Vipoma
Carcinoid Tumor
Neuroendocrine Tumors
Practice Guidelines as Topic
Neoplasm Staging
Guideline Adherence
Carcinoma, Neuroendocrine
Pancreatic polypeptide hyperplasia causing watery diarrhea syndrome: a case report. (1/23)
Neuroendocrine tumours of the pancreas can secrete numerous peptides, leading to various recognizable clinical syndromes. The secretion of pancreatic polypeptide has been used as a marker for neuroendocrine tumours but is considered to be a biologically inert peptide. A 37-year-old woman had watery diarrhea syndrome from pancreatic polypeptide hyperplasia. Only 2 other reported cases in the literature have described pancreatic polypeptide hyperplasia; however, this is the first reported case in which the patient was successfully treated by surgical resection, with a 2-year follow-up. This report and review of the literature illustrate that pancreatic polypeptide hypersecretion may present as a clinical endocrinopathy. (+info)Mutations of the DPC4/Smad4 gene in neuroendocrine pancreatic tumors. (2/23)
Tumors of the endocrine pancreas are extremely rare, and molecular mechanisms leading to their development are not well understood. A candidate tumor suppressor gene, DPC4, located at 18q21, has recently been shown to be inactivated in half of pancreatic adenocarcinoma xenografts. The close anatomical relationship of the exocrine and endocrine pancreas prompted us to determine the role of DPC4 in the tumorigenesis of 25 pancreatic islet cell tumors (11 insulinomas, nine non-functioning endocrine carcinomas, three gastrinomas, two vipomas). A mutation screening of the highly conserved COOH-terminal domain of DPC4 (exons 8-11) was performed by single-strand conformational variant (SSCP) analysis and a PCR-based deletion assay. Five of nine (55%) non-functioning endocrine pancreatic carcinomas revealed either point mutations, small intragenic deletions or homozygous deletion of DPC4 sequences compared to none of the insulinomas, gastrinomas or vipomas. These results suggest that DPC4 is an important target gene promoting tumorigenesis of non-functioning neuroendocrine pancreatic carcinomas. (+info)Putative tumor suppressor loci at 6q22 and 6q23-q24 are involved in the malignant progression of sporadic endocrine pancreatic tumors. (3/23)
Our previous comparative genomic hybridization study on sporadic endocrine pancreatic tumors (EPTs) revealed frequent losses on chromosomes 11q, 3p, and 6q. The aim of this study was to evaluate the importance of 6q losses in the oncogenesis of sporadic EPTs and to narrow down the smallest regions of allelic deletion. A multimodal approach combining polymerase chain reaction-based allelotyping, double-target fluorescence in situ hybridization, and comparative genomic hybridization was used in a collection of 109 sporadic EPTs from 93 patients. Nine polymorphic microsatellite markers (6q13 to 6q25-q27) were investigated, demonstrating a loss of heterozygosity (LOH) in 62.2% of the patients. A LOH was significantly more common in tumors >2 cm in diameter than below this threshold as well as in malignant than in benign tumors. We were able to narrow down the smallest regions of allelic deletion at 6q22.1 (D6S262) and 6q23-q24 (D6S310-UTRN) with LOH-frequencies of 50.0% and 41.2 to 56.3%, respectively. Several promising tumor suppressor candidates are located in these regions. Additional fluorescence in situ hybridization analysis on 46 EPTs using three locus-specific probes (6q21, 6q22, and 6q27) as well as a centromere 6-specific probe revealed complete loss of chromosome 6 especially in metastatic disease. We conclude that the two hot spots found on 6q may harbor putative tumor suppressor genes involved not only in the oncogenesis but maybe also in the malignant and metastatic progression of sporadic EPTs. (+info)Prevalence, characteristics and prognosis of MEN 1-associated glucagonomas, VIPomas, and somatostatinomas: study from the GTE (Groupe des Tumeurs Endocrines) registry. (4/23)
