Ovarian cancer stem cells express ROR1, which can be targeted for anti–cancer-stem-cell therapy
Although initially responsive to chemotherapy, many patients with ovarian cancer subsequently develop relapsed and potentially fatal metastatic disease, which is thought to develop from cancer stem cells (CSCs) that are relatively resistant to conventional therapy. Here, we show that CSCs express a...
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Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 111; no. 48; pp. 17266 - 17271 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
National Academy of Sciences
02.12.2014
National Acad Sciences |
Subjects | |
Online Access | Get full text |
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Abstract | Although initially responsive to chemotherapy, many patients with ovarian cancer subsequently develop relapsed and potentially fatal metastatic disease, which is thought to develop from cancer stem cells (CSCs) that are relatively resistant to conventional therapy. Here, we show that CSCs express a type I receptor tyrosine kinase-like orphan receptor (ROR1), which is expressed during embryogenesis and by many different cancers, but not normal postpartum tissues. Ovarian cancers with high levels of ROR1 had stem cell-like gene-expression signatures. Furthermore, patients with ovarian cancers with high levels of ROR1 had higher rates of relapse and a shorter median survival than patients with ovarian cancers that expressed low-to-negligible amounts of ROR1 . We found that ROR1-positive (ROR1 ⁺) cells isolated from primary tumor-derived xenografts (PDXs) also expressed aldehyde dehydrogenase 1 (ALDH1) and had a greater capacity to form spheroids and to engraft immune-deficient mice than did ROR1-negative (ROR1 ᴺᵉᵍ) ovarian cancer cells isolated from the same tumor population. Treatment with UC-961, an anti-ROR1 mAb, or shRNA silencing of ROR1 inhibited expression of the polycomb ring-finger oncogene, Bmi-1, and other genes associated with the epithelial–mesenchymal transition. Moreover, shRNA silencing of ROR1, depletion of ROR1 ⁺ cells, or treatment with UC-961 impaired the capacity of ovarian cancer cells to form spheroids or tumor xenografts. More importantly, treatment with anti-ROR1 affected the capacity of the xenograft to reseed a virgin mouse, indicating that targeting ROR1 may affect CSC self-renewal. Collectively, these studies indicate that ovarian CSCs express ROR1, which contributes to their capacity to form tumors, making ROR1 a potential target for the therapy of patients with ovarian cancer.
Significance This study demonstrates that the oncoembryonic surface antigen, receptor tyrosine kinase-like orphan receptor 1 (ROR1), is expressed on human ovarian cancer stem cells (CSCs), on which it seems to play a functional role in promoting migration/invasion or spheroid formation in vitro and tumor engraftment in immune-deficient mice. Treatment with a humanized mAb specific for ROR1 (UC-961) could inhibit the capacity of ovarian cancer cells to migrate, form spheroids, or engraft immune-deficient mice. Moreover, such treatment inhibited the growth of tumor xenografts, which in turn had a reduced capacity to engraft immune-deficient mice and were relatively depleted of cells with features of CSC, suggesting that treatment with UC-961 could impair CSC renewal. Collectively, these studies indicate that ovarian CSCs express ROR1, which may be targeted for anti-CSC therapy. |
