[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 169413
1. Tosello V, Mansour MR, Barnes K, Paganin M, Sulis ML, Jenkinson S, Allen CG, Gale RE, Linch DC, Palomero T, Real P, Murty V, Yao X, Richards SM, Goldstone A, Rowe J, Basso G, Wiernik PH, Paietta E, Pieters R, Horstmann M, Meijerink JP, Ferrando AA: WT1 mutations in T-ALL. Blood; 2009 Jul 30;114(5):1038-45
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The molecular mechanisms involved in disease progression and relapse in T-cell acute lymphoblastic leukemia (T-ALL) are poorly understood.
  • This analysis showed that diagnosis and relapsed cases have common genetic alterations, but also that relapsed samples frequently lose chromosomal markers present at diagnosis, suggesting that relapsed T-ALL emerges from an ancestral clone different from the major leukemic population at diagnosis.
  • [MeSH-major] Genes, Wilms Tumor. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adult. Child. Chromosome Aberrations. Clone Cells / chemistry. DNA Methylation. DNA Mutational Analysis. DNA, Neoplasm / genetics. Disease Progression. Genes, Homeobox. Humans. Kaplan-Meier Estimate. Neoplasm Proteins / chemistry. Neoplasm Proteins / genetics. Oncogenes. Polymorphism, Single Nucleotide. Prognosis. Recurrence. WT1 Proteins / chemistry. WT1 Proteins / genetics. Zinc Fingers / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 1992 Jul 1;89(13):6010-4 [1321431.001]
  • [Cites] Cell. 1991 Aug 23;66(4):649-61 [1831692.001]
  • [Cites] Hum Mol Genet. 1993 Mar;2(3):259-64 [8388765.001]
  • [Cites] Blood. 1994 May 15;83(10):2922-30 [8180387.001]
  • [Cites] Hum Mol Genet. 1995 Mar;4(3):351-8 [7795587.001]
  • [Cites] Blood. 1996 Mar 15;87(6):2171-9 [8630376.001]
  • [Cites] Hum Mutat. 1997;9(3):209-25 [9090524.001]
  • [Cites] Nucleic Acids Res. 1997 Jun 15;25(12):2532-4 [9171110.001]
  • [Cites] Eur J Haematol. 1997 May;58(5):346-9 [9222290.001]
  • [Cites] Blood. 1998 Apr 15;91(8):2961-8 [9531607.001]
  • [Cites] Kidney Int. 1998 Jun;53(6):1512-8 [9607183.001]
  • [Cites] Blood. 2005 Jul 1;106(1):274-86 [15774621.001]
  • [Cites] Pediatr Blood Cancer. 2006 Jan;46(1):18-25 [15929133.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1279-87 [16688224.001]
  • [Cites] Haematologica. 2006 Sep;91(9):1212-21 [16956820.001]
  • [Cites] Leukemia. 2007 Mar;21(3):550-1; author reply 552 [17205055.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Nat Genet. 2007 May;39(5):593-5 [17435759.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1258-66 [17443227.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1251-61 [17452517.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1825-35 [17646408.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1813-24 [17646409.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):9006-12 [17909001.001]
  • [Cites] Oncogene. 2007 Oct 15;26(47):6838-49 [17934490.001]
  • [Cites] Clin Cancer Res. 2007 Dec 1;13(23):6964-9 [18056171.001]
  • [Cites] J Exp Med. 2007 Dec 24;204(13):3059-66 [18070937.001]
  • [Cites] Leukemia. 2008 Jan;22(1):124-31 [17928886.001]
  • [Cites] Nat Rev Cancer. 2008 Feb;8(2):83-93 [18094723.001]
  • [Cites] Lancet. 2008 Mar 22;371(9617):1030-43 [18358930.001]
  • [Cites] Leukemia. 2008 Apr;22(4):762-70 [18185524.001]
  • [Cites] Nat Rev Immunol. 2008 May;8(5):380-90 [18421304.001]
  • [Cites] Blood. 2008 May 1;111(9):4668-80 [18299449.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 May 6;105(18):6708-13 [18458336.001]
  • [Cites] Blood. 2008 Aug 1;112(3):733-40 [18411416.001]
  • [Cites] J Clin Oncol. 2008 Oct 1;26(28):4595-602 [18559874.001]
  • [Cites] J Clin Oncol. 2008 Nov 20;26(33):5429-35 [18591546.001]
  • [Cites] Science. 2008 Nov 28;322(5906):1377-80 [19039135.001]
  • [Cites] Semin Hematol. 2000 Oct;37(4):381-95 [11071360.001]
  • [Cites] Genome Biol. 2001;2(8):RESEARCH0032 [11532216.001]
  • [Cites] Leukemia. 2001 Oct;15(10):1495-504 [11587205.001]
  • [Cites] J Pediatr Hematol Oncol. 2001 Oct;23(7):416-9 [11878574.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [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] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Clin Nephrol. 1985 Dec;24(6):269-78 [3000666.001]
  • [Cites] Genomics. 1989 Nov;5(4):685-93 [2556343.001]
  • [Cites] Cell. 1990 Jun 29;61(7):1257-69 [2163761.001]
  • [Cites] FEBS Lett. 1993 Feb 8;317(1-2):39-43 [8381368.001]
  • (PMID = 19494353.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE15931
  • [Grant] United States / NCI NIH HHS / CA / CA114737; United Kingdom / Medical Research Council / / MC/ U137686856; United States / NCI NIH HHS / CA / R01 CA129382; United Kingdom / Medical Research Council / / ; United States / NCI NIH HHS / CA / CA02111; United Kingdom / Medical Research Council / / G0500389; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / U24 CA114737; United States / NCI NIH HHS / CA / R01 CA120196-03
  • [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 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / WT1 Proteins
  • [Other-IDs] NLM/ PMC2721784
  •  go-up   go-down


2. Gu L, Zhou C, Liu H, Gao J, Li Q, Mu D, Ma Z: Rapamycin sensitizes T-ALL cells to dexamethasone-induced apoptosis. J Exp Clin Cancer Res; 2010;29:150
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.
  • BACKGROUND: Glucocorticoid (GC) resistance is frequently seen in acute lymphoblastic leukemia of T-cell lineage (T-ALL).
  • METHODS: Cell proliferation was detected by 3-(4,5-dimethylthiazol-2-yl)- 2,5-diphenyltetrazolium bromide (MTT) assay.
  • Fluorescence-activated cell sorting (FACS) analysis was used to analyze apoptosis and cell cycles.
  • Western blot analysis was performed to test the expression of the downstream effector proteins of mammalian target of rapamycin (mTOR), the cell cycle regulatory proteins, and apoptosis associated proteins.
  • Cell cycle arrest was associated with modulation of G1-S phase regulators.
  • Rapamycin enhanced GC-induced apoptosis and this was not achieved by modulation of glucocorticoid receptor (GR) expression, but synergistically up-regulation of pro-apoptotic proteins like caspase-3, Bax, and Bim, and down-regulation of anti-apoptotic protein of Mcl-1.
  • CONCLUSION: Our data suggests that rapamycin can effectively reverse GC resistance in T-ALL and this effect is achieved by inducing cell cycles arrested at G0/G1 phase and activating the intrinsic apoptotic program.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Dexamethasone / pharmacology. Drug Resistance, Neoplasm / drug effects. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Sirolimus / pharmacology
  • [MeSH-minor] Blotting, Western. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Separation. Drug Synergism. Flow Cytometry. Humans

  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. SIROLIMUS .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Leukemia. 2008 Jan;22(1):124-31 [17928886.001]
  • [Cites] Cancer Cell. 2007 Jul;12(1):9-22 [17613433.001]
  • [Cites] Leukemia. 2008 Nov;22(11):2091-6 [18685609.001]
  • [Cites] J Clin Oncol. 2009 May 1;27(13):2278-87 [19332717.001]
  • [Cites] Br J Haematol. 2009 Jun;145(5):569-80 [19344392.001]
  • [Cites] Pediatr Blood Cancer. 2009 Dec;53(6):984-91 [19621425.001]
  • [Cites] Semin Oncol. 2009 Dec;36 Suppl 3:S3-S17 [19963098.001]
  • [Cites] Leukemia. 2010 Feb;24(2):265-84 [20010625.001]
  • [Cites] Clin Cancer Res. 2001 Aug;7(8):2168-81 [11489790.001]
  • [Cites] Clin Cancer Res. 2002 Jun;8(6):1681-94 [12060604.001]
  • [Cites] Blood. 2004 Apr 15;103(8):3138-47 [15070696.001]
  • [Cites] Ann Hematol. 2004;83 Suppl 1:S121-3 [15124702.001]
  • [Cites] Clin Cancer Res. 2004 Jun 15;10(12 Pt 2):4270s-4275s [15217973.001]
  • [Cites] J Leukoc Biol. 2004 Jul;76(1):7-14 [15075361.001]
  • [Cites] Cell Death Differ. 2004 Jul;11 Suppl 1:S65-72 [15017388.001]
  • [Cites] Genes Dev. 2004 Aug 15;18(16):1926-45 [15314020.001]
  • [Cites] J Antibiot (Tokyo). 1975 Oct;28(10):721-6 [1102508.001]
  • [Cites] Leuk Lymphoma. 1994 Apr;13(3-4):187-201 [8049644.001]
  • [Cites] Ann Oncol. 2005 Apr;16(4):525-37 [15728109.001]
  • [Cites] Blood. 2005 Jul 1;106(1):274-86 [15774621.001]
  • [Cites] Blood. 2005 Sep 1;106(5):1801-7 [15886325.001]
  • [Cites] Cancer Res. 2006 Feb 15;66(4):2305-13 [16489035.001]
  • [Cites] Cancer Res. 2006 Jul 1;66(13):6589-97 [16818631.001]
  • [Cites] Ann N Y Acad Sci. 2006 Jun;1069:1-9 [16855130.001]
  • [Cites] Blood. 2006 Aug 1;108(3):1045-9 [16574952.001]
  • [Cites] Cancer Cell. 2006 Oct;10(4):331-42 [17010674.001]
  • [Cites] Am J Pathol. 2006 Dec;169(6):2171-80 [17148679.001]
  • [Cites] Cancer Treat Rev. 2007 Feb;33(1):78-84 [17161912.001]
  • [Cites] Curr Opin Hematol. 2008 Mar;15(2):88-94 [18300753.001]
  • (PMID = 21083937.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 7S5I7G3JQL / Dexamethasone; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC2998469
  •  go-up   go-down


3. Ferrando AA: The role of NOTCH1 signaling in T-ALL. Hematology Am Soc Hematol Educ Program; 2009;:353-61
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The identification of activating mutations in NOTCH1 in over 50% of T-cell acute lymphoblastic leukemias (T-ALL) has generated major interest in the elucidation of the mechanisms of transformation downstream of oncogenic NOTCH and in the targeting of the NOTCH signaling pathway in this disease.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Immunol. 2005 Sep;6(9):881-8 [16056227.001]
  • [Cites] Cancer Res. 2005 Aug 15;65(16):7159-68 [16103066.001]
  • [Cites] EMBO J. 2006 Jan 11;25(1):129-38 [16319921.001]
  • [Cites] Mol Cell Biol. 2006 Jun;26(12):4642-51 [16738328.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1279-87 [16688224.001]
  • [Cites] Genes Dev. 2006 Aug 1;20(15):2096-109 [16847353.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1151-7 [16614245.001]
  • [Cites] Haematologica. 2006 Sep;91(9):1212-21 [16956820.001]
  • [Cites] Mol Cell Biol. 2006 Nov;26(21):8022-31 [16954387.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18261-6 [17114293.001]
  • [Cites] Nat Immunol. 2007 May;8(5):451-6 [17440450.001]
  • [Cites] Blood. 2007 Jul 1;110(1):278-86 [17363738.001]
  • [Cites] Exp Cell Res. 2007 Aug 15;313(14):3141-52 [17560996.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1825-35 [17646408.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1813-24 [17646409.001]
  • [Cites] Nat Med. 2007 Oct;13(10):1203-10 [17873882.001]
  • [Cites] Clin Cancer Res. 2007 Dec 1;13(23):6964-9 [18056171.001]
  • [Cites] Blood. 2008 Jan 1;111(1):376-8 [17901244.001]
  • [Cites] Annu Rev Pathol. 2008;3:587-613 [18039126.001]
  • [Cites] EMBO Rep. 2008 Apr;9(4):377-83 [18274550.001]
  • [Cites] Haematologica. 2008 Apr;93(4):533-42 [18322257.001]
  • [Cites] Blood. 2008 Aug 1;112(3):733-40 [18411416.001]
  • [Cites] J Clin Invest. 2008 Sep;118(9):3181-94 [18677410.001]
  • [Cites] Oncogene. 2008 Oct 2;27(44):5833-44 [18560356.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Jan 6;106(1):244-9 [19118200.001]
  • [Cites] Nat Med. 2009 Jan;15(1):50-8 [19098907.001]
  • [Cites] Blood. 2009 Feb 19;113(8):1730-40 [18984862.001]
  • [Cites] Blood. 2009 Feb 19;113(8):1689-98 [19001083.001]
  • [Cites] Cancer Res. 2009 Apr 1;69(7):3060-8 [19318552.001]
  • [Cites] J Exp Med. 2009 Apr 13;206(4):779-91 [19349467.001]
  • [Cites] Blood. 2009 Apr 23;113(17):3918-24 [19109228.001]
  • [Cites] Blood. 2009 Apr 30;113(18):4381-90 [19075186.001]
  • [Cites] Blood. 2009 Jun 11;113(24):6172-81 [19246562.001]
  • [Cites] Br J Haematol. 2009 Apr;145(2):198-206 [19245433.001]
  • [Cites] J Clin Oncol. 2009 Sep 10;27(26):4352-6 [19635999.001]
  • [Cites] J Biol Chem. 2004 Jan 23;279(4):2937-44 [14583609.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Cell. 1991 Aug 23;66(4):649-61 [1831692.001]
  • [Cites] Cell Cycle. 2005 Oct;4(10):1356-9 [16131838.001]
  • (PMID = 20008221.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA120196-03; United States / NCI NIH HHS / CA / CA129382-02; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / CA120196-03; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / R01 CA129382-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / NOTCH1 protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptor, Notch1; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Number-of-references] 40
  • [Other-IDs] NLM/ NIHMS168983; NLM/ PMC2847371
  •  go-up   go-down


Advertisement
4. O'Neil J, Calvo J, McKenna K, Krishnamoorthy V, Aster JC, Bassing CH, Alt FW, Kelliher M, Look AT: Activating Notch1 mutations in mouse models of T-ALL. Blood; 2006 Jan 15;107(2):781-5
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent studies have demonstrated that most patients with T-cell acute lymphocytic leukemia (T-ALL) have activating mutations in NOTCH1.
  • We sequenced the heterodimerization domain and the PEST domain of Notch1 in our mouse model of TAL1-induced leukemia and found that 74% of the tumors harbor activating mutations in Notch1.
  • Cell lines derived from these tumors undergo G(0)/G(1) arrest and apoptosis when treated with a gamma-secretase inhibitor.
  • Thus, Notch1 mutations are often acquired as a part of the molecular pathogenesis of T-ALLs that develop in mice with known predisposing genetic alterations.
  • [MeSH-major] Disease Models, Animal. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma / genetics. Mutation / genetics. Receptor, Notch1 / genetics. Thymus Neoplasms / genetics
  • [MeSH-minor] Amyloid Precursor Protein Secretases. Animals. Apoptosis. Aspartic Acid Endopeptidases. Basic Helix-Loop-Helix Transcription Factors / genetics. Basic Helix-Loop-Helix Transcription Factors / physiology. DNA-Binding Proteins / genetics. DNA-Binding Proteins / physiology. Endopeptidases / chemistry. Enzyme Inhibitors / pharmacology. Female. G0 Phase. G1 Phase. Histones / genetics. Histones / physiology. Humans. Male. Mice. Mice, Transgenic. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / physiology. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / physiology

  • MedlinePlus Health Information. consumer health - Lymphoma.
  • MedlinePlus Health Information. consumer health - Thymus Cancer.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cell Biol. 2000 Jun;20(11):3831-42 [10805726.001]
  • [Cites] Oncogene. 2006 May 18;25(21):3023-31 [16407836.001]
  • [Cites] Immunity. 2000 Jul;13(1):73-84 [10933396.001]
  • [Cites] Blood. 2000 Sep 1;96(5):1906-13 [10961893.001]
  • [Cites] J Virol. 2000 Oct;74(20):9786-91 [11000255.001]
  • [Cites] Semin Hematol. 2000 Oct;37(4):381-95 [11071360.001]
  • [Cites] Blood. 2001 Mar 1;97(5):1211-8 [11222362.001]
  • [Cites] Science. 2002 May 3;296(5569):922-7 [11934988.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8173-8 [12034884.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] Cell. 2003 Aug 8;114(3):359-70 [12914700.001]
  • [Cites] Cell. 2003 Aug 8;114(3):371-83 [12914701.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2593-6 [12816868.001]
  • [Cites] Semin Hematol. 2003 Oct;40(4):274-80 [14582078.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1909-11 [14604958.001]
  • [Cites] Lancet. 2004 Feb 14;363(9408):535-6 [14975618.001]
  • [Cites] Cancer Cell. 2004 Jun;5(6):587-96 [15193261.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Cell. 1992 Mar 6;68(5):855-67 [1547487.001]
  • [Cites] Cell. 1996 Apr 5;85(1):27-37 [8620534.001]
  • [Cites] EMBO J. 1996 Oct 1;15(19):5160-6 [8895560.001]
  • [Cites] Oncogene. 1998 Jan 29;16(4):517-22 [9484841.001]
  • [Cites] Science. 1999 Apr 30;284(5415):770-6 [10221902.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3310-22 [10828010.001]
  • (PMID = 16166587.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096899
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / H2AX protein, mouse; 0 / Histones; 0 / NOTCH1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Rag2 protein, mouse; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse; 0 / Tumor Suppressor Protein p53; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.- / Endopeptidases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / BACE1 protein, human; EC 3.4.23.46 / Bace1 protein, mouse
  • [Other-IDs] NLM/ PMC1895623
  •  go-up   go-down


5. Dik WA, Nadel B, Przybylski GK, Asnafi V, Grabarczyk P, Navarro JM, Verhaaf B, Schmidt CA, Macintyre EA, van Dongen JJ, Langerak AW: Different chromosomal breakpoints impact the level of LMO2 expression in T-ALL. Blood; 2007 Jul 1;110(1):388-92

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The t(11;14)(p13;q11) is presumed to arise from an erroneous T-cell receptor delta TCRD V(D)J recombination and to result in LMO2 activation.
  • We performed combined in vivo, ex vivo, and in silico analyses on 9 new t(11;14)(p13;q11)-positive T-cell acute lymphoblastic leukemia (T-ALL) as well as normal thymocytes.
  • [MeSH-major] Chromosome Breakage. DNA-Binding Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Metalloproteins / genetics
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 14. Genes, T-Cell Receptor delta. Humans. LIM Domain Proteins. Proto-Oncogene Proteins / genetics. Translocation, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17360939.001).
  • [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


6. Cullion K, Draheim KM, Hermance N, Tammam J, Sharma VM, Ware C, Nikov G, Krishnamoorthy V, Majumder PK, Kelliher MA: Targeting the Notch1 and mTOR pathways in a mouse T-ALL model. Blood; 2009 Jun 11;113(24):6172-81
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Mutations in NOTCH1 are frequently detected in patients with T-cell acute lymphoblastic leukemia (T-ALL) and in mouse T-ALL models.
  • Treatment of mouse or human T-ALL cell lines in vitro with gamma-secretase inhibitors (GSIs) results in growth arrest and/or apoptosis.
  • T-ALL cell lines also exhibit PI3K/mTOR pathway activation, indicating that rapamycin may also have therapeutic benefit.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 2007 Jun 21;447(7147):966-71 [17515920.001]
  • [Cites] Blood. 2007 Jul 1;110(1):278-86 [17363738.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1813-24 [17646409.001]
  • [Cites] Nat Med. 2007 Oct;13(10):1203-10 [17873882.001]
  • [Cites] Blood. 2008 Aug 1;112(3):733-40 [18411416.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1825-35 [17646408.001]
  • [Cites] Blood. 2000 Sep 1;96(5):1906-13 [10961893.001]
  • [Cites] Nat Immunol. 2000 Aug;1(2):138-44 [11248806.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(2):655-64 [12509463.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1909-11 [14604958.001]
  • [Cites] J Biol Chem. 2004 Mar 26;279(13):12876-82 [14709552.001]
  • [Cites] Cancer Cell. 2004 Jun;5(6):587-96 [15193261.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Mol Cell Biol. 2004 Nov;24(21):9265-73 [15485896.001]
  • [Cites] Toxicol Sci. 2004 Nov;82(1):341-58 [15319485.001]
  • [Cites] Mol Cell Biol. 1989 May;9(5):2124-32 [2501659.001]
  • [Cites] EMBO J. 1990 Oct;9(10):3343-51 [2209547.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 May 15;88(10):4367-71 [2034676.001]
  • [Cites] Oncogene. 1991 Aug;6(8):1477-88 [1886719.001]
  • [Cites] Mol Cell Biol. 1991 Nov;11(11):5462-9 [1922059.001]
  • [Cites] Oncogene. 1991 Oct;6(10):1887-93 [1923511.001]
  • [Cites] Blood. 1992 Mar 1;79(5):1327-33 [1311214.001]
  • [Cites] Blood. 1995 Jul 15;86(2):666-76 [7605997.001]
  • [Cites] J Exp Med. 1996 May 1;183(5):2283-91 [8642337.001]
  • [Cites] EMBO J. 1996 Oct 1;15(19):5160-6 [8895560.001]
  • [Cites] Cell. 1996 Nov 1;87(3):483-92 [8898201.001]
  • [Cites] Cancer Res. 1996 Nov 15;56(22):5113-9 [8912842.001]
  • [Cites] EMBO J. 1997 May 1;16(9):2408-19 [9171354.001]
  • [Cites] Nature. 2005 Jun 16;435(7044):959-63 [15959515.001]
  • [Cites] Nature. 2005 Jun 16;435(7044):964-8 [15959516.001]
  • [Cites] Nat Immunol. 2005 Sep;6(9):881-8 [16056227.001]
  • [Cites] Mol Cell Biol. 2006 Jan;26(1):209-20 [16354692.001]
  • [Cites] Blood. 2006 Jan 15;107(2):781-5 [16166587.001]
  • [Cites] Blood. 2006 Mar 15;107(6):2540-3 [16282337.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 25;103(17):6688-93 [16618932.001]
  • [Cites] Blood. 2006 May 15;107(10):4115-21 [16449526.001]
  • [Cites] Oncogene. 2006 May 18;25(21):3023-31 [16407836.001]
  • [Cites] Mol Cell Biol. 2006 Jun;26(12):4642-51 [16738328.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jun 13;103(24):9262-7 [16751266.001]
  • [Cites] Genes Dev. 2006 Aug 1;20(15):2096-109 [16847353.001]
  • [Cites] Mol Cell Biol. 2006 Nov;26(21):8022-31 [16954387.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18261-6 [17114293.001]
  • [Cites] Nature. 2006 Dec 21;444(7122):1032-7 [17183313.001]
  • [Cites] Nature. 2006 Dec 21;444(7122):1083-7 [17183323.001]
  • [Cites] Curr Opin Genet Dev. 2007 Feb;17(1):52-9 [17178457.001]
  • [Cites] Nature. 2007 Feb 15;445(7129):781-4 [17259972.001]
  • [Cites] Chem Biol. 2007 Feb;14(2):209-19 [17317574.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Blood. 2007 Jun 1;109(11):4753-60 [17311993.001]
  • [Cites] Cancer Res. 2007 Jun 15;67(12):5611-6 [17575125.001]
  • [CommentIn] Blood. 2009 Jun 11;113(24):6044-5 [19520812.001]
  • (PMID = 19246562.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096899; United States / NCI NIH HHS / CA / CA096899; United States / NIDDK NIH HHS / DK / P30DK32529
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Carrier Proteins; 0 / Cyclic S-Oxides; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / MRK 003; 0 / Proto-Oncogene Proteins; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse; 0 / Thiadiazoles; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ PMC2699237
  •  go-up   go-down


7. Demarest RM, Ratti F, Capobianco AJ: It's T-ALL about Notch. Oncogene; 2008 Sep 1;27(38):5082-91
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.
  • T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive subset of ALL with poor clinical outcome compared to B-ALL.
  • Therefore, to improve treatment, it is imperative to delineate the molecular blueprint of this disease.
  • In addition to the activating mutations of Notch previously described, this review will outline combinations of mutations in pathways that contribute to Notch signaling and appear to drive T-ALL development by 'mimicking' Notch effects on cell cycle and apoptosis.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Neoplasm Proteins / physiology. Receptors, Notch / physiology. T-Lymphocytes / pathology
  • [MeSH-minor] Animals. Apoptosis / physiology. Cell Cycle / physiology. F-Box Proteins / physiology. Gene Expression Regulation, Leukemic. Genes, Tumor Suppressor. Humans. Ikaros Transcription Factor / genetics. Ikaros Transcription Factor / physiology. Ligands. Mice. Mice, Transgenic. Oncogenes. PTEN Phosphohydrolase / deficiency. PTEN Phosphohydrolase / genetics. PTEN Phosphohydrolase / physiology. Signal Transduction / physiology. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / physiology. Tumor Suppressor Proteins / physiology. Ubiquitin-Protein Ligases / physiology

  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18758476.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA09171
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / F-Box Proteins; 0 / Fbxw7 protein, mouse; 0 / IKZF1 protein, human; 0 / Ligands; 0 / Neoplasm Proteins; 0 / Receptors, Notch; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 148971-36-2 / Ikaros Transcription Factor; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Number-of-references] 84
  •  go-up   go-down


8. Chadwick N, Zeef L, Portillo V, Boros J, Hoyle S, van Doesburg JC, Buckle AM: Notch protection against apoptosis in T-ALL cells mediated by GIMAP5. Blood Cells Mol Dis; 2010 Oct 15;45(3):201-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent studies have highlighted the role of Notch signalling in the development of T cell acute lymphoblasic leukaemia (T-ALL).
  • The aims of this study were to determine the effect of Notch signalling on apoptosis in human T-ALL cell lines and to identify targets of Notch signalling that may mediate this effect.
  • Microarray analysis revealed that GIMAP5, a gene coding for an anti-apoptotic intracellular protein, is upregulated by Notch in T-ALL cell lines.
  • [MeSH-major] Apoptosis. GTP-Binding Proteins / biosynthesis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptor, Notch1 / metabolism. Receptors, Notch / metabolism. Signal Transduction

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20817506.001).
  • [ISSN] 1096-0961
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GIMAP5 protein, human; 0 / Glucocorticoids; 0 / NOTCH1 protein, human; 0 / NOTCH3 protein, human; 0 / Protease Inhibitors; 0 / Receptor, Notch1; 0 / Receptors, Notch; EC 3.6.1.- / GTP-Binding Proteins
  •  go-up   go-down


9. Van Vlierberghe P, Homminga I, Zuurbier L, Gladdines-Buijs J, van Wering ER, Horstmann M, Beverloo HB, Pieters R, Meijerink JP: Cooperative genetic defects in TLX3 rearranged pediatric T-ALL. Leukemia; 2008 Apr;22(4):762-70
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.
  • T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive neoplastic disorder, in which multiple genetic abnormalities cooperate in the malignant transformation of thymocytes.
  • [MeSH-major] Chromosome Aberrations. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Sequence Deletion
  • [MeSH-minor] Cell Cycle Proteins / genetics. Child. DNA Mutational Analysis. F-Box Proteins / genetics. Gene Dosage. Gene Rearrangement. Genome, Human. Humans. In Situ Hybridization, Fluorescence. Ubiquitin-Protein Ligases / genetics. WT1 Proteins / genetics

  • 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 = 18185524.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Homeodomain Proteins; 0 / TLX3 protein, human; 0 / WT1 Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  •  go-up   go-down


10. Liu S, Breit S, Danckwardt S, Muckenthaler MU, Kulozik AE: Downregulation of Notch signaling by gamma-secretase inhibition can abrogate chemotherapy-induced apoptosis in T-ALL cell lines. Ann Hematol; 2009 Jul;88(7):613-21
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] Downregulation of Notch signaling by gamma-secretase inhibition can abrogate chemotherapy-induced apoptosis in T-ALL cell lines.
  • Activation of Notch1 signaling plays an important role in the pathogenesis of precursor T-cell lymphoblastic leukemia (T-ALL).
  • In this study, we analyzed the response of four T-ALL cell lines to compound E, a potent gamma-secretase inhibitor, and to the combination of compound E with vincristine, daunorubicin, L-asparaginase (L-ASP), and dexamethasone (DEX).
  • We identified two distinct types of responses: In type 1 cell lines, represented by TALL1 and HSB2, GSI-induced apoptosis followed cell cycle arrest and enhanced the induction of apoptosis caused by DEX and L-ASP.
  • In type 2 cell lines, represented by CEM and Jurkat J6, GSI caused neither cell cycle block nor cell death.
  • In type 2 cells, GSI induced the upregulation of Bcl-xl mRNA and protein, which was thus identified as a candidate mechanism for the inhibition of apoptosis.
  • [MeSH-major] Amyloid Precursor Protein Secretases / physiology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Receptor, Notch1 / antagonists & inhibitors
  • [MeSH-minor] Asparaginase / pharmacology. Benzodiazepinones / pharmacology. Cell Line, Tumor. Daunorubicin / pharmacology. Dexamethasone / pharmacology. Down-Regulation. Humans. Signal Transduction. Vincristine / pharmacology

  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19057901.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 2-(((3,5-difluorophenyl)acetyl)amino)-N-(1-methyl-2-oxo-5-phenyl-2,3-dihydro-1H-1,4-benzodiazepin-3-yl)propanamide; 0 / Benzodiazepinones; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.5.1.1 / Asparaginase; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


11. Indraccolo S, Minuzzo S, Masiero M, Amadori A: Ligand-driven activation of the notch pathway in T-ALL and solid tumors: why Not(ch)? Cell Cycle; 2010 Jan 1;9(1):80-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ligand-driven activation of the notch pathway in T-ALL and solid tumors: why Not(ch)?
  • The Notch pathway is an evolutionally conserved cell-cell interaction signalling system involved in several key aspects of cell life, ranging from differentiation and proliferation to apoptosis.
  • The clearest example of oncogenic Notch signalling is observed in T acute lymphoblastic leukemia (T-ALL), an aggressive neoplasm of immature T-cells, due to genetic alterations leading to ligand-independent increased Notch1 receptor signalling.
  • In solid tumors, however, extrinsic regulation through canonical cell-cell interactions appears to drive activation of the pathway.
  • [MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptors, Notch / metabolism
  • [MeSH-minor] Animals. Humans. Intracellular Signaling Peptides and Proteins. Leukemia / metabolism. Membrane Proteins / metabolism. Models, Biological. Neovascularization, Pathologic / metabolism. Signal Transduction / genetics. Signal Transduction / physiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20016278.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / Receptors, Notch; 0 / delta protein
  •  go-up   go-down


