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Abstract

Introduction

Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) are a heterogeneous group of neoplasms with increasing incidence and variable clinical characteristics. This study aimed to describe the clinicopathological characteristics of surgically/endoscopically treated GEP-NETs and identify prognostic factors associated with overall survival (OS) in a single tertiary center.

Methods

In this retrospective, single-center cohort study, we reviewed the data of adult patients diagnosed with GEP-NETs and treated at the Department of General Surgery, Marmara University School of Medicine, between January 2018 and December 2024. Demographic, clinical, and pathological variables were collected, including histologic type (NET vs. NEC), tumor grade, tumor size, Ki-67 index, mitotic index, nodal status, and stage. The OS was analyzed using the Kaplan–Meier method and compared using the log-rank test. Cox proportional hazards models were used to identify the independent mortality predictors.

Results

Among the 96 patients included in the final analysis, 55% were female, with a median age of 55 years. The primary tumor sites were the pancreas (46%) and stomach (35%), followed by the appendix (6%), small intestine (5%), colorectal (3%), and hepatobiliary tract (4%). Surgical resection and lymph node dissection were performed in 90% and 72% of patients, respectively. NET and NEC accounted for 71% and 29%, respectively. Grades were G1 (48%), G2 (22%), G3 (16%), MiNEN (8%), and undefined (6%). The 5-year OS for the cohort was 79%. Patients with pancreatic and gastric tumors, higher-grade tumors, larger tumors, elevated Ki-67/mitotic indices, NEC histology, and advanced stage had significantly worse survival. In the multivariate analysis, older age, NEC histology, and advanced stage remained independent adverse prognostic factors.

Conclusion

In this single-center experience, GEP-NET prognosis was primarily driven by age, histologic type, and disease stage. These findings may support risk-adapted, multidisciplinary management tailored to tumor biology and disease extent.

Keywords

neuroendocrine neoplasms neuroendocrine tumors gastroenteropancreatic neuroendocrine tumors Ki-67 proliferation index prognostic factors

Introduction

Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) are rare tumors originating from the digestive system and pancreas, representing a heterogeneous clinical and pathological group. A significant increase in their incidence has been recently observed. This diversity complicates diagnosis and treatment and directly affects the disease course.^1,2

Clinical findings vary according to the organ of origin, hormone production status, degree of differentiation, and tumor spread extent. Functional tumors can cause hormone secretion-related syndromes, whereas nonfunctional tumors are mostly asymptomatic and incidentally detected. Although histopathological examination is the gold standard for diagnosis, endoscopic methods, advanced imaging techniques, and biochemical markers increase the accuracy of diagnosis.^3-6

Pathological classification is based on the degree of differentiation (well-differentiated NET, poorly differentiated NEC), proliferation index (mitotic count, Ki-67), and Tumor, Node, Metastasis (TNM) staging. Computed tomography (CT), magnetic resonance imaging (MRI), endoscopic ultrasound (EUS), and positron emission tomography/computed tomography (PET/CT) are used for diagnostic purposes. Radioisotope imaging methods that target somatostatin receptors (e.g., ^68Ga-DOTA-peptide PET/CT) offer high sensitivity for evaluating small lesions and their spread. Additionally, chromogranin A, 5-HIAA, and hormone levels are particularly important in functional tumors.^3,4,7

Molecular biology and genetic infrastructure are becoming increasingly important in understanding the pathogenesis and prognosis of GEP-NETs. Genetic and epigenetic differences between primary and metastatic lesions affect tumor biology and treatment response. In particular, heterogeneity in somatostatin receptor expression can limit the effectiveness of both diagnostic imaging and somatostatin analog treatment. Furthermore, differences in the Ki-67 proliferation index can lead to uncertainties in grading and prognosis prediction.^2,4

Functional status, differentiation grade, stage, and the presence of metastasis are key determinants of clinical management. While surgical curative treatment forms the basis for localized disease, somatostatin analogs, peptide receptor radionuclide therapy (PRRT), targeted therapies, and chemotherapy are prominent in advanced stages. Although somatostatin analogs can be used to achieve long-term control in well-differentiated, low-grade tumors, aggressive chemotherapy protocols are preferred for poorly differentiated, high-grade tumors.^8,9

A multidisciplinary approach is critical for accurately assessing tumor localization, spread, and biological behavior, especially in patients who are newly diagnosed. Genetic counseling is also important in patients with familial syndromes (e.g., MEN1 and VHL). However, resistance to treatment is a significant problem. Reactivation of targeted pathways, activation of alternative pathways, or dedifferentiation of tumor cells reduces treatment efficacy. This situation highlights the need to develop new treatment strategies.^5,8,10

This study aimed to analyze the clinical-pathological characteristics and prognosis of patients with GEP-NET in a single center.