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AbstractList | Although initially responsive to chemotherapy, many patients with ovarian cancer subsequently develop relapsed and potentially fatal metastatic disease, which is thought to develop from cancer stem cells (CSCs) that are relatively resistant to conventional therapy. Here, we show that CSCs express a type I receptor tyrosine kinase-like orphan receptor (ROR1), which is expressed during embryogenesis and by many different cancers, but not normal postpartum tissues. Ovarian cancers with high levels of ROR1 had stem cell-like gene-expression signatures. Furthermore, patients with ovarian cancers with high levels of ROR1 had higher rates of relapse and a shorter median survival than patients with ovarian cancers that expressed low-to-negligible amounts of ROR1. We found that ROR1-positive (ROR1(+)) cells isolated from primary tumor-derived xenografts (PDXs) also expressed aldehyde dehydrogenase 1 (ALDH1) and had a greater capacity to form spheroids and to engraft immune-deficient mice than did ROR1-negative (ROR1(Neg)) ovarian cancer cells isolated from the same tumor population. Treatment with UC-961, an anti-ROR1 mAb, or shRNA silencing of ROR1 inhibited expression of the polycomb ring-finger oncogene, Bmi-1, and other genes associated with the epithelial-mesenchymal transition. Moreover, shRNA silencing of ROR1, depletion of ROR1(+) cells, or treatment with UC-961 impaired the capacity of ovarian cancer cells to form spheroids or tumor xenografts. More importantly, treatment with anti-ROR1 affected the capacity of the xenograft to reseed a virgin mouse, indicating that targeting ROR1 may affect CSC self-renewal. Collectively, these studies indicate that ovarian CSCs express ROR1, which contributes to their capacity to form tumors, making ROR1 a potential target for the therapy of patients with ovarian cancer. Significance This study demonstrates that the oncoembryonic surface antigen, receptor tyrosine kinase-like orphan receptor 1 (ROR1), is expressed on human ovarian cancer stem cells (CSCs), on which it seems to play a functional role in promoting migration/invasion or spheroid formation in vitro and tumor engraftment in immune-deficient mice. Treatment with a humanized mAb specific for ROR1 (UC-961) could inhibit the capacity of ovarian cancer cells to migrate, form spheroids, or engraft immune-deficient mice. Moreover, such treatment inhibited the growth of tumor xenografts, which in turn had a reduced capacity to engraft immune-deficient mice and were relatively depleted of cells with features of CSC, suggesting that treatment with UC-961 could impair CSC renewal. Collectively, these studies indicate that ovarian CSCs express ROR1, which may be targeted for anti-CSC therapy. Although initially responsive to chemotherapy, many patients with ovarian cancer subsequently develop relapsed and potentially fatal metastatic disease, which is thought to develop from cancer stem cells (CSCs) that are relatively resistant to conventional therapy. Here, we show that CSCs express a type I receptor tyrosine kinase-like orphan receptor (ROR1), which is expressed during embryogenesis and by many different cancers, but not normal postpartum tissues. Ovarian cancers with high levels of ROR1 had stem cell-like gene-expression signatures. Furthermore, patients with ovarian cancers with high levels of ROR1 had higher rates of relapse and a shorter median survival than patients with ovarian cancers that expressed low-to-negligible amounts of ROR1 . We found that ROR1-positive (ROR1 + ) cells isolated from primary