Inflammation plays an important role in the pathogenesis of peritoneal carcinosis. Patients with elevated levels of different inflammation cytokines show a worse prognosis at the time of diagnosis. In women, ovarian and colon cancer are the main causes of peritoneal carcinosis and a comparison of these two different types of peritoneal invasion have not been conducted yet. We found interesting studying the role of immune response, in particular tumour-associated antigens (TAA) that modulate the metastatic process. We will investigate also mitochondrial defects, such as mutations in mt-DNA, potentially involved in carcinogenesis.
At the time of hospitalization all the patients will undergo a complete clinical evaluation with determination of biochemical parameters such as fasting blood glucose, blood count, hs-CRP, AST and ALT, uric acid, creatinine and BUN. An extra blood aliquot will be collected to assess the serum biomarkers under investigation. During surgery two samples of peritoneal tissue macroscopically undamaged will be collected. On those samples will be executed separation of adipocytes cells, RNA and protein extraction for measuring of inflammatory and neoplastic biomarkers, determination of P2X7R-inflammasome activity and mitochondrial DNA analyse.
Study Type
OBSERVATIONAL
Enrollment
30
Partial removal of peritoneal tissue involved by neoplastic invasion
University of Pisa
Pisa, Italy
Immune biomarkers level
Serum level of different immune related biomarkers (such as CD4, CD8, CUZD1, LAG3, PD1, PDL1, IMP1 and p62/IMP2) will be determined using ELISA.
Time frame: Each patients will be assessed at baseline
Metastatic mediators level
Peritoneal expression of cytokines related to metastatic process (such as IL6, IL2, TNFα, TGFβ1, VEGF, CD68, FGFR1, CCL2/MCP-1, CD73) will be determined using real time-PCR.
Time frame: Each patients will be assessed at baseline
P2X7R-inflammasome activity
Peritoneal expression of NLRP3-ASC will be determine using RT-PCR
Time frame: Each patients will be assessed at baseline
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