BioMedLib Search Engine [ goto HOMEPAGE ]

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] The evaluation of hTERT mRNA expression in acute leukemia children and 2 years follow-up of 40 cases.

The aim of this study is to evaluate (1) the human telomerase-specific reverse transcriptase (hTERT) mRNA expression in childhood acute leukemia, (2) the association between the hTERT mRNA expression with the patients' characteristics and the known prognostic factors and (3) the correlation of the patients' survival with the initial hTERT mRNA value at diagnosis.

A total of 40 newly diagnosed patients consist of children [31 cases with acute lymphoblastic leukemia (ALL) and 9 cases with acute myeloblastic leukemia (AML)] were prospectively included into the study.

The highest hTERT mRNA value was observed in Pre B-cell ALL patients followed by B-cell ALL, T-cell ALL and AML.

The hTERT mRNA relative ratio difference between the ALL and AML groups was significant.

Although DFS and OS was longer in AML patients with lower initial hTERT mRNA, the difference was not significant.

In conclusion, the hTERT mRNA expression values were not significantly associated with the known prognostic factors in children both with ALL and AML. hTERT mRNA value is a significant factor for childhood ALL at diagnosis in relation to the estimated survival.

[MeSH-major] Biomarkers, Tumor / genetics. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA, Messenger / metabolism. Telomerase / metabolism

[MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Follow-Up Studies. Humans. Infant. Male. Prospective Studies

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

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

[Cites] Leukemia. 2007 May;21(5):965-72 [17344921.001]

[Cites] Cancer. 2003 May 1;97(9):2212-7 [12712473.001]

[Cites] Virchows Arch. 2000 Jul;437(1):1-16 [10963374.001]

[Cites] Ann Oncol. 2004 Oct;15(10):1476-80 [15367406.001]

[Cites] Turk J Haematol. 2006 Jun 5;23(2):77-83 [27265287.001]

[Cites] Cancer Res. 1998 Nov 1;58(21):4918-22 [9810000.001]

[Cites] Am J Hum Genet. 1998 May;62(5):1003-7 [9545415.001]

[Cites] Stem Cells. 2007 Aug;25(8):1853-61 [17510216.001]

[Cites] Leuk Res. 2004 Jul;28(7):707-11 [15158092.001]

[Cites] Leuk Lymphoma. 2005 Mar;46(3):393-9 [15621829.001]

[Cites] Biochem Soc Trans. 2000 Feb;28(2):245-50 [10816136.001]

[Cites] Clin Cancer Res. 1996 May;2(5):799-803 [9816233.001]

[Cites] Br J Haematol. 1998 Jan;100(1):156-65 [9450805.001]

[Cites] Br J Haematol. 1998 Sep;102(5):1367-75 [9753073.001]

[Cites] Zhonghua Xue Ye Xue Za Zhi. 2001 Nov;22(11):592-4 [11855149.001]

[Cites] Crit Rev Oncol Hematol. 2002 Jan;41(1):29-40 [11796230.001]

[Cites] Sichuan Da Xue Xue Bao Yi Xue Ban. 2003 Jul;34(3):486-8 [12910697.001]

[Cites] J Pediatr Hematol Oncol. 2004 Jun;26(6):342-50 [15167346.001]

[Cites] Am J Hematol. 2005 Aug;79(4):267-73 [16044449.001]

[Cites] Blood. 1995 May 1;85(9):2315-20 [7727765.001]

[Cites] Hum Genet. 1998 Apr;102(4):397-402 [9600234.001]

[Cites] Clin Cancer Res. 1997 Apr;3(4):619-25 [9815729.001]

[Cites] Leuk Lymphoma. 2004 Dec;45(12):2477-80 [15621763.001]

(PMID = 18293058.001).

[ISSN] 0925-5710

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

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

[Publication-country] Japan

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[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 .

Hazardous Substances Data Bank. VIDARABINE .

[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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] 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 .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

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

(PMID = 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

   

Advertisement

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] Profile of infections in newly diagnosed patients with acute leukemia during the induction phase of treatment.

BACKGROUND AND PURPOSE: Acute leukemia is the most common pediatric malignancy.

The aim of the present study is to assess the type, frequency, and severity of infectious complications in a cohort of pediatric cancer patients treated at a single medical institution.

We also aim to identify factors affecting bloodstream infections in newly diagnosed ALL and AML pediatric patients during the induction phase of treatment.

PATIENTS AND METHODS: This study was carried out at the Department of Pediatric Oncology, National Cancer Institute, Cairo University, during the time period from January 1st to June 30th 2007.

Inclusion criteria were pediatric age group (from 0-16 years), newly diagnosed acute leukemia, positive blood culture and documented site of infection.

RESULTS: This is a retrospective study including 100 newly diagnosed cases of acute leukemia.

Fifty-four patients had ALL, and 46 patients had AML.

KEY WORDS: Acute leukemia - Blood stream infection - Bacterial infection - Pediatric cancer patients.

[Email] Email this result item

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

(PMID = 21415868.001).

[ISSN] 1110-0362

[Journal-full-title] Journal of the Egyptian National Cancer Institute

[ISO-abbreviation] J Egypt Natl Canc Inst

[Language] eng

[Publication-type] Journal Article

[Publication-country] Egypt

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] Characterization of 6q abnormalities in childhood acute myeloid leukemia and identification of a novel t(6;11)(q24.1;p15.5) resulting in a NUP98-C6orf80 fusion in a case of acute megakaryoblastic leukemia.

Chromosome abnormalities of 6q are not frequently observed in myeloid disorders.

In this article, we report the incidence of these chromosome changes in childhood myeloid leukemia as 2%-4% based on the cytogenetic database of a single institution.

We applied fluorescence in situ hybridization (FISH) to characterize precisely the types of 6q abnormalities in seven patients (six with acute myeloid leukemia and one with myelodysplastic syndrome).

Among these, we identified a novel translocation, t(6;11)(q24.1;p15.5), in a patient with acute megakaryoblastic leukemia.

Further studies will aim to fully characterize C6orf80 and will elucidate the role of this new NUP98 fusion in myeloid leukemia.

[MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 6 / genetics. Leukemia, Myeloid / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

[MeSH-minor] Acute Disease. Adolescent. Amino Acid Sequence. Base Sequence. Child. Child, Preschool. Chromosome Breakage. Chromosomes, Artificial, Bacterial. Cytogenetic Analysis. DNA, Neoplasm / analysis. Humans. In Situ Hybridization, Fluorescence. Infant. Molecular Sequence Data. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction

Genetic Alliance. consumer health - Acute Megakaryoblastic Leukemia.

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) 2005 Wiley-Liss, Inc.

(PMID = 16028218.001).

[ISSN] 1045-2257

[Journal-full-title] Genes, chromosomes & cancer

[ISO-abbreviation] Genes Chromosomes Cancer

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Neoplasm; 0 / nuclear pore complex protein 98

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[Title] Does modulation of P-glycoprotein have clinical relevance in pediatric acute myeloid leukemia?

[MeSH-major] Drug Resistance, Neoplasm. Gene Expression Regulation, Leukemic. Immunosuppressive Agents / therapeutic use. Leukemia, Myeloid, Acute / metabolism. P-Glycoprotein / biosynthesis

[MeSH-minor] Adult. Age Factors. Antibodies, Monoclonal / chemistry. Child. Child, Preschool. Cyclosporine / pharmacology. Female. Flow Cytometry. Humans. Male. Randomized Controlled Trials as Topic. Remission Induction

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

Hazardous Substances Data Bank. CYCLOSPORIN A .

[Email] Email this result item

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

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

(PMID = 16754781.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Comment; Letter

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunosuppressive Agents; 0 / P-Glycoprotein; 83HN0GTJ6D / Cyclosporine

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] Identification of NOM1, a nucleolar, eIF4A binding protein encoded within the chromosome 7q36 breakpoint region targeted in cases of pediatric acute myeloid leukemia.

In this report, we describe the characterization of a novel MIF4G/MA3 family member called NOM1 (nucleolar protein with MIF4G domain 1) that was identified at the chromosome 7q36 breakpoint involved in 7;12 translocations associated with certain acute leukemias of childhood.

[MeSH-major] Chromosomes, Human, Pair 7 / genetics. Eukaryotic Initiation Factor-4A / metabolism. Exons / genetics. Leukemia, Myeloid, Acute / genetics. Nuclear Proteins / genetics. RNA-Binding Proteins / genetics

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

COS Scholar Universe. author profiles.

Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

Saccharomyces Genome Database. Saccharomyces Genome Database .

[Email] Email this result item

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

(PMID = 15715967.001).

[ISSN] 0378-1119

[Journal-full-title] Gene

[ISO-abbreviation] Gene

[Language] eng

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

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Codon, Nonsense; 0 / Nom1 protein, human; 0 / Nuclear Proteins; 0 / RNA-Binding Proteins; EC 2.7.7.- / Eukaryotic Initiation Factor-4A

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] Allogeneic versus autologous versus peripheral stem cell transplantation in CR1 pediatric AML patients: a single center experience.

BACKGROUND: Treatment of childhood acute myelocytic leukemia (AML) in first remission, is still evolving.

PROCEDURE: Out of 81 pediatric patients with AML in first CR, 67 were biologically randomized for allogeneic (n = 31), autologous (n = 20), or peripheral stem cell transplant (n = 16) after completing consolidation treatment, with the remaining (n = 11) dropping out or receiving chemotherapy.

CONCLUSION: In pediatric AML patients without a donor, autologous BMT or autologous PBSCT appears to be an effective treatment option with low transplant related mortality especially in less privileged countries where the chemotherapy only results are still low.

[MeSH-major] Bone Marrow Transplantation. Leukemia, Myeloid / therapy. Peripheral Blood Stem Cell Transplantation

[MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Transplantation, Autologous. Transplantation, Homologous

Genetic Alliance. consumer health - Transplantation.

MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.

[Email] Email this result item

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

[Copyright] Copyright 2005 Wiley-Liss, Inc.

(PMID = 15700262.001).

[ISSN] 1545-5009

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] 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.

COS Scholar Universe. author profiles.

