A5020731473- Estrogen and related hormone effects
- Prostate Cancer Treatment and Research
- Inflammatory mediators and NSAID effects
- Hormonal Regulation and Hypertension
- Hormonal and reproductive studies
- Cancer Genomics and Diagnostics
- Lung Cancer Treatments and Mutations
- Lung Cancer Research Studies
The University of Texas Southwestern Medical Center
2023
Southwestern Medical Center
2023
University of Michigan
2023
Abstract In castration-resistant prostate cancer (CRPC), increased glucocorticoid receptor (GR) expression and ensuing transcriptional activity have been proposed as an oncogenic “bypass” mechanism in response to androgen (AR) signaling inhibition (ARSi). Here, we report that GR acquired following ARSi is associated with the upregulation of cyclic adenosine monophosphate (cAMP)-associated gene pathways both model systems metastatic patient samples. context ARSi, GR-mediated genes encoding...
<p>List of cAMP pathway genes n=224 (based on IPA) used in this study</p>
<p>Overlap of GR DEGs from Arora et al. and the present study</p>
<p>GR activation increases PKA substrate phosphorylation events in AR-antagonized CWR-22Rv1 cells</p>
<p>IPA-derived activation Z-scores in CWR-22Rv1 cells</p>
<p>IPA-derived activation Z-scores in CWR-22Rv1 cells</p>
<p>A downstream cAMP-activated transcription factor, CREB, is phosphorylated at Ser133 following GR activation</p>
<p>List of cAMP pathway genes n=224 (based on IPA) used in this study</p>
<p>Cyclic AMP pathway expression in GR high vs low mCRPC and PDX models</p>
<p>Western blot of PKIB in LAPC4 and CWR-22Rv1 cells</p>
<div>Abstract<p>In castration-resistant prostate cancer (CRPC), increased glucocorticoid receptor (GR) expression and ensuing transcriptional activity have been proposed as an oncogenic “bypass” mechanism in response to androgen (AR) signaling inhibition (ARSi). Here, we report that GR acquired following ARSi is associated with the upregulation of cyclic adenosine monophosphate (cAMP)-associated gene pathways both model systems metastatic patient samples. In context ARSi,...
<p>GR-mediated cAMP signaling pathway-related genes with co-treatment of SGRMs</p>
<p>IPA-derived activation Z-scores in LAPC4 cells</p>
<p>Overlap of GR DEGs from Arora et al. and the present study</p>
<p>Cyclic AMP pathway expression in GR high vs low mCRPC and PDX models</p>
<p>Western blot of PKIB in LAPC4 and CWR-22Rv1 cells</p>
<div>Abstract<p>In castration-resistant prostate cancer (CRPC), increased glucocorticoid receptor (GR) expression and ensuing transcriptional activity have been proposed as an oncogenic “bypass” mechanism in response to androgen (AR) signaling inhibition (ARSi). Here, we report that GR acquired following ARSi is associated with the upregulation of cyclic adenosine monophosphate (cAMP)-associated gene pathways both model systems metastatic patient samples. In context ARSi,...
<p>Supplementary figure legends</p>
<p>GR activation increases PKA substrate phosphorylation events in AR-antagonized CWR-22Rv1 cells</p>
<p>IPA-derived activation Z-scores in LAPC4 cells</p>
<p>A downstream cAMP-activated transcription factor, CREB, is phosphorylated at Ser133 following GR activation</p>
<p>Supplementary figure legends</p>
<p>GR-mediated cAMP signaling pathway-related genes with co-treatment of SGRMs</p>
Lung cancer (LC) remains the top cause of cancer-associated mortality worldwide, with a 10-year overall survival rate only 5%. While most LCs are smoking related, 25% non-small cell LC (NSCLC) diagnosed in patients little or no history. Fusions involving ALK oncogenic driver ∼3–7% NSCLC. inhibitors targeting kinase domain (TKI) have proven extremely effective, inevitably, resistance develops limited effective treatment options. We developed precision medicine-based platform (PMP) to screen...