Endometrial Cancer PDX Model – EC38

Model Overview

Model Details

Patient Information

Molecular Characterization

Patient Clinical History – Diagnosis and Treatment Timeline

Case Study: PDX-EC38 – Romidepsin Enhances Hormonal Therapy

Progesterone receptor (PR) downregulation is a key mechanism underlying endocrine resistance in endometrial cancer, and PR expression can be restored through epigenetic modulation via HDAC inhibitors. The PDX-EC38 model, derived from a 56-year-old patient with Stage II Grade 3 dedifferentiated endometrial carcinoma (MLH1/PMS2-deficient, p53 wild-type), represents an ideal platform for evaluating the efficacy of HDAC inhibitors in combination with progestin therapy.

In this study, PDX-EC38 tumor-bearing mice were divided into four groups: vehicle control, NETE monotherapy (1 mg/mouse, i.m.), romidepsin monotherapy (0.02 mg/mouse, i.p.), and the combination group. Tumor growth inhibition was assessed across groups to evaluate the synergistic anti-tumor effects of the combination regimen.

Results

• Inhibition of tumor proliferation: Romidepsin significantly suppressed tumor growth in PDX-EC38
• Restoration of PR expression: Romidepsin restored PR expression through transcriptional de-repression and prevented proteasomal degradation
• Synergistic anti-tumor efficacy: The NETE + romidepsin combination demonstrated superior tumor growth inhibition compared to either monotherapy

Fig. 1 Anti-tumor efficacy of NETE and romidepsin in the PDX-EC38 model. Data are presented as mean ± standard error (SEM). (Source: Alfa Cytology)

Conclusion

The PDX-EC38 model successfully validated that romidepsin restores PR expression and enhances hormonal therapy efficacy in dedifferentiated endometrial cancer. The significant tumor growth inhibition achieved with both monotherapy and combination treatment provides strong preclinical support for clinical trials evaluating HDAC inhibitors in combination with hormonal therapy in endometrial cancer.

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