BioMedLib Search Engine [ goto HOMEPAGE ]

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

Effective preventive strategies are needed to guarantee adequate vitamin D levels throughout childhood and adolescence, taking into account the geographical setting, season of the year, the level of environmental pollution, skin characteristics, eating habits and body weight, with a view to securing optimum health during these phases, and the prevention of complications in adulthood.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

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

[Cites] Pediatrics. 2008 Nov;122(5):1142-52 [18977996.001]

[Cites] J Clin Endocrinol Metab. 1999 Dec;84(12):4702-12 [10599739.001]

[Cites] J Am Diet Assoc. 2004 Jun;104(6):980-3 [15175600.001]

[Cites] N Engl J Med. 2007 Jul 19;357(3):266-81 [17634462.001]

[Cites] PLoS Genet. 2009 Feb;5(2):e1000369 [19197344.001]

[Cites] J Clin Endocrinol Metab. 2009 Sep;94(9):3200-6 [19549742.001]

[Cites] Med Hypotheses. 2008;70(4):750-9 [17920208.001]

[Cites] Can J Public Health. 2005 Nov-Dec;96(6):443-9 [16350869.001]

[Cites] Pediatrics. 2009 Sep;124(3):e371-9 [19661053.001]

[Cites] Endocrinol Metab Clin North Am. 2005 Sep;34(3):537-53, vii [16085158.001]

[Cites] Prog Biophys Mol Biol. 2006 Sep;92(1):33-8 [16618499.001]

[Cites] Maturitas. 2008 Feb 20;59(2):101-13 [18289805.001]

[Cites] Am J Clin Nutr. 2002 Dec;76(6):1446-53 [12450915.001]

[Cites] Arch Dis Child. 2005 Apr;90(4):373-8 [15781927.001]

[Cites] Ann Nutr Metab. 2009;54(1):15-21 [19194104.001]

[Cites] J Nutr. 2005 Feb;135(2):279-82 [15671226.001]

[Cites] Arch Intern Med. 2009 Mar 23;169(6):626-32 [19307527.001]

[Cites] Metabolism. 2008 Feb;57(2):183-91 [18191047.001]

[Cites] Am J Clin Nutr. 1995 Mar;61(3 Suppl):638S-645S [7879731.001]

[Cites] Bone. 2003 Aug;33(2):242-7 [14499358.001]

[Cites] Arch Phys Med Rehabil. 1999 Jan;80(1):54-8 [9915372.001]

[Cites] Mol Genet Metab. 2009 Mar;96(3):113-20 [19147383.001]

[Cites] Endocrinology. 2005 Apr;146(4):1956-64 [15637289.001]

[Cites] J Clin Endocrinol Metab. 1992 Oct;75(4):1060-5 [1400871.001]

[Cites] Clin Exp Immunol. 2008 Jan;151(1):76-85 [17983444.001]

[Cites] Calcif Tissue Int. 1998 Nov;63(5):369-74 [9799819.001]

[Cites] Atherosclerosis. 2009 Jul;205(1):255-60 [19091317.001]

[Cites] Endocrinol Nutr. 2009 Apr;56(4):164-9 [19627732.001]

[Cites] JAMA. 2006 Dec 20;296(23):2832-8 [17179460.001]

[Cites] J Clin Oncol. 2009 May 1;27(13):2117-9 [19349538.001]

[Cites] Osteoporos Int. 2009 Jan;20(1):133-40 [18458986.001]

[Cites] Arch Dermatol. 1991 Apr;127(4):536-8 [1848745.001]

[Cites] J Clin Endocrinol Metab. 2008 Jul;93(7):2693-701 [18445674.001]

[Cites] J Bone Miner Res. 1995 May;10(5):711-5 [7639106.001]

[Cites] J Bone Miner Res. 1998 Oct;13(10):1602-12 [9783549.001]

[Cites] Eur J Clin Nutr. 2005 Apr;59(4):533-41 [15714215.001]

[Cites] Environ Health Perspect. 2007 Aug;115(8):1132-9 [17687438.001]

[Cites] Bone. 2002 May;30(5):771-7 [11996918.001]

[Cites] N Engl J Med. 1998 Mar 19;338(12):777-83 [9504937.001]

[Cites] J Bone Miner Res. 2001 Nov;16(11):1962-71 [11697792.001]

[Cites] Pediatrics. 2008 Aug;122(2):398-417 [18676559.001]

[Cites] J Neurol. 2009 Sep;256(9):1468-79 [19399382.001]

[Cites] Eur J Clin Nutr. 1999 Sep;53(9):746-51 [10509773.001]

[Cites] JAMA. 1992 Nov 4;268(17):2403-8 [1404797.001]

[Cites] Curr Med Chem. 2010;17(5):453-66 [20015037.001]

[Cites] Arch Pediatr Adolesc Med. 2005 Apr;159(4):335-41 [15809385.001]

[Cites] Arch Dis Child. 2008 Jun;93(6):512-7 [18339654.001]

[Cites] J Nutr. 2005 Nov;135(11):2735S-8S [16251640.001]

[Cites] Bone. 1995 Dec;17(6):513-6 [8835303.001]

[Cites] J Bone Miner Res. 1996 Oct;11(10 ):1545-56 [8889856.001]

[Cites] Calcif Tissue Int. 2007 Nov;81(5):352-63 [17989943.001]

[Cites] Maturitas. 2009 Mar 20;62(3):248-62 [19211206.001]

[Cites] Maturitas. 2007 Oct 20;58(2):117-37 [17604580.001]

[Cites] Aten Primaria. 2008 Aug;40(8):393-9 [18755099.001]

[Cites] Diabetologia. 2008 Aug;51(8):1391-8 [18548227.001]

[Cites] J Clin Endocrinol Metab. 2009 Jan;94(1):26-34 [18854395.001]

[Cites] J Clin Endocrinol Metab. 2009 Feb;94(2):559-63 [19033372.001]

[Cites] Reprod Sci. 2009 Jan;16(1):7-19 [19144887.001]

[Cites] J Nutr. 2009 May;139(5):1002-7 [19321588.001]

[Cites] Am J Clin Nutr. 1998 Oct;68(4):854-8 [9771862.001]

[Cites] Ann Trop Paediatr. 2006 Mar;26(1):1-16 [16494699.001]

[Cites] Am J Clin Nutr. 2008 Apr;87(4):1039-44 [18400729.001]

[Cites] Photochem Photobiol Sci. 2004 Nov-Dec;3(11-12):1067-70 [15570398.001]

[Cites] Osteoporos Int. 2001;12(10):875-9 [11716192.001]

[Cites] Gynecol Endocrinol. 2007 Jan;23(1):13-24 [17484507.001]

[Cites] Cell Mol Neurobiol. 2010 Mar;30(2):161-71 [19774457.001]

[Cites] Arch Dis Child. 2004 Aug;89(8):781-4 [15269083.001]

[Cites] J Adolesc Health. 2005 Jul;37(1):75 [15963911.001]

[Cites] Diabetologia. 2004 Mar;47(3):451-62 [14758446.001]

[Cites] Am J Geriatr Psychiatry. 2006 Dec;14(12):1032-40 [17138809.001]

[Cites] Clin Chem. 2009 Jun;55(6):1163-70 [19359534.001]

[Cites] Osteoporos Int. 2006;17 (3):433-40 [16362145.001]

[Cites] Neurology. 2010 Jan 5;74(1):27-32 [19794127.001]

[Cites] J Nutr. 2005 Nov;135(11):2602-8 [16251618.001]

[Cites] J Immunol. 2009 Apr 1;182(7):4289-95 [19299728.001]

[Cites] J Clin Endocrinol Metab. 1991 Sep;73(3):555-63 [1874933.001]

[Cites] J Clin Endocrinol Metab. 2009 Jan;94(1):67-73 [18984659.001]

[Cites] J Steroid Biochem Mol Biol. 2004 May;89-90(1-5):491-5 [15225826.001]

[Cites] Pediatrics. 2009 Mar;123(3):797-803 [19255005.001]

[Cites] J Clin Endocrinol Metab. 1992 Oct;75(4):1099-103 [1328275.001]

[Cites] J Geriatr Psychiatry Neurol. 2009 Sep;22(3):188-95 [19073839.001]

[Cites] Pediatrics. 2001 Apr;107(4):E53 [11335774.001]

[Cites] Nature. 1973 Aug 24;244(5417):515-7 [4621128.001]

[Cites] Eur J Endocrinol. 2007 Aug;157(2):225-32 [17656603.001]

[Cites] J Trop Pediatr. 2004 Dec;50(6):364-8 [15537725.001]

[Cites] Child Care Health Dev. 2008 Mar;34(2):276-8 [18257797.001]

[Cites] J Nutr. 2006 Apr;136(4):1130-4 [16549494.001]

[Cites] Clin Chem. 2002 Oct;48(10):1731-8 [12324490.001]

[Cites] Am J Clin Nutr. 2003 Sep;78(3):485-92 [12936933.001]

[Cites] Osteoporos Int. 2005 Jan;16(1):109-13 [15175848.001]

[Cites] J Neurol Neurosurg Psychiatry. 2009 Jul;80(7):722-9 [19460797.001]

[Cites] Am J Clin Nutr. 2009 Sep;90(3):459-67 [19640956.001]

[Cites] Bone. 2009 Sep;45(3):423-6 [19465168.001]

[Cites] Am J Clin Nutr. 2007 Jul;86(1):150-8 [17616775.001]

[Cites] Am J Clin Nutr. 2004 Dec;80(6 Suppl):1748S-51S [15585799.001]

[Cites] J Clin Endocrinol Metab. 2000 Jul;85(7):2370-7 [10902781.001]

[Cites] Am J Clin Nutr. 2001 Aug;74(2):206-10 [11470722.001]

[Cites] J Pediatr. 2009 Jan;154(1):132-4 [19187735.001]

[Cites] Circulation. 2008 Jan 29;117(4):503-11 [18180395.001]

(PMID = 28028383.001).

[Journal-full-title] Adolescent health, medicine and therapeutics

[ISO-abbreviation] Adolesc Health Med Ther

[Language] eng

[Publication-type] Review; Journal Article

[Publication-country] New Zealand

[Keywords] NOTNLM ; Vitamin D / balanced diet / osteomalacia / osteoporosis supplements / rickets

   

[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

   

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

[Title] Mer receptor tyrosine kinase is a novel therapeutic target in pediatric B-cell acute lymphoblastic leukemia.

Acute lymphoblastic leukemia (ALL) is currently treated with an intense regimen of chemotherapy yielding cure rates near 80%.

Here, we report ectopic expression of the receptor tyrosine kinase Mer in pediatric B-cell ALL.