Methods

This retrospective, single-center cohort study was conducted in the Department of General Surgery at Marmara University School of Medicine. The study included adult patients diagnosed with GEP-NETs who were treated at our clinic between January 2018 and December 2024, with follow-up extending until June 2025. Eligible patients were retrospectively identified from institutional records and consecutively included if they met the study inclusion criteria.

The study protocol was approved by the Marmara University School of Medicine Clinical Research Ethics Committee (Approval No: 09.2025.25-0461). Due to the retrospective nature of the study and the use of anonymized patient data, the requirement for informed consent was waived by the Ethics Committee.

This study was conducted in accordance with the principles of the Declaration of Helsinki. The reporting of this study conforms to the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) guidelines.¹¹ All patient data were fully de-identified prior to analysis.

The study population consisted of only patients aged 18 years or older who had undergone surgical or endoscopic treatment and whose follow-up records were fully accessible. Patients with primary neuroendocrine tumors outside the gastroenteropancreatic system and those with incomplete records were excluded.

Patient demographics such as age and gender, comorbid diseases, American Society of Anesthesiologists (ASA) scores, functional tumors (insulinoma and VIPoma), primary tumor locations, resection procedure (surgical or endoscopic), systemic chemotherapies, and ablation therapies such as radiofrequency or microwave ablations were noted.

Pathological parameters included histologic type (neuroendocrine tumor [NET] vs neuroendocrine carcinoma [NEC]), tumor grade (G1–G3, MiNEN, undefined), tumor size, Ki-67 proliferation index, mitotic count, T and N stages, and overall pathological stage. Pathological staging was performed according to the American Joint Committee on Cancer 8th edition. Tumor size was evaluated as a continuous variable and categorized as 0–20, 20–40, and > 40 mm.^5,12-16 In accordance with the updated WHO classification, tumors previously categorized as mixed adeno-neuroendocrine carcinomas (MANECs) were classified as mixed neuroendocrine–non-neuroendocrine neoplasms (MiNENs), defined by the presence of both neuroendocrine and non-neuroendocrine components.

The primary outcome of this study was overall survival (OS), defined as the time from diagnosis to death from any cause or last follow-up. The survival status was confirmed using hospital records and national databases.

The secondary outcomes of this study were to evaluate the clinical and pathological characteristics of GEP-NETs treated surgically/endoscopically at a single center.

Statistical Analysis

Statistical analyses were conducted using SPSS version 28.0 (IBM, Chicago, IL, USA) and Jamovi (version 2.3; The jamovi project, Sydney, Australia). Categorical variables are presented as frequencies and percentages, and continuous variables are presented as medians with ranges. Overall survival (OS) was evaluated using the Kaplan–Meier method, and survival curves were compared using the log-rank test performed in Jamovi. Univariate Cox proportional hazards regression was performed for each clinical and pathological variable. Variables with p < 0.05 in the univariate analysis were included in a multivariate Cox regression model to identify independent predictors of mortality. Hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated. A two-sided p < 0.05 was considered statistically significant. No formal sample size calculation was performed due to the retrospective nature of the study.

Results

A total of 217 patients diagnosed with GEP-NET between January 2018 and December 2024 were analyzed. Of these, 81 patients who had only biopsy results were excluded. A total of 40 patients were excluded due to follow-up loss. Finally, 96 patients were included in the analysis. Among them, 53 (55%) were female. The median age was 55 years (range: 18–84 years). Most patients had an ASA score of 1–2 (71%), while 54% had at least one comorbid disease, with hypertension (35%) and diabetes mellitus (26%) being the most common (Table 1). One patient was classified as ASA 5 due to emergency presentation with perforated metastatic gastric NET.

Table 1.

