[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 182
1. Tomblyn MB, Arora M, Baker KS, Blazar BR, Brunstein CG, Burns LJ, DeFor TE, Dusenbery KE, Kaufman DS, Kersey JH, MacMillan ML, McGlave PB, Miller JS, Orchard PJ, Slungaard A, Tomblyn MR, Vercellotti GM, Verneris MR, Wagner JE, Weisdorf DJ: Myeloablative hematopoietic cell transplantation for acute lymphoblastic leukemia: analysis of graft sources and long-term outcome. J Clin Oncol; 2009 Aug 1;27(22):3634-41
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myeloablative hematopoietic cell transplantation for acute lymphoblastic leukemia: analysis of graft sources and long-term outcome.
  • PURPOSE: Analysis of hematopoietic cell transplantation (HCT) for high-risk or recurrent acute lymphoblastic leukemia (ALL) using different donor sources is confounded by variable conditioning and supportive care.
  • RESULTS: After median of 8.3 years of follow-up, 5-year overall survival (OS), leukemia-free survival (LFS), and relapse were 29% (95% CI, 26% to 32%), 26% (95% CI, 23% to 29%), and 43% (95% CI, 39% to 47%), respectively.
  • Acute graft-versus-host disease was associated with fewer relapses.
  • [MeSH-major] Graft vs Host Disease / diagnosis. Hematopoietic Stem Cell Transplantation / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / surgery. Transplantation Conditioning

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Transplantation.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Bone Marrow Transplant. 1997 May;19(10):963-8 [9169639.001]
  • [Cites] Biol Blood Marrow Transplant. 2002;8(4):213-20 [12014810.001]
  • [Cites] Blood. 2004 Nov 15;104(10):3028-37 [15256423.001]
  • [Cites] Blood. 2005 Feb 1;105(3):1343-7 [15466923.001]
  • [Cites] Biol Blood Marrow Transplant. 2005 Feb;11(2):149-60 [15682076.001]
  • [Cites] Eur J Cancer Care (Engl). 2005 Mar;14(1):53-62 [15698386.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1611-8 [12176879.001]
  • [Cites] J Clin Oncol. 2004 Jul 15;22(14):2816-25 [15254049.001]
  • [Cites] J Clin Oncol. 2004 Oct 15;22(20):4075-86 [15353542.001]
  • [Cites] N Engl J Med. 1987 Aug 20;317(8):461-7 [3302708.001]
  • [Cites] J Clin Oncol. 1987 Sep;5(9):1348-55 [3305794.001]
  • [Cites] Bone Marrow Transplant. 1990 Feb;5(2):83-9 [2107007.001]
  • [Cites] Bone Marrow Transplant. 1990 Jul;6(1):9-16 [2202462.001]
  • [Cites] Blood. 1991 Oct 15;78(8):1923-7 [1912575.001]
  • [Cites] Br J Haematol. 1994 Jan;86(1):62-9 [8011550.001]
  • [Cites] Br J Haematol. 1994 Sep;88(1):72-8 [7803259.001]
  • [Cites] Blood. 1995 Aug 15;86(4):1619-28 [7632972.001]
  • [Cites] Ann Intern Med. 1995 Sep 15;123(6):428-31 [7639442.001]
  • [Cites] Biol Blood Marrow Transplant. 2008 Jul;14(7):748-58 [18541193.001]
  • [Cites] Blood. 2008 Jul 15;112(2):426-34 [18398065.001]
  • [Cites] Br J Haematol. 1998 Apr;101(1):94-103 [9576189.001]
  • [Cites] Blood. 1997 Oct 15;90(8):2962-8 [9376576.001]
  • [Cites] Blood. 2006 Feb 1;107(3):1116-23 [16195338.001]
  • [Cites] Cancer. 2006 Jun 15;106(12):2657-63 [16703597.001]
  • [Cites] Blood. 2008 Feb 15;111(4):1827-33 [18048644.001]
  • [Cites] Bone Marrow Transplant. 2008 Apr;41(7):635-42 [18084335.001]
  • [Cites] Crit Rev Oncol Hematol. 2000 Oct;36(1):49-58 [10996522.001]
  • [Cites] Blood. 2001 Mar 15;97(6):1572-7 [11238093.001]
  • [Cites] Blood. 2001 May 15;97(10):2957-61 [11342417.001]
  • [Cites] Bone Marrow Transplant. 1998 Aug;22(3):253-7 [9720738.001]
  • (PMID = 19581540.001).
  • [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] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2720079
  •  go-up   go-down


2. Nowak NJ, Sait SN, Zeidan A, Deeb G, Gaile D, Liu S, Ford L, Wallace PK, Wang ES, Wetzler M: Recurrent deletion of 9q34 in adult normal karyotype precursor B-cell acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2010 May;199(1):15-20
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent deletion of 9q34 in adult normal karyotype precursor B-cell acute lymphoblastic leukemia.
  • The prognosis of adult normal karyotype (NK) precursor B-cell acute lymphoblastic leukemia (B-ALL) has not improved over the last decade, mainly because separation into distinct molecular subsets has been lacking and no targeted treatments are available.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • [Cites] Mol Biol Cell. 2000 Oct;11(10):3381-96 [11029043.001]
  • [Cites] J Hematol Oncol. 2009;2:3 [19166587.001]
  • [Cites] Nat Genet. 2001 Nov;29(3):263-4 [11687795.001]
  • [Cites] Blood. 2002 Jan 1;99(1):252-7 [11756179.001]
  • [Cites] Eur J Haematol. 2003 Jun;70(6):363-72 [12756018.001]
  • [Cites] Int Immunol. 2004 Oct;16(10):1377-89 [15302850.001]
  • [Cites] Nat Genet. 2004 Oct;36(10):1084-9 [15361874.001]
  • [Cites] Blood. 1995 Apr 15;85(8):2025-37 [7718875.001]
  • [Cites] Haematologica. 2007 Feb;92(2):232-5 [17296573.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1258-66 [17443227.001]
  • [Cites] Genet Med. 2007 Sep;9(9):585-95 [17873646.001]
  • [Cites] Br J Haematol. 2008 Mar;140(5):572-7 [18275435.001]
  • [Cites] Lancet. 2008 Mar 22;371(9617):1030-43 [18358930.001]
  • [Cites] Curr Protoc Hum Genet. 2005 Aug;Chapter 4:Unit 4.13 [18428377.001]
  • [Cites] Blood. 2008 May 1;111(9):4668-80 [18299449.001]
  • [Cites] Leuk Res. 2008 Aug;32(8):1228-35 [18328560.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 May 6;105(18):6708-13 [18458336.001]
  • [Cites] Curr Opin Hematol. 2008 Jul;15(4):400-7 [18536580.001]
  • [Cites] Best Pract Res Clin Haematol. 2001 Sep;14(3):593-607 [11640871.001]
  • (PMID = 20417863.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016056; None / None / / P30 CA016056-33; United States / NCI NIH HHS / CA / CA16056; United States / NCI NIH HHS / CA / P30 CA016056-33
  • [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 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Homeodomain Proteins; 157907-48-7 / HoxA protein
  • [Other-IDs] NLM/ NIHMS173834; NLM/ PMC2862995
  •  go-up   go-down


3. Brugnoletti F, Morris EB, Laningham FH, Patay Z, Pauley JL, Pui CH, Jeha S, Inaba H: Recurrent intrathecal methotrexate induced neurotoxicity in an adolescent with acute lymphoblastic leukemia: Serial clinical and radiologic findings. Pediatr Blood Cancer; 2009 Feb;52(2):293-5
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent intrathecal methotrexate induced neurotoxicity in an adolescent with acute lymphoblastic leukemia: Serial clinical and radiologic findings.
  • Systemic and intrathecal methotrexate (MTX) are integral components of acute lymphoblastic leukemia (ALL) therapy, but can be associated with neurotoxicity.
  • We describe here the case of an adolescent male with T-cell ALL who developed recurrent episodes of subacute neurotoxicity characterized by slurred speech, emotional lability, and hemiparesis after intrathecal MTX administration.
  • Serial magnetic resonance imaging with diffusion-weighted imaging showed recurrent areas of restricted diffusion within cerebral hemispheric white matter, which correlated chronologically with the administration of intrathecal therapy and severity of clinical symptoms.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • [Cites] J Natl Cancer Inst. 1992 Feb 19;84(4):252-6 [1734087.001]
  • [Cites] J Clin Oncol. 1986 Dec;4(12):1845-50 [3465876.001]
  • [Cites] Cancer. 1985 Sep 15;56(6):1356-60 [3875390.001]
  • [Cites] Radiology. 2003 Dec;229(3):659-69 [14576448.001]
  • [Cites] Radiology. 2000 Nov;217(2):331-45 [11058626.001]
  • [Cites] J Child Neurol. 2000 Sep;15(9):573-80 [11019787.001]
  • [Cites] Lancet Oncol. 2008 Mar;9(3):257-68 [18308251.001]
  • [Cites] AJNR Am J Neuroradiol. 2004 Nov-Dec;25(10):1688-95 [15569732.001]
  • [Cites] Ann Oncol. 2008 Jan;19(1):178-84 [17947226.001]
  • [Cites] Blood. 1949 Feb;4(2):160-7 [18107667.001]
  • [Cites] Leuk Lymphoma. 2007 Sep;48(9):1672-3 [17786701.001]
  • [Cites] Leukemia. 2007 Feb;21(2):238-47 [17170721.001]
  • [Cites] J Clin Oncol. 2006 Jul 1;24(19):3142-9 [16809737.001]
  • [Cites] J Neurooncol. 2006 Jan;76(2):153-7 [16132495.001]
  • [Cites] AJNR Am J Neuroradiol. 2005 May;26(5):1263-9 [15891195.001]
  • [Cites] Leukemia. 1998 Aug;12(8):1176-81 [9697870.001]
  • [Cites] J Clin Invest. 1993 Dec;92(6):2675-82 [8254024.001]
  • [Cites] J Clin Oncol. 1998 May;16(5):1712-22 [9586883.001]
  • [Cites] Lancet. 1995 Mar 4;345(8949):544-7 [7776773.001]
  • (PMID = 18831032.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; None / None / / P30 CA021765-29; United States / NCI NIH HHS / CA / CA 21765; United States / NCI NIH HHS / CA / P30 CA021765-29
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] YL5FZ2Y5U1 / Methotrexate
  • [Other-IDs] NLM/ NIHMS75296; NLM/ PMC2605174
  •  go-up   go-down


Advertisement
4. De Keersmaecker K, Marynen P, Cools J: Genetic insights in the pathogenesis of T-cell acute lymphoblastic leukemia. Haematologica; 2005 Aug;90(8):1116-27
SciCrunch. KEGG: Data: Disease Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic insights in the pathogenesis of T-cell acute lymphoblastic leukemia.
  • Over the past 20 years, a large number of genes involved in the pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL) has been identified by molecular characterization of recurrent chromosomal aberrations and more subtle genetic defects.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16079112.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Neoplasm Proteins
  • [Number-of-references] 129
  •  go-up   go-down


5. Cardone S, Yen MT, Chévez-Barrios P, Foroozan R, Yen KG: Recurrent acute lymphoblastic leukemia presenting in the lacrimal gland. Ophthal Plast Reconstr Surg; 2006 Jan-Feb;22(1):56-7
MedlinePlus Health Information. consumer health - Tears.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent acute lymphoblastic leukemia presenting in the lacrimal gland.
  • A 14-year-old girl with a history of acute lymphoblastic leukemia presented with periorbital swelling of the right eyelid associated with enlargement of the lacrimal gland and cervical lymphadenopathy.
  • The patient underwent an incisional biopsy of the lacrimal gland that showed atypical lymphocytes consistent with recurrent acute lymphoblastic leukemia.
  • [MeSH-major] Eye Neoplasms / diagnosis. Lacrimal Apparatus / pathology. Lacrimal Apparatus Diseases / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • MedlinePlus Health Information. consumer health - Eye Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16418669.001).
  • [ISSN] 0740-9303
  • [Journal-full-title] Ophthalmic plastic and reconstructive surgery
  • [ISO-abbreviation] Ophthal Plast Reconstr Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Different molecular mechanisms causing 9p21 deletions in acute lymphoblastic leukemia of childhood.
  • Deletion of chromosome 9p21 is a crucial event for the development of several cancers including acute lymphoblastic leukemia (ALL).
  • Four of the 46 breakpoints coincide with those reported in other cases, thus confirming the presence of recurrent deletion hotspots.
  • [MeSH-major] Chromosomes, Human, Pair 9 / genetics. Cyclin-Dependent Kinase Inhibitor p15 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Sequence Deletion / genetics

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


7. An Q, Wright SL, Moorman AV, Parker H, Griffiths M, Ross FM, Davies T, Harrison CJ, Strefford JC: Heterogeneous breakpoints in patients with acute lymphoblastic leukemia and the dic(9;20)(p11-13;q11) show recurrent involvement of genes at 20q11.21. Haematologica; 2009 Aug;94(8):1164-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Heterogeneous breakpoints in patients with acute lymphoblastic leukemia and the dic(9;20)(p11-13;q11) show recurrent involvement of genes at 20q11.21.
  • The dic(9;20)(p11-13;q11) is a recurrent chromosomal abnormality in patients with acute lymphoblastic leukemia.
  • From an initial cohort of 58 with acute lymphoblastic leukemia patients with this translocation, breakpoint mapping with fluorescence in situ hybridization on 26 of them revealed breakpoint heterogeneity of both chromosomes.
  • This study provides insight into the breakpoint complexity underlying dicentric chromosomal formation in acute lymphoblastic leukemia and highlights putative target gene loci.
  • [MeSH-major] Chromosomes, Human, Pair 20 / genetics. Chromosomes, Human, Pair 9 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Leukemia. 2008 Jan;22(1):114-23 [17972957.001]
  • [Cites] Genes Chromosomes Cancer. 2008 Feb;47(2):149-58 [17990329.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Nov 4;105(44):17050-4 [18957548.001]
  • [Cites] Leukemia. 2000 Feb;14(2):241-6 [10673740.001]
  • [Cites] Leukemia. 1995 Jan;9(1):102-6 [7845002.001]
  • [Cites] Genes Chromosomes Cancer. 1995 May;13(1):54-61 [7541644.001]
  • [Cites] Leukemia. 1995 Oct;9(10):1613-9 [7564498.001]
  • [Cites] Cancer Genet Cytogenet. 1996 Dec;92(2):111-5 [8976366.001]
  • [Cites] Nat Genet. 1997 Apr;15 Spec No:417-74 [9140409.001]
  • [Cites] Br J Haematol. 2004 Dec;127(5):509-18 [15566354.001]
  • [Cites] J Clin Invest. 2005 Sep;115(9):2351-62 [16127461.001]
  • [Cites] Nat Methods. 2006 Jun;3(6):447-53 [16721378.001]
  • [Cites] J Biol Chem. 2006 Jun 30;281(26):17588-98 [16606617.001]
  • [Cites] Cancer Genet Cytogenet. 2006 Sep;169(2):159-63 [16938575.001]
  • [Cites] Br J Haematol. 2006 Nov;135(4):492-9 [16999846.001]
  • [Cites] Leukemia. 2007 Mar;21(3):515-23 [17230227.001]
  • [Cites] Oncogene. 2007 Jun 21;26(29):4306-18 [17237825.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Aug 19;105(33):11921-6 [18697940.001]
  • (PMID = 19586940.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / ASXL1 protein, human; 0 / B-Cell-Specific Activator Protein; 0 / FRG1 protein, human; 0 / Nuclear Proteins; 0 / PAX5 protein, human; 0 / Repressor Proteins; 0 / Transcription Factors; 0 / ZCCHC7 protein, human
  • [Other-IDs] NLM/ PMC2719040
  •  go-up   go-down


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

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

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


9. Lowe T, Luu T, Shen J, Bhatia S, Shibata S, Stein A, Somlo G: Male breast cancer 15 years after allogeneic hematopoietic cell transplantation including total body irradiation for recurrent acute lymphoblastic leukemia. Onkologie; 2008 May;31(5):266-9
MedlinePlus Health Information. consumer health - Male Breast Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Male breast cancer 15 years after allogeneic hematopoietic cell transplantation including total body irradiation for recurrent acute lymphoblastic leukemia.
  • CASE REPORTS: We report here the case of a 34-year-old man who developed stage IIB node-positive breast cancer almost 15 years following total body irradiation and allogeneic hematopoietic cell transplantation for acute lymphoblastic leukemia.
  • [MeSH-major] Breast Neoplasms, Male / etiology. Hematopoietic Stem Cell Transplantation / adverse effects. Neoplasms, Radiation-Induced / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Whole-Body Irradiation / adverse effects


10. Gong H, Liu WL, Zhou JF, Xu HZ: [Expression of mitosis checkpoint gene CHFR in acute leukemia]. Zhonghua Yi Xue Za Zhi; 2005 Apr 27;85(16):1085-8
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of mitosis checkpoint gene CHFR in acute leukemia].
  • OBJECTIVE: To investigate the expression of mitosis checkpoint gene CHFR in adult patients with acute leukemia (AL) and its clinical significance.
  • METHODS: Four ml of bone marrow was extracted from 65 AL patients, 38 males and 27 females, with the median age of 35, 43 with acute myelocytic leukemia (AML) and 22 with acute lymphocytic leukemia (ALL), 45 de novo patients and 20 recurrent patients, and 8 normal donor of allogeneic bone marrow transplantation as controls.
  • (1) The levels of CHFR protein and mRNA were correlated with the cumulative percentages of cells in S phases. (2) The expression level of CHFR protein in 40.6% (13/32) of the AL patients and that of the CHFR mRNA in 60.0% (27/45) of the AL patients were both significantly lower than those of the normal controls. (3) The mean expression level of CHFR protein in the recurrent acute lymphoblastic leukemia (ALL) was 0.71, significantly higher than that of the de novo group (0.38, t = 2.54, P = 0.017). (4) The complete remission (CR) rates in the AL patients with high expression levels of CHFR protein and mRNA were 30.2% and 42.4% respectively, significantly lower than those in the AL patients with low expression levels (88.6% and 85.4% respectively, both P < 0.05).
  • CONCLUSION: By affecting mitotic checkpoint function, CHFR inactivation plays a key role in tumorigenesis in adult patients with acute leukemia.
  • Moreover, the aberrant expression of CHFR appears to be a good molecular marker to predict the sensitivity of acute leukemia to chemotherapy.
  • [MeSH-major] Cell Cycle Proteins / biosynthesis. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16029562.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CHFR protein, human; 0 / Cell Cycle Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
  •  go-up   go-down


16. Luong NV, Kantarjian HM, Faderl SH, Thomas DA, Vu KD: Occurence of venothromboembolism (VTE) in patients (pts) with acute lymphocytic leukemia (ALL), Burkitt's leukemia/lymphoma (BL), or lymphoblastic leukemia (LL). J Clin Oncol; 2009 May 20;27(15_suppl):7059

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Occurence of venothromboembolism (VTE) in patients (pts) with acute lymphocytic leukemia (ALL), Burkitt's leukemia/lymphoma (BL), or lymphoblastic leukemia (LL).
  • Although neoplastic diseases are known risk factors for the development of VTE, little is known about the incidence and predisposing factors of VTE among leukemia patients (pts).
  • Recurrent VTE occurred in 10 pts.
  • Further studies should be done in other leukemias to establish guidelines in the prevention and management of VTE in pts with leukemia.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27961450.001).
  • [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
  •  go-up   go-down


