[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 391
1. Teuffel O, Stanulla M, Cario G, Ludwig WD, Rottgers S, Schafer BW, Zimmermann M, Schrappe M, Niggli FK: Anemia and survival in childhood acute lymphoblastic leukemia. Haematologica; 2008 Nov;93(11):1652-7
MedlinePlus Health Information. consumer health - Anemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anemia and survival in childhood acute lymphoblastic leukemia.
  • BACKGROUND: Several studies have demonstrated that patients with childhood acute lymphoblastic leukemia presenting with mild anemia at diagnosis have an increased risk of poor outcome compared to patients with more severe anemia.
  • However, it has not been reported whether there is any correlation between degree of anemia and leukemia subtype.
  • DESIGN AND METHODS: In a cohort of 1162 patients with childhood acute lymphoblastic leukemia we analyzed whether there was a correlation between degree of anemia and leukemia subtype.
  • RESULTS: Hemoglobin levels at diagnosis were distributed in a non-random pattern.
  • The degree of anemia was significantly different for three distinct groups of patients compared to the remaining patients (mean hemoglobin; T-cell leukemia: 106 g/L versus 76 g/L (precursor B-cell acute lymphoblastic leukemia); within precursor B-cell ALL: TEL-AML1 positive: 68 g/L versus 79 g/L; BCR-ABL positive: 93 g/L versus 76 g/L; each p<0.05).
  • Furthermore, in contrast to the entire study group, patients with T-cell leukemia, TEL-AML1(+), and BCR-ABL(+) precursor B-cell leukemia had a more favorable prognosis if presenting with a higher hemoglobin level (>/=80 g/L).
  • CONCLUSIONS: These observations indicate that the formerly reported direct correlation between severity of anemia and survival in childhood acute lymphoblastic leukemia mainly reflects differences in the degree of anemia between distinct biological subgroups with different treatment outcomes.
  • [MeSH-major] Anemia / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality
  • [MeSH-minor] Burkitt Lymphoma / complications. Burkitt Lymphoma / genetics. Burkitt Lymphoma / mortality. Child. Cohort Studies. Core Binding Factor Alpha 2 Subunit / genetics. Disease-Free Survival. Fusion Proteins, bcr-abl / genetics. Hemoglobins / metabolism. Homeodomain Proteins / genetics. Humans. Leukemia, T-Cell / complications. Leukemia, T-Cell / genetics. Leukemia, T-Cell / mortality. Leukocyte Count. Mutation. Oncogene Proteins, Fusion / genetics. Risk Factors. Survival Analysis. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • Genetic Alliance. consumer health - Anemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18815194.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Hemoglobins; 0 / Homeodomain Proteins; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human; 146150-85-8 / E2A-Pbx1 fusion protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  •  go-up   go-down


2. Bhojwani D, Howard SC, Pui CH: High-risk childhood acute lymphoblastic leukemia. Clin Lymphoma Myeloma; 2009;9 Suppl 3:S222-30
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-risk childhood acute lymphoblastic leukemia.
  • Although most children with acute lymphoblastic leukemia (ALL) are cured, certain subsets have a high risk of relapse.
  • Infants with mixed-lineage leukemia (MLL)-rearranged ALL comprise a very poor-risk group wherein further intensification of chemotherapy causes significant toxicity.
  • Hybrid protocols incorporating drugs effective for acute myeloid leukemia could improve survival, a strategy being tested in international trials.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2008 Mar 15;111(6):2984-90 [18182569.001]
  • [Cites] Bone Marrow Transplant. 2008 Mar;41(5):447-53 [17968326.001]
  • [Cites] J Clin Oncol. 2008 Mar 20;26(9):1496-503 [18349402.001]
  • [Cites] Lancet. 2008 Mar 22;371(9617):1030-43 [18358930.001]
  • [Cites] Leukemia. 2008 Apr;22(4):771-82 [18239620.001]
  • [Cites] Blood. 2008 May 1;111(9):4477-89 [18285545.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5477-85 [18388178.001]
  • [Cites] Bone Marrow Transplant. 2008 Jun;41 Suppl 2:S71-4 [18545248.001]
  • [Cites] Clin Cancer Res. 2008 Jul 1;14(13):4027-31 [18593977.001]
  • [Cites] J Clin Oncol. 2008 Jul 1;26(19):3204-12 [18541900.001]
  • [Cites] Clin Cancer Res. 2008 Jul 15;14(14):4392-9 [18628453.001]
  • [Cites] Haematologica. 2008 Aug;93(8):1155-60 [18519521.001]
  • [Cites] Blood. 2008 Aug 15;112(4):1005-12 [18477770.001]
  • [Cites] J Clin Oncol. 2008 Sep 20;26(27):4376-84 [18802149.001]
  • [Cites] Blood. 2008 Nov 15;112(10):4318-27 [18723429.001]
  • [Cites] Semin Hematol. 2009 Jan;46(1):39-51 [19100367.001]
  • [Cites] Semin Hematol. 2009 Jan;46(1):100-6 [19100372.001]
  • [Cites] JAMA. 2009 Jan 28;301(4):393-403 [19176441.001]
  • [Cites] N Engl J Med. 2009 Jan 29;360(5):470-80 [19129520.001]
  • [Cites] Lancet Oncol. 2009 Feb;10(2):147-56 [19147408.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Jun 9;106(23):9414-8 [19470474.001]
  • [Cites] J Clin Oncol. 2009 Nov 1;27(31):5175-81 [19805687.001]
  • [Cites] Blood. 2006 Jul 1;108(1):97-102 [16537802.001]
  • [Cites] Blood. 2006 Jul 15;108(2):441-51 [16556894.001]
  • [Cites] Leukemia. 2006 Aug;20(8):1368-76 [16761017.001]
  • [Cites] Blood. 2006 Aug 1;108(3):1050-7 [16627760.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1469-77 [16638934.001]
  • [Cites] Clin Cancer Res. 2006 Sep 15;12(18):5329-35 [17000665.001]
  • [Cites] J Clin Oncol. 2006 Dec 20;24(36):5742-9 [17179108.001]
  • [Cites] J Clin Oncol. 2007 Jan 1;25(1):16-24 [17194902.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Feb;13(2):218-27 [17241927.001]
  • [Cites] Blood. 2007 Feb 1;109(3):896-904 [17003366.001]
  • [Cites] Blood. 2007 Feb 1;109(3):926-35 [17003380.001]
  • [Cites] Nat Rev Drug Discov. 2007 Feb;6(2):149-65 [17268486.001]
  • [Cites] Blood. 2007 Mar 15;109(6):2327-30 [17095619.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Lancet. 2007 Jun 9;369(9577):1947-54 [17560447.001]
  • [Cites] Blood. 2007 Jul 15;110(2):727-34 [17405907.001]
  • [Cites] Lancet. 2007 Jul 21;370(9583):240-50 [17658395.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1112-5 [17473063.001]
  • [Cites] J Clin Oncol. 2007 Oct 20;25(30):4813-20 [17947730.001]
  • [Cites] Leukemia. 2007 Nov;21(11):2258-63 [17690691.001]
  • [Cites] Nat Rev Cancer. 2007 Nov;7(11):823-33 [17957188.001]
  • [Cites] N Engl J Med. 2000 Apr 6;342(14):998-1006 [10749961.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3310-22 [10828010.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2223-33 [11187913.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2257-66 [11187917.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1038-42 [11287973.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]
  • [Cites] Blood. 2002 Jun 1;99(11):3885-91 [12010785.001]
  • [Cites] Lancet. 2002 Jun 1;359(9321):1909-15 [12057554.001]
  • [Cites] Blood. 2002 Jul 1;100(1):43-7 [12070006.001]
  • [Cites] Leukemia. 2002 Sep;16(9):1668-72 [12200679.001]
  • [Cites] Br J Haematol. 2002 Nov;119(2):445-53 [12406084.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):173-83 [12620411.001]
  • [Cites] Bone Marrow Transplant. 2003 May;31(10):909-18 [12748668.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2736-40 [12843002.001]
  • [Cites] Pediatr Blood Cancer. 2004 Jan;42(1):8-23 [14752789.001]
  • [Cites] Leukemia. 2004 Mar;18(3):521-9 [14712291.001]
  • [Cites] Leukemia. 2004 Mar;18(3):499-504 [14981525.001]
  • [Cites] Nat Genet. 2004 May;36(5):453-61 [15098032.001]
  • [Cites] Ann Hematol. 2004;83 Suppl 1:S124-6 [15124703.001]
  • [Cites] Nature. 2004 May 27;429(6990):464-8 [15164072.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2690-6 [15251979.001]
  • [Cites] J Clin Oncol. 1985 Nov;3(11):1513-21 [3863894.001]
  • [Cites] Blood. 1994 Nov 1;84(9):3122-33 [7949185.001]
  • [Cites] Cancer. 1997 Nov 1;80(9):1717-26 [9351539.001]
  • [Cites] J Clin Oncol. 1998 Feb;16(2):527-35 [9469337.001]
  • [Cites] N Engl J Med. 1998 Jun 4;338(23):1663-71 [9614257.001]
  • [Cites] Cancer. 1998 Nov 1;83(9):2030-9 [9806664.001]
  • [Cites] Lancet. 1998 Nov 28;352(9142):1731-8 [9848348.001]
  • [Cites] Leukemia. 1999 Aug;13(8):1221-6 [10450750.001]
  • [Cites] Blood. 2005 Jan 15;105(2):821-6 [15388585.001]
  • [Cites] JAMA. 2005 Mar 23;293(12):1485-9 [15784872.001]
  • [Cites] Blood. 2005 May 1;105(9):3749-56 [15637143.001]
  • [Cites] Lancet. 2005 Aug 20-26;366(9486):635-42 [16112299.001]
  • [Cites] Blood. 2005 Oct 1;106(7):2484-90 [15956279.001]
  • [Cites] Biol Blood Marrow Transplant. 2005 Dec;11(12):999-1005 [16338622.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] J Clin Oncol. 2006 Jan 20;24(3):460-6 [16344315.001]
  • [Cites] Leukemia. 2006 Feb;20(2):264-71 [16357833.001]
  • [Cites] J Clin Oncol. 2008 Jan 10;26(2):283-9 [18182669.001]
  • [Cites] Clin Cancer Res. 2008 Jan 15;14(2):352-9 [18223208.001]
  • [Cites] Curr Probl Pediatr Adolesc Health Care. 2008 Mar;38(3):78-94 [18279790.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2548-55 [18039957.001]
  • [Cites] Lancet Oncol. 2008 Mar;9(3):257-68 [18308251.001]
  • (PMID = 19778845.001).
  • [ISSN] 1938-0712
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / P30 CA021765-31; United States / NCI NIH HHS / CA / CA21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Glucocorticoids
  • [Number-of-references] 92
  • [Other-IDs] NLM/ NIHMS163517; NLM/ PMC2814411
  •  go-up   go-down


3. Attarbaschi A, Mann G, König M, Steiner M, Strehl S, Schreiberhuber A, Schneider B, Meyer C, Marschalek R, Borkhardt A, Pickl WF, Lion T, Gadner H, Haas OA, Dworzak MN: Mixed lineage leukemia-rearranged childhood pro-B and CD10-negative pre-B acute lymphoblastic leukemia constitute a distinct clinical entity. Clin Cancer Res; 2006 May 15;12(10):2988-94
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mixed lineage leukemia-rearranged childhood pro-B and CD10-negative pre-B acute lymphoblastic leukemia constitute a distinct clinical entity.
  • PURPOSE: Mixed lineage leukemia (MLL) abnormalities occur in approximately 50% of childhood pro-B acute lymphoblastic leukemia (ALL).
  • RESULTS: We found that 15 of 29 pro-B ALL, 7 of 11 CD10- pre-B ALL, and 1 of 2 French-American-British classification L1 mature B-cell leukemia cases had a MLL rearrangement.
  • [MeSH-major] Chromosome Aberrations. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16707593.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.4.24.11 / Neprilysin
  •  go-up   go-down


Advertisement
4. Dunwell TL, Hesson LB, Pavlova T, Zabarovska V, Kashuba V, Catchpoole D, Chiaramonte R, Brini AT, Griffiths M, Maher ER, Zabarovsky E, Latif F: Epigenetic analysis of childhood acute lymphoblastic leukemia. Epigenetics; 2009 Apr 1;4(3):185-93
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epigenetic analysis of childhood acute lymphoblastic leukemia.
  • We used a chromosome 3 wide NotI microarray for identification of epigenetically inactivated genes in childhood acute lymphoblastic leukemia (ALL).
  • Three novel genes demonstrated frequent methylation in childhood ALL.
  • In our series of childhood ALL BNC1 was frequently methylated in both T (77%) and B-ALL (79%), whilst MSX1 showed T-ALL (25%) specific methylation.
  • The methylation of the above five genes was cancer specific and expression of the genes could be restored in methylated leukemia cell lines treated with 5-aza-2'-deoxycytidine.
  • This is the first report demonstrating frequent epigenetic inactivation of PPP2R3A, FBLN2, THRB, BNC1 and MSX1 in leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 3 / genetics. DNA Methylation. Epigenesis, Genetic. Gene Expression Regulation, Leukemic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


5. Settin A, Al Haggar M, Al Dosoky T, Al Baz R, Abdelrazik N, Fouda M, Aref S, Al-Tonbary Y: Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia. Indian J Pediatr; 2007 Mar;74(3):255-63
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia.
  • OBJECTIVE: To evaluate children with acute lymphoblastic leukemia (ALL) showing resistance to immediate induction chemotherapy in relation to conventional and advanced cytogenetic analysis.
  • RESULTS: Cases aged 50.000/mm3 also showed better but non-significant remission rates.
  • CONCLUSION: Some cytogenetic and molecular characterizations of childhood ALL could add prognostic criteria for proper therapy allocation.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17401264.001).
  • [ISSN] 0973-7693
  • [Journal-full-title] Indian journal of pediatrics
  • [ISO-abbreviation] Indian J Pediatr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  •  go-up   go-down


6. Wehrli LA, Braun J, Buetti LN, Hagleitner N, Hengartner H, Kühne T, Lüer S, Ozsahin H, Popovic MB, Niggli FK, Betts DR, Bourquin JP: Non-classical karyotypic features in relapsed childhood B-cell precursor acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2009 Feb;189(1):29-36
Genetic Alliance. consumer health - Acute Non Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Non-classical karyotypic features in relapsed childhood B-cell precursor acute lymphoblastic leukemia.
  • Karyotype analysis of acute lymphoblastic leukemia (ALL) at diagnosis has provided valuable prognostic markers for treatment stratification.
  • Non-classical cytogenetic aberrations in these 29 patients were mostly found on chromosomes 1, 2, 7, 9, 13, 14, and 17.
  • From 29 patients with non-classical cytogenetic aberrations, only 8 (28%) had been stratified to a high risk-arm on the first treatment protocol, suggesting that this subgroup might benefit from the identification of new prognostic markers in future studies.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Chromosome Aberrations. Female. Humans. Infant. Karyotyping. Male. Recurrence. Translocation, Genetic. Treatment Outcome


7. Hosking FJ, Papaemmanuil E, Sheridan E, Kinsey SE, Lightfoot T, Roman E, Irving JA, Allan JM, Taylor M, Tomlinson IP, Greaves M, Houlston RS: Genome-wide homozygosity signatures and childhood acute lymphoblastic leukemia risk. Blood; 2010 Jun 3;115(22):4472-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genome-wide homozygosity signatures and childhood acute lymphoblastic leukemia risk.
  • To examine whether homozygosity is associated with an increased risk of developing childhood B-cell precursor acute lymphoblastic leukemia (BCP-ALL), we analyzed 824 ALL cases and 2398 controls genotyped for 292 200 tagging SNPs.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20231427.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / / 10417; United Kingdom / Cancer Research UK / / C1298/A8362
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Erythropoietin
  •  go-up   go-down


8. Sherborne AL, Hosking FJ, Prasad RB, Kumar R, Koehler R, Vijayakrishnan J, Papaemmanuil E, Bartram CR, Stanulla M, Schrappe M, Gast A, Dobbins SE, Ma Y, Sheridan E, Taylor M, Kinsey SE, Lightfoot T, Roman E, Irving JA, Allan JM, Moorman AV, Harrison CJ, Tomlinson IP, Richards S, Zimmermann M, Szalai C, Semsei AF, Erdelyi DJ, Krajinovic M, Sinnett D, Healy J, Gonzalez Neira A, Kawamata N, Ogawa S, Koeffler HP, Hemminki K, Greaves M, Houlston RS: Variation in CDKN2A at 9p21.3 influences childhood acute lymphoblastic leukemia risk. Nat Genet; 2010 Jun;42(6):492-4
SciCrunch. OMIM: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Variation in CDKN2A at 9p21.3 influences childhood acute lymphoblastic leukemia risk.
  • Using data from a genome-wide association study of 907 individuals with childhood acute lymphoblastic leukemia (cases) and 2,398 controls and with validation in samples totaling 2,386 cases and 2,419 controls, we have shown that common variation at 9p21.3 (rs3731217, intron 1 of CDKN2A) influences acute lymphoblastic leukemia risk (odds ratio = 0.71, P = 3.01 x 10(-11)), irrespective of cell lineage.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • 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] J Biol Chem. 2002 Nov 29;277(48):46289-97 [12228235.001]
  • [Cites] PLoS Genet. 2005 Dec;1(6):e78 [16362079.001]
  • [Cites] Haematologica. 2006 Jul;91(7):881-5 [16818274.001]
  • [Cites] Science. 2007 Jun 1;316(5829):1341-5 [17463248.001]
  • [Cites] Blood. 2009 Jan 1;113(1):100-7 [18838613.001]
  • [Cites] Leukemia. 2009 Jul;23(7):1209-18 [19242497.001]
  • [Cites] Science. 2007 Jun 8;316(5830):1488-91 [17478681.001]
  • [Cites] Nat Genet. 2009 Aug;41(8):920-5 [19578364.001]
  • [Cites] Nat Genet. 2009 Aug;41(8):915-9 [19578365.001]
  • [Cites] Nat Genet. 2009 Aug;41(8):899-904 [19578367.001]
  • [Cites] Nat Genet. 2009 Sep;41(9):1001-5 [19684603.001]
  • [Cites] Nat Genet. 2009 Sep;41(9):1006-10 [19684604.001]
  • [Cites] Leukemia. 2010 Jan;24(1):66-73 [19759560.001]
  • [Cites] Nat Genet. 2009 Aug;41(8):909-14 [19578363.001]
  • (PMID = 20453839.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] ENG
  • [Grant] United Kingdom / Medical Research Council / / MC/ U137686856; United States / NCI NIH HHS / CA / R01 CA026038-31; United Kingdom / Medical Research Council / / MC/ U137686861; United Kingdom / Cancer Research UK / / C1298/A8362; United States / NIGMS NIH HHS / GM / T32 GM008243; United States / NCI NIH HHS / CA / R01 CA026038-32; United States / NCI NIH HHS / CA / CA026038-30A2; United States / NCI NIH HHS / CA / R01 CA026038; United States / NCI NIH HHS / CA / R01 CA026038-30A2; United Kingdom / Cancer Research UK / / 10417
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS400186; NLM/ PMC3434228
  •  go-up   go-down


