Abstract
Background: Inflammation is a well-documented driver of cancer development and progression. However, little is known about its role in prostate carcinogenesis. Thus, we aimed to investigate the association of C-reactive protein (CRP), haptoglobin, albumin and white blood cells (WBC) with prostate cancer severity and progression.
Method: We selected 8471 men with newly diagnosed prostate cancer from the Swedish Apolipoprotein Mortality Risk (AMORIS) study who had exposure measurements taken approximately 14 years prior to diagnosis. We calculated multivariable odds ratio (OR) and 95% confidence interval (CI) for the associations between the inflammatory markers and prostate cancer severity using logistic regression, while Cox proportional hazard regression was used for the associations with overall and prostate cancer death.
Results: Serum CRP levels were positively associated with risk of high risk and metastatic prostate cancer, and high PSA levels (≥20 μg/L) (OR: 1.29; 95% CI: 1.06–1.56, 1.32; 1.05–1.65 and 1.51; 1.26–1.81 respectively). Similar positive associations were seen for haptoglobin with metastatic prostate cancer, high PSA level and possibly high grade prostate cancer (1.38; 1.10–1.74, 1.50; 1.17–1.93 and 1.25; 1.00–1.56 respectively). While albumin was positively associated with Gleason 4 + 3 tumour (1.38; 1.02–1.86), the associations with high risk prostate cancer and high PSA levels (≥20 μg/L) were inverse (0.71; 0.56–0.89 and 0.72; 0.59–0.90). However, none of these markers were associated with prostate cancer death or overall death. WBC was not associated with any of the outcomes.
Conclusion: Systemic inflammation as early as 14 years prior to diagnosis may influence prostate cancer severity, raising the question whether the host environment influences progression to a more malignant phenotype – or helps select more malignant cell-clones – early in the natural history of the disease.
Method: We selected 8471 men with newly diagnosed prostate cancer from the Swedish Apolipoprotein Mortality Risk (AMORIS) study who had exposure measurements taken approximately 14 years prior to diagnosis. We calculated multivariable odds ratio (OR) and 95% confidence interval (CI) for the associations between the inflammatory markers and prostate cancer severity using logistic regression, while Cox proportional hazard regression was used for the associations with overall and prostate cancer death.
Results: Serum CRP levels were positively associated with risk of high risk and metastatic prostate cancer, and high PSA levels (≥20 μg/L) (OR: 1.29; 95% CI: 1.06–1.56, 1.32; 1.05–1.65 and 1.51; 1.26–1.81 respectively). Similar positive associations were seen for haptoglobin with metastatic prostate cancer, high PSA level and possibly high grade prostate cancer (1.38; 1.10–1.74, 1.50; 1.17–1.93 and 1.25; 1.00–1.56 respectively). While albumin was positively associated with Gleason 4 + 3 tumour (1.38; 1.02–1.86), the associations with high risk prostate cancer and high PSA levels (≥20 μg/L) were inverse (0.71; 0.56–0.89 and 0.72; 0.59–0.90). However, none of these markers were associated with prostate cancer death or overall death. WBC was not associated with any of the outcomes.
Conclusion: Systemic inflammation as early as 14 years prior to diagnosis may influence prostate cancer severity, raising the question whether the host environment influences progression to a more malignant phenotype – or helps select more malignant cell-clones – early in the natural history of the disease.
Original language | English |
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Pages (from-to) | 2223-2224 |
Number of pages | 2 |
Journal | European Journal of Surgical Oncology |
Volume | 43 |
Issue number | 11 |
Early online date | 22 Nov 2017 |
DOIs | |
Publication status | Published - Nov 2017 |