ECP 2022 Abstract Book

Virchows Archiv (2022) 481 (Suppl 1):S1–S364 13 association between the markers and clinicopathological param- eters, including TSR, was evaluated. Results: Immunostaining of podoplanin was detected in CCs and CAFs, with positivity of 36.8% and 70%, respectively. Higher positivity of podoplanin in CCs was observed predominantly at TSR area: 64.3% of cases. Status podoplanin CAFs+ was higher in the desmoplasic region (71.6%). Stroma-high tumours showed increased expression of podoplanin in CCs and CAFs in compari- son with stroma-low tumours. The status of podoplanin in CCs was observed in association with women (p=0.042), angiolym- phatic involvement (p=0.021; p=0.047) and distant metastasis (p=0.014). Conclusion: In the CCR microenvironment, CAFs and CCs express podoplanin. Our research found an increase in podoplanin expression in high stromal tumours, known to be more aggressive than low stromal tumours, and an association with angioinvasion and distant metastasis. The expression of this marker, in CRA stratified by tumour-stroma ratio, contributes to aggressive behaviour. It may represent a patient stratification tool, in the prediction of possible outcomes. PS-07-002 IgG4 as a biomarker for inflammatory bowel disease D. Raduta*, S. Zurac, M. Busca, R. Ardeleanu, A. Vilaia, A. Din- culescu, M. Filip, L. Cristina, C. Popp *Colentina Clinical Hospital, Romania Background & objectives: Inflammatory bowel disease (IBD) is a non-specific inflammatory condition affecting the gastrointestinal tract. The pathogenesis of IBD is insufficiently understood, but a key role is attributed to immune dysregulation. Our objective was to approach the IgG4 contribution to mucosal injury. Methods: We conducted a case-control study comprising 12 patients with IBD with different stages of disease activity (remis- sion, mild, moderate, severe), and we focused our research on immunohistochemical identification and quantification of IgG4+ plasma cells found in lamina propria. The infiltration of IgG4+ plasma cells in patients with IBD was compared with plasma cells level of 12 healthy control individuals. Results: Patients with IBD had higher intestinal mucosal IgG4 counts than normal colonic mucosa (over 10 times more plasma cells IgG4+ in IBD per 10 HPF). Cases of ulcerative colitis (UC) showed higher numbers of IgG4+ plasma cells in lamina propria, compared to patients with Crohn disease (CD) for the same stage of activity. Mucosal infiltration of IgG4+ plasmocytes in active disease was higher comparative to remission stage of disease, as it follows: 5 IgG4+ per 10 HPF when CD is remitted and up to 25 IgG4+ in severely active CD, in contrast to 13 IgG4+ in remitted UC which goes up to 33-41 IgG4+ in moderately to severely active UC. Conclusion: Our study led to the following conclusions: The potential pathogenic involvement of B cell lineage in the pathogenesis of IBD deserves further research and in-depth stud- ies, as it may contribute to personalized therapy. PS-07-003 MMR proteins and PD-L1 status: impact on gastric adenocar- cinoma’s prognosis F. Sassi*, R. Jouini, F. Khanchel, I. Helal, R. Hedhli, H. Zaafouri, M. Sabbah, E. Ben Brahim, A. Chadli Debbiche *Department of Pathology, Charles Nicolle Hospital Tunis, Tunisia Background & objectives: Deficient MMR proteins and PD-L1 expression have been shown to be prognostic factors[H1] and predictive biomarkers for anti-PD-1 immunotherapy in gastric adenocarcinoma(GA). We aimed to assess the expression of MMR proteins and PD-L1 in GA with clinicopathological features and survival. Methods: This was a retrospective and descriptive study including 143 GA diagnosed at the Department of Pathology of Habib Thameur hospital (2001-2018). Evaluation of MMR proteins and PD-L1 status was carried out by immunohistochemistry. The combined positive score (CPS) was calculated for PD-L1 with a threshold of 1. Results: The frequency of deficient MMR proteins (dMMR) GA was 30.1%. There was no significant association, in uni- variate and multivariate analysis, between MMR proteins and clinicopathological parameters. dMMR GA were PD-L1+ in 24%. The frequency of PD-L1+ GA was 21.7%. Medullary histological subtype according to World Health Organisation classification (p<0.001), intestinal subtype according to Lauren classification (p=0.014), lymphoid stroma reaction (p=0.004) were predictors of PD-L1+ status. Median survival was 16 and 18 months for patients with dMMR and PD-L1+ GA, respec- tively, with no significant association. PD-L1- status was asso- ciated with a poor prognosis. Conclusion: One third of patients with GA have dMMR status. PD-L1- status is a factor of poor prognosis. Prognostic value of dMMR status should be investigated in a larger series. PS-07-004 Pathomorphological and molecular genetic features of serrated colorectal lesions L. Mikhaleva*, R. Vandysheva, N. Shakhpazyan, A. Biryukov, M. Guschin *A.P. Avtsyn Research Institute of Human Morphology, Russia Background & objectives: Morphological diagnosis of serrated neoplasms today is based on the identification of a specific struc- ture of formations in histological preparations. Therefore, the aim of our study was to identify molecular and biological fea- tures of serrated colorectal lesions (CSL). Methods: We studied 481 cases of CSL (GP - 238, SSL - 201, and TSA – 42), st ained wit h H&E and PAS-AB. For molecular-biological analysis, 69 observations of CSL were selected: SSL - 26, GP - 26, TSA - 17. The immu- noh i st o ch emi c a l p a n e l i n c l ud e d : CK20 , Ki 67 , MUC2 , MUC5AC , MUC6 , MLH1 , PMS 2 , MSH2 a n d MSH6 . KRAS/BRAF/NRAS gene mutations were determined by real-time PCR. Results: CSL show immunophenotypic signs of both colorectal dif- ferentiation (expressed expression of more than 50% of all cells of the markers MUC2 and CK20) and gastric differentiation (appearance of MUC5AC and MUC6 expression, focal positive PAS-AB staining). MUC6 expression is characteristic only for SSL. The malignisation pathway of SSL was associated with the presence of a BRAF gene mutation (53.8%) and high grade microsatellite instability (34.8%), while that of TSA was associated with a KRAS gene mutation (47.1%) and MSI-H (40%). The KRAS (15.4%), BRAF (38.5%) and MSI (60%) gene mutations detected in HP confirm their role in serrated carcino- genesis. The NRAS gene mutation was not detected in serrated colo- rectal lesions. Conclusion: CSL show immunophenotypic signs of both colorec- tal differentiation and gastric differentiation. The malignisation pathway of CSL was associated with the presence of a BRAF gene mutation and MSI-H. Genetic mutations found in hyperplastic pol- yps, in combination with immunophenotype confirm their role in serrated carcinogenesis S91