@prefix this: . @prefix rdfs: . @prefix xsd: . @prefix sio: . @prefix ncit: . @prefix lld: . @prefix miriam-gene: . @prefix miriam-pubmed: . @prefix eco: . @prefix wi: . @prefix prov: . @prefix pav: . @prefix prv: . @prefix dcterms: . @prefix np: . @prefix dgn-np: . @prefix dgn-gda: . @prefix dgn-void: . dgn-np:NP752255.RAeq-ik-fm3ASaUaYL0rvsCI73E_Z1yQAmUVo6zPmSQHM130_head { this: np:hasAssertion dgn-np:NP752255.RAeq-ik-fm3ASaUaYL0rvsCI73E_Z1yQAmUVo6zPmSQHM130_assertion; np:hasProvenance dgn-np:NP752255.RAeq-ik-fm3ASaUaYL0rvsCI73E_Z1yQAmUVo6zPmSQHM130_provenance; np:hasPublicationInfo dgn-np:NP752255.RAeq-ik-fm3ASaUaYL0rvsCI73E_Z1yQAmUVo6zPmSQHM130_publicationInfo; a np:Nanopublication . dgn-np:NP752255.RAeq-ik-fm3ASaUaYL0rvsCI73E_Z1yQAmUVo6zPmSQHM130_assertion a np:Assertion . dgn-np:NP752255.RAeq-ik-fm3ASaUaYL0rvsCI73E_Z1yQAmUVo6zPmSQHM130_provenance a np:Provenance . dgn-np:NP752255.RAeq-ik-fm3ASaUaYL0rvsCI73E_Z1yQAmUVo6zPmSQHM130_publicationInfo a np:PublicationInfo . } dgn-np:NP752255.RAeq-ik-fm3ASaUaYL0rvsCI73E_Z1yQAmUVo6zPmSQHM130_assertion { miriam-gene:7157 a ncit:C16612 . lld:C0242379 a ncit:C7057 . dgn-gda:DGNd747fc8f6dc65bec98be6e27be25f230 sio:SIO_000628 miriam-gene:7157, lld:C0242379; a sio:SIO_001121 . } dgn-np:NP752255.RAeq-ik-fm3ASaUaYL0rvsCI73E_Z1yQAmUVo6zPmSQHM130_provenance { dgn-np:NP752255.RAeq-ik-fm3ASaUaYL0rvsCI73E_Z1yQAmUVo6zPmSQHM130_assertion dcterms:description "[This model showed that: (i) the combination of five genetic alterations (CDK4, hTERT, sh-p53, KRAS(V12), and c-MYC) is sufficient for full tumorigenic conversion of HBECs; (ii) genetically identical clones of transformed HBECs exhibit pronounced differences in tumor growth, histology, and differentiation; (iii) HBECs from different individuals vary in their sensitivity to transformation by these oncogenic manipulations; (iv) high levels of KRAS(V12) are required for full malignant transformation of HBECs, however, prior loss of p53 function is required to prevent oncogene-induced senescence; (v) overexpression of c-MYC greatly enhances malignancy but only in the context of sh-p53+KRAS(V12); (vi) growth of parental HBECs in serum-containing medium induces differentiation, whereas growth of oncogenically manipulated HBECs in serum increases in vivo tumorigenicity, decreases tumor latency, produces more undifferentiated tumors, and induces epithelial-to-mesenchymal transition (EMT); (vii) oncogenic transformation of HBECs leads to increased sensitivity to standard chemotherapy doublets; (viii) an mRNA signature derived by comparing tumorigenic versus nontumorigenic clones was predictive of outcome in patients with lung cancer.]. 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:23449933; prov:wasDerivedFrom dgn-void:befree-20150227; prov:wasGeneratedBy eco:ECO_0000203 . dgn-void:befree-20150227 pav:importedOn "2015-02-27"^^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 . } dgn-np:NP752255.RAeq-ik-fm3ASaUaYL0rvsCI73E_Z1yQAmUVo6zPmSQHM130_publicationInfo { this: dcterms:created "2015-08-25T14:45:14+02:00"^^xsd:dateTime; dcterms:rights ; dcterms:rightsHolder dgn-void:IBIGroup; dcterms:subject sio:SIO_000983; prv:usedData dgn-void:disgenetv3.0rdf; pav:authoredBy , , , , ; pav:createdBy ; pav:version "v3.0.0.0" . dgn-void:disgenetv3.0rdf pav:version "v3.0.0" . }