My research in the Boutros Lab at UCLA focuses on understanding the molecular heterogeneity of prostate cancer to improve risk stratification and treatment. I use integrative genomic approaches — including whole-genome sequencing, transcriptomics, and clinical trial correlatives — to identify biomarkers with translational relevance.
Prostate-specific membrane antigen (PSMA) PET imaging has transformed how prostate cancer is staged and managed. My work investigates the molecular biology underlying PSMA PET visibility — asking what it means at a genomic level when a tumor “lights up” on PSMA PET.
In a study published in European Urology, we characterized PSMA levels as a reflection of cancer biology in treatment-naïve prostate cancer, correlating PSMA PET signal with gene expression, genomic alterations, and treatment sensitivities using a multi-omic approach. We found that PSMA expression is associated with distinct transcriptomic programs and may serve as a biomarker for treatment responsiveness beyond simply identifying disease location.
Key publication: Weiner, A.B., Agrawal, R., et al. (2024). Molecular Hallmarks of Prostate-specific Membrane Antigen in Treatment-naïve Prostate Cancer. Eur Urol.
Androgen deprivation therapy (ADT) is a cornerstone of prostate cancer treatment, yet resistance invariably develops. My work has focused on understanding the molecular mechanisms of ADT response and whether combination strategies can delay resistance.
As first author on a phase 2 randomized clinical trial published in European Urology Oncology, I led the molecular analysis of neoadjuvant enzalutamide + degarelix combined with either MEK inhibition (trametinib) or SRC inhibition (dasatinib) in patients with unfavorable-risk localized prostate cancer. We evaluated whether targeting epithelial-mesenchymal transition (EMT) pathways could mitigate ADT resistance. While the combination arms did not reduce EMT markers compared to ADT alone, the trial generated a rich molecular dataset characterizing the genomic landscape of treatment response.
Key publication: Agrawal, R., Weiner, A.B., et al. (2025). Neoadjuvant Antiandrogen Therapy With or Without MEK or SRC Inhibition for Unfavorable-risk Prostate Cancer: A Phase 2 Randomized Clinical Trial. Eur Urol Oncol.
An emerging area of cancer biology is the role of the microbiome in tumor initiation and progression. My work has explored whether colibactin — a genotoxin produced by certain strains of E. coli — contributes to prostate cancer development.
In a study published in European Urology Oncology, we showed that exposure to colibactin-producing pks+ E. coli was positively associated with prostate cancer diagnosis in a clinical cohort. In cell culture, colibactin 742 increased replication fork stalling and fusions, and when combined with dihydrotestosterone (DHT), induced more somatic mutations of all types — including kataegis (localized hypermutation). These findings suggest that microbial genotoxins may synergize with androgens to drive genomic instability in the prostate.
Key publication: Agrawal, R., Al-Hiyari, S., et al. (2025). Colibactin Exerts Androgen-Dependent and -Independent Effects on Prostate Cancer. Eur Urol Oncol.