BioMedLib Search Engine [ goto HOMEPAGE ]

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Prognostic impact of combined fludarabine, treosulfan and mitoxantrone resistance profile in childhood acute myeloid leukemia.

BACKGROUND: The role of cellular drug resistance in childhood acute myeloid leukemia (AML) has not yet been established.

The aim of the study was the analysis of the clinical value of ex vivo drug resistance in pediatric AML.

PATIENTS AND METHODS: A cohort of 90 children with de novo AML were assayed for drug resistance profile by the 3-4,5-dimethylthiazol-2-yl-2,5-difenyl tetrazolium bromide (MTT) assay and prognostic model of in vitro drug sensitivity was analyzed.

A combined in vitro drug resistance profile to fludarabine, treosulfan and mitoxantrone (FTM score) was defined and it had an independent prognostic significance for disease free survival in pediatric AML.

CONCLUSION: The combined fludarabine, treosulfan and mitoxantrone resistance profile to possibly may be used for better stratification of children with AML or indicate the necessity for additional therapy.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

[MeSH-minor] Busulfan / administration & dosage. Busulfan / analogs & derivatives. Child. Child, Preschool. Cohort Studies. Drug Resistance, Neoplasm. Drug Screening Assays, Antitumor. Female. Humans. Infant. Male. Mitoxantrone / administration & dosage. Prognosis. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

Hazardous Substances Data Bank. FLUDARABINE .

Hazardous Substances Data Bank. TREOSULFAN .

Hazardous Substances Data Bank. BUSULFAN .

Hazardous Substances Data Bank. VIDARABINE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18630483.001).

[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] BZ114NVM5P / Mitoxantrone; CO61ER3EPI / treosulfan; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The frequency of NPM1 mutations in childhood acute myeloid leukemia.

BACKGROUND: Mutations in the nucleophosmin (NPM1) gene have been solely associated with childhood acute myeloid leukemia (AML).

We evaluated the frequency of NPM1 mutations in childhood AML, their relation to clinical and cytogenetic features and the presence of common FLT3 and RAS mutations.

The role of different types of NPM1 mutations, either individually or in the presence of other common gene mutations may be essential for childhood AML prognosis.

[MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics

[MeSH-minor] Adolescent. Child. Child, Preschool. Cohort Studies. Gene Frequency. Humans. Infant. Prognosis. Survival Analysis

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Blood. 2005 Dec 1;106(12):3733-9 [16076867.001]

[Cites] Blood. 2005 Dec 1;106(12):3740-6 [16051734.001]

[Cites] Cancer Res. 2006 Mar 15;66(6):3310-6 [16540685.001]

[Cites] Blood. 2006 May 15;107(10):4011-20 [16455956.001]

[Cites] Leuk Res. 2007 Jan;31(1):109-11 [16678898.001]

[Cites] Leukemia. 2007 Feb;21(2):366-7 [17151698.001]

[Cites] APMIS. 2007 Apr;115(4):341-6 [17504301.001]

[Cites] Blood. 2007 Aug 1;110(3):979-85 [17440048.001]

[Cites] Leuk Lymphoma. 2007 Nov;48(11):2141-4 [17990177.001]

[Cites] Leuk Res. 2008 Jul;32(7):1141-3 [18180033.001]

[Cites] Haematologica. 2008 Oct;93(10):1565-9 [18641025.001]

[Cites] Ann Hematol. 2009 Feb;88(2):159-66 [18726096.001]

[Cites] Hematol Oncol. 2009 Jun;27(2):90-7 [19365794.001]

[Cites] Hematol Oncol. 2009 Dec;27(4):171-81 [19569254.001]

[Cites] Med Oncol. 2009 Dec;26(4):460-2 [19085113.001]

[Cites] Blood. 1999 Dec 1;94(11):3707-16 [10572083.001]

[Cites] Blood. 2002 Mar 15;99(6):1909-12 [11877259.001]

[Cites] Nat Med. 2002 Jul;8(7):743-50 [12091906.001]

[Cites] Nat Rev Cancer. 2003 Sep;3(9):650-65 [12951584.001]

[Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]

[Cites] Blood. 2005 Aug 15;106(4):1419-22 [15870172.001]

[Cites] Blood. 2005 Oct 15;106(8):2854-61 [15994285.001]

[Cites] Blood. 2005 Dec 1;106(12):3747-54 [16109776.001]

(PMID = 20979630.001).

[ISSN] 1756-8722

[Journal-full-title] Journal of hematology & oncology

[ISO-abbreviation] J Hematol Oncol

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin

[Other-IDs] NLM/ PMC2988697

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Mechanisms of synergistic antileukemic interactions between valproic acid and cytarabine in pediatric acute myeloid leukemia.

PURPOSE: To determine the possibility of synergistic antileukemic activity and the underlying molecular mechanisms associated with cytarabine combined with valproic acid (VPA; a histone deacetylase inhibitor and a Food and Drug Administration-licensed drug for treating both children and adults with epilepsy) in pediatric acute myeloid leukemia (AML).

EXPERIMENTAL DESIGN: The type and extent of antileukemic interactions between cytarabine and VPA in clinically relevant pediatric AML cell lines and diagnostic blasts from children with AML were determined by MTT assays and standard isobologram analyses.

RESULTS: We showed synergistic antileukemic activities between cytarabine and VPA in four pediatric AML cell lines and nine diagnostic AML blast samples. t(8;21) AML blasts were significantly more sensitive to VPA and showed far greater sensitivities to combined cytarabine and VPA than non-t(8;21) AML cases.

CONCLUSIONS: Our results establish global synergistic antileukemic activity of combined VPA and cytarabine in pediatric AML and provide compelling evidence to support the use of VPA in the treatment of children with this deadly disease.

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. CYTARABINE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] ©2010 AACR.

[Cites] Blood. 2008 Mar 1;111(5):2505-15 [18299451.001]

[Cites] J Pharmacol Exp Ther. 2001 Sep;298(3):865-72 [11504778.001]

[Cites] Clin Cancer Res. 2008 Jul 15;14(14):4500-10 [18628465.001]

[Cites] Blood. 2009 Sep 24;114(13):2744-52 [19638627.001]

[Cites] Mol Cell Biol. 2009 Dec;29(23):6149-69 [19805519.001]

[Cites] EMBO J. 2001 Dec 17;20(24):6969-78 [11742974.001]

[Cites] Leuk Res. 2002 May;26(5):495-502 [11916526.001]

[Cites] Leukemia. 2003 Jan;17(1):120-4 [12529668.001]

[Cites] Cancer Cell. 2003 Dec;4(6):425-9 [14706334.001]

[Cites] Leukemia. 2004 Jul;18(7):1246-51 [15116123.001]

[Cites] Blood. 2004 Sep 1;104(5):1266-9 [15155466.001]

[Cites] Br J Haematol. 2004 Nov;127(3):264-79 [15491285.001]

[Cites] Adv Cancer Res. 1998;72:197-233 [9338077.001]

[Cites] Blood. 1999 Aug 15;94(4):1393-400 [10438727.001]

[Cites] Nat Med. 2005 Jan;11(1):71-6 [15619634.001]

[Cites] J Natl Cancer Inst. 2005 Feb 2;97(3):226-31 [15687366.001]

[Cites] Leuk Res. 2005 Jul;29(7):739-48 [15927669.001]

[Cites] J Clin Oncol. 2005 Jun 10;23(17):3923-31 [15897550.001]

[Cites] Leuk Res. 2005 Nov;29(11):1335-42 [15936818.001]

[Cites] Trends Mol Med. 2005 Oct;11(10):442-4 [16150641.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Nov 1;102(44):16090-5 [16243973.001]

[Cites] Blood. 2006 Jan 1;107(1):241-9 [16141349.001]

[Cites] Cancer. 2006 Jan 1;106(1):112-9 [16323176.001]

[Cites] Blood. 2006 Aug 15;108(4):1174-82 [16675713.001]

[Cites] Mol Cancer Res. 2006 Aug;4(8):563-73 [16877702.001]

[Cites] Cancer Res. 2006 Sep 1;66(17):8903-11 [16951208.001]

[Cites] Nat Rev Drug Discov. 2006 Sep;5(9):769-84 [16955068.001]

[Cites] Pharmacol Rev. 2006 Sep;58(3):621-81 [16968952.001]

[Cites] Blood. 2006 Nov 15;108(10):3271-9 [16882711.001]

[Cites] Seizure. 2006 Dec;15(8):630-2 [17070075.001]

[Cites] Leukemia. 2007 Feb;21(2):248-52 [17122863.001]

[Cites] Oncologist. 2007 Mar;12(3):341-55 [17405900.001]

[Cites] J Clin Oncol. 2007 May 20;25(15):1979-85 [17513804.001]

[Cites] Blood. 2007 Jul 1;110(1):267-77 [17356134.001]

[Cites] Curr Drug Targets. 2007 Jun;8(6):727-37 [17584028.001]

[Cites] Blood. 2007 Oct 1;110(7):2302-8 [17596541.001]

[Cites] Haematologica. 2007 Nov;92(11):1519-32 [18024401.001]

[Cites] Curr Biol. 2000 Jul 27-Aug 10;10(15):886-95 [10959836.001]

[Cites] Cancer Treat Rev. 2008 May;34(3):206-22 [18226465.001]

(PMID = 20889917.001).

[ISSN] 1078-0432

[Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research

[ISO-abbreviation] Clin. Cancer Res.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA120772-01A2; United States / NCI NIH HHS / CA / R01 CA120772; United States / NCI NIH HHS / CA / CA120772; United States / NCI NIH HHS / CA / R01 CA120772-01A2

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 04079A1RDZ / Cytarabine; 614OI1Z5WI / Valproic Acid; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9

[Other-IDs] NLM/ NIHMS238223; NLM/ PMC3018695

   

Advertisement

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Translocation (10;11)(p12;q23) in childhood acute myeloid leukemia: incidence and complex mechanism.

This translocation represented 28% of all cases of childhood AML treated at our center in 2004, and 63% of AML with rearrangements of 11q23.

The median event-free survival of patients was 8.1 months, and we conclude that the t(10;11)(p12;q23) is associated with unfavorable prognosis in childhood acute myeloid leukemia.

[MeSH-major] Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 11. Leukemia, Myeloid / genetics. Translocation, Genetic

[MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Chromosome Banding. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Karyotyping. Male. Reverse Transcriptase Polymerase Chain Reaction

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16938568.001).

[ISSN] 0165-4608

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Beginning treatment for pediatric acute myeloid leukemia: the family connection.

There is a loud silence on psycho-oncology research in relation to pediatric Acute Myeloid Leukemia (AML).

The present article documents the less obvious, often hidden, aspect of beginning treatment for pediatric AML--the "behind the scenes" experience of the home and family connection.

The findings are from the first stage of a five year longitudinal study that examines through qualitative research the experience of childhood leukemia from the perspective of the child, siblings and parents.

The findings emphasise the need for support for families coping with childhood AML.

[MeSH-major] Adaptation, Psychological. Attitude to Health. Child, Hospitalized / psychology. Family / psychology. Leukemia, Myeloid / psychology

[MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Family Health. Health Services Needs and Demand. Holistic Health. Hospitals, Pediatric. Humans. Infant. Longitudinal Studies. Models, Psychological. Nursing Methodology Research. Parent-Child Relations. Qualitative Research. Queensland. Sibling Relations. Social Support. Surveys and Questionnaires

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Children's Health.

MedlinePlus Health Information. consumer health - Family Issues.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16006383.001).

[ISSN] 0146-0862

[Journal-full-title] Issues in comprehensive pediatric nursing

[ISO-abbreviation] Issues Compr Pediatr Nurs

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Complex karyotype abnormalities in pediatric acute myeloid leukemia].

A majority of the data on the prognostic significance of distinct chromosome changes and combinations of them in pediatric acute myeloid leukemia (AML) has been derived from adult studies, with not numerous published data in pediatric patients.

We investigated characteristic features of complex karyotype in newly diagnosed pediatric AML de novo.

