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With In the Clinic, The ASCO Post provides overviews of novel oncology agents, addressing indications, mechanisms, administration recommendations, safety profiles, and other essential information needed for the appropriate clinical use of these drugs. Indication—The oral kinase inhibitor sunitinib (Sutent) was recently granted approval for the treatment of progressive, well-differentiated pancreatic neuroendocrine tumors (pNET, Fig. How it works—Sunitinib inhibits cellular signaling by targeting multiple receptor tyrosine kinases.
How it is given—The recommended dose of sunitinib for pNET is 37.5 mg taken orally once daily continuously without a scheduled off-treatment period. Adverse events resulted in permanent discontinuation in 22% of sunitinib patients and in 17% of placebo patients.
Kulke MH, Lenz HJ, Meropol NJ, et al: Activity of sunitinib in patients with advanced neuroendocrine tumors.
Raymond E, Dahan L, Raoul JL, et al: Sunitinib malate for the treatment of pancreatic neuroendocrine tumors.
Indication—The kinase inhibitor everolimus (Afinitor) was also recently approved for treatment of unresectable, locally advanced or metastatic progressive neuroendocrine tumors of pancreatic origin (pNET). How it works—Everolimus inhibits mammalian target of rapamycin (mTOR), a serine-threonine kinase that stimulates cell growth, proliferation, and angiogenesis. How it is given—The recommended dose of everolimus is 10 mg once daily; it should be taken at the same time of day and consistently with or without food. Safety profile—Data from the trial supporting everolimus approval and 858 additional patients with advanced neuroendocrine tumors in the everolimus safety database indicate that the most common adverse reactions in patients receiving everolimus (> 30%) were stomatitis, rash, diarrhea, fatigue, edema, abdominal pain, nausea, fever, and headache. Find a doctor at The Johns Hopkins Hospital, Johns Hopkins Bayview Medical Center or Johns Hopkins Community Physicians. Neuroendocrine tumor cancer survivor Betsey Clark discusses her life-saving experience at The Johns Hopkins Hospital, which included a Whipple procedure and subsequent total pancreatectomy, or removal of her pancreas.
In the United States, 32,000 people are diagnosed with pancreatic cancer; in Europe over 60,000 people are diagnosed.
There are two types of pancreatic tumors one is an adenocarcinomas, which occur in 95% of patients, the other is neuroendocrine tumors which occur in 5 %of patients. Risk factors for pancreatic cancer are age, being male, African descent or ethnicity, smoking, diets that are high in meat, obesity, diabetes, daily exposure to certain chemicals, dyes and pesticides, a family history, Helicobacter pylori infection and chronic pancreatitis. Unfortunately, pancreatic cancer has the number one fatality rate of all cancers and is number 4 in cancer death for men and women in the United States. Be sure to tell your doctor of any allergies you have whether it is to medication or food, preservatives, or dyes.
Pancreatic neuroendocrine tumors: insulinoma - What radiological tests are helpful before surgery in localizing these tumors? Thank you for visiting the American Association of Endocrine Surgeons Patient Education web site. Once the diagnosis is unequivocally established biochemically, the next step in patient management is to localize the insulinoma. Which and in what order localization methods are chosen often depends on the equipment and expertise available at any particular institution. A sequential manner is usually elected, proceeding from the least complicated and generally less expensive, to more complex methods that may require more cooperation by the patient and often are more expensive.
The advantages include no radiation, least invasive (no IVs, blood sampling, etc.), relatively inexpensive, and when successful, the tumor is defined by precise anatomically location.
This test may be omitted by some since in some reports it is successful in only about 10% of patients. With recent advances in CT technology (speed, high resolution, and image-reconstruction software), triple-phase helical CT is usually the initially obtained imaging study (Figure 2).
Although requiring modest radiation exposure, an IV, and more expense, precise anatomic localization can be achieved in about 70% or more of these tumors.
Additionally, the remainder of the abdominal organs is imaged in the unusual case of malignant insulinoma that may have spread to other sites (see below). The stomach (S with green lines up and down) has air (black) and fluid (darker gray) with it (stomach wall at end of lower green line). Just to the right of the insulinoma is the portal vein (white with "tail"–vein from the spleen joining it) carrying blood from intestine and pancreas to liver. As with any ultrasound method, the success of this technique relies heavily on the expertise and experience of the endoscopist. It involves comfortable sedation for the patient using IV medication, and an endoscope (flexible lighted tube with a camera on the end) is inserted through the mouth, down the esophagus (swallowing tube), and into the stomach and duodenum. The specialized endoscope is equipped with high resolution ultrasound, and because the stomach is directly in front of the pancreas, and the duodenum wraps around the head and body of the pancreas, the ultrasound apparatus is right next to the pancreas. This allows very high resolution, detailed imaging of the pancreas, with a success rate of about 90% (Figure 3). Obviously, this is more "invasive" for the patient, is more expensive, and the images are not as readily interpreted by the surgeon.


