Excess late mortality among long-term gastric cancer survivors following gastrectomy: a population-based cohort study

Introduction

Gastric cancer (GC) remains a major global health challenge, ranking as the fifth most common malignancy and the fourth leading cause of cancer-related death worldwide (1). Advances in multimodal treatment strategies, particularly the refinement of surgical techniques such as gastrectomy, have significantly improved survival outcomes and led to a growing cohort of long-term survivors who achieve the critical 5-year survival milestone (2). While this progress highlights the effectiveness of contemporary management, it also shifts clinical focus toward understanding the long-term health trajectory of these individuals beyond the initial treatment phase.

Recent years have witnessed a growing body of research focused on late mortality among long-term cancer survivors, with particular attention given to pediatric and adolescent and young adult (AYA) populations. Studies in these cohorts have consistently demonstrated that survivors face significantly elevated risks of late mortality compared to the general population, not only from disease recurrence but also from non-cancer causes such as cardiovascular disease (CVD), second malignant neoplasms (SMNs), and infectious disease (3-10). While these investigations have effectively highlighted the vulnerability of younger survivors, there remains a notable gap in understanding similar long-term risks in older adult populations undergoing major oncological surgeries and extensive adjuvant therapies. Most existing studies have concentrated on perioperative outcomes or follow-up for at most 5 years, leaving a notable gap in the systematic evaluation of cause-specific late mortality in GC survivors who have achieved long-term survival (11-15).

To address this, we conducted a population-based cohort study utilizing data from the Surveillance, Epidemiology, and End Results (SEER) registry. Our objectives were to quantify excess late mortality among long-term GC survivors after gastrectomy, to delineate the spectrum of causes of death, particularly SMNs and non-cancer conditions, and to identify demographic and clinical subgroups at heightened risk. The findings aim to inform tailored survivorship care strategies and optimize long-term health monitoring for this expanding patient population. We present this article in accordance with the STROBE reporting checklist (available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-1-0141/rc).

Methods

Data source and study population

This retrospective cohort study utilized data from the SEER database of 12 registries [1992–2022], covering approximately 12.2% of the U.S. population. The inclusion criteria were as follows: (I) aged 15–89 years; (II) primary GC according to International Classification of Diseases for Oncology, 3rd Edition (ICD-O-3) site codes C16.0–C16.9; (III) adenocarcinoma with positive histology; (IV) underwent gastrectomy; (V) survival duration of at least 5 years post-diagnosis (long-term survivors). Patients with unknown age, pathology other than adenocarcinoma, and prior malignancies, or confirmed solely by death certificates or autopsy reports were excluded. The specific parameters and criteria for data acquisition are detailed in Table S1. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. For this study, we used deidentified, publicly available SEER data; thus, additional ethical review and participant consent were not required.

Assessment of demographic and clinicopathological characteristics

Demographic and clinicopathological characteristics were obtained and recategorized as follows: year of diagnosis (1992–2004 and 2005–2017), age at diagnosis (15–49, 50–69 and ≥70 years), sex (men and women), race (non-Hispanic White, non-Hispanic Black, Hispanic, and others), location (cardia and non-cardia), histological type [adenocarcinoma and signet ring cell carcinoma (SRCC)], grade (I/II and III/IV), stage (localized, regional and distant), radiotherapy (yes and no/unknown), and chemotherapy (yes and no/unknown) (Table S2).

Follow-up and causes of death

The follow-up of GC survivors extended from the date of GC diagnosis until death, loss to follow-up, or December 31, 2022, whichever occurred first. Causes of death were classified using the International Classification of Diseases (ICD), with ICD-9 for 1992–1998 and ICD-10 for 1999–2017. Mortality outcomes were classified into five categories: all-cause mortality, mortality due to recurrence or progression, mortality due to SMNs, non-cancer health-related mortality and mortality due to external injuries. Non-cancer health-related mortality were then grouped into diabetes mellitus, Alzheimer’s disease, CVDs, infectious diseases, respiratory diseases, gastrointestinal diseases, kidney diseases, and other causes of death (Table S3).