Few studies have concerned the rare functioning endocrine pancreatic tumors associated with multiple endocrine neoplasia type 1 (MEN 1). When sporadic, these tumors have a poor prognosis. AIM: To analyze the frequency, characteristics and prognosis of MEN 1-associated glucagonomas, VIPomas and somatostatinomas recorded in the GTE (Groupe des Tumeurs Endocrines) registry. METHODS: Records of the patients whose GTE registry codes included glucagonoma, VIPoma or somatostatinoma were reviewed. The diagnosis was confirmed when there were clinical signs of a functioning tumor and/or when blood levels of the peptide were higher than twice the upper limit of normal. RESULTS: Among 580 patients with MEN 1, duodeno-pancreatic involvement was present in 307 (52.9%). Five (1.6%) had a glucagonoma, 3 (0.98%) a VIPoma and 2 (0.65%) a somatostatinoma. A clinical syndrome was present in 1 patient with glucagonoma, in the 3 with VIPomas and in 1 with somatostatinoma. Tumor size was greater than 3 cm more often for these rare tumours (67%) than in patients with other type of duodeno-pancreatic involvement (28%) (P=0.02) and visceral metastases were more frequent (40% vs 15%; P=0.056). Ten-year survival of patients with glucagonomas, VIPomas or somatostatinomas (53.8%; CI95%: 15.5-92.1) was poorer than that of patients with insulinomas (91.4%; CI95%: 83.399.5; P=0.01) or gastrinomas (81.7%; CI95%: 74.9-88.5; P=0.20) and close to that of patients with non-functioning tumors (62.2%, CI95%: 41.0-83.9; NS). CONCLUSION: Glucagonomas, VIPomas and somatostatinomas, especially the functioning type, are very rare in patients with MEN 1. Prognosis is poor, probably because of large tumor size and high rate of metastasis. Survival is similar to that in patients with non-functioning tumors. (+info)BRAF gene mutations are rare events in gastroenteropancreatic neuroendocrine tumors. (5/23)
The BRAF gene, one of the human isoforms of RAF, is activated by ras, leading to cooperative effects in cells responsive to growth factor signals. We studied the frequency of BRAF and k-ras-2 mutations in primary neuroendocrine gastroenteropancreatic (GEP) tumors. Mutation analysis of the BRAF and k-ras-2 genes was performed in 40 primary neuroendocrine tumors of the GEP system. The expression of extracellular signaling-related kinase (ERK) 1/2, an important downstream point of convergence in the ras-RAF-mitogen-activated protein-ERK pathway was analyzed immunohistochemically. We detected one 1796 T-->A BRAF mutation that led to a substitution of valine by glutamic acid at position 599 (V599E) in 40 primary neuroendocrine GEP tumors (3%). We failed to detect specific mutation of the k-ras-2 gene. We identified constitutively activated ERK in almost all neuroendocrine tumor tissues tested irrespective of BRAF mutation or localization or functional activity. These results suggest that BRAF mutations do not have a role in tumorigenesis of neuroendocrine tumors. Nevertheless, activation of the RAF/mitogen-activated protein kinase pathway might have a causative role in the development of neuroendocrine tumors, independent of BRAF or k-ras-2 mutation. (+info)Outcome of duodenopancreatic resections in patients with multiple endocrine neoplasia type 1. (6/23)
OBJECTIVE: To evaluate the outcome of an aggressive surgical approach for duodenopancreatic neuroendocrine tumors (PETs) associated with multiple endocrine neoplasia type 1 (MEN1). SUMMARY BACKGROUND DATA: The management of PETs is still controversial in the setting of the autosomal dominant inherited MEN1 syndrome. METHODS: MEN1 patients that had either biochemical evidence of functioning PETs or visualized nonfunctioning PETs larger than 1 cm in size on imaging were operated. Since 1997, patients were followed annually by biochemical testing and imaging studies. RESULTS: Twenty-six genetically confirmed MEN1 patients underwent duodenopancreatic resection for functioning (n = 17) or nonfunctioning (n = 9) PETs. Ten (38%) patients had malignant PETs as characterized by the presence of lymph node (10 patients) and/or distant metastases (2 patients). The surgical approach was selected based on the type, location, and size of PETs. Four Zollinger-Ellison syndrome (ZES) patients required pylorus preserving pancreaticoduodenectomy (PPPD) as initial or redo procedure, 20 patients underwent other duodenopancreatic resections, and 2 patients had simple enucleations of PETs. After median 83 months (range, 5-241 months), 24 patients were alive and 2 patients died of an unrelated cause. All patients with insulinoma or vipoma and 7 of 11 patients with ZES were biochemically cured, including the ZES patients who underwent PPPD. However, 19 of 26 (73%) patients developed new small PETs (<1 cm) in the pancreatic remnant, but no patient had yet detectable metastases on imaging. CONCLUSIONS: Early and aggressive surgery of PETs in MEN1 patients prevents the development of liver metastases, which are the most life-threatening determinant. PPPD might be the procedure of choice for MEN1-ZES, which has to be proven in large scale studies. (+info)Watery diarrhea, hypokalemia and achlorhydria syndrome due to an adrenal pheochromocytoma. (7/23)
