6 islet-cell tumors of the pancreas

10 ■ APPLIED RADIOLOGY© www.appliedradiology.com November 2009

Although pancreatic islet-celltumors account for only 1% to5% of all pancreatic neoplasms,

they represent an important subset ofpancreatic neoplasms due to their sub-stantially improved prognosis com-pared to pancreatic adenocarcinoma.1,2

Pancreatic islet-cell tumors, alsoreferred to as neuroendocrine tumors,may present with a broad spectrum ofclinical and imaging manifestations,sometimes quite dramatic, dependingon whether lesions are solitary or multi-ple, syndromic or nonsyndromic, inher-ited or sporadic, or benign or malignant.The role of the radiologist in imagingpancreatic islet-cell tumors is to localizethe tumor and evaluate the extent of dis-ease, which in turn helps determinewhether the patient is an operative can-didate and helps guide therapy.

Ninety-five percent of pancreatic islet-cell tumors are solitary and sporadic.Generally, these do not exhibit hormonalhypersecretion (nonsyndromic) and areclinically silent until they grow largeenough to cause symptoms.

On the other hand, hyperfunctioningislet-cell tumors (referred to as syn-dromic islet-cell tumors) manifest muchearlier, and at a much smaller size due tosymptoms caused by hormonal over-secretion. Often these syndromictumors are barely visible by imaging, inspite of a dramatic clinical presentation.These tumors are classified according tothe predominant hormone of oversecre-tion: insulinoma, gastrinoma, vasoac-tive intestinal peptide-secreting tumors(VIPoma), glucagonoma, somatostatin-oma, and growth-hormone-releasingfactor-secreting tumors (GRFomas).

Insulinomas account for 50% of allislet-cell tumors and are the most com-mon islet-cell tumor subtype.6 Themajority of insulinomas (80% to 90%)

are benign, solitary and are <2 cm atpresentation.7 These tumors cause fluc-tuations in serum glucose levels inpatients, with associated morbidityrelated to severe hypoglycemia, occa-sionally leading to multiple seizures.Surgical resection of insulinomas is thetreatment of choice, with symptomspromptly resolving after resection.

Pancreatic islet-cell tumors otherthan insulinomas have a higher malig-nancy rate, approaching 60% to 90%.1

Gastrinomas are the second most com-mon islet-cell tumor, with approxi-mately 25% associated with multipleendocrine neoplasia (MEN-1).4 Resec-tion of gastrinomas is often difficultdue to locally invasive features ormetastatic disease in more than half of

Islet-cell tumors of the pancreas:Spectrum of MDCT findings. A pictorial essay.

David S. Lee, MD, R. Brooke Jeffrey, MD, and Aya Kamaya, MD

Dr. Lee is a Body Imaging Fellow, Dr.Kamaya is an Assistant Professor, andDr. Jeffrey is a Professor and Abdomi-nal Imaging Section Chief, Departmentof Radiology, Stanford University Med-ical Center, Stanford, CA.


patients.1 When a gastrinoma is sus-pected, one should carefully inspectthe “gastrinoma triangle,” an anatomictriangle bounded by the junction of thecystic duct insertion on the commonbile duct, the body of the pancreas, andthe junction of the second and thirdportions of the duodenum (Figure 1).About 85% to 90% of gastrinomas arepresent within the gastrinoma triangle;the search for this tumor should not belimited solely to the pancreas butshould include the boundaries of thisanatomic triangle. Similarly, VIPomas,somatostatinomas, and GRFomas mayalso arise outside of the pancreas.4

Unlike sporadic islet-cell tumors, inher-ited pancreatic islet-cell tumors are usuallymultiple in location and most often related to

ISLET-CELL TUMORS OF THE PANCREAS

FIGURE 1. “Gastrinoma triangle.” The gas-trinoma triangle is an anatomic trianglebounded by the junction of the cystic ductinsertion on the common bile duct, the bodyof the pancreas, and the junction of the sec-ond and third portions of the duodenum.Contents of the gastrinoma triangle arehighlighted in this diagram, whereas regionsoutside of the triangle are darkened. Illustra-tion courtesy of Amy N. Morris.

FIGURE 2. Hepatic metastases. Octreotidescan demonstrates several somatostatin-positive foci in the right-upper abdomen in apatient with history of pancreatic islet-celltumor, which is consistent with hepaticmetastases in distribution and appearance.