Inhibition of Mer prevented Erk 1/2 activation, increased the sensitivity of B-ALL cells to cytotoxic agents in vitro by promoting apoptosis, and delayed disease onset in a mouse model of leukemia.

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

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

[Email] Email this result item

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

[Cites] Blood. 2008 Jan 1;111(1):379-82 [17878402.001]

[Cites] Nature. 2008 Jan 10;451(7175):147-52 [18185580.001]

[Cites] Rapid Commun Mass Spectrom. 2008;22(4):519-25 [18228243.001]

[Cites] Biotechnol Bioeng. 2008 Apr 15;99(6):1443-52 [18023050.001]

[Cites] Adv Cancer Res. 2008;100:35-83 [18620092.001]

[Cites] Cancer Lett. 2008 Sep 18;268(2):314-24 [18502572.001]

[Cites] Semin Hematol. 2008 Jul;45(3 Suppl 2):S17-21 [18760705.001]

[Cites] J Clin Invest. 2008 Sep;118(9):3038-50 [18704194.001]

[Cites] Cancer Res. 2008 Sep 15;68(18):7409-18 [18794129.001]

[Cites] Pediatr Blood Cancer. 2009 Feb;52(2):177-81 [18816698.001]

[Cites] Clin Cancer Res. 2008 Dec 15;14(24):7971-4 [19088011.001]

[Cites] Leukemia. 2008 Dec;22(12):2142-50 [18818707.001]

[Cites] Cancer. 2000 Apr 1;88(7):1687-95 [10738228.001]

[Cites] Cancer Treat Rev. 2001 Dec;27(6):351-63 [11908928.001]

[Cites] Methods. 2002 Jan;26(1):57-75 [12054905.001]

[Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]

[Cites] J Biol Chem. 2002 Jul 5;277(27):24057-66 [11929866.001]

[Cites] J Biol Chem. 2002 Jul 5;277(27):23977-80 [11997383.001]

[Cites] Anticancer Res. 2002 Mar-Apr;22(2B):1071-8 [12168903.001]

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

[Cites] N Engl J Med. 2004 Aug 5;351(6):601-3 [15295054.001]

[Cites] Nature. 1977 Jun 30;267(5614):841-3 [197411.001]

[Cites] Blood. 1984 Mar;63(3):721-4 [6607758.001]

[Cites] Blood. 1990 Jul 1;76(1):117-22 [2364165.001]

[Cites] J Clin Oncol. 1990 Aug;8(8):1380-8 [2380759.001]

[Cites] Blood. 1991 Feb 15;77(4):687-93 [1671560.001]

[Cites] Leukemia. 1991 Apr;5(4):322-31 [2027299.001]

[Cites] Leukemia. 1993 Nov;7(11):1865-74 [8231254.001]

[Cites] Cell Growth Differ. 1994 Jun;5(6):647-57 [8086340.001]

[Cites] Mol Cell Biol. 1995 Dec;15(12):6582-92 [8524223.001]

[Cites] Blood. 1996 Feb 15;87(4):1211-24 [8608207.001]

[Cites] EMBO J. 1996 Dec 2;15(23):6541-51 [8978681.001]

[Cites] Oncogene. 1997 May 1;14(17):2033-9 [9160883.001]

[Cites] Mol Cell Biol. 1997 Aug;17(8):4442-53 [9234702.001]

[Cites] Mol Cell Biol. 1999 Feb;19(2):1171-81 [9891051.001]

[Cites] Leukemia. 1999 Sep;13(9):1352-8 [10482985.001]

[Cites] Cancer Res. 2005 Aug 15;65(16):7052-8 [16103051.001]

[Cites] Neoplasia. 2005 Dec;7(12):1058-64 [16354588.001]

[Cites] Cancer Res. 2006 Feb 1;66(3):1500-8 [16452206.001]

[Cites] Clin Cancer Res. 2006 May 1;12(9):2662-9 [16675557.001]

[Cites] N Engl J Med. 2006 Jun 15;354(24):2531-41 [16775234.001]

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

[Cites] Oncogene. 2006 Oct 5;25(45):6092-100 [16652142.001]

[Cites] Blood. 2007 Feb 1;109(3):1026-33 [17047157.001]

[Cites] J Chromatogr B Analyt Technol Biomed Life Sci. 2007 Jun 1;852(1-2):545-53 [17379584.001]

[Cites] Blood. 2007 Jun 15;109(12):5473-6 [17351113.001]

[Cites] Cancer Cell. 2007 Jul;12(1):9-22 [17613433.001]

[Cites] Brain Res. 2007 Jul 16;1158:39-49 [17559813.001]

[Cites] Eur J Cancer. 2007 Sep;43(14):2074-81 [17716890.001]

[RetractionIn] Blood. 2012 Aug 16;120(7):1533 [22753864.001]

(PMID = 19643988.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NHLBI NIH HHS / HL / F32 HL096416; United States / NCI NIH HHS / CA / CA98543; United States / NCI NIH HHS / CA / CA114766; United States / NCI NIH HHS / CA / U24 CA114766; United States / NHLBI NIH HHS / HL / F32HL096416; United States / NCI NIH HHS / CA / U10 CA098543

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; EC 2.7.10.1 / MERTK protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases

[Other-IDs] NLM/ PMC2927045

   

Advertisement

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

[Title] HLA-associated susceptibility to childhood B-cell precursor ALL: definition and role of HLA-DPB1 supertypes.

Childhood B-cell precursor (BCP) ALL is thought to be caused by a delayed immune response to an unidentified postnatal infection.

[Email] Email this result item

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

[Cites] Leukemia. 1995 Mar;9(3):440-3 [7885043.001]

[Cites] Immunogenetics. 1991;34(1):12-22 [1713190.001]

[Cites] Ann Hum Genet. 1995 Jan;59(Pt 1):97-105 [7762987.001]

[Cites] Leukemia. 1995 May;9(5):875-8 [7769851.001]

[Cites] Annu Rev Immunol. 1995;13:587-622 [7612235.001]

[Cites] Hum Immunol. 1995 Jul;43(3):219-26 [7558939.001]

[Cites] Tissue Antigens. 1996 Mar;47(3):212-21 [8740771.001]

[Cites] Immunol Cell Biol. 1996 Oct;74(5):444-8 [8912007.001]

[Cites] Adv Immunol. 1997;66:67-100 [9328640.001]

[Cites] J Immunol. 1997 Nov 15;159(10):4935-42 [9366419.001]

[Cites] J Immunol. 1998 Apr 1;160(7):3363-73 [9531296.001]

[Cites] J Gen Virol. 1998 Apr;79 ( Pt 4):697-704 [9568963.001]

[Cites] Am J Trop Med Hyg. 1998 Aug;59(2):302-6 [9715951.001]

[Cites] Curr Opin Immunol. 1998 Aug;10(4):478-82 [9722926.001]

[Cites] Br J Cancer. 1998 Sep;78(5):561-5 [9744491.001]

[Cites] Blood. 1999 Jul 15;94(2):694-700 [10397736.001]

[Cites] J Immunol. 1999 Aug 1;163(3):1647-53 [10415070.001]

[Cites] Eur J Immunol. 1999 Jul;29(7):2140-7 [10427976.001]

[Cites] Tissue Antigens. 1999 Aug;54(2):153-61 [10488742.001]

[Cites] Immunogenetics. 2005 Jan;56(10):754-9 [15565337.001]

[Cites] Paediatr Perinat Epidemiol. 2005 Mar;19(2):152-64 [15787890.001]

[Cites] J Immunol. 2005 Jun 1;174(11):7085-95 [15905552.001]

[Cites] Haematologica. 2006 Feb;91(2):240-3 [16461310.001]

[Cites] Nat Rev Cancer. 2006 Mar;6(3):193-203 [16467884.001]

[Cites] J Immunol. 2006 May 1;176(9):5401-8 [16622007.001]

[Cites] Am J Epidemiol. 2007 Mar 1;165(5):496-504 [17182983.001]

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

[Cites] Br J Cancer. 2000 Mar;82(5):1073-102 [10737392.001]

[Cites] J Virol. 2000 Dec;74(23):10930-8 [11069987.001]

[Cites] Nat Rev Genet. 2001 Dec;2(12):967-77 [11733749.001]

[Cites] Br Med Bull. 2002;61:13-28 [11997296.001]

[Cites] Hum Mol Genet. 2002 Jul 1;11(14):1585-97 [12075003.001]

[Cites] Am J Hum Genet. 2002 Oct;71(4):759-76 [12297984.001]

[Cites] J Immunol. 2002 Dec 15;169(12):6928-34 [12471126.001]

[Cites] Cancer Res. 2002 Dec 15;62(24):7195-9 [12499257.001]

[Cites] Paediatr Respir Rev. 2000 Sep;1(3):210-4 [12531081.001]

[Cites] Int Immunol. 2003 May;15(5):565-76 [12697658.001]

[Cites] Nat Med. 2003 Jul;9(7):928-35 [12819779.001]

[Cites] BMC Med Genet. 2003 Jan 24;4:2 [12542841.001]

[Cites] Tissue Antigens. 2003 Dec;62(6):459-71 [14617029.001]

[Cites] Am J Hum Genet. 2004 Jan;74(1):160-7 [14669136.001]

[Cites] J Virol. 2004 Feb;78(4):1775-81 [14747542.001]

[Cites] Virology. 2004 Sep 1;326(2):220-30 [15302208.001]

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

[Cites] Leuk Res. 1985;9(6):715-33 [3859718.001]

[Cites] J Immunol. 1992 Jan 1;148(1):249-58 [1727870.001]

[Cites] Leukemia. 1993 Jan;7(1):27-34 [8418376.001]

[Cites] J Virol. 1993 Oct;67(10):6285-8 [7690424.001]

[Cites] Leukemia. 1993 Oct;7(10):1630-4 [8412325.001]

[Cites] Leukemia. 1994 May;8(5):856-64 [8182942.001]

[Cites] Proc Natl Acad Sci U S A. 1994 Aug 2;91(16):7515-9 [8052611.001]

[Cites] Cancer Immunol Immunother. 2008 Jan;57(1):53-61 [17622527.001]

[Cites] Am J Epidemiol. 1986 Oct;124(4):590-4 [3463201.001]

[Cites] Cancer. 1988 Feb 1;61(3):475-7 [3422171.001]

[Cites] J Immunol. 1988 Dec 1;141(11):4024-30 [2460556.001]

[Cites] J Virol. 1989 Feb;63(2):747-52 [2463381.001]

[Cites] Genetics. 1990 Apr;124(4):967-78 [2323559.001]

[Cites] J Immunol. 1990 Jul 1;145(1):305-10 [1694205.001]

[Cites] J Immunol. 1995 May 1;154(9):4536-45 [7536773.001]

(PMID = 18334973.001).

