Development of a prognostic nomogram for colorectal cancer with peritoneal metastasis: a SEER database analysis
Original Article

Development of a prognostic nomogram for colorectal cancer with peritoneal metastasis: a SEER database analysis

Rouyan Zhong1#, Xiaoyan Wang2#, Dandan Gong1#, Changfeng Man1, Yu Fan1 ORCID logo

1Cancer Institute, Affiliated People’s Hospital of Jiangsu University, Zhenjiang, China; 2Department of Gastroenterology, Affiliated Suqian First People’s Hospital of Nanjing Medical University, Suqian, China

Contributions: (I) Conception and design: R Zhong, Y Fan; (II) Administrative support: Y Fan; (III) Provision of study materials or patients: R Zhong, D Gong, C Man; (IV) Collection and assembly of data: R Zhong, X Wang, D Gong; (V) Data analysis and interpretation: R Zhong; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

#These authors contributed equally to this work.

Correspondence to: Yu Fan. Cancer Institute, Affiliated People’s Hospital of Jiangsu University, No 8, Dianli Road, Zhenjiang 212002, China. Email: yuf12345@ujs.edu.cn.

Background: Colorectal cancer (CRC) is one of the most common malignant tumors worldwide. Advanced CRC patients often develop peritoneal metastasis (PM), which severely impairs prognosis. However, there is a lack of accurate prognostic prediction tools to guide clinical decision-making. This study aimed to develop and validate a nomogram for short-term prognostic assessment in CRC patients with PM using the Surveillance, Epidemiology, and End Results (SEER) database.

Methods: We retrospectively analyzed 2,425 eligible CRC patients with PM identified from the SEER database between 2018 and 2022. Patients were randomly assigned to a training cohort and an internal validation cohort at a ratio of 7:3. In addition, 58 patients from the Affiliated People’s Hospital of Jiangsu University (2011–2024) were included as an external validation cohort. The primary endpoint was cancer-specific survival (CSS). Univariate and multivariate Cox proportional hazards regression analyses combined with Kaplan-Meier (KM) survival curves were performed to identify independent prognostic factors and construct a nomogram for predicting 6-month and 1-year CSS. Model performance was evaluated using the concordance index (C-index), time-dependent receiver operating characteristic curves, the area under the curve (AUC), and calibration plots.

Results: Age, primary tumor location, N stage, carcinoembryonic antigen (CEA) level, surgical history, chemotherapy history, and number of lymph nodes examined were identified as independent prognostic factors. The nomogram’s C-index was 0.76 [95% confidence interval (CI): 0.74–0.77] in the training cohort and 0.73 (95% CI: 0.70–0.76) in the internal validation cohort. The AUC values for predicting 6-month and 1-year CSS were 0.84 and 0.80 in the training cohort, and 0.82 and 0.77 in the internal validation cohort, respectively. Calibration curves showed good agreement between predicted and actual CSS.

Conclusions: We developed a nomogram for short-term prognostic assessment in CRC patients with PM using routinely available clinicopathological variables. The model showed acceptable discrimination and calibration in the SEER-derived cohorts, and external calibration showed generally acceptable agreement in the preliminary external validation cohort. Further validation in larger multicenter cohorts is needed.

Keywords: Colorectal cancer (CRC); peritoneal metastasis (PM); Surveillance, Epidemiology, and End Results database (SEER database); prognosis; nomogram prediction model


Submitted Feb 13, 2026. Accepted for publication Apr 14, 2026. Published online May 27, 2026.

doi: 10.21037/tcr-2026-1-0348


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Key findings

• This study developed and validated a prognostic nomogram for colorectal cancer (CRC) patients with peritoneal metastasis (PM) using a large Surveillance, Epidemiology, and End Results (SEER) cohort (n=2,425) and an external validation cohort (n=58).

• The model showed good discrimination (C-index, 0.76 in the training cohort and 0.73 in the validation cohort; AUC 0.84/0.80 for 6/12-month survival) and good calibration.

What is known and what is new?

• PM confers poor prognosis in CRC.

• Several clinicopathological and treatment-related factors, including age, tumor location, N stage, carcinoembryonic antigen level, surgery, chemotherapy, and lymph node count, have been associated with survival outcomes in previous studies.

• This study developed a disease-focused nomogram for short-term prognostic assessment in CRC patients with PM using routinely available clinicopathological variables.

• The model showed stable performance in the SEER-derived cohorts, with preliminary support from external validation.

• In this cohort, N2 disease was associated with worse prognosis than N0–1 disease, whereas T stage and radiotherapy were not retained as independent prognostic factors in the multivariable model.

What is the implication, and what should change now?

• This nomogram may assist short-term individualized risk stratification in CRC patients with PM.

• The findings regarding N-stage grouping, T stage, and radiotherapy should be interpreted cautiously and require further validation in datasets with more detailed information on metastatic burden and treatment characteristics.

• Given the retrospective design and the limitations of registry-based variables, further prospective and multicenter validation is warranted before broad clinical implementation.


Introduction

Cancer was the second leading cause of death globally in 2023, second only to cardiovascular disease (1). According to authoritative data from the International Agency for Research on Cancer (IARC) in 2022, colorectal cancer (CRC) has become the third most common malignancy worldwide, with its mortality ranking second (2). Distant metastasis is one of the major factors affecting the prognosis of CRC patients. Peritoneal metastasis (PM) represents a particularly challenging metastatic pattern in clinical practice (3). Previous studies have reported that approximately 4–15% of patients have synchronous PM at initial diagnosis (4-6), while others develop metachronous PM after curative-intent resection of the primary tumor. Imaging plays an important role in the detection of PM (7). However, small peritoneal lesions are often difficult to identify on conventional imaging (8), which may lead to underestimation of the true incidence of PM.

