Table 2.

Association between increasing BMI (per 5 units)–predicted by a weighted^a 87-locus genetic risk score–and risk of ovarian cancer by histological subtype, stratified by study

Histological subtype	N studies	N controls	N cases	Odds ratios (95% CI)b
Primary outcomes
High-grade serous	39	23 003	7933	1.06 (0.88-1.27)
Non-high grade serous	39	23 003	4434	1.29 (1.03-1.61)
Borderline	20	16 463	1680	1.28 (0.86-1.90)
Secondary outcomes
Serous
High-grade ovary/tubal	39	23 003	7466	1.06 (0.89-1.27)
High-grade peritoneal c	37	22 026	447	1.77 (0.91-3.43)
Invasive low-grade and borderline	39	23 003	1411	1.93 (1.33-2.81)
Mucinous (invasive and borderline)	39	23 003	1563	1.18 (0.84-1.67)
Endometrioid	39	23 003	2059	1.17 (0.87-1.59)
Clear cell	39	23 003	962	1.27 (0.83-1.96)

^aWeights applied were β-coefficients for the relationship between each SNP and BMI as reported in a large meta-analysis of genome-wide association studies. BMI, body mass index; CI, confidence interval

^bPooled odds ratios are reported for primary outcomes.

^cExcludes two studies (AUS and SRO) where < 20% of women with primary peritoneal cancers were genotyped. BMI, body mass index; CI, confidence interval.