tumor-derived xenografts (PDXs) also expressed aldehyde dehydrogenase 1 (ALDH1) and had a greater capacity to form spheroids and to engraft immune-deficient mice than did ROR1-negative (ROR1 Neg ) ovarian cancer cells isolated from the same tumor population. Treatment with UC-961, an anti-ROR1 mAb, or shRNA silencing of ROR1 inhibited expression of the polycomb ring-finger oncogene, Bmi-1, and other genes associated with the epithelial–mesenchymal transition. Moreover, shRNA silencing of ROR1, depletion of ROR1 + cells, or treatment with UC-961 impaired the capacity of ovarian cancer cells to form spheroids or tumor xenografts. More importantly, treatment with anti-ROR1 affected the capacity of the xenograft to reseed a virgin mouse, indicating that targeting ROR1 may affect CSC self-renewal. Collectively, these studies indicate that ovarian CSCs express ROR1, which contributes to their capacity to form tumors, making ROR1 a potential target for the therapy of patients with ovarian cancer. This study demonstrates that the oncoembryonic surface antigen, receptor tyrosine kinase-like orphan receptor 1 (ROR1), is expressed on human ovarian cancer stem cells (CSCs), on which it seems to play a functional role in promoting migration/invasion or spheroid formation in vitro and tumor engraftment in immune-deficient mice. Treatment with a humanized mAb specific for ROR1 (UC-961) could inhibit the capacity of ovarian cancer cells to migrate, form spheroids, or engraft immune-deficient mice. Moreover, such treatment inhibited the growth of tumor xenografts, which in turn had a reduced capacity to engraft immune-deficient mice and were relatively depleted of cells with features of CSC, suggesting that treatment with UC-961 could impair CSC renewal. Collectively, these studies indicate that ovarian CSCs express ROR1, which may be targeted for anti-CSC therapy. Although initially responsive to chemotherapy, many patients with ovarian cancer subsequently develop relapsed and potentially fatal metastatic disease, which is thought to develop from cancer stem cells (CSCs) that are relatively resistant to conventional therapy. Here, we show that CSCs express a type I receptor tyrosine kinase-like orphan receptor (ROR1), which is expressed during embryogenesis and by many different cancers, but not normal postpartum tissues. Ovarian cancers with high levels of ROR1 had stem cell-like gene-expression signatures. Furthermore, patients with ovarian cancers with high levels of ROR1 had higher rates of relapse and a shorter median survival than patients with ovarian cancers that expressed low-to-negligible amounts of ROR1 . We found that ROR1-positive (ROR1 + ) cells isolated from primary tumor-derived xenografts (PDXs) also expressed aldehyde dehydrogenase 1 (ALDH1) and had a greater capacity to form spheroids and to engraft immune-deficient mice than did ROR1-negative (ROR1 Neg ) ovarian cancer cells isolated from the same tumor population. Treatment with UC-961, an anti-ROR1 mAb, or shRNA silencing of ROR1 inhibited expression of the polycomb ring-finger oncogene, Bmi-1, and other genes associated with the epithelial–mesenchymal transition. Moreover, shRNA silencing of ROR1, depletion of ROR1 + cells, or treatment with UC-961 impaired the capacity of ovarian cancer cells to form spheroids or tumor xenografts. More importantly, treatment with anti-ROR1 affected the capacity of the xenograft to reseed a virgin mouse, indicating that targeting ROR1 may affect CSC self-renewal. Collectively, these studies indicate that ovarian