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MeSH Review

Leukemia, Lymphocytic, Acute, L1

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Disease relevance of Leukemia, Lymphocytic, Acute, L1


High impact information on Leukemia, Lymphocytic, Acute, L1

  • Mutations in one gene, connexin 26 (CX26GJB2), are responsible for most cases of recessive non-syndromic deafness, accounting for 30-40% of all childhood genetic deafness in some populations (eg, white people of western European descent) [6].
  • Whatever the cause, in childhood ALL variable formation of intracellular mercaptopurine metabolites seems to be clinically important [7].
  • These results indicate that genetically determined TPMT activity may be a substantial regulator of the cytotoxic effect of 6-MP, an effect which in turn could be important in influencing the outcome of therapy for childhood ALL [8].
  • 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 [9].
  • In conclusion, our data support the hypothesis that the leukemia in TEL/AML1-positive childhood ALL originates in a CD19+ lymphoid progenitor [10].

Chemical compound and disease context of Leukemia, Lymphocytic, Acute, L1

  • CONCLUSION: These results clearly demonstrate a therapeutic systemic effect of low doses of IT MTX in childhood ALL, and response to prephase therapy should not be considered as an in vivo test for cortico-sensitivity only [11].
  • Improving outcome through two decades in childhood ALL in the Nordic countries: the impact of high-dose methotrexate in the reduction of CNS irradiation. Nordic Society of Pediatric Haematology and Oncology (NOPHO) [12].
  • We conclude that high VCP expression is associated with poor prednisone response in childhood ALL patients.Leukemia (2006) 20, 820-826. doi:10.1038/sj.leu.2404162; published online 16 March 2006 [13].
  • In conclusion, resistance to DNR in childhood ALL can not be explained by decreased levels of Topo II alpha gene expression, but additional Topo II activity studies in fresh leukemia samples may need further exploration [14].
  • In conclusion, PNA positivity, especially frequent in T cell ALL, is a marker for a subgroup of childhood ALL patients who are very likely to respond well to systemic PRD 'monotherapy'. In addition, PNA positivity is a favorable prognostic factor in T cell ALL [15].

Biological context of Leukemia, Lymphocytic, Acute, L1


Anatomical context of Leukemia, Lymphocytic, Acute, L1

  • To address this assumption and to investigate the prognostic significance of TEL-AML1 expression in relapsed childhood ALL, bone marrow samples of 146 children were analyzed by reverse-transcriptase (RT)-polymerase chain reaction (PCR) [21].
  • To address the significance of beta-tubulin and MAP4 alterations in childhood ALL, two CCRF-CEM-derived Vinca alkaloid resistant cell lines, VCR R (vincristine) and VLB100 (vinblastine), were examined [22].

Gene context of Leukemia, Lymphocytic, Acute, L1

  • We therefore conclude that the presence of a homozygous p16 deletion may well be an important risk factor for both relapse and death in childhood ALL, and that its prognostic effect is not a consequence of confounding by other factors already known to influence outcome in this disease [23].
  • To identify new partner breakpoints for ETV6 and CBFA2, we selected 30 patients with childhood ALL in whose leukemic cells a t(12;21) had been detected by RT-PCR [24].
  • Expression of LRP, but not of P-gp and MRP, significantly correlated with DNR resistance in childhood ALL (Rs 0. 33, P = 0.03) [25].
  • We recommend the use of the above mentioned fixation methods in order to study the clinical relevance of P-gp, MRP and LRP in childhood ALL [26].
  • These findings suggest that GSTP1 variants (alone or combined with other GSTs) represent significant genetic determinants of childhood ALL [27].

Analytical, diagnostic and therapeutic context of Leukemia, Lymphocytic, Acute, L1