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

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


18. Stanulla M, Schrappe M: Treatment of childhood acute lymphoblastic leukemia. Semin Hematol; 2009 Jan;46(1):52-63
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of childhood acute lymphoblastic leukemia.
  • Childhood acute lymphoblastic leukemia (ALL) is the most common malignancy of childhood.
  • While the goal of effective therapy for the majority of children with ALL has been achieved, significant numbers of patients still die due to recurrent disease or the toxicity of treatment.
  • Thus, future research must extend our molecular understanding of leukemia and host factors in order to even more specifically identify the mechanisms underlying the differences in treatment response and outcome, and to finally address the therapeutic needs of the individual child.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19100368.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 101
  •  go-up   go-down


19. Strefford JC, An Q, Harrison CJ: Modeling the molecular consequences of unbalanced translocations in cancer: lessons from acute lymphoblastic leukemia. Cell Cycle; 2009 Jul 15;8(14):2175-84
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modeling the molecular consequences of unbalanced translocations in cancer: lessons from acute lymphoblastic leukemia.
  • Chromosomal rearrangements are recurrent findings in human cancer and result in aberrant restructuring of the genome.
  • This review focuses on one such strategy, using traditional and innovative molecular technologies to characterize breakpoint heterogeneity within a series of acute lymphoblastic leukemia (ALL) patients with dicentric chromosomes.
  • [MeSH-major] Models, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19556891.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / PAX5 protein, human
  • [Number-of-references] 71
  •  go-up   go-down


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

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

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


21. Harrison CJ: Cytogenetics of paediatric and adolescent acute lymphoblastic leukaemia. Br J Haematol; 2009 Jan;144(2):147-56

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetics of paediatric and adolescent acute lymphoblastic leukaemia.
  • Cytogenetics has determined the incidence and prognostic significance of chromosomal abnormalities in acute lymphoblastic leukaemia (ALL).
  • (ii) intrachromosomal amplification of chromosome 21 is a new recurrent abnormality in precursor-B ALL (BCP-ALL);.
  • [MeSH-major] Chromosome Aberrations. Cytogenetic Analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19006567.001).
  • [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
  • [Number-of-references] 74
  •  go-up   go-down


22. Ponce-Torres E, Ruíz-Rodríguez Mdel S, Alejo-González F, Hernández-Sierra JF, Pozos-Guillén Ade J: Oral manifestations in pediatric patients receiving chemotherapy for acute lymphoblastic leukemia. J Clin Pediatr Dent; 2010;34(3):275-9
MedlinePlus Health Information. consumer health - Mouth Disorders.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oral manifestations in pediatric patients receiving chemotherapy for acute lymphoblastic leukemia.
  • The purpose of this study was to determine the prevalence of oral manifestations in pediatric patients with acute lymphoblastic leukemia (ALL) receiving chemotherapy, and to evaluate the significance of independent risk factors (oral health, gender, age, time and type of treatment, and phase of chemotherapy).
  • The prevalence of oral manifestations was: gingivitis, 91.84%; caries, 81.63%; mucositis, 38.77%; periodontitis, 16.32%; cheilitis, 18.36%; recurrent herpes, 12.24%; and primary herpetic gingivostomatitis, 2.04%.
  • The type of leukemia, gender and phase of chemotherapy were apparently associated with the presence of candidiasis, gingivitis, and periodontitis, and they could be considered risk factors for the development of oral manifestations.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Mouth Diseases / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20578668.001).
  • [ISSN] 1053-4628
  • [Journal-full-title] The Journal of clinical pediatric dentistry
  • [ISO-abbreviation] J Clin Pediatr Dent
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


23. Roberson JR, Raju S, Shelso J, Pui CH, Howard SC: Diabetic ketoacidosis during therapy for pediatric acute lymphoblastic leukemia. Pediatr Blood Cancer; 2008 Jun;50(6):1207-12
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diabetic ketoacidosis during therapy for pediatric acute lymphoblastic leukemia.
  • BACKGROUND: Hyperglycemia is common during therapy for acute lymphoblastic leukemia (ALL), but diabetic ketoacidosis (DKA) occurs rarely.
  • Race, sex, body mass index, leukemia immunophenotype, ALL risk category, white blood cell count at diagnosis, and treatment protocol were not associated with DKA.
  • No patient had recurrent DKA; only one of the six patients had a subsequent hyperglycemia episode.
  • [MeSH-major] Diabetic Ketoacidosis / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 18266226.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-36401; United States / NCI NIH HHS / CA / CA-51001; United States / NCI NIH HHS / CA / CA-60419; United States / NCI NIH HHS / CA / CA-78224; United States / NIGMS NIH HHS / GM / GM-61393
  • [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 / Antineoplastic Agents; 0 / Glucocorticoids; EC 3.5.1.1 / Asparaginase
  •  go-up   go-down


24. Tavil B, Secmeer G, Balc YI, Tezer H, Aksoy C, Alan S, Gumruk F, Yetgin S: Chronic recurrent multifocal osteomyelitis as the first presentation of acute lymphoblastic leukemia in a 2-year-old boy. J Pediatr Hematol Oncol; 2010 May;32(4):e151-2
Genetic Alliance. consumer health - Osteomyelitis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic recurrent multifocal osteomyelitis as the first presentation of acute lymphoblastic leukemia in a 2-year-old boy.
  • SUMMARY: We present herein a 2-year-old boy who suffered from chronic recurrent multifocal osteomyelitis for 6 months and was later diagnosed as acute lymphoblastic leukemia.
  • In view of the rarity of bilateral symmetric and multifocal lesions in osteomyelitis in children, we suggest that leukemia should be investigated with bone marrow aspiration in such patients, even if complete blood count parameters are normal, and there is no hepatosplenomegaly.
  • [MeSH-major] Osteomyelitis / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis


25. Meijerink JP, den Boer ML, Pieters R: New genetic abnormalities and treatment response in acute lymphoblastic leukemia. Semin Hematol; 2009 Jan;46(1):16-23
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New genetic abnormalities and treatment response in acute lymphoblastic leukemia.
  • Numerous genetic abnormalities have been identified in acute lymphoblastic leukemia (ALL).
  • Here we review the recurrent abnormalities with emphasis on those recently discovered, and discuss their association with chemotherapy resistance or sensitivity and with clinical response to therapy.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19100364.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Transcription Factors
  • [Number-of-references] 70
  •  go-up   go-down


26. Tomizawa D, Koh K, Hirayama M, Miyamura T, Hatanaka M, Saikawa Y, Ishii E: Outcome of recurrent or refractory acute lymphoblastic leukemia in infants with MLL gene rearrangements: A report from the Japan Infant Leukemia Study Group. Pediatr Blood Cancer; 2009 Jul;52(7):808-13
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcome of recurrent or refractory acute lymphoblastic leukemia in infants with MLL gene rearrangements: A report from the Japan Infant Leukemia Study Group.
  • BACKGROUND: Despite the poor outcome of recurrent or refractory acute lymphoblastic leukemia (ALL) in infants with MLL gene rearrangement, few studies have focused on this specific group.
  • We conducted a retrospective analysis of infants with recurrent or refractory ALL from two previous consecutive Japanese studies to clarify the characteristics and prognostic factors among these patients PROCEDURE: All recurrent or refractory ALL infants with MLL gene rearrangement (MLL-R) who were registered in two consecutive Japanese nation-wide multicentric trials (MLL96 and MLL98; between 1995 and 2001) were eligible for the study.
  • CONCLUSIONS: The prognosis of infants with recurrent or refractory MLL-R ALL is extremely poor despite alternative treatments including HSCT; therefore, it is necessary to develop novel treatment strategies.
  • [MeSH-major] Drug Resistance, Neoplasm. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Recurrence, Local / genetics. Neoplasm Recurrence, Local / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19229974.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down


27. Digiuseppe JA: Acute lymphoblastic leukemia: diagnosis and detection of minimal residual disease following therapy. Clin Lab Med; 2007 Sep;27(3):533-49, vi
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute lymphoblastic leukemia: diagnosis and detection of minimal residual disease following therapy.
  • Flow cytometric immunophenotyping (FCI) is an important diagnostic modality in the evaluation of patients who have suspected or known acute lymphoblastic leukemia (ALL).
  • Beyond facilitating the classification of ALL into fundamental diagnostic categories, FCI may anticipate recurrent cytogenetic and molecular abnormalities.
  • [MeSH-major] Flow Cytometry / methods. Immunophenotyping. Neoplasm, Residual / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17658406.001).
  • [ISSN] 0272-2712
  • [Journal-full-title] Clinics in laboratory medicine
  • [ISO-abbreviation] Clin. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 61
  •  go-up   go-down


28. Metzgeroth G, Walz C, Score J, Siebert R, Schnittger S, Haferlach C, Popp H, Haferlach T, Erben P, Mix J, Müller MC, Beneke H, Müller L, Del Valle F, Aulitzky WE, Wittkowsky G, Schmitz N, Schulte C, Müller-Hermelink K, Hodges E, Whittaker SJ, Diecker F, Döhner H, Schuld P, Hehlmann R, Hochhaus A, Cross NC, Reiter A: Recurrent finding of the FIP1L1-PDGFRA fusion gene in eosinophilia-associated acute myeloid leukemia and lymphoblastic T-cell lymphoma. Leukemia; 2007 Jun;21(6):1183-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent finding of the FIP1L1-PDGFRA fusion gene in eosinophilia-associated acute myeloid leukemia and lymphoblastic T-cell lymphoma.
  • Here, we report on seven FIP1L1-PDGFRA-positive patients who presented with acute myeloid leukemia (AML, n=5) or lymphoblastic T-cell non-Hodgkin-lymphoma (n=2) in conjunction with AML or Eos-MPD.
  • [MeSH-major] Eosinophilia / drug therapy. Leukemia, Myeloid / drug therapy. Oncogene Proteins, Fusion / analysis. Piperazines / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / administration & dosage. Receptor, Platelet-Derived Growth Factor alpha. mRNA Cleavage and Polyadenylation Factors
  • [MeSH-minor] Acute Disease. Adult. Aged. Benzamides. Disease-Free Survival. Humans. Imatinib Mesylate. Male. Middle Aged. Myeloproliferative Disorders / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Remission Induction / methods


29. Bhatt UK, Gregory ME, Madi MS, Fraser M, Woodruff GH: Sequential leukemic infiltration and human herpesvirus optic neuropathy in acute lymphoblastic leukemia. J AAPOS; 2008 Apr;12(2):200-2
MedlinePlus Health Information. consumer health - Optic Nerve Disorders.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sequential leukemic infiltration and human herpesvirus optic neuropathy in acute lymphoblastic leukemia.
  • Leukemic infiltration is a common cause of optic disk swelling in a patient with acute lymphoblastic leukemia (ALL).
  • Recurrence of optic disk swelling in a patient with previous leukemic infiltration carries a grave prognosis when it is associated with recurrent central nervous system disease.
  • We report a case of recurrent swelling of an optic disk in a patient with T-cell ALL who had previously been treated for CNS relapse with optic nerve involvement.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18329931.001).
  • [ISSN] 1528-3933
  • [Journal-full-title] Journal of AAPOS : the official publication of the American Association for Pediatric Ophthalmology and Strabismus
  • [ISO-abbreviation] J AAPOS
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


30. Pan J, Xue Y, Wu Y, Wang Y, Shen J: Dicentric (7;9)(p11;p11) is a rare but recurrent abnormality in acute lymphoblastic leukemia: a study of 7 cases. Cancer Genet Cytogenet; 2006 Sep;169(2):159-63
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dicentric (7;9)(p11;p11) is a rare but recurrent abnormality in acute lymphoblastic leukemia: a study of 7 cases.
  • A clinical and experimental study of acute lymphoblastic leukemia (ALL) with a dic(7;9)(p11;p11) included 7 patients (5 males and 2 females) with a median age of 32 years.
  • We consider the dic(7;9) a rare but recurrent abnormality, which may represent a distinct cytogenetic subgroup in B-ALL.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 9. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. 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 = 16938575.001).
  • [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
  •  go-up   go-down


31. Lad EM, Jain A, Lad SP, Lin RC, Alcorn DM, Moshfeghi DM: Orbital recurrence of B-progenitor acute lymphoblastic leukemia in a child. J Pediatr Ophthalmol Strabismus; 2010 Jan-Feb;47(1):46-50
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Orbital recurrence of B-progenitor acute lymphoblastic leukemia in a child.
  • Orbital mass is an exceedingly rare presentation of acute lymphoblastic leukemia.
  • This report describes a 12-year-old boy with recurrent orbital pre-B-cell acute lymphoblastic leukemia and reviews the literature on the incidence, presentation, prognosis, and management of orbital tumors in acute lymphoblastic leukemia.
  • Early diagnosis and treatment of orbital acute lymphoblastic leukemia with a multidisciplinary approach is essential to minimize or prevent deterioration of vision and optimize clinical outcomes.
  • [MeSH-major] Neoplasm Recurrence, Local / diagnosis. Orbital Neoplasms / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Acute Disease. Biopsy. Bone Marrow / pathology. Child. Combined Modality Therapy. Diagnosis, Differential. Disease Progression. Fatal Outcome. Humans. Magnetic Resonance Imaging. Male

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010, SLACK Incorporated.
  • (PMID = 20128555.001).
  • [ISSN] 0191-3913
  • [Journal-full-title] Journal of pediatric ophthalmology and strabismus
  • [ISO-abbreviation] J Pediatr Ophthalmol Strabismus
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


32. Russell LJ, Akasaka T, Majid A, Sugimoto KJ, Loraine Karran E, Nagel I, Harder L, Claviez A, Gesk S, Moorman AV, Ross F, Mazzullo H, Strefford JC, Siebert R, Dyer MJ, Harrison CJ: t(6;14)(p22;q32): a new recurrent IGH@ translocation involving ID4 in B-cell precursor acute lymphoblastic leukemia (BCP-ALL). Blood; 2008 Jan 01;111(1):387-91
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] t(6;14)(p22;q32): a new recurrent IGH@ translocation involving ID4 in B-cell precursor acute lymphoblastic leukemia (BCP-ALL).
  • Translocations involving the immunoglobulin heavy chain locus (IGH@) at chromosome band 14q32 are common in mature B-cell neoplasms, but are rare in B-cell precursor acute lymphoblastic leukemia (BCP-ALL).
  • Here, we report the translocation, t(6;14)(p22;q32), involving IGH@ as a novel recurrent translocation in 13 BCP-ALL patients.
  • [MeSH-major] Immunoglobulin Heavy Chains / genetics. Inhibitor of Differentiation Proteins / genetics. Leukemia, B-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17940204.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U132670597
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ID4 protein, human; 0 / Immunoglobulin Heavy Chains; 0 / Inhibitor of Differentiation Proteins; 0 / PAX5 Transcription Factor; 0 / PAX5 protein, human
  •  go-up   go-down


33. Le QH, Thomas X, Ecochard R, Iwaz J, Lhéritier V, Michallet M, Fiere D: Proportion of long-term event-free survivors and lifetime of adult patients not cured after a standard acute lymphoblastic leukemia therapeutic program: adult acute lymphoblastic leukemia-94 trial. Cancer; 2007 May 15;109(10):2058-67
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Proportion of long-term event-free survivors and lifetime of adult patients not cured after a standard acute lymphoblastic leukemia therapeutic program: adult acute lymphoblastic leukemia-94 trial.
  • BACKGROUND: In adult acute lymphoblastic leukemia, treatment results generally are expressed in terms of overall survival or disease-free survival at 3 years.
  • In this investigation, the authors attempted to express the results in terms of the proportion of long-term disease-free survivors and in terms of lifetime in patients who developed recurrent disease or died.
  • METHODS: Univariate and multivariate analyses were used to assess the influence of different covariates on the 2 result criteria in 922 participants in the Adult Acute Lymphoblastic Leukemia-94 multicenter trial.
  • CONCLUSIONS: The results of this study highlighted and specified the importance of some classic prognostic factors in patients with acute lymphoblastic leukemia.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Female. Follow-Up Studies. Genes, abl / genetics. Humans. Karyotyping. L-Lactate Dehydrogenase / blood. Leukocyte Count. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics. Odds Ratio. Oncogene Proteins, Fusion / genetics. Prognosis. Risk Factors. Survival Rate. Treatment Failure

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2007 American Cancer Society
  • (PMID = 17407135.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 1.1.1.27 / L-Lactate Dehydrogenase
  •  go-up   go-down


34. Quentmeier H, Schneider B, Röhrs S, Romani J, Zaborski M, Macleod RA, Drexler HG: SET-NUP214 fusion in acute myeloid leukemia- and T-cell acute lymphoblastic leukemia-derived cell lines. J Hematol Oncol; 2009;2:3
Cellosaurus - a cell line knowledge resource. culture/stock collections - Cellosaurus - a cell line knowledge resource .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] SET-NUP214 fusion in acute myeloid leukemia- and T-cell acute lymphoblastic leukemia-derived cell lines.
  • BACKGROUND: SET-NUP214 fusion resulting from a recurrent cryptic deletion, del(9)(q34.11q34.13) has recently been described in T-cell acute lymphoblastic leukemia (T-ALL) and in one case of acute myeloid leukemia (AML).
  • RESULTS: Of 141 human leukemia/lymphoma cell lines tested, only the T-ALL cell line LOUCY and the AML cell line MEGAL expressed the SET(TAF-Ibeta)-NUP214 fusion gene transcript.
  • [MeSH-major] Histone Chaperones / genetics. Leukemia, Myeloid, Acute / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics


35. Seegmiller AC, Kroft SH, Karandikar NJ, McKenna RW: Characterization of immunophenotypic aberrancies in 200 cases of B acute lymphoblastic leukemia. Am J Clin Pathol; 2009 Dec;132(6):940-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of immunophenotypic aberrancies in 200 cases of B acute lymphoblastic leukemia.
  • Morphologic distinction of leukemic lymphoblasts in B acute lymphoblastic leukemia (B-ALL) from their nonneoplastic counterparts in bone marrow (hematogones) can be difficult.
  • Specific aberrancies correlate with recurrent cytogenetic abnormalities in B-ALL.
  • [MeSH-major] Bone Marrow Cells / pathology. Immunophenotyping / methods. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Precursor Cells, B-Lymphoid / pathology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19926587.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


36. Strefford JC, Worley H, Barber K, Wright S, Stewart AR, Robinson HM, Bettney G, van Delft FW, Atherton MG, Davies T, Griffiths M, Hing S, Ross FM, Talley P, Saha V, Moorman AV, Harrison CJ: Genome complexity in acute lymphoblastic leukemia is revealed by array-based comparative genomic hybridization. Oncogene; 2007 Jun 21;26(29):4306-18
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genome complexity in acute lymphoblastic leukemia is revealed by array-based comparative genomic hybridization.
  • Chromosomal abnormalities are important for the classification and risk stratification of patients with acute lymphoblastic leukemia (ALL).
  • Other recurrent findings included dim(13q), dim(16q) and enh(17q).
  • [MeSH-major] Burkitt Lymphoma / genetics. Gene Expression Profiling. Genome, Human. Leukemia-Lymphoma, Adult T-Cell / genetics. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17237825.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