Watery diarrhea, hypokalemia and achlorhydria (WDHA) syndrome caused by vasoactive intestinal polypeptide (VIP) -producing tumor only rarely occurs in patients with nonpancreatic disease. A 49-year-old woman was referred for evaluation of a right adrenal tumor incidentally diagnosed by abdominal ultrasound during the investigation of chronic watery diarrhea. Laboratory findings showed hypokalemia and excessive production of VIP and catecholamines. After surgical resection of the tumor, diarrhea subsided and both electrolytes and affected hormone levels normalized. Immunohistochemical examination confirmed a diagnosis of pheochromocytoma, which contained VIP-positive ganglion-like cells. We herein present the clinical and histogenetic implications of this rare clinical entity, with literature review. (+info)Population-based study of islet cell carcinoma. (8/23)
BACKGROUND: We examine the epidemiology, natural history, and prognostic factors that affect the duration of survival for islet cell carcinoma by using population-based registries. METHODS: The Surveillance, Epidemiology, and End Results (SEER) Program database (1973-2003 release, April 2006) was used to identify cases of islet cell carcinoma by histology codes and tumor site. RESULTS: A total of 1310 (619 women and 691 men) cases with a median age of 59 years were identified. The annual age-adjusted incidence in the periods covered by SEER 9 (1973-1991), SEER 13 (1992-1999), and SEER 17 (2000-2003) were .16, .14, and .12 per 100,000, respectively. The estimated 28-year limited duration prevalence on January 1, 2003, in the United States was 2705 cases. Classified by SEER stage, localized, regional, and distant stages corresponded to 14%, 23%, and 54% of cases. The median survival was 38 months. By stage, median survival for patients with localized, regional, and distant disease were 124 (95% CI, 80-168) months, 70 (95% CI, 54-86) months, and 23 (95% CI, 20-26) months, respectively. By multivariate Cox proportional modeling, stage (P < .001), primary tumor location (P = .04), and age at diagnosis (P < .001) were found to be significant predictors of survival. CONCLUSIONS: Islet cell carcinomas account for approximately 1.3% of cancers arising in the pancreas. Most patients have advanced disease at the time of diagnosis. Despite the disease's reputation of being indolent, survival of patients with advanced disease remains only 2 years. Development of novel therapeutic approaches is needed. (+info)A vipoma, also known as a verner morrison syndrome or a non-insulin-secreting pancreatic tumor, is a rare medical condition characterized by the excessive production and secretion of vasoactive intestinal peptides (VIP) from a functional neuroendocrine tumor in the pancreas. This leads to a series of symptoms known as watery diarrhea, hypokalemia, and acidosis (WDHA) syndrome due to the effects of VIP on the gastrointestinal system. Symptoms include severe watery diarrhea, dehydration, electrolyte imbalances, and low blood pressure. Treatment typically involves surgical removal of the tumor, along with supportive care to manage symptoms and correct electrolyte abnormalities.
A carcinoid tumor is a type of slow-growing neuroendocrine tumor that usually originates in the digestive tract, particularly in the small intestine. These tumors can also arise in other areas such as the lungs, appendix, and rarely in other organs. Carcinoid tumors develop from cells of the diffuse endocrine system (also known as the neuroendocrine system) that are capable of producing hormones or biologically active amines.
Carcinoid tumors can produce and release various hormones and bioactive substances, such as serotonin, histamine, bradykinins, prostaglandins, and tachykinins, which can lead to a variety of symptoms. The most common syndrome associated with carcinoid tumors is the carcinoid syndrome, characterized by flushing, diarrhea, abdominal cramping, and wheezing or difficulty breathing.
Carcinoid tumors are typically classified as functional or nonfunctional based on whether they produce and secrete hormones that cause symptoms. Functional carcinoid tumors account for approximately 30% of cases and can lead to the development of carcinoid syndrome, while nonfunctional tumors do not produce significant amounts of hormones and are often asymptomatic until they grow large enough to cause local or distant complications.