9. Podgornik H, Debeljak M, Zontar D, Cernelc P, Prestor VV, Jazbec J: RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia. Cancer Genet Cytogenet; 2007 Oct 1;178(1):77-81
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia.
  • Amplification of RUNX1 (alias AML1) is a recurrent karyotypic abnormality in childhood acute lymphoblastic leukemia (ALL) that is generally associated with a poor outcome.
  • It does not occur with other primary chromosomal abnormalities in acute ALL.
  • AML1 amplification in acute myelogenous leukemia (AML) is a rare secondary event described mainly in therapy-related cases.
  • AML1 amplification was found in a 13-year-old patient with AML M4/M5 leukemia that occurred 5 years after she had been diagnosed with common B-cell ALL.
  • Conventional cytogenetic, fluorescent in situ hybridization (FISH), and polymerase chain reaction methods revealed no other chromosomal change expected to occur in a disease that we assumed to be a secondary leukemia.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Neoplastic. Leukemia, B-Cell / genetics. Leukemia, B-Cell / pathology. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology


10. Huang L, Lequin M, Pieters R, van den Heuvel-Eibrink MM: The clinical value of follow-up examinations in childhood T-cell acute lymphoblastic leukemia and T-cell non-Hodgkin's lymphoma. Pediatr Blood Cancer; 2007 Apr;48(4):468-72
Genetic Alliance. consumer health - Lymphoblastic lymphoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The clinical value of follow-up examinations in childhood T-cell acute lymphoblastic leukemia and T-cell non-Hodgkin's lymphoma.
  • BACKGROUND: The aim of this study was to evaluate the value of follow-up investigations of T-cell acute lymphoblastic leukemia (T-ALL) and T-cell non-Hodgkin's lymphoma (T-NHL), including cerebrospinal fluid (CSF) examination, bone marrow (BM) aspiration, peripheral blood (PB) count, serum lactate dehydrogenase (LDH) and chest X-rays in patients with an initial mediastinal enlargement.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / diagnosis. Lymphoma, T-Cell / diagnosis


11. Ye QD, Gu LJ, Tang JY, Xue HL, Chen J, Pan C, Chen J, Dong L, Zhou M: [ALL-XH-99 protocol in the treatment of childhood T-cell acute lymphoblastic leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2009 Jan;30(1):26-8
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [ALL-XH-99 protocol in the treatment of childhood T-cell acute lymphoblastic leukemia].
  • OBJECTIVE: To analyze the incidence, clinical characteristics and prognosis of childhood T-cell acute lymphoblastic leukemia (T-ALL).
  • RESULTS: Of 305 childhood ALL patients, 43 were T-ALL.
  • CONCLUSION: There were statistic differences between T-cell and B-cell childhood ALLs in age, initial WBC count, early response to therapy, and eight-year EFS and RFS.
  • Childhood T-ALL was associated with a worse prognosis than other sub-types of childhood ALL.
  • [MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Immunophenotyping. Infant. Karyotyping. Male. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / therapy. Prognosis

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19563031.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  •  go-up   go-down


12. Mansur MB, Emerenciano M, Splendore A, Brewer L, Hassan R, Pombo-de-Oliveira MS, Brazilian Collaborative Study Group of Infant Acute Leukemia: T-cell lymphoblastic leukemia in early childhood presents NOTCH1 mutations and MLL rearrangements. Leuk Res; 2010 Apr;34(4):483-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell lymphoblastic leukemia in early childhood presents NOTCH1 mutations and MLL rearrangements.
  • T-cell acute lymphoblastic leukemia (T-ALL) may affect children in very early age.
  • We used standard methods to explore NOTCH1 mutations and other specific molecular markers in 15 early childhood T-ALL cases.
  • Despite being found in a lower frequency than that described for overall pediatric T-ALL, NOTCH1 alterations were the most frequent ones.
  • [MeSH-major] Mutation. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19631984.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down


13. Park MJ, Taki T, Oda M, Watanabe T, Yumura-Yagi K, Kobayashi R, Suzuki N, Hara J, Horibe K, Hayashi Y: FBXW7 and NOTCH1 mutations in childhood T cell acute lymphoblastic leukaemia and T cell non-Hodgkin lymphoma. Br J Haematol; 2009 Apr;145(2):198-206
Genetic Alliance. consumer health - Non-Hodgkin Lymphoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FBXW7 and NOTCH1 mutations in childhood T cell acute lymphoblastic leukaemia and T cell non-Hodgkin lymphoma.
  • Mutation analysis of FBXW7 and NOTCH1 genes was performed in 55 T cell acute lymphoblastic leukaemia (T-ALL) and 14 T cell non-Hodgkin lymphoma (T-NHL) patients who were treated on the Japan Association of Childhood Leukaemia Study (JACLS) protocols ALL-97 and NHL-98.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Gene Expression Regulation, Leukemic. Lymphoma, T-Cell / genetics. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics. Ubiquitin-Protein Ligases / genetics


14. Nurmio M, Keros V, Lähteenmäki P, Salmi T, Kallajoki M, Jahnukainen K: Effect of childhood acute lymphoblastic leukemia therapy on spermatogonia populations and future fertility. J Clin Endocrinol Metab; 2009 Jun;94(6):2119-22
Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of childhood acute lymphoblastic leukemia therapy on spermatogonia populations and future fertility.
  • CONTEXT: Isolation of spermatogonial stem cells before potentially sterilizing cancer therapy, followed by transplantation of these cells into the testis after such treatment, may be an effective approach to prevent infertility among prepubertal boys suffering from acute lymphoblastic leukemia (ALL).
  • A key clinical consideration in this context is the timing of biopsy, if collection of spermatogonia could be delayed from diagnosis to the later phase of leukemia treatment, better patient selection could be offered.
  • OBJECTIVE: The objective of the study was to examine the routine testicular biopsy material collected to detect testicular leukemia to evaluate if treatment for leukemia affects numbers and maturation of the spermatogonia during the prepubertal period.
  • No significant alteration in spermatogonial numbers was associated with testicular leukemia.
  • CONCLUSION: Treatment for childhood leukemia without high-dose cyclophosphamide seldom depletes the spermatogonial stem cell pool totally.
  • [MeSH-major] Cyclophosphamide / adverse effects. Fertility / drug effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Sperm Count. Spermatogonia / pathology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19318447.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 8N3DW7272P / Cyclophosphamide
  •  go-up   go-down


15. Settin A, Al Haggar M, Al Dosoky T, Al Baz R, Abdelrazik N, Fouda M, Aref S, Al-Tonbary Y: Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia: cases from Mansoura, Egypt. Hematology; 2006 Oct;11(5):341-9
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia: cases from Mansoura, Egypt.
  • OBJECTIVE: To evaluate children with acute lymphoblastic leukemia (ALL) showing resistance to immediate induction chemotherapy in relation to conventional and advanced cytogenetic analysis.
  • Initially low Hb < 8 gm/dl, high WBCs and platelet counts > 50,000/mm(3) also showed better but non-significant remission rates.
  • CONCLUSIONS: Cytogenetic and molecular characterizations of childhood ALL may add prognostic criteria for optimal therapy allocation.
  • [MeSH-major] Cytogenetic Analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17607584.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers
  •  go-up   go-down


16. Liu Y, Chen J, Tang J, Ni S, Xue H, Pan C: Cost of childhood acute lymphoblastic leukemia care in Shanghai, China. Pediatr Blood Cancer; 2009 Oct;53(4):557-62
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cost of childhood acute lymphoblastic leukemia care in Shanghai, China.
  • BACKGROUND: Acute lymphoblastic leukemia (ALL) is the most common and curable malignant pediatric disease in children.
  • Here, we analyzed the overall costs for pediatric ALL therapies and their constitutive elements.
  • Average overall costs for childhood ALL in this study were less than US $11,000, with reasonable clinical results.
  • [MeSH-major] Health Care Costs. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19526524.001).
  • [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
  •  go-up   go-down


17. Wandroo F, Bell A, Darbyshire P, Pratt G, Stankovic T, Gordon J, Lawson S, Moss P: ZAP-70 is highly expressed in most cases of childhood pre-B cell acute lymphoblastic leukemia. Int J Lab Hematol; 2008 Apr;30(2):149-57
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ZAP-70 is highly expressed in most cases of childhood pre-B cell acute lymphoblastic leukemia.
  • ZAP-70 is, however, expressed in adult B cell chronic lymphocytic leukemia where it correlates with a poor prognosis.
  • We wished to determine if ZAP-70 is also expressed in pediatric B cell malignancy.
  • ZAP-70 expression was then determined in bone marrow lymphoblasts obtained from 12 patients with pre-B cell acute lymphoblastic leukemia (ALL).
  • ZAP-70 expression was strongly expressed in nine of the 12 cases of primary pre-B cell lymphoblastic leukemia.
  • The T cell-associated protein kinase ZAP-70 is highly expressed in pre-B lineage cells and most cases of pre-B acute lymphoblastic leukemia.
  • [MeSH-major] B-Lymphocytes / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cells, B-Lymphoid / metabolism. ZAP-70 Protein-Tyrosine Kinase / metabolism

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18333847.001).
  • [ISSN] 1751-5521
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
  •  go-up   go-down


18. Pakakasama S, Sirirat T, Kanchanachumpol S, Udomsubpayakul U, Mahasirimongkol S, Kitpoka P, Thithapandha A, Hongeng S: Genetic polymorphisms and haplotypes of DNA repair genes in childhood acute lymphoblastic leukemia. Pediatr Blood Cancer; 2007 Jan;48(1):16-20
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic polymorphisms and haplotypes of DNA repair genes in childhood acute lymphoblastic leukemia.
  • This study was performed to evaluate the effect of the polymorphisms of DNA repair genes on risk of childhood acute lymphoblastic leukemia (ALL).
  • CONCLUSION: The XRCC1 194Trp allele and haplotype B showed a protective effect against development of childhood ALL.
  • [MeSH-major] Alleles. DNA Repair. DNA-Binding Proteins / genetics. Genetic Predisposition to Disease. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16435384.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / X-ray repair cross complementing protein 1
  •  go-up   go-down


19. Settin A, Al Haggar M, Al Dosoky T, Al Baz R, Abdelrazik N, Fouda M, Aref S, Al-Tonbary Y: Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia: cases from Mansoura Egypt. Hematology; 2007 Apr;12(2):103-11
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic cytogenetic markers in childhood acute lymphoblastic leukemia: cases from Mansoura Egypt.
  • The objective of the work was to evaluate children with acute lymphoblastic leukemia (ALL) showing resistance to immediate induction chemotherapy in relation to conventional and advanced cytogenetic analysis.
  • Initially low HB < 8 gm/dl, high WBCs and platelet counts >50.000/mm(3) also showed better but non-significant remission rates.
  • Our conclusions were that cytogenetic and molecular characterizations of childhood ALL could add prognostic criteria for proper therapy allocation.
  • [MeSH-major] Aneuploidy. Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17454190.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Genetic Markers
  •  go-up   go-down


20. Banklau C, Jindadamrongwech S, Sawangpanich R, Apibal S, Hongeng S, Paisooksantivatana K, Pakakasama S: Effect of genetic alterations of cytarabine- metabolizing enzymes in childhood acute lymphoblastic leukemia. Hematol Oncol Stem Cell Ther; 2010;3(3):103-8
Hazardous Substances Data Bank. CYTARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of genetic alterations of cytarabine- metabolizing enzymes in childhood acute lymphoblastic leukemia.
  • Currently, treatment of childhood acute lymphoblastic leukemia (ALL) includes cytarabine, especially in high-risk patients.
  • PATIENTS AND METHODS: We included children diagnosed with ALL and lymphoblastic lymphoma (LL) stage III and IV.
  • CONCLUSION: The dCK-360G allele was found to increase the risk of mucositis after exposure to low-dose cytarabine in childhood ALL therapy.
  • [MeSH-major] Cytarabine / therapeutic use. Cytidine Deaminase / genetics. Deoxycytidine Kinase / genetics. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20890066.001).
  • [ISSN] 1658-3876
  • [Journal-full-title] Hematology/oncology and stem cell therapy
  • [ISO-abbreviation] Hematol Oncol Stem Cell Ther
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Saudi Arabia
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; EC 2.7.1.74 / Deoxycytidine Kinase; EC 3.1.3.48 / Antigens, CD45; EC 3.5.4.5 / Cytidine Deaminase
  •  go-up   go-down


21. Kikuchi A, Mori T, Fujimoto J, Kumagai M, Sunami S, Okimoto Y, Tsuchida M: Outcome of childhood B-cell non-Hodgkin lymphoma and B-cell acute lymphoblastic leukemia treated with the Tokyo Children's Cancer Study Group NHL B9604 protocol. Leuk Lymphoma; 2008 Apr;49(4):757-62
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcome of childhood B-cell non-Hodgkin lymphoma and B-cell acute lymphoblastic leukemia treated with the Tokyo Children's Cancer Study Group NHL B9604 protocol.
  • From June 1996 to January 2001, 91 patients with B-cell non-Hodgkin lymphoma or B-cell acute lymphoblastic leukemia up to 18 years of age were enrolled in Tokyo Children's Cancer Study Group (TCCSG) NHL B9604 protocol study.


22. Schmiegelow K, Vestergaard T, Nielsen SM, Hjalgrim H: Etiology of common childhood acute lymphoblastic leukemia: the adrenal hypothesis. Leukemia; 2008 Dec;22(12):2137-41
Hazardous Substances Data Bank. HYDROCORTISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Etiology of common childhood acute lymphoblastic leukemia: the adrenal hypothesis.
  • The pattern of infections in the first years of life modulates our immune system, and a low incidence of infections has been linked to an increased risk of common childhood acute lymphoblastic leukemia (ALL).
  • We here present a new interpretation of these observations--the adrenal hypothesis--that proposes that the risk of childhood ALL is reduced when early childhood infections induce qualitative and quantitative changes in the hypothalamus-pituitary-adrenal axis that increase plasma cortisol levels.
  • [MeSH-major] Hypothalamo-Hypophyseal System / immunology. Infection / immunology. Pituitary-Adrenal System / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18719616.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 50
  •  go-up   go-down


