ECP 2023 Abstracts

S391 Virchows Archiv (2023) 483 (Suppl 1):S1–S391 13 Methods: Characterization of patients subgroups (AML, age ≤/> 65 years- S1, S2; low BCL- Ann Arbor I-II tumoral stages-S1, high stage BCL- Ann Arbor III-IV tumoral stages-S2; match control healthy patients- C1; C2), CD4+, CD3+ T lymphocytes, platelet membrane glycoproteins (CD42b, CD61), and platelets derived microparticles (CD61-PMP) bio- markers from blood samples were performed by flow cytometry methods. Results: An intravascular platelets activation in AML patients was observed by increased CD61-PMP expressions than controls (S1- 63.97±0.88 vs. C1-34.96±0.82; S2-72.11±0.32 vs. C2-29.26±1.23; p<0.01). CD4+ and CD3+ lymphocytes biomarkers presented differ- ences in AML patients (S1-71.32±1.09 vs. C1-67.05±0.76; S2-64.94 ±0.88 vs. C2-59.92 ±1.33; S1-76.53 ±0.73 vs. C1-71.78±0.91; S2-69.17 ±0.35 vs. C2-58.53 ±1.80; p<0.01). Platelet activation in low-stage BCL patients manifests increased expressions of CD61, CD42 b glyco- proteins, and CD4+ lymphocytes reported to controls (S1-51.99±2.65 vs. C1-33.35±2.84; S1-60.74±3.62 vs. C1-48.66±0.76; p<0.01; S1-71.26±1.32 vs. C1-66.92±0.72, p< 0.05). High-stage BCL had lower values for CD-biomarkers reported to controls (CD61-S2-17.61±1.16 vs. C2-28.87±2.09; CD4+-S2-59.45±1.33 vs. C2-67.00±0.94; CD42b-S2-16.60±1.24 vs. C2-49.65±0.65; CD3+-S2-49.29±8.36 vs C2-72.02±1.76; CD 61 PMP-S2-9.30±0.60 vs. C2-35.16±0.81; p<0.01). Conclusion: Platelet–leukocyte interactions in AML and BCL patients may prove to be a useful tool in different diseases, as biomarkers by flow cytometry. Platelet microparticles show promise as a diagnostic bio- marker for diseases and potentially as a delivery system for therapeutics. E-PS-26-002 Biological mechanisms involved in the prostatic tumorigenesis by flow cytometry methods E. Matei*, M. Aschie, A. Mitroi, M. Deacu, G.I. Baltatescu, A.A. Nico- lau, L.A. Tuta, I.C. Iorga, M. Enciu *1 Center for Research and Development of the Morphological and Genetic Studies of Malignant Pathology, “Ovidius” University of Constanţa, Romania Background & objectives: Prostate intratumoral heterogeneity, driven by epithelial-mesenchymal plasticity, contributes to the limited treat- ment response and therefore is necessary to use the biomarkers to improve patient prognostic survival. Methods: Characterization of patients groups (prostate adenocarci- noma –PCa; benign prostatic hyperplasia-BPH; controls for experimen- tal groups using non-malignant adjacent tissue samples recovered from patients with PCa or BPH (controls, C), and biological mechanisms studies as cell cycle, cell proliferation by adhesion glycoproteins, and cell apoptosis involved in the evolution of the prostate tumour process were performed by flow cytometry methods. Results: Proliferative activity (S-phase) revealed lower values of prostate adenocarcinoma (PCa) and benign prostatic hyperpla- sia (BPH) reported at non-malignant adjacent cell samples (PCa- 4.32±4.91; BPH-2.35±1.37 vs. C-10.23±0.43, p<0.01). 68% of BPH cases and 88% of patients with PCa had aneuploidy. Increased values of cell proliferation (CD34+CD61+) were observed in pros- tate adenocarcinoma and hyperplasia cases reported to non-malig- nant adjacent cell samples (PCa-28.79±10.14; BPH-40.65±11.88 vs. C-16.15±2.58, p<0.05). CD42b+ cell population with a role in cell adhesion and metastasis had an increased value in PCa cases (38.39±11.23) reported to controls (C-26.24±0.62, p<0.01). The intratumoral expression of CD34 showed an increased pattern of PCa tissue samples reported to controls (PCa-26.12±6.84 vs. C-1.50±0.70, p<0.01). Conclusion: Flow cytometric analysis of cell cycle, apoptosis, and cell proliferation by adhesion glycoproteins, recommend as efficient methods in diagnostic and therapeutic targets for adenocarcinoma and hyperplasia prostate patients and should be explored in the future for others maligned affections. Publisher’s note  Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.