[ISSN] 0007-0920

[Journal-full-title] British journal of cancer

[ISO-abbreviation] Br. J. Cancer

[Language] ENG

[Grant] United Kingdom / Cancer Research UK / /

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

[Publication-country] England

[Chemical-registry-number] 0 / HLA-DP Antigens; 0 / HLA-DP beta-Chains; 0 / HLA-DPB1 antigen

[Other-IDs] NLM/ PMC2275491

   

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

[Title] [Clinical importance of minimal residual disease testing in the therapy of childhood B-cell acute lymphoblastic leukemia].

OBJECTIVE: To study the role of minimal residual disease (MRD) in the evaluation of therapeutic effectiveness of childhood B-cell acute lymphoblastic leukemia (ALL).

METHODS: MRD testing was performed in 124 children with B-cell ALL, who were newly diagnosed and enrolled in the ALL-XH-99 treatment protocol from September 2001 to April 2005MRD was determined by 4-color flow cytometry in the different time points during the treatment period.

Multivariate analysis confirmed that the MRD level after induction chemotherapy together with the reaction to prednisone, the bone marrow features on the 19th day of induction, and the fusion gene with BCR-ABL or MLL-AF4 had prognostic significance in childhood B-cell ALL.

CONCLUSIONS: The MRD level in the whole course of therapy is an important outcome indicator in childhood B cell ALL.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Burkitt Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

[Email] Email this result item

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

(PMID = 18554462.001).

[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

   

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

[Title] Prognostic significance of CD20 expression in childhood B-cell precursor acute lymphoblastic leukemia.

CD20 expression is associated with inferior survival in adults with acute lymphoblastic leukemia (ALL).

We analyzed the prognostic impact of CD20 expression in 353 children with B-cell precursor ALL treated in 3 consecutive St Jude Total Therapy studies.

There was no association between CD20 expression and E2A-PBX, TEL-AML1, ploidy, white blood cell count at diagnosis, or sex.

These data suggest that CD20 expression is not associated with inferior outcome in pediatric patients treated with contemporary regimens.

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] Ann Oncol. 2003 Apr;14(4):520-35 [12649096.001]

[Cites] J Clin Oncol. 2003 Aug 15;21(16):3084-91 [12915598.001]

[Cites] JAMA. 2003 Oct 15;290(15):2001-7 [14559953.001]

[Cites] Blood. 1998 Jul 15;92(2):411-5 [9657739.001]

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

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

[Cites] Blood. 1997 Jun 1;89(11):3960-6 [9166833.001]

[Cites] Blood. 2004 Jun 15;103(12):4396-407 [14551133.001]

(PMID = 16896151.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA21765

[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 / Antigens, CD20

[Other-IDs] NLM/ PMC1895438

   

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

Stable transgene expression is observed in a small percentage of hepatocytes, often in two- to eight-cell clusters, suggestive of genomic integration.

We conclude that successful use of rAAV to treat liver disease in early childhood will require optimally efficient vector constructs and probable re-administration.

[Email] Email this result item

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

[Copyright] Copyright © 2008 The American Society of Gene Therapy. Published by Elsevier Inc. All rights reserved.

(PMID = 28178471.001).

[ISSN] 1525-0024

[Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy

[ISO-abbreviation] Mol. Ther.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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

[Title] Replication analysis confirms the association of ARID5B with childhood B-cell acute lymphoblastic leukemia.

Although childhood acute lymphoblastic leukemia is the most common pediatric cancer, its etiology remains poorly understood.

In an attempt to replicate the findings of 2 recent genome-wide association studies in a French-Canadian cohort, we confirmed the association of 5 SNPs [rs7073837 (P=4.2 x 10(-4)), rs10994982 (P=3.8 x 10(-4)), rs10740055 (P=1.6 x 10(-5)), rs10821936 (P=1.7 x 10(-7)) and rs7089424 (P=3.6 x 10(-7))] in the ARID5B gene with childhood acute lymphoblastic leukemia.

We also confirmed a selective effect for B-cell acute lymphoblastic leukemia with hyperdiploidy and report a putative gender-specific effect of ARID5B SNPs on acute lymphoblastic leukemia risk in males.

This study provides a strong rationale for more detailed analysis to identify the causal variants at this locus and to better understand the overall functional contribution of ARID5B to childhood acute lymphoblastic leukemia susceptibility.

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] Leuk Res. 1997 Sep;21(9):817-23 [9393596.001]

[Cites] Nucleic Acids Res. 1996 May 1;24(9):1695-701 [8649988.001]

[Cites] Blood. 1999 Mar 1;93(5):1496-501 [10029576.001]

[Cites] Genetics. 2005 Nov;171(3):1321-30 [15944347.001]

[Cites] Blood. 2007 Jan 15;109(2):683-92 [17008550.001]

[Cites] Pediatr Clin North Am. 2008 Feb;55(1):1-20, ix [18242313.001]

[Cites] Blood. 2008 Jun 15;111(12):5515-23 [18334672.001]

[Cites] Leuk Res. 2009 Jun;33(6):759-63 [19101034.001]

[Cites] Nat Genet. 2009 Sep;41(9):1001-5 [19684603.001]

[Cites] Nat Genet. 2009 Sep;41(9):1006-10 [19684604.001]

[Cites] Blood. 2010 Mar 4;115(9):1765-7 [20042726.001]

[Cites] Leukemia. 2010 Apr;24(4):894-6 [20054350.001]

[Cites] Leuk Lymphoma. 2007 Apr;48(4):786-92 [17454638.001]

[Cites] Eur J Cancer. 1999 Dec;35(14):1941-53 [10711237.001]

[Cites] Int J Cancer. 2002 Jan 10;97(2):230-6 [11774269.001]

[Cites] Cell Growth Differ. 2002 Mar;13(3):95-106 [11959810.001]

[Cites] Genet Epidemiol. 2002 Nov;23(4):426-43 [12432508.001]

[Cites] Genet Epidemiol. 2004 Jul;27(1):21-32 [15185400.001]

[Cites] Am J Hum Genet. 1998 Jul;63(1):259-66 [9634505.001]

(PMID = 20460642.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] ENG

[Grant] Canada / Canadian Institutes of Health Research / /

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

[Publication-country] Italy

[Chemical-registry-number] 0 / ARID5B protein, human; 0 / DNA-Binding Proteins; 0 / Transcription Factors

[Other-IDs] NLM/ PMC2930966

   

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

[Title] [Prognostic value of minimal residual disease in childhood B-cell acute lymphoblastic leukemia].

OBJECTIVE: To assess the prognostic value of minimal residual disease (MRD) in childhood B-cell acute lymphoblastic leukemia (ALL) after induction chemotherapy.

CONCLUSION: The MRD level at achieving CR is one of important prognostic factor in the treatment of childhood B-cell ALL, and might be used to assess the early treatment response.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, B-Cell / drug therapy. Neoplasm, Residual

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

[Email] Email this result item

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

(PMID = 16732969.001).

[ISSN] 0253-2727

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

[ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi

[Language] chi

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

[Publication-country] China

   

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

[Title] Differential microRNA expression in childhood B-cell precursor acute lymphoblastic leukemia.

The analysis of differential microRNA expression profiles may be a powerful tool to allow us insight on the mechanisms of childhood B-cell precursor acute lymphoblastic leukemia (pre-B-ALL).

[MeSH-major] Gene Expression Regulation, Neoplastic. MicroRNAs / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

[MeSH-minor] Child. Child, Preschool. Computational Biology. Gene Expression Profiling. Hematopoiesis / genetics. Humans. Infant. 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 = 19206004.001).

[ISSN] 1521-0669

[Journal-full-title] Pediatric hematology and oncology

[ISO-abbreviation] Pediatr Hematol Oncol

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / MIRN222 microRNA, human; 0 / MIRN373 microRNA, human; 0 / MIRN451 microRNA, human; 0 / MicroRNAs

   

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

[Title] Expression of angiogenic factors in childhood B-cell precursor acute lymphoblastic leukemia.

In pediatric acute lymphocytic leukemia however, the expression of angiogenic molecules and its relation to prognosis and relapse are unknown.

Therefore, we prospectively analyzed 46 pediatric patients with precursor B cell acute lymphocytic leukemia by semi-quantitative RT-PCR for expression of the angiogenic molecules VEGF, VEGF-C, iNOS and TGF-beta and correlated relapse and survival data with the expression of these factors.

Angiogenic factors are expressed in the bone marrow of patients with pediatric B cell precursor ALL and VEGF is a potential candidate for therapeutic intervention as it is significantly higher expressed in children with late relapses.

The mRNA expression of iNOS in the surviving children possibly reflects an increased activity of the immune system against the leukemia which leads to a superior survival.

[MeSH-major] Angiogenic Proteins / biosynthesis. Burkitt Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

[Email] Email this result item

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

(PMID = 17143492.001).

[ISSN] 1021-335X

[Journal-full-title] Oncology reports

[ISO-abbreviation] Oncol. Rep.

[Language] eng

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

[Publication-country] Greece

[Chemical-registry-number] 0 / Angiogenic Proteins; 0 / RNA, Messenger; 0 / Transforming Growth Factor beta; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C; 103107-01-3 / Fibroblast Growth Factor 2; EC 1.14.13.39 / Nitric Oxide Synthase Type II

   

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

[Title] DNA methylation and miRNA expression profiling in childhood B-cell acute lymphoblastic leukemia.

Acute lymphoblastic leukemia (ALL) is the most common cancer in children in the modern world.

A number of DNA methylation and miRNA profiling studies have investigated the role of both in childhood ALL.

[MeSH-major] DNA Methylation / physiology. Epigenesis, Genetic / physiology. High-Throughput Screening Assays / methods. MicroRNAs / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

[Email] Email this result item

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

(PMID = 22122053.001).

[ISSN] 1750-192X

[Journal-full-title] Epigenomics

[ISO-abbreviation] Epigenomics

[Language] eng

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

[Publication-country] England

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

   

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

[Title] Amplification of RUNX1 gene in two new cases of childhood B-cell precursor acute lymphoblastic leukemia: A case report.

: e21000 Background: Chromosome abnormalities of leukemia cells have important prognostic significance in childhood acute lymphoblastic leukemia (ALL).

B-cell precursor acute lymphoblastic leukemia (BCP-ALL) ETV6/RUNX1 (alias TEL/AML1) is most frequent i.e.

We report two new cases with Pre B- cell ALL without ETV6/RUNX1 rearrangement, showing amplification of AML1 gene detected by FISH analysis.

RESULTS: In first case a 3-year girl with four copies of AML (RUNX1) gene were observed in 95% of the cell with normal two copies of TEL (ETV6) gene in both interphase and metaphase FISH.