37. Gorello P, La Starza R, Varasano E, Chiaretti S, Elia L, Pierini V, Barba G, Brandimarte L, Crescenzi B, Vitale A, Messina M, Grammatico S, Mancini M, Matteucci C, Bardi A, Guarini A, Martelli MF, Foà R, Mecucci C: Combined interphase fluorescence in situ hybridization elucidates the genetic heterogeneity of T-cell acute lymphoblastic leukemia in adults. Haematologica; 2010 Jan;95(1):79-86
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined interphase fluorescence in situ hybridization elucidates the genetic heterogeneity of T-cell acute lymphoblastic leukemia in adults.
  • BACKGROUND: Molecular lesions in T-cell acute lymphoblastic leukemias affect regulators of cell cycle, proliferation, differentiation, survival and apoptosis in multi-step pathogenic pathways.
  • DESIGN AND METHODS: We designed a combined interphase fluorescence in situ hybridization strategy to study 25 oncogenes/tumor suppressor genes in T-cell acute lymphoblastic leukemias and applied it in 23 adult patients for whom immunophenotyping, karyotyping, molecular studies, and gene expression profiling data were available.
  • The results were confirmed and integrated with those of multiplex-polymerase chain reaction analysis and gene expression profiling in another 129 adults with T-cell acute lymphoblastic leukemias.
  • It found abnormalities known to be associated with T-cell acute lymphoblastic leukemias, i.e.
  • Multiplex-polymerase chain reaction analysis and gene expression profiling of 129 further cases found five additional cases of TAF_I-NUP214-positive T-cell acute lymphoblastic leukemia.
  • CONCLUSIONS: Our combined interphase fluorescence in situ hybridization strategy greatly improved the detection of genetic abnormalities in adult T-cell acute lymphoblastic leukemias.
  • The estimated incidence of TAF_I-NUP214, a new recurrent fusion in adult T-cell acute lymphoblastic leukemias, was 4.6% (7/152).
  • [MeSH-major] Comparative Genomic Hybridization. Genetic Heterogeneity. In Situ Hybridization, Fluorescence. Leukemia-Lymphoma, Adult T-Cell / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Oncogene. 2007 Jun 21;26(29):4306-18 [17237825.001]
  • [Cites] Haematologica. 2007 May;92(5):619-26 [17488685.001]
  • [Cites] Nat Med. 2007 Oct;13(10):1203-10 [17873882.001]
  • [Cites] Blood. 2008 Apr 15;111(8):4322-8 [18172006.001]
  • [Cites] J Exp Med. 2008 Apr 14;205(4):751-8 [18362173.001]
  • [Cites] Blood. 2008 May 1;111(9):4668-80 [18299449.001]
  • [Cites] Br J Haematol. 2008 Oct;143(2):153-68 [18691165.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] Haematologica. 2003 Mar;88(3):275-9 [12651265.001]
  • [Cites] Blood. 2003 Jul 1;102(1):262-8 [12637319.001]
  • [Cites] Cancer Res. 2004 Jun 15;64(12):4089-98 [15205317.001]
  • [Cites] Nat Genet. 2004 Oct;36(10):1084-9 [15361874.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 May 15;88(10):4367-71 [2034676.001]
  • [Cites] Exp Cell Res. 1998 May 1;240(2):274-81 [9597000.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14863-8 [9843981.001]
  • [Cites] J Mol Biol. 1999 Jul 9;290(2):547-57 [10390352.001]
  • [Cites] Blood. 2005 Jun 15;105(12):4849-52 [15713800.001]
  • [Cites] Blood. 2005 Jul 1;106(1):274-86 [15774621.001]
  • [Cites] Haematologica. 2005 Aug;90(8):1116-27 [16079112.001]
  • [Cites] Leukemia. 2005 Nov;19(11):1948-57 [16107895.001]
  • [Cites] Leukemia. 2006 Jan;20(1):82-6 [16270038.001]
  • [Cites] Leukemia. 2006 Jun;20(6):1184-7 [16572206.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1238-44 [16673021.001]
  • [Cites] Haematologica. 2006 Sep;91(9):1248-51 [16956826.001]
  • [Cites] Haematologica. 2007 Feb;92(2):232-5 [17296573.001]
  • [Cites] Nat Genet. 2007 May;39(5):593-5 [17435759.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1251-61 [17452517.001]
  • (PMID = 20065082.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2805748
  •  go-up   go-down


38. Akasaka T, Balasas T, Russell LJ, Sugimoto KJ, Majid A, Walewska R, Karran EL, Brown DG, Cain K, Harder L, Gesk S, Martin-Subero JI, Atherton MG, Brüggemann M, Calasanz MJ, Davies T, Haas OA, Hagemeijer A, Kempski H, Lessard M, Lillington DM, Moore S, Nguyen-Khac F, Radford-Weiss I, Schoch C, Struski S, Talley P, Welham MJ, Worley H, Strefford JC, Harrison CJ, Siebert R, Dyer MJ: Five members of the CEBP transcription factor family are targeted by recurrent IGH translocations in B-cell precursor acute lymphoblastic leukemia (BCP-ALL). Blood; 2007 Apr 15;109(8):3451-61
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Five members of the CEBP transcription factor family are targeted by recurrent IGH translocations in B-cell precursor acute lymphoblastic leukemia (BCP-ALL).
  • Mutations of CEBPA are found in a subset of acute myeloid leukemia (AML) and in some cases of familial AML.
  • Here, using cytogenetics, fluorescence in situ hybridization (FISH), and molecular cloning, we show that 5 CEBP gene family members are targeted by recurrent IGH chromosomal translocations in BCP-ALL.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17170124.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U132670597
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / Immunoglobulin Heavy Chains
  •  go-up   go-down


39. Prabhu S, Gottlieb DJ, Varikatt W, St Heaps L, Diaz S, Smith A: Adult B-cell acute lymphoblastic leukemia with two unrelated abnormal cytogenetic clones. Cancer Genet Cytogenet; 2010 Aug;201(1):24-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult B-cell acute lymphoblastic leukemia with two unrelated abnormal cytogenetic clones.
  • On the basis of the morphology, flow cytometry, and lack of myeloid-associated markers, a diagnosis of precursor B-cell acute lymphoblastic leukemia (B-ALL) was made.
  • The dic(7;9) is a rare but recurrent abnormality in B-ALL, while trisomy 8 as a sole abnormality is most commonly associated with myeloid malignancies.
  • [MeSH-major] Leukemia, B-Cell / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20633764.001).
  • [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
  •  go-up   go-down


40. Levine RL, Loriaux M, Huntly BJ, Loh ML, Beran M, Stoffregen E, Berger R, Clark JJ, Willis SG, Nguyen KT, Flores NJ, Estey E, Gattermann N, Armstrong S, Look AT, Griffin JD, Bernard OA, Heinrich MC, Gilliland DG, Druker B, Deininger MW: The JAK2V617F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia, but not in acute lymphoblastic leukemia or chronic lymphocytic leukemia. Blood; 2005 Nov 15;106(10):3377-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The JAK2V617F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia, but not in acute lymphoblastic leukemia or chronic lymphocytic leukemia.
  • Recently, we and others identified a single recurrent somatic activating mutation (JAK2V617F) in the Janus kinase 2 (JAK2) tyrosine kinase in the myeloproliferative disorders (MPDs) polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis.
  • We used direct sequence analysis to determine if the JAK2V617F mutation was present in acute myeloid leukemia (AML), chronic myelomonocytic leukemia (CMML)/atypical chronic myelogenous leukemia (aCML), myelodysplastic syndrome (MDS), B-lineage acute lymphoblastic leukemia (ALL), T-cell ALL, and chronic lymphocytic leukemia (CLL).
  • These data indicate that the JAK2V617F allele is present in acute and chronic myeloid malignancies but not in lymphoid malignancies.


41. Yoshida Y, Toma Y, Arai M, Higashi R, Kashihara K, Kaizaki Y: [Primitive neuroectodermal tumor arising 8 years after chemotherapy and radiotherapy for acute lymphoblastic leukemia: case report]. No Shinkei Geka; 2005 Jul;33(7):717-22
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Primitive neuroectodermal tumor arising 8 years after chemotherapy and radiotherapy for acute lymphoblastic leukemia: case report].
  • We report a case of primitive neuroectodermal tumor (PNET) arising 8 years after chemotherapy and radiotherapy for acute lymphoblastic leukemia.
  • A 15-year-old boy with a history of acute lymphoblastic leukemia, at the age of 7, underwent chemotherapy and 14Gy of radiotherapy to the whole brain.
  • Follow-up MRI showed no evidence of recurrent tumor 4 months after the radiotherapy.
  • This tumor was thought to be a secondary brain tumor arising in this survivor of childhood acute lymphoblastic leukemia and it is a rare complication of successful leukemia treatment.
  • [MeSH-major] Brain Neoplasms / surgery. Cranial Irradiation. Neoplasms, Second Primary. Neuroectodermal Tumors, Primitive / surgery. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16001813.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Using adaptive model predictive control to customize maintenance therapy chemotherapeutic dosing for childhood acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is a common childhood cancer in which nearly one-quarter of patients experience a disease relapse.
  • During the course of treatment, the patient-specific parameters are adaptively identified using recurrent complete blood count measurements, which sufficiently constrain the patient parameter uncertainty to support customized adjustments of the drug dose.
  • [MeSH-major] 6-Mercaptopurine / therapeutic use. Dose-Response Relationship, Drug. Models, Biological. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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


43. Seif AE, Barrett DM, Milone M, Brown VI, Grupp SA, Reid GS: Long-term protection from syngeneic acute lymphoblastic leukemia by CpG ODN-mediated stimulation of innate and adaptive immune responses. Blood; 2009 Sep 17;114(12):2459-66
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term protection from syngeneic acute lymphoblastic leukemia by CpG ODN-mediated stimulation of innate and adaptive immune responses.
  • Acute lymphoblastic leukemia (ALL) is the most common childhood cancer and remains a major cause of mortality in children with recurrent disease and in adults.
  • Despite observed graft-versus-leukemia effects after stem cell transplantation, successful immune therapies for ALL have proven elusive.
  • CpG ODN induced early killing of leukemia by innate immune effectors both in vitro and in vivo.
  • Mice were treated with CpG ODN starting 7 days after injection with leukemia to mimic a minimal residual disease state and achieved T cell-dependent remissions of more than 6 months.
  • In addition, mice in remission after CpG ODN treatment were protected from leukemia rechallenge, and adoptive transfer of T cells from mice in remission conferred protection against leukemia growth.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2004 Aug 15;64(16):5850-60 [15313929.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):15113-8 [14657335.001]
  • [Cites] Blood. 1996 Jul 1;88(1):41-8 [8704200.001]
  • [Cites] Blood. 1998 Jul 1;92(1):273-82 [9639527.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3529-36 [9808544.001]
  • [Cites] Leukemia. 2005 Jan;19(1):44-8 [15496974.001]
  • [Cites] Exp Hematol. 2005 Mar;33(3):286-94 [15730852.001]
  • [Cites] Exp Hematol. 2005 Mar;33(3):344-52 [15730858.001]
  • [Cites] Blood. 2005 May 1;105(9):3641-7 [15650062.001]
  • [Cites] Br J Haematol. 2005 Jul;130(1):67-75 [15982346.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1332-41 [16249392.001]
  • [Cites] Leukemia. 2006 Apr;20(4):645-9 [16498391.001]
  • [Cites] Leukemia. 2007 Jan;21(1):110-20 [17024114.001]
  • [Cites] Blood. 2007 Feb 1;109(3):926-35 [17003380.001]
  • [Cites] Blood. 2007 Mar 1;109(5):2008-13 [17068155.001]
  • [Cites] Immunology. 2007 Mar;120(3):412-23 [17163960.001]
  • [Cites] Nat Med. 2007 Mar;13(3):354-60 [17334371.001]
  • [Cites] Environ Sci Technol. 2007 Mar 15;41(6):2064-8 [17410806.001]
  • [Cites] J Clin Invest. 2007 May;117(5):1184-94 [17476348.001]
  • [Cites] J Clin Invest. 2008 Mar;118(3):1165-75 [18259609.001]
  • [Cites] FASEB J. 2008 Jun;22(6):2053-63 [18180331.001]
  • [Cites] Ann Hematol. 2008 Sep;87(9):701-8 [18437383.001]
  • [Cites] Blood. 2008 Sep 15;112(6):2205-13 [18591383.001]
  • [Cites] Leukemia. 2008 Nov;22(11):2070-9 [18633431.001]
  • [Cites] Blood. 2009 Apr 9;113(15):3546-52 [18941113.001]
  • [Cites] J Cell Mol Med. 2009 Aug;13(8B):1962-76 [18624776.001]
  • [Cites] Blood. 2000 Mar 1;95(5):1572-9 [10688810.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3323-7 [10828011.001]
  • [Cites] Cytokine. 2001 Jan 7;13(1):39-50 [11145841.001]
  • [Cites] Br J Haematol. 2000 Dec;111(4):1130-7 [11167752.001]
  • [Cites] Cancer Res. 2001 Apr 15;61(8):3399-405 [11309299.001]
  • [Cites] Blood. 2002 May 1;99(9):3151-7 [11964277.001]
  • [Cites] Biol Blood Marrow Transplant. 2002;8(4):213-20 [12014810.001]
  • [Cites] Leukemia. 2002 Oct;16(10):2046-54 [12357356.001]
  • [Cites] Clin Cancer Res. 2003 Jan;9(1):76-83 [12538454.001]
  • [Cites] J Immunol. 2003 Jul 1;171(1):166-74 [12816995.001]
  • [Cites] Leukemia. 2003 Aug;17(8):1566-72 [12886244.001]
  • [Cites] Methods. 2003 Oct;31(2):135-42 [12957571.001]
  • [Cites] Trends Biotechnol. 1991 Apr;9(4):109-13 [1367388.001]
  • (PMID = 19636062.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K12 CA076931; United States / NCI NIH HHS / CA / 2K12CA076931-11; United States / NCI NIH HHS / CA / T32 CA009615; United States / NCI NIH HHS / CA / R03-CA123554; United States / NCI NIH HHS / CA / R03 CA123554
  • [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 / CPG-oligonucleotide; 0 / Oligodeoxyribonucleotides
  • [Other-IDs] NLM/ PMC2746473
  •  go-up   go-down


44. Van Vlierberghe P, van Grotel M, Tchinda J, Lee C, Beverloo HB, van der Spek PJ, Stubbs A, Cools J, Nagata K, Fornerod M, Buijs-Gladdines J, Horstmann M, van Wering ER, Soulier J, Pieters R, Meijerink JP: The recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-cell acute lymphoblastic leukemia. Blood; 2008 May 1;111(9):4668-80
Genetic Alliance. consumer health - Pediatric T-cell leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) is mostly characterized by specific chromosomal abnormalities, some occurring in a mutually exclusive manner that possibly delineate specific T-ALL subgroups.
  • Using a gene expression-based clustering analysis of 67 T-ALL cases with recurrent molecular genetic abnormalities and 25 samples lacking apparent aberrations, we identified 5 new patients with elevated HOXA levels.
  • Using microarray-based comparative genomic hybridization (array-CGH), a cryptic and recurrent deletion, del (9)(q34.11q34.13), was exclusively identified in 3 of these 5 patients.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128.001]
  • [Cites] Blood. 2007 Dec 15;110(13):4445-54 [17855633.001]
  • [Cites] Nat Genet. 2004 Oct;36(10):1084-9 [15361874.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Mol Cell Biol. 1990 Aug;10(8):4016-26 [2370860.001]
  • [Cites] Cancer Genet Cytogenet. 1990 Oct 15;49(2):241-8 [2208060.001]
  • [Cites] Stat Med. 1990 Jul;9(7):811-8 [2218183.001]
  • [Cites] Mol Cell Biol. 1992 Apr;12(4):1687-97 [1549122.001]
  • [Cites] Genes Chromosomes Cancer. 1992 Oct;5(3):227-34 [1384675.001]
  • [Cites] Oncogene. 1996 Oct 17;13(8):1801-8 [8895527.001]
  • [Cites] Mol Cell Biol. 1997 Jan;17(1):495-505 [8972230.001]
  • [Cites] EMBO J. 1997 Jun 2;16(11):3145-57 [9214632.001]
  • [Cites] EMBO J. 1998 Jul 1;17(13):3714-25 [9649441.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 21;101(51):17765-70 [15591353.001]
  • [Cites] FEBS Lett. 2005 Jan 31;579(3):757-62 [15670842.001]
  • [Cites] Leukemia. 2005 Mar;19(3):358-66 [15674412.001]
  • [Cites] Cell. 2005 Apr 22;121(2):167-78 [15851025.001]
  • [Cites] Blood. 2005 Jul 1;106(1):274-86 [15774621.001]
  • [Cites] Haematologica. 2005 Aug;90(8):1116-27 [16079112.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6306-15 [16155013.001]
  • [Cites] Leukemia. 2005 Nov;19(11):1948-57 [16107895.001]
  • [Cites] Leukemia. 2006 Jan;20(1):82-6 [16270038.001]
  • [Cites] Nat Rev Cancer. 2006 May;6(5):347-59 [16612405.001]
  • [Cites] Genes Dev. 2006 May 1;20(9):1123-36 [16618801.001]
  • [Cites] Genes Dev. 2006 Aug 1;20(15):2096-109 [16847353.001]
  • [Cites] Leukemia. 2006 Sep;20(9):1496-510 [16826225.001]
  • [Cites] Nat Cell Biol. 2006 Sep;8(9):1017-24 [16921363.001]
  • [Cites] Haematologica. 2006 Sep;91(9):1212-21 [16956820.001]
  • [Cites] Mol Cell Biol. 2006 Nov;26(21):8022-31 [16954387.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3520-9 [16873670.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18261-6 [17114293.001]
  • [Cites] Leukemia. 2007 Jan;21(1):121-8 [17039236.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] Bioinformatics. 2002;18 Suppl 1:S96-104 [12169536.001]
  • [Cites] Leukemia. 2003 Jun;17(6):1157-63 [12764384.001]
  • [Cites] Cell. 2001 Jan 12;104(1):119-30 [11163245.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1197-204 [11830466.001]
  • [Cites] Blood. 2003 Jul 1;102(1):262-8 [12637319.001]
  • [Cites] Leukemia. 2004 Feb;18(2):337-40 [14671643.001]
  • [Cites] Mol Cell Biol. 2004 Mar;24(6):2373-84 [14993277.001]
  • [Cites] Haematologica. 2007 Feb;92(2):232-5 [17296573.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Nat Genet. 2007 May;39(5):593-5 [17435759.001]
  • [Cites] Am J Pathol. 2007 Aug;171(2):654-66 [17569777.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1251-61 [17452517.001]
  • [Cites] J Cell Physiol. 2008 Feb;214(2):322-33 [17620317.001]
  • [Cites] Int J Cancer. 2004 Sep 10;111(4):501-7 [15239126.001]
  • (PMID = 18299449.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA11560
  • [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 / Chromosomal Proteins, Non-Histone; 0 / Histone Chaperones; 0 / Homeodomain Proteins; 0 / NUP214 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / SET protein, human; 0 / Transcription Factors; 157907-48-7 / HoxA protein
  • [Other-IDs] NLM/ PMC2343598
  •  go-up   go-down