12. Epenetos AA, Kousparou C, Stylianou S: Inhibition of Notch and tumor regression. J Clin Oncol; 2009 May 20;27(15_suppl):e14623

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e14623 Background: Notch signaling is an evolutionary-conserved pathway in vertebrates and invertebrates which is involved many developmental processes, including cell fate decisions, apoptosis, proliferation, and stem-cell self renewal.
  • Increasing evidence suggests that the Notch signaling pathway is frequently up regulated in many forms of cancer including acute T-cell lymphoblastic leukemia, cervical, prostate, lung, breast and others.
  • RESULTS: Our data show that ANTP/DN MAML fusion protein, TR4 contains signals for proper cell targeting, internalization and nuclear transport.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27964214.001).
  • [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


13. Řezáčová M, Vávrová J, Vokurková D: Ionizing Radiation Sensitizes Leukemic MOLT-4 Cells to TRAIL-induced Apoptosis. Acta Medica (Hradec Kralove); 2008;51(2):101-105

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • However, leukemia cells studied to date have shown variable susceptibility to TRAIL.
  • Our study demonstrates that cells of acute T-lymphoblastic leukemia MOLT-4 are resistant to TRAIL and that ionizing radiation in the therapeutically achievable dose of 1 Gy sensitizes TRAIL-resistant cells MOLT-4 to the TRAIL-induced apoptosis by increase in death receptors for TRAIL DR5.
  • When TRAIL is applied after the irradiation in the time of increased DR5 positivity more efficient cell killing is achieved.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 28550838.001).
  • [ISSN] 1211-4286
  • [Journal-full-title] Acta medica (Hradec Kralove)
  • [ISO-abbreviation] Acta Medica (Hradec Kralove)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Czech Republic
  • [Keywords] NOTNLM ; Apoptosis / DR5 / Ionizing radiation / Leukemia / TRAIL
  •  go-up   go-down


14. Mukhopadhyay A, Gupta P, Mukhopadhyay S, Dey S, Basak J, Pandey R: Result of adolescent acute lymphoblastic leukemia protocol (MCP 841) from a developing country. J Clin Oncol; 2009 May 20;27(15_suppl):10046

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Result of adolescent acute lymphoblastic leukemia protocol (MCP 841) from a developing country.
  • : 10046 Background: Acute Lymphatic Leukemia is a curable disease in the range of 80 - 90% in developed countries by aggressive protocol like BFM, St. Judes' but result is much less in adolescence age group (60-70%).
  • In a follow-up period of 24 - 88 months (with an average of 54 months) the disease-free survival ( DFS) was 42 (56%) patients with an overall survival of 46 (61.34%) patients.
  • The major cause of the mortality was infection 18% (24.0% patients) followed progressive disease 9 (12.0%) and hemorrhage 2 (2.7%).
  • CONCLUSIONS: The data of acute lymphatic leukemia in adolescent is not satisfactory as compared to other pediatric patients.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962472.001).
  • [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


15. Sharma H, Campbell AC, Thajam S, Singh BJ: Metal-on-metal surface hip arthroplasty in patients with abnormal Coxanatomy: preliminary results. Eur J Orthop Surg Traumatol; 2006 Jun;16(2):135-139

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Transliterated title] Arthroplastie de resurfaçage métal/métal en cas d’anatomie de hanche anormale.
  • These patients were defined to have abnormal coxanatomy by virtue of previous dysplastic disease of hip in three cases, previous Legg-Calve-Perthes disease, multiple epiphyseal dysplasia, T cell acute lymphoblastic leukaemia, trauma and sepsis in one case each.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Arthroplasty. 2001 Dec;16(8 Suppl 1):134-9 [11742465.001]
  • [Cites] Clin Orthop Relat Res. 1996 Aug;(329 Suppl):S89-98 [8769326.001]
  • [Cites] Clin Orthop Relat Res. 1996 Aug;(329 Suppl):S78-88 [8769325.001]
  • [Cites] Instr Course Lect. 1981;30:444-54 [6820656.001]
  • [Cites] Hip Int. 2002 Apr-Jun;12 (2):158-162 [28124361.001]
  • [Cites] Hip. 1982;:156-66 [7166497.001]
  • [Cites] Clin Orthop Relat Res. 1996 Aug;(329 Suppl):S106-14 [8769328.001]
  • (PMID = 28755114.001).
  • [ISSN] 1633-8065
  • [Journal-full-title] European journal of orthopaedic surgery & traumatology : orthopedie traumatologie
  • [ISO-abbreviation] Eur J Orthop Surg Traumatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Keywords] NOTNLM ; Anatomy / Arthroplasty / Hip / Metal-on-metal
  •  go-up   go-down


16. Andorsky DJ, Yamada R, Steward K, De Vos S, Said J, Timmerman J: Expression of programmed death ligand 1 (PD-L1) by non-Hodgkin's lymphomas (NHL) and effect on tumor-associated T cells. J Clin Oncol; 2009 May 20;27(15_suppl):8526

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: PD-L1 expression was analyzed in 16 NHL cell lines by flow cytometry (FC) and in 111 lymphoma specimens by immunohistochemistry (IHC) (n=92) or FC (n=19).
  • In functional studies, irradiated anaplastic large cell lymphoma (ALCL) cells were co-cultured with allogeneic T cells in the presence of anti-PD-L1 blocking antibody, and IFNγ secretion and thymidine incorporation was used to assess T cell function and proliferation.
  • To further test tumor-T cell interactions, malignant ascites from a patient with ALK+ ALCL and peripheral blood mononuclear cells from a patient with leukemic mantle cell lymphoma, both containing PD-L1-expressing tumor cells and tumor-associated T cells, were stimulated with phytohemagglutinin (a polyclonal T cell activator) and incubated with anti-PD-L1 antibody.
  • Levels of 16 inflammatory cytokines were measured as an assessment of T cell activity.
  • RESULTS: All 9 B cell lymphoma lines were negative for PD-L1, while all 5 ALCL cell lines were strongly positive.
  • One T-cell ALL line was positive, and one peripheral T cell lymphoma was negative.
  • Strong PD-L1 staining was detected by IHC in all 14 ALCL specimens and in 83% of diffuse large B cell lymphomas (DLBCL) analyzed (n=35).
  • In the autologous setting using cultures of ALCL and mantle cell lymphoma specimens containing host T cells, secretion of inflammatory cytokines by tumor-associated T cells, including GMCSF, IFNγ, IL-1, IL-6, IL-8, TNFα, and MIP1α, were increased by incubation with anti-PD-L1 antibody.
  • PD-L1 may play a role in thwarting an effective anti-tumor immune response and represents an attractive target for lymphoma immunotherapy.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27960901.001).
  • [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. Khattab TM, Jastaniah WA, Felimban SK, Elemam N, Abdullah K, Ahmed B: How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia. J Clin Oncol; 2009 May 20;27(15_suppl):10048

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia.
  • : 10048 Background: T-cell acute lymphoblastic leukemia (T-ALL) is representing 10-15% of pediatric ALL.
  • Our published data showed that T-ALL phenotype patients fared poorly with 5 year survival of 27% versus 83% for precursor B-ALL (Recent Advances Research Update: 2006, 7; 1, P 51-56).
  • OBJECTIVES: We reviewed all patients diagnosed with T-ALL to assess risk classification according to NCI criteria, type of therapy received, overall survival and causes of mortality.
  • METHODS: Retrospective review of all patients files diagnosed with T-ALL from 1989 until now with data collection including; sex, age, white cell count (WBCs), CNS disease, type of protocol used, length of survival, overall survival, cause of death (toxic, disease).
  • Median WBCs 50,000/Cmm (range: 1.500-619,000/Cmm) and positive CNS at diagnosis 10/52 (20%).
  • Overall survival 27/52 (52%) and 25 pts. died (48%); 15 secondary to disease recurrence (9 on UKALL, 4 BFM, 2 CCG 1961); 4 during induction, 1 fulminant hepatic failure, 1 tumor lysis syndrome, and 4 due to toxicities (mucormycosis, staphylococcal toxic shock syndrome, CMV pneumonia, pseudomonas sepsis).
  • Further risk and response stratification in addition to intensification of therapy for T-cell ALL in our center may prove to be beneficial.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962474.001).
  • [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


18. Faderl S, Thomas DA, Gandhi V, Huang X, Borthakur G, O'Brien S, Ravandi F, Plunkett W, Bretz JL, Kantarjian HM: Results of a phase I study of clofarabine (CLO) plus cyclophosphamide (CY) in adult patients (pts) with relapsed and/or refractory acute lymphoblastic leukemia (ALL). J Clin Oncol; 2009 May 20;27(15_suppl):7020

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Results of a phase I study of clofarabine (CLO) plus cyclophosphamide (CY) in adult patients (pts) with relapsed and/or refractory acute lymphoblastic leukemia (ALL).
  • The continual reassessment method (CRM) was used to determine the maximum tolerated dose (MTD) from 4 pre-defined dose levels.
  • Twenty-one pts had pre-B ALL, 5 pts pre-T/T ALL, 1 pt mature B ALL, and 3 pts biphenotypic acute leukemias.
  • All pts had pre-B ALL.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27961382.001).
  • [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


19. Xicoy B, Ribera JM, Oriol A, Sanz MA, Abella E, Tormo M, del Potro E, Bueno J, Grande C, Fernández-Calvo J, Orts M, Novo A, Rivas C, Hernández-Rivas JM, Feliu E, Ortega JJ: [Prognostic influence of immunological subtypes of T-cell acute lymphoblastic leukemia. Study of 81 patients]. Med Clin (Barc); 2006 Jan 21;126(2):41-6
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] [Prognostic influence of immunological subtypes of T-cell acute lymphoblastic leukemia. Study of 81 patients].
  • [Transliterated title] Significado pronóstico de los subtipos inmunológicos de la leucemia aguda linfoblástica T del adulto. Estudio de 81 pacientes.
  • BACKGROUND AND OBJECTIVE: T-cell acute lymphoblastic leukemia (ALL) includes 4 immunological subtypes: pro-T, pre-T, thymic or cortical and mature.
  • In some studies, pro-T and mature subtypes have a poor prognosis.
  • The objective of this study was to describe the clinical characteristics, the result of treatment and the prognosis of the immunological subtypes of T-cell ALL in 81 adult patients included in 2 protocols of the Spanish PETHEMA group (ALL-96 and ALL-93).
  • The main clinical and biological parameters as well as the rate of response to treatment, the frequency of complete remission , disease free survival and overall survival were compared in each T-cell ALL subtype.
  • RESULTS: Of the 64 evaluable patients the distribution of the immunological subtypes was: 3 pro-T, 17 pre-T, 22 thymic or cortical and 22 mature.
  • Patients with mature T-cell ALL had a slow rate of response to treatment in comparison with patients wit pre-T and mature T-cell ALL but this did not translate to significant differences in frequency of complete remission (77% vs 94%), disease free survival (42% vs 46%) and overall survival (29% vs 47%).
  • CONCLUSIONS: Although patients with mature T-cell ALL had a slow rate of response to treatment and their survival tended to be shorter, in the present study there were no statistically significant differences in the prognosis of the different subtypes of T-cell ALL.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / mortality

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16426542.001).
  • [ISSN] 0025-7753
  • [Journal-full-title] Medicina clínica
  • [ISO-abbreviation] Med Clin (Barc)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
  •  go-up   go-down


20. Imataki O, Koike A, Iwabu M, Shintani T, Waki F, Ohue Y, Ohnishi H, Ishida T: [Limited but potential efficacy by graft-versus-leukemia (GVL) for Pro T-ALL]. Gan To Kagaku Ryoho; 2008 Nov;35(11):1911-4
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] [Limited but potential efficacy by graft-versus-leukemia (GVL) for Pro T-ALL].
  • We present a 22-year-old male diagnosed with pro T-acute lymphoblastic leukemia (ALL).
  • Flow cytometry analysis of the leukemic cells showed cCD3+, CD7+, CD2+, CD1a-, CD3-, CD5-, CD4-, CD8-, CD34+, and HLA-DR+ as a pro T-cell phenotype.
  • He underwent up-front stem cell transplantation (SCT) from an HLA-full matched sibling, with early relapse just before transplantation.
  • Based on the immature T cell phenotype frequently with myeloid markers, a graft-versus- leukemic effect might be expected after allogeneic SCT for Pro T-ALL and a positive indication of SCT for this disease should be considered.
  • [MeSH-major] Graft vs Leukemia Effect / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19011341.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


21. Calzavara E, Chiaramonte R, Cesana D, Basile A, Sherbet GV, Comi P: Reciprocal regulation of Notch and PI3K/Akt signalling in T-ALL cells in vitro. J Cell Biochem; 2008 Apr 1;103(5):1405-12
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Our analyses indicate that the PI3K/Akt pathway is constitutively active in the four T-ALL cell lines tested.
  • PTEN expression was not detected in 3/4 cell lines tested, suggesting the loss of PTEN-mediated Akt activation.
  • We analysed the relationship between Notch-1 and the PI3K/Akt signalling and show that inhibition of the Akt pathway changes Notch expression; Notch-1 protein decreased in all the cell lines upon treatment with the inhibitor.
  • [MeSH-major] Phosphatidylinositol 3-Kinases / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptor, Notch1 / metabolism. Signal Transduction

  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2007 Wiley-Liss, Inc.
  • (PMID = 17849443.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / bcl-2-Associated X Protein; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 3.6.5.2 / ras Proteins
  •  go-up   go-down


22. Dohnal AM, Inthal A, Felzmann T, Glatt S, Sommergruber W, Mann G, Gadner H, Panzer-Grümayer ER: Leukemia-associated antigenic isoforms induce a specific immune response in children with T-ALL. Int J Cancer; 2006 Dec 15;119(12):2870-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukemia-associated antigenic isoforms induce a specific immune response in children with T-ALL.
  • The potential immunogenicity of acute lymphoblastic leukemia of the T cell (T-ALL), a small subgroup of childhood leukemia with increased risk for treatment failure and early relapse, was addressed by serological identification of leukemia-derived antigens by recombinant expression cloning (SEREX).
  • Further characterization of the 4 novel isoforms revealed that 3 (HECTD1Delta, CX-ORF-15Delta and hCAP-EDelta) had restricted mRNA expression in more than 70% of T-ALLs (n = 22) and that specific antibodies against these isoforms were detected in up to 30% of patients (n = 16), with the highest frequency for HECTD1Delta.
  • The latter protein was present at high abundance in T-ALLs but not in normal hematopoietic tissues.
  • Given that the leukemia-associated antigens detected in this study have an intracellular localization, the generation of immune effector responses most likely requires antigen presentation.
  • To test this assumption, dendritic cells were loaded with HECTD1Delta protein and used for T cell stimulation.
  • A specific T cell response was induced in vitro in all 3 healthy donors studied, including a former T-ALL patient.
  • [MeSH-major] Antigens, Neoplasm / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 17016825.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, Neoplasm; 0 / DNA, Complementary; 0 / Protein Isoforms; 0 / RNA, Messenger; 82115-62-6 / Interferon-gamma
  •  go-up   go-down


23. O'Neil J, Tchinda J, Gutierrez A, Moreau L, Maser RS, Wong KK, Li W, McKenna K, Liu XS, Feng B, Neuberg D, Silverman L, DeAngelo DJ, Kutok JL, Rothstein R, DePinho RA, Chin L, Lee C, Look AT: Alu elements mediate MYB gene tandem duplication in human T-ALL. J Exp Med; 2007 Dec 24;204(13):3059-66
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent studies have demonstrated that the MYB oncogene is frequently duplicated in human T cell acute lymphoblastic leukemia (T-ALL).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2000 Oct 1;60(19):5323-8 [11034064.001]
  • [Cites] Nat Genet. 2007 May;39(5):593-5 [17435759.001]
  • [Cites] Nat Rev Genet. 2002 May;3(5):370-9 [11988762.001]
  • [Cites] Nat Genet. 2002 Sep;32(1):160-5 [12185367.001]
  • [Cites] EMBO J. 2003 Sep 1;22(17):4478-88 [12941699.001]
  • [Cites] Nat Immunol. 2004 Jul;5(7):721-9 [15195090.001]
  • [Cites] Cancer Res. 2004 Jul 15;64(14):4744-8 [15256441.001]
  • [Cites] Genes Chromosomes Cancer. 2004 Nov;41(3):257-65 [15334549.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Oct 12;101(41):14853-8 [15466706.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Aug;79(15):4714-7 [6289315.001]
  • [Cites] Cell. 1982 Dec;31(2 Pt 1):453-63 [6297766.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Jul;81(14):4534-8 [6589609.001]
  • [Cites] Mol Cell Biol. 1988 Feb;8(2):884-92 [2832742.001]
  • [Cites] Cancer Lett. 1990 Jun 30;52(1):57-62 [2354420.001]
  • [Cites] J Exp Med. 1991 Oct 1;174(4):867-73 [1680958.001]
  • [Cites] Oncogene. 1992 Dec;7(12):2519-23 [1461655.001]
  • [Cites] Leukemia. 1995 Nov;9(11):1812-7 [7475267.001]
  • [Cites] Oncogene. 1996 Nov 21;13(10):2205-12 [8950988.001]
  • [Cites] Science. 1997 Nov 7;278(5340):1059-64 [9353180.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Mar 3;95(5):2390-5 [9482895.001]
  • [Cites] Am J Hum Genet. 1999 Jan;64(1):300-2 [9915971.001]
  • [Cites] Genes Dev. 1999 May 1;13(9):1073-8 [10323859.001]
  • [Cites] Nature. 2007 Jun 21;447(7147):966-71 [17515920.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1251-61 [17452517.001]
  • [Cites] Mol Genet Metab. 1999 Jul;67(3):183-93 [10381326.001]
  • [Cites] Genes Dev. 2005 Oct 1;19(19):2331-42 [16166372.001]
  • [Cites] Blood. 2006 Aug 1;108(3):896-903 [16597594.001]
  • [Cites] Genes Dev. 2006 Aug 1;20(15):2096-109 [16847353.001]
  • [Cites] DNA Repair (Amst). 2006 Sep 8;5(9-10):1065-74 [16815104.001]
  • [Cites] Mol Cell Biol. 2006 Nov;26(21):8022-31 [16954387.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18261-6 [17114293.001]
  • [Cites] EMBO J. 2000 Nov 15;19(22):6112-20 [11080157.001]
  • (PMID = 18070937.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE7615
  • [Grant] United States / NCI NIH HHS / CA / P01 CA109901; United States / NIGMS NIH HHS / GM / R37 GM050237; United States / NCI NIH HHS / CA / CA11560; United States / NIGMS NIH HHS / GM / GM067055; United States / NIGMS NIH HHS / GM / R01 GM067055; United States / NIGMS NIH HHS / GM / R01 GM050237; United States / NCI NIH HHS / CA / R01 CA111560; United States / NCI NIH HHS / CA / R21 CA115853; United States / NIGMS NIH HHS / GM / GM050237; United States / NCI NIH HHS / CA / CA115853; United States / NCI NIH HHS / CA / CA68484-11; United States / NCI NIH HHS / CA / P01 CA068484; United States / NCI NIH HHS / CA / CA109901
  • [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 / Proto-Oncogene Proteins c-myb
  • [Other-IDs] NLM/ PMC2150982
  •  go-up   go-down


24. Krieger D, Moericke A, Oschlies I, Zimmermann M, Schrappe M, Reiter A, Burkhardt B: Frequency and clinical relevance of DNA microsatellite alterations of the CDKN2A/B, ATM and p53 gene loci: a comparison between pediatric precursor T-cell lymphoblastic lymphoma and T-cell lymphoblastic leukemia. Haematologica; 2010 Jan;95(1):158-62
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] Frequency and clinical relevance of DNA microsatellite alterations of the CDKN2A/B, ATM and p53 gene loci: a comparison between pediatric precursor T-cell lymphoblastic lymphoma and T-cell lymphoblastic leukemia.
  • Although deletions of cell cycle regulatory gene loci have long been reported in various malignancies, little is known regarding their relevance in pediatric T-cell lymphoblastic lymphoma (T-LBL) and T-cell lymphoblastic leukemia (TALL).
  • [MeSH-major] Cell Cycle Proteins / genetics. Cyclin-Dependent Kinase Inhibitor p15 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. DNA-Binding Proteins / genetics. Genetic Loci / genetics. Leukemia, T-Cell / genetics. Microsatellite Repeats / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Protein-Serine-Threonine Kinases / genetics. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Proteins / genetics

  • Genetic Alliance. consumer health - Lymphoblastic lymphoma.
  • Genetic Alliance. consumer health - Pediatric T-cell 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
  • [Cites] Blood. 1997 Jun 1;89(11):4161-6 [9166859.001]
  • [Cites] Pediatr Hematol Oncol. 1997 Mar-Apr;14(2):141-50 [9089742.001]
  • [Cites] Leukemia. 1997 Aug;11(8):1201-6 [9264370.001]
  • [Cites] Haematologica. 1998 May;83(5):403-7 [9658723.001]
  • [Cites] Br J Haematol. 1998 Nov;103(2):536-8 [9827931.001]
  • [Cites] Leuk Res. 1999 Feb;23(2):115-26 [10071127.001]
  • [Cites] Blood. 1999 Sep 1;94(5):1537-44 [10477677.001]
  • [Cites] J Clin Oncol. 2006 Jan 20;24(3):491-9 [16421426.001]
  • [Cites] Pediatr Blood Cancer. 2006 Aug;47(2):130-40 [16358311.001]
  • [Cites] Leukemia. 2006 Aug;20(8):1422-9 [16738692.001]
  • [Cites] Leukemia. 2006 Sep;20(9):1496-510 [16826225.001]
  • [Cites] Leuk Lymphoma. 2007 Sep;48(9):1745-54 [17786710.001]
  • [Cites] Leuk Lymphoma. 2008 Mar;49(3):451-61 [18297521.001]
  • [Cites] Nat Rev Immunol. 2008 May;8(5):380-90 [18421304.001]
  • [Cites] Blood. 2008 May 1;111(9):4477-89 [18285545.001]
  • [Cites] Pediatr Blood Cancer. 2008 Oct;51(4):489-94 [18618503.001]
  • [Cites] Eur J Haematol. 2000 Dec;65(6):390-8 [11168496.001]
  • [Cites] Br J Haematol. 2001 Mar;112(3):680-90 [11260073.001]
  • [Cites] Leukemia. 2003 Jan;17(1):149-54 [12529672.001]
  • [Cites] Blood. 1995 May 1;85(9):2321-30 [7727766.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 15;93(21):11837-41 [8876224.001]
  • [Cites] Br J Haematol. 1997 Jul;98(1):147-50 [9233578.001]
  • (PMID = 19586936.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / CDKN2B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / Genetic Markers; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ PMC2805736
  •  go-up   go-down


25. Guo D, Ye J, Dai J, Li L, Chen F, Ma D, Ji C: Notch-1 regulates Akt signaling pathway and the expression of cell cycle regulatory proteins cyclin D1, CDK2 and p21 in T-ALL cell lines. Leuk Res; 2009 May;33(5):678-85
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] Notch-1 regulates Akt signaling pathway and the expression of cell cycle regulatory proteins cyclin D1, CDK2 and p21 in T-ALL cell lines.
  • Gain-of-function mutations in Notch-1 are common in T-cell lymphoblastic leukemia (T-ALL), making this receptor a promising target for drugs such as gamma-secretase inhibitors (GSIs).
  • However, GSIs seem to be active in only a small fraction of T-ALL cell lines with constitutive Notch-1 activity and the downstream response of Notch signaling is only partially understood.
  • To further investigate the molecular mechanisms underlying proliferation suppression and apoptosis and explore effective downstream target genes, we used RNA interference (RNAi) technology to down-regulate the expression of Notch-1 in GSIs-resistant T-ALL cell lines.
  • Results showed that down-regulation of Notch-1 by transfection of a small interfering RNA (siRNA) could cause SupT1 cells proliferation inhibition by inducing G(0)/G(1) cell cycle arrest and apoptosis.
  • The proliferation inhibitory and apoptotic effects resulting from down-regulation of Notch-1 may be mediated through regulating the expression of cell cycle regulatory proteins cyclin D1, CDK2 and p21 and the activity of Akt signaling.
  • Taken together, cell cycle regulatory proteins and Akt signaling may be attractive targets in T-ALL.
  • [MeSH-major] CDC2 Protein Kinase / genetics. Cyclin D1 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-akt / metabolism. Receptor, Notch1 / physiology. Signal Transduction / physiology
  • [MeSH-minor] Apoptosis. Base Sequence. Cell Cycle. Cell Line, Tumor. Cell Proliferation. Down-Regulation / physiology. Humans. Mutation. RNA Interference. RNA, Small Interfering. Reverse Transcriptase Polymerase Chain Reaction

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19091404.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / NOTCH1 protein, human; 0 / RNA, Small Interfering; 0 / Receptor, Notch1; 136601-57-5 / Cyclin D1; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.22 / CDC2 Protein Kinase
  •  go-up   go-down


26. Hernandez CP, Morrow K, Lopez-Barcons LA, Zabaleta J, Sierra R, Velasco C, Cole J, Rodriguez PC: Pegylated arginase I: a potential therapeutic approach in T-ALL. Blood; 2010 Jun 24;115(25):5214-21
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Adult patients with acute lymphoblastic T cell leukemia (T-ALL) have a very poor prognosis and few effective therapeutic options.
  • In addition, treatment of malignant T-cell lines with peg-Arg I significantly impaired their proliferation, which correlated with a decreased progression into the cell cycle, followed by the induction of apoptosis.
  • The results suggest the potential benefit of L-Arginine depletion by peg-Arg I in the treatment of T-cell malignancies.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. (L)-ARGININE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2007 Feb 15;109(4):1568-73 [17023580.001]
  • [Cites] Cancer Res. 2007 Jan 1;67(1):309-17 [17210712.001]
  • [Cites] Cancer Res. 2009 Feb 15;69(4):1553-60 [19201693.001]
  • [Cites] Blood. 2009 Feb 19;113(8):1689-98 [19001083.001]
  • [Cites] Cancer Lett. 2009 May 8;277(1):91-100 [19138817.001]
  • [Cites] Nat Rev Mol Cell Biol. 2009 Jun;10(6):430-6 [19461665.001]
  • [Cites] Leukemia. 2000 Jul;14(7):1215-24 [10914545.001]
  • [Cites] Trends Genet. 2000 Oct;16(10):469-73 [11050335.001]
  • [Cites] Blood. 2002 Mar 15;99(6):1986-94 [11877270.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 15;100(8):4843-8 [12655043.001]
  • [Cites] Trends Immunol. 2003 Jun;24(6):302-6 [12810105.001]
  • [Cites] J Immunol. 2003 Aug 1;171(3):1232-9 [12874210.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):451-61 [14706337.001]
  • [Cites] Cell Death Differ. 2004 Apr;11(4):381-9 [14685163.001]
  • [Cites] Curr Opin Clin Nutr Metab Care. 2004 Jan;7(1):45-51 [15090903.001]
  • [Cites] J Clin Oncol. 2004 May 15;22(10):1815-22 [15143074.001]
  • [Cites] Cancer Res. 2004 Aug 15;64(16):5839-49 [15313928.001]
  • [Cites] Clin Cancer Res. 2004 Aug 15;10(16):5335-41 [15328169.001]
  • [Cites] J Nutr. 2004 Oct;134(10 Suppl):2760S-2764S; discussion 2765S-2767S [15465781.001]
  • [Cites] J Clin Oncol. 2004 Oct 15;22(20):4075-86 [15353542.001]
  • [Cites] Cancer Res. 1979 Oct;39(10):3893-6 [383278.001]
  • [Cites] Leuk Res. 1992;16(5):475-83 [1625473.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Feb 6;93(3):1065-70 [8577715.001]
  • [Cites] Semin Oncol. 1997 Feb;24(1):70-82 [9045306.001]
  • [Cites] N Engl J Med. 1998 Aug 27;339(9):605-15 [9718381.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Apr;6(4):318-27 [15803138.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3044-8 [15833831.001]
  • [Cites] Cell Immunol. 2004 Nov-Dec;232(1-2):21-31 [15922712.001]
  • [Cites] Nat Rev Immunol. 2005 Aug;5(8):641-54 [16056256.001]
  • [Cites] J Exp Med. 2005 Oct 3;202(7):931-9 [16186186.001]
  • [Cites] J Clin Oncol. 2005 Oct 20;23(30):7660-8 [16234528.001]
  • [Cites] Cell. 2006 Jun 16;125(6):1111-24 [16777601.001]
  • [Cites] Cell Cycle. 2007 Nov 15;6(22):2768-72 [17986863.001]
  • (PMID = 20407034.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / P20RR021970; United States / NCRR NIH HHS / RR / P20 RR021970; United States / NCI NIH HHS / CA / R01 CA082689; United States / NIGMS NIH HHS / GM / P20 GM103501; United States / NCI NIH HHS / CA / R01 CA107974
  • [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 / CCND3 protein, human; 0 / Cyclin D3; 04079A1RDZ / Cytarabine; 30IQX730WE / Polyethylene Glycols; 94ZLA3W45F / Arginine; EC 3.5.3.1 / Arginase
  • [Other-IDs] NLM/ PMC2892956
  •  go-up   go-down


27. Eguchi-Ishimae M, Eguchi M, Kempski H, Greaves M: NOTCH1 mutation can be an early, prenatal genetic event in T-ALL. Blood; 2008 Jan 1;111(1):376-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • NOTCH1 mutations are common in T-lineage acute lymphoblastic leukemia (T-ALL).
  • Twin studies and retrospective screening of neonatal blood spots provide evidence that fusion genes and other chromosomal abnormalities associated with pediatric leukemias can originate prenatally.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17901244.001).
  • [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 / NOTCH1 protein, human; 0 / Receptor, Notch1
  •  go-up   go-down


28. Balgobind BV, Van Vlierberghe P, van den Ouweland AM, Beverloo HB, Terlouw-Kromosoeto JN, van Wering ER, Reinhardt D, Horstmann M, Kaspers GJ, Pieters R, Zwaan CM, Van den Heuvel-Eibrink MM, Meijerink JP: Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis. Blood; 2008 Apr 15;111(8):4322-8
MedlinePlus Health Information. consumer health - Neurofibromatosis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis.
  • Neurofibromatosis type 1 (NF1) is an autosomal dominant genetic disorder caused by mutations in the NF1 gene.
  • Patients with NF1 have a higher risk to develop juvenile myelomonocytic leukemia (JMML) with a possible progression toward acute myeloid leukemia (AML).
  • In an oligo array comparative genomic hybridization-based screening of 103 patients with pediatric T-cell acute lymphoblastic leukemia (T-ALL) and 71 patients with MLL-rearranged AML, a recurrent cryptic deletion, del(17)(q11.2), was identified in 3 patients with T-ALL and 2 patients with MLL-rearranged AML.
  • Since the NF1 protein is a negative regulator of the RAS pathway (RAS-GTPase activating protein), homozygous NF1 inactivation represent a novel type I mutation in pediatric MLL-rearranged AML and T-ALL with a predicted frequency that is less than 10%.
  • NF1 inactivation may provide an additional proliferative signal toward the development of leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation / genetics. Neurofibromatoses / genetics. Neurofibromin 1 / genetics