Statistical analysis

The sample size was determined by the available pool of eligible long-term cancer survivors within the SEER dataset rather than by formal power calculations. Person-years at risk were calculated from the date of 5-year survival until the date of death, loss to follow-up, or December 31, 2022, whichever occurred first. Cumulative all-cause mortality probabilities at 10-, 15- and 20-year follow-up were estimated using the Kaplan-Meier method, with 95% confidence intervals (CIs) derived via the log-log transformation. Cumulative cause-specific mortality was estimated using the cumulative incidence function (CIF), accounting for competing risks of death. To quantify excess mortality, standardized mortality ratios (SMRs) with 95% CIs were calculated as the ratio of observed deaths among cancer survivors to expected deaths in the age-, sex-, race- and calendar year-matched general U.S. population. Absolute excess risks (AERs) were computed as the difference between observed and expected deaths per 10,000 person-years. Subgroup analyses for all-cause, SMN-related and non-cancer health-related mortality were performed according to sociodemographic and clinicopathological characteristics. To assess effect modification, the relative-risk SMR (RRSMR) and its 95% CIs between subgroups were calculated using the delta method, which estimates the variance of the ratio based on the SMRs and the number of observed deaths.

All statistical analyses were performed using SEER*Stat software (version 9.0.42.2) and R software (version 4.5.2). Statistical significance was defined as a two-sided P value <0.05 or a 95% confidence interval excluding 1.

Results

Baseline characteristics

This study included 8,637 long-term GC survivors who had undergone gastrectomy, with a median age of 66 (interquartile range, 56–74) years. The majority of the cohort was male (61.7%), with 1,164 (13.5%) aged under 50 years and 3,459 (40.0%) aged 70 years or older. More than half of the patients (52.3%) were diagnosed in or after 2005. Regarding race, non-Hispanic Whites comprised 40.0% of the cohort, followed by other racial groups (33.9%), Hispanics (18.1%), and non-Hispanic Blacks (7.9%). Most cancers were poorly or undifferentiated (grade III/IV, 57.2%), localized (52.4%) and non-cardia (78.4%). SRCC accounted for 17.9% of the cohort, with the remaining 82.1% consisting of various adenocarcinomas. Treatment modalities included radiotherapy in 26.8% and chemotherapy in 39.7% of patients (Table S4).

Late mortality and causes of death

Long-term GC survivors were followed for a total of 61,003 person-years from 5-year survival, with a median follow-up of 126 (interquartile range, 87–187) months since the time of diagnosis. At the end of follow-up, 4,048 (46.9%) patients were alive and 4,589 (53.1%) were deceased, corresponding to an all-cause mortality of 663.6 per 10,000 person-years. The estimated all-cause cumulative mortality probabilities were 31.6% (95% CI: 30.6–32.7%) at 10 years, 51.5% (95% CI: 50.0–52.4%) at 15 years, and 67.7% (95% CI: 66.4–69.1%) at 20 years after diagnosis (Figure 1A and Table S5). The leading cause was non-cancer health-related conditions (n=2,685, 58.5%), followed by recurrence or progression (n=1,272, 27.7%), SMNs (n=535, 11.7%), and external injuries (n=97, 2.1%). A clear temporal trend was observed in the distribution of causes of death: as survival time increased, the proportion of deaths due to recurrence or progression declined steadily from 41.3% during years 5–9 to only 12% beyond 20 years. In contrast, the proportion of non-cancer health-related deaths rose substantially from 53.9% to 73.9% over the same intervals. Meanwhile, SMNs and external injuries represented relatively stable or slightly increased proportional causes in later periods (Figure 1B and Table S6).

Figure 1 Late mortality and causes of death among long-term gastric cancer survivors following gastrectomy. (A) The cumulative cause-specific mortality. (B) Causes of death during each latency period.