FIGURE 3. Ultrasound appearance of pan-creatic islet-cell tumor. Intraoperative ultra-sound image shows well-circumscribedhypoechoic pancreatic islet-cell tumor withhypervascular, predominantly peripheral,vascularity.

FIGURE 4. “Typical” hypervascular pancreatic islet-cell tumor on computed tomography (CT).(A) Typical appearance of well-circumscribed, small, hypervascular, pancreatic-tail, islet-celltumor (insulinoma) on arterial-phase imaging (arrow). (B) Tumor retains contrast on delayedimaging (arrow).

FIGURE 5. (A) The same insulinoma as seen in Figure 4 is shown on magnetic resonance imaging (MRI) with low T1 signal intensity on the pre-contrast image (arrow) and it enhances on T1-weighted (T1W) postcontrast images, approaching signal intensity of surrounding normal pancre-atic parenchyma on arterial-phase images (B, arrow). This tumor is difficult to identify on T2-weighted (T2W) fat-suppressed images (C),however, with only subtle signal abnormality noted (arrow).

A B

A B C



MEN-1. They can also be seen with othersyndromes such as Von Hippel-Lindau,tuberous sclerosis and neurofibromatosis type1.3Whether pancreatic lesions associated withMEN-1 are more likely benign or malignant isstill much debated. Differentiation betweeninherited and sporadic etiologies is importantnot only because of their different imagingpresentation, but also because they undergodifferent therapies.4,5

Imaging is helpful in determining

FIGURE 6. Intraoperative ultrasound of insulinoma for the same patient shown in Figures 4Aand 4B. (A) Well-circumscribed oval hypoechoic pancreatic mass is visible. (B) Both periph-eral and central vascular blood flow is demonstrated.

A B

FIGURE 7. Maximum intensity projection (MIP) appearance of pancreatic islet-cell tumor.Hypervascular pancreatic islet-cell tumor seen adjacent to SMV near portal confluence(arrow) on arterial-phase MIP.

FIGURE 8. Utility of multiplanar reforma-tions. (A) curved planar reformation (CPR)and MIP are often useful for delineating theanatomic relationship of tumor with adjacentpancreatic tissue and vessels. (B and C)Reformatted images show hypervascularpancreatic islet-cell tumor causing masseffect on the mid portion of pancreatic duct(arrow).

A

B

C

FIGURE 9. Differences in appearance based on phase of imaging. (A) Arterial-phase imagedemonstrates multiple hypervascular liver metastases from pancreatic islet-cell tumor. (B) Metastases are less conspicuous on venous-phase images.

A B

www.appliedradiology.com APPLIED RADIOLOGY©■ 17November 2009


extent of disease, with implications on thepat ient’s overal l prognosis . Tumorgrowth and spread is considered the majordeterminant of patient survival. Pan-creatic islet-cell tumors spread first toregional lymph nodes, then to the liver,bone, and rarely, to distant sites such as thelung or brain. Lymphovascular invasionis an important feature correlating tosurvival.8 Fifty percent to seventy percentof deaths in patients with metastaticdisease are thought to be caused by tumorFIGURE 10. Differences in appearance based on phase of imaging. (A) Axial CT in arterial

phase shows a large heterogeneous pancreatic islet-cell tumor. (B) Venous-phase imagedemonstrates late retention of contrast by tumor.

A B

FIGURE 11. Inherited syndromic patient withpancreatic islet-cell tumors. Coronal multi-planar reformation (MPR) image shows twowell-circumscribed hypervascular pancreaticislet-cell tumors in a patient with several gas-trinomas (arrows).

FIGURE 12. Inherited syndromic patient with cysts and pancreatic islet-cell tumors. (A and B)Axial CT images in arterial phase show multiple pancreatic cysts and hypervascular islet-celltumor (arrow) in a patient with Von Hippel-Lindau syndrome.

A B

FIGURE 13. Inherited syndromic patient with cysts and pancreatic islet-cell tumors. (A and B) CPR images demonstrate multiple pancreaticcysts as well as several heterogeneously enhancing pancreatic islet-cell tumors (arrows) in a patient with Von Hippel-Lindau syndrome.