Compared to metastatic CRC patients without PM, those with PM have significantly shorter median overall survival (3). Additionally, most untreated PM patients rapidly develop symptoms such as intestinal obstruction, ascites, abdominal pain, and malnutrition due to disease progression (9,10). Their median survival is only six months (11). Even with comprehensive treatment, there are still significant individual differences in prognosis.

Current treatment for CRC with PM has evolved into a multidisciplinary approach integrating systemic therapy and local precision interventions. Novel therapies such as cytoreductive surgery (CRS), hyperthermic intraperitoneal chemotherapy (HIPEC), targeted therapy, and immunotherapy have significantly improved outcomes. However, clinical practice remains controversial (12-14), and there is a lack of effective prognostic tools to guide treatment decisions. Therefore, it is crucial for optimizing treatment strategies, improving survival, and achieving individualized therapy to identify prognostic factors accurately and develop reliable prediction models.

Although research on CRC has largely focused on screening, early diagnosis, and treatment optimization, prognostic modeling specifically for CRC patients with PM remains relatively limited. Several studies have attempted to identify prognostic factors or develop prediction models for this population. However, many were based on selected populations, relatively small cohorts, or treatment-specific settings, which may limit generalizability (15). In addition, PM-specific disease burden indicators such as the peritoneal cancer index (PCI) are often available in some selected surgical series but are not routinely recorded in population-based registries such as Surveillance, Epidemiology, and End Results (SEER), which further complicates prognostic evaluation in this setting. These issues highlight the need for pragmatic prognostic tools based on readily accessible clinicopathological variables.

The SEER database is a population-based cancer registry supported by the National Cancer Institute and provides standardized data on cancer incidence, clinicopathological characteristics, treatment, and survival (16). This study used SEER data to develop and internally validate a nomogram for predicting 6-month and 1-year cancer-specific survival (CSS) in CRC patients with PM. We further performed preliminary external validation using an independent cohort from the Affiliated People’s Hospital of Jiangsu University. This study aimed to develop a practical tool for short-term prognostic assessment and risk stratification in CRC patients with PM. We present this article in accordance with the TRIPOD reporting checklist (available at https://tcr.amegroups.com/article/view/10.21037/tcr-2026-1-0348/rc).


Methods

Study population and data source

This study adopted a retrospective cohort study design. Data for the training and internal validation cohorts were obtained from the SEER database using SEER*Stat software. Because PM is not routinely recorded as an independent metastatic site variable in the conventional SEER metastatic-site fields, CRC patients with PM were identified based on the American Joint Committee on Cancer (AJCC) 8th edition M stage classification (17) and Extent of Disease (EOD) Mets Recode (2018+) coding available for cases diagnosed from 2018 onward. Therefore, patients diagnosed between January 2018 and December 2022 were screened.

The inclusion criteria were as follows: (I) pathologically confirmed CRC; (II) primary tumor site coded as C18.0–C20.9 according to the International Classification of Diseases for Oncology, Third Edition (ICD-O-3); (III) PM identified as M1c disease according to the AJCC 8th edition staging system and EOD Mets Recode (2018+) =50; and (IV) complete survival information. The exclusion criteria were as follows: (I) carcinoma in situ (Tis); (II) unclear T stage or N stage; and (III) appendiceal malignancies (C18.1), overlapping colon lesions (C18.8), or unspecified colon cancer (C18.9). A total of 2,425 eligible patients were included and randomly assigned to a training cohort (n=1,697) and an internal validation cohort (n=728) at a ratio of 7:3.

For preliminary external validation, 58 CRC patients with PM treated at the Affiliated People’s Hospital of Jiangsu University between January 2011 and December 2024 were included. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This study was approved by the institutional ethics committee of Affiliated People’s Hospital of Jiangsu University (Ethics No. K-20240143-Y). Written informed consent was obtained from all patients or their guardians.

Variable definitions

The extracted clinicopathological variables included sex (male or female), age (<50, 50–64, or ≥65 years), primary tumor site, T stage, N stage, carcinoembryonic antigen (CEA) level, history of surgery, history of chemotherapy, history of radiotherapy, and number of lymph nodes examined. Primary tumor site was categorized as right-sided colon (cecum, ascending colon, hepatic flexure, and transverse colon), left-sided colon (splenic flexure, descending colon, and sigmoid colon), and rectum. CEA level was classified as normal or elevated. History of surgery, chemotherapy, and radiotherapy were categorized as yes or no. The number of lymph nodes examined was grouped as <12 or ≥12.

The primary endpoint of this study was CSS, which was defined as the interval from diagnosis to death attributable to CRC or last follow-up. Deaths from causes other than CRC were treated as censored observations.

Statistical analysis

All statistical analyses were performed using R software (version 4.5.1). Categorical variables are presented as numbers and percentages, and comparisons between groups were performed using the χ2 test. A two-sided P value <0.05 was considered statistically significant.

Univariate Cox proportional hazards regression analysis was first performed in the training cohort to evaluate the association between each clinicopathological variable and CSS. Variables with P<0.05 in the univariate analysis were subsequently entered into the multivariate Cox proportional hazards regression model to identify independent prognostic factors. In addition, Kaplan-Meier (KM) survival analysis was performed for selected variables, and survival differences between groups were compared using the log-rank test.

