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Quelle: Fontanari Krause 2006 Seite(n): 22, 23, Zeilen: 22: 13-19 - 23: 1-6 |
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| [The fusion protein critical for the development of the chronic myelo-]monocytic leukemia is the ETV6/PDGFRB fusion and not the reciprocal PDGFRB/ETV6 fusion. In the ETV6/PDGFRB fusion protein the N terminal portion of ETV6, which includes the pointed domain, is fused to the C-terminal two thirds of the PDGFRB protein, conserving the tyrosine kinase domain of PDGFRB. The fusion of the pointed domain of ETV6 in the N-terminal half with the tyrosine kinase domain in the C-terminal half of the fusion partner is characteristic of the class of ETV6/PTK fusions and is found in the fusions of ETV6 with ABL1, ABL2, JAK2, NTRK3, FGFR3 and SYK (Fig. 11) (Table 2) (Papadopoulos et. al., 1995; Cazzaniga et. al., 1999; Knezevich et. al., 1998; Kuno et. al., 2001; Peeters et. al., 1997)
Table2. Tyrosine kinase fusion partners of ETV6
1.6.4 Transcription factors and other fusion partners of ETV6 The ETV6/RUNX1 (ETV6/AML1) fusion is the most common fusion gene in childhood acute B cell lymphoblastic leukemia (Shurtleff et. al., 1995). Cazzaniga, G., Tosi, S., Aloisi, A., Giudici, G., Daniotti, M., Pioltelli, P., Kearney, L., and Biondi, A. (1999). The tyrosine kinase abl-related gene ARG is fused to ETV6 in an AML-M4Eo patient with a t(1;12)(q25;p13): molecular cloning of both reciprocal transcripts. Blood 94, 4370- 4373. Knezevich, S. R., McFadden, D. E., Tao, W., Lim, J. F., and Sorensen, P. H. (1998). A novel ETV6-NTRK3 gene fusion in congenital fibrosarcoma. Nat Genet 18, 184-187. Kuno, Y., Abe, A., Emi, N., Iida, M., Yokozawa, T., Towatari, M., Tanimoto, M., and Saito, H. (2001). Constitutive kinase activation of the TEL-Syk fusion gene in myelodysplastic syndrome with t(9;12)(q22;p12). Blood 97, 1050-1055. Papadopoulos, P., Ridge, S. A., Boucher, C. A., Stocking, C., and Wiedemann, L. M. (1995). The novel activation of ABL by fusion to an ets-related gene, TEL. Cancer Res 55, 34-38. Peeters, P., Raynaud, S. D., Cools, J., Wlodarska, I., Grosgeorge, J., Philip, P., Monpoux, F., Van Rompaey, L., Baens, M., Van den Berghe, H., and Marynen, P. (1997a). Fusion of TEL, the ETS-variant gene 6 (ETV6), to the receptor-associated kinase JAK2 as a result of t(9;12) in a lymphoid and t(9;15;12) in a myeloid leukemia. Blood 90, 2535- 2540. Peeters, P., Wlodarska, I., Baens, M., Criel, A., Selleslag, D., Hagemeijer, A., Van den Berghe, H., and Marynen, P. (1997b). Fusion of ETV6 to MDS1/EVI1 as a result of t(3;12)(q26;p13) in myeloproliferative disorders. Cancer Res 57, 564-569. Shurtleff, S. A., Buijs, A., Behm, F. G., Rubnitz, J. E., Raimondi, S. C., Hancock, M. L., Chan, G. C., Pui, C. H., Grosveld, G., and Downing, J. R. (1995). TEL/AML1 fusion resulting from a cryptic t(12;21) is the most common genetic lesion in pediatric ALL and defines a subgroup of patients with an excellent prognosis. Leukemia 9, 1985-1989. |
The fusion protein critical for the development of the chronic myelomonocytic leukemia is the ETV6/PDGFRB fusion, and not the reciprocal PDGFRB/ETV6 fusion. In the ETV6/PDGFRB fusion protein the N terminal portion of ETV6, which includes the pointed domain, is fused to the C-terminal two thirds of the PDGFRB protein, conserving the tyrosine kinase domain of PDGFRB. The fusion of the pointed domain of ETV6 in the N-terminal half with the tyrosine kinase domain in the C-terminal half of the fusion partner is characteristic of the class of ETV6/PTK fusions
[page 23] and is found in the fusions of ETV6 with ABL1, ABL2, JAK2, NTRK3, FGFR3 and SYK (Table 4.2 adapted from Bohlander, 2005) (Papadopoulos, 1995; Cazzaniga, 1999; Kuno, 2001). Table 4.2: Protein tyrosine kinase fusion partner of ETV6
4.3.4. Transcription factors and other fusion partners of ETV6 The ETV6/RUNX1 (ETV6/AML1) fusion is the most common fusion gene in childhood acute B cell lymphoblastic leukemia (Shurtleff, 1995). Bohlander S. K. (2005). ETV6: A versatile player in leukemogenesis. Semin Cancer Biol. 15 (3), 162-74. Cazzaniga G., Tosi S., Aloisi A., et al. (1999). The tyrosine kinase abl-related gene ARG is fused to EYV6 in an AML-M4Eo patient with a t(1;12)(q25;p13): molecular cloning of both reciprocal transcripts. Blood. 94, 4370-73. Kuno Y., Abe a., Emi N., Iida M., Yokozawa t., towatari M., et al. (2001). Constitutive kinase activation of the TEL-Syk fusion gene in myelodysplastic syndrome with t(9;12)(q22;p12). Blood. 97, 1050-5. Papadopoulos P., Rigde S. A., Boucher C. A., Stocking C., Wiedemann L. M. (1995). The novel activation of ABL by fusion to an ets-related gene, TEL. Cancer Res. 55 (1), 34-8. Shurtleff S. A., Buijs A., Behm F. G., Rubnitz J. E., Raimondi S. C., Hancock M. L., Chan G. C., Pui C. H., Grosveld G., Downing J. R. (1995).TEL/AML1 fusion resulting from a cryptic t(12;21) is the most common genetic lesion in pediatric ALL and defines a subgroup of patients with an excellent. Leukemia. 9 (12), 1985-9. |
The source is not mentioned here. Note that the table in the source Fontanari Krause (2006) has the same columns as Vpr but a different order of the columns. The original source Bohlander (2005) has the same column order as Fontanari Krause (2006), but two additional columns that appear neither in Vpr nor in Fontanari Krause (2006). This can be interpreted as indication that Vpr copied from Fontanari Krause (2006) who copied from Bohlander (2005). Note that there are two publicationen "Peeters et. al., 1997" in the bibliography. Note also that Vpr is closer to Fontanari Krause (2006) than to Bohlander (2005), see Vpr/Dublette/Fragment_022_01. However, Vpr includes two references: Knezevich et al. (1998) and Peeters et al. (1997) that also Bohlander (2005) mentions, but Fontanari Krause (2006) does not. |
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