Molecular Signature of Endometrial Cancer with Coexistent Adenomyosis: A Multicentric Exploratory Analysis

Simple Summary The impact of the molecular signature on the favorable prognosis of endometrial cancer patients with coexistent adenomyosis is undefined. We aimed to compare the prevalence of molecular groups at poor and intermediate prognosis (p53-abn and MMR-d groups) between endometrial cancer patients with and without coexistent adenomyosis through a multicentric, observational, retrospective, cohort study. We included 147 endometrial cancer patients (38 in the adenomyosis group and 109 in the no adenomyosis group) and we found no significant difference in the prevalence of p53-abn (p = 1.000) and MMR-d (p = 0.2880) signatures between the two groups. Therefore, the molecular signature does not appear to explain the better prognosis associated with coexistent adenomyosis in endometrial cancer patients. Further investigation of the topic requires future larger studies.Abstract Adenomyosis has been associated with better survival outcomes in women with endometrial cancer. However, although the endometrial cancer patients' risk stratification has been revolutionized by molecular findings, the impact of the molecular signature on the favorable prognosis of endometrial cancer patients with coexistent adenomyosis is unknown. The aim of our study was to compare the prevalence of molecular groups at poor and intermediate prognosis between endometrial cancer patients with and without coexistent adenomyosis. A multicentric, observational, retrospective, cohort study was performed to assess the differences in the prevalence of p53-abnormal expression (p53-abn) and mismatch repair protein-deficient expression (MMR-d) signatures between endometrial cancer patients with and without coexistent adenomyosis. A total of 147 endometrial cancer patients were included in the study: 38 in the adenomyosis group and 109 in the no adenomyosis group. A total of 37 patients showed the MMR-d signature (12 in the adenomyosis group and 25 in the no adenomyosis group), while 12 showed the p53-abn signature (3 in the adenomyosis group and 9 in the no adenomyosis group). No significant difference was found in the prevalence of p53-abn (p = 1.000) and MMR-d (p = 0.2880) signatures between endometrial cancer patients with and without coexistent adenomyosis. In conclusion, the molecular signature does not appear to explain the better prognosis associated with coexistent adenomyosis in endometrial cancer patients. Further investigation of these findings is necessary through future larger studies.