45. Kearney SL, Dahlberg SE, Levy DE, Voss SD, Sallan SE, Silverman LB: Clinical course and outcome in children with acute lymphoblastic leukemia and asparaginase-associated pancreatitis. Pediatr Blood Cancer; 2009 Aug;53(2):162-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical course and outcome in children with acute lymphoblastic leukemia and asparaginase-associated pancreatitis.
  • BACKGROUND: Asparaginase, an agent used in the treatment of acute lymphoblastic leukemia (ALL), is associated with the development of pancreatitis.
  • CONCLUSION: Asparaginase-associated pancreatitis was more common in older children, and caused significant acute morbidity.
  • Re-treatment with asparaginase after an episode of pancreatitis was associated with a high risk of recurrent pancreatitis.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Pancreatitis.
  • MedlinePlus Health Information. consumer health - Pancreatitis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • [Cites] Med Pediatr Oncol. 2000 Mar;34(3):200-5 [10696127.001]
  • [Cites] Pediatr Blood Cancer. 2007 Oct 15;49(5):634-9 [16937362.001]
  • [Cites] Blood. 2001 Mar 1;97(5):1211-8 [11222362.001]
  • [Cites] Dis Markers. 2001;17(2):77-88 [11673654.001]
  • [Cites] J Clin Oncol. 2002 Jan 1;20(1):237-46 [11773175.001]
  • [Cites] Blood. 2002 Mar 15;99(6):1986-94 [11877270.001]
  • [Cites] Blood. 2002 Apr 15;99(8):2734-9 [11929760.001]
  • [Cites] Science. 1968 May 3;160(3827):533-5 [5689413.001]
  • [Cites] J Exp Med. 1968 Jun 1;127(6):1055-72 [4871211.001]
  • [Cites] N Engl J Med. 1969 Nov 6;281(19):1028-34 [4898857.001]
  • [Cites] Cancer. 1970 Feb;25(2):306-20 [4905155.001]
  • [Cites] Cancer Res. 1971 Jul;31(7):942-9 [4327086.001]
  • [Cites] Biochem Pharmacol. 1969 Oct;18(10):2578-80 [4935103.001]
  • [Cites] Cancer. 1972 Aug;30(2):339-47 [4626307.001]
  • [Cites] J Pediatr. 1972 Dec;81(6):1220-1 [4643049.001]
  • [Cites] Cancer. 1974 Sep;34(3):780-5 [4527863.001]
  • [Cites] Med Pediatr Oncol. 1976;2(4):387-95 [1004382.001]
  • [Cites] Med Pediatr Oncol. 1977;3(4):387-400 [337095.001]
  • [Cites] Am J Pediatr Hematol Oncol. 1979 Spring;1(1):9-13 [295576.001]
  • [Cites] Cancer Res. 1983 Nov;43(11):5601-7 [6352020.001]
  • [Cites] N Engl J Med. 1986 Sep 11;315(11):657-63 [2943992.001]
  • [Cites] Br J Haematol. 1990 Apr;74(4):465-70 [2189489.001]
  • [Cites] Eur J Haematol. 1992 Aug;49(2):63-6 [1397242.001]
  • [Cites] Thromb Haemost. 1993 Jan 11;69(1):12-5 [8446931.001]
  • [Cites] J Clin Oncol. 1994 Apr;12(4):740-7 [8151317.001]
  • [Cites] Blood. 1997 Mar 15;89(6):1886-95 [9058708.001]
  • [Cites] Blood. 2007 Feb 1;109(3):896-904 [17003366.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2247-56 [11187916.001]
  • (PMID = 19405141.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA068484-13; United States / NCI NIH HHS / CA / P01 CA068484-13; United States / NCI NIH HHS / CA / P01 CA068484-139001; United States / NCI NIH HHS / CA / CA068484-139001; United States / NCI NIH HHS / CA / P01 CA068484; United States / NCI NIH HHS / CA / 5P01CA68484
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 3.5.1.1 / Asparaginase
  • [Other-IDs] NLM/ NIHMS110197; NLM/ PMC2721691
  •  go-up   go-down


46. Gmidène A, Elghezal H, Sennana H, Ben Youssef Y, Meddeb B, Elloumi M, Khlif A, Saad A: ETV6-RUNX1 Rearrangement in Tunisian Pediatric B-Lineage Acute Lymphoblastic Leukemia. Adv Hematol; 2009;2009:924301

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ETV6-RUNX1 Rearrangement in Tunisian Pediatric B-Lineage Acute Lymphoblastic Leukemia.
  • In this study, Forty-one out of fifty-seven Tunisian children with B-lineage acute lymphoblastic leukemia (B-ALL), and without cytogenetically detectable recurrent abnormalities at the time of the diagnosis, were evaluated by fluorescence in situ hybridization (FISH) for the t(12;21).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Hematol Oncol. 2008 Jun;26(2):91-7 [18271061.001]
  • [Cites] Br J Haematol. 1999 Dec;107(3):667-9 [10583273.001]
  • [Cites] Cancer Genet Cytogenet. 2005 Jan 15;156(2):129-33 [15642392.001]
  • [Cites] Cancer Genet Cytogenet. 1999 Apr;110(1):7-13 [10198615.001]
  • [Cites] Leukemia. 1997 Sep;11(9):1459-64 [9305598.001]
  • [Cites] Leukemia. 1997 Aug;11(8):1220-3 [9264373.001]
  • [Cites] Blood. 1997 Jul 15;90(2):571-7 [9226156.001]
  • [Cites] Br J Haematol. 1996 Jul;94(1):105-11 [8757516.001]
  • [Cites] Blood. 1996 Apr 1;87(7):2891-9 [8639909.001]
  • [Cites] Leukemia. 1995 Dec;9(12):1985-9 [8609706.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 May 23;92(11):4917-21 [7761424.001]
  • [Cites] Genes Chromosomes Cancer. 1994 Mar;9(3):186-91 [7515661.001]
  • [Cites] Blood. 1993 May 1;81(9):2237-51 [8481506.001]
  • [Cites] Leuk Res. 2004 Oct;28(10):1033-8 [15289014.001]
  • [Cites] Chin Med J (Engl). 2003 Sep;116(9):1298-303 [14527352.001]
  • [Cites] Cancer Genet Cytogenet. 2003 Jul 15;144(2):143-7 [12850377.001]
  • [Cites] Leukemia. 2002 Jun;16(6):1131-4 [12040444.001]
  • [Cites] Leukemia. 2002 Apr;16(4):658-68 [11960347.001]
  • [Cites] Cancer Genet Cytogenet. 2002 Jan 1;132(1):61-4 [11801311.001]
  • [Cites] Haematologica. 2001 Dec;86(12):1245-53 [11726315.001]
  • [Cites] Genes Chromosomes Cancer. 2001 Nov;32(3):244-9 [11579464.001]
  • [Cites] Leukemia. 2001 Sep;15(9):1442-7 [11516105.001]
  • [Cites] Leuk Lymphoma. 2000 Dec;40(1-2):39-47 [11426627.001]
  • [Cites] Genes Chromosomes Cancer. 2001 Apr;30(4):407-9 [11241794.001]
  • [Cites] Haematologica. 2000 Apr;85(4):362-6 [10756360.001]
  • [Cites] Hematol Oncol. 1999 Sep;17(3):91-105 [10641030.001]
  • [Cites] Cancer Genet Cytogenet. 2008 Jan 15;180(2):129-34 [18206538.001]
  • (PMID = 20049174.001).
  • [ISSN] 1687-9112
  • [Journal-full-title] Advances in hematology
  • [ISO-abbreviation] Adv Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2799269
  •  go-up   go-down


47. Yamamoto K, Nagata K, Morita Y, Inagaki K, Hamaguchi H: Isodicentric Philadelphia chromosome in acute lymphoblastic leukemia with der(7;12)(q10;q10). Leuk Res; 2007 May;31(5):713-8
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Isodicentric Philadelphia chromosome in acute lymphoblastic leukemia with der(7;12)(q10;q10).
  • We describe here the first case of acute lymphoblastic leukemia (ALL) with an isodicentric Philadelphia [idic(Ph)] chromosome.
  • The idic(Ph) chromosome was spindle-shaped and supposed to be formed by two Ph chromosomes joined at their q terminals, whereas idic(Ph) chromosomes in chronic myelogenous leukemia (CML) have been shown to be fused at the satellite regions of p arms.
  • Furthermore, considering other three reported cases, der(7;12)(q10;q10) may be one of the recurrent translocations in ALL.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 7. Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16979235.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  •  go-up   go-down


48. Hah JO: Anaplastic oligodendroglioma after childhood acute lymphoblastic leukemia: chemotherapy and autologous peripheral blood stem cell transplantation. J Pediatr Hematol Oncol; 2008 Oct;30(10):764-7
Genetic Alliance. consumer health - Transplantation.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic oligodendroglioma after childhood acute lymphoblastic leukemia: chemotherapy and autologous peripheral blood stem cell transplantation.
  • Secondary brain tumors after cranial irradiation occur in survivors of childhood acute lymphoblastic leukemia (ALL).
  • High-dose chemotherapy with stem cell rescue seems to be potentially effective for multiple recurrent anaplastic oligodendroglioma occurring after childhood ALL.
  • [MeSH-major] Neoplasms, Second Primary / therapy. Oligodendroglioma / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications


49. Karst C, Gross M, Haase D, Wedding U, Höffken K, Liehr T, Mkrtchyan H: Novel cryptic chromosomal rearrangements detected in acute lymphoblastic leukemia detected by application of new multicolor fluorescent in situ hybridization approaches. Int J Oncol; 2006 Apr;28(4):891-7
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel cryptic chromosomal rearrangements detected in acute lymphoblastic leukemia detected by application of new multicolor fluorescent in situ hybridization approaches.
  • However, it is often difficult to obtain good karyotypes, especially of cells from cases with acute lymphoblastic leukemia (ALL) because of poor morphology and spreading.
  • Thus, we detected the following recurrent cryptic chromosomal aberrations: del(12)(pter) [8 cases], del(9)(qter) [3 cases], and del(11)(pter) [2 cases].
  • [MeSH-major] Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Spectral Karyotyping / methods. Translocation, Genetic / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16525638.001).
  • [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
  •  go-up   go-down


50. Kwon YJ, Lee JW, Kim MS, Jang PS, Chung NG, Jeong DC, Kim YG, Han KJ, Lee SJ, Cho B, Kim HK: Cytogenetic analysis in childhood acute lymphoblastic leukemia: experience at a single institution in Korea. Int J Hematol; 2009 Mar;89(2):150-8
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic analysis in childhood acute lymphoblastic leukemia: experience at a single institution in Korea.
  • We evaluated major cytogenetic abnormalities associated with childhood acute lymphoblastic leukemia (ALL) through both fluorescent in situ hybridization and conventional chromosomal analysis for 132 ALL patients diagnosed at St Mary's Hospital in Korea.
  • Of the patients with abnormal karyotypes, recurrent structural abnormalities were determined in 103 (78%) cases. t(12;21)(q13;q22) was found in 29 (22%) out of 132 patients, 9p abnormalities in 13 (10%) patients, t(1;19)(q23;p13.3) in 11 (8%) patients, t(9;22)(q34;q11.2) in 11 (8%) patients, and 11q23 abnormalities in 7 (5%) patients.
  • [MeSH-major] Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Genes Chromosomes Cancer. 1994 Mar;9(3):186-91 [7515661.001]
  • [Cites] Cancer. 2001 Oct 1;92(7):1977-83 [11745273.001]
  • [Cites] Genes Chromosomes Cancer. 2004 Jan;39(1):88-92 [14603446.001]
  • [Cites] Blood. 2008 May 1;111(9):4477-89 [18285545.001]
  • [Cites] J Clin Oncol. 1994 May;12(5):909-15 [8164041.001]
  • [Cites] Hematol Oncol. 2003 Mar;21(1):1-9 [12605417.001]
  • [Cites] Leukemia. 2001 Aug;15(8):1256-61 [11480568.001]
  • [Cites] Br J Haematol. 2001 Apr;113(1):3-10 [11328273.001]
  • [Cites] Oncologist. 2000;5(4):321-8 [10965000.001]
  • [Cites] Rev Clin Exp Hematol. 2002 Jun;6(2):91-113; discussion 200-2 [12196211.001]
  • [Cites] Blood. 1994 Apr 15;83(8):2274-84 [8161794.001]
  • [Cites] Cancer Genet Cytogenet. 1996 May;88(1):57-65 [8630981.001]
  • [Cites] Blood. 1996 Apr 1;87(7):2870-7 [8639906.001]
  • [Cites] J Korean Med Sci. 2005 Feb;20(1):36-41 [15716599.001]
  • [Cites] Cancer Genet Cytogenet. 2001 Apr 1;126(1):73-7 [11343784.001]
  • [Cites] Blood. 1997 Jul 15;90(2):571-7 [9226156.001]
  • [Cites] Blood. 1999 Dec 15;94(12):4036-45 [10590047.001]
  • [Cites] Cancer Genet Cytogenet. 1999 Apr;110(1):7-13 [10198615.001]
  • [Cites] Blood. 1995 May 1;85(9):2321-30 [7727766.001]
  • [Cites] Blood. 2000 Oct 1;96(7):2543-9 [11001909.001]
  • [Cites] N Engl J Med. 1998 Aug 27;339(9):605-15 [9718381.001]
  • [Cites] Eur J Haematol. 2002 Jan;68(1):31-41 [11952819.001]
  • [Cites] J Pediatr Hematol Oncol. 2001 Oct;23(7):411-5 [11878573.001]
  • [Cites] Blood. 1999 Sep 1;94(5):1537-44 [10477677.001]
  • [Cites] Cancer Genet Cytogenet. 2001 Feb;125(1):27-9 [11297764.001]
  • [Cites] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128.001]
  • [Cites] Cancer Cell. 2002 Jun;1(5):417-20 [12124171.001]
  • [Cites] Blood. 2002 Sep 15;100(6):1957-64 [12200352.001]
  • [Cites] Br J Haematol. 1997 Mar;96(3):601-10 [9054669.001]
  • [Cites] Pediatr Hematol Oncol. 2006 Sep;23(6):495-506 [16849281.001]
  • [Cites] Br J Haematol. 1997 Oct;99(1):93-100 [9359508.001]
  • [Cites] Leukemia. 2005 May;19(5):734-40 [15789069.001]
  • [Cites] Blood. 1997 Mar 1;89(5):1716-22 [9057655.001]
  • [Cites] Eur J Haematol. 2001 May;66(5):297-304 [11422408.001]
  • [Cites] Blood. 1993 May 1;81(9):2237-51 [8481506.001]
  • (PMID = 19109731.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Relapsed childhood high hyperdiploid acute lymphoblastic leukemia: presence of preleukemic ancestral clones and the secondary nature of microdeletions and RTK-RAS mutations.
  • Although childhood high hyperdiploid acute lymphoblastic leukemia is associated with a favorable outcome, 20% of patients still relapse.
  • No single aberration was linked to relapse, but four deletions, involving IKZF1, PAX5, CDKN2A/B or AK3, were recurrent.
  • [MeSH-major] Chromosome Deletion. Diploidy. Genes, ras / genetics. Mutation / genetics. Neoplasm Recurrence, Local / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor Protein-Tyrosine Kinases / genetics


52. Speleman F, Cauwelier B, Dastugue N, Cools J, Verhasselt B, Poppe B, Van Roy N, Vandesompele J, Graux C, Uyttebroeck A, Boogaerts M, De Moerloose B, Benoit Y, Selleslag D, Billiet J, Robert A, Huguet F, Vandenberghe P, De Paepe A, Marynen P, Hagemeijer A: A new recurrent inversion, inv(7)(p15q34), leads to transcriptional activation of HOXA10 and HOXA11 in a subset of T-cell acute lymphoblastic leukemias. Leukemia; 2005 Mar;19(3):358-66
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A new recurrent inversion, inv(7)(p15q34), leads to transcriptional activation of HOXA10 and HOXA11 in a subset of T-cell acute lymphoblastic leukemias.
  • Chromosomal translocations with breakpoints in T-cell receptor (TCR) genes are recurrent in T-cell malignancies.
  • Here, we describe a new recurrent chromosomal inversion of chromosome 7, inv(7)(p15q34), in a subset of patients with T-cell acute lymphoblastic leukemia characterized by CD2 negative and CD4 positive, CD8 negative blasts.
  • This is the first report of a recurrent chromosome rearrangement targeting the HOXA gene cluster in T-cell malignancies resulting in deregulated HOXA gene expression (particularly HOXA10 and HOXA11) and is in keeping with a previous report suggesting HOXA deregulation in MLL-rearranged T- and B cell lymphoblastic leukemia as the key factor in leukaemic transformation.
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 7 / genetics. DNA-Binding Proteins / genetics. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Transcriptional Activation / genetics

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15674412.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / HOXA11 protein, human; 0 / Homeodomain Proteins; 140441-81-2 / HOXA10 protein, human
  •  go-up   go-down


53. Kirschner-Schwabe R, Lottaz C, Tödling J, Rhein P, Karawajew L, Eckert C, von Stackelberg A, Ungethüm U, Kostka D, Kulozik AE, Ludwig WD, Henze G, Spang R, Hagemeier C, Seeger K: Expression of late cell cycle genes and an increased proliferative capacity characterize very early relapse of childhood acute lymphoblastic leukemia. Clin Cancer Res; 2006 Aug 1;12(15):4553-61
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of late cell cycle genes and an increased proliferative capacity characterize very early relapse of childhood acute lymphoblastic leukemia.
  • PURPOSE: In childhood acute lymphoblastic leukemia (ALL), approximately 25% of patients suffer from relapse.
  • In recurrent disease, despite intensified therapy, overall cure rates of 40% remain unsatisfactory and survival rates are particularly poor in certain subgroups.
  • [MeSH-major] Cell Cycle Proteins / genetics. Gene Expression Profiling. 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 = 16899601.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins
  •  go-up   go-down


54. Wang HY, Tirado CA: t(8;21)(q22;q22) Translocation involving AML1 and ETO in B lymphoblastic leukemia [corrected]. Hum Pathol; 2010 Feb;41(2):286-92

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] t(8;21)(q22;q22) Translocation involving AML1 and ETO in B lymphoblastic leukemia [corrected].
  • t(8;21)(q22;q22) giving rise to RUNX1/RUNX1T1 fusion transcript is a recurrent non-random chromosomal translocation, accounting for approximately 5% of cases of acute myeloid leukemia and 10% of acute myeloid leukemia with maturation.
  • Studies have demonstrated so far that t(8;21)(q22;q22) occurs only in acute myeloid leukemia, and B lymphoblastic leukemia with t(8;21)(q22;q22) has not been reported in the literature.
  • In the present study, we report a 44-year-old woman with a diagnosis of a B lymphoblastic leukemia based on morphology and immunophenotype.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics. Translocation, Genetic / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • [ErratumIn] Hum Pathol. 2010 Apr;41(4):620
  • (PMID = 19896694.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors
  •  go-up   go-down


55. Han Y, Xue Y, Zhang J, Wu Y, Pan J, Wang Y, Shen J, Dai H, Bai S: Translocation (14;14)(q11;q32) with simultaneous involvement of the IGH and CEBPE genes in B-lineage acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2008 Dec;187(2):125-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Translocation (14;14)(q11;q32) with simultaneous involvement of the IGH and CEBPE genes in B-lineage acute lymphoblastic leukemia.
  • Translocation (14;14)(q11;q32) is one of the recurrent chromosome aberrations in ataxia-teleangiectasia (AT) and T-cell malignancies.
  • However, t(14;14)(q11;q32) is an exceedingly rare phenomenon in B-lineage acute lymphoblastic leukemia (B-ALL).
  • We suggest that t(14;14)(q11;q32) involving the IGH and CEBPE genes in B-ALL is rare, but it is a recurrent abnormality that could identify a new subgroup of B-ALL.
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / genetics. Chromosomes, Human, Pair 14 / genetics. Immunoglobulin Heavy Chains / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19027493.001).
  • [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 / Biomarkers, Tumor; 0 / CCAAT-Enhancer-Binding Proteins; 0 / Immunoglobulin Heavy Chains; 142805-41-2 / CEBPE protein, human; 5J49Q6B70F / Vincristine; VB0R961HZT / Prednisone; ZS7284E0ZP / Daunorubicin; VDP protocol
  •  go-up   go-down


