Pancreatic cancer circulating tumour cells express a cell motility gene signature that predicts survival after surgery
Background Most cancer deaths are caused by metastases, resulting from circulating tumor cells (CTC) that detach from the primary cancer and survive in distant organs. The aim of the present study was to develop a CTC gene signature and to assess its prognostic relevance after surgery for pancreatic...
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| Veröffentlicht in: | BMC cancer Jg. 12; H. 1; S. 527 |
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| Format: | Journal Article |
| Sprache: | Englisch |
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BioMed Central
16.11.2012
BioMed Central Ltd Springer Nature B.V |
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| ISSN: | 1471-2407, 1471-2407 |
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| Abstract | Background
Most cancer deaths are caused by metastases, resulting from circulating tumor cells (CTC) that detach from the primary cancer and survive in distant organs. The aim of the present study was to develop a CTC gene signature and to assess its prognostic relevance after surgery for pancreatic ductal adenocarcinoma (PDAC).
Methods
Negative depletion fluorescence activated cell sorting (FACS) was developed and validated with spiking experiments using cancer cell lines in whole human blood samples. This FACS-based method was used to enrich for CTC from the blood of 10 patients who underwent surgery for PDAC. Total RNA was isolated from 4 subgroup samples, i.e. CTC, haematological cells (G), original tumour (T), and non-tumoural pancreatic control tissue (P). After RNA quality control, samples of 6 patients were eligible for further analysis. Whole genome microarray analysis was performed after double linear amplification of RNA. ‘Ingenuity Pathway Analysis’ software and AmiGO were used for functional data analyses. A CTC gene signature was developed and validated with the nCounter system on expression data of 78 primary PDAC using Cox regression analysis for disease-free (DFS) and overall survival (OS).
Results
Using stringent statistical analysis, we retained 8,152 genes to compare expression profiles of CTC vs. other subgroups, and found 1,059 genes to be differentially expressed. The pathway with the highest expression ratio in CTC was p38 mitogen-activated protein kinase (p38 MAPK) signaling, known to be involved in cancer cell migration. In the p38 MAPK pathway, TGF-β1, cPLA2, and MAX were significantly upregulated. In addition, 9 other genes associated with both p38 MAPK signaling and cell motility were overexpressed in CTC. High co-expression of TGF-β1 and our cell motility panel (≥ 4 out of 9 genes for DFS and ≥ 6 out of 9 genes for OS) in primary PDAC was identified as an independent predictor of DFS (p=0.041, HR (95% CI) = 1.885 (1.025 – 3.559)) and OS (p=0.047, HR (95% CI) = 1.366 (1.004 – 1.861)).
Conclusions
Pancreatic CTC isolated from blood samples using FACS-based negative depletion, express a cell motility gene signature. Expression of this newly defined cell motility gene signature in the primary tumour can predict survival of patients undergoing surgical resection for pancreatic cancer.
Trial Registration
Clinical trials.gov NCT00495924 |
|---|---|
| AbstractList | Most cancer deaths are caused by metastases, resulting from circulating tumor cells (CTC) that detach from the primary cancer and survive in distant organs. The aim of the present study was to develop a CTC gene signature and to assess its prognostic relevance after surgery for pancreatic ductal adenocarcinoma (PDAC).BACKGROUNDMost cancer deaths are caused by metastases, resulting from circulating tumor cells (CTC) that detach from the primary cancer and survive in distant organs. The aim of the present study was to develop a CTC gene signature and to assess its prognostic relevance after surgery for pancreatic ductal adenocarcinoma (PDAC).Negative depletion fluorescence activated cell sorting (FACS) was developed and validated with spiking experiments using cancer cell lines in whole human blood samples. This FACS-based method was used to enrich for CTC from the blood of 10 patients who underwent surgery for PDAC. Total RNA was isolated from 4 subgroup samples, i.e. CTC, haematological cells (G), original tumour (T), and non-tumoural pancreatic control tissue (P). After RNA quality control, samples of 6 patients were eligible for further analysis. Whole genome microarray analysis was performed after double linear amplification of RNA. 