  1. Expression of interleukin-10 splicing variants is a positive prognostic feature in relapsed childhood acute lymphoblastic leukemia. Wu, S., Gessner, R., Taube, T., von Stackelberg, A., Henze, G., Seeger, K. J. Clin. Oncol. (2005) [Pubmed]
  2. ETV6 is the target of chromosome 12p deletions in t(12;21) childhood acute lymphocytic leukemia. Cavé, H., Cacheux, V., Raynaud, S., Brunie, G., Bakkus, M., Cochaux, P., Preudhomme, C., Laï, J.L., Vilmer, E., Grandchamp, B. Leukemia (1997) [Pubmed]
  3. Influence of two different Escherichia coli asparaginase preparations on fibrinolytic proteins in childhood ALL. Nowak-Göttl, U., Werber, G., Ziemann, D., Ahlke, E., Boos, J. Haematologica (1996) [Pubmed]
  4. FLT3 inhibitors: a paradigm for the development of targeted therapeutics for paediatric cancer. Brown, P., Small, D. Eur. J. Cancer (2004) [Pubmed]
  5. The prevalence and incidence of convulsive disorders in children. Hauser, W.A. Epilepsia (1994) [Pubmed]
  6. Advances in hereditary deafness. Tekin, M., Arnos, K.S., Pandya, A. Lancet (2001) [Pubmed]
  7. Mercaptopurine metabolism and risk of relapse in childhood lymphoblastic leukaemia. Lilleyman, J.S., Lennard, L. Lancet (1994) [Pubmed]
  8. Genetic variation in response to 6-mercaptopurine for childhood acute lymphoblastic leukaemia. Lennard, L., Lilleyman, J.S., Van Loon, J., Weinshilboum, R.M. Lancet (1990) [Pubmed]
  9. 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]
  10. Immature CD34+CD19- progenitor/stem cells in TEL/AML1-positive acute lymphoblastic leukemia are genetically and functionally normal. Hotfilder, M., Röttgers, S., Rosemann, A., Jürgens, H., Harbott, J., Vormoor, J. Blood (2002) [Pubmed]
  11. Systemic effect of intrathecal methotrexate during the initial phase of treatment of childhood acute lymphoblastic leukemia. The European Organization for Research and Treatment of Cancer Children's Leukemia Cooperative Group. Thyss, A., Suciu, S., Bertrand, Y., Mazingue, F., Robert, A., Vilmer, E., Mechinaud, F., Benoit, Y., Brock, P., Ferster, A., Lutz, P., Boutard, P., Marguerite, G., Plouvier, E., Michel, G., Plantaz, D., Munzer, M., Rialland, X., Chantraine, J.M., Norton, L., Solbu, G., Philippe, N., Otten, J. J. Clin. Oncol. (1997) [Pubmed]
  12. Improving outcome through two decades in childhood ALL in the Nordic countries: the impact of high-dose methotrexate in the reduction of CNS irradiation. Nordic Society of Pediatric Haematology and Oncology (NOPHO). Gustafsson, G., Schmiegelow, K., Forestier, E., Clausen, N., Glomstein, A., Jonmundsson, G., Mellander, L., Mäkipernaa, A., Nygaard, R., Saarinen-Pihkala, U.M. Leukemia (2000) [Pubmed]
  13. Unsupervised proteome analysis of human leukaemia cells identifies the Valosin-containing protein as a putative marker for glucocorticoid resistance. Lauten, M., Schrauder, A., Kardinal, C., Harbott, J., Welte, K., Schlegelberger, B., Schrappe, M., von Neuhoff, N. Leukemia (2006) [Pubmed]
  14. Topoisomerase II alpha gene expression in childhood acute lymphoblastic leukemia. Klumper, E., Giaccone, G., Pieters, R., Broekema, G., van Ark-Otte, J., van Wering, E.R., Kaspers, G.J., Veerman, A.J. Leukemia (1995) [Pubmed]
  15. Prognostic significance of peanut agglutinin binding in childhood acute lymphoblastic leukemia. Kaspers, G.J., Veerman, A.J., Van Wering, E.R., Van Der Linden-Schrever, B.E., Van Zantwijk, C.H., Van Der Does-Van Den Berg, A., Pieters, R. Leukemia (1996) [Pubmed]
  16. Rearrangement of the MLL gene confers a poor prognosis in childhood acute lymphoblastic leukemia, regardless of presenting age. Behm, F.G., Raimondi, S.C., Frestedt, J.L., Liu, Q., Crist, W.M., Downing, J.R., Rivera, G.K., Kersey, J.H., Pui, C.H. Blood (1996) [Pubmed]
  17. Frequent loss of heterozygosity at the TEL gene locus in acute lymphoblastic leukemia of childhood. Stegmaier, K., Pendse, S., Barker, G.F., Bray-Ward, P., Ward, D.C., Montgomery, K.T., Krauter, K.S., Reynolds, C., Sklar, J., Donnelly, M. Blood (1995) [Pubmed]
