The t(8;17)(p11;q23) in the 8p11 myeloproliferative syndrome fuses MYO18A to FGFR1

Walz, Christoph; Chase, Andrew; Schoch, Claudia; Weisser, A.; Schlegel, Frank; Hochhaus, Andreas; Fuchs, Roland J.; Schmitt-Gräff, A.; Hehlmann, Rüdiger; Cross, Nicholas C. P.; Reiter, Andreas

doi:10.1038/sj.leu.2403712

Cited by 76 publications

(54 citation statements)

References 23 publications

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“…26 MYO18B, encoded by a paralogue of MYO18A, is found at the centrosome. 21 Moreover, we have found that MYO18A interacts with CEP1 (L Daviet and D Birnbaum, unpublished).…”

Section: How Many Mpds Are Centrosomal Diseases?mentioning

confidence: 99%

Myeloproliferative disorders: the centrosome connection

2005

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Some myeloproliferative disorders (MPD) result from a reciprocal translocation that involves the FGFR1 gene and a partner gene. The event creates a chimeric gene that encodes a fusion protein with constitutive FGFR1 tyrosine kinase activity. FGFR1-MPD is a rare disease, but its study may provide interesting clues on different processes such as cell signalling, oncogenesis and stem cell renewal. Some partners of FGFR1 are centrosomal proteins. The corresponding oncogenic fusion kinases are targeted to the centrosome. Constitutive phosphorylation at this site may perturbate centrosome function and the cell cycle. Direct attack at this small organelle may be an efficient way for oncogenes to alter regulation of signalling for proliferation and survival and get rid of checkpoints in cell cycle progression. The same effect might be triggered by other fusion kinases in other MPD and non-MPD malignancies.

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“…26 MYO18B, encoded by a paralogue of MYO18A, is found at the centrosome. 21 Moreover, we have found that MYO18A interacts with CEP1 (L Daviet and D Birnbaum, unpublished).…”

Section: How Many Mpds Are Centrosomal Diseases?mentioning

confidence: 99%

Myeloproliferative disorders: the centrosome connection

2005

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“…[37][38][39][40] Additional fusion partners for FGFR1, including BCR, have since been described (Table 5). [41][42][43][44][45][46][47] The FGFR1 rearrangement can be found in both myeloid and lymphoid cells, suggesting an origin in a multipotent hematopoietic progenitor, and thus the basis for the disease's alternate designation of 'stem cell leukemia/ lymphoma syndrome.' EMS manifests an aggressive course and therefore early allogeneic transplantation is often recommended.…”

Section: Terminology and Classificationmentioning

confidence: 99%

Five years since the discovery of FIP1L1–PDGFRA: what we have learned about the fusion and other molecularly defined eosinophilias

Gotlib¹,

2008

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“…3,6 Markedly, many of the translocation partner proteins identified to date are localized to the centrosome, a cell organelle, which contributes to cell-cycle control and organizes the mitotic spindle apparatus. [7][8][9][10][11][12][13][14][15][16][17][18] As the primary microtubule organizing center of most eukaryotic cells, the centrosome ensures symmetry and bipolarity of the cell division process, a function that is essential for accurate chromosome segregation. 19 Furthermore, cell-cycle progression into mitosis is initiated and controlled by cell-cycle regulatory proteins localized to the centrosome.…”

Section: Introductionmentioning

confidence: 99%

Centrosomal targeting of tyrosine kinase activity does not enhance oncogenicity in chronic myeloproliferative disorders

et al. 2011

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Constitutive tyrosine kinase activation by reciprocal chromosomal translocation is a common pathogenetic mechanism in chronic myeloproliferative disorders. Since centrosomal proteins have been recurrently identified as translocation partners of tyrosine kinases FGFR1, JAK2, PDGFRa and PDGFRb in these diseases, a role for the centrosome in oncogenic transformation has been hypothesized. In this study, we addressed the functional role of centrosomally targeted tyrosine kinase activity. First, centrosomal localization was not routinely found for all chimeric fusion proteins tested. Second, targeting of tyrosine kinases to the centrosome by creating artificial chimeric fusion kinases with the centrosomal targeting domain of AKAP450 failed to enhance the oncogenic transforming potential in both Ba/F3 and U2OS cells, although phospho-tyrosine-mediated signal transduction pathways were initiated at the centrosome. We conclude that the centrosomal localization of constitutively activated tyrosine kinases does not contribute to disease pathogenesis in chronic myeloproliferative disorders.

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The t(8;17)(p11;q23) in the 8p11 myeloproliferative syndrome fuses MYO18A to FGFR1

Cited by 76 publications

References 23 publications

Myeloproliferative disorders: the centrosome connection

Myeloproliferative disorders: the centrosome connection

Five years since the discovery of FIP1L1–PDGFRA: what we have learned about the fusion and other molecularly defined eosinophilias

Centrosomal targeting of tyrosine kinase activity does not enhance oncogenicity in chronic myeloproliferative disorders

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