'Ingenuity Pathway Analysis' software and AmiGO were used for functional data analyses. A CTC gene signature was developed and validated with the nCounter system on expression data of 78 primary PDAC using Cox regression analysis for disease-free (DFS) and overall survival (OS).METHODSNegative depletion fluorescence activated cell sorting (FACS) was developed and validated with spiking experiments using cancer cell lines in whole human blood samples. This FACS-based method was used to enrich for CTC from the blood of 10 patients who underwent surgery for PDAC. Total RNA was isolated from 4 subgroup samples, i.e. CTC, haematological cells (G), original tumour (T), and non-tumoural pancreatic control tissue (P). After RNA quality control, samples of 6 patients were eligible for further analysis. Whole genome microarray analysis was performed after double linear amplification of RNA. 'Ingenuity Pathway Analysis' software and AmiGO were used for functional data analyses. A CTC gene signature was developed and validated with the nCounter system on expression data of 78 primary PDAC using Cox regression analysis for disease-free (DFS) and overall survival (OS).Using stringent statistical analysis, we retained 8,152 genes to compare expression profiles of CTC vs. other subgroups, and found 1,059 genes to be differentially expressed. The pathway with the highest expression ratio in CTC was p38 mitogen-activated protein kinase (p38 MAPK) signaling, known to be involved in cancer cell migration. In the p38 MAPK pathway, TGF-β1, cPLA2, and MAX were significantly upregulated. In addition, 9 other genes associated with both p38 MAPK signaling and cell motility were overexpressed in CTC. High co-expression of TGF-β1 and our cell motility panel (≥ 4 out of 9 genes for DFS and ≥ 6 out of 9 genes for OS) in primary PDAC was identified as an independent predictor of DFS (p=0.041, HR (95% CI) = 1.885 (1.025 - 3.559)) and OS (p=0.047, HR (95% CI) = 1.366 (1.004 - 1.861)).RESULTSUsing stringent statistical analysis, we retained 8,152 genes to compare expression profiles of CTC vs. other subgroups, and found 1,059 genes to be differentially expressed. The pathway with the highest expression ratio in CTC was p38 mitogen-activated protein kinase (p38 MAPK) signaling, known to be involved in cancer cell migration. In the p38 MAPK pathway, TGF-β1, cPLA2, and MAX were significantly upregulated. In addition, 9 other genes associated with both p38 MAPK signaling and cell motility were overexpressed in CTC. High co-expression of TGF-β1 and our cell motility panel (≥ 4 out of 9 genes for DFS and ≥ 6 out of 9 genes for OS) in primary PDAC was identified as an independent predictor of DFS (p=0.041, HR (95% CI) = 1.885 (1.025 - 3.559)) and OS (p=0.047, HR (95% CI) = 1.366 (1.004 - 1.861)).Pancreatic CTC isolated from blood samples using FACS-based negative depletion, express a cell motility gene signature. Expression of this newly defined cell motility gene signature in the primary tumour can predict survival of patients undergoing surgical resection for pancreatic cancer.CONCLUSIONSPancreatic CTC isolated from blood samples using FACS-based negative depletion, express a cell motility gene signature. Expression of this newly defined cell motility gene signature in the primary tumour can predict survival of patients undergoing surgical resection for pancreatic cancer.Clinical trials.gov NCT00495924.TRIAL REGISTRATIONClinical trials.gov NCT00495924. Most cancer deaths are caused by metastases, resulting from circulating tumor cells (CTC) that detach from the primary cancer and survive in distant organs. The aim of the present study was to develop a CTC gene signature and to assess its prognostic relevance after surgery for pancreatic ductal adenocarcinoma (PDAC). Negative depletion fluorescence activated cell sorting (FACS) was developed and validated with spiking experiments using cancer cell lines in whole human blood samples. This FACS-based method was used to enrich for CTC from the blood of 10 patients who underwent surgery for PDAC. Total RNA was isolated from 4 subgroup samples, i.e. CTC, haematological cells (G), original tumour (T), and non-tumoural pancreatic control tissue (P). After RNA quality control, samples of 6 patients were eligible for further analysis. Whole genome microarray analysis was performed after double linear amplification of RNA. 