  18. Clinical relevance of BCL-2 overexpression in childhood acute lymphoblastic leukemia. Coustan-Smith, E., Kitanaka, A., Pui, C.H., McNinch, L., Evans, W.E., Raimondi, S.C., Behm, F.G., Aricò, M., Campana, D. Blood (1996) [Pubmed]
  19. Mutations of the E2F4 gene in hematological malignancies having microsatellite instability. Komatsu, N., Takeuchi, S., Ikezoe, T., Tasaka, T., Hatta, Y., Machida, H., Williamson, I.K., Bartram, C.R., Koeffler, H.P., Taguchi, H. Blood (2000) [Pubmed]
  20. Molecular quantification of response to therapy and remission status in TEL-AML1-positive childhood ALL by real-time reverse transcription polymerase chain reaction. Seeger, K., Kreuzer, K.A., Lass, U., Taube, T., Buchwald, D., Eckert, C., Körner, G., Schmidt, C.A., Henze, G. Cancer Res. (2001) [Pubmed]
  21. TEL-AML1 fusion transcript in relapsed childhood acute lymphoblastic leukemia. The Berlin-Frankfurt-Münster Study Group. Seeger, K., Adams, H.P., Buchwald, D., Beyermann, B., Kremens, B., Niemeyer, C., Ritter, J., Schwabe, D., Harms, D., Schrappe, M., Henze, G. Blood (1998) [Pubmed]
  22. Multiple microtubule alterations are associated with Vinca alkaloid resistance in human leukemia cells. Kavallaris, M., Tait, A.S., Walsh, B.J., He, L., Horwitz, S.B., Norris, M.D., Haber, M. Cancer Res. (2001) [Pubmed]
  23. Homozygous deletion of the p16/MTS1 gene in pediatric acute lymphoblastic leukemia is associated with unfavorable clinical outcome. Kees, U.R., Burton, P.R., Lü, C., Baker, D.L. Blood (1997) [Pubmed]
  24. Novel cryptic, complex rearrangements involving ETV6-CBFA2 (TEL-AML1) genes identified by fluorescence in situ hybridization in pediatric patients with acute lymphoblastic leukemia. Mathew, S., Shurtleff, S.A., Raimondi, S.C. Genes Chromosomes Cancer (2001) [Pubmed]
  25. Relationship between the intracellular daunorubicin concentration, expression of major vault protein/lung resistance protein and resistance to anthracyclines in childhood acute lymphoblastic leukemia. Den Boer, M.L., Pieters, R., Kazemier, K.M., Janka-Schaub, G.E., Henze, G., Veerman, A.J. Leukemia (1999) [Pubmed]
  26. Optimal immunocytochemical and flow cytometric detection of P-gp, MRP and LRP in childhood acute lymphoblastic leukemia. Den Boer, M.L., Zwaan, C.M., Pieters, R., Kazemier, K.M., Rottier, M.M., Flens, M.J., Scheper, R.J., Veerman, A.J. Leukemia (1997) [Pubmed]
  27. Glutathione S-transferase P1 genetic polymorphisms and susceptibility to childhood acute lymphoblastic leukaemia. Krajinovic, M., Labuda, D., Sinnett, D. Pharmacogenetics (2002) [Pubmed]
  28. Altered expression of p53 and mdm-2 proteins at diagnosis is associated with early treatment failure in childhood acute lymphoblastic leukemia. Marks, D.I., Kurz, B.W., Link, M.P., Ng, E., Shuster, J.J., Lauer, S.J., Carroll, D., Brodsky, I., Haines, D.S. J. Clin. Oncol. (1997) [Pubmed]
  29. Incidence and relevance of secondary chromosome abnormalities in childhood TEL/AML1+ acute lymphoblastic leukemia: an interphase FISH analysis. Attarbaschi, A., Mann, G., König, M., Dworzak, M.N., Trebo, M.M., Mühlegger, N., Gadner, H., Haas, O.A. Leukemia (2004) [Pubmed]
  30. The management of adult acute lymphoblastic leukaemia. Woodruff, R. Cancer Treat. Rev. (1978) [Pubmed]
  31. Remission induction therapy for childhood acute lymphoblastic leukaemia: clinical and cellular pharmacology of vincristine, corticosteroids, L-asparaginase and anthracyclines. Ronghe, M., Burke, G.A., Lowis, S.P., Estlin, E.J. Cancer Treat. Rev. (2001) [Pubmed]
  32. Matched-pair analysis comparing allogeneic PBPCT and BMT from HLA-identical relatives in childhood acute lymphoblastic leukemia. Vicent, M.G., Madero, L., Ortega, J.J., Martinez, A., Gomez, P., Verdeguer, A., Badell, I., Muñoz, A., Olive, T., Maldonado, M.S., Bureo, E., Cubells, J., Diaz, M.A. Bone Marrow Transplant. (2002) [Pubmed]
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