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1. Lönnerholm G, Thörn I, Sundström C, Frost BM, Abrahamsson J, Behrendtz M, Heldrup J, Jacobsson S, Li A, Olofsson T, Porwit A, Söderhäll S, Larsson R, Forestier E: In vitro cellular drug sensitivity at diagnosis is correlated to minimal residual disease at end of induction therapy in childhood acute lymphoblastic leukemia. Leuk Res; 2009 Jan;33(1):46-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro cellular drug sensitivity at diagnosis is correlated to minimal residual disease at end of induction therapy in childhood acute lymphoblastic leukemia.
  • Leukemic cells from 85 children with newly diagnosed precursor B-lineage ALL were tested for in vitro drug sensitivity to a panel of anti-cancer drugs.
  • There was a significant correlation between MRD day 29 and in vitro sensitivity to prednisolone (p<0.001) and doxorubicin (p=0.017), drugs administered during induction therapy.
  • Thus, data show that in vitro drug sensitivity at diagnosis is correlated to cell kill during induction therapy as measured by MRD day 29.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoplasm, Residual. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


2. Styczynski J: Drug resistance in childhood acute myeloid leukemia. Curr Pharm Biotechnol; 2007 Apr;8(2):59-75
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  • [Title] Drug resistance in childhood acute myeloid leukemia.
  • Therapy results in childhood AML differ from those of ALL.
  • The development of drug resistance is the limiting factor in the therapy of AML.
  • Different problems of drug resistance in childhood AML, with emphasis to age and in comparison to adult AML are presented.
  • In vitro and in vivo aspects are discussed, together with mechanisms of resistance to cytostatic drugs, focused on clinical relevance of cellular drug resistance profile and its prognostic value.
  • Possibilities of modulation and circumvention of drug resistance are reviewed, with stress on new drugs being tested.
  • Taking into account both children and adults, it seems that age is adversely related to therapy outcome in AML, and the percentage of patients with favorable cytogenetics decreases with age; however, age is positively correlated with multi-drug resistance and the proportion of patients with unfavorable cytogenetics.
  • BCRP, PGP and MRP's are preferentially expressed in leukemic stem cells, making this disease drug resistant.
  • Cellular drug resistance in AML cells seems to be similar throughout all other age groups, however the higher the age, the worse the outcome.
  • In childhood AML, no drug is more effective in comparison to ALL, and cellular drug resistance is partially related to chromosomal abnormalities.
  • Pediatric and adult AML, respectively, are possibly equally drug resistant on initial diagnosis and at relapse.
  • In contrast to ALL, the prognostic value of in vitro drug resistance in childhood AML has not been well documented yet.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / epidemiology. Neoplasm Recurrence, Local / epidemiology. Neoplasm Recurrence, Local / prevention & control


3. Clausen OP, Olsen G, Tjønnfjord GE: [Flow cytometry--use in cell biology and benefits in clinical medicine]. Tidsskr Nor Laegeforen; 2000 Feb 10;120(4):489-95
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  • [Title] [Flow cytometry--use in cell biology and benefits in clinical medicine].
  • The method has been increasingly used in the context of medical diagnosis and prognosis over the last ten years.
  • For immunophenotyping of acute leukaemias, flow cytometry is used routinely in all university hospitals in Norway.
  • In diagnostic pathology, DNA flow cytometry is used for analysis of DNA ploidy and S-phase fractions in malignant tumours.
  • DNA aneuploidy is a strong prognostic factor in some childhood tumours and in gynaecological malignant tumours, and flow cytometry is used in tumour biology for measurements of growth and apoptotic cell death.
  • Furthermore, the method is an important research tool in many areas of biomedical research for detection of structural and functional cellular features.
  • [MeSH-minor] Animals. DNA / analysis. DNA, Neoplasm / genetics. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Leukemia / genetics. Leukemia / immunology. Leukemia / pathology. Lymphoma / genetics. Lymphoma / immunology. Lymphoma / pathology. Ploidies. Prognosis

