In our clinical institute of pathology, tumor sections are processed from the capsule, every 1–2 cm of tumor tissue and from tumor regions, which appear different on gross inspection. However, our immunohistochemical analyses were done on selected slides from one block per patient that represented the main tumor component with a very homogenous histology.
Formaldehyde-fixed and paraffin embedded human specimens of all patients (n = 95) with TETs were available for immunohistochemical stainings. Staining was performed by using the automated Ventana Benchmark® platform (Ventana Medical Systems, Tucson, AZ, USA) according to standard protocol of the Clinical Institute of Pathology46 (link). We used monoclonal rabbit anti-human Anti-Activin A Receptor Type IB antibody (ab204655, Abcam, Cambridge, UK) and monoclonal mouse anti-human Follistatin antibody IgG2a (MAB669, R&D Systems, Minneapolis, MN, USA) as primary antibodies to assess Activin A and Follistatin expression in TETs. In addition, we used monoclonal mouse anti-human CD34 antibody (LEICA, NovoCastra, Clone QBEnd/10, Nussloch, Germany) to assess microvascular density.
Formaldehyde-fixed and paraffin embedded human specimens of all patients (n = 95) with TETs were available for immunohistochemical stainings. Staining was performed by using the automated Ventana Benchmark® platform (Ventana Medical Systems, Tucson, AZ, USA) according to standard protocol of the Clinical Institute of Pathology46 (link). We used monoclonal rabbit anti-human Anti-Activin A Receptor Type IB antibody (ab204655, Abcam, Cambridge, UK) and monoclonal mouse anti-human Follistatin antibody IgG2a (MAB669, R&D Systems, Minneapolis, MN, USA) as primary antibodies to assess Activin A and Follistatin expression in TETs. In addition, we used monoclonal mouse anti-human CD34 antibody (LEICA, NovoCastra, Clone QBEnd/10, Nussloch, Germany) to assess microvascular density.
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