Ricerc@Sapienza

Cancer Cachexia (CC) occurs in almost 80% of cancer patients and is the leading cause of death in about 20% of this population. The cause of the pathogenesis of cachexia is complex and involves different organs, cell types, hormones, cytokines/chemokines, growth factors, and interorgan crosstalk. During CC, several alterations occur in peripheral tissues, and the adipose tissue (AT) may be involved during the catabolic stimuli, such as increased lipid mobilization due to increased lipolysis, reduced lipogenesis and impairment of fat cell turnover. Moreover, AT inflammation plays an important role in the metabolic alterations of this organ. Macrophages are crucial drivers of tumor-promoting inflammation. Also, tumor-associated macrophages (TAMs) contribute to the tumor progression at different levels: by promoting genetic instability, nurturing cancer stem cells, supporting metastasis, and taming protective adaptive immunity. In response to signals from the extracellular environment, macrophages can be activated towards the pro-inflammatory (M1) or anti-inflammatory (M2) phenotype. Recent data suggest a protective role of macrophages in the loss of AT during cancer.
We will enroll colon cancer patients and controls with non-malignant diseases, undergoing surgery. We will collect AT during surgery, and tumor tissue after diagnosis to perform histomorphological analyses (cross-sectional area-CSA and percent of fibrosis) and immunohistochemistry to characterize macrophages M1/M2 population, identified by anti iNOS and anti CD163 antibodies, respectively. By CT-scan, we will calculate subcutaneous and visceral AT. The results of this project will provide useful indications on the different distribution of M1/M2 macrophages in subcutaneous, peritumoral AT and into the tumor tissue. Moreover, they will give information about the morphological difference of subcutaneous and peritumoral AT in a population of colorectal cancer patients.