Next Article in Journal
PROX1 Expression in Resected Non-Small Cell Lung Cancer: Immunohistochemical Profile and Clinicopathological Correlates
Previous Article in Journal
An Interventional Study Exploring the Effects of Nutritional Psychoeducation on Emotional Eating After 3 Months
 
 
Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
Journals
Medical Sciences
Volume 13
Issue 3
10.3390/medsci13030139
medsci-logo
Submit to this Journal Review for this Journal Propose a Special Issue
► Article Menu

Article Menu

share Share announcement Help format_quote Cite question_answer Discuss in SciProfiles
first_page
settings
Order Article Reprints
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Article

Survival Patterns and Mortality Causes in Patients with Invasive Ependymoma: A Retrospective Cohort Analysis from 2000 to 2019

by
Anas Elgenidy
1,†,
Khaled Saad
2,*,†,
Amir Aboelgheet
2,
Eman F. Gad
2,
Usama El-Shokhaiby
3,
Thamer A. M. Alruwaili
4,
Abdelrahman N. Abdelal
5,
Kawashty R. Mohamed
5,
Mohammad Bazzazeh
6,
Mohamed Hesn
7,
Abdelrahman H. Elshimy
6,
Aya Sayed
8,
Sara Magdy
9,
Doaa Ali Gamal
10,
Amira A. Elhoufey
11,12,
Shymaa Adel Ismael
13,
Ahmed M. Afifi
14,
Mohamed Fahmy M. Ibrahim
15 and
Amany Ragab
1
1
Department of Neurology, Faculty of Medicine, Cairo University, Cairo 12613, Egypt
2
Pediatric Department, Faculty of Medicine, Assiut University, Assiut 71516, Egypt
3
Department of Neurosurgery, Al Azhar University, Cairo 11884, Egypt
4
Department of Pediatrics, College of Medicine, Jouf University, Sakaka 75741, Saudi Arabia
5
Department of Neurology, Al-Azhar University, Assiut 71111, Egypt
6
Faculty of Medicine, Alexandria University, Alexandria 21526, Egypt
7
Faculty of Medicine, Al Azhar University, Damietta 25242, Egypt
8
Medical Research Institute, Alexandria University, Alexandria 21526, Egypt
9
Faculty of Medicine, Ain Shams University, Cairo 11591, Egypt
10
Department of Clinical Oncology, Faculty of Medicine, Assiut University, Assiut 71516, Egypt
11
Department of Community Health Nursing, Alddrab University College, Jazan University, Jazan 45142, Saudi Arabia
12
Department of Community Health Nursing, Faculty of Nursing, Assiut University, Assiut 71516, Egypt
13
Department of Neurosurgery, Al-Azhar University for Girls, Cairo 11754, Egypt
14
Department of Surgery, University of Toledo Medical Center, Toledo, OH 44192, USA
15
Department of Pediatrics, Al-Azhar University, Assiut 71111, Egypt
 
add Show full affiliation list
 
remove Hide full affiliation list
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Med. Sci. 2025, 13(3), 139; https://doi.org/10.3390/medsci13030139
Submission received: 19 June 2025 / Revised: 24 July 2025 / Accepted: 12 August 2025 / Published: 16 August 2025
(This article belongs to the Section Cancer and Cancer-Related Research)
Versions Notes

Abstract

Background: Ependymomas are primary CNS neoplasms that arise from the ependymal cells of the brain and spinal cord, accounting for 3–6% of all CNS tumors. Aims: This study provides a comprehensive analysis of ependymoma survival patterns and examines non-cancer causes of death in the US. Methods: This retrospective study used data from SEER 17 registries between 2000 and 2019 to evaluate the incidence of ependymoma, as well as the survival and mortality trends in the US. Results: A total of 3821 patients were included, with 842 (22%) deaths. The highest mortality was observed in younger patients (<18 years) within one year of diagnosis (SMR, 54.77; 95% CI, 38.95–74.88). Brain and other nervous system cancers were the leading causes of death, followed by non-cancer causes, particularly cerebrovascular diseases, pneumonia, influenza, and septicemia. The survival rates observed at one, three, and five years were 94% (95% CI: 0.94–0.95), 88% (95% CI: 0.87–0.89), and 84% (95% CI: 0.82–0.85), respectively. Conditional survival improved over time, with a three-year conditional relative survival rate of 92% after one year of diagnosis and 96% for those who survived five years. Conclusion: The death rate was highest among pediatric patients under 18 years of age. Cerebrovascular disorders were the leading non-cancer cause of death across all time intervals. The probability of surviving for three years increases for patients who have already survived one, three, or five years post-diagnosis.

1. Introduction

Ependymomas are neuroepithelial tumors that arise from ependymal cells that form the walls of the ventricles and the central canal of the spinal cord. While the radial glial cells in the embryonic phase are considered the primary origin of the ependymomas, their etiology has not been completely elucidated [1]. Ependymomas are a diverse group of cancers with unknown oncogenic determinants. In contrast to other central nervous system (CNS) tumors, point mutations are quite rare but significantly negatively impact the patient’s condition. However, dealing with fusion genes and copy number aberrations is critical in the generation of cancers [2]. Ependymomas constitute 3–6% of all CNS tumors, with over 50% coming from the spinal cord [3,4]. Primary spinal cord tumors are relatively infrequent, contributing to 4–10% of all CNS tumors, but ependymomas are the most common primary intramedullary spinal tumors that are seen in 30–45% of cases [3,5]. More than half of ependymomas occur in children under the age of five years [6]
Traditionally, ependymomas have been classified histologically into three grades by the World Health Organization (WHO): grade I (subependymoma and myxopapillary ependymoma), grade II (ependymoma, not otherwise specified [NOS]), and grade III (anaplastic ependymoma). However, this histological grading system has shown limited prognostic consistency. More recently, molecular classification based on DNA methylation profiling has identified nine distinct ependymoma groups across anatomical compartments (supratentorial, posterior fossa, spinal), with superior clinical and prognostic relevance. Notably, supratentorial ependymomas are now divided into ZFTA-rearranged (formerly RELA-fused) and YAP1-rearranged subtypes, while posterior fossa ependymomas are classified as PFA (posterior fossa group A) and PFB (posterior fossa group B), with PFA associated with significantly worse outcomes. Spinal ependymomas often harbor MYCN amplification or NF2 mutations. This evolving molecular framework is expected to be integrated into future WHO classifications and is increasingly guiding risk stratification and therapeutic decisions [7,8]. Thus, an integrated model was constructed based on the methylation data and clinicopathological characteristics to estimate progression-free survival. The groups with the worst 10-year overall survival were the patients diagnosed with ependymoma (PFA), ependymoma (ZFTA), and ependymoma (MYCN) tumors, with respective rates of 56%, 62%, and 32% [8]. On average, patients with ependymomas have a 5-year survival rate of 60–70% [7].
The incidence rate decreases with the patient’s age at diagnosis. The data indicate a slight male majority in ependymomas, with a ratio of 1.35:1. As the Central Brain Tumor Registry of the United States recommends, the rate of ependymomas per the human population annually is about 0.29 and 0.6 per 100,000 people [9]. Furthermore, few studies have examined the updated population-level survival of all patients diagnosed with at least one of the various subcategories of ependymoma [10]. More research that investigated ependymoma survival—depending on characteristics such as histology, tumor location, or specific age—has found contrastive survival patterns [11,12]. Also, the assessment of prognostic variables for ependymoma has remained uncertain. Earlier studies were commonly based on a cohort statistical experiment of a small number of people, and the predicted outcomes are rather diverse. Predicting patient mortality and survival times is difficult for experienced physicians, who may meet many challenges. Additionally, medical technologies differ from one institution to another, making it hard to develop a prognosis prediction of ependymoma [13]. Therefore, this study aims to provide an up-to-date and comprehensive investigation of ependymoma incidence rates, survival patterns, and mortality causes in the US.