Patient Characteristics

Variables	All patients (n = 96)
Age (years; median, IQR)	55 (25)
Sex, n (%)
Male	43 (45%)
Female	53 (55%)
Tumor functionality, n (%)
Insulinoma	7 (7%)
VIPoma	1 (1%)
ASA score, n (%)
1	25 (26%)
2	43 (45%)
3	17 (18%)
4	10 (10%)
5	1 (1%)
Comorbidities, n (%)
Present	52 (54%)
Absent	44 (46%)
Comorbidities, n (%)
Diabetes mellitus	25 (26%)
Hypertension	34 (35%)
Ischemic heart disease	14 (15%)
COPD	4 (4%)
Others	24 (25%)
Primary tumor location, n (%)
Appendix	6 (6%)
Colorectal	3 (3%)
Hepatobiliary	4 (4%)
Pancreas	44 (46%)
Small Intestine	5 (5%)
Stomach	34 (35%)
Resection type, n (%)
Surgical	86 (90%)
Endoscopic	10 (10%)
Lymph node dissection, n (%)	69 (72%)
Systemic chemotherapy, n (%)	24 (25%)
Ablation therapies, n (%)	3 (3%)

ASA: American Society of Anesthesiologists physical status, VIP: Vasoactive Intestinal Peptide, COPD: Chronic Obstructive Pulmonary Disease. IQR: interquartile range.

The most common primary tumor sites were the pancreas (46%) and stomach (35%), followed by appendix (6%), small intestine (5%), colorectal region (3%), and hepatobiliary tract (4%). Most patients underwent surgical resection (90%), and 72% underwent lymph node dissection. Systemic chemotherapy and ablation therapies were administered to 25% and 3% of the patients, respectively.

NETs were observed in 68 (71%) patients, whereas 28 (29%) had NECs. The tumor grades were as follows: G1 (48%), G2 (22%), G3 (16%), MiNEN (8%), and undefined (6%). The median tumor size was 21.5 mm (range: 0.2–210 mm), with 48% measuring 0–20 mm, 19% measuring 20–40 mm, and 33% exceeding 40 mm.

Regarding the Ki-67 proliferative index, 43% had an index <2%, 24% had 3–20%, and 24% had >20%. The mitotic index was <2 in 46% of cases, 2–20 in 7%, and >20 in 4%, while 43% were not clearly defined. Among the 86 staged patients, T1 (34%) and T3 (29%) were the most common T stages. Lymph node metastasis (N1 or N2) was found in 39 (45%) of these patients. The overall pathological stages were as follows: Stage I (44%), Stage II (15%), Stage III (29%), and Stage IV (12%) (Table 2).

Table 2.

Pathological Outcomes of the Patients

Variables	All patients (n = 96)
Histologic type, n (%)
Neuroendocrine Tumor	68 (71%)
Neuroendocrine Carcinoma	28 (29%)
Tumor grade, n (%)
Grade 1	46 (48%)
Grade 2	21 (22%)
Grade 3	15 (16%)
MiNEN	8 (8%)
Undefined	6 (6%)
Tumor size (mm; median, IQR)	21.5 (47)
Tumor size (mm)
0-20	46 (48%)
20-40	18 (19%)
> 40	32 (33%)
Ki67 proliferative index, n (%)
< 2%	41 (43%)
3-20%	23 (24%)
> 20%	23 (24%)
Undefined	9 (9%)
Mitotic index, n (%)
< 2	44 (46%)
2-20	7 (7%)
> 20	4 (4%)
Undefined	41 (43%)
T stage, n (%) (n = 86)*
T1	29 (34%)
T2	15 (17%)
T3	25 (29%)
T4	17 (20%)
N Stage, n (%) (n = 86)*
N0	47 (55%)
N1	24 (28%)
N2	15 (17%)
Stage, n (%)
Stage 1	42 (44%)
Stage 2	14 (15%)
Stage 3	28 (29%)
Stage 4	12 (12%)

MiNEN: Mixed neuroendocrine non-neuroendocrine neoplasm, IQR: interquartile range; *Patients with endoscopic resection excluded.

In univariate Cox regression analysis, age, sex, histological type (NET vs NEC), tumor grade, tumor size, Ki-67 proliferative index, mitotic index, and TNM stage were significantly associated with overall survival. In the multivariate model, age, NEC histology, and advanced stage remained independent predictors of mortality (Table 3).

Table 3.

