Objective:　To　evaluate　the　mutation　rates　of　homologous　recombination　repair　(HRR)　genes　and　the　impact　of　these　mutations　on　the　clinical　characteristics　of　metastatic　endometrial　cancer　(EC).　Methods:　Somatic　DNA　from　895　patients　with　metastatic　EC　in　the　Memorial　Sloan　Kettering-Metastatic　Events　and　Tropisms　cohort　was　assessed　for　mutations　in　10　HRR　genes　(BRCA1,　BRCA2,　ATM,　BARD1,　BRIP1,　PALB2,　RAD51C,　RAD51D,　CHEK2,　and　CDK12).　The　correlation　between　the　mutation　status　of　HRR　genes　and　the　clinical　characteristics　of　patients　with　metastatic　EC　was　evaluated.　Results:　Somatic　mutations　in　HRR　genes　were　detected　in　106　(11.8%)　patients　with　metastatic　EC.　Compared　with　nonmutation　carriers,　a　greater　proportion　of　carriers　had　endometrioid　carcinoma　(76.4%　vs.　50.3%,　p＜0.001).　Regarding　the　TCGA　classification,　the　proportions　of　the　POLE-ultramutated　(POLEmut)　and　mismatch　repair-deficient　(dMMR)　subtypes　were　significantly　greater　among　mutation　carriers　than　noncarriers　(20.8%　vs.　0.4%,　p＜0.001;　34.9%　vs.　11.9%,　p＜0.001,　respectively).　The　carriers　had　a　significantly　lower　frequency　of　TP53　mutations　than　noncarriers　(25.5%　vs.　54.1%,　p＜0.001).　Fewer　mutation　carriers　than　noncarriers　had　intra-abdominal　and　lung　metastases　(41.5%　vs.　54.2%,　p=0.014;　19.8%　vs.　30.3%,　p=0.026,　respectively).　The　mutation　status　of　HRR　genes　did　not　significantly　affect　the　overall　survival　of　patients　with　metastatic　EC.　Conclusion:　Somatic　HRR　mutations　are　detected　in　11.8%　of　metastatic　EC.　Compared　with　noncarriers,　HRR　mutation　carriers　in　metastatic　EC　have　higher　proportions　of　endometrioid　carcinoma,　POLEmut,　and　dMMR　subtypes,　and　unique　metastatic　patterns.　However,　the　prognoses　are　similar　regardless　of　HRR　status.