Bone marrow karyotype in combination with molecular cytogenetic techniques like FISH should be done for improvement in sensitivity and accurate cytogenetic analysis in childhood ALL patients for proper identification of prognostic group for optimum treatment.

This is one of the few reported studies worldwide for amplification of RUNX1 gene from Indian subcontinent in childhood BCP-ALL.

[Email] Email this result item

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

(PMID = 27960689.001).

[ISSN] 1527-7755

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

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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

: 10021 Background: Pilocytic astrocytoma (WHO grade I) comprises the most frequent brain tumor in childhood.

Genes contained in the signature most interestingly included three homeobox family genes (HOXB1, HOXD3, and HOXD4), and NES, a tumor stem cell marker.

[Email] Email this result item

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

(PMID = 27962622.001).

[ISSN] 1527-7755

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

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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

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

: 10034 Background: In the setting of hematopoietic stem cell transplantation (HSCT), donor natural killer (NK) cells exhibit potent anti-leukemic effects without causing graft-versus-host disease.

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

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

Leukemic cell genetic abnormalities included CBFβ-MYH11in 4 cases, RBM15-MKL1in 2 cases, MLL-ENL and MLL-AF9 in 1 case each; 2 cases had no detectable abnormalities.

All patients had detectable donor NK cells at one or more time points: donor NK cell chimerism ranged from 0% to 30% during the first 4 weeks after the infusions and was greater than 1% in 9 cases at week 1, 4 cases at week 2, 5 cases at week 3, and 3 cases at week 4.

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

[Email] Email this result item

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

(PMID = 27962581.001).

[ISSN] 1527-7755

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

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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

[Title] Burkitt lymphoma in children: The Israel Society of Pediatric Hematology Oncology retrospective study.

: 10051 Background: From 2000 to 2005, the Israel Society of Pediatric Hematology Oncology studied the results of the FAB-LMB 96 protocol in children with B cell lymphoma.

Fifty patients (57%) were classified as burkitt lymphoma, 5 (5.7%) as burkitt-like lymphoma, 22 (25%) as diffuse large B cell (DLBC), 9 (10.2%) as burkitt leukemia.

CONCLUSIONS: In nonresected mature B cell lymphoma of childhood and adolescence with no BM or CNS involvement, a 93% cure rate was achieved.

[Email] Email this result item

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

(PMID = 27962447.001).

[ISSN] 1527-7755

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

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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

[Title] Ovarian function after high-dose chemotherapy in childhood: Risk factors for developing partial ovarian failure and how to identify them early.

: e20665 Background: During the last 30 years, polychemotherapies, surgery and radiotherapy have been established as standard therapies for treating pediatric cancers thus leading to a significant improvement in terms of 5-year-overall-survival which is now around 70% among children and adolescents.

Eligibility criteria: age >12 years at time of analysis; peripheral stem cell graft between 2-20 years; high dose chemotherapy.

[Email] Email this result item

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

(PMID = 27961711.001).

[ISSN] 1527-7755

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

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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

[Title] Pediatric Preclinical Testing Program (PPTP) testing of the CENP-E inhibitor GSK923295A.

METHODS: The PPTP includes a molecularly characterized in vitro panel of cell lines (n = 27) and in vivo panel of xenografts (n = 60) representing most of the common types of childhood solid tumors and childhood acute lymphoblastic leukemia (ALL).

RESULTS: GSK923295A demonstrated potent in vitro activity against the PPTP cell line panel with a median IC50 of 27 nM (range 12 nM to > 10 μM).

[Email] Email this result item

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

(PMID = 27962529.001).

[ISSN] 1527-7755

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

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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

[Title] Resistance of stem-like cells from neuroblastoma cell lines to commonly used anticancer drugs.

: 10054 Background: Neuroblastoma is the most common extra-cranial solid tumor of childhood.

For this study, we investigated the cytotoxicity of 4 commonly used anti-cancer drugs on stem-like cells isolated from neuroblastoma cell lines.

METHODS: Cell surface marker CD133 positivity was used to define stem-like cells.

Three neuroblastoma lines were screened for the expression of stem cell marker CD133 by FACS analysis.

CONCLUSIONS: This study suggests that CD133+ cells in neuroblastoma cell lines are more resistant to conventional anti-cancer drugs compared to CD133- cells.

Targeting these stem-like cell populations could lead to development of more effective treatment for neuroblastoma.

[Email] Email this result item

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

(PMID = 27962450.001).

[ISSN] 1527-7755

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

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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

[Title] 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.

While the first course of chemotherapy successfully eradicated the cell line with the t(12;21), the second cell line with AML1 amplification remained latent during the time of complete remission and reappeared with a different immunophenotype.

[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

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

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

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

[Email] Email this result item

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

(PMID = 17889714.001).

[ISSN] 0165-4608

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human

   

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

[Title] Chromosome 14 copy number-dependent IGH gene rearrangement patterns in high hyperdiploid childhood B-cell precursor ALL: implications for leukemia biology and minimal residual disease analysis.

Childhood B-cell precursor acute lymphoblastic leukemia (BCP ALL) is generally a clonal disease in which the number of IGH rearrangements per cell does not exceed the number of the IGH alleles on chromosome 14.

[MeSH-major] Chromosomes, Human, Pair 14 / genetics. Gene Dosage / genetics. Gene Rearrangement. Immunoglobulin Heavy Chains / genetics. Neoplasm, Residual / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

[Email] Email this result item

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

(PMID = 19148138.001).

[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 / Immunoglobulin Heavy Chains

   

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

[Title] [The clinical significance of detecting minimal residual disease in acute childhood B-cell lymphoblastic leukemia with flow cytometry].

OBJECTIVE: Flow cytometry may be used to detect minimal residual disease (MRD) in acute lymphoblastic leukemia because leukemic cells often display aberrant phenotypes when compared to normal cells.

The investigators also aimed to study the value of the detection of MRD by flow cytometry in childhood B-ALL without effective antibody combinations.

METHODS: Thirty-six cases of childhood B-ALL with effective antibody combinations were performed MRD analysis after induction therapy.

(1) Forty-two cases of childhood B-ALL were screened for antibody combinations of interest and were identified in 86% (36/42) of the cases.

CONCLUSION:. (1) Flow cytometry is a sensitive and specific method for detecting MRD of childhood ALL, and could predict the coming relapse. (2) Patients with MRD levels > 10(-3) had poor prognosis. (3) The levels of MRD at month 9 and 12 had prognostic value. (4) The value of antibody combinations consisting of CD(45)/CD(19)/CD(10)/CD(34) and CD(45)/CD(19)/CD(20)/CD(22) should be further investigated in patients without effective antibody combinations.

[MeSH-major] B-Lymphocyte Subsets / immunology. Flow Cytometry. Immunophenotyping. Neoplasm, Residual / diagnosis. 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 = 16083543.001).

[ISSN] 0578-1310

[Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics

[ISO-abbreviation] Zhonghua Er Ke Za Zhi

[Language] chi

[Publication-type] English Abstract; Evaluation Studies; Journal Article

[Publication-country] China

   

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

[Title] Immunohistochemical analyses of phosphatases in childhood B-cell lymphoma: lower expression of PTEN and HePTP and higher number of positive cells for nuclear SHP2 in B-cell lymphoma cases compared to controls.

Although many pediatric B-cell lymphoma patients are being cured today, much is still unknown about the pathogenesis of this disease.

The authors have analyzed 26 pediatric B-cell lymphoma cases for the expression of a panel of phosphatases and report a statistically significant lower expression intensity of PTEN and HePTP and higher nuclear SHP2 expression in B-cell lymphoma cases compared to lymphoid tissue.

Knowledge about the expression of key regulatory proteins in pediatric B-cell lymphomas is necessary for revealing the complex molecular background of this disease.

[MeSH-major] Lymphoma, B-Cell / genetics. PTEN Phosphohydrolase / metabolism. Protein Tyrosine Phosphatase, Non-Receptor Type 11 / biosynthesis. Protein Tyrosine Phosphatases, Non-Receptor / metabolism

[Email] Email this result item

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

(PMID = 18728972.001).

[ISSN] 1521-0669

[Journal-full-title] Pediatric hematology and oncology

[ISO-abbreviation] Pediatr Hematol Oncol

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] EC 3.1.3.48 / PTPN7 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / Protein Tyrosine Phosphatases, Non-Receptor; EC 3.1.3.67 / PTEN Phosphohydrolase

   

[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.

We compared the karyotypes from 436 nonselected B-cell precursor ALL patients at initial diagnosis and of 76 patients at first relapse.

[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

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 = 19167609.001).

[ISSN] 1873-4456

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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

[Title] Identification of candidate target antigens for antibody-based immunotherapy in childhood B-cell precursor ALL.

BACKGROUND: Contemporary risk adapted treatment protocols for childhood acute lymphoblastic leukemia (ALL) rely on accurate risk assessment strategies for disease re-occurrence by incorporating clinical parameters as well as immunological, molecular and cytogenetic features of the blasts at initial manifestation.

PATIENTS AND METHODS: In order to identify target antigen structures, we analyzed the immunological expression profiles of blasts from 181 patients with B-cell precursor ALL treated at our institution in 11 years according to the CoALL-92/97/03 protocols.

CD20 was expressed on 11-37 % of B-cell precursor ALL samples.

CONCLUSIONS: These analyses clearly identified the three antigens CD19, CD22 and HLA-DR present on blasts in more than 90 % of patients as potential target structures for targeted therapies with native or toxin-bound monoclonal antibodies in childhood ALL.

[MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, CD19 / analysis. Burkitt Lymphoma / immunology. HLA-DR Antigens / analysis. Immunotherapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Sialic Acid Binding Ig-like Lectin 2 / analysis

[Email] Email this result item

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

(PMID = 17080335.001).

[ISSN] 0300-8630

[Journal-full-title] Klinische Pädiatrie

[ISO-abbreviation] Klin Padiatr

[Language] eng

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

[Publication-country] Germany

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD19; 0 / HLA-DR Antigens; 0 / Sialic Acid Binding Ig-like Lectin 2

   

[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).

All patients were classified according to their immunophenotype, and only B-cell precursor and T-lineage were analyzed.

The frequency of B-cell precursor ALL was 76.1%, whereas T lineage ALL showed a frequency of 23.6%.

B-cell precursor ALL was the major contributor to peak age; T lineage ALL showed a peak among 1 and 3 years of age.

We conclude that the age peak for children with ALL in MC is within the ranges reported for developed countries and that B-cell precursor ALL is the main contributor to these peak.

[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

   

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

[Title] The efficacy of rituximab in high-grade pediatric B-cell lymphoma/leukemia: a review of available evidence.

PURPOSE OF REVIEW: This review evaluates whether rituximab has efficacy in high-grade pediatric B-cell lymphoma/leukemia.

