Presentation Type
Oral Presentation
Discipline Track
Biomedical Science
Abstract Type
Research/Clinical
Abstract
Background: Cancer health disparities represent a significant public health concern in the United States. Prostate cancer is one such disease with a higher incidence and death rate in African American (AA) men than in Whites. This study aimed to understand the role of systemic inflammation in association with prostate cancer disparity among AA and White men.
Methods: We used a 40-plex human chemokine assay kit to determine the differential level of cytokines-chemokines associated with prostate cancer disparity among AA and White men. A total of 211 serum samples from prostate cancer patients and healthy donors were tested. Differential expression of the selected chemokines was also analyzed using IHC (immunohistochemistry) in a representative group of prostate tumor tissues of two races.
Results: Race-specific differences were observed for significantly higher serum levels of CXCL2, CXCL5, and IL-6 and lower levels of CCL23 and CCL27 in AA prostate cancer patients (n = 14) compared to Whites (n = 14). Further extension of the analysis to 211 serum samples showed significantly higher levels of CXCL2 and CXCL5 in AA men than in Whites, whereas CCL23 differed significantly within and between the races with a lower level in AA cancer cases than healthy donors. Patient age, PSA, or Gleason scores were not significantly associated with these chemokines. IHC for CXCL5 and CCL23 in prostate tissues displayed higher CXCL5 in prostate tumors than in benign tissues, while CCL23 was non-detectable in tumor tissues. In contrast, independent of racial composition, serum levels of C-C chemokines CCL1, CCL7, CCL8, CCL11, CCL13, CXCL9, CXCL10, and the cytokine IL-2, and TNF-α were significantly lower in prostate cancer patients (n = 28) compared to healthy controls (n = 11).
Conclusions: This study observed that serum chemokines CXCL2, CXCL5, and CCL23 are the most distinguished chemokines differentially expressed in men of AA and White races. The impact of such chemokines contributing to the disparity in prostate cancer biology among races needs further investigation. The establishment of such disproportionate levels of serum chemokines may help guide the therapeutic approaches in targeting aggressive prostate cancer as often diagnosed in men of AA race.
Recommended Citation
Karan, Dev, "Analysis of serum cytokines-chemokines in association with prostate cancer disparity." (2024). Research Symposium. 32.
https://scholarworks.utrgv.edu/somrs/2024/talks/32
Included in
Analysis of serum cytokines-chemokines in association with prostate cancer disparity.
Background: Cancer health disparities represent a significant public health concern in the United States. Prostate cancer is one such disease with a higher incidence and death rate in African American (AA) men than in Whites. This study aimed to understand the role of systemic inflammation in association with prostate cancer disparity among AA and White men.
Methods: We used a 40-plex human chemokine assay kit to determine the differential level of cytokines-chemokines associated with prostate cancer disparity among AA and White men. A total of 211 serum samples from prostate cancer patients and healthy donors were tested. Differential expression of the selected chemokines was also analyzed using IHC (immunohistochemistry) in a representative group of prostate tumor tissues of two races.
Results: Race-specific differences were observed for significantly higher serum levels of CXCL2, CXCL5, and IL-6 and lower levels of CCL23 and CCL27 in AA prostate cancer patients (n = 14) compared to Whites (n = 14). Further extension of the analysis to 211 serum samples showed significantly higher levels of CXCL2 and CXCL5 in AA men than in Whites, whereas CCL23 differed significantly within and between the races with a lower level in AA cancer cases than healthy donors. Patient age, PSA, or Gleason scores were not significantly associated with these chemokines. IHC for CXCL5 and CCL23 in prostate tissues displayed higher CXCL5 in prostate tumors than in benign tissues, while CCL23 was non-detectable in tumor tissues. In contrast, independent of racial composition, serum levels of C-C chemokines CCL1, CCL7, CCL8, CCL11, CCL13, CXCL9, CXCL10, and the cytokine IL-2, and TNF-α were significantly lower in prostate cancer patients (n = 28) compared to healthy controls (n = 11).
Conclusions: This study observed that serum chemokines CXCL2, CXCL5, and CCL23 are the most distinguished chemokines differentially expressed in men of AA and White races. The impact of such chemokines contributing to the disparity in prostate cancer biology among races needs further investigation. The establishment of such disproportionate levels of serum chemokines may help guide the therapeutic approaches in targeting aggressive prostate cancer as often diagnosed in men of AA race.