[Email] Email this result item

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

[Cites] Blood. 2006 Jul 1;108(1):74-80 [16537811.001]

[Cites] Curr Opin Hematol. 2005 Jan;12(1):62-7 [15604893.001]

[Cites] J Clin Oncol. 2006 Aug 20;24(24):3904-11 [16921041.001]

[Cites] Blood. 2009 May 7;113(19):4505-11 [19221039.001]

[Cites] Blood. 2008 Mar 1;111(5):2527-37 [17965322.001]

[Cites] J Clin Oncol. 2005 Aug 20;23(24):5705-17 [16110030.001]

[Cites] Leukemia. 2002 May;16(5):776-84 [11986937.001]

[Cites] Ann Hematol. 2004;83 Suppl 1:S108-12 [15124698.001]

[Cites] Blood. 2006 May 1;107(9):3463-8 [16384925.001]

[Cites] J Clin Oncol. 2001 Mar 1;19(5):1279-87 [11230469.001]

[Cites] Blood. 2007 Jan 15;109(2):431-48 [16960150.001]

[Cites] Best Pract Res Clin Haematol. 2008 Dec;21(4):621-8 [19041601.001]

[Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]

[Cites] Blood. 2007 Jun 1;109(11):4641-7 [17299091.001]

[Cites] Blood. 2006 Mar 1;107(5):1806-9 [16291592.001]

[Cites] Blood. 1985 Feb;65(2):298-304 [3881140.001]

[Cites] Cancer. 2008 Jan 15;112(2):407-15 [18058809.001]

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

[Cites] Br J Haematol. 2003 Oct;123(2):243-52 [14531905.001]

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

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

[Cites] Br J Haematol. 1999 Oct;107(1):69-79 [10520026.001]

[Cites] J Clin Oncol. 2008 Oct 1;26(28):4595-602 [18559874.001]

[Cites] Hematology Am Soc Hematol Educ Program. 2009;:385-95 [20008224.001]

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

[Cites] Pediatr Blood Cancer. 2007 Jan;48(1):10-5 [16642489.001]

[Cites] Blood. 2009 Sep 17;114(12):2489-96 [19528532.001]

[Cites] J Clin Oncol. 2006 Aug 1;24(22):3686-92 [16877738.001]

[Cites] Blood. 2007 Dec 15;110(13):4172-4 [17909077.001]

[Cites] J Clin Oncol. 2003 Sep 15;21(18):3415-22 [12885836.001]

[Cites] Blood. 2010 Mar 25;115(12):2372-9 [20056794.001]

[Cites] J Clin Oncol. 2008 Oct 20;26(30):4944-51 [18606980.001]

[Cites] N Engl J Med. 1999 Sep 30;341(14):1051-62 [10502596.001]

[Cites] Pediatr Blood Cancer. 2009 Dec;53(6):1136-9 [19618455.001]

[Cites] J Clin Oncol. 2010 Feb 1;28(4):578-85 [20038731.001]

[Cites] J Clin Oncol. 2004 Feb 15;22(4):624-33 [14726504.001]

[Cites] J Clin Oncol. 2003 Dec 15;21(24):4642-9 [14673054.001]

[Cites] J Clin Oncol. 2008 Oct 10;26(29):4791-7 [18695255.001]

[Cites] Leukemia. 2009 Feb;23(2):262-70 [19020547.001]

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

[Cites] Leukemia. 2002 Apr;16(4):601-7 [11960339.001]

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

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

[Cites] Blood. 2009 Jun 25;113(26):6558-66 [19304957.001]

[Cites] Best Pract Res Clin Haematol. 2009 Dec;22(4):523-8 [19959103.001]

[Cites] J Clin Oncol. 2004 Apr 15;22(8):1404-12 [15084614.001]

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[Title] Ethnicity and survival in childhood acute myeloid leukemia: a report from the Children's Oncology Group.

We evaluated differences in outcome by ethnicity among children with acute myeloid leukemia (AML).

In conclusion, Hispanic and black children with AML have worse survival than white children.

Access to chemotherapy, differences in supportive care or leukemia phenotype, and reduced compliance are unlikely explanations for this difference because therapy was given intravenously according to CCG protocols.

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

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.

COS Scholar Universe. author profiles.

[Email] Email this result item

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

[Cites] Transplant Proc. 1991 Oct;23(5):2531-2 [1926465.001]

[Cites] Blood. 1984 Mar;63(3):694-700 [6696996.001]

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

[Cites] J Clin Oncol. 1997 Jul;15(7):2644-51 [9215836.001]

[Cites] Br J Haematol. 1998 Apr;101(1):130-40 [9576193.001]

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

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

[Cites] Biol Blood Marrow Transplant. 2001;7(1):45-8 [11215698.001]

[Cites] J Clin Oncol. 2001 May 15;19(10):2705-13 [11352963.001]

[Cites] Blood. 2002 Sep 15;100(6):1957-64 [12200352.001]

[Cites] Arch Intern Med. 2002 Sep 23;162(17):1985-93 [12230422.001]

[Cites] Am J Hematol. 2003 Feb;72(2):127-34 [12555217.001]

[Cites] N Engl J Med. 2003 Mar 20;348(12):1166-70 [12646675.001]

[Cites] N Engl J Med. 2003 Mar 20;348(12):1170-5 [12646676.001]

[Cites] N Engl J Med. 2003 Jun 19;348(25):2581-2; author reply 2581-2 [12815151.001]

[Cites] N Engl J Med. 2003 Jun 19;348(25):2581-2; author reply 2581-2 [12816115.001]

[Cites] Curr Oncol Rep. 2003 Nov;5(6):489-97 [14521808.001]

[Cites] JAMA. 2003 Oct 15;290(15):2008-14 [14559954.001]

[Cites] Blood. 2004 Jun 1;103(11):4036-42 [14976037.001]

[Cites] JAMA. 1995 Feb 22;273(8):633-7 [7844873.001]

(PMID = 16537811.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / 1 U10 CA98413-01

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

[Publication-country] United States

[Other-IDs] NLM/ PMC1895824

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[Title] Fms-like tyrosine kinase 3 mutations in childhood acute leukemias and their association with prognosis.

OBJECTIVE: In this study, the presence of FLT3 mutations in childhood acute leukemias patients and their association with prognosis were investigated.

MATERIALS AND METHODS: A total of 120 patients, 80 with acute lymphoblastic leukemia (ALL) and 40 with acute myeloblastic leukemia (AML), were included.

RESULTS: FLT3/ITD (internal tandem duplication) mutations were found in 6 (7.5%) of the patients with ALL and in 9 (22.5%) of those with AML, whereas no FLT3/TKD (trans kinase domain) mutation was evident in any case.

However, in FLT3/ITD positive and negative AML patients, there was a statistically significant difference in OS (p=0.0041), but not EFS and DFS (p=0.09, p=0.095, respectively).

CONCLUSION: We found that FLT3/ITD positivity increased with age and that it was associated with decrease in OS in AML patients, providing further evidence that it is an independent factor negatively influencing prognosis.

[MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / mortality. Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. fms-Like Tyrosine Kinase 3 / genetics

[MeSH-minor] Adolescent. Age Factors. Child. Child, Preschool. Disease-Free Survival. Humans. Infant. Kaplan-Meier Estimate. Male. Prognosis. Recurrence

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 = 21133602.001).

[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] EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[Title] Maternal alcohol consumption during pregnancy and risk of childhood leukemia: systematic review and meta-analysis.

BACKGROUND: Leukemia is the most frequently occurring cancer in children.

Although its etiology is largely unknown, leukemia is believed to result from an interaction between genetic and environmental factors.

METHODS: To assess the association between maternal alcohol consumption during pregnancy and childhood leukemia, a systematic review and meta-analysis of published studies was done.

Analyses were conducted by type of leukemia, children's age at diagnosis, and type of alcoholic beverage and trimester of pregnancy at alcohol use.

Alcohol intake during pregnancy (yes versus no) was statistically significantly associated with childhood acute myeloid leukemia (AML) [odds ratio (OR), 1.56; 95% confidence interval (CI), 1.13-2.15] but not with acute lymphoblastic leukemia (OR, 1.10; 95% CI, 0.93-1.29).

The OR of AML for an increase of a drink per week was 1.24 (95% CI, 0.94-1.64).

The association of alcohol intake during pregnancy with AML was observed for cancers diagnosed at age 0 to 4 years (OR, 2.68; 95% CI, 1.85-3.89) in five studies without heterogeneity (I2<or=0.1%).

CONCLUSIONS: The results of case-control studies indicate that maternal alcohol consumption during pregnancy is associated with a significantly increased risk of AML in young children.

IMPACT: Avoidance of maternal alcohol drinking during pregnancy might contribute to a decrease in the risk of childhood AML.

[MeSH-major] Alcohol Drinking / adverse effects. Leukemia / chemically induced. Prenatal Exposure Delayed Effects

[MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Mothers. Pregnancy. Risk Factors. Young Adult

Genetic Alliance. consumer health - Pregnancy.

MedlinePlus Health Information. consumer health - Alcohol.

MedlinePlus Health Information. consumer health - Childhood Leukemia.

MedlinePlus Health Information. consumer health - Leukemia.

[Email] Email this result item

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

[Copyright] Copyright (c) 2010 AACR

(PMID = 20447918.001).

[ISSN] 1538-7755

[Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology

[ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.

[Language] eng

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

[Publication-country] United States

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] Inversion (11)(p15q22) with NUP98-DDX10 fusion gene in pediatric acute myeloid leukemia.

The inv(11)(p15q22), a rare but recurrent chromosome abnormality that creates a NUP98-DDX10 fusion gene, is associated with de novo or secondary myeloid malignancies.

We report a case of acute monocytic leukemia presenting this rearrangement, studied using fluorescence in situ hybridization (FISH) and reverse transcriptase-PCR (RT-PCR).

[MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 11 / genetics. DEAD-box RNA Helicases / genetics. Gene Fusion. Leukemia, Myeloid, Acute / genetics. Nuclear Pore Complex Proteins / genetics

[MeSH-minor] Child. Humans. Male. Molecular Sequence Data

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 = 17116492.001).

[ISSN] 0165-4608

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Databank-accession-numbers] GENBANK/ AB040537/ AB040538

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

[Publication-country] United States

[Chemical-registry-number] 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; EC 3.6.1.- / DDX10 protein, human; EC 3.6.4.13 / DEAD-box RNA Helicases

[Number-of-references] 12

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] Defective in vitro growth of primitive hematopoietic cells from pediatric patients with acute myeloid leukemia.

BACKGROUND: Acute myeloid leukemia (AML) is a neoplastic hematologic disorder that arises at the level of a primitive stem/progenitor cell.

Most studies on the biology of the hematopoietic system in AML have focused on cells from adult patients; much less is known about hematopoietic cells from childhood AML.

PROCEDURE: By using a negative immunoselection system, we have obtained a primitive cell population (enriched for CD34(+) Lin(-) cells) from the bone marrow (BM) of 17 pediatric AML patients and characterized its proliferation, expansion, and differentiation potentials in liquid cultures supplemented with a mixture of 8 different recombinant stimulatory cytokines.

RESULTS: The proportion of CD34(+) cells in AML patients was extremely heterogeneous, ranging from 0% to 74%.

Regardless of their CD34(+) cell content, and in contrast to normal cells, AML cells showed a deficient capacity to proliferate even in the presence of the stimulatory cytokines.

AML progenitors were unable to generate new progenitor cells, indicating their inability to expand.

Interestingly, AML cells were able to differentiate in culture, giving rise to morphologically recognizable precursors.

A major difference, however, as compared to hematopoietic progenitors from normal subjects, was the fact that whereas in cultures of normal cells both myeloid and erythroid precursors were produced, in AML cultures the vast majority of the cells generated corresponded to myeloid cells, mostly mature macrophages.

CONCLUSION: As compared to their normal counterparts, primitive hematopoietic cells from pediatric patients with AML possess impaired proliferation, expansion, and differentiation potentials in vitro.

[MeSH-major] Bone Marrow Cells / pathology. Hematopoietic Stem Cells / pathology. Leukemia, Myeloid, Acute / blood

[MeSH-minor] Adolescent. Antigens, CD34 / blood. Cell Differentiation. Cell Proliferation. Cells, Cultured. Child. Child, Preschool. Cytokines / metabolism. Female. Humans. In Vitro Techniques. Male

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

MedlinePlus Health Information. consumer health - Stem Cells.

[Email] Email this result item

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

(PMID = 18680148.001).

[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 / Antigens, CD34; 0 / Cytokines

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[Title] Minimal residual disease-directed therapy for childhood acute myeloid leukaemia: results of the AML02 multicentre trial.

BACKGROUND: We sought to improve outcome in patients with childhood acute myeloid leukaemia (AML) by applying risk-directed therapy that was based on genetic abnormalities of the leukaemic cells and measurements of minimal residual disease (MRD) done by flow cytometry during treatment.