A B



progression.4

Imaging optionsComputed tomography (CT) is the

initial imaging modality of choice, but isestimated to detect only 60% to 70% ofprimary pancreatic insulinomas andgastrinomas.9,10 Magnetic resonance

imaging (MRI), intraoperative ultra-sound, endoscopic ultrasound, selectiveangiography and portal venous samplingmay serve as adjunct ive methods ofevaluating disease.11 Recent literaturesuggests that MRI may be at least assensitive as multiphasic CT in detectingpancreatic islet-cell tumors.12 In our

experience, a multimodality approach isuseful for diagnosing and staging pan-creatic islet-cell tumors as well as helpingto guide surgery (Figures 2-6).

TreatmentPreoperative imaging evaluation is

important for surgical planning because

FIGURE 14. Typical hypervascular liver metastases.Axial CT image in arterial phase shows multiple smallhypervascular liver metastases from pancreatic islet-celltumor (arrows).

FIGURE 15. Necrotic liver metastases and changes ofchronic pancreatitis. Axial image shows two large, het-erogeneously enhancing, centrally necrotic liver masseswith several small hypervascular liver lesions, compatiblewith metastatic disease in a patient with known pancre-atic islet-cell tumor. There are several punctate pancre-atic-tail calcifications as well as pancreatic duct dilationand parenchymal atrophy, suggesting changes of chronicpancreatitis.

FIGURE 16. Regional lymphadenopathy. (A and B) Axial CT images showregional adenopathy around the abdominal aorta near the origin of the celiacartery in a patient with pancreatic islet-cell tumor (arrows).

A

B



FIGURE 17. Bone metastases. Axial CTimage viewed in bone algorithm shows scle-rotic bone lesions in lumbar vertebra of apatient with pancreatic islet-cell tumor, pre-sumed to represent metastatic disease.

FIGURE 18. Isoattenuating pancreatic islet-cell tumor. CPR image shows isoattenuating pan-creatic-head mass (arrow) exerting mass effect upon the pancreatic duct.

FIGURE 19. Necrotic islet-cell tumor with liver metastases. Axial CT shows large necrotic pancreatic islet-cell tumor (white arrow). Several smallhypervascular liver metastases are present (black arrows). (B) Coronal reformation image demonstrates large peripherally enhancing, centrallynecrotic pancreatic mass and several hypervascular liver metastases (arrows).

A B

FIGURE 20. Hypoattenuating appearance of pancreatic islet-cell tumor. Axial CT shows small peripherally hypervascular pancreatic uncinateislet-cell tumor containing two small central hypoattenuating regions (arrow). (B) Coronal MIP better demonstrates peripheral enhancement andcentral low attenuation of mass (arrow).

A B


resection is the only definitive curativet rea tment , regard less of benign ormal ignant pa thology. One shoulddetermine the location of the tumor withinthe pancreas, and assess presence of

mul t ip le tumors , inc luding tumorsoutside of the pancreas, and looking forevidence of local invasion or metastaticdisease. 13 These findings will affect surgical candidacy and help guide the type


FIGURE 21. Unusual “cystic” appearance of pancreatic islet-cell tumor. (A) Axial CT in arterial phase demonstrates round, low-attenuation, well-circumscribed lesion within pancreatic tail; this is an extremely atypical appearance for pancreatic islet-cell tumor. (B) Cystic-appearing lesion isredemonstrated on coronal MPR image. Lesion was confirmed pathologically as pancreatic islet-cell tumor.

A B

FIGURE 22. Partially calcified pancreatic islet-cell tumor. Axial image demonstrates large het-erogeneous pancreatic islet-cell tumor containing calcifications. There is heterogeneousattenuation of the liver with large, round hypodensity in the posterior right hepatic lobe, com-patible with diffuse liver metastases. A large right renal cyst is incidentally seen.

FIGURE 23. Partially calcified pancreaticislet-cell tumor. (A) On axial CT imaging, thetumor contains chunky central calcifications.(B) Mass interrupts pancreatic duct on coro-nal MPR image. MPR image also demon-strates course of distal common bile ductand remainder of pancreatic duct.