Based on the independent prognostic factors identified in the multivariate Cox regression model, a nomogram for predicting 6-month and 1-year CSS in CRC patients with PM was constructed using the “rms” package in R. Model performance was evaluated by discrimination and calibration. Discrimination was assessed using the concordance index (C-index) with 95% confidence intervals (CIs) and time-dependent receiver operating characteristic (ROC) curves with calculation of the area under the curve (AUC). Calibration curves were generated to evaluate the agreement between the predicted and observed survival probabilities.


Results

Baseline characteristics

Comparisons of baseline characteristics between the training cohort and the internal validation cohort, including sex, age, primary tumor site, T stage, N stage, history of surgery, history of radiotherapy, history of chemotherapy, number of lymph nodes examined, and CEA level, showed no statistically significant differences (all P>0.05), suggesting that the two cohorts were generally comparable at baseline (Table 1). In contrast, statistically significant differences were observed between the training cohort and the external validation cohort in primary tumor site, CEA level, and number of lymph nodes examined (all P<0.05) (Table 2).

Table 1

Comparison of baseline characteristics between the training cohort and the internal validation cohort

Characteristic Overall, N=2,425 Training cohort, N=1,697 Validation cohort, N=728 P value
Sex 0.80
   Male 1,207 (50%) 847 (50%) 360 (49%)
   Female 1,218 (50%) 850 (50%) 368 (51%)
Age, years 0.80
   <50 440 (18%) 305 (18%) 135 (19%)
   50–64 822 (34%) 583 (34%) 239 (33%)
   ≥65 1,163 (48%) 809 (48%) 354 (49%)
Tumor site 0.50
   Right colon 1,351 (56%) 935 (55%) 416 (57%)
   Left colon 742 (31%) 532 (31%) 210 (29%)
   Rectum 332 (14%) 230 (14%) 102 (14%)
T stage 0.051
   T1 152 (6.3%) 108 (6.4%) 44 (6.0%)
   T2 34 (1.4%) 18 (1.1%) 16 (2.2%)
   T3 550 (23%) 402 (24%) 148 (20%)
   T4 1,689 (70%) 1,169 (69%) 520 (71%)
Surgery 2,006 (83%) 1,407 (83%) 599 (82%) 0.70
Radiation therapy 144 (5.9%) 102 (6.0%) 42 (5.8%) 0.80
Chemotherapy 1,708 (70%) 1,197 (71%) 511 (70%) 0.90
Number of lymph nodes examined 1,702 (70%) 1,191 (70%) 511 (70%) >0.9
CEA level 0.20
   Low 594 (24%) 402 (24%) 192 (26%)
   High 1,831 (76%) 1,295 (76%) 536 (74%)
N stage 0.80
   N0 624 (26%) 431 (25%) 193 (27%)
   N1 734 (30%) 512 (30%) 222 (30%)
   N2 1,067 (44%) 754 (44%) 313 (43%)

, Pearson’s χ2 test. CEA, carcinoembryonic antigen; N, node; T, tumor.

Table 2

Comparison of baseline characteristics between the training cohort and the external validation cohort

Characteristic Overall, N=1,755 Training cohort, N=1,697 Validation cohort, N=58 P value
Age, years 0.60
   <50 313 (18%) 305 (18%) 8 (14%)
   50–64 602 (34%) 583 (34%) 19 (33%)
   ≥65 840 (48%) 809 (48%) 31 (53%)
Tumor site 0.02
   Right colon 957 (55%) 935 (55%) 22 (38%)
   Left colon 560 (32%) 532 (31%) 28 (48%)
   Rectum 238 (14%) 230 (14%) 8 (14%)
Surgery 1,450 (83%) 1,407 (83%) 43 (74%) 0.08
Chemotherapy 1,243 (71%) 1,197 (71%) 46 (79%) 0.15
Number of lymph nodes examined 1,223 (70%) 1,191 (70%) 32 (55%) 0.01
CEA level 0.03
   Low 423 (24%) 402 (24%) 21 (36%)
   High 1,332 (76%) 1,295 (76%) 37 (64%)
N stage 0.10
   N0 442 (25%) 431 (25%) 11 (19%)
   N1 525 (30%) 512 (30%) 13 (22%)
   N2 788 (45%) 754 (44%) 34 (59%)

, Pearson’s χ2 test. CEA, carcinoembryonic antigen; N, node; T, tumor.

Identification of prognostic factors

Univariate Cox proportional hazards regression analysis showed that age, primary tumor site, T stage, N stage, CEA level, history of surgery, history of chemotherapy, and number of lymph nodes examined were associated with CSS in CRC patients with PM (all P<0.05); sex and history of radiotherapy showed no significant association with CSS (both P>0.05) (Table 3).

Table 3

Univariate Cox proportional hazards regression analysis for CSS in CRC patients with PM

Variables HR 95% CI P
Sex, female 1.03 0.92–1.14 0.62
Age, years
   50–64 1.45 1.22–1.71 <0.001
   ≥65 1.98 1.68–2.33 <0.001
Tumor site
   Left colon 0.66 0.59–0.75 <0.001
   Rectum 0.73 0.63–0.86 <0.001
T stage
   T2 0.48 0.28–0.82 0.008
   T3 0.53 0.42–0.67 <0.001
   T4 0.64 0.52–0.79 <0.001
N stage
   N1 0.57 0.49–0.66 <0.001
   N2 0.94 0.83–1.07 0.34
Surgery, yes 0.54 0.47–0.61 <0.001
Radiation therapy, yes 0.92 0.73–1.15 0.45
Chemotherapy, yes 0.29 0.26–0.33 <0.001
Number of lymph nodes examined, regional yes 0.57 0.51–0.64 <0.001
CEA level, high 1.22 1.07–1.38 0.002

CEA, carcinoembryonic antigen; CI, confidence interval; CRC, colorectal cancer; CSS, cancer-specific survival; HR, hazard ratio; N, node; PM, peritoneal metastasis; T, tumor.