23. Chang JS, Wiemels JL, Chokkalingam AP, Metayer C, Barcellos LF, Hansen HM, Aldrich MC, Guha N, Urayama KY, Scélo G, Green J, May SL, Kiley VA, Wiencke JK, Buffler PA: Genetic polymorphisms in adaptive immunity genes and childhood acute lymphoblastic leukemia. Cancer Epidemiol Biomarkers Prev; 2010 Sep;19(9):2152-63
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic polymorphisms in adaptive immunity genes and childhood acute lymphoblastic leukemia.
  • BACKGROUND: Childhood acute lymphoblastic leukemia (ALL) has been hypothesized to have an infection- and immune-related etiology.
  • The lack of immune priming in early childhood may result in abnormal immune responses to infections later in life and increase ALL risk.
  • METHODS: The current analyses examined the association between childhood ALL and 208 single-nucleotide polymorphisms (SNP) of 29 adaptive immune function genes among 377 ALL cases and 448 healthy controls.
  • This increased risk was stronger among firstborn children of all ethnicities and among non-Hispanic children with less day care attendance, consistent with the hypothesis about the role of early immune modulation in the development of childhood ALL.
  • Haplotype analyses identified additional regions of CD28, FCGR2, GATA3, IL2RA, STAT4, and STAT6 associated with childhood ALL.
  • CONCLUSION: Polymorphisms of genes on the adaptive immunity pathway are associated with childhood ALL risk.
  • IMPACT: Results of this study support an immune-related etiology of childhood ALL.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2010 AACR.
  • [Cites] Br J Cancer. 2000 Jan;82(1):234-40 [10638995.001]
  • [Cites] Int J Epidemiol. 2010 Jun;39(3):718-32 [20110276.001]
  • [Cites] Am J Epidemiol. 2000 Dec 15;152(12):1136-44 [11130619.001]
  • [Cites] Am J Hum Genet. 2001 Jul;69(1):138-47 [11404819.001]
  • [Cites] Eur J Immunol. 2001 Nov;31(11):3394-402 [11745358.001]
  • [Cites] Int J Epidemiol. 2001 Dec;30(6):1428-37 [11821358.001]
  • [Cites] Br J Cancer. 2002 Apr 8;86(7):1064-9 [11953850.001]
  • [Cites] Br J Cancer. 2002 May 6;86(9):1419-24 [11986774.001]
  • [Cites] Med Pediatr Oncol. 2002 Jun;38(6):391-7 [11984799.001]
  • [Cites] Science. 2002 Jun 21;296(5576):2225-9 [12029063.001]
  • [Cites] Nat Rev Immunol. 2003 Feb;3(2):133-46 [12563297.001]
  • [Cites] Int J Cancer. 2003 Jun 10;105(2):255-60 [12673688.001]
  • [Cites] Nature. 2003 Dec 18;426(6968):789-96 [14685227.001]
  • [Cites] Br J Cancer. 2004 Jan 12;90(1):139-45 [14710221.001]
  • [Cites] Am J Epidemiol. 2004 May 15;159(10):915-21 [15128601.001]
  • [Cites] Immunology. 2004 Jul;112(3):352-63 [15196202.001]
  • [Cites] Am J Phys Anthropol. 1986 Aug;70(4):433-41 [3766713.001]
  • [Cites] Am J Phys Anthropol. 1986 Aug;70(4):489-503 [3766715.001]
  • [Cites] BMJ. 1989 Nov 18;299(6710):1259-60 [2513902.001]
  • [Cites] J Epidemiol Community Health. 1989 Dec;43(4):352-5 [2614325.001]
  • [Cites] Br J Cancer. 1995 Jan;71(1):1-5 [7819022.001]
  • [Cites] J Natl Cancer Inst. 1997 Jul 2;89(13):939-47 [9214673.001]
  • [Cites] Br J Cancer. 1997;76(9):1241-7 [9365177.001]
  • [Cites] J Immunol. 1998 May 15;160(10):4730-7 [9590218.001]
  • [Cites] Vaccine. 1998 Aug-Sep;16(14-15):1415-9 [9711781.001]
  • [Cites] Clin Exp Allergy. 1998 Nov;28 Suppl 5:39-44; discussion 50-1 [9988446.001]
  • [Cites] Br J Cancer. 1999 May;80(3-4):585-90 [10408870.001]
  • [Cites] Br J Cancer. 1999 Aug;80(11):1844-51 [10468308.001]
  • [Cites] Bioinformatics. 2005 Jan 15;21(2):263-5 [15297300.001]
  • [Cites] Paediatr Perinat Epidemiol. 2005 Mar;19(2):152-64 [15787890.001]
  • [Cites] BMJ. 2005 Jun 4;330(7503):1294 [15849205.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Aug;14(8):1928-34 [16103439.001]
  • [Cites] Nucleic Acids Res. 2006 Jan 1;34(Database issue):D617-21 [16381944.001]
  • [Cites] Nat Rev Cancer. 2006 Mar;6(3):193-203 [16467884.001]
  • [Cites] BMC Genet. 2006;7:38 [16774684.001]
  • [Cites] Clin Exp Allergy. 2006 Nov;36(11):1357-66 [17083345.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Dec;15(12):2533-6 [17164381.001]
  • [Cites] Am J Hum Genet. 2007 Feb;80(2):273-90 [17236132.001]
  • [Cites] Am J Epidemiol. 2007 Mar 1;165(5):496-504 [17182983.001]
  • [Cites] Int J Cancer. 2007 Aug 15;121(4):819-24 [17390373.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Aug;16(8):1686-90 [17684147.001]
  • [Cites] Am J Epidemiol. 2008 Mar 1;167(5):598-606 [18079130.001]
  • [Cites] Adv Genet. 2008;60:335-405 [18358327.001]
  • [Cites] Br J Cancer. 2008 Nov 4;99(9):1529-33 [18827817.001]
  • [Cites] Cancer Causes Control. 2000 Apr;11(4):303-7 [10843442.001]
  • (PMID = 20716621.001).
  • [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
  • [Grant] United States / NIEHS NIH HHS / ES / R01 ES009137-08; United States / NIEHS NIH HHS / ES / ES009137-10; United States / NIEHS NIH HHS / ES / P42 ES004705-22S10023; United States / NIEHS NIH HHS / ES / R01 ES009137-01A1; United States / NIEHS NIH HHS / ES / P42 ES004705-22S20023; United States / NIEHS NIH HHS / ES / ES009137-05S1; United States / NIEHS NIH HHS / ES / P42 ES004705-200023; United States / NIEHS NIH HHS / ES / P42 ES004705-220023; United States / NIEHS NIH HHS / ES / ES009137-02; United States / NIEHS NIH HHS / ES / ES009137-05; United States / NIEHS NIH HHS / ES / ES009137-04; United States / NIEHS NIH HHS / ES / ES009137-01A1; United States / NIEHS NIH HHS / ES / R01 ES009137-02; United States / NIEHS NIH HHS / ES / R01 ES009137-03; United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NCI NIH HHS / CA / R25 CA112355; United States / NIEHS NIH HHS / ES / ES004705-22S30023; United States / NIEHS NIH HHS / ES / R01 ES009137-10S1; United States / NIEHS NIH HHS / ES / ES009137-03S1; United States / NIEHS NIH HHS / ES / R01 ES009137-07; United States / NIEHS NIH HHS / ES / ES004705-190023; United States / NIEHS NIH HHS / ES / ES004705-200023; United States / NIEHS NIH HHS / ES / R01 ES009137-05S1; United States / NIEHS NIH HHS / ES / R01 ES009137-10; United States / NIEHS NIH HHS / ES / ES004705-230023; United States / NIEHS NIH HHS / ES / PS42ES04705; United States / NIEHS NIH HHS / ES / ES004705-210023; United States / NIEHS NIH HHS / ES / ES009137-06A1; United States / NIEHS NIH HHS / ES / P42 ES004705-22S30023; United States / NIEHS NIH HHS / ES / P42 ES004705-210023; United States / NIEHS NIH HHS / ES / R01 ES009137-03S1; United States / NIEHS NIH HHS / ES / P42 ES004705-230023; United States / NIEHS NIH HHS / ES / ES009137-07; United States / NIEHS NIH HHS / ES / R01 ES009137-04; United States / NIEHS NIH HHS / ES / ES009137-09; United States / NIEHS NIH HHS / ES / ES004705-220023; United States / NIEHS NIH HHS / ES / R01ES09137; United States / NIEHS NIH HHS / ES / ES004705-22S10023; United States / NIEHS NIH HHS / ES / R01 ES009137-06A1; United States / NIEHS NIH HHS / ES / ES004705-22S20023; United States / NIEHS NIH HHS / ES / R01 ES009137; United States / NIEHS NIH HHS / ES / ES009137-10S1; United States / NIEHS NIH HHS / ES / R01 ES009137-05; United States / NIEHS NIH HHS / ES / ES009137-03; United States / NIEHS NIH HHS / ES / P42 ES004705-190023; United States / NIEHS NIH HHS / ES / R01 ES009137-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS220398; NLM/ PMC3257312
  •  go-up   go-down


24. Novara F, Beri S, Bernardo ME, Bellazzi R, Malovini A, Ciccone R, Cometa AM, Locatelli F, Giorda R, Zuffardi O: Different molecular mechanisms causing 9p21 deletions in acute lymphoblastic leukemia of childhood. Hum Genet; 2009 Oct;126(4):511-20
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Different molecular mechanisms causing 9p21 deletions in acute lymphoblastic leukemia of childhood.
  • Deletion of chromosome 9p21 is a crucial event for the development of several cancers including acute lymphoblastic leukemia (ALL).
  • We have cloned 23 breakpoint junctions for a total of 46 breakpoints in 17 childhood ALL (9 B- and 8 T-lineages) showing different size deletions at one or both homologous chromosomes 9 to investigate which particular sequences make the region susceptible to interstitial deletion.
  • We found that half of 9p21 deletion breakpoints were mediated by ectopic V(D)J recombination mechanisms whereas the remaining half were associated to repeated sequences, including some with potential for non-B DNA structure formation.
  • [MeSH-major] Chromosomes, Human, Pair 9 / genetics. Cyclin-Dependent Kinase Inhibitor p15 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Sequence Deletion / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Oncogene. 2003 Jun 12;22(24):3792-8 [12802286.001]
  • [Cites] Nat Genet. 2009 Apr;41(4):385-6 [19338077.001]
  • [Cites] Proc Natl Acad Sci U S A. 1971 Apr;68(4):820-3 [5279523.001]
  • [Cites] Genes Dev. 1989 Jul;3(7):1053-61 [2777075.001]
  • [Cites] Mol Cell Biol. 1989 Jul;9(7):3049-57 [2550794.001]
  • [Cites] Med Pediatr Oncol. 1992;20(6):497-505 [1435520.001]
  • [Cites] Mol Cell Biol. 1993 Feb;13(2):1078-92 [8380891.001]
  • [Cites] J Immunol. 1994 Nov 15;153(10):4520-9 [7963524.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jun 11;93(12):6203-8 [8650244.001]
  • [Cites] Blood. 1997 Nov 1;90(9):3720-6 [9345058.001]
  • [Cites] Leukemia. 1998 Jun;12(6):845-59 [9639410.001]
  • [Cites] Biochim Biophys Acta. 1998 Oct 14;1378(2):F115-77 [9823374.001]
  • [Cites] Am J Pathol. 1999 Jul;155(1):105-13 [10393843.001]
  • [Cites] Carcinogenesis. 1999 Aug;20(8):1403-10 [10426784.001]
  • [Cites] J Biol Chem. 2004 Nov 12;279(46):47411-4 [15326170.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3053-8 [15833833.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Sep;7(9):667-77 [16921403.001]
  • [Cites] DNA Repair (Amst). 2006 Sep 8;5(9-10):1273-81 [16931177.001]
  • [Cites] Br J Dermatol. 2006 Nov;155(5):999-1005 [17034532.001]
  • [Cites] Trends Biochem Sci. 2007 Jun;32(6):271-8 [17493823.001]
  • [Cites] Oncogene. 2007 Jun 21;26(29):4306-18 [17237825.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jun 26;104(26):10950-5 [17573529.001]
  • [Cites] Lancet. 2007 Jul 21;370(9583):240-50 [17658395.001]
  • [Cites] Genome Res. 2007 Sep;17(9):1296-303 [17675364.001]
  • [Cites] Hum Mol Genet. 2007 Dec 1;16(23):2783-94 [17666407.001]
  • [Cites] Nat Genet. 2008 Jan;40(1):90-5 [18059269.001]
  • [Cites] Leukemia. 1999 Dec;13(12):1901-28 [10602411.001]
  • [Cites] Nat Rev Cancer. 2001 Nov;1(2):157-62 [11905807.001]
  • [Cites] J Biol Chem. 2002 Nov 29;277(48):46289-97 [12228235.001]
  • [Cites] Genes Chromosomes Cancer. 2003 May;37(1):44-57 [12661005.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Jun;37(2):141-8 [12696062.001]
  • [Cites] Am J Hum Genet. 2008 Mar;82(3):763-71 [18304490.001]
  • [Cites] Leuk Res. 2008 Aug;32(8):1228-35 [18328560.001]
  • [Cites] Nat Genet. 2008 Oct;40(10):1199-203 [18776910.001]
  • [Cites] Genes Chromosomes Cancer. 2009 Jan;48(1):22-38 [18803328.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Nov 11;105(45):17453-6 [18988746.001]
  • [Cites] PLoS Biol. 2009 Feb 17;7(2):e36 [19226189.001]
  • [Cites] Nat Genet. 2009 Apr;41(4):446-9 [19287382.001]
  • [Cites] Nat Genet. 2009 Apr;41(4):455-9 [19287384.001]
  • [Cites] Nat Genet. 2009 Apr;41(4):450-4 [19287385.001]
  • [Cites] Nat Genet. 2004 Sep;36(9):949-51 [15286789.001]
  • (PMID = 19484265.001).
  • [ISSN] 1432-1203
  • [Journal-full-title] Human genetics
  • [ISO-abbreviation] Hum. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / CDKN2B protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA Primers
  • [Other-IDs] NLM/ PMC2762534
  •  go-up   go-down


25. Aricó M, Baruchel A, Bertrand Y, Biondi A, Conter V, Eden T, Gadner H, Gaynon P, Horibe K, Hunger SP, Janka-Schaub G, Masera G, Nachman J, Pieters R, Schrappe M, Schmiegelow K, Valsecchi MG, Pui CH: The seventh international childhood acute lymphoblastic leukemia workshop report: Palermo, Italy, January 29--30, 2005. Leukemia; 2005 Jul;19(7):1145-52
Pharmacogenomics Knowledge Base. meta-databases - Pharmacogenomic Annotation 1183701929 for PMID:15902295 [PharmGKB] .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The seventh international childhood acute lymphoblastic leukemia workshop report: Palermo, Italy, January 29--30, 2005.
  • Between 1995 and 2004, six International Childhood Acute Lymphoblastic Leukemia (ALL) Workshop have been held, and the completion of several collaborative projects has established the clinical relevance and treatment options for several specific genetic subtypes of ALL.
  • [MeSH-major] Neoplasm, Residual / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15902295.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-29139; United States / NCI NIH HHS / CA / CA-31566; United States / NCI NIH HHS / CA / CA-37379; United States / NCI NIH HHS / CA / CA-51001; United States / NCI NIH HHS / CA / CA-78824; United States / NIGMS NIH HHS / GM / GM-61393; United States / NIGMS NIH HHS / GM / GM61374
  • [Publication-type] Congresses; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


26. Bernaldez-Rios R, Ortega-Alvarez MC, Perez-Saldivar ML, Alatoma-Medina NE, Del Campo-Martinez Mde L, Rodriguez-Zepeda Mdel C, Montero-Ponce I, Franco-Ornelas S, Fernandez-Castillo G, Nuñez-Villegas NN, Taboada-Flores MA, Flores-Lujano J, Argüelles-Sanchez ME, Juarez-Ocaña S, Fajardo-Gutierrez A, Mejia-Arangure JM: The age incidence of childhood B-cell precursor acute lymphoblastic leukemia in Mexico City. J Pediatr Hematol Oncol; 2008 Mar;30(3):199-203
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The age incidence of childhood B-cell precursor acute lymphoblastic leukemia in Mexico City.
  • The objective of this population-based survey was to assess the peak age of incidence of B-cell precursor acute lymphoblastic leukemia (ALL) in children in Mexico City (MC).
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18376281.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


27. Schotte D, Chau JC, Sylvester G, Liu G, Chen C, van der Velden VH, Broekhuis MJ, Peters TC, Pieters R, den Boer ML: Identification of new microRNA genes and aberrant microRNA profiles in childhood acute lymphoblastic leukemia. Leukemia; 2009 Feb;23(2):313-22
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of new microRNA genes and aberrant microRNA profiles in childhood acute lymphoblastic leukemia.
  • To identify miRNAs relevant to pediatric acute lymphoblastic leukemia (ALL), we cloned 105 known and 8 new miRNA genes expressed in patients' leukemia cells.
  • Eight miRNAs were differentially expressed between MLL and non-MLL precursor B-ALL cases (P<0.05).
  • The expression did not correlate with the maturation status of leukemia cells based on immunoglobulin and T-cell receptor rearrangements, immunophenotype or MLL-fusion partner.
  • [MeSH-major] MicroRNAs / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA, Neoplasm / genetics
  • [MeSH-minor] Cloning, Molecular. Gene Expression Regulation, Neoplastic. Humans. Infant. Infant, Newborn. Myeloid-Lymphoid Leukemia Protein / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18923441.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / RNA, Neoplasm; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  •  go-up   go-down


28. Savaşan S, Buck S, Ozdemir O, Hamre M, Asselin B, Pullen J, Ravindranath Y: Evaluation of cytotoxicity by flow cytometric drug sensitivity assay in childhood T-cell acute lymphoblastic leukemia. Leuk Lymphoma; 2005 Jun;46(6):833-40
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of cytotoxicity by flow cytometric drug sensitivity assay in childhood T-cell acute lymphoblastic leukemia.
  • Risk-based treatment strategies have improved outcome in childhood B-precursor acute lymphoblastic leukemia, and in vitro drug sensitivity assessment using methyl-thiazol-tetrazolium (MTT) assay has been shown to be an independent prognostic marker.
  • To date, such strategies in childhood T-cell acute lymphoblastic leukemia (T-ALL) have proved elusive, and in vitro drug sensitivity testing has had limited success in T-ALL due to poor T-cell lymphoblast survival in vitro.
  • We studied 68 cases of childhood T-ALL for cytarabine (Ara-C) and daunorubicin sensitivity by FCDSA and compared the results with those obtained by MTT assay.
  • Comparison of T-ALL sensitivity with acute myeloid leukemia (AML) cases revealed a unique pattern difference.
  • [MeSH-major] Drug Screening Assays, Antitumor. Flow Cytometry / methods. Medical Oncology / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Apoptosis. Bone Marrow Cells / cytology. Bone Marrow Cells / metabolism. Child. Daunorubicin / pharmacology. Humans. Immunophenotyping / methods. Inhibitory Concentration 50. Leukemia, T-Cell / diagnosis. Leukemia, T-Cell / drug therapy. Reproducibility of Results. Sensitivity and Specificity. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. METHYLTHIAZOLETETRAZOLIUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16019527.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U10-CA29691
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tetrazolium Salts; 0 / Thiazoles; 298-93-1 / thiazolyl blue; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


29. Hu R, Yan Y, Li Q, Lin Y, Jin W, Li H, Lu Y, Pang T: Increased drug efflux along with midkine gene high expression in childhood B-lineage acute lymphoblastic leukemia cells. Int J Hematol; 2010 Jul;92(1):105-10
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased drug efflux along with midkine gene high expression in childhood B-lineage acute lymphoblastic leukemia cells.
  • Multidrug resistance (MDR) induced by drug efflux has been identified as the major clinical obstacle in the treatment of childhood acute lymphoblastic leukemia (ALL).
  • In the Rhodamine 123 (Rh123) efflux test, mean fluorescence intensity (MFI) in the leukemia cells was obviously lower than that in normal pre-B cells (p < 0.01).
  • We concluded that there was powerful drug efflux ability in lymphoblastic leukemia cells with high MK gene expression.
  • [MeSH-major] Drug Resistance, Multiple / genetics. Gene Expression Regulation, Leukemic. Nerve Growth Factors / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20544404.001).
  • [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] United States
  • [Chemical-registry-number] 0 / MDK protein, human; 0 / Nerve Growth Factors
  •  go-up   go-down