  • Genetic Alliance. consumer health - Neurofibromatosis.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18172006.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neurofibromin 1; 0 / RNA, Messenger
  •  go-up   go-down


29. Clappier E, Cuccuini W, Kalota A, Crinquette A, Cayuela JM, Dik WA, Langerak AW, Montpellier B, Nadel B, Walrafen P, Delattre O, Aurias A, Leblanc T, Dombret H, Gewirtz AM, Baruchel A, Sigaux F, Soulier J: The C-MYB locus is involved in chromosomal translocation and genomic duplications in human T-cell acute leukemia (T-ALL), the translocation defining a new T-ALL subtype in very young children. Blood; 2007 Aug 15;110(4):1251-61
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] The C-MYB locus is involved in chromosomal translocation and genomic duplications in human T-cell acute leukemia (T-ALL), the translocation defining a new T-ALL subtype in very young children.
  • The C-Myb transcription factor is essential for hematopoiesis, including in the T-cell lineage.
  • Here, we identified 2 types of genomic alterations involving the C-MYB locus at 6q23 in human T-cell acute leukemia (T-ALL).
  • Expression analysis, including allele-specific approaches, showed stronger C-MYB expression in the MYB-rearranged cases compared with other T-ALLs, and a dramatically skewed C-MYB allele expression in the TCRB-MYB cases, which suggests that a translocation-driven deregulated expression may overcome a cellular attempt to down-regulate C-MYB.
  • Strikingly, profiling of the T-ALLs by clinical, genomic, and large-scale gene expression analyses shows that the TCRB-MYB translocation defines a new T-ALL subtype associated with a very young age for T-cell leukemia (median, 2.2 years) and with a proliferation/mitosis expression signature.
  • [MeSH-major] Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 7 / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Proto-Oncogene Proteins c-myb / genetics. Translocation, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17452517.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA101859
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myb
  •  go-up   go-down


30. van Grotel M, Meijerink JP, van Wering ER, Langerak AW, Beverloo HB, Buijs-Gladdines JG, Burger NB, Passier M, van Lieshout EM, Kamps WA, Veerman AJ, van Noesel MM, Pieters R: Prognostic significance of molecular-cytogenetic abnormalities in pediatric T-ALL is not explained by immunophenotypic differences. Leukemia; 2008 Jan;22(1):124-31

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Pediatric T-cell acute lymphoblastic leukemia (T-ALL) is characterized by chromosomal rearrangements possibly enforcing arrest at specific development stages.
  • We studied the relationship between molecular-cytogenetic abnormalities and T-cell development stage to investigate whether arrest at specific stages can explain the prognostic significance of specific abnormalities.
  • HOX11 cases were CD1 positive consistent with a cortical stage, but as 4/5 cases lacked cytoplasmatic-beta expression, developmental arrest may precede beta-selection.
  • HOX11L2 was especially confined to immature and pre-AB developmental stages, but 3/17 HOX11L2 mature cases were restricted to the gammadelta-lineage.
  • Classification into T-cell developmental subgroups was not predictive for outcome.
  • [MeSH-major] Gene Rearrangement / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Neoplasm Recurrence, Local / genetics. Receptor, Notch1 / genetics
  • [MeSH-minor] Basic Helix-Loop-Helix Transcription Factors / genetics. Cell Lineage. Child. Female. Homeodomain Proteins / genetics. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Mutation / genetics. Oncogene Proteins, Fusion / genetics. Prognosis. Proto-Oncogene Proteins / genetics. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Receptors, Antigen, T-Cell, alpha-beta / genetics. Receptors, Antigen, T-Cell, gamma-delta / genetics. Reverse Transcriptase Polymerase Chain Reaction

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17928886.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AF10-CALM fusion protein, human; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Homeodomain Proteins; 0 / NOTCH1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Antigen, T-Cell, gamma-delta; 0 / TLX3 protein, human; 135471-20-4 / TAL1 protein, human
  •  go-up   go-down


31. Burmeister T, Gökbuget N, Reinhardt R, Rieder H, Hoelzer D, Schwartz S: NUP214-ABL1 in adult T-ALL: the GMALL study group experience. Blood; 2006 Nov 15;108(10):3556-9
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.
  • The NUP214-ABL1 fusion gene in T-cell acute lymphoblastic leukemia (T-ALL) has recently been identified as a possible target for imatinib and related tyrosine kinase inhibitors, but exact data regarding the prognostic impact and frequency of the several putative NUP214-ABL1 mRNA transcripts are still missing.
  • Eleven (3.9%) patients were NUP214-ABL1 positive, and 5 different transcripts were observed; 8 patients had a thymic immunophenotype, 1 had an early T-cell immunophenotype, and 2 had a mature T-cell immunophenotype.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-abl / genetics

  • 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
  • (PMID = 16873673.001).
  • [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 / Benzamides; 0 / NUP214 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
  •  go-up   go-down


32. Cauwelier B, Dastugue N, Cools J, Poppe B, Herens C, De Paepe A, Hagemeijer A, Speleman F: Molecular cytogenetic study of 126 unselected T-ALL cases reveals high incidence of TCRbeta locus rearrangements and putative new T-cell oncogenes. Leukemia; 2006 Jul;20(7):1238-44

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular cytogenetic study of 126 unselected T-ALL cases reveals high incidence of TCRbeta locus rearrangements and putative new T-cell oncogenes.
  • Chromosomal aberrations of T-cell receptor (TCR) gene loci often involve the TCRalphadelta (14q11) locus and affect various known T-cell oncogenes.
  • Therefore, we initiated a screening of 126 T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma cases and 19 T-ALL cell lines using FISH break-apart assays for the different TCR loci.
  • Some of these chromosome aberrations target new putative T-cell oncogenes at chromosome 11q24, 20p12 and 6q22.
  • Five patients and one cell line carried chromosomal rearrangements affecting both TCRbeta and TCRalphadelta loci.
  • In conclusion, this study presents the first inventory of chromosomal rearrangements of TCR loci in T-ALL, revealing an unexpected high number of cryptic chromosomal rearrangements of the TCRbeta locus and further broadening the spectrum of genes putatively implicated in T-cell oncogenesis.
  • [MeSH-major] Gene Rearrangement, T-Lymphocyte / genetics. Genes, T-Cell Receptor beta / genetics. Leukemia-Lymphoma, Adult T-Cell / epidemiology. Leukemia-Lymphoma, Adult T-Cell / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Genes, T-Cell Receptor alpha / genetics. Genes, T-Cell Receptor delta / genetics. Humans. In Situ Hybridization, Fluorescence. Incidence. Male. Middle Aged. Retrospective Studies. Translocation, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16673021.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


33. Gordon WR, Roy M, Vardar-Ulu D, Garfinkel M, Mansour MR, Aster JC, Blacklow SC: Structure of the Notch1-negative regulatory region: implications for normal activation and pathogenic signaling in T-ALL. Blood; 2009 Apr 30;113(18):4381-90
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The NRR includes the 3 Lin12/Notch repeats and the juxtamembrane heterodimerization domain, the region of Notch1 most frequently mutated in T-cell acute lymphoblastic leukemia lymphoma (T-ALL).
  • [MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Receptor, Notch1 / chemistry. Receptor, Notch1 / metabolism. Regulatory Sequences, Nucleic Acid. Signal Transduction

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 2000 Sep 7;407(6800):48-54 [10993067.001]
  • [Cites] Cell. 1997 Jul 25;90(2):281-91 [9244302.001]
  • [Cites] Cell. 1991 Aug 23;66(4):649-61 [1831692.001]
  • [Cites] Cell. 2006 Mar 10;124(5):973-83 [16530044.001]
  • [Cites] Mol Cell Biol. 2000 Oct;20(20):7505-15 [11003647.001]
  • [Cites] J Biol Chem. 2008 Feb 22;283(8):4674-81 [18048354.001]
  • [Cites] Cell. 1990 May 4;61(3):523-34 [2185893.001]
  • [Cites] Nat Struct Mol Biol. 2007 Apr;14(4):295-300 [17401372.001]
  • [Cites] J Appl Crystallogr. 2007 Aug 1;40(Pt 4):658-674 [19461840.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Feb 20;93(4):1683-8 [8643690.001]
  • [Cites] Nat Struct Mol Biol. 2006 Jan;13(1):71-6 [16369486.001]
  • [Cites] Annu Rev Pathol. 2008;3:587-613 [18039126.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Haematologica. 2008 Apr;93(4):533-42 [18322257.001]
  • [Cites] Development. 2000 Apr;127(7):1373-85 [10704384.001]
  • [Cites] Leukemia. 2006 Mar;20(3):537-9 [16424867.001]
  • [Cites] Annu Rev Neurosci. 2003;26:565-97 [12730322.001]
  • [Cites] FEBS J. 2005 May;272(9):2118-31 [15853797.001]
  • [Cites] Acta Crystallogr D Biol Crystallogr. 1998 Sep 1;54(Pt 5):905-21 [9757107.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Mar 31;95(7):3408-12 [9520379.001]
  • [Cites] Mol Cell. 2000 Feb;5(2):207-16 [10882063.001]
  • [Cites] Acta Crystallogr D Biol Crystallogr. 1997 May 1;53(Pt 3):240-55 [15299926.001]
  • [Cites] Mol Cell Biol. 2006 Aug;26(16):6261-71 [16880534.001]
  • [Cites] J Cell Sci. 2008 Oct 1;121(Pt 19):3109-19 [18799787.001]
  • [Cites] Blood. 2008 Aug 1;112(3):733-40 [18411416.001]
  • [Cites] J Mol Biol. 1987 Aug 5;196(3):641-56 [3681970.001]
  • [Cites] Cell. 2006 Mar 10;124(5):985-96 [16530045.001]
  • [Cites] Nature. 1999 Apr 8;398(6727):518-22 [10206645.001]
  • [Cites] Nature. 1999 Apr 8;398(6727):522-5 [10206646.001]
  • [Cites] Mol Cell Biol. 2006 Jun;26(12):4642-51 [16738328.001]
  • [Cites] Bioinformatics. 2000 Jun;16(6):566-7 [10980157.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Sep;7(9):678-89 [16921404.001]
  • [Cites] J Mol Biol. 2007 Sep 21;372(3):774-97 [17681537.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1151-7 [16614245.001]
  • [Cites] J Biol Chem. 2004 Dec 3;279(49):50864-73 [15448134.001]
  • [Cites] Clin Cancer Res. 2006 May 15;12(10):3043-9 [16707600.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):8108-12 [9653148.001]
  • [Cites] Acta Crystallogr D Biol Crystallogr. 2004 Dec;60(Pt 12 Pt 1):2126-32 [15572765.001]
  • [Cites] Mol Cell. 2000 Feb;5(2):197-206 [10882062.001]
  • [Cites] Nature. 1998 May 28;393(6683):382-6 [9620803.001]
  • [Cites] J Biol Chem. 2008 Mar 21;283(12):8046-54 [18182388.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jan 2;98(1):229-34 [11134525.001]
  • [Cites] Clin Cancer Res. 2007 Dec 1;13(23):6964-9 [18056171.001]
  • [Cites] Mol Cell Biol. 2004 Nov;24(21):9265-73 [15485896.001]
  • [Cites] J Biol Chem. 2004 Mar 26;279(13):13174-82 [14764598.001]
  • [Cites] J Cell Biol. 2007 Feb 12;176(4):445-58 [17296795.001]
  • (PMID = 19075186.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R56 CA092433; United States / NCI NIH HHS / CA / P01 CA119070-030003; United States / NCI NIH HHS / CA / R01 CA092433-05S1; United States / NCI NIH HHS / CA / CA092433; United States / NCI NIH HHS / CA / R56 CA092433-06A1; United States / NCI NIH HHS / CA / R01 CA092433; United States / NCI NIH HHS / CA / P01 CA119070-03; United States / NCI NIH HHS / CA / P01 CA119070-039001; United States / NCI NIH HHS / CA / P01 CA119070-029001; United States / NCI NIH HHS / CA / P01 CA119070-020003; United States / NCI NIH HHS / CA / R01 CA092433-05; United Kingdom / Medical Research Council / / G0500389; United States / NCI NIH HHS / CA / R01 CA092433-04; United States / NCI NIH HHS / CA / P01 CA119070
  • [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 / NOTCH1 protein, human; 0 / NOTCH2 protein, human; 0 / Receptor, Notch1; 0 / Receptor, Notch2; EC 1.13.12.- / Luciferases
  • [Other-IDs] NLM/ PMC2676092
  •  go-up   go-down


34. Estes DA, Lovato DM, Khawaja HM, Winter SS, Larson RS: Genetic alterations determine chemotherapy resistance in childhood T-ALL: modelling in stage-specific cell lines and correlation with diagnostic patient samples. Br J Haematol; 2007 Oct;139(1):20-30
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] Genetic alterations determine chemotherapy resistance in childhood T-ALL: modelling in stage-specific cell lines and correlation with diagnostic patient samples.
  • Acquired drug resistance eventually leads to treatment failure in T-cell acute lymphoblastic leukaemia (T-ALL).
  • Immunophenotypic and cytogenetic heterogeneities within T-ALL influence susceptibility to cytotoxic therapy, and little is known about the mechanisms of drug resistance at specific stages of T-cell ontogeny.
  • We developed tolerance to therapeutic concentrations of daunorubicin (DNR) and L-asparaginase (L-asp) in Jurkat (CD1a(-), sCD3(+)) and Sup T1 (CD1a(+), sCD3(-)) cell lines, having respective 'mature' and 'cortical' stages of developmental arrest.
  • Microarray analysis identified upregulation of asparagine synthetase (ASNS) and argininosuccinate synthase 1 (ASS1) to cell lines with acquired resistance to L-asp, and in the case of DNR, upregulation of ATP-binding cassette B1 (ABCB1).
  • This study expands the pool of available drug resistant cell lines having cortical and mature stages of developmental arrest, introduces three new drug resistant T-ALL cell lines, and identifies gene interactions leading to L-asp and DNR resistance.
  • [MeSH-major] Cell Line, Tumor. Drug Resistance, Neoplasm / genetics. Gene Expression Regulation, Leukemic. Genes, MDR. Leukemia-Lymphoma, Adult T-Cell / genetics

  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17854304.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1 R01 CA114589; United States / NCI NIH HHS / CA / U10 CA98543-03-14305
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / P-Glycoprotein; 0 / RNA, Small Interfering; 5J49Q6B70F / Vincristine; 9PHQ9Y1OLM / Prednisolone; EC 3.5.1.1 / Asparaginase; EC 6.3.1.1 / Aspartate-Ammonia Ligase; EC 6.3.4.5 / Argininosuccinate Synthase; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


35. Marçais A, Jeannet R, Hernandez L, Soulier J, Sigaux F, Chan S, Kastner P: Genetic inactivation of Ikaros is a rare event in human T-ALL. Leuk Res; 2010 Apr;34(4):426-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The Ikaros (Ikzf1) gene, encoding a transcription regulator, is a major tumor suppressor in B-cell acute lymphoblastic leukemia (B-ALL).
  • [MeSH-major] Gene Silencing. Ikaros Transcription Factor / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • [CommentIn] Leuk Res. 2010 Apr;34(4):416-7 [19892402.001]
  • (PMID = 19796813.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / IKZF1 protein, human; 0 / Protein Isoforms; 148971-36-2 / Ikaros Transcription Factor
  •  go-up   go-down


36. Xu SN, Chen JP: [Research advance on the pathogenesis of T-ALL induced by notch 1 activating mutations]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Feb;18(1):242-5
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • T-cell acute lymphoblastic leukemia (T-ALL) is the hematological malignancy of bone marrow characterized by the rapid proliferation and subsequent accumulation of immature T lymphocyte and mainly occurs in children and adolescents.
  • This review briefly discusses the four main subtypes of Notch 1 activating mutations, also focuses on how these mutations change the normal signaling pathways and genes expression during their participation in the pathogenesis of T-ALL, and how these insights will promote the development of newly targeting therapies for patients with this aggressive form of leukemia.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20137156.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Receptor, Notch1
  •  go-up   go-down


37. Jeannet R, Mastio J, Macias-Garcia A, Oravecz A, Ashworth T, Geimer Le Lay AS, Jost B, Le Gras S, Ghysdael J, Gridley T, Honjo T, Radtke F, Aster JC, Chan S, Kastner P: Oncogenic activation of the Notch1 gene by deletion of its promoter in Ikaros-deficient T-ALL. Blood; 2010 Dec 16;116(25):5443-54
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.
  • The Notch pathway is frequently activated in T-cell acute lymphoblastic leukemias (T-ALLs).
  • Of the Notch receptors, Notch1 is a recurrent target of gain-of-function mutations and Notch3 is expressed in all T-ALLs, but it is currently unclear how these receptors contribute to T-cell transformation in vivo.
  • While deletion of Notch3 has little effect, T cell-specific deletion of floxed Notch1 promoter/exon 1 sequences significantly accelerates leukemogenesis.
  • Further, spontaneous deletion of 5' Notch1 sequences occurs in approximately 75% of Ikaros-deficient T-ALLs.
  • [MeSH-major] Ikaros Transcription Factor / physiology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic / genetics. Receptor, Notch1 / genetics. Transcriptional Activation / physiology
  • [MeSH-minor] Animals. Blotting, Northern. Blotting, Western. Cell Transformation, Neoplastic. DNA Primers / chemistry. DNA Primers / genetics. Flow Cytometry. Gene Expression Regulation, Neoplastic. Immunoglobulin J Recombination Signal Sequence-Binding Protein / physiology. Mice. Mice, Knockout. Mutation / genetics. RNA, Messenger / genetics. Receptors, Notch / physiology. Reverse Transcriptase Polymerase Chain Reaction. Sequence Deletion. Survival Rate

  • COS Scholar Universe. author profiles.
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • 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] Mol Cell. 2005 Dec 22;20(6):971-8 [16364921.001]
  • [Cites] Mol Cell Biol. 2000 Jun;20(11):3831-42 [10805726.001]
  • [Cites] Blood. 2000 Jun 15;95(12):3891-9 [10845925.001]
  • [Cites] EMBO J. 2000 Jul 3;19(13):3337-48 [10880446.001]
  • [Cites] Immunity. 2000 Jul;13(1):73-84 [10933396.001]
  • [Cites] Nat Immunol. 2001 Mar;2(3):235-41 [11224523.001]
  • [Cites] Genes Dev. 2002 Feb 1;16(3):295-300 [11825871.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3788-93 [11891328.001]
  • [Cites] Int Immunol. 2002 Jun;14(6):637-45 [12039915.001]
  • [Cites] Immunity. 2002 Jun;16(6):869-79 [12121668.001]
  • [Cites] Carcinogenesis. 2003 Jul;24(7):1257-68 [12807718.001]
  • [Cites] Science. 2003 Aug 22;301(5636):1096-9 [12934008.001]
  • [Cites] Genesis. 2003 Nov;37(3):139-43 [14595837.001]
  • [Cites] Mol Cell Biol. 2004 Jan;24(2):757-64 [14701747.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 6;101(14):4936-41 [15044701.001]
  • [Cites] Immunity. 2004 May;20(5):611-22 [15142529.001]
  • [Cites] Semin Cancer Biol. 2004 Oct;14(5):329-40 [15288258.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Cell. 1991 Aug 23;66(4):649-61 [1831692.001]
  • [Cites] Nature. 1995 Sep 28;377(6547):355-8 [7566092.001]
  • [Cites] J Exp Med. 1996 May 1;183(5):2283-91 [8642337.001]
  • [Cites] Mol Cell Biol. 1997 Nov;17(11):6265-73 [9343387.001]
  • [Cites] Immunity. 1999 Mar;10(3):345-55 [10204490.001]
  • [Cites] Immunity. 1999 May;10(5):547-58 [10367900.001]
  • [Cites] Blood. 2005 Jul 1;106(1):274-86 [15774621.001]
  • [Cites] Cell. 2005 Nov 18;123(4):581-92 [16286007.001]
  • [Cites] Cell. 2005 Nov 18;123(4):593-605 [16286008.001]
  • [Cites] Mol Cell Biol. 2006 Jan;26(1):209-20 [16354692.001]
  • [Cites] Mol Cell. 2007 Jan 12;25(1):31-42 [17218269.001]
  • [Cites] EMBO J. 2007 Mar 21;26(6):1670-80 [17332745.001]
  • [Cites] J Biol Chem. 2007 Oct 12;282(41):30227-38 [17681952.001]
  • [Cites] Lancet. 2008 Mar 22;371(9617):1030-43 [18358930.001]
  • [Cites] J Biol Chem. 2008 Apr 18;283(16):10476-84 [18287091.001]
  • [Cites] Nat Rev Immunol. 2008 May;8(5):380-90 [18421304.001]
  • [Cites] J Clin Invest. 2008 Sep;118(9):3181-94 [18677410.001]
  • [Cites] Mol Cell Biol. 2008 Dec;28(24):7465-75 [18852286.001]
  • [Cites] Genes Dev. 2009 Jul 15;23(14):1665-76 [19605688.001]
  • [Cites] Bioinformatics. 2009 Aug 1;25(15):1952-8 [19505939.001]
  • [Cites] Leuk Res. 2010 Apr;34(4):426-9 [19796813.001]
  • [Cites] Blood. 2010 Dec 16;116(25):5455-64 [20852131.001]
  • [CommentIn] Blood. 2010 Dec 16;116(25):5436-8 [21163932.001]
  • (PMID = 20829372.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / R01 HD034883
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Immunoglobulin J Recombination Signal Sequence-Binding Protein; 0 / Notch1 protein, mouse; 0 / Notch3 protein, mouse; 0 / RNA, Messenger; 0 / Rbpj protein, mouse; 0 / Receptor, Notch1; 0 / Receptors, Notch; 0 / Zfpn1a1 protein, mouse; 148971-36-2 / Ikaros Transcription Factor
  • [Other-IDs] NLM/ PMC3100247
  •  go-up   go-down


38. Ashworth TD, Pear WS, Chiang MY, Blacklow SC, Mastio J, Xu L, Kelliher M, Kastner P, Chan S, Aster JC: Deletion-based mechanisms of Notch1 activation in T-ALL: key roles for RAG recombinase and a conserved internal translational start site in Notch1. Blood; 2010 Dec 16;116(25):5455-64
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Point mutations that trigger ligand-independent proteolysis of the Notch1 ectodomain occur frequently in human T-cell acute lymphoblastic leukemia (T-ALL) but are rare in murine T-ALL, suggesting that other mechanisms account for Notch1 activation in murine tumors.
  • Here we show that most murine T-ALLs harbor Notch1 deletions that fall into 2 types, both leading to ligand-independent Notch1 activation.
  • Type 1 deletions remove exon 1 and the proximal promoter, appear to be RAG-mediated, and are associated with mRNA transcripts that initiate from 3' regions of Notch1.
  • Type 2 deletions remove sequences between exon 1 and exons 26 to 28 of Notch1, appear to be RAG-independent, and are associated with transcripts in which exon 1 is spliced out of frame to 3' Notch1 exons.
  • [MeSH-major] Homeodomain Proteins / physiology. Peptide Chain Initiation, Translational / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic / genetics. Receptor, Notch1 / genetics. Transcriptional Activation / physiology

  • COS Scholar Universe. author profiles.
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell. 2002 Jun 28;109(7):811-21 [12110179.001]
  • [Cites] Radiat Res. 2002 Mar;157(3):331-40 [11839096.001]
  • [Cites] Nat Immunol. 2003 Feb;4(2):168-74 [12514733.001]
  • [Cites] Cancer Cell. 2003 Jun;3(6):551-64 [12842084.001]
  • [Cites] Carcinogenesis. 2003 Jul;24(7):1257-68 [12807718.001]
  • [Cites] Science. 2003 Aug 22;301(5636):1096-9 [12934008.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Cell. 1991 Aug 23;66(4):649-61 [1831692.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Feb 20;93(4):1683-8 [8643690.001]
  • [Cites] Genes Dev. 1996 Aug 1;10(15):1930-44 [8756350.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3780-92 [9808572.001]
  • [Cites] Cancer Res. 2004 Dec 15;64(24):8882-90 [15604248.001]
  • [Cites] Nature. 2005 Jul 14;436(7048):221-6 [16015321.001]
  • [Cites] Cell. 2005 Aug 12;122(3):435-47 [16096062.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3898-906 [16118316.001]
  • [Cites] Mol Cell Biol. 2006 Jan;26(1):209-20 [16354692.001]
  • [Cites] Blood. 2006 Jan 15;107(2):781-5 [16166587.001]
  • [Cites] Blood. 2006 Mar 15;107(6):2540-3 [16282337.001]
  • [Cites] Mol Cell Biol. 2006 Jun;26(12):4642-51 [16738328.001]
  • [Cites] Mol Cell Biol. 2000 Jun;20(11):3831-42 [10805726.001]
  • [Cites] Mol Cell Biol. 2000 Oct;20(20):7505-15 [11003647.001]
  • [Cites] Mol Cell. 2000 Oct;6(4):939-45 [11090631.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1279-87 [16688224.001]
  • [Cites] Nat Struct Mol Biol. 2007 Apr;14(4):295-300 [17401372.001]
  • [Cites] Nature. 2007 Jun 21;447(7147):966-71 [17515920.001]
  • [Cites] Nat Med. 2007 Oct;13(10):1203-10 [17873882.001]
  • [Cites] Oncogene. 2008 Jan 10;27(3):404-8 [17621273.001]
  • [Cites] J Biol Chem. 2008 Mar 21;283(12):8046-54 [18182388.001]
  • [Cites] Annu Rev Pathol. 2008;3:587-613 [18039126.001]
  • [Cites] J Clin Invest. 2008 Sep;118(9):3181-94 [18677410.001]
  • [Cites] Immunity. 2009 Jan 16;30(1):67-79 [19110448.001]
  • [Cites] Mutat Res. 2009 Jan 15;660(1-2):22-32 [19000702.001]
  • [Cites] Cell. 2009 Apr 17;137(2):216-33 [19379690.001]
  • [Cites] Blood. 2009 Apr 30;113(18):4381-90 [19075186.001]
  • [Cites] J Biol Chem. 2009 May 8;284(19):13013-22 [19254953.001]
  • [Cites] Blood. 2009 Jun 11;113(24):6172-81 [19246562.001]
  • [Cites] Genes Dev. 2009 Jul 15;23(14):1665-76 [19605688.001]
  • [Cites] Mol Cell Biol. 2009 Nov;29(21):5679-95 [19704010.001]
  • [Cites] Nature. 2009 Nov 12;462(7270):182-8 [19907488.001]
  • [Cites] J Neurosci. 2010 Feb 3;30(5):1648-56 [20130175.001]
  • [Cites] PLoS One. 2010;5(2):e9094 [20161710.001]
  • [Cites] Proc Natl Acad Sci U S A. 2010 Mar 16;107(11):5106-11 [20194733.001]
  • [Cites] Cell. 2010 Apr 30;141(3):419-31 [20398922.001]
  • [Cites] Blood. 2010 Dec 16;116(25):5443-54 [20829372.001]
  • [CommentIn] Blood. 2010 Dec 16;116(25):5436-8 [21163932.001]
  • (PMID = 20852131.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096899
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Notch1 protein, mouse; 0 / RNA, Messenger; 0 / Receptor, Notch1; 0 / Zfpn1a1 protein, mouse; 128559-51-3 / RAG-1 protein; 148971-36-2 / Ikaros Transcription Factor
  • [Other-IDs] NLM/ PMC3031398
  •  go-up   go-down


39. Przybylski GK, Dik WA, Wanzeck J, Grabarczyk P, Majunke S, Martin-Subero JI, Siebert R, Dölken G, Ludwig WD, Verhaaf B, van Dongen JJ, Schmidt CA, Langerak AW: Disruption of the BCL11B gene through inv(14)(q11.2q32.31) results in the expression of BCL11B-TRDC fusion transcripts and is associated with the absence of wild-type BCL11B transcripts in T-ALL. Leukemia; 2005 Feb;19(2):201-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Disruption of the BCL11B gene through inv(14)(q11.2q32.31) results in the expression of BCL11B-TRDC fusion transcripts and is associated with the absence of wild-type BCL11B transcripts in T-ALL.
  • T-cell acute lymphoblastic leukemia (T-ALL) is associated with chromosomal aberrations characterized by juxtaposition of proto-oncogenes to T-cell receptor gene loci (TCR), resulting in the deregulated transcription of these proto-oncogenes.
  • The TRDV1-BCL11B joining region was 1344 bp long and contained fragments derived from 20q11.22, 3p21.33 and from 11p12, indicating the complex character of this aberration.
  • A strong expression of in-frame transcripts with truncated BCL11B and TCRD constant region (TRDC) were observed, but in contrast to normal T cells and other T-ALL samples, no wild-type BCL11B transcripts were detected in the T-ALL sample.
  • Screening of 37 other T-ALLs revealed one additional case with expression of the BCL11B-TRDC fusion transcript.
  • As BCL11B appears to play a key role in T-cell differentiation, BCL11B disruption and disturbed expression may contribute to the development of T-cell malignancies in man.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 14. Leukemia-Lymphoma, Adult T-Cell / genetics. Translocation, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15668700.001).
  • [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 / BCL11B protein, human; 0 / DNA-Binding Proteins; 0 / Repressor Proteins; 0 / Tumor Suppressor Proteins
  •  go-up   go-down


40. Asnafi V, Buzyn A, Le Noir S, Baleydier F, Simon A, Beldjord K, Reman O, Witz F, Fagot T, Tavernier E, Turlure P, Leguay T, Huguet F, Vernant JP, Daniel F, Béné MC, Ifrah N, Thomas X, Dombret H, Macintyre E: NOTCH1/FBXW7 mutation identifies a large subgroup with favorable outcome in adult T-cell acute lymphoblastic leukemia (T-ALL): a Group for Research on Adult Acute Lymphoblastic Leukemia (GRAALL) study. Blood; 2009 Apr 23;113(17):3918-24
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NOTCH1/FBXW7 mutation identifies a large subgroup with favorable outcome in adult T-cell acute lymphoblastic leukemia (T-ALL): a Group for Research on Adult Acute Lymphoblastic Leukemia (GRAALL) study.
  • Many somatic genetic abnormalities have been identified in T-cell acute lymphoblastic leukemia (T-ALL) but each individual abnormality accounts for a small proportion of cases; therapeutic stratification consequently still relies on classical clinical markers.
  • We screened 141 adult diagnostic T-ALL samples from patients treated on either the Lymphoblastic Acute Leukemia in Adults (LALA)-94 (n = 87) or the GRAALL-2003 (n = 54) trials.
  • In 88 cases (62%) there were demonstrated NOTCH1 mutations (42% heterodimerization [HD], 10% HD+proline glutamate serine threonine [PEST], 6% PEST, 2% juxtamembrane mutations, 2% transactivation domain [TAD]) and 34 cases (24%) had FBXW7 mutations (21 cases had both NOTCH1 and FBXW7 mutations); 40 cases (28%) were wild type for both.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics. Ubiquitin-Protein Ligases / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19109228.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Receptor, Notch1; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  •  go-up   go-down


41. Cauwelier B, Cavé H, Gervais C, Lessard M, Barin C, Perot C, Van den Akker J, Mugneret F, Charrin C, Pagès MP, Grégoire MJ, Jonveaux P, Lafage-Pochitaloff M, Mozzicconacci MJ, Terré C, Luquet I, Cornillet-Lefebvre P, Laurence B, Plessis G, Lefebvre C, Leroux D, Antoine-Poirel H, Graux C, Mauvieux L, Heimann P, Chalas C, Clappier E, Verhasselt B, Benoit Y, Moerloose BD, Poppe B, Van Roy N, Keersmaecker KD, Cools J, Sigaux F, Soulier J, Hagemeijer A, Paepe AD, Dastugue N, Berger R, Speleman F: Clinical, cytogenetic and molecular characteristics of 14 T-ALL patients carrying the TCRbeta-HOXA rearrangement: a study of the Groupe Francophone de Cytogénétique Hématologique. Leukemia; 2007 Jan;21(1):121-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical, cytogenetic and molecular characteristics of 14 T-ALL patients carrying the TCRbeta-HOXA rearrangement: a study of the Groupe Francophone de Cytogénétique Hématologique.
  • Recently, we and others described a new chromosomal rearrangement, that is, inv(7)(p15q34) and t(7;7)(p15;q34) involving the T-cell receptor beta (TCRbeta) (7q34) and the HOXA gene locus (7p15) in 5% of T-cell acute lymphoblastic leukemia (T-ALL) patients leading to transcriptional activation of especially HOXA10.
  • To further address the clinical, immunophenotypical and molecular genetic findings of this chromosomal aberration, we studied 330 additional T-ALLs.
  • In conclusion, this study defines TCRbeta-HOXA rearranged T-ALLs as a distinct cytogenetic subgroup by clinical, immunophenotypical and molecular genetic characteristics.
  • [MeSH-major] Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Receptors, Antigen, T-Cell, alpha-beta / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17039236.001).
  • [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 / Homeodomain Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell, alpha-beta; 140441-81-2 / HOXA10 protein, human
  •  go-up   go-down


42. Rodig SJ, Payne EG, Degar BA, Rollins B, Feldman AL, Jaffe ES, Androkites A, Silverman LB, Longtine JA, Kutok JL, Fleming MD, Aster JC: Aggressive Langerhans cell histiocytosis following T-ALL: clonally related neoplasms with persistent expression of constitutively active NOTCH1. Am J Hematol; 2008 Feb;83(2):116-21
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aggressive Langerhans cell histiocytosis following T-ALL: clonally related neoplasms with persistent expression of constitutively active NOTCH1.
  • Langerhans cell histiocytosis (LCH) and related entities are neoplasms of unknown pathogenesis.
  • Here, we describe studies assessing the role of NOTCH1 mutations in LCH, which were based on a case of fatal Langerhans cell tumor after T-cell acute lymphoblastic leukemia (T-ALL).
  • Although the two types of neoplasm in this patient were temporally and pathologically distinct, molecular analyses showed that they harbored the same T-cell receptor gene rearrangements and two activating NOTCH1 mutations involving exons 27 and 34.
  • Analysis of cDNA prepared from the aggressive Langerhans cell tumor showed that the NOTCH1 mutations were aligned in cis, a configuration that caused synergistic increases in NOTCH1 signal strength in reporter gene assays.
  • Immunohistochemistry confirmed that the Langerhans cell tumor also expressed NOTCH1 protein.
  • Although these data suggested that NOTCH1 mutations might contribute to the pathogenesis of typical sporadic LCH and related neoplasms occurring in the absence of T-ALL, an analysis of 24 cases of LCH and Rosai-Dorfman Disease occurring in patients without an antecedent history of T-ALL revealed no mutations.
  • Thus, activating NOTCH1 mutations appear to be unique to aggressive Langerhans cell tumors occurring after T-ALL.

