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000128376 0247_ $$2doi$$a10.1158/0008-5472.CAN-13-1885
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000128376 0247_ $$2ISSN$$a0008-5472
000128376 0247_ $$2ISSN$$a0099-7013
000128376 0247_ $$2ISSN$$a0099-7374
000128376 0247_ $$2ISSN$$a1538-7445
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000128376 037__ $$aDKFZ-2017-04393
000128376 041__ $$aeng
000128376 082__ $$a610
000128376 1001_ $$aSteinert, Gunnar$$b0
000128376 245__ $$aImmune escape and survival mechanisms in circulating tumor cells of colorectal cancer.
000128376 260__ $$aPhiladelphia, Pa.$$bAACR$$c2014
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000128376 520__ $$aThe prognosis of colorectal cancer is closely linked to the occurrence of distant metastases. Systemic dissemination is most likely caused by circulating tumor cells (CTC). Despite the fundamental role of CTC within the metastatic cascade, technical obstacles have so far prevented detailed genomic and, in particular, phenotypic analyses of CTC, which may provide molecular targets to delay or prevent distant metastases. We show here a detailed genomic analysis of single colorectal cancer-derived CTC by array comparative genomic hybridization (aCGH), mutational profiling, and microsatellite instability (MSI) analysis. Furthermore, we report the first gene expression analysis of manually selected colorectal cancer-derived CTC by quantitative real-time PCR (qRT-PCR) to investigate transcriptional changes, enabling CTC to survive in circulation and form distant metastases. aCGH confirmed the tumor cell identity of CellSearch-isolated colorectal cancer-derived CTC. Mutational and MSI analyses revealed mutational profiles of CTC to be similar, but not identical to the corresponding tumor tissue. Several CTC exhibited mutations in key genes such as KRAS or TP53 that could not be detected in the tumor. Gene expression analyses revealed both a pronounced upregulation of CD47 as a potential immune-escape mechanism and a significant downregulation of several other pathways, suggesting a dormant state of viable CTC. Our results suggest mutational heterogeneity between tumor tissue and CTC that should be considered in future trials on targeted therapy and monitoring of response. The finding of upregulated immune-escape pathways, which may be responsible for survival of CTC in circulation, could provide a promising target to disrupt the metastatic cascade in colorectal cancer. Cancer Res; 74(6); 1694-704. ©2014 AACR.
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000128376 7001_ $$aSchölch, Sebastian$$b1
000128376 7001_ $$aNiemietz, Thomas$$b2
000128376 7001_ $$aIwata, Naoki$$b3
000128376 7001_ $$aGarcía, Sebastián A$$b4
000128376 7001_ $$aBehrens, Bianca$$b5
000128376 7001_ $$aVoigt, Anita$$b6
000128376 7001_ $$0P:(DE-HGF)0$$aKloor, Matthias$$b7
000128376 7001_ $$0P:(DE-He78)e15dfa1260625c69d6690a197392a994$$aBenner, Axel$$b8$$udkfz
000128376 7001_ $$aBork, Ulrich$$b9
000128376 7001_ $$aRahbari, Nuh N$$b10
000128376 7001_ $$aBüchler, Markus W$$b11
000128376 7001_ $$aStoecklein, Nikolas H$$b12
000128376 7001_ $$aWeitz, Jürgen$$b13
000128376 7001_ $$aKoch, Moritz$$b14
000128376 773__ $$0PERI:(DE-600)2036785-5$$a10.1158/0008-5472.CAN-13-1885$$gVol. 74, no. 6, p. 1694 - 1704$$n6$$p1694 - 1704$$tCancer research$$v74$$x1538-7445$$y2014
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