2. Materials and Methods

2.1. Study Design and Data Source

This retrospective study utilized SEER*Stat software (version 8.4.3) to extract data from the SEER 17 registries [14,15], which cover approximately 26.5% of the US population from 1 January 2000 to 31 December 2019.

2.2. Study Population

The authors selected patients of known age with invasive ependymoma from 1 January 2000 to 31 December 2019; for site and morphology, we used the AYA site recode 2020 revision = 3.1.3.2 ependymoma-invasive. To eliminate any potential confounding effects from secondary malignancies and keep the emphasis on the original cancer diagnosis, this study was limited to cases that were classified as “first primary only (Sequence Number 0 or 1).” This option includes the first tumor of the patient if that tumor meets the inclusion criteria and has a sequence of 0 or 1. A sequence number equal to 0 means that it is the only tumor in the patient’s history. A sequence number equal to 1 is the first tumor of two or more tumors [16]. We also included only patients with invasive malignant behavior and excluded patients with unknown survival time or other criteria.

2.3. Outcomes

The authors evaluated non-cancer causes of death in individuals with invasive ependymoma, considering the following variables: sex, age at diagnosis, and race. The authors categorized causes of death by latency period: within one year, one to five years, and more than five years following the diagnosis of invasive ependymoma. Using the International Classification of Diseases 10th Revision (ICD-10)-World Health Organization (WHO) codes, the authors identified the causes of death [Supplementary Table S1]. Pregnancy, puerperium, childhood difficulties, homicide, stomach and duodenal ulcers, and perinatal disorders are included in the definition of other causes of death.

2.4. Statistical Analysis

We used SEER*Stat software, version 8.4.3, to calculate our survival and mortality outcomes. To estimate expected survival, we used the Ederer II method, in which the matched individuals are considered at risk until the corresponding patient dies or is censored [17]. Regarding survival outcomes, we calculated the following:

2.5. Relative Survival

It is the ratio of the actual survival rate of a group of patients over a certain period and the expected survival rate within the general population. Relative survival helps to isolate the effect of cancer alone on survival [17].

2.6. Observed Survival

It is the probability of surviving from all causes of death for a group of cancer patients. Observed survival gives a direct indication of survival rates but includes deaths from all causes, not just the cancer under study [17].

2.7. Conditional Survival

It is the probability of a patient surviving for a specific time, given that the patient has already survived for a particular time [18]. Conditional survival provides insight into how prognosis improves for patients who have already survived a certain period after diagnosis. We calculated conditional survival of four years for those who survived for one year, six years for those who survived for three years, and eight years for those who survived for five years.
Regarding mortality outcomes, we calculated standardized mortality ratios (SMRs), which are used to compare the mortality rate of a study population to the mortality rate of a standard or general population by dividing the number of invasive ependymoma deaths observed by the number of deaths predicted by the age- and sex-matched population in the same period to ensure comparability between groups. SMRs are used to compare the study population’s mortality rate to the general population’s mortality rate [19]. Moreover, our survival and mortality outcomes were stratified by age (<18, 18–44, 45–59, 60–74, >75), sex, and race (black, white, American Indian/Alaska Native, and Isan or pacific islander).

3. Results

3.1. Baseline Characteristics

This study included a total of 3821 patients. The study sample comprised 1960 males (51%) and 1861 females (49%). The largest proportion of patients (1269, 33%) was between 18 and 44 years of age. White patients made up the majority of the patient population (3153, 83%), and the most common ependymoma site was the spinal cord (C72.0) (1649 patients, 43%). Histologically, most of the tumors were diagnosed as ependymoma, not otherwise specified (NOS) (2980 patients, 78%), and anaplastic ependymoma accounted for a lower proportion (738 patients, 19%) [Table 1].

3.2. Mortality Rate and Causes of Death

This study included a total of 3821 patients, with 842 (22%) deaths [Table 2]. The highest mortality rate (244 deaths, 29%) was seen in pediatric patients younger than 18. Most of the deaths (688 deaths, 83%) were white people. Patients with cancers in the spinal cord had the greatest mortality rate (229 deaths, 43%). Patients with ependymoma NOS accounted for the majority of histological deaths (572 deaths, 78%). Among the total deaths, 424 (52%) resulted from brain and other nervous system cancers, 75 (9%) from non-CNS cancers, and 321 (39%) from non-cancer causes. The most common non-cancer causes included cerebrovascular diseases, pneumonia, and septicemia, with respective SMRs of 2.84 (95% CI, 1.86–4.17), 3.05 (95% CI, 1.52–5.45), and 3.35 (95% CI, 1.61–6.61).

3.3. Causes of Death Within One Year of the Diagnosis

A total of 198 deaths, representing 24.1% of all deaths, occurred within one year following the diagnosis of invasive ependymoma. Among these, 102 patients (52%) died of brain and other nervous system cancers, 13 patients (7%) died from non-CNS cancers, and 83 patients (42%) died due to non-cancer causes. Cerebrovascular diseases (seven deaths; SMR, 8.76; 95% CI, 3.52–18.05) were the most prevalent non-cancer causes, followed by infectious and parasitic diseases (five deaths; SMR, 17.57; 95% CI, 5.71–41.01). Patients under 18 who were diagnosed with invasive ependymoma had a greater risk of mortality within one year compared to those without the disease at the same age (SMR, 54.77; 95% CI, 38.95–74.88). Non-cancer causes were responsible for 30% of deaths among patients under the age of 18 and for 48% of deaths among patients aged 18 to 44 within one year following their diagnosis [Supplementary Table S2].

3.4. Causes of Death from One to Five Years After the Diagnosis

Between one and five years after being diagnosed with invasive ependymoma, 342 patients died. Among them, 211 patients (62%) died of brain and other nervous system malignancies, 30 (9%) died of non-CNS cancers, and 101 (30%) died of non-cancer causes. Cerebrovascular diseases (nine deaths, SMR, 3.18; 95% CI, 1.46–6.04) were the most common non-cancer causes. Brain and other nervous system cancers accounted for 82% of mortality in patients under 18 between one and five years following diagnosis.

3.5. Causes of Death After Five Years Following the Diagnosis

A total of 280 patients died over five years after being diagnosed with invasive ependymoma. Among them, 111 patients (40%) died of brain and other nervous system cancers, 32 (11%) died of non-CNS cancers, and 137 (49%) died of non-cancer causes. In patients aged 60–74 years, cerebrovascular disorders (eight deaths, SMR, 3.27; 95% CI, 1.41–6.45) were the most frequent non-cancer causes after five years following invasive ependymoma diagnosis.

3.6. Overall Survival Rate

In total, the observed survival rates at one, three, and five years were 94% (95% CI: 0.94–0.95), 88% (95%CI: 0.87–0.89), and 84% (95%CI: 0.82–0.85). For patients who survived the first year, three-year conditional survival was 91% (95% CI: 0.90–0.92), with a relative survival of 92% (95% CI: 0.91–0.93). For those who survived three years, three-year conditional survival was 94% (95% CI: 0.93–0.95), with a relative survival rate of 95% (95% CI: 0.94–0.96). For those who survived 5 years, 3-year conditional and relative survival rates were 94% (95%CI: 0.93–0.95) and 96% (95%CI: 0.95–0.97), respectively [Table 3].