Excess late all-cause mortality

Compared to the general population, long-term GC survivors experienced a significantly elevated overall mortality, with a SMR of 1.66 (95% CI: 1.61–1.70) and an AER of 297.8 per 10,000 person-years (Figure 2). Excess late mortality risks persisted across follow-up and varied substantially among subgroups. Men had a higher SMR (1.70, 95% CI: 1.64–1.76) compared to women (1.59, 95% CI: 1.51–1.66), with a RRSMR of 1.07 (95% CI: 1.01–1.14). Risk was most pronounced in the 5–9 years post-diagnosis (SMR =1.89, 95% CI: 1.82–1.97), declining thereafter, though remaining elevated even beyond 20 years (SMR =1.40, 95% CI: 1.26–1.56). Patients diagnosed at a younger age faced substantially higher relative mortality, with the highest SMR observed in the 15–49 years age group (4.51, 95% CI: 4.04–5.02; RRSMR =3.18, 95% CI: 2.84–3.56). Cardia cancer had a higher SMR (2.09, 95% CI: 1.96–2.22) compared to non-cardia cancer (1.57, 95% CI: 1.52–1.62), with a RRSMR of 1.33 (95% CI: 1.24–1.43). In terms of clinical characteristics, survivors with regional or distant disease had significantly higher SMRs compared to those with localized disease, with RRSMRs of 1.27 (95% CI: 1.20–1.35) and 1.31 (95% CI: 1.11–1.55), respectively. Those with SRCC histology also exhibited a 1.12-fold (95% CI: 1.03–1.21) late mortality relative to adenocarcinoma. Notably, radiotherapy and chemotherapy increased the excess mortality risks by 51% (95% CI: 41–61%) and 46% (95% CI: 37–55%), respectively. There were no significant differences in SMRs by diagnostic era or tumor grade (Table 1).

Figure 2 Relative and absolute excess risks for late mortality among long-term gastric cancer survivors following gastrectomy. AERs, absolute excess risks; CI, confidence interval; COPD, chronic obstructive pulmonary disease; CVDs, cardiovascular diseases; SMNs, second malignant neoplasms; SMR, standardized mortality ratio.

Excess late mortality due to SMNs

Long-term GC survivors faced a significantly elevated risk of death from SMNs compared to the general population, with an overall SMR of 1.30 (95% CI: 1.20–1.42) and an AER of 22.1 per 10,000 person-years (Figure 2). The risk of SMN-related excess late mortality was higher in men (SMR =1.38, 95% CI: 1.25–1.52) than in women (SMR =1.15, 95% CI: 0.97–1.34), with a RRSMR of 1.20 (95% CI: 1.00–1.44). Risk remained consistently elevated across all survival intervals, with no significant trend over time. Survivors diagnosed at a younger age had a markedly higher relative risk, particularly in the 15–49 years age group (SMR =2.41, 95% CI: 1.74–3.25; RRSMR =2.03, 95% CI: 1.47–2.80). Cardia cancer had a higher SMR (1.49, 95% CI: 1.25–1.77) compared to non-cardia cancer (1.15, 95% CI: 1.04–1.27), with a RRSMR of 1.30 (95% CI: 1.07–1.57). Regarding clinical factors, patients with higher-grade tumors (grade III/IV) exhibited a lower SMR for SMN-related death (SMR =1.15, 95% CI: 1.02–1.30) than those with lower-grade tumors (grade I/II) (1.51, 95% CI: 1.33–1.71), with a significant RRSMR of 0.76 (95% CI: 0.64–0.90). Although the SMN-related excess late mortality increased significantly regardless of grade or histological types, the differences between these subgroups were not significant. Survivors who received radiotherapy had a significantly increased risk (SMR =1.67, 95% CI: 1.41–1.95; RRSMR =1.40, 95% CI: 1.16–1.69), as did those who received chemotherapy (SMR =1.47, 95% CI: 1.27–1.70; RRSMR =1.20, 95% CI: 1.01–1.44) (Table 2).