Current pediatric protocols for CD20+ B-cell lymphoma/leukemia significantly improve survival, but with major morbidity.

To assess whether rituximab has efficacy in very high-grade pediatric disease, all published data on rituximab therapy for Burkitt's lymphoma/B acute lymphoblastic leukaemia (B-ALL) and pediatric patients with relapsed/refractory large B-cell lymphoma were reviewed.

Minimal pediatric data have been published, but 19 children with mature B-cell lymphoma/B-ALL received rituximab, alone or in combination with chemotherapy, as salvage therapy, after failure of intensive chemotherapy.

Although positive reporting bias is suspected, it appears that rituximab, even as monotherapy, has efficacy in heavily pretreated pediatric patients with high-grade B-lymphoma/B-ALL.

[MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Lymphoma, B-Cell / drug therapy

MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

[Email] Email this result item

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

(PMID = 18197034.001).

[ISSN] 1040-8703

[Journal-full-title] Current opinion in pediatrics

[ISO-abbreviation] Curr. Opin. Pediatr.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab

[Number-of-references] 53

   

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

[Title] Prognostic effect of chromosomal abnormalities in childhood B-cell precursor acute lymphoblastic leukaemia: results from the UK Medical Research Council ALL97/99 randomised trial.

BACKGROUND: Chromosomal abnormalities in childhood acute lymphoblastic leukaemia are well established disease markers and indicators of outcomes.

METHODS: We analysed cytogenetic data from 1725 children with B-cell precursor acute lymphoblastic leukaemia who were included in the UK Medical Research Council ALL97/99 study and followed up for a median time of 8.2 years.

Multivariate analysis incorporating age, white-cell count, and treatment parameters showed that six cytogenetic abnormalities (ETV6-RUNX1, high hyperdiploidy, iAMP21, t(9;22), loss of 13q, and abnormal 17p) retained their significance for effect on relapse risk.

[MeSH-major] Chromosome Aberrations. 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

[Copyright] 2010 Elsevier Ltd. All rights reserved.

[CommentIn] Lancet Oncol. 2010 May;11(5):403-4 [20409755.001]

[ErratumIn] Lancet Oncol. 2010 Jun;11(6):516

(PMID = 20409752.001).

[ISSN] 1474-5488

[Journal-full-title] The Lancet. Oncology

[ISO-abbreviation] Lancet Oncol.

[Language] eng

[Grant] United Kingdom / Medical Research Council / / MRC/ G0300130; United Kingdom / Medical Research Council / / MRC/ MC/ U137686856

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

[Publication-country] England

   

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

[Title] [Intrachromosomal amplification of AML1 gene in childhood acute lymphoblastic leukemia].

[Transliterated title] AML1-gén intrakromoszomális amplifikációja gyermekkori acut lymphoid leukaemiában.

The introduction of routine molecular cytogenetic assays enabled us to reveal hitherto unknown genetic disorders of childhood acute leukemias.

In our present study we review a novel cytogenetic mutation typical for childhood B-cell ALL, the intrachromosomal amplification of chromosome 21, which requires high-risk therapy irrespective of other risk factors, and which is associated with a cryptic 12;21 translocation of good prognostic value.

[MeSH-major] Biomarkers, Tumor / genetics. Chromosomes, Human, Pair 21. Core Binding Factor Alpha 2 Subunit / genetics. Gene Amplification. Genetic Markers. 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 = 18539581.001).

[ISSN] 0030-6002

[Journal-full-title] Orvosi hetilap

[ISO-abbreviation] Orv Hetil

[Language] hun

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Hungary

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Genetic Markers; 0 / RUNX1 protein, human

   

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

[Title] The t(12:21) is underrepresented in childhood B-lineage acute lymphoblastic leukemia in Kerala, Southern India.

t(12;21) (TEL/AML1) is the most common genetic event in childhood B-cell acute lymphoblastic leukemia (B-ALL) in Western countries.

[MeSH-major] Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 21. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

[MeSH-minor] Child. Humans. Incidence. India / epidemiology. Leukemia, B-Cell. Molecular Epidemiology

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

[Email] Email this result item

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

(PMID = 15749681.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Letter

[Publication-country] Italy

   

[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.

The TCCSG NHL B9604 protocol achieved an excellent treatment outcome especially in patients with the most advanced disease (Group D: high BM blast cell burden and/or central nervous system involvement).

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Burkitt Lymphoma / drug therapy. Lymphoma, B-Cell / drug therapy

Genetic Alliance. consumer health - Childhood Cancer.

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

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

Genetic Alliance. consumer health - Acute Non Lymphoblastic Leukemia.

Genetic Alliance. consumer health - Hodgkin lymphoma.

Genetic Alliance. consumer health - Hodgkin lymphoma, childhood.

Genetic Alliance. consumer health - Lymphoblastic lymphoma.

Genetic Alliance. consumer health - Non-Hodgkin lymphoma, childhood.

Genetic Alliance. consumer health - Non-Hodgkin Lymphoma.

Hazardous Substances Data Bank. CYTARABINE .

Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

[Email] Email this result item

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

(PMID = 18398744.001).

[ISSN] 1029-2403

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Clinical Trial; Journal Article

[Publication-country] England

[Chemical-registry-number] 04079A1RDZ / Cytarabine; 8N3DW7272P / Cyclophosphamide; YL5FZ2Y5U1 / Methotrexate

   

[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.

Fluorescence in situ hybridization revealed that eight of the nine B-cell precursor (BCP) cases and none of the three T-cell ALL cases had an ETV6/RUNX1 rearrangement.

[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

   

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

[Title] Detection of prognostically relevant genetic abnormalities in childhood B-cell precursor acute lymphoblastic leukaemia: recommendations from the Biology and Diagnosis Committee of the International Berlin-Frankfürt-Münster study group.

Treatment of childhood acute lymphoblastic leukaemia (ALL) has improved considerably in recent years.

Here we review the current diagnostic criteria of genetic abnormalities in precursor B-ALL (BCP-ALL), including the relevant technical approaches and the application of the most appropriate methods for the detection of each abnormality.

[MeSH-major] Chromosome Aberrations. Leukemia, B-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

[Email] Email this result item

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

[Copyright] © 2010 Blackwell Publishing Ltd.

(PMID = 20701601.001).

[ISSN] 1365-2141

[Journal-full-title] British journal of haematology

[ISO-abbreviation] Br. J. Haematol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

   

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

[Title] Interleukin-23 acts as antitumor agent on childhood B-acute lymphoblastic leukemia cells.

The aim of this study was to investigate the potential direct antitumor activity of IL-23 in pediatric B-acute lymphoblastic leukemia (B-ALL) cells and to unravel the molecular mechanisms involved.

Here, we show, for the first time, that IL-23R is up-regulated in primary B-ALL cells, compared with normal early B lymphocytes, and that IL-23 dampens directly tumor growth in vitro and in vivo through the inhibition of tumor cell proliferation and induction of apoptosis.

The latter finding is related to IL-23-induced up-regulation of miR15a expression and the consequent down-regulation of BCL-2 protein expression in pediatric B-ALL cells.

[MeSH-major] Interleukin-23 Subunit p19 / immunology. Interleukin-23 Subunit p19 / pharmacology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology

[MeSH-minor] Animals. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Child. Child, Preschool. Female. Gene Expression / drug effects. Genes, bcl-2 / drug effects. Humans. In Vitro Techniques. Infant. Male. Mice. Mice, Inbred NOD. Mice, SCID. MicroRNAs / antagonists & inhibitors. MicroRNAs / genetics. Recombinant Proteins / genetics. Recombinant Proteins / immunology. Recombinant Proteins / pharmacology. Signal Transduction / immunology

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

[Email] Email this result item

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

(PMID = 20671120.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / IL23A protein, human; 0 / Interleukin-23 Subunit p19; 0 / MIRN15 microRNA, human; 0 / MicroRNAs; 0 / Recombinant Proteins

   

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

[Title] The role of hematopoietic stem cell transplantation with relapsed or primary refractory childhood B-cell non-Hodgkin lymphoma and mature B-cell leukemia: a retrospective analysis of enrolled cases in Japan.

BACKGROUND: There have been excellent treatment results for children with B-cell non-Hodgkin lymphoma (B-NHL) and mature B-cell leukemia (B-ALL) in the last few decades.

Among 18 patients who had a chemotherapy-sensitive disease, 4 of 5 patients who underwent hematopoietic stem cell transplantation (HSCT) during remission survived without progression, while 3 of 12 patients who did not receive HSCT were alive without disease progression.

[MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, B-Cell / therapy. Lymphoma, B-Cell / therapy

Genetic Alliance. consumer health - Hodgkin lymphoma.

Genetic Alliance. consumer health - Hodgkin lymphoma, childhood.

Genetic Alliance. consumer health - Non-Hodgkin lymphoma, childhood.

Genetic Alliance. consumer health - Transplantation.

[Email] Email this result item

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

(PMID = 18428432.001).

[ISSN] 1545-5017

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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

[Title] Characterisation of dic(9;20)(p11-13;q11) in childhood B-cell precursor acute lymphoblastic leukaemia by tiling resolution array-based comparative genomic hybridisation reveals clustered breakpoints at 9p13.2 and 20q11.2.

Although the dic(9;20)(p11-13;q11) is a recurrent chromosomal abnormality in paediatric B-cell precursor acute lymphoblastic leukaemia (BCP ALL), occurring in approximately 2% of the cases, its molecular genetic consequences have not been elucidated.

In the present study, high-resolution genome-wide array-based comparative genomic hybridisation (array-CGH) and fluorescence in situ hybridisation (FISH) were used to characterise the 9p and 20q breakpoints (BPs) in seven childhood BCP ALLs with dic(9;20), which was shown to be unbalanced in all of them, resulting in loss of 9p13.2-pter.

One of the ALLs, shown to have a complex dic(9;20), was further investigated by FISH, revealing a rearrangement of the haemapoietic cell kinase isoform p61 (HCK) gene at 20q11.

[Email] Email this result item

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

(PMID = 16999846.001).

[ISSN] 0007-1048

[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 / DNA, Neoplasm

   

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

[Title] Prognostic relevance of dic(9;20)(p11;q13) in childhood B-cell precursor acute lymphoblastic leukaemia treated with Berlin-Frankfurt-Münster (BFM) protocols containing an intensive induction and post-induction consolidation therapy.

The presence of a dicentric chromosome dic(9;20) has been reported to have an unfavourable prognosis in children with B-cell precursor acute lymphoblastic leukaemia (BCP-ALL).

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Chromosomes, Human, Pair 20 / genetics. Chromosomes, Human, Pair 9 / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

Hazardous Substances Data Bank. DAUNORUBICIN .

