Abstract 246P
Background
C-reactive protein (CRP) is the inflammation-responsible protein and a significant rise of the plasma concentration of CRP is pervasive in the progress of ovarian cancer. However, there are few studies that comprehensively evaluate the correlation between CRP concentrations and ovarian cancer and the causal effect remains unknown. With a Mendelian randomization (MR) approach, we were able to investigate the causal relationship between genetically predicted CRP levels and ovarian cancer risk.
Methods
Utilizing 32 CRP-related single nucleotide polymorphisms as instrumental variables identified by the latest genome-wide association studies, we investigated the correlation between genetically predicted CRP and ovarian cancer risk using summary statistics from the Ovarian Cancer Association Consortium (25,509 cases and 40,941 controls). The Inverse variance weighted (IVW) method was applied to estimate the causality between genetically elevated CRP concentrations and ovarian cancer risk. To further evaluate the pleiotropy, the weighted median and the MR-Egger regression method were implemented. Subgroup analyses according to different histotypes of ovarian cancer were also conducted.
Results
An inverse association was observed between genetically predicted one-unit increase in the log-transformed CRP concentrations and ovarian cancer (OR = 0.93, 95%CI = 0.87-1.00 p = 0.047). When results were examined by histotypes, an inverse association was observed between genetically predicted one-unit increase in the log-transformed CRP concentrations and endometrioid ovarian cancer (OR = 0.80, 95%CI = 0.70-0.91 p = 0.001), low-grade serous ovarian cancer (OR = 0.70, 95%CI = 0.58-0.86 p = 0.001) and serous ovarian cancer (OR = 0.84, 95%CI = 0.74-0.96 p = 0.012). Additionally, the results demonstrated the absence of the horizontal pleiotropy.
Conclusions
MR findings provide evidence for a causal relationship between genetically predicted one-unit increase in the log-transformed CRP concentrations and reduced ovarian cancer risk, overall and among specific histotypes. Further studies are warranted to investigate the underlying mechanism.
Clinical trial identification
Editorial acknowledgement
Resources from the same session
434P - Pan-Canadian evidence-based, consensus-driven cancer treatment protocols/information for use at the point of care by medical oncologists? Is there a need?
Presenter: Kiran Virik
Session: e-Poster Display Session
435P - Hypnotics and risk of cancer: A meta-analysis of observational studies
Presenter: Tzu Rong Peng
Session: e-Poster Display Session
436P - Clinicopathological characteristics and outcomes of adolescent and young adult (AYA) melanoma: Results from an Asian perspective
Presenter: Wei Lin Goh
Session: e-Poster Display Session
437P - Long-term efficacy and toxicity outcome of adjuvant external beam radiotherapy for medullary thyroid cancer: A single institution cohort study
Presenter: Ka Man Cheung
Session: e-Poster Display Session
438P - Real-world data of relapse after adjuvant treatment (Tx) in high-risk melanoma
Presenter: Carolina Ortiz Velez
Session: e-Poster Display Session
439P - Immunohistochemical analysis of p53 and Ki-67 in glioblastoma (GBM) and their correlations with patient survival
Presenter: Paulo Luz
Session: e-Poster Display Session
440P - Blinded independent central review of oncology trials: The monitoring of readers' performance
Presenter: Hubert Beaumont
Session: e-Poster Display Session
441P - Influence of radiation therapy of patients with somatotropic pituitary adenomas depending on the age of patients
Presenter: Saodat Issaeva
Session: e-Poster Display Session
442P - Results from the registrational phase I/II ARROW trial of pralsetinib (BLU-667) in patients (pts) with advanced RET mutation-positive medullary thyroid cancer (RET+ MTC)
Presenter: Bhumsuk Keam
Session: e-Poster Display Session