3.7. Survival Rate According to Age, Sex and Race

At one, three, and five years, the observed survival rates were higher for females: 95% (95%CI: 0.94–0.96), 90% (95%CI: 0.88–0.91), and 86% (95%CI: 0.84–0.87), respectively. American Indian/Alaska Native patients had the lowest survival rates, with 91% (95%CI: 0.68–0.98), 86% (95%CI: 0.62–0.95), and 74% (95%CI: 0.48–0.89) observed survival at one, three, and five years. Patients aged 18–44 showed the highest observed survival rates of 97% (95%CI: 0.96–0.98), 94% (95%CI: 0.92–0.95), and 91% (95%CI: 0.89–0.93) [Table 4].

4. Discussion

Ependymoma is a neoplasm that arises from progenitor cells lining the ventricular system and the central canal of the spinal cord [9]. It is typically a benign tumor that arises from the ependymal cells of the central nervous system [20]. It represents 3–6% of all CNS tumors, and about 50% of them occur in the spine, although primary spinal cord tumors are relatively infrequent and represent only 4–10% of all CNS tumors [3,5,21,22,23].
The present study included 3821 patients, 51% (1960) of whom were males. The largest age group was those between 18 and 44 years old and represented 33% (1269) of the included population. Most of the patients were white (3153, 83%). Ryu et al., 2019, included a comparable sample, with males representing 53.5% and white people at 88.2% [3]. McGuire et al., 2009, reported that the incidence was higher among males and older adults above 40 years old [24]. Previous studies have reported increased male incidence compared to females [24,25,26,27]. A previous study conducted on patients from the US diagnosed with anaplastic ependymoma and ependymoma NOS in the period between 2000 and 2006 found that the incidence rate of both anaplastic ependymoma and ependymoma NOS was significantly higher in white people compared to all other races, except for anaplastic ependymoma, in which the incidence was not significantly higher in white people compared to Asia/Pacific Islanders, and in that study, the white population comprised 86.8% of the patients, which is comparable to this study [10]. The same study reported that the incidence of anaplastic ependymoma was not significantly different among males and females, while ependymoma NOS incidence was significantly higher in male patients [10]. According to this study, the most common ependymoma site was the spinal cord (C72.0) (1649 patients, 43%). This aligns with previous studies that reported ependymoma as the commonest primary intramedullary spinal cord tumor and that the spine represents 30–45% of the ependymoma site or about 50%, according to other studies [2,3,4,9,10]. Ryu et al., 2019, reported that 94.1% of all spine ependymomas were explicitly located in the spinal cord [3]. In pediatrics, about 90% of ependymomas are intracranial; in adults, about 60% are spinal, according to McGuire et al., 2009 [24].
The incidence of anaplastic ependymoma was the highest in the supratentorial location, followed by the infratentorial location, and lowest in the spinal cord, while ependymoma NOS was highest in the spinal cord, followed by the infratentorial and then the supratentorial locations [10].
The most common histological type was ependymoma NOS (2980 patients, 78%), followed by anaplastic ependymoma (738 patients, 19%). The annual percent change in the overall incidence of ependymoma increased by 2.1% from 2000 to 2010 [25]. In Ryu et al., 2019, which studied the spinal ependymomas, only 2.1% were anaplastic, while 65.1% of the cases were non-myxo papillary low grade and 32.8% were myxo papillary [3].
According to a previous study, the incidence of anaplastic ependymoma and ependymoma NOS was similar in the pediatric population aged 0–4 years, but, on the other hand, the ependymoma NOS had a significantly higher incidence in other pediatric age groups, 5–9 and 10–14 years [10]. The anaplastic-type incidence plateaued in adults and then declined in geriatrics above 85 years old. At the same time, ependymoma NOS peaked in the 45–69 age group and declined in those in the 80s [10]. This is consistent with previous reports on ependymoma incidence trends in the USA [9,25,26].
Of this study’s 3821 participants, 842 (22%) died. Ryu et al., 2019, reported a 10-year survival of 85% [3]. The 10-year survival of the spinal ependymomas was reported to be excellent, exceeding 90% [28,29,30]. A retrospective study conducted on patients treated for ependymoma between 1990 and 2009 found that the death rate was 15% during the follow-up period [31].
According to this study, the highest mortality rate was among patients younger than 18 (244 deaths, 29%), white (688 deaths, 83%), and those with cancer in the spinal cord (229 deaths, 43%). This could be aligned with the fact that 83% of this study population was white, and 43% of the disease was in the spinal cord.
The observed survival rates were higher among females; the patients aged 18–44 showed the highest observed survival rates, and American Indian/Alaska Native patients had the lowest survival rates.
A previous study reported that anaplastic ependymoma and ependymoma NOS had a 78% and 91% increased risk of death, respectively, in African Americans compared to the white population, which aligns with our findings in Supplementary Table S3 [10]. Another study reported that in gliomas, non-Hispanic white people had a lower survival rate than African Americans, contrary to our results [32]. A study reported that children had a worse prognosis when compared to adults [33]. In anaplastic ependymoma, adults older than 40 years had a 5-times greater risk of death compared to children aged 0–14 years, while in ependymoma NOS, young adults aged 15–39 years had a lower risk of death compared to children [10]. Supratentorial ependymoma and infratentorial ependymoma had 2.5- and 2.76-times greater risk of mortality than spinal cord ependymoma [10]. These results align with our findings, explaining the higher mortality rate in patients under 18, as approximately 90% of pediatric ependymomas are intracranial. In contrast, about 60% of adults are spinal, according to McGuire et al., 2009 [27]. The aggressive nature of the tumor in children may be due to the immaturity of neural tissue and unfavorable histopathological findings [20,34]. Many studies concluded that the patient’s gender is not a significant prognostic factor [35,36,37,38], while others have reported worse survival for female patients [39,40]. On the contrary, the results of the present study, in accordance with two previous studies, reported better survival for female patients [33,41].
Patients under 18 diagnosed with invasive ependymoma had a greater risk of mortality within one year compared to those without the disease at the same age (SMR, 54.77; 95% CI, 38.95–74.88). Within one year of diagnosis, the non-cancer causes were responsible for 30% of deaths of patients under 18 and 48% of patients aged 18–44. Brain and other nervous system cancers accounted for 82% of mortality in patients under 18 within one to five years following diagnosis, while in patients aged 60–74 years, cerebrovascular disorders (eight deaths, SMR, 3.27; 95% CI, 1.41–6.45) were the most frequent non-cancer causes after five years following invasive ependymoma diagnosis.
The most common pediatric solid malignancy is brain tumors, which are the leading cause of mortality related to cancers [42,43], with the ependymoma being the third most common pediatric brain tumor after astrocytoma and medulloblastoma, with over 50% arising before the age of 5 [44,45]. The very limited outcomes in younger patients may be due to the higher incidence of high-grade ependymoma and the higher rate of lateral and posterior fossa tumors, which infiltrate the nearby vital structures, complicating the gross total resection of the tumor and the mandatory delay of the radiotherapy below 3 years of age [31]. In adolescents and young adults, the mortality rate associated with cancer has declined by 0.8%, but survival rates with CNS tumors have not improved [46].
We found that ependymoma NOS accounted for 78% of all histological deaths. Previous studies found that the tumor site, histology, age, and sex are significant predictors of the patient’s survival [6,47,48,49]. A previous study reported that those with anaplastic ependymoma had a 2-times higher risk of death compared to ependymoma NOS [10].
The most frequent cause of death in this study was brain and other nervous system cancers, accounting for 52% of all deaths. The non-cancer causes accounted for 39% of all deaths, and 9% of deaths were due to non-CNS cancers.
We found that the predominant non-cancer causes were cerebrovascular diseases (26 deaths, SMR, 2.84; 95% CI, 1.86–4.17), pneumonia and influenza (11 deaths, SMR, 3.05; 95% CI, 1.52–5.45), septicemia (10 deaths, SMR, 3.35; 95% CI, 1.61–6.61), and other infectious and parasitic diseases (8 deaths, SMR, 2.99; 95% CI, 1.29–5.9). A study reported that in the last 4 weeks of life, 85% of patients with brain tumors presented with dysphagia [50]. Dysphagia associated with brain tumors can cause dehydration, undernutrition, and precipitate aspiration pneumonia [51].
In total, the observed survival rates in this study at one, three, and five years were 94%, 88%, and 84%, respectively. The 10-year survival of the spinal ependymomas was reported to be excellent, exceeding 90% [28,29,30].
In this study, 24.1% of deaths occurred within one year of diagnosis with invasive ependymoma, while 41.7% of deaths occurred from one to five years and 34.1% after five years. Brain and other nervous system cancers accounted for 52% of deaths within one year, 62% from one to five years, and 40% after five years. At the same time, non-cancer causes accounted for 42% of deaths within one year, 30% from one to five years, and 49% after five years. Further, 7% of deaths within one year, 9% from one to five years, and 11% after five years were the result of non-CNS cancers. Cerebrovascular diseases were the most common non-cancer causes of death within one year, from one to five years, and after five years of diagnosis with invasive ependymoma.
This study highlights the scarcity of evidence on the causes of death in ependymoma patients, making it a valuable starting point for addressing this topic. This will help move towards a more personalized healthcare approach in dealing with ependymoma patients, improving survival and decreasing mortality and morbidity. It also reveals the necessity for high-quality, dedicated research to address the causes of death in ependymoma patients.
This study has several limitations that should be considered when interpreting the findings. First, our analysis relies on the SEER database, which, while population-based and nationally representative, lacks detailed clinical information, such as the extent of surgical resection, radiation therapy parameters, chemotherapy regimens, molecular or genetic profiling, performance status, and comorbidities. The absence of these data limits our ability to adjust for key prognostic variables and may introduce residual confounding, particularly in subgroup comparisons across age, sex, and racial categories. Second, treatment details—especially the completeness of tumor resection and adjuvant therapy—are not consistently captured in SEER. Although the database includes some treatment variables (e.g., radiation), these are often incomplete or not applicable for CNS tumors, and there is no reliable coding for chemotherapy administration in many cases. As a result, we were unable to incorporate treatment modalities into our survival models, which may affect the generalizability and clinical interpretability of our results. Third, the causes of death in SEER data were derived from death certificates, which may lead to underreporting, especially for non-cancer causes, such as septicemia, cerebrovascular disease, and infections. While the use of SMRs helps contextualize excess mortality relative to the general population, inaccuracies in coding could influence the precision of these estimates. Fourth, despite the large sample size, some subgroup analyses—particularly for minority racial groups such as American Indian/Alaska Native and Asian/Pacific Islander populations—were based on small numbers, which may reduce statistical power and increase variability in survival estimates. Finally, the retrospective nature of the study design inherently limits causal inference. Unmeasured socioeconomic, access-to-care, and healthcare utilization factors may contribute to observed disparities in survival and should be explored in future prospective or linked healthcare database studies.
On the other hand, the relatively large sample size, being a population-based study from a high-quality database (SEER), which includes about 28% of the cancer patients in the USA and the independent, prospective collection of data, which decreases the recall bias, increases the credibility of our study.

