sub:provenance {
  sub:assertion dcterms:description "[In bone metastases, tumor cells interact with the bone microenvironment to induce osteoclastogenesis, leading to bone destruction and the growth factor release.� RANK ligand (RANKL) is essential for osteoclast formation, function, and survival.� Tumor cell-mediated osteolysis is thought to occur ultimately via induction of RANKL within the bone stroma, and inhibition of RANKL in models of breast cancer bone metastases blocks tumor-induced osteolysis and reduces skeletal tumor burden.� In addition, the skeleton is co-opted by tumor cells and functions as a supportive tumor microenvironment.� Inhibition of RANKL, by reducing tumor-induced osteoclastogenesis, may reduce the local release of growth factors and calcium which may potentially enhance the anti-tumor activity of cytotoxic or direct tumor apoptotic agents.� Recombinant human Apo2 ligand/ TNF-related apoptosis-inducing ligand (rhApo2L/TRAIL/dulanermin) is a dual pro-apoptotic receptor agonist that preferentially induces apoptosis in cancer cells versus normal cells.� We therefore examined RANKL inhibition (using RANK-Fc) in combination with rhApo2L/TRAIL on tumor-induced osteolysis and skeletal tumor burden in a murine intracardiac injection model of MDA-MB-231 breast carcinoma bone metastasis.� rhApo2L/TRAIL treatment resulted in a rapid reduction of skeletal tumor burden.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine."@en ;
    wi:evidence dgn-void:source_evidence_literature ;
    sio:SIO_000772 miriam-pubmed:20150760 ;
    prov:wasDerivedFrom dgn-void:BEFREE ;
    prov:wasGeneratedBy eco:ECO_0000203 .
  dgn-void:BEFREE pav:importedOn "2017-02-19"^^xsd:date .
  dgn-void:source_evidence_literature a eco:ECO_0000212 ;
    rdfs:comment "Gene-disease associations inferred from text-mining the literature."@en ;
    rdfs:label "DisGeNET evidence - LITERATURE"@en .
}