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Transcriptomic profiling of triple-negative breast cancer (TNBC) patient-derived xenografts (PDX) sensitive and resistant to docetaxel.

ABSTRACT: SurePrint G3 Human Gene Expression Microarray v2 was used to obtain gene expression profiles of two different TNBC PDX models sensitive to docetaxel and in the docetaxel resistant TNBC PDX models derived from both initially sensitive.

ORGANISM(S): Homo sapiens

PROVIDER: GSE110153 | GEO | 2019/07/30

REPOSITORIES: GEO

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Transcriptomic profiling of triple-negative breast cancer (TNBC) patient-derived xenografts (PDX) sensitive and resistant to docetaxel.

Project description:Transcriptomic profiling of triple-negative breast cancer (TNBC) patient-derived xenografts (PDX) sensitive and resistant to docetaxel.

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Epigenetic profiling of docetaxel resistance in Breast Cancer

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Expression data from Docetaxel-resistant prostate cancer cells

Project description:Docetaxel is the standard first line therapy for hormone-refractory prostate cancer patients. Here we generated models of Docetaxel resistance in prostate cancer cells to study the molecular pathways that drive the acquisition of resistance to this therapy. We used microarrays to detail the global program of gene expression underlying the acquisition of Docetaxel resistance in prostate cancer cells. Parental Docetaxel-sensitive prostate cancer cell lines (DU145 and 22Rv1) and selected Docetaxel-resistant cells (DU145-DR and 22Rv1-DR) were harvested for RNA extraction and hybridization on Affymetrix microarrays. Samples were analyzed in triplicates in order to increase the resolution of expression profiles.

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17 Models: Buparlisib-treated Patient Derived Xenograft (PDX) Reversed Phase Protein Array (RPPA) Data

Project description:Aberrant activation of PI3K pathway is frequently observed in triple negative breast cancer (TNBC). However single agent PI3K inhibitors have shown limited anti-tumor activity. To investigate biomarkers of response and resistance mechanisms, we tested 17 TNBC patient-derived xenograft (PDX) models representing diverse genomic backgrounds and varying degrees of PI3K pathway signaling activities for their tumor growth response to the pan-PI3K inhibitor BKM120. Baseline and post-treatment PDX tumors harvested following 3 days of BKM120 or vehicle administration were subjected to reverse phase protein array (RPPA) to identify protein markers associated with tumor growth response. While BKM120 consistently reduced PI3K pathway activity, as demonstrated by reduced levels of phosphorylated AKT, percentage tumor growth inhibition (%TGI) ranged from 35% in the least sensitive to 84% in the most sensitive PDX model at the completion of approximately 3-4 weeks of treatment. Several biomarkers showed significant association with resistance, including elevated baseline levels of growth factor receptors (EGFR, pHER3 Y1197), PI3Kp85 regulatory subunit, anti-apoptotic protein BclXL, EMT (Vimentin, MMP9, IntegrinaV), NFKB pathway (IkappaB, RANKL), and intracellular signaling molecules including Caveolin, CBP, and KLF4, as well as treatment-induced increase in the levels of phosphorylated forms of Aurora kinases. Sensitivity to BKM120 was associated with higher baseline levels of proapoptotic markers (Bak and Caspase 3) and a greater number of markers differentially changed following BKM120 therapy. Interestingly, markers indicating PI3K pathway signaling activation or PTEN loss at baseline were not significantly correlated to %TGI. These results provide important insights into biomarker development for PI3K inhibitors in TNBC.

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