The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
MeSH Review

Leukemia, T-Cell, Acute

Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of Leukemia, T-Cell, Acute


High impact information on Leukemia, T-Cell, Acute

  • NUP214-ABL1 expression defines a new subgroup of individuals with T-ALL who could benefit from treatment with imatinib [1].
  • Our results implicate PI3K as a major effector of IL-7-induced viability, metabolic activation, growth and proliferation of T-ALL cells, and suggest that PI3K and its downstream effectors may represent molecular targets for therapeutic intervention in T-ALL [6].
  • Two models have been proposed for the molecular mechanism by which the Tal1 oncogene causes T cell acute lymphoblastic leukemia (T-ALL) [7].
  • Analysis of the 134 T-ALL suggested that the occurrence of tal-1 deletions is associated with the CD3 phenotype, because no tal-1 deletions were found in 25 TCR-gamma/delta + T-ALL, whereas 8 of the 69 CD3- T-ALL and 11 of the 40 TCR-alpha/beta + T-ALL contained such a deletion [8].
  • We also show that in B-lineage ALL, the cells probably use the same V gamma genes for TRG gamma rearrangements as the malignant cells in T-ALL and the polyclonal T cells [9].

Chemical compound and disease context of Leukemia, T-Cell, Acute

  • To this end, leukemic blasts from pediatric patients with T-ALL were prospectively investigated as to their responsiveness to IL-7, IL-4, and IL-2 (in terms of modulation of spontaneous apoptosis, assessed by flow cytometry), cytokine receptor expression profiles, and expression levels of Bcl-2 and Bax proteins [10].
  • We therefore examined 81 de novo childhood T-lineage acute lymphoblastic leukemias (T-ALL) including 54 steroid-poor responders, 10 relapsed T-ALL, and 10 leukemic T-cell lines, for the presence of CD95 mutations using single-strand confirmation polymorphism and sequence analysis [11].
  • When compared to cortical T-ALL, mature (CD1a(-), surface CD3(+)) T-ALL were significantly more resistant to doxorubicin, and immature, pro-/pre-T-ALL were more resistant to both drugs (P <.05) [12].
  • A single T-ALL case had a codon 11 mutation resulting in substitution of alanine with threonine [13].
  • One patient revealed a unique profile with high expression of the chemokine receptor CCR9 and the integrin CD103 on the T-ALL cells [14].

Biological context of Leukemia, T-Cell, Acute

  • Careful examination of all TCR genes revealed that tal-1 deletions exclusively occurred in CD3- or CD3+ T-ALL of the alpha/beta lineage with a frequency of 18% in T-ALL with one deleted TCR-delta allele, and a frequency of 34% in T-ALL with TCR-delta gene deletions on both alleles [8].
  • We have characterized a case of T-ALL with t(1;14)(p32;q11) in which, unlike the majority of t(1;14), the recombination with the T cell receptor delta elements affected the 3' side of the tal-1 locus [15].
  • We now report that an additional 25% of T-ALL patients bear tal-1 gene rearrangements that are not detected by karyotype analysis [16].
  • The TAL2 gene is located 33 kilobase pairs from the chromosome 9 breakpoint of t(7;9)(q34;q32), a recurring translocation specifically associated with T-ALL [17].
  • Similar to what occurs in normal immature thymocytes, prevention of spontaneous apoptosis by IL-7 in precursor T-cell acute lymphoblastic leukemia (T-ALL) cells correlates with up-regulation of bcl-2 [18].

Anatomical context of Leukemia, T-Cell, Acute

  • One T-ALL, which demonstrated a different staining pattern with monoclonal antibodies against the products of the TCR gamma/delta genes than the PEER cell line, rearranges J delta 1 to a currently unidentified variable region [19].
  • We performed sensitive polymerase chain reaction-based minimal residual disease (MRD) analyses on bone marrow samples at 9 follow-up time points in 71 children with T-lineage acute lymphoblastic leukemia (T-ALL) and compared the results with the precursor B-lineage ALL (B-ALL) results (n = 210) of our previous study [20].
  • Systemic high-dose methotrexate (MTX) and intrathecal chemotherapy is a safe and effective method of CNS prophylaxis in the context of BFM-oriented treatment for all children with ALL, regardless of the risk group (with the possible exception of T-ALL patients with high white blood cell counts) [21].
  • In CD7+CD4-CD8- ALL, which is thought to originate from the lymphohematopoietic stem cell, expressed the MDR1 gene with a high incidence (six of eight patients), whereas three surface CD3+ and one CD4+CD8+ T-cell ALL (T-ALL) did not have detectable MDR1 transcripts [22].
  • The tal-1 gene, frequently activated in human T-cell acute lymphoblastic leukemia (T-ALL), is expressed in the erythroid, megakaryocytic, and mast cell lineages during normal hematopoiesis [23].