KM survival analysis showed significant differences in CSS among patients with different age groups, primary tumor sites, T stages, N stages, history of surgery, history of chemotherapy, number of lymph nodes examined, and CEA levels (all P<0.05). Among them, patients aged ≥65 years, those with right-sided colon tumors, T1 stage disease, N2 stage disease, no history of surgery, no history of chemotherapy, fewer than 12 lymph nodes examined, and elevated CEA levels showed lower survival probabilities (Figure 2).

Figure 2 KM survival curves for age (A), primary tumor site (B), T stage (C), N stage (D), history of surgery (E), history of chemotherapy (F), number of lymph nodes examined (G), and CEA level (H), respectively. CEA, carcinoembryonic antigen; KM, Kaplan-Meier; N, node; NLND; T, tumor.

Multivariate Cox proportional hazards regression analysis identified older age, primary tumor site in the right-sided colon, higher N stage, no history of surgery, no history of chemotherapy, fewer than 12 lymph nodes examined, and elevated CEA level as independent prognostic factors for CSS in CRC patients with PM (all P<0.05) (Figure 3).

Figure 3 Forest plot of multivariate Cox regression analysis. CEA, carcinoembryonic antigen; N, node; NLND, T, tumor.

T stage was significantly associated with CSS in the univariate Cox regression analysis (P<0.05) but did not remain significant in the multivariate Cox regression analysis (P>0.05); therefore, it was not included in the final model. In addition, no statistically significant difference in CSS was observed between patients with N0 stage disease and those with N1 stage disease in the multivariate analysis (P=0.222). Accordingly, N0 and N1 were combined into an N0–1 group for model construction.

Nomogram development and validation

Nomogram model construction

Based on the independent prognostic factors identified in the multivariate Cox regression analysis, a nomogram was constructed to predict 6-month and 1-year CSS in CRC patients with PM (Figure 4). Each independent prognostic factor was assigned a corresponding score, and the total score was used to estimate the predicted 6-month and 1-year CSS probabilities on the nomogram.

Figure 4 Nomogram for predicting 6-month and 1-year CSS in CRC patients with PM. CEA, carcinoembryonic antigen; CRC, colorectal cancer; CSS, cancer-specific survival; N, node; NLND; PM, peritoneal metastasis; T, tumor.

Model validation

The C-index was 0.76 (95% CI: 0.74–0.77) in the training cohort and 0.73 (95% CI: 0.70–0.76) in the internal validation cohort.

Time-dependent ROC analysis showed that the AUCs for predicting 6-month and 1-year CSS were 0.84 and 0.80, respectively, in the training cohort, and 0.82 and 0.77, respectively, in the internal validation cohort (Figure 5).

Figure 5 ROC curves for the training cohort and internal validation cohort. (A,B) ROC curves for 6-month and 1-year survival rates in the training cohort, respectively; (C,D) ROC curves for 6-month and 1-year survival rates in the internal validation cohort, respectively. AUC, area under the curve; ROC, receiver operating characteristic.

Calibration curves for the training cohort, internal validation cohort, and external validation cohort showed generally good agreement between the predicted and observed survival probabilities (Figure 6).

Figure 6 (A,B) The calibration curves for 6-month and 1-year survival rates in the training cohort, respectively; (C,D) the calibration curves for 6-month and 1-year survival rates in the internal validation cohort, respectively; (E,F) the calibration curves for 6-month and 1-year survival rates in the external validation cohort, respectively.

Discussion

As a challenging area in clinical treatment, the prognostic assessment of PM in CRC has always been a research focus. Although PM is generally associated with poor outcomes, the clinical course is not the same in every patient. Some patients may still achieve relatively prolonged survival after standardized treatment, whereas others experience rapid disease progression and poor outcomes (18). This heterogeneity suggests that prognosis in CRC patients with PM is not determined by a single factor (19), but is instead influenced by multiple dimensions, including primary tumor location, tumor biology, disease burden, treatment strategy, and overall patient condition (20). In the present study, we developed a nomogram for predicting 6-month and 1-year CSS in CRC patients with PM using a population-based SEER cohort, followed by preliminary external validation in an independent single-center cohort. The final model incorporated 7 independent prognostic factors identified by multivariate Cox regression analysis. The model showed acceptable performance in the SEER-derived cohorts, with preliminary support from calibration in the external cohort, suggesting that it may serve as a practical adjunct for short-term prognostic assessment in this setting.

Among the 7 independent prognostic factors identified in this study, older age, tumor origin in the right-sided colon, higher N stage, no surgical treatment, no chemotherapy, <12 lymph nodes examined, and elevated CEA level have all been reported to be associated with poorer outcomes in CRC, including studies focused on CRC-PM (15,21-25).

Age, as a classic factor influencing cancer prognosis, is reaffirmed in this study. Our findings showed that older patients tended to have poorer CSS, which may partly reflect reduced physiological reserve, greater comorbidity burden, and lower tolerance to intensive treatment (26). From a clinical perspective, this finding supports more individualized treatment planning in elderly patients with PM (21), particularly when balancing treatment intensity against overall functional status and treatment tolerance.

