Solid pseudopapillary neoplasm of the pancreas with postoperative multiple liver metastases in an older woman: a case report

Introduction

An extremely rare tumor entity, solid pseudopapillary neoplasm of the pancreas (SPN) was first proposed by Virginia K. Frantz in 1959, and is also known as Frantz’s tumor (1). In the 2019 World Health Organization (WHO) Classification of Tumours, Digestive System Tumours (5th edition), SPN is recognized as a distinct pancreatic epithelial neoplasm with low-grade malignant potential (2). SPN is a rare neoplasm accounting for less than 2% of exocrine pancreatic tumors (3,4); however, it has attracted increasing attention due to its apparent increase in incidence, which may be attributed to advances in imaging techniques. Currently, the origins of SPN remain largely unclear. Thus, additional information needs to be collected regarding not only its pathogenic mechanisms but also its clinical aspects.

SPN is more common in young females, while male patients tend to be older and present with smaller tumors than female patients (4). The CTNNB1 gene mutation, observed in most patients, is considered a hallmark feature of SPN (5,6). Among common imaging methods and routine laboratory tests, endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) with complementary immunohistochemistry can be used for the preoperative diagnosis of this tumor (7). Nevertheless, in the early stages of SPN, clinical presentations are often non-specific, such as upper abdominal pain and bloating discomfort, and some patients (approximately 35%) are even asymptomatic (4,8). Recently, SPN has been reported in extra-pancreatic locations (e.g., the testis) (9). Accordingly, the accurate diagnosis of this rare disease will benefit from increased clinical experience and comprehensive case information, including clinical, histological, and immunohistochemical (IHC) findings (10).

Early detection and complete surgical resection of the tumor may be the most effective treatment for the prevention of metastasis. A previous study thoroughly reviewed and summarized the common surgical procedures and organ preservation surgeries for SPN. Due to the relatively low-grade malignancy of most SPNs, early detection and treatment can achieve a high survival rate and long life expectancy. However, in the present study, we report a rare SPN case with postoperative metastases and a poor prognosis. This case may serve as a reference for the diagnosis, long-term surveillance, and post-recurrence management of aggressive SPN, potentially contributing to the prevention and management of malignant postoperative metastases in SPN patients. We present this article in accordance with the CARE reporting checklist (available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-0296/rc).

Case presentation

A 68-year-old female patient, who had her first consultation in February 2017, complained of abdominal pain and vomiting after eating (lasting for more than one month). On examination, the abdomen was soft and non-tender; however, rebound pain or a positive Murphy’s sign was observed. Some 10 years ago, the patient had been diagnosed with coronary heart disease. However, she had no history of fever, diarrhea, abdominal distension, weight loss, hepatitis virus infection, diabetes mellitus, or mental disorder. The patient also reported no personal or family history of cancer or related surgeries.

No significant abnormalities were found after laboratory tests, including tumor markers (Table 1). An ultrasound examination from the referring facility showed a hypoechoic, irregular mass originating from the pancreatic tail and adjacent to the splenic hilum. Computed tomography (CT) revealed that the tail of the pancreas was enlarged, and hyperdense plaque was observed. Magnetic resonance imaging (MRI) detected a lesion (44 mm × 25 mm × 33 mm in size), which was considered a neuroendocrine neoplasm, but malignancy could not be excluded (11-13).

Further, there was no evidence of metastases in other organs or lymph node involvement. The patient had no contraindications to surgical treatment. Therefore, the laparoscopic resection of the pancreatic body and tail, as well as the spleen (laparoscopic distal pancreatectomy with splenectomy), was performed after thorough preoperative preparation (no preoperative biopsy was performed). After the operation, the surgical specimen was submitted for histopathological and IHC evaluations (Figure 1, Table 2). Histopathological examination of the resected pancreatic tumor supported the diagnosis of SPN. On hematoxylin and eosin staining, the tumor exhibited a mixture of solid and pseudopapillary structures with delicate fibrovascular cores. The neoplastic cells were relatively uniform and polygonal, with eosinophilic to lightly vacuolated cytoplasm, finely granular chromatin, and inconspicuous nucleoli. Cytologic atypia was not prominent, mitotic figures were rare (<1/10 high-power fields), and no tumor necrosis was identified. The tumor invaded the peripancreatic fat and showed perineural invasion, whereas lymphovascular invasion was not detected. The pancreatic resection margin was negative, and no metastatic involvement was found in the examined lymph node (0/1). The Ki-67 proliferation index was approximately 5%. These findings confirmed the diagnosis of SPN. After the successful R0 resection, no further adjuvant chemotherapy was required. Having a smooth and uneventful postoperative course, the patient was discharged six days later and was followed up regularly.

