Eva Corey

This study identifies proteomic signatures of prostate cancer bone metastasis subtypes, revealing distinct molecular states of bone-tumor microenvironment remodeling.

This study identifies a functional cooperation between nuclear pore complexes and m6A signaling that promotes castration-resistant prostate cancer by linking mRNA export to cholesterol biosynthesis and androgen production.

This paper identifies FOXJ1 as a mediator of taxane resistance in prostate cancer by regulating microtubule dynamics, with clinical implications for patient stratification.

The paper identifies global 3'UTR lengthening in SCNC through APA and develops a neural network model to classify SCNC using APA signatures.

This study shows that AR inhibition does not enhance PARP inhibitor efficacy in HR-proficient prostate cancer and instead impairs response in castration-sensitive cells.

This study identifies TRIM24 as a target for preventing prostate cancer progression by degrading it to counteract AR inhibition adaptation and tumor relapse.

The paper identifies a subgroup of mCRPC characterized by LINE1 repeat DNA elements flanking the AR gene, which drive AR overexpression and confer resistance to androgen signaling inhibitors.

This study identifies BET inhibitors as effective against GI transcriptome-positive CRPC by targeting HNF1A and HNF4G, improving outcomes in preclinical models.

This study shows that TMPRSS2-ERG fusion promotes resistance to antiandrogens by interacting with GR, suggesting combined GR and AR inhibition could benefit tERG-positive prostate cancer patients.

This study shows that ARv7 drives AR activity in castration-resistant prostate cancer through increased chromatin accessibility mediated by NFI factors.

This study shows that acute CDK12 loss in prostate cancer causes HR deficiency via polyadenylation, but chronic loss leads to adaptation, making PARP inhibitors ineffective and suggesting CDK13 targeting as a new therapeutic approach.

This study uses PS-OCT to differentiate bone tissue types in prostate cancer metastases by analyzing collagen organization and quantifying structural features.

This study shows MYC overexpression disrupts AR transcriptional pause release, promoting aggressive prostate cancer progression.