56. Iacobucci I, Storlazzi CT, Cilloni D, Lonetti A, Ottaviani E, Soverini S, Astolfi A, Chiaretti S, Vitale A, Messa F, Impera L, Baldazzi C, D'Addabbo P, Papayannidis C, Lonoce A, Colarossi S, Vignetti M, Piccaluga PP, Paolini S, Russo D, Pane F, Saglio G, Baccarani M, Foà R, Martinelli G: Identification and molecular characterization of recurrent genomic deletions on 7p12 in the IKZF1 gene in a large cohort of BCR-ABL1-positive acute lymphoblastic leukemia patients: on behalf of Gruppo Italiano Malattie Ematologiche dell'Adulto Acute Leukemia Working Party (GIMEMA AL WP). Blood; 2009 Sep 3;114(10):2159-67
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification and molecular characterization of recurrent genomic deletions on 7p12 in the IKZF1 gene in a large cohort of BCR-ABL1-positive acute lymphoblastic leukemia patients: on behalf of Gruppo Italiano Malattie Ematologiche dell'Adulto Acute Leukemia Working Party (GIMEMA AL WP).
  • The BCR-ABL1 fusion gene defines the subgroup of acute lymphoblastic leukemia (ALL) with the worst clinical prognosis.
  • The IKZF1 deletion also was identified in the progression of chronic myeloid leukemia to lymphoid blast crisis (66%) but never in myeloid blast crisis or chronic-phase chronic myeloid leukemia or in patients with acute myeloid leukemia.
  • [MeSH-major] Base Sequence / genetics. Chromosomes, Human, Pair 7 / genetics. Fusion Proteins, bcr-abl / genetics. Ikaros Transcription Factor / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Sequence Deletion
  • [MeSH-minor] Adolescent. Adult. Aged. Blast Crisis / genetics. Blast Crisis / metabolism. Cell Line, Tumor. Codon, Initiator / genetics. Codon, Initiator / metabolism. Cohort Studies. Exons / genetics. Female. Gene Expression Regulation, Leukemic / genetics. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Male. Microarray Analysis. Middle Aged. Polymorphism, Single Nucleotide

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Blood. 2010 Sep 23;116(12):2196
  • (PMID = 19589926.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon, Initiator; 0 / IKZF1 protein, human; 148971-36-2 / Ikaros Transcription Factor; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  •  go-up   go-down


57. Paulsson K, Cazier JB, Macdougall F, Stevens J, Stasevich I, Vrcelj N, Chaplin T, Lillington DM, Lister TA, Young BD: Microdeletions are a general feature of adult and adolescent acute lymphoblastic leukemia: Unexpected similarities with pediatric disease. Proc Natl Acad Sci U S A; 2008 May 06;105(18):6708-13
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Microdeletions are a general feature of adult and adolescent acute lymphoblastic leukemia: Unexpected similarities with pediatric disease.
  • We present here a genome-wide map of abnormalities found in diagnostic samples from 45 adults and adolescents with acute lymphoblastic leukemia (ALL).
  • Furthermore, several genes not previously implicated in the pathogenesis of ALL were identified as possible recurrent targets of deletion.
  • [MeSH-major] Gene Deletion. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2005 May 1;105(9):3434-41 [15650057.001]
  • [Cites] Cancer Res. 2005 Jan 15;65(2):375-8 [15695375.001]
  • [Cites] Cancer Genet Cytogenet. 2005 Oct 15;162(2):176-8 [16213368.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3760-7 [16105981.001]
  • [Cites] Leukemia. 2006 May;20(5):840-6 [16498392.001]
  • [Cites] Pediatr Blood Cancer. 2006 Nov;47(6):748-56 [16470520.001]
  • [Cites] Blood. 2007 Feb 1;109(3):926-35 [17003380.001]
  • [Cites] Ann Oncol. 2007 Jan;18 Suppl 1:i3-i8 [17311819.001]
  • [Cites] Blood. 2007 Mar 15;109(6):2327-30 [17095619.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3189-97 [17170120.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Cancer. 2007 May 15;109(10):2058-67 [17407135.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1258-66 [17443227.001]
  • [Cites] Oncogene. 2007 Jun 21;26(29):4306-18 [17237825.001]
  • [Cites] Hum Mol Genet. 2007 Sep 15;16(18):2215-25 [17613536.001]
  • [Cites] Immunol Cell Biol. 2008 Jan;86(1):47-53 [17998914.001]
  • [Cites] Blood. 2008 Jan 15;111(2):776-84 [17890455.001]
  • [Cites] Genes Chromosomes Cancer. 2008 Sep;47(9):729-39 [18506749.001]
  • [Cites] Leukemia. 2000 Mar;14(3):356-63 [10720126.001]
  • [Cites] Cancer. 2000 Nov 1;89(9):1976-82 [11064355.001]
  • [Cites] Blood. 2002 Feb 1;99(3):863-71 [11806988.001]
  • [Cites] Cancer. 2003 Oct 1;98(7):1337-54 [14508819.001]
  • [Cites] Bioinformatics. 2004 May 22;20(8):1233-40 [14871870.001]
  • [Cites] Nat Genet. 2004 Sep;36(9):949-51 [15286789.001]
  • [Cites] Blood. 2004 Oct 15;104(8):2492-8 [15198948.001]
  • [Cites] Ann Med. 2004;36(7):492-503 [15513300.001]
  • [Cites] Blood. 1996 Apr 15;87(8):3135-42 [8605327.001]
  • [Cites] Genes Chromosomes Cancer. 1996 Jul;16(3):155-63 [8814447.001]
  • [Cites] Blood. 1999 Jun 1;93(11):3983-93 [10339508.001]
  • [Cites] Nat Genet. 2005 Jun;37 Suppl:S11-7 [15920524.001]
  • (PMID = 18458336.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE9611
  • [Grant] United Kingdom / Cancer Research UK / / A6438; United Kingdom / Cancer Research UK / / A6789
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2373322
  •  go-up   go-down


58. Sørensen GV, Helgestad J, Rosthøj S: [Herpes zoster-associated morbidity in children undergoing chemotherapy for acute lymphoblastic leukaemia]. Ugeskr Laeger; 2009 Nov 9;171(46):3350-4
Hazardous Substances Data Bank. ACYCLOVIR .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Herpes zoster-associated morbidity in children undergoing chemotherapy for acute lymphoblastic leukaemia].
  • We aimed to assess morbidity from herpes zoster in children with acute lymphoblastic leukemia (ALL).
  • Three children on prolonged intensive chemotherapy had recurrent zoster episodes.
  • CONCLUSION: Chemotherapy causes zoster eruptions in approximately one quarter of children with ALL, and with intensive protocols recurrent zoster can cause significant morbidity.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Herpes Zoster / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

  • MedlinePlus Health Information. consumer health - Shingles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19925740.001).
  • [ISSN] 1603-6824
  • [Journal-full-title] Ugeskrift for laeger
  • [ISO-abbreviation] Ugeskr. Laeg.
  • [Language] dan
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antiviral Agents; X4HES1O11F / Acyclovir
  •  go-up   go-down


59. Rabin KR, Man TK, Yu A, Folsom MR, Zhao YJ, Rao PH, Plon SE, Naeem RC: Clinical utility of array comparative genomic hybridization for detection of chromosomal abnormalities in pediatric acute lymphoblastic leukemia. Pediatr Blood Cancer; 2008 Aug;51(2):171-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical utility of array comparative genomic hybridization for detection of chromosomal abnormalities in pediatric acute lymphoblastic leukemia.
  • BACKGROUND: Accurate detection of recurrent chromosomal abnormalities is critical to assign patients to risk-based therapeutic regimens for pediatric acute lymphoblastic leukemia (ALL).

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Genes Chromosomes Cancer. 1995 May;13(1):54-61 [7541644.001]
  • [Cites] Leukemia. 2004 May;18(5):939-47 [14999294.001]
  • [Cites] Cancer Genet Cytogenet. 1998 May;103(1):20-4 [9595040.001]
  • [Cites] Bioinformatics. 2004 Dec 12;20(18):3413-22 [15381628.001]
  • [Cites] J Med Genet. 2005 Feb;42(2):121-8 [15689449.001]
  • [Cites] Br J Haematol. 2005 May;129(4):520-30 [15877734.001]
  • [Cites] Nat Genet. 2005 Jun;37 Suppl:S11-7 [15920524.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] Genes Chromosomes Cancer. 2006 May;45(5):482-94 [16425296.001]
  • [Cites] Br J Haematol. 2006 Nov;135(4):492-9 [16999846.001]
  • [Cites] J Mol Diagn. 2006 Nov;8(5):528-33 [17065418.001]
  • [Cites] PLoS One. 2007;2(3):e327 [17389918.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Genes Chromosomes Cancer. 2007 Sep;46(9):805-12 [17539022.001]
  • [Cites] Leukemia. 1995 Oct;9(10):1613-9 [7564498.001]
  • [CommentIn] Pediatr Blood Cancer. 2008 Aug;51(2):153-4 [18300321.001]
  • (PMID = 18253961.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K12 CA090433; United States / NCI NIH HHS / CA / CA90433-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS570929; NLM/ PMC4063297
  •  go-up   go-down


60. Dalle JH, Moghrabi A, Rousseau P, Leclerc JM, Barrette S, Bernstein ML, Champagne J, David M, Demers J, Duval M, Hume H, Meyer P, Champagne MA: Second induction in pediatric patients with recurrent acute lymphoid leukemia using DFCI-ALL protocols. J Pediatr Hematol Oncol; 2005 Feb;27(2):73-9
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Second induction in pediatric patients with recurrent acute lymphoid leukemia using DFCI-ALL protocols.
  • Between 15% and 30% of children with acute lymphoblastic leukemia (ALL) experience disease recurrence.
  • The authors report their institutional experience in the management of children with recurrent ALL using the Dana Farber Cancer Institute (DFCI) ALL protocol in patients treated initially with that same protocol.
  • Between April 1986 and May 2003, 34 patients with recurrent ALL, treated at initial diagnosis with DFCI-ALL protocol therapy, were given the same protocol as repeat induction chemotherapy.
  • The treatment of children with recurrent ALL using the DFCI-ALL protocol induction regimen after initial use of the same protocol is associated with a high rate of second CR with no excess toxicity.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • 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 = 15701980.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate
  •  go-up   go-down


61. Schraders M, van Reijmersdal SV, Kamping EJ, van Krieken JH, van Kessel AG, Groenen PJ, Hoogerbrugge PM, Kuiper RP: High-resolution genomic profiling of pediatric lymphoblastic lymphomas reveals subtle differences with pediatric acute lymphoblastic leukemias in the B-lineage. Cancer Genet Cytogenet; 2009 May;191(1):27-33
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-resolution genomic profiling of pediatric lymphoblastic lymphomas reveals subtle differences with pediatric acute lymphoblastic leukemias in the B-lineage.
  • Lymphoblastic lymphoma (LBL) is one of the most frequent occurring pediatric non-Hodgkin lymphomas.
  • In the WHO classification scheme, pediatric LBL is considered to be the same disease entity as pediatric acute lymphoblastic leukemia (ALL).
  • Similar to what previously has been found in T-ALL, T-LBL exhibited recurrent deletions of the CDKN2A locus, occurring in 92% of the cases.
  • [MeSH-major] B-Lymphocytes / pathology. Cell Lineage. Gene Expression Profiling. Genome, Human / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Cell Cycle. Child. Chromosomes, Human, Pair 13 / genetics. Chromosomes, Human, Pair 9 / genetics. Gene Duplication. Gene Expression Regulation, Leukemic. Humans. Polyploidy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. T-Lymphocytes / pathology

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19389505.001).
  • [ISSN] 1873-4456
  • [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
  •  go-up   go-down


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

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

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


63. Gaikwad A, Rye CL, Devidas M, Heerema NA, Carroll AJ, Izraeli S, Plon SE, Basso G, Pession A, Rabin KR: Prevalence and clinical correlates of JAK2 mutations in Down syndrome acute lymphoblastic leukaemia. Br J Haematol; 2009 Mar;144(6):930-2
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence and clinical correlates of JAK2 mutations in Down syndrome acute lymphoblastic leukaemia.
  • Recurrent, prognostically significant chromosomal abnormalities occur in approximately 75% of paediatric acute lymphoblastic leukaemia (ALL), but only infrequently in children with Down syndrome (DS) and ALL.

  • Genetic Alliance. consumer health - Down Syndrome.
  • MedlinePlus Health Information. consumer health - Down Syndrome.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2007 Mar 1;109(5):2202-4 [17068151.001]
  • [Cites] Lancet. 2008 Oct 25;372(9648):1484-92 [18805579.001]
  • [Cites] Br J Cancer. 1977 Jan;35(1):1-39 [831755.001]
  • [Cites] Lancet. 2000 Jan 15;355(9199):165-9 [10675114.001]
  • [Cites] Nat Genet. 2002 Sep;32(1):148-52 [12172547.001]
  • [Cites] Blood. 2009 Jan 15;113(3):646-8 [18927438.001]
  • (PMID = 19120350.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K12 CA090433; United States / NCI NIH HHS / CA / K12 CA090433-06; United States / NCI NIH HHS / CA / CA90433-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / Janus Kinase 2
  • [Other-IDs] NLM/ NIHMS127709; NLM/ PMC2724897
  •  go-up   go-down


64. Thomas DA, Sarris AH, Cortes J, Faderl S, O'Brien S, Giles FJ, Garcia-Manero G, Rodriguez MA, Cabanillas F, Kantarjian H: Phase II study of sphingosomal vincristine in patients with recurrent or refractory adult acute lymphocytic leukemia. Cancer; 2006 Jan 1;106(1):120-7
Hazardous Substances Data Bank. VINCRISTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of sphingosomal vincristine in patients with recurrent or refractory adult acute lymphocytic leukemia.
  • BACKGROUND: Outcomes with salvage therapy for patients with recurrent or refractory acute lymphocytic leukemia (ALL) are poor, with complete response (CR) rates reported to be 20-30% and a median survival ranging from 2-6 months.
  • METHODS: A Phase II clinical trial of single-agent SV given at a dose of 2.0 mg/m2 every 2 weeks was conducted in patients with recurrent or refractory ALL.
  • Five patients (36%) had transient reductions in bone marrow leukemia infiltrate with subsequent regrowth of the leukemia between SV infusions.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Salvage Therapy. Vincristine / therapeutic use

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2005 American Cancer Society.
  • [ErratumIn] Cancer. 2006 Apr 1;106(7):1641
  • (PMID = 16331634.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Liposomes; 0 / Sphingomyelins; 5J49Q6B70F / Vincristine
  •  go-up   go-down


65. Hamaki T, Kami M, Kanda Y, Yuji K, Inamoto Y, Kishi Y, Nakai K, Nakayama I, Murashige N, Abe Y, Ueda Y, Hino M, Inoue T, Ago H, Hidaka M, Hayashi T, Yamane T, Uoshima N, Miyakoshi S, Taniguchi S: Reduced-intensity stem-cell transplantation for adult acute lymphoblastic leukemia: a retrospective study of 33 patients. Bone Marrow Transplant; 2005 Mar;35(6):549-56
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reduced-intensity stem-cell transplantation for adult acute lymphoblastic leukemia: a retrospective study of 33 patients.
  • Efficacy of reduced-intensity stem-cell transplantation (RIST) for acute lymphoblastic leukemia (ALL) was investigated in 33 patients (median age, 55 years).
  • Acute and chronic graft-versus-host disease (GVHD) developed in 45 and 64%, respectively.
  • Six patients received donor lymphocyte infusion (DLI), for prophylaxis (n=1) or treatment of recurrent ALL (n=5).
  • These findings suggest the presence of a graft-versus-leukemia effect for ALL.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15756282.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


66. Stanulla M, Cario G, Meissner B, Schrauder A, Möricke A, Riehm H, Schrappe M: Integrating molecular information into treatment of childhood acute lymphoblastic leukemia--a perspective from the BFM Study Group. Blood Cells Mol Dis; 2007 Sep-Oct;39(2):160-3
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Integrating molecular information into treatment of childhood acute lymphoblastic leukemia--a perspective from the BFM Study Group.
  • Acute lymphoblastic leukemia (ALL) is the most common malignancy of childhood and is treated with chemotherapy alone or, in particular subgroups, with additional radiation therapy and/or stem cell transplantation.
  • However, although overall long-term cure rates for childhood ALL treated on risk-adapted protocols have dramatically improved over the last decades and, to date, are higher than 75%, a significant number of patients still die due to recurrent disease or the toxicity of treatment applied.
  • One goal in future BFM trials will be to take advantage of a better molecular understanding of leukemia and host characteristics to dissect the mechanisms underlying the differences in treatment response.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17532236.001).
  • [ISSN] 1079-9796
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 18
  •  go-up   go-down


67. Kato K, Kobayashi C, Kudo K, Hara T, Masuko K, Koike K, Tsuchida M: Late recurrence of precursor B-cell acute lymphoblastic leukemia 9 years and 7 months after allogeneic hematopoietic stem cell transplantation. J Pediatr Hematol Oncol; 2010 Oct;32(7):e290-3
Genetic Alliance. consumer health - Transplantation.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Late recurrence of precursor B-cell acute lymphoblastic leukemia 9 years and 7 months after allogeneic hematopoietic stem cell transplantation.
  • We present the case of a 15-year-old adolescent boy with recurrent precursor B-cell acute lymphoblastic leukemia, which appeared 9 years and 7 months after a first unrelated allogeneic hematopoietic stem cell transplantation (HSCT).
  • [MeSH-major] Gene Rearrangement, B-Lymphocyte. Hematopoietic Stem Cell Transplantation. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / therapy

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20881873.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


68. Tsuzuki S, Karnan S, Horibe K, Matsumoto K, Kato K, Inukai T, Goi K, Sugita K, Nakazawa S, Kasugai Y, Ueda R, Seto M: Genetic abnormalities involved in t(12;21) TEL-AML1 acute lymphoblastic leukemia: analysis by means of array-based comparative genomic hybridization. Cancer Sci; 2007 May;98(5):698-706
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic abnormalities involved in t(12;21) TEL-AML1 acute lymphoblastic leukemia: analysis by means of array-based comparative genomic hybridization.
  • The TEL (ETV6)-AML1 (RUNX1) chimeric gene fusion is the most common genetic abnormality in childhood acute lymphoblastic leukemias.
  • Evidence suggests that this chimeric gene fusion constitutes an initiating mutation that is necessary but insufficient for the development of leukemia.
  • In a search for additional genetic events that could be linked to the development of leukemia, we applied a genome-wide array-comparative genomic hybridization technique to 24 TEL-AML1 leukemia samples and two cell lines.
  • Recurrent regions of chromosomal imbalance (>10% of cases) and representative involved genes were gain of chromosomes 10 (17%) and 21q (25%; RUNX1) and loss of 12p13.2 (87%; TEL), 9p21.3 (29%; p16INK4a/ARF), 9p13.2 (25%; PAX5), 12q21.3 (25%; BTG1), 3p21 (21%; LIMD1), 6q21 (17%; AIM1 and BLIMP1), 4q31.23 (17%; NR3C2), 11q22-q23 (13%;.
  • Together, these findings suggest that some of the genes identified as lost by array-comparative genomic hybridization may partly account for the development of leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 21. Core Binding Factor Alpha 2 Subunit / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17374122.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 146835-72-5 / BTG1 protein, human
  •  go-up   go-down


69. Reid AG, Seppa L, von der Weid N, Niggli FK, Betts DR: A t(12;17)(p13;q12) identifies a distinct TEL rearrangement-negative subtype of precursor-B acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2006 Feb;165(1):64-9
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A t(12;17)(p13;q12) identifies a distinct TEL rearrangement-negative subtype of precursor-B acute lymphoblastic leukemia.
  • Structural rearrangements involving the short arm of chromosome 12 are common in acute lymphoblastic leukemia (ALL) and often involve the TEL locus at 12p13.
  • The balanced t(12;17)(p13;q12) is a rare but recurrent aberration in ALL.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16490598.001).
  • [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 / ETS translocation variant 6 protein; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins; 0 / TEL-AML1 fusion protein
  •  go-up   go-down