Prior to reoperation, using the EUS, a needle was inserted into the insulinoma and a tiny sample was taken to verify under the microscope that this was the tumor.
Dating back to the 1970s, arteriography with specialized subtraction views was considered the gold standard of localization, but succeeded in only 50% with few exceptions. Today, arteriography with SACS is generally held in reserve until the final effort at localization because it involves the highest degree of radiologist expertise, the most invasive for the patient, and considerably more expensive.
Because most insulinomas have an excellent blood supply, they may show up by their "blush" during the injection of contrast into the arteries feeding the pancreas (Figure 4). As an extension of this technique, because insulin secretion is stimulated by calcium, each of the 3 principal arteries that feed different regions of the pancreas can be injected with calcium. Blood is sampled from draining veins after the "calcium-stimulation" and marked increases in the measured insulin narrows the location of the insulinoma to the region fed by that particular artery (Figure 5).
Therefore, this technique is not as anatomically precise, but can direct the intraoperative surgical exploration to that region of the pancreas.
Arteriogram with special "subtraction" view–making the insulinoma looking black (lower left). The catheter can be seen tracking up the middle of the picture before curling into the specific artery feeding the insulinoma. After calcium injection, blood is sampled through the second catheter positioned in a vein draining the liver. In this case, the tumor is seen in the head of the pancreas, and injection of the artery serving that region would stimulate a much higher level in the sampled blood than the other 2 arteries. Intraoperative US showing the small insulinoma (black arrow head) with the pancreatic duct (pd, arrow) bending over the tumor, touching one side. Together with the surgeon's ability to feel the insulinomas, IOUS is perhaps the most helpful localization technique of all—the combination exceeding 95% success (Figure 6). In difficult situations if not routinely, the expertise of a radiologist in the OR is necessary. This is not the only test obtained, however, because surgeons and patients alike are far more comfortable knowing the location of the insulinoma prior to proceeding to the OR. IOUS also helps define critical anatomic relationships such as the arteries, veins, common bile duct, and most importantly, the main pancreatic duct (See below under Complications).
Decisions regarding the safest and most effect technique for surgical removal of the insulinoma may be directed by the IOUS findings.
NEXT SECTION: What are the treatment options for insulinoma, both the benign and the malignant?
Nonfunctional tumors tend to present at later clinical stages with symptoms attributable to mass effect or metastases. Tumor localization and staging studies include imaging with computed tomography (CT) with or without magnetic resonance imaging (MRI), and endoscopic ultrasound.
Elevated human chorionic gonadotropin levels.InsulinomaInsulinomas are far more likely to be benign than malignant. In the era of proton pump inhibitors and H2 blocking agents, the potentially lethal hyperacidity and hypersecretory states induced by excessive gastrin production can usually be controlled. Necrotizing erythema of glucagonoma may be relieved in 24 hours with somatostatin analogue, with nearly complete disappearance within 1 week. About This PDQ SummaryPurpose of This SummaryThis PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the treatment of pancreatic neuroendocrine tumors (islet cell tumors). Improved progression-free survival was seen in multiple patient subgroups, including those with prior somatostatin analog treatment. Vascular endothelial growth factor (VEGF) is a key driver of angiogenesis in pancreatic neuroendocrine tumors, and malignant pancreatic endocrine tumors also show widespread expression of platelet-derived growth factor receptors (PDGFRs) ? and ?, stem-cell factor receptor (c-kit), and VEGF receptor (VEGFR)-2 and VEGFR-3.
During the double-blind phase of the trial supporting approval of sunitinib in pNET, the most common (? 30%) adverse reactions were diarrhea, nausea, asthenia, vomiting, and fatigue.
The safety and efficacy of everolimus in treatment of carcinoid tumors have not been established. Autocrine activation of the mTOR signaling pathway, which is mediated by insulin-like growth factor 1, is implicated in the proliferation of pancreatic neuroendocrine tumor cells, and inhibition of mTOR has been shown to result in an antiproliferative effect. Causes of death in the everolimus group included acute renal failure, acute respiratory distress, cardiac arrest, death (cause unknown), hepatic failure, pneumonia, sepsis, and death from unknown cause. Vincent Rajkumar, MD, and Sagar Lonial, MD, on Treating Multiple Myeloma - VideoOlanzapine Combination Reduces Nausea and Vomiting in Patients Receiving Highly Emetogenic Chemotherapy - NewsDavid G.