METHODS: From Oct 13, 2002, to June 19, 2008, 232 patients with de-novo AML (n=206), therapy-related or myelodysplasia-related AML (n=12), or mixed-lineage leukaemia (n=14) were enrolled at eight centres.

Other analyses were limited to the 216 patients with AML, excluding those with mixed-lineage leukaemia.

INTERPRETATION: Our findings suggest that the use of targeted chemotherapy and HSCT, in the context of a comprehensive risk-stratification strategy based on genetic features and MRD findings, can improve outcome in patients with childhood AML.

[MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / pathology

[MeSH-minor] Adolescent. Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Cytarabine / administration & dosage. Cytogenetic Analysis. Daunorubicin / administration & dosage. Disease-Free Survival. Etoposide / administration & dosage. Female. Flow Cytometry. Humans. Infant. Infant, Newborn. Male. Neoplasm, Residual. Remission Induction. Survival Rate. Young Adult

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

COS Scholar Universe. author profiles.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

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

[Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.

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

[Cites] J Clin Oncol. 2010 Feb 20;28(6):955-9 [20085940.001]

[Cites] Blood. 2001 Jun 15;97(12):3727-32 [11389009.001]

[Cites] J Clin Oncol. 2002 May 1;20(9):2302-9 [11981001.001]

[Cites] Lancet. 2002 May 11;359(9318):1686-9 [12020548.001]

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

[Cites] Br J Haematol. 2003 Jun;121(6):823-38 [12786792.001]

[Cites] Br J Haematol. 2003 Oct;123(2):243-52 [14531905.001]

[Cites] Cancer. 2003 Dec 15;98(12):2715-22 [14669294.001]

[Cites] J Chronic Dis. 1974 Sep;27(7-8):365-75 [4612056.001]

[Cites] Br J Cancer. 1977 Jan;35(1):1-39 [831755.001]

[Cites] Biometrics. 1979 Sep;35(3):549-56 [497341.001]

[Cites] Blood. 1996 Mar 1;87(5):1710-7 [8634416.001]

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

[Cites] Blood. 1996 Oct 15;88(8):2841-51 [8874180.001]

[Cites] Br J Haematol. 1998 Apr;101(1):130-40 [9576193.001]

[Cites] Leukemia. 2005 Dec;19(12):2090-100 [16304571.001]

[Cites] Leukemia. 2005 Dec;19(12):2130-8 [16304572.001]

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

[Cites] Cancer. 2006 Jun 1;106(11):2495-502 [16639734.001]

[Cites] Blood. 2006 Jul 1;108(1):74-80 [16537811.001]

[Cites] Cancer. 2006 Jul 1;107(1):116-24 [16721819.001]

[Cites] J Clin Oncol. 2006 Aug 1;24(22):3686-92 [16877738.001]

[Cites] J Clin Oncol. 2006 Sep 20;24(27):4499-506 [16983120.001]

[Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]

[Cites] Cancer. 2008 Jul 15;113(2):376-82 [18459178.001]

[Cites] J Clin Oncol. 2008 Oct 20;26(30):4944-51 [18606980.001]

[Cites] Blood. 2009 May 21;113(21):5083-9 [19131545.001]

[Cites] N Engl J Med. 2009 Jun 25;360(26):2730-41 [19553647.001]

[Cites] Blood. 2009 Jul 30;114(5):937-51 [19357394.001]

[Cites] Leukemia. 2009 Aug;23(8):1410-6 [19242495.001]

[Cites] J Clin Oncol. 2009 Aug 20;27(24):4007-13 [19620491.001]

[Cites] Hematology Am Soc Hematol Educ Program. 2009;:385-95 [20008224.001]

[CommentIn] Lancet Oncol. 2010 Jun;11(6):502-3 [20522371.001]

(PMID = 20451454.001).

[ISSN] 1474-5488

[Journal-full-title] The Lancet. Oncology

[ISO-abbreviation] Lancet Oncol.

[Language] eng

[Databank-accession-numbers] ClinicalTrials.gov/ NCT00136084

[Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01 CA115422; United States / NCI NIH HHS / CA / R01 CA115422-02

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

[Publication-country] England

[Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 93NS566KF7 / gemtuzumab; ZS7284E0ZP / Daunorubicin; DAV regimen

[Other-IDs] NLM/ NIHMS319127; NLM/ PMC3171799

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] 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.

MedlinePlus Health Information. consumer health - Acute Myeloid 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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] No nucleophosmin mutations in pediatric acute myeloid leukemia with normal karyotype: a study of the Japanese Childhood AML Cooperative Study Group.

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

[MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. DNA Mutational Analysis. Humans. Infant. Infant, Newborn. Japan. Karyotyping. Mutation

Genetic Alliance. consumer health - Acute Myelocytic Leukemia.

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 = 17315018.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

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

[Publication-country] England

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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] Cytogenetics of childhood acute myeloid leukemia: United Kingdom Medical Research Council Treatment trials AML 10 and 12.

PURPOSE: Karyotype is an independent indicator of prognosis in acute myeloid leukemia (AML) that is widely applied to risk-adapted therapy.

Because AML is rare in children, the true prognostic significance of individual chromosomal abnormalities in this age group remains unclear.

PATIENTS AND METHODS: This cytogenetic study of 729 childhood patients classified them into 22 subgroups and evaluated their incidence and risk.

Abnormalities of 3q and complex karyotypes, in the absence of favorable-risk features, have been associated with an adverse outcome in adults, but the results were not significant in this childhood series.

CONCLUSION: Because the spectrum of chromosomal changes and their risk association seem to differ between children and adults with AML, biologic differences are emerging, which will contribute to the redefinition of risk stratification for different age groups in the future.

[MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 12. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / mortality

[MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Transplantation. Child. Child, Preschool. Confidence Intervals. Cytogenetic Analysis. Disease-Free Survival. Female. Fluorescence. Genetic Predisposition to Disease / epidemiology. Humans. In Situ Hybridization. Infant. Kaplan-Meier Estimate. Karyotyping. Logistic Models. Male. Multivariate Analysis. Odds Ratio. Probability. Prognosis. Proportional Hazards Models. Registries. Retrospective Studies. Risk Assessment. Survival Analysis. Treatment Outcome. United Kingdom

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.

COS Scholar Universe. author profiles.

[Email] Email this result item

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

(PMID = 20439644.001).

[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

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

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

[Publication-country] United States

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] Low frequency of KIT gene mutation in pediatric acute myeloid leukemia with inv(16)(p13q22): a study of the Japanese Childhood AML Cooperative Study Group.

[MeSH-major] Chromosome Inversion. Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins c-kit / genetics

[MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease-Free Survival. Female. Follow-Up Studies. Humans. Infant. Male. Survival Rate

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

[Cites] J Clin Oncol. 2006 Aug 20;24(24):3904-11 [16921041.001]

[Cites] Leukemia. 2006 Jun;20(6):965-70 [16598313.001]

[Cites] Blood. 2006 Mar 1;107(5):1806-9 [16291592.001]

[Cites] Leukemia. 2000 May;14(5):945-7 [10803532.001]

[Cites] Br J Haematol. 2003 Jun;121(5):775-7 [12780793.001]

[Cites] Blood. 2000 Jan 15;95(2):726-7 [10660321.001]

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

[Cites] Pediatr Blood Cancer. 2007 Apr;48(4):393-8 [16550530.001]

[Cites] Leukemia. 2005 Sep;19(9):1536-42 [16015387.001]

[Cites] Br J Haematol. 2003 May;121(4):566-77 [12752097.001]

[Cites] Blood. 1995 Mar 1;85(5):1313-22 [7858261.001]

[Cites] Br J Haematol. 2005 Jan;128(1):18-34 [15606546.001]

(PMID = 17989000.001).

[ISSN] 0925-5710

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

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

[Publication-country] Japan

[Chemical-registry-number] EC 2.7.10.1 / Proto-Oncogene Proteins c-kit

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[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 .

Hazardous Substances Data Bank. NOVANTRONE .

[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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[Title] Preliminary results of the safety of immunotherapy with gemtuzumab ozogamicin following reduced intensity allogeneic stem cell transplant in children with CD33+ acute myeloid leukemia.

PURPOSE: Myeloablative allogeneic stem cell transplantation (SCT) has been successful in the treatment of childhood acute myeloid leukemia (AML), but may be associated with significant toxicity and recurrent disease.

Reduced-intensity allogeneic SCT may offer a less toxic approach to patients with AML.

Targeted immunotherapy with gemtuzumab ozogamicin has been shown to be safe, well tolerated in children, and, as a single agent, gemtuzumab ozogamicin has induced responses in 30% of patients with recurrent CD33+ AML.

Therefore, we explored the feasibility and toxicity of targeted immunotherapy following reduced-intensity allogeneic SCT in children with CD33+ AML.

EXPERIMENTAL DESIGN: Eight patients with CD33+ AML received a reduced-intensity allogeneic SCT following fludarabine 30 mg/m2 for 6 days and busulfan 3.2 mg/kg (<4 years, 4 mg/kg/d) for 2 days.

CONCLUSIONS: The administration of gemtuzumab ozogamicin post reduced-intensity allogeneic SCT in children with average risk AML is feasible and well tolerated with minimal toxicity.

The maximal tolerated dose has yet to be determined for gemtuzumab ozogamicin post reduced-intensity allogeneic SCT in children with CD33+ AML.

[MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antigens, CD / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis. Immunotherapy / methods. Leukemia, Myeloid, Acute / therapy. Stem Cell Transplantation / methods

[MeSH-minor] Adolescent. Antibodies, Monoclonal, Humanized. Busulfan / administration & dosage. Child. Child, Preschool. Combined Modality Therapy. Female. Graft vs Host Disease / prevention & control. Histocompatibility Testing. Humans. Infant. Male. Pilot Projects. Recurrence. Sialic Acid Binding Ig-like Lectin 3. Time Factors. Transplantation Conditioning. Transplantation, Homologous. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. FLUDARABINE .

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 = 16203817.001).

[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 / NHLBI NIH HHS / HL / T32 HL07968

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

[Publication-country] United States

[Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[Title] Clinical effectiveness and cost-effectiveness of stem cell transplantation in the management of acute leukaemia: a systematic review.

BACKGROUND: Acute leukaemia is a group of rapidly progressing cancers of bone marrow and blood classified as either acute myeloid leukaemia (AML) or acute lymphoblastic leukaemia (ALL).

OBJECTIVES: A systematic overview of the best available evidence on the clinical effectiveness and cost-effectiveness of SCT in the treatment of acute leukaemia.

Included randomised controlled trials (RCTs) and donor versus no donor (DvND) studies were mapped to the evidence covered in existing systematic reviews and meta-analyses according to a framework of 12 decision problems (DPs): DP1 related to SCT in adults with AML in first complete remission (CR1); DP2 to adults with AML in second or subsequent remission or with refractory disease (CR2+); DP3 to children with AML in CR1; DP4 to children with AML in CR2+; DP5 to adults with ALL in CR1; DP6 to adults with ALL in CR2+; DP7 to children with ALL in CR1; DP8 to children with ALL in CR2+; DP9 to comparison of different sources of stem cells in transplantation; DP10 to different conditioning regimens; DP11 to the use of purging in autologous SCT; and DP12 to the use of T-cell depletion in allogeneic SCT.