Figure 1 Histopathological findings of the primary pancreatic tumor (magnification ×200; H&E stained). H&E staining shows tumor cells arranged in nests, cords, and solid sheets. Decreased cellular cohesiveness is observed locally, forming focal cystic spaces. High-power field view demonstrates characteristic pseudopapillary structures where tumor cells are layered around delicate fibrovascular cores. The neoplastic cells are uniform in size, with rich eosinophilic cytoplasm, finely granular chromatin, and inconspicuous nucleoli. H&E, hematoxylin and eosin.

After surgery, the patient underwent regular postoperative follow-up. Imaging surveillance was performed at routine intervals using abdominal CT (Figure 2). On February 13, 2017, the first postoperative unenhanced abdominal CT revealed no definite signs of metastatic lesions (Figure 2A). However, an abdominal MRI performed on October 23, 2020, indicated that the liver size and shape were within the normal range, but multiple mixed cystic-solid metastatic lesions were observed in the liver. These lesions demonstrated low signal intensity on T1-weighted imaging and high signal intensity on coronal T2-weighted imaging. Additionally, the lesions exhibited restricted diffusion with high signal intensity on diffusion-weighted imaging (DWI) and demonstrated rim-like enhancement on contrast-enhanced sequences (Figure 2B-2D). Nevertheless, laboratory tests still revealed no significant abnormalities, including liver and renal function abnormalities, coagulation defects, and tumor marker alterations (Table 1).

Figure 2 Representative imaging findings of postoperative surveillance and liver metastases. (A) First postoperative unenhanced abdominal CT on February 13, 2017, showing no definite metastatic lesion. (B) Coronal T2-weighted MRI on October 23, 2020, demonstrating multiple mixed cystic-solid liver metastases. (C) DWI on October 23, 2020, showing multiple hepatic lesions with high signal intensity. (D) Contrast-enhanced MRI on October 23, 2020, demonstrating rim enhancement of the metastatic lesions. (E,F) Contrast-enhanced abdominal CT on April 22, 2021, showing progression of the hepatic metastatic disease. CT, computed tomography; DWI, diffusion-weighted imaging; MRI, magnetic resonance imaging.

Following multidisciplinary consultation, the liver lesions were considered multiple metastases based on the patient’s clinical history and related examination data. Given the suspicion of hepatic metastasis, an ultrasound-guided percutaneous liver biopsy was conducted to confirm the diagnosis (Table 2). Ultrasound-guided liver biopsy was performed. Histologically, the liver lesion showed tumor cells arranged in nests, cords, solid sheets and pseudopapillary structures with delicate fibrovascular cores, resembling the morphology of the previously resected pancreatic tumor. Decreased cellular cohesiveness was observed away from the vessels, and focal cystic spaces were present. The neoplastic cells were relatively uniform, with eosinophilic cytoplasm and round to oval nuclei with finely granular chromatin and inconspicuous nucleoli. IHC findings were concordant with metastatic SPN, including nuclear β-catenin expression and positive staining for Vimentin. Based on the morphologic and immunophenotypic similarity to the primary pancreatic lesion, the liver lesion was diagnosed as metastatic SPN. A gene mutation analysis of the liver biopsy specimen (Figure 3) revealed a missense mutation (p.S33P) in exon 3 of the CTNNB1 gene, and a tissue abundance of 45.1%. No BRCA1/BRCA2 mutations were detected. KRAS, CDKN2A, TP53, and SMAD4 were not included in the sequencing panel used in this case. Therefore, although the morphologic and immunophenotypic findings strongly supported metastatic SPN rather than pancreatic ductal adenocarcinoma, the absence of these pancreatic ductal adenocarcinoma-related molecular data should be acknowledged as a limitation. She was thus diagnosed with multiple metastases in the liver.

Figure 3 Histopathological and genetic findings of the liver metastasis (magnification ×200; H&E stained). H&E staining of the ultrasound-guided liver biopsy specimen reveals morphological features highly similar to the primary pancreatic tumor. The metastatic tumor cells are also arranged in solid sheets and pseudopapillary structures with delicate fibrovascular cores. The cytological characteristics, including uniform nuclei, fine chromatin, and eosinophilic cytoplasm, are concordant with the primary SPN lesion, confirming the diagnosis of metastatic SPN. H&E, hematoxylin and eosin; SPN, solid pseudopapillary neoplasm of the pancreas.

