk of t-AML/MDS.
  • The molecular pathogenesis of therapy-related acute myeloid leukaemia/myelodysplastic syndrome (t-AML/MDS) remains uncertain.
  • Moreover, accelerated telomere shortening may be induced by replicative stress or oxidative damage, leading to genomic instability, and inactivating polymorphisms of the gene encoding NADPH-quinone oxidoreductase (NQO1) are more frequently observed in patients with t-AML.
  • We studied clonal haemopoiesis, telomere length and NQO1 status in 146 patients receiving conventional chemotherapy for non-myeloid malignancies.
  • Telomere length was reduced in patients following chemotherapy (n = 52) compared with controls (n = 42) (P < 0.001), particularly in those with clonal haemopoiesis (P < 0.002).
  • Whilst there was a trend towards telomere shortening in control subjects polymorphic for NQO1-187Ser (n = 12), chemotherapy-exposed patients polymorphic for the NQO1-187Ser allele (n = 29) had significantly shorter telomeres (P < 0.001).
  • Furthermore, chemotherapy-treated patients with the NQO1-187Ser, polymorphism were more likely to develop clonal haemopoiesis than patients with wild type NQO1 (odds ratio = 7; 1.16-42.6).
  • We conclude that a switch to clonal haemopoiesis may occur after conventional chemotherapy and lead to accelerated telomere shortening.
  • [MeSH-major] Hematopoiesis. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. NAD(P)H Dehydrogenase (Quinone) / genetics. Stem Cell Transplantation / adverse effects. Telomere / ultrastructure

  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15198733.001).
  • [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] EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human
  •  go-up   go-down






Advertisement