  • Genetic Alliance. consumer health - Histiocytosis.
  • Genetic Alliance. consumer health - Langerhans cell histiocytosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17874453.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI050225; United States / NCI NIH HHS / CA / CA082308; United States / NCI NIH HHS / CA / CA119070-02; United States / NCI NIH HHS / CA / P01 CA119070-02; United States / NCI NIH HHS / CA / P01 CA119070
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
  •  go-up   go-down


43. Remke M, Pfister S, Kox C, Toedt G, Becker N, Benner A, Werft W, Breit S, Liu S, Engel F, Wittmann A, Zimmermann M, Stanulla M, Schrappe M, Ludwig WD, Bartram CR, Radlwimmer B, Muckenthaler MU, Lichter P, Kulozik AE: High-resolution genomic profiling of childhood T-ALL reveals frequent copy-number alterations affecting the TGF-beta and PI3K-AKT pathways and deletions at 6q15-16.1 as a genomic marker for unfavorable early treatment response. Blood; 2009 Jul 30;114(5):1053-62
SciCrunch. ArrayExpress: Data: Microarray .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Precursor T-cell acute lymphoblastic leukemia (T-ALL) in children represents a clinical challenge, because relapses are usually fatal.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Deletion. Chromosomes, Human, Pair 6 / genetics. Neoplasm Proteins / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Signal Transduction / genetics

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19406988.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GPL5713/ GSE8738
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / NOTCH1 protein, human; 0 / Neoplasm Proteins; 0 / Receptor, Notch1; 0 / Transforming Growth Factor beta; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  •  go-up   go-down


44. Cecchinato V, Erba E, Basile A, Scarpati B, Fazi C, Brando B, Comi P, Chiaramonte R: Hexamethylene bisacetamide inhibits malignant phenotype in T-ALL cell lines. Leuk Res; 2008 May;32(5):791-7
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hexamethylene bisacetamide inhibits malignant phenotype in T-ALL cell lines.
  • T acute lymphoblastic leukemia cell lines treated with hexamethylene bisacetamide (HMBA) undergo a delay in cell cycle progression and increase susceptibility to apoptosis, although they never overcome the differentiation block.
  • In accordance with changes in cell cycle and apoptosis, transitory p53 pathway activation commonly occurs.
  • Bcl-2 inhibition further favours the pro-apoptotic effect of HMBA.
  • Even if HMBA generally reduces Notch1 level in T acute lymphoblastic leukemia (T-ALL) cell lines, this does not commonly influence the biological response; in fact all the analysed cell lines, except CEM cells, display no biological effect following DAPT-induced Notch inhibition.
  • [MeSH-major] Acetamides / pharmacology. Antineoplastic Agents / pharmacology. Leukemia-Lymphoma, Adult T-Cell / drug therapy
  • [MeSH-minor] Cell Line, Tumor. Cyclin-Dependent Kinase 4 / analysis. Humans. Proto-Oncogene Proteins c-bcl-2 / physiology. Receptor, Notch1 / physiology. Signal Transduction. Triglycerides / pharmacology. Tumor Suppressor Protein p53 / physiology. gamma-Aminobutyric Acid / analogs & derivatives. gamma-Aminobutyric Acid / pharmacology

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Leuk Res. 2008 May;32(5):689-90 [18164760.001]
  • (PMID = 17964649.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Acetamides; 0 / Antineoplastic Agents; 0 / NOTCH1 protein, human; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptor, Notch1; 0 / Triglycerides; 0 / Tumor Suppressor Protein p53; 56-12-2 / gamma-Aminobutyric Acid; 93349-26-9 / 1,2-dilinolenoyl-3-(4-aminobutyryl)propane-1,2,3-triol; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; LA133J59VU / hexamethylene bisacetamide
  •  go-up   go-down


45. Matsuoka S, Oike Y, Onoyama I, Iwama A, Arai F, Takubo K, Mashimo Y, Oguro H, Nitta E, Ito K, Miyamoto K, Yoshiwara H, Hosokawa K, Nakamura Y, Gomei Y, Iwasaki H, Hayashi Y, Matsuzaki Y, Nakayama K, Ikeda Y, Hata A, Chiba S, Nakayama KI, Suda T: Fbxw7 acts as a critical fail-safe against premature loss of hematopoietic stem cells and development of T-ALL. Genes Dev; 2008 Apr 15;22(8):986-91
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Common molecular machineries between hematopoietic stem cell (HSC) maintenance and leukemia prevention have been highlighted.
  • The tumor suppressor Fbxw7 (F-box and WD-40 domain protein 7), a subunit of an SCF-type ubiquitin ligase complex, induces the degradation of positive regulators of the cell cycle.
  • We demonstrate that inactivation of Fbxw7 in hematopoietic cells causes premature depletion of HSCs due to active cell cycling and p53-dependent apoptosis.
  • Interestingly, Fbxw7 deletion also confers a selective advantage to cells with suppressed p53 function, eventually leading to development of T-cell acute lymphoblastic leukemia (T-ALL).
  • [MeSH-major] F-Box Proteins / metabolism. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / enzymology. Leukemia-Lymphoma, Adult T-Cell / etiology. Ubiquitin-Protein Ligases / metabolism
  • [MeSH-minor] Animals. Cell Cycle. Cells, Cultured. Mice. Mice, Transgenic. Tumor Suppressor Protein p53 / metabolism

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Genes Dev. 1999 Oct 15;13(20):2658-69 [10541552.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Aug;6(8):599-609 [16064136.001]
  • [Cites] Cancer Res. 2002 Aug 15;62(16):4535-9 [12183400.001]
  • [Cites] Nature. 2003 Oct 23;425(6960):836-41 [14574412.001]
  • [Cites] Nature. 2003 Oct 23;425(6960):841-6 [14574413.001]
  • [Cites] Cancer Res. 2004 Feb 1;64(3):795-800 [14871801.001]
  • [Cites] J Biol Chem. 2004 Mar 5;279(10):9417-23 [14672936.001]
  • [Cites] Nature. 2004 Mar 4;428(6978):77-81 [14999283.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 9;101(10):3338-45 [14766969.001]
  • [Cites] Cell. 2004 Jul 23;118(2):149-61 [15260986.001]
  • [Cites] Nature. 2005 Aug 4;436(7051):642 [16079833.001]
  • [Cites] Cancer Biol Ther. 2005 May;4(5):506-8 [15908780.001]
  • [Cites] Cancer Res. 2005 Aug 15;65(16):7159-68 [16103066.001]
  • [Cites] Clin Adv Hematol Oncol. 2004 Dec;2(12):779-80 [16166953.001]
  • [Cites] Cell Cycle. 2005 Oct;4(10):1356-9 [16131838.001]
  • [Cites] Nat Rev Cancer. 2006 May;6(5):347-59 [16612405.001]
  • [Cites] Nat Rev Cancer. 2006 May;6(5):369-81 [16633365.001]
  • [Cites] Nature. 2006 May 25;441(7092):475-82 [16598206.001]
  • [Cites] Nature. 2006 May 25;441(7092):518-22 [16633340.001]
  • [Cites] Genes Dev. 2006 Aug 1;20(15):2096-109 [16847353.001]
  • [Cites] Cell. 2007 Jan 26;128(2):325-39 [17254970.001]
  • [Cites] Ann N Y Acad Sci. 2007 Apr;1100:312-5 [17460193.001]
  • [Cites] Nature. 2007 Jun 21;447(7147):966-71 [17515920.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1825-35 [17646408.001]
  • [Cites] J Exp Med. 2007 Nov 26;204(12):2875-88 [17984302.001]
  • [Cites] Science. 2000 Mar 10;287(5459):1804-8 [10710306.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Nature. 2004 Oct 21;431(7011):1002-7 [15457180.001]
  • [Cites] Nature. 2004 Oct 21;431(7011):997-1002 [15496926.001]
  • [Cites] Genes Dev. 1998 Aug 1;12(15):2424-33 [9694806.001]
  • [Cites] Immunity. 1999 Sep;11(3):299-308 [10514008.001]
  • [Cites] Genes Dev. 2004 Nov 15;18(22):2747-63 [15545632.001]
  • [Cites] Nature. 2004 Dec 9;432(7018):775-9 [15592418.001]
  • [CommentIn] Genes Dev. 2008 May 1;22(9):1107-9 [18451101.001]
  • (PMID = 18367647.001).
  • [ISSN] 0890-9369
  • [Journal-full-title] Genes & development
  • [ISO-abbreviation] Genes Dev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / F-Box Proteins; 0 / Fbxw7 protein, mouse; 0 / Tumor Suppressor Protein p53; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Other-IDs] NLM/ PMC2335330
  •  go-up   go-down


46. Li X, Gounari F, Protopopov A, Khazaie K, von Boehmer H: Oncogenesis of T-ALL and nonmalignant consequences of overexpressing intracellular NOTCH1. J Exp Med; 2008 Nov 24;205(12):2851-61
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.
  • Mutations resulting in overexpression of intracellular Notch1 (ICN1) are frequently observed in human T cell acute lymphoblastic leukemia (T-ALL).
  • Early consequences are the generation of polyclonal nontumorigenic CD4(+)8(+) T cell receptor (TCR)-alphabeta(+) cells that do not qualify as tumor precursors despite the observation that they overexpress Notch 1 and c-Myc and degrade the tumor suppressor E2A by posttranslational modification.
  • The first tumorigenic cells are detected among more immature CD4(-)8(+)TCR-alphabeta(-) cells that give rise to monoclonal tumors with a single, unique TCR-beta chain and diverse TCR-alpha chains, pinpointing malignant transformation to a stage after pre-TCR signaling and before completion of TCR-alpha rearrangement.

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 2007 Jun 21;447(7147):966-71 [17515920.001]
  • [Cites] Nature. 1985 Mar 7-13;314(6006):103-7 [2983227.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1813-24 [17646409.001]
  • [Cites] Cell. 2007 Jun 1;129(5):879-90 [17540169.001]
  • [Cites] Genes Dev. 1999 Oct 15;13(20):2658-69 [10541552.001]
  • [Cites] Genes Dev. 1999 Oct 15;13(20):2678-90 [10541554.001]
  • [Cites] Blood. 2000 Mar 15;95(6):2104-10 [10706881.001]
  • [Cites] Immunity. 2001 Jan;14(1):45-55 [11163229.001]
  • [Cites] Nat Immunol. 2001 Mar;2(3):235-41 [11224523.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3788-93 [11891328.001]
  • [Cites] Nat Immunol. 2002 May;3(5):483-8 [11927911.001]
  • [Cites] Nature. 1985 May 16-22;315(6016):232-3 [3873615.001]
  • [Cites] Cell. 1991 Aug 9;66(3):533-40 [1868548.001]
  • [Cites] Nature. 1995 Jun 29;375(6534):795-8 [7596413.001]
  • [Cites] Genes Dev. 1996 Aug 1;10(15):1930-44 [8756350.001]
  • [Cites] Annu Rev Immunol. 1997;15:433-52 [9143695.001]
  • [Cites] Mol Cell Biol. 1997 Aug;17(8):4782-91 [9234734.001]
  • [Cites] Science. 1999 Apr 30;284(5415):770-6 [10221902.001]
  • [Cites] Mol Cell. 1999 Aug;4(2):199-207 [10488335.001]
  • [Cites] Curr Opin Hematol. 2004 Nov;11(6):426-33 [15548998.001]
  • [Cites] Nat Rev Immunol. 2005 Jun;5(6):497-508 [15928681.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Aug;6(8):635-45 [16064138.001]
  • [Cites] Nat Immunol. 2005 Sep;6(9):881-8 [16056227.001]
  • [Cites] J Exp Med. 2006 May 15;203(5):1329-42 [16682500.001]
  • [Cites] Blood. 2006 Jul 1;108(1):305-10 [16507772.001]
  • [Cites] Genes Dev. 2006 Aug 1;20(15):2096-109 [16847353.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18261-6 [17114293.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Apr 30;99(9):6274-9 [11983916.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]
  • [Cites] Cell. 2002 Jun 28;109(7):811-21 [12110179.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Aug 20;99(17):11322-7 [12172006.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(2):655-64 [12509463.001]
  • [Cites] Blood. 2003 Apr 1;101(7):2797-803 [12517816.001]
  • [Cites] EMBO J. 2003 Nov 3;22(21):5780-92 [14592976.001]
  • [Cites] EMBO Rep. 2003 Nov;4(11):1067-72 [14566327.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):451-61 [14706337.001]
  • [Cites] Blood. 2004 Sep 15;104(6):1696-702 [15187027.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1825-35 [17646408.001]
  • (PMID = 18981238.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE12948
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI045846; United States / NCI NIH HHS / CA / P01 CA109901; United States / NCI NIH HHS / CA / T32 CA070083; United States / NCI NIH HHS / CA / T32-CA70083; United States / NIAID NIH HHS / AI / R01 AI45846; United States / NCI NIH HHS / CA / CA109901
  • [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 / Notch1 protein, mouse; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC2585834
  •  go-up   go-down


47. Kox C, Zimmermann M, Stanulla M, Leible S, Schrappe M, Ludwig WD, Koehler R, Tolle G, Bandapalli OR, Breit S, Muckenthaler MU, Kulozik AE: The favorable effect of activating NOTCH1 receptor mutations on long-term outcome in T-ALL patients treated on the ALL-BFM 2000 protocol can be separated from FBXW7 loss of function. Leukemia; 2010 Dec;24(12):2005-13
Hazardous Substances Data Bank. PREDNISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Precursor T-cell acute lymphoblastic leukemia (T-ALL) remains an important challenge in pediatric oncology.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Prednisone / therapeutic use. Receptor, Notch1 / genetics. Ubiquitin-Protein Ligases / genetics

  • MedlinePlus Health Information. consumer health - Steroids.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2004 Apr 1;103(7):2771-8 [14684422.001]
  • [Cites] Science. 2004 Feb 27;303(5662):1374-8 [14739463.001]
  • [Cites] Br J Haematol. 2004 Jul;126(2):231-43 [15238145.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Klin Padiatr. 1987 May-Jun;199(3):151-60 [3306129.001]
  • [Cites] Blood. 1989 Oct;74(5):1762-7 [2676018.001]
  • [Cites] Blood. 1991 Jan 15;77(2):331-9 [1824678.001]
  • [Cites] Leukemia. 1995 Oct;9(10):1783-6 [7564526.001]
  • [Cites] Blood. 1998 Sep 15;92(6):1898-909 [9731046.001]
  • [Cites] Lancet. 1998 Nov 28;352(9142):1731-8 [9848348.001]
  • [Cites] Blood. 2010 Apr 22;115(16):3206-14 [20154213.001]
  • [Cites] Leukemia. 2010 Dec;24(12):2014-22 [20861909.001]
  • [Cites] EMBO J. 2004 May 19;23(10):2116-25 [15103331.001]
  • [Cites] Ann Hematol. 1999 Apr;78(4):157-62 [10348146.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2004;:118-45 [15561680.001]
  • [Cites] Nature. 2004 Dec 9;432(7018):775-9 [15592418.001]
  • [Cites] Cell Metab. 2005 Jun;1(6):379-91 [16054087.001]
  • [Cites] Clin Cancer Res. 2006 May 15;12(10):3043-9 [16707600.001]
  • [Cites] Genes Dev. 2006 Aug 1;20(15):2096-109 [16847353.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1151-7 [16614245.001]
  • [Cites] Mol Cell. 2007 Apr 13;26(1):131-43 [17434132.001]
  • [Cites] Cancer Res. 2007 Jun 15;67(12):5611-6 [17575125.001]
  • [Cites] Nature. 2007 Jun 21;447(7147):966-71 [17515920.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1825-35 [17646408.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1813-24 [17646409.001]
  • [Cites] Leukemia. 2008 Jan;22(1):124-31 [17928886.001]
  • [Cites] Leukemia. 2008 Apr;22(4):771-82 [18239620.001]
  • [Cites] Blood. 2008 May 1;111(9):4477-89 [18285545.001]
  • [Cites] Science. 2008 Sep 12;321(5895):1499-502 [18787170.001]
  • [Cites] Blood. 2009 Apr 23;113(17):3918-24 [19109228.001]
  • [Cites] Br J Haematol. 2009 Apr;145(2):198-206 [19245433.001]
  • [Cites] Nature. 2009 Jun 18;459(7249):1000-4 [19536265.001]
  • [Cites] N Engl J Med. 2009 Jun 25;360(26):2730-41 [19553647.001]
  • [Cites] Blood. 2009 Jul 16;114(3):647-50 [19458356.001]
  • [Cites] Blood. 2009 Jul 30;114(5):1053-62 [19406988.001]
  • [Cites] Leukemia. 2009 Aug;23(8):1417-25 [19340001.001]
  • [Cites] J Clin Oncol. 2009 Sep 10;27(26):4352-6 [19635999.001]
  • [Cites] Haematologica. 2009 Oct;94(10):1383-90 [19794083.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3310-22 [10828010.001]
  • [Cites] J Biol Chem. 2001 Sep 21;276(38):35847-53 [11461910.001]
  • [Cites] Mol Cell Biol. 2001 Nov;21(21):7403-15 [11585921.001]
  • [Cites] Science. 2001 Oct 5;294(5540):173-7 [11533444.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4386-93 [12036866.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] J Neurochem. 2002 Sep;82(6):1540-8 [12354302.001]
  • [Cites] Leukemia. 2003 Jun;17(6):1013-34 [12764363.001]
  • [Cites] J Clin Oncol. 2004 Feb 1;22(3):569-70; author reply 570-1 [14752084.001]
  • [CommentIn] Leukemia. 2010 Dec;24(12):2003-4 [21157484.001]
  • (PMID = 20944675.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Receptor, Notch1; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases; VB0R961HZT / Prednisone
  • [Other-IDs] NLM/ PMC3035973
  •  go-up   go-down


48. Dik WA, Brahim W, Braun C, Asnafi V, Dastugue N, Bernard OA, van Dongen JJ, Langerak AW, Macintyre EA, Delabesse E: CALM-AF10+ T-ALL expression profiles are characterized by overexpression of HOXA and BMI1 oncogenes. Leukemia; 2005 Nov;19(11):1948-57
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The t(10;11)(p13;q14-21) is found in T-ALL and acute myeloid leukemia and fuses CALM (Clathrin-Assembly protein-like Lymphoid-Myeloid leukaemia gene) to AF10.
  • Microarray results were validated by quantitative RT-PCR on an independent group of T-ALL and compared to mixed lineage leukemia-translocated acute leukemias (MLL-t AL).
  • We propose to define a HOXA+ leukemia group composed of at least MLL-t, CALM-AF10 and HOXA-t AL, which may benefit from adapted management.
  • [MeSH-major] Homeodomain Proteins / biosynthesis. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Nuclear Proteins / biosynthesis. Oncogene Proteins, Fusion / biosynthesis. Proto-Oncogene Proteins / biosynthesis. Repressor Proteins / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Cell Proliferation. Cell Transformation, Neoplastic. Child. Gene Expression Profiling. Humans. Oligonucleotide Array Sequence Analysis. Polycomb Repressive Complex 1. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic. Up-Regulation

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16107895.001).
  • [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 / AF10-CALM fusion protein, human; 0 / BMI1 protein, human; 0 / Homeodomain Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 157907-48-7 / HoxA protein; EC 6.3.2.19 / Polycomb Repressive Complex 1
  •  go-up   go-down


49. Chen LJ, Li JY, Wu YJ, Yang H, Qian SX, Wu HX, Lu H, Xu W, Sheng RL: [Immunophenotyping characteristics of T-cell acute lymphoblastic leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Aug;15(4):692-5
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Immunophenotyping characteristics of T-cell acute lymphoblastic leukemia].
  • The objective of this study was to investigate the immunophenotypic characteristics of T-cell acute lymphoblastic leukemia (T-ALL).
  • It is concluded that immunophenotyping is an important tool for diagnosis of T-ALL.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17708784.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD3; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3
  •  go-up   go-down


50. Tremblay CS, Hoang T, Hoang T: Early T cell differentiation lessons from T-cell acute lymphoblastic leukemia. Prog Mol Biol Transl Sci; 2010;92:121-56
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] Early T cell differentiation lessons from T-cell acute lymphoblastic leukemia.
  • T cells develop from bone marrow-derived self-renewing hematopoietic stem cells (HSC).
  • Upon entering the thymus, these cells undergo progressive commitment and differentiation driven by the thymic stroma and the pre-T cell receptor (pre-TCR).
  • These processes are disrupted in T-cell acute lymphoblastic leukemia (T-ALL).
  • For example, bHLH oncoproteins inhibit E2A and HEB, revealing their tumor suppressor function in the thymus.
  • The induction of T-ALL, nonetheless, requires collaboration with constitutive NOTCH1 signaling and the pre-TCR, as well as loss-of-function mutations for CDKN2A and PTEN.
  • Significantly, NOTCH1, the pre-TCR pathway, and E2A/HEB proteins control critical checkpoints and branchpoints in early thymocyte development whereas several oncogenic transcription factors, HOXA9, c-MYB, SCL, and LYL-1 control HSC self-renewal.
  • Together, these genetic lesions alter key regulatory processes in the cell, favoring self-renewal and subvert the normal control of thymocyte homeostasis.
  • [MeSH-major] Cell Differentiation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Signal Transduction. T-Lymphocytes / cytology. Thymus Gland / cytology

  • 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 © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20800819.001).
  • [ISSN] 1877-1173
  • [Journal-full-title] Progress in molecular biology and translational science
  • [ISO-abbreviation] Prog Mol Biol Transl Sci
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Oncogene Proteins; 0 / Transcription Factors
  •  go-up   go-down


51. Uyttebroeck A, Vanhentenrijk V, Hagemeijer A, Boeckx N, Renard M, Wlodarska I, Vandenberghe P, Depaepe P, De Wolf-Peeters C: Is there a difference in childhood T-cell acute lymphoblastic leukaemia and T-cell lymphoblastic lymphoma? Leuk Lymphoma; 2007 Sep;48(9):1745-54
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Is there a difference in childhood T-cell acute lymphoblastic leukaemia and T-cell lymphoblastic lymphoma?
  • To distinguish the similarities or differences between T-cell acute lymphoblastic leukaemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LBL), we retrospectively analyzed the clinical, immunophenotypic, cytogenetic, and molecular characteristics in 37 children diagnosed between December 1990 and December 2003.
  • The clinical presentation and cytogenetic characteristics are largely similar for T-ALL and T-LBL supporting the concept that both represent a spectrum of one single disease.
  • The differences that were found between both neoplasms, in particular in their phenotype and in their expression profile may suggest that most T-ALL derive from a T-cell progenitor of the bone marrow, while thymocytes represent the normal counterpart of T-LBL.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Lymphoblastic lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17786710.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  •  go-up   go-down


52. Gutierrez A, Sanda T, Ma W, Zhang J, Grebliunaite R, Dahlberg S, Neuberg D, Protopopov A, Winter SS, Larson RS, Borowitz MJ, Silverman LB, Chin L, Hunger SP, Jamieson C, Sallan SE, Look AT: Inactivation of LEF1 in T-cell acute lymphoblastic leukemia. Blood; 2010 Apr 08;115(14):2845-51
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] Inactivation of LEF1 in T-cell acute lymphoblastic leukemia.
  • To further unravel the molecular pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL), we performed high-resolution array comparative genomic hybridization on diagnostic specimens from 47 children with T-ALL and identified monoallelic or biallelic LEF1 microdeletions in 11% (5 of 47) of these primary samples.
  • Gene expression microarrays showed increased expression of MYC and MYC targets in cases with LEF1 inactivation, as well as differentiation arrest at an early cortical stage of thymocyte development characterized by expression of CD1B, CD1E, and CD8, with absent CD34 expression.
  • LEF1 inactivation was associated with a younger age at the time of T-ALL diagnosis, as well as activating NOTCH1 mutations, biallelic INK4a/ARF deletions, and PTEN loss-of-function mutations or activating mutations of PI3K or AKT genes.
  • [MeSH-major] Codon, Terminator. Lymphoid Enhancer-Binding Factor 1 / genetics. Neoplasm Proteins / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Sequence Deletion

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 2000 Feb 17;403(6771):781-5 [10693808.001]
  • [Cites] Blood. 2009 Jul 16;114(3):647-50 [19458356.001]
  • [Cites] Nucleic Acids Res. 2001 Apr 1;29(7):1410-9 [11266540.001]
  • [Cites] Nat Genet. 2001 May;28(1):53-7 [11326276.001]
  • [Cites] Stem Cells. 2001;19(3):165-79 [11359942.001]
  • [Cites] Mol Cell Biol. 2001 Nov;21(22):7537-44 [11604490.001]
  • [Cites] Development. 2002 Jan;129(1):95-109 [11782404.001]
  • [Cites] Dev Biol. 2002 Apr 1;244(1):1-8 [11900454.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] Blood. 2003 Jul 1;102(1):262-8 [12637319.001]
  • [Cites] Nat Genet. 2003 Jul;34(3):267-73 [12808457.001]
  • [Cites] J Clin Oncol. 2003 Oct 1;21(19):3616-22 [14512392.001]
  • [Cites] Crit Rev Oncol Hematol. 2004 Jun;50(3):223-61 [15182827.001]
  • [Cites] N Engl J Med. 2004 Aug 5;351(6):552-9 [15295048.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Genes Dev. 1994 Nov 15;8(22):2691-703 [7958926.001]
  • [Cites] Leukemia. 1995 Oct;9(10):1783-6 [7564526.001]
  • [Cites] Immunity. 1998 Jan;8(1):11-20 [9462507.001]
  • [Cites] Science. 1998 Sep 4;281(5382):1509-12 [9727977.001]
  • [Cites] J Exp Med. 2005 Jun 6;201(11):1715-23 [15928199.001]
  • [Cites] Blood. 2005 Jul 1;106(1):274-86 [15774621.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] Cell. 2006 Mar 24;124(6):1283-98 [16564017.001]
  • [Cites] Nat Med. 2006 Apr;12(4):395-7 [16565724.001]
  • [Cites] Nat Genet. 2006 May;38(5):500-1 [16642009.001]
  • [Cites] Leukemia. 2006 Jun;20(6):1184-7 [16572206.001]
  • [Cites] J Cell Sci. 2007 May 1;120(Pt 9):1646-53 [17452626.001]
  • [Cites] Blood. 2007 Jun 15;109(12):5463-72 [17317856.001]
  • [Cites] Nature. 2007 Jun 21;447(7147):966-71 [17515920.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1825-35 [17646408.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1813-24 [17646409.001]
  • [Cites] Blood. 2007 Sep 1;110(5):1429-38 [17495134.001]
  • [Cites] Leukemia. 2007 Nov;21(11):2344-53 [17690692.001]
  • [Cites] J Exp Med. 2007 Dec 24;204(13):3059-66 [18070937.001]
  • [Cites] J Exp Med. 2008 Mar 17;205(3):515-22 [18316418.001]
  • [Cites] Cell. 2008 May 30;133(5):864-77 [18510930.001]
  • [Cites] Sci Signal. 2008;1(45):ra12 [19001663.001]
  • [Cites] Mol Cell Biol. 2008 Dec;28(24):7368-79 [18852287.001]
  • [Cites] Lancet Oncol. 2009 Feb;10(2):147-56 [19147408.001]
  • [Cites] Nucleic Acids Res. 2000 May 1;28(9):1994-2003 [10756202.001]
  • (PMID = 20124220.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1K08CA133103; United States / NCI NIH HHS / CA / CA98543; United States / NCI NIH HHS / CA / K08 CA133103-04; United States / NCI NIH HHS / CA / K08 CA133103-01; United States / NCI NIH HHS / CA / CA114766; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U24 CA114766; United States / NCI NIH HHS / CA / K08 CA133103; United States / NCI NIH HHS / CA / K08 CA133103-03; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA98413; United States / NCI NIH HHS / CA / K08 CA133103-02; 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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Codon, Terminator; 0 / LEF1 protein, human; 0 / Lymphoid Enhancer-Binding Factor 1; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ PMC2854430
  •  go-up   go-down


