Publications by authors named "C A Sweeney"
Background And Objective: Owing to the expansion of treatment options for metastatic hormone-sensitive prostate cancer (mHSPC) and an appreciation of clinical subgroups with differential prognosis and treatment responses, prognostic and predictive biomarkers are needed to personalize care in this setting. Our aim was to evaluate a multimodal artificial intelligence (MMAI) biomarker for prognostic ability in mHSPC.
Methods: We used data from the phase 3 CHAARTED trial; 456/790 patients with mHSPC had evaluable digital histopathology images and requisite clinical variables to generate MMAI scores for inclusion in our analysis.
This Letter reports a search for charge-parity (CP) symmetry violating nonstandard interactions (NSI) of neutrinos with matter using the NOvA Experiment, and examines their effects on the determination of the standard oscillation parameters. Data from ν_{μ}(ν[over ¯]_{μ})→ν_{μ}(ν[over ¯]_{μ}) and ν_{μ}(ν[over ¯]_{μ})→ν_{e}(ν[over ¯]_{e}) oscillation channels are used to measure the effect of the NSI parameters ϵ_{eμ} and ϵ_{eτ}. With 90% CL the magnitudes of the NSI couplings are constrained to be |ϵ_{eμ}|≲0.
View Article and Find Full Text PDFThe CHAARTED study showed that adding docetaxel (Doc) to androgen deprivation therapy (ADT) in men initiating treatment for metastatic hormone sensitive prostate cancer (mHSPC) prolongs survival, particularly in high-volume disease. Androgens drive both mHSPC and metastatic castration resistant prostate cancer (mCRPC). Lower nadir serum testosterone (T) concentrations are associated with better outcomes in men treated with ADT for biochemical relapse, while higher androgens at mCRPC are associated with better prognosis and increased benefit from abiraterone.
View Article and Find Full Text PDFArticle Synopsis
- - Phenotypic plasticity in cancer, particularly prostate cancer (PCa), leads to resistance against androgen receptor-targeted therapies, highlighting the need to understand its driving mechanisms to prevent resistance emergence.
- - The study found that loss of the tristetraprolin (TTP) gene (ZFP36) increases NF-κB activation, correlating with more aggressive disease and recurrence, especially when PTEN, another key driver in PCa, is also lost.
- - Targeting the NF-κB pathway with an inhibitor (DMAPT) showed promising therapeutic effects in tumors exhibiting co-loss of ZFP36 and PTEN, suggesting a potential new treatment strategy for castration-resistant PCa.