OBJECTIVE: Uterine sarcomas are a rare group of uterine malignancies. Due to the low incidence and changes in uterine sarcoma classification, risk factors are not well characterized. Our objective was to evaluate risk factors for uterine sarcoma and compare risk factors between uterine sarcoma, malignant mixed Mullerian tumors (MMMTs), and type I endometrial carcinomas.
METHODS: This nested case-control study utilized linked data from population-based medical birth and cancer registries in Denmark, Finland, Norway, and Sweden. Up to 10 controls were matched on country and birth year for each uterine cancer case. Using multivariable adjusted multinomial logistic regression, estimates of the associations between pregnancy-related factors and risk of uterine sarcoma, MMMTs, and type I endometrial carcinomas were determined.
RESULTS: Having a very-low-birth-weight infant (< 1500 vs. 2500-3999 g: OR [95% CI] 2.83 [1.61-4.96]) was associated with an increased risk of uterine sarcoma. Whereas, having a more recent pregnancy was associated with reduced risks of MMMT (< 10 vs. ≥ 30 years: 0.66 [0.20-2.23]) and type 1 endometrial carcinomas (0.35 [0.30-0.41]) but not uterine sarcomas (1.33 [0.90-1.98], p-heterogeneity < 0.01).
CONCLUSIONS: Our study provides evidence that risk factors for uterine sarcoma and MMMT, previously grouped with uterine sarcomas, vary substantially. Additionally, MMMT and type I endometrial carcinomas are more similar than uterine sarcoma in that pregnancy complications like gestational hypertension and preeclampsia were associated with reduced risks of both but not uterine sarcoma, suggesting different etiologies.

This study aimed to assess the association between ABO blood type and incident of type I endometrial cancer (EC), as well as the stage and differentiation. 213 patients with type I EC and 300 healthy controls were included. As a result, the frequencies of A, B, O, and AB blood types among patients with type I EC were 51 (23.9%), 59 (27.7%), 93 (43.7%) and 10 (4.7%), respectively. There were no significant differences in age, body mass index, and other baseline covariates between groups of ABO blood types (p > .05). Logistic regression model showed that women with blood type O was more likely to develop type I EC than those with type A (odds ratio (OR): 1.66, 95% confidence interval (CI): 1.05-2.63). However, there was no significant association of ABO blood type with stage and differentiation of type I EC (p > .05). In conclusion, blood type O was the most prevalent ABO blood type among patients with type I EC and was associated with increased risk of type I EC, while ABO blood type was not significantly associated with stage or differentiation of type I EC.IMPACT STATEMENTWhat is already known on this subject? Previous studies have produced inconsistent findings on association of ABO blood type with EC. Those studies also did not explore the relationship between ABO blood type and stage or differentiation of type I EC.What the results of this study add? The present study showed that women with blood type O was more likely to develop type I EC than those with type A and there was no significant association of ABO blood type with stage or differentiation of type I EC.What the implications are of these findings for clinical practice and/or further research? Gynaecologists should pay more attention to women with blood type O, who should undergo more active EC screening.

POLE-mutated endometrial cancer (EC) frequently shows high-grade endometrioid histology, which represents heterogeneity in the dualistic classification of EC. This study aimed to assess the clinicopathology and pathogenesis of POLE-mutated EC due to the scarcity of related information for Asian women. POLE variants were sequenced in tissues of Japanese women with EC. The tumor mutation burden (TMB) was assessed in tissues with a POLE variant of unknown significance. In the POLE-mutated EC tissues, the immunostaining expression of CD8, hormonal receptors, and p53 was evaluated, and the POLE variants in cancer and atypical endometrial hyperplasia (AEH) lesions were assessed by laser-capture microdissection. POLE variants were identified in five patients (3.9%) with high-grade endometrioid carcinoma among 127 patients with EC (S459F in two tissues and P441P in three tissues with a high TMB). The five cancer tissues coexisted with normal endometrium and/or AEH. Both AEH and cancer cells showed hormonal receptor positivity and harbored the same POLE mutation. Two patients showed a subclonal overexpression pattern of p53 in cancer and AEH lesions. In conclusion, POLE-mutated EC progresses through the type I pathway, even though it frequently shows high-grade endometrioid morphology. The common POLE mutation sites in EC might vary among races.