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Annals of Surgical Oncology 9:35-40 (2002)
© 2002 Society of Surgical Oncology

ORIGINAL ARTICLES

Solid-Pseudopapillary Tumor of the Pancreas: A Surgical Enigma?

Robert C. G. Martin, MD, David S. Klimstra, MD, Murray F. Brennan, MD and Kevin C. Conlon, MD

From the Gastric and Mixed Tumor Service, Department of Surgery (RCGM, MFB, KCC), and the Department of Pathology (DSK), Memorial Sloan-Kettering Cancer Center, New York, New York.

Correspondence: Address correspondence and reprint requests to: Kevin C. Conlon, MD, Memorial Sloan-Kettering Cancer Center, Department of Surgery, 1275 York Ave., New York, NY 10021; Fax: 212-717-3097; E-mail: conlonk{at}mskcc.org


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSION
 REFERENCES
 
Background: Solid-pseudopapillary tumors (SPTs) of the pancreas have been reported as rare lesions with "low malignant potential" occurring mainly in young women. This study was designed to define the clinicopathological characteristics and the effect of surgical intervention.

Methods: A retrospective review from January 1985 to July 2000 was performed. Clinicopathological, operative, and survival data were obtained. The Kaplan-Meier method and {chi}2 analysis were performed. All cases were re-reviewed by a senior pathologist.

Results: During this time, 24 patients were diagnosed as having SPTs (0.9%). Twenty females and four males were identified, with a median age of 39 years (range, 12–79). The median size of the lesions was 8.0 cm (range, 1–20). Two patients’ tumors were found to be unresectable at initial presentation because of vascular invasion; both patients have remained alive with disease, one for 13 years and the other 1 year. At a median follow-up of 8 years, one recurrence occurred in 17 patients who underwent complete resection. Microscopic margin positive (P = .26), invasion of surrounding structures (P = .51), and size >5 cm (P = .20) were not significant predictors of survival. Four patients presented with synchronous liver metastasis and underwent resection of the primary tumor and the liver metastasis, with one patient dying of progression of metastatic disease at 8 months, another alive with recurrence in the liver at 6 years, and the last two alive without evidence of disease at 1 month and 11 years.

Conclusions: SPT occurs predominantly in women (82%), although it can occur in men; all age groups are affected. Complete resection is associated with long-term survival even in the presence of metastatic disease.

Key Words: Solid-pseudopapillary tumor • Peripancreatic malignancy • Liver metastasis • Tumor resection


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 CONCLUSION
 REFERENCES
 
Solid-pseudopapillary tumors (SPTs) of the pancreas were first described by Frantz in 1959.1 They are considered a rare pathologic entity with low malignant potential,2 affecting primarily young women.3

Recently there has been a steady increase in the number of SPTs of the pancreas, with more than two thirds of the total cases described in the last 10 years. Despite the increase in recognition, the pathogenesis and apparent therapeutic algorithm remain unclear. This study was designed to examine the clinicopathological characteristics of the disease and to define the effect of surgical intervention by examining a single institution’s experience.


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 CONCLUSION
 REFERENCES
 
A review of the Memorial Sloan-Kettering Cancer Center Department of Surgery’s prospective pancreatic database from January 1, 1985, to July 31, 2000, was performed. Patients admitted to our institution with a diagnosis of SPT of the pancreas were identified. Clinicopathological, operative, and survival data were obtained. The Kaplan-Meier method and {chi}2 analysis were performed. All cases were re-reviewed by a senior pathologist (D.S.K.).