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  • (PMID = 10833942.001).
  • [ISSN] 0029-2001
  • [Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række
  • [ISO-abbreviation] Tidsskr. Nor. Laegeforen.
  • [Language] nor
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] NORWAY
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 9007-49-2 / DNA
  • [Number-of-references] 20
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4. Casale F, D'Angelo V, Addeo R, Caraglia M, Crisci S, Rondelli R, Di Tullio MT, Indolfi P: P-glycoprotein 170 expression and function as an adverse independent prognostic factor in childhood acute lymphoblastic leukemia. Oncol Rep; 2004 Dec;12(6):1201-7
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  • [Title] P-glycoprotein 170 expression and function as an adverse independent prognostic factor in childhood acute lymphoblastic leukemia.
  • Little is known about the prognostic role of multidrug resistance (MDR) in newly diagnosed childhood acute lymphoblastic leukemia (ALL).
  • P-glycoprotein 170 (MDR1), a cellular drug efflux pump, is thought to be one of the major causes of MDR.
  • The aim of this retrospective study was to evaluate in 85 children with ALL the impact of the MDR1 product of the mdr-1 gene on the achievement of complete remission (CR) and outcome.
  • At diagnosis, 40 patients (47%) expressed MDR1 protein at significant levels, and 45 (53%) were MDR1 negative.
  • Our results, derived from a monocentric study, demonstrate that MDR1 expression in childhood ALL is an independent adverse prognostic factor on outcome, and could be a useful biological marker of response in these patients.
  • [MeSH-major] Biomarkers, Tumor / analysis. P-Glycoprotein / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology


5. Ramakers-van Woerden NL, Pieters R, Slater RM, Loonen AH, Beverloo HB, van Drunen E, Heyman M, Moreno TC, Rots MG, van Wering ER, Kamps WA, Janka-Schaub GE, Veerman AJ: In vitro drug resistance and prognostic impact of p16INK4A/P15INK4B deletions in childhood T-cell acute lymphoblastic leukaemia. Br J Haematol; 2001 Mar;112(3):680-90
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  • [Title] In vitro drug resistance and prognostic impact of p16INK4A/P15INK4B deletions in childhood T-cell acute lymphoblastic leukaemia.
  • p16 gene deletions are present in about 70% of primary paediatric T-cell acute lymphoblastic leukaemia (T-ALL) and 20% of common/precursor B-cell ALL cases.
  • We studied the relationship between p16/p19ARF deletions, using fluorescence in situ hybridization, and in vitro drug resistance and prognosis in childhood T-ALL at diagnosis.
  • The cellular drug resistance was measured with the methyl thiazol tetrazoliumbromide assay using a panel of drugs and the thymidylate synthase inhibition assay for methotrexate.
  • There was a complete overlap of individual LC50 values of p16 gene homozygously deleted and p16 germ-line cases for most of the nine classes of drugs tested.
  • The homozygously deleted p16 T-ALL patients (n = 34) treated with the modern multiagent chemotherapy schemes of the Dutch Childhood Leukaemia Study Group ALL-VII/-VIII or Co-operative ALL-92/-97 protocols have a significantly lower 5-year disease-free survival (DFS) than germ-line p16 T-ALL (n = 25) (65.1 +/- 9.1% vs. 95.5 +/- 4.4%, Plog rank = 0.021).
  • Hence, this study identifies a subpopulation of primary childhood T-ALL that appears to have an extremely high DFS.
  • However, the observed differences in outcome do not seem to be related to intrinsic resistance for the tested drugs.
  • [MeSH-major] Dexamethasone. Drug Resistance / genetics. Genes, p16. Glucocorticoids. Leukemia-Lymphoma, Adult T-Cell / genetics. Prednisolone

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  • (PMID = 11260073.001).
  • [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 / Glucocorticoids; 7S5I7G3JQL / Dexamethasone; 9PHQ9Y1OLM / Prednisolone
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6. Schmiegelow K, Al-Modhwahi I, Andersen MK, Behrendtz M, Forestier E, Hasle H, Heyman M, Kristinsson J, Nersting J, Nygaard R, Svendsen AL, Vettenranta K, Weinshilboum R, Nordic Society for Paediatric Haematology and Oncology: Methotrexate/6-mercaptopurine maintenance therapy influences the risk of a second malignant neoplasm after childhood acute lymphoblastic leukemia: results from the NOPHO ALL-92 study. Blood; 2009 Jun 11;113(24):6077-84
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  • [Title] Methotrexate/6-mercaptopurine maintenance therapy influences the risk of a second malignant neoplasm after childhood acute lymphoblastic leukemia: results from the NOPHO ALL-92 study.
  • Among 1614 children with acute lymphoblastic leukemia (ALL) treated with the Nordic Society for Paediatric Haematology and Oncology (NOPHO) ALL-92 protocol, 20 patients developed a second malignant neoplasm (SMN) with a cumulative risk of 1.6% at 12 years from the diagnosis of ALL.
  • Nine of the 16 acute myeloid leukemias or myelodysplastic syndromes had monosomy 7 (n = 7) or 7q deletions (n = 2).
  • Thiopurine methyltransferase (TPMT) methylates 6MP and its metabolites, and thus reduces cellular levels of cytotoxic 6-thioguanine nucleotides.
  • Among 427 TPMT wild-type patients for whom the 6MP dose was registered, those who developed SMN received higher average 6MP doses than the remaining patients (69.7 vs 60.4 mg/m2; P = .03).
  • This study indicates that the duration and intensity of 6MP/MTX maintenance therapy of childhood ALL may influence the risk of SMNs in childhood ALL.