70. Wolach B, Ash S, Gavrieli R, Stark B, Yaniv I, Roos D: Acute lymphoblastic leukemia in a patient with chronic granulomatous disease and a novel mutation in CYBB: first report. Am J Hematol; 2005 Sep;80(1):50-4
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute lymphoblastic leukemia in a patient with chronic granulomatous disease and a novel mutation in CYBB: first report.
  • We report for the first time a child with chronic granulomatous disease (CGD) who developed acute lymphoblastic leukemia (ALL).
  • During the course of ALL and later, he suffered from recurrent severe pyogenic infections, but careful detection of the etiological agent and promptly instituted specific treatment resulted in his complete recovery.
  • [MeSH-major] Granulomatous Disease, Chronic / genetics. Membrane Glycoproteins / genetics. Mutation. NADPH Oxidase / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Chronic Granulomatous Disease.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16138344.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CYBB protein, human; 0 / Membrane Glycoproteins; EC 1.6.3.1 / NADPH Oxidase
  •  go-up   go-down


71. Alexander BM, Wechsler D, Braun TM, Levine J, Herman J, Yanik G, Hutchinson R, Pierce LJ: Utility of cranial boost in addition to total body irradiation in the treatment of high risk acute lymphoblastic leukemia. Int J Radiat Oncol Biol Phys; 2005 Nov 15;63(4):1191-6
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Utility of cranial boost in addition to total body irradiation in the treatment of high risk acute lymphoblastic leukemia.
  • PURPOSE: Total body irradiation (TBI) as part of a conditioning regimen before hematopoietic stem cell transplant (HSCT) is an important component in the management of acute lymphoblastic leukemia (ALL) that has relapsed or has other certain high-risk features.
  • RESULTS: At the time of analysis, 30 (45%) patients were alive with no evidence of disease, 8 (12%) were alive with recurrence of leukemia, 7 (10.5%) had recurrent ALL but with successful salvage, 7 (11%) died subsequent to recurrence, 14 (21%) died from complications related to HCST, and 1 patient was lost to follow-up (1.5%).
  • [MeSH-major] Brain Neoplasms / prevention & control. Cranial Irradiation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / prevention & control. Whole-Body Irradiation


72. Pan JL, Xue YQ, Jiang HY, Zhu YJ, Ma L, Li TY, Wang Y, Wu YF: [Clinical and experimental study of 7 cases of acute lymphoblastic leukemia with dic(7;9) (pll;pll)]. Zhonghua Xue Ye Xue Za Zhi; 2005 Aug;26(8):485-8
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical and experimental study of 7 cases of acute lymphoblastic leukemia with dic(7;9) (pll;pll)].
  • OBJECTIVE: To investigate the laboratory and clinical features of 7 cases of acute lymphoblastic leukemia (ALL) with dic(7;9) (pll;pll).
  • CONCLUSION: dic(7;9) was a rare, but recurrent chromosome abnormality in ALL and had some clinical and laboratory features.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16383241.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  •  go-up   go-down


73. Van Vlierberghe P, van Grotel M, Beverloo HB, Lee C, Helgason T, Buijs-Gladdines J, Passier M, van Wering ER, Veerman AJ, Kamps WA, Meijerink JP, Pieters R: The cryptic chromosomal deletion del(11)(p12p13) as a new activation mechanism of LMO2 in pediatric T-cell acute lymphoblastic leukemia. Blood; 2006 Nov 15;108(10):3520-9
Genetic Alliance. consumer health - Pediatric T-cell leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The cryptic chromosomal deletion del(11)(p12p13) as a new activation mechanism of LMO2 in pediatric T-cell acute lymphoblastic leukemia.
  • To identify new cytogenetic abnormalities associated with leukemogenesis or disease outcome, T-cell acute lymphoblastic leukemia (T-ALL) patient samples were analyzed by means of the array-comparative genome hybridization technique (array-CGH).
  • Here, we report the identification of a new recurrent and cryptic deletion on chromosome 11 (del(11)(p12p13)) in about 4% (6/138) of pediatric T-ALL patients.
  • LMO2 rearrangements, including this del(11)(p12p13) and t(11;14) (p13;q11) or t(7;11)(q35;p13), were found in the absence of other recurrent cytogenetic abnormalities involving HOX11L2, HOX11, CALM-AF10, TAL1, MLL, or MYC.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 11. DNA-Binding Proteins / metabolism. Metalloproteins / metabolism. 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 = 16873670.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LMO2 protein, human; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins
  •  go-up   go-down


74. Einsiedel HG, von Stackelberg A, Hartmann R, Fengler R, Schrappe M, Janka-Schaub G, Mann G, Hählen K, Göbel U, Klingebiel T, Ludwig WD, Henze G: Long-term outcome in children with relapsed ALL by risk-stratified salvage therapy: results of trial acute lymphoblastic leukemia-relapse study of the Berlin-Frankfurt-Münster Group 87. J Clin Oncol; 2005 Nov 1;23(31):7942-50
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term outcome in children with relapsed ALL by risk-stratified salvage therapy: results of trial acute lymphoblastic leukemia-relapse study of the Berlin-Frankfurt-Münster Group 87.
  • PURPOSE: Approximately 20% of children with acute lymphoblastic leukemia (ALL) suffer a relapse, and their prognosis is unfavorable.
  • Between 1987 and 1990, the multicenter trial Acute Lymphoblastic Leukemia-Relapse Study of the Berlin-Frankfurt-Münster Group (ALL-REZ BFM) 87 was conducted to establish a uniform treatment for these children in Germany and Austria.
  • CONCLUSION: With the ALL-REZ BFM 87 protocol, more than one-third of patients may be regarded as cured from recurrent ALL with second complete remissions lasting more than 10 years.
  • [MeSH-major] Neoplasm Recurrence, Local / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Salvage Therapy

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Hazardous Substances Data Bank. THIOGUANINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] J Clin Oncol. 2008 May 1;26(13):2238
  • (PMID = 16258094.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] FTK8U1GZNX / Thioguanine; YL5FZ2Y5U1 / Methotrexate
  •  go-up   go-down


75. van Grotel M, Meijerink JP, Beverloo HB, Langerak AW, Buys-Gladdines JG, Schneider P, Poulsen TS, den Boer ML, Horstmann M, Kamps WA, Veerman AJ, van Wering ER, van Noesel MM, Pieters R: The outcome of molecular-cytogenetic subgroups in pediatric T-cell acute lymphoblastic leukemia: a retrospective study of patients treated according to DCOG or COALL protocols. Haematologica; 2006 Sep;91(9):1212-21
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The outcome of molecular-cytogenetic subgroups in pediatric T-cell acute lymphoblastic leukemia: a retrospective study of patients treated according to DCOG or COALL protocols.
  • BACKGROUND AND OBJECTIVES: Subgroups of T-cell acute lymphoblastic leukemia (T-ALL), defined according to recurrent cytogenetic aberrations, may have different prognoses.
  • Our data on CALM-AF10 rearranged T-ALL, albeit based on only three patients, suggest that this type of leukemia is associated with a poor outcome.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Cytogenetic Analysis. Leukemia-Lymphoma, Adult T-Cell / diagnosis

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Pediatric T-cell leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Haematologica. 2006 Sep;91(9):1156A [16956809.001]
  • (PMID = 16956820.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / AF10-CALM fusion protein, human; 0 / Oncogene Proteins, Fusion
  •  go-up   go-down


76. Pérez-Vera P, Salas C, Montero-Ruiz O, Frías S, Dehesa G, Jarquín B, Rivera-Luna R: Analysis of gene rearrangements using a fluorescence in situ hybridization method in Mexican patients with acute lymphoblastic leukemia: experience at a single institution. Cancer Genet Cytogenet; 2008 Jul 15;184(2):94-8
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of gene rearrangements using a fluorescence in situ hybridization method in Mexican patients with acute lymphoblastic leukemia: experience at a single institution.
  • We evaluated the prevalence of BCR/ABL, MLL, and ETV6/RUNX1 rearrangements as well as CDKN2A (alias p16) deletion in a group of Mexican children with acute lymphoblastic leukemia (ALL) to determine whether the changes coexist, and to compare the incidences found with other reports in the literature.
  • The coexistence of two recurrent abnormalities with specific prognostic significance in the same patient was not found.
  • [MeSH-major] Chromosome Aberrations. In Situ Hybridization, Fluorescence / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Child. Child, Preschool. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 19. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 9. Core Binding Factor Alpha 2 Subunit / genetics. Female. Gene Frequency. Genes, abl. Genes, p16. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Male. Mexico. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18617057.001).
  • [ISSN] 1873-4456
  • [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 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down


77. Abbas S, Lugthart S, Kavelaars FG, Schelen A, Koenders JE, Zeilemaker A, van Putten WJ, Rijneveld AW, Löwenberg B, Valk PJ: Acquired mutations in the genes encoding IDH1 and IDH2 both are recurrent aberrations in acute myeloid leukemia: prevalence and prognostic value. Blood; 2010 Sep 23;116(12):2122-6
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acquired mutations in the genes encoding IDH1 and IDH2 both are recurrent aberrations in acute myeloid leukemia: prevalence and prognostic value.
  • Somatic mutations in isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) were recently demonstrated in acute myeloid leukemia (AML), but their prevalence and prognostic impact remain to be explored in large extensively characterized AML series, and also in various other hematologic malignancies.
  • Moreover, we identified IDH mutations in 2 JAK2 V617F myeloproliferative neoplasias (n = 96), a single case of acute lymphoblastic leukemia (n = 96), and none in chronic myeloid leukemias (n = 81).
  • [MeSH-major] Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics. Mutation

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20538800.001).
  • [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] EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human; EC 1.1.1.42. / IDH1 protein, human; EC 2.7.10.2 / Janus Kinase 2
  •  go-up   go-down


78. Kim MJ, Yoon HS, Lim G, Kim SY, Lee HJ, Suh JT, Lee J, Lee WI, Park TS: ABL1 gene deletion without BCR/ABL1 rearrangement in a young adolescent with precursor B-cell acute lymphoblastic leukemia: clinical study and literature review. Cancer Genet Cytogenet; 2010 Jan 15;196(2):184-8
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ABL1 gene deletion without BCR/ABL1 rearrangement in a young adolescent with precursor B-cell acute lymphoblastic leukemia: clinical study and literature review.
  • Here we describe a fifth case of ABL1 deletion without BCR/ABL1 rearrangement in an adolescent patient with precursor B-cell lymphoblastic leukemia (B-ALL) and review the relevant literature.
  • It is not clear how ABL1 deletion affects leukemogenesis; however, it is plausible that ABL1 deletion without BCR/ABL1 rearrangement is a rare but recurrent genetic abnormality in precursor B-ALL patients.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Gene Deletion. Gene Rearrangement. Leukemia, B-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20082857.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 24
  •  go-up   go-down


79. Scandura JM: Advances in the molecular genetics of acute leukemia. Curr Oncol Rep; 2005 Sep;7(5):323-32
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Advances in the molecular genetics of acute leukemia.
  • Acute leukemias are characterized by the unrestrained clonal proliferation of hematopoietic precursor cells coupled with aberrant or arrested differentiation.
  • The molecular basis of hematopoiesis and leukemogenesis is still being defined, yet it is increasingly evident that acute leukemias have recurrent molecular features that can be exploited for diagnostic, prognostic, and therapeutic purposes.
  • Modern molecular technologies already influence treatment strategies for these diseases, and it is likely that as such technology matures it will have an increasing impact on all aspects of acute leukemia management.
  • This article reviews recent developments in the molecular classification, prognostication, and treatment of the acute leukemias.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Leukemia / genetics
  • [MeSH-minor] Cell Line, Tumor. Epigenesis, Genetic. Humans. Immunophenotyping. Karyotyping. Medical Oncology / trends. Mutation. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis. Pharmacogenetics / methods. Phenotype. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Prognosis. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic

  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2003 Oct 1;102(7):2705-6 [14504076.001]
  • [Cites] Blood. 2004 Oct 15;104(8):2492-8 [15198948.001]
  • [Cites] Blood. 2004 Dec 1;104(12):3679-87 [15226186.001]
  • [Cites] Nat Rev Cancer. 2005 Mar;5(3):223-31 [15719030.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2771-8 [14684422.001]
  • [Cites] Science. 2003 May 9;300(5621):949 [12738854.001]
  • [Cites] BMC Genomics. 2004 Sep 23;5:71 [15387886.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Ann Hematol. 2005 Apr;84(4):236-44 [15538567.001]
  • [Cites] Pharmacogenetics. 2002 Apr;12(3):183-90 [11927833.001]
  • [Cites] Br J Haematol. 2003 Jun;121(5):775-7 [12780793.001]
  • [Cites] Ann Hematol. 2004;83 Suppl 1:S124-6 [15124703.001]
  • [Cites] Nat Rev Cancer. 2004 Dec;4(12 ):988-93 [15573120.001]
  • [Cites] Blood. 1997 May 1;89(9):3323-9 [9129038.001]
  • [Cites] Am J Clin Pathol. 2004 Dec;122 Suppl:S47-57 [15690642.001]
  • [Cites] Leukemia. 2005 Apr;19(4):628-35 [15744351.001]
  • [Cites] Bioinformatics. 2003 Jan;19(1):71-8 [12499295.001]
  • [Cites] Blood. 2003 Feb 15;101(4):1270-6 [12406912.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4372-80 [12393388.001]
  • [Cites] Trends Genet. 2004 Feb;20(2):87-94 [14746990.001]
  • [Cites] Blood. 2000 Jan 15;95(2):726-7 [10660321.001]
  • [Cites] N Engl J Med. 2004 Aug 5;351(6):533-42 [15295046.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] J Clin Oncol. 1999 Dec;17(12):3835-49 [10577857.001]
  • [Cites] J Clin Oncol. 2003 Sep 1;21(17):3262-8 [12947061.001]
  • [Cites] Curr Oncol Rep. 2003 Sep;5(5):391-8 [12895391.001]
  • [Cites] Oncol Rep. 2004 Dec;12(6):1201-7 [15547738.001]
  • [Cites] Leukemia. 2003 Oct;17(10):1990-7 [14513049.001]
  • [Cites] Science. 2005 Feb 25;307(5713):1182 [15731412.001]
  • [Cites] J Clin Oncol. 2004 Feb 15;22(4):624-33 [14726504.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1617-28 [15084694.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • [Cites] Leuk Res. 2002 Jul;26(7):621-9 [12008078.001]
  • [Cites] Blood. 2005 Jun 1;105(11):4445-54 [15718413.001]
  • [Cites] Blood. 2000 Dec 15;96(13):4075-83 [11110676.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1883-90 [14592841.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1605-16 [15084693.001]
  • [Cites] Blood Rev. 2004 Jun;18(2):115-36 [15010150.001]
  • [Cites] Curr Opin Hematol. 2005 Jan;12(1):7-13 [15604885.001]
  • [Cites] Ann Intern Med. 1997 Apr 15;126(8):608-14 [9103127.001]
  • [Cites] Nat Med. 2001 Apr;7(4):444-51 [11283671.001]
  • [Cites] Clin Cancer Res. 2002 Oct;8(10):3118-30 [12374679.001]
  • [Cites] J Clin Oncol. 2004 Mar 15;22(6):1078-86 [15020609.001]
  • [Cites] Science. 1999 Oct 15;286(5439):531-7 [10521349.001]
  • [Cites] Oncogene. 2002 May 13;21(21):3422-44 [12032780.001]
  • (PMID = 16091192.001).
  • [ISSN] 1523-3790
  • [Journal-full-title] Current oncology reports
  • [ISO-abbreviation] Curr Oncol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger
  • [Number-of-references] 50
  •  go-up   go-down


80. Griffin TC, Weitzman S, Weinstein H, Chang M, Cairo M, Hutchison R, Shiramizu B, Wiley J, Woods D, Barnich M, Gross TG, Children's Oncology Group: A study of rituximab and ifosfamide, carboplatin, and etoposide chemotherapy in children with recurrent/refractory B-cell (CD20+) non-Hodgkin lymphoma and mature B-cell acute lymphoblastic leukemia: a report from the Children's Oncology Group. Pediatr Blood Cancer; 2009 Feb;52(2):177-81
Hazardous Substances Data Bank. CARBOPLATIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A study of rituximab and ifosfamide, carboplatin, and etoposide chemotherapy in children with recurrent/refractory B-cell (CD20+) non-Hodgkin lymphoma and mature B-cell acute lymphoblastic leukemia: a report from the Children's Oncology Group.
  • BACKGROUND: To estimate the response rate and therapy related toxicities of the anti-CD20 monoclonal antibody rituximab when combined with chemotherapy including ifosfamide, carboplatin, and etoposide (ICE) in patients with relapsed and refractory B-cell non-Hodgkin lymphoma and mature B-cell acute lymphoblastic leukemia (B-ALL).


81. Jones D, Thomas D, Yin CC, O'Brien S, Cortes JE, Jabbour E, Breeden M, Giles FJ, Zhao W, Kantarjian HM: Kinase domain point mutations in Philadelphia chromosome-positive acute lymphoblastic leukemia emerge after therapy with BCR-ABL kinase inhibitors. Cancer; 2008 Sep 1;113(5):985-94
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Kinase domain point mutations in Philadelphia chromosome-positive acute lymphoblastic leukemia emerge after therapy with BCR-ABL kinase inhibitors.
  • BACKGROUND: BCR-ABL kinase domain (KD) mutations are detected in approximately 45% of patients with imatinib-resistant chronic myeloid leukemia.
  • Patterns of KD mutations in Philadelphia chromosome (Ph)-positive acute lympho- blastic leukemia (ALL) are less well studied.
  • METHODS: The authors assessed KD mutations in patients with recurrent Ph-positive ALL after treatments that included 1 or more kinase inhibitors (n = 24 patients) or no prior kinase inhibitor (KI) therapy (n = 12 patients).
  • RESULTS: ABL KD mutations were detected by direct sequencing in 15 of 17 patients (88%) who had recurrent Ph-positive ALL and received prior imatinib (n = 16) or dasatinib (n = 1) treatment and in 6 of 7 patients (86%) who had resistant/recurrent tumors treated with >or=2 KIs compared with 0 of 12 patients with recurrent Ph-positive ALL who never received KIs.
  • Using a more sensitive pyrosequencing method, mutations were not detected at codons 315 and 253 in the diagnostic samples from those 12 patients or in 30 patients with Ph-positive ALL who never developed recurrent disease.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2008 American Cancer Society.
  • (PMID = 18615627.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / P50 CA100632-010007; United States / NCI NIH HHS / CA / P50 CA100707; United States / NCI NIH HHS / CA / 1P50CA100707-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ NIHMS58345; NLM/ PMC4204653
  •  go-up   go-down


82. Clappier E, Cuccuini W, Cayuela JM, Vecchione D, Baruchel A, Dombret H, Sigaux F, Soulier J: Cyclin D2 dysregulation by chromosomal translocations to TCR loci in T-cell acute lymphoblastic leukemias. Leukemia; 2006 Jan;20(1):82-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cyclin D2 dysregulation by chromosomal translocations to TCR loci in T-cell acute lymphoblastic leukemias.
  • Here, we identified chromosomal translocations targeting the CCND2 locus at 12p13, and the T-cell receptor beta (TCRB) or the TCRA/D loci in T-cell acute lymphoblastic leukemias (T-ALLs).
  • This report is the first clear evidence of a direct involvement of cyclin D2 in human cancer due to recurrent somatic genetic alterations.
  • [MeSH-major] Chromosomes, Human, Pair 12 / genetics. Cyclins / biosynthesis. Cyclins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Receptors, Antigen, T-Cell / genetics. Translocation, Genetic

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16270038.001).
  • [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 / CCND2 protein, human; 0 / Cyclin D2; 0 / Cyclins; 0 / Receptors, Antigen, T-Cell
  •  go-up   go-down


83. Mody R, Li S, Dover DC, Sallan S, Leisenring W, Oeffinger KC, Yasui Y, Robison LL, Neglia JP: Twenty-five-year follow-up among survivors of childhood acute lymphoblastic leukemia: a report from the Childhood Cancer Survivor Study. Blood; 2008 Jun 15;111(12):5515-23
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Twenty-five-year follow-up among survivors of childhood acute lymphoblastic leukemia: a report from the Childhood Cancer Survivor Study.
  • Survivors of childhood acute lymphoblastic leukemia (ALL) are at risk for late effects of cancer therapy.
  • Recurrent ALL (n = 483) and second neoplasms (SNs; n = 89) were the major causes of death.
  • Survivors who received radiation therapy as part of their treatment or had a leukemia relapse are at greatest risk for adverse outcomes.