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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FBXW7 and NOTCH1 mutations in childhood T cell acute lymphoblastic leukaemia and T cell non-Hodgkin lymphoma.
  • Mutation analysis of FBXW7 and NOTCH1 genes was performed in 55 T cell acute lymphoblastic leukaemia (T-ALL) and 14 T cell non-Hodgkin lymphoma (T-NHL) patients who were treated on the Japan Association of Childhood Leukaemia Study (JACLS) protocols ALL-97 and NHL-98.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Gene Expression Regulation, Leukemic. Lymphoma, T-Cell / genetics. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics. Ubiquitin-Protein Ligases / genetics
  • [MeSH-minor] Chi-Square Distribution. Child. Chromatography, High Pressure Liquid. DNA Mutational Analysis. Disease-Free Survival. Female. Humans. Kaplan-Meier Estimate. Male. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate


54. Sulis ML, Williams O, Palomero T, Tosello V, Pallikuppam S, Real PJ, Barnes K, Zuurbier L, Meijerink JP, Ferrando AA: NOTCH1 extracellular juxtamembrane expansion mutations in T-ALL. Blood; 2008 Aug 1;112(3):733-40
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Heterodimerization domain (HD) mutations in NOTCH1 induce ligand-independent activation of the receptor and contribute to the pathogenesis of one-third of human T-cell lymphoblastic leukemias (T-ALLs).
  • Here we report a novel class of activating mutations in NOTCH1 leading to aberrant activation of NOTCH1 signaling in T-cell lymphoblasts.
  • Notably, structure-function analysis of leukemia-derived and synthetic JME mutants demonstrated that the aberrant activation of NOTCH1 signaling is dependent on the number of residues introduced in the extracellular juxtamembrane region of the receptor and not on the specific amino acid sequence of these insertions.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Curr Opin Immunol. 2000 Apr;12(2):166-72 [10712939.001]
  • [Cites] Annu Rev Pathol. 2008;3:587-613 [18039126.001]
  • [Cites] Mol Cell. 2000 Feb;5(2):197-206 [10882062.001]
  • [Cites] Mol Cell. 2000 Feb;5(2):207-16 [10882063.001]
  • [Cites] Immunity. 2001 Mar;14(3):253-64 [11290335.001]
  • [Cites] J Exp Med. 2001 Oct 1;194(7):991-1002 [11581320.001]
  • [Cites] Immunity. 2002 Jun;16(6):869-79 [12121668.001]
  • [Cites] J Immunol. 2002 Aug 15;169(4):1817-21 [12165504.001]
  • [Cites] Cancer Cell. 2003 Mar;3(3):203-5 [12676578.001]
  • [Cites] Semin Immunol. 2003 Apr;15(2):69-79 [12681943.001]
  • [Cites] J Exp Med. 2004 Aug 16;200(4):469-79 [15314075.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Cell. 1991 Aug 23;66(4):649-61 [1831692.001]
  • [Cites] Cell. 1996 Nov 1;87(3):483-92 [8898201.001]
  • [Cites] Cell. 1997 Mar 21;88(6):833-43 [9118226.001]
  • [Cites] Development. 1997 Dec;124(23):4759-67 [9428412.001]
  • [Cites] Genes Dev. 1998 Jun 15;12(12):1751-62 [9637676.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):8108-12 [9653148.001]
  • [Cites] Science. 1999 Jan 1;283(5398):91-4 [9872749.001]
  • [Cites] Nature. 1999 Apr 8;398(6727):522-5 [10206646.001]
  • [Cites] Immunity. 1999 May;10(5):547-58 [10367900.001]
  • [Cites] Immunity. 1999 Sep;11(3):299-308 [10514008.001]
  • [Cites] Nat Immunol. 2005 Mar;6(3):314-22 [15665828.001]
  • [Cites] Cell. 2005 Aug 12;122(3):435-47 [16096062.001]
  • [Cites] Nat Rev Cancer. 2006 May;6(5):347-59 [16612405.001]
  • [Cites] Mol Cell Biol. 2006 Jun;26(12):4642-51 [16738328.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1279-87 [16688224.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1151-7 [16614245.001]
  • [Cites] Nat Struct Mol Biol. 2007 Apr;14(4):295-300 [17401372.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1825-35 [17646408.001]
  • [Cites] Nucleic Acids Res. 2008 Jan;36(Database issue):D25-30 [18073190.001]
  • [CommentIn] Blood. 2008 Aug 1;112(3):457-8 [18650457.001]
  • (PMID = 18411416.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA120196-03; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / CA120196; United States / NCI NIH HHS / CA / R01 CA120196-03
  • [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 / Receptor, Notch1; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ PMC2481531
  •  go-up   go-down


55. Van Vlierberghe P, Palomero T, Khiabanian H, Van der Meulen J, Castillo M, Van Roy N, De Moerloose B, Philippé J, González-García S, Toribio ML, Taghon T, Zuurbier L, Cauwelier B, Harrison CJ, Schwab C, Pisecker M, Strehl S, Langerak AW, Gecz J, Sonneveld E, Pieters R, Paietta E, Rowe JM, Wiernik PH, Benoit Y, Soulier J, Poppe B, Yao X, Cordon-Cardo C, Meijerink J, Rabadan R, Speleman F, Ferrando A: PHF6 mutations in T-cell acute lymphoblastic leukemia. Nat Genet; 2010 Apr;42(4):338-42
SciCrunch. OMIM: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PHF6 mutations in T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy with an increased incidence in males.
  • Mutational loss of PHF6 is importantly associated with leukemias driven by aberrant expression of the homeobox transcription factor oncogenes TLX1 and TLX3.
  • Overall, these results identify PHF6 as a new X-linked tumor suppressor in T-ALL and point to a strong genetic interaction between PHF6 loss and aberrant expression of TLX transcription factors in the pathogenesis of this disease.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 7;96(25):14440-4 [10588724.001]
  • [Cites] Blood. 2009 Dec 10;114(25):5136-45 [19828704.001]
  • [Cites] Nat Genet. 2002 Dec;32(4):661-5 [12415272.001]
  • [Cites] J Clin Oncol. 2003 Oct 1;21(19):3616-22 [14512392.001]
  • [Cites] Clin Genet. 2004 Mar;65(3):226-32 [14756673.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jun 22;96(13):7364-9 [10377420.001]
  • [Cites] Acta Med Scand. 1962 Jan;171:13-21 [13871358.001]
  • [Cites] Curr Biol. 2005 Feb 8;15(3):R99-R102 [15694301.001]
  • [Cites] Nature. 2005 Mar 17;434(7031):400-4 [15772666.001]
  • [Cites] Blood. 2005 Jul 1;106(1):274-86 [15774621.001]
  • [Cites] Cell. 2006 Mar 24;124(6):1283-98 [16564017.001]
  • [Cites] Haematologica. 2006 Sep;91(9):1212-21 [16956820.001]
  • [Cites] Cytogenet Genome Res. 2006;115(3-4):247-53 [17124407.001]
  • [Cites] Nat Genet. 2007 May;39(5):593-5 [17435759.001]
  • [Cites] Science. 2007 May 25;316(5828):1160-6 [17525332.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1251-61 [17452517.001]
  • [Cites] Gene Expr Patterns. 2007 Oct;7(8):858-71 [17698420.001]
  • [Cites] Lancet. 2008 Mar 22;371(9617):1030-43 [18358930.001]
  • [Cites] Nat Rev Immunol. 2008 May;8(5):380-90 [18421304.001]
  • [Cites] Blood. 2008 May 1;111(9):4668-80 [18299449.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Aug 5;105(31):10762-7 [18669648.001]
  • [Cites] Annu Rev Genet. 2008;42:733-72 [18729722.001]
  • [Cites] Mutat Res. 2008 Dec 1;647(1-2):3-12 [18682256.001]
  • [Cites] Nat Biotechnol. 2009 Feb;27(2):182-9 [19182786.001]
  • [Cites] J Exp Med. 2009 Apr 13;206(4):779-91 [19349467.001]
  • [Cites] PLoS Comput Biol. 2009 May;5(5):e1000386 [19461883.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • (PMID = 20228800.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA120196-03; United States / NIAID NIH HHS / AI / U54-AI057158; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / R01 CA129382-03; United States / NCI NIH HHS / CA / CA129382-03; United States / NCI NIH HHS / CA / CA120196-03; United States / NCI NIH HHS / CA / R01CA120196; United States / NIAID NIH HHS / AI / U54 AI057158; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NLM NIH HHS / LM / 1R01LM010140-01; United States / NCI NIH HHS / CA / U24 CA114737; United States / NLM NIH HHS / LM / R01 LM010140; United States / NCI NIH HHS / CA / R01 CA155743
  • [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 / Carrier Proteins; 0 / Homeodomain Proteins; 0 / PHF6 protein, human; 0 / Proto-Oncogene Proteins; 0 / TLX3 protein, human; 143275-75-6 / TLX1 protein, human
  • [Other-IDs] NLM/ NIHMS176587; NLM/ PMC2847364
  •  go-up   go-down


56. Dos Santos NR, Ghezzo MN, da Silva RC, Fernandes MT: NF-κB in T-cell Acute Lymphoblastic Leukemia: Oncogenic Functions in Leukemic and in Microenvironmental Cells. Cancers (Basel); 2010;2(4):1838-60

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NF-κB in T-cell Acute Lymphoblastic Leukemia: Oncogenic Functions in Leukemic and in Microenvironmental Cells.
  • T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy of thymocytes that despite significant therapeutic advances can still be fatal.
  • Although mutations in NF-κB genes have not been reported in T-ALL, NF-κB constitutive activation in human T-ALL and in acute T-cell leukemia mouse models has been observed.
  • Although these studies revealed activation of members of both canonical and noncanonical NF-κB pathways in acute T-cell leukemia, only inhibition of canonical NF-κB signaling was shown to impair leukemic T cell growth.
  • Besides playing an important pro-oncogenic role in leukemic T cells, NF-κB signaling also appears to modulate T-cell leukemogenesis through its action in microenvironmental stromal cells.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 24281204.001).
  • [ISSN] 2072-6694
  • [Journal-full-title] Cancers
  • [ISO-abbreviation] Cancers (Basel)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Other-IDs] NLM/ PMC3840450
  •  go-up   go-down


57. Lahortiga I, De Keersmaecker K, Van Vlierberghe P, Graux C, Cauwelier B, Lambert F, Mentens N, Beverloo HB, Pieters R, Speleman F, Odero MD, Bauters M, Froyen G, Marynen P, Vandenberghe P, Wlodarska I, Meijerink JP, Cools J: Duplication of the MYB oncogene in T cell acute lymphoblastic leukemia. Nat Genet; 2007 May;39(5):593-5
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] Duplication of the MYB oncogene in T cell acute lymphoblastic leukemia.
  • We identified a duplication of the MYB oncogene in 8.4% of individuals with T cell acute lymphoblastic leukemia (T-ALL) and in five T-ALL cell lines.
  • The duplication is associated with a threefold increase in MYB expression, and knockdown of MYB expression initiates T cell differentiation.
  • [MeSH-major] Cell Differentiation / genetics. Gene Duplication. Genes, myb / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. T-Lymphocytes / pathology
  • [MeSH-minor] Cell Line, Tumor. Chromosomes, Artificial / genetics. Flow Cytometry. Gene Dosage. Gene Expression Regulation, Neoplastic / genetics. Genetic Testing. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Mutation / genetics. Nucleic Acid Hybridization / genetics. RNA, Small Interfering / genetics. Statistics, Nonparametric


58. Bremer E, ten Cate B, Samplonius DF, de Leij LF, Helfrich W: CD7-restricted activation of Fas-mediated apoptosis: a novel therapeutic approach for acute T-cell leukemia. Blood; 2006 Apr 1;107(7):2863-70
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] CD7-restricted activation of Fas-mediated apoptosis: a novel therapeutic approach for acute T-cell leukemia.
  • Consequently, new antileukemia strategies based on Fas activation have to meet the criterion of strictly localized action at the tumor-cell surface.
  • We report on a novel fusion protein, designated scFvCD7:sFasL, that is designed to have leukemia-restricted activity.
  • ScFvCD7:sFasL consists of sFasL genetically linked to a high-affinity single-chain fragment of variable regions (scFv) antibody fragment specific for the T-cell leukemia-associated antigen CD7.
  • Soluble homotrimeric scFvCD7:sFasL is inactive and acquires tumoricidal activity only after specific binding to tumor cell-surface-expressed CD7.
  • Treatment of T-cell acute lymphoblastic leukemia (T-ALL) cell lines and patient-derived T-ALL, peripheral T-cell lymphoma (PTCL), and CD7-positive acute myeloid leukemia (AML) cells with homotrimeric scFvCD7:sFasL revealed potent CD7-restricted induction of apoptosis that was augmented by conventional drugs, farnesyl transferase inhibitor L-744832, and the proteasome inhibitor bortezomib (Velcade; Millenium, Cambridge, MA).
  • CD7-restricted activation of Fas in T-cell leukemic cells by scFvCD7:sFasL revitalizes interest in the applicability of Fas signaling in leukemia therapy.
  • [MeSH-major] Antigens, CD7 / immunology. Apoptosis / immunology. Leukemia-Lymphoma, Adult T-Cell / therapy. Membrane Glycoproteins / immunology. Tumor Necrosis Factors / immunology
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Bystander Effect. Cell Line, Tumor. DNA Primers. Fas Ligand Protein. Humans. Jurkat Cells

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16332967.001).
  • [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 / Antigens, CD7; 0 / Antineoplastic Agents; 0 / DNA Primers; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Tumor Necrosis Factors
  •  go-up   go-down


59. Weng AP, Lau A: Notch signaling in T-cell acute lymphoblastic leukemia. Future Oncol; 2005 Aug;1(4):511-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Notch signaling in T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) is a form of pediatric leukemia that is thought to be caused by approximately 12 distinct chromosomal translocations that lead to aberrant expression of as many different cellular genes.
  • Recent studies, however, have identified a large fraction of T-ALL cases carrying mutations in one of these genes, Notch1, suggesting for the first time that many cases may share a common pathogenic etiology, and perhaps may allow the development of targeted therapies that benefit the majority of patients with this disease.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Receptors, Notch / physiology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16556027.001).
  • [ISSN] 1479-6694
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Notch
  • [Number-of-references] 118
  •  go-up   go-down


60. Palomero T, Ferrando A: Therapeutic targeting of NOTCH1 signaling in T-cell acute lymphoblastic leukemia. Clin Lymphoma Myeloma; 2009;9 Suppl 3:S205-10
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] Therapeutic targeting of NOTCH1 signaling in T-cell acute lymphoblastic leukemia.
  • The recent identification of activating mutations in NOTCH1 in the majority of T-cell acute lymphoblastic leukemias (T-ALLs) has brought major interest toward targeting the NOTCH signaling pathway in this disease.
  • However, the clinical development of GSIs has been hampered by their low cytotoxicity against human T-ALL and the development of significant gastrointestinal toxicity derived from the inhibition of NOTCH signaling in the gut.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Exp Med. 1996 May 1;183(5):2283-91 [8642337.001]
  • [Cites] Genes Dev. 1996 Aug 1;10(15):1930-44 [8756350.001]
  • [Cites] Cell. 1997 Mar 21;88(6):833-43 [9118226.001]
  • [Cites] Nature. 1998 May 28;393(6683):382-6 [9620803.001]
  • [Cites] N Engl J Med. 1998 Aug 27;339(9):605-15 [9718381.001]
  • [Cites] Nature. 1999 Apr 8;398(6727):518-22 [10206645.001]
  • [Cites] Nature. 1999 Apr 8;398(6727):522-5 [10206646.001]
  • [Cites] Bone Marrow Transplant. 1999 Mar;23(6):555-60 [10217185.001]
  • [Cites] Blood. 1999 Jun 1;93(11):3931-9 [10339502.001]
  • [Cites] Immunity. 1999 May;10(5):547-58 [10367900.001]
  • [Cites] Immunity. 1999 Sep;11(3):299-308 [10514008.001]
  • [Cites] Blood. 2004 Nov 15;104(10):3028-37 [15256423.001]
  • [Cites] Blood. 2008 Jan 1;111(1):376-8 [17901244.001]
  • [Cites] Blood. 2008 Feb 15;111(4):1827-33 [18048644.001]
  • [Cites] Annu Rev Pathol. 2008;3:587-613 [18039126.001]
  • [Cites] Blood. 2008 Aug 1;112(3):733-40 [18411416.001]
  • [Cites] Oncogene. 2008 Oct 2;27(44):5833-44 [18560356.001]
  • [Cites] Mol Cell. 2004 Nov 19;16(4):509-20 [15546612.001]
  • [Cites] Curr Opin Investig Drugs. 2005 Jan;6(1):35-47 [15675602.001]
  • [Cites] Oncogene. 2005 Feb 3;24(6):992-1000 [15592506.001]
  • [Cites] Nature. 2005 Jun 16;435(7044):959-63 [15959515.001]
  • [Cites] Blood. 2005 Jul 1;106(1):274-86 [15774621.001]
  • [Cites] Cell. 2005 Aug 12;122(3):435-47 [16096062.001]
  • [Cites] EMBO J. 2006 Jan 11;25(1):129-38 [16319921.001]
  • [Cites] Cancer Res. 2006 May 1;66(9):4715-24 [16651424.001]
  • [Cites] Mol Cell Biol. 2006 Jun;26(12):4642-51 [16738328.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1279-87 [16688224.001]
  • [Cites] Genes Dev. 2006 Aug 1;20(15):2096-109 [16847353.001]
  • [Cites] Mol Cell Biol. 2006 Nov;26(21):8022-31 [16954387.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18261-6 [17114293.001]
  • [Cites] Blood. 2007 Feb 1;109(3):944-50 [17032921.001]
  • [Cites] Cancer Res. 2007 Jun 15;67(12):5611-6 [17575125.001]
  • [Cites] Blood. 2007 Jul 1;110(1):278-86 [17363738.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1825-35 [17646408.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1813-24 [17646409.001]
  • [Cites] Nat Med. 2007 Oct;13(10):1203-10 [17873882.001]
  • [Cites] Clin Cancer Res. 2007 Dec 1;13(23):6964-9 [18056171.001]
  • [Cites] Lab Invest. 2008 Jan;88(1):11-7 [18059366.001]
  • [Cites] Mol Cell Biol. 2000 Mar;20(5):1825-35 [10669757.001]
  • [Cites] Curr Opin Immunol. 2000 Apr;12(2):166-72 [10712939.001]
  • [Cites] J Exp Med. 2000 Apr 3;191(7):1085-94 [10748227.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3310-22 [10828010.001]
  • [Cites] Mol Cell. 2000 Feb;5(2):197-206 [10882062.001]
  • [Cites] Mol Cell. 2000 Feb;5(2):207-16 [10882063.001]
  • [Cites] Blood. 2000 Sep 1;96(5):1906-13 [10961893.001]
  • [Cites] Nature. 2000 Sep 7;407(6800):48-54 [10993067.001]
  • [Cites] Semin Hematol. 2000 Oct;37(4):381-95 [11071360.001]
  • [Cites] Dev Biol. 2000 Dec 15;228(2):151-65 [11112321.001]
  • [Cites] Blood. 2001 Mar 1;97(5):1211-8 [11222362.001]
  • [Cites] J Exp Med. 2001 Jul 2;194(1):99-106 [11435476.001]
  • [Cites] Nat Cell Biol. 2001 Aug;3(8):751-4 [11483961.001]
  • [Cites] J Exp Med. 2001 Oct 1;194(7):991-1002 [11581320.001]
  • [Cites] J Exp Med. 2001 Oct 1;194(7):1003-12 [11581321.001]
  • [Cites] Blood. 2002 Feb 1;99(3):863-71 [11806988.001]
  • [Cites] Curr Biol. 2002 Jan 22;12(2):R74-8 [11818085.001]
  • [Cites] Curr Opin Immunol. 2002 Apr;14(2):192-9 [11869892.001]
  • [Cites] J Clin Oncol. 2002 May 15;20(10):2464-71 [12011123.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] Biochemistry. 2003 Jan 14;42(1):137-44 [12515548.001]
  • [Cites] Semin Immunol. 2003 Apr;15(2):69-79 [12681943.001]
  • [Cites] Cancer Cell. 2003 Jun;3(6):551-64 [12842084.001]
  • [Cites] Mol Cell. 2003 Aug;12(2):425-35 [14536082.001]
  • [Cites] Annu Rev Cell Dev Biol. 2003;19:367-95 [14570574.001]
  • [Cites] J Biol Chem. 2003 Nov 14;278(46):46107-16 [12949072.001]
  • [Cites] J Biol Chem. 2004 Mar 26;279(13):12876-82 [14709552.001]
  • [Cites] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128.001]
  • [Cites] J Exp Med. 2004 Aug 16;200(4):469-79 [15314075.001]
  • [Cites] Blood. 2004 Sep 15;104(6):1696-702 [15187027.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] J Clin Oncol. 2004 Oct 15;22(20):4075-86 [15353542.001]
  • [Cites] Mol Cell Biol. 2004 Nov;24(21):9265-73 [15485896.001]
  • [Cites] Toxicol Sci. 2004 Nov;82(1):341-58 [15319485.001]
  • [Cites] Lancet. 1991 Jan 12;337(8733):61-6 [1670723.001]
  • [Cites] J Clin Oncol. 1991 Sep;9(9):1570-4 [1875218.001]
  • [Cites] Cell. 1991 Aug 23;66(4):649-61 [1831692.001]
  • [Cites] Blood. 1992 Aug 15;80(4):1090-3 [1498326.001]
  • [Cites] Blood. 1991 Nov 15;78(10):2780-4 [1824271.001]
  • [Cites] N Engl J Med. 1994 Nov 10;331(19):1253-8 [7935682.001]
  • [Cites] Baillieres Clin Haematol. 1994 Jun;7(2):365-76 [7803907.001]
  • [Cites] Lancet. 1995 Jan 21;345(8943):143-8 [7823668.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 1994;59:125-36 [7587062.001]
  • (PMID = 19778842.001).
  • [ISSN] 1938-0712
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA120196-03; United States / NCI NIH HHS / CA / CA129382-02; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / CA120196-03; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / R01 CA129382-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Ligands; 0 / NOTCH1 protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptor, Notch1; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Number-of-references] 85
  • [Other-IDs] NLM/ NIHMS153170; NLM/ PMC2814179
  •  go-up   go-down


61. Real PJ, Ferrando AA: NOTCH inhibition and glucocorticoid therapy in T-cell acute lymphoblastic leukemia. Leukemia; 2009 Aug;23(8):1374-7
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] NOTCH inhibition and glucocorticoid therapy in T-cell acute lymphoblastic leukemia.
  • Inhibition of NOTCH1 signaling with gamma-secretase inhibitors (GSIs) has been proposed as a molecularly targeted therapy in T-cell acute lymphoblastic leukemia (T-ALL).

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • MedlinePlus Health Information. consumer health - Steroids.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 1997 Apr 15;89(8):2959-65 [9108416.001]
  • [Cites] Nature. 2006 Dec 21;444(7122):1083-7 [17183323.001]
  • [Cites] Blood. 1998 Oct 15;92(8):2730-41 [9763557.001]
  • [Cites] Immunity. 1998 Dec;9(6):777-86 [9881968.001]
  • [Cites] Cancer Res. 1999 Mar 15;59(6):1378-85 [10096574.001]
  • [Cites] Blood. 1999 Aug 15;94(4):1209-17 [10438708.001]
  • [Cites] Cancer Res. 2005 Mar 15;65(6):2353-63 [15781650.001]
  • [Cites] Eur J Cancer. 2005 Jun;41(9):1300-3 [15869873.001]
  • [Cites] Nature. 2005 Jun 16;435(7044):959-63 [15959515.001]
  • [Cites] Leukemia. 2005 Oct;19(10):1841-3 [16079893.001]
  • [Cites] Carcinogenesis. 2006 Jan;27(1):23-31 [16219632.001]
  • [Cites] Cancer Res. 2006 Feb 1;66(3):1517-25 [16452208.001]
  • [Cites] Mol Cancer Ther. 2006 Mar;5(3):483-93 [16546962.001]
  • [Cites] Blood. 2006 Aug 1;108(3):1045-9 [16574952.001]
  • [Cites] Blood. 2007 Feb 1;109(3):944-50 [17032921.001]
  • [Cites] Cancer Sci. 2007 Feb;98(2):155-62 [17297654.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1112-5 [17473063.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1825-35 [17646408.001]
  • [Cites] Cancer Res. 2007 Sep 1;67(17):8051-7 [17804716.001]
  • [Cites] Nat Med. 2007 Oct;13(10):1203-10 [17873882.001]
  • [Cites] Cancer Res. 2007 Dec 1;67(23):11244-53 [18056450.001]
  • [Cites] Annu Rev Pathol. 2008;3:587-613 [18039126.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3310-22 [10828010.001]
  • [Cites] Mol Cell. 2000 Feb;5(2):197-206 [10882062.001]
  • [Cites] Mol Cell. 2000 Feb;5(2):207-16 [10882063.001]
  • [Cites] Semin Hematol. 2000 Oct;37(4):381-95 [11071360.001]
  • [Cites] Blood. 2001 Mar 1;97(5):1211-8 [11222362.001]
  • [Cites] Development. 2002 Jun;129(11):2619-28 [12015290.001]
  • [Cites] Leukemia. 2003 Jan;17(1):17-25 [12529655.001]
  • [Cites] Biochemistry. 2003 Sep 23;42(37):10978-90 [12974633.001]
  • [Cites] J Biol Chem. 2003 Nov 14;278(46):46107-16 [12949072.001]
  • [Cites] J Biol Chem. 2004 Mar 26;279(13):12876-82 [14709552.001]
  • [Cites] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128.001]
  • [Cites] Semin Cancer Biol. 2004 Oct;14(5):365-73 [15288262.001]
  • [Cites] Biochemistry. 2004 Aug 31;43(34):10851-8 [15323545.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Toxicol Sci. 2004 Nov;82(1):341-58 [15319485.001]
  • [Cites] Cancer Res. 1981 Nov;41(11 Pt 2):4861-2 [6975165.001]
  • [Cites] Leuk Res. 1985;9(8):993-9 [4046634.001]
  • [Cites] J Biol Chem. 1988 Aug 25;263(24):12044-8 [3261297.001]
  • [Cites] Lancet. 1991 Jan 12;337(8733):61-6 [1670723.001]
  • [Cites] Leuk Lymphoma. 1994 Apr;13(3-4):187-201 [8049644.001]
  • [Cites] Lancet. 1995 Jan 21;345(8943):143-8 [7823668.001]
  • [Cites] Blood. 1995 Nov 15;86(10):3861-8 [7579354.001]
  • [Cites] Blood. 2008 Aug 1;112(3):733-40 [18411416.001]
  • [Cites] Oncogene. 2008 Sep 1;27(38):5132-7 [18758482.001]
  • [Cites] Br J Cancer. 2008 Oct 21;99(8):1204-9 [18827808.001]
  • [Cites] Curr Oncol Rep. 2008 Nov;10(6):453-8 [18928659.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Jan 6;106(1):244-9 [19118200.001]
  • [Cites] Nat Med. 2009 Jan;15(1):50-8 [19098907.001]
  • [Cites] Blood. 2009 Feb 5;113(6):1375-82 [18988865.001]
  • [Cites] Dev Cell. 2009 Feb;16(2):196-208 [19217422.001]
  • [Cites] Blood. 2009 Apr 23;113(17):3918-24 [19109228.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1151-7 [16614245.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18261-6 [17114293.001]
  • [Cites] Nature. 2006 Dec 21;444(7122):1032-7 [17183313.001]
  • [Cites] N Engl J Med. 1998 Aug 27;339(9):605-15 [9718381.001]
  • (PMID = 19357700.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA120196-03; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / CA120196-03; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Enzyme Inhibitors; 0 / GKLF protein; 0 / Glucocorticoids; 0 / Hes1 protein, mouse; 0 / Homeodomain Proteins; 0 / Kruppel-Like Transcription Factors; 0 / NOTCH1 protein, human; 0 / Neoplasm Proteins; 0 / Notch1 protein, mouse; 0 / Receptor, Notch1; 149348-15-2 / HES1 protein, human; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Number-of-references] 58
  • [Other-IDs] NLM/ NIHMS153167; NLM/ PMC2814171
  •  go-up   go-down