30. Lightfoot T: Aetiology of childhood leukemia. Bioelectromagnetics; 2005;Suppl 7:S5-S11
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aetiology of childhood leukemia.
  • Leukemia is the most common cancer to affect children, accounting for approximately a third of all childhood cancers.
  • The major morphological subtypes of leukemia, acute lymphoblastic leukemia (ALL), and acute myeloblastic leukemia (AML), are characterized by chromosomal translocations involving over 200 genes including mixed lineage leukemia (MLL), TEL, and AML1.
  • Chromosomal translocations involving the MLL gene at 11q23 are a common feature of infant acute leukemia, found in up to 80% of all cases, and there is strong evidence that rearrangements involving the MLL gene or the TEL-AML1 gene fusion can originate in utero.
  • As with most other cancers, the mechanism by which leukemia arises is likely to involve gene-environment interactions.
  • Exposures acting before birth and early in life has long been thought to be important determinants of leukemia, and the list of suspected chemical, physical, and biological agents continues to increase.
  • Unfortunately, the evidence regarding the majority of suggested exposures is limited and often contradictory, and there are areas, which clearly warrant further investigation in order to further our understanding of the aetiology of childhood leukemia.
  • [MeSH-major] Electromagnetic Fields / adverse effects. Environmental Exposure / adverse effects. Leukemia, Radiation-Induced / etiology. Leukemia, Radiation-Induced / physiopathology. Prenatal Exposure Delayed Effects / etiology. Prenatal Exposure Delayed Effects / physiopathology

  • MedlinePlus Health Information. consumer health - Electromagnetic Fields.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2005 Wiley-Liss, Inc
  • (PMID = 16059922.001).
  • [ISSN] 0197-8462
  • [Journal-full-title] Bioelectromagnetics
  • [ISO-abbreviation] Bioelectromagnetics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 54
  •  go-up   go-down


31. Hu RH, Lu Y, Li QH, Ma L, Li B, Zhu XF, Wang JX, Pang TX: [Relationship between midkine expression and drug efflux in childhood acute lymphoblastic leukemia cells]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Dec;17(6):1502-6
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Relationship between midkine expression and drug efflux in childhood acute lymphoblastic leukemia cells].
  • This study was aimed to investigate the expression of midkine gene in childhood acute lymphoblastic leukemia patients (ALL) and to explore the possible effects of midkine gene on the chemotherapeutic drug efflux.
  • The rhodamine 123 efflux test revealed that MFI in the leukemia cells was obviously lower than that in normal cells (p < 0.01), furthermore, there was an evident negative correlation between the MFI and MK mRNA expression (r = -0.869, p < 0.001).
  • It is concluded that there is powerful drug efflux ability in lymphoblastic leukemia cells with high midkine gene expression.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20030935.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / MDK protein, human; 0 / Nerve Growth Factors; 0 / RNA, Messenger
  •  go-up   go-down


32. Pui CH, Campana D, Pei D, Bowman WP, Sandlund JT, Kaste SC, Ribeiro RC, Rubnitz JE, Raimondi SC, Onciu M, Coustan-Smith E, Kun LE, Jeha S, Cheng C, Howard SC, Simmons V, Bayles A, Metzger ML, Boyett JM, Leung W, Handgretinger R, Downing JR, Evans WE, Relling MV: Treating childhood acute lymphoblastic leukemia without cranial irradiation. N Engl J Med; 2009 Jun 25;360(26):2730-41
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treating childhood acute lymphoblastic leukemia without cranial irradiation.
  • BACKGROUND: Prophylactic cranial irradiation has been a standard treatment in children with acute lymphoblastic leukemia (ALL) who are at high risk for central nervous system (CNS) relapse.
  • CNS leukemia (CNS-3 status) or a traumatic lumbar puncture with blast cells at diagnosis and a high level of minimal residual disease (> or = 1%) after 6 weeks of remission induction were significantly associated with poorer event-free survival.
  • CONCLUSIONS: With effective risk-adjusted chemotherapy, prophylactic cranial irradiation can be safely omitted from the treatment of childhood ALL. (ClinicalTrials.gov number, NCT00137111. )
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • 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. DAUNORUBICIN .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. MERCAPTOPURINE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • Hazardous Substances Data Bank. METHOTREXATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2009 Massachusetts Medical Society
  • [Cites] Leukemia. 2002 Jun;16(6):1099-111 [12040440.001]
  • [Cites] JAMA. 2002 Oct 23-30;288(16):2001-7 [12387652.001]
  • [Cites] J Natl Cancer Inst. 2008 Sep 17;100(18):1301-9 [18780868.001]
  • [Cites] J Clin Oncol. 2003 Jan 15;21(2):184-8 [12525508.001]
  • [Cites] Blood. 2003 May 15;101(10):3809-17 [12531809.001]
  • [Cites] N Engl J Med. 2003 Aug 14;349(7):640-9 [12917300.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2736-40 [12843002.001]
  • [Cites] JAMA. 2003 Oct 15;290(15):2001-7 [14559953.001]
  • [Cites] Br J Haematol. 2004 Jan;124(1):33-46 [14675406.001]
  • [Cites] Leukemia. 2004 May;18(5):934-8 [15029212.001]
  • [Cites] Nature. 2004 May 27;429(6990):464-8 [15164072.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2690-6 [15251979.001]
  • [Cites] N Engl J Med. 1993 Jul 29;329(5):314-9 [8321259.001]
  • [Cites] J Clin Oncol. 1995 Jan;13(1):177-9 [7799017.001]
  • [Cites] J Clin Oncol. 1997 Aug;15(8):2786-91 [9256120.001]
  • [Cites] N Engl J Med. 1998 Feb 19;338(8):499-505 [9468466.001]
  • [Cites] Blood. 1998 Jul 15;92(2):411-5 [9657739.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3310-22 [10828010.001]
  • [Cites] Leukemia. 2000 Aug;14(8):1354-61 [10942229.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2691-6 [11023499.001]
  • [Cites] Blood. 2000 Nov 15;96(10):3381-4 [11071631.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2196-204 [11187911.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2223-33 [11187913.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2257-66 [11187917.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2267-75 [11187918.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2286-94 [11187920.001]
  • [Cites] Cancer Chemother Pharmacol. 2001 Sep;48(3):235-40 [11592346.001]
  • [Cites] Blood. 2002 Feb 1;99(3):825-33 [11806983.001]
  • [Cites] Blood. 2002 Apr 15;99(8):2734-9 [11929760.001]
  • [Cites] N Engl J Med. 1998 Aug 27;339(9):605-15 [9718381.001]
  • [Cites] Blood. 1999 May 1;93(9):2817-23 [10216075.001]
  • [Cites] J Clin Invest. 2005 Jan;115(1):110-7 [15630450.001]
  • [Cites] Br J Haematol. 2005 Jun;129(6):734-45 [15952999.001]
  • [Cites] J Clin Oncol. 2005 Oct 1;23(28):7161-7 [16192600.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] J Clin Oncol. 2006 May 20;24(15):2332-6 [16710032.001]
  • [Cites] J Clin Oncol. 2006 Jul 1;24(19):3142-9 [16809737.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1165-73 [16609069.001]
  • [Cites] N Engl J Med. 2006 Oct 12;355(15):1572-82 [17035650.001]
  • [Cites] Blood. 2007 Feb 1;109(3):896-904 [17003366.001]
  • [Cites] JAMA. 2007 Mar 21;297(11):1207-15 [17374815.001]
  • [Cites] Blood. 2007 May 15;109(10):4151-7 [17264302.001]
  • [Cites] JAMA. 2007 Jun 27;297(24):2705-15 [17595271.001]
  • [Cites] J Clin Oncol. 2007 Nov 1;25(31):4914-21 [17971588.001]
  • [Cites] Blood. 2007 Dec 1;110(12):4022-9 [17720883.001]
  • [Cites] Lancet Oncol. 2008 Mar;9(3):257-68 [18308251.001]
  • [Cites] J Clin Oncol. 2008 Apr 20;26(12):1932-9 [18421047.001]
  • [Cites] Blood. 2008 May 1;111(9):4477-89 [18285545.001]
  • [CommentIn] N Engl J Med. 2009 Sep 24;361(13):1310; author reply 1311-2 [19776415.001]
  • [CommentIn] N Engl J Med. 2009 Sep 24;361(13):1310-1; author reply 1311-2 [19780213.001]
  • (PMID = 19553647.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00137111
  • [Grant] United States / NIGMS NIH HHS / GM / U01 GM061393; United States / NCI NIH HHS / CA / R01 CA078224; United States / NCI NIH HHS / CA / R37 CA036401; United States / NCI NIH HHS / CA / CA36401; United States / NCI NIH HHS / CA / R01 CA051001-13; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA78224; United States / NCI NIH HHS / CA / R01 CA060419; United States / NCI NIH HHS / CA / CA60419; United States / NIGMS NIH HHS / GM / GM61393; United States / NCI NIH HHS / CA / P30 CA021765; United States / NIGMS NIH HHS / GM / U01 GM061393-090007; United States / NCI NIH HHS / CA / R01 CA051001; United States / NCI NIH HHS / CA / R01 CA036401; United States / NCI NIH HHS / CA / CA51001; United States / NCI NIH HHS / CA / U01 CA060419
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 8N3DW7272P / Cyclophosphamide; E7WED276I5 / 6-Mercaptopurine; EC 3.5.1.1 / Asparaginase; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ NIHMS118392; NLM/ PMC2754320
  •  go-up   go-down


33. Fais F, Tenca C, Cimino G, Coletti V, Zanardi S, Bagnara D, Saverino D, Zarcone D, De Rossi G, Ciccone E, Grossi CE: CD1d expression on B-precursor acute lymphoblastic leukemia subsets with poor prognosis. Leukemia; 2005 Apr;19(4):551-6
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD1d expression on B-precursor acute lymphoblastic leukemia subsets with poor prognosis.
  • Acute lymphoblastic leukemia (ALL) is the most frequent malignancy of childhood.
  • We investigated CD1d expression in 80 pediatric B-cell precursor (BCP) ALL cases defined according to immunophenotype, cytogenetic features and age at onset.
  • CD1d+ ALLs were significantly associated with infant leukemia, pro-B phenotype and mixed-lineage leukemia (MLL)/AF4 gene rearrangement.
  • [MeSH-major] Antigens, CD1 / metabolism. Hematopoietic Stem Cells / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15744356.001).
  • [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 / Antigens, CD1; 0 / Antigens, CD1d; 0 / Biomarkers, Tumor; 0 / CD1D protein, human; 0 / Galactosylceramides; 0 / alpha-galactosylceramide
  •  go-up   go-down


34. Zhu YM, Zhao WL, Fu JF, Shi JY, Pan Q, Hu J, Gao XD, Chen B, Li JM, Xiong SM, Gu LJ, Tang JY, Liang H, Jiang H, Xue YQ, Shen ZX, Chen Z, Chen SJ: NOTCH1 mutations in T-cell acute lymphoblastic leukemia: prognostic significance and implication in multifactorial leukemogenesis. Clin Cancer Res; 2006 May 15;12(10):3043-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NOTCH1 mutations in T-cell acute lymphoblastic leukemia: prognostic significance and implication in multifactorial leukemogenesis.
  • PURPOSE: NOTCH signaling pathway is essential in T-cell development and NOTCH1 mutations are frequently present in T-cell acute lymphoblastic leukemia (T-ALL).
  • Interestingly, the statistically significant difference of survival according to NOTCH1 mutations was only observed in adult patients (>18 years) but not in pediatric patients (< or = 18 years), possibly due to the relatively good overall response of childhood T-ALL to the current chemotherapy.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Receptor, Notch1 / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Clin Cancer Res. 2009 Feb 15;15(4):1506
  • (PMID = 16707600.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
  •  go-up   go-down


35. Yamamoto T, Isomura M, Xu Y, Liang J, Yagasaki H, Kamachi Y, Kudo K, Kiyoi H, Naoe T, Kojma S: PTPN11, RAS and FLT3 mutations in childhood acute lymphoblastic leukemia. Leuk Res; 2006 Sep;30(9):1085-9
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PTPN11, RAS and FLT3 mutations in childhood acute lymphoblastic leukemia.
  • Recently, PTPN11 mutations have been reported in children with acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Burkitt Lymphoma / genetics. Intracellular Signaling Peptides and Proteins / genetics. Mutation, Missense. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Protein Tyrosine Phosphatases / genetics. fms-Like Tyrosine Kinase 3 / genetics. ras Proteins / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Down Syndrome / complications. Down Syndrome / genetics. Female. Humans. Infant. Japan. Male. Noonan Syndrome / genetics. Protein Tyrosine Phosphatase, Non-Receptor Type 11

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16533526.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.6.5.2 / ras Proteins
  •  go-up   go-down


36. Goshen Y, Stark B, Kornreich L, Michowiz S, Feinmesser M, Yaniv I: High incidence of meningioma in cranial irradiated survivors of childhood acute lymphoblastic leukemia. Pediatr Blood Cancer; 2007 Sep;49(3):294-7
Genetic Alliance. consumer health - Meningioma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High incidence of meningioma in cranial irradiated survivors of childhood acute lymphoblastic leukemia.
  • BACKGROUND: Most survivors of childhood acute lymphoblastic leukemia (ALL) and T-cell lymphoma (T-NHL) treated before 1990 received cranial radiation.
  • This study assessed the occurrence of second tumors in irradiated and non-irradiated survivors.
  • Imaging (MRI, CT) was performed every 3-6 years in 76/88 irradiated and 74/122 non-irradiated patients for the last 20 years.
  • Only one of the 74 non-irradiated patients (median follow-up 14 years) developed meningioma.
  • CONCLUSIONS: Survivors of childhood ALL treated with cranial radiation require prolonged surveillance because of a high incidence of late meningiomas.
  • [MeSH-major] Cranial Irradiation / adverse effects. Meningeal Neoplasms / epidemiology. Meningioma / epidemiology. Neoplasms, Radiation-Induced / epidemiology. Neoplasms, Second Primary / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy


37. Schmiegelow K, Forestier E, Hellebostad M, Heyman M, Kristinsson J, Söderhäll S, Taskinen M, Nordic Society of Paediatric Haematology and Oncology: Long-term results of NOPHO ALL-92 and ALL-2000 studies of childhood acute lymphoblastic leukemia. Leukemia; 2010 Feb;24(2):345-54
Pharmacogenomics Knowledge Base. meta-databases - Pharmacogenomic Annotation 1183701935 for PMID:20010622 [PharmGKB] .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term results of NOPHO ALL-92 and ALL-2000 studies of childhood acute lymphoblastic leukemia.
  • Analysis of 2668 children with acute lymphoblastic leukemia (ALL) treated in two successive Nordic clinical trials (Nordic Society of Paediatric Haematology and Oncology (NOPHO) ALL-92 and ALL-2000) showed that 75% of all patients are cured by first-line therapy, and 83% are long-term survivors.
  • Improved risk stratification and chemotherapy have eliminated the previous independent prognostic significance of gender, CNS leukemia and translocation t(1;19)(q23;p13), whereas the post-induction level of minimal residual disease (MRD) has emerged as a new risk grouping feature.
  • Infant leukemia, high leukocyte count, T-lineage immunophenotype, translocation t(4;11)(q21;q23) and hypodiploidy persist to be associated with lower cure rates.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy


38. He J, Chen ZX, Xue YQ, Li JQ, He HL, Huang YP, He YX, Chai YH, Zhu LL: [Detection of fusion genes resulting from chromosome abnormalities in childhood acute lymphoblastic leukemia]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2005 Oct;22(5):551-3
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Detection of fusion genes resulting from chromosome abnormalities in childhood acute lymphoblastic leukemia].
  • OBJECTIVE: To detect the expression of the fusion genes resulting from chromosome abnormalities in childhood acute lymphoblastic leukemia(ALL) and its conformity to WHO classification.
  • The multiplex RT-PCR in combination with chromosome analysis revealed genetic abnormalities in 69.4%(43/62) of childhood ALL.
  • CONCLUSION: Multiplex RT-PCR combined with chromosome analysis and immunophenotyping can provide reliable and helpful information for the diagnosis, therapy evaluation and prognosis prediction in childhood ALL, which may also serve as a basis on which to implement the criteria of WHO classification.
  • [MeSH-major] Chromosome Aberrations. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit / genetics. Core Binding Factor Alpha 2 Subunit / metabolism. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Flow Cytometry. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Immunophenotyping. Infant. Karyotyping. Myeloid-Lymphoid Leukemia Protein / genetics. Myeloid-Lymphoid Leukemia Protein / metabolism. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. RNA-Binding Protein FUS / genetics. RNA-Binding Protein FUS / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transcription Factors / genetics. Transcription Factors / metabolism

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16215946.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / E2a-Hlf fusion protein, human; 0 / Homeodomain Proteins; 0 / MLL-AF10 fusion protein, human; 0 / MLL-AF4 fusion protein, human; 0 / MLL-AF9 fusion protein, human; 0 / MLL-ELL fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RNA-Binding Protein FUS; 0 / TEL-AML1 fusion protein; 0 / TLS-ERG fusion protein, human; 0 / Transcription Factors; 143275-75-6 / TLX1 protein, human; 146150-85-8 / E2A-Pbx1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  •  go-up   go-down


39. Schrauder A, Reiter A, Gadner H, Niethammer D, Klingebiel T, Kremens B, Peters C, Ebell W, Zimmermann M, Niggli F, Ludwig WD, Riehm H, Welte K, Schrappe M: Superiority of allogeneic hematopoietic stem-cell transplantation compared with chemotherapy alone in high-risk childhood T-cell acute lymphoblastic leukemia: results from ALL-BFM 90 and 95. J Clin Oncol; 2006 Dec 20;24(36):5742-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Superiority of allogeneic hematopoietic stem-cell transplantation compared with chemotherapy alone in high-risk childhood T-cell acute lymphoblastic leukemia: results from ALL-BFM 90 and 95.
  • PURPOSE: The role of hematopoietic stem-cell transplantation (SCT) in first complete remission (CR1) for children with very high-risk (VHR) acute lymphoblastic leukemia (ALL) is still under critical discussion.
  • CONCLUSION: SCT in CR1 is superior to treatment with chemotherapy alone for childhood HR-T-ALL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