  • Genetic Alliance. consumer health - Childhood Cancer.
  • 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] J Clin Oncol. 2006 Aug 20;24(24):3858-64 [16921038.001]
  • [Cites] J Clin Epidemiol. 2004 Sep;57(9):933-44 [15504636.001]
  • [Cites] Cancer. 2006 Sep 15;107(6):1303-12 [16894525.001]
  • [Cites] N Engl J Med. 2006 Oct 12;355(15):1572-82 [17035650.001]
  • [Cites] J Clin Oncol. 2006 Nov 20;24(33):5277-82 [17088567.001]
  • [Cites] Pediatr Blood Cancer. 2007 Apr;48(4):460-7 [16767717.001]
  • [Cites] J Pediatr. 2007 Apr;150(4):370-5, 375.e1 [17382112.001]
  • [Cites] Pediatr Blood Cancer. 2007 Jul;49(1):65-73 [16628558.001]
  • [Cites] Pediatr Blood Cancer. 2007 Jul;49(1):47-51 [16755550.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Jul;16(7):1356-63 [17627001.001]
  • [Cites] Am J Obstet Gynecol. 2002 Oct;187(4):1070-80 [12389007.001]
  • [Cites] Cancer. 2002 Dec 1;95(11):2431-41 [12436452.001]
  • [Cites] Cancer. 2000 Apr 1;88(7):1687-95 [10738228.001]
  • [Cites] Blood. 2000 May 1;95(9):2770-5 [10779419.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3310-22 [10828010.001]
  • [Cites] J Natl Cancer Inst. 2001 Apr 18;93(8):618-29 [11309438.001]
  • [Cites] J Clin Oncol. 2001 Jul 1;19(13):3163-72 [11432882.001]
  • [Cites] J Clin Oncol. 2001 Jul 1;19(13):3173-81 [11432883.001]
  • [Cites] Cancer. 2001 Oct 1;92(7):1977-83 [11745273.001]
  • [Cites] Med Pediatr Oncol. 2002 Apr;38(4):229-39 [11920786.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4257-64 [12036851.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jul;87(7):3136-41 [12107213.001]
  • [Cites] Cancer. 1986 Jul 15;58(2 Suppl):598-602 [3719551.001]
  • [Cites] N Engl J Med. 1987 Sep 3;317(10):588-93 [3475572.001]
  • [Cites] JAMA. 1989 Nov 17;262(19):2693-9 [2810602.001]
  • [Cites] Cancer. 1991 Jan 1;67(1):206-13 [1985719.001]
  • [Cites] Am J Pediatr Hematol Oncol. 1990 Winter;12(4):454-61 [2285126.001]
  • [Cites] Acta Paediatr Scand. 1991 Dec;80(12):1220-8 [1785295.001]
  • [Cites] J Clin Oncol. 1992 Sep;10(9):1397-406 [1517782.001]
  • [Cites] Am J Pediatr Hematol Oncol. 1994 May;16(2):143-52 [8166367.001]
  • [Cites] JAMA. 1994 Nov 9;272(18):1427-32 [7933424.001]
  • [Cites] Child Care Health Dev. 1994 Sep-Oct;20(5):309-22 [7988001.001]
  • [Cites] J Dev Behav Pediatr. 1994 Oct;15(5):353-66 [7868704.001]
  • [Cites] Cancer. 1995 Apr 15;75(8):2186-95 [7697611.001]
  • [Cites] N Engl J Med. 1995 Jun 15;332(24):1618-30 [7753142.001]
  • [Cites] Arch Dis Child. 1995 Aug;73(2):136-40 [7574857.001]
  • [Cites] J Child Psychol Psychiatry. 1996 Jul;37(5):597-607 [8807440.001]
  • [Cites] Oncology (Williston Park). 1997 Feb;11(2):259-64; discussion 264-5 [9057179.001]
  • [Cites] J Clin Oncol. 1997 Jun;15(6):2205-13 [9196132.001]
  • [Cites] Pediatr Clin North Am. 1997 Aug;44(4):1021-42 [9286298.001]
  • [Cites] J Clin Oncol. 1998 Aug;16(8):2848-53 [9704738.001]
  • [Cites] N Engl J Med. 1998 Aug 27;339(9):605-15 [9718381.001]
  • [Cites] Eur J Cancer. 1998 Apr;34(5):694-8 [9713276.001]
  • [Cites] Curr Probl Pediatr. 1998 Oct;28(9):273-97 [9794096.001]
  • [Cites] Stat Med. 1999 Mar 30;18(6):695-706 [10204198.001]
  • [Cites] Br J Cancer. 2004 Nov 29;91(11):1905-10 [15534607.001]
  • [Cites] Lancet. 2005 Jun 11-17;365(9476):2014-23 [15950715.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9187-97 [16361621.001]
  • [Cites] J Clin Oncol. 2006 Jun 1;24(16):2536-43 [16735706.001]
  • [Cites] J Natl Cancer Inst. 2006 Jul 5;98(13):890-6 [16818852.001]
  • [Cites] Turk J Pediatr. 2006 Apr-Jun;48(2):101-4 [16848106.001]
  • [Cites] Acta Paediatr. 2006 Aug;95(8):922-8 [16882563.001]
  • [Cites] Eur J Cancer. 2003 Feb;39(3):359-65 [12565989.001]
  • [Cites] Cancer. 2003 Feb 15;97(4):1115-26 [12569614.001]
  • [Cites] J Clin Oncol. 2003 Apr 1;21(7):1359-65 [12663727.001]
  • [Cites] Cancer. 2003 May 15;97(10):2554-64 [12733155.001]
  • [Cites] N Engl J Med. 2003 Aug 14;349(7):640-9 [12917300.001]
  • [Cites] JAMA. 2003 Sep 24;290(12):1583-92 [14506117.001]
  • [Cites] Ann Intern Med. 2004 Oct 19;141(8):590-7 [15492338.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Sep;91(9):3494-8 [16822820.001]
  • (PMID = 18334672.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / PHS HHS / / U24 55727; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2424150
  •  go-up   go-down


84. Lilljebjörn H, Soneson C, Andersson A, Heldrup J, Behrendtz M, Kawamata N, Ogawa S, Koeffler HP, Mitelman F, Johansson B, Fontes M, Fioretos T: The correlation pattern of acquired copy number changes in 164 ETV6/RUNX1-positive childhood acute lymphoblastic leukemias. Hum Mol Genet; 2010 Aug 15;19(16):3150-8
SciCrunch. ArrayExpress: Data: Microarray .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The correlation pattern of acquired copy number changes in 164 ETV6/RUNX1-positive childhood acute lymphoblastic leukemias.
  • The ETV6/RUNX1 fusion gene, present in 25% of B-lineage childhood acute lymphoblastic leukemia (ALL), is thought to represent an initiating event, which requires additional genetic changes for leukemia development.
  • In total, 45 recurrent CNAs were identified with an average number of 3.5 recurrent changes per case (range 0-13).
  • Twenty-six percent of cases displayed a set of recurrent CNAs identical to that of other cases in the data set.
  • The majority (74%), however, displayed a unique pattern of recurrent CNAs, indicating a large heterogeneity within this ALL subtype.

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Haematol. 2008 Mar;140(6):665-72 [18241254.001]
  • [Cites] Genes Chromosomes Cancer. 2008 Apr;47(4):333-40 [18181181.001]
  • [Cites] Genes Chromosomes Cancer. 2008 Dec;47(12):1118-25 [18767146.001]
  • [Cites] Genes Chromosomes Cancer. 2009 Jan;48(1):1-9 [18767147.001]
  • [Cites] Int J Cancer. 2009 Jun 15;124(12):2864-71 [19267402.001]
  • [Cites] Genes Chromosomes Cancer. 2009 Aug;48(8):637-60 [19415723.001]
  • [Cites] Leukemia. 2009 Jul;23(7):1209-18 [19242497.001]
  • [Cites] Hum Genet. 2009 Oct;126(4):511-20 [19484265.001]
  • [Cites] Leukemia. 2007 Oct;21(10):2137-44 [17690704.001]
  • [Cites] Lancet. 1999 Oct 30;354(9189):1499-503 [10551495.001]
  • [Cites] Cancer Res. 2000 Nov 15;60(22):6503-9 [11103820.001]
  • [Cites] J Comput Biol. 2000;7(6):789-803 [11382362.001]
  • [Cites] Nucleic Acids Res. 2002 Jan 1;30(1):207-10 [11752295.001]
  • [Cites] Bioinformatics. 2004 May 22;20(8):1233-40 [14871870.001]
  • [Cites] Cancer Genet Cytogenet. 1982 Oct;7(2):137-52 [7172163.001]
  • [Cites] Nature. 1995 Jul 20;376(6537):263-7 [7542362.001]
  • [Cites] Leukemia. 1995 Dec;9(12):1985-9 [8609706.001]
  • [Cites] Mol Cell Biol. 1996 Jun;16(6):2898-905 [8649400.001]
  • [Cites] Blood. 1996 Dec 1;88(11):4252-8 [8943861.001]
  • [Cites] J Comput Biol. 1999 Spring;6(1):37-51 [10223663.001]
  • [Cites] Nature. 1999 Oct 7;401(6753):556-62 [10524622.001]
  • [Cites] Mol Cell Biol. 2005 Jan;25(1):324-35 [15601853.001]
  • [Cites] Bioinformatics. 2007 Mar 15;23(6):657-63 [17234643.001]
  • [Cites] Cancer Sci. 2007 May;98(5):698-706 [17374122.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1258-66 [17443227.001]
  • [Cites] Blood. 2008 Jan 15;111(2):776-84 [17890455.001]
  • [Cites] Science. 2008 Jan 18;319(5861):336-9 [18202291.001]
  • [Cites] Nature. 2008 May 1;453(7191):110-4 [18408710.001]
  • (PMID = 20513752.001).
  • [ISSN] 1460-2083
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA026038-31; United States / NCI NIH HHS / CA / R01 CA026038-32; United States / NCI NIH HHS / CA / CA026038-30A2; United States / NCI NIH HHS / CA / R01 CA026038; United States / NCI NIH HHS / CA / R01 CA026038-30A2
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
  • [Other-IDs] NLM/ PMC3146010
  •  go-up   go-down


85. Kawamata N, Ogawa S, Zimmermann M, Kato M, Sanada M, Hemminki K, Yamatomo G, Nannya Y, Koehler R, Flohr T, Miller CW, Harbott J, Ludwig WD, Stanulla M, Schrappe M, Bartram CR, Koeffler HP: Molecular allelokaryotyping of pediatric acute lymphoblastic leukemias by high-resolution single nucleotide polymorphism oligonucleotide genomic microarray. Blood; 2008 Jan 15;111(2):776-84
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular allelokaryotyping of pediatric acute lymphoblastic leukemias by high-resolution single nucleotide polymorphism oligonucleotide genomic microarray.
  • Pediatric acute lymphoblastic leukemia (ALL) is a malignant disease resulting from accumulation of genetic alterations.
  • Three common genetic alterations were found: deletion of ETV6, deletion of p16INK4A, and hyperdiploidy, as well as a number of novel recurrent genetic alterations.
  • [MeSH-major] Chromosomes, Human, Pair 9 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Gene Deletion. Polymorphism, Single Nucleotide. 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
  • [Cites] Blood. 2000 Jun 1;95(11):3310-22 [10828010.001]
  • [Cites] Am J Hum Genet. 2007 Jul;81(1):114-26 [17564968.001]
  • [Cites] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128.001]
  • [Cites] Nat Genet. 2004 Oct;36(10):1084-9 [15361874.001]
  • [Cites] Blood. 1982 Oct;60(4):959-67 [7115962.001]
  • [Cites] Cell. 1987 Jul 31;50(3):509-17 [3607877.001]
  • [Cites] Blood. 1992 Sep 1;80(5):1316-23 [1381244.001]
  • [Cites] Genes Chromosomes Cancer. 1995 May;13(1):54-61 [7541644.001]
  • [Cites] Leukemia. 1995 Oct;9(10):1783-6 [7564526.001]
  • [Cites] Am J Med Genet. 1995 Nov 6;59(2):174-81 [8588582.001]
  • [Cites] Cancer Genet Cytogenet. 1996 Dec;92(2):111-5 [8976366.001]
  • [Cites] Blood. 1998 Sep 15;92(6):1898-909 [9731046.001]
  • [Cites] Cancer Res. 2005 Jan 15;65(2):375-8 [15695375.001]
  • [Cites] Lancet. 2005 Mar 19-25;365(9464):1054-61 [15781101.001]
  • [Cites] Nat Methods. 2004 Nov;1(2):109-11 [15782172.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):387-97 [15837627.001]
  • [Cites] Leukemia. 2005 May;19(5):734-40 [15789069.001]
  • [Cites] N Engl J Med. 2005 Apr 28;352(17):1779-90 [15858187.001]
  • [Cites] Nat Genet. 2005 May;37(5):549-54 [15838508.001]
  • [Cites] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] Nature. 2005 Jul 7;436(7047):117-22 [16001072.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6071-9 [16024607.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6306-15 [16155013.001]
  • [Cites] Br J Haematol. 2005 Sep;130(6):964-5 [16156866.001]
  • [Cites] Nat Rev Cancer. 2005 Oct;5(10):773-85 [16195750.001]
  • [Cites] Cancer Res. 2005 Oct 1;65(19):8597-603 [16204023.001]
  • [Cites] Nature. 2005 Oct 27;437(7063):1299-320 [16255080.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3377-9 [16081687.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] N Engl J Med. 2007 Feb 1;356(5):459-68 [17267906.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1258-66 [17443227.001]
  • [Cites] J Med Genet. 2001 Aug;38(8):497-507 [11483637.001]
  • (PMID = 17890455.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [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 / Cyclin-Dependent Kinase Inhibitor p16; 0 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins
  • [Other-IDs] NLM/ PMC2200831
  •  go-up   go-down


86. Kim IS, Kim HJ, Yoo KH, Sung KW, Kim SH: A boy with acute lymphoblastic leukemia acquired clonal and nonclonal cytogenetic abnormalities including del(7q) and del(20q) without clinical evidence of disease after sex-mismatched cord blood transplantation. J Pediatr Hematol Oncol; 2006 Aug;28(8):540-3
Genetic Alliance. consumer health - Transplantation.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A boy with acute lymphoblastic leukemia acquired clonal and nonclonal cytogenetic abnormalities including del(7q) and del(20q) without clinical evidence of disease after sex-mismatched cord blood transplantation.
  • An 8-year-old boy was diagnosed with precursor B-cell acute lymphoblastic leukemia.
  • Del(7q) and del(20q), 2 recurrent chromosomal aberrations in myeloid neoplasia, might represent underlying genomic instability in this patient, not the direct culprits of dysplasia or leukemogenesis.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16912597.001).
  • [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
  •  go-up   go-down


87. Baysal BE: A recurrent stop-codon mutation in succinate dehydrogenase subunit B gene in normal peripheral blood and childhood T-cell acute leukemia. PLoS One; 2007 May 09;2(5):e436
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A recurrent stop-codon mutation in succinate dehydrogenase subunit B gene in normal peripheral blood and childhood T-cell acute leukemia.
  • Here, I describe that succinate dehydrogenase (SDH; mitochondrial complex II) subunit B gene (SDHB) is somatically mutated at a cytidine residue in normal peripheral blood mononuclear cells (PBMCs) and T-cell acute leukemia.
  • Transcript sequence analyses in leukemic cell lines derived from monocyte, NK, T and B cells indicate that the mutational mechanism targeting SDHB is operational in T-cell acute leukemia.
  • Accordingly, substantial levels (more than 3%) of the mutant SDHB transcripts are detected in five of 20 primary childhood T-cell acute lymphoblastic leukemia (T-ALL) bone marrow samples, but in none of 20 B-ALL samples.
  • CONCLUSIONS: The identification of a recurrent, inactivating stop-codon mutation in the SDHB gene in normal blood cells suggests that SDHB is targeted by a cytidine deaminase enzyme.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2004 Oct 15;104(8):2224-34 [15231578.001]
  • [Cites] Hum Genet. 2003 Aug;113(3):228-37 [12811540.001]
  • [Cites] Eur J Haematol. 1999 Sep;63(3):180-91 [10485273.001]
  • [Cites] Mol Cell Biol. 2004 Dec;24(24):10933-40 [15572694.001]
  • [Cites] Nat Rev Cancer. 2005 Nov;5(11):857-66 [16327764.001]
  • [Cites] BMC Med Genet. 2005;6:39 [16288654.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Jun;7(6):415-25 [16723977.001]
  • [Cites] Cancer Res. 2006 Aug 1;66(15):7615-20 [16885361.001]
  • [Cites] Anal Biochem. 2007 Jan 1;360(1):84-91 [17107651.001]
  • [Cites] J Exp Med. 2007 Jan 22;204(1):7-10 [17190841.001]
  • [Cites] BMC Biol. 2007;5:12 [17376234.001]
  • [Cites] J Appl Physiol (1985). 2005 Feb;98(2):715-21 [15649883.001]
  • [Cites] Science. 2000 Feb 4;287(5454):848-51 [10657297.001]
  • [Cites] Nat Genet. 2000 Aug;25(4):375-6 [10932175.001]
  • [Cites] Am J Hum Genet. 2002 Jan;70(1):38-50 [11727199.001]
  • [Cites] Annu Rev Immunol. 2002;20:165-96 [11861601.001]
  • [Cites] J Med Genet. 2002 Mar;39(3):178-83 [11897817.001]
  • [Cites] Trends Genet. 2003 Apr;19(4):207-16 [12683974.001]
  • [Cites] Annu Rev Genet. 1990;24:305-26 [2088171.001]
  • (PMID = 17487275.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA98543; United States / NCI NIH HHS / CA / CA114766; United States / NCI NIH HHS / CA / U24 CA114766; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA11236
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon, Terminator; 0 / DNA Primers; 0 / RNA, Messenger; EC 1.3.99.1 / Succinate Dehydrogenase
  • [Other-IDs] NLM/ PMC1855983
  • [General-notes] NLM/ Original DateCompleted: 20070727
  •  go-up   go-down


