AuthOr’s VIew

Tumors develop in constant interaction with the immune system, which influences both oncogenesis and tumor progression. This process has been conceptualized by the theory of cancer immunoediting, which involves an elimination, an equilib-rium and an escape phase.1 During can-cer immunoediting, tumors eventually develop ways to escape efficient antitu-mor immunity. One such ways is to cre-ate immunomodulatory conditions within the tumor microenvironment.2 The local production of immunosuppressive fac-tors such as transforming growth factor β (TGFβ) and interleukin-10 (IL-10), the induction of enzymes that consume essen-tial nutrients for immune cell function (e.g., IDO, Arg-I), and the local activa-tion or recruitment of immunosuppressive cell types (e.g., regulatory T cells, myeloid derived suppressor cells) can all contribute to limit immune responses. In many clinical settings, the presence of tumor-associated antigens in the serum of patients is being used for diagnostic and sometimes prognostic purposes. For instance, in colorectal carcinoma (CRC) patients, the levels of the carcinoembryonic antigen (CEA) in the serum has clinical rel-evance3 and is used as a prognostic maker. We hypothesized that the release of such antigens by tumor cells into the blood-stream might influence antitumor immu-nity. This strategy would add up to local Antigen shedding into the circulation contributes to tumor immune escape Bastian höchst and Linda Diehl