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While the bulk of this web site is dedicated to the more common adenocarcinomas of the pancreas, the research team at Johns Hopkins also extensively studies islet cell tumors (also known as well-differentiated pancreatic endocrine neoplasms). Multiple Endocrine Neoplasia Type 1, abbreviated MEN-1, is a familial syndrome caused by inherited mutations in the MEN1 gene on chromosome 11. Clinical genetic testing is now available for these syndromes, but such testing is best done with the help of a trained genetic counselor.
Should the CT scan fail to detect the primary tumor, the next step in radiographic assessment may be visceral angiography, focusing upon selective visualization of the arterial supply to the pancreas and peripancreatic regions (26). Another technique that holds promise for the imaging of pancreatic endocrine tumors is somatostatin receptor imaging. At the time of surgical exploration for pancreatic endocrine neoplasm, a complete evaluation of the pancreas and peripancreatic regions is performed.
Because these tumors are so slow growing they often do not respond to conventional chemotherapy (which usually targets fast growing cells).
Afinitor was approved for the treatment of patients with progressive pancreatic neuroendocrine tumors that are not resectable surgically, that are locally advanced or metastatic. Sunitinib belongs to the class of drugs called "tyrosine kinase inhibitors," and it has both effects against blood vessels in tumors (antiangiogenic) and effects against the tumor itself (antitumor properties).
In some instance metastases to the liver can be treated by destroying their blood supply using techniques such as hepatic artery embolisation and chemoembolisation.
The most important prognostic factor is whether or not the tumor can be removed surgically.
After the diagnosis of insulinoma is confirmed by biochemical analyses, the appropriate localization and staging studies as described above are performed. In approximately 10% of all cases insulinoma will be found to have spread (metastasized) to peripancreatic lymph nodes or to the liver, justifying a diagnosis of malignant insulinoma. Chemotherapeutic agents with some efficacy against malignant insulinoma include streptozocin, dacarbazine (DTIC), doxorubicin and 5-fluorouracil (60-62).
Peptic ulceration of the upper GI tract and abdominal pain are seen in up to 90% of patients. The diagnosis of gastrinoma should be suspected in several clinical settings, and the liberal use of serum gastrin measurement for screening is encouraged.
Following the biochemical confirmation of the diagnosis of gastrinoma, two steps are important in patient management. Gastrinomas within the pancreas are usually surgically resected either by distal pancreatectomy or pancreaticoduodenectomy (54, 76). Patients with gastrinomas that cannot be removed surgically can be treated long-term omeprazole therapy to alleviate their symptoms. The overall results in patients with gastrinoma have improved markedly since the initial description of the syndrome. Most patients with incurable metastatic gastrinoma succumb to eventual tumor growth and dissemination. Hepatic transplantation, hepatic artery embolization, and interferon therapy have all been used in small numbers of patients with gastrinoma metastatic to the liver (89-91). The diagnosis of VIPoma is typically made after excluding other more common causes of diarrhea. After biochemical documentation of elevated VIP levels, tumor localization and staging begins with abdominal CT scan with intravenous and oral contrast. The preparation for surgical exploration in patients with VIPoma must include correction of fluid and electrolyte losses involving vigorous intravenous fluid administration and appropriate electrolyte replacement. Surgical excision of the VIPoma is appropriate in all patients with the Verner-Morrison syndrome.
In patients with recurrent or unresectable VIPoma, octreotide therapy is used to reduce circulating VIP levels and control diarrhea. The diagnosis of glucagonoma may be suggested by the clinical presentation and biopsy of the skin lesions, but is secured by the documentation of elevated levels of fasting serum glucagon.
Patients with biochemical documentation of hyperglucagonemia in the appropriate clinical setting should undergo radiographic localization and staging with contrast-enhanced abdominal CT scan. Glucagonoma patients with incurable or recurrent disease appear to have low response rates to standard chemotherapeutic agents such as streptozocin and dacarbazine (97).
At surgery resection for cure has been uncommon, because of the presence of metastatic disease in most cases.
Localization and staging studies are performed in similar fashion to patients with the more common diagnosis of ductal adenocarcinoma of the exocrine pancreas. At surgery most of these nonfunctional neoplasms are larger than 2 cm, and are not safely excised by local techniques. The overall 5-year survival rate in all patients with resected nonfunctional pancreatic neoplasms approaches 50% (108).
