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000153784 1001_ $$0P:(DE-He78)79e92bc6260b7a24abe4daf4378bf19c$$aMöhrmann, Lino$$b0$$eFirst author
000153784 245__ $$aA Perivascular Niche in the Bone Marrow Hosts Quiescent and Proliferating Tumorigenic Colorectal Cancer Cells.
000153784 260__ $$aBognor Regis$$bWiley-Liss$$c2020
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000153784 520__ $$aDisseminated tumor cells (dTCs) can frequently be detected in the bone marrow (BM) of colorectal cancer (CRC) patients, raising the possibility that the BM serves as a reservoir for metastatic tumor cells. Identification of dTCs in BM aspirates harbors the potential of assessing therapeutic outcome and directing therapy intensity with limited risk and effort. Still, the functional and prognostic relevance of dTCs is not fully established. We have previously shown that CRC cell clones can be traced to the bone marrow (BM) of mice carrying patient-derived xenografts. However, cellular interactions, proliferative state and tumorigenicity of dTCs remain largely unknown. Here, we applied a co-culture system modeling the microvascular niche and used immunofluorescence imaging of the murine BM to show that primary CRC cells migrate towards endothelial tubes. dTCs in the BM were rare, but detectable in mice with xenografts from most patient samples (8/10) predominantly at perivascular sites. Comparable to primary tumors, a substantial fraction of proliferating dTCs were detected in the BM. However, most dTCs were found as isolated cells, indicating that dividing dTCs rather separate than aggregate to metastatic clones - a phenomenon frequently observed in the microvascular niche model. Clonal tracking identified subsets of self-renewing tumor-initiating cells in the BM that formed tumors out of BM transplants, including one subset that did not drive primary tumor growth. Our results indicate an important role of the perivascular BM niche for CRC cell dissemination and show that dTCs can be a potential source for tumor relapse and tumor heterogeneity. This article is protected by copyright. All rights reserved.
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000153784 7001_ $$0P:(DE-He78)77c840a683146ceba3c47a339f6fbff6$$aZowada, Martina K$$b1$$eFirst author
000153784 7001_ $$0P:(DE-He78)0922b09fe35a55ae6cf8cd5f01870a58$$aStrakerjahn, Hendrik$$b2
000153784 7001_ $$0P:(DE-He78)be98d27bcd782f4e5961b646107dc14b$$aSiegl, Christine$$b3
000153784 7001_ $$0P:(DE-He78)bb6a7a70f976eb8df1769944bf913596$$aKopp-Schneider, Annette$$b4
000153784 7001_ $$0P:(DE-He78)2214defe87d04a849413e5eed47c415e$$aKrunic, Damir$$b5
000153784 7001_ $$aStrunk, Dirk$$b6
000153784 7001_ $$aSchneider, Martin$$b7
000153784 7001_ $$aKriegsmann, Mark$$b8
000153784 7001_ $$aKriegsmann, Katharina$$b9
000153784 7001_ $$0P:(DE-He78)13dc15153ce40f775007112548f34d79$$aHerbst, Friederike$$b10
000153784 7001_ $$0P:(DE-He78)7a10ea1b9b2872da9f375002c44ddfce$$aBall, Claudia R$$b11
000153784 7001_ $$0P:(DE-He78)157277fe62f07df1732f9d126a51d1b9$$aGlimm, Hanno$$b12
000153784 7001_ $$0P:(DE-He78)34c336827b750ba10a020fd62ec4664f$$aDieter, Sebastian$$b13$$eLast author
000153784 773__ $$0PERI:(DE-600)1474822-8$$a10.1002/ijc.32933$$gp. ijc.32933$$n2$$p519-531$$tInternational journal of cancer$$v147$$x1097-0215$$y2020
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