Treatment options for carcinoid tumors depend on the location, size, and extent of the tumor, as well as whether it is functional or nonfunctional. Treatment may include surgery, medications (such as somatostatin analogs, chemotherapy, or targeted therapies), and radiation therapy. Regular follow-up with imaging studies and biochemical tests is essential to monitor for recurrence and assess treatment response.
Neuroendocrine tumors (NETs) are a diverse group of neoplasms that arise from cells of the neuroendocrine system, which is composed of dispersed neuroendocrine cells throughout the body, often in close association with nerves and blood vessels. These cells have the ability to produce and secrete hormones or hormone-like substances in response to various stimuli. NETs can occur in a variety of organs, including the lungs, pancreas, small intestine, colon, rectum, stomach, and thyroid gland, as well as in some less common sites such as the thymus, adrenal glands, and nervous system.
NETs can be functional or nonfunctional, depending on whether they produce and secrete hormones or hormone-like substances that cause specific symptoms related to hormonal excess. Functional NETs may give rise to a variety of clinical syndromes, such as carcinoid syndrome, Zollinger-Ellison syndrome, pancreatic neuroendocrine tumor syndrome (also known as Verner-Morrison or WDHA syndrome), and others. Nonfunctional NETs are more likely to present with symptoms related to the size and location of the tumor, such as abdominal pain, intestinal obstruction, or bleeding.
The diagnosis of NETs typically involves a combination of imaging studies, biochemical tests (e.g., measurement of serum hormone levels), and histopathological examination of tissue samples obtained through biopsy or surgical resection. Treatment options depend on the type, location, stage, and grade of the tumor, as well as the presence or absence of functional symptoms. They may include surgery, radiation therapy, chemotherapy, targeted therapy, and/or peptide receptor radionuclide therapy (PRRT).
Lung neoplasms refer to abnormal growths or tumors in the lung tissue. These tumors can be benign (non-cancerous) or malignant (cancerous). Malignant lung neoplasms are further classified into two main types: small cell lung carcinoma and non-small cell lung carcinoma. Lung neoplasms can cause symptoms such as cough, chest pain, shortness of breath, and weight loss. They are often caused by smoking or exposure to secondhand smoke, but can also occur due to genetic factors, radiation exposure, and other environmental carcinogens. Early detection and treatment of lung neoplasms is crucial for improving outcomes and survival rates.
Practice guidelines, also known as clinical practice guidelines, are systematically developed statements that aim to assist healthcare professionals and patients in making informed decisions about appropriate health care for specific clinical circumstances. They are based on a thorough evaluation of the available scientific evidence, consensus of expert opinion, and consideration of patient preferences. Practice guidelines can cover a wide range of topics, including diagnosis, management, prevention, and treatment options for various medical conditions. They are intended to improve the quality and consistency of care, reduce unnecessary variations in practice, and promote evidence-based medicine. However, they should not replace clinical judgment or individualized patient care.
Neoplasm staging is a systematic process used in medicine to describe the extent of spread of a cancer, including the size and location of the original (primary) tumor and whether it has metastasized (spread) to other parts of the body. The most widely accepted system for this purpose is the TNM classification system developed by the American Joint Committee on Cancer (AJCC) and the Union for International Cancer Control (UICC).
In this system, T stands for tumor, and it describes the size and extent of the primary tumor. N stands for nodes, and it indicates whether the cancer has spread to nearby lymph nodes. M stands for metastasis, and it shows whether the cancer has spread to distant parts of the body.
Each letter is followed by a number that provides more details about the extent of the disease. For example, a T1N0M0 cancer means that the primary tumor is small and has not spread to nearby lymph nodes or distant sites. The higher the numbers, the more advanced the cancer.
Staging helps doctors determine the most appropriate treatment for each patient and estimate the patient's prognosis. It is an essential tool for communication among members of the healthcare team and for comparing outcomes of treatments in clinical trials.
Guideline adherence, in the context of medicine, refers to the extent to which healthcare professionals follow established clinical practice guidelines or recommendations in their daily practice. These guidelines are systematically developed statements designed to assist practitioners and patient decisions about appropriate health care for specific clinical circumstances. Adherence to evidence-based guidelines can help improve the quality of care, reduce unnecessary variations in practice, and promote optimal patient outcomes. Factors that may influence guideline adherence include clinician awareness, familiarity, agreement, self-efficacy, outcome expectancy, and the complexity of the recommendation.
