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http://purl.uniprot.org/citations/31307406http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31307406http://www.w3.org/2000/01/rdf-schema#comment"

Background

The protease uPA and its inhibitor PAI-1 play major roles in hemostasis and are also involved in cancer progression. This is mainly caused by their ability to degrade extracellular matrix-facilitating tumor cell migration. This study aimed to investigate the impact of uPA/PAI-1 and disseminated cytokeratin-positive cells (dCK+) on the outcome and the existence of synergistic effects.

Methods

We retrospectively analyzed a cohort of 480 breast cancer cases with known uPA/PAI-1 and dCK+ status. uPA/PAI-1 was tested on fresh tumor samples using a commercial ELISA test. Bone marrow aspirates were investigated immunocytochemically for CK18.

Results

DCK+ cells were identified in 23% of cases. uPA positivity was significantly associated with the occurrence of dCK+ cells (P = 0.028). uPA and PAI-1 were significantly associated with outcome in the subgroup of early-stage cases without chemotherapy. DCK+ cells alone were not prognostic. However, we found synergistic effects. In the subgroup of node-negative cases with and without chemotherapy, the prognostic impact of uPA and PAI-1 was enhanced in cases with additional dCK-positivity (triple +). In cases without chemotherapy, triple-positive status was independently prognostic (HR: 9.3 CI: 1.1-75) next to T stage.

Conclusions

uPA and PAI-1 seem to influence the metastatic potential of dCK+ cells, which underlines its important role in tumor progression."xsd:string
http://purl.uniprot.org/citations/31307406http://purl.org/dc/terms/identifier"doi:10.1186/s12885-019-5857-0"xsd:string
http://purl.uniprot.org/citations/31307406http://purl.uniprot.org/core/author"Hoffmann R."xsd:string
http://purl.uniprot.org/citations/31307406http://purl.uniprot.org/core/author"Jung T."xsd:string
http://purl.uniprot.org/citations/31307406http://purl.uniprot.org/core/author"Harbeck N."xsd:string
http://purl.uniprot.org/citations/31307406http://purl.uniprot.org/core/author"Jakubowicz E."xsd:string
http://purl.uniprot.org/citations/31307406http://purl.uniprot.org/core/author"Schlimok G."xsd:string
http://purl.uniprot.org/citations/31307406http://purl.uniprot.org/core/author"Markl B."xsd:string
http://purl.uniprot.org/citations/31307406http://purl.uniprot.org/core/author"Oruzio D."xsd:string
http://purl.uniprot.org/citations/31307406http://purl.uniprot.org/core/author"Schenkirsch G."xsd:string
http://purl.uniprot.org/citations/31307406http://purl.uniprot.org/core/author"Kazik M."xsd:string
http://purl.uniprot.org/citations/31307406http://purl.uniprot.org/core/author"Steinfeld D."xsd:string
http://purl.uniprot.org/citations/31307406http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/31307406http://purl.uniprot.org/core/name"BMC Cancer"xsd:string
http://purl.uniprot.org/citations/31307406http://purl.uniprot.org/core/pages"692"xsd:string
http://purl.uniprot.org/citations/31307406http://purl.uniprot.org/core/title"Impact of uPA/PAI-1 and disseminated cytokeratin-positive cells in breast cancer."xsd:string
http://purl.uniprot.org/citations/31307406http://purl.uniprot.org/core/volume"19"xsd:string
http://purl.uniprot.org/citations/31307406http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31307406
http://purl.uniprot.org/citations/31307406http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/31307406
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http://purl.uniprot.org/uniprot/#_P00749-mappedCitation-31307406http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31307406
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