Univariate and Multivariate Cox Regression Analyses of Overall Survival

Variables	All patients (n = 96)
Variables	HR	95% CI	p-value	HR	95% CI	p-value
Sex	5.759	2.106-15.748	<0.001	2.708	0.836-8.772	0.097
Age	1.082	1.040-1.126	<0.001	1.054	1.011-1.099	0.014
Comorbidities	2.385	0.929-6.123	0.073
Histologic type	5.085	2.753-9.291	<0.001	4.444	1.306-15.123	0.017
Tumor functionality	0.043	0.000-21.651	0.321
Tumor grading			<0.001			0.963
Grade 1	Ref.			Ref.
Grade 2	0.550	0.061-4.949		0.495	0.022-11.207
Grade 3	9.104	2.562-32.345		0.312	0.013-7.514
MiNEN	27.665	7.333-35.943		0.271	0.009-7.947
Undefined	7.751	1.672-35.943		0.316	0.011-9.260
Tumor size	1.011	1.004-1.018	0.001			0.178
Ki-67 proliferative index			<0.001			0.738
< 2%	Ref.			Ref.
3-20%	0.459	0.051-4.116		0.358	0.016-7.776
> 20%	7.833	2.483-24.709		0.637	0.052-7.758
Undefined	8.752	2.343-32.702		1.205	0.107-13.547
Mitotic index	2.143	1.422-3.228	<0.001	1.325	0.737-2.380	0.347
Stage			<0.001
Stage 1	Ref.			Ref.		0.096
Stage 2	3.051	0.430-21.651		1.398	0.113-17.358	0.794
Stage 3	13.071	2.939-58.120		6.065	1.020-36.074	0.048
Stage 4	9.249	1.793-47.711		4.766	0.574-39.580	0.148
Systemic chemotherapy	2.083	0.707-6.139	0.183

Bold values indicate statistical significance (p < 0.05).

The median follow-up time for the entire cohort was 32.5 (range, 1–90) months. The 5-year overall survival (OS) rate was 79%. Kaplan–Meier survival curves according to primary tumor localization are shown in Figure 1. Patients with pancreatic and gastric tumors had significantly worse OS compared with those with appendiceal and small intestinal GEP-NETs (log-rank p = 0.001).

Figure 1.

Analysis of overall survival by tumor location

Subgroup Kaplan–Meier analyses are presented in Figure 2. Tumor grade was significantly associated with survival outcomes (log-rank p < 0.001) (Figure 2A). Patients with low-grade (G1) tumors had the most favorable prognosis, whereas those with G3 and MiNEN histologies demonstrated reduced survival rates. Similarly, patients with a Ki-67 index <2% had significantly better OS compared with those with intermediate (3%–20%) or high (>20%) proliferative indices (log-rank p < 0.001) (Figure 2B). A comparable survival pattern was observed according to mitotic index (log-rank p < 0.001) (Figure 2C).

Figure 2.

Kaplan–Meier analysis of overall survival by pathological and clinical variables. Survival curves are shown for (A) tumor grade, (B) Ki-67 proliferation index, (C) mitotic index, (D) tumor size categories, (E) histological type, and (F) TNM stage

Tumor size also had a significant impact on survival (log-rank p < 0.001), with progressively worse outcomes observed in patients with larger tumors (Figure 2D). Survival differed significantly between NET and NEC histologies (log-rank p < 0.001), with NEC associated with higher mortality risk (Figure 2E). Finally, advanced TNM stage was significantly associated with poorer OS (log-rank p < 0.001) (Figure 2F).

Discussion

The clinicopathological characteristics and long-term survival outcomes of patients with gastroenteropancreatic neuroendocrine tumors (GEP-NETs) were evaluated, and the key prognostic factors were analyzed. Our findings show that GEP-NETs exhibit marked biological and clinical heterogeneity, and that histological type, grade, proliferative activity, and stage play decisive roles in survival. In particular, advanced disease stage, neuroendocrine carcinoma histology, and high proliferation indices were strongly associated with poor prognosis. These results support the notion that a single approach is insufficient in the clinical management of GEP-NETs and that patient-based assessment is necessary.