A

B


of surgery to be performed, such as enu-cleation, partial, or rarely, total pancre-atectomy.14

There are several therapeutic optionsfor treating advanced disease from islet-cell tumor. Liver metastases in patientswith insulinomas and gastrinomas areestimated to be present in up to 35% to74% of cases.4 Chemotherapy has beenused for metastatic disease with somesuccess in limited trials.15 Interferon andoctreotide, as well as hepatic ar teryembolization or ligation, have also beenused.16,17In select cases liver transplan-tation has been performed.14 There issome controversy over the efficacy ofdebulking for treatment of metastaticdisease.15

CT techniqueAt our institution, most patients are

initially evaluated with a pancreatic-protocol CT. We use 8- and 16-detectorCT scanners in our hospital (Lightspeed,GE Healthcare, Chalfont St. Giles, U.K.)and a 64-detector scanner at our outpatientfaci l i ty (SOMATOM Sensat ion 64,Siemens Healthcare, Malvern, PA).Fifteen to thirty minutes prior to the study,patients drink 1350 cc of VoLumen, a


FIGURE 24. Splenic artery encasement and narrowing. (A) CPR showssplenic artery encasement by hypodense pancreatic islet cell tumor. (B) Splenic artery encasement and mild narrowing also demonstrated onthin-slab MIP.

FIGURE 25. Splenic vein thrombus. AxialCT image in venous phase demonstratesfocal filling defect within splenic vein (arrow)presumed to be due to patientʼs pancreaticislet-cell tumor.

FIGURE 26. SMV encasement by tumor.SMV narrowing (“teardrop” sign) with flatten-ing and acute angulation of the right lateralwall of the superior mesenteric vein (arrow)indicates presence of isoattenuating pancre-atic islet-cell tumor. Appearance more com-monly seen with pancreatic adenocarcinoma.

FIGURE 27. Venous occlu-sion without arterial encase-ment. Coronal MPR imagedemonstrates occlusion ofsplenic vein with venouscollateral formation aroundproximal splenic artery, butno encasement, in a patientwith pancreatic islet-celltumor.

A B



neutral oral contrast agent, (BraccoDiagnostics, Princeton, N.J.) and another450 cc immediately prior to scanning.Oral contrast facilitates luminal dis-tention of the stomach and duodenum. Ascout image of the abdomen is initiallyacquired, followed by limited non-con t ras t images o f the abdomen to

localize the pancreas (5 mm thickness).Approx imate ly 140 cc o f non ion iccon t ras t ( ISOVUE-370 , BraccoDiagnostics) is subsequently admin-istered intravenously at an injection rateof 4 cc/sec, with arterial-phase imagesacquired 40 seconds after injection (1.25mm thickness, helical acquisition, 0.6

mm interval, 1.35:1 pitch) from the levelof the diaphragm to the top of the iliaccrests. Portal venous-phase images areobtained at a 60-second delay followinginjection (2.5 mm thickness, 1.25 mminterval, 1.35:1 pitch). Delayed imagesare routinely acquired through the kid-neys 3 minutes after contrast adminis-

FIGURE 28. Portal vein with tumor thrombus. (A) Axial CT image in venous phase, shows portal vein expanded and filled with enhancing mater-ial, as well as numerous periportal and gastrohepatic venous collaterals, consistent with tumor thrombus within the portal vein from pancreaticislet-cell tumor. (B) Coronal MPR image confirms portal vein invasion (black arrow) with cavernous transformation (white arrow).

A B

FIGURE 29. Portal vein with tumor invasion. (A) CPR image shows islet-cell tumor directly invading the portal vein (arrow). (B) Coronal reforma-tion image demonstrates venous invasion (black arrow) of the portal vein extending directly from a large heterogeneous pancreatic body islet-cell tumor (white arrow).

A B


tration (5 mm thickness).The helically acquired volumetric data

is postprocessed by specially trainedtechnologis ts in our dedicated 3-dimensional laboratory to generatemultiplanar reconstruction images in-cluding maximum intensity projections(MIPs), minimum intensity projections(MINIPs) and curved planar reformations(CPRs). These reconstructions providebetter anatomic definition of key struc-tures commonly affected by locallyinvasive pancreatic neoplasms (Figure 7),including thin-slab MIPs of the celiacorigin, portal and splenic veins; CPRs ofthe superior mesenteric vein and artery,hepatic artery, gastroduodenal artery,splenic artery, distal common bile duct andpancreatic ducts; thin-slab MINIPs of thepancreatic ducts; and, coronal MPRs in theplane of the main portal vein through theentirety of the pancreas.