'Ingenuity Pathway Analysis' software and AmiGO were used for functional data analyses. A CTC gene signature was developed and validated with the nCounter system on expression data of 78 primary PDAC using Cox regression analysis for disease-free (DFS) and overall survival (OS). Using stringent statistical analysis, we retained 8,152 genes to compare expression profiles of CTC vs. other subgroups, and found 1,059 genes to be differentially expressed. The pathway with the highest expression ratio in CTC was p38 mitogen-activated protein kinase (p38 MAPK) signaling, known to be involved in cancer cell migration. In the p38 MAPK pathway, TGF-β1, cPLA2, and MAX were significantly upregulated. In addition, 9 other genes associated with both p38 MAPK signaling and cell motility were overexpressed in CTC. High co-expression of TGF-β1 and our cell motility panel (≥ 4 out of 9 genes for DFS and ≥ 6 out of 9 genes for OS) in primary PDAC was identified as an independent predictor of DFS (p=0.041, HR (95% CI) = 1.885 (1.025 - 3.559)) and OS (p=0.047, HR (95% CI) = 1.366 (1.004 - 1.861)). Pancreatic CTC isolated from blood samples using FACS-based negative depletion, express a cell motility gene signature. Expression of this newly defined cell motility gene signature in the primary tumour can predict survival of patients undergoing surgical resection for pancreatic cancer. Clinical trials.gov NCT00495924. Background: Most cancer deaths are caused by metastases, resulting from circulating tumor cells (CTC) that detach from the primary cancer and survive in distant organs. The aim of the present study was to develop a CTC gene signature and to assess its prognostic relevance after surgery for pancreatic ductal adenocarcinoma (PDAC). Methods: Negative depletion fluorescence activated cell sorting (FACS) was developed and validated with spiking experiments using cancer cell lines in whole human blood samples. This FACS-based method was used to enrich for CTC from the blood of 10 patients who underwent surgery for PDAC. Total RNA was isolated from 4 subgroup samples, i.e. CTC, haematological cells (G), original tumour (T), and non-tumoural pancreatic control tissue (P). After RNA quality control, samples of 6 patients were eligible for further analysis. Whole genome microarray analysis was performed after double linear amplification of RNA. 'Ingenuity Pathway Analysis' software and AmiGO were used for functional data analyses. A CTC gene signature was developed and validated with the nCounter system on expression data of 78 primary PDAC using Cox regression analysis for disease-free (DFS) and overall survival (OS). Results: Using stringent statistical analysis, we retained 8,152 genes to compare expression profiles of CTC vs. other subgroups, and found 1,059 genes to be differentially expressed. The pathway with the highest expression ratio in CTC was p38 mitogen-activated protein kinase (p38 MAPK) signaling, known to be involved in cancer cell migration. In the p38 MAPK pathway, TGF-[beta]1, cPLA2, and MAX were significantly upregulated. In addition, 9 other genes associated with both p38 MAPK signaling and cell motility were overexpressed in CTC. High co-expression of TGF-[beta]1 and our cell motility panel (> or = 4 out of 9 genes for DFS and > or = 6 out of 9 genes for OS) in primary PDAC was identified as an independent predictor of DFS (p=0.041, HR (95% CI) = 1.885 (1.025 - 3.559)) and OS (p=0.047, HR (95% CI) = 1.366 (1.004 - 1.861)). Conclusions: Pancreatic CTC isolated from blood samples using FACS-based negative depletion, express a cell motility gene signature. Expression of this newly defined cell motility gene signature in the primary tumour can predict survival of patients undergoing surgical resection for pancreatic cancer. Trial Registration: Clinical trials.gov NCT00495924 Background Most cancer deaths are caused by metastases, resulting from circulating tumor cells (CTC) that detach from the primary cancer and survive in distant organs. The aim of the present study was to develop a CTC gene signature and to assess its prognostic relevance after surgery for pancreatic ductal adenocarcinoma (PDAC). Methods Negative depletion fluorescence activated cell sorting (FACS) was developed and validated with spiking experiments using cancer cell lines in whole human blood samples. This FACS-based method was used to enrich for CTC from the blood of 10 patients who underwent surgery for PDAC. Total RNA was isolated from 4 subgroup samples, i.e. CTC, haematological cells (G), original tumour (T), and non-tumoural pancreatic control tissue (P). After RNA quality control, samples of 6 patients were eligible for further analysis. Whole genome microarray analysis was performed after double linear amplification of RNA. 