Tumor grade and proliferation index (Ki-67) are among the most important factors in the prognosis of GEP-NET. A high Ki-67 index is associated with more aggressive biological behavior and poor prognosis.^17-19 Multiple studies have demonstrated that tumor grade and the Ki-67 index significantly affect survival, and that high-grade (G3) tumors have a significantly shorter disease-free survival.^20-23 Furthermore, a large-scale study involving 759 patients showed that the 5-year recurrence rate increased significantly according to tumor grade and that high-grade tumors had more frequent distant recurrences.²⁴ The results of our study, consistent with the literature, suggest that tumor grade and Ki-67 index are key biomarkers in predicting prognosis. In addition, emerging evidence suggests that metabolic alterations, particularly in lipid metabolism, may contribute to tumor development, progression, and therapeutic resistance in neuroendocrine neoplasms, highlighting potential future therapeutic targets.²⁵

GEP-NET primary localization is an important determinant of clinical behavior and prognosis. The pancreas and stomach were identified as the most common primary tumor sites in our cohort. However, several large epidemiological studies have reported different distributions, with the small intestine and rectum being among the most frequently involved sites.^1,26-29 Differences between studies may be related to referral patterns in tertiary surgical centers, geographic variations in tumor distribution, and differences in diagnostic practices and screening strategies across populations.^18,30,31 In addition, the primary tumor location may influence recurrence patterns; for example, peritoneal recurrence has been reported to be less common in pancreatic NETs.²⁴ Therefore, tumor localization plays a critical role in prognostic assessment, surgical planning, and the selection of appropriate treatment strategies.

The presence of metastasis and lymph node involvement are major factors that negatively affect GEP-NET survival. Studies in the literature report that metastatic disease is detected in >50% of patients at diagnosis and that this significantly reduces survival.³² Lymph node involvement and the presence of distant metastasis have been emphasized as independent prognostic factors in survival analyses.^23,33 Our study also demonstrated a relationship between advanced disease and poor survival.

The majority of patients in this study underwent surgical resection, reflecting the central role of surgery in the management of localized GEP-NETs. Accordingly, survival outcomes should be interpreted within the context of a predominantly surgically treated cohort. Similarly, another study reported that patients who underwent minimally invasive surgery experienced fewer postoperative complications, shorter hospital stays, and better survival outcomes.²⁰ However, systemic therapies, targeted agents, and radionuclide therapies may be used in addition to surgery in advanced or metastatic disease.³² These findings emphasize the need for a multidisciplinary approach and patient-based treatment strategies for treating GEP-NETs.^34-37

Various biomarkers are used in GEP-NET diagnosis and follow-up. Immunohistochemical markers, such as chromogranin A (CgA) and synaptophysin (Syn), have been shown to have high sensitivity in diagnosis in clinicopathological analyses.³³ In addition, the Ki-67 proliferation index is a key biomarker in tumor grading and prognosis prediction. Artificial intelligence-based analyses can assist pathologists in the automatic and accurate calculation of the Ki-67 index and can achieve a 95% accuracy rate in tumor grading.³⁸ These developments contribute to the standardization and increased objectivity of diagnostic processes.

The development of treatment resistance and tumor heterogeneity in GEP-NETs is a significant challenge in clinical management.^10,39 The tumor microenvironment (TME) is gaining increasing importance in GEP-NET biology and treatment response. Targeting the TME may enable the development of new treatment strategies, particularly in advanced-stage and high-grade tumors.⁴⁰

The main factors affecting the prognosis of GEP-NETs include age, tumor location, tumor grade, Ki-67 index, lymph node involvement, distant metastasis, tumor diameter, lymphovascular and perineural invasion, mitotic index, and treatment modality.^23,41,42 In large-scale series, age, tumor location, distant metastasis, and tumor grade at diagnosis have been shown to significantly affect survival.³³ Similarly, another study emphasized that tumor grade and metastasis are the two most important factors affecting survival.⁴³ Furthermore, large tumor size, lymphovascular and perineural invasion, and high mitotic and Ki-67 indices are associated with increased recurrence and mortality rates.³¹ The postoperative recurrence rates vary depending on the tumor grade and location. In a large-scale study, the 5-year postoperative recurrence rates for G1, G2, and G3 tumors were 22%, 46%, and 59%, respectively.²⁴ Consistent with these data, our study identified advanced age, poor histology, and advanced stage as factors associated with poor prognosis.