5. Conclusions

The death rate was highest among pediatric patients under 18 years of age. Cerebrovascular disorders were the leading non-cancer cause of death across all time intervals. The probability of surviving for three years increases for patients who have already survived one, three, or five years post-diagnosis of invasive ependymoma. We present our findings to medical professionals to explore the potential development of future guidelines for the management of invasive ependymoma.

Supplementary Materials

The following supporting information can be downloaded at: https://www.mdpi.com/article/10.3390/medsci13030139/s1, Table S1: Definition of each cause of death and corresponding codes in the ICD-10 of Diseases and Related Health. Table S2. Shows the standardized mortality ratios (SMRs) for each cause of death following diagnosis of Invasive ependymoma according to age. Table S3. Survival of each age-specific group according to sex and race.

Author Contributions

The study was designed, and the data were analyzed by A.E., K.S., A.A., U.E.-S., T.A.M.A., A.N.A., K.R.M., M.B., M.H., A.H.E., A.S., S.M., and A.R. The manuscript was drafted by A.A.E., E.F.G., D.A.G., M.F.M.I., A.E., S.A.I., and A.M.A. All authors contributed to the critical review of the final version of the manuscript.

Funding

This research received no external Funding.

Institutional Review Board Statement

This study was conducted in compliance with the ethical guidelines established by the World Medical Association’s Declaration of Helsinki. Approval for all procedures was granted by the Ethical Committee of Al-Azhar Faculty of Medicine, Egypt (PED025/12/275/9/2022).

Informed Consent Statement

All data used in the study were obtained from the anonymized SEER database. As the study utilized de-identified data, informed consent was not required, and the need for consent was waived.

Data Availability Statement

Data are available through the SEER Program (www.seer.cancer.gov, accessed on 31 January 2025).

Conflicts of Interest

The authors declare no conflicts of interest.

Abbreviations

CNSCentral Nervous system
HIVHuman Immunodeficiency Virus
ICD-OInternational Classification of Diseases for Oncology
NOSNot otherwise specified
SEERSurveillance Epidemiology and End Results
SMRStandardized mortality ratio