Although there is a wealth of information on costs and some information on cost-effectiveness of allogeneic SCT in adults with AML (DPs 1 and 2), there is very limited evidence on relative costs and cost-effectiveness for other DPs.

CONCLUSIONS: Bearing in mind the limitations, existing evidence suggests that sibling donor allogeneic SCT may be more effective than chemotherapy in adult AML (except in good-risk patients) in CR1, childhood AML in CR1 and adult ALL in CR1, and that autologous SCT is equal to or less effective than chemotherapy.

[MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / surgery. Precursor Cell Lymphoblastic Leukemia-Lymphoma / surgery

[MeSH-minor] Adult. Child. Cost-Benefit Analysis. Humans

Genetic Alliance. consumer health - Transplantation.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

PubMed Health. PubMed Health .

[Email] Email this result item

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

(PMID = 21138675.001).

[ISSN] 2046-4924

[Journal-full-title] Health technology assessment (Winchester, England)

[ISO-abbreviation] Health Technol Assess

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[Title] Infections and association with different intensity of chemotherapy in children with acute myeloid leukemia.

BACKGROUND: The objectives were to compare infections during different intensities of therapy in children with acute myeloid leukemia (AML).

METHODS: Subjects were children enrolled in Children's Cancer Group 2891 with AML.

This information sheds insight into the mechanisms behind susceptibility and outcome of infections in pediatric AML.

Genetic Alliance. consumer health - Leukemia, Myeloid.

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

[Copyright] (c) 2009 American Cancer Society.

[Cites] J Clin Oncol. 2000 May;18(9):1845-55 [10784625.001]

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

[Cites] Clin Infect Dis. 2002 Jan 1;34(1):7-14 [11731939.001]

[Cites] J Pediatr Hematol Oncol. 2002 Nov;24(8):627-35 [12439034.001]

[Cites] Leukemia. 2004 Jan;18(1):72-7 [14586478.001]

[Cites] J Clin Oncol. 2004 Nov 1;22(21):4384-93 [15514380.001]

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

[Cites] J Clin Oncol. 1998 Mar;16(3):1179-87 [9508206.001]

[Cites] Br J Haematol. 1999 Aug;106(2):436-44 [10460604.001]

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

[Cites] Ann Intern Med. 2005 Jun 21;142(12 Pt 1):979-95 [15968013.001]

[Cites] J Clin Oncol. 2006 Nov 20;24(33):5207-15 [17114653.001]

[Cites] Blood. 2007 Nov 15;110(10):3532-9 [17660380.001]

[Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]

[ErratumIn] Cancer. 2009 Jun 15;115(12):2807

(PMID = 19156894.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / U10 CA098543-06; United States / NCI NIH HHS / CA / U10 CA098413-06; United States / NCI NIH HHS / CA / U10 CA095861-08; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U10 CA095861; United States / NCI NIH HHS / CA / U10 CA098543; None / None / / U10 CA098413-06; United States / NCI NIH HHS / CA / U10 CA095861-06; United States / NCI NIH HHS / CA / CA095861-06; None / None / / U10 CA098543-06

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

[Publication-country] United States

[Other-IDs] NLM/ NIHMS107661; NLM/ PMC2677372

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] 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.

MedlinePlus Health Information. consumer health - Organ Donation.

[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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] Recent advances in management of acute myeloid leukemia (AML).

Acute myeloid leukemia (AML) is the most common childhood malignancy.

AML has therapeutically been difficult to treat.

In 2001, the World Health Organization (WHO), in conjunction with the Society for Hematopathology and the European Association of Hematopathology, published a new classification for myeloid neoplasms.

A number of chromosomal abnormalities are used to predict outcome and stratify therapeutic risk groups in children with AML.

Recently, alterations in receptor tyrosine kinases, tyrosine phosphatases and in oncogenes such as RAS have been implicated in the pathogenesis of AML.

This article aims to review the recent development in diagnosis, treatment and monitoring of AML.

Better understanding of the molecular pathogenesis of AML has led to the development of target-specific therapies.

The role of allogenic SCT, particularly whether it should be done during first CR or reserved for second remission, remains the most controversial issue in pediatric AML.

There is a need of collaboration with international pediatric cooperative oncology groups and definitive clinical trials in order to establish use of these newer molecules in pediatric populations.

[MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Immunologic Factors / therapeutic use. Leukemia, Myeloid, Acute / therapy. Neoplasm, Residual / drug therapy

[MeSH-minor] Antigens, CD / blood. Antigens, Differentiation, Myelomonocytic / blood. Child. Child, Preschool. Humans. Prognosis. Remission Induction. Sialic Acid Binding Ig-like Lectin 3. fms-Like Tyrosine Kinase 3 / antagonists & inhibitors. fms-Like Tyrosine Kinase 3 / genetics

Genetic Alliance. consumer health - Acute Myelocytic Leukemia.

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

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

[Cites] Blood. 2002 Oct 1;100(7):2292-302 [12239137.001]

[Cites] Blood. 2003 Feb 15;101(4):1494-504 [12406902.001]

[Cites] Br J Haematol. 1998 Apr;101(1):130-40 [9576193.001]

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

[Cites] Blood. 2007 Feb 15;109 (4):1387-94 [17082323.001]

[Cites] Haematologica. 1990 Mar-Apr;75(2):159-69 [2192943.001]

[Cites] Clin Cancer Res. 2001 Jun;7(6):1490-6 [11410481.001]

[Cites] Blood. 2003 Aug 1;102(3):795-801 [12649163.001]

[Cites] Blood. 2005 Aug 15;106(4):1183-8 [15886328.001]

[Cites] Leukemia. 2005 Dec;19(12):2130-8 [16304572.001]

[Cites] Leukemia. 2001 Mar;15(3):348-54 [11237056.001]

[Cites] Blood. 1991 Nov 15;78(10):2520-6 [1824249.001]

[Cites] Blood. 1992 Jun 15;79(12):3267-73 [1596567.001]

[Cites] Curr Opin Oncol. 2003 Jan;15(1):23-35 [12490758.001]

[Cites] Blood. 2004 May 15;103(10):3669-76 [14726387.001]

[Cites] Blood. 2005 Jan 1;105(1):54-60 [15345597.001]

[Cites] Cancer Res. 1998 Sep 15;58(18):4173-9 [9751631.001]

[Cites] Pediatr Clin North Am. 2008 Feb;55(1):21-51, ix [18242314.001]

[Cites] Blood. 2005 Feb 1;105(3):986-93 [15459012.001]

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

[Cites] Blood Cells Mol Dis. 2008 Mar-Apr;40(2):192-9 [17905612.001]

[Cites] Leuk Lymphoma. 2002 Sep;43(9):1843-8 [12685842.001]

[Cites] Klin Padiatr. 2002 Jul-Aug;214(4):188-94 [12165900.001]

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

[Cites] Leukemia. 2005 Dec;19(12):2025-9 [16304569.001]

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

[Cites] Br J Haematol. 1999 Sep;106(4):860-9 [10519985.001]

[Cites] Leukemia. 1996 Oct;10(10):1563-9 [8847890.001]

[Cites] J Clin Oncol. 2002 Oct 15;20(20):4217-24 [12377965.001]

[Cites] Br J Clin Pharmacol. 2003 Oct;56(4):370-7 [12968981.001]

[Cites] Blood. 2002 Oct 15;100(8):2708-16 [12351376.001]

[Cites] Haematologica. 2006 Mar;91(3):419-21 [16531270.001]

[Cites] N Engl J Med. 2008 May 1;358(18):1919-28 [18450603.001]

[Cites] Haematol Blood Transfus. 1987;30:71-5 [3305225.001]

[Cites] Onkologie. 2004 Jun;27(3):269-72 [15249716.001]

[Cites] Leuk Res. 2004 Apr;28(4):349-52 [15109533.001]

[Cites] Pediatr Blood Cancer. 2007 Aug;49(2):127-32 [16807916.001]

[Cites] Cancer Res. 1990 Oct 15;50(20):6525-8 [2208112.001]

[Cites] Eur J Cancer. 2004 Mar;40(5):707-21, discussion 722-4 [15010072.001]

[Cites] Bone Marrow Transplant. 2002 May;29(10):843-52 [12058234.001]

[Cites] N Engl J Med. 2008 May 1;358(18):1909-18 [18450602.001]

[Cites] J Clin Oncol. 2001 Jun 1;19(11):2804-11 [11387351.001]

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

(PMID = 18769895.001).

[ISSN] 0973-7693

[Journal-full-title] Indian journal of pediatrics

[ISO-abbreviation] Indian J Pediatr

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] India

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Immunologic Factors; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

[Number-of-references] 43

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] Complex karyotype defined by molecular cytogenetic FISH and M-FISH in an infant with acute megakaryoblastic leukemia and neurofibromatosis.

Acute myeloid leukemia in childhood is a heterogeneous group of diseases, and different epidemiologic factors are involved in the etiopathogenesis.

Genetic syndromes are one of the predisposing factors of acute myeloid leukemia (AML), including Down syndrome, Bloom syndrome, and neurofibromatosis.

Acute megakaryoblastic leukemia (AMKL) is the main subtype in Down syndrome infants, and acquired chromosomal anomalies are closely related to the physiopathology of the illness.

[MeSH-major] In Situ Hybridization, Fluorescence / methods. Leukemia, Megakaryoblastic, Acute / genetics. Neurofibromatoses / genetics

[MeSH-minor] Female. Genes, p53. Histone-Lysine N-Methyltransferase. Humans. Infant. Karyotyping. Myeloid-Lymphoid Leukemia Protein / genetics

Genetic Alliance. consumer health - Acute Megakaryoblastic Leukemia.

Genetic Alliance. consumer health - Neurofibromatosis.

MedlinePlus Health Information. consumer health - Neurofibromatosis.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

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

[Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.

(PMID = 20620601.001).

[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, 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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[Title] FAS promoter polymorphism: outcome of childhood acute myeloid leukemia. A children's oncology group report.

Previous work has shown increased risk of developing acute myeloid leukemia (AML) in adult patients with a variant allele at this site.

The same authors have shown that the presence of an adenine residue rather than a guanine residue at -1,377 bp significantly attenuates transcription factor stimulatory protein 1 binding and may contribute to a reduction in FAS expression and ultimately to the enrichment of apoptosis-resistant clones in AML.

We hypothesized that FAS genotype by altering susceptibility to apoptosis might affect outcome of childhood AML therapy.

EXPERIMENTAL DESIGN: Four hundred forty-four children treated for de novo AML on a uniform protocol were genotyped for FAS 1377.

CONCLUSIONS: FAS 1377 genotype does not alter outcome of de novo AML in children.

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

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

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

[Cites] J Mol Med (Berl). 2000;78(6):312-25 [11001528.001]

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

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

[Cites] J Exp Med. 1989 May 1;169(5):1747-56 [2469768.001]

[Cites] Cell. 1991 Jul 26;66(2):233-43 [1713127.001]

[Cites] Blood. 1992 Mar 1;79(5):1291-8 [1536952.001]

[Cites] J Biol Chem. 1992 May 25;267(15):10709-15 [1375228.001]

[Cites] J Biol Chem. 1993 May 25;268(15):10932-7 [7684370.001]

[Cites] Cell. 1994 Mar 25;76(6):969-76 [7511063.001]

[Cites] Science. 1995 Jun 2;268(5215):1347-9 [7539157.001]

[Cites] Blood. 1995 Nov 15;86(10):3848-60 [7579353.001]

[Cites] J Exp Med. 1998 Jun 1;187(11):1825-38 [9607923.001]

[Cites] Immunity. 1998 Jul;9(1):47-57 [9697835.001]

[Cites] Exp Hematol. 1999 May;27(5):868-74 [10340403.001]

[Cites] Cancer Res. 1999 Jul 1;59(13):3068-72 [10397246.001]

[Cites] Cancer Res. 2004 Nov 1;64(21):8101-8 [15520222.001]

[Cites] Cancer Res. 2003 Aug 1;63(15):4327-30 [12907599.001]

(PMID = 19047119.001).