New data were obtained for complex karyotype differences of adult and pediatric AML.

In the great majority (76%) of complex karyotypes in our adult patients chromosome abnormalities associated with adverse risk were found but in pediatric patients their frequency was significantly less (30%).

Complex karyotype is considered to be characteristic of older AML patients and in the majority of the patients the karyotype contains markers of adverse risk.

Possibly, worse outcome in older AML patients is connected with the markers but not with multiple chromosome changes.

New data of frequency and the peculiarities of complex karyotype in pediatric AML are important for understanding of AML pathogenesis and for development a more effective AML treatment.

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18589906.001).

[ISSN] 0869-6047

[Journal-full-title] Vestnik Rossiiskoi akademii meditsinskikh nauk

[ISO-abbreviation] Vestn. Akad. Med. Nauk SSSR

[Language] RUS

[Publication-type] Comparative Study; English Abstract; Journal Article; Multicenter Study

[Publication-country] Russia (Federation)

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Prenatal origin of childhood AML occurs less frequently than in childhood ALL.

BACKGROUND: While there is enough convincing evidence in childhood acute lymphoblastic leukemia (ALL), the data on the pre-natal origin in childhood acute myeloid leukemia (AML) are less comprehensive.

Our study aimed to screen Guthrie cards (neonatal blood spots) of non-infant childhood AML and ALL patients for the presence of their respective leukemic markers.

In AML patients (n = 13, age 1-14 years) PML/RARalpha (n = 4), CBFbeta/MYH11 (n = 3), AML1/ETO (n = 2), MLL/AF6 (n = 1), MLL/AF9 (n = 1) and MLL/AF10 (n = 1) fusion genes and/or internal tandem duplication of FLT3 gene (FLT3/ITD) (n = 2) were used as clonotypic markers.

We did not find patient-specific molecular markers in any patient with AML.

CONCLUSION: In the largest cohort examined so far we used identical approach for the backtracking of non-infant childhood ALL and AML.

Our data suggest that either the prenatal origin of AML is less frequent or the load of pre-leukemic cells is significantly lower at birth in AML compared to ALL cases.

[MeSH-major] Biomarkers, Tumor / blood. DNA, Neoplasm / blood. Fetal Blood / chemistry. Gene Rearrangement, B-Lymphocyte. Gene Rearrangement, T-Lymphocyte. Leukemia, Myeloid / embryology. Oncogene Proteins, Fusion / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / embryology

[MeSH-minor] Bone Marrow Cells / chemistry. Child. Child, Preschool. Clone Cells / chemistry. Cohort Studies. Core Binding Factor Alpha 2 Subunit / blood. Core Binding Factor Alpha 2 Subunit / genetics. Female. Gene Duplication. Humans. Infant. Infant, Newborn. Male. Myeloid-Lymphoid Leukemia Protein / blood. Myeloid-Lymphoid Leukemia Protein / genetics. Neonatal Screening. Neoplasm Proteins / blood. Neoplasm Proteins / genetics. Polymerase Chain Reaction. Tandem Repeat Sequences. fms-Like Tyrosine Kinase 3 / blood. fms-Like Tyrosine Kinase 3 / genetics

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Br J Haematol. 2003 Jul;122(1):24-9 [12823342.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Jan 11;102(2):449-54 [15626757.001]

[Cites] Blood. 2003 Oct 1;102(7):2321-33 [12791663.001]

[Cites] Lancet. 1999 Oct 30;354(9189):1499-503 [10551495.001]

[Cites] Blood. 1999 Dec 1;94(11):3707-16 [10572083.001]

[Cites] Blood. 2000 Jul 1;96(1):264-8 [10891460.001]

[Cites] Blood. 2001 Jan 1;97(1):89-94 [11133746.001]

[Cites] Blood. 2001 Jul 15;98(2):478-82 [11435320.001]

[Cites] Blood. 2001 Oct 1;98(7):2272-4 [11568017.001]

[Cites] Blood. 2002 Apr 15;99(8):2992-6 [11929791.001]

[Cites] Blood. 2002 May 15;99(10):3801-5 [11986239.001]

[Cites] Blood. 2002 Oct 1;100(7):2387-92 [12239146.001]

[Cites] Blood. 2002 Oct 1;100(7):2393-8 [12239147.001]

[Cites] Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):15101-6 [12415113.001]

[Cites] Br J Cancer. 2002 Oct 21;87(9):994-9 [12434291.001]

[Cites] Genes Chromosomes Cancer. 2003 May;37(1):36-43 [12661004.001]

[Cites] Blood. 2003 Jun 1;101(11):4640-1 [12756163.001]

[Cites] Genes Chromosomes Cancer. 2003 Aug;37(4):406-11 [12800152.001]

[Cites] Leukemia. 2003 Nov;17(11):2202-6 [12931229.001]

[Cites] Leuk Lymphoma. 2003 Dec;44(12):2099-102 [14959854.001]

[Cites] Genes Chromosomes Cancer. 2004 Apr;39(4):335-40 [14978794.001]

[Cites] Nucleic Acids Res. 1988 Feb 11;16(3):1215 [3344216.001]

[Cites] Nucleic Acids Res. 1995 Sep 25;23(18):3788-9 [7479012.001]

[Cites] Blood. 1997 Jan 1;89(1):281-5 [8978302.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):13950-4 [9391133.001]

[Cites] Proc Natl Acad Sci U S A. 1998 May 26;95(11):6413-8 [9600980.001]

[Cites] J Pediatr Hematol Oncol. 1998 May-Jun;20(3):264-7 [9628441.001]

[Cites] Leukemia. 1999 Jan;13(1):110-8 [10049045.001]

[Cites] Blood. 1999 May 1;93(9):3074-80 [10216104.001]

[Cites] Blood. 1999 Jun 15;93(12):4079-85 [10361104.001]

[Cites] Blood. 1999 Aug 1;94(3):1057-62 [10419898.001]

[Cites] Leukemia. 2003 Aug;17(8):1667-9 [12886258.001]

(PMID = 16630339.001).

[ISSN] 1471-2407

[Journal-full-title] BMC cancer

[ISO-abbreviation] BMC Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Biomarkers, Tumor; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA, Neoplasm; 0 / MLL-AF10 fusion protein, human; 0 / MLL-AF6 fusion protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

[Other-IDs] NLM/ PMC1463004

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Prognostic factors and outcome of recurrence in childhood acute myeloid leukemia.

BACKGROUND: Outcome after recurrence of childhood acute myeloid leukemia (AML) is poor.

We performed this study to identify prognostic factors for recurrence and for survival after recurrence of AML.

METHODS: The clinical characteristics, biological features, treatment modalities, and outcomes of children with de novo AML who were enrolled on 3 consecutive clinical protocols from 1987 to 2002 at St. Jude Children's Research Hospital were studied.

CONCLUSIONS: Survival after recurrence was poor in children with AML.

Novel therapies are urgently needed to prevent or to treat recurring AML.

[MeSH-major] Leukemia, Myeloid / mortality

[MeSH-minor] Acute Disease. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Male. Multivariate Analysis. Prognosis. Recurrence. Sex Factors. Stem Cell Transplantation. Survival Rate. Time Factors. Transplantation, Autologous

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] (c) 2006 American Cancer Society.

(PMID = 17133407.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P30 CA-21765

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Outcomes in childhood AML in the absence of transplantation in first remission--Children's Cancer Group (CCG) studies 2891 and CCG 213.

BACKGROUND: The majority of childhood acute myeloid leukemia (AML) patients lack a matched-related bone marrow transplant (BMT) donor in first remission.

PROCEDURE: Disease-free survival (DFS), overall survival (OS), relapse-free survival (RFS), and post-relapse outcome were evaluated for children with de novo AML on CCG 213 and the standard timing (ST) and intensive timing (IT) induction arms of CCG 2891 who were randomized to (intent-to-treat, ITT) or who received (as-treated, AT) only chemotherapy intensification.

Overall survival for childhood AML in the absence of BMT in CR1 is influenced by duration of CR1 and by race.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

[MeSH-minor] Child. Disease-Free Survival. Female. Humans. Male. Remission Induction. Survival Analysis. Survival Rate

Genetic Alliance. consumer health - Childhood Cancer.

Genetic Alliance. consumer health - Transplantation.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] (c) 2007 Wiley-Liss, Inc.

(PMID = 17252564.001).

[ISSN] 1545-5017

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA 13539; United States / NCI NIH HHS / CA / CA 98543

[Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] High WT1 expression after induction therapy predicts high risk of relapse and death in pediatric acute myeloid leukemia.

PURPOSE: To determine whether minimal residual disease (MRD) measured by Wilms' tumor gene 1 (WT1) expression is a prognostic marker in pediatric acute myeloid leukemia (AML), we quantified WT1 transcript by real-time quantitative-polymerase chain reaction in 92 AML at diagnosis and during follow-up.

PATIENTS AND METHODS: Patients (median age, 6 years; cytogenetics, favorable 27%, intermediate 59%, poor 13%) were treated between 1995 and 2002 and enrolled in Leucémie aiguë Myéloblastique Enfant (LAME) 89/91, LAME 99 pilot study and Acute Promyelocytic Leukemia French collaborative protocols.

CONCLUSION: WT1 quantification is an informative molecular marker for MRD in pediatric AML and is now performed as prospective analysis in ELAM02 protocol.

[MeSH-major] Genes, Wilms Tumor. Leukemia, Myeloid, Acute / genetics

[MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit / genetics. Female. Gene Dosage. Humans. Infant. Infant, Newborn. Male. Multivariate Analysis. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. RNA, Messenger / analysis. Recurrence. Reverse Transcriptase Polymerase Chain Reaction

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16575000.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Treatment of childhood acute myeloid leukemia.

Childhood acute myeloid leukemia is rare, but accounts for a significant number of malignancy-related deaths in this age group.

Therefore, there is a need for further improved treatment of pediatric acute myeloid leukemia.

Subgroup-directed treatment has become a reality for acute myeloid leukemia in young children with Down's syndrome and in acute promyelocytic leukemia.

In addition to tailoring therapy according to biologic features and especially monitoring treatment by measurements of minimal residual disease, targeted therapy for subgroups with activating mutations in receptor tyrosine kinases will further optimize the treatment of pediatric acute myeloid leukemia.

Together with the development of many novel agents that have different mechanisms of action than the currently available anticancer agents, and improved supportive care, it is realistic that the prognosis of acute myeloid leukemia in children and adolescents will improve further in the next 5-10 years.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy. Stem Cell Transplantation

[MeSH-minor] Acute Disease. Antineoplastic Agents / pharmacology. Child. Clinical Trials as Topic. Cranial Irradiation. Down Syndrome / complications. Humans. Neoplasm, Residual. Prognosis. Quality of Life. Remission Induction. Risk Assessment. Transplantation, Homologous

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16221060.001).

[ISSN] 1744-8328

[Journal-full-title] Expert review of anticancer therapy

[ISO-abbreviation] Expert Rev Anticancer Ther

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents

[Number-of-references] 90

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Correlatoin of apoptosis signaling in primary pediatric BCP-ALL xenograft cells with the kinetics of engraftment in vivo in a NOD/SCID model and patient outcome.

: 10043 Background: We previously identified the importance of intact apoptosis signaling for treatment response in pediatric ALL and AML by analyzing two key apoptogenic events, caspase-3 activation and cytochrome c release.

Using a NOD/SCID mouse model for pediatric BCP-ALL we found that short time from transplant to overt leukemia in the recipient mice (short time to leukemia, TTLshort) determines poor patient outcome.

METHODS: In this study we investigated the importance of deficient apoptosis signaling for leukemia engraftment in this model.

CONCLUSIONS: Our finding in the NOD/SCID/huALL model matches our results in pediatric ALL and AML to conclude that the functional integrity of a downstream apoptotic checkpoint is an important feature regulating leukemia biology.

Thus, deficient apoptosis signaling appears to determine rapid engraftment of leukemia cells in the NOD/SCID model in vivo and consequently poor patient outcome.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 27962469.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Promoter DNA methylation of CD10 in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene.