References

  1. Taylor, M.D.; Poppleton, H.; Fuller, C.; Su, X.; Liu, Y.; Jensen, P.; Magdaleno, S.; Dalton, J.; Calabrese, C.; Board, J. Radial glia cells are candidate stem cells of ependymoma. Cancer Cell 2005, 8, 323–335. [Google Scholar] [CrossRef]
  2. Pajtler, K.W.; Witt, H.; Sill, M.; Jones, D.T.; Hovestadt, V.; Kratochwil, F.; Wani, K.; Tatevossian, R.; Punchihewa, C.; Johann, P.; et al. Molecular classification of ependymal tumors across all CNS compartments, histopathological grades, and age groups. Cancer Cell 2015, 27, 728–743. [Google Scholar] [CrossRef]
  3. Ryu, S.M.; Lee, S.H.; Kim, E.S.; Eoh, W. Predicting survival of patients with spinal ependymoma using machine learning algorithms with the SEER database. World Neurosurg 2018, 124, e331–e339. [Google Scholar] [CrossRef]
  4. Ostrom, Q.T.; Patil, N.; Cioffi, G.; Waite, K.; Kruchko, C.; Barnholtz-Sloan, J.S. CBTRUS statistical report: Primary brain and other central nervous system tumors diagnosed in the United States in 2013–2017. Neuro Oncol. 2020, 22, iv1–iv96. [Google Scholar] [CrossRef] [PubMed]
  5. Bertero, L.; Ricci, A.A.; Tampieri, C.; Cassoni, P.; Modena, P. Ependymomas. Pathologica 2022, 114, 436–446. [Google Scholar] [CrossRef] [PubMed]
  6. Amirian, E.S.; Armstrong, T.S.; Aldape, K.D.; Gilbert, M.R.; Scheurer, M.E. Predictors of survival among pediatric and adult ependymoma cases: A study using Surveillance, Epidemiology, and End Results data from 1973 to 2007. Neuroepidemiology 2012, 39, 116–124. [Google Scholar] [CrossRef]
  7. Lampros, M.; Vlachos, N.; Alexiou, G.A. Ependymomas in children and adults. Adv. Exp. Med. Biol. 2023, 1405, 99–116. [Google Scholar] [PubMed]
  8. Pohl, L.C.; Leitheiser, M.; Obrecht, D.; Schweizer, L.; Wefers, A.K.; Eckhardt, A.; Raffeld, M.; Sturm, D.; Pajtler, K.W.; Rutkowski, S.; et al. Molecular characteristics and improved survival prediction in a cohort of 2023 ependymomas. Acta Neuropathol. 2024, 147, 24. [Google Scholar] [CrossRef]
  9. Ostrom, Q.T.; Cioffi, G.; Waite, K.; Kruchko, C.; Barnholtz-Sloan, J.S. CBTRUS statistical report: Primary brain and other central nervous system tumors diagnosed in the United States in 2014–2018. Neuro Oncol. 2021, 23 (Suppl. S2), iii1–iii105. [Google Scholar] [CrossRef]
  10. Achey, R.L.; Vo, S.; Cioffi, G.; Gittleman, H.; Schroer, J.; Khanna, V.; Buerki, R.; Kruchko, C.; Barnholtz-Sloan, J.S. Ependymoma NOS and anaplastic ependymoma incidence and survival in the United States varies widely by patient and clinical characteristics, 2000–2016. Neuro-Oncol Pract 2020, 7, 549–558. [Google Scholar] [CrossRef]
  11. Khalid, S.I.; Adogwa, O.; Kelly, R.; Metha, A.; Bagley, C.; Cheng, J.; O’Toole, J. Adult spinal ependymomas: An epidemiologic study. World Neurosurg. 2018, 111, e53–e61. [Google Scholar] [CrossRef]
  12. Khalid, S.I.; Kelly, R.; Adogwa, O.; Carlton, A.; Woodward, J.; Ahmed, S.; Khanna, R.; Bagley, C.; Cheng, J.; Shah, S.; et al. Pediatric spinal ependymomas: An epidemiologic study. World Neurosurg. 2018, 115, e119–e128. [Google Scholar] [CrossRef]
  13. Jia, Z.; Yan, Y.; Wang, J.; Yang, H.; Zhan, H.; Chetn, Q.; He, Y.; Hualng, C.; Hu, Y. Development and validation of prognostic nomogram in ependymoma: A retrospective analysis of the SEER database. Cancer Med. 2021, 10, 6140–6148. [Google Scholar] [CrossRef] [PubMed]
  14. Surveillance Research Program, National Cancer Institute. SEER*Stat Software Version 8.4.3. Available online: https://seer.cancer.gov/seerstat/ (accessed on 31 January 2025).
  15. Surveillance, Epidemiology, and End Results (SEER) Program. SEER*Stat Database: Incidence—SEER Research Plus Data, 17 Registries, Nov 2021 Sub (2000–2019)—Linked to County Attributes—Total US, 1969–2020 Counties, National Cancer Institute, DCCPS, Surveillance Research Program, Released April 2022. Available online: https://seer.cancer.gov/data/ (accessed on 31 January 2025).
  16. National Cancer Institute. Multiple Primary Selections for Prevalence. SEER*Stat Help System. Available online: https://seer.cancer.gov/help/seerstat/limited-duration-prevalence-session/ld-prevalence-selection-tab/multiple-primary-selections-for-prevalence (accessed on 31 January 2025).
  17. Cho, H.; Howlader, N.; Mariotto, A.B.; Cronin, K.A. Estimating Relative Survival for Cancer Patients from the SEER Program Using Expected Rates Based on Ederer I Versus Ederer II Method, Published 2011. Available online: http://surveillance.cancer.gov/reports/ (accessed on 31 January 2025).
  18. Wang, S.J.; Emery, R.; Fuller, C.D.; Kim, J.S.; Sittig, D.F.; Thomas, C.R. Conditional survival in gastric cancer: A SEER database analysis. Gastric Cancer 2007, 10, 153–158. [Google Scholar] [CrossRef] [PubMed]
  19. Sonbol, Y.T.; Elgenidy, A.; Awad, A.K.; Elmehrath, A.O.; Kobeissi, H.; Afifi, A.M.; Ghozy, S. Stroke as a cause of death in patients with cancer: A SEER-based study. J. Stroke Cerebrovasc. Dis. 2023, 32, 107154. [Google Scholar] [CrossRef] [PubMed]
  20. Reni, M.; Gatta, G.; Mazza, E.; Vecht, C. Ependymoma. Crit. Rev. Oncol. Hematol. 2007, 63, 81–89. [Google Scholar] [CrossRef]
  21. Chamberlain, M.C. Ependymomas. Curr. Neurol. Neurosci. Rep. 2003, 3, 193–199. [Google Scholar] [CrossRef]
  22. Gilbert, M.R.; Ruda, R.; Soffietti, R. Ependymomas in adults. Curr. Neurol. Neurosci. Rep. 2010, 10, 240–247. [Google Scholar] [CrossRef]
  23. Rudà, R.; Gilbert, M.; Soffietti, R. Ependymomas of the adult: Molecular biology and treatment. Curr. Opin. Neurol. 2008, 21, 754–761. [Google Scholar] [CrossRef]
  24. McGuire, C.S.; Sainani, K.L.; Fisher, P.G. Incidence patterns for ependymoma: A Surveillance, Epidemiology, and End Results study. J. Neurosurg. 2009, 110, 725–729. [Google Scholar] [CrossRef]
  25. Gittleman, H.R.; Ostrom, Q.T.; Rouse, C.D.; Dowling, J.A.; De Blank, P.M.; Kruchko, C.A.; Elder, J.B.; Rosenfeld, S.S.; Selman, W.R.; Sloan, A.E.; et al. Trends in central nervous system tumor incidence relative to other common cancers in adults, adolescents, and children in the United States, 2000 to 2010. Cancer 2015, 121, 102–112. [Google Scholar] [CrossRef]
  26. Villano, J.L.; Parker, C.K.; Dolecek, T.A. Descriptive epidemiology of ependymal tumors in the United States. Br. J. Cancer 2013, 108, 2367–2371. [Google Scholar] [CrossRef]
  27. McGuire, C.S.; Sainani, K.L.; Fisher, P.G. Both location and age predict survival in ependymoma: A SEER study. Pediatr. Blood Cancer 2009, 52, 65–69. [Google Scholar] [CrossRef]
  28. Tsai, C.J.; Wang, Y.; Allen, P.K.; Mahajan, A.; McCutcheon, I.E.; Rao, G.; Rhines, L.D.; Tatsui, C.E.; Armstrong, T.S.; Maor, M.H.; et al. Outcomes after surgery and radiotherapy for spinal myxopapillary ependymoma: Update of the MD Anderson Cancer Center experience. Neurosurgery 2014, 75, 205–214. [Google Scholar] [CrossRef]
  29. Kukreja, S.; Ambekar, S.; Sharma, M.; Sin, A.H.; Nanda, A. Outcome predictors in the management of spinal myxopapillary ependymoma: An integrative survival analysis. World Neurosurg 2015, 83, 852–859. [Google Scholar] [CrossRef]
