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Ojala Lab

Contact Information:

Päivi Ojala

Biomedicum Helsinki, B530b2
PO Box 63 (Haartmaninkatu 8)
FI-00014 University of Helsinki

Tel. +358 9 191 25548
Fax. +358 9 191 25554

e-mail :

Viral tumorigenesis group

The group is a member in the new Centre of Excellence for Translational
Genome-Scale Biology
and in the EU-funded INCA Project "The role of chronic infections in the development of cancer".

About the research

KSHV infection is the causative agent in three different tumor types; Kaposi’s sarcoma (KS), a plasmablastic variant of multicentric Castelman’s disease and an AIDS-related form of B cell lymphoproliferative disorder called primary effusion lymphoma (PEL). While the mechanisms involved in the pathogenesis are not fully understood, it is intriguing that the KSHV genome contains several potential oncogenes pirated from the human genome. All tumor cells are latently infected by KSHV and express latent genes such as viral cyclin (v-cyclin), vFLIP, the latent nuclear antigen (LANA-1), and the viral interferon regulatory factor 3 (vIRF3). Interestingly, KSHV was recently identified to also encode for 12 viral micro-RNAs (miRNAs), most of them during the latency

The association of KSHV with a human neoplasm and the large number of cellular counterparts in the KSHV genome make it of tremendous interest to determine which of its genes are contributing to its pathogenicity, and which pathways are activated in the host cell upon KSHV tumorigenesis. The goal of the research group is to provide tools for targeted therapy studies and translate novel findings to potential clinical applications. To this end we study the in vivo function of KSHV latent gene products by several molecular biology, cell biology and biochemical techniques, use functional genomics to screen for cellular factors involved in viral reactivation and KSHV-induced cell transformation, generate novel animal models to mimic human endothelium originating KS and identify molecules specific for this human neoplasm. Deciphering the pathways leading to viral oncogenesis will help in the development of novel, highly selective treatment modalities for virus-induced cancers.

Our recent studies have demonstrated mechanisms how KSHV evades inhibition by CDK inhibitors in naturally infected lymphoma cells as wells as findings on the first effective treatment for currently incurable KSHV- lymphoma in mouse models . We have also recently demonstrated that DNA damage checkpoint response functions as an anti-cancer barrier in this virally induced cancer. More recently our studies have revealed novel cellular regulators for reactivation of KSHV from the latency.

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