Typical imaging findingsThe typical appearance of a pan-

crea t ic i s le t -ce l l tumor i s a wel l -circumscribed, solitary, hypervascularmass (Figure 4) . Because i s le t -ce l ltumors a re genera l ly sof t , and lackassociated desmoplastic reaction, theydo not usually cause pancreatic ductobstruction or dilation. Mild distortion

of the duct may be seen due to adjacentmass effect or if the tumor is located nearthe main pancreatic duct (Figure 8).

Typically, pancreatic islet-cell tumorsand metastases are best seen during thelate arterial phase (Figures 4, 9). Onpor ta l -venous phase , tumors wi l lcharacterist ical ly demonstrate lateretention of contrast (Figures 4, 10).While arterial enhancement patterns areaccepted as the most common imagingappearance, a typical enhancementpatterns do occur, and varying opinionson optimal phase of enhancement havebeen reported.9,12,18,19,20 Given the vari-ab i l i ty in peak enhancement andenhancement patterns, mult iphasicimaging is generally accepted as the bestmethod to ensure optimal detection ofpancreatic islet-cell tumors.

On ultrasound, pancreatic islet-celltumors are generally hypoechoic andwell c ircumscribed. Color Dopplerimaging will reveal prominent vascu-larity of the tumor. Often the tumor isdifficult to palpate surgically due to itssoft texture. Intraoperative ultrasound ishelpful in localizing small tumors anddelineating their relationship to the mainpancreatic duct and adjacent vessels(Figure 6).

In patients with inherited islet-cell


FIGURE 30. “Interrupted duct” from pancreatic islet-cell tumor. CPR shows abrupt terminationof dilated pancreatic duct with isoattenuating pancreatic-head mass (arrow). A biliary stenthad been placed.

FIGURE 31. Isoattenuating islet-cell tumorcausing “double duct” sign. (A) On CPR, alarge, infiltrative, isoattenuating, pancreaticislet-cell tumor causes abrupt interruptionand dilation of the pancreatic duct. (B) Massand pancreatic duct dilation is confirmed oncoronal minimum intensity projection imag-ing. (C) There is biliary duct dilation, which inconjunction with pancreatic duct dilation,causes a “double duct” sign; these imagingfeatures are more typically associated withpancreatic adenocarcinoma.

A

B

C


tumors, multiple hypervascular pan-creatic masses are often present (Figures11 and 12). Additionally, other pancreaticlesions are commonly seen, such asmultiple pancreatic cysts in patients withVon Hippel-Lindau syndrome (Figures12 and 13).

Metastatic lesions occurring in theliver are generally hypervascular inappearance on late arterial-phase scans,with similar enhancement character-istics as the primary pancreatic neoplasm

(Figure 14). Rapid washout from hepaticmetastases may render them isodense onvenous-phase acquisitions. It is thereforeessent ia l to perform ar ter ia l -phaseimaging to detect liver metastases. Aswith the primary tumor, liver metastasescan become centrally necrotic as theyincrease in size (Figure 15). Regionaladenopathy, liver, bone and pulmonarymetas tases a re addi t iona l imagingfeatures of advanced disease (Figures 16and 17).

A commonly cited reason for difficultyin visual iz ing pancreat ic i s le t -cel ltumors i s the p resence o f ad jacen tenhancing vessels. Because pancreaticislet-cell tumors are often intenselyvascular, their appearance in the axialcross-section can either mimic, or beobscured by, adjacent vessels of similarcaliber.9 Multiplanar reformations aswel l as mul t iphas ic imaging can behelpful to avoid this potential pitfall.Occasionally, hypervascular metastasesto the pancreas can occur, most com-monly from renal-cell carcinoma. Whilerare, these can be mistaken for a pan-creatic islet-cell tumor due to similarenhancement characteristics.21

Atypical imaging findingsAtypical imaging appearances of

pancreat ic is le t-cel l tumors are notuncommon. While most islet-cell tumorsare well-visualized on CT due to theirhypervascular nature, some may beisoattenuating to the rest of the pancreasand challenging to visualize. In caseswhere the lesion is not immediatelyapparen t , sub t l e pancrea t i c duc tindentation or subtle changes in pan-creatic duct caliber may be helpful clues


FIGURE 32. Regional lymphadenopathy suggesting local recurrence. (A) Patient underwent Whipple surgery for pancreatic islet-cell tumor. (A)Hypervascular aortocaval (arrow) and (B) portocaval lymph nodes (arrow) are seen on follow-up imaging, suggesting local recurrence.