  30. Weber, D.C.; Wang, Y.; Miller, R.; Villà, S.; Zaucha, R.; Pica, A.; Poortmans, P.; Anacak, Y.; Ozygit, G.; Baumert, B.; et al. Long-term outcome of patients with spinal myxopapillary ependymoma: Treatment results from the MD Anderson Cancer Center and institutions from the Rare Cancer Network. Neuro Oncol. 2015, 17, 588–595. [Google Scholar] [CrossRef] [PubMed]
  31. Merchant, T.E. Current management of childhood ependymoma. Oncology 2006, 16, 629–642, 644–645. [Google Scholar]
  32. Ostrom, Q.T.; Cote, D.J.; Ascha, M.; Kruchko, C.; Barnholtz-Sloan, J.S. Adult glioma incidence and survival by race or ethnicity in the United States from 2000 to 2014. JAMA Oncol. 2018, 4, 1254–1262. [Google Scholar] [CrossRef] [PubMed]
  33. Rodríguez, D.; Cheung, M.C.; Housri, N.; Quinones-Hinojosa, A.; Camphausen, K.; Koniaris, L.G. Outcomes of malignant CNS ependymomas: An examination of 2408 cases through the Surveillance, Epidemiology, and End Results (SEER) database (1973–2005). J. Surg. Res. 2009, 156, 340–351. [Google Scholar] [CrossRef]
  34. Korshunov, A.; Golanov, A.; Timirgaz, V. Immunohistochemical markers for intracranial ependymoma recurrence: An analysis of 88 cases. J. Neurol. Sci. 2000, 177, 72–82. [Google Scholar] [CrossRef]
  35. Kovalic, J.J.; Flaris, N.; Grigsby, P.W.; Pirkowski, M.; Simpson, J.R.; Roth, K.A. Intracranial ependymoma long-term outcome, patterns of failure. J. Neurooncol. 1993, 15, 125–131. [Google Scholar] [CrossRef]
  36. Rousseau, P.; Habrand, J.L.; Sarrazin, D.; Kalifa, C.; Terrier-Lacombe, M.J.; Rekacewicz, C.; Rey, A. Treatment of intracranial ependymomas of children: Review of a 15-year experience. Int. J. Radiat. Oncol. Biol. Phys. 1994, 28, 381–386. [Google Scholar] [CrossRef]
  37. Shaw, E.G.; Evans, R.G.; Scheithauer, B.W.; Ilstrup, D.M.; Earle, J.D. Postoperative radiotherapy of intracranial ependymoma in pediatric and adult patients. Int. J. Radiat. Oncol. Biol. Phys. 1987, 13, 1457–1462. [Google Scholar] [CrossRef]
  38. Figarella-Branger, D.; Gambarelli, D.; Dollo, C.; Devictor, B.; Perez-Castillo, A.M.; Genitori, L.; Lena, G.; Choux, M.; Pellissier, J.F. Infratentorial ependymomas of childhood: Correlation between histological features, immunohistological phenotype, silver nucleolar organizer region staining values, and post-operative survival in 16 cases. Acta Neuropathol. 1991, 82, 208–216. [Google Scholar] [CrossRef] [PubMed]
  39. West, C.R.; Bruce, D.A.; Duffner, P.K. Ependymomas: Factors in clinical and diagnostic staging. Cancer 1985, 56 (Suppl. S7), 1812–1816. [Google Scholar] [CrossRef] [PubMed]
  40. Chiu, J.K.; Woo, S.Y.; Ater, J.; Connetlly, J.; Bruner, J.M.; Maor, M.H.; van Eys, J.; Oswald, M.J.; Shallenberger, R. Intracranial ependymoma in children: Analysis of prognostic factors. J. Neurooncol. 1992, 13, 283–290. [Google Scholar] [CrossRef]
  41. Vanuytsel, L.J.; Bessell, E.M.; Ashley, S.E.; Bloom, H.J.G.; Brada, M. Intracranial ependymoma: Long-term results of a policy of surgery and radiotherapy. Int. J. Radiat. Oncol. Biol. Phys. 1992, 23, 313–319. [Google Scholar] [CrossRef]
  42. Bleyer, W.A. Epidemiologic impact of children with brain tumors. Child′s Nerv. Syst. 1999, 15, 758–763. [Google Scholar] [CrossRef]
  43. Baldwin, R.T.; Preston-Martin, S. Epidemiology of brain tumors in childhood: A review. Toxicol. Appl. Pharmacol. 2004, 199, 118–131. [Google Scholar] [CrossRef] [PubMed]
  44. Hasselblatt, M. Ependymal tumors. Fortschr Krebsforsch. 2009, 171, 51–66. [Google Scholar]
  45. Kilday, J.P.; Rahman, R.; Dyer, S.; Ridlety, L.; Lowe, J.; Coyle, B.; Grundy, R. Pediatric ependymoma: Biological perspectives. Mol. Cancer Res. 2009, 7, 765–786. [Google Scholar] [CrossRef] [PubMed]
  46. Close, A.G.; Dreyzin, A.; Miller, K.D.; Seynnaeve, B.K.N.; Rapkin, L.B. Adolescent and young adult oncology: Past, present, and future. CA Cancer J. Clin. 2019, 69, 485–496. [Google Scholar] [CrossRef] [PubMed]
  47. Merchant, T.E.; Kiehna, E.N.; Thompson, S.J.; Heideman, R.; Sanford, R.A.; Kun, L.E. Pediatric low-grade and ependymal spinal cord tumors. Pediatr. Neurosurg. 2000, 32, 30–36. [Google Scholar] [CrossRef] [PubMed]
  48. Nuño, M.; Yu, J.J.; Varshneya, K.; Alexander, J.; Mukherjee, D.; Black, K.L.; Patil, C.G. Treatment and survival of supratentorial and posterior fossa ependymomas in adults. J. Clin. Neurosci. 2016, 28, 24–30. [Google Scholar] [CrossRef]
  49. Safaee, M.; Oh, M.C.; Kim, J.M.; Aranda, D.; Tarapore, P.E.; Cage, T.A.; Gupta, N.; Parsa, A.T. Histologic grade and extent of resection are associated with survival in pediatric spinal cord ependymomas. Child′s Nerv. Syst. 2013, 29, 2057–2064. [Google Scholar] [CrossRef]
  50. Pace, A.; Di Lorenzo, C.; Guariglia, L.; Jandolo, B.; Carapella, C.M.; Pompili, A. End of life issues in brain tumor patients. J. Neurooncol. 2009, 91, 39–43. [Google Scholar] [CrossRef]
  51. Walbert, T.; Khan, M. End-of-life symptoms and care in patients with primary malignant brain tumors: A systematic literature review. J. Neurooncol. 2014, 117, 217–224. [Google Scholar] [CrossRef]
Table 1. Baseline characteristics of patients with invasive ependymoma and mortality outcomes.
Table 1. Baseline characteristics of patients with invasive ependymoma and mortality outcomes.
CharacteristicsDiagnosed Cases No (%)Deaths No (%)
All patients 3821 (100%)842 (22%)
Age at diagnosis
less than 18 years1004 (26%)244 (29%)
18–441269 (33%)174 (21%)
45–59949 (25%)174 (21%)
60–75504 (13%)180 (21%)
more than 7595 (2%)70 (8%)
Sex
Male1960 (51%)477 (51%)
Female 1861 (49%)365 (49%)
Race
American Indian/Alaska Native22 (1%)6 (1%)
Asian or Pacific Islander252 (7%)41 (7%)
white3153 (83%)688 (83%)
Black344 (9%)105 (9%)
Unknown50 (1%)2 (1%)
Primary site—labeled
C41.2—Vertebral column7 (0%)2 (0%)
C48.0—Retroperitoneum1 (0%)-
C49.0—Connective, subcutaneous, other soft tissue: head, face, neck1 (0%)1 (0%)
C49.5—Connective, subcutaneous, other soft tissue: pelvis3 (0%)-
C49.6—Connective, subcutaneous, other soft tissue: trunk, NOS2 (0%)-
C56.9—Ovary1 (0%)-
C57.4—Uterine adnexa1 (0%)-
C70.0—Cerebral meninges1 (0%)-
C70.1—Spinal meninges35 (1%)5 (1%)
C70.9—Meninges, NOS2 (0%)-
C71.0—Cerebrum39 (1%)18 (1%)
C71.1—Frontal lobe155 (4%)46 (4%)
C71.2—Temporal lobe70 (2%)38 (2%)
C71.3—Parietal lobe127 (3%)37 (3%)
C71.4—Occipital lobe59 (2%)12 (2%)
C71.5—Ventricle, NOS384 (10%)99 (10%)
C71.6—Cerebellum, NOS215 (6%)75 (6%)
C71.7—Brain stem610 (16%)151 (16%)
C71.8—Overlapping lesion of the brain107 (3%)35 (3%)
C71.9—Brain, NOS285 (7%)82 (7%)
C72.0—Spinal cord1649 (43%)229 (43%)
C72.1—Cauda equina51 (1%)8 (1%)
C72.5—Cranial nerve, NOS1 (0%)-
C72.8—Overlapping lesion of brain & CNS2 (0%)-
C72.9—Nervous system, NOS5 (0%)1 (0%)
C75.3—Pineal gland8 (0%)3 (0%)
ICD-O-3 Histological Behavior, malignant
Sub ependymoma, malignant3 (0%)-
Ependymoma NOS2980 (78%)572 (78%)
Ependymoma, anaplastic738 (19%)260 (19%)
Papillary ependymoma NOS57 (1%)7 (1%)
Myxopapillary ependymoma, malignant35 (1%)3 (1%)
Ependymoma, RELA fusion-positive8 (0%)-
Table 2. Standardized mortality ratios for causes of death following the diagnosis of invasive ependymoma.