'Ingenuity Pathway Analysis' software and AmiGO were used for functional data analyses. A CTC gene signature was developed and validated with the nCounter system on expression data of 78 primary PDAC using Cox regression analysis for disease-free (DFS) and overall survival (OS). Results Using stringent statistical analysis, we retained 8,152 genes to compare expression profiles of CTC vs. other subgroups, and found 1,059 genes to be differentially expressed. The pathway with the highest expression ratio in CTC was p38 mitogen-activated protein kinase (p38 MAPK) signaling, known to be involved in cancer cell migration. In the p38 MAPK pathway, TGF-[beta]1, cPLA2, and MAX were significantly upregulated. In addition, 9 other genes associated with both p38 MAPK signaling and cell motility were overexpressed in CTC. High co-expression of TGF-[beta]1 and our cell motility panel ([greater than or equai to] 4 out of 9 genes for DFS and [greater than or equai to] 6 out of 9 genes for OS) in primary PDAC was identified as an independent predictor of DFS (p=0.041, HR (95% CI) = 1.885 (1.025 - 3.559)) and OS (p=0.047, HR (95% CI) = 1.366 (1.004 - 1.861)). Conclusions Pancreatic CTC isolated from blood samples using FACS-based negative depletion, express a cell motility gene signature. Expression of this newly defined cell motility gene signature in the primary tumour can predict survival of patients undergoing surgical resection for pancreatic cancer. Trial Registration Clinical trials.gov NCT00495924 Keywords: Circulating tumour cells, Pancreatic ductal adenocarcinoma, Gene expression profiling, p38 - MAPK signaling, Transforming growth factor - [beta]1, Cancer cell migration, Cell motility Background Most cancer deaths are caused by metastases, resulting from circulating tumor cells (CTC) that detach from the primary cancer and survive in distant organs. The aim of the present study was to develop a CTC gene signature and to assess its prognostic relevance after surgery for pancreatic ductal adenocarcinoma (PDAC). Methods Negative depletion fluorescence activated cell sorting (FACS) was developed and validated with spiking experiments using cancer cell lines in whole human blood samples. This FACS-based method was used to enrich for CTC from the blood of 10 patients who underwent surgery for PDAC. Total RNA was isolated from 4 subgroup samples, i.e. CTC, haematological cells (G), original tumour (T), and non-tumoural pancreatic control tissue (P). After RNA quality control, samples of 6 patients were eligible for further analysis. Whole genome microarray analysis was performed after double linear amplification of RNA. ‘Ingenuity Pathway Analysis’ software and AmiGO were used for functional data analyses. A CTC gene signature was developed and validated with the nCounter system on expression data of 78 primary PDAC using Cox regression analysis for disease-free (DFS) and overall survival (OS). Results Using stringent statistical analysis, we retained 8,152 genes to compare expression profiles of CTC vs. other subgroups, and found 1,059 genes to be differentially expressed. The pathway with the highest expression ratio in CTC was p38 mitogen-activated protein kinase (p38 MAPK) signaling, known to be involved in cancer cell migration. In the p38 MAPK pathway, TGF-β1, cPLA2, and MAX were significantly upregulated. In addition, 9 other genes associated with both p38 MAPK signaling and cell motility were overexpressed in CTC. High co-expression of TGF-β1 and our cell motility panel (≥ 4 out of 9 genes for DFS and ≥ 6 out of 9 genes for OS) in primary PDAC was identified as an independent predictor of DFS (p=0.041, HR (95% CI) = 1.885 (1.025 – 3.559)) and OS (p=0.047, HR (95% CI) = 1.366 (1.004 – 1.861)). Conclusions Pancreatic CTC isolated from blood samples using FACS-based negative depletion, express a cell motility gene signature. Expression of this newly defined cell motility gene signature in the primary tumour can predict survival of patients undergoing surgical resection for pancreatic cancer. Trial Registration Clinical trials.gov NCT00495924 Most cancer deaths are caused by metastases, resulting from circulating tumor cells (CTC) that detach from the primary cancer and survive in distant organs. The aim of the present study was to develop a CTC gene signature and to assess its prognostic relevance after surgery for pancreatic ductal adenocarcinoma (PDAC). Negative depletion fluorescence activated cell sorting (FACS) was developed and validated with spiking experiments using cancer cell lines in whole human blood samples. This FACS-based method was used to enrich for CTC from the blood of 10 patients who underwent surgery for PDAC. Total RNA was isolated from 4 subgroup samples, i.e. CTC, haematological cells (G), original tumour (T), and non-tumoural pancreatic control tissue (P). After RNA quality control, samples of 6 patients were eligible for further analysis. Whole genome microarray analysis was performed after double linear amplification of RNA. 