International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · 2026
Should lymph node staging be tailored according to molecular profile in endometrial cancer?
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Dzyubak Oleksandra, Moshkovich Michal, Watts Megan, Tarafdar Oishika, Wei-Jia Lim Justin, Maganti Manjula, Han Kathy, Hodgson Anjelica, Ferguson Sarah E, Kim Soyoun Rachel
Аннотация
OBJECTIVE: This study investigates whether the specific molecular profile of endometrial cancer is associated with propensity for lymph node metastasis.
METHODS: Patients undergoing primary surgery between 2015 and 2023 were reviewed. Clinicopathological, lymph node metastasis, recurrence, and survival patterns were compared between molecular sub-groups: no specific molecular profile, p53-abnormal, POLE-mutated, and mismatch repair-deficient, with a sub-group analysis of MLH1 promoter methylated and non-MLH1 promoter methylated mismatch repair-deficient cases.
RESULTS: Of 537 patients, 239 (45%) were no specific molecular profile, 145 (27%) were p53-abnormal, 109 (20%) were MLH1 promoter methylated, 40 (7%) were non-MLH1 promoter methylated mismatch repair-deficient, and 4 (1%) were POLE-mutated. Lymph node assessment was done in 420 patients (78%), with lymph node metastases present in 92 (22%). There was no significant difference in lymph node metastasis between molecular groups (p =.080). However, MLH1 promoter methylated tumors had the highest incidence of lymphovascular space invasion (48%, p <.001) and microcystic, elongated, and fragmented pattern of invasion (17%, p <.001). The p53-abnormal sub-group had the highest median tumor volume (12.7 cm3, 0.0-781.5, p =.013), followed by MLH1 promoter methylated (12.2 cm3, 0.0-375.8). The median follow-up was 2.4 years (0.05-7.67). Two-year estimated progression-free survival was as follows: non-MLH1 promoter methylated mismatch repair-deficient (92.1%, 95% confidence interval 83.9% to 100%), no specific molecular profile (92.3%, 95% confidence interval 88.7% to 96.0%), MLH1 promoter methylated (83.1%, 95% confidence interval 76.0% to 90.8%), and p53-abnormal (75.0%, 95% confidence interval 67.9% to 82.9%) (p <.001). Two-year estimated overall survival was as follows: non-MLH1 promoter methylated mismatch repair-deficient (100%), no specific molecular profile (98.2%, 95% confidence interval 96.5 to 100.0), MLH1 promoter methylated (92.6%, 95% confidence interval 87.4% to 98.1%), and p53-abnormal (92.0%, 95% confidence interval 87.3% to 96.9%) (p <.001).
CONCLUSIONS: Currently, there is not enough evidence to tailor lymph node staging according to molecular profile. Special attention should be paid to MLH1 promoter methylated tumors due to high-risk features and poor outcomes.
METHODS: Patients undergoing primary surgery between 2015 and 2023 were reviewed. Clinicopathological, lymph node metastasis, recurrence, and survival patterns were compared between molecular sub-groups: no specific molecular profile, p53-abnormal, POLE-mutated, and mismatch repair-deficient, with a sub-group analysis of MLH1 promoter methylated and non-MLH1 promoter methylated mismatch repair-deficient cases.
RESULTS: Of 537 patients, 239 (45%) were no specific molecular profile, 145 (27%) were p53-abnormal, 109 (20%) were MLH1 promoter methylated, 40 (7%) were non-MLH1 promoter methylated mismatch repair-deficient, and 4 (1%) were POLE-mutated. Lymph node assessment was done in 420 patients (78%), with lymph node metastases present in 92 (22%). There was no significant difference in lymph node metastasis between molecular groups (p =.080). However, MLH1 promoter methylated tumors had the highest incidence of lymphovascular space invasion (48%, p <.001) and microcystic, elongated, and fragmented pattern of invasion (17%, p <.001). The p53-abnormal sub-group had the highest median tumor volume (12.7 cm3, 0.0-781.5, p =.013), followed by MLH1 promoter methylated (12.2 cm3, 0.0-375.8). The median follow-up was 2.4 years (0.05-7.67). Two-year estimated progression-free survival was as follows: non-MLH1 promoter methylated mismatch repair-deficient (92.1%, 95% confidence interval 83.9% to 100%), no specific molecular profile (92.3%, 95% confidence interval 88.7% to 96.0%), MLH1 promoter methylated (83.1%, 95% confidence interval 76.0% to 90.8%), and p53-abnormal (75.0%, 95% confidence interval 67.9% to 82.9%) (p <.001). Two-year estimated overall survival was as follows: non-MLH1 promoter methylated mismatch repair-deficient (100%), no specific molecular profile (98.2%, 95% confidence interval 96.5 to 100.0), MLH1 promoter methylated (92.6%, 95% confidence interval 87.4% to 98.1%), and p53-abnormal (92.0%, 95% confidence interval 87.3% to 96.9%) (p <.001).
CONCLUSIONS: Currently, there is not enough evidence to tailor lymph node staging according to molecular profile. Special attention should be paid to MLH1 promoter methylated tumors due to high-risk features and poor outcomes.