Gene expression signature-based chemical genomic prediction identifies a novel class of HSP90 pathway modulators.

By H. Hieronymus, J. Lamb, K. Ross, Xiao Peng, Cristina C. Clement, A. Rodina, M. Nieto, Jinyan Du, K. Stegmaier, Srilakshmi M. Raj and 5 more. Cancer Cell, 2006

604 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/3fd9f1ea94a4363e720f81a6ad52b6124a708d11

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Citations in the corpus

Integrative genomic profiling of human prostate cancer (2010, methodology): “0001), as assessed by an independent signature of 29 androgen-responsive genes (Hieronymus et al., 2006).”
The molecular taxonomy of primary prostate cancer (2015, methodology): “To address these questions, we sought to infer the AR output of tumors by calculating an AR activity score from the expression pattern of 20 genes that are experimentally validated AR transcriptional targets (Hieronymus et al., 2006).”
Treatment of Obesity with Celastrol (2015, neutral): “Celastrol has also been proposed as a heat-shock protein 90 kDa (HSP90) inhibitor (Hieronymus et al., 2006).”
RNA-Seq of Single Prostate CTCs Implicates Noncanonical Wnt Signaling in Antiandrogen Resistance (2015, neutral): “Non-canonical Wnt signature is from reference (14), glucocorticoid receptor (GR) signature is from reference (28), and AR signature is from reference (30) (Table S7).”
A review of connectivity map and computational approaches in pharmacogenomics (2017, background): “Furthermore, their results also justified that the HSF1 level and HSF1-related signatures impact on carcinogenesis during disease progression and found that HSF1 can be used for developing new therapeutic targets [17].”
Genomic correlates of clinical outcome in advanced prostate cancer (2019, methodology): “NEPC and AR signaling scores were computed by the Pearson’s correlation coefficient between the log2-transformed FPKM values of each score’s gene list and a reference gene expression vector, as previously described (7, 32).”
Reciprocal feedback regulation of PI3K and androgen receptor signaling in PTEN-deficient prostate cancer. (2011, methodology): “We then analyzed AR pathway activation by PTEN status using a previously reported mRNA signature of AR target genes (Hieronymus et al., 2006).”
Molecular understanding and modern application of traditional medicines: triumphs and trials. (2007, background): “…effects, including gene expression modulation likely mediated through inhibition of NF-κB via TAK1 and IκBα kinase (Sethi et al., 2007 and references therein), proteasome inhibition, topoisomerase II inhibition, and heat shock response activation (Hieronymus et al., 2006 and references therein).”
Rank–rank hypergeometric overlap: identification of statistically significant overlap between gene-expression signatures (2010, methodology): “Similarly, mean Cmap scores were calculated for each drug using the top 50 genes that increased and decreased by gedunin treatment relative to controls—the exact same gedunin signature-based gene sets used in the original Cmap analysis (43).”
Androgen Receptor Pathway-Independent Prostate Cancer Is Sustained through FGF Signaling (2017, methodology): “Gene expression programs of the tumors classified by immunohistochemistry (IHC) supported these distinct subtypes using 10-gene signatures that were concordant with previously published gene sets indicative of NE and AR pathway activity (Figures 1C, S1A, and S1B) (Beltran et al., 2016; Hieronymus et”
Systems biology approaches for advancing the discovery of effective drug combinations (2015, methodology): “This method assumes gene expression changes can be used as a “ universal language ” to connect distinct biological states (e.g. diseases), allowing for the successful repurposing of compounds [51,52].”