The impact of primary tumor site on prognosis is also significant. Some studies have pointed out that among recurrent CRC patients, the prognosis of rectal cancer is often better than that of right-sided colon cancer but worse than left-sided colon cancer (27). This is consistent with the results of the KM survival curves and nomogram in this study. In this study, patients with right-sided colon tumors showed poorer outcomes than those with left-sided colon or rectal tumors. This observation is generally consistent with previous studies in CRC and may be related to biological heterogeneity across tumor locations, including differences in embryologic origin (28), molecular characteristics, and clinical presentation. In addition, right-sided tumors often present with less specific early symptoms and may therefore be diagnosed at a more advanced stage.

Among treatment-related factors, surgery can remove the primary tumor and part of the metastases, reducing tumor burden; chemotherapy can inhibit or kill tumor cells throughout the body, delaying disease progression. In our cohort, both surgery and chemotherapy were linked to better CSS. This is consistent with the current view that management of CRC with PM should be multidisciplinary and individualized. Contemporary guidelines and expert consensus generally emphasize individualized multimodal management for PM, combining systemic therapy with selected local treatment when appropriate (29). CRS may be considered a local treatment option in carefully selected patients, but the additional value of HIPEC has not been uniformly established (6,13,30,31). Accordingly, decisions regarding HIPEC should remain individualized and should take into account disease burden, resectability, treatment protocol, and institutional experience (32). More broadly, treatment decisions for PM are complex and depend on disease burden, general condition, and resectability. Our findings suggest that active treatment may be associated with improved survival in appropriately selected patients, although the treatment variables available in SEER do not allow detailed evaluation of specific treatment strategies or treatment intensity. Therefore, the surgical variable in the present model should be interpreted as a broad treatment-related indicator rather than evidence for the prognostic effect of any specific surgical strategy, because the SEER-derived surgery variable used in this study did not allow reliable distinction of surgical intent or comprehensive characterization of surgical strategy, including whether surgery was performed for curative or palliative purposes.

Previous studies have suggested that the burden of nodal involvement, particularly when assessed by lymph node ratio, may retain prognostic value even in stage IV CRC (23). This study found that the prognosis of CRC patients with PM may be affected by lymph node status. In this study, patients with N2 stage disease had poorer outcomes, whereas no statistically significant difference was observed between N0 and N1 stage disease in the multivariate analysis. Accordingly, N0 and N1 were combined into an N0-1 group during model construction. This finding suggests that, in patients with PM, the prognostic contribution of regional nodal involvement may differ from that observed in earlier-stage CRC. Because PM represents stage IV disease, the prognostic impact of intra-abdominal tumor burden and treatment-related factors may outweigh the incremental difference between N0 and N1 disease (33). Nevertheless, this result should be interpreted with caution and warrants further validation.

Elevated CEA level was also identified as an independent adverse prognostic factor, which is consistent with its established role as a marker of tumor burden and disease activity in CRC. In this study, examining fewer than 12 lymph nodes was associated with poorer prognosis. This finding may reflect both suboptimal staging accuracy and variability in surgical or pathological evaluation, and is also broadly consistent with current guideline recommendations emphasizing evaluation of at least 12 lymph nodes for adequate nodal staging in CRC. This observation further underscores the importance of standardized management in this population. The specific result regarding T stage in this study deserves in-depth discussion: T stage was associated with prognosis in univariate analysis but did not become an independent risk factor in multivariate analysis, and the KM survival curve showed that T1 stage patients had a worse prognosis than T2–4 stage patients (with no significant difference in prognosis among T2–4 stage patients). This pattern differs from the conventional expectation in non-metastatic CRC (34), and robust prior evidence supporting this observation in CRC with PM remains limited. A possible explanation is that, in the setting of PM, the prognostic contribution of primary tumor invasion depth may be attenuated by metastatic burden and treatment-related factors. Another possibility is that a subset of T1 tumors presenting with PM may have particularly aggressive biological behavior. In addition, the relatively small number of T1 cases and potential case-selection effects may have introduced instability into the subgroup analysis. Therefore, this finding should be interpreted cautiously and requires further confirmation.

Some previous studies have suggested that radiotherapy may improve outcomes in selected patients with rectal cancer, although its impact on survival remains context-dependent (35). This study suggests that radiotherapy was not significantly associated with CSS in CRC patients with PM, which may reflect the specific clinical context of PM. First, the proportion of patients receiving radiotherapy in the training cohort was low (only 6.0%, 102/1,697), which may lead to insufficient statistical power. Second, radiotherapy in patients with PM is usually applied in selected clinical scenarios, such as symptom palliation or control of localized disease, which introduces potential selection bias. Third, the SEER database lacks detailed radiotherapy information, including dose, target volume, and technique, preventing further evaluation of treatment quality and intent. In addition, the diffuse distribution pattern of peritoneal metastases may further limit the effectiveness of radiotherapy in this setting, and potential differences in treatment response between PM lesions and primary tumors may also have contributed to the observed findings. Therefore, the role of radiotherapy in CRC with PM could not be fully evaluated in the present study. It is also noteworthy that significant differences were observed between the training cohort and the external validation cohort in primary tumor site, CEA level, and number of lymph nodes examined. These differences likely reflect, at least in part, variation in patient composition, clinical practice patterns, and underlying population characteristics between a population-based registry cohort and a single-center institutional cohort. Although such heterogeneity may reduce direct comparability between cohorts, it also reflects real-world clinical diversity. Therefore, the preliminary external validation may still provide additional information regarding the potential applicability of the model across different practice settings (36), although this interpretation should remain cautious given the limited external sample size.

