Colon carcinoma and the possible significance of T-cell population, including FOXP3-positive lymphocytes
Authors | |
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Year of publication | 2007 |
Type | Article in Proceedings |
Conference | Proceedings of the American Association for Cancer Research |
MU Faculty or unit | |
Citation | |
Field | Oncology and hematology |
Keywords | colon carcinoma;T-cell lymphocytes;FOXP3 |
Description | Tumor-infiltrating lymphocytes (TIL) of colon carcinoma (CC) include also cytotoxic T-cells that are generally considered as prognostically favourable because of their ability to exert anti-tumor immunity. As progression of CC occurs, the question arises whether the CC microenvironment may have some suppressive capabilities. We were interested if a recently discovered subgroup of T-cells, namely regulatory T-cells (TREG, CD4+ CD25+ FOXP3+), which are able to functionally suppress immune responses and are supposed to lead to tumor progression, makes part of TIL of CC. We used immunohistochemical staining to detect lymphocytes co-expressing CD4+ and FOXP3+ in 44 cases of CC primary tumors, using formalin-fixed and paraffin-embedded sections, and commercially available monoclonal antibodies. We were first indeed to show the occurence of FOXP3+ TREG lymphocytes in CC. What we found interesting in futher studies was the localization of FOXP3+ cells. We observed them in stroma, within the epitelium, but above all they formed invasive fragment between cancer and non-cancer tissue. This localization is very suspicious to play a role in local immune system, although to explain this fact there are futher experiments undergoing in our laboratory. Investigations, in fact, are in progress on: (i) differences in TREG distribution between left/right side-localized CC, (ii) differences in TREG distribution among CC in clinical stage I-IV, (iii) TREG behaviour in cases asssociated with microsatelite instability, which is known to have more favourable clinical outcome. This project is supported by Internal Grant Agency, Ministry of Health, Czech Republic. No.: NR/9076-4. |