This study has several limitations related to its retrospective, single-center design. Patients with biopsy-only diagnoses were excluded because the study aimed to analyze the clinicopathological characteristics and survival outcomes of patients who underwent surgical or endoscopic treatment for GEP-NETs. Consequently, the study population may be enriched with patients with resectable disease, which may introduce selection bias and limit the generalizability of the findings to the broader population of patients with GEP-NETs. Mitotic index data were unavailable in a substantial proportion of cases, reflecting variability in historical pathology reporting and potentially affecting proliferation-based prognostic assessment robustness. The relatively limited sample size, together with heterogeneity in tumor localization and treatment modalities, may have reduced the statistical power of certain subgroup analyses. In addition, the limited number of events may have contributed to wider confidence intervals in the multivariate Cox regression analysis. The median follow-up duration was relatively short, which may restrict the strength of long-term prognostic conclusions. Therefore, these findings are most applicable to surgically managed patients treated in tertiary referral centers, and further multicenter prospective studies with longer follow-up are needed to validate these observations.

Despite these limitations, the present study provides a detailed clinicopathological evaluation of surgically and endoscopically treated GEP-NETs in a tertiary referral center. This study provides additional real-world data and highlights the clinicopathological characteristics of surgically managed GEP-NETs in a well-characterized cohort, in addition to confirming previously reported prognostic factors.

Conclusion

Numerous factors influence the clinical and pathological characteristics and prognosis of GEP-NETs, primarily the tumor’s histological type and grade, proliferation index, primary location, lymph node involvement, presence of distant metastasis, and advanced stage. In the present study, advanced age, NEC histology, and advanced disease stage were independently associated with poor survival. These findings may support the need for patient-based, multidisciplinary assessment and treatment strategies informed by tumor biology and disease extent, rather than a single standard approach to the management of GEP-NETs.

Footnotes

ORCID iDs

Muhammer Ergenç

Hilmi Yazıcı

Ethical Considerations

This study was conducted in accordance with the principles of the Declaration of Helsinki. The study protocol was approved by the Marmara University School of Medicine Clinical Research Ethics Committee (Approval No: 09.2025.25-0461). Due to the retrospective design of the study and the use of anonymized patient data, the requirement for informed consent was waived by the Ethics Committee.

Author Contributions

All listed authors meet the ICMJE criteria. We attest that all authors contributed significantly to the creation of this manuscript, each having fulfilled criteria as established by the ICMJE. We confirm that the manuscript has been read and approved by all named authors.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article: This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work.

Declaration of Conflicting Interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Data Availability Statement

The datasets generated during and/or analysed during the current study are available from the corresponding author on reasonable request.*

CrediT Authorship Contribution Statement

Conceptualization: ME, HY, MÜU, AC, ÖG, CY. Methodology: ME, HY, MÜU, AC, ÖG, CY. Formal analysis and investigation: ME, HY, FY, AA, AB, ŞK, MC, EB, TKU, AEA, MÜU, AC, ÖG, CY. Writing – Original Draft Preparation: ME, HY, FY, AA, AB, ŞK, MC, EB, TKU, AEA, MÜU, AC, ÖG, CY. Writing – review and editing: ME, HY, FY, AA, AB, ŞK, MC’, EB, TKU, AEA, MÜU, AC, ÖG, CY. Funding acquisition: ME, HY, FY, AA, AB, ŞK, MC, EB, TKU, AEA, MÜU, AC, ÖG, CY. Resources: ME, HY, FY, AA, AB, ŞK, MC, EB, TKU, AEA, MÜU, AC, ÖG, CY. Supervision: ME, HY, MÜU, AC, ÖG, CY.

Declaration

A portion of the data included in this manuscript was presented as an oral presentation at the 24th National Surgical Congress (Antalya, Turkey, April 8–12, 2026).

Declaration of Generative AI and AI-Assisted Technologies in the Writing Process

The initial draft of the manuscript was prepared in Turkish and translated into English using DeepL (deepl.com). AI-assisted language tools, including Grammarly (grammarly.com), Trinka (trinka.ai), and ChatGPT (), were used solely to improve grammar, clarity, and readability. The authors reviewed and edited the manuscript and take full responsibility for the content of the article.

Appendix

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Clinicopathological Features and Prognostic Factors of Gastroenteropancreatic Neuroendocrine Tumors: A Single-Center Experience

Abstract

Introduction

Methods

Results

Conclusion

Keywords

Introduction

Methods

Statistical Analysis

Results

Discussion

Conclusion

Footnotes

ORCID iDs

Ethical Considerations

Author Contributions

Funding

Declaration of Conflicting Interests

Data Availability Statement

CrediT Authorship Contribution Statement

Declaration

Declaration of Generative AI and AI-Assisted Technologies in the Writing Process

Appendix

References