Abstract
Aim: Fibrosis is observed both in pancreatic cancer (PDAC) and chronic pancreatitis (CP). The main cells involved in fibrosis are pancreatic stellate cells (PSCs), which activate alpha smooth muscle actin (αSMA), which is considered to be the best-known fibrosis marker. The aim of the study was to evaluate the expression of the αSMA in patients with PDAC and CP as the possible differentiation marker. Methods: We enrolled 114 patients undergoing pancreatic resection: 83 with PDAC and 31 with CP. Normal fragments of resected specimen from 21 patients represented the control tissue. The immunoexpressions of αSMA were detected in tissue specimens with immunohistochemistry (Abcam antibodies, GB). Results: Mean cytoplasmatic expression of αSMA protein in PDAC stromal cells was significantly higher compared to CP: 2.42 ± 0.37 vs 1.95 ± 0.45 (p < 0.01) and control group 0.61 ± 0.45 (p < 0.01). Strong immunoexpression of the αSMA protein was found in the vast majority (80.7%) of patients with PDAC, in about half (58%) of patients with CP, and not at all in healthy tissue. The expression of αSMA of different intensity was found in all patients with PDAC and CP, while in healthy tissue was minimal or absent. In PDAC patients, αSMA expression was significantly higher in tumors of diameter higher than 3 cm compared to smaller ones (p = 0.017). Conclusions: Presented findings confirm the significant role of fibrosis in both PDAC and CP; however, they do not confirm the role of αSMA as a marker of differentiation.
Highlights
Chronic pancreatitis is a long-term inflammatory process that leads to irreversible morphological changes in the pancreatic parenchyma, its gradual fibrosis, and calcification [1,2,3,4]
Mean fasting glucose (p = 0.05) and BMI index (p < 0.05) were statistically significantly higher in pancreatic ductal ductaladenocarcinoma adenocarcinoma (PDAC) patients compared to patients with chronic pancreatitis (CP)
We revealed the highest expression of αSMA protein in G-3 tumors 2.54 ±
Summary
Chronic pancreatitis is a long-term inflammatory process that leads to irreversible morphological changes in the pancreatic parenchyma, its gradual fibrosis, and calcification [1,2,3,4]. Long-term CP is an important risk factor for the development of pancreatic cancer, the mechanisms leading to cancer transformation are still poorly understood [9,10]. It is believed that chronic inflammatory process underlies malignant transformation [9,10,11,12]. Pancreatic chronic inflammatory process leads to the activation of stellate cells. Activated stellate cells can proliferate and migrate, are a source of extracellular matrix (ECM) proteins, pro-inflammatory cytokines (IL-1, IL-6, IL-8, IL-18, IL-33, TNFα), chemokines and growth factors IGF-1, PDGF, TGF-β1) [6,7,8]
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