[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 / U10 CA098543-06; United States / NCI NIH HHS / CA / R01 CA093552-01; United States / NCI NIH HHS / CA / R01 CA093552; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / R01 CA 76326-01; None / None / / U10 CA098543-06; United States / NCI NIH HHS / CA / CA093552-01

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD95

[Other-IDs] NLM/ NIHMS103099; NLM/ PMC2787450

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] Maternal alcohol and coffee drinking, parental smoking and childhood leukaemia: a French population-based case-control study.

We investigated the role of maternal alcohol and coffee drinking during pregnancy and that of parental smoking in the aetiology of childhood leukaemia.

A French, population-based, case-control study was conducted, comparing 472 [407 acute lymphoblastic leukaemia (ALL) and 62 acute myeloblastic leukaemia] cases of childhood acute leukaemia (AL) and 567 population controls, frequency-matched with cases on age, gender and region of residence.

The present results suggest a possible role of the highest consumption of alcohol by the mother during pregnancy in the aetiology of childhood AL.

[MeSH-major] Alcohol Drinking / adverse effects. Caffeine / adverse effects. Central Nervous System Stimulants / adverse effects. Leukemia, Myeloid, Acute / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Smoking / adverse effects

[MeSH-minor] Adolescent. Case-Control Studies. Child. Child, Preschool. Female. France / epidemiology. Humans. Infant. Male. Mothers. Pregnancy. Risk Factors

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

MedlinePlus Health Information. consumer health - Alcohol.

MedlinePlus Health Information. consumer health - Caffeine.

MedlinePlus Health Information. consumer health - Smoking.

MedlinePlus Health Information. consumer health - Smoking and Youth.

Hazardous Substances Data Bank. CAFFEINE .

[Email] Email this result item

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

(PMID = 17564585.001).

[ISSN] 0269-5022

[Journal-full-title] Paediatric and perinatal epidemiology

[ISO-abbreviation] Paediatr Perinat Epidemiol

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Central Nervous System Stimulants; 3G6A5W338E / Caffeine

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] 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.

COS Scholar Universe. author profiles.

[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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] Treatment strategy and results in children treated on three Dutch Childhood Oncology Group acute myeloid leukemia trials.

This report describes the long-term follow-up data of three consecutive Dutch Childhood Oncology Group acute myeloid leukemia (AML) protocols.

A total of 303 children were diagnosed with AML, of whom 209 were eligible for this report.

The first study was the AML-82 protocol.

Study AML-87 was based on the BFM-87 protocol, with prophylactic cranial irradiation in high-risk patients only, and without maintenance therapy.

The subsequent study AML-92/94 consisted of a modified BFM-93 protocol, that is, without maintenance therapy and prophylactic cranial irradiation.

Our results demonstrate that outcome in childhood AML is still unsatisfactory, and that further intensification of therapy carries the risk of enhanced toxicity.

Our patients are currently included in the MRC AML studies, based on the results of their AML 10 trial.

[MeSH-major] Antineoplastic Protocols / standards. Leukemia, Myeloid / therapy

[MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Cranial Irradiation. Female. Follow-Up Studies. Hematopoietic Stem Cell Transplantation. Humans. Infant. Infant, Newborn. Male. Recurrence. Risk Assessment. Survival Analysis. 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 = 16107896.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Clinical Trial, Phase III; Journal Article; Randomized Controlled Trial

[Publication-country] England

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] Natural killer cell allorecognition of missing self in allogeneic hematopoietic transplantation: a tool for immunotherapy of leukemia.

Donor-versus-recipient natural killer (NK) cell alloreactivity has been established as a key therapeutic element in HLA haplotype mismatched hematopoietic transplants in adult AML and pediatric ALL and as a possible beneficial effector in cord blood transplant for AML.

At present NK cell allotherapy for leukemia is deployed through stem cell transplantation (and ensuing NK cell reconstitution) across KIR ligand mismatches.

[MeSH-major] Hematopoietic Stem Cell Transplantation. Killer Cells, Natural / immunology. Leukemia, Myeloid / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

[MeSH-minor] Acute Disease. Adult. Child. Humans. Immunotherapy / methods. Transplantation, Homologous

Genetic Alliance. consumer health - Transplantation.

COS Scholar Universe. author profiles.

[Email] Email this result item

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

(PMID = 19717293.001).

[ISSN] 1879-0372

[Journal-full-title] Current opinion in immunology

[ISO-abbreviation] Curr. Opin. Immunol.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / 1 PO1 CA100265

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

[Publication-country] England

[Number-of-references] 46

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] Standardization of WT1 mRNA quantitation for minimal residual disease monitoring in childhood AML and implications of WT1 gene mutations: a European multicenter study.

A standardized, sensitive and universal method for minimal residual disease (MRD) detection in acute myeloid leukemia (AML) is still pending.

Although hyperexpression of Wilms' tumor (WT1) gene transcript has been frequently proposed as an MRD marker in AML, wide comparability of the various methods used for evaluating WT1 expression has not been given.

In a series of quality-control rounds, we analyzed 69 childhood AML samples and 47 normal bone marrow (BM) samples from 4 participating centers.

In AML samples, the median WT1/1E+04 Abelson (ABL) expression was 3.5E+03 compared with that of 2.3E+01 in healthy BM samples.

As 11.5% of childhood AML samples in this cohort harbored WT1 mutations in exon 7, the effect of mutations on WT1 expression has been investigated, showing that mutated cases expressed significantly higher WT1 levels than wild-type cases.

[MeSH-major] Bone Marrow Examination / standards. Genes, Wilms Tumor. Leukemia, Myeloid / pathology. RNA, Messenger / analysis. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction / standards

[MeSH-minor] Acute Disease. Adolescent. Adult. Child. Child, Preschool. Cohort Studies. DNA Primers. Exons / genetics. Female. Gene Expression Regulation, Leukemic. Humans. Infant. Male. Middle Aged. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Neoplasm, Residual. Sensitivity and Specificity. WT1 Proteins / biosynthesis. Young Adult

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

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

(PMID = 19322206.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

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

[Publication-country] England

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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] Common genetic variants in the interleukin-6 and chitotriosidase genes are associated with the risk for serious infection in children undergoing therapy for acute myeloid leukemia.

Infectious complications represent a substantial cause of morbidity and mortality in children undergoing therapy for acute myeloid leukemia (AML).

Since it has been shown that alterations in innate immune pathways contribute to the risk for serious infections, we analyzed well-characterized variants in innate immune genes (TNF, IL6, IL8, MPO, CHIT, FCGR2A, TLR2, and TLR4) to determine their possible contribution to infectious complications during therapy for pediatric AML.

The study population consisted of 168 North European Caucasian children enrolled on the clinical trial AML-BFM 93.

Our data suggest that variant alleles of both IL6 and CHIT could influence susceptibility to infection with Gram-negative bacteria in children undergoing therapy for AML.

[MeSH-major] Gram-Negative Bacterial Infections / etiology. Hexosaminidases / genetics. Interleukin-6 / genetics. Leukemia, Myeloid / genetics. Polymorphism, Genetic. Promoter Regions, Genetic / genetics

[MeSH-minor] Acute Disease. Adolescent. Alleles. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Clinical Trials as Topic. Female. Genetic Variation. Genotype. Gram-Negative Bacteria / isolation & purification. Humans. Infant. Infant, Newborn. Male

Genetic Alliance. consumer health - Leukemia, Myeloid.

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

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

(PMID = 16107886.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Interleukin-6; EC 3.2.1.- / Hexosaminidases; EC 3.2.1.- / chitotriosidase

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] 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 .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

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

[Cites] Blood. 2006 Oct 15;108(8):2764-9 [16809615.001]

[Cites] Cancer Res. 2006 Jun 15;66(12):6361-9 [16778214.001]

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

[Cites] Leukemia. 2003 May;17 (5):995-7 [12750723.001]

[Cites] Blood. 1992 Apr 1;79(7):1811-6 [1373089.001]

[Cites] Cancer Res. 2005 Feb 15;65(4):1277-84 [15735013.001]

[Cites] Cancer Cell. 2003 Aug;4(2):99-110 [12957285.001]

[Cites] Leuk Lymphoma. 2006 Feb;47(2):207-22 [16321850.001]

[Cites] Blood. 2006 Nov 15;108(10):3262-70 [16857985.001]

[Cites] Blood. 2007 Feb 15;109 (4):1387-94 [17082323.001]

[Cites] Blood. 2001 Oct 15;98 (8):2301-7 [11588023.001]

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

[Cites] Int J Hematol. 2005 Aug;82(2):100-7 [16146839.001]

[Cites] N Engl J Med. 2003 Mar 27;348(13):1201-14 [12660384.001]

[Cites] Blood. 1999 Mar 15;93(6):2043-56 [10068678.001]

[Cites] Blood. 2003 Mar 1;101(5):1692-7 [12411300.001]

[Cites] Blood. 2005 Aug 15;106(4):1183-8 [15886328.001]

[Cites] N Engl J Med. 2002 Aug 15;347(7):472-80 [12181401.001]

[Cites] Blood. 2007 May 15;109 (10 ):4168-70 [17227830.001]

[Cites] Blood. 1995 Apr 15;85(8):2005-12 [7718872.001]

[Cites] Curr Hematol Rep. 2004 May;3(3):203-9 [15087069.001]

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

[Cites] Blood. 2004 Sep 15;104(6):1841-9 [15166029.001]

[Cites] Blood. 2002 Jun 1;99(11):4222-4 [12010830.001]

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

[Cites] Cancer Res. 1997 Mar 1;57(5):837-41 [9041182.001]

[Cites] Blood. 1999 May 15;93(10):3302-8 [10233882.001]

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

[Cites] Blood. 2004 May 15;103(10):3669-76 [14726387.001]

[Cites] Clin Cancer Res. 2007 Mar 1;13(5):1516-22 [17332297.001]

[Cites] Blood. 2005 Apr 15;105(8):3058-65 [15626743.001]

[Cites] Clin Cancer Res. 2006 Sep 1;12(17):5165-73 [16951235.001]

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

[Cites] Blood. 2004 Jun 1;103(11):4276-84 [14962898.001]

[Cites] Blood. 1997 Jul 15;90(2):489-519 [9226149.001]

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

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

[Cites] Leukemia. 2003 Feb;17(2):350-8 [12592335.001]

[Cites] N Engl J Med. 2001 Apr 5;344(14):1031-7 [11287972.001]

[Cites] Cancer Res. 2001 Oct 1;61(19):7233-9 [11585760.001]

[Cites] J Pharmacol Exp Ther. 2007 Jun;321(3):953-60 [17389244.001]

[Cites] J Clin Oncol. 2004 Dec 1;22(23 ):4816-22 [15570084.001]

[Cites] Nature. 2005 Jun 30;435(7046):1267-70 [15988530.001]

[Cites] Blood. 2004 Nov 1;104(9):2690-6 [15251979.001]