40. Urayama KY, Wiencke JK, Buffler PA, Chokkalingam AP, Metayer C, Wiemels JL: MDR1 gene variants, indoor insecticide exposure, and the risk of childhood acute lymphoblastic leukemia. Cancer Epidemiol Biomarkers Prev; 2007 Jun;16(6):1172-7
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MDR1 gene variants, indoor insecticide exposure, and the risk of childhood acute lymphoblastic leukemia.
  • Among children enrolled in the Northern California Childhood Leukemia Study, we examined the susceptibility conferred by MDR1 single nucleotide polymorphisms (SNP) and predicted haplotypes and whether they modify the association between indoor insecticide exposure and risk of childhood acute lymphoblastic leukemia (ALL).
  • RESULTS: Allele frequencies in non-Hispanic White and Hispanic controls were similar, and with the exception of T-129C, seemed to be in strong linkage disequilibrium.
  • Overall, the SNPs considered individually or within haplotypes (C1236T-G2677T/A-C3435T) were not significantly associated with childhood ALL.
  • [MeSH-major] Air Pollution, Indoor / adverse effects. Genes, MDR. Insecticides / adverse effects. P-Glycoprotein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • MedlinePlus Health Information. consumer health - Indoor Air Pollution.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17548681.001).
  • [ISSN] 1055-9965
  • [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
  • [Grant] United States / NIEHS NIH HHS / ES / P42 ES04705; United States / NIEHS NIH HHS / ES / R01 ES09137
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insecticides; 0 / P-Glycoprotein
  •  go-up   go-down


41. Ceppi F, Brown A, Betts DR, Niggli F, Popovic MB: Cytogenetic characterization of childhood acute lymphoblastic leukemia in Nicaragua. Pediatr Blood Cancer; 2009 Dec 15;53(7):1238-41
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic characterization of childhood acute lymphoblastic leukemia in Nicaragua.
  • BACKGROUND: Within the frame of a twinning programme with Nicaragua, The La Mascota project, we evaluated in our study the contribution of cytogenetic characterization of acute lymphoblastic leukemia (ALL) as prognostic factor compared to clinical, morphological, and immunohistochemical parameters.
  • METHODS: All patients with ALL treated at the only cancer pediatric hospital in Nicaragua during 2006 were studied prospectively.
  • [MeSH-major] Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Aneuploidy. Child. Child, Preschool. Chromosome Banding. Core Binding Factor Alpha 2 Subunit / genetics. Female. Fusion Proteins, bcr-abl / genetics. Hepatomegaly / epidemiology. Hepatomegaly / etiology. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Nicaragua / epidemiology. Oncogene Proteins, Fusion / genetics. Prognosis. Prospective Studies. Risk. Splenomegaly / epidemiology. Splenomegaly / etiology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19672974.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  •  go-up   go-down


42. Raimondi SC, Zhou Y, Shurtleff SA, Rubnitz JE, Pui CH, Behm FG: Near-triploidy and near-tetraploidy in childhood acute lymphoblastic leukemia: association with B-lineage blast cells carrying the ETV6-RUNX1 fusion, T-lineage immunophenotype, and favorable outcome. Cancer Genet Cytogenet; 2006 Aug;169(1):50-7
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Near-triploidy and near-tetraploidy in childhood acute lymphoblastic leukemia: association with B-lineage blast cells carrying the ETV6-RUNX1 fusion, T-lineage immunophenotype, and favorable outcome.
  • The prognostic significance of near-triploidy (68-80 chromosomes) and near-tetraploidy (>80 chromosomes) in childhood acute lymphoblastic leukemia (ALL) is unclear.
  • [MeSH-major] B-Lymphocytes / immunology. Core Binding Factor Alpha 2 Subunit / genetics. Oncogene Proteins, Fusion / genetics. Polyploidy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. T-Lymphocytes / immunology


43. Noble SL, Sherer E, Hannemann RE, Ramkrishna D, Vik T, Rundell AE: Using adaptive model predictive control to customize maintenance therapy chemotherapeutic dosing for childhood acute lymphoblastic leukemia. J Theor Biol; 2010 Jun 7;264(3):990-1002
Hazardous Substances Data Bank. MERCAPTOPURINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Using adaptive model predictive control to customize maintenance therapy chemotherapeutic dosing for childhood acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is a common childhood cancer in which nearly one-quarter of patients experience a disease relapse.
  • However, it has been shown that individualizing therapy for childhood ALL patients by adjusting doses based on the blood concentration of active drug metabolite could significantly improve treatment outcome.
  • An adaptive model predictive control (MPC) strategy is presented in which maintenance therapy for childhood ALL is personalized using routine patient measurements of red blood cell mean corpuscular volume as a surrogate for the active drug metabolite concentration.
  • [MeSH-major] 6-Mercaptopurine / therapeutic use. Dose-Response Relationship, Drug. Models, Biological. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20138060.001).
  • [ISSN] 1095-8541
  • [Journal-full-title] Journal of theoretical biology
  • [ISO-abbreviation] J. Theor. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, American Recovery and Reinvestment Act; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; E7WED276I5 / 6-Mercaptopurine
  •  go-up   go-down


44. Liu M, Ge Y, Payton SG, Aboukameel A, Buck S, Flatley RM, Haska C, Mohammad R, Taub JW, Matherly LH: Transcriptional regulation of the human reduced folate carrier in childhood acute lymphoblastic leukemia cells. Clin Cancer Res; 2006 Jan 15;12(2):608-16
Hazardous Substances Data Bank. FOLIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transcriptional regulation of the human reduced folate carrier in childhood acute lymphoblastic leukemia cells.
  • PURPOSE: The transcriptional regulation of the human reduced folate carrier (hRFC), involved in cellular uptake of methotrexate and reduced folates, was studied in childhood acute lymphoblastic leukemia (ALL).
  • In 40 ALL and 17 non-ALL specimens, 2 cosegregating high-frequency polymorphisms (T-1309/C-1217 and C-1309/T-1217; allelic frequencies of 36% and 64%, respectively) were detected in the A1/A2 promoter; none were detected in promoter B.
  • [MeSH-major] DNA Methylation. Gene Expression Regulation. Membrane Transport Proteins / genetics. Membrane Transport Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16428507.001).
  • [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 / CA 76641
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / Membrane Transport Proteins; 0 / Protein Isoforms; 0 / Reduced Folate Carrier Protein; 0 / SLC19A1 protein, human; 0 / Slc19a1 protein, mouse; 0 / Sp1 Transcription Factor; 0 / USF1 protein, human; 0 / Upstream Stimulatory Factors; 148971-36-2 / Ikaros Transcription Factor; 935E97BOY8 / Folic Acid
  •  go-up   go-down


45. Tassano E, Acquila M, Tavella E, Micalizzi C, Panarello C, Morerio C: MicroRNA-125b-1 and BLID upregulation resulting from a novel IGH translocation in childhood B-Cell precursor acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2010 Aug;49(8):682-7
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA-125b-1 and BLID upregulation resulting from a novel IGH translocation in childhood B-Cell precursor acute lymphoblastic leukemia.
  • Recent findings have also revealed their significant role in B-cell precursor acute lymphoblastic leukemia.
  • In this study, we describe a pediatric case of B-cell precursor acute lymphoblastic leukemia showing microRNA-125b-1 (MIR125B1) and BLID gene overexpression, resulting from a novel t(11;14)(q24.1;q32) translocation involving IGH.
  • [MeSH-major] BRCA2 Protein / genetics. Immunoglobulin Heavy Chains / genetics. MicroRNAs / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Apoptosis Regulatory Proteins. Child. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 14 / genetics. Female. Humans. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20544842.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BLID protein, human; 0 / BRCA2 Protein; 0 / BRCA2 protein, human; 0 / Immunoglobulin Heavy Chains; 0 / MIRN125 microRNA, human; 0 / MicroRNAs; 0 / RNA, Messenger
  •  go-up   go-down


46. Lemez P, Attarbaschi A, Béné MC, Bertrand Y, Castoldi G, Forestier E, Garand R, Haas OA, Kagialis-Girard S, Ludwig WD, Matutes E, Mejstríková E, Pages MP, Pickl W, Porwit A, Orfao A, Schabath R, Starý J, Strobl H, Talmant P, van't Veer MB, Zemanová Z, European Group for the Immunological Characterization of Leukemias (EGIL): Childhood near-tetraploid acute lymphoblastic leukemia: an EGIL study on 36 cases. Eur J Haematol; 2010 Oct;85(4):300-8
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Childhood near-tetraploid acute lymphoblastic leukemia: an EGIL study on 36 cases.
  • OBJECTIVES: Patients with near-tetraploid (karyotype: 81 - 103 chromosomes) acute lymphoblastic leukemia (NT-ALL) constitute about 1% of childhood ALL and data reported on them are limited and controversial.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] © 2010 John Wiley & Sons A/S.
  • (PMID = 20561032.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  •  go-up   go-down


47. Ariffin H, Chen SP, Kwok CS, Quah TC, Lin HP, Yeoh AE: Ethnic differences in the frequency of subtypes of childhood acute lymphoblastic leukemia: results of the Malaysia-Singapore Leukemia Study Group. J Pediatr Hematol Oncol; 2007 Jan;29(1):27-31
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ethnic differences in the frequency of subtypes of childhood acute lymphoblastic leukemia: results of the Malaysia-Singapore Leukemia Study Group.
  • Childhood acute lymphoblastic leukemia (ALL) is clinically heterogeneous with prognostically and biologically distinct subtypes.
  • Although racial differences in frequency of different types of childhood ALL have been reported, many are confounded by selected or limited population samples.
  • The Malaysia-Singapore (MA-SPORE) Leukemia Study Group provided a unique platform for the study of the frequency of major subgroups of childhood ALL in a large cohort of unselected multiethnic Asian children.
  • Our study suggests that there are indeed significant and important racial differences in the frequency of subtypes of childhood ALL.
  • Comprehensive subgrouping of childhood ALL may reveal interesting population frequency differences of the various subtypes, their risk factors and hopefully, its etiology.
  • [MeSH-major] Asian Continental Ancestry Group. Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / ethnology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Pediatr Hematol Oncol. 2007 Aug;29(8):585 [17762503.001]
  • (PMID = 17230064.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins
  •  go-up   go-down


48. Imanishi H, Okamura N, Yagi M, Noro Y, Moriya Y, Nakamura T, Hayakawa A, Takeshima Y, Sakaeda T, Matsuo M, Okumura K: Genetic polymorphisms associated with adverse events and elimination of methotrexate in childhood acute lymphoblastic leukemia and malignant lymphoma. J Hum Genet; 2007;52(2):166-71
Nature Publishing Group. Nature Publishing Group (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic polymorphisms associated with adverse events and elimination of methotrexate in childhood acute lymphoblastic leukemia and malignant lymphoma.
  • Methotrexate is administered in high doses to treat childhood acute lymphoblastic leukemia and malignant lymphoma.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Liver Diseases / genetics. Lymphoma / genetics. Methotrexate / therapeutic use. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


49. Mullighan CG, Zhang J, Harvey RC, Collins-Underwood JR, Schulman BA, Phillips LA, Tasian SK, Loh ML, Su X, Liu W, Devidas M, Atlas SR, Chen IM, Clifford RJ, Gerhard DS, Carroll WL, Reaman GH, Smith M, Downing JR, Hunger SP, Willman CL: JAK mutations in high-risk childhood acute lymphoblastic leukemia. Proc Natl Acad Sci U S A; 2009 Jun 9;106(23):9414-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] JAK mutations in high-risk childhood acute lymphoblastic leukemia.
  • Pediatric acute lymphoblastic leukemia (ALL) is a heterogeneous disease consisting of distinct clinical and biological subtypes that are characterized by specific chromosomal abnormalities or gene mutations.
  • We recently identified a poor prognostic subgroup of pediatric BCR-ABL1-negative ALL patients characterized by deletion of IKZF1 (encoding the lymphoid transcription factor IKAROS) and a gene expression signature similar to BCR-ABL1-positive ALL, raising the possibility of activated tyrosine kinase signaling within this leukemia subtype.
  • Here, we report activating mutations in the Janus kinases JAK1 (n = 3), JAK2 (n = 16), and JAK3 (n = 1) in 20 (10.7%) of 187 BCR-ABL1-negative, high-risk pediatric ALL cases.
  • The JAK-mutated cases had a gene expression signature similar to BCR-ABL1 pediatric ALL, and they had a poor outcome.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • COS Scholar Universe. author profiles.
  • 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).
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Oncogene. 2001 Sep 27;20(43):6188-95 [11593427.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]
  • [Cites] J Biol Chem. 2002 Dec 6;277(49):47954-63 [12351625.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2951-9 [12730115.001]
  • [Cites] Cancer Chemother Rep. 1966 Mar;50(3):163-70 [5910392.001]
  • [Cites] Nature. 1996 Jul 25;382(6589):325-31 [8684460.001]
  • [Cites] N Engl J Med. 1998 Jun 4;338(23):1663-71 [9614257.001]
  • [Cites] Nature. 1998 Sep 17;395(6699):237-43 [9751050.001]
  • [Cites] Nature. 1998 Sep 17;395(6699):244-50 [9751051.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):387-97 [15837627.001]
  • [Cites] N Engl J Med. 2005 Apr 28;352(17):1779-90 [15858187.001]
  • [Cites] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] J Biol Chem. 2005 Dec 23;280(51):41893-9 [16239216.001]
  • [Cites] Blood. 2006 Jan 1;107(1):176-83 [16174768.001]
  • [Cites] Cancer Res. 2006 Jul 1;66(13):6468-72 [16818614.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Nat Rev Cancer. 2007 Sep;7(9):673-83 [17721432.001]
  • [Cites] Mol Cell Biol. 2008 Mar;28(5):1792-801 [18160720.001]
  • [Cites] Lancet. 2008 Mar 22;371(9617):1030-43 [18358930.001]
  • [Cites] J Exp Med. 2008 Apr 14;205(4):751-8 [18362173.001]
  • [Cites] Nature. 2008 May 1;453(7191):110-4 [18408710.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5477-85 [18388178.001]
  • [Cites] Blood. 2008 Sep 15;112(6):2190-8 [18779404.001]
  • [Cites] Cancer Cell. 2008 Oct 7;14(4):335-43 [18835035.001]
  • [Cites] Lancet. 2008 Oct 25;372(9648):1484-92 [18805579.001]
  • [Cites] Semin Cell Dev Biol. 2008 Aug;19(4):385-93 [18682296.001]
  • [Cites] Blood. 2009 Jan 15;113(3):646-8 [18927438.001]
  • [Cites] N Engl J Med. 2009 Jan 29;360(5):470-80 [19129520.001]
  • [Cites] Lancet. 2005 Mar 19-25;365(9464):1054-61 [15781101.001]
  • (PMID = 19470474.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA118100; United States / NCI NIH HHS / CA / U10 CA98413; United States / NCI NIH HHS / CA / L40 CA142226; United States / NCI NIH HHS / CA / U01 CA114762; United States / NCI NIH HHS / CA / CA114762; United States / NCI NIH HHS / CA / U10 CA098413; United States / PHS HHS / / N01-C0-12400; United States / NCI NIH HHS / CA / CA098543; United States / Howard Hughes Medical Institute / / ; United States / NICHD NIH HHS / HD / T32 HD044331; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / T32 CA128583; United States / NCI NIH HHS / CA / U10 CA98543
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IKZF1 protein, human; 148971-36-2 / Ikaros Transcription Factor; EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / Janus Kinase 3; EC 2.7.10.2 / Janus Kinases
  • [Other-IDs] NLM/ PMC2695045
  •  go-up   go-down


50. Cox CV, Martin HM, Kearns PR, Virgo P, Evely RS, Blair A: Characterization of a progenitor cell population in childhood T-cell acute lymphoblastic leukemia. Blood; 2007 Jan 15;109(2):674-82
MedlinePlus Health Information. consumer health - Stem Cells.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of a progenitor cell population in childhood T-cell acute lymphoblastic leukemia.
  • A significant proportion of children with T-cell acute lymphoblastic leukemia (T-ALL) continue to fail therapy.
  • Cells from 13 pediatric cases were maintained in vitro for at least 4 weeks and expanded in 8 cases.
  • The immunophenotype and genotype of the original leukemia cells were preserved with serial passage in the NOD/SCID mice.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Stem Cells / immunology. Stem Cells / pathology


51. Meleshko AN, Lipay NV, Stasevich IV, Potapnev MP: Rearrangements of IgH, TCRD and TCRG genes as clonality marker of childhood acute lymphoblastic leukemia. Exp Oncol; 2005 Dec;27(4):319-24
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rearrangements of IgH, TCRD and TCRG genes as clonality marker of childhood acute lymphoblastic leukemia.
  • AIM: Immunoglobulin (Ig) and T-cell receptor (TCR) gene rearrangements are excellent patient-specific targets for clonality studies and monitoring of acute lymphoblastic leukemia (ALL).
  • Seven pair cases of patients with de novo leukemia and relapses were analyzed and revealed subclonal deviation in rearrangements of IgH or TCR genes during disease evolution.
  • [MeSH-major] Gene Rearrangement, B-Lymphocyte, Heavy Chain. Gene Rearrangement, delta-Chain T-Cell Antigen Receptor. Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


52. Gadner H, Masera G, Schrappe M, Eden T, Benoit Y, Harrison C, Nachman J, Pui CH: The Eighth International Childhood Acute Lymphoblastic Leukemia Workshop ('Ponte di legno meeting') report: Vienna, Austria, April 27-28, 2005. Leukemia; 2006 Jan;20(1):9-17
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The Eighth International Childhood Acute Lymphoblastic Leukemia Workshop ('Ponte di legno meeting') report: Vienna, Austria, April 27-28, 2005.
  • The International Acute Lymphoblastic Leukemia Working Group, the so-called 'Ponte di Legno Workshop' has led to substantial progress in international collaboration in leukemia research.
  • Furthermore, collaborative projects of clinical relevance with special emphasis on rare genetic subtypes of Childhood ALL were established.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16281070.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-29139; United States / NCI NIH HHS / CA / CA-31566; United States / NCI NIH HHS / CA / CA-37379; United States / NCI NIH HHS / CA / CA-51001; United States / NCI NIH HHS / CA / CA-78824; United States / NIGMS NIH HHS / GM / GM-61374; United States / NIGMS NIH HHS / GM / GM-61393
  • [Publication-type] Congresses; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


