2007
DOI: 10.1182/blood-2007-01-066076
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Flt3-dependent transformation by inactivating c-Cbl mutations in AML

Abstract: IntroductionReceptor tyrosine kinases (RTKs) bind extracellular growth factors and activate intracellular signaling networks. The magnitude and kinetics of RTKs activation are tightly regulated, since they determine the quality and extent of the biologic response. 1 Attenuation of RTK signaling occurs by endocytosis and subsequent protein degradation. [2][3][4] Cbl proteins have been shown to be central players in these processes. [5][6][7] The members of the Cbl family, c-Cbl, Cbl-b, and Cbl-3, contain an N-t… Show more

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Cited by 187 publications
(232 citation statements)
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“…The prevalence and clinical significance of these mutations in AML remains to be determined. 102,103 Mutations that impair myeloid differentiation…”
Section: Ptpn11mentioning
confidence: 99%
“…The prevalence and clinical significance of these mutations in AML remains to be determined. 102,103 Mutations that impair myeloid differentiation…”
Section: Ptpn11mentioning
confidence: 99%
“…In the past few years, several groups have reported mutations of the CBL gene in a subset of patients with myeloid neoplasms (4)(5)(6)(7)(8)(9)(10)(11)(12)(13). A large proportion of CBL mutations is associated with myelodysplastic syndrome/myeloproliferative disorder (MDS/ MPD), a heterogeneous group of hematopoietic malignancies characterized by deregulated hematopoiesis and a high propensity to develop acute myeloid leukemia (AML).…”
mentioning
confidence: 99%
“…Recently, CBL has been identified as a frequent target of gain-of-function mutations in several myeloid neoplasias, including juvenile and chronic myelomonocytic leukemias (JMML and CMML), AML, myelodysplastic syndromes and myeloproliferative neoplasms (Caligiuri et al, 2007;Sargin et al, 2007;Dunbar et al, 2008;Grand et al, 2009;Loh et al, 2009;Makishima et al, 2009;Reindl et al, 2009;Sanada et al, 2009). Mutations between the TKB and ring-finger domains, associated with acquired 11q uniparental disomy (Dunbar et al, 2008;Grand et al, 2009;Makishima et al, 2009;Sanada et al, 2009), lead to a loss of the E3 ligase activity (Sargin et al, 2007). Even though these mutations require the expression of a functional RTK for factor-independent growth (Sargin et al, 2007;Grand et al, 2009), it is not known whether a loss of E3 activity is sufficient for this phenotype.…”
Section: Gain-of-function Mutations In Cblmentioning
confidence: 99%
“…Mutations between the TKB and ring-finger domains, associated with acquired 11q uniparental disomy (Dunbar et al, 2008;Grand et al, 2009;Makishima et al, 2009;Sanada et al, 2009), lead to a loss of the E3 ligase activity (Sargin et al, 2007). Even though these mutations require the expression of a functional RTK for factor-independent growth (Sargin et al, 2007;Grand et al, 2009), it is not known whether a loss of E3 activity is sufficient for this phenotype. In this context, it should be noted that mice with CBL gene disruption are not known to be associated with ligand-independent RTK activation (Murphy et al, 1998;Naramura et al, 1998).…”
Section: Gain-of-function Mutations In Cblmentioning
confidence: 99%