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Rabinowits, Guilherme

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Rabinowits

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Guilherme

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Rabinowits, Guilherme
Author's Publications: search.filters.isAuthorOfPublication.6cd7a125-36db-41bb-95ba-92f17cbc71c7

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    Systemic Therapy for Merkel Cell Carcinoma: What’s on the Horizon?
    (MDPI, 2014) Rabinowits, Guilherme
    Merkel cell carcinoma is an aggressive neuroendocrine skin cancer that usually affects elderly patients. Despite being uncommon, incidence has been steadily increasing over the last two decades, likely due to increased awareness, better diagnostic methods and aging of the population. It is currently one of the most lethal cutaneous malignancies, with a five-year overall survival of approximately 50%. With the better understanding of the molecular pathways that lead to the development of Merkel cell carcinoma, there has been an increasing excitement and optimism surrounding novel targeted therapies, in particular to immunotherapy. Some of the concepts surrounding the novel targeted therapies and currently ongoing clinical trials are reviewed here.
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    Merkel Cell Polyomavirus Exhibits Dominant Control of the Tumor Genome and Transcriptome in Virus-Associated Merkel Cell Carcinoma
    (American Society for Microbiology, 2017) Starrett, Gabriel J.; Marcelus, Christina; Cantalupo, Paul G.; Katz, Joshua P.; Cheng, Jingwei; Akagi, Keiko; Thakuria, Manisha; Rabinowits, Guilherme; Wang, Linda C.; Symer, David E.; Pipas, James M.; Harris, Reuben S.; DeCaprio, James
    ABSTRACT Merkel cell polyomavirus is the primary etiological agent of the aggressive skin cancer Merkel cell carcinoma (MCC). Recent studies have revealed that UV radiation is the primary mechanism for somatic mutagenesis in nonviral forms of MCC. Here, we analyze the whole transcriptomes and genomes of primary MCC tumors. Our study reveals that virus-associated tumors have minimally altered genomes compared to non-virus-associated tumors, which are dominated by UV-mediated mutations. Although virus-associated tumors contain relatively small mutation burdens, they exhibit a distinct mutation signature with observable transcriptionally biased kataegic events. In addition, viral integration sites overlap focal genome amplifications in virus-associated tumors, suggesting a potential mechanism for these events. Collectively, our studies indicate that Merkel cell polyomavirus is capable of hijacking cellular processes and driving tumorigenesis to the same severity as tens of thousands of somatic genome alterations.