METHODS: CD10-negative infant ALL with MLL/AF4, CD10-positive infant ALL with germ-line MLL, CD10-positive pre-B ALL cell line, infant AML (M5) with MLL/AF9 and pediatric AML (M2) with AML1/ETO were analyzed for VDJ_H status and methylation of CD10 gene promoters.

In contrast, none or a few of the CpG dinucleotides were methylated in the CD10-positive ALL, AML (M5) with MLL/AF9 or AML (M2) with AML1/ETO.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 27962471.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Pilot study of haploidentical natural killer cell transplantation in childhood acute myeloid leukemia.

We hypothesized that the transplantation of purified haploidentical NK cells may be a safe and effective form of consolidation therapy that will reduce the risk of relapse among children with acute myeloid leukemia (AML) who are not treated with HSCT.

In this pilot study, we assessed the safety, feasibility, and engraftment of NK cell infusions in 10 patients with AML in first remission.

CONCLUSIONS: Haploidentical NK cells can be safely administered to AML patients who are in remission.

We have recently opened a new trial to evaluate the efficacy of NK cell therapy in children in first remission of AML.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 27962581.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] A case of childhood acute myeloid leukemia AML (M5) with a neocentric chromosome neo(1)(qter-->q23 approximately 24::q23 approximately 24-->q43-->neo-->q43-->qter) and tetrasomy of chromosomes 8 and 21.

Hyperdiploidy is rarely observed in childhood acute myeloid leukemia (AML).

Described here is the case of a 2(1/2)-year-old girl with AML-M5 and 51 chromosomes characterized by double tetrasomy of chromosomes 8 and 21 and also a neocentric derivative chromosome neo(1)(qter-->q23 approximately 24::q23 approximately 24-->q43-->neo-->q43-->qter).

Little is known about the prognostic significance of these chromosomal abnormalities in childhood AML.

[MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics

[MeSH-minor] Child, Preschool. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping

Genetic Alliance. consumer health - Acute Myelocytic Leukemia.

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19665076.001).

[ISSN] 1873-4456

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Long-term outcome of childhood acute myeloid leukemia in a developing country: experience from a children's hospital in China.

Data on childhood acute myeloid leukemia (AML) in developing countries are limited.

Herein we report the outcome of childhood AML treated with modified NPCLC-AML97 in our institution from 1997 to 2005.

One hundred and eighty-five children with newly diagnosed AML were admitted.

Thirty-one patients (25.2%) relapsed, but no central nervous system leukemia was observed.

Although the cure rate of childhood AML in China was low, the treatment outcome for patients who could adhere to the treatment protocol was satisfactory.

[MeSH-major] Developing Countries. Hospitals, Pediatric / statistics & numerical data. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy

[MeSH-minor] Adolescent. Child. Child, Preschool. China. Cohort Studies. Female. Humans. Infant. Male. Survival Analysis. Time Factors. Treatment Outcome

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[ErratumIn] Leuk Lymphoma. 2011 Mar;52(3):544

(PMID = 20929322.001).

[ISSN] 1029-2403

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Repetitive cycles of high-dose cytarabine are effective for childhood acute myeloid leukemia: long-term outcome of the children with AML treated on two consecutive trials of Tokyo Children's Cancer Study Group.

BACKGROUND: Various methods of intensive chemotherapy have contributed to an improved survival in pediatric acute myeloid leukemia (AML).

PROCEDURE: A total of 216 eligible children with newly diagnosed AML were treated in the two consecutive multi-center trials of TCCSG, M91-13 and M96-14, from August 1991 to September 1998.

Among patients without Down syndrome (DS) or acute promyelocytic leukemia (APL), the presence of t(8;21) or inv(16) was a significant good prognostic factor both in the univariate and multivariate analyses.

CONCLUSIONS: These results suggest that repetitive use of HD-Ara-C was effective and safe for childhood AML.

However, further optimization of AML therapy is required.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy

[MeSH-minor] Acute Disease. Adolescent. Antimetabolites, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / therapeutic use. Child. Child, Preschool. Combined Modality Therapy. Cytarabine / administration & dosage. Cytarabine / therapeutic use. Disease-Free Survival. Down Syndrome / complications. Doxorubicin / administration & dosage. Doxorubicin / analogs & derivatives. Drug Administration Schedule. Etoposide / administration & dosage. Female. Hematopoietic Stem Cell Transplantation. Humans. Hydrocortisone / administration & dosage. Infant. Infection / etiology. Infection / mortality. Japan / epidemiology. Kaplan-Meier Estimate. Male. Methotrexate / administration & dosage. Mitoxantrone / administration & dosage. Remission Induction. Survival Analysis. Transplantation, Autologous. Transplantation, Homologous. Treatment Outcome. Tretinoin / administration & dosage. Vincristine / administration & dosage

Genetic Alliance. consumer health - Childhood Cancer.

Genetic Alliance. consumer health - Acute Myelocytic Leukemia.

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

Hazardous Substances Data Bank. CYTARABINE .

Hazardous Substances Data Bank. DOXORUBICIN .

Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

Hazardous Substances Data Bank. ETOPOSIDE .

Hazardous Substances Data Bank. HYDROCORTISONE .

Hazardous Substances Data Bank. VINCRISTINE .

Hazardous Substances Data Bank. METHOTREXATE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16807916.001).

[ISSN] 1545-5009

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; BZ114NVM5P / Mitoxantrone; D58G680W0G / pirarubicin; WI4X0X7BPJ / Hydrocortisone; YL5FZ2Y5U1 / Methotrexate

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Childhood acute myeloid leukemia with hemophagocytosis by the blasts and inv(8)(p11q13) with MOZ-TIF2 fusion transcripts.

We describe a unique case of de novo childhood acute myeloid leukemia in which the blasts showed evidence of hemophagocytosis and harbored inv(8) (p11q13) chromosomal abnormality.

To our knowledge, this is the eighth overall and the fourth childhood case of acute myeloid leukemia with inv(8) (p11q13) with MOZ-TIF2 fusion.

[MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 11 / genetics. Leukemia, Myeloid / genetics. Lymphohistiocytosis, Hemophagocytic / genetics. Oncogene Proteins, Fusion / genetics

[MeSH-minor] Acute Disease. Child. Female. Humans. Transcription, Genetic

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17805042.001).

[ISSN] 1077-4114

[Journal-full-title] Journal of pediatric hematology/oncology

[ISO-abbreviation] J. Pediatr. Hematol. Oncol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / MOZ-TIF2 protein, human; 0 / Oncogene Proteins, Fusion

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Genetic changes including gene copy number alterations and their relation to prognosis in childhood acute myeloid leukemia.

We studied a series of 68 subjects diagnosed with childhood acute myeloid leukemia (AML) using conventional cytogenetics and fluorescence in situ hybridization (FISH), polymerase chain reaction (PCR) to analyze mutations in FLT3 and NPM1 genes, and/or array comparative genomic hybridization (CGH).

Six genes (AKT1, RUNX1, LTB, SDC1, RUNX1T1, and JAK2) from the imbalanced regions have been reported to be involved in AML, whereas other 30 cancer genes, not previously reported in an AML context, were identified as imbalanced.

[MeSH-major] Gene Dosage. Leukemia, Myeloid, Acute / genetics. Mutation

[MeSH-minor] Adolescent. Bone Marrow Cells / cytology. Child. Child, Preschool. Cytogenetics. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Infant, Newborn. Karyotyping. Male. Polymerase Chain Reaction. Prognosis. Translocation, Genetic

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20001230.001).

[ISSN] 1029-2403

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Analysis of prognostic variables in childhood acute myeloid leukemia].

OBJECTIVE: To assess the prognostic value of the biological features and therapy-related factors in childhood acute myeloid leukemia (AML).

METHODS: From January 1998 to May 2003, 75 patients with newly diagnosed AML were enrolled on the protocol AML-XH-99.

Univariate analysis also demonstrated that the 5-year pEFS for patients with age < 1 year or > 10 years, platelet count < 20 x 10(9)/L, FAB M(5), hepatomegaly, BM blasts >or= 0.150 at 48 h after the first induction course and no response to the first induction course, central nervous system (CNS) leukemia was unfavorable, while the outcome of patients with cytogenetic abnormalities of t (8;.

17) were better. (2) Multivariate analysis suggested that cytogenetic abnormality of t (15; 17), achieved CR after the first induction course and no CNS leukemia were independent favorable prognostic factors.

[MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / therapy

[MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Karyotyping. Male. Prognosis. Treatment Outcome

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16732931.001).

[ISSN] 0253-2727

[Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi

[ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Prognostic factors in pediatric acute myeloid leukemia.

Acute myeloid leukemia (AML), a heterogeneous group of diseases with variable responses to the same therapy, comprises nearly a quarter of childhood acute leukemias.

Although historically very few prognostic markers have been incorporated into therapeutic decision making in AML, recent advances in technology have enabled identification of numerous factors associated with disease outcome.

This review provides a detailed analysis of most clinically relevant factors associated with disease outcome in childhood AML.

[MeSH-major] Leukemia, Myeloid, Acute / diagnosis

[MeSH-minor] Age Factors. Biomarkers, Tumor. Body Mass Index. Child. Cytogenetics. Humans. Polymorphism, Genetic. Prognosis. Risk Factors. Sex Factors

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20652454.001).

[ISSN] 1558-822X

[Journal-full-title] Current hematologic malignancy reports

[ISO-abbreviation] Curr Hematol Malig Rep

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Low efficacy of methotrexate in childhood acute myeloid leukemia (AML): single-agent therapeutic window study in relapsed AML.

BACKGROUND: The efficacy in pediatric acute myeloid leukemia (AML) of single-agent methotrexate (MTX) at a higher dose than previously applied, 1,000 mg/m2, given as a theoretically beneficial 36-hr continuous infusion, is unknown, but may be beneficial based on preclinical data.

PROCEDURE: We performed a therapeutic window study in children with first relapsed AML treated in four different countries.

By that time, another four patients had been enrolled, of which one patient with a late relapsed AML FAB type M7 showed a good response.

CONCLUSIONS: This study shows that single-agent MTX in the applied regimen in pediatric relapsed AML has limited efficacy.

However, it also demonstrates the feasibility of an international and therapeutic window phase II study in pediatric relapsed AML.

[MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Methotrexate / therapeutic use

[MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Dose-Response Relationship, Drug. Female. Humans. Infant. Infusions, Intravenous. Male. Maximum Tolerated Dose. Recurrence. Treatment Outcome

Genetic Alliance. consumer health - Acute Myelocytic Leukemia.

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright (c) 2005 Wiley-Liss, Inc.

[CommentIn] Pediatr Blood Cancer. 2006 Oct 15;47(5):535-6 [16453297.001]

(PMID = 16358301.001).

[ISSN] 1545-5009

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial

[Publication-country] United States

[Chemical-registry-number] YL5FZ2Y5U1 / Methotrexate

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cytogenetics of pediatric acute myeloid leukemia.

Acute myeloid leukemia (AML) is a clinically and genetically heterogeneous disease accounting for 15-20% of all childhood acute leukemias, while it is responsible for more than half of the leukemic deaths in these patients.

This article focuses on the significance of cytogenetic analysis in pediatric AML supporting the importance of cytogenetic analysis in the pathogenesis, diagnosis, prognosis, follow-up and treatment selection in childhood AML.

Furthermore, it discusses the association of specific chromosome rearrangements with prenatal exposure to carcinogenic agents or therapeutic agents and highlights the ongoing and future research on pediatric AML in the evolving field of Cytogenetics.

[MeSH-major] Cytogenetics / methods. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19563518.001).

[ISSN] 1600-0609

[Journal-full-title] European journal of haematology

[ISO-abbreviation] Eur. J. Haematol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Carcinogens, Environmental

[Number-of-references] 123

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Risk factors and therapy for isolated central nervous system relapse of pediatric acute myeloid leukemia.