'Ingenuity Pathway Analysis' software and AmiGO were used for functional data analyses. A CTC gene signature was developed and validated with the nCounter system on expression data of 78 primary PDAC using Cox regression analysis for disease-free (DFS) and overall survival (OS). Using stringent statistical analysis, we retained 8,152 genes to compare expression profiles of CTC vs. other subgroups, and found 1,059 genes to be differentially expressed. The pathway with the highest expression ratio in CTC was p38 mitogen-activated protein kinase (p38 MAPK) signaling, known to be involved in cancer cell migration. In the p38 MAPK pathway, TGF-[beta]1, cPLA2, and MAX were significantly upregulated. In addition, 9 other genes associated with both p38 MAPK signaling and cell motility were overexpressed in CTC. High co-expression of TGF-[beta]1 and our cell motility panel ([greater than or equai to] 4 out of 9 genes for DFS and [greater than or equai to] 6 out of 9 genes for OS) in primary PDAC was identified as an independent predictor of DFS (p=0.041, HR (95% CI) = 1.885 (1.025 - 3.559)) and OS (p=0.047, HR (95% CI) = 1.366 (1.004 - 1.861)). Pancreatic CTC isolated from blood samples using FACS-based negative depletion, express a cell motility gene signature. Expression of this newly defined cell motility gene signature in the primary tumour can predict survival of patients undergoing surgical resection for pancreatic cancer. Doc number: 527 Abstract Background: Most cancer deaths are caused by metastases, resulting from circulating tumor cells (CTC) that detach from the primary cancer and survive in distant organs. The aim of the present study was to develop a CTC gene signature and to assess its prognostic relevance after surgery for pancreatic ductal adenocarcinoma (PDAC). Methods: Negative depletion fluorescence activated cell sorting (FACS) was developed and validated with spiking experiments using cancer cell lines in whole human blood samples. This FACS-based method was used to enrich for CTC from the blood of 10 patients who underwent surgery for PDAC. Total RNA was isolated from 4 subgroup samples, i.e. CTC, haematological cells (G), original tumour (T), and non-tumoural pancreatic control tissue (P). After RNA quality control, samples of 6 patients were eligible for further analysis. Whole genome microarray analysis was performed after double linear amplification of RNA. 'Ingenuity Pathway Analysis' software and AmiGO were used for functional data analyses. A CTC gene signature was developed and validated with the nCounter system on expression data of 78 primary PDAC using Cox regression analysis for disease-free (DFS) and overall survival (OS). Results: Using stringent statistical analysis, we retained 8,152 genes to compare expression profiles of CTC vs. other subgroups, and found 1,059 genes to be differentially expressed. The pathway with the highest expression ratio in CTC was p38 mitogen-activated protein kinase (p38 MAPK) signaling, known to be involved in cancer cell migration. In the p38 MAPK pathway, TGF-β1, cPLA2, and MAX were significantly upregulated. In addition, 9 other genes associated with both p38 MAPK signaling and cell motility were overexpressed in CTC. High co-expression of TGF-β1 and our cell motility panel (≥ 4 out of 9 genes for DFS and ≥ 6 out of 9 genes for OS) in primary PDAC was identified as an independent predictor of DFS (p=0.041, HR (95% CI) = 1.885 (1.025 - 3.559)) and OS (p=0.047, HR (95% CI) = 1.366 (1.004 - 1.861)). Conclusions: Pancreatic CTC isolated from blood samples using FACS-based negative depletion, express a cell motility gene signature. Expression of this newly defined cell motility gene signature in the primary tumour can predict survival of patients undergoing surgical resection for pancreatic cancer. Trial Registration: Clinical trials.gov NCT00495924 |
| ArticleNumber | 527 |
| Audience | Academic |
| Author | van Eijsden, Rudy Roskams, Tania Topal, Baki Sergeant, Gregory Van Duppen, Victor |
| AuthorAffiliation | 2 VIB Nucleomics Core, KU Leuven, Herestraat 49, Leuven, 3000, Belgium 1 Department of Abdominal Surgery, University Hospitals Leuven, Herestraat 49, Leuven, 3000, Belgium 4 Laboratory of Experimental Hematology, KU Leuven, Herestraat 49, Leuven, 3000, Belgium 3 Department of Pathology, University Hospitals Leuven, Herestraat 49, Leuven, 3000, Belgium |
| AuthorAffiliation_xml | – name: 2 VIB Nucleomics Core, KU Leuven, Herestraat 49, Leuven, 3000, Belgium – name: 3 Department of Pathology, University Hospitals Leuven, Herestraat 49, Leuven, 3000, Belgium – name: 4 Laboratory of Experimental Hematology, KU Leuven, Herestraat 49, Leuven, 3000, Belgium – name: 1 Department of Abdominal Surgery, University Hospitals Leuven, Herestraat 49, Leuven, 3000, Belgium |