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 CONCLUSION
 REFERENCES
 
During the time this study reviewed, 2486 patients with peripancreatic malignancy were admitted to our institution, with 24 diagnosed as having SPTs (.9%). There were 20 females and 4 males with a median age of 39 years (range, 12–79). The median size of the lesions was 8.0 cm (range, 1–20). Eight patients had their primary tumors within the head, 6 in the body, and 10 in the tail of the gland. The predominant presenting symptom was abdominal pain (58%); seven patients (29%) were asymptomatic

A total of 18 patients presented with local disease and underwent resection. Eleven patients underwent a distal pancreatectomy; seven patients underwent pancreaticoduodenectomy for treatment of their primary disease. One of these patients was found to have a single focus of metastatic disease in a single lymph node after complete resection. This patient’s disease recurred 1 year after resection, and the patient died of systemic recurrence.

At a median follow-up of 8 years, no patient who underwent an R0 resection and was node negative (n = 17) had evidence of recurrence. Microscopic margin positive (P = .26), invasion of surrounding structures (P = .51), and size >5 cm (P = .20) were not significant predictors of survival in this group, although the numbers are very small.

Four patients presented with synchronous liver metastasis, and all four underwent resection of both the primary lesion and the liver metastasis. Of these four patients with liver involvement, one patient died of progression of metastatic disease at 8 months, another was alive with recurrence in the liver at 6 years, and two were alive without evidence of disease at 6 months and 11 years. Two patients were found to have unresectable disease at initial presentation because of vascular invasion, and both patients have remained alive with disease: one for 13 years and the other for 1 year.

Tumors were generally large, varied from tan to yellow, and showed irregular cystic cavities lined by soft, friable tissue. Foci of hemorrhage were common. Some examples also demonstrated firm, fibrotic regions within the tumor. Most cases appeared to be grossly well circumscribed or even partially encapsulated.

The microscopic appearance of all the cases demonstrated the characteristic microscopic features of SPT. The solid areas were composed of monotonous polygonal epithelioid cells, often with minimal intervening stroma, accompanied by innumerable capillary-sized vessels (Fig. 1A). Some areas showed more extensive stromal fibrosis, with round aggregates of perivascular hyalinized stroma imparting a cylindromatous appearance. In the pseudopapillary regions, the cells located away from the small vessels appeared to have dropped away, leaving an irregular cuff of cells surrounding each vascular core (Fig. 1B). There was evidence of cellular degeneration, including aggregates of foamy histiocytes, cholesterol clefts, and cytoplasmic vacuolization. Clusters of cells demonstrated large eosinophilic cytoplasmic globules. The nuclei were generally uniform and round to oval, with longitudinal grooves. Despite the apparent gross circumscription, the microscopic interface between the tumors and the adjacent pancreas commonly showed an infiltrative growth pattern, with islands of nonneoplastic pancreatic parenchyma entrapped within the tumor and nests of tumor cells extending into the adjacent pancreas.



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  		FIG. 1 Histologically (A), solid-pseudopapillary tumors exhibit solid, cellular areas that lack gland formation or other specific architectural features (lower left). Characteristically pseudopapillary formations are formed when the cells located distant from the rich capillary network degenerate. The resulting pseudopapillae (arrows) consist of irregular cuffs of cells clinging to the central fibrovascular cores. At high power (B), the polygonal tumor cells are relatively uniform and exhibit round to oval nuclei with nuclear grooves. Clusters of cells contain large eosinophilic globules (arrows).

 
Two of the cases showed unusual histological features in some regions, in addition to exhibiting the typical morphology described previously. In these cases, there were large regions demonstrating a diffuse, sheetlike growth pattern (Fig. 2A). The tumor cells in these regions showed increased nuclear pleomorphism (a higher nucleus to cytoplasm ratio) when the miotic rate was increased (up to 20 mitoses per 10 high-power microscopic fields). In addition, both cases exhibited some spindling of the tumor cells (Fig. 2B). In fact, in one of these cases a discrete 1.0-cm focus in the center of the tumor was composed of a highly pleomorphic spindle cell population that showed anaplastic tumor giant cells and atypical mitotic figures; this focus had the appearance of sarcomatoid carcinoma. One of these two cases also exhibited a lymph node metastasis, a finding not encountered in any of the other cases under study.



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  		FIG. 2 Two cases exhibited a more diffuse, sheetlike arrangement of tumor cells (A), with relatively few pseudopapillae. At high power (B) the tumor cells have increased nuclear atypia, a high nucleus to cytoplasm ratio, and readily identifiable mitotic figures (arrows). Some of the cells are spindle shaped.

 
Although the diagnosis was based largely on the presence of typical histological features, the immunohistochemical staining performed on these cases displayed a consistent pattern of reactivity for vimentin and {alpha}1-antitrypsin, with inconsistent, generally focal positivity for keratin. Stains for the pancreatic enzymes trypsin and chymotrypsin were consistently negative, as was the specific endocrine marker chromogranin. Some cases did display focal positivity for synaptophysin and for the less specific marker neuron-specific enolase.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
CONCLUSION
 REFERENCES
 
SPT has been described by many other terms, such as papillary epithelial neoplasm, solid and cystic acinar cell tumor, papillary cystic neoplasm, papillary cystic carcinoma, solid and cystic tumor, low-grade papillary tumor, and Frantz’s tumor. SPT has also been misdiagnosed as adenocarcinoma, islet cell tumors, cystadenomas, papillary cystadenocarcinoma, or cystadenocarcinoma.

A total of 450 cases of SPT of the pancreas have been reported in the literature since it was first described in 1959.1,4–15 SPT of the pancreas is a rare tumor and represents <1.0% of all pancreatic admissions at Memorial Sloan-Kettering Cancer Center. There has been an increasing incidence of this entity in recent years, both in reported cases and in our institution (Fig. 3). A possible explanation is a greater awareness of this disease, as well as a better understanding of pancreatic pathology with the 1996 new classifications of pancreatic neoplasms from the World Health Organization.16 Our own experience has led to a greater awareness of the pathologic characteristics and the radiographical and clinical presentation and has led to an increase in diagnosis, as well as an improved understanding of the natural history of these lesions.



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  		FIG. 3 Incidence of pseudopapillary tumors of the pancreas. (A) Total reported cases of solid-pseudopapillary tumors of the pancreas; (B) Memorial Sloan-Kettering Cancer Center experience with solid-pseudopapillary tumors of the pancreas.

 
The majority of SPTs of the pancreas have been diagnosed in young women. However, this series has demonstrated the incidence of male patients diagnosed with this disease. A majority of reports have found the greatest incidence of SPT of the pancreas in the third decade of life; however, our patients presented with a median age of 39 years, which is significantly older than in the two large single institutional series and in the total number of cases reported (median age of 26 years).6,10,17 Our series found only seven patients who were under the age of 25 years, of whom five were female.

Almost all of the patients in this series presented with vague mild abdominal pain or early satiety. Symptoms, when they occur, are often vague and nonspecific, leading to a delay in diagnosis. As a result of these subtle symptoms, tumor presentation can be quite large, as demonstrated in our experience. Size of the lesion is not a predictor of unresectability, as seen in this series and in others, with lesions 20 to 30 cm in size still being resectable.11,18,19 These lesions rarely invade contiguous structures or occlude the bile ducts. Vascular invasion, although uncommon, does occur, as evidenced by our two patients who presented with superior mesenteric encasement. Reports have demonstrated resectability and long-term survival with isolated portal vein and arterial resection and reconstruction.

The pathologic diagnosis of SPT is based on the presence of characteristic light microscopic features. Solid areas alternating with pseudopapillary formations; evidence of cellular degeneration, including cholesterol clefts and aggregates of foamy histiocytes; nuclear grooves; and aggregates of hyaline cytoplasmic globules are found, at least focally, in every case. The line of cellular differentiation reflected in SPTs remains unclear, so immunohistochemical staining for specific cell lineage markers is of marginal utility in proving the diagnosis of SPT. Markers of acinar differentiation (the pancreatic enzymes trypsin and chymotrypsin) are consistently negative, as are glycoprotein markers of ductal differentiation. Some cases do express the neuroendocrine marker synaptophysin, although the most specific marker of neuroendocrine differentiation, chromogranin, is always negative. Despite the lack of specific lines of differentiation, SPT does display a characteristic immunophenotype. Vimentin is consistently expressed, and the hyaline cytoplasmic globules contain {alpha}1-antitrypsin. In many examples, keratins are not expressed or are found only focally. Thus, the staining pattern of most examples of SPT is distinctive and differs from that of other primary pancreatic tumors that could be considered the differential diagnosis, such as pancreatic endocrine neoplasms and acinar cell carcinomas.20

In most studies of the clinical outcome of SPTs, no pathologic factors predictive of prognosis have been identified, in part because of the favorable prognosis. In fact, the occurrence of long-term survival in the presence of stable metastatic disease4 and the rarity of death from this tumor make it difficult to identify any clinicopathological features predictive of survival. In the largest clinicopathological study to date (published only in abstract form), pathologic factors including mitotic rate, nuclear pleomorphism, and vascular invasion were not found to correlate with prognosis.21 It is of interest that two patients in this study died of tumor, both within 1 year of diagnosis. In both of these tumors, the histological appearance was somewhat unusual, with large areas exhibiting a more diffuse, sheetlike growth pattern, increased nuclear pleomorphism, and a markedly increased mitotic rate. One of these tumors contained a focus of sarcomatoid carcinoma, and the other exhibited lymph node metastasis, both exceptional (if not singular) findings in this neoplasm. The fact that both of these patients died of progressive disease raises the possibility that these histological findings may allow identification of a variant of SPT associated with aggressive behavior, although definitive conclusions cannot be drawn on the basis of these small numbers. Attention to these histological features in the future may allow a more specific statement to be made regarding their prospective prognostic significance.

Metastatic disease does occur with SPTs, with 20 previously reported cases.4,17–19,22–33 The most common site of distant disease is the liver; very rare cases of lymph node (n = 5) and peritoneal spread (n = 4) have been reported. Disseminated disease is also not a negative predictor of survival. Long-term survival, 7 to 10 years, has been reported in patients undergoing complete resection, but it is more important to note that it has also been reported in patients with residual disease.11,17 In this series, two patients with liver metastasis had significant overall survival, with one alive at 11 years and the other alive with liver recurrence at 4 years.

Experience with adjuvant therapy has been used only in a small number of patients because the resectability rate for SPT of the pancreas is so high. Many different regimens of chemotherapy have been used without any demonstration of response. One patient in this series was treated with complete cycles of 5-fluorouracil, doxorubicin, and streptozocin and interferon, cisplatin, and topotecan without any response to the primary lesion. Radiotherapy has been used infrequently. Only one case report indicates significant success in a locally advanced lesion involving the porta hepatis; it responded to 4000 cGy over 6 weeks with a 3-year follow-up.13 Other reports have also looked at estrogen receptor status and have found no indication that overexpression exists in these lesions.10

Recurrence of SPT of the pancreas has not been reported with complete resection of local disease. Neither local, nor vascular, nor perineural invasion has been a factor to predict recurrence or overall survival. This series did not demonstrate any factors significant for overall survival.


   CONCLUSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSION
REFERENCES
 
We believe that SPT of the pancreas should be treated aggressively, with attempts made for complete resection, even if this requires metastasectomy. Long-term survival can be achieved with an aggressive approach to both the primary lesion and to the synchronous or metachronous metastatic lesion, predominantly found in the liver.


   Footnotes
 
Presented at the 54th Annual Cancer Symposium of the Society of Surgical Oncology, Washington, DC, March 15–18, 2001.

Received for publication February 27, 2001. Accepted for publication August 29, 2001.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSION
 REFERENCES
 

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