Several limitations should be acknowledged in this study. First, this was a retrospective study, and inherent selection bias and residual confounding could not be avoided. In addition, in the SEER database, PM was identified using the AJCC 8th edition M1c classification together with EOD Mets Recode (2018+) =50. Although this approach helps improve the specificity of PM identification in the 2018+ cohort, it indicates the presence of PM but does not allow complete exclusion of coexisting distant metastases in other organs. Therefore, isolated PM could not be reliably distinguished from PM accompanied by other distant metastatic sites in this study. Although some common metastatic sites can be partially assessed using site-specific variables available in SEER, the database does not allow comprehensive exclusion of all coexisting distant metastatic sites for every patient in this cohort. Therefore, we did not define the study population as patients with definitively isolated PM. This issue should also be interpreted in the context of real-world clinical practice, in which PM often coexists with other distant metastatic sites in a proportion of CRC patients. Moreover, although all included CRC cases were pathologically confirmed at the primary tumor level, the SEER database does not provide lesion-level information to determine whether PM itself was confirmed by biopsy or surgical pathology. Second, a substantial proportion of initially screened patients were not included in the final cohort because of missing T stage or N stage information. In the original SEER dataset, 5,269 patients were screened, whereas only 2,425 met the final eligibility criteria. One possible explanation is that some patients had already developed PM at diagnosis and therefore did not undergo surgery with adequate pathological staging, making complete and standardized tumor-node-metastasis (TNM) classification difficult to obtain. Because T stage and N stage are important variables in prognostic assessment, we attempted multiple imputation for the missing data. However, the imputed T stage and N stage did not show prognostic significance in subsequent analyses, and their stability and clinical interpretability were limited. Therefore, these imputed data were not retained in the final model. Although this approach helped preserve the relative reliability of staging information in the analyzed cohort, it inevitably reduced the sample size and may have introduced selection bias.

Third, PM-specific disease burden indicators, such as the PCI and the Japanese P classification, were not available in SEER and therefore could not be incorporated into the model. PCI remains a commonly used measure of peritoneal disease burden in CRC patients with PM and is frequently considered in prognostic assessment and treatment decision-making (18). Although T stage, N stage, and metastatic classification may partly reflect overall disease status, they cannot substitute for PM-specific burden measures. In addition, the SEER database does not capture several clinically important variables, including specific chemotherapy regimens, targeted therapy, immunotherapy, CRS-HIPEC, completeness of cytoreduction, molecular markers such as RAS/BRAF and microsatellite instability (MSI) status, and patient-related factors such as performance status, body mass index, and comorbidities. The type and intent of surgery also could not be adequately distinguished. Treatment timing could not be assessed either. Previous studies have suggested that perioperative or postoperative systemic chemotherapy may be associated with improved survival in selected CRC patients with PM, but the optimal timing remains controversial (37,38). Because SEER does not provide sufficiently detailed information on treatment sequence or perioperative treatment strategy, this issue could not be explored in the present study. In addition, some pathological factors with potential prognostic importance could not be evaluated because of substantial missing data. Lymph-vascular invasion was entirely unavailable in our cohort, while tumor deposits and perineural invasion were excluded because of excessive missingness. Inclusion of these variables would have markedly reduced the effective sample size and potentially compromised the robustness of the analysis. Therefore, residual confounding related to pathological aggressiveness and tumor burden could not be fully avoided.

Finally, the model was designed for short-term prognostic prediction and was not intended to predict long-term survival. The 6-month and 1-year time horizons were selected because CRC patients with PM generally have poor survival and short-term prognostic assessment is clinically relevant for initial treatment planning and early risk stratification. We also explored longer-term prediction, including 3-year and 5-year endpoints. However, the corresponding calibration performance was unsatisfactory. This may indicate that longer-term prognostic prediction in CRC patients with PM requires more detailed treatment-related, molecular, and disease-burden information, which is not adequately captured in the SEER database. In addition, the external validation cohort was relatively small and covered a long inclusion period, which may have introduced treatment heterogeneity.

Despite these limitations, the present study may still provide clinically relevant information for short-term risk stratification in CRC patients with PM. Although the variables included in the model are largely established prognostic factors, their integration into a disease-focused nomogram may still offer practical value in this setting. The nomogram was developed using a relatively large population-based cohort and incorporated variables that are readily available in routine practice. Therefore, it may serve as a practical adjunct for short-term prognostic assessment and clinical risk stratification in this population.


Conclusions

We developed and validated a nomogram for predicting 6-month and 1-year CSS in CRC patients with PM based on 7 independent prognostic factors. The model showed acceptable discrimination and calibration in the training, internal validation, and preliminary external validation cohorts. This nomogram may serve as a practical tool for short-term prognostic assessment and risk stratification in this population. Future studies should focus on prospective multicenter validation and incorporate more detailed treatment, imaging, molecular, and disease-burden data to refine the model and improve the prediction of long-term outcomes.

Figure 1 Global incidence and mortality of major malignant tumors in 2022. The distributions of cancer incidence (A) and mortality (B) in 2022, respectively. Colorectal cancer ranked third in incidence and second in mortality worldwide.

Acknowledgments

None.