Carcinoma, neuroendocrine is a type of cancer that arises from the neuroendocrine cells, which are specialized cells that have both nerve and hormone-producing functions. These cells are found throughout the body, but neuroendocrine tumors (NETs) most commonly occur in the lungs, gastrointestinal tract, pancreas, and thyroid gland.
Neuroendocrine carcinomas can be classified as well-differentiated or poorly differentiated based on how closely they resemble normal neuroendocrine cells under a microscope. Well-differentiated tumors tend to grow more slowly and are less aggressive than poorly differentiated tumors.
Neuroendocrine carcinomas can produce and release hormones and other substances that can cause a variety of symptoms, such as flushing, diarrhea, wheezing, and heart palpitations. Treatment for neuroendocrine carcinoma depends on the location and extent of the tumor, as well as the patient's overall health. Treatment options may include surgery, radiation therapy, chemotherapy, targeted therapy, or a combination of these approaches.
VIPoma
Vasoactive intestinal peptide
Apudoma
Olivia Williams
Adenocarcinoma
Multiple endocrine neoplasia type 1
Endocrine oncology
List of MeSH codes (C04)
List of syndromes
List of MeSH codes (C19)
List of MeSH codes (C06)
International Classification of Diseases for Oncology
Pancreatic neuroendocrine tumor
Carcinoma
List of diseases (V)
VIPoma - Wikipedia
vipoma - Flashcard Collection
Vipoma - Cancer Therapy Advisor
Neuroendocrine Tumors Guidelines: Initial Evaluation, Grading and Staging, Gastrointestinal and Pulmonary Carcinoid Tumors
Vipoma - Gastrointestinal Disorders - MSD Manual Professional Edition
Multi-visceral resection of pancreatic VIPoma in a patient with sinistral portal hypertension<...
Pancreatic Neuroendocrine Neoplasms (pNENs) - Symptoms, Causes, Treatment | NORD
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Emergent Treatment of Gastroenteritis: Background, Pathophysiology, Etiology
Article - Billing and Coding: Octreotide Acetate for Injectable Suspension (Sandostatin® LAR Depot) (A56531)
Multiple Endocrine Neoplasias - MEN | Choose the Right Test
Sandostatin LAR Depot - Drug Information from Guideline Central
Flashcards - ABSITE ch 33 pancreas.txt
Nutrients | Free Full-Text | Potassium Metabolism and Management in Patients with CKD
Oncologic Therapies
Notes from Dr. RW: June 2009
Sepsecs Mouse Gene Details | Sep (O-phosphoserine) tRNA:Sec (selenocysteine) tRNA synthase | International Mouse Phenotyping...
Diarrhea - Gastrointestinal Disorders - Merck Manuals Professional Edition
Bio2Vec
Uses of Sandostatin | Vinmec
Antidiarrheal Drugs | Concise Medical Knowledge
Erika+2211969 Shared 'Gastrointestinal' - 64 Picmonics
Why You Keep Getting Diarrhea On, and Off: Possible causes, Doctor Explains. - Oh My Gut
DeCS 2011 - January 06, 2011 version
Chromogranin A: Reference Range, Interpretation, Collection and Panels
Insulinoma1
- They can be functional, exhibiting a hormonal hypersecretion syndrome, but can be non-functional presenting with non-specific symptoms and include insulinoma, glucagonoma, VIPoma, somatostatinoma (SSoma), PPoma and Zollinger-Ellison syndrome (ZES, or gastrinoma) and other ectopic hormone producing tumors (such as GRFoma) (see these terms). (findzebra.com)
Tumor3
- A VIPoma or vipoma (/vɪˈpoʊmə/) is a rare endocrine tumor that overproduces vasoactive intestinal peptide (thus VIP + -oma). (wikipedia.org)
- A vipoma is a non-beta pancreatic islet cell tumor secreting vasoactive intestinal peptide (VIP), resulting in a syndrome of watery diarrhea, hypokalemia, and achlorhydria (WDHA syndrome). (msdmanuals.com)
- During a ct scan and pet scan for a vipoma -pancreatic tumor, my left lung showed a growth, I also have sleep apnea. (candacesilversstudios.com)
Pancreatic2
- Vipoma (Verner-Morrison syndrome, pancreatic cholera, WDHA syndrome - for watery diarrhea, hypokalemia, and achlorhydria) is one of several rare types of functioning pancreatic neuroendocrine tumors (NETs) and accounts for 2-4% of all pancreatic NETs. (cancertherapyadvisor.com)