53. Paulsson K, Heidenblad M, Mörse H, Borg A, Fioretos T, Johansson B: Identification of cryptic aberrations and characterization of translocation breakpoints using array CGH in high hyperdiploid childhood acute lymphoblastic leukemia. Leukemia; 2006 Nov;20(11):2002-7
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of cryptic aberrations and characterization of translocation breakpoints using array CGH in high hyperdiploid childhood acute lymphoblastic leukemia.
  • High hyperdiploidy, characterized by non-random trisomies, is the largest cytogenetic subgroup in childhood acute lymphoblastic leukemia (ALL).
  • We performed array comparative genome hybridization (CGH) analyses, with a resolution of 100 kb, of eight cases of high hyperdiploid childhood ALL to characterize structural abnormalities found with G-banding/multicolor fluorescence in situ hybridization (FISH) and to detect novel changes.
  • The non-centromeric breakpoints of four rearrangements, including three translocations and one 1q duplication, were narrowed down to <0.2 Mb.
  • In conclusion, the array CGH analyses revealed putative leukemia-associated submicroscopic imbalances and rearrangements in 2/8 (25%) hyperdiploid ALLs.
  • The detection and characterization of these additional genetic aberrations will most likely increase our understanding of the pathogenesis of high hyperdiploid childhood ALL.
  • [MeSH-major] Genomics / methods. In Situ Hybridization, Fluorescence / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic


54. Mussolin L, Pillon M, Conter V, Piglione M, Lo Nigro L, Pierani P, Micalizzi C, Buffardi S, Basso G, Zanesco L, Rosolen A: Prognostic role of minimal residual disease in mature B-cell acute lymphoblastic leukemia of childhood. J Clin Oncol; 2007 Nov 20;25(33):5254-61
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic role of minimal residual disease in mature B-cell acute lymphoblastic leukemia of childhood.
  • PURPOSE: To study the prevalence of t(8;14) at diagnosis and the response kinetics to treatment of minimal residual disease (MRD) in B-cell acute lymphoblastic leukemia (B-ALL) patients and determine its impact on prognosis.
  • PATIENTS AND METHODS: A total of 68 children affected by de novo B-ALL enrolled onto the Berlin-Frankfurt-Muenster-based Italian Association of Pediatric Hematology and Oncology LNH-97 clinical protocol were studied.
  • [MeSH-major] Burkitt Lymphoma / mortality. Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 8. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Translocation, Genetic

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18024872.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.1.1.27 / L-Lactate Dehydrogenase
  •  go-up   go-down


55. Paulsson K, Mörse H, Fioretos T, Behrendtz M, Strömbeck B, Johansson B: Evidence for a single-step mechanism in the origin of hyperdiploid childhood acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2005 Oct;44(2):113-22
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evidence for a single-step mechanism in the origin of hyperdiploid childhood acute lymphoblastic leukemia.
  • High hyperdiploidy (>50 chromosomes) in childhood acute lymphoblastic leukemia (ALL) is characterized by nonrandom multiple trisomies and tetrasomies involving in particular chromosomes X, 4, 6, 8, 10, 14, 17, 18, and 21.
  • This characteristic karyotypic pattern, the most common in pediatric ALL, may arise via a tetraploid state with subsequent loss of chromosomes, by sequential gains of chromosomes in consecutive cell divisions, or by simultaneous gain of chromosomes in a single mitosis.
  • These data strongly suggest that hyperdiploidy in childhood ALL generally arises by a simultaneous gain of all additional chromosomes in a single abnormal mitosis.
  • [MeSH-major] Diploidy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15942938.001).
  • [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 / Genetic Markers
  •  go-up   go-down


56. Zhang YT, Luo ZF, Fang JP, Guo HX, Huang K, Li CK: [Detection of minimal residual disease in childhood acute lymphoblastic leukemia by using real-time quantitative PCR]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Oct;18(5):1235-9
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Detection of minimal residual disease in childhood acute lymphoblastic leukemia by using real-time quantitative PCR].
  • This study was purposed to detect the minimal residual disease (MRD) in childhood acute lymphoblastic leukemia (ALL) by using real time quantitative PCR (RQ-PCR) .
  • It is concluded that Ig/TCR gene rearrangements can be used as a marker to detect MRD in childhood ALL; the technique of QR-PCR with SYBR green dye staining is reliable, relatively sensitive and easy performable method which can be used in routine detection for childhood ALL.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21129267.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA Primers
  •  go-up   go-down


57. Meleshko AN, Belevtsev MV, Savitskaja TV, Potapnev MP: The incidence of T-cell receptor gene rearrangements in childhood B-lineage acute lymphoblastic leukemia is related to immunophenotype and fusion oncogene expression. Leuk Res; 2006 Jul;30(7):795-800
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The incidence of T-cell receptor gene rearrangements in childhood B-lineage acute lymphoblastic leukemia is related to immunophenotype and fusion oncogene expression.
  • TCR genes rearrangements were reported to occur at high frequency in B-lineage acute lymphoblastic leukemia (ALL).
  • Therefore, we have analyzed 83 children with acute B-lineage ALL (67 de novo patients and 19 relapses) by PCR analysis for clonal IgH, incomplete TCRD (Vdelta2-Ddelta3 and Ddelta2-Ddelta3) and TCRG rearrangements.
  • [MeSH-major] Burkitt Lymphoma / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Fusion Proteins, bcr-abl / genetics. Homeodomain Proteins / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16386788.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Homeodomain Proteins; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Antigen, T-Cell; 0 / TEL-AML1 fusion protein; 146150-85-8 / E2A-Pbx1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  •  go-up   go-down


58. Otsubo K, Kanegane H, Eguchi M, Eguchi-Ishimae M, Tamura K, Nomura K, Abe A, Ishii E, Miyawaki T: ETV6-ARNT fusion in a patient with childhood T lymphoblastic leukemia. Cancer Genet Cytogenet; 2010 Oct 1;202(1):22-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ETV6-ARNT fusion in a patient with childhood T lymphoblastic leukemia.
  • Leukemia with t(1;12)(q21;p13) was previously described in a 5-year-old boy with acute myeloblastic leukemia (AML-M2) who exhibited a novel ETV6-aryl hydrocarbon receptor nuclear translocator (ARNT) fusion protein.
  • We herein report the case of a 2-year-old boy with T-cell lymphoblastic leukemia (T-ALL) harboring t(1;12)(q21;p13).
  • To our knowledge, the current report is novel in its report of the ETV6-ARNT fusion in childhood T-ALL.
  • [MeSH-major] ARNTL Transcription Factors / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20804916.001).
  • [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 / ARNTL Transcription Factors; 0 / DNA Primers; 0 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins
  •  go-up   go-down


59. Tie LJ, Gu LJ, Jiang LM, Zhao JC, Chen J, Pan C, Dong L, Chen J, Xue HL, Tang JY, Wang YP: [Tandem application of flow cytometry and polymerase chain reaction for choice targets of minimal residual disease in childhood acute lymphoblastic leukemia]. Zhongguo Dang Dai Er Ke Za Zhi; 2009 Apr;11(4):246-50
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Tandem application of flow cytometry and polymerase chain reaction for choice targets of minimal residual disease in childhood acute lymphoblastic leukemia].
  • OBJECTIVE: Minimal residual disease (MRD) is one of the most important prognostic factors in childhood acute lymphoblastic leukemia (ALL).
  • Using sets of combined antibodies, immunophenotypic expression of leukemia cells was observed in 95 of 106 B-lineage ALL cases (89.6%).
  • [MeSH-major] Flow Cytometry / methods. Polymerase Chain Reaction / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19374803.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  •  go-up   go-down


60. Gast A, Bermejo JL, Flohr T, Stanulla M, Burwinkel B, Schrappe M, Bartram CR, Hemminki K, Kumar R: Folate metabolic gene polymorphisms and childhood acute lymphoblastic leukemia: a case-control study. Leukemia; 2007 Feb;21(2):320-5
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Folate metabolic gene polymorphisms and childhood acute lymphoblastic leukemia: a case-control study.
  • We genotyped six folate metabolic pathway genes for 11 polymorphisms in 460 cases of childhood acute lymphoblastic leukemia (ALL) and 552 ethnically matched controls.
  • Our results suggest that, besides a weak association of childhood ALL with the 66A>G polymorphism, haplotypes within the MTRR gene may, in part, account for population-based differences in risk.
  • [MeSH-major] Folic Acid / genetics. Folic Acid / metabolism. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


61. Holleman A, den Boer ML, Kazemier KM, Beverloo HB, von Bergh AR, Janka-Schaub GE, Pieters R: Decreased PARP and procaspase-2 protein levels are associated with cellular drug resistance in childhood acute lymphoblastic leukemia. Blood; 2005 Sep 1;106(5):1817-23
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Decreased PARP and procaspase-2 protein levels are associated with cellular drug resistance in childhood acute lymphoblastic leukemia.
  • Drug resistance in childhood acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) is associated with impaired ability to induce apoptosis.
  • To elucidate causes of apoptotic defects, we studied the protein expression of Apaf-1, procaspases-2, -3, -6, -7, -8, -10, and poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP) in cells from children with acute lymphoblastic leukemia (ALL; n = 43) and acute myeloid leukemia (AML; n = 10).
  • In conclusion, low baseline expression of PARP and procaspase-2 is related to cellular drug resistance in childhood acute lymphoblastic leukemia.
  • [MeSH-major] Caspases / metabolism. Drug Resistance, Neoplasm / physiology. Poly(ADP-ribose) Polymerases / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15899912.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspase 2; EC 3.4.22.- / Caspases
  •  go-up   go-down


62. Ning F, Cai SJ, Zhang TJ, Liu XX, Zhang YM: [Expression of nm23 H(1) gene in childhood acute lymphoblastic leukemia and the relationship between nm23 H(1) expression and immunophenotype]. Zhongguo Dang Dai Er Ke Za Zhi; 2009 Nov;11(11):881-4
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of nm23 H(1) gene in childhood acute lymphoblastic leukemia and the relationship between nm23 H(1) expression and immunophenotype].
  • OBJECTIVE: To study the expression of nm23-H(1) gene in children with acute lymphoblastic leukemia (ALL) and the relationship between nm23-H(1) expression and immunophenotype.
  • [MeSH-major] NM23 Nucleoside Diphosphate Kinases / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20113651.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / NM23 Nucleoside Diphosphate Kinases
  •  go-up   go-down


63. Plasschaert SL, de Bont ES, Boezen M, vander Kolk DM, Daenen SM, Faber KN, Kamps WA, de Vries EG, Vellenga E: Expression of multidrug resistance-associated proteins predicts prognosis in childhood and adult acute lymphoblastic leukemia. Clin Cancer Res; 2005 Dec 15;11(24 Pt 1):8661-8
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of multidrug resistance-associated proteins predicts prognosis in childhood and adult acute lymphoblastic leukemia.
  • PURPOSE: Patients with acute lymphoblastic leukemia (ALL) are treated with a variety of chemotherapeutic drugs, which can be transported by six multidrug resistance-associated proteins (MRP).
  • [MeSH-major] Multidrug Resistance-Associated Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16361551.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Multidrug Resistance-Associated Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm
  •  go-up   go-down


64. Horinouchi M, Yagi M, Imanishi H, Mori T, Yanai T, Hayakawa A, Takeshima Y, Hijioka M, Okamura N, Sakaeda T, Matsuo M, Okumura K, Nakamura T: Association of genetic polymorphisms with hepatotoxicity in patients with childhood acute lymphoblastic leukemia or lymphoma. Pediatr Hematol Oncol; 2010 Aug;27(5):344-54
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of genetic polymorphisms with hepatotoxicity in patients with childhood acute lymphoblastic leukemia or lymphoma.
  • The objective of this study was to identify novel pharmacogenetic determinants of treatment-related hepatotoxicity during the maintenance phase in children with acute lymphoblastic leukemia (ALL) or lymphoblastic lymphoma (LBL).
  • This study suggested rs1966862 (ARHGAP24) and the other SNPs to be predictive factors for drug-induced hepatotoxicity during the maintenance phase in pediatric patients with ALL or LBL.
  • [MeSH-major] Drug-Induced Liver Injury / genetics. Genetic Association Studies. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications


65. Kaddar T, Chien WW, Bertrand Y, Pages MP, Rouault JP, Salles G, Ffrench M, Magaud JP: Prognostic value of miR-16 expression in childhood acute lymphoblastic leukemia relationships to normal and malignant lymphocyte proliferation. Leuk Res; 2009 Sep;33(9):1217-23
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic value of miR-16 expression in childhood acute lymphoblastic leukemia relationships to normal and malignant lymphocyte proliferation.
  • We then explored its expression in 93 childhood acute lymphoblastic leukemia (ALL) cases.
  • The prognostic value of miR-16 in childhood ALL highlighted the complexity of miR-16 functions.
  • [MeSH-major] Cell Proliferation. Lymphocytes / cytology. MicroRNAs / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19195700.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs
  •  go-up   go-down


66. Balduzzi A, De Lorenzo P, Schrauder A, Conter V, Uderzo C, Peters C, Klingebiel T, Stary J, Felice MS, Magyarosy E, Schrappe M, Dini G, Gadner H, Valsecchi MG: Eligibility for allogeneic transplantation in very high risk childhood acute lymphoblastic leukemia: the impact of the waiting time. Haematologica; 2008 Jun;93(6):925-9
MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Eligibility for allogeneic transplantation in very high risk childhood acute lymphoblastic leukemia: the impact of the waiting time.
  • The advantage of allogeneic transplant from compatible related donors versus chemotherapy in children with very-high-risk acute lymphoblastic leukemia in first complete remission was previously demonstrated in an international prospective trial.
  • Of 357 pediatric patients with very-high-risk acute lymphoblastic leukemia, 259 received chemotherapy, 55 transplantation from compatible related and 43 from unrelated donors.
  • The relative advantage of transplant from compatible related donors in very-high-risk childhood acute lymphoblastic leukemia was consistent for any time elapsed in first remission.
  • [MeSH-major] Bone Marrow Transplantation / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Transplantation, Homologous / methods


67. Batar B, Güven M, Bariş S, Celkan T, Yildiz I: DNA repair gene XPD and XRCC1 polymorphisms and the risk of childhood acute lymphoblastic leukemia. Leuk Res; 2009 Jun;33(6):759-63
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA repair gene XPD and XRCC1 polymorphisms and the risk of childhood acute lymphoblastic leukemia.
  • In this study, we aimed to determine the four polymorphisms in two DNA repair genes, xeroderma pigmentosum complementation group D (XPD) and X-ray repair cross-complementing group 1 (XRCC1), in a sample of Turkish patients with childhood acute lymphoblastic leukemia (ALL), and evaluate their association with childhood ALL development.
  • We used polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP), to analyze XPD Asp312Asn, XPD Lys751Gln, XRCC1 Arg194Trp, and XRCC1 Arg399Gln polymorphisms in 70 patients with childhood ALL and in 75 disease-free controls, who were of a similar age.
  • This finding indicates that females carrying XRCC1 194Trp allele are at increased risk of developing childhood ALL.
  • These results suggest that the risk of childhood ALL may be associated with DNA repair mechanisms, and understanding these mechanisms will help identify individuals at increased risk of developing childhood ALL, and also should be lead to improved treatment of ALL.
  • [MeSH-major] DNA Repair / genetics. DNA-Binding Proteins / genetics. Genetic Predisposition to Disease. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Xeroderma Pigmentosum Group D Protein / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19101034.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Codon; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / X-ray repair cross complementing protein 1; EC 3.6.4.12 / Xeroderma Pigmentosum Group D Protein; EC 5.99.- / ERCC2 protein, human
  •  go-up   go-down


68. Milani L, Lundmark A, Kiialainen A, Nordlund J, Flaegstad T, Forestier E, Heyman M, Jonmundsson G, Kanerva J, Schmiegelow K, Söderhäll S, Gustafsson MG, Lönnerholm G, Syvänen AC: DNA methylation for subtype classification and prediction of treatment outcome in patients with childhood acute lymphoblastic leukemia. Blood; 2010 Feb 11;115(6):1214-25
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA methylation for subtype classification and prediction of treatment outcome in patients with childhood acute lymphoblastic leukemia.
  • Despite improvements in the prognosis of childhood acute lymphoblastic leukemia (ALL), subgroups of patients would benefit from alternative treatment approaches.
  • We also identified 20 individual genes with DNA methylation levels that predicted relapse of leukemia.
  • [MeSH-major] CpG Islands. DNA Methylation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


69. Stanulla M, Schäffeler E, Arens S, Rathmann A, Schrauder A, Welte K, Eichelbaum M, Zanger UM, Schrappe M, Schwab M: GSTP1 and MDR1 genotypes and central nervous system relapse in childhood acute lymphoblastic leukemia. Int J Hematol; 2005 Jan;81(1):39-44
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] GSTP1 and MDR1 genotypes and central nervous system relapse in childhood acute lymphoblastic leukemia.
  • The probability of event-free survival of childhood acute lymphoblastic leukemia (ALL) approaches 80% or more with the use of modern multiagent chemotherapeutic regimens.
  • In a matched case-control study, we investigated the associations between CNS relapse in childhood ALL and the presence of phenotypically relevant single nucleotide polymorphisms within the GSTP1 (codon 105 and 114) and MDR1 genes (ABCB1; coding for Pgp; exon 26, C3435T).
  • These results suggested a modulating role for host genetic variation in the development of CNS relapse in childhood ALL treated according to Berlin-Frankfurt-Münster protocols.
  • [MeSH-major] Central Nervous System Neoplasms / genetics. Glutathione Transferase / genetics. Isoenzymes / genetics. P-Glycoprotein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15717687.001).
  • [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] United States
  • [Chemical-registry-number] 0 / Isoenzymes; 0 / P-Glycoprotein; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi; EC 2.5.1.18 / Glutathione Transferase
  •  go-up   go-down