PURPOSE: CNS relapse of pediatric acute myeloid leukemia (AML) is an infrequent occurrence.

PATIENTS AND METHODS: Records of 886 patients with de novo AML were reviewed, and patients who entered remission at the end of one course of therapy and developed an isolated CNS relapse as their first event were analyzed (n = 690).

[MeSH-major] Central Nervous System Neoplasms / drug therapy. Central Nervous System Neoplasms / radiotherapy. Leukemia, Myeloid / pathology

[MeSH-minor] Acute Disease. Adolescent. Adult. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Male. Prognosis. Recurrence. Retrospective Studies. Risk Factors. Survival Analysis

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16361619.001).

[ISSN] 0732-183X

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Successive clinical trials for childhood acute myeloid leukemia at St Jude Children's Research Hospital, from 1980 to 2000.

Despite substantial progress in the management of childhood acute myeloid leukemia (AML), only about 50% of patients are cured by intensive chemotherapy.

From 1980 to 2000, 251 patients <15 years of age with newly diagnosed AML were enrolled on one of the five consecutive St Jude AML studies.

With the exception of one protocol (AML-83), outcomes improved in general over the two decades.

The estimated 5-year event-free survival (+/-s.e.) was 30.8+/-5.6% for AML-80; 11.1+/-4.3% for AML-83; 35.9+/-7.4% for AML-87; 43.5+/-6.2% for AML-91; and 45.0+/-11.1% for AML-97.

Resistant or relapsed AML caused the great majority of treatment failures.

Increasing the intensity of chemotherapy (AML-87) did not improve outcome, partially because of toxicity, nor did prolonging postremission therapy by adding sequential myeloablative (AML-80) or nonmyeloablative (AML-83) chemotherapy cycles.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Antineoplastic Protocols / standards. Leukemia, Myeloid / therapy

[MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Dose-Response Relationship, Drug. Female. Follow-Up Studies. Humans. Infant. Infant, Newborn. Male. Remission Induction / methods. Survival Analysis. Treatment Failure. Treatment Outcome

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16281077.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA-21765

[Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Fludarabine, treosulfan and etoposide sensitivity and the outcome of hematopoietic stem cell transplantation in childhood acute myeloid leukemia.

BACKGROUND: The prognostic role of the ex vivo drug resistance profile has not yet been proved in childhood acute myeloid leukemia (AML).

The aim of the study was the analysis of the impact of the ex vivo drug resistance profile in a cohort of 44 children with AML undergoing hematopoietic stem cell transplantation (HSCT).

CONCLUSION: The combined drug resistance profile to fludarabine, treosulfan and etoposide may be useful for better stratification of children with AML undergoing stem cell transplantation or to indicate the necessity for additional post-transplant therapy.

[MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm. Granulocyte Precursor Cells / drug effects. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / surgery

[MeSH-minor] Acute Disease. Adolescent. Busulfan / analogs & derivatives. Busulfan / pharmacology. Child. Child, Preschool. Etoposide / pharmacology. Female. Humans. Infant. Male. Prognosis. Recurrence. Treatment Outcome. Vidarabine / analogs & derivatives. Vidarabine / pharmacology

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

Genetic Alliance. consumer health - Transplantation.

Hazardous Substances Data Bank. FLUDARABINE .

Hazardous Substances Data Bank. TREOSULFAN .

Hazardous Substances Data Bank. ETOPOSIDE .

Hazardous Substances Data Bank. BUSULFAN .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17595774.001).

[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; 6PLQ3CP4P3 / Etoposide; CO61ER3EPI / treosulfan; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Outpatient consolidation chemotherapy in pediatric acute myeloid leukemia: a retrospective analysis.

BACKGROUND: To assess the outcomes of outpatient high dose cytosine arabinoside consolidation cycles in pediatric acute myeloid leukemia (AML) patients in comparison to inpatient treatment.

METHODS: We retrospectively analyzed 90 cycles of AML consolidation given to 30 patients between July 2003 and July 2007.

CONCLUSIONS: Outpatient AML consolidation therapy is safe and feasible in children.

To our knowledge, this report is the first of its kind looking specifically at outpatient consolidation chemotherapy in AML.

[MeSH-major] Leukemia, Myeloid, Acute / therapy

[MeSH-minor] Adolescent. Anti-Infective Agents / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Child. Child, Preschool. Female. Granulocyte-Macrophage Colony-Stimulating Factor / administration & dosage. Humans. Infant. Leukocyte Count. Male. Neutropenia / blood. Neutropenia / drug therapy. Platelet Count. Recombinant Proteins. Retrospective Studies

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19843379.001).

[ISSN] 1607-8454

[Journal-full-title] Hematology (Amsterdam, Netherlands)

[ISO-abbreviation] Hematology

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Recombinant Proteins; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Residual disease monitoring in childhood acute myeloid leukemia by multiparameter flow cytometry: the MRD-AML-BFM Study Group.

PURPOSE: Monitoring of residual disease (RD) by flow cytometry in childhood acute myeloid leukemia (AML) may predict outcome.

PATIENTS AND METHODS: Five hundred forty-two specimens of 150 children enrolled in the AML-Berlin-Frankfurt-Muenster (BFM) 98 study were analyzed by four-color immunophenotyping at up to four predefined time points during treatment.

For each of the 12 leukemia-associated immunophenotypes and time points, a threshold level based on a previous retrospective analysis of another cohort of children with AML and on control bone marrows was determined.

Compared with commonly defined risk factors in the AML-BFM studies, flow cytometry does not provide additional information for outcome prediction, but may be helpful to evaluate the remission status at day 28.

[MeSH-major] Flow Cytometry. Leukemia, Myeloid, Acute / diagnosis. Neoplasm, Residual / diagnosis

[MeSH-minor] Adolescent. Adult. Analysis of Variance. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow / pathology. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Predictive Value of Tests. Prognosis. Proportional Hazards Models. Retrospective Studies. Risk Factors. Survival Analysis. Treatment Outcome

Genetic Alliance. consumer health - Acute Myelocytic Leukemia.

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16877738.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] EVI1 overexpression in distinct subtypes of pediatric acute myeloid leukemia.

Overexpression of the ecotropic virus integration-1 (EVI1) gene (EVI1+), localized at chromosome 3q26, is associated with adverse outcome in adult acute myeloid leukemia (AML).

In pediatric AML, 3q26 abnormalities are rare, and the role of EVI1 is unknown.

We studied 228 pediatric AML samples for EVI1+ using gene expression profiling and RQ-PCR.

EVI1+ was found in 20/213 (9%) of children with de novo AML, and in 4/8 with secondary AML.

It was predominantly found in MLL-rearranged AML (13/47), monosomy 7 (2/3), or FAB M6/7 (6/10), and mutually exclusive with core-binding factor AML, t(15;17), and NPM1 mutations.

Although significant differences in 4 years pEFS for EVI1+ and EVI1- pediatric AML were observed (28%+/-11 vs 44%+/-4, P=0.04), multivariate analysis did not identify EVI1+ as an independent prognostic factor.

We conclude that EVI1+ can be found in approximately 10% of pediatric AML.

Although EVI1+ was not an independent prognostic factor, it was predominantly found in subtypes of pediatric AML that are related with an intermediate to unfavorable prognosis.

Remarkably, no 3q26 abnormalities were identified in EVI1+ pediatric AML.

[MeSH-major] Biomarkers, Tumor / genetics. Chromosomes, Human, Pair 3 / genetics. DNA-Binding Proteins / genetics. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics

[MeSH-minor] Child. Child, Preschool. Chromosome Aberrations. Female. Gene Expression Profiling. Humans. In Situ Hybridization, Fluorescence. Male. Oligonucleotide Array Sequence Analysis. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20357826.001).

[ISSN] 1476-5551

[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 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / RNA, Messenger; 0 / Transcription Factors

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] CEBPalpha mutations in childhood acute myeloid leukemia.

CEBPalpha: mutations have been described in adult acute myeloid leukemia (AML) and conferred a favorable prognosis.

We investigated 117 children with de novo AML using DNA PCR assay followed by sequencing for each PCR product.

Our results showed that CEBPalpha mutations occurred in 6% of childhood AML and most exhibited combined mutations in both N-terminal part and bZIP domain.

[MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / genetics. Leukemia, Myeloid, Acute / genetics. Mutation

[MeSH-minor] Adolescent. Child. Child, Preschool. Clone Cells. DNA Mutational Analysis / methods. Gene Frequency. Humans. Infant. Infant, Newborn. Polymerase Chain Reaction / methods

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15618961.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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.

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.

AML is considered a stem cell disease.

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 AML is equally resistant as adult AML.

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

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17430154.001).

[ISSN] 1873-4316

[Journal-full-title] Current pharmaceutical biotechnology

[ISO-abbreviation] Curr Pharm Biotechnol

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antineoplastic Agents

[Number-of-references] 165

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Incidence of FLT3 and nucleophosmin gene mutations in childhood acute myeloid leukemia: Serbian experience and the review of the literature.

Mutations in the fms-like tyrosine kinase 3 (FLT3) gene (internal tandem duplication (ITD) and point mutation in the tyrosine kinase domain, FLT3/D835) as well as the nucleophosmin (NPM1) gene are the most common abnormalities in adult acute myeloid leukemia (AML).

Their significance in pediatric AML is still unclear.

In this study we evaluated the frequency of FLT3 and NPM1 mutations in childhood AML.

FLT3 and NPM1 mutations were analysed in 42 and 37 childhood AML patients, respectively, using polymerase chain reaction (PCR) and direct sequencing.

Here we report the results of the study of FLT3 and NPM1 gene mutations in childhood AML patients in Serbia.

Comparative study of data on NPM1 mutations in childhood AML revealed that various NPM1 gene mutation types are associated with childhood AML.

Our findings as well as previously reported data, contributes to a hypothesis of different biology and etiology of adult and childhood AML.

More extensive studies of NPM1 and FLT3 mutations in childhood AML are needed to determine their biological and clinical importance.

[MeSH-major] Leukemia, Myeloid / genetics. Mutation. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. fms-Like Tyrosine Kinase 3 / genetics

[MeSH-minor] Acute Disease. Child. Child, Preschool. DNA Mutational Analysis. DNA, Neoplasm / genetics. Female. Humans. Male. Serbia

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19557552.001).

[ISSN] 1559-131X

[Journal-full-title] Medical oncology (Northwood, London, England)

[ISO-abbreviation] Med. Oncol.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] WT1 expression at diagnosis does not predict survival in pediatric AML: a report from the Children's Oncology Group.

WT1 is a transcription factor that is aberrantly overexpressed in acute and chronic leukemias.

Overexpression of WT1 in pediatric acute myeloid leukemia has been reported, but the prognostic significance is unclear because sample sizes in these studies have been relatively small.

WT1 expression was measured by quantitative RT-PCR in samples obtained at diagnosis from 155 pediatric AML patients treated on a cooperative group protocol.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Clin Oncol. 2008 Jan 20;26(3):414-20 [18202418.001]

[Cites] J Clin Oncol. 2008 Nov 20;26(33):5429-35 [18591546.001]

[Cites] Blood. 2009 Jun 4;113(23):5951-60 [19171881.001]

[Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]

[Cites] Leukemia. 2002 Jul;16(7):1381-9 [12094264.001]

[Cites] Leukemia. 2003 May;17(5):965-71 [12750711.001]

[Cites] Haematologica. 2004 Aug;89(8):926-33 [15339675.001]

[Cites] Blood. 1994 Nov 1;84(9):3071-9 [7949179.001]

[Cites] Blood. 1997 Feb 15;89(4):1405-12 [9028964.001]

[Cites] Leukemia. 1997 May;11(5):639-43 [9180285.001]

[Cites] Blood. 1997 Aug 1;90(3):1217-25 [9242555.001]

[Cites] Blood. 1998 Apr 15;91(8):2969-76 [9531608.001]

[Cites] Leukemia. 1998 Dec;12(12):1886-94 [9844919.001]

[Cites] Ann Hematol. 2004 Dec;83(12):745-50 [15340762.001]

[Cites] Leukemia. 2005 Dec;19(12):2101-16 [16136167.001]

[Cites] Leukemia. 2006 Feb;20(2):254-63 [16341043.001]

[Cites] J Clin Oncol. 2006 Apr 1;24(10):1507-15 [16575000.001]

[Cites] Leuk Res. 2007 Apr;31(4):570-2 [16876863.001]

[Cites] Pediatr Blood Cancer. 2007 Aug;49(2):133-8 [16883592.001]

(PMID = 19618455.001).

