ECP 2023 Abstracts

S289 Virchows Archiv (2023) 483 (Suppl 1):S1–S391 13 *Department of Pathology, University of Turku and Turku University Hospital, Finland Background & objectives: Our aim was to study the immunohisto- chemical (IHC) staining patterns of p53 in head and heck squamous cell carcinomas (HNSCC) and compare p53 IHC staining patterns to TP53 mutation status and p16 IHC staining. Methods: We stained 31 HNSCCs (22 oropharynx, six larynx/ hypopharynx, three other sites) by IHC for p53 and p16, and performed next-generation sequencing (FoundationOne©CDx) on all cases. p53 IHC patterns were assessed as described in SCCs: wildtype, and abnormal patterns: overexpression, null and cytoplasmic staining. p53 wildtype staining patterns in p16+ tumours were assessed separately. p53 IHC was compared to TP53 status. Results: Of the 31 tumours, 18 showed abnormal p53 expression (11 parabasal/diffuse overexpression, seven null) and had a TP53 muta- tion. 10 tumours showed p16 positivity without TP53 mutations. Of the remaining cases, two were p53 wildtype but had a TP53 mutation (one p16 positive, one p16 negative) and one was p53 wildtype and p16 negative. One p53 overexpressing tumour showed p16 positivity and was originally assigned as p16 positive. Of the ten p16 positive cases nine showed p53 wildtype IHC staining patterns described in HPV-associated SCCs; four showed single positive cells i.e. “null- like” pattern or single positive clusters and five showed basal sparing pattern of which two had only scattered positivity. Conclusion: There is excellent correlation between p53 abnormal IHC staining and the presence of a TP53 mutation. Although p53 abnormal pattern and p16 positivity are almost mutually exclusive, mutations in TP53 can occasionally be associated with p16 positivity and lead to misclassification as p16 positive HNSCC. p16 positivity is often associated with wildtype p53 patterns that can mimic abnormal p53 staining. In conclusion, performing p16 and p53 together improves the accurate interpretation of both stainings. E-PS-12-029 Primary PNET/Ewing’s sarcoma of trachea in an adolescent girl – case report M. Jikurashvili*, R. Davitashvili *CSD-Georgia, Georgia Background & objectives: PNET/Ewing’s sarcoma is a malignant small round blue cell tumour found mostly in bone and soft tissue of the extremities and the axial skeleton. The involvement of the trachea has rarely been reported. Methods: We present a case of a 12 year old female patient who presented with a stridor and pneumonia signs. Bronchoscopy revealed intraluminal movable polypoid round mass attached to the wall of trachea clinically thought to be an adenoma. The mass was excised en toto and delivered for routine pathologic examination at our laboratory. Results: H&E sections showed a wall of trachea with a tumour com- posed of atypical small round blue cells infiltrated within a myxoid stroma having a focal necrosis. One could easily notice pseudovascu- lar/pseudocystic spaces too. Mitotic figures were numerous. Surface epithelium was focally ulcerated but not connected to the tumour. Immunohistochemistry revealed positive CD99, NSE, CD56 and Vimentin positivity. Mitotic index of Ki67 was around 30%. Other markers like S100, desmin, sma, p63, synaptophysin, chromogranin A, TTF1, CD34, CKs, CD45, OCT3/4 were negative. The results obtained were consistent with the diagnosis of PNET. The recom- mendation to confirm the pathology with further molecular studies was given. FISH analysis reported EWSR1-FLI1 fusion. Conclusion: Ewing sarcoma of the trachea is a rare entity, especially in the paediatric age group. The diagnostic challenge lies in differenti- ating it from other location-specific tumours. Extensive immunostain- ing and FISH confirm the diagnosis. The therapeutic approach requires a combination of surgical resection, followed by chemotherapy and radiotherapy to achieve disease-free survival. Presently newer modalities of targeted immunotherapy against EWSR1-FLI1 chimeric fusion transcript are being explored. E-PS-12-030 PDL1 and p16 immunohistochemical expression in oral squamous cell carcinoma J. Kini*, N. Prasad, H. Kini *Kasturba Medical College, Mangalore, Manipal Academy of Higher education, Manipal, India Background & objectives: Programmed cell death ligand 1 (PD-L1) is an immune checkpoint molecule that weakens the host response against tumours. The aim of this study was to evaluate PDL-1 and p16 expres- sion by immunohistochemistry in oral squamous cell carcinoma (OSCC) Methods: A retrospective study was conducted including all resected specimens of OSCC received in the Pathology department over a three year period. Clinical and morphological features were correlated with immunohistochemical expression of PD-L1 and p16. PD-L1 staining was quantified by percentage of tumour positive cells and PD-L1 posi- tive inflammatory cells assessed by tumour proportion score (TPS) and combined positive score (CPS). Results: Of a total of 101 resected cases of OSCC, paraffin blocks with tumour were available for 94 cases. p16 expression was seen in 5.3% of the cases. Increased expression of PD-L1 was found in 38.3% cases. The tumour proportion score (TPS) (p value= 0.019) and combined positive score (CPS) (p value=0.009) were significantly associated with PDL1 staining intensity. Nearly one third of well, moderately and poorly differentiated OSCC were positive for PDL-1. Marked lym- phocytic response was present in 53% of the positive PDL1 cases. A highly significant association was seen between CPS, TPS and lympho- vascular invasion (p value = 0.005) and TPS with perineural invasion (p value = 0.030). Conclusion: PD-L1 expression was seen in nearly two- fifths of the cases of OSCC. There was no significant association between PD-L1 and p16 expression. Intensity of p16 expression was significantly associated with tumour thickness, nodal status and eosinophilic host response. Perineural and lymphovascular invasion were seen to be sig- nificantly associated with PDL1 expression, indicating an aggressive nature of these tumours. E-PS-12-031 A case of renal cell–like sinonasal adenocarcinoma: rare entity A. Kret*, M. Pankhania, A. Al-Omari *Histopathology Department, Sheffield Teaching Hospitals NHS Trust, United Kingdom Background & objectives: A 84-year-old male presented with epistaxis. He was found to have a mass primarily in the left sinonasal cav- ity with radiological evidence of infiltration into the anterior skull base. Methods: The lesional tissue was excised in piecemeal. Histological assessment demonstrated nasal mucosa largely infiltrated by a neoplasm showing a predominant clear cell morphology arranged in cohesive lobules and sheets. The lesional cells were monomorphous and cuboidal in nature, lacking mitotic activity, necrosis, lympho-vascular and perineural invasion. Results: Immunohistochemistry demonstrated expression of AE1/3, SOX10, CK7, Vimentin, PAS positive and diastase resistant. The CK20, p63, TTF1, Synaptophysin, S100, CD10, AMACR, DOG1, RCC, PAX8, SMA, CD56, HMB45, and TFE3 were not expressed. The diagnosis of Renal cell–like sinonasal adenocarcinoma (RCLSA) was made. RCLSA is a rare entity and it is one of the variants of non- intestinal type sinonasal adenocarcinoma which arises in nasal cavity, paranasal sinuses and nasopharynx.