Hazardous Substances Data Bank. PREDNISONE .

[Email] Email this result item

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

(PMID = 20067563.001).

[ISSN] 1365-2141

[Journal-full-title] British journal of haematology

[ISO-abbreviation] Br. J. Haematol.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 5J49Q6B70F / Vincristine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; ZS7284E0ZP / Daunorubicin; PVDA protocol

   

[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

   

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

[Title] [Acute T cells lymphoblastic leukemia with a t(1;19)(q23;p13) and E2A-PBX1 in an adult: one case report and literature review].

OBJECTIVE: To report a case of T cell acute lymphoblastic leukemia (ALL) with t(1;19)(q23;pl3) and E2A-PBX1 fusion gene, which is a characteristic translocation of childhood B cell ALL (B-ALL).

The leukemic cells expressed T cell markers.

CONCLUSION: t(1;19)E2A-PBX1(+) can be implicated in adult T-ALL, besides childhood B-ALL.

[MeSH-major] Homeodomain Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

[Email] Email this result item

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

(PMID = 19954663.001).

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

[Publication-country] China

[Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Oncogene Proteins, Fusion; 146150-85-8 / E2A-Pbx1 fusion protein

   

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

[Title] [Prognostic significance of lymphocyte function associated anti-gen-3 (CD58) in childhood B cell-acute lymphocytic leukemia].

This study was aimed to investigate the value of CD58 in evaluation of early therapeutic effect on childhood B-ALL.

The expression features of CD58 in 135 cases of childhood B-ALL were analyzed by four-color flow cytometry; MRD detection protocol for B-ALL using CD58/CD10/CD34/CD19 combination was established; the correlation between the expression features of CD58 and MRD detection was analyzed for the early therapeutic response in childhood B-ALL.

The CD58 over expression may be considered as a marker of a favorable prognosis in childhood B-ALL.

[Email] Email this result item

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

(PMID = 16928307.001).

[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

[Publication-country] China

[Chemical-registry-number] 0 / Antigens, CD58; 0 / Biomarkers, Tumor

   

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

The human ETS family gene TEL2/ETV7 is highly homologous to TEL1/ETV6, a frequent target of chromosome translocations in human leukemia and specific solid tumors.

Although TEL2 is infrequently up-regulated in human sporadic Burkitt's lymphoma, analysis of pediatric B-cell acute lymphocytic leukemia (B-ALL) samples showed increased coexpression of TEL2 and MYC and/or MYCN in over one-third of B-ALL patients.

Therefore, TEL2 and MYC also appear to cooperate in provoking a cadre of human B-cell malignancies.

COS Scholar Universe. author profiles.

KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

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

[Cites] EMBO J. 1998 Sep 1;17(17):5001-14 [9724636.001]

[Cites] Genes Dev. 1998 Aug 1;12(15):2424-33 [9694806.001]

[Cites] Clin Cancer Res. 1997 Jul;3(7):1067-76 [9815785.001]

[Cites] Oncol Rep. 1999 Jul-Aug;6(4):859-63 [10373671.001]

[Cites] J Pathol. 1999 Mar;187(4):403-9 [10398098.001]

[Cites] J Biol Chem. 1999 Oct 15;274(42):30132-8 [10514502.001]

[Cites] Genes Dev. 1999 Oct 15;13(20):2658-69 [10541552.001]

[Cites] Genes Dev. 1999 Oct 15;13(20):2670-7 [10541553.001]

[Cites] Biochem Biophys Res Commun. 1999 Nov 2;264(3):871-7 [10544023.001]

[Cites] Blood. 2000 Jun 1;95(11):3341-8 [10828014.001]

[Cites] Neoplasia. 1999 Dec;1(6):526-36 [10935500.001]

[Cites] Oncogene. 2000 Sep 28;19(41):4802-6 [11032031.001]

[Cites] Oncogene. 2000 Dec 18;19(55):6524-32 [11175368.001]

[Cites] J Biol Chem. 2001 Mar 23;276(12):9421-36 [11108721.001]

[Cites] Histol Histopathol. 2001 Apr;16(2):595-601 [11332715.001]

[Cites] Mol Cell Biol. 2001 Aug;21(15):5063-70 [11438662.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Aug 14;98(17):9654-9 [11481442.001]

[Cites] J Mol Med (Berl). 2002 Mar;80(3):137-46 [11894140.001]

[Cites] Cancer Cell. 2002 Nov;2(5):367-76 [12450792.001]

[Cites] Blood. 2003 Feb 15;101(4):1220-35 [12393483.001]

[Cites] Gene. 2003 Jan 16;303:11-34 [12559563.001]

[Cites] Mol Cell. 2003 Apr;11(4):905-14 [12718877.001]

[Cites] Cold Spring Harb Symp Quant Biol. 2000;65:499-510 [12760067.001]

[Cites] J Biol Chem. 2003 Nov 21;278(47):46378-86 [12960174.001]

[Cites] Cancer Res. 2004 Sep 1;64(17):6091-100 [15342392.001]

[Cites] Science. 1983 Oct 28;222(4622):390-3 [6414084.001]

[Cites] Nature. 1984 Jan 26-Feb 1;307(5949):334-40 [6420706.001]

[Cites] Nature. 1985 Dec 12-18;318(6046):533-8 [3906410.001]

[Cites] Cell. 1986 Oct 10;47(1):11-8 [3093082.001]

[Cites] Mol Cell Biol. 1987 Apr;7(4):1436-44 [3037318.001]

[Cites] Nature. 1990 Nov 22;348(6299):331-3 [2250704.001]

[Cites] Curr Top Microbiol Immunol. 1992;182:37-43 [1490376.001]

[Cites] Nature. 1994 Nov 10;372(6502):143-9 [7969446.001]

[Cites] Oncogene. 1995 May 4;10(9):1717-23 [7753548.001]

[Cites] Mol Cell Biol. 1995 Jul;15(7):3840-7 [7791791.001]

[Cites] Blood. 1995 Dec 1;86(11):4263-9 [7492786.001]

[Cites] J Exp Med. 1996 Feb 1;183(2):381-91 [8627151.001]

[Cites] Blood. 1996 Apr 1;87(7):2891-9 [8639909.001]

[Cites] Curr Top Microbiol Immunol. 1997;220:67-79 [9103676.001]

[Cites] Nat Genet. 1997 Apr;15 Spec No:417-74 [9140409.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Jul 8;94(14):7245-50 [9207076.001]

[Cites] Oncogene. 1997 Jul 10;15(2):203-11 [9244355.001]

[Cites] EMBO J. 1997 Jul 16;16(14):4374-83 [9250681.001]

[Cites] Blood. 1997 Sep 1;90(5):1777-86 [9292510.001]

[Cites] Cell. 1997 Nov 28;91(5):649-59 [9393858.001]

[Cites] Biochim Biophys Acta. 1998 Apr 17;1377(2):F1-11 [9606973.001]

[Cites] Genes Dev. 1998 Aug 1;12(15):2392-402 [9694803.001]

[Cites] Nature. 1998 Sep 10;395(6698):124-5 [9744267.001]

(PMID = 15743832.001).

[ISSN] 0270-7306

[Journal-full-title] Molecular and cellular biology

[ISO-abbreviation] Mol. Cell. Biol.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA076379; United States / NCI NIH HHS / CA / R01 CA76379-07; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01-CA72999-08

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

[Publication-country] United States

[Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / ETV7 protein, human; 0 / Proto-Oncogene Proteins c-ets; 0 / Proto-Oncogene Proteins c-myc; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53

[Other-IDs] NLM/ PMC1061619

   

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

[Title] A primitive cell origin for B-cell precursor ALL?

A stem cell origin has been described for both acute and chronic myelogenous leukemias.

In contrast, childhood B-cell precursor acute lymphoblastic leukemia (ALL) is thought to arise in committed B-lineage cells.

Evidence suggests that some subtypes of childhood ALL have a primitive cell origin and share many immunophenotypic characteristics with normal progenitor cells.

These leukemic stem cells may be resistant to current therapeutic strategies designed to kill the bulk ALL cell population and subsequent relapses may arise from this population.

[MeSH-major] Antigens, Neoplasm / immunology. Biomarkers, Tumor / immunology. Burkitt Lymphoma / immunology. Gene Expression Regulation, Leukemic / immunology. Neoplastic Stem Cells / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

[MeSH-minor] Animals. B-Lymphocytes / immunology. B-Lymphocytes / pathology. Cell Proliferation. Humans. Recurrence

[Email] Email this result item

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

(PMID = 17142855.001).

[ISSN] 1550-8943

[Journal-full-title] Stem cell reviews

[ISO-abbreviation] Stem Cell Rev

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

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

[Number-of-references] 54

   

[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.

In comparison with that of B cell ALL (B-ALL), the percentages of age older than 10 years, initial WBC count more than 50 x 10(9)/ L, prednisone poor response (PPR), and failed to achieve remission at day 19 of induction chemotherapy in the T-ALLs were all higher.

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

   

[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

   

[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.

A quantitative PCR assay for ZAP-70 expression was established and ZAP-70 expression in a range of human B cell lines was compared with expression in the Jurkat T cell line.

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 not detected in mature B cell lines but was detected in pre-B cell lines at a level comparable to that seen in T cells.

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.

ZAP-70 expression may hold prognostic value for pre-B ALL and raises the prospect of a novel therapeutic target.

[MeSH-major] B-Lymphocytes / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cells, B-Lymphoid / metabolism. ZAP-70 Protein-Tyrosine Kinase / metabolism

[MeSH-minor] Adolescent. Blotting, Western. Bone Marrow Cells / metabolism. Cell Line, Transformed. Cell Line, Tumor. Child. Child, Preschool. Female. Flow Cytometry. Gene Expression. Humans. Jurkat Cells. Male. Polymerase Chain Reaction

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

   

[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.

Chromosomal translocations involving the immunoglobulin heavy chain (IGH) locus are common abnormalities in mature B-cell neoplasms.

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

   

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

[Title] Rituximab combined with CHOP for successful treatment of aggressive recurrent, pediatric B-cell large cell non-Hodgkin's lymphoma.

This report is the first to describe the successful treatment of a 14-year-old boy with aggressive recurrent, CD20-positive, B-cell large cell non-Hodgkin's lymphoma.

Rituximab and CHOP in addition to chemotherapy may be an alternative treatment for aggressive recurrent, pediatric CD20-positive B-cell large cell non-Hodgkin's lymphoma if highly intensive chemotherapy and stem cell transplantation are not available.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, B-Cell / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy. Neoplasm Recurrence, Local / drug therapy

Genetic Alliance. consumer health - Lymphoma, large-cell.

Hazardous Substances Data Bank. RITUXIMAB .

