Molecular determinants of resistance to antiandrogen therapy

By C. Chen, Derek S. Welsbie, C. Tran, S. H. Baek, Randolph A Chen, R. Vessella, Michael G. Rosenfeld, C. Sawyers. Nature Medicine, 2004

2,387 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Genetics, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/3ae33edf612d738c1cca1375749ea375b906c8a0

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Endocrinology, Diabetes and Metabolism

1. John Wongvipat
2. C. Sawyers

In Genetics

1. C. Sawyers
2. John Wongvipat
3. Jason S. Carroll
4. Christopher Sander
5. Debashis Ghosh
6. Olivier Elemento
7. X. Chen
8. Zhaohui S. Qin

In Pulmonary and Respiratory Medicine

1. Arul M. Chinnaiyan
2. John Wongvipat
3. C. Sawyers
4. Celestia S. Higano
5. Mark A. Rubin
6. R. Vessella
7. Ethan G. Cerami
8. David M. Sabatini

Citations in the corpus

• Therapeutic Targeting of BET Bromodomain Proteins in Castration-Resistant Prostate Cancer (2014, methodology): “(2) Aligned reads were sorted using NovoSort and exact duplicates were removed using Samtools33.”
• Integrative molecular concept modeling of prostate cancer progression (2007, background): “Hormone-refractory metastatic cancers select for mechanisms to maintain androgen signaling (such as androgen receptor amplifications or mutation”
• Androgen Receptor Regulates a Distinct Transcription Program in Androgen-Independent Prostate Cancer (2009, background): “As AR is expressed in the vast majority of both ADPC and AIPC (Heinlein and Chang, 2004; Scher and Sawyers, 2005) and decreasing levels of AR protein expression reduces both ADPC and AIPC growth in model systems (Chen et al., 2004; Haag et al., 2005; Heinlein and Chang, 2004), it appears AR signalin”
• Androgen-Induced Differentiation and Tumorigenicity of Human Prostate Epithelial Cells (2004, result): “Consistent with these observations, a recent study showed that increases in AR mRNA and protein levels was necessary and sufficient to convert prostate cancer cells from a hormone-sensitive to a hormone-refractory state and that these effects required a functional ligand-binding domain (3).”
• Androgen-Independent Prostate Cancer Is a Heterogeneous Group of Diseases (2004, background): “Chen et al. ( 37 ) have recently demonstrated that the AR in androgen-independent prostate cancer can still be active and fueled by submicromolar amount of testosterone.”
• Molecular genetics of prostate cancer: new prospects for old challenges. (2010, background): “These findings have been most strongly supported by key experiments showing that xenografts that have been selected for castration resistance primarily differ from their parental androgen-dependent lines with respect to levels of AR expression (Chen et al. 2004).”
• Resistance to CYP17A1 inhibition with abiraterone in castration resistant prostate cancer: Induction of steroidogenesis and androgen receptor splice variants (2011, neutral): “Importantly, a 2to 3-fold increase in expression of AR is known to render low androgen levels physiologically relevant in promoting AR driven growth (2), suggesting clinical treatment of Abi-R patients with more stringent ligand inhibition may be of benefit.”
• Androgen levels increase by intratumoral de novo steroidogenesis during progression of castration-resistant prostate cancer. (2008, background): “We and others (14, 15, 29, 30) found that androgen-dependent genes become constitutively reexpressed in the absence of testicular androgens during CRPC progression and that down-regulation of AR expression following castration with small interfering RNA can suppress prostate cancer tumor growth (29,”
• ARN-509: a novel anti-androgen for prostate cancer treatment (2012, positive): “This cell-line was engineered to over-express AR (3–5 fold higher than parental LNCaP), thus mimicking the castration-resistant clinical state (2, 13).”
• Identification of human triple-negative breast cancer subtypes and preclinical models for selection of targeted therapies. (2011, methodology): “We performed hierarchical clustering using an AR-activated gene signature (28) on the training and validation TNBC tumor data sets.”
• Dual role of FoxA1 in androgen receptor binding to chromatin, androgen signalling and prostate cancer (2011, background): “AR amplification and overexpression are also major features of castration-resistant prostate cancers (Visakorpi et al, 1995; Chen et al, 2004), and retinoblastoma tumour suppressor controls prostate cancer progression through modulation of AR expression (Sharma et al, 2010).”
• Integrative genomic profiling of human prostate cancer (2010, methodology): “Common Genomic Alterations in Androgen Receptor Signaling Pathway Members We also conducted a core pathway analysis of AR, which is essential for growth and differentiation of the normal prostate and is responsible for treatment failure in castration-resistant, metastatic disease (Chen et al., 2004;”
• Maintenance of intratumoral androgens in metastatic prostate cancer: a mechanism for castration-resistant tumor growth. (2008, background): “Furthermore, Chen et al. have shown that increased AR expression is instrumental in the progression from androgen-dependent to castration-resistant growth in a xenograft model, with the degree of AR up-regulation observed sufficient to allow tumor cell proliferation in 80% lower androgen concentrati”