Endometrial Cancer PDX Model – EC38
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Model Overview
Model Details
- Model:Endometrial Cancer PDX Model – EC38
- Animal: NSG Mice
- Weight: 18-22 g
- Passage: P3 (stable)
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- Cancer Type: Endometrial Dedifferentiated Carcinoma
- Age: 6-8 Weeks
- Molecular Profile: dMMR (MLH1/PMS2-deficient), MLH1 Promoter Methylation+, p53 Wild-type, HER2 IHC Score 0.
- Matched PDC Model: PDC-EC38
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Patient Information
- Sex: Female
- Race/Ethnicity: /
- Age at Diagnosis: 56 years
- BMI: 50.11
- Diagnosis: Dedifferentiated carcinoma, Grade 3, Stage II
- Treatment History: Chemotherapy and consideration of radiation therapy; progesterone therapy
- Comorbidities: Essential hypertension, Morbid obesity, Type 2 diabetes
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Molecular Characterization
Immunohistochemistry (IHC) Profile
- ER: Not specified
- PR: Not specified
- p53: Wild-type
- p16: Not specified
- MLH1: Not expressed (loss in tumor cells)
- PMS2: Not expressed (loss in tumor cells)
- MSH2: Intact
- MSH6: Intact
- HER2: IHC Score 0 (negative)
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Molecular Classification
- MMR Status: Deficient (dMMR) – MLH1/PMS2 loss
- MLH1 Promoter Methylation: Positive
- p53 Status: Wild-type
- HER2 Status: Negative (IHC Score 0)
- MSI Status: MSI-H (inferred from dMMR)
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Patient Clinical History – Diagnosis and Treatment Timeline
- Jan 18, 2024: Serum calcium: 9.4; Glucose: 216
- Feb 12, 2024: Sample receipt date; Glucose: 234
- Post-surgery: Hysterectomy and bilateral salpingo-oophorectomy
- Jun 12, 2025: CT Chest: Postsurgical changes without evidence of local recurrence
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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.
Accelerate Your Endometrial Cancer Drug Development
From model establishment to preclinical validation, Alfa Cytology provides PDX models with comprehensive molecular characterization and pharmacodynamic validation. Whether you are exploring novel immunotherapies, combination strategies, or screening effective drug candidates, our models deliver reliable preclinical data to support your research programs. Please don't hesitate to contact us to discuss your specific research needs and request a complete model list.
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