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      Circulating and disseminated tumour cells — mechanisms of immune surveillance and escape

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      Nature Reviews Clinical Oncology

      Springer Nature

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          Abstract

          To form metastases, cancer cells must leave the immunosuppressive tumour microenvironment and traffic, predominantly in the circulation, to new tissue sites, where they must then expand. During this process, the tumour cells are open to attack by the immune system. This Review highlights the possible mechanisms used by circulating tumour cells in the blood and disseminated tumour cells in other tissues to evade, escape, or subvert the immune system in order to survive and form metastatic lesions.

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          Most cited references 102

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          The catalog of human cytokeratins: patterns of expression in normal epithelia, tumors and cultured cells.

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            Detection of mutations in EGFR in circulating lung-cancer cells.

            The use of tyrosine kinase inhibitors to target the epidermal growth factor receptor gene (EGFR) in patients with non-small-cell lung cancer is effective but limited by the emergence of drug-resistance mutations. Molecular characterization of circulating tumor cells may provide a strategy for noninvasive serial monitoring of tumor genotypes during treatment. We captured highly purified circulating tumor cells from the blood of patients with non-small-cell lung cancer using a microfluidic device containing microposts coated with antibodies against epithelial cells. We performed EGFR mutational analysis on DNA recovered from circulating tumor cells using allele-specific polymerase-chain-reaction amplification and compared the results with those from concurrently isolated free plasma DNA and from the original tumor-biopsy specimens. We isolated circulating tumor cells from 27 patients with metastatic non-small-cell lung cancer (median number, 74 cells per milliliter). We identified the expected EGFR activating mutation in circulating tumor cells from 11 of 12 patients (92%) and in matched free plasma DNA from 4 of 12 patients (33%) (P=0.009). We detected the T790M mutation, which confers drug resistance, in circulating tumor cells collected from patients with EGFR mutations who had received tyrosine kinase inhibitors. When T790M was detectable in pretreatment tumor-biopsy specimens, the presence of the mutation correlated with reduced progression-free survival (7.7 months vs. 16.5 months, P<0.001). Serial analysis of circulating tumor cells showed that a reduction in the number of captured cells was associated with a radiographic tumor response; an increase in the number of cells was associated with tumor progression, with the emergence of additional EGFR mutations in some cases. Molecular analysis of circulating tumor cells from the blood of patients with lung cancer offers the possibility of monitoring changes in epithelial tumor genotypes during the course of treatment. 2008 Massachusetts Medical Society
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              Tumor self-seeding by circulating cancer cells.

              Cancer cells that leave the primary tumor can seed metastases in distant organs, and it is thought that this is a unidirectional process. Here we show that circulating tumor cells (CTCs) can also colonize their tumors of origin, in a process that we call "tumor self-seeding." Self-seeding of breast cancer, colon cancer, and melanoma tumors in mice is preferentially mediated by aggressive CTCs, including those with bone, lung, or brain-metastatic tropism. We find that the tumor-derived cytokines IL-6 and IL-8 act as CTC attractants whereas MMP1/collagenase-1 and the actin cytoskeleton component fascin-1 are mediators of CTC infiltration into mammary tumors. We show that self-seeding can accelerate tumor growth, angiogenesis, and stromal recruitment through seed-derived factors including the chemokine CXCL1. Tumor self-seeding could explain the relationships between anaplasia, tumor size, vascularity and prognosis, and local recurrence seeded by disseminated cells following ostensibly complete tumor excision. Copyright 2009 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Nature Reviews Clinical Oncology
                Nat Rev Clin Oncol
                Springer Nature
                1759-4774
                1759-4782
                September 20 2016
                September 20 2016
                :
                :
                Article
                10.1038/nrclinonc.2016.144
                27644321
                © 2016

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