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1. Elie BT, Gocheva V, Shree T, Dalrymple SA, Holsinger LJ, Joyce JA: Identification and pre-clinical testing of a reversible cathepsin protease inhibitor reveals anti-tumor efficacy in a pancreatic cancer model. Biochimie; 2010 Nov;92(11):1618-24
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  • [Title] Identification and pre-clinical testing of a reversible cathepsin protease inhibitor reveals anti-tumor efficacy in a pancreatic cancer model.
  • Therefore, the discovery of effective cathepsin inhibitors has considerable potential for anti-cancer therapy.
  • VBY-825 was tested in a pre-clinical model of pancreatic islet cancer and found to significantly decrease tumor burden and tumor number.
  • Thus, the identification of VBY-825 as a new and effective anti-tumor drug encourages the therapeutic application of cathepsin inhibitors in cancer.

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  • [Copyright] Copyright © 2010 Elsevier Masson SAS. All rights reserved.
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  • (PMID = 20447439.001).
  • [ISSN] 1638-6183
  • [Journal-full-title] Biochimie
  • [ISO-abbreviation] Biochimie
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA125162; United States / NCI NIH HHS / CA / CA125162-04; United States / NCI NIH HHS / CA / P30 CA008748; United States / NCI NIH HHS / CA / R01-CA125162; United States / NCI NIH HHS / CA / 3P30CA008748-44S4; United States / NCI NIH HHS / CA / R01 CA125162-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hydrocarbons, Fluorinated; 0 / JPM 565; 0 / Protease Inhibitors; 0 / Sulfones; 0 / VBY-825; EC 3.4.- / Cathepsins; GMW67QNF9C / Leucine
  • [Other-IDs] NLM/ NIHMS202086; NLM/ PMC3814225
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2. Pautrat K, Bretagnol F, de Muret A, de Calan L: [Recurrent glucagonoma 20 years after surgical resection]. Gastroenterol Clin Biol; 2003 Dec;27(12):1163-5
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  • Glucagonoma is a rare islet alpha-cell pancreatic tumor.
  • Diagnosis is based on the presence of a pancreatic tumor in association with hyperglucagonemia.
  • Tumor characterization is made by computed tomography and/or pancreatic endoscopic ultrasonic and indium-labeled octreo-scan.
  • Surgery is the main component of the treatment, in some cases in association with chemotherapy.
  • We report the case of a 72-year-old patient who developed a recurrent glucagonoma, 20 years after surgical resection.
  • [MeSH-major] Glucagonoma / pathology. Glucagonoma / surgery. Neoplasm Recurrence, Local. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Aged. Female. Humans. Time Factors

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  • (PMID = 14770122.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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3. Shah MH, Young D, Kindler HL, Webb I, Kleiber B, Wright J, Grever M: Phase II study of the proteasome inhibitor bortezomib (PS-341) in patients with metastatic neuroendocrine tumors. Clin Cancer Res; 2004 Sep 15;10(18 Pt 1):6111-8
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  • PURPOSE: This phase II study was undertaken to assess objective response, toxicity, tumor marker response, and pharmacodynamics of bortezomib in patients with metastatic neuroendocrine (carcinoid and islet cell) tumors.
  • EXPERIMENTAL DESIGN: A total of 16 patients with measurable metastatic carcinoid (n=12) or islet cell (n=4) tumors received i.v. bolus of single agent bortezomib at a dose of 1.5 mg/m2 on days 1, 4, 8, and 11 every 21 days.
  • All patients were chemotherapy naïve and had Eastern Cooperative Oncology Group performance status of 0 to 1.
  • The patients received total of 264 doses of therapy with a median of 15 doses per patient.
  • CONCLUSIONS: Despite achieving the surrogate biologic end point, single-agent bortezomib did not induce any objective responses in patients with metastatic carcinoid or islet cell tumors.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Boronic Acids / therapeutic use. Carcinoid Tumor / drug therapy. Neuroendocrine Tumors / drug therapy. Pancreatic Neoplasms / drug therapy. Protease Inhibitors / therapeutic use. Pyrazines / therapeutic use
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor. Bortezomib. Female. Humans. Male. Maximum Tolerated Dose. Middle Aged. Neoplasm Metastasis. Proteasome Inhibitors. Time Factors. Treatment Outcome