62. Staal FJ, van Dongen JJ, Langerak AW: Novel insights into the development of T-cell acute lymphoblastic leukemia. Curr Hematol Malig Rep; 2007 Jul;2(3):176-82
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 insights into the development of T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) results from malignant transformation of immature cells of the T-cell lineage.
  • T-ALL is a heterogeneous disease both clinically and genetically.
  • It is generally accepted that T-ALL cells are the malignant counterpart of normally developing T cells in the thymus (thymocytes).
  • Recent data using genome-wide gene expression profiling and assessment of the rearrangement status of the T-cell receptor loci confirm this notion.
  • [MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / etiology
  • [MeSH-minor] Adult. Animals. Antigens, Differentiation, T-Lymphocyte / analysis. Antigens, Neoplasm / analysis. Antineoplastic Agents / pharmacology. Cell Transformation, Neoplastic. Child. Drug Delivery Systems. Gene Expression Profiling. Gene Expression Regulation, Developmental. Gene Expression Regulation, Leukemic. Humans. Lymphopoiesis / physiology. Mice. Oncogene Proteins, Fusion / antagonists & inhibitors. Oncogene Proteins, Fusion / biosynthesis. Oncogene Proteins, Fusion / genetics. Oncogenes. Receptors, Antigen, T-Cell / genetics. Receptors, Notch / physiology. T-Lymphocytes / immunology. T-Lymphocytes / pathology. Thymus Gland / pathology. Translocation, Genetic. Wnt Proteins / physiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Trends Immunol. 2006 Mar;27(3):125-31 [16473042.001]
  • [Cites] J Exp Med. 2001 Jul 2;194(1):99-106 [11435476.001]
  • [Cites] Bioessays. 1997 Jul;19(7):607-13 [9230693.001]
  • [Cites] Nat Rev Immunol. 2005 Jan;5(1):21-30 [15630426.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 24;101(34):12682-7 [15314234.001]
  • [Cites] Cell. 1991 Aug 23;66(4):649-61 [1831692.001]
  • [Cites] Biochim Biophys Acta. 2003 Jun 5;1653(1):1-24 [12781368.001]
  • [Cites] Nat Rev Cancer. 2006 May;6(5):347-59 [16612405.001]
  • [Cites] Chem Biol. 2007 Feb;14(2):209-19 [17317574.001]
  • [Cites] J Biol Chem. 2004 Mar 26;279(13):12876-82 [14709552.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] Curr Opin Immunol. 2003 Apr;15(2):204-8 [12633671.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3462-9 [17148581.001]
  • [Cites] Science. 1986 Nov 21;234(4779):982-5 [3490692.001]
  • [Cites] Nat Genet. 2004 Oct;36(10):1084-9 [15361874.001]
  • [Cites] Leukemia. 2007 Apr;21(4):754-63 [17268520.001]
  • [Cites] Leukemia. 2006 Nov;20(11):1967-77 [16990763.001]
  • [Cites] Nat Immunol. 2004 Mar;5(3):247-53 [14985712.001]
  • [Cites] Leukemia. 2005 Feb;19(2):201-8 [15668700.001]
  • [Cites] Blood. 2003 Jul 1;102(1):262-8 [12637319.001]
  • [Cites] Blood. 2003 Apr 1;101(7):2693-703 [12446444.001]
  • [Cites] Nature. 2006 Sep 21;443(7109):E5; discussion E6-7 [16988660.001]
  • [Cites] Nat Med. 2007 Jan;13(1):70-7 [17173050.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3322-6 [16492759.001]
  • [Cites] Nature. 2005 Jun 16;435(7044):959-63 [15959515.001]
  • [Cites] Mol Cell Biol. 1997 Nov;17(11):6265-73 [9343387.001]
  • [Cites] J Allergy Clin Immunol. 2005 Apr;115(4):834-40 [15806007.001]
  • [Cites] Leukemia. 2006 Nov;20(11):1963-6 [17008890.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3788-93 [11891328.001]
  • [Cites] Immunity. 1999 May;10(5):547-58 [10367900.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1245-53 [16673019.001]
  • [Cites] Blood. 2006 Apr 15;107(8):3313-20 [16368887.001]
  • [Cites] J Exp Med. 2005 Jun 6;201(11):1715-23 [15928199.001]
  • [Cites] Leukemia. 2005 Nov;19(11):1948-57 [16107895.001]
  • [Cites] Blood. 2007 Jul 1;110(1):388-92 [17360939.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1197-205 [16688226.001]
  • [Cites] EMBO J. 1998 Aug 17;17(16):4594-605 [9707419.001]
  • [Cites] Blood. 2007 Jun 15;109(12):5463-72 [17317856.001]
  • [Cites] Nature. 2005 Apr 14;434(7035):843-50 [15829953.001]
  • [Cites] Eur J Immunol. 2001 Jan;31(1):285-93 [11265645.001]
  • [Cites] Cancer Cell. 2004 Jun;5(6):587-96 [15193261.001]
  • [Cites] Blood. 2005 Jul 1;106(1):274-86 [15774621.001]
  • [Cites] Nat Immunol. 2001 Mar;2(3):235-41 [11224523.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Apr 26;102(17):6068-73 [15827121.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18261-6 [17114293.001]
  • [Cites] Oncogene. 1996 Aug 1;13(3):617-24 [8760303.001]
  • [Cites] Annu Rev Immunol. 2006;24:287-320 [16551251.001]
  • [Cites] Am J Clin Pathol. 2002 Mar;117(3):380-9 [11888077.001]
  • [Cites] Leukemia. 2007 Mar;21(3):462-71 [17252014.001]
  • (PMID = 20425367.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Notch; 0 / Wnt Proteins
  • [Number-of-references] 50
  •  go-up   go-down


63. Soulier J, Clappier E, Cayuela JM, Regnault A, García-Peydró M, Dombret H, Baruchel A, Toribio ML, Sigaux F: HOXA genes are included in genetic and biologic networks defining human acute T-cell leukemia (T-ALL). Blood; 2005 Jul 1;106(1):274-86
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] HOXA genes are included in genetic and biologic networks defining human acute T-cell leukemia (T-ALL).
  • Using a combination of molecular cytogenetic and large-scale expression analysis in human T-cell acute lymphoblastic leukemias (T-ALLs), we identified and characterized a new recurrent chromosomal translocation, targeting the major homeobox gene cluster HOXA and the TCRB locus.
  • Real-time quantitative polymerase chain reaction (RQ-PCR) analysis showed that the expression of the whole HOXA gene cluster was dramatically dysregulated in the HOXA-rearranged cases, and also in MLL and CALM-AF10-related T-ALL cases, strongly suggesting that HOXA genes are oncogenic in these leukemias.
  • Inclusion of HOXA-translocated cases in a general molecular portrait of 92 T-ALLs based on large-scale expression analysis shows that this rearrangement defines a new homogeneous subgroup, which shares common biologic networks with the TLX1- and TLX3-related cases.
  • Because T-ALLs derive from T-cell progenitors, expression profiles of the distinct T-ALL subgroups were analyzed with respect to those of normal human thymic subpopulations.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Differentiation / genetics. Child. Child, Preschool. Female. Gene Expression Profiling. Humans. Infant. Male. Middle Aged. Multigene Family. T-Lymphocytes / cytology. T-Lymphocytes / physiology

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15774621.001).
  • [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 / Homeodomain Proteins; 157907-48-7 / HoxA protein
  •  go-up   go-down


64. Youns M, Fu YJ, Zu YG, Kramer A, Konkimalla VB, Radlwimmer B, Sültmann H, Efferth T: Sensitivity and resistance towards isoliquiritigenin, doxorubicin and methotrexate in T cell acute lymphoblastic leukaemia cell lines by pharmacogenomics. Naunyn Schmiedebergs Arch Pharmacol; 2010 Sep;382(3):221-34
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sensitivity and resistance towards isoliquiritigenin, doxorubicin and methotrexate in T cell acute lymphoblastic leukaemia cell lines by pharmacogenomics.
  • In the present investigation, we compared the cytotoxicity of the chalcone flavonoide, isoliquiritigenin (ISL), with that of doxorubicin (DOX) and methotrexate (MTX) in five T cell acute lymphoblastic leukaemia (T-ALL) cell lines (Jurkat, J-Jhan, J16, HUT78 and Karpas 45).
  • To gain insight into the molecular mechanisms which determine the response of T-ALL cells towards ISL, DOX and MTX, we applied array-based matrix comparative genomic hybridisation and microarray-based mRNA expression profiling and compared the genomic and transcriptomic profiles of the cell lines with their 50% inhibition (IC(50)) values for these three drugs.
  • The IC(50) values for ISL did not correlate with those for DOX or MTX, indicating that ISL was still active in DOX- or MTX-unresponsive cell lines.
  • In conclusion, ISL represents a cytotoxic natural product with activity towards T-ALL cell lines.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm / genetics. Leukemia, T-Cell / drug therapy. Pharmacogenetics / methods
  • [MeSH-minor] Antimetabolites, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / pharmacology. Cell Line, Tumor. Chalcones / administration & dosage. Chalcones / pharmacology. Doxorubicin / administration & dosage. Doxorubicin / pharmacology. Gene Expression Profiling. Humans. Inhibitory Concentration 50. Jurkat Cells. Methotrexate / administration & dosage. Methotrexate / pharmacology. Microarray Analysis. RNA, Messenger / metabolism

  • Hazardous Substances Data Bank. DOXORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Life Sci. 2005 Jun 3;77(3):279-92 [15878356.001]
  • [Cites] Arthritis Rheum. 2006 Mar;54(3):1009-19 [16508983.001]
  • [Cites] Pharmacol Rev. 1998 Jun;50(2):151-96 [9647865.001]
  • [Cites] Reprod Sci. 2008 Jul;15(6):552-8 [18487228.001]
  • [Cites] Clin Exp Pharmacol Physiol. 2004 Jul;31(7):414-8 [15236626.001]
  • [Cites] Genome Biol. 2003;4(10):R70 [14519205.001]
  • [Cites] Cancer. 2009 Jun 15;115(12):2684-92 [19396818.001]
  • [Cites] J Cell Biochem. 2002;85(4):714-20 [11968011.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Mar;87(5):1663-7 [1689846.001]
  • [Cites] Lab Invest. 2002 Jan;82(1):47-60 [11796825.001]
  • [Cites] Oncogene. 2003 Mar 6;22(9):1425-9 [12618769.001]
  • [Cites] J Med Food. 2009 Feb;12(1):8-14 [19298190.001]
  • [Cites] Drugs. 1997;54 Suppl 4:1-7 [9361955.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10787-92 [11553813.001]
  • [Cites] Invest New Drugs. 2010 Feb;28(1):1-13 [19139819.001]
  • [Cites] Free Radic Biol Med. 2009 Mar 15;46(6):731-6 [19110051.001]
  • [Cites] Cancer Res. 1988 Sep 1;48(17):4827-33 [3409223.001]
  • [Cites] Nat Cell Biol. 2000 Feb;2(2):62-9 [10655584.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6567-72 [12011421.001]
  • [Cites] Cancer Lett. 2009 May 18;277(2):174-81 [19167809.001]
  • [Cites] Cancer Metastasis Rev. 2007 Mar;26(1):153-81 [17333344.001]
  • [Cites] Cancer Res. 2004 Jul 1;64(13):4428-33 [15231651.001]
  • [Cites] Prostate. 1999 Dec 1;41(4):275-80 [10544301.001]
  • [Cites] Adv Exp Med Biol. 2007;608:87-100 [17993234.001]
  • [Cites] Cancer Res. 2001 Mar 1;61(5):2301-6 [11280802.001]
  • [Cites] Oncogene. 2000 Nov 20;19(49):5614-9 [11114742.001]
  • [Cites] Breast Cancer Res. 2000;2(5):335-44 [11250726.001]
  • [Cites] Surg Oncol Clin N Am. 2001 Apr;10(2):271-88, viii [11382587.001]
  • [Cites] Clin Cancer Res. 2004 Aug 1;10(15):5145-50 [15297418.001]
  • [Cites] Clin Cancer Res. 2003 Feb;9(2):613-8 [12576426.001]
  • [Cites] Bioinformatics. 2007 Sep 1;23(17):2273-80 [17599933.001]
  • [Cites] Eur Urol. 2003 May;43(5):580-6 [12706007.001]
  • [Cites] Cancer Lett. 2004 Apr 15;207(1):27-35 [15050731.001]
  • [Cites] J Nat Prod. 2007 Mar;70(3):461-77 [17309302.001]
  • [Cites] Curr Cancer Drug Targets. 2008 Mar;8(2):87-97 [18336191.001]
  • [Cites] Hematol Oncol Clin North Am. 1995 Apr;9(2):451-73 [7642473.001]
  • [Cites] J Steroid Biochem Mol Biol. 2002 Nov;82(4-5):315-22 [12589938.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Jun;6(6):462-75 [15928710.001]
  • [Cites] Mol Nutr Food Res. 2009 Jul;53(7):826-35 [19536869.001]
  • [Cites] Am J Pathol. 2003 Apr;162(4):1037-42 [12651595.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]
  • [Cites] J Steroid Biochem Mol Biol. 2001 Sep;78(3):291-8 [11595510.001]
  • [Cites] Bioinformatics. 2002;18 Suppl 1:S96-104 [12169536.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Sep 4;104(36):14442-7 [17726105.001]
  • [Cites] Nat Genet. 2000 May;25(1):25-9 [10802651.001]
  • [Cites] Z Naturforsch C. 2005 Jul-Aug;60(7-8):649-56 [16163844.001]
  • [Cites] Curr Cancer Drug Targets. 2008 Sep;8(6):473-9 [18781894.001]
  • [Cites] Cancer Res. 2003 Jun 15;63(12):3425-9 [12810680.001]
  • [Cites] BMC Genomics. 2004 Apr 30;5(1):29 [15119961.001]
  • [Cites] Clin Cancer Res. 2005 Jan 15;11(2 Pt 1):646-55 [15701852.001]
  • (PMID = 20668838.001).
  • [ISSN] 1432-1912
  • [Journal-full-title] Naunyn-Schmiedeberg's archives of pharmacology
  • [ISO-abbreviation] Naunyn Schmiedebergs Arch. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Chalcones; 0 / RNA, Messenger; 80168379AG / Doxorubicin; B9CTI9GB8F / isoliquiritigenin; YL5FZ2Y5U1 / Methotrexate
  •  go-up   go-down


65. Nagel S, Venturini L, Przybylski GK, Grabarczyk P, Schmidt CA, Meyer C, Drexler HG, Macleod RA, Scherr M: Activation of miR-17-92 by NK-like homeodomain proteins suppresses apoptosis via reduction of E2F1 in T-cell acute lymphoblastic leukemia. Leuk Lymphoma; 2009 Jan;50(1):101-8
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] Activation of miR-17-92 by NK-like homeodomain proteins suppresses apoptosis via reduction of E2F1 in T-cell acute lymphoblastic leukemia.
  • The NK-like family of homeobox genes includes TLX1, TLX3 and NKX2-5, which are ectopically activated in distinct subsets of T-cell acute lymphoblastic leukemia (T-ALL) cells.
  • Quantification of pri-miR-17-92 in T-ALL cell lines suggested an implication of the NK-like homeodomain proteins in transcriptional regulation.
  • Lentiviral-mediated overexpression of NKX2-5 in the T-ALL cell line MOLT-4 consistently resulted in increased miR-17-92 pri-miRNA levels and decreased amounts of E2F1 protein.
  • Induction of apoptosis by treating miR17-92 or E2F1 transduced T-ALL cells with etoposide led to reduced or enhanced cell viability, respectively.
  • [MeSH-major] Apoptosis / genetics. E2F1 Transcription Factor / metabolism. Homeodomain Proteins / metabolism. Killer Cells, Natural / immunology. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / pathology. MicroRNAs / genetics
  • [MeSH-minor] Cell Line. Gene Expression Regulation, Neoplastic / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19148830.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / E2F1 Transcription Factor; 0 / Homeodomain Proteins; 0 / MicroRNAs
  •  go-up   go-down


66. Erbilgin Y, Sayitoglu M, Hatirnaz O, Dogru O, Akcay A, Tuysuz G, Celkan T, Aydogan G, Salcioglu Z, Timur C, Yuksel-Soycan L, Ure U, Anak S, Agaoglu L, Devecioglu O, Yildiz I, Ozbek U: Prognostic significance of NOTCH1 and FBXW7 mutations in pediatric T-ALL. Dis Markers; 2010;28(6):353-60

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The NOTCH signaling pathway plays important role in the development of multicellular organisms, as it regulates cell proliferation, survival, and differentiation.
  • In this study, the mutation analysis of NOTCH1 and FBXW7 genes was performed in 87 pediatric T-ALLs who were treated on the ALL-BFM protocols.
  • NOTCH1 and FBXW7, NOTCH1 alone were found correlated with lower initial leucocyte counts which was independent from the sex and T- cell immunophenotype.
  • However, NOTCH1 and FBXW7 mutations were not predictive of outcome in the overall cohort of pediatric T-ALLs.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Mutation / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics. Ubiquitin-Protein Ligases / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20683149.001).
  • [ISSN] 1875-8630
  • [Journal-full-title] Disease markers
  • [ISO-abbreviation] Dis. Markers
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / NOTCH1 protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptor, Notch1; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Other-IDs] NLM/ PMC3833232
  •  go-up   go-down


67. Hoang T: Of mice and men: how an oncogene transgresses the limits and predisposes to T cell acute lymphoblastic leukemia. Sci Transl Med; 2010 Mar 3;2(21):21ps10
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] Of mice and men: how an oncogene transgresses the limits and predisposes to T cell acute lymphoblastic leukemia.
  • The gene encoding LIM-only 2 (LMO2), an oncogenic transcription factor, is frequently activated in T cell acute lymphoblastic leukemia (T-ALL), but how LMO2 transforms primary hematopoietic cells to induce T-ALL remains an open question.
  • These leukemia-initiating cells are resistant to irradiation, indicating the need to develop new therapeutic drugs that specifically target the oncogene itself.
  • [MeSH-major] DNA-Binding Proteins / genetics. Genetic Predisposition to Disease. Metalloproteins / genetics. Oncogenes / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • 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
  • (PMID = 20374994.001).
  • [ISSN] 1946-6242
  • [Journal-full-title] Science translational medicine
  • [ISO-abbreviation] Sci Transl Med
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [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 / Lmo2 protein, mouse; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins
  •  go-up   go-down


68. Dawidowska M, Derwich K, Szczepański T, Jółkowska J, Witt M, Wachowiak J: [Identification of immunoglobulin and T-cell receptor gene rearrangements--prerequisite for monitoring of minimal residual disease in Polish acute lymphoblastic leukemia patients based on European standards. Preliminary results]. Med Wieku Rozwoj; 2006 Jan-Mar;10(1 Pt 2):323-34
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] [Identification of immunoglobulin and T-cell receptor gene rearrangements--prerequisite for monitoring of minimal residual disease in Polish acute lymphoblastic leukemia patients based on European standards. Preliminary results].
  • [Transliterated title] Identyfikacja rearranzacji genów kodujacych immunoglobuliny i receptory limfocytów T--podstawa monitorowania minimalnej choroby resztkowej u polskich pacjentów z ostra białaczka limfoblastyczna w oparciu o standardy europejskie. Wstepne wyniki badań własnych.
  • OBJECTIVE: Initiation and popularization of routine molecular diagnostics of minimal residual disease (MRD) are currently one of the most urgent challenges in Polish hemato-oncology.
  • The paper is aimed to present preliminary results of identification of immunoglobulin (Ig) and T-cell receptor (TCR) gene rearrangements and quantitative assessment of MRD levels in Polish children with acute lymphoblastic leukemia (ALL).
  • MATERIAL: DNA isolated from bone marrow / bone marrow mononuclear cells obtained at diagnosis from 26 children (25 B-precursor ALL, 1 T-ALL) aged 1.3-16.5 years.
  • CONCLUSIONS: There is an urgent need to broaden the scope of minimal residual disease study in Poland and to develop Polish standards of MRD diagnostics, based on current European experience and standards.
  • [MeSH-major] Gene Rearrangement, T-Lymphocyte / genetics. Genes, Immunoglobulin / genetics. Neoplasm, Residual / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Burkitt Lymphoma / genetics. Burkitt Lymphoma / immunology. Child. Child, Preschool. Europe. Female. Gene Rearrangement, B-Lymphocyte / genetics. Humans. Infant. Male. Poland. Polymerase Chain Reaction / methods. Reproducibility of Results. Sensitivity and Specificity

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17028396.001).
  • [Journal-full-title] Medycyna wieku rozwojowego
  • [ISO-abbreviation] Med Wieku Rozwoj
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  •  go-up   go-down


69. Barata JT, Cardoso AA, Boussiotis VA: Interleukin-7 in T-cell acute lymphoblastic leukemia: an extrinsic factor supporting leukemogenesis? Leuk Lymphoma; 2005 Apr;46(4):483-95
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] Interleukin-7 in T-cell acute lymphoblastic leukemia: an extrinsic factor supporting leukemogenesis?
  • The malignant transformation and expansion of tumor cells involve both cell-autonomous mechanisms and microenvironment signals that regulate viability, nutrient utilization, metabolic activity and cell growth.
  • In T-cell acute lymphoblastic leukemia (T-ALL), the co-culture of leukemic cells with stroma or the addition of particular cytokines prevents ex vivo spontaneous apoptosis.
  • PI3K signaling is required for the induction of Bcl-2, the down-regulation of p27(kip1) and cell cycle progression.
  • PI3K signaling is also required for the expression of the glucose transporter Glut1, uptake of glucose, activation of the metabolic machinery, increase in cell size, and maintenance of mitochondrial integrity.
  • [MeSH-major] Interleukin-7 / metabolism. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / metabolism
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Humans. Mitogen-Activated Protein Kinases / drug effects. Mitogen-Activated Protein Kinases / metabolism. Phosphatidylinositol 3-Kinases / drug effects. Phosphatidylinositol 3-Kinases / metabolism. Protein-Serine-Threonine Kinases / drug effects. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / drug effects. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Signal Transduction / drug effects. Signal Transduction / physiology. Trans-Activators / drug effects. Trans-Activators / metabolism

  • 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 .
  • 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 = 16019476.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI 46548; United States / NCI NIH HHS / CA / P01-CA68484
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-7; 0 / Proto-Oncogene Proteins; 0 / Trans-Activators; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Number-of-references] 125
  •  go-up   go-down


70. Li MO, Flavell RA: TGF-beta: a master of all T cell trades. Cell; 2008 Aug 08;134(3):392-404
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] TGF-beta: a master of all T cell trades.
  • A functional adaptive immune system depends on a diverse and self-tolerant population of T lymphocytes that are generated in the thymus and maintained in the peripheral lymphoid organs.
  • Recent studies have defined the cytokine transforming growth factor-beta (TGF-beta) as a critical regulator of thymic T cell development as well as a crucial player in peripheral T cell homeostasis, tolerance to self antigens, and T cell differentiation during the immune response.
  • The unique mechanism of TGF-beta activation and the plasticity of TGF-beta signaling create a stage for TGF-beta to integrate signals from multiple cell types and environmental cues to regulate T cells.
  • [MeSH-minor] Animals. Cell Differentiation. Humans. Mice. Thymus Gland / cytology. Thymus Gland / immunology

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 2003 Oct 9;425(6958):577-84 [14534577.001]
  • [Cites] J Exp Med. 2003 Dec 15;198(12):1951-7 [14662908.001]
  • [Cites] J Exp Med. 2003 Dec 15;198(12):1875-86 [14676299.001]
  • [Cites] J Immunol. 2004 Apr 1;172(7):4275-84 [15034041.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 30;101(13):4572-7 [15070759.001]
  • [Cites] J Immunol. 2004 May 1;172(9):5149-53 [15100250.001]
  • [Cites] J Immunol. 2004 May 15;172(10):5967-72 [15128778.001]
  • [Cites] FEBS Lett. 2006 May 22;580(12):2811-20 [16678165.001]
  • [Cites] Lab Invest. 2006 Aug;86(8):815-28 [16751781.001]
  • [Cites] Immunity. 2006 Jul;25(1):129-41 [16860762.001]
  • [Cites] Immunity. 2006 Sep;25(3):455-71 [16973386.001]
  • [Cites] Immunity. 2006 Sep;25(3):441-54 [16973387.001]
  • [Cites] Lab Invest. 2006 Oct;86(10):1008-19 [16865088.001]
  • [Cites] Cell. 2006 Sep 22;126(6):1121-33 [16990136.001]
  • [Cites] Nat Immunol. 2006 Nov;7(11):1151-6 [16998492.001]
  • [Cites] J Immunol. 2007 Jan 1;178(1):280-90 [17182565.001]
  • [Cites] J Exp Med. 2006 Dec 25;203(13):2785-91 [17130300.001]
  • [Cites] J Immunol. 2007 Feb 15;178(4):2018-27 [17277105.001]
  • [Cites] Curr Opin Immunol. 2007 Apr;19(2):176-85 [17306520.001]
  • [Cites] J Cell Biol. 2007 Mar 12;176(6):787-93 [17353357.001]
  • [Cites] J Immunol. 2007 Apr 1;178(7):4022-6 [17371955.001]
  • [Cites] J Biol Chem. 2007 Mar 30;282(13):9358-63 [17277312.001]
  • [Cites] Annu Rev Immunol. 2006;24:99-146 [16551245.001]
  • [Cites] Nature. 2006 May 11;441(7090):231-4 [16648837.001]
  • [Cites] Nature. 2006 May 11;441(7090):235-8 [16648838.001]
  • [Cites] Immunity. 2000 Feb;12(2):171-81 [10714683.001]
  • [Cites] J Exp Med. 2000 Apr 3;191(7):1187-96 [10748236.001]
  • [Cites] N Engl J Med. 2000 May 4;342(18):1350-8 [10793168.001]
  • [Cites] Eur J Immunol. 2000 Sep;30(9):2639-49 [11009098.001]
  • [Cites] J Immunol. 2000 Nov 1;165(9):4773-7 [11045997.001]
  • [Cites] Nat Genet. 2001 Jan;27(1):68-73 [11138001.001]
  • [Cites] Science. 2002 Jan 11;295(5553):336-8 [11786643.001]
  • [Cites] Nat Rev Immunol. 2002 Jan;2(1):11-9 [11908514.001]
  • [Cites] J Cell Biol. 2002 Apr 29;157(3):493-507 [11970960.001]
  • [Cites] J Exp Med. 2002 May 6;195(9):1129-43 [11994418.001]
  • [Cites] J Exp Med. 2002 Jun 3;195(11):1499-505 [12045248.001]
  • [Cites] Cytokine. 2002 Apr 7;18(1):43-50 [12090759.001]
  • [Cites] J Immunol. 2002 Oct 15;169(8):4183-9 [12370347.001]
  • [Cites] Nat Rev Immunol. 2002 Dec;2(12):933-44 [12461566.001]
  • [Cites] J Cell Sci. 2003 Jan 15;116(Pt 2):217-24 [12482908.001]
  • [Cites] Nature. 2003 Feb 13;421(6924):744-8 [12610626.001]
  • [Cites] Annu Rev Immunol. 2003;21:139-76 [12414722.001]
  • [Cites] Nat Rev Immunol. 2003 Mar;3(3):253-7 [12658273.001]
  • [Cites] Nat Immunol. 2003 Apr;4(4):330-6 [12612578.001]
  • [Cites] Cell. 2003 Jun 13;113(6):685-700 [12809600.001]
  • [Cites] J Exp Med. 2003 Jun 16;197(12):1689-99 [12810687.001]
  • [Cites] Nature. 2003 Jul 3;424(6944):88-93 [12840763.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Sep 16;100(19):10878-83 [12949259.001]
  • [Cites] Immunity. 2007 May;26(5):579-91 [17481928.001]
  • [Cites] J Immunol. 2007 Jul 1;179(1):71-9 [17579023.001]
  • [Cites] Science. 2007 Jul 13;317(5835):256-60 [17569825.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1757-64 [17620361.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1775-85 [17620362.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1765-74 [17620363.001]
  • [Cites] Nature. 2007 Sep 20;449(7160):361-5 [17694047.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15823-8 [17895374.001]
  • [Cites] J Exp Med. 2007 Oct 29;204(11):2545-52 [17938236.001]
  • [Cites] Nat Immunol. 2007 Dec;8(12):1390-7 [17994024.001]
  • [Cites] Nat Immunol. 2008 Feb;9(2):194-202 [18157133.001]
  • [Cites] Immunity. 2008 Apr;28(4):445-53 [18400187.001]
  • [Cites] Nature. 2008 May 8;453(7192):236-40 [18368049.001]
  • [Cites] Nat Immunol. 2008 Jun;9(6):632-40 [18438410.001]
  • [Cites] Cell. 2008 May 30;133(5):775-87 [18510923.001]
  • [Cites] Immunity. 2004 May;20(5):509-16 [15142520.001]
  • [Cites] Immunity. 2004 Oct;21(4):527-38 [15485630.001]
  • [Cites] Nature. 1992 Oct 22;359(6397):693-9 [1436033.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Jan 15;90(2):770-4 [8421714.001]
  • [Cites] J Clin Invest. 1996 Nov 1;98(9):2109-19 [8903331.001]
  • [Cites] Annu Rev Immunol. 1997;15:535-62 [9143699.001]
  • [Cites] Transgenic Res. 1997 May;6(3):197-202 [9167267.001]
  • [Cites] Cell. 1999 Feb 5;96(3):319-28 [10025398.001]
  • [Cites] Genetics. 1999 Jun;152(2):783-95 [10353918.001]
  • [Cites] J Immunol. 1999 Oct 1;163(7):4013-9 [10491004.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 11;102(2):419-24 [15623559.001]
  • [Cites] J Exp Med. 2005 Jan 17;201(2):233-40 [15657292.001]
  • [Cites] J Exp Med. 2005 Mar 7;201(5):737-46 [15753207.001]
  • [Cites] Science. 2005 Mar 11;307(5715):1603-9 [15761148.001]
  • [Cites] J Exp Med. 2005 Apr 4;201(7):1061-7 [15809351.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Apr 5;102(14):5126-31 [15795373.001]
  • [Cites] Semin Immunol. 2005 Jun;17(3):183-91 [15826823.001]
  • [Cites] Semin Immunol. 2005 Jun;17(3):231-7 [15826828.001]
  • [Cites] Nature. 2005 Jun 2;435(7042):598-604 [15931212.001]
  • [Cites] J Exp Med. 2005 Oct 3;202(7):901-6 [16203863.001]
  • [Cites] Nat Immunol. 2005 Nov;6(11):1133-41 [16200068.001]
  • [Cites] Nat Immunol. 2005 Nov;6(11):1123-32 [16200070.001]
  • [Cites] Cancer Cell. 2005 Nov;8(5):369-80 [16286245.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4234-40 [16131565.001]
  • [Cites] Nat Immunol. 2006 Jan;7(1):83-92 [16311599.001]
  • [Cites] Nat Immunol. 2005 Dec;6(12):1219-27 [16244650.001]
  • [Cites] Immunity. 2006 Feb;24(2):179-89 [16473830.001]
  • (PMID = 18692464.001).
  • [ISSN] 1097-4172
  • [Journal-full-title] Cell
  • [ISO-abbreviation] Cell
  • [Language] eng
  • [Grant] United States / Howard Hughes Medical Institute / / ; United States / NIAMS NIH HHS / AR / R01 AR060723; United States / NIDDK NIH HHS / DK / R01 DK051665; United States / NIDDK NIH HHS / DK / DK51656
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Transforming Growth Factor beta
  • [Number-of-references] 67
  • [Other-IDs] NLM/ NIHMS470791; NLM/ PMC3677783
  •  go-up   go-down


71. Wang D, Claus CL, Vaccarelli G, Braunstein M, Schmitt TM, Zúñiga-Pflücker JC, Rothenberg EV, Anderson MK: The basic helix-loop-helix transcription factor HEBAlt is expressed in pro-T cells and enhances the generation of T cell precursors. J Immunol; 2006 Jul 1;177(1):109-19
SciCrunch. OMIM: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The basic helix-loop-helix transcription factor HEBAlt is expressed in pro-T cells and enhances the generation of T cell precursors.
  • We have cloned a new transcription factor, called HEBAlt, from a pro-T cell cDNA library.
  • Retroviral transduction of HEBAlt or HEBCan into hemopoietic stem cells followed by OP9-DL1 coculture revealed that HEBAlt-transduced precursors generated more early T lineage precursors and more DP pre-T cells than control transduced cells.
  • By contrast, HEBCan-transduced cells that maintained high level expression of the HEBCan transgene were inhibited in expansion and progression through T cell development.
  • HEB(-/-) fetal liver precursors transduced with HEBAlt were rescued from delayed T cell specification, but HEBCan-transduced HEB(-/-) precursors were not.
  • Therefore, HEBAlt and HEBCan are functionally distinct transcription factors, and HEBAlt is specifically required for the efficient generation of early T cell precursors.
  • [MeSH-major] Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / biosynthesis. Basic Helix-Loop-Helix Transcription Factors / biosynthesis. Cell Differentiation / immunology. Stem Cells / cytology. Stem Cells / metabolism. T-Lymphocyte Subsets / cytology. T-Lymphocyte Subsets / metabolism
  • [MeSH-minor] Amino Acid Sequence. Animals. Conserved Sequence. Evolution, Molecular. Mice. Mice, Inbred C57BL. Mice, Knockout. Mice, SCID. Molecular Sequence Data. Peptide Fragments / biosynthesis. Peptide Fragments / chemistry. Peptide Fragments / physiology. Protein Isoforms / biosynthesis. Protein Isoforms / chemistry. Protein Isoforms / physiology. Protein Structure, Tertiary. Thymus Gland / cytology. Thymus Gland / immunology. Thymus Gland / metabolism

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • Institute for Transcriptional Informatics. gene/protein/disease-specific - Institute for Transcriptional Informatics (registration required).
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16785505.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 90233
  • [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 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Peptide Fragments; 0 / Protein Isoforms; 0 / Tcf12 protein, mouse
  •  go-up   go-down


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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NOTCH1 mutations in T-cell acute lymphoblastic leukemia: prognostic significance and implication in multifactorial leukemogenesis.
  • PURPOSE: NOTCH signaling pathway is essential in T-cell development and NOTCH1 mutations are frequently present in T-cell acute lymphoblastic leukemia (T-ALL).
  • These mutations were significantly associated with elevated WBC count at diagnosis and independently linked to short survival time.
  • CONCLUSION: NOTCH1 mutation is an important prognostic marker in T-ALL and its predictive value could be even further increased if coevaluated with other T-cell-related regulatory genes.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Receptor, Notch1 / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Clin Cancer Res. 2009 Feb 15;15(4):1506
  • (PMID = 16707600.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
  •  go-up   go-down


73. Raetz EA, Perkins SL, Bhojwani D, Smock K, Philip M, Carroll WL, Min DJ: Gene expression profiling reveals intrinsic differences between T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma. Pediatr Blood Cancer; 2006 Aug;47(2):130-40
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression profiling reveals intrinsic differences between T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma.
  • BACKGROUND: T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LL) and are often thought to represent a spectrum of a single disease.
  • The malignant cells in T-ALL and T-LL are morphologically indistinguishable, and they share the expression of common cell surface antigens and cytogenetic characteristics.
  • CONCLUSIONS: Despite significant similarities between the malignant T-cell precursors, clear differences in the gene expression profiles were observed between T-ALL and T-LL implying underlying differences in the biology of the two entities.
  • [MeSH-major] Gene Expression Profiling. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Lymphoblastic lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16358311.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01 CA88361
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  •  go-up   go-down


74. Aifantis I, Raetz E, Buonamici S: Molecular pathogenesis of T-cell leukaemia and lymphoma. Nat Rev Immunol; 2008 May;8(5):380-90
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] Molecular pathogenesis of T-cell leukaemia and lymphoma.
  • T-cell acute lymphoblastic leukaemia (T-ALL) is induced by the transformation of T-cell progenitors and mainly occurs in children and adolescents.
  • Although treatment outcome in patients with T-ALL has improved in recent years, patients with relapsed disease continue to have a poor prognosis.
  • It is therefore important to understand the molecular pathways that control both the induction of transformation and the treatment of relapsed disease.
  • In this Review, we focus on the molecular mechanisms responsible for disease induction and maintenance.
  • We also compare the physiological progression of T-cell differentiation with T-cell transformation, highlighting the close relationship between these two processes.