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  • (PMID = 19224761.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM028157; United States / NIGMS NIH HHS / GM / U01 GM061388; United States / NIGMS NIH HHS / GM / R01-GM28157; United States / NIGMS NIH HHS / GM / U01 GM61388
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.- / Methyltransferases; EC 2.1.1.67 / thiopurine methyltransferase; YL5FZ2Y5U1 / Methotrexate
  • [Other-IDs] NLM/ PMC2699230
  • [Investigator] Schmiegelow K; Hejl M; Østergård M; Schrøder H; Pihkala U; Ilanmaa E; Antila K; Korpela K; Vuorinen O; Perkkiö M; Kojo N; Nyman R; Pere M; Lanning M; Niemi A; Vuoristo A; Niemi S; Isotalo J; Laapas H; Mäkipernaa A; Salmi T; Varsamäki T; Kristinsson J; Zeller B; Danielsen O; Madsen B; Nielsen B; Stensvold K; Lund JH; Danielsen K; Brekke P; Stamnes O; Glomstein A; Widing E; Hapnes C; Stokland T; Kolmannskog S; Halvorsen B; Spangen S; Carlsson G; Bergkvist M; Skanka N; Korlén B; Dimberg A; Adrian BA; Mellander L; Aronson S; Jensen D; Winiarski J; Lagerwall A; Jonsson NO; Cervin T; Samuelsson U; Berg A; Nilsson H; Behrendtz M; Wiebe T; Ljung R; Tessin I; Ljungren CG; Dohlwitz A; Christensen HO; Ronge E; Berglund M; Björk O; Fransson D; Eriksson M; Forestier E; Kreuger A; Blomgren M; Rönnblad B; Eriksson B; Berg T; Hedling L; Forsberg T; Lindquist B; Kriström B; Hjalmars U
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7. Styczynski J, Wysocki M, Debski R, Juraszewska E, Malinowska I, Stanczak E, Ploszynska A, Stefaniak J, Mazur B, Szczepanski T: Ex vivo drug resistance profile in childhood acute myelogenous leukemia: no drug is more effective in comparison to acute lymphoblastic leukemia. Leuk Lymphoma; 2002 Sep;43(9):1843-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ex vivo drug resistance profile in childhood acute myelogenous leukemia: no drug is more effective in comparison to acute lymphoblastic leukemia.
  • Therapy results in childhood acute myelogenous leukemia (AML) differ from those of acute lymphoblastic leukemia (ALL).
  • Cellular drug resistance might be one of the reasons of therapy failure in AML.
  • The aim of the study was the analysis of ex vivo drug resistance profile in childhood initial and relapsed AML in comparison to initial ALL.
  • Ex vivo drug resistance was tested by means of the MTT assay.
  • Up to 29 cytotoxic drugs were tested for each patient.
  • When compared to de nova ALL samples, myeloblasts from initial AML samples were significantly more resistant to most tested drugs, except cytarabine, mercaptopurine and thioguanine.
  • Patients, who have died due to refractory or relapsing disease, were already on first diagnosis 2-fold more resistant to cytarabine, 6.4-fold more resistant to cisplatin and 3-fold more resistant to carboplatin, when compared to those who stay in remission.
  • Resistance to cytarabine occurred in 2.1% of ALL and 12% of AML cases while a patient with Down syndrome presented the most sensitive drug resistance profile.
  • In conclusion this study shows that no drug was found which, on average, was more effective in AML than in ALL samples.
  • [MeSH-major] Drug Resistance, Neoplasm. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Carboplatin / therapeutic use. Cell Survival. Child. Cisplatin / therapeutic use. Coloring Agents / pharmacology. Humans. Recurrence. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology. Time Factors. Treatment Outcome. Tumor Cells, Cultured


