Oncogenic FGFR Fusions Produce Centrosome and Cilia Defects by Ectopic Signaling
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985904%3A_____%2F21%3A00544015" target="_blank" >RIV/67985904:_____/21:00544015 - isvavai.cz</a>
Alternative codes found
RIV/00159816:_____/21:00075127 RIV/00216224:14110/21:00122060
Result on the web
<a href="https://www.mdpi.com/2073-4409/10/6/1445" target="_blank" >https://www.mdpi.com/2073-4409/10/6/1445</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3390/cells10061445" target="_blank" >10.3390/cells10061445</a>
Alternative languages
Result language
angličtina
Original language name
Oncogenic FGFR Fusions Produce Centrosome and Cilia Defects by Ectopic Signaling
Original language description
A single primary cilium projects from most vertebrate cells to guide cell fate decisions. A growing list of signaling molecules is found to function through cilia and control ciliogenesis, including the fibroblast growth factor receptors (FGFR). Aberrant FGFR activity produces abnormal cilia with deregulated signaling, which contributes to pathogenesis of the FGFR-mediated genetic disorders. FGFR lesions are also found in cancer, raising a possibility of cilia involvement in the neoplastic transformation and tumor progression. Here, we focus on FGFR gene fusions, and discuss the possible mechanisms by which they function as oncogenic drivers. We show that a substantial portion of the FGFR fusion partners are proteins associated with the centrosome cycle, including organization of the mitotic spindle and ciliogenesis. The functions of centrosome proteins are often lost with the gene fusion, leading to haploinsufficiency that induces cilia loss and deregulated cell division. We speculate that this complements the ectopic FGFR activity and drives the FGFR fusion cancers.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
10603 - Genetics and heredity (medical genetics to be 3)
Result continuities
Project
Result was created during the realization of more than one project. More information in the Projects tab.
Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2021
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Cells
ISSN
2073-4409
e-ISSN
2073-4409
Volume of the periodical
10
Issue of the periodical within the volume
6
Country of publishing house
CH - SWITZERLAND
Number of pages
25
Pages from-to
1445
UT code for WoS article
000667840600001
EID of the result in the Scopus database
2-s2.0-85110309511