Dr Giulia de Falco
Reader in Pathology and Molecular Clinical Microbiology, Nanchang Joint Programme
Email: email@example.comTelephone: +44 (0)20 7882 3206Room Number: Room 3.12, Fogg Building
Molecular mechanisms of viral-associated malignant transformation
I am interested in the mechanisms used by viruses to drive malignant transformation, with a particular attention to the viral molecular mimicry. My research of last years has been focused on investigating the role of HIV and Epstein-Barr (EBV) in B-cell lymphomagenesis, being both viruses often associated with B-cell tumors.
The results of this research show that both viruses have a direct involvement in cancer, due to viral-encoded genes and/or microRNAs. I have investigated the role of HIV in contributing to transformation focusing on its major transactivator, the Tat protein. My findings show that Tat is able to dysregulate the cell cycle by binding to the RB family of proteins, forcing even uninfected B-cells towards an uncontrolled cell proliferation. Tat is also able to dysregulate the expression of cellular genes and microRNAs and to induce the aberrant over-expression of DNA methyltransferases, resulting in an unbalanced epigenetic control of gene expression in HIV-positive tumors.
In respect with EBV, I have investigated the differences existing between EBV-positive and –negative B-cell tumors in terms of gene and microRNA expression, to understand at which extent the virus interferes with the host cell gene expression. By using next-generation sequencing platforms I have observed the expression pattern of EBV-encoded products and then demonstrated that viral-encoded genes and microRNAs (viRNAs) interfere with the host cell gene expression. In particular, the viral pattern of gene and viRNA expression depends on EBV latency program, which is therefore able to influence host cell gene expression profile. As EBV expresses a different latency program in different B-cell tumor types, the expression pattern of the virus may critically contribute to the development of a distinct B-cell tumor.
Future goals will be to further investigate the complex interplay existing between viruses and host cells, which may lead to malignant transformation.
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