[eng] Obesity is strongly linked to a higher risk of developing colon cancer, and both pathologies
are growing on an international scale. However, the underlying mechanism of this association is
poorly understood. While biomedical research conventionally tried to explain the dysfunctions in
cancerous epithelial colonocytes, an interest for the role of visceral adipose tissue (VAT) in this
problematic has recently emerged. Firstly, because VAT is anatomically localized in proximity to
colon, so colon cancer metastasizes primarily in this tissue; and secondly, because obesity causes fat
cells hypertrophy, leading to an excessive secretion of adipokines and fatty acids, and a chronic lowgrade inflammation in the tumor microenvironment, finally prompting colon cancer cells
malignization. The objective of our study was to examine whether the lipidomic profile of distal
mesenteric VAT (mVAT) adipocytes was altered at pT3 stage, and whether colon cancer infiltration
into peritumoral VAT (pVAT) influences the immunologic signature of this fat-depot. Hence, we
described fatty acids composition of mVAT adipocytes of 11 colon cancer patients at pT2 and pT3
stages using gas chromatography-mass spectrometry (GC-MS). We did not observe differences in
fatty acids profile and average proportion between both groups. Then, we performed flow cytometry
analysis of immune cells in pVAT and mVAT. Although only three patients were analyzed, we
identified a consistent increase of T and B lymphocytes and pro-inflammatory macrophages in
peritumoral fat. Our preliminary data indicate that colon cancer stage did not affect the lipid content
of adipocytes in the mVAT, and that colon cancer was associated with a change in the inflammatory
status of pVAT, suggesting a crosstalk between colon cancer cells and immune cells.