Footnote

Reporting Checklist: The authors have completed the TRIPOD reporting checklist. Available at https://tcr.amegroups.com/article/view/10.21037/tcr-2026-1-0348/rc

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Funding: This work was partially supported by grants from the Key Project Fund of Jiangsu Provincial Health Commission (No. ZD2023016) and the Zhenjiang Social Development Fund (Nos. SH2024002, SH2024075, and JC2024031).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tcr.amegroups.com/article/view/10.21037/tcr-2026-1-0348/coif). All authors report receiving grants from the Key project fund of Jiangsu Provincial Health Commission and the Zhenjiang Social Development Fund. The authors have no other conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This study was approved by the institutional ethics committee of Affiliated People’s Hospital of Jiangsu University (Ethics No. K-20240143-Y). Written informed consent was obtained from all patients or their guardians.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.


References

  1. GBD 2023 Cancer Collaborators. The global, regional, and national burden of cancer, 1990-2023, with forecasts to 2050: a systematic analysis for the Global Burden of Disease Study 2023. Lancet 2025;406:1565-86. [Crossref] [PubMed]
  2. Bray F, Laversanne M, Sung H, et al. Global cancer statistics 2022: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin 2024;74:229-63. [Crossref] [PubMed]
  3. Young J, Edwards J, Park JH. The epidemiology, current evidence and controversies in diagnosis and management of patients with colorectal peritoneal metastases. Surgeon 2025;S1479-666X(25)00157-X.
  4. Lurvink RJ, Bakkers C, Rijken A, et al. Increase in the incidence of synchronous and metachronous peritoneal metastases in patients with colorectal cancer: A nationwide study. Eur J Surg Oncol 2021;47:1026-33. [Crossref] [PubMed]
  5. Quere P, Facy O, Manfredi S, et al. Epidemiology, Management, and Survival of Peritoneal Carcinomatosis from Colorectal Cancer: A Population-Based Study. Dis Colon Rectum 2015;58:743-52. [Crossref] [PubMed]
  6. Hübner M, van Der Speeten K, Govaerts K, et al. 2022 Peritoneal Surface Oncology Group International Consensus on HIPEC Regimens for Peritoneal Malignancies: Colorectal Cancer. Ann Surg Oncol 2024;31:567-76. [Crossref] [PubMed]
  7. Vandecaveye V, Rousset P, Nougaret S, et al. Imaging of peritoneal metastases of ovarian and colorectal cancer: joint recommendations of ESGAR, ESUR, PSOGI, and EANM. Eur Radiol 2025;35:2712-22. [Crossref] [PubMed]
  8. Stańczak M, Kruszewski W, Ciesielski M, et al. What is worth knowing about peritoneal metastases in colorectal cancer? Front Surg 2025;12:1719153. [Crossref] [PubMed]
  9. Foster JM, Zhang C, Rehman S, et al. The contemporary management of peritoneal metastasis: A journey from the cold past of treatment futility to a warm present and a bright future. CA Cancer J Clin 2023;73:49-71. [Crossref] [PubMed]
  10. Liu JL, Wang CX, Wang HL. Advances in the management of cancer-related incomplete intestinal obstruction: Therapeutic strategies and emerging interventions. World J Gastroenterol 2026;32:115030. [Crossref] [PubMed]
  11. Rijsemus CJV, Kok NFM, Aalbers AGJ, et al. Staging peritoneal metastases in colorectal cancer: The correlation between MRI, surgical and histopathological peritoneal cancer index. Eur J Surg Oncol 2024;50:108611. [Crossref] [PubMed]
  12. Somashekhar SP, Surendran AK, Goyal D, et al. Current Status of Hyperthermic Intraperitoneal Chemotherapy (HIPEC) in Colorectal Cancer (CRC). South Asian J Cancer 2024;13:267-73. [Crossref] [PubMed]
  13. Quénet F, Elias D, Roca L, et al. Cytoreductive surgery plus hyperthermic intraperitoneal chemotherapy versus cytoreductive surgery alone for colorectal peritoneal metastases (PRODIGE 7): a multicentre, randomised, open-label, phase 3 trial. Lancet Oncol 2021;22:256-66. [Crossref] [PubMed]
  14. Hayler R, Garrett C, Guo J, et al. Overall survival post secondary cytoreductive surgery and hyperthermic intraperitoneal chemotherapy for recurrent colorectal cancer with peritoneal metastases. World J Surg Oncol 2025;23:297. [Crossref] [PubMed]
  15. Ge X, Yang G, Wu H, et al. Prognostic Factors and Nomogram-Based Prediction Models for Colorectal Cancer Patients With Synchronous Peritoneal Metastasis Undergoing Cytoreductive Surgery: A Retrospective Cohort Study. Cancer Med 2026;15:e71464. [Crossref] [PubMed]
  16. Hong YD, Mariotto AB, Lewis DR, et al. Compliance With Recommendations of the Surveillance, Epidemiology, and End Results (SEER) Treatment Data Use Agreement: A Review of Published Studies. Med Care 2025;63:899-906. [Crossref] [PubMed]
  17. Weiser MR. AJCC 8th edition: colorectal cancer. Ann Surg Oncol 2018;25:1454-5.
