as PR-like eruptions may have peripheral eosinophilia, interface dermatitis and eosinophils on histopathology, with no evidence of HHV-6 and HHV-7 systemic reactivation. 3 Our cases had overlapping features of both PR and PR-like eruptions.COVID-19 has been associated with cases of PR and PRlike eruptions following the acute infection. 6,7 Skin biopsies may demonstrate positivity for the SARS-CoV-2 virus spike protein on endothelial cells and lymphocytes suggesting a direct relationship between SARS-CoV-2 infection and PR. 7 SARS-CoV-2 may also trigger PR by reactivation of HHV-6 or HHV-7. 5 PR eruptions have developed following vaccination for influenza and H1N1 8-10 and may be secondary to reactivation of HHV-6 and HHV-7, which may be detected in skin biopsies via in situ hybridization and immunohistochemistry. 9 Another possible cause for PR in the setting of vaccination is a T-cell-mediated response triggered by molecular mimicry from a viral epitope. 8 Given worldwide vaccination efforts against COVID-19 with mRNA vaccines, it is important for doctors and patients to recognize possible adverse events including PR. Further study is required to confirm the causative link, including direct examination of tissue and serological studies for evidence of HHV-6 and HHV-7 reactivation.
In epithelial ovarian cancer (EOC), response to platinum (PT)-based chemotherapy dictates subsequent treatments and predicts patients' prognosis. Alternative splicing is often deregulated in human cancers and can be altered by chemotherapy. Whether and how changes in alternative splicing regulation could impact on the response of EOC to PT-based chemotherapy is still not clarified. We identified the splicing factor proline and glutamine rich (SFPQ) as a critical mediator of response to PT in an unbiased functional genomic screening in EOC cells and, using a large cohort of primary and recurrent EOC samples, we observed that it is frequently overexpressed in recurrent PT-treated samples and that its overexpression correlates with PT resistance. At mechanistic level, we show that, under PT treatment, SFPQ, in complex with p54 nrb , binds and regulates the activity of the splicing factor SRSF2. SFPQ/p54 nrb complex decreases SRSF2 binding to caspase-9 RNA, favoring the expression of its alternative spliced antiapoptotic form. As a consequence, SFPQ/p54 nrb protects cells from PTinduced death, eventually contributing to chemoresistance. Overall, our work unveils a previously unreported SFPQ/p54 nrb / SRSF2 pathway that in EOC cells plays a central role in regulating alternative splicing and PT-induced apoptosis and that could result in the design of new possible ways of intervention to overcome PT resistance.
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