70. Cario G, Stanulla M, Fine BM, Teuffel O, Neuhoff NV, Schrauder A, Flohr T, Schäfer BW, Bartram CR, Welte K, Schlegelberger B, Schrappe M: Distinct gene expression profiles determine molecular treatment response in childhood acute lymphoblastic leukemia. Blood; 2005 Jan 15;105(2):821-6
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distinct gene expression profiles determine molecular treatment response in childhood acute lymphoblastic leukemia.
  • Treatment resistance, as indicated by the presence of high levels of minimal residual disease (MRD) after induction therapy and induction consolidation, is associated with a poor prognosis in childhood acute lymphoblastic leukemia (ALL).
  • Because treatment response could be predicted with high accuracy, gene expression profiling could become a clinically relevant tool for treatment stratification in the early course of childhood ALL.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Gene Expression Profiling. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


71. Marquis A, Kuehni CE, Strippoli MP, Kühne T, Brazzola P, Swiss Pediatric Oncology Group: Sperm analysis of patients after successful treatment of childhood acute lymphoblastic leukemia with chemotherapy. Pediatr Blood Cancer; 2010 Jul 15;55(1):208-10
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sperm analysis of patients after successful treatment of childhood acute lymphoblastic leukemia with chemotherapy.
  • Survivors of childhood acute lymphoblastic leukemia (ALL) treated with radiotherapy are at risk for impaired fertility.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Sperm Count. Spermatozoa / drug effects

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20310003.001).
  • [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
  •  go-up   go-down


72. Yamaji K, Okamoto T, Yokota S, Watanabe A, Horikoshi Y, Asami K, Kikuta A, Hyakuna N, Saikawa Y, Ueyama J, Watanabe T, Okada M, Taga T, Kanegane H, Kogawa K, Chin M, Iwai A, Matsushita T, Shimomura Y, Hori T, Tsurusawa M, Japanese Childhood Cancer Leukemia Study Group: Minimal residual disease-based augmented therapy in childhood acute lymphoblastic leukemia: a report from the Japanese Childhood Cancer and Leukemia Study Group. Pediatr Blood Cancer; 2010 Dec 15;55(7):1287-95
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Minimal residual disease-based augmented therapy in childhood acute lymphoblastic leukemia: a report from the Japanese Childhood Cancer and Leukemia Study Group.
  • BACKGROUND: The majority of minimal residual disease (MRD)-positive patients with acute lymphoblastic leukemia (ALL) have poor outcomes.
  • The ALL2000 study was performed to evaluate the efficacy of augmented chemotherapy based on MRD-restratification in childhood ALL.
  • The EFS rate of the MRD stratifiable (MRD) group was 82.5 ± 2.6%, considerably superior to the 74.7 ± 5.7% of MRD non-stratifiable (Non-MRD) group (P = 0.084) and the 74.4 ± 2.1% for ALL 941 (P = 0.012).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

  • Genetic Alliance. consumer health - Childhood Cancer.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Wiley-Liss, Inc.
  • (PMID = 20535816.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


73. Stanulla M, Schaeffeler E, Flohr T, Cario G, Schrauder A, Zimmermann M, Welte K, Ludwig WD, Bartram CR, Zanger UM, Eichelbaum M, Schrappe M, Schwab M: Thiopurine methyltransferase (TPMT) genotype and early treatment response to mercaptopurine in childhood acute lymphoblastic leukemia. JAMA; 2005 Mar 23;293(12):1485-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Thiopurine methyltransferase (TPMT) genotype and early treatment response to mercaptopurine in childhood acute lymphoblastic leukemia.
  • CONTEXT: Early response to multiagent chemotherapy, including mercaptopurine, as measured by minimal residual disease is an important prognostic factor for children with acute lymphoblastic leukemia (ALL).
  • OBJECTIVE: To assess the association of TPMT genotype with minimal residual disease load before and after treatment with mercaptopurine in the early treatment course of childhood ALL.
  • DESIGN, SETTING, AND PATIENTS: TPMT genotyping of childhood ALL patients (n = 814) in Germany consecutively enrolled in the ALL-BFM (Berlin-Frankfurt-Münster) 2000 study from October 1999 to September 2002.
  • CONCLUSIONS: TPMT genotype has a substantial impact on minimal residual disease after administration of mercaptopurine in the early course of childhood ALL, most likely through modulation of mercaptopurine dose intensity.


74. Assumpção JG, Ganazza MA, de Araújo M, Silva AS, Scrideli CA, Brandalise SR, Yunes JA: Detection of clonal immunoglobulin and T-cell receptor gene rearrangements in childhood acute lymphoblastic leukemia using a low-cost PCR strategy. Pediatr Blood Cancer; 2010 Dec 15;55(7):1278-86
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of clonal immunoglobulin and T-cell receptor gene rearrangements in childhood acute lymphoblastic leukemia using a low-cost PCR strategy.
  • BACKGROUND: Immunoglobulin (Ig) and T-cell receptor (TCR) gene rearrangements function as specific markers for minimal residual disease (MRD), which is one of the best predictors of outcome in childhood acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Gene Rearrangement. Gene Rearrangement, T-Lymphocyte. Genes, T-Cell Receptor / genetics. Immunoglobulins / genetics. Polymerase Chain Reaction / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Child. Clone Cells. Humans. Neoplasm, Residual. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Prognosis

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Wiley-Liss, Inc.
  • (PMID = 20730889.001).
  • [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 / Immunoglobulins
  •  go-up   go-down


75. Haltrich I, Kost-Alimova M, Kovács G, Dobos M, Klein G, Fekete G, Imreh S: Multipoint interphase FISH in childhood T-acute lymphoblastic leukemia detects subpopulations that carry different chromosome 3 aberrations. Cancer Genet Cytogenet; 2007 Jan 1;172(1):54-60
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multipoint interphase FISH in childhood T-acute lymphoblastic leukemia detects subpopulations that carry different chromosome 3 aberrations.
  • We examined chromosome 3 in 32 childhood acute lymphoblastic leukemia (ALL) bone marrow samples.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 3 / genetics. DNA, Neoplasm / genetics. Interphase / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17175380.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm
  •  go-up   go-down


76. Attarbaschi A, Mann G, König M, Steiner M, Dworzak MN, Gadner H, Haas OA, Austrian Berlin-Frankfurt-Münster Cooperative Study Group: Near-tetraploidy in childhood B-cell precursor acute lymphoblastic leukemia is a highly specific feature of ETV6/RUNX1-positive leukemic cases. Genes Chromosomes Cancer; 2006 Jun;45(6):608-11
Genetic Alliance. consumer health - Tetraploidy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Near-tetraploidy in childhood B-cell precursor acute lymphoblastic leukemia is a highly specific feature of ETV6/RUNX1-positive leukemic cases.
  • Near-tetraploidy (82-94 chromosomes) makes up fewer than 1% of childhood acute lymphoblastic leukemia (ALL) cases and has been reportedly associated with a possibly poorer prognosis compared with other ploidy groups.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / analysis. Polyploidy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / analysis. Repressor Proteins / analysis

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16552772.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins
  •  go-up   go-down


77. Teitell MA, Pandolfi PP: Molecular genetics of acute lymphoblastic leukemia. Annu Rev Pathol; 2009;4:175-98
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular genetics of acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is mainly a disease of childhood that arises from recurrent genetic insults that block precursor B and T cell differentiation and drive aberrant cell proliferation and survival.
  • Recent discoveries arising from genome-wide surveys and adoptive transfer of leukemia-initiating cells have uncovered multiple gene copy number aberrations and have yielded new insight into at least one type of ALL-originating cell.
  • Here, we review the spectrum of genetic aberrations that promote acute B and T cell leukemias and the mechanisms of cell transformation and malignant progression that are reinforced by mouse models of human ALL.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Gene Expression Regulation, Leukemic. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18783329.001).
  • [ISSN] 1553-4014
  • [Journal-full-title] Annual review of pathology
  • [ISO-abbreviation] Annu Rev Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 153
  •  go-up   go-down


78. Styczynski J, Wysocki M, Debski R, Czyzewski K, Kolodziej B, Rafinska B, Kubicka M, Koltan S, Koltan A, Pogorzala M, Kurylak A, Olszewska-Slonina D, Balwierz W, Juraszewska E, Wieczorek M, Olejnik I, Krawczuk-Rybak M, Kuzmicz M, Kowalczyk J, Stefaniak J, Badowska W, Sonta-Jakimczyk D, Szczepanski T, Matysiak M, Malinowska I, Stanczak E, Wachowiak J, Konatkowska B, Gil L, Balcerska A, Maciejka-Kapuscinska L: Predictive value of multidrug resistance proteins and cellular drug resistance in childhood relapsed acute lymphoblastic leukemia. J Cancer Res Clin Oncol; 2007 Nov;133(11):875-93
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Predictive value of multidrug resistance proteins and cellular drug resistance in childhood relapsed acute lymphoblastic leukemia.
  • PURPOSE: Cellular resistance in childhood acute leukemias might be related to profile and function of multidrug resistance proteins and apoptosis regulating proteins.
  • (2) correlation with ex vivo drug resistance, and (3) analysis of their prognostic impact on clinical outcome in childhood acute lymphoblastic (ALL) and acute myeloid (AML) leukemia.
  • CONCLUSIONS: The phenomenon of cellular drug resistance in childhood acute leukemias is multifactorial and plays an important role in response to therapy.
  • Expression of MRP1, PGP and LRP proteins, as well as their co-expression play possible role in childhood relapsed ALL.
  • [MeSH-major] Drug Resistance, Multiple. Drug Resistance, Neoplasm. Multidrug Resistance-Associated Proteins / metabolism. P-Glycoprotein / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Vault Ribonucleoprotein Particles / metabolism

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] J Cancer Res Clin Oncol. 2007 Nov;133(11):895. Wachowiak, Jacek [added]; Konatkowska, Benigna [added]; Gil, Lidia [added]; Balcerska, Anna [added]; Maciejka-Kapuscinska, Lucyna [added]
  • (PMID = 17671794.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein
  •  go-up   go-down


79. Poppe B, Cauwelier B, Van Limbergen H, Yigit N, Philippé J, Verhasselt B, De Paepe A, Benoit Y, Speleman F: Novel cryptic chromosomal rearrangements in childhood acute lymphoblastic leukemia detected by multiple color fluorescent in situ hybridization. Haematologica; 2005 Sep;90(9):1179-85
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel cryptic chromosomal rearrangements in childhood acute lymphoblastic leukemia detected by multiple color fluorescent in situ hybridization.
  • BACKGROUND AND OBJECTIVES: It is often difficult to obtain good karyotypes of cells from children with acute lymphoblastic leukemia (ALL) because of poor morphology and spreading.
  • Our objective was to search for cryptic rearrangements in childhood ALL.
  • DESIGN AND METHODS: A series of eight cases of childhood ALL with at least two structural defects were selected and studied by multiple color fluorescent in situ hybridization (M-FISH).
  • [MeSH-major] In Situ Hybridization, Fluorescence / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16154840.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  •  go-up   go-down


80. Möricke A, Zimmermann M, Reiter A, Henze G, Schrauder A, Gadner H, Ludwig WD, Ritter J, Harbott J, Mann G, Klingebiel T, Zintl F, Niemeyer C, Kremens B, Niggli F, Niethammer D, Welte K, Stanulla M, Odenwald E, Riehm H, Schrappe M: Long-term results of five consecutive trials in childhood acute lymphoblastic leukemia performed by the ALL-BFM study group from 1981 to 2000. Leukemia; 2010 Feb;24(2):265-84
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term results of five consecutive trials in childhood acute lymphoblastic leukemia performed by the ALL-BFM study group from 1981 to 2000.
  • Between 1981 and 2000, 6609 children (<18 years of age) were treated in five consecutive trials of the Berlin-Frankfurt-Münster (BFM) study group for childhood acute lymphoblastic leukemia (ALL).
  • In parallel to relapse reduction, major efforts focused on reducing acute and late toxicity through advanced risk adaptation of treatment.
  • (1) preventive cranial radiotherapy could be safely reduced to 12 Gy in T-ALL and high-risk (HR) ALL patients, and eliminated in non- HR non-T-ALL patients, if it was replaced by high-dose and intrathecal (IT) MTX;.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cranial Irradiation. Neoplasm Recurrence, Local / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Stem Cell Transplantation


81. Papaemmanuil E, Hosking FJ, Vijayakrishnan J, Price A, Olver B, Sheridan E, Kinsey SE, Lightfoot T, Roman E, Irving JA, Allan JM, Tomlinson IP, Taylor M, Greaves M, Houlston RS: Loci on 7p12.2, 10q21.2 and 14q11.2 are associated with risk of childhood acute lymphoblastic leukemia. Nat Genet; 2009 Sep;41(9):1006-10
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).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loci on 7p12.2, 10q21.2 and 14q11.2 are associated with risk of childhood acute lymphoblastic leukemia.
  • To identify risk variants for childhood acute lymphoblastic leukemia (ALL), we conducted a genome-wide association study of two case-control series, analyzing the genotypes with respect to 291,423 tagging SNPs in a total of 907 ALL cases and 2,398 controls.
  • These data show that common low-penetrance susceptibility alleles contribute to the risk of developing childhood ALL and provide new insight into disease causation of this specific hematological cancer.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19684604.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / / 10417; United Kingdom / Bloodwise / / 13027; United Kingdom / Medical Research Council / / G0000934; United Kingdom / Cancer Research UK / / C1298/A8362
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ARID5B protein, human; 0 / CCAAT-Enhancer-Binding Proteins; 0 / DNA-Binding Proteins; 0 / IKZF1 protein, human; 0 / Transcription Factors; 142805-41-2 / CEBPE protein, human; 148971-36-2 / Ikaros Transcription Factor
  • [Other-IDs] NLM/ EMS27409; NLM/ PMC4915548
  •  go-up   go-down


82. Koppen IJ, Hermans FJ, Kaspers GJ: Folate related gene polymorphisms and susceptibility to develop childhood acute lymphoblastic leukaemia. Br J Haematol; 2010 Jan;148(1):3-14
Hazardous Substances Data Bank. FOLIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Folate related gene polymorphisms and susceptibility to develop childhood acute lymphoblastic leukaemia.
  • Acute lymphoblastic leukaemia (ALL) is the most common paediatric cancer, accounting for nearly 30% of all paediatric cancers and 80% of childhood leukaemias.
  • Polymorphisms in folate-related genes may influence the susceptibility to childhood ALL.
  • The total group consisted of 729 children and 1821 adults or non age-defined patients.
  • Based on several studies, it is plausible that polymorphisms in the MTHFR gene, 677C>T and 1298A>C, are associated with a decreased susceptibility to childhood ALL in non-Asian populations.
  • In general, it is clear that susceptibility to (childhood) ALL is partly related to constitutional differences in folate gene polymorphisms.
  • [MeSH-major] Folic Acid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • MedlinePlus Health Information. consumer health - Folic Acid.
  • Pharmacogenomics Knowledge Base. meta-databases - Pharmacogenomic Annotation 827858523 for PMID:19775302 [PharmGKB] .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Br J Haematol. 2010 Jun;149(5):797-8; author reply 799-800 [20148884.001]
  • (PMID = 19775302.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] England
  • [Chemical-registry-number] 935E97BOY8 / Folic Acid; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
  • [Number-of-references] 43
  •  go-up   go-down


83. Nebral K, König M, Harder L, Siebert R, Haas OA, Strehl S: Identification of PML as novel PAX5 fusion partner in childhood acute lymphoblastic leukaemia. Br J Haematol; 2007 Oct;139(2):269-74

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of PML as novel PAX5 fusion partner in childhood acute lymphoblastic leukaemia.
  • In B-cell precursor acute lymphoblastic leukaemia (ALL), PAX5 is involved in several chromosome translocations that fuse the N-terminal paired DNA-binding domain of PAX5 with the C-terminal regulatory sequences of ETV6, FOXP1, ZNF521 or ELN.
  • Herein, we describe the identification of a novel recurrent t(9;15)(p13;q24) in two cases of childhood ALL, which results in an in-frame fusion of PAX5 to the promyelocytic leukaemia (PML) gene.
  • [MeSH-major] B-Cell-Specific Activator Protein / genetics. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics. Tumor Suppressor Proteins / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17897302.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / PAX5 protein, human; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human
  •  go-up   go-down


84. Aricò M, Conter V, Valsecchi MG, Rizzari C, Boccalatte MF, Barisone E, Messina C, De Rossi G, Lo Nigro L, Pession A, Locatelli F, Micalizzi C, Basso G: Treatment reduction in highly selected standard-risk childhood acute lymphoblastic leukemia. The AIEOP ALL-9501 study. Haematologica; 2005 Sep;90(9):1186-91
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment reduction in highly selected standard-risk childhood acute lymphoblastic leukemia. The AIEOP ALL-9501 study.
  • BACKGROUND AND OBJECTIVES: Treatment of childhood standard-risk (SR) acute lymphoblastic leukemia (ALL) is generally successful.
  • DESIGN AND METHODS: The population of patients with SR ALL included children aged between 1 and 6 years with less than 20,000 WBC/mm3, non-T immunophenotype, DNA index between 1.16 and 1.6, absence of t(9;22) and t(4;11) clonal translocations, no extramedullary leukemia, good response to prednisone and complete remission (CR) at the end of induction therapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16154841.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; ZS7284E0ZP / Daunorubicin; PVDA protocol
  •  go-up   go-down


85. Ek T, Mellander L, Hahn-Zoric M, Abrahamsson J: Avidity of tetanus and Hib antibodies after childhood acute lymphoblastic leukaemia - implications for vaccination strategies. Acta Paediatr; 2006 Jun;95(6):701-6
Genetic Alliance. consumer health - Tetanus.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Avidity of tetanus and Hib antibodies after childhood acute lymphoblastic leukaemia - implications for vaccination strategies.
  • AIM: To investigate the possible relationship between serum levels and avidities of antibodies against tetanus toxoid (TT) and Haemophilus influenzae type b (Hib) in children that were vaccinated after treatment for childhood acute lymphoblastic leukaemia (ALL).
  • CONCLUSION: The vaccination strategy after childhood ALL must be different for low-risk and high-risk ALL groups, since the high-risk group fail to elicit a recall response to tetanus.
  • [MeSH-major] Antibodies, Bacterial / immunology. Antibody Affinity. Haemophilus Vaccines / immunology. Haemophilus influenzae / immunology. Polysaccharides, Bacterial / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Tetanus Toxoid / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16754551.001).
  • [ISSN] 0803-5253
  • [Journal-full-title] Acta paediatrica (Oslo, Norway : 1992)
  • [ISO-abbreviation] Acta Paediatr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Antibodies, Bacterial; 0 / Haemophilus Vaccines; 0 / Haemophilus influenzae type b polysaccharide vaccine; 0 / Polysaccharides, Bacterial; 0 / Tetanus Toxoid
  •  go-up   go-down


86. Liu XP, Zhu XF, Wang JX, Mi YC, Zou Y, Chen YM, Li CW, Dai Y, Qin S, Xiao JG, Xu FY, Gong JY, Wang SP, Yu CL, Fan J: [A comparative cytogenetic analysis in large scale between adult and childhood patients with acute lymphoblastic leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Dec;17(6):1399-404
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A comparative cytogenetic analysis in large scale between adult and childhood patients with acute lymphoblastic leukemia].
  • This study was purposed to comparatively analyze the cytogenetic characteristics between 566 cases of adult acute lymphoblastic leukemia (aALL) and 586 cases of childhood acute lymphoblastic leukemia (cALL).