Excess late mortality due to non-cancer health-related causes

GC survivors exhibited a significantly elevated risk of death from non-cancer health-related conditions compared to the general population, with an overall SMR of 1.21 (95% CI: 1.16–1.26) and an AER of 74.6 per 10,000 person-years. With the exception of diabetes mellitus (SMR =1.09, 95% CI: 0.87–1.35), the risk of death from all other examined non-cancer diseases was significantly increased. The most pronounced excess mortality was observed for gastrointestinal diseases (SMR =2.30, 95% CI: 1.68–3.07), infectious diseases (SMR =1.76, 95% CI: 1.53–2.00), and hypertension without disease of heart (SMR =1.60, 95% CI: 1.22–2.05) (Figure 2). The increased non-cancer health-related excess late mortality was observed in the majority of investigated subgroups. Cancer diagnosed at younger ages (aged 15–49 years) had a notably higher relative risk (SMR =1.69, 95% CI: 1.34–2.11; RRSMR =1.41, 95% CI: 1.12–1.77). A significant reduction in risk was observed among patients diagnosed in 2005 or later (SMR =1.11, 95% CI: 1.03–1.19) compared to those diagnosed in 1992–2004 (SMR =1.26, 95% CI: 1.20–1.32), with an RRSMR of 0.88 (95% CI: 0.81–0.96). Cardia cancer had a higher SMR (1.33, 95% CI: 1.21–1.45) compared to non-cardia cancer (1.14, 95% CI: 1.10–1.19), with a RRSMR of 1.17 (95% CI: 1.05–1.29). In terms of clinical characteristics, survivors with grade III/IV tumors had a lower SMR (1.15, 95% CI: 1.09–1.21) compared to those with grade I/II tumors (SMR =1.28, 95% CI: 1.21–1.36), with a significant RRSMR of 0.90 (95% CI: 0.83–0.97). Similarly, survivors with adenocarcinoma histology had a higher risk (SMR =1.23, 95% CI: 1.18–1.28) compared to those with SRCC (SMR =1.08, 95% CI: 0.96–1.21, RRSMR =0.88, 95% CI: 0.78–0.99). Patients who received radiotherapy also had a significantly elevated risk (SMR =1.33, 95% CI: 1.21–1.46; RRSMR =1.12, 95% CI: 1.01–1.24). No significant risk difference was observed by chemotherapy exposure (Table 3).

Discussion

This population-based study comprehensively evaluated the long-term mortality patterns among 8,637 GC survivors who underwent gastrectomy and achieved 5-year survival. Our analysis reveals several significant findings with important clinical and public health implications. First, GC survivors experienced a 66% higher all-cause mortality compared to the general population, with this excess risk persisting beyond 20 years post-diagnosis. Second, while cancer recurrence or progression contributed substantially to deaths in earlier survivorship periods, non-cancer health-related conditions became the predominant cause of late mortality, accounting for nearly three-quarters of deaths after 20 years. Third, the risk profile varied considerably across subgroups, with particularly elevated mortality observed in younger patients, those with specific clinical characteristics, and those receiving certain treatment modalities.

Current clinical practice and research in GC, including follow-up protocols, therapeutic trials, and surveillance guidelines, mainly set the 5-year survival as the primary outcomes (11-15). Consequently, there is a notable gap in understanding the long-term mortality patterns and causes of death among patients who survive beyond 5 years after gastrectomy. Recent years have witnessed growing research interest in late mortality among long-term cancer survivors, particularly within pediatric and AYA oncology, where studies have consistently demonstrated elevated risks of late morbidity and mortality that rarely returns to population levels (3-10). To our knowledge, this study represents the first comprehensive, population-based assessment of excess late mortality specifically in long-term GC survivorship cohort. Our findings reveal that these survivors face significantly elevated risks of death from multiple causes, including SMNs, CVDs, and other non-cancer conditions, with risks persisting for decades post-diagnosis. The persistent elevation suggests that factors beyond the initial cancer diagnosis continue to influence mortality in this population, possibly including long-term effects of treatment, physiological changes from gastrectomy, or shared etiological factors for multiple conditions. Previous studies on patients gastrectomized for benign diseases have shown variable long-term mortality outcomes, suggesting that gastrectomy itself may confer some long-term health risks (16,17). However, the excess mortality observed in our GC cohort likely reflects a combination of cancer-specific factors, treatment effects, and post-gastrectomy physiological changes.

