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Updated: May 17, 2025

An Orthotopic Endometrial Cancer Model with Retroperitoneal Lymphadenopathy Made From In Vivo Propagated and Cultured VX2 Cells
Published on: September 12, 2019
Abdominal fat distribution in endometrial cancer: from diagnosis to follow-up
Kristine E Fasmer1,2, Jostein Sæterstøl3,4, Maria B S Ljunggren3
1Mohn Medical Imaging and Visualization Centre (MMIV), Department of Radiology, Haukeland University Hospital, Bergen, Norway. kristine.fasmer@helse-bergen.no.
Background:
The objective of this study is to quantify abdominal obesity markers from computed tomography (CT) scans at primary diagnosis and follow-up in a large endometrial cancer cohort, and to assess temporal change in obesity markers in relation to surgicopathological patient characteristics and outcome.
Methods:
Total- (TAV), subcutaneous- (SAV), visceral (VAV) abdominal fat volumes, and visceral-to-total fat percentage (VAV%) were derived from CT scans acquired in an endometrial cancer patient cohort at primary diagnosis (nprimary=293). Temporal (delta, δ) changes in CT obesity markers from primary diagnosis to follow-up were assessed for all patients with a follow-up CT 13 (7, 19) [median (interquartile range)] months after diagnosis (nfollow-up=152/293 patients). The CT obesity markers were assessed in relation to clinicopathological features and progression-free survival (PFS) using Mann-Whitney U-test, and Cox hazard ratios (HRs), respectively.
Results:
At primary diagnosis, VAV% was the only marker significantly associated with high-risk histology (median of 33% for endometrioid endometrial carcinoma (EEC) grade 1-2, 36% for EEC grade 3 and 36% for non-endometrioid EC, p = 0.003), myometrial invasion (MI) (median of 34% for MI < 50% vs. 35% for MI ≥ 50%, p = 0.03) and lymphovascular space invasion (LVSI) (median of 34% for no LVSI vs. 36% for LVSI, p = 0.009). High VAV% (≥ 35%) also predicted poor PFS both in univariable analysis (HR = 1.8, p = 0.02), and when stratified for surgicopathological FIGO stage (HR = 3.1, p = 0.03). At follow-up, median TAV, VAV, SAV, and VAV% were significantly lower than at primary diagnosis (p < 0.001 for all). Furthermore, patients with progression had larger reductions in visceral fat compartments (δVAV=-24%, δVAV% =-3%), than patients with no progression (δVAV=-17%, δVAV%=-2%, p ≤ 0.006 for both).
Conclusion:
Visceral abdominal obesity (high VAV%) is associated with high-risk histologic features, myometrial invasion, and poor prognosis. Furthermore, high visceral fat loss during/following therapy is associated with disease progression.
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