[ISSN] 1545-5017

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / 5T32CA060441-15; United States / NCI NIH HHS / CA / T32 CA060441; United States / NCI NIH HHS / CA / CA060441-15; United States / NCI NIH HHS / CA / L40 CA117542; United States / NCI NIH HHS / CA / CA120535; United States / NCI NIH HHS / CA / T32 CA060441-15; United States / NCI NIH HHS / CA / R01 CA120535

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / RNA, Messenger; 0 / WT1 Proteins

[Other-IDs] NLM/ NIHMS123739; NLM/ PMC2926132

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Clinical significance of flowcytometric minimal residual disease detection in pediatric acute myeloid leukemia patients treated according to the DCOG ANLL97/MRC AML12 protocol.

Analysis of minimal residual disease (MRD) in childhood acute myeloid leukemia (AML) may predict for clinical outcome.

MRD levels were assessed by flowcytometric immunophenotyping in 94 children with AML enrolled into a single trial (United Kingdom Medical Research Council AML12 and similar Dutch Childhood Oncology Group ANLL97).

In conclusion, flowcytometric MRD detection is possible in children with AML.

[MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Neoplasm, Residual / diagnosis

[MeSH-minor] Child. Clinical Protocols. Flow Cytometry. Humans. Immunophenotyping. Probability. Prognosis. RNA, Messenger / genetics. Recurrence

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20668473.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Grant] United Kingdom / Medical Research Council / / G0300133

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / RNA, Messenger

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Prognostic factors and risk-based therapy in pediatric acute myeloid leukemia.

Acute myeloid leukemia (AML) has posed significant therapeutic challenges to pediatric oncologists.

Despite intensive therapy, half of the children with AML relapse and die from their disease.

Efforts to identify risk factors in AML are directed toward defining populations who may benefit from alternative therapies.

Management of high-risk patients may prove more difficult, as the nearly myeloablative nature of AML therapy leaves little room for therapy escalation short of stem cell transplantation.

This review evaluates prognostic factors in pediatric AML and discusses the feasibility of using these factors in risk-adapted therapy regimens.

[MeSH-major] Leukemia, Myeloid / therapy

[MeSH-minor] Acute Disease. Antineoplastic Agents / therapeutic use. Child. Humans. Neoplasm Recurrence, Local. Prognosis. Risk Assessment. Risk Factors. Stem Cell Transplantation

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17405900.001).

[ISSN] 1083-7159

[Journal-full-title] The oncologist

[ISO-abbreviation] Oncologist

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents

[Number-of-references] 133

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Incidence and prognostic importance of molecular genetic defects in children with acute myeloblastic leukemia.

INTRODUCTION: Acute myeloblastic leukemia (AML) accounts for 15 to 25 percent of childhood acute leukemias.

The most common genetic abnormalities seen in pediatric AML patients are AML1-ETO, PML-RARα and CBFB-MYH11 genes resulting in t(8;21), t(15;17) and inv(16).

These genetic defects are seen in approximately 20-25% of AML patients.

OBJECTIVE: We investigated in this study, incidence and prognostic significance of the AML1-ETO, PML-RARα and CBFB-MYH11 genes in children with AML.

MATERIALS AND METHODS: The authors analyzed 34 children with AML using the real time-polymerase chain reaction for AML1-ETO, PML-RARα and CBFB-MYH11 genes.

[MeSH-major] Leukemia, Myeloid, Acute / genetics

[MeSH-minor] Adolescent. Child. Child, Preschool. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 8. Core Binding Factor Alpha 2 Subunit / genetics. Female. Humans. Infant. Kaplan-Meier Estimate. Male. Mutation / genetics. Oncogene Proteins, Fusion / genetics. Polymerase Chain Reaction. Prognosis. Survival Rate

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 21198299.001).

[ISSN] 2476-762X

[Journal-full-title] Asian Pacific journal of cancer prevention : APJCP

[ISO-abbreviation] Asian Pac. J. Cancer Prev.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Thailand

[Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Clinical implications of FLT3 mutations in pediatric AML.

FLT3 mutation status of 630 children with de novo acute myeloid leukemia (AML) treated on CCG-2941 and -2961 was determined, and ITD-AR was calculated for patients with FLT3/ITD.

ITD-AR defines the prognostic significance in FLT3/ITD-positive AML, and ITD-AR greater than 0.4 is a significant and independent prognostic factor for relapse in pediatric AML.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Mol Diagn. 2003 May;5(2):96-102 [12707374.001]

[Cites] Blood. 2003 May 1;101(9):3398-406 [12506020.001]

[Cites] Blood. 2003 Oct 1;102(7):2387-94 [12816873.001]

[Cites] J Clin Oncol. 2004 Jan 1;22(1):150-6 [14701777.001]

[Cites] Blood. 2004 Nov 1;104(9):2646-54 [15251987.001]

[Cites] Leukemia. 1997 Sep;11(9):1447-52 [9305596.001]

[Cites] Leukemia. 1999 Jan;13(1):38-43 [10049058.001]

[Cites] Blood. 1999 May 1;93(9):3074-80 [10216104.001]

[Cites] JAMA. 2005 Jan 12;293(2):203-11 [15644547.001]

[Cites] Blood. 2005 Jun 15;105(12):4792-9 [15718420.001]

[Cites] Blood. 2005 Jul 1;106(1):265-73 [15769897.001]

[Cites] Leukemia. 2005 Aug;19(8):1345-9 [15959528.001]

[Cites] Blood. 2005 Nov 15;106(10):3658-65 [16076872.001]

[Cites] Blood. 2006 Jul 1;108(1):400; author reply 400-1 [16790584.001]

[Cites] Med Pediatr Oncol. 1999 Dec;33(6):525-9 [10573574.001]

[Cites] Br J Haematol. 2000 Feb;108(2):322-30 [10691863.001]

[Cites] Br J Haematol. 2000 Oct;111(1):190-5 [11091200.001]

[Cites] Blood. 2001 Jan 1;97(1):89-94 [11133746.001]

[Cites] Blood. 2001 Apr 15;97(8):2434-9 [11290608.001]

[Cites] Blood. 2001 Jun 1;97(11):3589-95 [11369655.001]

[Cites] Br J Haematol. 2001 Jun;113(4):983-8 [11442493.001]

[Cites] Leukemia. 2001 Jul;15(7):1001-10 [11455967.001]

[Cites] Blood. 2001 Sep 15;98(6):1752-9 [11535508.001]

[Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]

[Cites] Blood. 2003 Aug 15;102(4):1474-9 [12702504.001]

(PMID = 16912228.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / K23 CA092405; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / R01 CA114563-01; United States / NCI NIH HHS / CA / R21 CA10262-01

[Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

[Other-IDs] NLM/ PMC1895470

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Prognostic significance of myeloperoxidase expression in childhood acute myeloid leukemia.

BACKGROUND: The percentage of myeloperoxidase (MPO)-positive blast cells is associated with prognosis in adult acute myeloid leukemia (AML), but this association is unsubstantiated in pediatric AML.

PROCEDURE: We retrospectively compared cytochemical MPO results with outcome in 154 patients younger than 21 years treated on three consecutive institutional protocols for newly diagnosed AML (1987-2001).

Patients with FAB M0 and M7 AML (no MPO expression) or M3 AML (100% MPO expression) and Down's syndrome were excluded.

CONCLUSIONS: The percentage of MPO-positive blast cells is related to FAB subtype in pediatric AML but has limited prognostic relevance.

[MeSH-major] Leukemia, Myeloid / blood. Myeloid Cells / enzymology. Neoplastic Stem Cells / enzymology. Peroxidase / blood

[MeSH-minor] Acute Disease. Adolescent. Adult. Biomarkers. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Kaplan-Meier Estimate. Karyotyping. Male. Prognosis. Retrospective Studies. Risk. Survival Analysis

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] (c) 2007 Wiley-Liss, Inc.

(PMID = 17763467.001).

[ISSN] 1545-5017

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA-21765

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers; EC 1.11.1.7 / Peroxidase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Adiponectin in relation to childhood myeloblastic leukaemia.

Adiponectin, an adipocyte-specific secretory protein known to induce apoptosis, has been reported to be inversely related to breast and endometrial cancers and recently found to inhibit proliferation of myeloid but not lymphoid cell lines.

We hypothesised that adiponectin may be inversely associated with acute myeloblastic leukaemia (AML), but not with acute lymphoblastic leukaemia of B (ALL-B) or T (ALL-T) cell origin in children.

Blood samples and clinical information were collected over the period 1996-2000 from 201 children (0-14 years old) with leukaemia (22 AML, 161 ALL-B and 18 ALL-T cases) through a national network of childhood Hematology-Oncology units in Greece and from 201 controls hospitalised for minor pediatric ailments.

Adiponectin was inversely associated with AML (OR=0.56; 95% CI, 0.34-0.94), whereas it was not significantly associated with either ALL-B (OR=0.88; 95% CI, 0.71-1.10) or ALL-T (OR=1.08; 95% CI, 0.67-1.72).

Biological plausibility and empirical evidence point to the importance of this hormone in the pathogenesis of childhood AML.

[MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / physiopathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology

[MeSH-minor] Adiponectin / analysis. Adiponectin / biosynthesis. Adolescent. Apoptosis. Body Height. Body Weight. Case-Control Studies. Cell Proliferation. Child. Child, Preschool. Female. Gene Expression Profiling. Greece. Humans. Infant. Infant, Newborn. Leukemia, B-Cell. Leukemia, T-Cell. Male. Odds Ratio

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Br J Haematol. 2004 Nov;127(3):243-63 [15491284.001]

[Cites] J Clin Endocrinol Metab. 2004 Mar;89(3):1160-3 [15001602.001]

[Cites] BMJ. 1993 Sep 25;307(6907):774 [8219951.001]

[Cites] Nature. 1996 Jul 25;382(6589):352-3 [8684463.001]

[Cites] Cancer Causes Control. 1996 Sep;7(5):553-9 [8877054.001]

[Cites] Biochem Biophys Res Commun. 1999 Apr 2;257(1):79-83 [10092513.001]

[Cites] Proc Natl Acad Sci U S A. 1999 May 11;96(10):5728-33 [10318952.001]

[Cites] Clin Lab Sci. 2004 Fall;17(4):235-45 [15559730.001]

[Cites] Eur J Endocrinol. 2004 Dec;151(6):741-6 [15588241.001]

[Cites] Am J Epidemiol. 2005 Jan 1;161(1):27-32 [15615910.001]

[Cites] J Natl Cancer Inst. 2005 Aug 3;97(15):1154-7 [16077074.001]

[Cites] Circulation. 1999 Dec 21-28;100(25):2473-6 [10604883.001]

[Cites] Blood. 2000 Sep 1;96(5):1723-32 [10961870.001]

[Cites] Cancer Causes Control. 2000 Sep;11(8):765-71 [11065014.001]

[Cites] Circulation. 2001 Feb 27;103(8):1057-63 [11222466.001]

[Cites] Diabetes. 2002 Jun;51(6):1884-8 [12031977.001]

[Cites] J Clin Endocrinol Metab. 2002 Dec;87(12):5662-7 [12466369.001]

[Cites] J Clin Endocrinol Metab. 2003 Mar;88(3):993-7 [12629074.001]

[Cites] Diabetologia. 2003 Apr;46(4):459-69 [12687327.001]

[Cites] J Clin Endocrinol Metab. 2003 Oct;88(10):4823-31 [14557461.001]

[Cites] Am J Epidemiol. 2003 Oct 15;158(8):724-35 [14561661.001]

[Cites] Clin Cancer Res. 2003 Nov 15;9(15):5699-704 [14654554.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Feb 24;101(8):2476-81 [14983034.001]

[Cites] J Clin Endocrinol Metab. 2004 Mar;89(3):1102-7 [15001594.001]

[Cites] J Natl Cancer Inst. 2004 Oct 20;96(20):1549-56 [15494605.001]

(PMID = 16404369.001).