In patients with unresectable disease, partial responses to combination chemotherapy have been reported. The highest response rate of 69% was seen in patients receiving streptozocin plus doxorubicin. The MEN-1 gene codes for the menin protein, and patients with an inherited mutation in the MEN1 are predisposed to develop tumors of the pituitary (the small "master" gland at the base of the brain), the parathyroids (four small glands in neck which help control blood calcium levels), and the pancreas. Patients with von Hippel-Lindau are predisposed to developing tumors in a number of organs including the the brain (hemagioblastoma), the eye (hemagioblastoma), the kidney (renal cell carcinoma), and the adrenals (pheochromocytoma). Tuberous sclerosis complex is caused by inherited mutations in one of two genes- TSC1 or TSC2.
Individuals found to have one of these genetic syndromes may benefit from increased screening for early tumors, and, it is our hope, that a better understanding of the genetics of these syndromes will lead to novel gene-specific therapies in the future. The accuracy of the CT scan in tumor localization is improved by the use of both oral and intravenous contrast. Rosch and colleagues were able to correctly localize 32 of 39 tumors (82%) using endoscopic ultrasound, after a prior CT scan had failed to locate the tumor.
These approaches involve the selective cannulation of the blood vessels leading to the liver. During a monitored fast, blood is sampled every four to six hours for glucose and insulin determinations, and at the time of symptom occurrence. For insulinoma the standard imaging studies include abdominal CT, endoscopic ultrasound and visceral angiography. Under these circumstances, cautious and safe resection of the primary tumor and accessible metastases should be considered (56-58). Fifty percent of patients have some degree of diarrhea, while about 10% of patients present with diarrhea as the solitary symptom.
Gastric acid analysis is an important test in the evaluation of patients with suspected gastrinoma, as it can differentiate between ulcerogenic (high gastric acid) causes of hypergastrinemia and nonulcerogenic (low gastric acid) causes of hypergastrinemia. At the time of exploration the entire abdomen is carefully assessed for tumors within the pancreas and outside of the pancreas (72).

Gastrinomas may also arise within the duodenum and they often can be surgically resected with primary closure of the duodenal defect (78, 79).
Up to 35% of patients explored for gastrinoma with curative intent have been rendered eugastrinemic at follow-up, and considering only those patients explored and thought to be successfully resected, the cure rates approach 60 to 70%. Multiple modalities have been utilized in an effort to treat patients with such metastatic gastrinoma. None of these therapies appears to be associated with reproducible improvements in survival. Synonyms for this syndrome include the WDHA syndrome (watery diarrhea, hypokalemia (low potassium levels in the blood), and either achlorhydria or hypochlorhydria (low chloride)) and the pancreatic cholera syndrome.
The active agent in the VIPoma syndrome is the hormone vasoactive intestinal polypeptide (VIP) (93), with a minority of patients having elevations of other candidate mediators such as peptide histidine-isoleucine (PHI) or prostaglandins (94). Therapy with octreotide can be an important adjunct in the preoperative setting, as octreotide leads to a reduction in circulating VIP levels with a resultant decrease in the volume of diarrhea. The majority of VIPomas have been located in the tail of the pancreas, where they are amenable to resection via distal pancreatectomy. In the presence of metastatic disease, safe palliative surgical debulking of metastatic tumor is indicated (95).
Chemotherapy specific for VIPoma patients has not been studied prospectively, although small numbers of patients have appeared to show partial responses to streptozocin, combination chemotherapy or interferon. Because these tumors are usually large and solitary, the CT scan localizes the tumor in the majority of patients. These tumors are typically large and bulky, and surgical resection has required distal pancreatectomy. Octreotide can be successful in reducing elevated glucagon levels, and in controlling the hyperglycemia and dermatitis associated with incurable glucagonoma (98, 99).
The most useful test for localization and staging has been the abdominal CT scan, which has been used to identify and stage these typically large tumors. Safe resection of the primary tumor and careful debulking of liver metastases appear indicated.
The abdominal CT scan is used for evaluation of the primary tumor and to assess for hepatic metastases. Tumors in the head, neck or uncinate process of the pancreas typically require pancreaticoduodenectomy (the Whipple resection) for safe resection, while tumors arising in the body or tail of the pancreas are treated by distal pancreatectomy. Dysinsulinism: convulsions and coma due to islet cell tumor of the pancreas, with operation and cure. Primary peptic ulcerations of the jejunum associated with islet cell tumors of the pancreas. Comparisons of mutations of ras oncogene in human pancreatic exocrine and endocrine tumors. Gs alpha - Identification of a gene highly expressed by insulinoma and other endocrine tumors.
Putative tumor-suppressor gene on chromosome 11 is important in sporadic endocrine tumor formation. Prospective study of the ability of computed axial tomography to localize gastrinomas in patients with Zollinger-Ellison syndrome.