During the overall long-term survival period, non-cancer health-related conditions contributed to the majority of late mortality, and with the survival time increasing, deaths due to recurrence or progression declined steadily, whereas non-cancer health-related deaths increased markedly. This pattern has important implications for survivorship care. In contrast to traditional post-gastrectomy surveillance paradigms that primarily target 5-year survival endpoints with an emphasis on detecting cancer recurrence or progression, our findings underscore the necessity of shifting clinical focus toward the comprehensive monitoring of non-cancer health conditions in long-term survivors. The most pronounced elevations in non-cancer mortality were observed for gastrointestinal diseases, infectious diseases, and hypertension without heart disease, suggesting that physiological changes following gastrectomy may create specific vulnerabilities in these organ systems. However, mortality from diabetes mellitus was not significantly elevated. This finding contrasts with studies of other cancer survivors and warrants further investigation (18-21). Potential explanations include differences in baseline diabetes prevalence, altered glucose metabolism following gastrectomy (particularly after total gastrectomy), or competing mortality risks that preclude the development of long-term diabetic complications. Alternatively, the nutritional challenges and weight loss common after gastrectomy may paradoxically reduce diabetes risk in some patients, though this hypothesis requires validation in studies with more detailed metabolic data (22-24).

This study also found some demographic and clinicopathological features may be associated with excess late mortality. Younger patients experienced dramatically elevated all-cause mortality, primarily driven by higher relative risks of both SMNs and non-cancer health-related causes. This finding aligns with research in other cancer types showing that younger age at diagnosis is associated with greater long-term health burden, possibly due to more aggressive disease, intensive chemotherapy and or radiation therapy, longer exposure to treatment effects, different tumor biology, or the interaction of cancer treatments with normal developmental processes (25,26). The clinical implication is clear: younger GC survivors require particularly vigilant long-term follow-up that extends well beyond cancer surveillance to include comprehensive health monitoring. Interestingly, we found survivors with GC that has worse pathological characteristics, such as grade III/IV, more advanced stage and SRCC, showed lower excess mortality due to SMNs and non-cancer health-related conditions. This finding may reflect competing risks, as patients with more aggressive cancers may die from recurrence before developing non-cancer conditions. In recent years, gastroesophageal junction (GEJ) adenocarcinoma has been recognized as a distinct entity from distal GC, differing in tumor biology and treatment paradigms. Although the SEER database does not directly identify GEJ tumors, we used cardia location as a proxy for GEJ cancer. Our analysis revealed that cardia cancer survivors experienced significantly higher excess mortality compared to non-cardia survivors, suggesting that patients with cardia tumors may receive more intensive treatment yet still have a poorer prognosis than those with distal GC (27). In addition, a significant reduction in excess non-cancer health-related mortality was observed among patients diagnosed since 2005, from then the surgical techniques, chemotherapy regimen (more anthracycline-based regimen in early years), perioperative care, and management of treatment complications for GC patients have been markedly advanced (2,28). The adoption of minimally invasive approaches, enhanced recovery protocols, and better nutritional support may have reduced long-term sequelae of gastrectomy. However, the lack of improvement in all-cause or SMN-related excess mortality over the same period suggests that while we may be getting better at preventing some non-cancer deaths, challenges remain in preventing cancer-related deaths in long-term survivors.