CSCs express ROR1, which contributes to their capacity to form tumors, making ROR1 a potential target for the therapy of patients with ovarian cancer. Although initially responsive to chemotherapy, many patients with ovarian cancer subsequently develop relapsed and potentially fatal metastatic disease, which is thought to develop from cancer stem cells (CSCs) that are relatively resistant to conventional therapy. Here, we show that CSCs express a type I receptor tyrosine kinase-like orphan receptor (ROR1), which is expressed during embryogenesis and by many different cancers, but not normal postpartum tissues. Ovarian cancers with high levels of ROR1 had stem cell-like gene-expression signatures. Furthermore, patients with ovarian cancers with high levels of ROR1 had higher rates of relapse and a shorter median survival than patients with ovarian cancers that expressed low-to-negligible amounts of ROR1. We found that ROR1-positive (ROR1⁺) cells isolated from primary tumor-derived xenografts (PDXs) also expressed aldehyde dehydrogenase 1 (ALDH1) and had a greater capacity to form spheroids and to engraft immune-deficient mice than did ROR1-negative (ROR1Neg) ovarian cancer cells isolated from the same tumor population. Treatment with UC-961, an anti-ROR1 mAb, or shRNA silencing of ROR1 inhibited expression of the polycomb ring-finger oncogene, Bmi-1, and other genes associated with the epithelial-mesenchymal transition. Moreover, shRNA silencing of ROR1, depletion of ROR1⁺ cells, or treatment with UC-961 impaired the capacity of ovarian cancer cells to form spheroids or tumor xenografts. More importantly, treatment with anti-ROR1 affected the capacity of the xe nog raft to reseed a virgin mouse, indicating that targeting ROR1 may affect CSC self-renewal. Collectively, these studies indicate that ovarian CSCs express ROR1, which contributes to their capacity to form tumors, making ROR1 a potential target for the therapy of patients with ovarian cancer. Although initially responsive to chemotherapy, many patients with ovarian cancer subsequently develop relapsed and potentially fatal metastatic disease, which is thought to develop from cancer stem cells (CSCs) that are relatively resistant to conventional therapy. Here, we show that CSCs express a type I receptor tyrosine kinase-like orphan receptor (ROR1), which is expressed during embryogenesis and by many different cancers, but not normal postpartum tissues. Ovarian cancers with high levels of ROR1 had stem cell-like gene-expression signatures. Furthermore, patients with ovarian cancers with high levels of ROR1 had higher rates of relapse and a shorter median survival than patients with ovarian cancers that expressed low-to-negligible amounts of ROR1 . We found that ROR1-positive (ROR1 ⁺) cells isolated from primary tumor-derived xenografts (PDXs) also expressed aldehyde dehydrogenase 1 (ALDH1) and had a greater capacity to form spheroids and to engraft immune-deficient mice than did ROR1-negative (ROR1 ᴺᵉᵍ) ovarian cancer cells isolated from the same tumor population. Treatment with UC-961, an anti-ROR1 mAb, or shRNA silencing of ROR1 inhibited expression of the polycomb ring-finger oncogene, Bmi-1, and other genes associated with the epithelial–mesenchymal transition. Moreover, shRNA silencing of ROR1, depletion of ROR1 ⁺ cells, or treatment with UC-961 impaired the capacity of ovarian cancer cells to form spheroids or tumor xenografts. More importantly, treatment with anti-ROR1 affected the capacity of the xenograft to reseed a virgin mouse, indicating that targeting ROR1 may affect CSC self-renewal. Collectively, these studies indicate that ovarian CSCs express ROR1, which contributes to their capacity to form tumors, making ROR1 a potential target for the therapy of patients with ovarian cancer. Significance This study demonstrates that the oncoembryonic surface antigen, receptor tyrosine kinase-like orphan receptor 1 (ROR1), is expressed on human ovarian cancer stem cells (CSCs), on which it seems to play a functional role in promoting migration/invasion or spheroid formation in vitro and tumor engraftment in immune-deficient mice. Treatment with a humanized mAb specific for ROR1 (UC-961) could inhibit the capacity of ovarian cancer cells to migrate, form spheroids, or engraft immune-deficient mice. Moreover, such treatment inhibited the growth of tumor xenografts, which in turn had a reduced capacity to engraft immune-deficient mice and were relatively depleted of cells with features of CSC, suggesting that treatment with UC-961 could impair CSC renewal. Collectively, these studies indicate that ovarian CSCs express ROR1, which may be targeted for anti-CSC therapy. Although initially responsive to chemotherapy, many patients with ovarian cancer subsequently develop relapsed and potentially fatal metastatic disease, which is thought to develop from cancer stem cells (CSCs) that are relatively resistant to conventional therapy. Here, we show that CSCs express a type I receptor tyrosine kinase-like orphan receptor (ROR1), which is expressed during embryogenesis and by many different cancers, but not normal postpartum tissues. Ovarian cancers with high levels of ROR1 had stem cell-like gene-expression signatures. Furthermore, patients with ovarian cancers with high levels of ROR1 had higher rates of relapse and a shorter median survival than patients with ovarian cancers that expressed low-to-negligible amounts of ROR1. We found that ROR1-positive (ROR1+) cells isolated from primary tumor-derived xenografts (PDXs) also expressed aldehyde dehydrogenase 1 (ALDH1) and had a greater capacity to form spheroids and to engraft immune-deficient mice than did ROR1-negative (...) ovarian cancer cells isolated from the same tumor population. Treatment with UC-961, an anti-ROR1 mAb, or shRNA silencing of ROR1 inhibited expression of the polycomb ring-finger oncogene, Bmi-1, and other genes associated with the epithelial-mesenchymal transition. Moreover, shRNA silencing of ROR1, depletion of ROR1+ cells, or treatment with UC-961 impaired the capacity of ovarian cancer cells to form spheroids or tumor xenografts. More importantly, treatment with anti-ROR1 affected the capacity of the xenograft to reseed a virgin mouse, indicating that targeting ROR1 may affect CSC self-renewal. Collectively, these studies indicate that ovarian CSCs express ROR1, which contributes to their capacity to form tumors, making ROR1 a potential target for the therapy of patients with ovarian cancer. (ProQuest: ... denotes formulae/symbols omitted.) |
Author | Zhang, Zhuhong Widhopf, George F. Wu, Rongrong Carson, Dennis A. Zhang, Suping Lai, Hsien Ghia, Emanuela M. Cui, Bing Wu, Christina C. N. Schwab, Richard Kipps, Thomas J. Chen, Liguang Liu, Grace |
Author_xml | – sequence: 1 givenname: Suping surname: Zhang fullname: Zhang, Suping – sequence: 2 givenname: Bing surname: Cui fullname: Cui, Bing – sequence: 3 givenname: Hsien surname: Lai fullname: Lai, Hsien – sequence: 4 givenname: Grace surname: Liu fullname: Liu, Grace – sequence: 5 givenname: Emanuela M. surname: Ghia fullname: Ghia, Emanuela M. – sequence: 6 givenname: George F. surname: Widhopf fullname: Widhopf, George F. – sequence: 7 givenname: Zhuhong surname: Zhang fullname: Zhang, Zhuhong – sequence: 8 givenname: Christina C. N. surname: Wu fullname: Wu, Christina C. N. – sequence: 9 givenname: Liguang surname: Chen fullname: Chen, Liguang – sequence: 10 givenname: Rongrong surname: Wu fullname: Wu, Rongrong – sequence: 11 givenname: Richard surname: Schwab fullname: Schwab, Richard – sequence: 12 givenname: Dennis A. surname: Carson fullname: Carson, Dennis A. – sequence: 13 givenname: Thomas J. surname: Kipps fullname: Kipps, Thomas J. |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25411317$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1002/cncr.26215 10.1200/JCO.1996.14.6.1895 10.1158/1535-7163.MCT-10-0788 10.1158/0008-5472.CAN-08-0364 10.1016/j.critrevonc.2010.07.004 10.1371/journal.pone.0084941 10.1056/NEJM199601043340101 10.1158/1078-0432.CCR-08-0196 10.1158/1535-7163.MCT-10-0563 10.1038/nm.3418 10.1016/S0046-8177(98)90066-1 10.1038/onc.2008.374 10.1002/path.2793 10.1159/000112847 10.1186/1757-2215-3-28 10.1038/ng.127 10.4161/cc.8.1.7533 10.1371/journal.pone.0029079 10.1200/JCO.2006.10.2517 10.2741/3693 10.1038/srep05811 10.1016/j.leukres.2011.06.021 10.1371/journal.pone.0010277 10.1016/j.semcancer.2012.04.001 10.1186/1471-2407-9-221 10.1158/0008-5472.CAN-07-6341 10.1073/pnas.0712148105 10.1172/JCI200420800 10.1016/j.ajpath.2011.11.015 10.1073/pnas.0603672103 10.1172/JCI69815 10.1073/pnas.0506580102 10.2217/nnm.12.22 10.1016/j.ccr.2012.02.008 10.1371/journal.pone.0057799 10.1002/stem.236 10.1016/j.ajpath.2012.08.024 10.1158/0008-5472.CAN-10-3175 10.1158/0008-5472.CAN-12-3832 10.1073/pnas.1308374111 10.1002/hon.948 10.1046/j.1432-1327.1998.2510549.x 10.1371/journal.pone.0031127 10.1158/0008-5472.CAN-10-2662 10.1186/1476-4598-12-24 10.1158/0008-5472.CAN-07-6595 10.1158/1078-0432.CCR-09-2317 10.1158/0008-5472.CAN-06-3126 |
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Keywords | PDX mice model ovarian cancer stem cell ROR1 monoclonal antibody |
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Notes | http://dx.doi.org/10.1073/pnas.1419599111 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Author contributions: S.Z. and T.J.K. designed research; S.Z., B.C., H.L., G.L., Z.Z., C.C.N.W., L.C., and R.W. performed research; G.F.W. and R.S. contributed new reagents/analytic tools; S.Z., B.C., H.L., G.L., E.M.G., D.A.C., and T.J.K. analyzed data; and S.Z., H.L., and T.J.K. wrote the paper. Contributed by Dennis A. Carson, October 22, 2014 (sent for review September 15, 2014; reviewed by Brunhilde H. Felding) Reviewers included: B.H.F., The Scripps Research Institute. 1S.Z. and B.C. contributed equally to this work. |
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References | 18698038 - Clin Cancer Res. 2008 Aug 15;14(16):5198-208 22471722 - Nanomedicine (Lond). 2012 Apr;7(4):597-615 18593951 - Cancer Res. 2008 Jul 1;68(13):5478-86 18287027 - Proc Natl Acad Sci U S A. 2008 Feb 26;105(8):3047-52 18443585 - Nat Genet. 2008 May;40(5):499-507 9490025 - Eur J Biochem. 1998 Feb 1;251(3):549-57 25056203 - Sci Rep. 2014;4:5811 23593543 - Am J Cancer Res. 2013 Apr 03;3(2):221-9 20422001 - PLoS One. 2010;5(4):e10277 21079657 - Iran Biomed J. 2010 Jul;14(3):77-82 18836486 - Oncogene. 2009 Jan 15;28(2):209-18 24292392 - Nat Med. 2014 Jan;20(1):29-36 17704411 - J Clin Oncol. 2007 Aug 20;25(24):3621-7 20889728 - Mol Cancer Ther. 2010 Dec;9(12):3186-99 22554795 - Semin Cancer Biol. 2012 Oct;22(5-6):396-403 24409314 - PLoS One. 2014;9(1):e84941 19158483 - Cell Cycle. 