Abstract
<h3>Background</h3> Colon carcinoma is a malignant tumour showing a marked preference to metastasise to distant organs. The presence of circulating tumour cells in the peripheral blood is a prerequisite for the formation of distant metastases. However, whether circulating cytokines are linked to the circulation of tumour cells, as individual cells or clusters, remains unclear. In this study, we investigated the circulating levels of TGF-<i>β</i>, CXCL1, VEGF, and PAI-1 as potential bioindicators of the presence of CTCs in patients with metastatic colon cancer. <h3>Methods</h3> CTCs were isolated from peripheral blood by immunomagnetic separation and phenotypically characterised in a cohort of 103 patients with metastatic colon cancer. TGF-<i>β</i>, CXCL1, VEGF, and PAI-1 concentrations were determined by immunoassay in plasma samples from the same patients. <h3>Findings</h3> We detected two different populations of CTCs, single cells or clusters, in patients with metastatic colon cancer. Within the single-cell population and according to the number of cells, we classified two groups of patients: 27 patients with a number of CTCs<10 (CK1+/−) and 43 patients with CTCs⩾10 (CK2+). Patients (<i>n</i>=33) with clusters represented a unique group because we were unable to make any distinction. Presence of clusters is significantly associated with high plasma levels of TGF-beta and CXCL1 (<i>p</i>< 0.0001) and with reduced overall survival (OS); the median OS was 12, 27, and 54months, respectively, in clustered, CK2+, and CK1+/− patient groups (<i>p</i><0.0001). <h3>Interpretation</h3> These findings show that detection of clustered CTCs represents a negative prognostic factor in patients with metastatic colon cancer. The presence of clustered CTCs is associated with elevated circulating levels of cytokines such as TGF-<i>β</i> and CXCL1. This finding suggests an additional role for circulating cytokines as a predictive tool for cancer prognosis and diagnosis of minimal residual disease, as well as assessment of tumour sensitivity to anticancer therapy.
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