- A three-dimensional (3-D) pancreas protocol computed tomography scan revealed an 18 × 12 cm pancreatic VIPoma abutting the liver, stomach, spleen, left adrenal, colon that also invaded the distal duodenum - proximal jejunum at the ligament of Treitz in association with sinistral portal hypertension. (elsevierpure.com)
Tumors1
- Aggressive resection of patients with advanced VIPoma neuroendocrine tumors has rarely been reported. (elsevierpure.com)
Diarrhea3
- Order fasting serum VIP for patients suspected of having vipoma (presenting with otherwise unexplained high volume secretory diarrhea, supported by low osmotic gap in a stool specimen). (cancertherapyadvisor.com)
- A single elevated fasting VIP concentration in the presence of secretory diarrhea should be repeated to establish the diagnosis of vipoma. (cancertherapyadvisor.com)
- Diagnosis of vipoma requires demonstration of secretory diarrhea (stool osmolality is close to plasma osmolality, and twice the sum of sodium and potassium concentration in the stool accounts for all measured stool osmolality). (msdmanuals.com)
Syndrome1
- Although false ves being reported, alzheimers disease chromosome codes for non-numerical data may be justied to make sure responses are consistent with the vipoma syndrome. (familytreecounseling.com)
Serum1
- In vipoma, fasting serum VIP concentrations are usually greater than 75 pg/mL. (cancertherapyadvisor.com)
Left1
- Following preoperative proximal splenic artery embolization, the patient with underwent successful en bloc resection of the locally advanced VIPoma in conjunction with a diaphragmatic resection, total gastrectomy, splenectomy, left adrenalectomy, as well as small and large bowel resection. (elsevierpure.com)
Vasoactive7
- A VIPoma or vipoma (/vɪˈpoʊmə/) is a rare endocrine tumor that overproduces vasoactive intestinal peptide (thus VIP + -oma). (wikipedia.org)
- VIPoma causes cells in the pancreas to produce a high level of a hormone called vasoactive intestinal peptide (VIP). (medlineplus.gov)
- A doctor bases the diagnosis of vipoma on the person's diarrhea symptoms and finding elevated levels of vasoactive intestinal peptide (VIP) in the blood. (msdmanuals.com)
- We report a patient with MEN-I who exhibited rapid growth of multiple collagenomas after pancreatic enucleation of a vasoactive intestinal peptide-secreting tumor (VIPoma) and excision of multiple pancreatic masses. (nih.gov)
- Pancreatic neuroendocrine tumors can overproduce hormones such as insulin (insulinoma), gastrin (gastrinoma), glucagon (glucagonoma), or vasoactive peptide protein (VIPoma). (news-medical.net)
- Vipoma is an acronym which stands for vasoactive intestinal polypeptide (VIP), which is otherwise known as Verner Morrison syndrome. (cancerwall.com)
- VIPoma - the over-production of vasoactive intestinal peptide by a VIPoma can cause severe watery diarrhoea and fatigue, muscle weakness and palpitations due to a low blood potassium level. (yourhormones.info)
Insulinoma1
- The primary pathology was tumour (benign insulinoma 3, malignant vipoma 3, mixed endocrine tumours 3, cystadenoma 1 and cystadenocarcinoma 1), pancreatitis (acute 5, chronic 2) and trauma (2). (ox.ac.uk)
Pancreatic VIPoma2
Islet1
- VIPoma is a very rare cancer that usually grows from cells in the pancreas called islet cells. (medlineplus.gov)
Excision1
- 9. Cure of intractable watery diarrhoea by excision of a vipoma. (nih.gov)
Diagnosis1
- Despite of continuous octreotide therapy, interferon and two courses of combination chemotherapy, the hepatic metastases failed to regress and the patient died 10 months after the diagnosis of a metastatic VIPoma. (e-enm.org)
People2
- Some people seem to respond to a combination chemo called capecitabine and temozolomide but there is no report that it totally cured people of VIPoma. (wikipedia.org)
- Each year, only about 1 in 1 million people are diagnosed with a VIPoma. (medlineplus.gov)