They are relatively rare tumors and are best managed in centers with extensive expertise.Neuroendocrine tumors may arise in various places, most commonly the pancreas. CT scan showing an insulinoma (white dot pointed to by yellow arrow) in the body of the pancreas (P with arrows pointing to the body and tail of the pancreas). CT scan showing insulinoma (white dot pointed to by yellow arrow) in junction of head and uncinate portions of pancreas. Two catheters are inserted, 1 into the aorta (red) then selectively threaded into the 3 arteries feeding the pancreas.


About 15% to 35% of gastrinomas are associated with the MEN-1 syndrome and up to 50% are malignant. In a retrospective case series of 30 patients with 32 pancreatic insulinomas, the combination of preoperative dual-phase thin-section multidetector CT and endoscopic sonography correctly identified and localized all of the tumors.
Treatment with proton pump inhibitors or H2 blocking agents may aid in control of peptic symptoms.
In a series of 212 patients with Zollinger-Ellison syndrome (ZES), no patients died of causes related to acid hypersecretion. Sunitinib has earlier indications in gastrointestinal stromal tumors (GIST) after disease progression on imatinib (Gleevec) or in patients intolerant of imatinib and in advanced renal cell carcinoma.
Sunitinib inhibits these kinases, and has been shown to delay tumor growth in a RIP1-Tag2 transgenic mouse model of pancreatic islet cell tumors by reducing endothelial cell density and pericyte coverage of tumor vessels. Everolimus has prior indications in advanced renal cell carcinoma after failure of sunitinib or sorafenib and in subependymal giant cell astrocytoma associated with tuberous sclerosis that requires intervention but cannot be treated by curative resection. In total, 73% of placebo patients crossed over to everolimus after disease progression, as permitted by study protocol. The dose should be reduced to 5 mg once daily in patients with moderate (Child-Pugh class B) hepatic impairment. The most common (? 3%) grade 3 or 4 laboratory abnormalities were hyperglycemia, lymphopenia, decreased hemoglobin, hypophosphatemia, increased ALP, neutropenia, increased AST, decreased potassium, and thrombocytopenia. After crossover to open-label everolimus, there were 3 additional deaths, 1 due to hypoglycemia and cardiac arrest in a patient with insulinoma, 1 due to myocardial infarction with congestive heart failure, and 1 due to sudden death. The trial was discontinued early, after the independent data and safety monitoring committee observed more serious adverse events and deaths in the placebo group, as well as a difference in progression-free survival favoring sunitinib.
Five patients receiving sunitinib and nine receiving placebo died on-study; of the five sunitinib on-study deaths, one was due to cardiac failure and four were due to disease progression. Adverse events resulted in permanent discontinuation in 20% and 6% of patients in the everolimus and placebo groups, respectively. Although 32% of the patients died during the course of the study, only 50% of the 67 deaths were attributable to ZES-related causes.
An additional sunitinib patient was taken off study due to cardiac failure and died 2 months later. Improvements in progression-free survival were observed across all patient subgroups, irrespective of prior somatostatin analog use.
If strong inducers of CYP3A4 are required, the dose can be increased in 5-mg increments to a maximum of 20 mg once daily.
Dose delays or reductions were necessary in 61% of everolimus patients and 29% of placebo patients. Those causes were mainly liver metastases with progressive anorexia and cachexia (67%) or secondary endocrine tumors consequent to MEN-1 syndrome. An interim analysis showed no difference between groups in overall survival (HR = 1.05, P = NS).
Opportunistic infections in patients with advanced neuroendocrine tumors included hepatitis B reactivation (resulting in death), mycobacterial infection, and invasive aspergillus. The development of bone or liver metastases (especially diffuse liver disease) or of ectopic Cushing syndrome during the study period predicted for decreased survival times.
Last accessed July 12, 2016.Treatment Option OverviewLocalized DiseaseIf technically and medically feasible, primary management of endocrine tumors of the pancreas involves surgical resection with curative intent. Muggia, MD (New York University Medical Center)Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website's Email Us. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.Levels of EvidenceSome of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Adult Treatment Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.Permission to Use This SummaryPDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. Siperstein AE, Berber E: Cryoablation, percutaneous alcohol injection, and radiofrequency ablation for treatment of neuroendocrine liver metastases.



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