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Exon array analysis of the response to bevacizumab/erlotinib in advanced non-small cell lung cancer

ABSTRACT: In the current study, we used exon arrays and clinical samples from a previous trial (SAKK 19/05) to investigate the expression variations at the exon-level of 3 genes potentially playing a key role in modulating treatment response (EGFR, KRAS, VEGFA). Exon-level biomarkers for the response to targeted therapy bevacizumab/erlotinib were identified in patients with metastatic non-small cell lung cancer

ORGANISM(S): Homo sapiens

PROVIDER: GSE37138 | GEO | 2013/07/30

SECONDARY ACCESSION(S): PRJNA158417

REPOSITORIES: GEO

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Exon array analysis of the response to bevacizumab/erlotinib in advanced non-small cell lung cancer

Project description:In the current study, we used exon arrays and clinical samples from a previous trial (SAKK 19/05) to investigate the expression variations at the exon-level of 3 genes potentially playing a key role in modulating treatment response (EGFR, KRAS, VEGFA). Exon-level biomarkers for the response to targeted therapy bevacizumab/erlotinib were identified in patients with metastatic non-small cell lung cancer Multicenter, prospective, open-label, single-arm, phase II trial.

2013-07-30 | E-GEOD-37138 | biostudies-arrayexpress

24h-response to bevacizumab erlortinib in non-small cell lung cancer from blood-based exon array profiling

Project description:The mechanisms of action of the combined targeted therapy bevacizumab erlotinib in late stage non-squamous non-small cell lung cancer was investigated by means of whole genome exon arrays. mRNA from peripherial blood was extracted at baseline and 24h after initiation of the therapy and hybridized on Affymetrix Human Exon 1.0 ST Arrays

2016-12-31 | GSE61676 | GEO

Transcription profiling of human xenografts produced from an endometrial cell line treated with bevacizumab (Avastin)

Project description:Microarrays were used to determine the efficacy of bevacizumab (a monoclonal antibody against the vascular endothelial growth factor and its receptors.) on endometrial cancer cells. Endometrial cancer is the most frequent gynecologic cancer in women. Long term outcomes for patients with advanced stage or recurrent disease are poor. Targeted molecular therapy against the vascular endothelial growth factor (VEGF) and its receptors constitute a new therapeutic option for these patients. The goal of our work was to assess the potential effectiveness of inhibition of VEGF/VEGFR signaling in a xenograft model of endometrial cancer using bevacizumab (Avastin, a humanized antibody against VEGFA). We also aimed to identify molecular markers of sensitivity or resistance to this agent. We show that bevacizumab retards tumor growth in athymic mice by inhibiting molecular components of signaling pathways that sustain cell survival and proliferation. We also demonstrate that resistance to bevacizumab may involve up-regulation of antiapoptotic genes and certain proto-oncogenes. Experiment Overall Design: Human xenografts produced from endometrial cell line, grown in athymic mice, were treated in vivo with bevacizumab.

2009-11-16 | E-GEOD-18195 | biostudies-arrayexpress

Effects of bevacizumab (avastin) in mouse model of endometrial cancer

2009-09-22 | GSE18195 | GEO

Charaterization of genetic alterations and gene expression signatures found in erlotinib-resistant and erlotinib/crizotinib dual-resistant HCC827 subpopulations

Project description:The non-small cell lung cancer (NSCLC) cell line HCC827 harbors an activating EGFR mutation (exon 19 deletion) that confers sensitivity to the FDA-approved EGFR inhibitor erlotinib. By applying the ClonTracer barcoding system, we were able to show the presence of pre-existing sub-populations in HCC827 that contribute to erlotinib resistance. Prior studies implicated that MET amplification confers resistance to erlotinib in this cell line. Therefore we examined the effects of the c-Met inhibitor crizotinib on the barcoded HCC827 population when treated either sequentially or simultaneously with both inhibitors. Despite the significant reduction in barcode complexity, the erlotinib/crizotinib combination treatment failed to eradicate all of the resistant clones implying the presence of an erlotinib/crizotinib dual resistant subpopulation. We performed transcriptome profiling (RNA-seq) to elucidate the potential resistance mechanisms of the dual resistant subpopulation in comparison to vehicle-treated or single agent erlotinib-resistant HCC827 cell populations as controls.

2014-10-07 | GSE62118 | GEO

Charaterization of genetic alterations and gene expression signatures found in erlotinib-resistant and erlotinib/crizotinib dual-resistant HCC827 subpopulations

2014-10-07 | E-GEOD-62118 | biostudies-arrayexpress

Immuno-priming with bevacizumab: durvalumab plus bevacizumab after prolonged exposition to bevacizumab in breast cancer

Project description:Purpose: To study the potential priming benefit of bevacizumab from subsequent immunotherapy (durvalumab) in advanced breast cancer patients Methods: We tested this hypothesis by adding durvalumab after progression to maintenance single-agent bevacizumab treatment in advanced HER2-negative patients (average 3 treatment lines). In order to study the potential priming benefit, patients had to experience disease progression while on bevacizumab maintenance prior to entering the trial. In addition, we sought to find traits in peripheral-blood mononuclear cells (PBMCs) and tumor biopsies that informed about this immuno-priming, in an attempt to search for novel biomarkers of efficacy of the combo and obtain a better understanding of the biology of this clinical scenario. Results: Patients that experienced clinical benefit, compared with the remaining patients, displayed a lymphocyte pattern in PBMCs consisting on increased T-effector subpopulations (CD4- and CD8- effector and effector-memory) and decreased immunosuppressive T-regulatory cells. Gene-expression studies in tumor samples showed a congruent pattern, with increased T-effector and memory T cell signatures in responders, and increased T-regulatory and decreased active dendritic cells in non-responders. These events were observed in patients that displayed vascular normalization features as a result of previous bevacizumab, supporting the immuno-priming effects of this strategy.

2020-10-15 | GSE139050 | GEO

Immuno-priming with bevacizumab: durvalumab plus bevacizumab after prolonged exposition to bevacizumab in breast cancer

Project description:Immuno-priming with bevacizumab: durvalumab plus bevacizumab after prolonged exposition to bevacizumab in breast cancer

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Differential Gene Expression in Erlotinib-Treated Fibroblasts

Project description:Analysis of human, adult, dermal fibroblasts following treatment with 100nM or 1 uM of erlotinib, a tryrosine kinase inhibitor (TKI) that targets the epidermal growth factor receptor (EGFR) inhibiting EGFR activation and signaling. Erlotinib is widely used to effectively treat patients with advanced non-small cell lung cancer but treatment with erlotinib and other EGFR TKIs are associated with a painful skin rash. Results identified significantly differentially expressed genes in fibroblasts treated with erlotinib providing insight into how the drug alters the transcriptome in ways that may contribute to the TKI-related rash.

2019-01-01 | GSE106151 | GEO

TMT analysis of tissue proteomics in bevacizumab-resistant xenograft tumor tissuein nude mice

Project description:TMT proteomics was used to detect the difference in protein expression of bevacizumab-resistant xenograft tumor tissue in nude mice.

2022-10-13 | PXD030202 | Pride

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