Introduction Trastuzumab emtansine is an antibody-drug conjugate targeting the human epidermal growth factor receptor 2 use in recurrent metastatic breast cancer. Cases of trastuzumab emtansine-induced nodular regenerative hyperplasia are often reported as overt noncirrhotic portal hypertension with ascites and variceal bleeding. Case report We report the case of a 61-year-old woman who present multiple stellate angiomas with gradual increased liver transaminases and reduced platelet count during a 27-months course on trastuzumab emtansine therapy for recurrent metastatic breast cancer. After the nodular regenerative hyperplasia was histologically confirmed, the trastuzumab emtansine was stopped. After two months, trastuzumab was restarted together with exemestane. During trastuzumab therapy, the patient had a normalization of liver transaminases, platelet count and a gradual improvement of her stellate angiomas. Trastuzumab was continued for 15 months without any reoccurrence of nodular regenerative hyperplasia. Management and outcome Nodular regenerative hyperplasia should be suspected after one year of trastuzumab emtansine treatment in patients with signs of portal hypertension without cirrhosis. Definitive cessation of trastuzumab emtansine is required after a diagnosis of nodular regenerative hyperplasia and complete resolution of symptoms generally takes several months. Discussion Based on fundamental studies, nodular regenerative hyperplasia is probably caused by the emtansine (DM1) part of the trastuzumab emtansine. It is still unclear if trastuzumab therapy can be reintroduced after nodular regenerative hyperplasia induced by trastuzumab emtansine, depriving the patient of a HER2-targeted therapy. Only one case reported having given trastuzumab in this situation over one month. In our case, trastuzumab was reintroduced without any complications for a long extent following TDM1-associated nodular regenerative hyperplasia.

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In this study, we evaluated the presence of early and late Human Papillomavirus (HPV) proteins in retinoblastoma Brazilian patients. For this, 8 formalin-fixed paraffin-embedded retinoblastoma tissue blocks were used. HPV DNA presence was determined by in situ hybridization (ISH). Immunohistochemistry were performed to verify HPV16/18 E6, E1^E4, and L1 proteins. HPV was detected in all retinoblastoma tumors and viral DNA was labeled in tumor cells, retinal layers and optical nerve structures. In addition, E1^E4, E6 and L1 proteins were detected in all samples in the same areas where HPV DNA was detected. Our data showed the presence and expression of early and late HPV proteins in retinoblastoma tumors from Brazilian children. However, further studies should be performed to clarify the role of HPV infection in retinoblastoma tumor.