8. Meier M, den Boer ML, Meijerink JP, Broekhuis MJ, Passier MM, van Wering ER, Janka-Schaub GE, Pieters R: Differential expression of p73 isoforms in relation to drug resistance in childhood T-lineage acute lymphoblastic leukaemia. Leukemia; 2006 Aug;20(8):1377-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential expression of p73 isoforms in relation to drug resistance in childhood T-lineage acute lymphoblastic leukaemia.
  • The T-lineage phenotype of childhood acute lymphoblastic leukaemia (ALL) is associated with an increased relapse-risk and in vitro resistance to drugs as compared to a precursor B phenotype.
  • Antiapoptotic isoforms of p73 that lack part of the transactivation (TA) domain (DeltaTA-p73, i.e. p73Deltaex2, p73Deltaex3, p73Deltaex2/3 and DeltaN-p73) may cause resistance to anticancer agents through inhibition of p53 and/or proapoptotic p73 family members (TA-p73).
  • We demonstrate in our study that the expression of total p73 mRNA was higher in childhood T-ALL compared to controls (P=0.004).
  • Leukaemic cells of T-ALL patients expressing higher levels of antiapoptotic p73 were more resistant to the DNA-damaging drug daunorubicin compared to cells of patients with low or negative expression or these isoforms (P(trend)=0.045).
  • Our results suggest that childhood T-ALL is associated with a high expression of DeltaTA-p73.
  • These isoforms may play a role in cellular resistance to DNA-damaging drugs in children at initial diagnosis of T-ALL.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Nuclear Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Cell Lineage. Child. Child, Preschool. DNA Methylation. Drug Resistance, Neoplasm. Genes, Tumor Suppressor. Humans. Infant. Loss of Heterozygosity. Protein Isoforms. RNA, Messenger / analysis. Tumor Suppressor Proteins

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  • (PMID = 16791269.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins; 0 / tumor suppressor protein p73
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9. Germain DP: Fabry disease. Orphanet J Rare Dis; 2010;5:30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Deficient activity of lysosomal α-galactosidase A results in progressive accumulation of globotriaosylceramide within lysosomes, believed to trigger a cascade of cellular events.
  • Demonstration of marked α-galactosidase A deficiency is the definitive method for the diagnosis of hemizygous males.
  • In childhood, other possible causes of pain such as rheumatoid arthritis and 'growing pains' must be ruled out.
  • Prenatal diagnosis, available by determination of enzyme activity or DNA testing in chorionic villi or cultured amniotic cells is, for ethical reasons, only considered in male fetuses.
  • Pre-implantation diagnosis is possible.
  • Conventional management consists of pain relief with analgesic drugs, nephroprotection (angiotensin converting enzyme inhibitors and angiotensin receptors blockers) and antiarrhythmic agents, whereas dialysis or renal transplantation are available for patients experiencing end-stage renal failure.
  • End-stage renal disease and life-threatening cardiovascular or cerebrovascular complications limit life-expectancy of untreated males and females with reductions of 20 and 10 years, respectively, as compared to the general population.

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  • (PMID = 21092187.001).
  • [ISSN] 1750-1172
  • [Journal-full-title] Orphanet journal of rare diseases
  • [ISO-abbreviation] Orphanet J Rare Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.2.1.22 / alpha-Galactosidase
  • [Other-IDs] NLM/ PMC3009617
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10. Holleman A, den Boer ML, de Menezes RX, Cheok MH, Cheng C, Kazemier KM, Janka-Schaub GE, Göbel U, Graubner UB, Evans WE, Pieters R: The expression of 70 apoptosis genes in relation to lineage, genetic subtype, cellular drug resistance, and outcome in childhood acute lymphoblastic leukemia. Blood; 2006 Jan 15;107(2):769-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The expression of 70 apoptosis genes in relation to lineage, genetic subtype, cellular drug resistance, and outcome in childhood acute lymphoblastic leukemia.
  • Childhood acute lymphoblastic leukemia (ALL) consists of various subtypes that respond differently to cytotoxic drugs and therefore have a markedly different clinical outcome.
  • We used microarrays to investigate, in 190 children with ALL at initial diagnosis, whether 70 key apoptosis genes were differentially expressed between leukemic subgroups defined by lineage, genetic subtype, in vitro drug resistance, and clinical outcome.
  • In conclusion, ALL subtypes have a unique expression pattern of apoptosis genes and our data suggest that selective genes are linked to cellular drug resistance and prognosis in childhood B-lineage ALL.
  • [MeSH-major] Apoptosis. Cell Lineage. Drug Resistance, Neoplasm / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