Role of selective angiography in the management of patients with Zollinger-Ellison syndrome. Preoperative localization of gastrointestinal endocrine tumors using somatostatin-receptor scintigraphy. Hormone-producing gastrointestinal tumors contain a high density of somatostatin receptors. Intraoperative localization of neuroendocrine tumors with 125I-tyr3-octreotide and a hand-held gamma-detecting probe.
Detection of occult gastrinomas with iodine 125-labeled lanreotide and intraoperative gamma detection. Vasoactive intestinal peptide-receptor imaging for the localization of intestinal adenocarcinomas and endocrine tumors. Transhepatic portal vein catheterization for localization of sporadic and MEN gastrinomas: A ten year experience. Transhepatic portal vein catheterization for localization of insulinomas: A ten year experience. Usefulness of selective arterial secretin injection test for localization of gastrinoma in the Zollinger-Ellison syndrome. Prospective study of the use of intraarterial secretin injection and portal venous sampling to localize duodenal gastrinomas. Synthesis and secretion of insulin-like growth factor II by a leiomyosarcoma with associated hypoglycemia. Functioning insulinoma - Incidence, recurrence, and long-term survival of patients: A 60-year study. Streptozocin-doxorubicin, streptozocin-fluorouracil, or chlorozotocin in the treatment of advanced islet-cell carcinoma. Streptozocin alone compared with streptozocin plus fluorouracil in the treatment of advanced islet-cell carcinoma. Symptomatic secondary hormone syndromes in patients with established malignant pancreatic endocrine tumors.
Long-term efficacy and safety of omeprazole in patients with Zollinger-Ellison syndrome: A prospective study. Role of pancreatoduodenectomy in the management of primary duodenal wall gastrinomas in patients with Zollinger-Ellison syndrome.
Microgastrinomas of the duodenum: A cause of failed operations for the Zollinger-Ellison syndrome. Treatment of Zollinger-Ellison syndrome with exploratory laparotomy, proximal gastric vagotomy, and H2-receptor antagonists.
The place for curative surgical procedures in the treatment of sporadic and familial Zollinger-Ellison syndrome.
Effect of somatostatin analog on peptide release and tumor growth in the Zollinger-Ellison syndrome. Transplantation of the liver for metastatic endocrine tumors of the intestine and pancreas.
Islet cell tumors metastatic to the liver: Effective palliation by sequential hepatic artery embolization.
Gastrinomas in the duodenums of patients with multiple endocrine neoplasia type 1 and the Zollinger-Ellison syndrome.
Pancreatic cholera syndrome due to a vasoactive intestinal polypeptide-producing tumor: Further insights into the pathophysiology.
Treatment of inoperable glucagonoma with the long-acting somatostatin analogue SMS 201-955.

Calcitonin immunoreactivity and hypercalcitoninemia in two patients with sporadic, nonfamilial, gastroenteropancreatic neuroendocrine tumors.
Malignant islet cell tumor of the pancreas associated with high plasma calcitonin and somatostatin levels. The utility of circulating levels of human pancreatic polypeptide as a marker for islet cell tumors. Charles Yeo, ("Neoplasms of the Endocrine Pancreas" from Greenfield et al, Surgery: Scientific Principles in Practice, Second Edition published by Lippincott-Raven Publishers, abstracted with permission). First, because these genetic syndromes are caused by genetic changes that can be inherited, other family members may be at risk. Pancreatic disease may be the first manifestation of VHL, and most patients with VHL eventually develop a pancreatic tumor.
Patients with neurofibromatosis develop dark patches of skin (cafe-au-lait spots), and benign (non-cancerous) and malignant (cancerous) tumors of the nervous system. The CT scan is also used to assess for peripancreatic lymph node enlargement and for the presence of hepatic metastases.
In their experience, endoscopic ultrasonography was more sensitive than the combination of CT and visceral angiography. In these cases, localization of the occult neoplasm may be assisted by the performance of selective transhepatic portal venous hormone sampling (37-41). Potential extrapancreatic sites of tumor are evaluated in all cases, with particular attention being paid to the duodenum, the area of the spleen (splenic hilum), small bowel and its blood vessels (mesentery), the lymph nodes around the pancreas and the reproductive tract in women. Food and Drug Administration (FDA) recently approved the drugs Sutent (sunitinib) and Afinitor (Everolimus) for the treatment of advanced pancreatic endocrine tumors (also known as islet cell tumors or pancreatic neuroendocrine tumors [PanNETs]). Symptoms include confusion, seizure, obtundation, personality change and coma, as well as palpitations, tremulousness, diaphoresis (sweating) and tachycardia (fast heart rate).