  18. Kazanowski M, Lesiak P, Wierzbicki J, et al. Peritoneal Cancer Index Dominates Prognosis After CRS-HIPEC for Colorectal Peritoneal Metastases: A Consecutive Single-Centre Cohort with 3-Year Follow-Up. Cancers (Basel) 2025;17:3614. [Crossref] [PubMed]
  19. Simkens GA, Wintjens AGWE, Rovers KP, et al. Effective Strategies to Predict Survival of Colorectal Peritoneal Metastases Patients Eligible for Cytoreductive Surgery and HIPEC. Cancer Manag Res 2021;13:5239-49. [Crossref] [PubMed]
  20. Lemmens VE, Klaver YL, Verwaal VJ, et al. Predictors and survival of synchronous peritoneal carcinomatosis of colorectal origin: a population-based study. Int J Cancer 2011;128:2717-25. [Crossref] [PubMed]
  21. Soler-González G, Sastre-Valera J, Viana-Alonso A, et al. Update on the management of elderly patients with colorectal cancer. Clin Transl Oncol 2024;26:69-84. [Crossref] [PubMed]
  22. de Boer NL, Rovers K, Burger JWA, et al. A population-based study on the prognostic impact of primary tumor sidedness in patients with peritoneal metastases from colon cancer. Cancer Med 2020;9:5851-9. [Crossref] [PubMed]
  23. Naidu K, Chapuis PH, Connell L, et al. Lymph node ratio prognosticates overall survival in patients with stage IV colorectal cancer. Tech Coloproctol 2024;28:115. [Crossref] [PubMed]
  24. Yang Z, Li Y, Qin X, et al. Development and Validation of a Prognostic Nomogram for Colorectal Cancer Patients With Synchronous Peritoneal Metastasis. Front Oncol 2021;11:615321. [Crossref] [PubMed]
  25. Gramkow MH, Mosgaard CS, Schou JV, et al. The prognostic role of circulating CA19-9 and CEA in patients with colorectal cancer. Cancer Treat Res Commun 2025;43:100907. [Crossref] [PubMed]
  26. Ohta R, Tanaka Y, Tanaka K, et al. Impact of Comorbidity Burden on Clinical Outcomes in Older Adults With Metastatic Colorectal Cancer: A Systematic Review and Meta-Analysis. Cureus 2025;17:e94099. [Crossref] [PubMed]
  27. Shida D, Inoue M, Tanabe T, et al. Prognostic impact of primary tumor location in Stage III colorectal cancer-right-sided colon versus left-sided colon versus rectum: a nationwide multicenter retrospective study. J Gastroenterol 2020;55:958-68. [Crossref] [PubMed]
  28. Mendoza-Moreno F, Díez-Alonso M, Matías-García B, et al. Does Tumor Sidedness Matter After Curative Surgery in Colorectal Cancer? A Retrospective Cohort Study on Recurrence Patterns and Post Recurrence Survival. Clin Colorectal Cancer 2026;25:87-96.
  29. Colorectal Cancer Professional Committee, Chinese Medical Doctor Association. Expert consensus on the diagnosis and treatment of colorectal cancer peritoneal metastasis (2025 edition). Chinese Journal of Gastrointestinal Surgery 2025;28:441-9.
  30. Tonello M, Cenzi C, Pizzolato E, et al. National Guidelines for Cytoreductive Surgery and Hyperthermic Intraperitoneal Chemotherapy (HIPEC) in Peritoneal Malignancies: A Worldwide Systematic Review and Recommendations of Strength Analysis. Ann Surg Oncol 2025;32:5795-806. [Crossref] [PubMed]
  31. Taqi K, Lee J, Hurton S, et al. Long-Term Outcomes following Cytoreductive Surgery and Hyperthermic Intraperitoneal Chemotherapy for Peritoneal Carcinomatosis of Colorectal Origin. Curr Oncol 2024;31:3657-68. [Crossref] [PubMed]
  32. Schultz KS, Bansal VV, Wach MM, et al. Consensus Guideline for the Management of Colorectal Cancer with Peritoneal Metastases. Ann Surg Oncol 2026;33:5260-82. [Crossref] [PubMed]
  33. Cervantes A, Adam R, Roselló S, et al. Metastatic colorectal cancer: ESMO Clinical Practice Guideline for diagnosis, treatment and follow-up. Ann Oncol 2023;34:10-32. [Crossref] [PubMed]
  34. Bhutiani N, Hu CY, Palis B, et al. Lack of Hierarchical Survival Prognosis in AJCC Staging for Colon and Rectal Cancer-Implications for Future Summary Stage Classification. Clin Colorectal Cancer 2025;24:159-165.e2. [Crossref] [PubMed]
  35. Pennel K, Dutton L, Melissourgou-Syka L, et al. Novel radiation and targeted therapy combinations for improving rectal cancer outcomes. Expert Rev Mol Med 2024;26:e14. [Crossref] [PubMed]
  36. Ramspek CL, Jager KJ, Dekker FW, et al. External validation of prognostic models: what, why, how, when and where? Clin Kidney J 2021;14:49-58. [Crossref] [PubMed]
  37. Tonello M, Cenzi C, Pizzolato E, et al. Systemic Chemotherapy in Colorectal Peritoneal Metastases Treated with Cytoreductive Surgery: Systematic Review and Meta-Analysis. Cancers (Basel) 2024;16:1182. [Crossref] [PubMed]
  38. Cashin PH, Esquivel J, Larsen SG, et al. Perioperative chemotherapy in colorectal cancer with peritoneal metastases: A global propensity score matched study. EClinicalMedicine 2023;55:101746. [Crossref] [PubMed]
Cite this article as: Zhong R, Wang X, Gong D, Man C, Fan Y. Development of a prognostic nomogram for colorectal cancer with peritoneal metastasis: a SEER database analysis. Transl Cancer Res 2026;15(5):384. doi: 10.21037/tcr-2026-1-0348

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