  • MedlinePlus Health Information. consumer health - Lymphoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18421304.001).
  • [ISSN] 1474-1741
  • [Journal-full-title] Nature reviews. Immunology
  • [ISO-abbreviation] Nat. Rev. Immunol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA105129; United States / NCI NIH HHS / CA / R01CA105129; United States / NCI NIH HHS / CA / T32 CA-09161
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Homeodomain Proteins; 0 / NF-kappa B; 0 / Receptor, Notch1; 0 / Transcription Factors; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Number-of-references] 101
  •  go-up   go-down


75. Hoelzer D, Gökbuget N: T-cell lymphoblastic lymphoma and T-cell acute lymphoblastic leukemia: a separate entity? Clin Lymphoma Myeloma; 2009;9 Suppl 3:S214-21
Genetic Alliance. consumer health - Lymphoblastic lymphoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell lymphoblastic lymphoma and T-cell acute lymphoblastic leukemia: a separate entity?
  • T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LBL) are considered the same disease, differing by the extent of bone marrow infiltration.
  • Immunophenotypes of T-LBL and T-ALL are identical but differ in frequency, with a higher rate of cortical or mature immunophenotypes in T-LBL, which is probably related to the higher rate (> 90%) of mediastinal tumors.
  • Treatment approaches in T-LBL changed from conventional non-Hodgkin lymphoma (NHL) protocols to intensive NHL protocols but recently to ALL-designed protocols.
  • Strategies for stem cell transplantation (SCT) in T-LBL and T-ALL differ.
  • MRD may guide further treatment strategies in T-ALL and probably also in T-LBL as indications for a SCT or for the evaluation of novel, particularly T-cell-specific, drugs.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19778844.001).
  • [ISSN] 1938-0712
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 39
  •  go-up   go-down


76. Sanda T, Li X, Gutierrez A, Ahn Y, Neuberg DS, O'Neil J, Strack PR, Winter CG, Winter SS, Larson RS, von Boehmer H, Look AT: Interconnecting molecular pathways in the pathogenesis and drug sensitivity of T-cell acute lymphoblastic leukemia. Blood; 2010 Mar 4;115(9):1735-45
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] Interconnecting molecular pathways in the pathogenesis and drug sensitivity of T-cell acute lymphoblastic leukemia.
  • To identify dysregulated pathways in distinct phases of NOTCH1-mediated T-cell leukemogenesis, as well as small-molecule inhibitors that could synergize with or substitute for gamma-secretase inhibitors (GSIs) in T-cell acute lymphoblastic leukemia (T-ALL) therapy, we compared gene expression profiles in a Notch1-induced mouse model of T-ALL with those in human T-ALL.
  • The overall patterns of NOTCH1-mediated gene expression in human and mouse T-ALLs were remarkably similar, as defined early in transformation in the mouse by the regulation of MYC and its target genes and activation of nuclear factor-kappaB and PI3K/AKT pathways.
  • Later events in murine Notch1-mediated leukemogenesis included down-regulation of genes encoding tumor suppressors and negative cell cycle regulators.
  • When tested in vitro, histone deacetylase, PI3K and proteasome inhibitors synergized with GSI in suppressing T-ALL cell growth in GSI-sensitive cells.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 2009 Jan 6;106(1):244-9 [19118200.001]
  • [Cites] J Exp Med. 2008 Nov 24;205(12):2851-61 [18981238.001]
  • [Cites] Blood. 2009 Jul 16;114(3):647-50 [19458356.001]
  • [Cites] Blood. 2009 Jul 30;114(5):1053-62 [19406988.001]
  • [Cites] Leukemia. 2000 Mar;14(3):399-402 [10720133.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] Nat Genet. 2003 Jul;34(3):267-73 [12808457.001]
  • [Cites] Cancer Cell. 2004 Jun;5(6):587-96 [15193261.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Blood. 1994 Dec 15;84(12):4038-44 [7994022.001]
  • [Cites] Blood. 1995 Feb 1;85(3):854 [7833489.001]
  • [Cites] Blood. 1995 Aug 15;86(4):1269-75 [7632931.001]
  • [Cites] J Exp Med. 1996 May 1;183(5):2283-91 [8642337.001]
  • [Cites] Genes Dev. 1996 Aug 1;10(15):1930-44 [8756350.001]
  • [Cites] Oncogene. 1997 Nov 20;15(21):2609-14 [9399648.001]
  • [Cites] EMBO J. 1999 May 17;18(10):2803-11 [10329626.001]
  • [Cites] Mol Cell. 1999 Aug;4(2):199-207 [10488335.001]
  • [Cites] Curr Opin Hematol. 2004 Nov;11(6):426-33 [15548998.001]
  • [Cites] Nat Immunol. 2005 Aug;6(8):800-9 [16025118.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6306-15 [16155013.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] EMBO J. 2006 Jan 11;25(1):129-38 [16319921.001]
  • [Cites] Nat Rev Cancer. 2006 May;6(5):347-59 [16612405.001]
  • [Cites] Genes Dev. 2006 Aug 1;20(15):2096-109 [16847353.001]
  • [Cites] Science. 2006 Sep 29;313(5795):1929-35 [17008526.001]
  • [Cites] Mol Cell Biol. 2006 Nov;26(21):8022-31 [16954387.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18261-6 [17114293.001]
  • [Cites] Nat Med. 2007 Jan;13(1):70-7 [17173050.001]
  • [Cites] Leukemia. 2007 Mar;21(3):462-71 [17252014.001]
  • [Cites] Chem Biol. 2007 Feb;14(2):209-19 [17317574.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1258-66 [17443227.001]
  • [Cites] Blood. 2007 Jun 15;109(12):5463-72 [17317856.001]
  • [Cites] Cancer Res. 2007 Jun 15;67(12):5611-6 [17575125.001]
  • [Cites] Nature. 2007 Jun 21;447(7147):966-71 [17515920.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1825-35 [17646408.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1813-24 [17646409.001]
  • [Cites] Blood. 2007 Sep 1;110(5):1429-38 [17495134.001]
  • [Cites] Nat Med. 2007 Oct;13(10):1203-10 [17873882.001]
  • [Cites] Oncogene. 2007 Oct 15;26(47):6838-49 [17934490.001]
  • [Cites] Leukemia. 2007 Nov;21(11):2344-53 [17690692.001]
  • [Cites] Blood. 2008 May 15;111(10):5093-100 [18349321.001]
  • [Cites] Cell Cycle. 2008 Apr 15;7(8):965-70 [18414037.001]
  • [Cites] Curr Opin Pharmacol. 2008 Aug;8(4):370-4 [18644253.001]
  • [Cites] Cancer Res. 2009 Apr 1;69(7):3060-8 [19318552.001]
  • (PMID = 20007543.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA109901; United States / NCI NIH HHS / CA / CA98543; United States / NCI NIH HHS / CA / 5P01CA109901-040001; None / None / / K08 CA133103-03; United States / NCI NIH HHS / CA / K08 CA133103-04; United States / NCI NIH HHS / CA / CA114766; United States / NCI NIH HHS / CA / K08 CA133103-03; United States / NCI NIH HHS / CA / U24 CA114766; None / None / / K08 CA133103-01; None / None / / K08 CA133103-04; United States / NCI NIH HHS / CA / K08 CA133103; United States / NCI NIH HHS / CA / K08 CA133103-02; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / K08 CA133103-01; None / None / / K08 CA133103-02
  • [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 / Enzyme Inhibitors; 0 / NOTCH1 protein, human; 0 / Notch1 protein, mouse; 0 / Receptor, Notch1; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ PMC2832805
  •  go-up   go-down


77. Espinosa L, Cathelin S, D'Altri T, Trimarchi T, Statnikov A, Guiu J, Rodilla V, Inglés-Esteve J, Nomdedeu J, Bellosillo B, Besses C, Abdel-Wahab O, Kucine N, Sun SC, Song G, Mullighan CC, Levine RL, Rajewsky K, Aifantis I, Bigas A: The Notch/Hes1 pathway sustains NF-κB activation through CYLD repression in T cell leukemia. Cancer Cell; 2010 Sep 14;18(3):268-81
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 Notch/Hes1 pathway sustains NF-κB activation through CYLD repression in T cell leukemia.
  • It was previously shown that the NF-κB pathway is downstream of oncogenic Notch1 in T cell acute lymphoblastic leukemia (T-ALL).
  • Here, we visualize Notch-induced NF-κB activation using both human T-ALL cell lines and animal models.
  • Finally, we demonstrate that IKK inhibition is a promising option for the targeted therapy of T-ALL as specific suppression of IKK expression and function affected both the survival of human T-ALL cells and the maintenance of the disease in vivo.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / metabolism. Homeodomain Proteins / metabolism. Leukemia, T-Cell / metabolism. NF-kappa B / metabolism. Receptors, Notch / metabolism. Tumor Suppressor Proteins / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Differentiation / physiology. Cell Growth Processes / physiology. Cell Survival / physiology. Genes, Tumor Suppressor. Humans. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Knockout. Signal Transduction. Transcription Factor HES-1. Transcription Factor RelA / metabolism

  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • SciCrunch. ArrayExpress: Data: Microarray .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • [Cites] J Nucl Med. 2006 Jul;47(7):1136-43 [16818948.001]
  • [Cites] Nature. 2006 May 25;441(7092):431-6 [16724054.001]
  • [Cites] Nat Med. 2007 Jan;13(1):70-7 [17173050.001]
  • [Cites] J Exp Med. 2007 Jun 11;204(6):1475-85 [17548520.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1813-24 [17646409.001]
  • [Cites] Cancer Cell. 2007 Aug;12(2):115-30 [17692804.001]
  • [Cites] Cancer Cell. 2007 Aug;12(2):131-44 [17692805.001]
  • [Cites] Science. 2008 Mar 21;319(5870):1676-9 [18323416.001]
  • [Cites] Nat Rev Immunol. 2008 May;8(5):380-90 [18421304.001]
  • [Cites] J Exp Med. 2008 Nov 24;205(12):2851-61 [18981238.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 30;105(52):20840-5 [19088189.001]
  • [Cites] J Exp Med. 2009 Jan 16;206(1):221-32 [19124656.001]
  • [Cites] Annu Rev Immunol. 2009;27:693-733 [19302050.001]
  • [Cites] Mol Cell. 2009 May 14;34(4):461-72 [19481526.001]
  • [Cites] Nature. 2009 Jun 4;459(7247):712-6 [19412163.001]
  • [Cites] Nature. 2009 Jun 4;459(7247):717-21 [19412164.001]
  • [Cites] Nature. 2009 Jun 18;459(7249):1000-4 [19536265.001]
  • [Cites] Blood. 2009 Jul 30;114(5):1046-52 [19436050.001]
  • [Cites] Nature. 2009 Nov 5;462(7269):104-7 [19847165.001]
  • [Cites] Nature. 2009 Nov 5;462(7269):108-12 [19847166.001]
  • [Cites] Science. 2010 Apr 9;328(5975):232-5 [20299548.001]
  • [Cites] Nat Genet. 2000 Jun;25(2):160-5 [10835629.001]
  • [Cites] Mol Cell. 2000 Feb;5(2):197-206 [10882062.001]
  • [Cites] Mol Cell. 2000 Jun;5(6):981-92 [10911992.001]
  • [Cites] Science. 2000 Sep 1;289(5484):1550-4 [10968790.001]
  • [Cites] Nat Immunol. 2001 May;2(5):403-9 [11323693.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] Science. 2002 Nov 8;298(5596):1241-5 [12424381.001]
  • [Cites] Trends Mol Med. 2003 Jan;9(1):30-5 [12524208.001]
  • [Cites] J Cell Physiol. 2003 Mar;194(3):237-55 [12548545.001]
  • [Cites] Bioinformatics. 2003 Feb 12;19(3):368-75 [12584122.001]
  • [Cites] Mol Biol Cell. 2003 Feb;14(2):491-502 [12589049.001]
  • [Cites] Nature. 2003 Aug 14;424(6950):793-6 [12917689.001]
  • [Cites] Nature. 2003 Aug 14;424(6950):797-801 [12917690.001]
  • [Cites] Immunity. 2003 Sep;19(3):377-89 [14499113.001]
  • [Cites] Nature. 2004 Aug 5;430(7000):694-9 [15258597.001]
  • [Cites] Science. 1995 Sep 8;269(5229):1427-9 [7660125.001]
  • [Cites] Nature. 1995 Sep 28;377(6547):355-8 [7566092.001]
  • [Cites] Oncogene. 1996 Jun 6;12(11):2425-35 [8649784.001]
  • [Cites] J Cell Sci. 1997 Feb;110 ( Pt 3):369-78 [9057089.001]
  • [Cites] EMBO J. 1997 Jul 16;16(14):4226-37 [9250666.001]
  • [Cites] Curr Top Microbiol Immunol. 1998;228:273-324 [9401210.001]
  • [Cites] Mol Cell Biol. 1998 Apr;18(4):2324-33 [9528802.001]
  • [Cites] J Biol Chem. 1999 Mar 12;274(11):7238-44 [10066785.001]
  • [Cites] Nature. 1999 Mar 18;398(6724):252-6 [10094049.001]
  • [Cites] J Neurosci Res. 1999 May 1;56(3):229-40 [10336252.001]
  • [Cites] Cell Res. 1999 Sep;9(3):179-88 [10520600.001]
  • [Cites] J Exp Med. 2005 Feb 21;201(4):603-14 [15728238.001]
  • [Cites] EMBO J. 2006 Jan 11;25(1):129-38 [16319921.001]
  • [Cites] Nat Immunol. 2006 Apr;7(4):411-7 [16501569.001]
  • [Cites] Mol Cell Biol. 2006 Aug;26(16):6261-71 [16880534.001]
  • (PMID = 20832754.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA133379; United States / NCIPC CDC HHS / CE / R01CE149655; United States / NCI NIH HHS / CA / R01CA133379; United States / NLM NIH HHS / LM / R56 LM007948; United States / NCI NIH HHS / CA / R21CA141399; United States / NCRR NIH HHS / RR / UL1 RR029893; United States / NCRR NIH HHS / RR / 1UL1RR029893; United States / NCI NIH HHS / CA / R01 CA149655; United States / NCI NIH HHS / CA / R01 CA105129; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / R21 CA141399; United States / NCI NIH HHS / CA / R01CA105129; United States / NLM NIH HHS / LM / R56LM007948
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / CYLD protein, human; 0 / Homeodomain Proteins; 0 / NF-kappa B; 0 / Receptors, Notch; 0 / Transcription Factor HES-1; 0 / Transcription Factor RelA; 0 / Tumor Suppressor Proteins; 149348-15-2 / HES1 protein, human
  • [Other-IDs] NLM/ HHMIMS237725; NLM/ PMC2963042
  •  go-up   go-down


78. Vitale A, Guarini A, Ariola C, Mancini M, Mecucci C, Cuneo A, Pane F, Saglio G, Cimino G, Tafuri A, Meloni G, Fabbiano F, Recchia A, Kropp MG, Krampera M, Cascavilla N, Ferrara F, Romano A, Mazza P, Fozza C, Paoloni F, Vignetti M, Foà R: Adult T-cell acute lymphoblastic leukemia: biologic profile at presentation and correlation with response to induction treatment in patients enrolled in the GIMEMA LAL 0496 protocol. Blood; 2006 Jan 15;107(2):473-9
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] Adult T-cell acute lymphoblastic leukemia: biologic profile at presentation and correlation with response to induction treatment in patients enrolled in the GIMEMA LAL 0496 protocol.
  • Between 1996 and 2000, 90 newly diagnosed adult patients with T-acute lymphoblastic leukemia (T-ALL) were registered in the Gruppo Italiano Malattie Ematologiche dell'Adulto (GIMEMA) Leucemia Acuta Limfoide (LAL) 0496 protocol.
  • Four percent of cases were pro-T, 47% pre-T, 39% cortical T, and 10% mature T-ALL.
  • Fifty-six percent of patients with pro-T + pre-T-ALL achieved complete remission (CR) compared with 91% for cortical + mature cases (P = .002).
  • Thirty-one (36.5%) of 85 patients had an abnormal karyotype, the most common abnormality (15%) being a partial del(6q).
  • [MeSH-major] Chromosome Aberrations. Leukemia-Lymphoma, Adult T-Cell. Oncogene Proteins, Fusion / metabolism. P-Glycoprotein / metabolism
  • [MeSH-minor] Adolescent. Adult. Cytogenetic Analysis. Drug Resistance, Multiple. Female. Humans. Immunophenotyping. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Prognosis. Remission Induction. Treatment Outcome

  • 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 = 16179376.001).
  • [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 / Oncogene Proteins, Fusion; 0 / P-Glycoprotein
  •  go-up   go-down


79. Bourette RP, Grasset MF, Mouchiroud G: E2a/Pbx1 oncogene inhibits terminal differentiation but not myeloid potential of pro-T cells. Oncogene; 2007 Jan 11;26(2):234-47
Hazardous Substances Data Bank. ESTRADIOL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] E2a/Pbx1 oncogene inhibits terminal differentiation but not myeloid potential of pro-T cells.
  • E2a/Pbx1 is a fusion oncoprotein resulting from the t(1;19) translocation found in human pre-B acute lymphocytic leukemia and in a small number of acute T-lymphoid and myeloid leukemias.
  • To address this question, we introduced the receptor of the macrophage-colony-stimulating factor (M-CSF-R) in pro-T cells immortalized by a conditional, estradiol-dependent, E2a/Pbx1-protein, and continuously proliferating in response to stem cell factor and interleukin-7.
  • We asked whether M-CSF-R would be functional in an early T progenitor cell and influence the fate of E2a/Pbx1-immortalized cells.
  • E2a-Pbx1 immortalized pro-T cells could proliferate and shifted from lymphoid to myeloid lineage after signaling through exogenously expressed M-CSF-R, irrespective of the presence of estradiol.
  • This demonstrated that M-CSF-R is functional for proliferation and differentiation signaling in a T-lymphoid progenitor cell, which, in addition, unveiled myeloid potential of pro-T progenitors.
  • [MeSH-major] Cell Differentiation. Cell Lineage. Cell Transformation, Neoplastic. Homeodomain Proteins / physiology. Oncogene Proteins, Fusion / physiology. T-Lymphocytes / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Cell Proliferation. Estradiol / pharmacology. Female. Flow Cytometry. Genes, fms / genetics. Genes, fms / physiology. Green Fluorescent Proteins / metabolism. Interleukin-7 / pharmacology. Lymphocytes / metabolism. Male. Mice. Mice, Inbred C57BL. Mice, Inbred DBA. Myeloid Cells / metabolism. Phagocytosis. Receptor, Macrophage Colony-Stimulating Factor / genetics. Receptor, Macrophage Colony-Stimulating Factor / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Stem Cell Factor / pharmacology. Stem Cells / metabolism. Stem Cells / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16819510.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Interleukin-7; 0 / Oncogene Proteins, Fusion; 0 / Stem Cell Factor; 0 / enhanced green fluorescent protein; 146150-85-8 / E2A-Pbx1 fusion protein; 147336-22-9 / Green Fluorescent Proteins; 4TI98Z838E / Estradiol; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
  •  go-up   go-down


80. Rüdiger T, Zettl A, Adam P, Bonzheim I, Geissinger E, Müller-Hermelink HK: [Peripheral NK/T-cell lymphoma]. Pathologe; 2007 Feb;28(1):55-8
SciCrunch. The Antibody Registry: Reagent: Antibodies .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Peripheral NK/T-cell lymphoma].
  • [Transliterated title] Periphere NK/T-Zell-Lymphome.
  • Peripheral T-cell lymphomas comprise 8% of the malignant lymphomas in Germany.
  • Such localizations are typical for the respective disease and form the basis for the classification of extranodal peripheral T-cell lymphoma.
  • Extranodal NK/T-cell lymphomas of the nasal type are characterized by an angiocentric growth pattern and large confluent areas of necrosis.
  • In the differential diagnosis, B-cell lymphomas are more frequent at all localizations than T- or NK-cell lymphomas.
  • [MeSH-major] Killer Cells, Natural / pathology. Lymphoma, T-Cell / pathology. T-Lymphocytes / immunology
  • [MeSH-minor] Diagnosis, Differential. Humans. Immunophenotyping. Lymphoma, B-Cell / classification. Lymphoma, B-Cell / immunology. Lymphoma, B-Cell / pathology

  • Genetic Alliance. consumer health - Peripheral T-cell lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Haematol. 2003 Jun;121(5):805-14 [12780797.001]
  • [Cites] Cancer. 1986 Jul 1;58(1):67-71 [2423228.001]
  • [Cites] Blood. 1994 Sep 1;84(5):1361-92 [8068936.001]
  • [Cites] Cancer Sci. 2006 Jul;97(7):605-10 [16827800.001]
  • [Cites] Int J Cancer. 1996 Nov 4;68(3):285-90 [8903467.001]
  • [Cites] Am J Surg Pathol. 1995 Mar;19(3):284-96 [7532919.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3628-30 [10828054.001]
  • [Cites] Hum Pathol. 1996 Jul;27(7):701-7 [8698315.001]
  • [Cites] Ann Oncol. 2002 Jan;13(1):140-9 [11863096.001]
  • [Cites] Semin Hematol. 2003 Jul;40(3):175-84 [12876666.001]
  • [Cites] J Clin Oncol. 2006 Feb 1;24(4):612-8 [16380410.001]
  • [Cites] Blood. 1997 Nov 15;90(10):4099-105 [9354680.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Nov 26;93(24):13791-6 [8943014.001]
  • [Cites] Blood. 2003 May 1;101(9):3590-3 [12506019.001]
  • (PMID = 17195040.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


81. Akahane K, Inukai T, Zhang X, Hirose K, Kuroda I, Goi K, Honna H, Kagami K, Nakazawa S, Endo K, Kubota T, Yagita H, Koyama-Okazaki T, Sugita K: Resistance of T-cell acute lymphoblastic leukemia to tumor necrosis factor--related apoptosis-inducing ligand-mediated apoptosis. Exp Hematol; 2010 Oct;38(10):885-95
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] Resistance of T-cell acute lymphoblastic leukemia to tumor necrosis factor--related apoptosis-inducing ligand-mediated apoptosis.
  • OBJECTIVE: Cytotoxic ligands are involved in tumor immunity and graft-vs.-leukemia effect after allogeneic stem cell transplantation for leukemia.
  • To clarify the susceptibility of T-cell acute lymphoblastic leukemia (T-ALL) to tumor immunity, sensitivity to recombinant human soluble Fas ligand (rhsFasL) and tumor necrosis factor-related apoptosis-inducing ligand (rhsTRAIL) was determined.
  • MATERIALS AND METHODS: Sensitivity to rhsFasL and rhsTRAIL and cell surface expression of their receptors were tested in T-ALL cell lines (n = 7) and patients' samples (n = 17) and compared with those in B-precursor ALL cell lines (n = 30).
  • Expression of components of the death-inducing signaling complex and the TRAIL receptor genes (DR4/DR5), and the methylation status and promoter activity of the DR4/DR5 gene were tested in T-ALL cell lines.
  • RESULTS: T-ALL cell lines showed higher level of Fas expression and higher sensitivity to rhsFasL than did B-precursor ALL cell lines.
  • Despite comparable expression of components of death-inducing signaling complex, cell lines and patients' samples of T-ALL showed TRAIL-resistance associated with low cell surface expression of DR4/DR5.
  • Gene expression of DR4/DR5 in T-ALL cell lines was significantly lower than that in B-precursor ALL cell lines, and the methylation status of the gene promoter in T-ALL cell lines was associated with the gene expression level at least for DR4.
  • [MeSH-major] Apoptosis / drug effects. Cell Proliferation / drug effects. Fas Ligand Protein / pharmacology. TNF-Related Apoptosis-Inducing Ligand / pharmacology
  • [MeSH-minor] Antigens, CD95 / metabolism. Cell Line, Tumor. Cells, Cultured. DNA Methylation / drug effects. Dose-Response Relationship, Drug. Drug Resistance. Flow Cytometry. Gene Expression / drug effects. Humans. Immunoblotting. Jurkat Cells. Luciferases / genetics. Luciferases / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Promoter Regions, Genetic / genetics. Receptors, TNF-Related Apoptosis-Inducing Ligand / genetics. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20670671.001).
  • [ISSN] 1873-2399
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / FAS protein, human; 0 / Fas Ligand Protein; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / TNF-Related Apoptosis-Inducing Ligand; EC 1.13.12.- / Luciferases
  •  go-up   go-down


82. De Keersmaecker K: ABL1 fusions in T-cell acute lymphoblastic leukemia. Verh K Acad Geneeskd Belg; 2008;70(4):245-55
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 fusions in T-cell acute lymphoblastic leukemia.
  • To obtain insight in the contribution of activated kinases to the pathogenesis ofT-cell acute lymphoblastic leukemia (T-ALL), we studied the NUP214-ABL1 fusion gene that is found in 6% of T-ALL and EML1-ABL1 that we identified in one T-ALL patient.
  • [MeSH-major] Leukemia, T-Cell / genetics. Leukemia, T-Cell / metabolism. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / antagonists & inhibitors

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19166098.001).
  • [ISSN] 0302-6469
  • [Journal-full-title] Verhandelingen - Koninklijke Academie voor Geneeskunde van België
  • [ISO-abbreviation] Verh. K. Acad. Geneeskd. Belg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Belgium
  • [Chemical-registry-number] 0 / Benzamides; 0 / EML1-ABL1 fusion protein, human; 0 / NUP214 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 17
  •  go-up   go-down


83. Grabher C, von Boehmer H, Look AT: Notch 1 activation in the molecular pathogenesis of T-cell acute lymphoblastic leukaemia. Nat Rev Cancer; 2006 May;6(5):347-59
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] Notch 1 activation in the molecular pathogenesis of T-cell acute lymphoblastic leukaemia.
  • The chromosomal translocation t(7;9) in human T-cell acute lymphoblastic leukaemia (T-ALL) results in deregulated expression of a truncated, activated form of Notch 1 (TAN1) under the control of the T-cell receptor-beta (TCRB) locus.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia-Lymphoma, Adult T-Cell / metabolism. Receptor, Notch1 / metabolism

  • COS Scholar Universe. author profiles.
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16612405.001).
  • [ISSN] 1474-175X
  • [Journal-full-title] Nature reviews. Cancer
  • [ISO-abbreviation] Nat. Rev. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
  • [Number-of-references] 175
  •  go-up   go-down


84. Real PJ, Tosello V, Palomero T, Castillo M, Hernando E, de Stanchina E, Sulis ML, Barnes K, Sawai C, Homminga I, Meijerink J, Aifantis I, Basso G, Cordon-Cardo C, Ai W, Ferrando A: Gamma-secretase inhibitors reverse glucocorticoid resistance in T cell acute lymphoblastic leukemia. Nat Med; 2009 Jan;15(1):50-8
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] Gamma-secretase inhibitors reverse glucocorticoid resistance in T cell acute lymphoblastic leukemia.
  • Gamma-secretase inhibitors (GSIs) block the activation of the oncogenic protein Notch homolog-1 (NOTCH1) in T cell acute lymphoblastic leukemia (T-ALL).
  • Inhibition of NOTCH1 signaling in glucocorticoid-resistant T-ALL restored glucocorticoid receptor autoupregulation and induced apoptotic cell death through induction of the gene encoding BCL-2-like apoptosis initiator-11 (BCL2L11).
  • GSI treatment resulted in cell cycle arrest and accumulation of goblet cells in the gut mediated by upregulation of the gene encoding the transcription factor Krüppel-like factor-4 (Klf4), a negative regulator of the cell cycle required for goblet cell differentiation.
  • In contrast, glucocorticoid treatment induced transcriptional upregulation of cyclin D2 (Ccnd2) and protected mice from developing the intestinal goblet cell metaplasia typically induced by inhibition of NOTCH signaling with GSIs.