11. Styczynski J, Wysocki M, Debski R, Czyzewski K, Kolodziej B, Rafinska B, Kubicka M, Koltan S, Koltan A, Pogorzala M, Kurylak A, Olszewska-Slonina D, Balwierz W, Juraszewska E, Wieczorek M, Olejnik I, Krawczuk-Rybak M, Kuzmicz M, Kowalczyk J, Stefaniak J, Badowska W, Sonta-Jakimczyk D, Szczepanski T, Matysiak M, Malinowska I, Stanczak E, Wachowiak J, Konatkowska B, Gil L, Balcerska A, Maciejka-Kapuscinska L: Predictive value of multidrug resistance proteins and cellular drug resistance in childhood relapsed acute lymphoblastic leukemia. J Cancer Res Clin Oncol; 2007 Nov;133(11):875-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Predictive value of multidrug resistance proteins and cellular drug resistance in childhood relapsed acute lymphoblastic leukemia.
  • PURPOSE: Cellular resistance in childhood acute leukemias might be related to profile and function of multidrug resistance proteins and apoptosis regulating proteins.
  • (1) analysis of expression of MRP1, PGP1, LRP, BCL-2 and p53 proteins;.
  • (2) correlation with ex vivo drug resistance, and (3) analysis of their prognostic impact on clinical outcome in childhood acute lymphoblastic (ALL) and acute myeloid (AML) leukemia.
  • Drug resistance for up to 30 anticancer agents was performed by the MTT assay.
  • Expression of all proteins was tested by flow cytometry.
  • RESULTS: Both initial AML and relapsed ALL samples showed higher drug resistance than initial ALL samples.
  • No significant differences were found in drug resistance between initial and relapsed AML samples.
  • The presence of multidrug resistance and apoptosis proteins had no impact on pDFS in iALL and iAML, however strong trend towards adverse prognostic impact of MRP1, PGP and LRP on pDFS in rALL was observed.
  • The same trend was observed for each of analyzed co-expressions of tested multidrug resistance proteins.
  • CONCLUSIONS: The phenomenon of cellular drug resistance in childhood acute leukemias is multifactorial and plays an important role in response to therapy.
  • Expression of MRP1, PGP and LRP proteins, as well as their co-expression play possible role in childhood relapsed ALL.
  • [MeSH-major] Drug Resistance, Multiple. Drug Resistance, Neoplasm. Multidrug Resistance-Associated Proteins / metabolism. P-Glycoprotein / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Vault Ribonucleoprotein Particles / metabolism
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / pharmacology. Child. Child, Preschool. Female. Flow Cytometry. Gene Expression Regulation, Leukemic. Humans. Immunophenotyping. Infant. Infant, Newborn. Male. Neoplasm Recurrence, Local / diagnosis. Prognosis