Table 2. Standardized mortality ratios for causes of death following the diagnosis of invasive ependymoma.
Deaths by Time After Diagnosis
<1 Year1–5 Years>5 YearsTotal
Observed No (%)SMR (95% CI)Observed No (%)SMR (95% CI)Observed No (%)SMR (95% CI)Observed No (%)SMR (95% CI)
All Causes of Death198 (100%)10.54 (9.12–12.11)342 (100%)5.24 (4.7–5.83)280 (100%)2.28 (2.02–2.56)820 (100%)3.96 (3.69–4.24)
Brain and Other Nervous System102 (52%)655 (534–795)211 (62%)392 (341–449)111 (40%)114 (93.57–137)424 (52%)254 (230–279)
Non-CNS cancers13 (7%)2.66 (1.41–4.54)30 (9%)1.77 (1.19–2.52)32 (11%)1.02 (0.7–1.44)75 (9%)1.41 (1.11–1.76)
Non-cancer causes83 (42%)6.04 (4.81–7.49)101 (30%)2.12 (1.72–2.57)137 (49%)1.51 (1.27–1.79)321 (39%)2.11 (1.89–2.35)
Septicemia4 (2%)15.4 (4.2–39.42)2 (1%)2.17 (0.26–7.84)4 (1%)2.22 (0.6–5.67)10 (1%)3.35 (1.61–6.16)
Other Infectious and Parasitic Diseases, including HIV5 (3%)17.57 (5.71–41.01)0 (0%)0 (0–3.93)3 (1%)2.07 (0.43–6.05)8 (1%)2.99 (1.29–5.9)
Diabetes Mellitus2 (1%)3.37 (0.41–12.16)3 (1%)1.44 (0.3–4.21)5 (2%)1.26 (0.41–2.94)10 (1%)1.5 (0.72–2.77)
Alzheimer’s (ICD-9 and 10 only) 0 (0%)0 (0–3.08)6 (2%)1.91 (0.7–4.16)6 (1%)1.3 (0.48–2.83)
Cardiovascular Diseases8 (4%)1.79 (0.77–3.52)18 (5%)1.14 (0.68–1.81)32 (11%)1.08 (0.74–1.52)58 (7%)1.16 (0.88–1.5)
Cerebrovascular Diseases7 (4%)8.76 (3.52–18.05)9 (3%)3.18 (1.46–6.04)10 (4%)1.81 (0.87–3.33)26 (3%)2.84 (1.86–4.17)
Pneumonia and Influenza3 (2%)9.43 (1.94–27.56)4 (1%)3.54 (0.96–9.06)4 (1%)1.85 (0.5–4.74)11 (1%)3.05 (1.52–5.45)
Chronic Obstructive Pulmonary Disease and Allied Cond4 (2%)4.04 (1.1–10.35)5 (1%)1.39 (0.45–3.25)10 (4%)1.34 (0.64–2.46)19 (2%)1.57 (0.95–2.46)
Chronic Liver Disease and Cirrhosis1 (1%)2.52 (0.06–14.05)0 (0%)0 (0–2.68)1 (0%)0.4 (0.01–2.21)2 (0%)0.47 (0.06–1.68)
Nephritis, Nephrotic Syndrome and Nephrosis0 (0%)0 (0–12.7)1 (0%)0.95 (0.02–5.3)4 (1%)1.92 (0.52–4.91)5 (1%)1.46 (0.47–3.41)
Accidents and Adverse Effects0 (0%)0 (0–2.88)4 (1%)0.94 (0.26–2.4)10 (4%)1.42 (0.68–2.61)14 (2%)1.11 (0.61–1.87)
Suicide and Self-inflicted Injury1 (1%)2.23 (0.06–12.4)2 (1%)1.33 (0.16–4.79)1 (0%)0.41 (0.01–2.31)4 (0%)0.92 (0.25–2.34)
Other Cause of Death48 (24%)14.44 (11–19.14)53 (15%)4.78 (3.58–6.25)47 (17%)2.21 (1.62–2.93)148 (18%)4.14 (3.5–4.87)
CNS: central nervous system; HIV: Human Immunodeficiency Virus; SMRs: standardized mortality ratios.
Table 3. Overall survival and survival according to gender and race.
Table 3. Overall survival and survival according to gender and race.
YearsNo of PatientsObserved Survival 95% CI (Lower-Upper)Relative Survival 95% CI (Lower-Upper)
Overall
1 Year382194% (0.94–0.95)95% (0.94–0.96)
3 years382188% (0.87–0.89)89% (0.88–0.9)
5 years382184% (0.82–0.85)86% (0.85–0.87)
3 years survival after 1 year survival 337491% (0.90–0.92)92% (0.91–0.93)
3 years survival after 3 years survival274194% (0.93–0.95)95% (0.94–0.96)
3 years survival after 5 years survival228194% (0.93–0.95)96% (0.95–0.97)
Male
1 Year196094% (0.92–0.95)94% (0.93–0.95)
3 Years196086% (0.84–0.87)85% (0.86–0.89)
5 Years196082% (0.80–0.83)84% (0.82–0.86)
3 years survival after 1 year survival171689% (0.88–0.91)91% (0.89–0.92)
3 years survival after 3 years survival138393% (0.92–0.95)95% (0.94–0.97)
3 years survival after 5 years survival 114293% (0.92–0.95)95% (0.93–0.97)
Female
1 Year186195% (0.94–0.96)96% (0.95–0.97)
3 Years186190% (0.88–0.91)91% (0.89–0.92)
5 Years186186% (0.84–0.87)88% (0.86–0.89)
3 years survival after 1 year survival165892% (0.91–0.93)93% (0.92–0.95)
3 years survival after 3 years survival135894% (0.93–0.95)95% (0.94–0.97)
3 years survival after 5 years survival113995% (0.93–0.96)97% (0.95–0.98)
White
1 Year315394% (0.94–0.95)95% (0.94–0.96)
3 Years315388% (0.87–0.89)90% (0.88–0.91)
5 Years315384% (0.83–0.86)87% (0.85–0.88)
3 years survival after 1 year survival278891% (0.90–0.92)93% (0.91–0.94)
3 years survival after 3 years survival228894% (0.93–0.95)96% (0.94–0.96)
3 years survival after 5 years survival192195% (0.93–0.956)96% (0.95–0.97)
Black
1 Year34493% (0.89–0.95)93% (0.90–0.95)
3 Years34481% (0.76–0.85)82% (0.77–0.86)
5 Years34477% (0.72–0.81)79% (0.74–0.84)
3 years survival after 1 year survival30086% (0.81–0.89)87% (0.82–0.91)
3 years survival after 3 years survival23493% (0.89–0.96)95% (0.90–0.97)
3 years survival after 5 years survival18289% (0.83–0.93)91% (0.84–0.95)
American Indian/Alaska Native
1 Year2291% (0.68–0.98)91% (0.67–0.98)
3 Years2286% (0.62–0.95)86% (0.61–0.96)
5 Years2274% (0.48–0.89)76% (0.49–0.91)
3 years survival after 1 year survival1888% (0.60–0.97)89% (0.59–0.98)
3 years survival after 3 years survival1587% (0.56–0.97)88% (0.55–0.97)
3 years survival after 5 years survival1392% (0.57–0.99)93% (0.52–0.99)
Asian or Pacific Islander
1 Year25296% (0.93–0.98)96% (0.93–0.98)
3 Years25290% (0.85–0.93)90% (0.86–0.94)
5 Years25285% (0.80–0.90)86% (0.80–0.90)
3 years survival after 1 year survival22892% (0.87–0.95)93% (0.88–0.96)
3 years survival after 3 years survival17694% (0.88–0.97)94% (0.89–0.97)
3 years survival after 5 years survival14196% (0.91–0.98)96% (0.91–0.99)
Table 4. Survival rate according to age.
Table 4. Survival rate according to age.
YearsNo of PatientsObserved Survival 95% CI
(Lower–Upper)		Relative Survival 95% CI
(Lower–Upper)
Age < 18
1 Year100496% (0.94–0.97)96% (0.94–0.97)
3 Years100485% (0.82–0.87)85% (0.82–0.87)
5 Years100478% (0.75–0.81)78% (0.75–0.81)
3 years survival after 1 year survival89885% (0.82–0.87)85% (0.82–0.87)
3 years survival after 3 years survival67689% (0.87–0.92)90% (0.87–0.92)
3 years survival after 5 years survival54192% (0.89–0.94)92% (0.89–0.94)
Age 18–44
1 Year126997% (0.96–0.98)98% (0.97–0.98)
3 Years126994% (0.92–0.95)94% (0.92–0.95)
5 Years126991% (0.89–0.93)92% (0.90–0.93)
3 years survival after 1 year survival115595% (0.93–0.96)95% (0.93–0.96)
3 years survival after 3 years survival98296% (0.95–0.98)97% (0.95–0.98)
3 years survival after 5 years survival82697% (0.96–0.98)98% (0.96–0.99)
Age 45–59
1 Year94995% (0.93–0.96)96% (0.94–0.97)
3 Years94990% (0.88–0.92)92% (0.90–0.94)
5 Years94988% (0.85–0.90)90% (0.88–0.92)
3 years survival after 1 year survival84694% (0.92–0.95)96% (0.94–0.97)
3 years survival after 3 years survival71796% (0.94–0.97)98% (0.96–0.99)
3 years survival after 5 years survival61896% (0.94–0.98)98% (0.96–0.99)
Age 60–74
1 Year48489% (0.86–0.92)90% (0.87–0.93)
3 Years48481% (0.77–0.85)85% (0.81–0.89)
5 Years48478% (0.74–0.82)84% (0.80–0.88)
3 years survival after 1 year survival40289% (0.85–0.92)93% (0.89–0.96)
3 years survival after 3 years survival31894% (0.91–0.96)99% (0.94–1)
3 years survival after 5 years survival26387% (0.82–0.91)93% (0.87–0.96)
Age > 75
1 Year11566% (0.57–0.74)70% (0.60–0.78)
3 Years11552% (0.42–0.61)62% (0.49–0.72)
5 Years11539% (0.30–0.49)54% (0.40–0.67)
3 years survival after 1 year survival7366% (0.53–0.76)80% (0.62_0.90)
3 years survival after 3 years survival4867% (0.51–0.78)83% (0.57–0.94)
3 years survival after 5 years survival3365% (0.46–0.79)85% (0.46–0.96)
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content.