2009 Jan 1;8(1):158-66 21196176 - Front Biosci (Landmark Ed). 2011;16:368-92 16849428 - Proc Natl Acad Sci U S A. 2006 Jul 25;103(30):11154-9 23536770 - PLoS One. 2013;8(3):e57799 19583859 - BMC Cancer. 2009;9:221 9596274 - Hum Pathol. 1998 May;29(5):498-504 22272227 - PLoS One. 2012;7(1):e29079 20674385 - Crit Rev Oncol Hematol. 2011 Jul;79(1):17-23 24762435 - J Clin Invest. 2014 Jun;124(6):2611-25 21216927 - Mol Cancer Ther. 2011 Feb;10(2):325-35 20597086 - Hematol Oncol. 2011 Mar;29(1):17-21 19816957 - Stem Cells. 2009 Dec;27(12):2875-83 16199517 - Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 21125672 - J Pathol. 2011 Jan;223(2):147-61 21813176 - Leuk Res. 2011 Oct;35(10):1390-4 8656258 - J Clin Oncol. 1996 Jun;14(6):1895-902 14722607 - J Clin Invest. 2004 Jan;113(2):175-9 18519691 - Cancer Res. 2008 Jun 1;68(11):4311-20 21487037 - Cancer Res. 2011 Apr 15;71(8):3132-41 21176222 - J Ovarian Res. 2010 Dec 22;3:28 22403610 - PLoS One. 2012;7(3):e31127 21498635 - Cancer Res. 2011 Jun 1;71(11):3991-4001 22222226 - Am J Pathol. 2012 Mar;180(3):1159-69 23041612 - Am J Pathol. 2012 Dec;181(6):1903-10 19996211 - Clin Cancer Res. 2009 Dec 15;15(24):7593-7601 18160824 - Cells Tissues Organs. 2008;188(1-2):127-38 23771907 - Cancer Res. 2013 Jun 15;73(12):3649-60 16990346 - Cancer Res. 2006 Oct 1;66(19):9339-44 23537295 - Mol Cancer. 2013;12:24 21692061 - Cancer. 2011 Dec 15;117(24):5519-28 22439932 - Cancer Cell. 2012 Mar 20;21(3):348-61 18632618 - Cancer Res. 2008 Jul 15;68(14):5658-68 24379361 - Proc Natl Acad Sci U S A. 2014 Jan 14;111(2):793-8 7494563 - N Engl J Med. 1996 Jan 4;334(1):1-6 e_1_3_3_50_2 e_1_3_3_16_2 e_1_3_3_18_2 e_1_3_3_39_2 e_1_3_3_12_2 e_1_3_3_37_2 e_1_3_3_14_2 e_1_3_3_35_2 e_1_3_3_33_2 e_1_3_3_10_2 e_1_3_3_31_2 e_1_3_3_40_2 Rabbani H (e_1_3_3_27_2) 2010; 14 Ricci F (e_1_3_3_44_2) 2013; 3 e_1_3_3_5_2 e_1_3_3_7_2 e_1_3_3_9_2 e_1_3_3_29_2 e_1_3_3_23_2 e_1_3_3_48_2 e_1_3_3_25_2 e_1_3_3_46_2 e_1_3_3_1_2 e_1_3_3_3_2 e_1_3_3_21_2 e_1_3_3_42_2 e_1_3_3_17_2 e_1_3_3_19_2 e_1_3_3_38_2 e_1_3_3_13_2 e_1_3_3_36_2 e_1_3_3_15_2 e_1_3_3_34_2 e_1_3_3_32_2 e_1_3_3_11_2 e_1_3_3_30_2 e_1_3_3_6_2 e_1_3_3_8_2 e_1_3_3_28_2 e_1_3_3_49_2 e_1_3_3_24_2 e_1_3_3_47_2 e_1_3_3_26_2 e_1_3_3_45_2 e_1_3_3_2_2 e_1_3_3_20_2 e_1_3_3_43_2 e_1_3_3_4_2 e_1_3_3_22_2 e_1_3_3_41_2 |
References_xml | – ident: e_1_3_3_49_2 doi: 10.1002/cncr.26215 – ident: e_1_3_3_2_2 doi: 10.1200/JCO.1996.14.6.1895 – ident: e_1_3_3_42_2 doi: 10.1158/1535-7163.MCT-10-0788 – ident: e_1_3_3_18_2 doi: 10.1158/0008-5472.CAN-08-0364 – ident: e_1_3_3_3_2 doi: 10.1016/j.critrevonc.2010.07.004 – ident: e_1_3_3_22_2 doi: 10.1371/journal.pone.0084941 – ident: e_1_3_3_1_2 doi: 10.1056/NEJM199601043340101 – ident: e_1_3_3_35_2 doi: 10.1158/1078-0432.CCR-08-0196 – ident: e_1_3_3_9_2 doi: 10.1158/1535-7163.MCT-10-0563 – ident: e_1_3_3_39_2 doi: 10.1038/nm.3418 – ident: e_1_3_3_47_2 doi: 10.1016/S0046-8177(98)90066-1 – ident: e_1_3_3_7_2 doi: 10.1038/onc.2008.374 – ident: e_1_3_3_13_2 doi: 10.1002/path.2793 – ident: e_1_3_3_46_2 doi: 10.1159/000112847 – ident: e_1_3_3_11_2 doi: 10.1186/1757-2215-3-28 – ident: e_1_3_3_23_2 doi: 10.1038/ng.127 – ident: e_1_3_3_5_2 doi: 10.4161/cc.8.1.7533 – ident: e_1_3_3_16_2 doi: 10.1371/journal.pone.0029079 – ident: e_1_3_3_41_2 doi: 10.1200/JCO.2006.10.2517 – ident: e_1_3_3_6_2 doi: 10.2741/3693 – ident: e_1_3_3_34_2 doi: 10.1038/srep05811 – ident: e_1_3_3_50_2 doi: 10.1016/j.leukres.2011.06.021 – ident: e_1_3_3_10_2 doi: 10.1371/journal.pone.0010277 – ident: e_1_3_3_25_2 doi: 10.1016/j.semcancer.2012.04.001 – ident: e_1_3_3_19_2 doi: 10.1186/1471-2407-9-221 – ident: e_1_3_3_15_2 doi: 10.1158/0008-5472.CAN-07-6341 – ident: e_1_3_3_26_2 doi: 10.1073/pnas.0712148105 – volume: 3 start-page: 221 year: 2013 ident: e_1_3_3_44_2 article-title: ALDH enzymatic activity and CD133 positivity and response to chemotherapy in ovarian cancer patients publication-title: Am J Cancer Res contributor: fullname: Ricci F – ident: e_1_3_3_38_2 doi: 10.1172/JCI200420800 – ident: e_1_3_3_17_2 doi: 10.1016/j.ajpath.2011.11.015 – ident: e_1_3_3_14_2 doi: 10.1073/pnas.0603672103 – ident: e_1_3_3_21_2 doi: 10.1172/JCI69815 – ident: e_1_3_3_37_2 doi: 10.1073/pnas.0506580102 – ident: e_1_3_3_43_2 doi: 10.2217/nnm.12.22 – ident: e_1_3_3_32_2 doi: 10.1016/j.ccr.2012.02.008 – ident: e_1_3_3_24_2 doi: 10.1371/journal.pone.0057799 – ident: e_1_3_3_8_2 doi: 10.1002/stem.236 – volume: 14 start-page: 77 year: 2010 ident: e_1_3_3_27_2 article-title: Expression of ROR1 in patients with renal cancer: A potential diagnostic marker publication-title: Iran Biomed J contributor: fullname: Rabbani H – ident: e_1_3_3_30_2 doi: 10.1016/j.ajpath.2012.08.024 – ident: e_1_3_3_45_2 doi: 10.1158/0008-5472.CAN-10-3175 – ident: e_1_3_3_33_2 doi: 10.1158/0008-5472.CAN-12-3832 – ident: e_1_3_3_40_2 doi: 10.1073/pnas.1308374111 – ident: e_1_3_3_28_2 doi: 10.1002/hon.948 – ident: e_1_3_3_12_2 doi: 10.1046/j.1432-1327.1998.2510549.x – ident: e_1_3_3_31_2 doi: 10.1371/journal.pone.0031127 – ident: e_1_3_3_29_2 doi: 10.1158/0008-5472.CAN-10-2662 – ident: e_1_3_3_20_2 doi: 10.1186/1476-4598-12-24 – ident: e_1_3_3_36_2 doi: 10.1158/0008-5472.CAN-07-6595 – ident: e_1_3_3_48_2 doi: 10.1158/1078-0432.CCR-09-2317 – ident: e_1_3_3_4_2 doi: 10.1158/0008-5472.CAN-06-3126 |
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Snippet | Although initially responsive to chemotherapy, many patients with ovarian cancer subsequently develop relapsed and potentially fatal metastatic disease, which... Significance This study demonstrates that the oncoembryonic surface antigen, receptor tyrosine kinase-like orphan receptor 1 (ROR1), is expressed on human... This study demonstrates that the oncoembryonic surface antigen, receptor tyrosine kinase-like orphan receptor 1 (ROR1), is expressed on human ovarian cancer... |
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SubjectTerms | Animals Antibodies, Monoclonal - immunology Antibodies, Monoclonal - pharmacology Biological Sciences Cancer Cancer therapies Cell Line, Tumor Cell lines Cellular immunity Female Gene Expression Profiling Gene Expression Regulation, Neoplastic Heterologous transplantation Humans Immunoblotting Kaplan-Meier Estimate Mice Mice, Inbred NOD Mice, Knockout Mice, SCID Microscopy, Confocal Molecular Targeted Therapy - methods Neoplastic Stem Cells - metabolism Neoplastic Stem Cells - pathology Ovarian cancer Ovarian Neoplasms - genetics Ovarian Neoplasms - metabolism Ovarian Neoplasms - prevention & control Prognosis Receptor Tyrosine Kinase-like Orphan Receptors - genetics Receptor Tyrosine Kinase-like Orphan Receptors - immunology Receptor Tyrosine Kinase-like Orphan Receptors - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA Interference Rodents Signatures Spheroids Spheroids, Cellular - drug effects Spheroids, Cellular - metabolism Stem cells Transplantation, Heterologous Tumors |
Title | Ovarian cancer stem cells express ROR1, which can be targeted for anti–cancer-stem-cell therapy |
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