After recurrence was confirmed by liver biopsy, the patient was re-evaluated for further management. Because multiple liver metastases were present at the time of recurrence, curative-intent hepatic resection was not considered feasible. After multidisciplinary evaluation, liver-directed local treatment was also not prioritized, as the extent of hepatic disease suggested limited benefit from local control alone. Therefore, systemic treatment was initiated with palliative intent.

In the absence of an established standard systemic regimen for metastatic SPN, treatment decisions were individualized. Subsequently, systemic treatment was adopted to control the progression of the postoperative metastases of SPN, based on the willingness and physical condition of the patient. The patients received two cycles of nab-paclitaxel (130 mg/m², intravenously on days 1 and 8) plus S-1 (60 mg orally on days 1-14, every 21 days); unfortunately, the patient’s hepatic metastatic lesions continued to progress, and the result of the efficacy evaluation was disease progression.

To further control the disease progression, a second-line treatment started on January 14, 2021, including gemcitabine (1,000 mg/m² intravenously on day 1) plus capecitabine (1,000 mg/m² orally twice daily on days 1–14, every 21 days). After two cycles of treatment, the CT result suggested that multiple metastatic foci of the liver were further increased, and multiple metastases were observed in the intra-abdominal lymph nodes.

Given the patient’s physical condition and limited ability to tolerate the side effects of chemotherapy, and based on a review of the latest literature, a combination strategy of immune checkpoint inhibitors and targeted therapy was implemented. Anlotinib combined with programmed cell death protein 1 (PD-1) antibody has been shown to contribute to the normalization of tumor vasculature via CD4 T cells, which can remodel the tumor immune microenvironment and improve the suppression of the systemic immune system. Thus, on March 21, 2021, she received a third-line PD-1 antibody therapy combined with a tyrosine kinase inhibitor (TKI) tislelizumab (200 mg intravenously on day 1) plus anlotinib (8 mg orally once daily on days 1–21). However, unfortunately, after two cycles of treatment, the repeated CT suggested disease re-progression. An abdominal contrast-enhanced CT performed on April 22, 2021, revealed further progression of the multiple intrahepatic metastases (Figure 2E,2F). The patient ultimately died of progressive disease. Overall survival was 52 months, calculated from the date of diagnosis/resection of the primary pancreatic tumor to death. Survival after the diagnosis of liver metastases was 8 months. The detailed clinical course, diagnostic timeline, and treatment sequences are summarized in Table 3. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient while she was alive for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

SPN is an uncommon pancreatic neoplasm with generally favorable outcomes after complete surgical resection (14). The present case is notable for four features: older age at presentation, delayed liver recurrence 44 months after R0 resection, persistently normal tumor markers despite progressive metastatic disease, and refractoriness to three lines of systemic therapy (15). These findings suggest that normal laboratory results do not exclude relapse and that long-term radiologic surveillance remains necessary even after apparently curative surgery.

Older age at presentation and delayed postoperative recurrence may indicate biological heterogeneity within SPN (16-18). Although most SPNs follow an indolent course, a subset behaves aggressively, with local recurrence or distant metastasis occurring months to years after curative-intent surgery (19-24).

The mechanisms underlying SPN remain largely unclear. Recently, several hypotheses based on the characteristics of SPN have been proposed to illustrate the etiological factors and development of the disease. Among them, the Wnt/β-catenin signaling pathway has been shown to be significantly associated with SPN occurrence (25). The β-catenin protein encoded by the CTNNB1 gene is an important effector molecule in the Wnt signaling pathway, which has been shown to be involved in the regulation of the cell cycle, metastatic potential, tumorigenicity, and some other processes involved in tumor genesis and development.

Therapeutics have already targeted this pathway in the drug development pipelines (26). The alteration of the Wnt/β-catenin signaling pathway has been demonstrated to promote the occurrence of SPN, and this signaling pathway is most commonly abnormally activated by mutations in exon 3 of the CTNNB1 gene. Hotspot mutations in CTNNB1 can result in the unusual stabilization and nuclear localization of β-catenin; thus, targeted medicines aimed at disrupting β-catenin may exert therapeutic effects in such patients (26). In this rare case, a CTNNB1 mutation and its related characteristics were identified. Further explorations targeting the Wnt/β-catenin signaling pathway are urgently needed to establish a basis for novel treatment strategies. The diagnosis of metastatic SPN in this patient was supported by the characteristic morphology of both the primary tumor and the liver biopsy, including poorly cohesive uniform cells forming solid and pseudopapillary structures around delicate fibrovascular cores, together with concordant immunophenotypic findings such as nuclear β-catenin expression. The CTNNB1 exon 3 mutation identified in the liver metastasis is consistent with the known molecular hallmark of SPN and supports activation of the Wnt/β-catenin pathway. However, because CTNNB1 alterations are common in SPN, this finding alone should not be interpreted as sufficient evidence of aggressive biological behavior.