FIGURE 33. Response to chemotherapy. (A) Axial CT image shows several peripherallyenhancing, centrally hypoattenuating liver masses and large hypodense pancreatic islet-celltumor prior to chemotherapy. (B) Following chemotherapy, significant improvement withdecrease in size of pancreatic-head mass as well as size of liver metastases. Majority of liverparenchyma returned to normal attenuation and enhancement pattern. A metallic biliary stentwas placed in the interim.

A B

A B

in identifying the location of the lesion(Figure 18). Indeed, small isoattenuatinglesions can be particularly difficult todelineate by CT and in some cases may bebetter seen on endoscopic ultrasound orintraoperative ultrasound.

Another atypical appearance of islet-cell tumors is that of cystic or necroticchange. Central necrosis is more com-monly seen in larger nonsyndromicpancreatic islet-cell tumors that outgrowtheir blood supply. Often the lesionperiphery will remain hypervascularwhi le the cen te r does no t enhance(Figures 19 and 20).22 In our experience inone very rare instance, a pancreatic islet-cell tumor presented with a purely cysticappearance (Figure 21).

Ca lc i f i ca t ions a re no t a typ ica limaging feature of pancreatic islet-celltumors but can be seen in up to 20%, bestdelineated on CT (Figures 22 and 23). Thepresence o f ca lc i f i ca t ions i s more sugges t ive o f a pancrea t i c islet-cell tumor and can be helpful indifferentiating a lesion from adeno-carcinoma of the pancreas.6

Vascular encasement, narrowing,and /or f rank vascu la r invas ion a reaggressive findings commonly seen inpancreatic adenocarcinoma. Occa-sionally, these findings may also be seenwith pancreatic islet-cell tumors. In these

atypical islet-cell tumors, the degree ofvascular encasement or occlusion is oftendisproportionally less than that found in asimilarly sized pancreatic adenocar-c inoma (F igures 24-28) . Beyondencasement, direct invasion of the portalvein with resulting tumor thrombus canrarely occur in islet-cell tumors, againmimicking an adenocarcinoma of thepancreas (Figure 29).

Another uncommon appearance ofis le t -cel l tumors is pancreat ic ductinvolvement. While mild mass effectupon the pancreatic duct is commonlyseen, occasionally significant narrowingor pancreatic duct obstruction and sub-sequent dilatation can be present (Fig-ure30). Obstruction may be so severe thatintrahepatic biliary ductal dilatation mayalso be present (Figure 31). In these cases,the degree of obstruction is again usuallyless than would be expected with adeno-carcinoma.

Once the diagnosis and staging of apancreatic islet-cell tumor is performed,imaging is helpful in determining thesuccess o f su rg ica l t r ea tment andmonitoring for s igns of recurrence.Recurrence may occur locally in thepostoperative site, present as regionallymphadenopathy, or appear as distantmetastatic disease in the liver, lungs orbone (Figure 32). Patients who are not

surgical candidates are also imaged toassess for therapy response (Figure 33).

ConclusionThe radiologist should be familiar with

bo th typ ica l and a typ ica l imagingappearances of pancreatic islet-celltumors and the appearance of metastaticdisease to help determine whether apatient is a surgical candidate. The classicappearance of pancreat ic is le t -cel ltumors is a solitary, well-circumscribedhypervascular lesion that does not disruptthe pancreatic duct. Advanced diseasemay present as regional adenopathy ordistant metastases to liver, bone and/orlungs. Atypical appearances includeisodense lesions, cyst ic change andinternal calcifications. Rarely, islet-celltumors may mimic a pancreatic ade-nocarc inoma by nar rowing o robs t ruc t ing the pancrea t i c duc t o rcausing vascular encasement, occlusionor invasion.

AcknowledgmentsThe authors wish to thank Jeslyn A.

Rumbold for editorial assistance.

REFERENCES1. Kumar V AA, Fausto N. Robbins Basic Pathology.8thEdition. Philadelphia: Saunders Elsevier, 2007.2. Bartsch DK, Schill ing T, Ramaswamy A, et al.Management of nonfunctioning islet cell carcinomas.World J Surg.2000;24:1418-1424.


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6 islet-cell tumors of the pancreas

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