↓ Figure 1. Histopathologic and immunophenotypic features of classical Hodgkin lymphoma in dyskeratosis congenita: (a) Low-power view of lymph node architecture (H&E, × 5) showing partial effacement by nodular proliferation. (b) Higher-power field (H&E, × 20) demonstrating scattered large, atypical Hodgkin/Reed–Sternberg cells with prominent nucleoli in an inflammatory background rich in small lymphocytes and eosinophils. (c) CD30 shows strong membranous and paranuclear positivity in the large, atypical cells (× 10). (d) CD15 highlights the same large, atypical cells with cytoplasmic/membranous staining (× 10). (e) PAX5 demonstrates weak nuclear staining in the neoplastic cells with strong positivity in background B cells (× 10). (f) CD20 shows loss of expression in the Hodgkin cells (× 10). (g) EBER in situ hybridization reveals nuclear positivity within Hodgkin cells (× 10). (h) Ki-67 immunostaining shows a high proliferative index within the atypical cells and peripheral reactive germinal centers (× 10). H&E: hematoxylin and eosin; PAX5: paired box 5; EBER: Epstein-Barr virus-encoded small RNAs.

↓ Figure 2. Pre-BV-AVD imaging. Pre-BV-AVD FDG positron emission tomography-computed tomography (PET-CT) maximum intensity projection (axial and coronal, left) and transverse section (right) demonstrating an intensely FDG-avid left retropectoral lymph node conglomerate (indicated by arrows). BV-AVD: brentuximab vedotin, adriamycin, vinblastine, and dacarbazine; FDG: fluorodeoxyglucose.

↓ Figure 3. Post-BV-AVD imaging. Post-BV-AVD FDG positron emission tomography-computed tomography (PET-CT) maximum intensity projection (axial and coronal, left) and transverse section (right) showing interval reduction in nodal size and FDG uptake (indicated by arrows). BV-AVD: brentuximab vedotin, adriamycin, vinblastine, and dacarbazine; FDG: fluorodeoxyglucose.