[ISSN] 0007-0920

[Journal-full-title] British journal of cancer

[ISO-abbreviation] Br. J. Cancer

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / ADIPOQ protein, human; 0 / Adiponectin

[Other-IDs] NLM/ PMC2361080

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cathepsins B and L in peripheral blood mononuclear cells of pediatric acute myeloid leukemia: potential poor prognostic markers.

However, their significance in acute leukemias is lacking.

This study was planned to investigate expression and significance of these proteases in peripheral blood mononuclear cells (PBMCs) of patients with pediatric acute myeloid leukemia (AML).

CTSL and CTSB activities were assayed in PBMCs of 24 children with AML and ten healthy controls by spectrofluorimetry.

CTSL and CTSB protease activity and their mRNA expression were significantly higher in AML patients compared to controls (p ≤ 0.001).

Cystatin expression though significantly high (p ≤ 0.001) in AML was negatively correlated with CTSL (r = -0.920; p ≤ 0.001) and CTSB (r = -0.580, p ≤ 0.001) expression.

AML patients with higher CTSL and CTSB activity exhibited an inferior EFS (CTSL: p = 0.045; CTSB: p = 0.002) and overall survival (OS; CTSL: p = 0.05; CTSB: p = 0.004) compared to patients with lower levels of these proteases.

This is the first report demonstrating increased expression of CTSL and CTSB in AML, mechanism of their increased expression in relation to VEGF, and their association with poor EFS and OS.

[MeSH-major] Cathepsin B / metabolism. Cathepsin L / metabolism. Leukemia, Myeloid / enzymology. Leukocytes, Mononuclear / enzymology

[MeSH-minor] Acute Disease. Adolescent. Biomarkers, Tumor / blood. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Child. Child, Preschool. Cystatin C / genetics. Female. Gene Expression Regulation, Leukemic. Humans. Infant. Kaplan-Meier Estimate. Male. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Vascular Endothelial Growth Factor A / genetics

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20567828.001).

[ISSN] 1432-0584

[Journal-full-title] Annals of hematology

[ISO-abbreviation] Ann. Hematol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cystatin C; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; EC 3.4.22.1 / Cathepsin B; EC 3.4.22.15 / Cathepsin L

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Health and risk behaviors in survivors of childhood acute myeloid leukemia: a report from the Children's Oncology Group.

BACKGROUND: Survivors of childhood acute myeloid leukemia (AML) face increased risks of chronic disease and secondary malignancies.

PROCEDURES: Participants were diagnosed with AML at <21 years of age and survived > or =5 years following diagnosis.

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Oncol Nurs Forum. 1999 Oct;26(9):1475-86 [11064879.001]

[Cites] Drug Alcohol Depend. 2008 Nov 1;98(1-2):13-23 [18585871.001]

[Cites] J Clin Oncol. 2001 Jul 1;19(13):3163-72 [11432882.001]

[Cites] Med Pediatr Oncol. 2001 Jul;37(1):42-6 [11466722.001]

[Cites] Med Pediatr Oncol. 2002 Apr;38(4):229-39 [11920786.001]

[Cites] J Clin Oncol. 2003 Jan 15;21(2):189-96 [12525509.001]

[Cites] JAMA. 2003 Sep 24;290(12):1583-92 [14506117.001]

[Cites] Ann Intern Med. 2004 Apr 6;140(7):557-68 [15068985.001]

[Cites] Semin Oncol. 1982 Mar;9(1):34-51 [6176027.001]

[Cites] J Clin Oncol. 1993 Aug;11(8):1448-57 [8336184.001]

[Cites] J Clin Oncol. 1994 Jan;12(1):127-35 [8270968.001]

[Cites] J Natl Cancer Inst. 1994 Jan 19;86(2):131-7 [8271296.001]

[Cites] J Clin Oncol. 1994 Nov;12(11):2367-77 [7964952.001]

[Cites] Blood. 1996 Jun 15;87(12):4979-89 [8652810.001]

[Cites] J Natl Cancer Inst. 1998 Feb 4;90(3):219-25 [9462679.001]

[Cites] Ann Epidemiol. 2005 Mar;15(3):202-6 [15723765.001]

[Cites] J Clin Oncol. 2005 Sep 20;23(27):6516-23 [16116148.001]

[Cites] Semin Hematol. 2006 Jan;43(1):42-52 [16412788.001]

[Cites] J Clin Oncol. 2006 Jan 20;24(3):476-83 [16421424.001]

[Cites] Pediatr Blood Cancer. 2006 May 1;46(5):565-9 [16261562.001]

[Cites] Prev Med. 2006 Jun;42(6):435-42 [16626797.001]

[Cites] Cancer. 2006 Sep 15;107(6):1303-12 [16894525.001]

[Cites] N Engl J Med. 2006 Oct 12;355(15):1572-82 [17035650.001]

[Cites] MMWR Morb Mortal Wkly Rep. 2007 Nov 9;56(44):1157-61 [17989644.001]

[Cites] Cancer. 2008 May 1;112(9):2071-9 [18327823.001]

[Cites] J Natl Cancer Inst. 2001 Apr 18;93(8):618-29 [11309438.001]

(PMID = 20232426.001).

[ISSN] 1545-5017

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / U24 CA055727; United States / NCI NIH HHS / CA / U10 CA98413; United States / NCI NIH HHS / CA / 5U10CA78960; United States / NCI NIH HHS / CA / U24 CA55727; United States / NCI NIH HHS / CA / U10 CA007306-39; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U10 CA098543-08; None / None / / U10 CA098543-08; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA078960-04; United States / NCI NIH HHS / CA / CA007306-39; United States / NCI NIH HHS / CA / U10 CA098413-08; None / None / / U10 CA098413-08; United States / NCI NIH HHS / CA / U10 CA98543; United States / NCI NIH HHS / CA / 5U10 CA07306; United States / NCI NIH HHS / CA / R01 CA078960-04

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Other-IDs] NLM/ NIHMS166508; NLM/ PMC3152207

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Monosomy 7 associated with pediatric acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS): successful management by allogeneic hematopoietic stem cell transplant (HSCT).

Pediatric acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS) with monosomy 7 is associated with poor disease-free survival when treated by conventional chemotherapy, immunosuppression or supportive measures.

To better understand the curative potential of HSCT in these patients, all cases of AML and MDS with monosomy 7 treated by two transplant programs (1992 to present) were reviewed.

Primary diagnoses were MDS (N = 5), therapy-related MDS (N = 3), AML (N = 5) and therapy-related AML (N = 3).

Toxicity caused deaths of the five nonsurviving patients, four of whom were transplanted with active leukemia.

Allogeneic HSCT is effective therapy for childhood AML and MDS associated with monosomy 7, particularly for patients with AML in complete remission and MDS.

[MeSH-major] Chromosomes, Human, Pair 7. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / therapy. Monosomy. Myelodysplastic Syndromes / therapy

[MeSH-minor] Acute Disease. Adolescent. Cause of Death. Child. Child, Preschool. Disease Management. Female. Humans. Male. Neoplasms, Second Primary / mortality. Neoplasms, Second Primary / therapy. Remission Induction. Retrospective Studies. Survival Rate. Transplantation, Homologous. Treatment Outcome

Genetic Alliance. consumer health - Acute Myelocytic Leukemia.

Genetic Alliance. consumer health - Leukemia, Myeloid.

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 .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15558042.001).

[ISSN] 0268-3369

[Journal-full-title] Bone marrow transplantation

[ISO-abbreviation] Bone Marrow Transplant.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Molecularly targeted therapies for pediatric acute myeloid leukemia: progress to date.

While acute myeloid leukemia (AML) is significantly less common than acute lymphoblastic leukemia (ALL) in childhood, it is significantly more deadly with only half as many children likely to be cured with standard therapy.

In addition, the typical treatment for AML is among the most toxic of treatments for pediatric cancer; it includes intensive multiagent chemotherapy and, often, hematopoietic stem cell transplantation.

Given the poor prognosis of pediatric AML and the significant toxicity of standard AML therapy, novel therapies are needed.

Improved understanding of the molecular and cellular biology of leukemia has facilitated the development of molecularly targeted therapies.

In this article, we review progress to date with agents that are showing promise in the treatment of pediatric AML including targeted immunoconjugates, inhibitors of signaling molecules (e.g.

For the specific agents in each of these classes, we summarize the published preclinical data and the clinical trials that have been completed, are in progress, or are being planned for children with AML.

Finally, we discuss potential challenges to the success of molecularly targeted therapy including demonstrating adequate targeting of leukemia stem cells, developing synergistic and tolerable combinations of agents, and designing adequately powered clinical trials to test efficacy in molecularly defined subsets of patients.

[MeSH-major] Leukemia, Myeloid, Acute

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18345718.001).

[ISSN] 1174-5878

[Journal-full-title] Paediatric drugs

[ISO-abbreviation] Paediatr Drugs

[Language] eng

[Grant] United States / NCI NIH HHS / CA / K23 CA111728

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review

[Publication-country] New Zealand

[Chemical-registry-number] 0 / Histone Deacetylase Inhibitors; 0 / Proteasome Inhibitors; 0 / Protein Kinase Inhibitors; EC 2.5.1.29 / Farnesyltranstransferase; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

[Number-of-references] 92

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Pediatric acute myeloid leukemia: towards high-quality cure of all patients.

Prognosis of childhood acute myeloid leukemia (AML) has improved significantly over the past decades, from nearly no child surviving to a present probability of cure of approximately 60%.

This review summarizes current and future classification of pediatric AML, ongoing phase III studies, and subgroup-directed treatment.

These include minimal residual disease monitoring, pharmacogenomics and the detection of AML-specific molecular abnormalities.

Finally, we discuss the opportunities for innovative therapy in pediatric AML, such as the use of novel analogues, monoclonal antibody-mediated drugs, and receptor tyrosine kinase inhibitors.

Given the enormous increase in our understanding of the underlying biology of AML, and the development of many new targeted drugs, it should be possible to achieve high-quality cure in nearly all children and adolescents with AML within the next few decades.

[MeSH-major] Leukemia, Myeloid / therapy

[MeSH-minor] Acute Disease. Antineoplastic Agents / therapeutic use. Child. Humans. Neoplasm, Residual / diagnosis. Pharmacogenetics. Prognosis. Treatment Outcome

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18024401.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Italy

[Chemical-registry-number] 0 / Antineoplastic Agents

[Number-of-references] 147

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The incidence and clinical significance of nucleophosmin mutations in childhood AML.

Frameshift mutations in exon 12 of the nucleophosmin gene (NPM1) result in aberrant cytoplasmic localization of the NPM protein (NPMc(+)) and occur in 25% to 35% of adult acute myeloid leukemia (AML).

In adults with AML, NPMc(+) has been associated with normal karyotype, FLT3/ITD mutations, high remission induction rates, and improved survival (particularly in patients lacking FLT3/ITD).

NPMc(+) has not been well characterized in childhood AML.

This study examines the incidence and clinical significance of NPMc(+) in 295 children with newly diagnosed AML treated on a large cooperative group clinical trial (POG-9421).

We find that NPMc(+) is relatively uncommon in childhood AML (23 of 295 patients, 8%); and is significantly associated with FLT3/ITD mutations (P = .046), female sex (P = .029), older age (P = .047), and normal cytogenetics (P < .001).

