The Cyclin-like Protein Spy1 Regulates Growth and Division Characteristics of the CD133+ Population in Human Glioma
Document Type
Article
Publication Date
2014
Publication Title
Cancer Cell
Volume
25
Issue
1
First Page
64
Last Page
76
Abstract
Summary The heterogeneity of brain cancers, as most solid tumors, complicates diagnosis and treatment. Identifying and targeting populations of cells driving tumorigenesis is a top priority for the cancer biology field. This is not a trivial task; considerable variance exists in the driving mutations, identifying markers, and evolutionary pressures influencing initiating cells in different individual tumors. Despite this, the ability to self-renew and differentiate must be conserved to reseed a heterogeneous tumor mass. Focusing on one example of a tumor-initiating cell population, we demonstrate that the atypical cyclin-like protein Spy1 plays a role in balancing the division properties of glioma cells with stemness properties. This mechanistic insight may provide new opportunities for therapeutic intervention of brain cancer.
DOI
10.1016/j.ccr.2013.12.006
Recommended Citation
Lubanska, Dorota; Market-Velker, Brenna A.; deCarvalho, Ana C.; Mikkelsen, Tom; Fidalgo da Silva, Elizabeth; and Porter, Lisa A., "The Cyclin-like Protein Spy1 Regulates Growth and Division Characteristics of the CD133+ Population in Human Glioma" (2014). Cancer Cell, 25, 1, 64-76.
https://scholar.uwindsor.ca/biologypub/786