| Author_xml | – sequence: 1 givenname: Gregory surname: Sergeant fullname: Sergeant, Gregory organization: Department of Abdominal Surgery, University Hospitals Leuven – sequence: 2 givenname: Rudy surname: van Eijsden fullname: van Eijsden, Rudy organization: VIB Nucleomics Core, KU Leuven – sequence: 3 givenname: Tania surname: Roskams fullname: Roskams, Tania organization: Department of Pathology, University Hospitals Leuven – sequence: 4 givenname: Victor surname: Van Duppen fullname: Van Duppen, Victor organization: Laboratory of Experimental Hematology, KU Leuven – sequence: 5 givenname: Baki surname: Topal fullname: Topal, Baki email: baki.topal@med.kuleuven.be organization: Department of Abdominal Surgery, University Hospitals Leuven |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23157946$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1091/mbc.E08-09-0898 10.1038/nm1469 10.1189/jlb.1008647 10.1093/bioinformatics/btn615 10.1038/ncb1507 10.1093/bioinformatics/btg405 10.1038/nrclinonc.2009.23 10.1007/978-3-642-59349-9_13 10.1002/ijc.2910150505 10.1038/ng1215 10.1111/j.1749-6632.2009.04911.x 10.1038/nbt1385 10.1186/gb-2004-5-10-r80 10.1038/nrc1275 10.1016/S0092-8674(00)81683-9 10.1038/ncb1973 10.1002/cyto.10161 10.1002/jcp.21783 10.1111/j.2517-6161.1995.tb02031.x 10.2202/1544-6115.1027 10.2144/03356rr01 |
| ContentType | Journal Article |
| Copyright | Sergeant et al; licensee BioMed Central Ltd. 2012 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. COPYRIGHT 2012 BioMed Central Ltd. 2012 Sergeant et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright ©2012 Sergeant et al; licensee BioMed Central Ltd. 2012 Sergeant et al; licensee BioMed Central Ltd. |
| Copyright_xml | – notice: Sergeant et al; licensee BioMed Central Ltd. 2012 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. – notice: COPYRIGHT 2012 BioMed Central Ltd. – notice: 2012 Sergeant et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. – notice: Copyright ©2012 Sergeant et al; licensee BioMed Central Ltd. 2012 Sergeant et al; licensee BioMed Central Ltd. |
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| DOI | 10.1186/1471-2407-12-527 |
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| Discipline | Medicine |
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| EndPage | 527 |
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| Keywords | Cell motility Transforming growth factor - β1 Gene expression profiling Pancreatic ductal adenocarcinoma p38 – MAPK signaling Circulating tumour cells Cancer cell migration |
| Language | English |
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| References | Gertler, Rosenberg, Fuehrer, Dahm, Nekarda, Siewert (CR3) 2003; 162 Ehrchen, Sunderkotter, Foell, Vogl, Roth (CR15) 2009; 86 Zuo, Chen (CR16) 2009; 20 Hanahan, Weinberg (CR1) 2000; 100 Carbon, Ireland, Mungall, Shu, Marshall, Lewis (CR11) 2009; 25 Gentleman, Carey, Bates, Bolstad, Dettling, Dudoit, Ellis, Gautier, Ge, Gentry (CR7) 2004; 5 Chuang, Yang, Chen, Huang, Tan, Lin, Hsu, Fong, Tang (CR18) 2009; 220 Yu, Jove (CR19) 2004; 4 Pantel, Riethdorf (CR2) 2009; 6 Gautier, Cope, Bolstad, Irizarry (CR6) 2004; 20 CR9 Geiss, Bumgarner, Birditt, Dahl, Dowidar, Dunaway, Fell, Ferree, George, Grogan, James, Maysuria, Mitton, Oliveri, Osborn, Peng, Ratcliffe, Webster, Davidson, Hood, Dimitrov (CR22) 2008; 26 Schoor, Weinschenk, Hennenlotter, Corvin, Stenzl, Rammensee, Stevanovic (CR13) 2003; 35 Aggarwal, Kunnumakkara, Harikumar, Gupta, Tharakan, Koca, Dey, Sung (CR20) 2009; 1171 Lieber, Mazzetta, Nelson-Rees, Kaplan, Todaro (CR5) 1975; 15 Hiratsuka, Watanabe, Aburatani, Maru (CR14) 2006; 8 Giampieri, Manning, Hooper, Jones, Hill, Sahai (CR17) 2009; 11 Albertson, Collins, McCormick, Gray (CR12) 2003; 34 Smyth (CR8) 2004; 3 Benjamini, Hochberg (CR10) 1995; 57 Steeg (CR21) 2006; 12 Rosenberg, Gertler, Friederichs, Fuehrer, Dahm, Phelps, Thorban, Nekarda, Siewert (CR4) 2002; 49 BB Aggarwal (3727_CR20) 2009; 1171 GK Smyth (3727_CR8) 2004; 3 W Zuo (3727_CR16) 2009; 20 R Rosenberg (3727_CR4) 2002; 49 S Hiratsuka (3727_CR14) 2006; 8 O Schoor (3727_CR13) 2003; 35 RC Gentleman (3727_CR7) 2004; 5 S Giampieri (3727_CR17) 2009; 11 3727_CR9 Y Benjamini (3727_CR10) 1995; 57 D Hanahan (3727_CR1) 2000; 100 H Yu (3727_CR19) 2004; 4 R Gertler (3727_CR3) 2003; 162 K Pantel (3727_CR2) 2009; 6 PS Steeg (3727_CR21) 2006; 12 DG Albertson (3727_CR12) 2003; 34 L Gautier (3727_CR6) 2004; 20 JM Ehrchen (3727_CR15) 2009; 86 JY Chuang (3727_CR18) 2009; 220 M Lieber (3727_CR5) 1975; 15 GK Geiss (3727_CR22) 2008; 26 S Carbon (3727_CR11) 2009; 25 |