We conclude that NPMc(+) is relatively rare in childhood AML, particularly in younger children.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Cell. 2000 Sep 29;103(1):127-40 [11051553.001]

[Cites] Mutat Res. 2002 Nov 30;509(1-2):79-91 [12427532.001]

[Cites] Blood. 2001 Jun 1;97(11):3589-95 [11369655.001]

[Cites] Blood. 2001 Sep 15;98(6):1752-9 [11535508.001]

[Cites] Nat Cell Biol. 2002 Jul;4(7):529-33 [12080348.001]

[Cites] Blood. 2002 Oct 15;100(8):2717-23 [12351377.001]

[Cites] Biosci Biotechnol Biochem. 2002 Oct;66(10):2239-42 [12450141.001]

[Cites] Blood. 2002 Dec 15;100(13):4372-80 [12393388.001]

[Cites] Hematol J. 2003;4(1):31-40 [12692518.001]

[Cites] Mol Cell Biol. 2004 Nov;24(21):9327-38 [15485902.001]

[Cites] Blood. 2004 Nov 1;104(9):2646-54 [15251987.001]

[Cites] Biometrics. 1979 Mar;35(1):25-39 [497336.001]

[Cites] Biochemistry. 1986 Jan 28;25(2):484-91 [3955008.001]

[Cites] Science. 1994 Mar 4;263(5151):1281-4 [8122112.001]

[Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]

[Cites] Blood. 1999 Jan 15;93(2):632-42 [9885226.001]

[Cites] Protein Sci. 1999 Apr;8(4):905-12 [10211837.001]

[Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]

[Cites] Blood. 2005 Aug 15;106(4):1419-22 [15870172.001]

[Cites] Blood. 2005 Oct 15;106(8):2854-61 [15994285.001]

[Cites] Blood. 2005 Nov 15;106(10):3618-20 [16046528.001]

[Cites] Blood. 2005 Dec 1;106(12):3740-6 [16051734.001]

[Cites] Blood. 2005 Dec 1;106(12):3733-9 [16076867.001]

[Cites] Blood. 2005 Dec 1;106(12):3747-54 [16109776.001]

[Cites] Leukemia. 2006 Feb;20(2):368-71 [16341033.001]

[Cites] Blood. 2006 Feb 15;107(4):1315-24 [16254147.001]

[Cites] Cancer Res. 2006 Mar 15;66(6):3310-6 [16540685.001]

[Cites] Blood. 2006 May 15;107(10):4011-20 [16455956.001]

[Cites] Leukemia. 2006 Jun;20(6):1103-8 [16541144.001]

[Cites] Mutat Res. 2006 Sep 28;608(2):136-56 [16829162.001]

[Cites] Blood. 2006 Dec 1;108(12):3654-61 [16912228.001]

[Cites] Leukemia. 2007 Feb;21(2):366-7 [17151698.001]

[Cites] Leukemia. 2007 May;21(5):998-1004 [17361227.001]

[Cites] Blood. 2001 Jan 1;97(1):89-94 [11133746.001]

(PMID = 17440048.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / K23 CA111728; United States / NCI NIH HHS / CA / K23 CA 111728

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

[Other-IDs] NLM/ PMC1924773

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Intact apoptosis signaling in myeloid leukemia cells determines treatment outcome in childhood AML.

Recently we reported that intact apoptosis signaling is indicative of favorable outcome in childhood acute lymphoblastic leukemia.

Here we addressed this issue in 45 pediatric acute myeloid leukemia patients analyzing 2 core apoptogenic events: cytochrome c release and caspase-3 activation.

Thus, the propensity to undergo apoptosis of leukemia cells is an important feature for favorable treatment outcome and may serve as an additional stratification tool for pediatric AML patients.

[MeSH-major] Apoptosis. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / therapy. Signal Transduction

[MeSH-minor] Caspase 3 / metabolism. Child. Cytochromes c / metabolism. Disease-Free Survival. Enzyme Activation. Humans. Remission Induction. Risk Factors. Treatment Outcome

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18083847.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Databank-accession-numbers] ClinicalTrials.gov/ NCT00111345

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 9007-43-6 / Cytochromes c; EC 3.4.22.- / Caspase 3

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Prognostic significance of WT1 gene expression in pediatric acute myeloid leukemia.

High expression of WT1 at diagnosis has been associated with unfavorable prognosis in adult acute myeloid leukemia (AML).

The prognostic relevance of WT1 expression in pediatric AML was evaluated in only one study, including 47 patients, which showed that very low levels of WT1 at presentation were associated with an excellent outcome.

To test the validity of these findings we measured levels of WT1 in 41 newly diagnosed pediatric AML of the non-M3 FAB subtype.

PROCEDURE: Patients were treated according to an AML-BFM 83-based protocol in a single institution.

CONCLUSIONS: Higher WT1 expression was associated with favorable cytogenetics subtypes and accordingly with better outcome in children with AML in this study.

[MeSH-major] Genes, Wilms Tumor. Leukemia, Myeloid / genetics

[MeSH-minor] Acute Disease. Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brazil / epidemiology. Child. Child, Preschool. Chromosome Inversion. Chromosomes, Human, Pair 16 / ultrastructure. Chromosomes, Human, Pair 21 / ultrastructure. Chromosomes, Human, Pair 8 / ultrastructure. Cytarabine / therapeutic use. Daunorubicin / therapeutic use. Etoposide / therapeutic use. Female. Follow-Up Studies. Gene Expression Regulation, Leukemic. Humans. Infant. Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / mortality. Male. Neoplasm Proteins / biosynthesis. Prognosis. Proportional Hazards Models. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Translocation, Genetic. WT1 Proteins / biosynthesis

Genetic Alliance. consumer health - Leukemia, Myeloid.

Hazardous Substances Data Bank. CYTARABINE .

Hazardous Substances Data Bank. DAUNORUBICIN .

Hazardous Substances Data Bank. ETOPOSIDE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16883592.001).

[ISSN] 1545-5009

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Neoplasm Proteins; 0 / WT1 Proteins; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; ZS7284E0ZP / Daunorubicin; DAV regimen

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Unusual type of TLS/FUS-ERG chimeric transcript in a pediatric acute myelocytic leukemia with 47,XX,+10,t(16;21)(p11;q22).

We report on a case of pediatric acute myelocytic leukemia showing 47,XX,+10,t(16;21)(p11;q22) that resulted in an unusual TLS/FUS-ERG chimeric transcript.

The leukemic cells showed erythrophagocytosis, positive reactions for myeloperoxidase and Sudan black B stains, and negative reactions for periodic acid-Schiff and alpha-naphtyl butyrate esterase stains as well as expression of myeloid antigens.

[MeSH-major] Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. RNA-Binding Protein FUS / genetics. Translocation, Genetic

[MeSH-minor] Bone Marrow Cells / cytology. Child, Preschool. Chromosomes, Human, Pair 10. Female. Humans. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Sequence Analysis, DNA. Trisomy

Genetic Alliance. consumer health - Acute Myelocytic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16737920.001).

[ISSN] 0165-4608

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA-Binding Protein FUS; 0 / TLS-ERG fusion protein, human

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Immunophenotypic differences between diagnosis and relapse in childhood AML: Implications for MRD monitoring.

BACKGROUND: Determination of antigen expression patterns is, in addition to morphologic analysis, essential to the diagnosis of acute myeloid leukemia (AML).

The present study was performed to determine (a) the degree of changes in immunophenotype and their consequences on the monitoring of minimal residual disease (MRD) in childhood AML and (b) whether certain clusters of changes in antigen expression patterns exist between diagnosis and relapse.

METHODS: Bone marrow specimens of 48 children enrolled in the German AML-BFM-93/98 (Acute Myeloid Leukemia-Berlin-Frankfurt-Munster) studies were analyzed immunologically, morphologically, and genetically at diagnosis and at first relapse.

We did not observe significant changes for lineage specific markers, with comparable occurrences of loss or gain of myeloid and lymphoid antigens in the sample pairs.

The antibody panels used for MRD monitoring in childhood AML should therefore not be restricted to the immunophenotype detected at presentation but should include in particular markers of lineage immaturity.

[MeSH-major] Antigens, Neoplasm / immunology. Immunophenotyping / methods. Leukemia, Myeloid / diagnosis. Neoplasm, Residual / diagnosis

[MeSH-minor] Acute Disease. Adolescent. Biomarkers, Tumor / genetics. Biomarkers, Tumor / immunology. Bone Marrow / immunology. Bone Marrow / pathology. Child. Child, Preschool. Clone Cells. Flow Cytometry. Humans. Infant. Karyotyping. Recurrence

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] (c) 2004 Wiley-Liss, Inc.

(PMID = 15624201.001).

[ISSN] 1552-4949

[Journal-full-title] Cytometry. Part B, Clinical cytometry

[ISO-abbreviation] Cytometry B Clin Cytom

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Tandem duplications of MLL and FLT3 are correlated with poor prognoses in pediatric acute myeloid leukemia: a study of the Japanese childhood AML Cooperative Study Group.

BACKGROUND: Mixed-lineage leukemia (MLL)-partial tandem duplication (PTD) is associated with poor prognosis in adult acute myeloid leukemia (AML), but its relationship to pediatric AML is unknown.

PROCEDURE: One hundred fifty-eight newly diagnosed AML patients, including 13 FAB-M3 and 10 Down syndrome (DS) patients, who were treated on the Japanese Childhood AML Cooperative Treatment Protocol AML 99 were analyzed for MLL-PTD, as well as internal tandem duplication (ITD) and the kinase domain mutation (D835Mt) in the FLT3 gene.

RESULTS: We found MLL-PTD in 21 (13.3%) of 158 AML patients, but not in FAB-M3 or DS patients.

The differences between patients with and without MLL-PTD were significant for 3-year overall survival (OS) (56.3% vs. 83.2%, P = 0.018), disease-free survival (DFS) (41.7% vs. 69.6%, P = 0.010), and relapse rate (RR) (54.3% vs. 27.6%, P = 0.0085) of 135 AML patients excluding the FAB-M3 and DS patients.

CONCLUSION: AML patients with FLT3-ITD, but not D835Mt, showed a poor prognosis.

AML patients with MLL-PTD were also correlated with poor prognosis in this study.

[MeSH-major] Gene Duplication. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. fms-Like Tyrosine Kinase 3 / genetics

[MeSH-minor] Adolescent. Child. Child, Preschool. DNA Mutational Analysis. Down Syndrome / complications. Down Syndrome / genetics. Female. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Male. Mutation. Prognosis. Tandem Repeat Sequences. Treatment Outcome

Genetic Alliance. consumer health - Acute Myelocytic Leukemia.

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] (c) 2007 Wiley-Liss, Inc.

(PMID = 17763464.001).

[ISSN] 1545-5017

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] A review on allogeneic stem cell transplantation for newly diagnosed pediatric acute myeloid leukemia.

Survival of pediatric acute myeloid leukemia (AML) has improved considerably over the past decades.

However, it remains controversial whether allo-SCT is superior to chemotherapy for children with newly diagnosed AML.

This review summarizes phase 3 clinical trials that compared allo-SCT with chemotherapy (including autologous SCT) in pediatric AML, excluding studies that did not use the intention-to-treat analysis or correct for time-to-transplantation.

Because allo-SCT also gives more severe side effects and results more often in secondary malignancies than chemotherapy, we do not recommend allo-SCT in first remission for pediatric AML in general.

Further research should focus on the possibility that subgroups might benefit from allo-SCT, aiming at further improvements in the prognosis of pediatric AML.

[MeSH-major] Leukemia, Myeloid, Acute / therapy. Stem Cell Transplantation

[MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Clinical Trials, Phase III as Topic. Cost-Benefit Analysis. Disease-Free Survival. Humans. Remission Induction. Survival Analysis. Transplantation, Autologous. Transplantation, Homologous. Treatment Outcome

Genetic Alliance. consumer health - Leukemia, Myeloid.