Hazardous Substances Data Bank. DOXORUBICIN .

Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

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 = 15838396.001).

[ISSN] 1077-4114

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

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

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol

   

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

[Title] Aberrant expression of B203.13 antigen in acute lymphoid leukemia of B-cell origin.

The B203.13 monoclonal antibody was developed by immunizing mice with the B/monocyte biphenotypic cell line B1b.

We tested this antibody as a marker of childhood B-acute lymphoblastic leukemia (B-ALL).

The CD10(+)/B203.13(+) phenotype was specific to B-ALL, since CD10(+)/CD20(+) cells from common acute lymphoblastic leukemia (c-ALL) did not express B203.13.

We concluded that the use of B203.13 in association with CD10 and CD20 provides meaningful information for distinguishing normal residual B-cells from leukemic B-lymphoblasts and that recurrence of a CD10(+)/B203.13(+) phenotype after transplantation may be a very early relapse indicator of early B-acute lymphoblastic leukemia.

[MeSH-major] Antigens, Neoplasm / biosynthesis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

[Email] Email this result item

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

(PMID = 18636158.001).

[ISSN] 1019-6439

[Journal-full-title] International journal of oncology

[ISO-abbreviation] Int. J. Oncol.

[Language] eng

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

[Publication-country] Greece

[Chemical-registry-number] 0 / Antigens, CD20; 0 / Antigens, Neoplasm; EC 3.4.24.11 / Neprilysin

   

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

[Title] High hyperdiploid childhood acute lymphoblastic leukemia.

High hyperdiploidy (51-67 chromosomes) is the most common cytogenetic abnormality pattern in childhood B-cell precursor acute lymphoblastic leukemia (ALL), occurring in 25-30% of such cases.

Despite the high frequency of this karyotypic subgroup, many questions remain regarding the epidemiology, etiology, presence of other genetic changes, the time and cell of origin, and the formation and pathogenetic consequences of high hyperdiploidy.

However, during the last few years, several studies have addressed some of these important issues, and these, as well as previous reports on high hyperdiploid childhood ALL, are reviewed herein.

[MeSH-major] Chromosome Aberrations. Diploidy. Precursor Cell Lymphoblastic Leukemia-Lymphoma

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 = 19415723.001).

[ISSN] 1098-2264

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

[ISO-abbreviation] Genes Chromosomes Cancer

[Language] eng

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

[Publication-country] United States

[Number-of-references] 195

   

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

[Title] CD20 up-regulation in pediatric B-cell precursor acute lymphoblastic leukemia during induction treatment: setting the stage for anti-CD20 directed immunotherapy.

CD20 is expressed in approximately one- half of pediatric acute lymphoblastic leukemia (ALL) cases with B-cell precursor (BCP) origin.

To understand the impact of this on the potential effectiveness of anti-CD20 immunotherapy, we studied 237 CD10(+) pediatric BCP-ALL patients with Berlin-Frankfurt-Munster (BFM)-type therapy.

[MeSH-major] Antibodies, Monoclonal / administration & dosage. Antigens, CD20 / biosynthesis. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Gene Expression Regulation, Leukemic / drug effects. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

Hazardous Substances Data Bank. RITUXIMAB .

Hazardous Substances Data Bank. DAUNORUBICIN .

Hazardous Substances Data Bank. PREDNISONE .

[Email] Email this result item

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

[Cites] Ann Oncol. 1998 Sep;9(9):995-1001 [9818074.001]

[Cites] Exp Hematol. 1998 Apr;26(4):305-13 [9546313.001]

[Cites] Leuk Res. 2005 Jun;29(6):679-83 [15863209.001]

[Cites] J Immunol. 2005 Jun 15;174(12):7859-68 [15944291.001]

[Cites] Eur J Immunol. 2005 Jul;35(7):2175-83 [15971270.001]

[Cites] Clin Cancer Res. 2005 Aug 15;11(16):5971-80 [16115941.001]

[Cites] Cytometry B Clin Cytom. 2005 Nov;68(1):18-24 [16184615.001]

[Cites] Haematologica. 2005 Nov;90 Suppl:ECR24 [16266915.001]

[Cites] Haematologica. 2006 Feb;91(2):272-3 [16461321.001]

[Cites] Haematologica. 2006 Mar;91(3):322-30 [16531255.001]

[Cites] Cancer. 2006 Jun 15;106(12):2645-51 [16688777.001]

[Cites] Best Pract Res Clin Haematol. 2006;19(4):701-13 [16997178.001]

[Cites] Blood. 2006 Nov 15;108(10):3302-4 [16896151.001]

[Cites] Clin Cancer Res. 2006 Dec 1;12(23):7174-9 [17145843.001]

[Cites] Leukemia. 2007 May;21(5):897-905 [17330098.001]

[Cites] Br J Haematol. 2007 Oct;139(2):344-5 [17897313.001]

[Cites] Pediatr Blood Cancer. 2008 Feb;50(2):372-5 [17973316.001]

[Cites] Leukemia. 2008 Apr;22(4):771-82 [18239620.001]

[Cites] Cytometry B Clin Cytom. 2008 May;74(3):150-5 [18271020.001]

[Cites] Blood. 2008 Jun 15;111(12):5477-85 [18388178.001]

[Cites] Leukemia. 2000 Jul;14(7):1225-31 [10914546.001]

[Cites] Oncologist. 2000;5(5):376-84 [11040273.001]

[Cites] Blood. 2001 Dec 1;98(12):3383-9 [11719378.001]

[Cites] Cancer Immunol Immunother. 2002 Mar;51(1):15-24 [11845256.001]

[Cites] Blood. 2002 Mar 15;99(6):1952-8 [11877265.001]

[Cites] Haematologica. 2002 Sep;87(9):918-25 [12217803.001]

[Cites] Blood. 2003 Feb 1;101(3):1045-52 [12393541.001]

[Cites] Br J Haematol. 2003 Mar;120(5):846-9 [12614220.001]

[Cites] Blood. 2003 May 1;101(9):3413-5 [12522009.001]

[Cites] Haematologica. 2003 Nov;88(11):1245-52 [14607753.001]

[Cites] Leukemia. 2004 Apr;18(4):676-84 [14961035.001]

[Cites] Lancet Oncol. 2004 May;5(5):292-302 [15120666.001]

[Cites] Blood. 1997 Jun 1;89(11):3960-6 [9166833.001]

[Cites] Leukemia. 1997 Aug;11(8):1266-73 [9264380.001]

[Cites] Leukemia. 2005 Jan;19(1):49-56 [15538405.001]

(PMID = 18780832.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Databank-accession-numbers] ClinicalTrials.gov/ NCT00430118

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; ZS7284E0ZP / Daunorubicin; PVDA protocol

[Other-IDs] NLM/ PMC2581996

   

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

[Title] Implications of infectious diseases and the adrenal hypothesis for the etiology of childhood acute lymphoblastic leukemia.

Acute leukemia is the most frequent cancer in children.

Recently, a new hypothesis was proposed for the pathogenesis of childhood acute lymphoblastic leukemia (ALL).

The so-called 'adrenal hypothesis' emphasized the role of endogenous cortisol in the etiology of B-cell precursor ALL.

The adrenal hypothesis proposes that the risk of childhood B-cell precursor ALL is reduced when early childhood infections induce qualitative and quantitative changes in the hypothalamus-pituitary-adrenal axis.

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

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

Genetic Alliance. consumer health - Adrenal Diseases.

MedlinePlus Health Information. consumer health - Infectious Diseases.

[Email] Email this result item

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

(PMID = 20401428.001).

[ISSN] 1414-431X

[Journal-full-title] Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas

[ISO-abbreviation] Braz. J. Med. Biol. Res.

[Language] ENG

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

[Publication-country] Brazil

[Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone

   

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

[Title] Chemo-sensitivity in a panel of B-cell precursor acute lymphoblastic leukemia cell lines, YCUB series, derived from children.

Sensitivity to 10 anticancer drugs was evaluated in 6 childhood B-cell precursor acute lymphoblastic leukemia (BCP-ALL) cell lines.

Authenticity of newly established cell lines was confirmed by genomic fingerprinting.

This cell line panel offers an in vitro model for the development of new therapies for childhood BCP-ALL.

[MeSH-major] B-Lymphocytes / pathology. DNA Fingerprinting / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

[MeSH-minor] Antineoplastic Agents / therapeutic use. Cell Division / drug effects. Cell Line, Tumor / drug effects. Cell Survival / drug effects. Child. Child, Preschool. Flow Cytometry. Humans. Immunophenotyping. Leukocyte Count. Male. Prednisolone / pharmacology

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

Cellosaurus - a cell line knowledge resource. culture/stock collections - Cell lines described in this publication .

[Email] Email this result item

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

(PMID = 19157546.001).

[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 / Antineoplastic Agents; 9PHQ9Y1OLM / Prednisolone

   

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

[Title] Clinical characteristics and treatment results of pediatric B-cell non-Hodgkin lymphoma patients in a single center.

The aim of this study was to evaluate and compare the clinical characteristics of the B-cell non-Hodgkin lymphoma (NHL) patients and therapeutic efficacy of modified NHL BFM-90 and NHL BFM-95 protocols in the authors' center.

Forty-five patients were treated with modified B-cell BFM-90 and 16 patients were treated with B-cell BFM-95 regimens.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, B-Cell / drug therapy

Genetic Alliance. consumer health - Hodgkin lymphoma.

Genetic Alliance. consumer health - Non-Hodgkin Lymphoma.

Hazardous Substances Data Bank. SODIUM BICARBONATE .

Hazardous Substances Data Bank. Allopurinol .

Hazardous Substances Data Bank. VINCRISTINE .

Hazardous Substances Data Bank. LEUCOVORIN .

[Email] Email this result item

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

(PMID = 17710659.001).

[ISSN] 1521-0669

[Journal-full-title] Pediatric hematology and oncology

[ISO-abbreviation] Pediatr Hematol Oncol

[Language] eng

[Publication-type] Evaluation Studies; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Diuretics; 0 / Neoplasm Proteins; 5J49Q6B70F / Vincristine; 63CZ7GJN5I / Allopurinol; 8MDF5V39QO / Sodium Bicarbonate; EC 1.1.1.27 / L-Lactate Dehydrogenase; Q573I9DVLP / Leucovorin; YL5FZ2Y5U1 / Methotrexate

   

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

Monoclonal antibodies have provided new promise for patients with B-cell malignancies.

Rituximab is a monoclonal antibody against B-lymphocytes that express CD20; it is used for the treatment of patients with relapsed or refractory B-cell non-Hodgkin lymphoma.

In this article, we reported three children with primary refractory/relapsed B-cell-non-Hodgkin lymphoma, who were successfully treated with a combination of intensive chemotherapy protocol plus rituximab.