Our findings regarding treatment effects are particularly noteworthy. Patients who received radiotherapy experienced 51% higher excess mortality, while those receiving chemotherapy had 46% higher excess mortality compared to those not receiving these treatments. These associations likely reflect both treatment selection bias (patients with more advanced disease receiving more aggressive treatment) and potential long-term treatment toxicity (10,26). For radiotherapy, the increased mortality from SMNs supports the hypothesis of radiation-induced carcinogenesis, while the elevated non-cancer mortality suggests possible effects on cardiovascular, pulmonary, or gastrointestinal systems (29-31). The persistence of these elevated risks decades after treatment emphasizes the need for careful consideration of long-term consequences when making initial treatment decisions, particularly for patients with favorable prognoses and distal GC, in which the addition of radiotherapy is not routinely recommended based on recent trials (32,33).

Our findings have several actionable implications. First, as non-cancer conditions become the predominant cause of death after 20 years, surveillance should extend beyond recurrence monitoring to include gastrointestinal and infectious diseases. We recommend annual nutritional assessments, low-threshold infection evaluation, and vaccination campaigns for gastrectomy survivors. Second, younger patients and those receiving radiotherapy or chemotherapy warrant risk-adapted, intensified long-term follow-up. Third, the reduced non-cancer excess mortality in patients diagnosed since 2005 suggests that modern surgical techniques and perioperative care are improving outcomes. Finally, we advocate for dedicated, multidisciplinary survivorship clinics integrating oncologists, gastroenterologists, and primary care providers to address the unique post-gastrectomy health risks identified in this study.

Limitations

Several limitations of this study should be acknowledged. First, the SEER database does not provide detailed information on specific treatment regimens, such as chemotherapy protocols, radiation fields and doses, or perioperative care, which precludes identification of potentially modifiable treatment-related risk factors. Second, in our analysis, only deaths attributed to gastric and esophageal malignancies were conservatively classified as recurrence or progression whereas other cancers as SMNs, which may lead to an overestimation of mortality from SMNs. Third, the RRSMRs were calculated using the delta method in a univariate framework, which does not adjust for potential confounding or interactions between variables. Consequently, the observed associations should be interpreted as exploratory rather than causal. Future studies employing multivariable Poisson regression or other modeling approaches that account for covariate interplay would help to clarify the independent effects of each risk factor on excess late mortality. Fourth, the SEER database uses a summary staging system rather than detailed pathological TNM categories, making detailed staging data for risk stratification unavailable, as reduced life expectancy was observed even in patients with pT1 diseases (34,35). Finally, as our cohort was derived from the U.S. SEER database, which predominantly comprises non-Hispanic White individuals and reflects U.S. healthcare delivery patterns, the generalisability of our findings to other racial/ethnic groups or countries with different healthcare systems, surgical practices, and adjuvant therapy regimens remains uncertain. Further validation studies using diverse, international cohorts are warranted to confirm the external validity of these results.

Conclusions

Long-term GC survivors who have undergone gastrectomy face substantially elevated and persistent mortality risks compared to the general population, with particular vulnerabilities in SMNs and non-cancer health-related diseases. Younger patients and those receiving radiotherapy or chemotherapy represent especially vulnerable subgroups. These findings underscore the need for comprehensive, risk-adapted survivorship care that extends beyond recurrence surveillance to address the broad spectrum of health risks in this population. As GC treatment continues to improve and the population of long-term survivors grows, developing evidence-based strategies to optimize their long-term health outcomes represents an important priority for clinicians, researchers, and healthcare systems.

Acknowledgments

We gratefully acknowledge the participants and investigators of the SEER program for their willingness to contribute their data. We also gratefully thank researchers for their work in online database building and data sharing.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-1-0141/rc

Peer Review File: Available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-1-0141/prf

Funding: None.

Conflicts of Interest: Both authors have completed the ICMJE uniform disclosure form (available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-1-0141/coif). The authors have no 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. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments.

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/.

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