  • MedlinePlus Health Information. consumer health - Steroids.
  • COS Scholar Universe. author profiles.
  • Nuclear Receptor Signaling Atlas (NURSA). supplemental materials - Curated dataset for this article .
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • SciCrunch. Nuclear Receptor Signaling Atlas: Data: Gene Expression .
  • SciCrunch. OMIM: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 2005 Jun 16;435(7044):959-63 [15959515.001]
  • [Cites] J Biol Chem. 2004 Dec 31;279(53):55809-17 [15509554.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4131-8 [16118324.001]
  • [Cites] Carcinogenesis. 2006 Jan;27(1):23-31 [16219632.001]
  • [Cites] J Biol Chem. 2005 Dec 30;280(52):43264-71 [16263717.001]
  • [Cites] CNS Drugs. 2006;20(5):351-72 [16696577.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1279-87 [16688224.001]
  • [Cites] Cell Death Differ. 2006 Sep;13(9):1495-505 [16341126.001]
  • [Cites] Cancer Cell. 2006 Oct;10(4):331-42 [17010674.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18261-6 [17114293.001]
  • [Cites] FASEB J. 2006 Dec;20(14):2600-2 [17077285.001]
  • [Cites] Curr Opin Genet Dev. 2007 Feb;17(1):52-9 [17178457.001]
  • [Cites] Chem Biol. 2007 Feb;14(2):209-19 [17317574.001]
  • [Cites] Endocrinology. 2007 Aug;148(8):3987-97 [17495001.001]
  • [Cites] Nat Med. 2007 Oct;13(10):1203-10 [17873882.001]
  • [Cites] Annu Rev Pathol. 2008;3:587-613 [18039126.001]
  • [Cites] Cell Cycle. 2008 Apr 15;7(8):965-70 [18414037.001]
  • [Cites] Clin Cancer Res. 2008 Sep 1;14(17):5314-7 [18765521.001]
  • [Cites] Nat Immunol. 2005 Sep;6(9):881-8 [16056227.001]
  • [Cites] Cancer Res. 1999 Mar 15;59(6):1378-85 [10096574.001]
  • [Cites] Nat Genet. 2000 Jan;24(1):36-44 [10615124.001]
  • [Cites] J Biol Chem. 2000 Nov 3;275(44):34086-91 [10915801.001]
  • [Cites] Mol Endocrinol. 2001 Aug;15(8):1381-95 [11463861.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10267-72 [11504912.001]
  • [Cites] Science. 2001 Sep 7;293(5536):1829-32 [11546872.001]
  • [Cites] Development. 2002 Jun;129(11):2619-28 [12015290.001]
  • [Cites] Int Immunol. 2002 Jun;14(6):637-45 [12039915.001]
  • [Cites] Mol Cell Endocrinol. 2002 Mar 28;189(1-2):191-9 [12039077.001]
  • [Cites] Semin Immunol. 2003 Apr;15(2):69-79 [12681943.001]
  • [Cites] J Biol Chem. 2003 Jun 27;278(26):23861-7 [12676946.001]
  • [Cites] Biochemistry. 2003 Sep 23;42(37):10978-90 [12974633.001]
  • [Cites] Annu Rev Neurosci. 2003;26:565-97 [12730322.001]
  • [Cites] J Biol Chem. 2003 Nov 14;278(46):46107-16 [12949072.001]
  • [Cites] Curr Mol Med. 2003 Dec;3(8):707-17 [14682492.001]
  • [Cites] J Biol Chem. 2004 Mar 26;279(13):12876-82 [14709552.001]
  • [Cites] Biochemistry. 2004 Aug 31;43(34):10851-8 [15323545.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Toxicol Sci. 2004 Nov;82(1):341-58 [15319485.001]
  • [Cites] Cancer Res. 1981 Nov;41(11 Pt 2):4861-2 [6975165.001]
  • [Cites] Leuk Res. 1985;9(8):993-9 [4046634.001]
  • [Cites] J Biol Chem. 1988 Aug 25;263(24):12044-8 [3261297.001]
  • [Cites] Cancer Res. 1996 Nov 1;56(21):5033-8 [8895760.001]
  • [Cites] Nature. 1996 Dec 5;384(6608):470-4 [8945475.001]
  • [Cites] J Exp Med. 1997 May 19;185(10):1827-36 [9151708.001]
  • [Cites] Immunity. 1998 Dec;9(6):777-86 [9881968.001]
  • [Cites] Curr Opin Cell Biol. 1998 Dec;10(6):702-9 [9914172.001]
  • [CommentIn] Cancer Cell. 2009 Feb 3;15(2):85-7 [19185842.001]
  • [CommentIn] Nat Med. 2009 Jan;15(1):20-1 [19129776.001]
  • (PMID = 19098907.001).
  • [ISSN] 1546-170X
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE11184/ GSE7067
  • [Grant] United States / NCI NIH HHS / CA / 1R01 CA105129; United States / NCI NIH HHS / CA / CA133379-01A1; United States / NCI NIH HHS / CA / R01 CA120196-03; United States / NCI NIH HHS / CA / R01 CA133379; United States / NCI NIH HHS / CA / R01 CA105129-04; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / 1R01 CA133379; United States / NCI NIH HHS / CA / R01 CA149655; United States / NCI NIH HHS / CA / R01 CA105129; United States / NCI NIH HHS / CA / R01 CA133379-01A1; United States / NCI NIH HHS / CA / CA120196-03; United States / NIAID NIH HHS / AI / R56 AI070310-01A1; United States / NCI NIH HHS / CA / R01 CA120196; United States / NIAID NIH HHS / AI / AI070310-01A1; United States / NIAID NIH HHS / AI / R56 AI070310; United States / NCI NIH HHS / CA / CA105129-04
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Ccnd2 protein, mouse; 0 / Cyclin D2; 0 / Cyclins; 0 / Enzyme Inhibitors; 0 / Glucocorticoids; 0 / Membrane Proteins; 0 / NR3C1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptor, Notch1; 0 / Receptors, Glucocorticoid; 7S5I7G3JQL / Dexamethasone; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ NIHMS103250; NLM/ PMC2692090
  •  go-up   go-down


85. Dalmazzo LF, Jácomo RH, Marinato AF, Figueiredo-Pontes LL, Cunha RL, Garcia AB, Rego EM, Falcão RP: The presence of CD56/CD16 in T-cell acute lymphoblastic leukaemia correlates with the expression of cytotoxic molecules and is associated with worse response to treatment. Br J Haematol; 2009 Jan;144(2):223-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The presence of CD56/CD16 in T-cell acute lymphoblastic leukaemia correlates with the expression of cytotoxic molecules and is associated with worse response to treatment.
  • Some cases of T-cell acute lymphoblastic leukaemia (ALL) express markers found in natural-killer (NK) cells, such as CD56 and CD16.
  • Out of 84 T-cell ALL cases diagnosed at our Institution, CD56 and/or CD16 was detected in 24 (28.5%), which we designated T/NK-ALL group.
  • The mean overall survival (863 vs. 1869 d, P = 0.02) and disease-free survival (855 vs. 2095 d, P = 0.002) were shorter in patients expressing CD56/CD16.
  • [MeSH-major] Antigens, CD56 / analysis. Killer Cells, Natural / immunology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Receptors, IgG / analysis
  • [MeSH-minor] Adolescent. Adult. Age Factors. Antigens, CD / analysis. Antigens, CD3 / analysis. Antigens, CD34 / analysis. Antigens, CD45 / analysis. Antigens, Differentiation, Myelomonocytic / analysis. Biomarkers / analysis. Disease-Free Survival. Female. Flow Cytometry. Granzymes / analysis. Humans. Immunophenotyping. Kaplan-Meier Estimate. Male. Perforin / analysis. Platelet Count. Poly(A)-Binding Proteins / analysis. Sialic Acid Binding Ig-like Lectin 3. Survival Rate. Treatment Outcome. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19016721.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD3; 0 / Antigens, CD34; 0 / Antigens, CD56; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Biomarkers; 0 / CD33 protein, human; 0 / Poly(A)-Binding Proteins; 0 / Receptors, IgG; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / TIA1 protein, human; 126465-35-8 / Perforin; EC 3.1.3.48 / Antigens, CD45; EC 3.4.21.- / Granzymes
  •  go-up   go-down


86. Frey O, Kamradt T: [Effector function plasticity of T helper lymphocytes]. Z Rheumatol; 2009 Dec;68(10):834-5
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • However, a number of recent findings show a much higher degree of Th cell plasticity and interconvertibility than previously assumed.

  • MedlinePlus Health Information. consumer health - Autoimmune Diseases.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Immunity. 2009 Jan 16;30(1):155-67 [19144320.001]
  • [Cites] Nat Immunol. 2008 Dec;9(12):1341-6 [18931678.001]
  • [Cites] Nat Rev Immunol. 2008 Jul;8(7):523-32 [18566595.001]
  • [Cites] Nat Immunol. 2009 Aug;10(8):857-63 [19578369.001]
  • [Cites] Nat Immunol. 2009 Sep;10(9):1000-7 [19633673.001]
  • [Cites] Immunity. 2009 Jan 16;30(1):92-107 [19119024.001]
  • [Cites] Immunity. 2009 Mar 20;30(3):324-35 [19303387.001]
  • [Cites] Immunity. 2009 May;30(5):673-83 [19409816.001]
  • [Cites] Springer Semin Immunopathol. 1999;21(3):317-38 [10666776.001]
  • [Cites] Nat Immunol. 2009 Apr;10(4):385-93 [19252490.001]
  • [Cites] Science. 2009 Mar 13;323(5920):1488-92 [19286559.001]
  • [Cites] Immunity. 2008 Apr;28(4):454-67 [18400188.001]
  • (PMID = 19847446.001).
  • [ISSN] 1435-1250
  • [Journal-full-title] Zeitschrift fur Rheumatologie
  • [ISO-abbreviation] Z Rheumatol
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-2; 0 / Transcription Factors; 0 / Transforming Growth Factor beta; 207137-56-2 / Interleukin-4
  • [Number-of-references] 12
  •  go-up   go-down


87. Hagemeijer A, Graux C: ABL1 rearrangements in T-cell acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2010 Apr;49(4):299-308
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 rearrangements in T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) is the result of multiple oncogenic insults of thymocytes.
  • [MeSH-major] Gene Rearrangement. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-abl / 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 = 20073070.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
  • [Number-of-references] 60
  •  go-up   go-down


88. Palomero T, Odom DT, O'Neil J, Ferrando AA, Margolin A, Neuberg DS, Winter SS, Larson RS, Li W, Liu XS, Young RA, Look AT: Transcriptional regulatory networks downstream of TAL1/SCL in T-cell acute lymphoblastic leukemia. Blood; 2006 Aug 1;108(3):986-92
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transcriptional regulatory networks downstream of TAL1/SCL in T-cell acute lymphoblastic leukemia.
  • Aberrant expression of 1 or more transcription factor oncogenes is a critical component of the molecular pathogenesis of human T-cell acute lymphoblastic leukemia (T-ALL); however, oncogenic transcriptional programs downstream of T-ALL oncogenes are mostly unknown.
  • TAL1/SCL is a basic helix-loop-helix (bHLH) transcription factor oncogene aberrantly expressed in 60% of human T-ALLs.
  • Promoters occupied by TAL1 were also frequently bound by the class I bHLH proteins E2A and HEB, suggesting that TAL1/E2A as well as TAL1/HEB heterodimers play a role in transformation of T-cell precursors.
  • In addition, oligonucleotide microarray analysis of RNA from 47 primary T-ALL samples showed specific expression signatures involving TAL1 targets in TAL1-expressing compared with -nonexpressing human T-ALLs.
  • Our results indicate that TAL1 may act as a bifunctional transcriptional regulator (activator and repressor) at the top of a complex regulatory network that disrupts normal T-cell homeostasis and contributes to leukemogenesis.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cell. 2004 Nov 19;16(4):521-35 [15546613.001]
  • [Cites] Mol Cell Biol. 1999 Jul;19(7):5025-35 [10373552.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 22;102(12):4459-64 [15753290.001]
  • [Cites] PLoS Genet. 2005 Aug;1(2):e16 [16110340.001]
  • [Cites] Cell. 2000 Jul 7;102(1):109-26 [10929718.001]
  • [Cites] Nat Immunol. 2000 Aug;1(2):138-44 [11248806.001]
  • [Cites] Genes Dev. 2002 Jan 15;16(2):235-44 [11799066.001]
  • [Cites] Genes Dev. 2002 Jan 15;16(2):245-56 [11799067.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2430-40 [12239153.001]
  • [Cites] Science. 2002 Oct 25;298(5594):799-804 [12399584.001]
  • [Cites] Oncogene. 2003 Mar 13;22(10):1445-60 [12629508.001]
  • [Cites] J Biol Chem. 2003 Apr 11;278(15):12680-7 [12566462.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8164-9 [12808131.001]
  • [Cites] Mol Cell Biol. 2003 Nov;23(21):7585-99 [14560005.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Dec 26;312(4):1073-81 [14651981.001]
  • [Cites] Mol Cell Biol. 2004 Feb;24(4):1439-52 [14749362.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1909-11 [14604958.001]
  • [Cites] Lancet. 2004 Feb 14;363(9408):535-6 [14975618.001]
  • [Cites] Science. 2004 Feb 27;303(5662):1378-81 [14988562.001]
  • [Cites] J Cell Sci. 2004 Mar 1;117(Pt 7):1161-71 [14970264.001]
  • [Cites] Cancer Cell. 2004 Jun;5(6):587-96 [15193261.001]
  • [Cites] Mol Cell Biol. 1991 Jun;11(6):3037-42 [2038315.001]
  • [Cites] Oncogene. 1993 Mar;8(3):677-83 [8437851.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Apr 12;91(8):3181-5 [8159721.001]
  • [Cites] Mol Cell Biol. 1994 May;14(5):3403-13 [8164688.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jun 21;91(13):5947-51 [8016094.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jun 21;91(13):5952-6 [8016095.001]
  • [Cites] EMBO J. 1994 Oct 17;13(20):4831-9 [7957052.001]
  • [Cites] Blood. 1995 Jan 15;85(2):465-71 [7812000.001]
  • [Cites] Blood. 1995 Jun 1;85(11):3356-7 [7756670.001]
  • [Cites] Blood. 1995 Jul 15;86(2):666-76 [7605997.001]
  • [Cites] J Biol Chem. 1996 Feb 2;271(5):2683-8 [8576241.001]
  • [Cites] Cell. 1996 Jul 12;86(1):47-57 [8689686.001]
  • [Cites] J Biol Chem. 1996 Dec 6;271(49):31463-9 [8940159.001]
  • [Cites] EMBO J. 1997 Jun 2;16(11):3145-57 [9214632.001]
  • [Cites] Bioessays. 1997 Jul;19(7):607-13 [9230693.001]
  • [Cites] Mol Cell Biol. 1997 Aug;17(8):4782-91 [9234734.001]
  • [Cites] J Biol Chem. 1998 Mar 20;273(12):7030-7 [9507011.001]
  • [Cites] Mol Cell Biol. 1998 Dec;18(12):6939-50 [9819382.001]
  • [Cites] Oncogene. 1998 Nov 26;17(21):2799-803 [9840944.001]
  • [Cites] Cell. 2004 Dec 29;119(7):1041-54 [15620361.001]
  • (PMID = 16621969.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK68655; United States / NCI NIH HHS / CA / CA114589-01; United States / NIDDK NIH HHS / DK / DK070813; United States / NHGRI NIH HHS / HG / HG002668; United States / NCI NIH HHS / CA / CA109901
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / TCF3 protein, human; 135471-20-4 / TAL1 protein, human; 142661-93-6 / TCF12 protein, human
  • [Other-IDs] NLM/ PMC1895859
  •  go-up   go-down


89. Chadwick N, Zeef L, Portillo V, Fennessy C, Warrander F, Hoyle S, Buckle AM: Identification of novel Notch target genes in T cell leukaemia. Mol Cancer; 2009;8:35
SciCrunch. ArrayExpress: Data: Microarray .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of novel Notch target genes in T cell leukaemia.
  • BACKGROUND: Dysregulated Notch signalling is believed to play an important role in the development and maintenance of T cell leukaemia.
  • At a cellular level, Notch signalling promotes proliferation and inhibits apoptosis of T cell acute lymphoblastic leukaemia (T-ALL) cells.
  • In this study we aimed to identify novel transcriptional targets of Notch signalling in the T-ALL cell line, Jurkat.
  • A subset of genes found to be regulated by Notch was chosen for real-time PCR validation and in some cases, validation at the protein level, using several Notch-transduced T-ALL and non-T-ALL leukaemic cell lines.
  • These included the T cell costimulatory molecule CD28, the anti-apoptotic protein GIMAP5, and inhibitor of DNA binding 1 (1D1).
  • CONCLUSION: The identification of such downstream Notch target genes provides insights into the mechanisms of Notch function in T cell leukaemia, and may help identify novel therapeutic targets in this disease.
  • [MeSH-major] Gene Expression Profiling. Leukemia, T-Cell / genetics. Leukemia, T-Cell / metabolism. Receptors, Notch / genetics. Signal Transduction / genetics

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] EMBO J. 2000 Jul 3;19(13):3337-48 [10880446.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1279-87 [16688224.001]
  • [Cites] Immunology. 2000 Nov;101(3):309-15 [11106933.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jan 2;98(1):31-6 [11134512.001]
  • [Cites] J Immunol. 2001 Mar 1;166(5):3468-75 [11207305.001]
  • [Cites] Bioinformatics. 2001 Jun;17(6):509-19 [11395427.001]
  • [Cites] Mol Cell Biol. 2001 Sep;21(17):6071-9 [11486044.001]
  • [Cites] Anticancer Res. 2001 Jul-Aug;21(4A):2281-6 [11724283.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Mar 8;291(4):775-9 [11866432.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3788-93 [11891328.001]
  • [Cites] Genes Dev. 2006 Aug 1;20(15):2096-109 [16847353.001]
  • [Cites] Eur J Immunol. 2006 Aug;36(8):2223-34 [16838279.001]
  • [Cites] Mol Cell Biol. 2006 Nov;26(21):8022-31 [16954387.001]
  • [Cites] J Immunol. 2006 Nov 1;177(9):6098-107 [17056536.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18261-6 [17114293.001]
  • [Cites] Chem Biol. 2007 Feb;14(2):209-19 [17317574.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Sep 21;361(2):481-6 [17655828.001]
  • [Cites] Nat Med. 2007 Oct;13(10):1203-10 [17873882.001]
  • [Cites] Stem Cells. 2008 Mar;26(3):715-23 [18055449.001]
  • [Cites] Blood. 2008 Aug 1;112(3):733-40 [18411416.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Jan 6;106(1):244-9 [19118200.001]
  • [Cites] Science. 2002 Oct 25;298(5594):840-3 [12399594.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(2):655-64 [12509463.001]
  • [Cites] Bioinformatics. 2003 Jan 22;19(2):185-93 [12538238.001]
  • [Cites] Cancer Cell. 2003 Jun;3(6):525-30 [12842081.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9440-5 [12883005.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Sep 2;100(18):10382-7 [12930893.001]
  • [Cites] J Immunol. 2003 Nov 1;171(9):4504-11 [14568923.001]
  • [Cites] EMBO Rep. 2003 Nov;4(11):1067-72 [14566327.001]
  • [Cites] Mol Endocrinol. 2004 Mar;18(3):687-95 [14701943.001]
  • [Cites] Nat Rev Immunol. 2004 May;4(5):336-47 [15122199.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Cell. 1991 Aug 23;66(4):649-61 [1831692.001]
  • [Cites] Cancer Res. 1995 Sep 15;55(18):4140-5 [7545086.001]
  • [Cites] Nature. 1995 Sep 28;377(6547):355-8 [7566092.001]
  • [Cites] J Exp Med. 1996 May 1;183(5):2283-91 [8642337.001]
  • [Cites] Immunobiology. 1997 Dec;198(1-3):299-306 [9442401.001]
  • [Cites] Mol Cell Biol. 1998 Dec;18(12):7423-31 [9819428.001]
  • [Cites] Immunity. 1998 Dec;9(6):777-86 [9881968.001]
  • [Cites] Nat Immunol. 2005 Feb;6(2):152-62 [15640801.001]
  • [Cites] Semin Immunol. 2005 Apr;17(2):121-7 [15737573.001]
  • [Cites] Eur J Immunol. 2005 Nov;35(11):3287-96 [16224812.001]
  • [Cites] EMBO J. 2006 Jan 11;25(1):129-38 [16319921.001]
  • [Cites] J Biol Chem. 2006 Feb 24;281(8):5106-19 [16365048.001]
  • [Cites] PLoS Biol. 2006 Apr;4(4):e103 [16509771.001]
  • [Cites] Cancer Res. 2006 May 1;66(9):4715-24 [16651424.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Jun 23;345(1):446-52 [16682003.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Sep 16;276(1):189-96 [11006105.001]
  • (PMID = 19508709.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD28; 0 / ID1 protein, human; 0 / Inhibitor of Differentiation Protein 1; 0 / Receptors, Notch; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 3.6.1.- / GTP Phosphohydrolases
  • [Other-IDs] NLM/ PMC2698846
  •  go-up   go-down


90. Huang X, Chen S, Shen Q, Yang L, Li B, Zhong L, Geng S, Du X, Li Y: Analysis of the expression pattern of the BCL11B gene and its relatives in patients with T-cell acute lymphoblastic leukemia. J Hematol Oncol; 2010;3(1):44
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of the expression pattern of the BCL11B gene and its relatives in patients with T-cell acute lymphoblastic leukemia.
  • BACKGROUND: In a human T-cell acute lymphoblastic leukemia (T-ALL) cell line (Molt-4), siRNA-mediated suppression of BCL11B expression was shown to inhibit proliferation and induce apoptosis, functions which may be related to genes involved in apoptosis (such as TNFSF10 and BCL2L1) and TGF-β pathways (such as SPP1and CREBBP).
  • [MeSH-major] CREB-Binding Protein / biosynthesis. Gene Expression Regulation, Neoplastic / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Repressor Proteins / biosynthesis. Tumor Suppressor Proteins / biosynthesis. bcl-X Protein / biosynthesis

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Am J Physiol Renal Physiol. 2010 Jul;299(1):F234-42 [20392802.001]
  • [Cites] Nat Immunol. 2003 Jun;4(6):525-32 [12717432.001]
  • [Cites] Exp Oncol. 2004 Sep;26(3):179-84 [15494684.001]
  • [Cites] Nat Genet. 1996 Sep;14(1):33-41 [8782817.001]
  • [Cites] Leukemia. 1997 Dec;11(12):2087-96 [9447825.001]
  • [Cites] Blood. 1998 Feb 1;91(3):735-46 [9446631.001]
  • [Cites] Curr Opin Cell Biol. 2004 Dec;16(6):647-52 [15530776.001]
  • [Cites] FASEB J. 2004 Dec;18(15):1826-33 [15576486.001]
  • [Cites] Leukemia. 2005 Feb;19(2):201-8 [15668700.001]
  • [Cites] Trends Cell Biol. 2006 Feb;16(2):79-87 [16406521.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4500-7 [16484591.001]
  • [Cites] Cancer Gene Ther. 2006 Sep;13(9):819-29 [16424918.001]
  • [Cites] Blood. 2006 Dec 15;108(13):4198-201 [16926283.001]
  • [Cites] Oncogene. 2007 Feb 26;26(9):1324-37 [17322918.001]
  • [Cites] Oncogene. 2007 May 31;26(26):3797-810 [17173069.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Jun;16(6):1087-97 [17548669.001]
  • [Cites] Oncogene. 2007 Aug 30;26(40):5840-50 [17369851.001]
  • [Cites] J Cell Physiol. 2008 Jan;214(1):192-200 [17579344.001]
  • [Cites] BMC Cancer. 2007;7:195 [17941976.001]
  • [Cites] J Immunotoxicol. 2008 Apr;5(2):235-48 [18569395.001]
  • [Cites] Nat Rev Drug Discov. 2009 Feb;8(2):129-38 [19180106.001]
  • [Cites] Adv Drug Deliv Rev. 2009 Aug 10;61(10):850-62 [19422869.001]
  • [Cites] Nucleic Acids Res. 2002 May 1;30(9):e36 [11972351.001]
  • (PMID = 21080944.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BCL11B protein, human; 0 / BCL2L1 protein, human; 0 / CREBBP protein, human; 0 / Repressor Proteins; 0 / Tumor Suppressor Proteins; 0 / bcl-X Protein; EC 2.3.1.48 / CREB-Binding Protein
  • [Other-IDs] NLM/ PMC2992472
  •  go-up   go-down


91. Hussain AR, Al-Rasheed M, Manogaran PS, Al-Hussein KA, Platanias LC, Al Kuraya K, Uddin S: Curcumin induces apoptosis via inhibition of PI3'-kinase/AKT pathway in acute T cell leukemias. Apoptosis; 2006 Feb;11(2):245-54
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Curcumin induces apoptosis via inhibition of PI3'-kinase/AKT pathway in acute T cell leukemias.
  • The mechanism by which curcumin inhibit cell proliferation remains poorly understood.
  • In the present report, we investigated the effect of curcumin on the activation of apoptotic pathway in T-cell acute lymphoblastic leukemia (T-ALL) malignant cells.
  • Our data demonstrate that curcumin causes dose dependent suppression of proliferation in several T cell lines.
  • Curcumin treatment causes the de-phosphorylation/inactivation of constitutively active AKT, FOXO transcription factor and GSK3.
  • In addition, zVAD-fmk, a universal inhibitor of caspases, prevents caspase-3 activation and abrogates cell death induced by curcumin treatment.
  • Taken together, our finding suggest that curcumin suppresses constitutively activated targets of PI3'-kinase (AKT, FOXO and GSK3) in T cells leading to the inhibition of proliferation and induction of caspase-dependent apoptosis.
  • [MeSH-minor] Cell Proliferation / drug effects. Cells, Cultured. Dose-Response Relationship, Drug. Humans. Jurkat Cells. Time Factors

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CURCUMIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16502262.001).
  • [ISSN] 1360-8185
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; IT942ZTH98 / Curcumin
  •  go-up   go-down


92. Mansour MR, Duke V, Foroni L, Patel B, Allen CG, Ancliff PJ, Gale RE, Linch DC: Notch-1 mutations are secondary events in some patients with T-cell acute lymphoblastic leukemia. Clin Cancer Res; 2007 Dec 01;13(23):6964-9
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] Notch-1 mutations are secondary events in some patients with T-cell acute lymphoblastic leukemia.
  • PURPOSE: Activating Notch-1 mutations are frequent in T-cell acute lymphoblastic leukemia (T-ALL), occurring in >50% of patients.
  • In murine models of T-ALL, Notch-1 activation can both directly initiate leukemia and cooperate secondarily to other primary events.
  • Of 16 matched presentation-relapse samples studied, 7 were wild-type at both presentation and relapse.
  • One lost a PEST mutation and became wild-type.
  • Two others lost mutations at relapse but acquired different mutations, despite unchanged T-cell receptor rearrangements, suggesting that the latter event predated the acquisition of the Notch-1 mutation.
  • One relapsed with a secondary T-cell leukemia and different Notch mutation.
  • CONCLUSIONS: These results suggest that Notch-1 mutations can sometimes be acquired as secondary events in leukemogenesis and must be used cautiously as solitary minimal residual disease markers.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation. Receptor, Notch1 / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18056171.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0500389
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
  •  go-up   go-down


93. Rajnics P, Krenács L, Kenéz A, Járay Z, Bagdi E, Demeter J: [Long-term survival after nasal NK/T cell lymphoma]. Orv Hetil; 2008 Apr 27;149(17):801-5
Hazardous Substances Data Bank. VINCRISTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Long-term survival after nasal NK/T cell lymphoma].
  • [Transliterated title] Nazális NK/T-sejtes lymphoma hosszú túlélése.
  • The nasal NK/T cell lymphoma is a rare, extranodal non-Hodgkin lymphoma in western civilizations, which has poor prognosis.
  • [MeSH-major] Killer Cells, Natural. Lymphoma, T-Cell, Peripheral / diagnosis. Lymphoma, T-Cell, Peripheral / therapy. Nose Neoplasms / diagnosis. Nose Neoplasms / therapy
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Cyclophosphamide / therapeutic use. Diagnosis, Differential. Doxorubicin / therapeutic use. Female. Herpesvirus 4, Human / isolation & purification. Humans. Prednisone / therapeutic use. Tomography, X-Ray Computed. Vincristine / therapeutic use

  • MedlinePlus Health Information. consumer health - Nasal Cancer.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18426762.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
  • [Number-of-references] 10
  •  go-up   go-down


94. Burkhardt B, Moericke A, Klapper W, Greene F, Salzburg J, Damm-Welk C, Zimmermann M, Strauch K, Ludwig WD, Schrappe M, Reiter A: Pediatric precursor T lymphoblastic leukemia and lymphoblastic lymphoma: Differences in the common regions with loss of heterozygosity at chromosome 6q and their prognostic impact. Leuk Lymphoma; 2008 Mar;49(3):451-61
Genetic Alliance. consumer health - Lymphoblastic lymphoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric precursor T lymphoblastic leukemia and lymphoblastic lymphoma: Differences in the common regions with loss of heterozygosity at chromosome 6q and their prognostic impact.
  • This study analyzed loss of heterozygosity (LOH) at chromosome 6q and compared the LOH findings in pediatric precursor T lymphoblastic lymphoma (T-LBL) with the LOH findings in precursor-T lymphoblastic leukemia (T-ALL).
  • All patients were treated uniformly according to ALL-BFM-type treatment-strategy.
  • [MeSH-major] Chromosomes, Human, Pair 6. Loss of Heterozygosity. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Child. Chromosome Deletion. Diagnosis, Differential. Humans. Microsatellite Repeats. Prognosis. Recurrence. Retrospective Studies. Survival Analysis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18297521.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


95. Aifantis I, Vilimas T, Buonamici S: Notches, NFkappaBs and the making of T cell leukemia. Cell Cycle; 2007 Feb 15;6(4):403-6
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Notches, NFkappaBs and the making of T cell leukemia.
  • T cell lymphoblastic leukemia (T-ALL) is an aggressive hematological cancer frequent within pediatric ALL patients.
  • In these cases activating mutations of NOTCH1 are responsible for the transformation of developing T cell progenitors.
  • These observations prompted us to study the mechanisms of Notch1-induced T cell transformation.
  • Using parallel studies in T cell progenitors and established T-ALL lines we have demonstrated that the NFkappaB signaling pathway is targeted and induced by Notch1 activation.
  • NFkappaB appears to be important for the development of the disease as suppression of the pathway antagonizes T cell transformation both in vitro and in vivo, using animal models of T-ALL.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. NF-kappa B / physiology. Receptor, Notch1 / physiology. Signal Transduction
  • [MeSH-minor] Cell Transformation, Neoplastic. Humans. Models, Biological. T-Lymphocytes

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17329966.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA105129
  • [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 / NF-kappa B; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
  •  go-up   go-down


96. Graux C, Cools J, Michaux L, Vandenberghe P, Hagemeijer A: Cytogenetics and molecular genetics of T-cell acute lymphoblastic leukemia: from thymocyte to lymphoblast. Leukemia; 2006 Sep;20(9):1496-510
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] Cytogenetics and molecular genetics of T-cell acute lymphoblastic leukemia: from thymocyte to lymphoblast.
  • For long, T-cell acute lymphoblastic leukemia (T-ALL) remained in the shadow of precursor B-ALL because it was more seldom, and showed a normal karyotype in more than 50% of cases.
  • The genes deregulated by translocations or mutations appear to encode proteins that are also implicated in T-cell development, which prompted us to review the 'normal' and 'leukemogenic' functions of these transcription regulators.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphocytes / pathology. Thymus Gland / pathology
  • [MeSH-minor] Cell Lineage. Chromosome Aberrations. Genes, Homeobox. Humans. Protein-Tyrosine Kinases / genetics. Receptors, Antigen, T-Cell / metabolism. Signal Transduction

  • 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 = 16826225.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 158
  •  go-up