88. Reiter A, Walz C, Watmore A, Schoch C, Blau I, Schlegelberger B, Berger U, Telford N, Aruliah S, Yin JA, Vanstraelen D, Barker HF, Taylor PC, O'Driscoll A, Benedetti F, Rudolph C, Kolb HJ, Hochhaus A, Hehlmann R, Chase A, Cross NC: The t(8;9)(p22;p24) is a recurrent abnormality in chronic and acute leukemia that fuses PCM1 to JAK2. Cancer Res; 2005 Apr 1;65(7):2662-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The t(8;9)(p22;p24) is a recurrent abnormality in chronic and acute leukemia that fuses PCM1 to JAK2.
  • We have identified a t(8;9)(p21-23;p23-24) in seven male patients (mean age 50, range 32-74) with diverse hematologic malignancies and clinical outcomes: atypical chronic myeloid leukemia/chronic eosinophilic leukemia (n = 5), secondary acute myeloid leukemia (n = 1), and pre-B-cell acute lymphoblastic leukemia (n = 1).
  • We conclude that human autoantigen pericentriolar material (PCM1)-JAK2 is a novel, recurrent fusion gene in hematologic malignancies.
  • [MeSH-major] Cell Cycle Proteins / genetics. Chromosomes, Human, Pair 8 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Aged. Amino Acid Sequence. Autoantigens. Base Sequence. Humans. Janus Kinase 2. Male. Middle Aged. Molecular Sequence Data. Reverse Transcriptase Polymerase Chain Reaction

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15805263.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantigens; 0 / Cell Cycle Proteins; 0 / Oncogene Proteins, Fusion; 0 / PCM1 protein, human; 0 / PCM1-JAK2 fusion protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  •  go-up   go-down


89. Yasar D, Karadogan I, Alanoglu G, Akkaya B, Luleci G, Salim O, Timuragaoglu A, Toruner GA, Berker-Karauzum S: Array comparative genomic hybridization analysis of adult acute leukemia patients. Cancer Genet Cytogenet; 2010 Mar;197(2):122-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Array comparative genomic hybridization analysis of adult acute leukemia patients.
  • We have performed a retrospective array-based comparative hybridization (array-CGH) study on 41 acute leukemia samples [n=17 acute lymphoblastic leukemia (ALL) patients only at diagnosis, n=3 ALL patients both at diagnosis and relapse; n=20 acute myeloid leukemia (AML) patients only at diagnosis and n=1 AML patient both at diagnosis and relapse] using an Agilent 44K array.
  • ALL-specific recurrent abnormalities were RB1 (n=3), PAX5 (n=4), and CDKN2B (n=3) deletions; AML-specific recurrent abnormalities were HOXA9 and HOXA10 (n=2) deletions and NOTCH1 duplication (n=2).
  • Recurrent duplication of the ELK1 oncogene was observed in both ALL (n=2) and AML (n=3) cases.
  • [MeSH-major] Comparative Genomic Hybridization / methods. Oligonucleotide Array Sequence Analysis / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosome Aberrations. Female. Humans. In Situ Hybridization, Fluorescence. Leukemia, Myeloid, Acute / genetics. Male. Middle Aged. Mutation. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20193845.001).
  • [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
  •  go-up   go-down


90. Lundin C, Heidenblad M, Strombeck B, Borg A, Hovland R, Heim S, Johansson B: Tiling resolution array CGH of dic(7;9)(p11 approximately 13;p11 approximately 13) in B-cell precursor acute lymphoblastic leukemia reveals clustered breakpoints at 7p11.2 approximately 12.1 and 9p13.1. Cytogenet Genome Res; 2007;118(1):13-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tiling resolution array CGH of dic(7;9)(p11 approximately 13;p11 approximately 13) in B-cell precursor acute lymphoblastic leukemia reveals clustered breakpoints at 7p11.2 approximately 12.1 and 9p13.1.
  • The dic(7;9)(p11 approximately 13;p11 approximately 13) is a recurrent chromosomal abnormality in acute lymphoblastic leukemia (ALL), mainly of B-lineage.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2007 S. Karger AG, Basel.
  • (PMID = 17901695.001).
  • [ISSN] 1424-859X
  • [Journal-full-title] Cytogenetic and genome research
  • [ISO-abbreviation] Cytogenet. Genome Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  •  go-up   go-down


91. De Braekeleer M, Morel F, Le Bris MJ, Herry A, Douet-Guilbert N: The MLL gene and translocations involving chromosomal band 11q23 in acute leukemia. Anticancer Res; 2005 May-Jun;25(3B):1931-44
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The MLL gene and translocations involving chromosomal band 11q23 in acute leukemia.
  • Reciprocal chromosomal translocations are recurrent features of many hematological malignancies.
  • The cloning of the genes located at the breakpoints of chromosomal translocations in leukemia and lymphoma has led to the identification of new genes involved in carcinogenesis.
  • Based on 7969 cases of acute myeloblastic leukemia (AML) and 1252 cases of acute lymphoblastic leukemia (ALL) taken from the literature, band 11q23 and/or the MLL gene was involved in 5.2% of AML and 22% of ALL.
  • Differences in the frequency and the distribution of translocations were noted according to the type of acute leukemia and age of the patients.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Chromosome Banding. Histone-Lysine N-Methyltransferase. Humans. Myeloid-Lymphoid Leukemia Protein. Translocation, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16158928.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 55
  •  go-up   go-down


92. Sandler ES, Homans A, Mandell L, Amylon M, Wall DA, Devidas M, Buchanan GR, Lipton JM, Billett AL: Hematopoietic stem cell transplantation after first marrow relapse of non-T, non-B acute lymphoblastic leukemia: a pediatric oncology group pilot feasibility study. J Pediatr Hematol Oncol; 2006 Apr;28(4):210-5
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hematopoietic stem cell transplantation after first marrow relapse of non-T, non-B acute lymphoblastic leukemia: a pediatric oncology group pilot feasibility study.
  • BACKGROUND: Relapsed acute lymphoblastic leukemia (ALL) in children is associated with a poor outcome, especially for those patients whose relapse occurs during the first 36 months after diagnosis.
  • This study was designed to evaluate the feasibility of enrolling children with recurrent ALL in a standardized treatment protocol that included receipt of a hematopoietic stem cell transplant (HSCT).
  • CONCLUSION: We conclude that well designed and controlled prospective studies are necessary to define the role of HSCTs in children with recurrent ALL.
  • [MeSH-major] Bone Marrow / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Stem Cell Transplantation


93. Karrman K, Andersson A, Björgvinsdóttir H, Strömbeck B, Lassen C, Olofsson T, Nguyen-Khac F, Berger R, Bernard O, Fioretos T, Johansson B: Deregulation of cyclin D2 by juxtaposition with T-cell receptor alpha/delta locus in t(12;14)(p13;q11)-positive childhood T-cell acute lymphoblastic leukemia. Eur J Haematol; 2006 Jul;77(1):27-34
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Deregulation of cyclin D2 by juxtaposition with T-cell receptor alpha/delta locus in t(12;14)(p13;q11)-positive childhood T-cell acute lymphoblastic leukemia.
  • OBJECTIVES: The t(12;14)(p13;q11)--a recurrent translocation in childhood T-cell acute lymphoblastic leukemia (T-ALL)--has very recently been molecularly characterized in one case, which displayed overexpression of the cyclin D2 gene (CCND2).
  • CONCLUSION: We have confirmed, in two additional cases, that the recurrent T-ALL-associated t(12;14) results in overexpression of cyclin D2.
  • [MeSH-major] Cyclins / genetics. Gene Expression Regulation, Neoplastic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell, alpha-beta / genetics. Receptors, Antigen, T-Cell, gamma-delta / genetics. Translocation, Genetic

  • 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 = 16548914.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / CCND2 protein, human; 0 / Cyclin D2; 0 / Cyclins; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Antigen, T-Cell, gamma-delta
  •  go-up   go-down


94. Tibes R, Keating MJ, Ferrajoli A, Wierda W, Ravandi F, Garcia-Manero G, O'Brien S, Cortes J, Verstovsek S, Browning ML, Faderl S: Activity of alemtuzumab in patients with CD52-positive acute leukemia. Cancer; 2006 Jun 15;106(12):2645-51
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activity of alemtuzumab in patients with CD52-positive acute leukemia.
  • BACKGROUND: Alemtuzumab is a humanized monoclonal antibody directed against the cell surface antigen CD52 and has demonstrated activity in chronic lymphocytic leukemia and other CD52-positive lymphoproliferative disorders.
  • Because CD52 also is expressed on acute leukemic blasts, the authors investigated the safety and efficacy of alemtuzumab in patients with acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL).
  • METHODS: Fifteen patients with CD52-positive (> or = 20%), recurrent or refractory acute leukemia (9 patients with AML and 6 patients with ALL) received alemtuzumab at a dose of 30 mg intravenously given 3 times a week (dose escalation during Week 1) for a total of 4 to 12 weeks.
  • CONCLUSIONS: Single-agent alemtuzumab was found to have limited activity in recurrent or refractory acute leukemia.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antigens, CD / immunology. Antigens, Neoplasm / immunology. Glycoproteins / immunology. Leukemia, Myeloid / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antibodies, Monoclonal, Humanized. Bacteremia / diagnosis. Bacteremia / etiology. Bone Marrow / drug effects. Bone Marrow / pathology. Disease Progression. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Female. Fungemia / diagnosis. Fungemia / etiology. Humans. Male. Middle Aged. Pneumonia / diagnosis. Pneumonia / etiology. Treatment Outcome

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2006 American Cancer Society.
  • (PMID = 16688777.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CD52 antigen; 0 / Glycoproteins; 3A189DH42V / alemtuzumab
  •  go-up   go-down


95. Moorman AV, Harrison CJ, Buck GA, Richards SM, Secker-Walker LM, Martineau M, Vance GH, Cherry AM, Higgins RR, Fielding AK, Foroni L, Paietta E, Tallman MS, Litzow MR, Wiernik PH, Rowe JM, Goldstone AH, Dewald GW, Adult Leukaemia Working Party, Medical Research Council/National Cancer Research Institute: Karyotype is an independent prognostic factor in adult acute lymphoblastic leukemia (ALL): analysis of cytogenetic data from patients treated on the Medical Research Council (MRC) UKALLXII/Eastern Cooperative Oncology Group (ECOG) 2993 trial. Blood; 2007 Apr 15;109(8):3189-97
Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Karyotype is an independent prognostic factor in adult acute lymphoblastic leukemia (ALL): analysis of cytogenetic data from patients treated on the Medical Research Council (MRC) UKALLXII/Eastern Cooperative Oncology Group (ECOG) 2993 trial.
  • However, its usefulness in adult acute lymphoblastic leukemia (ALL) is generally limited to the presence of the Philadelphia (Ph) chromosome because of the low incidence of other recurrent abnormalities.
  • [MeSH-major] Chromosome Deletion. Philadelphia Chromosome. Ploidies. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17170120.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U137686856
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


96. Sinclair P, Harrison CJ, Jarosová M, Foroni L: Analysis of balanced rearrangements of chromosome 6 in acute leukemia: clustered breakpoints in q22-q23 and possible involvement of c-MYB in a new recurrent translocation, t(6;7)(q23;q32 through 36). Haematologica; 2005 May;90(5):602-11
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of balanced rearrangements of chromosome 6 in acute leukemia: clustered breakpoints in q22-q23 and possible involvement of c-MYB in a new recurrent translocation, t(6;7)(q23;q32 through 36).
  • BACKGROUND AND OBJECTIVES: Many clinically important oncogenes and tumor suppressor genes have been identified through analysis of recurrent chromosomal rearrangements in acute leukemia.
  • In this study we investigated the significance of novel translocations and inversions of 6q in acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).
  • INTERPRETATION AND CONCLUSIONS: We identified a new primary recurrent translocation t(6;7) (q22;q23 through q26) in pediatric T-ALL.
  • Other translocations interrupting the 6q22-q23 breakpoint cluster region did not appear to be recurrent and may contribute to leukemogenesis through a novel mechanism.
  • [MeSH-major] Chromosome Breakage. Chromosome Inversion / genetics. Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 7 / genetics. Genes, myb. Leukemia, Myeloid / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adaptor Proteins, Signal Transducing / genetics. Adolescent. Bone Marrow Cells / ultrastructure. Child. Child, Preschool. Chromosome Banding. Clone Cells / pathology. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Male. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15921375.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / AHI1 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Oncogene Proteins, Fusion
  •  go-up   go-down


97. Pihan G: Detection of gene fusions in acute leukemia using bead microarrays. Curr Protoc Cytom; 2006 Feb;Chapter 13:Unit13.7
MedlinePlus Health Information. consumer health - Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of gene fusions in acute leukemia using bead microarrays.
  • This unit describes a method for the rapid and simultaneous detection of hybrid mRNAs (hRNA; also known as gene fusions, RNA fusions, or chimeric RNA), resulting from recurrent chromosome translocations or inversions in acute leukemia.
  • The assay is designed to detect the most common risk-stratifying translocation in pediatric acute lymphoblastic leukemia, satisfying the demand for inclusion of genetic data in the diagnosis of acute leukemia as predicated by the current WHO classification of hematopoietic and lymphoid neoplasms.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18770837.001).
  • [ISSN] 1934-9300
  • [Journal-full-title] Current protocols in cytometry
  • [ISO-abbreviation] Curr Protoc Cytom
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / RNA, Messenger; 0 / RNA, Neoplasm
  •  go-up   go-down


98. Chang HH, Lu MY, Jou ST, Lin KH, Tien HF, Lin DT: Cytogenetics in childhood acute lymphoblastic leukemia in Taiwan: a single-institutional experience. Pediatr Hematol Oncol; 2006 Sep;23(6):495-506
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetics in childhood acute lymphoblastic leukemia in Taiwan: a single-institutional experience.
  • Of the patients with abnormal karyotypes, recurrent structural abnormalities were determined in 31 (50%) cases, with the most frequent t(9;22).
  • [MeSH-major] Chromosome Aberrations / statistics & numerical data. 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 = 16849281.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


99. Radtke I, Mullighan CG, Ishii M, Su X, Cheng J, Ma J, Ganti R, Cai Z, Goorha S, Pounds SB, Cao X, Obert C, Armstrong J, Zhang J, Song G, Ribeiro RC, Rubnitz JE, Raimondi SC, Shurtleff SA, Downing JR: Genomic analysis reveals few genetic alterations in pediatric acute myeloid leukemia. Proc Natl Acad Sci U S A; 2009 Aug 4;106(31):12944-9
SciCrunch. ArrayExpress: Data: Microarray .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genomic analysis reveals few genetic alterations in pediatric acute myeloid leukemia.
  • Pediatric de novo acute myeloid leukemia (AML) is an aggressive malignancy with current therapy resulting in cure rates of only 60%.
  • Our data demonstrate that, in contrast to pediatric acute lymphoblastic leukemia (ALL), de novo AML is characterized by a very low burden of genomic alterations, with a mean of only 2.38 somatic copy-number alterations per leukemia, and less than 1 nonsynonymous point mutation per leukemia in the 25 genes analyzed.
  • Even more surprising was the observation that 34% of the leukemias lacked any identifiable copy-number alterations, and 28% of the leukemias with recurrent translocations lacked any identifiable sequence or numerical abnormalities.
  • The only exception to the presence of few mutations was acute megakaryocytic leukemias, with the majority of these leukemias being characterized by a high number of copy-number alterations but rare point mutations.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mutat Res. 2008 Apr 2;640(1-2):97-106 [18243251.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1534-42 [17954704.001]
  • [Cites] Leukemia. 2008 May;22(5):915-31 [18288131.001]
  • [Cites] Genes Chromosomes Cancer. 2008 Sep;47(9):729-39 [18506749.001]
  • [Cites] Leuk Lymphoma. 2008 Jun;49(6):1178-83 [18452069.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1807-12 [18772396.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1801-6 [18772397.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Oct 21;105(42):16224-9 [18852474.001]
  • [Cites] Nature. 2008 Oct 23;455(7216):1061-8 [18772890.001]
  • [Cites] Nature. 2008 Nov 6;456(7218):66-72 [18987736.001]
  • [Cites] Cancer Res. 2008 Dec 15;68(24):10349-57 [19074904.001]
  • [Cites] Nature. 2009 Mar 12;458(7235):223-7 [19182780.001]
  • [Cites] Cancer. 2007 Jan 1;109(1):157-63 [17133407.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Genes Dev. 2000 Jul 15;14(14):1810-23 [10898795.001]
  • [Cites] Nature. 2001 Nov 1;414(6859):105-11 [11689955.001]
  • [Cites] Annu Rev Genomics Hum Genet. 2002;3:179-98 [12194988.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2387-94 [12816873.001]
  • [Cites] J Clin Oncol. 2004 Feb 15;22(4):624-33 [14726504.001]
  • [Cites] Nat Rev Cancer. 2004 Mar;4(3):177-83 [14993899.001]
  • [Cites] Oncogene. 2004 Jun 17;23(28):4903-10 [15077163.001]
  • [Cites] Oncogene. 2004 Aug 26;23(39):6612-20 [15208665.001]
  • [Cites] Leukemia. 2004 Nov;18(11):1831-4 [15385933.001]
  • [Cites] Oncogene. 1996 Nov 21;13(10):2121-30 [8950979.001]
  • [Cites] Cancer Res. 2005 Jan 15;65(2):375-8 [15695375.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1361-6 [15902284.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2101-16 [16136167.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2125-9 [16281077.001]
  • [Cites] Blood. 2006 May 15;107(10):3847-53 [16434492.001]
  • [Cites] PLoS Comput Biol. 2006 May;2(5):e41 [16699594.001]
  • [Cites] Oncogene. 2006 Jun 22;25(26):3735-44 [16449964.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3887-94 [16864856.001]
  • [Cites] DNA Repair (Amst). 2006 Sep 8;5(9-10):1282-97 [16893685.001]
  • [Cites] Science. 2006 Oct 13;314(5797):268-74 [16959974.001]
  • [Cites] Curr Oncol Rep. 2006 Nov;8(6):430-6 [17040621.001]
  • [Cites] Am J Hum Genet. 2007 Nov;81(5):906-12 [17924334.001]
  • [Cites] Nature. 2007 Dec 6;450(7171):893-8 [17982442.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):20007-12 [18077431.001]
  • [Cites] J Pharmacol Exp Ther. 2008 Jan;324(1):86-94 [17959747.001]
  • [Cites] Br J Haematol. 2008 Jan;140(2):123-32 [18173751.001]
  • [Cites] Nature. 2008 May 1;453(7191):110-4 [18408710.001]
  • (PMID = 19651601.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / PHS HHS / / 21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCDC26 protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / MLLT4 protein, human; 0 / Proto-Oncogene Proteins; 0 / RUNX1T1 protein, human; 0 / Transcription Factors; EC 3.6.1.- / Kinesin; EC 3.6.4.1 / Myosins
  • [Other-IDs] NLM/ PMC2716382
  •  go-up   go-down


100. Sino US Leukemia Cooperative Group of Shanghai: [Clinical study of 572 adult acute leukemia patients in Shanghai according to WHO classification]. Zhonghua Xue Ye Xue Za Zhi; 2007 Jul;28(7):444-8
MedlinePlus Health Information. consumer health - Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical study of 572 adult acute leukemia patients in Shanghai according to WHO classification].
  • OBJECTIVE: To evaluate WHO classification of acute leukemia (AL) in Shanghai and compare the difference between WHO and FAB classification.
  • METHODS: Successive and unselected leukemia patients were referred to Sino-US Leukemia Cooperative Group of Shanghai from 2003 to 2006.
  • RESULTS: Of the 572 AL patients, 436 (76.2%) were diagnosed as acute myeloid leukemia (AML), 119 (20.8%) acute lymphoblastic leukemia (ALL).
  • AML with recurrent cytogenetic abnormalities accounted for 35.3%, and with multilineage dysplasia for 13.1%, therapy-related AML accounted for 0.9%, and AML not otherwise categorized for 50.7%.
  • Comparing to the AL data of Shanghai Leukemia Group between 1984 and 1994, the percentage of AML-M4 was increased, but that of AML-M1 and M5 were decreased.
  • [MeSH-major] Leukemia / classification
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. China. Female. Humans. Karyotyping. Male. Middle Aged

  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18072625.001).
  • [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
  • [Publication-country] China
  •  go-up   go-down






Advertisement