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20030914.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  •  go-up   go-down


87. Steinemann D, Cario G, Stanulla M, Karawajew L, Tauscher M, Weigmann A, Göhring G, Ludwig WD, Harbott J, Radlwimmer B, Bartram C, Lichter P, Schrappe M, Schlegelberger B: Copy number alterations in childhood acute lymphoblastic leukemia and their association with minimal residual disease. Genes Chromosomes Cancer; 2008 Jun;47(6):471-80
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Copy number alterations in childhood acute lymphoblastic leukemia and their association with minimal residual disease.
  • In vivo response to initial therapy, as assessed by determination of minimal residual disease (MRD) after 5 and 12 weeks of treatment, has evolved as a strong prognostic factor in children with acute lymphoblastic leukemia (ALL) treated according to the BFM regime.
  • This is the first study evaluating the clinical significance of CNA as detected by array-CGH in childhood ALL and the first to suggest that such analyses may provide clinically important data.
  • [MeSH-major] Gene Dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


88. Moreno DA, Scrideli CA, Cortez MA, de Paula Queiroz R, Valera ET, da Silva Silveira V, Yunes JA, Brandalise SR, Tone LG: Differential expression of HDAC3, HDAC7 and HDAC9 is associated with prognosis and survival in childhood acute lymphoblastic leukaemia. Br J Haematol; 2010 Sep;150(6):665-73
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential expression of HDAC3, HDAC7 and HDAC9 is associated with prognosis and survival in childhood acute lymphoblastic leukaemia.
  • We evaluated the mRNA gene expression profile of 12 HDAC genes by quantitative real-time polymerase chain reaction in 94 consecutive childhood acute lymphoblastic leukaemia (ALL) samples and its association with clinical/biological features and survival.
  • Our data suggest that higher expression of HDAC7 and HDAC9 is associated with poor prognosis in childhood ALL and could be promising therapeutic targets for the treatment of refractory childhood ALL.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Histone Deacetylases / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] © 2010 Blackwell Publishing Ltd.
  • (PMID = 20636436.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Repressor Proteins; EC 3.5.1.98 / HDAC7 protein, human; EC 3.5.1.98 / HDAC9 protein, human; EC 3.5.1.98 / Histone Deacetylases; EC 3.5.1.98 / histone deacetylase 3
  •  go-up   go-down


89. Prasad RB, Hosking FJ, Vijayakrishnan J, Papaemmanuil E, Koehler R, Greaves M, Sheridan E, Gast A, Kinsey SE, Lightfoot T, Roman E, Taylor M, Pritchard-Jones K, Stanulla M, Schrappe M, Bartram CR, Houlston RS, Kumar R, Hemminki K: Verification of the susceptibility loci on 7p12.2, 10q21.2, and 14q11.2 in precursor B-cell acute lymphoblastic leukemia of childhood. Blood; 2010 Mar 4;115(9):1765-7
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).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Verification of the susceptibility loci on 7p12.2, 10q21.2, and 14q11.2 in precursor B-cell acute lymphoblastic leukemia of childhood.
  • Recent genome-wide association data have implicated genetic variation at 7p12.2 (IKZF1), 10q21.2 (ARIDB5), and 14q11.2 (CEBPE) in the etiology of B-cell childhood acute lymphoblastic leukemia (ALL).
  • To verify and further examine the relationship between these variants and ALL risk, we genotyped 1384 cases of precursor B-cell childhood ALL and 1877 controls from Germany and the United Kingdom.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, Pair 7 / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20042726.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ARID5B protein, human; 0 / CCAAT-Enhancer-Binding Proteins; 0 / DNA-Binding Proteins; 0 / IKZF1 protein, human; 0 / Transcription Factors; 142805-41-2 / CEBPE protein, human; 148971-36-2 / Ikaros Transcription Factor
  •  go-up   go-down


90. Davidsson J, Paulsson K, Lindgren D, Lilljebjörn H, Chaplin T, Forestier E, Andersen MK, Nordgren A, Rosenquist R, Fioretos T, Young BD, Johansson B: Relapsed childhood high hyperdiploid acute lymphoblastic leukemia: presence of preleukemic ancestral clones and the secondary nature of microdeletions and RTK-RAS mutations. Leukemia; 2010 May;24(5):924-31
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Relapsed childhood high hyperdiploid acute lymphoblastic leukemia: presence of preleukemic ancestral clones and the secondary nature of microdeletions and RTK-RAS mutations.
  • Although childhood high hyperdiploid acute lymphoblastic leukemia is associated with a favorable outcome, 20% of patients still relapse.
  • [MeSH-major] Chromosome Deletion. Diploidy. Genes, ras / genetics. Mutation / genetics. Neoplasm Recurrence, Local / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor Protein-Tyrosine Kinases / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20237506.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
  •  go-up   go-down


91. Santamaría-Quesada C, Vargas M, Venegas P, Calvo M, Obando C, Valverde B, Cartín W, Carrillo JM, Jimenez R, González M: Molecular and epidemiologic findings of childhood acute leukemia in Costa Rica. J Pediatr Hematol Oncol; 2009 Feb;31(2):131-5
MedlinePlus Health Information. consumer health - Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular and epidemiologic findings of childhood acute leukemia in Costa Rica.
  • In Central America, nearly 70% of pediatric cancer is related to hemato-oncologic disorders, especially acute lymphoblastic leukemia (ALL).
  • Preliminary studies have described a high incidence of childhood leukemia in these countries; however, no molecular analyses of these malignancies have yet been carried out.
  • We studied diagnostic samples from 84 patients from the National Children's Hospital in San Jose, Costa Rica (65 precursor B-ALL, 5 T-cell ALL, and 14 acute myeloblastic leukemia).
  • The observed rate of leukemia was 52.2 cases per million children per year.
  • Within 14 acute myeloblastic leukemia patients, we confirmed 2 cases with FLT3-internal tandem duplication+, 1 patient with AML1-ETO, and only 1 case carrying a PML-RARalpha rearrangement.
  • The present study confirms the relatively high incidence of pediatric leukemia in Costa Rica and constitutes the first report regarding the incidence of the main molecular alterations of childhood leukemia in our region.
  • [MeSH-major] Leukemia / epidemiology. Leukemia / genetics
  • [MeSH-minor] Acute Disease. Child. Costa Rica / epidemiology. Cytogenetic Analysis. Gene Rearrangement. Humans. Mutation. Oncogene Proteins, Fusion / analysis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19194200.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion
  •  go-up   go-down


92. Meier M, den Boer ML, Meijerink JP, Broekhuis MJ, Passier MM, van Wering ER, Janka-Schaub GE, Pieters R: Differential expression of p73 isoforms in relation to drug resistance in childhood T-lineage acute lymphoblastic leukaemia. Leukemia; 2006 Aug;20(8):1377-84
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential expression of p73 isoforms in relation to drug resistance in childhood T-lineage acute lymphoblastic leukaemia.
  • The T-lineage phenotype of childhood acute lymphoblastic leukaemia (ALL) is associated with an increased relapse-risk and in vitro resistance to drugs as compared to a precursor B phenotype.
  • We demonstrate in our study that the expression of total p73 mRNA was higher in childhood T-ALL compared to controls (P=0.004).
  • Our results suggest that childhood T-ALL is associated with a high expression of DeltaTA-p73.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Nuclear Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16791269.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins; 0 / tumor suppressor protein p73
  •  go-up   go-down


93. Shalapour S, Eckert C, Seeger K, Pfau M, Prada J, Henze G, Blankenstein T, Kammertoens T: Leukemia-associated genetic aberrations in mesenchymal stem cells of children with acute lymphoblastic leukemia. J Mol Med (Berl); 2010 Mar;88(3):249-65
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukemia-associated genetic aberrations in mesenchymal stem cells of children with acute lymphoblastic leukemia.
  • Childhood acute lymphoblastic leukemia (ALL) is caused by malignant immature lymphocytes.
  • Even though childhood ALL can be cured in a large number of patients, around 20% of the patients suffer a relapse after chemotherapy.
  • Given the high plasticity of cells, we searched for leukemia-associated genetic aberrations and immunoglobulin (IG) gene rearrangements in mesenchymal stem cells (MSC) from childhood B-cell precursor ALL patients.
  • MSC from all ten ALL patients analyzed presented the chromosomal translocations that had been detected in leukemia cells (TEL-AML1, E2A-PBX1, or MLL rearrangement).
  • Leukemia-specific IG gene rearrangements were detected in the MSC from three ALL patients.
  • The detection of leukemia-associated genetic aberrations in MSC indicates a clonal relationship between MSC and leukemia cells and suggests their involvement in the pathogenesis and/or pathophysiology of childhood ALL.
  • [MeSH-major] Mesenchymal Stromal Cells / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Mol Med (Berl). 2010 Mar;88(3):219-22 [20135087.001]
  • (PMID = 20155409.001).
  • [ISSN] 1432-1440
  • [Journal-full-title] Journal of molecular medicine (Berlin, Germany)
  • [ISO-abbreviation] J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
  •  go-up   go-down


94. Norén-Nyström U, Heyman M, Frisk P, Golovleva I, Sundström C, Porwit A, Roos G, Bergh A, Forestier E: Vascular density in childhood acute lymphoblastic leukaemia correlates to biological factors and outcome. Br J Haematol; 2009 Sep;146(5):521-30
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vascular density in childhood acute lymphoblastic leukaemia correlates to biological factors and outcome.
  • The issue of angiogenesis and its clinical relevance in childhood acute lymphoblastic leukaemia (ALL) is controversial.
  • One possible implication is that different subtypes of childhood ALL may respond differently to anti-angiogenic drugs as a supplement in first-line treatment.
  • [MeSH-major] Microvessels / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adolescent. Bone Marrow Examination. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit / genetics. Cytogenetic Analysis. Female. Humans. Leukocyte Count. Male. Neovascularization, Pathologic. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Prognosis. Proportional Hazards Models. Reticulin / ultrastructure. Reverse Transcriptase Polymerase Chain Reaction / methods. Risk. Survival Analysis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19594745.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Reticulin; 0 / TEL-AML1 fusion protein
  •  go-up   go-down


95. Rivera GK, Zhou Y, Hancock ML, Gajjar A, Rubnitz J, Ribeiro RC, Sandlund JT, Hudson M, Relling M, Evans WE, Pui CH: Bone marrow recurrence after initial intensive treatment for childhood acute lymphoblastic leukemia. Cancer; 2005 Jan 15;103(2):368-76
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bone marrow recurrence after initial intensive treatment for childhood acute lymphoblastic leukemia.
  • BACKGROUND: The authors studied the clinical outcome of 106 children with acute lymphoblastic leukemia (ALL) who developed a bone marrow recurrence as the first adverse event after contemporary intensified therapy.
  • CONCLUSIONS: Despite acceptable long-term second EFS rates for certain subgroups, overall bone marrow recurrence after intensified first-line therapy for childhood ALL signals a poor outcome.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Blast Crisis / epidemiology. Bone Marrow / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2004 American Cancer Society.
  • (PMID = 15599932.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA21765
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  •  go-up   go-down


96. Guastadisegni MC, Lonoce A, Impera L, Albano F, D'Addabbo P, Caruso S, Vasta I, Panagopoulos I, Leszl A, Basso G, Rocchi M, Storlazzi CT: Bone marrow ectopic expression of a non-coding RNA in childhood T-cell acute lymphoblastic leukemia with a novel t(2;11)(q11.2;p15.1) translocation. Mol Cancer; 2008;7:80
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bone marrow ectopic expression of a non-coding RNA in childhood T-cell acute lymphoblastic leukemia with a novel t(2;11)(q11.2;p15.1) translocation.
  • T-cell acute lymphoblastic leukemia (T-ALL) is associated with a large number of such rearrangements.
  • We report the ectopic expression of the 3' portion of EST DA926692 in the bone marrow of a childhood T-ALL case showing a t(2;11)(q11.2;p15.1) translocation as the sole chromosome abnormality.
  • Bioinformatic analysis excluded that this small non-coding RNA is a precursor of micro-RNA, although it is conceivable that it has a different, yet unknown, functional role.
  • To the best of our knowledge, this is the first report, in cancer, of the activation of a small non-coding RNA as a result of a chromosomal translocation.
  • [MeSH-major] Bone Marrow / metabolism. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 2 / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA, Untranslated / genetics. Translocation, Genetic


97. Campana D: Minimal residual disease in acute lymphoblastic leukemia. Hematology Am Soc Hematol Educ Program; 2010;2010:7-12
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Minimal residual disease in acute lymphoblastic leukemia.
  • In patients with acute lymphoblastic leukemia (ALL), treatment response is increasingly evaluated with minimal residual disease (MRD) assays.
  • ALL cells can be recognized by their clonal rearrangement of immunoglobulin and T-cell receptor genes, expression of gene fusions, and leukemia-associated immunophenotypes.
  • The vast majority of cases have antigen-receptor gene rearrangements and leukemia immunophenotypes for MRD monitoring; about half of the cases currently have suitable gene fusions.
  • The clinical significance of MRD has been conclusively demonstrated in both childhood and adult ALL.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21239764.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA60419
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


98. Troeger A, Siepermann M, Escherich G, Meisel R, Willers R, Gudowius S, Moritz T, Laws HJ, Hanenberg H, Goebel U, Janka-Schaub GE, Mahotka C, Dilloo D: Survivin and its prognostic significance in pediatric acute B-cell precursor lymphoblastic leukemia. Haematologica; 2007 Aug;92(8):1043-50
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Survivin and its prognostic significance in pediatric acute B-cell precursor lymphoblastic leukemia.
  • To date, however, there is no information available on the prognostic role of survivin in pediatric precursor B-cell acute lymphocytic leukemia (BCP-ALL), the most frequent malignancy in childhood.
  • DESIGN AND METHODS: In a retrospective study including 66 pediatric patients we analyzed the impact of survivin protein levels on outcome in BCP-ALL.
  • RESULTS: Survivin overexpression, with an up to ten-fold increase of the normal level, was detected in 65% of the leukemic samples in contrast to negligible expression in non-malignant hematopoietic cells.
  • [MeSH-major] Inhibitor of Apoptosis Proteins / analysis. Microtubule-Associated Proteins / analysis. Neoplasm Proteins / analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17640858.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
  •  go-up   go-down


99. Roman E, Simpson J, Ansell P, Kinsey S, Mitchell CD, McKinney PA, Birch JM, Greaves M, Eden T, United Kingdom Childhood Cancer Study Investigators: Childhood acute lymphoblastic leukemia and infections in the first year of life: a report from the United Kingdom Childhood Cancer Study. Am J Epidemiol; 2007 Mar 1;165(5):496-504
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Childhood acute lymphoblastic leukemia and infections in the first year of life: a report from the United Kingdom Childhood Cancer Study.
  • The United Kingdom Childhood Cancer Study was designed to examine the relation between childhood cancer and preceding exposure to infectious diseases.
  • The authors analyzed the relation between diagnosis (1991-1996) of acute lymphoblastic leukemia (ALL) at ages 2-5 years and clinically diagnosed infections in infancy.
  • Almost all study children (96% of both cases and controls) were taken to a general practitioner for a non-immunization-associated visit at least once before their first birthday.
  • These findings support the hypothesis that a dysregulated immune response to infection in the first few months of life promotes transition to overt ALL later in childhood.
  • [MeSH-major] Infection / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology


100. Bateman CM, Colman SM, Chaplin T, Young BD, Eden TO, Bhakta M, Gratias EJ, van Wering ER, Cazzaniga G, Harrison CJ, Hain R, Ancliff P, Ford AM, Kearney L, Greaves M: Acquisition of genome-wide copy number alterations in monozygotic twins with acute lymphoblastic leukemia. Blood; 2010 Apr 29;115(17):3553-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acquisition of genome-wide copy number alterations in monozygotic twins with acute lymphoblastic leukemia.
  • Chimeric fusion genes are highly prevalent in childhood acute lymphoblastic leukemia (ALL) and are mostly prenatal, early genetic events in the evolutionary trajectory of this cancer.
  • Recurrent CNAs are probably "driver" events contributing critically to clonal diversification and selection, but at diagnosis, their developmental timing is "buried" in the leukemia's covert natural history.
  • [MeSH-major] Gene Dosage. Genome-Wide Association Study. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Twins, Monozygotic

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Blood. 2010 Apr 29;115(17):3424-5 [20430963.001]
  • (PMID = 20061556.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Twin Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
  •  go-up   go-down






Advertisement