Genomic profiles in prostate cancer patients of varying measured socioeconomic inequality: A retrospective cohort study.

R Rishab Srivastava (University of Arizona Internal Medicine Residency, Tucson, AZ) M Megan Taylor (University of Arizona College of Medicine Tucson, Tucson, AZ) K Kenneth Barker (Mayo Clinic Arizona, Phoenix, AZ) T Tom Marco (University of Arizona Internal Medicine Residency - Banner University Medical Center, Tucson, AZ) J Jose Guillen-Rodriguez (University of Arizona Cancer Center, Tucson, AZ) A Aaron Bertolo (H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL) A Alejandro Recio-Boiles (University of Arizona College of Medicine, Department of Hematology & Oncology, Tucson, AZ) R Ricardo Medizabal-Estrada (Mayo Clinic Arizona, Scottsdale, AZ) J Juan J. Chipollini (University of Arizona College of Medicine Tucson Department of Urology, Tucson, AZ)

Abstract

e17159 Background: Socioeconomic inequality (SI) is a recognized risk factor for negative outcomes in prostate cancer (PCa), influenced by biology, healthcare access, and lifestyle. This study aims to explore the molecular impact of SI on PCa, focusing on targetable and prognostic biomarkers. Methods: We conducted a retrospective analysis of 100 metastatic hormone-sensitive PCa patients (2016-2023), with 97 undergoing next-generation sequencing (NGS). We examined only pathogenic variants alongside clinical variables. The Area Deprivation Index (ADI) assessed neighborhood SI, with higher scores indicating greater disadvantage. Patients were divided into tertiles. Chi-square and Fisher’s exact tests evaluated the relationships between tertiles and genomic alterations, while ordinal logistic regression analyzed outcomes by various stratifications. Results: Of the 97 patients, 29 were in tertile 1, 34 in tertile 2, and 35 in tertile 3. Tertile 1 had a significantly higher percentage of non-Hispanic patients (90%) compared to tertile 2 (62%) and tertile 3 (37%), p=0.0001. Other demographic factors, such as age, comorbidities, and cancer history, showed no significant differences by tertile. Median PSA levels increased from tertile 1 (22 ng/mL) to tertile 3 (95 ng/mL), although this was not statistically significant (p=0.14). Tumor volume and visceral metastasis were notably higher in tertile 3 (p=0.029 and p=0.02). BRCA1/2 mutations were more prevalent in tertile 3 (11%, p=0.03) via liquid biopsy compared to tertiles 1 and 2 (0%). TMPRSS2-ERG fusion mutations were significantly more common in tertile 3 (66.6%) compared to tertile 2 (19.1%) and tertile 1 (14.2%), p=0.009. The association between ADI tertile and TMPRSS2 approached significance when controlled for ethnicity (p=0.061), with Hispanic ethnicity having 3.5 times the odds of the fusion compared to non-Hispanics (p=0.02). Tertile 1 patients were more associated with receiving progressive therapy lines (2L p=0.01, 3L p=0.03, 4L p=0.04), but median time to subsequent treatment at 5 years was similar across tertiles (p=0.84). Conclusions: Higher SI was linked to increased PSA, tumor volume, visceral metastasis risk, and higher prevalence of BRCA1/2 and TMPRSS2-ERG mutations. This study highlights the need for further research on the molecular impacts of SI on adverse PCa outcomes, particularly among Hispanic populations.

Article Details

Volume / Issue Vol. 43, Issue 16_suppl
Published June 01, 2025
ISSN 0732-183X
Publisher Lippincott Williams & Wilkins

Journal Info

Journal of Clinical Oncology

Lippincott Williams & Wilkins

ISSN: 0732-183X Health Sciences

Authors (9)

R

Rishab Srivastava

University of Arizona Internal Medicine Residency, Tucson, AZ

M

Megan Taylor

University of Arizona College of Medicine Tucson, Tucson, AZ

K

Kenneth Barker

Mayo Clinic Arizona, Phoenix, AZ

T

Tom Marco

University of Arizona Internal Medicine Residency - Banner University Medical Center, Tucson, AZ

J

Jose Guillen-Rodriguez

University of Arizona Cancer Center, Tucson, AZ

A

Aaron Bertolo

H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL

A

Alejandro Recio-Boiles

University of Arizona College of Medicine, Department of Hematology & Oncology, Tucson, AZ

R

Ricardo Medizabal-Estrada

Mayo Clinic Arizona, Scottsdale, AZ

J

Juan J. Chipollini

University of Arizona College of Medicine Tucson Department of Urology, Tucson, AZ