Additional support for the diagnosis of insulinoma comes from the calculation of the insulin to glucose ratio (I:G ratio) at different time points during the monitored fast. Such tumor debulking can be helpful in reducing problematic hypoglycemic symptoms which can threaten long-term survival. In a small percentage of patients gastrinoma may be found only in peripancreatic lymph nodes, with these lymph nodes harboring the primary tumor. These recent results represent a major improvement in the management of gastrinoma patients over the past decades, and support the practice of initial pharmacologic control of gastric hypersecretion using omeprazole, followed by tumor localization and staging, in hopes of curative resection.
Metastases have been found in the majority of patients, and safe surgical debulking of these metastatic lesions should be considered.
At the time of exploration, cholecystectomy (removal of the gallbladder) is indicated even in the absence of documented gallstones, because of the concern about the development of gallstones with persistently elevated somatostatin levels. Second, these genetic syndromes predispose to (increase the risk of) more than one tumor type. The pancreatic tumors in patients with VHL are interesting because they can have unique appearances. Basically, a radioactive form of octreotide, a drug similar to somatostatin, is injected into the blood stream. One technique that provides additional information in the intraoperative setting is real time ultrasonography, which can assist in tumor identification (47, 48). In some instances drugs can be used to block the symptoms causes by the release of hormones from the tumor.
In most cases, patients consume carbohydrate-rich meals and snacks to relieve or prevent these symptoms. Insulinomas are found evenly distributed within the pancreas, with approximately one-third being located in the head and uncinate process of the pancreas, one-third in the body of the gland, and one-third in the tail of the gland (51). The average patient survives several years following diagnosis and treatment of malignant islet cell tumors, indicating that the natural history of these malignant tumors typically follows an indolent course (25, 59). Second, after the initiation of proton pump therapy, all gastrinoma patients should undergo imaging studies in an effort to localize the primary tumor and to assess for metastatic disease. Resection of these apparent lymph node primary gastrinomas has been associated with long-term eugastrinemia (normal gastrin levels) and biochemical cure in up to 50% of cases (80). Individuals with one of these syndromes therefore have an increased risk of developing pancreatic and extra-pancreatic neuroendocrine tumors. Patients with tuberous sclerosis complex can suffer from developmental delay, mental retardation and even autism, and they are predisposed to develop a number of different tumors. In general surgeons can perform a Whipple resection for tumors of the head of the pancreas and a distal pancreatectomy for tumors of the tail of the pancreas. For example, proton pump inhibitors can be used to counteract the high levels of stomach acid produced in patients with gastrinomas.
Ninety percent of patients will be found to have small solitary tumors amenable to surgical cure. The modalities appropriate for localization and staging of gastrinoma patients have already been discussed and include dynamic abdominal CT scanning with intravenous and oral contrast, endoscopic ultrasonography, somatostatin receptor imaging, percutaneous transhepatic portal venous sampling for gastrin, and the selective arterial secretin stimulation test. Finally, these syndromes are important because they provide insight into the biology of pancreatic neuroendocrine neoplasms. They are predisposed to develop three different brain lesions- "tubers," subependymal giant cell astrocytomas and subependymal nodules.
Prognosis is typically determined by the presence of local invasion, spread to regional lymph nodes, or the existence of hepatic or distant metastases.
The goals of surgical therapy for pancreatic endocrine neoplasms include control of symptoms from hormone excess, safe resection of maximal tumor mass and preservation of maximal pancreatic parenchyma.
The research team at Johns Hopkins has played a role in understanding the likely mechanism by which Afinitor works. Less than 10% of patients with insulinoma will be found to have some form of the multiple endocrine neoplasia-1 (MEN-1) syndrome (see below). Because the genes that cause these genetic syndromes are known, scientists can understand the cellular pathways which lead to the development of pancreatic neuroendocrine neoplasms. In fact, the name tuberous sclerosis comes from the brain lesions that these patients develop- Tuber in Latin means swelling and skleros in Greek means hard. They also can develop distinctive lesions of the skin (hypomelanotic macules and facial angiofibromas), kidney (angiomyolipomas), lungs (lymphangioleiomatosis), heart (rhabdomyomas), and eye tumors ( hamartomas). Most of these are entirely benign growths, but they can cause symptoms depending on their location. Although less common than the other manifestations of tuberous sclerosis, several patients with tuberous sclerosis complex have been reported who developed pancreatic neuroendocrine neoplasms.

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