[Cites] Eur J Clin Invest. 2007 Jan;37(1):73-82 [17181570.001]

[Cites] Blood. 2003 Aug 1;102(3):972-80 [12702506.001]

[Cites] Leukemia. 1998 Sep;12(9):1333-7 [9737679.001]

[Cites] Leukemia. 2003 Jan;17 (1):83-8 [12529664.001]

[Cites] Blood. 2005 Jul 15;106(2):673-80 [15797998.001]

[Cites] Blood. 2004 Mar 15;103(6):2325-31 [14644997.001]

[Cites] Nature. 1998 Feb 19;391(6669):811-4 [9486654.001]

[Cites] J Clin Oncol. 2001 Jul 1;19(13):3244-54 [11432892.001]

[Cites] Blood. 2003 Aug 15;102(4):1466-73 [12689934.001]

[Cites] Proc Natl Acad Sci U S A. 2002 Dec 10;99(25):16220-5 [12451177.001]

[Cites] Blood. 2005 Jul 1;106(1):345-52 [15774615.001]

[Cites] Blood. 2000 Jan 15;95(2):639-45 [10627474.001]

[Cites] Blood. 2004 Oct 1;104(7):1995-9 [15187030.001]

[Cites] Cell Growth Differ. 1992 Jul;3(7):461-9 [1419908.001]

[Cites] Leukemia. 2002 May;16(5):813-9 [11986941.001]

[Cites] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128.001]

[Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]

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

[Cites] Blood. 2004 Aug 15;104(4):1145-50 [15126317.001]

[Cites] Science. 2002 Feb 8;295(5557):1079-82 [11834837.001]

[Cites] Nat Clin Pract Oncol. 2005 Dec;2 Suppl 1:S30-5 [16341238.001]

[Cites] Leukemia. 2006 Aug;20(8):1368-76 [16761017.001]

[Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]

[Cites] Clin Cancer Res. 2004 May 15;10(10):3371-6 [15161691.001]

[Cites] Cancer. 2005 Oct 1;104(7):1442-52 [16116598.001]

[Cites] Adv Exp Med Biol. 2003;532:121-40 [12908554.001]

[Cites] Blood. 2001 Jun 1;97(11):3361-9 [11369625.001]

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

[Cites] Br J Haematol. 1991 Mar;77(3):323-7 [2012756.001]

[Cites] Leukemia. 1999 Dec;13(12):1932-42 [10602413.001]

[Cites] Blood. 2002 Jun 1;99(11):3885-91 [12010785.001]

[Cites] Blood. 2005 Mar 15;105(6):2527-34 [15550488.001]

[Cites] Leukemia. 1987 Oct;1(10):697-705 [3312833.001]

[Cites] Blood. 2001 Aug 15;98 (4):988-94 [11493443.001]

[Cites] Eur J Cancer. 2004 Mar;40(5):707-21, discussion 722-4 [15010072.001]

[Cites] J Clin Invest. 2006 Oct;116(10):2707-16 [16981007.001]

[Cites] Cell Cycle. 2006 Feb;5(3):271-3 [16397415.001]

[Cites] Blood. 2005 Aug 15;106(4):1154-63 [15870183.001]

[Cites] Semin Hematol. 2004 Apr;41(2 Suppl 4):27-32 [15190513.001]

[Cites] Leukemia. 2004 Mar;18(3):375-84 [14737069.001]

[Cites] Blood. 2007 Jun 15;109 (12 ):5151-6 [17351110.001]

[Cites] Blood. 1996 Feb 1;87(3):1089-96 [8562934.001]

[Cites] Blood. 2002 Jan 1;99(1):319-25 [11756187.001]

[Cites] Blood. 1993 Aug 1;82(3):792-9 [8338945.001]

[Cites] Lancet. 2007 Jul 28;370(9584):342-50 [17662883.001]

[Cites] Nature. 1998 Feb 19;391(6669):815-8 [9486655.001]

(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] Switzerland

[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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[Title] High-frequency type I/II mutational shifts between diagnosis and relapse are associated with outcome in pediatric AML: implications for personalized medicine.

Although virtually all pediatric patients with acute myeloid leukemia (AML) achieve a complete remission after initial induction therapy, 30%-40% of patients will encounter a relapse and have a dismal prognosis.

To determine relevance of established AML type I/II mutations that may serve as therapeutic targets, we assessed frequencies of these mutations and their persistence during disease progression in a large group (n = 69) of paired diagnosis and relapse pediatric AML specimens.

[MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Precision Medicine

[MeSH-minor] Adolescent. Base Sequence. Biomarkers, Tumor / genetics. Child. Child, Preschool. Cohort Studies. DNA Mutational Analysis. DNA Primers / genetics. DNA, Neoplasm / genetics. Female. Follow-Up Studies. Genes, Wilms Tumor. Genes, ras. Humans. Infant. Male. Prognosis. Recurrence. Time Factors. Treatment Outcome. fms-Like Tyrosine Kinase 3 / genetics

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

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

[CommentIn] Blood. 2010 Oct 14;116(15):2622-3 [20947687.001]

(PMID = 20592250.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA Primers; 0 / DNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] Comparable outcomes of HLA-matched unrelated and HLA-identical sibling donor bone marrow transplantation for childhood acute myeloid leukemia in first remission.

We retrospectively investigated the outcomes of HLA-matched unrelated BMT (MU-BMT, n = 13) and HLA-identical sibling donor BMT (MS-BMT, n = 17) for childhood AML in CR1 between June 2002 and August 2005.

The cumulative incidence of grade II-IV acute GVHD and any chronic GVHD at three yr was not different between MS-BMT and MU-BMT.

The outcome of HLA-matched unrelated BMT is comparable to that of HLA-identical sibling BMT for childhood AML in CR1.

HLA-matched unrelated BMT may be recommended for patients who have AML in CR1 without an HLA-matched sibling donor.

[MeSH-major] Bone Marrow Transplantation / methods. HLA Antigens / metabolism. Leukemia, Myeloid, Acute / therapy

[MeSH-minor] Adolescent. Adult. Blood Platelets / metabolism. Child. Child, Preschool. Female. Humans. Living Donors. Male. Neutrophils / metabolism. Remission Induction. Retrospective Studies. Siblings. Treatment Outcome

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

Genetic Alliance. consumer health - Leukemia, Myeloid.

Genetic Alliance. consumer health - Transplantation.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

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

(PMID = 18627512.001).

[ISSN] 1399-3046

[Journal-full-title] Pediatric transplantation

[ISO-abbreviation] Pediatr Transplant

[Language] eng

[Publication-type] Journal Article

[Publication-country] Denmark

[Chemical-registry-number] 0 / HLA Antigens

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] Prognostic significance of the BAALC isoform pattern and CEBPA mutations in pediatric acute myeloid leukemia with normal karyotype: a study by the Japanese Childhood AML Cooperative Study Group.

High BAALC (brain and acute leukemia, cytoplasmic) gene expression may indicate an adverse prognosis for adults who have acute myeloid leukemia (AML) and a normal karyotype, but its prognostic significance for pediatric AML cases is unclear.

Newly diagnosed AML patients with normal karyotype who were treated by the Japanese Childhood AML Cooperative Treatment Protocol AML 99 were analyzed in terms of their BAALC expression levels (n = 29), BAALC isoforms (n = 29), and CEBPA mutations (n = 49).

Thus, 1-5-6-8 isoform expression may be associated with an adverse prognosis in pediatric AML with normal karyotype.

[MeSH-major] Asian Continental Ancestry Group / genetics. CCAAT-Enhancer-Binding Proteins. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / diagnosis. Mutation. Neoplasm Proteins

[MeSH-minor] Adolescent. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Karyotyping. Male. Prognosis. Protein Isoforms / genetics

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

[Cites] Blood. 2007 Jan 15;109(2):431-48 [16960150.001]

[Cites] Blood. 2006 May 15;107(10):3847-53 [16434492.001]

[Cites] Blood. 2003 Sep 1;102(5):1613-8 [12750167.001]

[Cites] J Clin Oncol. 2005 Dec 20;23 (36):9234-42 [16275934.001]

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

[Cites] Clin Cancer Res. 2005 Feb 15;11(4):1416-24 [15746041.001]

[Cites] Exp Hematol. 2003 Nov;31(11):1051-6 [14585369.001]

[Cites] Blood. 2006 Dec 1;108(12):3898-905 [16912223.001]

[Cites] Haematologica. 2006 Jun;91(6):825-8 [16704962.001]

[Cites] Br J Haematol. 2006 Nov;135(4):438-49 [16965385.001]

[Cites] Blood. 2006 Mar 1;107(5):1806-9 [16291592.001]

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

[Cites] Blood. 2001 Nov 1;98(9):2651-6 [11675334.001]

[Cites] Blood. 2009 Mar 26;113(13):3088-91 [19171880.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13901-6 [11707601.001]

[Cites] Curr Opin Hematol. 2005 Jan;12(1):68-75 [15604894.001]

[Cites] Blood. 2006 Sep 1;108(5):1677-83 [16670265.001]

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

[Cites] Blood. 2002 Feb 15;99(4):1332-40 [11830484.001]

[Cites] J Neurochem. 2005 Feb;92(3):647-59 [15659234.001]

[Cites] Br J Haematol. 2007 Jun;137(5):387-400 [17488484.001]

[Cites] J Cell Biochem. 2006 Aug 1;98(5):1203-20 [16514668.001]

[Cites] Nat Genet. 2001 Mar;27(3):263-70 [11242107.001]

[Cites] Blood. 2003 Feb 1;101(3):837-45 [12393383.001]

[Cites] Nat Med. 2006 Aug;12(8):945-9 [16892037.001]

[Cites] Int J Cancer. 1999 Jun 11;81(6):897-901 [10362136.001]

[Cites] Leukemia. 2005 Mar;19(3):410-4 [15618961.001]

[Cites] Blood. 2002 Feb 15;99(4):1350-5 [11830486.001]

[Cites] J Biol Chem. 2006 Sep 22;281(38):28122-30 [16698800.001]

[Cites] J Clin Oncol. 2004 Feb 15;22(4):624-33 [14726504.001]

[Cites] Pediatr Blood Cancer. 2008 Feb;50(2):264-9 [17763464.001]

[Cites] Leukemia. 2007 Jun;21(6):1307 [17315018.001]

[Cites] J Clin Oncol. 2009 Aug 20;27(24):4007-13 [19620491.001]

[Cites] J Clin Oncol. 2006 Feb 10;24(5):790-7 [16418499.001]

[Cites] Gene Expr Patterns. 2005 Apr;5(4):463-73 [15749074.001]

[Cites] Int J Hematol. 2010 May;91(4):636-45 [20376583.001]

[Cites] Leukemia. 2005 Mar;19(3):329-34 [15674366.001]

(PMID = 20495894.001).

[ISSN] 1865-3774

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

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

[Publication-country] Japan

[Chemical-registry-number] 0 / BAALC protein, human; 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Neoplasm Proteins; 0 / Protein Isoforms

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[Title] XPD Lys751Gln polymorphism in the etiology and outcome of childhood acute myeloid leukemia: a Children's Oncology Group report.

Polymorphisms in XPD, a member of the nucleotide excision repair pathway, have been associated with development of treatment-related acute myeloid leukemia (AML) and with poor outcome of AML in elderly patients.

We hypothesized that XPD Lys751Gln polymorphism may play a role in causation of AML in children and, as shown in adults, may affect the outcome of childhood AML therapy.

Genotyping of 456 children treated for de novo AML was performed at XPD exon 23.