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  • [ErratumIn] J Cancer Res Clin Oncol. 2007 Nov;133(11):895. Wachowiak, Jacek [added]; Konatkowska, Benigna [added]; Gil, Lidia [added]; Balcerska, Anna [added]; Maciejka-Kapuscinska, Lucyna [added]
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  • (PMID = 17671794.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein
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12. Zwaan CM, Kaspers GJ, Pieters R, Hählen K, Huismans DR, Zimmermann M, Harbott J, Slater RM, Creutzig U, Veerman AJ: Cellular drug resistance in childhood acute myeloid leukemia is related to chromosomal abnormalities. Blood; 2002 Nov 1;100(9):3352-60
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  • [Title] Cellular drug resistance in childhood acute myeloid leukemia is related to chromosomal abnormalities.
  • Specific cytogenetic abnormalities predict prognosis in childhood acute myeloid leukemia (AML).
  • However, it is unknown why they are predictive and whether this is related to drug resistance.
  • Here, we successfully analyzed drug resistance and (cyto-) genetic abnormalities of 109 untreated childhood AML samples using the 4-day total cell-kill methyl-thiazolyl tetrazolium (MTT) assay.
  • Overall, we found no differences in drug resistance in samples taken at diagnosis between patients remaining in continuous complete remission (CCR) versus the refractory/relapsed patients.
  • We conclude that some, but not all, cytogenetic subgroups in childhood AML display specific drug-resistance profiles.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Chromosome Aberrations. Drug Resistance, Neoplasm / genetics. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Antibiotics, Antineoplastic / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Chromosome Inversion. Chromosomes, Human / ultrastructure. Cladribine / pharmacology. Cytarabine / pharmacology. Drug Resistance, Multiple / genetics. Etoposide / pharmacology. Female. Humans. Infant. Male. Neoplastic Stem Cells / drug effects. Recurrence. Remission Induction. Tetrazolium Salts. Thiazoles. Translocation, Genetic. Trisomy

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  • (PMID = 12384437.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 0 / Tetrazolium Salts; 0 / Thiazoles; 04079A1RDZ / Cytarabine; 298-93-1 / thiazolyl blue; 47M74X9YT5 / Cladribine; 6PLQ3CP4P3 / Etoposide
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13. Miketova P, Kaemingk K, Hockenberry M, Pasvogel A, Hutter J, Krull K, Moore IM: Oxidative changes in cerebral spinal fluid phosphatidylcholine during treatment for acute lymphoblastic leukemia. Biol Res Nurs; 2005 Jan;6(3):187-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oxidative changes in cerebral spinal fluid phosphatidylcholine during treatment for acute lymphoblastic leukemia.
  • Central nervous system (CNS) treatment contributes to improved long-term disease-free survival from childhood acute lymphoblastic leukemia (ALL) by significantly decreasing the rate of disease relapse.
  • Methotrexate (MTX), a drug commonly used for CNS treatment, has been associated with cognitive and academic problems, white-matter changes, perfusion defects, and brain atrophy.
  • Unoxidized and oxidized components of phosphatidylcholine (PC), the most prevalent phospholipid in CNS cellular membranes, were measured in cerebral spinal fluid (CSF) samples obtained from 21 children diagnosed with low (n = 7), standard (n= 7), or high (n= 7) risk ALL.
  • Phospholipids were extracted from CSF samples obtained at diagnosis and during the induction, consolidation, and continuation treatment phases.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Methotrexate / adverse effects. Phosphatidylcholines / cerebrospinal fluid. Precursor Cell Lymphoblastic Leukemia-Lymphoma / cerebrospinal fluid. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Injections, Spinal. Lipid Peroxidation / drug effects. Male. Oxidative Stress / drug effects

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  • (PMID = 15583359.001).
  • [ISSN] 1099-8004
  • [Journal-full-title] Biological research for nursing
  • [ISO-abbreviation] Biol Res Nurs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Phosphatidylcholines; YL5FZ2Y5U1 / Methotrexate
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14. Styczynski J, Gil L, Derwich K, Wachowiak J, Balwierz W, Badowska W, Krawczuk-Rybak M, Matysiak M, Wieczorek M, Balcerska A, Sonta-Jakimczyk D, Stefaniak J, Kowalczyk J, Urasinski T, Sobol G, Komarnicki M, Wysocki M: Comparison of clofarabine activity in childhood and adult acute leukemia: individual tumor response study. Anticancer Res; 2009 May;29(5):1643-50
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  • [Title] Comparison of clofarabine activity in childhood and adult acute leukemia: individual tumor response study.
  • The aim of the study was the analysis of ex vivo activity of clofarabine and 14 other anticancer drugs in pediatric and adult acute lymphoblastic (ALL) and myeloid (AML) leukemia.
  • PATIENTS AND METHODS: The ex vivo drug resistance profile was analyzed in 282 patients, including 201 children with ALL de novo, 24 children with relapsed ALL, 25 children with AML de novo and 32 adults with AML.
  • Cellular ex vivo drug resistance was tested by means of the MTT assay.
  • RESULTS: Clofarabine had comparable ex vivo activity against lymphoblasts and myeloblasts, both on initial diagnosis and at relapse, both in children and in adults.
  • Its activity in acute myeloid leukemia was independent of patient age.
  • No significant differences in drug resistance to clofarabine between pediatric age-based subgroups of ALL were detected, while it was observed for most of other drugs.
  • CONCLUSION: In comparison to childhood acute lymphoblastic leukemia, lack of differences in ex vivo activity gives rationale for use of clofarabine in refractory and relapsed pediatric and adult patients with acute myeloid leukemia.
  • [MeSH-major] Adenine Nucleotides / therapeutic use. Antineoplastic Agents / therapeutic use. Arabinonucleosides / therapeutic use. Leukemia / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Child. Child, Preschool. Humans. Infant. Middle Aged. Treatment Outcome. Young Adult

