Pauline Hascoet, Franck Chesnel, Cathy Le Goff, Xavier Le Goff, Yannick Arlot-Bonnemains
Abstract
Human tumors exhibit a variety of genetic alterations, including point mutations, translocations, gene amplifications and deletions, as well as aneuploid chromosome numbers. For carcinomas, aneuploidy is associated with poor patient outcome for a large variety of tumor types, including breast, colon, and renal cell carcinoma. The Renal cell carcinoma (RCC) is a heterogeneous carcinoma consisting of different histologic types. The clear renal cell carcinoma (ccRCC) is the most common subtype and represents 85% of the RCC. Central to the biology of the ccRCC is the loss of function of the Von Hippel-Lindau gene, but is also associated with genetic instability that could be caused by abrogation of the cell cycle mitotic spindle checkpoint and may involve the Aurora kinases, which regulate centrosome maturation. Aneuploidy can also result from the loss of cell-cell adhesion and apical-basal cell polarity that also may be regulated by the mitotic kinases (polo-like kinase 1, casein kinase 2, doublecortin-like kinase 1, and Aurora kinases). In this review, we describe the "non-mitotic" unconventional functions of these kinases in renal tumorigenesis.
Pharmacology, Toxicology and Pharmaceutical Science
2
9%
Nursing and Health Professions
1
5%
Other
0
0%
Unknown
4
18%
Attention Score in Context
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 27 October 2015.
All research outputs
#21,110,894
of 25,932,719 outputs
Outputs from Frontiers in oncology
#11,578
of 22,839 outputs
Outputs of similar age
#217,749
of 296,276 outputs
Outputs of similar age from Frontiers in oncology
#49
of 77 outputs
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