ECP 2023 Abstracts

S230 Virchows Archiv (2023) 483 (Suppl 1):S1–S391 13 its good response to local radiotherapy. Recognizing these lesions is important as it will save patients from unnecessary surgery. E-PS-07-044 Should we process all gallbladder specimens? An analysis of poten- tial clues to a diagnosis of incidental carcinoma C. Scicluna*, L. McElroy, F. Roberts, V. Gough, G. Kohnen *Department of Histopathology, Queen Elizabeth University Hospital, United Kingdom Background & objectives: Gallbladder cancer is rare and often first diagnosed in the cholecystectomy specimen. The aim of this study to identify any criteria that are suggestive of carcinoma to reduce process- ing of these specimens, which average £42,000 per year at QEUH. Methods: Gallbladder specimen report data at QEUH between May 2012 and September 2022 was split by outcomes (benign vs malignant), and correlated to specimen structural integrity, presence of gallstones and age at surgery. Cases with clinical suspicion of cancer or with suspicious findings at macroscopic examination were excluded. Cases with outcomes of only dysplasia were considered with the benign cases. Results: Out of 16,788 eligible reports, 16,756 had benign outcomes and 32 had malignant outcomes. The median age for benign outcomes was 50 (range 15 – 93), whereas for malignant outcomes it was 71 (range 51 – 84). Out of a total of 10,165 benign intact specimens, 8,803 had gallstones. Out of a total of 6,581 benign fragmented specimens, 5,119 had gallstones. Results from the malignant specimens revealed that 5 specimens were intact with gallstones, 3 specimens were intact without gallstones, 15 specimens were fragmented with gallstones and 5 specimens were frag- mented without gallstones. 30 of the malignant cases were of adeno- carcinoma with 2 were of adenosquamous carcinoma. Conclusion: Fragmented specimens with gallstones were more likely to harbour incidental carcinoma, however, no single feature completely predicted or excluded the presence of cancer. The lower age limit for malignancy was 51, a consideration could be made for not process- ing specimens from patients under the age of 45 as the likelihood of diagnosing incidental carcinoma is extremely unlikely. Therefore, a more selective approach to specimen selection would reduce yearly processing by 37% and save up to £15,500 per year. E-PS-07-045 Combined loss of numb and p53 promotes glycogen cumulative hepatomegaly and hepatocarcinogenesis Y. Shu*, Y. Shi *Department of Pathology & Institute of clinical Pathology, West China Hospital, Sichuan University, Chengdu, China Background & objectives: Hepatocyte glycogen accumulation always leads to hepatomegaly, and it has recently been reported to drive liver tumour initiation. Our previous study suggested that Numb may play an important role in glycogen metabolism, which requires further exploration. Methods: Glycogen accumulation index and glucose metabolism related pathways were measured in liver-specific Numb deletion mice(Numb−/−) by PAS staining and RNA-seq respectively. p53 can regulate cancer glycogen metabolism, and it has a complex reciprocal regulatory mechanism with Numb. Therefore, we constructed liver- specific Numb&p53 double deletion mice to investigate the effect of Numb&p53 on glycogen accumulation induced liver cancer. Results: RNA-seq analysis demonstrated that differential genes are significantly enriched in glucose metabolism related pathways in Numb−/− liver. PAS and HE staining revealed slight glycogen accumu- lation and hepatocellular hypertrophy in Numb−/− liver at 12 months. In Numb&p53−/− liver, significant hepatomegaly developed at 7 months accompanied by severe hepatocyte glycogen accumulation and hepatocyte hypertrophy. Further, tumour nodules could be observed in part of the 9-month-old Numb&p53−/− liver. After 6 months of DEN induction, tumours with a significant number and large size developed in all Numb&p53−/− mice liver but not in WT mice, which predicted that Numb and p53 double deletion could induce glycogen accumula- tion hepatomegaly and promote the development of HCC. Conclusion: In this study, we demonstrated the critical role of Numb- p53 on glycogen metabolism in the liver. We found that Numb-p53 deletion cause glycogen accumulation and induces hepatomegaly, and further promote hepatocarcinogenesis. E-PS-07-046 Porto-sinusoidal vascular disorder in patients with Turner’s syndrome E. Stoupi*, I. Grypari, S. Siasiakou, E. Stravodimou, K. Syrigos, D. Tiniakos *Department of Pathology, Aretaieion Hospital, Medical School, National and Kapodistrian University of Athens, Greece Background & objectives: The novel term porto-sinusoidal vascular disorder (PSVD) describes vascular liver diseases affecting the (peri) portal venules and sinusoids in the absence of cirrhosis. PSVD is fre- quently associated with various underlying conditions. We present two cases of PSVD in Turner’s syndrome. Methods: Case 1: An 18-year-old female with Turner’s syndrome phenotype (awaiting genetic confirmation), presented with elevated aminotransferase levels and an increased platelet count without other significant clinical findings. Case 2: A 30-year-old female with mosaic-Τurner’s syndrome, pre- sented with persistently elevated serum liver enzymes without other significant clinical findings. An adequately-sized needle liver biopsy was performed in both cases. Results: On histology, both cases had similar morphology. The liver parenchyma showed foci of regenerative hyperplasia (reticulin stain) and mild non-zonal sinusoidal dilatation. Abnormal periportal vessels, portal venule herniation and/or slit-like portal venules were noted in few portal tracts, while rare others were hypervascularised. Masson trichrome stain highlighted mild portal fibrosis and delicate sinusoidal fibrosis. The above histological findings were consistent with PSVD. The main features of PSVD include the absence of cirrhosis docu- mented in a liver biopsy and the detection of specific or non-specific histological findings, including those described above, with or without portal hypertension. Mild zone 3 steatosis and mild portal inflammation were additionally observed in Case 2. Conclusion: Turner’s syndrome has been linked το various liver abnor- malities but only few cases with PSVD have been described. Liver biopsy is required for PSVD diagnosis. Microcirculatory disturbances in addi- tion to immunological dysregulation, which both occur in patients with Turner’s syndrome, may be the driving force in the pathogenesis of PSVD in these cases. We highlight the importance of the assessment of vascular changes in liver biopsies from patients with known or suspected Turner’s syndrome and unexplained abnormal liver function tests. E-PS-07-047 Primary mixed adenoneuroendocrine carcinoma (MANEC) of the gallbladder and synchronous renal cell carcinoma of the right kid- ney. A co-existence never described before H. Trihia*, G.M. Stanc, E. Kontis, K. Stefanidis, E. Souka, M. Paraskevaides *Pathology Department Metaxa Cancer Hospital, Greece Background & objectives: Mixed adenoneuroendocrine carcinomas (MANEC) rarely arise in the gallbladder (GB-MANEC). The simulta- neous diagnosis of renal cell carcinoma (RCC) with a gastrointestinal malignancy, is a rare, well documented phenomenon. The coexistence of GB-MANEC and RCC, has never been described before. Methods: A 63-year-old woman was investigated for an MRI-detected 8cm liver mass and a coexistent 3,5cm tumour of the right kidney. She