Share and Cite

MDPI and ACS Style

Elgenidy, A.; Saad, K.; Aboelgheet, A.; Gad, E.F.; El-Shokhaiby, U.; Alruwaili, T.A.M.; Abdelal, A.N.; Mohamed, K.R.; Bazzazeh, M.; Hesn, M.; et al. Survival Patterns and Mortality Causes in Patients with Invasive Ependymoma: A Retrospective Cohort Analysis from 2000 to 2019. Med. Sci. 2025, 13, 139. https://doi.org/10.3390/medsci13030139

AMA Style

Elgenidy A, Saad K, Aboelgheet A, Gad EF, El-Shokhaiby U, Alruwaili TAM, Abdelal AN, Mohamed KR, Bazzazeh M, Hesn M, et al. Survival Patterns and Mortality Causes in Patients with Invasive Ependymoma: A Retrospective Cohort Analysis from 2000 to 2019. Medical Sciences. 2025; 13(3):139. https://doi.org/10.3390/medsci13030139

Chicago/Turabian Style

Elgenidy, Anas, Khaled Saad, Amir Aboelgheet, Eman F. Gad, Usama El-Shokhaiby, Thamer A. M. Alruwaili, Abdelrahman N. Abdelal, Kawashty R. Mohamed, Mohammad Bazzazeh, Mohamed Hesn, and et al. 2025. "Survival Patterns and Mortality Causes in Patients with Invasive Ependymoma: A Retrospective Cohort Analysis from 2000 to 2019" Medical Sciences 13, no. 3: 139. https://doi.org/10.3390/medsci13030139

APA Style

Elgenidy, A., Saad, K., Aboelgheet, A., Gad, E. F., El-Shokhaiby, U., Alruwaili, T. A. M., Abdelal, A. N., Mohamed, K. R., Bazzazeh, M., Hesn, M., Elshimy, A. H., Sayed, A., Magdy, S., Gamal, D. A., Elhoufey, A. A., Ismael, S. A., Afifi, A. M., Ibrahim, M. F. M., & Ragab, A. (2025). Survival Patterns and Mortality Causes in Patients with Invasive Ependymoma: A Retrospective Cohort Analysis from 2000 to 2019. Medical Sciences, 13(3), 139. https://doi.org/10.3390/medsci13030139

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop