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  Table of Contents    
Year : 2015  |  Volume : 58  |  Issue : 2  |  Page : 163-169
Solid-pseudopapillary neoplasm of the pancreas: A clinicopathological and immunohistochemical study of 33 cases from a single institution in Southern India

1 Department of Pathology, Nizam's Institute of Medical Sciences, Hyderabad, Telangana, India
2 Department of Surgical Gastroenterology, Nizam's Institute of Medical Sciences, Hyderabad, Telangana, India
3 Department of Surgical Gastroenterology, Nizam's Institute of Medical Sciences, Hyderabad, Telangana; Department of Surgical Gastroenterology, KIMS Hospital, Hyderabad, Telangana, India

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Date of Web Publication17-Apr-2015


Background: The clinicopathological and immunohistochemical data of solid-pseudopapillary neoplasm (SPN) from India are limited. Our objectives were to evaluate various histopathological parameters and immunomarkers to elucidate the best possible immunomarker combination that can accurately diagnose these tumors. Materials and Methods: Clinicopathological features of 33 consecutive cases of SPN were retrospectively analyzed. Immunohistochemistry (IHC) was performed on a tissue microarray of 31 of these cases with antibodies to pan-cytokeratin (CK), vimentin, CD 10, E-cadherin, β-catenin, estrogen receptor (ER), progesterone receptor (PR), chromogranin. Results: Totally, 32 of 33 patients were females with a mean age of 26 years (range 12-62 years). Majority presented with abdominal pain (93.93%) and/or abdominal mass (48.48%). Location in pancreas included tail (14), head (7), body and tail (6), body (5) and neck (1). The mean diameter of the tumor was 8.6 cm (range 0.5-16 cm). Surgical exploration was done in all cases. On IHC, tumor cells were consistently positive for vimentin and negative for chromogranin (100%). CK was positive in 12 cases (38.7%), CD 10 showed perinuclear dot positivity in 14 (45.16%) cases and cytoplasmic positivity in 05 (16.12%) cases. All cases showed loss of membranous staining for both β-catenin and E-cadherin with nuclear positivity in 90.32% and 70.16% cases, respectively. PR was positive in 20 (64.51%) cases, while all of them were negative for ER. Conclusion: Solid-pseudopapillary neoplasm is a tumor commonly affecting young females. Loss of membrane expression of β-catenin and E-cadherin with nuclear positivity can be used confirm the diagnosis of SPN.

Keywords: Immunohistochemistry, pancreas, pathology, solid-pseudopapillary neoplasm

How to cite this article:
Uppin SG, Hui M, Thumma V, Challa S, Uppin MS, Bheerappa N, Sastry RA, Paul TR, Prayaga AK. Solid-pseudopapillary neoplasm of the pancreas: A clinicopathological and immunohistochemical study of 33 cases from a single institution in Southern India. Indian J Pathol Microbiol 2015;58:163-9

How to cite this URL:
Uppin SG, Hui M, Thumma V, Challa S, Uppin MS, Bheerappa N, Sastry RA, Paul TR, Prayaga AK. Solid-pseudopapillary neoplasm of the pancreas: A clinicopathological and immunohistochemical study of 33 cases from a single institution in Southern India. Indian J Pathol Microbiol [serial online] 2015 [cited 2023 Sep 30];58:163-9. Available from:

   Introduction Top

Solid-pseudopapillary neoplasm (SPN) of the pancreas is a rare tumor and is considered to be a low-grade malignant neoplasm. [1] It was first described by Frantz Virginia in 1959 as "papillary cystic tumor of the pancreas" in the Armed Forces Institute of Pathology band on tumors of the pancreas. [2] It was incorporated by World Health Organization in 1996 as "solid pseudopapillary tumor" in the histologic classification of exocrine tumor of the pancreas. [3] The term SPN gained wide acceptance and is now an internationally accepted entity. The typical histological features have been described well in literature. It is sometimes difficult to differentiate it from the other pancreatic neoplasms like ductal adenocarcinoma and pancreatic neuroendocrine tumor (NET) solely based on histology. There are many large series of SPN in world literature, and these are reported mainly from USA, Europe, China, and Japan. [4],[5] To the best of our knowledge, this is the largest series of SPN from India. Till now, the only large series from India was of 14 cases by Patil et al. In their study, they have focused on clinicopathological and treatment outcome of the tumors. [6] In the present study, we have evaluated the various histopathological parameters and their frequency of occurrence. In addition, we have analyzed a wide a panel of immunomarkers by tissue microarray (TMA) methodology to elucidate the best possible immunomarker combination that can accurately diagnose these tumors and differentiate it from other pancreatic neoplasms.

   Materials and Methods Top

Thirty-three consecutive cases of SPN of pancreas diagnosed at Department of Pathology at Nizam's Institute of Medical Sciences over a period of 20 years from 1993 to 2013 were retrospectively analyzed. The demographic data, clinical details, radiological features, and laboratory investigations were retrieved from the medical records. The gross features including location, size, color, consistency, and infiltration into the adjacent areas as well as necrosis, hemorrhage, and cystic change on cut section were noted. The hematoxylin and eosin (H and E) stained sections of all the cases were reviewed by two pathologists to confirm the diagnosis. The histomorphological features analyzed include cellular arrangement, cell morphology, nuclear atypia, nuclear grooves, eosinophilic hyaline globules, foamy histiocytes, hyalinization, calcification, giant cells, and inflammatory infiltrate. Immunohistochemistry (IHC) was done on TMA prepared from 31 of these cases. In the remaining two cases, paraffin blocks were not available for array preparation and IHC.

Tissue microarray preparation

The original H and E sections of the tumor were reviewed; representative areas were identified and marked on the corresponding tissue blocks. Care was taken to avoid the area with necrosis and or hemorrhage. The tissue cores were extracted from the marked area and transferred into corresponding tissue block. Marked tissues were extracted from the donor block using Quick-Ray needle with 5 mm tip. Two cores were taken per case subject to availability of material. Tissue cores were delivered into corresponding holes of the recipient block. Recipient block was put in embedding mold with cutting section faced down and incubated at 60°C for 30 min. Then, recipient block was embedded; sections were cut at 4 µm thickness and taken on to charged slides for H and E and IHC studies.

Immunohistochemistry technique

The IHC was performed by semi-automated immunostainer (i6000, Bio Genex) using poly horseradish peroxidase (HRP) technique. To fix, the sections were kept at 60°c for 30 min. Dewaxing was done in three changes of xylene followed by hydration in graded alcohol and water. Antigen retrieval was done in citrate buffer at pH 6.0 using a pressure cooker. After cooling to room temperature, sections were washed with three changes of distilled water replacing the citrate buffer gradually. Then the slides were rinsed in phosphate buffer saline thrice for 5 min each followed by immersion in 3% methanol H 2 O 2 for 10 min to block endogenous peroxidase activity and treated with power block for 10 min to inhibit binding to nonspecific sites. Sections were incubated with primary antibody for 90 min, then secondary antibody (super-enhancer) for 20 min and HRP-polymer for 30 min. In between each of these above steps, two rinses of Phosphate Buffered Saline for 5 min each were applied. The antigen-antibody complex was visualized using diaminobenzidine as chromogen for 7 min. Sections were counterstained with Harris' hematoxylin for 1 min. Then they were dehydrated through alcohol, cleared in xylene and mounted in DPX. The IHC markers (primary antibodies) used included vimentin (clone; V9), pan cytokeratin (CK) (clone; AE1 and AE3), β-catenin (clone; E247), E-cadherin (clone; 36), CD10 (clone; 56c6), estrogen receptor (ER) (clone; ID5), progesterone receptor (PR) (clone; PR88) and chromogranin (clone; LK2H1). All the antibodies were ready to use, mouse monoclonal antibodies supplied by Bio Genex, CA.

   Results Top

There were 33 patients diagnosed with SPN of pancreas during the study period. There was a striking female preponderance with 32 females and 1 male. The age of the patients ranged from 12 to 62 years (mean 26.6 years). Majority of the patients (27 cases, 81.82%) were <30 years of age. The duration of clinical symptoms ranged from 3 days to 4 years. The only male patient was asymptomatic, and the tumor was detected incidentally on routine imaging done for an unrelated cause. The most common clinical features were abdominal discomfort/pain (93.93%) and palpable abdominal mass (48.48%). The location of the tumor in the pancreas included tail (14 cases), head (7 cases), body and tail (6 cases) and body (5 cases). The tumor was located in the neck of the pancreas in one case.


The patients underwent various radiological investigations including ultrasonography (USG), computed tomography (CT), and magnetic resonance imaging (MRI). The diagnosis was suggested on imaging in 23 cases. Rest of the cases were diagnosed as cystic neoplasm (6 cases), NET (2 cases), and carcinoma of tail of pancreas (2 cases).

Fine-needle aspiration cytology

The preoperative fine-needle aspiration cytology (FNAC) was performed in only 1 case and was diagnosed as papillary neoplasm.

Surgical treatment

Surgical exploration was done in all the cases. For the tumors primarily located in head or neck of the pancreas, pancreaticoduodenectomy (7 cases, 21.21%) was done and those located predominantly in body or tail, underwent distal pancreatectomy with or without splenectomy (20 cases, 60.61%). Central pancreatectomy was done in 2 cases located in the body of the pancreas. Subtotal resection and partial resection was done in 1 case each for pancreatic tail tumors. Debulking of the tumor was done in one case where the tumor was located in the pancreatic tail with retroperitoneal extension and laparoscopic biopsy without resection was done for one tumor located in the head of the pancreas.


Grossly, the tumors were predominantly encapsulated and globular. The mean diameter of the tumor was 8.6 cm (range 0.5-16 cm). Cut section was heterogeneous with solid and cystic component. The cystic component showed hemorrhage and reddish brown necrotic material. Five tumors showed extensive necrosis and cystic degeneration. The gross and histomorphological features are summarized in [Table 1].
Table 1: Gross and histomorphological features of solid pseudopapillary neoplasm of the pancreas (n = 33)

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Microscopic findings

Though the majority of the tumors had mixed solid and pseudo papillary arrangement on the histomorphology, 8 cases (24.24%) had a predominant solid component simulating NETs of the pancreas [Figure 1]a-c. The tumor cells were poorly cohesive uniform polyhedral arranged around delicate fibrovascular core. Clear cell change and oncocytic change were observed in 7 (21.21%) and 8 cases (24.24%), respectively. It was also observed that the tumors which had predominantly oncocytic cells had plenty of eosinophilic hyaline globules. In fact, the oncocytic appearance was due to intracellular accumulation of hyaline globules [Figure 1]d-g. In one case where the tumor was located in the head of the pancreas, the cells had eccentrically located nucleus with clear cytoplasm simulating signet ring cells [Figure 1]h. On frozen section, this was mistaken as signet ring cell carcinoma. The characteristic features like nuclear grooves were seen in almost all the cases [Figure 1]i. The other features included cholesterol clefts (12 cases, 36.36%), calcification (6 cases, 18.18%), ossification (2 cases, 6.06%), giant cells (6 cases, 18.18%), foamy histiocytes (12 cases, 36.36%) and dense inflammatory infiltrate especially eosinophils (4 cases, 12.12%) [Figure 2]a-f. Stromal changes such as hyalinization and myxoid change in the core of the pseudopapillae were also observed in 7 cases and 11 cases, respectively [Figure 2]g. Infiltration into the adjacent pancreas was noted in 4 (12.12%) cases [Figure 2]h. One of the cases showed bizarre hyperchromatic nuclei and multinucleated giant cells [Figure 2]i.
Figure 1: (a) Encapsulated tumor with adjacent normal pancreas (×40), (b) Pseudopapillary (×100) and (c) Solid pattern of arrangement of tumor cells (×100), (d) Clear cell change (×100), (e) Oncocytic change (×100), (f) Oncocytic cell with cytoplasm packed with hyaline globules; at places there is disruption of cytoplasm with extracellular release of hyaline globules (×400), (g) PAS with diastase stain showing hyaline globules (×400), (h) Signet ring appearance of tumor cells (×100) and (i) Nuclear grooves and indentations (×400)

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Figure 2: (a) Cholesterol clefts with surrounding giant cells (×40), (b) Calcification (×40), (c) Gamna Gandy body like sidero-calcific foci (×40), (d) Ossification (×40), (e) Aggregates of foamy histiocytes (×40), (f) Eosinophilic infiltrate within the fibrotic cyst wall (×100), (g) Myxo hyaline stromal cores of pseudopapillae (×40), (h) Tumor infiltration into adjacent pancreas (×40) and (i) Tumor cells with pleomorphic hyperchromatic nuclei (×100)

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Immunohistochemistry was done in 31/33 cases, and results are summarized in [Table 2]. In the remaining two cases, paraffin blocks were not available for array preparation and IHC study. The tumor cells were consistently positive for vimentin [Figure 3]a and negative for chromogranin in all the cases (100%) [Figure 3]b. Pan CK was positive in 12 cases (38.7%), [Figure 3]c and d CD 10 showed perinuclear dot positivity in 45.16% cases and cytoplasmic positivity in 16.12% cases [Figure 3]e and f. There was a complete loss of membrane expression for β-catenin in all the cases; nuclear positivity of β-catenin was seen in 28 cases of which 4 had cytoplasmic positivity in addition to nuclear positivity. Three cases showed only cytoplasmic staining. [Figure 4]a and b Loss of membrane expression of E-cadherin was seen in all cases with 22 (70.96%) of these showing nuclear positivity. [Figure 4]c and d PR was positive in 20 cases (64.51%) [Figure 4]e whereas ER was negative in all the cases [Figure 4]f.
Figure 3: Immunohistochemistry results show (a) Vimentin positivity (×100) (b) Chromogranin negativity (×100), (c) Tumors cells negative for pan cytokeratin (CK) With positive staining entrapped normal pancreatic acini (×100), (d) Pan CK positivity in tumor cells (×100), tumor cells showing cytoplasmic and perinuclear dot positivity for CD10 (e) (×100); (f) (×400)

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Figure 4: Immunohistochemistry results show (a) Nuclear and (×100) (b) Cytoplasmic staining for b-catenin (×100), (c) Loss of membrane expression of E-cadherin in tumors cells with preserved membranous expression in entrapped normal pancreatic acini (×40), (d) Nuclear positivity for E-cadherin (×100), (e) Positive nuclear staining for progesterone receptor (×100) and (f) Negative staining for estrogen receptor (×100)

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Table 2: Immunohistochemical features of solid pseudopapillary pancreatic neoplasm (n = 31)

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   Discussion Top

Solid-pseudopapillary neoplasm is an uncommon neoplasm of the pancreas and accounts for 0.13-2.7% of all primary pancreatic tumors. [4] Majority of these tumors are seen in young patients with a mean age of 28 years and a female to male ratio of 10:1. [5] The demographic profile in our study was similar to that described in the literature. There are very few reported cases in males. In our series as well there was only a single male patient aged 29 years. Machado et al. have reported greater incidence of SPN in males in comparison to other studies. These tumors in males were generally seen in elderly patients and were more aggressive. [7]

The clinical features are generally nonspecific comprising of abdominal discomfort, pain, and a palpable abdominal lump. Similar findings were noted in the present study. They are often asymptomatic due to slow growth and are detected incidentally on imaging for unrelated diseases or routine investigation as seen in one of the cases in the present series. The tumor size is often quite large at presentation owing to its slow growth and thus delaying early detection. The routine laboratory parameters and tumor markers are generally unremarkable. Advances in imaging modalities have led to increase in number of cases diagnosed in recent years. It can be diagnosed preoperatively by USG, CT scan, and MRI. Radiography shows well-circumscribed heterogeneous mass comprising of varying degree of solid and cystic components with peripheral capsule and calcification. MRI is superior to CT scan in view of its ability to detect marked degenerative changes such as cystic change, hemorrhage, and integrity of the capsule. [8] The ductal carcinomas in comparison are infiltrative with poorly defined margins and invade into the surrounding tissues. In an appropriate clinical setting, radiology helps in preoperative diagnosis which may obviate the need of a biopsy before planning surgical resection. In our study 23 (69.69%) cases were accurately diagnosed on imaging. Machado et al. in their case series found that 80% of cases have typical features on imageological study. [7] Ultrasound-guided FNAC may also be used as an alternative modality to distinguish SPN from other pancreatic tumors. The pseudopapillary arrangement of bland appearing tumor cells is characteristically seen on aspirations smear. The presence of large clear cytoplasmic vacuoles has been recently emphasized as a distinctive finding on cytology. [9] Preoperative FNAC was done in a single case, and it was broadly categorized as papillary neoplasm. However, FNAC is not recommended due to the possible spread of tumor cells along the needle tract. [10] Since the prognosis is good after an adequate resection; accurate preoperative diagnosis helps in surgical planning.

The most common sites of localization of these tumors are pancreatic tail followed by head and body. [11] The present study also showed similar localization of the tumors. Rare cases have been reported outside pancreas. [12] In our study, only one case which was located in the tail of pancreas had a retroperitoneal extension and a debulking surgery was done in this case.

As the name indicates the tumors have varying solid and cystic components. They range in size from 0.5 cm to 34.5 cm with a mean diameter of 6.8 cm. [13] The mean diameter of the tumor was slightly higher (8.6 cm) in the present study. The smaller tumors are predominantly solid but as they enlarge these tumors show fibrous pseudo capsule with extensive friable areas comprising of hemorrhage and necrosis simulating an appearance of pancreatic pseudocyst. In the present study, there were five such cases which were entirely cystic filled with necrotic and hemorrhagic material. Extensive sampling was done in these cases to demonstrate small viable foci of tumor.

The typical histologic features of conventional SPN have been described well in literature. Microscopically these tumors have solid and cystic areas with pseudopapillary growth pattern. As enumerated in literature periodic acid-schiff positive diastase resistant eosinophilic hyaline globules, uniform nuclei with grooves were frequently encountered in our study as well. Interestingly we noted that the cases showing large number of oncocytic cells had numerous eosinophilic hyaline globules. In fact, the oncocytic appearance was due to the conglomeration of numerous eosinophilic hyaline globules intra-cellularly. Based on our observation, we hypothesize that these globules are formed intracellularly and are later released outside following rupture of the cell membrane. Though these globules are classically associated with SPN, they are also reported to occur in 5% of pancreatic NETs. [14]

A clear cell variant of SPN has been described where the tumor cells have clear cytoplasm. This has been attributed to distended mitochondria and endoplasmic reticulum. This creates a diagnostic challenge in distinguishing it from other clear cell tumors of the pancreas such as metastatic renal cell carcinoma, ectopic adrenocortical nodules, clear-cell variant of pancreatic endocrine neoplasm, and ductal adenocarcinoma. IHC helpful in making a definitive diagnosis in such cases. [15] SPN which is characterized by vacuolated cytoplasm and signet ring morphology has also been described. This can be mistaken for signet ring cell adenocarcinoma as it happened in one of our case on initial frozen section. This was later correctly diagnosed on the routine sections with the help of IHC. Zhao et al., similarly misdiagnosed a case of clear cell variant as signet ring cell carcinoma on FNAC, which was also confirmed later with imunocytochemistry on the cell block and resected specimen. They suggested that an important clue to histological diagnosis of such cases of SPN on H and E sections is the orientation of the vacuolated cells away from the vascular core and that ischemia may play an important role in vacuolization. [16]

The other histological features such as foamy macrophages, hemorrhage, cholesterol clefts, and giant cells were commonly seen in large tumors ranging from 7 cm to 14 cm. Another interesting finding that we noted in largely necrotic tumor was extensive eosinophilic infiltrate in the dense fibrous stroma bordering these necrotic areas. This could represent inflammatory response to necrotic tumor tissue. Stromal degeneration such as myxoid change, calcification, and ossification were also noted. One of the cases showed bizarre cells with nuclear atypia comprising of >20% of the total tumor area. A diagnosis of malignancy is not warranted in such cases as nuclear atypia is not a criterion for malignancy in this tumor subtype. This may be a problem in evaluating cytology specimens and frozen section. Pleomorphic SPN has been described as SPN in which 20% of the total area shows significant nuclear pleomorphism. Nuclear pleomorphism is defined as more than fourfold variation in nuclear size. However, Kim et al. in their study on 18 pleomorphic SPN have found no difference in their behavior when compared to conventional SPN. [17]

Though these tumors are predominantly well-encapsulated, four cases had infiltrative margins. [1] On follow-up, these patients did not show any difference behavior of these tumors in comparison with others. Venous or perineural invasion, which are considered as definite criteria of malignancy were not demonstrated in any of the cases in the present series. It is important to differentiate these tumors from the much more common ductal adenocarcinomas which have an aggressive clinical course. They can be distinguished based on histological features like haphazardly arranged glands, nuclear atypia, and dense desmoplastic stroma.

In the present study, the IHC was performed on TMA as it facilitates simultaneous analysis of large number of specimens with decreased assay volume, time, and cost. To minimize problems pertaining to intratumoral heterogeneity, we have taken two cores of larger size (5 mm) from each case. Immunohistochemically these tumors show diffuse positivity for vimentin and are variably positive for CK. These results were consistent with the findings seen in our study. E-cadherin and β-catenin are the two key components of the Wnt signal transduction pathway and are involved in cellular differentiation and growth. [18] Almost all the cases harbor mutations in the CTNNB1 gene which encodes for the β-catenin protein and is considered to be the major molecular event in the tumorigenesis of SPN. [17] All the cases in our study showed complete loss of membrane expression for β-catenin with nuclear positivity in 28 of these cases. E-cadherin is a transmembrane protein closely related to β-catenin and plays an important role in cell adhesion; loss of membrane expression of E-cadherin explains the dyscohesive nature of these cells as well as cystic change. This pattern of immunoreactivity has been consistently observed in other studies as well. [19] Serra et al. first noted the nuclear expression of E-cadherin protein associated with a concomitant loss of membrane staining. [18] Similar findings were also noted in 22 cases in our study. β-catenin is an integral component of the E-cadherin complexes and the cytoplasmic tail of E-cadherin protein binds to β-catenin that in turn complexes with alpha-catenin to form the E-cadherin-catenin unit and activates transcription in the nucleus. The adjacent pancreatic acinar cells in few of the cores served as internal positive control with prominent membranous staining. The comparative analysis of the immunohistochemical findings of the present study with other studies is given in [Table 3].
Table 3: Comparative analysis of immunohistochemical features of solid pseudopapillary pancreatic neoplasm

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Notohara et al. reported expression of cytoplasmic CD10 positivity with some tumor cells displaying intensified membrane staining in all cases of SPN. [20] Chen et al. reported that the tumor cells of SPN showed strong cell membrane staining for CD10. [21] In contrast, Liu et al. reported a distinct juxtanuclear dot-like pattern in addition to cytoplasmic and membranous CD10 positivity in their study of 3 cases. The reason for this discrepancy was not clear. [22] In our study, 14 cases showed the perinuclear dot-like positivity and 5 cases showed cytoplasmic positivity. Notohara et al. have reported that CD10, CD56, vimentin, synaptophysin, chromogranin, and Pan CK are useful in distinguishing between SPNs and NETs. [20] In our study, all cases showed loss of membrane expression of β-catenin and E-cadherin with nuclear positivity in most; this can be used confirm the diagnosis of SPN. Positivity of CK, E-cadherin with membranous expression of β-catenin and negative chromogranin immunoreactivity supports the findings of adenocarcinoma. Kim et al. suggested that CD10 immunopositivity should be carefully interpreted as pancreatic adenocarcinoma (9.9%), or NET (10.7%) can also stain for CD10. [17] Notohara et al. opined that CD10 may be diagnostically useful only when used in conjunction with other neuroendocrine markers. [20]

Machado et al. reported PR positivity in 80% of their cases with negative ER staining in all. [7] Though the percentage of PR positive cases in the present series was slightly lower (64.5% vs. 80%) than that reported by Machado et al., all our cases were similarly negative for ER. The frequent expression of PR and a strong predilection for females hints toward a hormone dependency of the tumor. But the tumor in the only male patient in the present study also showed PR positivity. Liu et al. reported PR positivity in 90% of tumor cells in a male patient. [22] However Klφppel et al. showed lack of PR expression in two of their cases in males. [12] Though progesterone is also produced by the adrenal glands and testes, the origin of male SPN might be different from that of females and requires further studies. [22] The lack of ER expression by IHC in most of the studies including ours has been attributed to the type of anti-ER antibodies (specific for ER-a) used in IHC. Recent studies have shown that monoclonal antibodies directed against ER-b shows positivity in SPN. [23]

These tumors are consistently negative for chromogranin which helps to differentiate them from other NETs. In our study also, all the cases were negative for chromogranin. The other neuroendocrine markers such as neuron-specific enolase and synaptophysin are variably expressed in SPN. However, in our study, we have not included these markers.

   Conclusion Top

It is important to be familiar with the clinicopathological features of SPN to differentiate it from other pancreatic neoplasm. A diagnosis of SPN should be highly suspected in young women with the pancreatic mass comprising of solid and cystic components. The unusual morphological features like signet ring morphology and nuclear pleomorphism should be kept in mind to avoid potential diagnostic pitfalls. Loss of membrane expression of β-catenin and E-cadherin with nuclear positivity can be used confirm the diagnosis of SPN.

   Acknowledgments Top

Authors would like to acknowledge Mr. Madhavan, Mr. Vivekanand, and Mrs. Hema Shukla for their help in performing IHC.[24]

   References Top

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Correspondence Address:
Dr. Shantveer G Uppin
Department of Pathology, Nizam's Institute of Medical Sciences, Punjagutta, Hyderabad - 500 082, Telangana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0377-4929.155305

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

  [Table 1], [Table 2], [Table 3]

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