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Genetically-Induced Aberrant Chromatin States in Prostate Cancer – Biology and Therapy

People

 

Theurillat J. P.

(Responsible)

Abstract

Mutations in genes encoding epigenetic regulators have been observed to promote hematologic and pediatric malignancies by preventing terminal differentiation. Accumulating evidence suggests a similar role for mutation of epigenetic regulators in solid tumors. In prostate cancer, we discovered a genetically defined subclass of tumors characterized by point-mutations in SPOP (speckle-type POZ protein, a substrate-binding subunit of an E3 ubiquitin ligase) and deletions in CHD1 (chromodomain helicase DNA binding protein 1). These alterations conceivably alter chromatin-related biological processes such as cell differentiation and genomic stability. However, the precise roles these mutated genes play in tumorigenesis, and any therapeutic implications, remain elusive. This proposal aims (i) to establish disease-relevant cell culture models for SPOP and CHD1-mutated tumors in order to (ii) study the biological function of these newly discovered mutations and (iii) to design therapeutic strategies for this new subtype of prostate cancer.

Additional information

Start date
01.09.2014
End date
31.08.2018
Duration
48 Months
Funding sources
SNSF
Status
Ended
Category
Swiss National Science Foundation / SNSF Professorships