Gene context of Leukemia, T-Cell, Acute

  • Hence, TAL2, TAL1, and LYL1 constitute a discrete subgroup of helix-loop-helix proteins, each of which can potentially contribute to the development of T-ALL [17].
  • TAL2 sequences are actively transcribed in SUP-T3, a T-ALL cell line that harbors the t(7;9)(q34;q32) [17].
  • We have created a stable transgenic rag2-EGFP-mMyc zebrafish line that develops GFP-labeled T cell acute lymphoblastic leukemia (T-ALL), allowing visualization of the onset and spread of this disease [24].
  • IL-7 or IL-2 induced the proliferation of some leukemic cells, whereas sequential cell treatment with CD2-MoAb and then IL-2 promoted CD3/TCR expression on nearly all CD2+ cells (15 of 16), except for 1 T-ALL that developed into CD3-CD16+CD56+ cells [25].
  • IL-7-dependent human leukemia T-cell line as a valuable tool for drug discovery in T-ALL [26].

Analytical, diagnostic and therapeutic context of Leukemia, T-Cell, Acute


  1. Fusion of NUP214 to ABL1 on amplified episomes in T-cell acute lymphoblastic leukemia. Graux, C., Cools, J., Melotte, C., Quentmeier, H., Ferrando, A., Levine, R., Vermeesch, J.R., Stul, M., Dutta, B., Boeckx, N., Bosly, A., Heimann, P., Uyttebroeck, A., Mentens, N., Somers, R., MacLeod, R.A., Drexler, H.G., Look, A.T., Gilliland, D.G., Michaux, L., Vandenberghe, P., Wlodarska, I., Marynen, P., Hagemeijer, A. Nat. Genet. (2004) [Pubmed]
  2. The multidrug resistance-associated protein 3 (MRP3) is associated with a poor outcome in childhood ALL and may account for the worse prognosis in male patients and T-cell immunophenotype. Steinbach, D., Wittig, S., Cario, G., Viehmann, S., Mueller, A., Gruhn, B., Haefer, R., Zintl, F., Sauerbrey, A. Blood (2003) [Pubmed]
  3. Selective toxicity of deoxyguanosine and arabinosyl guanine for T-leukemic cells. Cohen, A., Lee, J.W., Gelfand, E.W. Blood (1983) [Pubmed]
  4. Role of folylpolyglutamate synthetase and folylpolyglutamate hydrolase in methotrexate accumulation and polyglutamylation in childhood leukemia. Rots, M.G., Pieters, R., Peters, G.J., Noordhuis, P., van Zantwijk, C.H., Kaspers, G.J., Hählen, K., Creutzig, U., Veerman, A.J., Jansen, G. Blood (1999) [Pubmed]
  5. EFA (9-beta-D-erythrofuranosyladenine) is an effective salvage agent for methylthioadenosine phosphorylase-selective therapy of T-cell acute lymphoblastic leukemia with L-alanosine. Batova, A., Cottam, H., Yu, J., Diccianni, M.B., Carrera, C.J., Yu, A.L. Blood (2006) [Pubmed]
  6. Activation of PI3K is indispensable for interleukin 7-mediated viability, proliferation, glucose use, and growth of T cell acute lymphoblastic leukemia cells. Barata, J.T., Silva, A., Brandao, J.G., Nadler, L.M., Cardoso, A.A., Boussiotis, V.A. J. Exp. Med. (2004) [Pubmed]
  7. Growth inhibition and apoptosis due to restoration of E2A activity in T cell acute lymphoblastic leukemia cells. Park, S.T., Nolan, G.P., Sun, X.H. J. Exp. Med. (1999) [Pubmed]
  8. Site-specific deletions involving the tal-1 and sil genes are restricted to cells of the T cell receptor alpha/beta lineage: T cell receptor delta gene deletion mechanism affects multiple genes. Breit, T.M., Mol, E.J., Wolvers-Tettero, I.L., Ludwig, W.D., van Wering, E.R., van Dongen, J.J. J. Exp. Med. (1993) [Pubmed]