Our aim is to emphasize the importance of use of rituximab in the treatment of childhood B-cell non-Hodgkin lymphoma.

[Email] Email this result item

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

(PMID = 20859698.001).

[ISSN] 1776-260X

[Journal-full-title] Targeted oncology

[ISO-abbreviation] Target Oncol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] France

[Chemical-registry-number] 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab

   

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

[Title] Disruption of ETV6 in intron 2 results in upregulatory and insertional events in childhood acute lymphoblastic leukaemia.

We describe four cases of childhood B-cell progenitor acute lymphoblastic leukaemia (BCP-ALL) and one of T-cell (T-ALL) with unexpected numbers of interphase signals for ETV6 with an ETV6-RUNX1 fusion probe.

Fluorescence in situ hybridisation (FISH), array comparative genomic hybridization (aCGH) and Molecular Copy-Number Counting (MCC) results were concordant for the T-cell case.

[MeSH-major] Chromosome Aberrations. Introns / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor 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

(PMID = 17972957.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / Homeodomain Proteins; 0 / Proto-Oncogene Proteins c-ets; 0 / RUNX1 protein, human; 0 / Repressor Proteins; 0 / TLX3 protein, human

   

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

[Title] Potentiating effects of RAD001 (Everolimus) on vincristine therapy in childhood acute lymphoblastic leukemia.

Despite advances in the treatment of acute lymphoblastic leukemia (ALL), the majority of children who relapse still die of ALL.

We investigated the effects of the mammalian target of rapamycin inhibitor, RAD001 (Everolimus), in a nonobese diabetic/severe combined immunodeficiency model of human childhood B-cell progenitor ALL.

RAD001 induced a cell-cycle arrest in the G(0/1) phase with associated dephosphorylation of the retinoblastoma protein, and reduced levels of cyclin-dependent kinases 4 and 6.

In conclusion, we have demonstrated activity of RAD001 in an in vivo leukemia model supporting further clinical development of target of rapamycin inhibitors for the treatment of patients with ALL.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Sirolimus / analogs & derivatives. Vincristine / administration & dosage

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

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

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. SIROLIMUS .

Hazardous Substances Data Bank. VINCRISTINE .

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

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

[Email] Email this result item

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

(PMID = 19196656.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Placebos; 5J49Q6B70F / Vincristine; 9HW64Q8G6G / Everolimus; W36ZG6FT64 / Sirolimus

   

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

[Title] Clinical characteristics and outcome analysis of pediatric B-cell non-Hodgkin's lymphoma. Experience with FAB-LMB 96 and UKCCSG B-cell NHL guidelines in a developing country.

AIM: To analyze the clinical characteristics of B-cell non-Hodgkin's lymphoma (NHL) patients and the therapeutic efficacy of French-American-British Lymphoma Malins de Burkitt 96 and the recent United Kingdom Children's Cancer Study Group B-cell NHL guidelines in the tertiary care hospital of a developing country.

METHODS: Patients aged < or =18 years registered at our hospital between January 1995 and December 2006 with histologically proved B-Cell NHL were selected for retrospective analysis.

Of these 95 had Burkitt's lymphoma, 22 diffuse large B-cell lymphoma and five had B-cell NHL not otherwise specified.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / mortality. Practice Guidelines as Topic

[Email] Email this result item

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

(PMID = 20398038.001).

[ISSN] 1743-7563

[Journal-full-title] Asia-Pacific journal of clinical oncology

[ISO-abbreviation] Asia Pac J Clin Oncol

[Language] eng

[Publication-type] Journal Article

[Publication-country] Australia

   

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

[Title] The presence of TEL/AML1 rearrangement and cryptic deletion of the TEL gene in adult acute lymphoblastic leukemia (ALL).

TEL/AML1 (also known as ETV6/RUNX1) rearrangement is the most frequent genetic change in childhood B-acute lymphoblastic leukemia (ALL) and is associated with a favorable prognosis.

TEL/AML1 rearrangement is not unique in childhood ALL, and cryptic TEL deletion without TEL/AML1 rearrangement was more frequent than the TEL/AML1 rearrangement in adult ALL.

[MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Deletion. Gene Rearrangement. Oncogene Proteins, Fusion / genetics. Precursor 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

(PMID = 16213368.001).

[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 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins; 0 / TEL-AML1 fusion protein

   

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

[Title] Cytogenetic patterns in ETV6/RUNX1-positive pediatric B-cell precursor acute lymphoblastic leukemia: A Nordic series of 245 cases and review of the literature.

Between 1992 and 2004, 1,140 children (1 to<15 years) were diagnosed with B-cell precursor acute lymphoblastic leukemia (ALL) in the Nordic countries.

[MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. DNA-Binding Proteins / genetics. Leukemia, Lymphoid / genetics. Transcription Factors / genetics

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

MedlinePlus Health Information. consumer health - Chronic Lymphocytic Leukemia.

[Email] Email this result item

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

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

(PMID = 17285576.001).

[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 / DNA-Binding Proteins; 0 / ETV1 protein, human; 0 / RUNX1 protein, human; 0 / Transcription Factors

   

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

[Title] A complex rearrangement involving cryptic deletion of ETV6 and CDKN1B genes in a case of childhood acute lymphoblastic leukemia.

We report on a case of childhood B-cell lineage acute lymphoblastic leukemia (ALL).

The deleted segment on 12p contains several genes, among the tumor suppressor genes ETV6 and CDKN1B, which are frequently involved in 12p abnormalities in childhood ALL.

Thus, the present study documents the loss of both ETV6 and CDKN1B genes accompanying the occurrence of a complex rearrangement involving chromosomes 3 and 12 in a case of childhood ALL.

[MeSH-major] Gene Deletion. Intracellular Signaling Peptides and Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

[Email] Email this result item

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

[ErratumIn] Cancer Genet Cytogenet. 2010 Apr 1;198(1):76

(PMID = 19963112.001).

[ISSN] 1873-4456

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / CDKN1B protein, human; 0 / ETS translocation variant 6 protein; 0 / Intracellular Signaling Peptides and Proteins; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27

   

[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

[MeSH-minor] Antigens, CD1d. B-Lymphocytes / cytology. Biomarkers, Tumor / metabolism. Cell Communication. Cell Line. Child. Galactosylceramides / metabolism. Humans. Infant. Killer Cells, Natural / cytology. Killer Cells, Natural / metabolism. Predictive Value of Tests. Prognosis. Survival Rate

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

   

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

[Title] Strong association of the HLA-DP6 supertype with childhood leukaemia is due to a single allele, DPB1*0601.

We previously reported that susceptibility to childhood B cell precursor ALL (BCP ALL) is associated with HLA-DPB1 alleles having glutamic acid (E) rather than lysine (K) in the P4 antigenic peptide-binding pocket.

Here, we report that only one of seven alleles with the DP6 supertype (DPB1(*)0601) is associated with childhood leukaemia (leukaemia vs controls: odds ratio, 95% confidence interval [OR, CI]: 4.6, 2.0-10.4; corrected P=0.019), but not with childhood solid tumours or lymphomas.

DPB1(*)0601 is also significantly associated with leukaemia subtypes, including BCP ALL, Pro-B ALL, T-ALL and AML.

Sequencing the coding region of DPB1(*)0601 revealed an exon 1-4 haplotype [T-DEAV-KIL-RVI] shared with DPB1(*)0301 and 0901, but no evidence of germline mutations in childhood leukaemia.

These results suggest that the DPbeta0601 molecule may be functionally involved in childhood leukaemia.

Analysis of peptide binding and T-cell activation by DPbeta0601-peptide complexes should help determine its role in childhood leukaemia causation.

[MeSH-major] HLA-DP Antigens / genetics. Haplotypes / genetics. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

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

(PMID = 19148140.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Grant] United Kingdom / Cancer Research UK / /

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

[Publication-country] England

[Chemical-registry-number] 0 / HLA-DP Antigens; 0 / HLA-DP beta-Chains; 0 / HLA-DPB1 antigen

   

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

[Title] HLA-DPB1 supertype-associated protection from childhood leukaemia: relationship to leukaemia karyotype and implications for prevention.

Most childhood B cell precursor (BCP) acute lymphoblastic leukaemia (ALL) cases carry the reciprocal translocation t(12;21)(p13;q22) ( approximately 25%), or a high hyperdiploid (HeH) karyotype (30%).

Based on our previous analysis of HLA-DP in childhood ALL, and evidence from in vitro studies that TEL-AML1 can activate HLA-DP-restricted T cell responses, we hypothesised that the development of TEL-AML1+ ALL might be influenced by the child's DPB1 genotype.

To test this, we analysed the frequency of six HLA-DPB1 supertypes in a population-based series of childhood leukaemias (n = 776) classified by their karyotype (TEL-AML1+, HeH and others), in comparison with newborn controls (n = 864).

[MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Genetic Predisposition to Disease. HLA-DP Antigens / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / prevention & control

[Email] Email this result item

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

(PMID = 17622527.001).

[ISSN] 0340-7004

[Journal-full-title] Cancer immunology, immunotherapy : CII

[ISO-abbreviation] Cancer Immunol. Immunother.

[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 / HLA-DP Antigens; 0 / HLA-DP beta-Chains; 0 / HLA-DPB1 antigen; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein

   

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

[Title] Clinical and cytogenetic features of pediatric dic(9;20)(p13.2;q11.2)-positive B-cell precursor acute lymphoblastic leukemias: a Nordic series of 24 cases and review of the literature.

Although dic(9;20)(p13.2;q11.2) is a characteristic abnormality in childhood B-cell precursor acute lymphoblastic leukemias (BCP ALL), little is known about its clinical impact or the type and frequency of additional aberrations it may occur together with.

We here review the clinical and cytogenetic features of a Nordic pediatric series of 24 patients with dic(9;20)-positive BCP ALL diagnosed 1996-2006, constituting 1.3% of the BCP ALL, as well as 47 childhood cases from the literature.

Consistent immunophenotypic features of the Nordic cases included positivity for HLA-DR, CD10, CD19, CD20, and CD22 and negativity for T-cell and myeloid markers; no detailed immunophenotypes were reported for the previously published cases.

The median patient age was 3 years, the female/male ratio was 2.0, the median white blood cell count was 24 x 10(9)/l, 11% had central nervous system involvement, and 5% had a mediastinal mass at diagnosis.

[MeSH-major] Chromosomes, Human, Pair 20 / genetics. Chromosomes, Human, Pair 9 / genetics. Cytogenetics. Leukemia, B-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

COS Scholar Universe. author profiles.

[Email] Email this result item

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

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

(PMID = 17990329.001).

[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; Review

[Publication-country] United States

[Number-of-references] 38