DNA ploidy in curettage specimens identifies high-risk patients and lymph node metastasis in endometrial cancer

Abstract

Background: Preoperative risk stratification is essential in tailoring endometrial cancer treatment, and biomarkers predicting lymph node metastasis and aggressive disease are aspired in clinical practice. DNA ploidy assessment in hysterectomy specimens is a well-established prognostic marker. DNA ploidy assessment in preoperative curettage specimens is less studied, and in particular in relation to the occurrence of lymph node metastasis.

Methods: Curettage image cytometry DNA ploidy in relation to established clinicopathological variables and outcome was investigated in 785 endometrial carcinoma patients prospectively included in the MoMaTEC multicentre trial.

Results: Diploid curettage status was found in 72.0%, whereas 28.0% were non-diploid. Non-diploid status significantly correlated with traditional aggressive postoperative clinicopathological features, and was an independent predictor of lymph node metastasis among FIGO stage I-III patients in multivariate analysis (OR 1.94, P=0.033). Non-diploid status was related to shorter disease-specific survival (5-year DSS of 74.4% vs 88.8% for diploid curettage, P<0.001). When stratifying by FIGO stage and lymph node status, the prognostic effect remained. However, in multivariate regression analysis, preoperative histological risk classification was a stronger predictor of DSS than DNA ploidy.

Conclusions: Non-diploid curettage is significantly associated with aggressive clinicopathological phenotype, lymph node metastasis, and poor survival in endometrial cancer. The prognostic effect was also observed among subgroups with (presumably) less aggressive traits, such as low FIGO stage and negative lymph node status. Our results indicate curettage DNA ploidy as a possible supplement to existing parameters used to tailor surgical treatment.

Figure 1

Disease-specific survival (DSS) for endometrial cancer patients related to curettage specimens classified according to DNA ploidy. (A) Disease-specific survival for all patients, grouped according to DNA ploidy (n=733). (B) Disease-specific survival for patients with FIGO stage I/II according to curettage DNA ploidy (n=623). Patients with aneuploid, tetraploid, and polyploid tumours were merged because of similar survival, and classified as non-diploid. The number of cases followed by the number of endometrial carcinoma-related deaths is given in parenthesis. P-values are by Kaplan–Meier estimation by the log-rank test.

Figure 2

Disease-specific survival (DSS) for endometrial cancer patients in relation to curettage specimen DNA ploidy and lymph node status. (A) Disease-specific survival for patients with positive lymph node status (n=66); (B) DSS for patients with negative lymph node status (n=485); (C) DSS for patients with unevaluated lymph node status (n=182); (D) DSS for patients with FIGO stage I/II and unevaluated lymph node status (n=152). Patients with aneuploid, tetraploid, and polyploid tumours were merged because of similar survival, and classified as non-diploid. The number of cases followed by the number of endometrial carcinoma related deaths is given in parenthesis. All P-values are by Kaplan–Meier estimation by the log-rank test.