# Nomogram Prediction Model and Prognostic Comparison of Cervical Clear Cell Carcinoma and Cervical Endometrioid Adenocarcinoma: A SEER Database Study

**Authors:** Jimiao Huang, Xiaoyan Li, Yiling Zhuang, Zhonghai Zhang, Junjie You, Hongwei Zhang, Jiamin Chen, Nianquan You, Rui Tang, Wuyuan Pan, Ruqi Fang, Suyu Li, Xiangqin Zheng

PMC · DOI: 10.1002/cam4.71699 · 2026-03-11

## TL;DR

This study creates a predictive model to help doctors assess survival risks for two rare cervical cancers using data from the SEER database.

## Contribution

A novel nomogram model is developed and validated for predicting survival in cervical clear cell and endometrioid adenocarcinomas.

## Key findings

- The model showed strong performance with AUCs of 0.894 and 0.857 for 12- and 24-month survival predictions in the development cohort.
- The model effectively stratified patients into risk groups with significantly different survival outcomes (p < 0.0001).
- Decision Curve Analysis and Clinical Impact Curve confirmed the model's clinical usefulness in identifying high-risk patients.

## Abstract

Cervical clear cell adenocarcinoma (CCAC) and cervical endometrioid adenocarcinoma (CEAC) are rare and aggressive non‐HPV‐associated malignancies. Despite their histological similarities, these subtypes demonstrate distinct biological behaviors, presenting challenges in treatment and prognosis.

To develop and validate a multivariable prognostic model for CCAC and CEAC, utilizing the SEER database to enhance clinical decision‐making.

A total of 775 CEAC and 421 CCAC cases were analyzed using a multivariable nomogram. Patients were randomly allocated to model‐development (n = 838) and validation (n = 358) cohorts in a 7:3 ratio. The model's performance was evaluated through AUC, Brier score, and Calibration. Decision Curve Analysis (DCA) and Clinical Impact Curve (CIC) were assessed in both development and internal validation cohorts.

The model exhibited excellent calibration and discrimination in predicting overall survival (OS). In the development cohort, the 12‐ and 24‐month prediction models had AUCs of 0.894 (95% CI: 0.860–0.928) and 0.857 (95% CI: 0.821–0.892), respectively. In the internal validation cohort, the 12‐ and 24‐month models achieved AUCs of 0.814 (95% CI: 0.788–0.840) and 0.798 (95% CI: 0.775–0.822), respectively. The model effectively stratified patients into low‐, intermediate‐, and high‐risk groups, with significantly different median survival times (p < 0.0001). DCA and CIC further validated the model's clinical utility.

We developed a robust nomogram for quantifying OS risk in CCAC and CEAC patients. This model provides clinicians with a tool for identifying high‐risk patients and implementing timely interventions.

## Linked entities

- **Diseases:** cervical clear cell adenocarcinoma (MONDO:0006135), cervical endometrioid adenocarcinoma (MONDO:0003665)

## Full-text entities

- **Genes:** ERBB2 (erb-b2 receptor tyrosine kinase 2) [NCBI Gene 2064] {aka CD340, HER-2, HER-2/neu, HER2, MLN 19, MLN-19}, ARID1A (AT-rich interaction domain 1A) [NCBI Gene 8289] {aka B120, BAF250, BAF250a, BM029, C1orf4, CSS2}, TP53 (tumor protein p53) [NCBI Gene 7157] {aka BCC7, BMFS5, LFS1, P53, TRP53}, EREG (epiregulin) [NCBI Gene 2069] {aka EPR, ER, Ep}, MYC (MYC proto-oncogene, bHLH transcription factor) [NCBI Gene 4609] {aka MRTL, MYCC, bHLHe39, c-Myc}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, CEACAM3 (CEA cell adhesion molecule 3) [NCBI Gene 1084] {aka CD66D, CEA, CGM1, CGM1a, W264, W282}, IGKV3-20 (immunoglobulin kappa variable 3-20) [NCBI Gene 28912] {aka 13K18, A27, IGKV320}, PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) [NCBI Gene 5290] {aka CCM4, CLAPO, CLOVE, CWS5, HMH, MCAP}, CD274 (CD274 molecule) [NCBI Gene 29126] {aka ADMIO5, B7-H, B7H1, PD-L1, PDCD1L1, PDCD1LG1}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, MUC16 (mucin 16, cell surface associated) [NCBI Gene 94025] {aka CA125}, MTOR (mechanistic target of rapamycin kinase) [NCBI Gene 2475] {aka FRAP, FRAP1, FRAP2, RAFT1, RAPT1, SKS}
- **Diseases:** carcinogenesis (MESH:D063646), SCC (MESH:D002294), CIC (MESH:D004834), HPV infection (MESH:D030361), cervical cancer (MESH:D002583), cervical endometriosis (MESH:D004715), adenocarcinoma (MESH:D000230), Tumor (MESH:D009369), CEAC (MESH:D018269), lymph node metastasis (MESH:D008207), Cervical Clear Cell Carcinoma (MESH:D002292), cysts (MESH:D003560), Stage (MESH:D062706), SEER (MESH:D003643), endometrial tumors (MESH:D016889), CCAC (MESH:D018262), lung metastasis (MESH:D009362), toxicity (MESH:D064420), DERIVED (MESH:C536408)
- **Chemicals:** TC (MESH:D013667), platinum (MESH:D010984), TV (MESH:C000707142), paclitaxel (MESH:D017239), DES (MESH:D004054), Pap (MESH:D010724), doxorubicin (MESH:D004317), Carbo (MESH:D016190), cisplatin (MESH:D002945)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12976804/full.md

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Source: https://tomesphere.com/paper/PMC12976804