Genetic Alliance. consumer health - Transplantation.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20538803.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Treatment of childhood acute myeloblastic leukemia: dose intensification improves outcome and maintenance therapy is of no benefit--multicenter studies of the French LAME (Leucémie Aiguë Myéloblastique Enfant) Cooperative Group.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Antineoplastic Protocols / standards. Leukemia, Myeloid, Acute / therapy

[MeSH-minor] Adolescent. Bone Marrow Transplantation. Child. Child, Preschool. Dose-Response Relationship, Drug. Follow-Up Studies. France. Humans. Infant. Infant, Newborn. Remission Induction. Risk Assessment. Survival Analysis. Treatment Outcome

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16121218.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial

[Publication-country] England

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The presence of central nervous system disease at diagnosis in pediatric acute myeloid leukemia does not affect survival: a Children's Oncology Group study.

BACKGROUND: The presence of central nervous system (CNS) disease in pediatric acute myeloid leukemia (AML) is often thought to confer a worse prognosis.

This study examined the outcome of children with AML who had CNS disease at diagnosis.

METHODS: Patients enrolled on Children's Cancer Group protocols 2861, 2891, 2941, and 2961 being treated for de novo AML were classified for the presence of CNS disease at diagnosis as CNS1 (<5 WBC in the CSF without blasts), CNS2 (<5 WBC in the CSF with blasts), or CNS3 (> or =5 WBC in the CSF with blasts).

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] 2010 Wiley-Liss, Inc.

[Cites] Blood. 1999 Dec 1;94(11):3707-16 [10572083.001]

[Cites] Lancet Oncol. 2008 Mar;9(3):257-68 [18308251.001]

[Cites] Leukemia. 2000 Apr;14(4):684-7 [10764155.001]

[Cites] Leukemia. 2000 Jul;14(7):1201-7 [10914543.001]

[Cites] Blood. 2001 Jan 1;97(1):56-62 [11133742.001]

[Cites] Leukemia. 2001 Jan;15(1):46-9 [11243398.001]

[Cites] Blood. 2001 Sep 15;98(6):1714-20 [11535502.001]

[Cites] Br J Haematol. 2002 Aug;118(2):365-77 [12139720.001]

[Cites] Br J Haematol. 2002 Aug;118(2):378-84 [12139721.001]

[Cites] J Clin Oncol. 2003 Sep 15;21(18):3415-22 [12885836.001]

[Cites] J Pediatr Hematol Oncol. 2003 Oct;25(10):760-8 [14528097.001]

[Cites] Leukemia. 2003 Nov;17(11):2090-6 [14523477.001]

[Cites] J Clin Oncol. 2004 Jan 1;22(1):150-6 [14701777.001]

[Cites] Leuk Res. 2004 Oct;28(10):1007-11 [15289011.001]

[Cites] Blood. 1985 Nov;66(5):1062-7 [3840394.001]

[Cites] J Clin Oncol. 1987 Jul;5(7):1026-32 [3474356.001]

[Cites] J Clin Oncol. 1990 Jan;8(1):75-83 [2295913.001]

[Cites] J Clin Oncol. 1991 Apr;9(4):572-80 [2066754.001]

[Cites] J Clin Oncol. 1993 Aug;11(8):1448-57 [8336184.001]

[Cites] Blood. 1994 Jul 15;84(2):355-66 [8025264.001]

[Cites] Blood. 1998 Jan 15;91(2):608-15 [9427716.001]

[Cites] J Pediatr Hematol Oncol. 1999 Mar-Apr;21(2):91-102 [10206454.001]

[Cites] Leukemia. 2005 Aug;19(8):1355-60 [15920490.001]

[Cites] Leukemia. 2005 Dec;19(12):2030-42 [16304570.001]

[Cites] Leukemia. 2005 Dec;19(12):2130-8 [16304572.001]

[Cites] J Clin Oncol. 2005 Dec 20;23(36):9172-8 [16361619.001]

[Cites] Cancer. 2007 Jan 1;109(1):157-63 [17133407.001]

[Cites] Pediatr Blood Cancer. 2007 Apr;48(4):393-8 [16550530.001]

[Cites] Oncologist. 2007 Mar;12(3):341-55 [17405900.001]

[Cites] Pediatr Blood Cancer. 2007 Jul;49(1):17-22 [16856158.001]

[Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]

[CommentIn] Pediatr Blood Cancer. 2010 Sep;55(3):399-400 [20658608.001]

(PMID = 20658610.001).

[ISSN] 1545-5017

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / U10 CA98413; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / U10 CA098543-01; United States / NCI NIH HHS / CA / U10 CA98543

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Other-IDs] NLM/ NIHMS218661; NLM/ PMC2990693

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Place of HSCT in treatment of childhood AML.

This short review focuses on the role of hematopoietic SCT (HSCT) in childhood AML.

Data on haploidentical HSCT and on cord blood HSCT are still lacking in the case of AML.

[MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Living Donors

[MeSH-minor] Adolescent. Child. Child, Preschool. Clinical Trials as Topic. Disease-Free Survival. Humans. Infant. Remission Induction. Siblings. Survival Rate. Transplantation, Autologous. Transplantation, Homologous

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18978749.001).

[ISSN] 1476-5365

[Journal-full-title] Bone marrow transplantation

[ISO-abbreviation] Bone Marrow Transplant.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Number-of-references] 15

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Determination of leukemia stem cells in childhood acute myeloid leukemia and its clinical significance].

The aim of this study was to detect the presence of human AML leukemia stem cells (LSC) in childhood patients with acute leukemia (AL) and analyze the correlation between LSC concentrations and minimal residual disease (MRD) levels in AML cases after remission.

The multi-parameter flow cytometry (FCM) and a panel of monoclonal antibody combination were used to detect the AML LSC or AML LSC immunophenotype-identical cell (AML LSC-IPIC) concentrations in childhood AML or ALL leukemia both at new diagnosis and at remission and correlated AML LSC to the MRD levels at different time points after remission.

The results indicated that the AML LSC or AML LSC-IPIC concentrations [in average 166 (range 14 - 1459)/100 000 mononuclear cells (MNCs)] in AML at initial diagnosis were significantly higher than those in ALL [7 (range 0 - 560)/100 000 MNCs, p < 0.017] and control [0 (range 0 - 6)/100 000 MNCs, p < 0.017], respectively.

The AML LSC concentrations in AML at non-CR were in average 36 (range 5 - 224)/100 000 MNCs.

No statistical difference (p > 0.05) was found between the AML LSC or AML LSC-IPIC concentrations in AML (in average 6 (range 0 - 41)/100, 000 MNCs) and ALL [10 (range 0 - 105)/100, 000 MNCs] after CR.

The significantly negative correlation was noticed between AML LSC concentrations and MRD levels.

It is concluded that the AML LSCs exist in newly diagnosed AML, which are significantly reduced when complete remission has achieved, but the low levels of these populations still remain.

The phenotypically similar (CD34(+)CD38⁻CD123(+)) AML LSC populations have also been found in the bone marrow from ALL patients, but their concentrations are not significantly different when CR has achieved.

The significantly negative correlation between AML LSC concentrations and MRD levels is observed in AML patients after remission.

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20723307.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Combination of cladribine and cytarabine is effective for childhood acute myeloid leukemia: results of the St Jude AML97 trial.

Because cladribine can increase cytarabine triphosphate levels, we tested a cladribine-cytarabine combination in the St Jude AML97, trial in which this combination was administered before standard chemotherapy to 96 children with acute myeloid leukemia (AML) or myelodysplastic syndrome.

Our results suggest that cladribine in combination with continuous-infusion cytarabine is effective therapy for childhood AML.

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. CYTARABINE .

Hazardous Substances Data Bank. DAUNORUBICIN .

Hazardous Substances Data Bank. ETOPOSIDE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Blood. 1994 Aug 15;84(4):1237-42 [7914104.001]

[Cites] Leukemia. 2005 Dec;19(12):2130-8 [16304572.001]

[Cites] Leukemia. 2005 Dec;19(12):2025-9 [16304569.001]

[Cites] Br J Haematol. 1998 Apr;101(1):130-40 [9576193.001]

[Cites] Leukemia. 1996 Oct;10(10):1563-9 [8847890.001]

[Cites] Blood. 2006 Feb 15;107(4):1315-24 [16254147.001]

[Cites] Leuk Lymphoma. 2000 Sep;39(1-2):121-9 [10975390.001]

[Cites] J Clin Oncol. 2001 Jun 1;19(11):2804-11 [11387351.001]

[Cites] J Clin Oncol. 2002 Oct 15;20(20):4217-24 [12377965.001]

[Cites] Br J Haematol. 2003 Jul;122(2):217-25 [12846889.001]

[Cites] Br J Haematol. 2003 Oct;123(2):243-52 [14531905.001]

[Cites] Leukemia. 2004 Jan;18(1):72-7 [14586478.001]

[Cites] Leuk Res. 2004 Apr;28(4):349-52 [15109533.001]

[Cites] J Clin Oncol. 2004 Nov 1;22(21):4384-93 [15514380.001]

[Cites] J Clin Invest. 1990 Nov;86(5):1480-8 [1700795.001]

[Cites] J Clin Oncol. 1991 Mar;9(3):416-22 [1671875.001]

[Cites] J Clin Oncol. 1992 Mar;10(3):364-70 [1346800.001]

[Cites] Blood. 1993 Jan 1;81(1):143-50 [8093345.001]

[Cites] Blood. 1996 Jan 1;87(1):256-64 [8547650.001]

[Cites] Cancer. 2008 Jul 15;113(2):376-82 [18459178.001]

[Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]

[Cites] Blood. 2007 Nov 15;110(10):3532-9 [17660380.001]

[Cites] J Clin Oncol. 2006 Sep 20;24(27):4499-506 [16983120.001]

(PMID = 19242495.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / P30 CA021765-30; United States / NCI NIH HHS / CA / P30 CA-21765

[Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 04079A1RDZ / Cytarabine; 47M74X9YT5 / Cladribine; 6PLQ3CP4P3 / Etoposide; EC 3.5.1.1 / Asparaginase; ZS7284E0ZP / Daunorubicin

[Other-IDs] NLM/ NIHMS90802; NLM/ PMC2726271

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Multipoint interphase FISH analysis of chromosome 3 abnormalities in 28 childhood AML patients.

To examine chromosome 3 abnormalities, in 28 childhood acute myeloid leukemia bone marrow samples, we performed interphase multipoint-fluorescence in situ hybridization using 84 chromosome 3-specific probes and detected clonal chromosome 3 aberrations in nine cases, which is of a higher frequency than the previously reported one.

We identified rare structural rearrangements in childhood acute myeloblastic leukemia, involving 3q21 and 3q26 loci around RPN1 and MDS1/EVI1 respectively.

The poor outcome in pediatric patients with 3q rearrangements appears to be quite uniform.

[MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 3. In Situ Hybridization, Fluorescence / methods. Interphase. Leukemia, Myeloid / genetics

[MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Female. Humans. Infant. Male

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16405433.001).

[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

[Publication-country] Denmark

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] FLT3 and KIT mutated pediatric acute myeloid leukemia (AML) samples are sensitive in vitro to the tyrosine kinase inhibitor SU11657.

New treatment strategies to improve the outcome of pediatric acute myeloid leukemia (AML) are required as 40% of children diagnosed with AML do not survive.

Around 30% of pediatric AML patients harbour a mutation in the tyrosine kinases FLT3 (+/-20%) or KIT (+/-10%).

In this study we investigated whether pediatric AML samples (N=61) were sensitive to the tyrosine kinase inhibitor SU11657 (similar to the clinically available drug sunitinib) in vitro, and whether sensitivity was related to expression of, and mutations in, FLT3 and KIT.

[MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Mutation. Organic Chemicals / pharmacology. Proto-Oncogene Proteins c-kit / genetics. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. fms-Like Tyrosine Kinase 3 / genetics

[MeSH-minor] Adolescent. Cell Line, Tumor. Child. Child, Preschool. Female. Humans. Male

Genetic Alliance. consumer health - Acute Myelocytic Leukemia.

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.

(PMID = 20435347.001).

[ISSN] 1873-5835

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Organic Chemicals; 0 / SU 11657; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3