Gene frequencies in AML patients and healthy controls were similar.

There were no significant differences in overall survival (P = .82), event-free survival (P = .78), treatment-related mortality (P = .43), or relapse rate (RR) (P = .92) between patients with XPD751AA versus 751AC versus 751CC genotypes, in contrast to reports in adult AML.

These data, representing the only data in pediatric AML, suggest that XPD genotype does not affect the etiology or outcome of childhood AML.

[MeSH-major] Leukemia, Myeloid / genetics. Polymorphism, Single Nucleotide. Xeroderma Pigmentosum Group D Protein / genetics

[MeSH-minor] Acute Disease. Adolescent. Adult. Case-Control Studies. Child. Child, Preschool. Female. Gene Frequency. Genetic Testing. Genotype. Humans. Infant. Infant, Newborn. Male. Mutation, Missense. Survival Analysis. 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 = 16150943.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] EC 3.6.4.12 / Xeroderma Pigmentosum Group D Protein; EC 5.99.- / ERCC2 protein, human

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[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.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[Title] Pediatric acute myeloid leukemia: international progress and future directions.

[MeSH-major] Leukemia, Myeloid / therapy

[MeSH-minor] Acute Disease. Child. Forecasting. Humans. 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 = 16304569.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Editorial; Review

[Publication-country] England

[Number-of-references] 30

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[Title] High expression of the very late antigen-4 integrin independently predicts reduced risk of relapse and improved outcome in pediatric acute myeloid leukemia: a report from the children's oncology group.

PURPOSE: To evaluate the prognostic significance of the integrin cell adhesion molecule very late antigen-4 (VLA-4) in acute myeloid leukemia (AML).

Subgroup analyses indicated that the prognostic role of VLA-4 expression was most prominent in patients with standard-risk AML, in whom low VLA-4 expression was associated with inferior DFS (34% +/- 16% v 69% +/- 14% for high expression; P = .011) and higher RR (61% +/- 16% v 26% +/- 14% for high expression; P = .009).

CONCLUSION: High VLA-4 expression is associated with better clinical outcome in pediatric AML and is an independent predictor of relapse that may refine our abilities to stratify patients without identifiable cytogenetic or molecular risk factors.

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

COS Scholar Universe. author profiles.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

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

[Cites] Blood. 2001 Apr 1;97(7):2121-9 [11264180.001]

[Cites] Cell. 2002 Sep 20;110(6):673-87 [12297042.001]

[Cites] Br J Haematol. 2003 Aug;122(4):579-89 [12899713.001]

[Cites] Nat Med. 2003 Sep;9(9):1158-65 [12897778.001]

[Cites] Blood. 1993 Nov 15;82(10):3125-32 [7693037.001]

[Cites] Leukemia. 1996 Apr;10(4):682-6 [8618447.001]

[Cites] Blood. 2009 Oct 1;114(14):3008-17 [19636064.001]

[Cites] Nat Rev Immunol. 2007 Sep;7(9):678-89 [17717539.001]

[Cites] Leuk Res. 2008 Jun;32(6):845-6 [18023867.001]

[Cites] Blood. 2009 Jan 22;113(4):866-74 [18927435.001]

[Cites] Annu Rev Immunol. 2009;27:339-62 [19302044.001]

[Cites] Leuk Res. 2009 Jun;33(6):764-8 [19042019.001]

[Cites] Genome Biol. 2007;8(5):215 [17543136.001]

(PMID = 20421533.001).

[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

[Grant] United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U24 CA114766; United States / NCI NIH HHS / CA / K23 CA137161; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / U10 CA098543

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Integrin alpha4beta1

[Other-IDs] NLM/ PMC2903318

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[Title] Prevalence and prognostic implications of WT1 mutations in pediatric acute myeloid leukemia (AML): a report from the Children's Oncology Group.

Recent studies of WT1 mutations in acute myeloid leukemia (AML) mostly report an association with unfavorable clinical outcome.

We screened 842 patients treated on 3 consecutive pediatric AML trials for WT1 zinc-finger mutations.

In current risk stratification schemes incorporating cytogenetics and FLT3/ITD status, the presence of WT1 mutations has no independent prognostic significance in predicting outcome in pediatric AML.

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

[MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Cohort Studies. DNA Mutational Analysis. DNA, Neoplasm / genetics. Exons / genetics. Female. Humans. Infant. Infant, Newborn. Kaplan-Meier Estimate. Karyotyping. Male. Prevalence. Prognosis. Proportional Hazards Models. Retrospective Studies. Tandem Repeat Sequences / genetics. Treatment Outcome. Young Adult. fms-Like Tyrosine Kinase 3 / genetics

Genetic Alliance. consumer health - Acute Myelocytic Leukemia.

Genetic Alliance. consumer health - Leukemia, Myeloid.

COS Scholar Universe. author profiles.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

The Lens. Cited by Patents in .

[Email] Email this result item

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

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

[Cites] Leukemia. 2007 May;21(5):868-76 [17361230.001]

[Cites] Br J Haematol. 2004 Jun;125(5):590-600 [15147374.001]

[Cites] J Clin Oncol. 2004 Oct 15;22(20):4140-6 [15483024.001]

[Cites] Leukemia. 1992 May;6(5):405-9 [1317488.001]

[Cites] Hum Mol Genet. 1994 Sep;3(9):1633-7 [7833922.001]

[Cites] Hum Mol Genet. 1995 Mar;4(3):351-8 [7795587.001]

[Cites] Biochemistry. 1996 Sep 17;35(37):12070-6 [8810912.001]

[Cites] Hum Mutat. 1997;9(3):209-25 [9090524.001]

[Cites] Cancer Res. 2005 Oct 15;65(20):9152-4 [16230371.001]

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

[Cites] Curr Opin Hematol. 2007 Mar;14(2):106-14 [17255787.001]

[Cites] Leukemia. 2007 Mar;21(3):550-1; author reply 552 [17205055.001]

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

[Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]

[Cites] Leukemia. 2008 May;22(5):915-31 [18288131.001]

[Cites] Semin Oncol. 2008 Aug;35(4):346-55 [18692685.001]

[Cites] J Clin Oncol. 2008 Oct 1;26(28):4595-602 [18559874.001]

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

[Cites] Blood. 2009 May 7;113(19):4505-11 [19221039.001]

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

[Cites] Blood. 2009 Jun 25;113(26):6558-66 [19304957.001]

[Cites] Cancer. 2009 Aug 15;115(16):3719-27 [19536888.001]

[Cites] Leukemia. 2009 Aug;23(8):1472-9 [19322206.001]

[Cites] Pediatr Blood Cancer. 2009 Dec;53(6):1136-9 [19618455.001]

[Cites] Blood. 2010 Mar 25;115(12):2372-9 [20056794.001]

[Cites] Gene. 2001 Aug 8;273(2):141-61 [11595161.001]

(PMID = 20413658.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Databank-accession-numbers] ClinicalTrials.gov/ NCT00002798/ NCT00070174

[Grant] United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / R21CA10262-01; United States / NCI NIH HHS / CA / U10 CA98543

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

[Publication-country] United States

[Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

[Other-IDs] NLM/ PMC2918327

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[Title] Twenty years of follow-up among survivors of childhood and young adult acute myeloid leukemia: a report from the Childhood Cancer Survivor Study.

BACKGROUND: Limited data exist on the comprehensive assessment of late medical and social effects experienced by survivors of childhood and young adult acute myeloid leukemia (AML).

METHODS: This analysis included 272 5-year AML survivors who participated in the Childhood Cancer Survivor Study (CCSS).

The cumulative incidence of recurrent AML was 6.6% at 10 years (95% CI, 3.7%-9.6%) and 8.6% at 20 years (95% CI, 5.1%-12.1%).

CONCLUSIONS: Long-term survival from childhood AML > or =5-years after diagnosis was favorable.

Genetic Alliance. consumer health - Childhood Cancer.

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

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

Genetic Alliance. consumer health - Leukemia, Myeloid.

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

(PMID = 18327823.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] ENG

[Grant] United States / NCRR NIH HHS / RR / K12 RR023247; United States / NCI NIH HHS / CA / U24 CA055727; United States / NCRR NIH HHS / RR / 1 K12 RR 023247; United States / NCI NIH HHS / CA / U24 CA 55727

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

[Publication-country] United States

[Investigator] Robison LL; Hudson M; Armstrong G; Perkins J; O'Leary M; Friedman D; Pendergrass T; Greffe B; Odom L; Ruccione K; Mulvihill J; Ginsberg J; Meadows A; Tersak J; Ritchey A; Blatt J; Reaman G; Packer R; Davies S; Bhatia S; Qualman S; Hammond S; Termuhlen A; Ruymann F; Diller L; Grier H; Li F; Meacham L; Mertens A; Leisenring W; Potter J; Greenberg M; Nathan PC; Boice J; Rodriguez V; Smithson WA; Gilchrist G; Sklar C; Oeffinger K; Finklestein J; Anderson B; Inskip P; Vik TA; Weetman R; Green DM; Hayashi R; Vietti T; Marina N; Donaldson SS; Link MP; Dreyer Z; Whelan K; Sande J; Berkow R; Yasui Y; Casallis J; Zeltzer L; Goldsby R; Ablin A; Hutchinson R; Neglia J; Deapen D; Breslow N; Bowers D; Tomlinson G; Buchanan GR; Strong L; Stovall M

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[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.

COS Scholar Universe. author profiles.

[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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[Title] Risk factors for acute leukemia in children: a review.

Although overall incidence is rare, leukemia is the most common type of childhood cancer.

Within this population, acute lymphocytic leukemia (ALL) occurs approximately five times more frequently than acute myelogenous leukemia (AML) and accounts for approximately 78% of all childhood leukemia diagnoses.

Epidemiologic studies of acute leukemias in children have examined possible risk factors, including genetic, infectious, and environmental, in an attempt to determine etiology.

Only one environmental risk factor (ionizing radiation) has been significantly linked to ALL or AML.

Most environmental risk factors have been found to be weakly and inconsistently associated with either form of acute childhood leukemia.

Our review focuses on the demographics of childhood leukemia and the risk factors that have been associated with the development of childhood ALL or AML.

