RGD Reference Report - Patient-derived ovarian cancer xenografts re-growing after a cisplatinum treatment are less responsive to a second drug re-challenge: a new experimental setting to study response to therapy. - Rat Genome Database

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Patient-derived ovarian cancer xenografts re-growing after a cisplatinum treatment are less responsive to a second drug re-challenge: a new experimental setting to study response to therapy.

Authors: Ricci, Francesca  Fratelli, Maddalena  Guffanti, Federica  Porcu, Luca  Spriano, Filippo  Dell'Anna, Tiziana  Fruscio, Robert  Damia, Giovanna 
Citation: Ricci F, etal., Oncotarget. 2017 Jan 31;8(5):7441-7451. doi: 10.18632/oncotarget.7465.
RGD ID: 18337281
Pubmed: PMID:26910918   (View Abstract at PubMed)
PMCID: PMC5352333   (View Article at PubMed Central)
DOI: DOI:10.18632/oncotarget.7465   (Journal Full-text)

Even if ovarian cancer patients are very responsive to a cisplatinum-based therapy, most will relapse with a resistant disease. New experimental animal models are needed to explore the mechanisms of resistance, to better tailor treatment and improve patient prognosis. To address these aims, seven patient-derived high-grade serous/endometrioid ovarian cancer xenografts were characterized for the antitumor response after one and two cycles of cisplatinum and classified as Very Responsive, Responsive, and Low Responsive to drug treatment. Xenografts re-growing after the first drug cycle were much less responsive to the second one. The expression of epithelial-mesenchymal transition (EMT) and cancer stem cells (CSCs) genes was investigated in cisplatinum-treated and not-treated tumors. We found that different EMT (TCF3, CAMK2N1, EGFR, and IGFBP4) and CSCs (SMO, DLL1, STAT3, and ITGA6) genes were expressed at higher levels in Low Responsive than in Responsive and Very Responsive xenografts. The expression of STAT3 was found to be associated with lower survival (HR = 13.7; p = 0.013) in the TCGA patient data set. MMP9, CD44, DLL4, FOXP1, MERTK, and PTPRC genes were found more expressed in tumors re-growing after cisplatinum treatment than in untreated tumors. We here describe a new in vivo ovarian carcinoma experimental setting that will be instrumental for specific trials of combination therapy to counteract cisplatinum resistance in order to improve the prognosis of ovarian patients.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
ovarian carcinoma treatmentIDA 18337281 RGD 
ovarian carcinoma treatmentISOCAMK2N1 (Homo sapiens)18337281; 18337281 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Camk2n1  (calcium/calmodulin-dependent protein kinase II inhibitor 1)

Genes (Mus musculus)
Camk2n1  (calcium/calmodulin-dependent protein kinase II inhibitor 1)

Genes (Homo sapiens)
CAMK2N1  (calcium/calmodulin dependent protein kinase II inhibitor 1)


Additional Information