  9. Human T cell gamma genes are frequently rearranged in B-lineage acute lymphoblastic leukemias but not in chronic B cell proliferations. Chen, Z., Le Paslier, D., Dausset, J., Degos, L., Flandrin, G., Cohen, D., Sigaux, F. J. Exp. Med. (1987) [Pubmed]
  10. Inhibition of in vitro spontaneous apoptosis by IL-7 correlates with bcl-2 up-regulation, cortical/mature immunophenotype, and better early cytoreduction of childhood T-cell acute lymphoblastic leukemia. Karawajew, L., Ruppert, V., Wuchter, C., Kösser, A., Schrappe, M., Dörken, B., Ludwig, W.D. Blood (2000) [Pubmed]
  11. CD95 (APO-1/Fas) mutations in childhood T-lineage acute lymphoblastic leukemia. Beltinger, C., Kurz, E., Böhler, T., Schrappe, M., Ludwig, W.D., Debatin, K.M. Blood (1998) [Pubmed]
  12. In vitro susceptibility to dexamethasone- and doxorubicin-induced apoptotic cell death in context of maturation stage, responsiveness to interleukin 7, and early cytoreduction in vivo in childhood T-cell acute lymphoblastic leukemia. Wuchter, C., Ruppert, V., Schrappe, M., Dörken, B., Ludwig, W.D., Karawajew, L. Blood (2002) [Pubmed]
  13. The pattern of mutational involvement of RAS genes in human hematologic malignancies determined by DNA amplification and direct sequencing. Ahuja, H.G., Foti, A., Bar-Eli, M., Cline, M.J. Blood (1990) [Pubmed]
  14. Possible link between unique chemokine and homing receptor expression at diagnosis and relapse location in a patient with childhood T-ALL. Annels, N.E., Willemze, A.J., van der Velden, V.H., Faaij, C.M., van Wering, E., Sie-Go, D.M., Egeler, R.M., van Tol, M.J., Révész, T. Blood (2004) [Pubmed]
  15. A third tal-1 promoter is specifically used in human T cell leukemias. Bernard, O., Azogui, O., Lecointe, N., Mugneret, F., Berger, R., Larsen, C.J., Mathieu-Mahul, D. J. Exp. Med. (1992) [Pubmed]
  16. Site-specific recombination of the tal-1 gene is a common occurrence in human T cell leukemia. Brown, L., Cheng, J.T., Chen, Q., Siciliano, M.J., Crist, W., Buchanan, G., Baer, R. EMBO J. (1990) [Pubmed]
  17. TAL2, a helix-loop-helix gene activated by the (7;9)(q34;q32) translocation in human T-cell leukemia. Xia, Y., Brown, L., Yang, C.Y., Tsan, J.T., Siciliano, M.J., Espinosa, R., Le Beau, M.M., Baer, R.J. Proc. Natl. Acad. Sci. U.S.A. (1991) [Pubmed]
  18. Interleukin-7 promotes survival and cell cycle progression of T-cell acute lymphoblastic leukemia cells by down-regulating the cyclin-dependent kinase inhibitor p27(kip1). Barata, J.T., Cardoso, A.A., Nadler, L.M., Boussiotis, V.A. Blood (2001) [Pubmed]
  19. T cell receptor gamma and delta rearrangements in hematologic malignancies. Relationship to lymphoid differentiation. Griesinger, F., Greenberg, J.M., Kersey, J.H. J. Clin. Invest. (1989) [Pubmed]
  20. Detection of minimal residual disease identifies differences in treatment response between T-ALL and precursor B-ALL. Willemse, M.J., Seriu, T., Hettinger, K., d'Aniello, E., Hop, W.C., Panzer-Grümayer, E.R., Biondi, A., Schrappe, M., Kamps, W.A., Masera, G., Gadner, H., Riehm, H., Bartram, C.R., van Dongen, J.J. Blood (2002) [Pubmed]