Routine laboratory tests, including tumor markers, often show no significant abnormalities in patients without complications or other diseases (24). One feature of this case was the persistently normal serum tumor marker profile despite metastatic progression, as well as following the development of metastasis. Further, no obvious abnormality in liver function was observed during the postoperative development of multiple liver metastases. Thus, tumor markers are not recommended for diagnosing or monitoring the occurrence, progression, metastasis, or prognosis of SPN. Due to the limited value of laboratory tests in diagnosing and predicting the prognosis of SPN, imaging is recommended for diagnosis and follow-up.

Currently, imaging examinations play crucial roles in the diagnosis and differential diagnosis of many diseases, including SPN. The most useful and predominant imaging modality is CT, as it can help to evaluate the tumor size, elucidate the mass structure, define the pancreatic anatomy, and detect the presence of local invasion and metastasis (27). In addition, this radiomics tool can improve the diagnostic accuracy of SPN and assist in differentiating between SPNs and pancreatic neuroendocrine tumors, facilitating targeted and appropriate treatment strategies (24).

Fluorodeoxyglucose positron emission tomography (FDG-PET) can be useful in the differential diagnosis of SPN, as it enables the monitoring of FDG uptake in a small-diameter neoplasms (25). However, imaging examinations usually provide limited information, and the definitive diagnosis of SPN is ultimately established through the clinicopathological and IHC analyses of surgical or biopsy specimens (8).

The diagnosis of metastatic SPN in this patient was supported by the characteristic morphology of both the primary tumor and the liver biopsy, including poorly cohesive uniform cells forming solid and pseudopapillary structures around delicate fibrovascular cores, together with concordant immunophenotypic findings such as nuclear β-catenin expression. The CTNNB1 exon 3 mutation identified in the liver metastasis is consistent with the known molecular hallmark of SPN and supports activation of the Wnt/β-catenin pathway. However, because CTNNB1 alterations are common in SPN, this finding alone should not be interpreted as sufficient evidence of aggressive biological behavior.

Management after recurrence was challenging. Because multiple liver metastases were present at the time of relapse, curative-intent hepatic resection was not considered feasible after multidisciplinary evaluation. Liver-directed local treatment was also not prioritized because local control alone was unlikely to provide meaningful benefit in the setting of multifocal hepatic disease. In the absence of a standard systemic regimen for metastatic SPN, treatment was individualized. Nab-paclitaxel plus S-1 was selected as the initial palliative regimen, gemcitabine plus capecitabine was administered after early progression, and tislelizumab plus anlotinib was attempted after failure of cytotoxic therapy and declining tolerance to further chemotherapy. Nevertheless, the disease remained refractory, highlighting the limited and non-standardized evidence supporting systemic therapy in advanced SPN.

This report has several limitations. First, KRAS, CDKN2A, TP53, and SMAD4 were not included in the sequencing panel used in this case; therefore, molecular exclusion of pancreatic ductal adenocarcinoma-related driver alterations was incomplete. Second, although preoperative CT and MRI examinations were performed and are described in the manuscript, the archived original contrast-enhanced imaging files of the primary pancreatic lesion were not retrievable, which precluded a direct side-by-side radiologic comparison with the metastatic liver lesions. Nevertheless, the diagnosis of metastatic SPN was strongly supported by the concordant morphology, immunophenotype, and CTNNB1 mutation detected in the liver metastasis. In summary, SPN is an inexplicable neoplasm characterized by low-grade malignancy, non-specific clinical presentation, a low preoperative diagnostic rate, and a low propensity for recurrence and metastasis. Long-term survival can be achieved following complete surgical resection, even in cases of relapse or metastasis. Multidisciplinary collaborations and investigations are expected to advance the diagnostic and therapeutic management of SPN.

Conclusions

SPN is generally associated with a favorable prognosis; however, rare cases may exhibit aggressive behavior with delayed metastasis. This case highlights that postoperative recurrence can occur even after R0 resection and may not be accompanied by abnormal tumor markers. Comprehensive imaging follow-up is therefore essential. In addition, conventional chemotherapy and immunotherapy may show limited efficacy in aggressive SPN subsets. Further studies focusing on the molecular mechanisms, particularly the Wnt/β-catenin pathway, are warranted to develop effective targeted therapies.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-0296/rc

Peer Review File: Available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-0296/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-0296/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. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient while she was alive for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal. A copy of the written consent is available for review by the editorial office of this journal.

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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(English Language Editor: L. Huleatt)