| References_xml | – volume: 20 start-page: 1020 year: 2009 end-page: 1029 ident: CR16 article-title: Specific activation of mitogen-activated protein kinase by transforming growth factor-beta receptors in lipid rafts is required for epithelial cell plasticity publication-title: Mol Biol Cell doi: 10.1091/mbc.E08-09-0898 – volume: 12 start-page: 895 year: 2006 end-page: 904 ident: CR21 article-title: Tumour metastasis: mechanistic insights and clinical challenges publication-title: Nat Med doi: 10.1038/nm1469 – volume: 86 start-page: 557 year: 2009 end-page: 566 ident: CR15 article-title: The endogenous Toll-like receptor 4 agonist S100A8/S100A9 (calprotectin) as innate amplifier of infection, autoimmunity, and cancer publication-title: J Leukoc Biol doi: 10.1189/jlb.1008647 – volume: 25 start-page: 288 year: 2009 end-page: 289 ident: CR11 article-title: AmiGO: online access to ontology and annotation data publication-title: Bioinformatics doi: 10.1093/bioinformatics/btn615 – volume: 8 start-page: 1369 year: 2006 end-page: 1375 ident: CR14 article-title: Tumour-mediated upregulation of chemoattractants and recruitment of myeloid cells predetermines lung metastasis publication-title: Nat Cell Biol doi: 10.1038/ncb1507 – volume: 20 start-page: 307 year: 2004 end-page: 315 ident: CR6 article-title: affy--analysis of Affymetrix GeneChip data at the probe level publication-title: Bioinformatics doi: 10.1093/bioinformatics/btg405 – ident: CR9 – volume: 6 start-page: 190 year: 2009 end-page: 191 ident: CR2 article-title: Pathology: are circulating tumour cells predictive of overall survival? publication-title: Nat Rev Clin Oncol doi: 10.1038/nrclinonc.2009.23 – volume: 162 start-page: 149 year: 2003 end-page: 155 ident: CR3 article-title: Detection of circulating tumour cells in blood using an optimized density gradient centrifugation publication-title: Recent Results Cancer Res doi: 10.1007/978-3-642-59349-9_13 – volume: 15 start-page: 741 year: 1975 end-page: 747 ident: CR5 article-title: Establishment of a continuous tumour-cell line (panc-1) from a human carcinoma of the exocrine pancreas publication-title: Int J Cancer doi: 10.1002/ijc.2910150505 – volume: 3 start-page: Article3 year: 2004 ident: CR8 article-title: Linear models and empirical bayes methods for assessing differential expression in microarray experiments publication-title: Stat Appl Genet Mol Biol – volume: 57 start-page: 289 year: 1995 end-page: 300 ident: CR10 article-title: Controlling the false discovery rate: a practical and powerful approach to multiple testing publication-title: J R Stat Soc Ser B – volume: 34 start-page: 369 year: 2003 end-page: 376 ident: CR12 article-title: Chromosome aberrations in solid tumours publication-title: Nat Genet doi: 10.1038/ng1215 – volume: 35 start-page: 1192 year: 2003 end-page: 1196 ident: CR13 article-title: Moderate degradation does not preclude microarray analysis of small amounts of RNA publication-title: Biotechniques – volume: 1171 start-page: 59 year: 2009 end-page: 76 ident: CR20 article-title: Signal transducer and activator of transcription-3, inflammation, and cancer: how intimate is the relationship? publication-title: Ann N Y Acad Sci doi: 10.1111/j.1749-6632.2009.04911.x – volume: 26 start-page: 317 year: 2008 end-page: 325 ident: CR22 article-title: Direct multiplexed measurement of gene expression with color-coded probe pairs publication-title: Nat Biotechnol doi: 10.1038/nbt1385 – volume: 5 start-page: R80 year: 2004 ident: CR7 article-title: Bioconductor: open software development for computational biology and bioinformatics publication-title: Genome Biol doi: 10.1186/gb-2004-5-10-r80 – volume: 4 start-page: 97 year: 2004 end-page: 105 ident: CR19 article-title: The STATs of cancer–new molecular targets come of age publication-title: Nat Rev Cancer doi: 10.1038/nrc1275 – volume: 100 start-page: 57 year: 2000 end-page: 70 ident: CR1 article-title: The hallmarks of cancer publication-title: Cell doi: 10.1016/S0092-8674(00)81683-9 – volume: 11 start-page: 1287 year: 2009 end-page: 1296 ident: CR17 article-title: Localized and reversible TGFbeta signalling switches breast cancer cells from cohesive to single cell motility publication-title: Nat Cell Biol doi: 10.1038/ncb1973 – volume: 49 start-page: 150 year: 2002 end-page: 158 ident: CR4 article-title: Comparison of two density gradient centrifugation systems for the enrichment of disseminated tumour cells in blood publication-title: Cytometry doi: 10.1002/cyto.10161 – volume: 220 start-page: 418 year: 2009 end-page: 426 ident: CR18 article-title: CCL5/CCR5 axis promotes the motility of human oral cancer cells publication-title: J Cell Physiol doi: 10.1002/jcp.21783 – volume: 20 start-page: 307 year: 2004 ident: 3727_CR6 publication-title: Bioinformatics doi: 10.1093/bioinformatics/btg405 – volume: 8 start-page: 1369 year: 2006 ident: 3727_CR14 publication-title: Nat Cell Biol doi: 10.1038/ncb1507 – volume: 4 start-page: 97 year: 2004 ident: 3727_CR19 publication-title: Nat Rev Cancer doi: 10.1038/nrc1275 – volume: 12 start-page: 895 year: 2006 ident: 3727_CR21 publication-title: Nat Med doi: 10.1038/nm1469 – volume: 34 start-page: 369 year: 2003 ident: 3727_CR12 publication-title: Nat Genet doi: 10.1038/ng1215 – volume: 220 start-page: 418 year: 2009 ident: 3727_CR18 publication-title: J Cell Physiol doi: 10.1002/jcp.21783 – volume: 100 start-page: 57 year: 2000 ident: 3727_CR1 publication-title: Cell doi: 10.1016/S0092-8674(00)81683-9 – volume: 57 start-page: 289 year: 1995 ident: 3727_CR10 publication-title: J R Stat Soc Ser B doi: 10.1111/j.2517-6161.1995.tb02031.x – volume: 5 start-page: R80 year: 2004 ident: 3727_CR7 publication-title: Genome Biol doi: 10.1186/gb-2004-5-10-r80 – volume: 3 start-page: Article3 year: 2004 ident: 3727_CR8 publication-title: Stat Appl Genet Mol Biol doi: 10.2202/1544-6115.1027 – volume: 35 start-page: 1192 year: 2003 ident: 3727_CR13 publication-title: Biotechniques doi: 10.2144/03356rr01 – volume: 6 start-page: 190 year: 2009 ident: 3727_CR2 publication-title: Nat Rev Clin Oncol doi: 10.1038/nrclinonc.2009.23 – volume: 26 start-page: 317 year: 2008 ident: 3727_CR22 publication-title: Nat Biotechnol doi: 10.1038/nbt1385 – volume: 1171 start-page: 59 year: 2009 ident: 3727_CR20 publication-title: Ann N Y Acad Sci doi: 10.1111/j.1749-6632.2009.04911.x – volume: 162 start-page: 149 year: 2003 ident: 3727_CR3 publication-title: Recent Results Cancer Res doi: 10.1007/978-3-642-59349-9_13 – volume: 25 start-page: 288 year: 2009 ident: 3727_CR11 publication-title: Bioinformatics doi: 10.1093/bioinformatics/btn615 – volume: 86 start-page: 557 year: 2009 ident: 3727_CR15 publication-title: J Leukoc Biol doi: 10.1189/jlb.1008647 – volume: 49 start-page: 150 year: 2002 ident: 3727_CR4 publication-title: Cytometry doi: 10.1002/cyto.10161 – volume: 15 start-page: 741 year: 1975 ident: 3727_CR5 publication-title: Int J Cancer doi: 10.1002/ijc.2910150505 – ident: 3727_CR9 – volume: 11 start-page: 1287 year: 2009 ident: 3727_CR17 publication-title: Nat Cell Biol doi: 10.1038/ncb1973 – volume: 20 start-page: 1020 year: 2009 ident: 3727_CR16 publication-title: Mol Biol Cell doi: 10.1091/mbc.E08-09-0898 |
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Most cancer deaths are caused by metastases, resulting from circulating tumor cells (CTC) that detach from the primary cancer and survive in distant... Most cancer deaths are caused by metastases, resulting from circulating tumor cells (CTC) that detach from the primary cancer and survive in distant organs.... Background Most cancer deaths are caused by metastases, resulting from circulating tumor cells (CTC) that detach from the primary cancer and survive in distant... Doc number: 527 Abstract Background: Most cancer deaths are caused by metastases, resulting from circulating tumor cells (CTC) that detach from the primary... Background: Most cancer deaths are caused by metastases, resulting from circulating tumor cells (CTC) that detach from the primary cancer and survive in... |
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| SubjectTerms | Adenocarcinoma - diagnosis Adenocarcinoma - metabolism Adenocarcinoma - mortality Adenocarcinoma - surgery Aged Analysis Biomarkers, Tumor - metabolism Biomedical and Life Sciences Biomedicine Bone morphogenetic proteins Cancer Cancer Research Cancer therapies Carcinoma, Pancreatic Ductal - diagnosis Carcinoma, Pancreatic Ductal - genetics Carcinoma, Pancreatic Ductal - mortality Carcinoma, Pancreatic Ductal - surgery Care and treatment Cell Line, Tumor DNA microarrays Female Fluorescence Gene expression Gene Expression Profiling Genes Genetic aspects Genomics Health Promotion and Disease Prevention Hematology Humans Information management Male Medical research Medicine/Public Health Metastasis Microarray Analysis Middle Aged Mitogens Motility Neoplastic Cells, Circulating - metabolism Oncology Oncology, Experimental Pancreas Pancreatic cancer Pancreatic Neoplasms - diagnosis Pancreatic Neoplasms - genetics Pancreatic Neoplasms - mortality Pancreatic Neoplasms - surgery Patient outcomes Predictive Value of Tests Prognosis Protein kinases Proteins Research Article RNA Statistical analysis Surgery Surgical Oncology Survival Analysis Transforming growth factors Translational oncology |
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| Title | Pancreatic cancer circulating tumour cells express a cell motility gene signature that predicts survival after surgery |
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