Abstract
C-Reactive Protein (CRP) is associated with diverse outcomes in patients with, or suspected to have, genitourinary malignancies. CRP levels have been shown to be associated with the probability of a prostate cancer diagnosis in patients with elevated PSA, the probability of biochemical recurrence following definitive treatment for localized prostate cancer, and decreased overall survival for patients with advanced disease. In patients with bladder and kidney cancers, CRP levels have been associated with disease progression, stage, and cancer-specific survival. Despite the abundance of correlative studies, the relationship between CRP levels and genitourinary cancer pathogenesis is not clearly understood. Here, we review the evidence for CRP as a biomarker in genitourinary (GU) cancers, with specific focus on potential clinical applications.
Highlights
C-reactive protein (CRP) is an acute phase reactant that is widely considered to be a marker of both acute and chronic systemic inflammation
Elevations in IL-6 and CRP correlate with cancer related anemia, and it has been postulated that states of persistent inflammation may induce a hypermetabolic state leading to malnutrition and cachexia [3]
Worse response to ICI, tyrosine kinase inhibitors (TKIs), and cytokine therapies; CRP “flare” predicts tumor shrinkage [12, 13] Persistent CRP elevation is associated with disease progression after BCG [14] Failure of CRP to normalize with GC or MVAC predicts shorter OS [20, 21] For castration-resistant prostate cancer (CRPC) on docetaxel, higher CRP is associated with shorter OS [25]
Summary
C-reactive protein (CRP) is an acute phase reactant that is widely considered to be a marker of both acute and chronic systemic inflammation. Because CRP’s half-life is long (19 hours) it is a stable marker for inflammation, unlike many cytokines whose half-lives can be as short as several minutes [1]. Elevations in IL-6 and CRP correlate with cancer related anemia, and it has been postulated that states of persistent inflammation may induce a hypermetabolic state leading to malnutrition and cachexia [3]. Two main hypotheses exist regarding CRP elevation in cancer pathogenesis; one hypothesis suggests that CRP elevation. CRP in Genitourinary Cancers occurs secondary to the inflammation of tumor growth, whereas the second suggests that CRP elevation is caused by the tumor itself [5]
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