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  • (PMID = 19443380.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 762RDY0Y2H / clofarabine
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15. Campana D: Status of minimal residual disease testing in childhood haematological malignancies. Br J Haematol; 2008 Nov;143(4):481-9
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  • [Title] Status of minimal residual disease testing in childhood haematological malignancies.
  • In children with acute leukaemia, measurements of minimal residual disease (MRD) provide unique information on treatment response and have become a crucial component of contemporary treatment protocols.
  • In acute lymphoblastic leukaemia (ALL), the most useful MRD assays are based on polymerase chain reaction (PCR) amplification of antigen-receptor genes, and on flow cytometric detection of abnormal immunophenotypes.
  • The latter is the only MRD assay available for most patients with acute myeloid leukaemia (AML).
  • Treatment de-intensification for patients with early MRD clearance is also being tested.
  • In addition to their direct clinical application, MRD measurements can be used to better understand the molecular and cellular mechanisms of drug resistance in vivo.
  • The identification of new markers of leukaemia and the use of increasingly sophisticated technologies for detection of rare cells should further facilitate routine monitoring of MRD and elucidate the features of drug-resistant leukaemic cells.

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  • (PMID = 18710378.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA115422-04; United States / NCI NIH HHS / CA / CA115422; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / U01 CA060419-04; United States / NCI NIH HHS / CA / R01 CA060419; United States / NCI NIH HHS / CA / CA60419; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA060419-04; United States / NCI NIH HHS / CA / R01 CA115422-04; United States / NCI NIH HHS / CA / R01 CA115422; United States / NCI NIH HHS / CA / U01 CA060419
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Number-of-references] 72
  • [Other-IDs] NLM/ NIHMS154353; NLM/ PMC2784675
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16. Dhooge C, De Moerloose B, Laureys G, Ferster A, De Bacquer D, Philippe J, Leroy J, Benoit Y: Expression of the multidrug transporter P-glycoprotein is highly correlated with clinical outcome in childhood acute lymphoblastic leukemia: results of a long-term prospective study. Leuk Lymphoma; 2002 Feb;43(2):309-14
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  • [Title] Expression of the multidrug transporter P-glycoprotein is highly correlated with clinical outcome in childhood acute lymphoblastic leukemia: results of a long-term prospective study.
  • The improved cure rate in childhood ALL may be attributed largely to the effective multidrug regimens currently applied in well-designed clinical trials.
  • However, in a minority of patients with ALL, chemotherapy failure remains a leading cause of cancer related death, most probably due to cellular drug resistance.
  • In a long term prospective study (mean time of follow-up: 65 months) the multidrug efflux pump P-gp was examined immunocytochemically in leukemic cells of 102 protocol-treated children with de novo acute lymphoblastic leukemia (ALL) and of 37 children with relapsed ALL.
  • Fourteen percent expressed P-gp at initial diagnosis and 35% were P-gp positive at relapse.
  • The patients being P-gp positive at initial diagnosis had a higher rate of leukemic relapse than the P-gp negative patients (P = 0.02).
  • Paired analysis on diagnostic and relapsed samples from 20 patients did not support the hypothesis of P-gp mediated expression being a chemotherapy induced phenomenon.
  • The cumulative event free survival for de novo ALL patients was significantly higher in the P-gp negative patient group.
  • In conclusion we strongly advise that tests for P-gp in leukemic blasts should be conducted for every child with ALL, since this parameter selects a subgroup of patients with increased risk for leukemic relapse.
  • [MeSH-major] P-Glycoprotein / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Drug Resistance, Multiple. Female. Humans. Infant. Longitudinal Studies. Male. Matched-Pair Analysis. Prognosis. Prospective Studies. Recurrence. Risk Factors. Survival Analysis






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