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

[MeSH-minor] Child. Communicable Diseases / complications. Environmental Exposure. Genetic Predisposition to Disease. Humans. Risk Factors

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

[Cites] Cancer Res. 1989 Jul 15;49(14):4030-7 [2736544.001]

[Cites] BMJ. 1990 Feb 17;300(6722):423-9 [2107892.001]

[Cites] Am J Hum Genet. 1990 Jun;46(6):1041-52 [2160192.001]

[Cites] Pediatr Hematol Oncol. 1987;4(1):63-72 [3152913.001]

[Cites] Br J Cancer. 1990 Dec;62(6):1008-14 [2257204.001]

[Cites] Environ Health Perspect. 1990 Aug;88:325-37 [2272330.001]

[Cites] Med J Aust. 1991 Apr 1;154(7):483-7 [2005848.001]

[Cites] BMJ. 1991 Mar 23;302(6778):681-7 [2021741.001]

[Cites] BMJ. 1991 Mar 23;302(6778):687-92 [2021742.001]

[Cites] Cancer. 1991 Sep 15;68(6):1351-5 [1873786.001]

[Cites] Br J Cancer. 1991 Sep;64(3):549-54 [1911197.001]

[Cites] Br J Cancer. 2001 Feb 2;84(3):406-12 [11161408.001]

[Cites] Int J Epidemiol. 2001 Feb;30(1):125-9 [11171872.001]

[Cites] Am J Epidemiol. 2001 Mar 15;153(6):615-7 [11257071.001]

[Cites] Cancer Res. 2001 Mar 15;61(6):2542-6 [11289128.001]

[Cites] Am J Public Health. 2001 Apr;91(4):564-7 [11291366.001]

[Cites] Cancer Causes Control. 2001 Aug;12(6):483-90 [11519756.001]

[Cites] Paediatr Perinat Epidemiol. 2001 Oct;15(4):338-45 [11703681.001]

[Cites] Radiat Res. 2001 Dec;156(6):718-23 [11741495.001]

[Cites] Environ Health Perspect. 1991 Aug;94:5-7 [1954939.001]

[Cites] Eur J Cancer. 1992;29A(1):87-95 [1445751.001]

[Cites] BMJ. 1993 Jan 9;306(6870):89-94 [8435648.001]

[Cites] Leukemia. 1993 Mar;7(3):349-60 [8445941.001]

[Cites] BMJ. 1993 Mar 6;306(6878):615-21 [8461811.001]

[Cites] BMJ. 1993 May 1;306(6886):1153-8 [8499814.001]

[Cites] Leukemia. 1993 Aug;7 Suppl 2:S146-7 [8361221.001]

[Cites] BMJ. 1993 Oct 16;307(6910):959-66 [8241906.001]

[Cites] Med Pediatr Oncol. 1994;22(2):78-83 [8259105.001]

[Cites] Nature. 1994 Feb 24;367(6465):678-80 [8107860.001]

[Cites] BMJ. 1994 Jul 16;309(6948):154-7 [8044093.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1994 Sep;3(6):457-60 [8000294.001]

[Cites] Br J Cancer. 1995 Jan;71(1):1-5 [7819022.001]

[Cites] Am J Public Health. 1995 Feb;85(2):249-52 [7856787.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1994 Dec;3(8):645-53 [7881337.001]

[Cites] Cancer. 1995 Apr 15;75(8):2186-95 [7697611.001]

[Cites] Epidemiol Rev. 1994;16(2):243-72 [7713179.001]

[Cites] Environ Health Perspect. 1995 Jun;103(6):550-4 [7556005.001]

[Cites] Eur J Cancer Prev. 1995 Sep;4 Suppl 1:3-107 [7496333.001]

[Cites] J Natl Cancer Inst. 1996 Jan 3;88(1):24-31 [8847721.001]

[Cites] Ann Epidemiol. 1995 Sep;5(5):354-9 [8653207.001]

[Cites] Environ Health Perspect. 1995 Sep;103 Suppl 6:177-84 [8549470.001]

[Cites] Epidemiology. 1999 Sep;10(5):481-7 [10468419.001]

[Cites] JAMA. 2003 Oct 15;290(15):2001-7 [14559953.001]

[Cites] Curr Opin Pediatr. 2004 Feb;16(1):9-14 [14758108.001]

[Cites] Environ Mol Mutagen. 2004;43(2):100-9 [14991750.001]

[Cites] Cancer Detect Prev. 2004;28(2):83-7 [15068830.001]

[Cites] Cancer Res. 1967 Dec;27(12):2420-3 [4230121.001]

[Cites] J Natl Cancer Inst. 1968 May;40(5):1079-85 [5648133.001]

[Cites] Nature. 1971 Apr 9;230(5293):370-3 [4927726.001]

[Cites] Lancet. 1971 Apr 3;1(7701):699-701 [4101637.001]

[Cites] Science. 1973 Dec 28;182(4119):1355-6 [4586464.001]

[Cites] J Med Genet. 1977 Apr;14(2):81-90 [856959.001]

[Cites] Cancer Res. 1978 Mar;38(3):485-93 [203382.001]

[Cites] Cancer. 1980 Apr 1;45(7):1675-8 [6929216.001]

[Cites] J Pediatr. 1981 Sep;99(3):425-8 [7264801.001]

[Cites] Am J Ind Med. 1981;2(3):217-45 [7345926.001]

[Cites] J Occup Med. 1984 Sep;26(9):679-82 [6207280.001]

[Cites] Leuk Res. 1985;9(6):817-23 [3159943.001]

[Cites] Am J Epidemiol. 1985 Feb;121(2):216-24 [3860001.001]

[Cites] Nature. 1987 Jan 22-28;325(6102):355-7 [3808031.001]

[Cites] Br J Cancer. 1987 Feb;55(2):179-90 [3814487.001]

[Cites] J Natl Cancer Inst. 1987 Jul;79(1):39-46 [3474448.001]

[Cites] Prog Clin Biol Res. 1987;246:19-32 [2958880.001]

[Cites] Am J Epidemiol. 1988 Apr;127(4):713-25 [3354538.001]

[Cites] Int J Epidemiol. 2001 Dec;30(6):1428-37 [11821358.001]

[Cites] BMJ. 2002 Feb 2;324(7332):283-7 [11823363.001]

[Cites] Lancet. 2002 Feb 2;359(9304):431-4 [11844534.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2002 Feb;11(2):177-85 [11867505.001]

[Cites] Environ Health Perspect. 2002 Mar;110(3):319-24 [11882484.001]

[Cites] Rev Environ Health. 2001 Jul-Sep;16(4):263-79 [12041882.001]

[Cites] Lancet Oncol. 2002 May;3(5):269-79 [12067803.001]

[Cites] Environ Health Perspect. 2002 Sep;110(9):955-60 [12204832.001]

[Cites] Br J Cancer. 2002 Sep 23;87(7):740-5 [12232757.001]

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

[Cites] Pharmacogenetics. 2002 Nov;12(8):655-8 [12439226.001]

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

[Cites] Br J Cancer. 1998 Mar;77(5):842-9 [9514068.001]

[Cites] Epidemiology. 1998 May;9(3):234-45 [9583414.001]

[Cites] Leukemia. 1998 May;12(5):645-51 [9593260.001]

[Cites] Environ Health Perspect. 1998 Jun;106 Suppl 3:893-908 [9646054.001]

[Cites] Br J Cancer. 1998 Jul;78(1):119-24 [9662261.001]

[Cites] Radiat Environ Biophys. 1998 Jul;37(2):87-93 [9728740.001]

[Cites] Radiat Res. 1998 Nov;150(5 Suppl):S30-41 [9806607.001]

[Cites] Cancer. 1999 Mar 15;85(6):1380-8 [10189146.001]

[Cites] Teratology. 1999 Apr;59(4):227-33 [10331524.001]

[Cites] J Natl Cancer Inst. 1999 Jun 16;91(12):1051-8 [10379968.001]

[Cites] Int J Radiat Biol. 1999 Jul;75(7):801-10 [10489891.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1999 Sep;8(9):783-91 [10498397.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1999 Sep;8(9):793-9 [10498398.001]

[Cites] Br J Cancer. 1999 Oct;81(3):549-53 [10507784.001]

[Cites] N Engl J Med. 1955 Jul 21;253(3):88-90 [14394332.001]

[Cites] Lancet. 1956 Sep 1;271(6940):447 [13358242.001]

[Cites] Arch Intern Med. 1961 Jul;108:86-90 [13720079.001]

[Cites] N Engl J Med. 1965 Apr 29;272:882-7 [14274439.001]

[Cites] N Engl J Med. 1959 Sep 17;261:585-9 [14425443.001]

[Cites] J Epidemiol Community Health. 2005 Feb;59(2):101-5 [15650139.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):651-5 [15767345.001]

[Cites] Environ Health. 2004;3(1):12 [15533260.001]

[Cites] Occup Environ Med. 2006 Feb;63(2):131-4 [16421392.001]

[Cites] Environ Health Perspect. 2003 Apr;111(4):663-8 [12676632.001]

[Cites] Hematol Oncol. 2003 Jun;21(2):51-5 [12802809.001]

[Cites] Environ Health Perspect. 2003 Jun;111(7):962-70 [12782499.001]

[Cites] Epidemiology. 2003 Jul;14(4):437-41 [12843769.001]

[Cites] Epidemiology. 2003 Sep;14(5):569-77 [14501272.001]

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

[Cites] Lancet. 1988 Sep 17;2(8612):665-9 [2901525.001]

[Cites] Lancet. 1988 Dec 10;2(8624):1323-7 [2904050.001]

[Cites] Cancer. 1989 May 15;63(10):1904-11 [2649219.001]

[Cites] Radiat Res. 1996 May;145(5):595-601 [8619025.001]

[Cites] Br J Cancer. 1996 Apr;73(8):1006-12 [8611419.001]

[Cites] Med Pediatr Oncol Suppl. 1996;1:29-34 [8643045.001]

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

[Cites] Int J Cancer. 1996 Jul 29;67(3):343-52 [8707407.001]

[Cites] Cancer. 1995 Apr 1;75(7):1718-27 [8826933.001]

[Cites] Cancer Causes Control. 1996 Nov;7(6):581-90 [8932918.001]

[Cites] J Natl Cancer Inst. 1997 Feb 5;89(3):238-44 [9017004.001]

[Cites] Br J Cancer. 1997;75(3):457-63 [9020498.001]

[Cites] Semin Oncol. 1997 Feb;24(1):3-16 [9045302.001]

[Cites] Occup Environ Med. 1996 Nov;53(11):773-81 [9038803.001]

[Cites] Br J Radiol. 1997 Feb;70:130-9 [9135438.001]

[Cites] Ann Epidemiol. 1997 Apr;7(3):172-9 [9141639.001]

[Cites] Cancer. 1997 May 15;79(10):2045-51 [9149034.001]

[Cites] Nature. 1997 May 15;387(6630):246 [9153387.001]

[Cites] Occup Environ Med. 1997 Mar;54(3):152-66 [9155776.001]

[Cites] N Engl J Med. 1997 Jul 3;337(1):1-7 [9203424.001]

[Cites] J Natl Cancer Inst. 1997 Jul 2;89(13):939-47 [9214673.001]

[Cites] Pediatr Clin North Am. 1997 Aug;44(4):831-46 [9286287.001]

[Cites] Environ Health Perspect. 1997 Oct;105(10):1068-77 [9349828.001]

[Cites] J Natl Cancer Inst. 1999 Oct 20;91(20):1765-72 [10528028.001]

[Cites] J Clin Oncol. 2000 Feb;18(4):813-23 [10673523.001]

[Cites] Curr Opin Oncol. 2000 Jan;12(1):3-12 [10687723.001]

[Cites] Am J Epidemiol. 2000 Mar 1;151(5):512-5 [10707920.001]

[Cites] CA Cancer J Clin. 2000 Jan-Feb;50(1):7-33 [10735013.001]

[Cites] Br J Cancer. 2000 Sep;83(5):692-8 [10944614.001]

[Cites] Am J Epidemiol. 2000 Sep 1;152(5):480-6 [10981463.001]

[Cites] Epidemiology. 2000 Nov;11(6):624-34 [11055621.001]

[CommentIn] Environ Health Perspect. 2007 Aug;115(8):A395-6 [17687418.001]

[CommentIn] Environ Health Perspect. 2007 Aug;115(8):A395 [17687419.001]

[ErratumIn] Environ Health Perspect. 2010 Sep;118(9):A380

(PMID = 17366834.001).

[ISSN] 0091-6765

[Journal-full-title] Environmental health perspectives

[ISO-abbreviation] Environ. Health Perspect.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Number-of-references] 145

[Other-IDs] NLM/ PMC1817663