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Accession of Tumor Heterogeneity by Multiplex Transcriptome Profiling of Single Circulating Tumor Cells
TM. Gorges, A. Kuske, K. Röck, O. Mauermann, V. Müller, S. Peine, K. Verpoort, V. Novosadova, M. Kubista, S. Riethdorf, K. Pantel,
Language English Country United States
Document type Journal Article
NLK
ProQuest Central
from 2002-12-01 to 2022-04-30
Open Access Digital Library
from 1955-02-01
Medline Complete (EBSCOhost)
from 2010-01-01 to 1 year ago
Nursing & Allied Health Database (ProQuest)
from 2002-12-01 to 2022-04-30
Health & Medicine (ProQuest)
from 2002-12-01 to 2022-04-30
Public Health Database (ProQuest)
from 2002-12-01 to 2022-04-30
- MeSH
- Epithelial-Mesenchymal Transition genetics MeSH
- Humans MeSH
- Tumor Cells, Cultured MeSH
- Neoplastic Cells, Circulating metabolism pathology MeSH
- RNA, Neoplasm genetics MeSH
- Gene Expression Profiling * MeSH
- Transcriptome genetics MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
BACKGROUND: Transcriptome analysis of circulating tumor cells (CTCs) holds great promise to unravel the biology of cancer cell dissemination and identify expressed genes and signaling pathways relevant to therapeutic interventions. METHODS: CTCs were enriched based on their EpCAM expression (CellSearch(®)) or by size and deformability (Parsortix(TM)), identified by EpCAM and/or pan-keratin-specific antibodies, and isolated for single cell multiplex RNA profiling. RESULTS: Distinct breast and prostate CTC expression signatures could be discriminated from RNA profiles of leukocytes. Some CTCs positive for epithelial transcripts (EpCAM and KRT19) also coexpressed leukocyte/mesenchymal associated markers (PTPRC and VIM). Additional subsets of CTCs within individual patients were characterized by divergent expression of genes involved in epithelial-mesenchymal transition (e.g., CDH2, MMPs, VIM, or ZEB1 and 2), DNA repair (RAD51), resistance to cancer therapy (e.g., AR, AR-V7, ERBB2, EGFR), cancer stemness (e.g., CD24 and CD44), activated signaling pathways involved in tumor progression (e.g., PIK3CA and MTOR) or cross talks between tumors and immune cells (e.g., CCL4, CXCL2, CXCL9, IL15, IL1B, or IL8). CONCLUSIONS: Multimarker RNA profiling of single CTCs reveals distinct CTC subsets and provides important insights into gene regulatory networks relevant for cancer progression and therapy.
Department of Biotechnology Czech Academy of Sciences Prague Czech Republic
Department of Gynecology University Hospital Hamburg Eppendorf Hamburg Germany
Department of Transfusion Medicine University Hospital Hamburg Eppendorf Hamburg Germany
Department of Tumor Biology University Medical Center Hamburg Eppendorf Hamburg Germany
References provided by Crossref.org
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- $a BACKGROUND: Transcriptome analysis of circulating tumor cells (CTCs) holds great promise to unravel the biology of cancer cell dissemination and identify expressed genes and signaling pathways relevant to therapeutic interventions. METHODS: CTCs were enriched based on their EpCAM expression (CellSearch(®)) or by size and deformability (Parsortix(TM)), identified by EpCAM and/or pan-keratin-specific antibodies, and isolated for single cell multiplex RNA profiling. RESULTS: Distinct breast and prostate CTC expression signatures could be discriminated from RNA profiles of leukocytes. Some CTCs positive for epithelial transcripts (EpCAM and KRT19) also coexpressed leukocyte/mesenchymal associated markers (PTPRC and VIM). Additional subsets of CTCs within individual patients were characterized by divergent expression of genes involved in epithelial-mesenchymal transition (e.g., CDH2, MMPs, VIM, or ZEB1 and 2), DNA repair (RAD51), resistance to cancer therapy (e.g., AR, AR-V7, ERBB2, EGFR), cancer stemness (e.g., CD24 and CD44), activated signaling pathways involved in tumor progression (e.g., PIK3CA and MTOR) or cross talks between tumors and immune cells (e.g., CCL4, CXCL2, CXCL9, IL15, IL1B, or IL8). CONCLUSIONS: Multimarker RNA profiling of single CTCs reveals distinct CTC subsets and provides important insights into gene regulatory networks relevant for cancer progression and therapy.
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