ArticleBMC medical genomics2010
Molecular signature of response and potential pathways related to resistance to the HSP90 inhibitor, 17AAG, in breast cancer.
Article in BMC medical genomics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Targeting HSP90 in cancer: advances in the development of inhibitors, mechanisms of action, and therapeutic applications.Molecular cancer · 2026Review
- Connective tissue growth factor: Role in trabecular meshwork remodeling and intraocular pressure lowering.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Secretome profiling ofFrontiers in oncology · 2023Article
- Molecular markers associated with the outcome of tamoxifen treatment in estrogen receptor-positive breast cancer patients: scoping review and in silico analysis.Discover oncology · 2021Article
- GRP94 promotes brain metastasis by engaging pro-survival autophagy.Neuro-oncology · 2020Article
- The Mitochondrial Chaperone TRAP1 as a Candidate Target of Oncotherapy.Frontiers in oncology · 2020Review
- Dihydropyrimidine Dehydrogenase Levels in Colorectal Cancer Cells Treated with a Combination of Heat Shock Protein 90 Inhibitor and Oxaliplatin or Capecitabine.Advanced pharmaceutical bulletin · 2019Article
- Phenotype-based variation as a biomarker of sensitivity to molecularly targeted therapy in melanoma.MedChemComm · 2017Article
- Mitochondrial unfolded protein response controls matrix pre-RNA processing and translation.Nature · 2016Article
- 17-AAG suppresses growth and invasion of lung adenocarcinoma cells via regulation of the LATS1/YAP pathway.Journal of cellular and molecular medicine · 2015Article
- Could the Anti-Chaperone VER155008 Replace Temozolomide for Glioma Treatment.Journal of Cancer · 2015Article
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- Targeting HSF1 sensitizes cancer cells to HSP90 inhibition.Oncotarget · 2013Article
- Fluorescent ligand for human progesterone receptor imaging in live cells.Bioconjugate chemistry · 2013Article
- Exposure to ionizing radiation induced persistent gene expression changes in mouse mammary gland.Radiation oncology (London, England) · 2012Article
- Combination therapy with HSP90 inhibitor 17-DMAG reconditions the tumor microenvironment to improve recruitment of therapeutic T cells.Cancer research · 2012Article
- NAD(P)H:quinone oxidoreductase 1 (NQO1) in the sensitivity and resistance to antitumor quinones.Biochemical pharmacology · 2012Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHSP90 may be a favorable target for investigational therapy in breast cancer. In fact, the HSP90 inhibitor, 17AAG, currently has entered in phase II clinical trials as an anticancer agent in breast and other tumors. Since HSP90 inhibition leads to global depletion of oncogenic proteins involved in multiple pathways we applied global analysis using gene array technology to study new genes and pathways involved in the drug response in breast cancer.
methodsGene expression profiling using Whole Human Genome Agilent array technology was applied to a total of six sensitive and two resistant breast cancer cell lines pre-treatment and treated with the 17AAG for 24 and 48 hours.
resultsWe have identified a common molecular signature of response to 17AAG composed of 35 genes which include novel pharmacodynamic markers of this drug. In addition, different patterns of HSP90 client transcriptional changes after 17AAG were identified associated to the sensitive cell lines, which could be useful to evaluate drug effectiveness. Finally, we have found differentially expressed pathways associated to resistance to 17AAG. We observed significant activation of NF-κB and MAPK pathways in resistant cells upon treatment, indicating that these pathways could be potentially targeted to overcome resistance.
conclusionsOur study shows that global mRNA expression analysis is a useful strategy to examine molecular effects of drugs, which allowed us the discovery of new biomarkers of 17AAG activity and provided more insights into the complex mechanism of 17AAG resistance.
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