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. 2021 Aug 3;13(8):1536. doi: 10.3390/v13081536

Figure 1.

Figure 1

Clinical presentation and histology of primary and metastatic OPSCC. (A) A positron-emission tomography (PET) scan of Case 1 at the time of initial diagnosis, showing the primary tumor and spread to local lymph nodes. (B) A magnetic resonance imaging (MRI) scan was taken 16 months later, showing a right parietal mass in the brain. (C) A PET scan of Case 2 at the time of initial diagnosis, showing the neck mass and local spread to lymph nodes. (D) An MRI was taken 33 months later, showing a metastatic tumor in the left centrum. (E–P) Serial tissue sections from Case 1 (E,F,I,J,M,N) and Case 2 (G,H,K,L,O,P) were used for immunohistochemistry (IHC) and in situ hybridization analysis. (E–H) Primary and metastatic brain tumors were stained with hematoxylin and eosin. (I–L) Adjacent sections were assayed for p16INK4a protein expression by IHC. All tumors displayed high levels of nuclear and cytoplasmic staining of p16INK4a, a hallmark of HPV+ tumors. (M–P) Tumors were assayed for HPV16 and HPV18 RNA using the RNAscope HPV16/18 probe set. The presence of HPV RNA is evident in both initial (M,O) and metastatic brain tumors (N,P). This pattern directly matches the pattern of p16INK4a overexpression from the adjacent slides. L = left side, R = right side, A = anterior, P = posterior. Scale bar = 50 μm.