  21. Intensive treatment of children with acute lymphoblastic leukemia according to ALL-BFM-86 without cranial radiotherapy: results of Dutch Childhood Leukemia Study Group Protocol ALL-7 (1988-1991). Kamps, W.A., Bökkerink, J.P., Hählen, K., Hermans, J., Riehm, H., Gadner, H., Schrappe, M., Slater, R., van den Berg-de Ruiter, E., Smets, L.A., de Vaan, G.A., Weening, R.S., van Weerden, J.F., van Wering, E.R., den der Does-van den Berg, A. Blood (1999) [Pubmed]
  22. Expression of MDR1 gene in acute leukemia cells: association with CD7+ acute myeloblastic leukemia/acute lymphoblastic leukemia. Miwa, H., Kita, K., Nishii, K., Morita, N., Takakura, N., Ohishi, K., Mahmud, N., Kageyama, S., Fukumoto, M., Shirakawa, S. Blood (1993) [Pubmed]
  23. Distinct DNase-I hypersensitive sites are associated with TAL-1 transcription in erythroid and T-cell lines. Leroy-Viard, K., Vinit, M.A., Lecointe, N., Mathieu-Mahul, D., Roméo, P.H. Blood (1994) [Pubmed]
  24. Cre/lox-regulated transgenic zebrafish model with conditional myc-induced T cell acute lymphoblastic leukemia. Langenau, D.M., Feng, H., Berghmans, S., Kanki, J.P., Kutok, J.L., Look, A.T. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  25. Maturation of acute T-lymphoblastic leukemia cells after CD2 ligation and subsequent treatment with interleukin-2. Mentz, F., Ouaaz, F., Michel, A., Blanc, C., Hervé, P., Bismuth, G., Debré, P., Merle-Béral, H., Mossalayi, M.D. Blood (1994) [Pubmed]
  26. IL-7-dependent human leukemia T-cell line as a valuable tool for drug discovery in T-ALL. Barata, J.T., Boussiotis, V.A., Yunes, J.A., Ferrando, A.A., Moreau, L.A., Veiga, J.P., Sallan, S.E., Look, A.T., Nadler, L.M., Cardoso, A.A. Blood (2004) [Pubmed]
  27. Frequent aberration of FHIT gene expression in acute leukemias. Iwai, T., Yokota, S., Nakao, M., Nakazawa, N., Taniwaki, M., Kimura, T., Sonoda, Y., Kaneko, H., Okuda, T., Azuma, H., Oka, T., Takeda, T., Watanabe, A., Kikuta, A., Asami, K., Sekine, I., Matsushita, T., Tsuchiya, T., Mimaya, J., Koizumi, S., Ohta, S., Miyake, M., Takaue, Y., Iwai, A., Fujimoto, T. Cancer Res. (1998) [Pubmed]
  28. Products of the TAL1 oncogene: basic helix-loop-helix proteins phosphorylated at serine residues. Cheng, J.T., Hsu, H.L., Hwang, L.Y., Baer, R. Oncogene (1993) [Pubmed]
  29. Reduced folate carrier gene expression in childhood acute lymphoblastic leukemia: relationship to immunophenotype and ploidy. Zhang, L., Taub, J.W., Williamson, M., Wong, S.C., Hukku, B., Pullen, J., Ravindranath, Y., Matherly, L.H. Clin. Cancer Res. (1998) [Pubmed]
  30. Relation between genetic variants of the ataxia telangiectasia-mutated (ATM) gene, drug resistance, clinical outcome and predisposition to childhood T-lineage acute lymphoblastic leukaemia. Meier, M., den Boer, M.L., Hall, A.G., Irving, J.A., Passier, M., Minto, L., van Wering, E.R., Janka-Schaub, G.E., Pieters, R. Leukemia (2005) [Pubmed]
  31. Therapy with OKT3 monoclonal antibody in refractory T cell acute lymphoblastic leukemia induces interleukin-2 responsiveness. Gramatzki, M., Burger, R., Strobel, G., Trautmann, U., Bartram, C.R., Helm, G., Horneff, G., Alsalameh, S., Jonker, M., Gebhart, E. Leukemia (1995) [Pubmed]
WikiGenes - Universities