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  • (PMID = 15447997.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA63185
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
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4. Moore AS, Nelson RW, Henry CJ, Rassnick KM, Kristal O, Ogilvie GK, Kintzer P: Streptozocin for treatment of pancreatic islet cell tumors in dogs: 17 cases (1989-1999). J Am Vet Med Assoc; 2002 Sep 15;221(6):811-8
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  • [Title] Streptozocin for treatment of pancreatic islet cell tumors in dogs: 17 cases (1989-1999).
  • OBJECTIVE: To determine toxic effects of streptozocin given in combination with a diuresis protocol in dogs and establish whether streptozocin is efficacious in treatment of pancreatic islet cell tumors in dogs.
  • PROCEDURE: Medical records were reviewed to obtain information regarding signalment, tumor stage and staging tests performed, number of streptozocin treatments, adverse effects, results of biochemical and hematologic monitoring during streptozocin treatment, tumor dimensions, duration of normoglycemia, and date of death, when applicable.
  • RESULTS: 58 treatments were administered to the 17 dogs.
  • Only 1 dog developed azotemia.
  • Serum alanine aminotransferase activity increased in some dogs but decreased when treatment was discontinued.
  • Two dogs developed diabetes mellitus after receiving 5 doses.
  • CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that streptozocin can be administered safely to dogs at a dosage of 500 mg/m2, IV, every 3 weeks when combined with a protocol for induction of diuresis and may be efficacious in the treatment of dogs with metastatic pancreatic islet cell tumors.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Carcinoma, Islet Cell / veterinary. Dog Diseases / drug therapy. Pancreatic Neoplasms / veterinary. Streptozocin / therapeutic use
  • [MeSH-minor] Animals. Dogs. Female. Male. Neoplasm Staging / veterinary. Retrospective Studies. Treatment Outcome

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  • (PMID = 12322919.001).
  • [ISSN] 0003-1488
  • [Journal-full-title] Journal of the American Veterinary Medical Association
  • [ISO-abbreviation] J. Am. Vet. Med. Assoc.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 5W494URQ81 / Streptozocin
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5. Pittenger GL, Taylor-Fishwick DA, Johns RH, Burcus N, Kosuri S, Vinik AI: Intramuscular injection of islet neogenesis-associated protein peptide stimulates pancreatic islet neogenesis in healthy dogs. Pancreas; 2007 Jan;34(1):103-11
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  • [Title] Intramuscular injection of islet neogenesis-associated protein peptide stimulates pancreatic islet neogenesis in healthy dogs.
  • It has been proposed that islet neogenesis from pancreatic progenitor cells may restore insulin secretion in diabetic mammals.
  • Islet neogenesis- associated protein (INGAP) stimulates islet neogenesis; therefore, we hypothesized that it would stimulate islet neogenesis in dogs.
  • After 30 days, pancreatic tissues were collected, and RNA and histological sections were analyzed.
  • There was a trend to increased insulin-positive cells and gene expression with treatments of 0.5 and 10 mg/kg peptide.
  • Protein gene product 9.5-positive cells were increased with treatment.
  • CONCLUSIONS: These results indicate that INGAP stimulates cells in the pancreatic duct epithelium of healthy dogs (putative islet progenitor cells) to develop along a neuroendocrine pathway and form new islets in response to INGAP peptide.
  • The INGAP might be an effective therapy for diabetes.
  • [MeSH-major] Antigens, Neoplasm / pharmacology. Biomarkers, Tumor / pharmacology. Islets of Langerhans / cytology. Islets of Langerhans / drug effects
  • [MeSH-minor] Animals. Cell Division / drug effects. Cricetinae. Diabetes Mellitus, Type 1 / drug therapy. Diabetes Mellitus, Type 2 / drug therapy. Dogs. Female. Fluorescent Antibody Technique. Injections, Intramuscular. Injections, Intravenous. Lectins, C-Type / genetics. Male. Mesocricetus. RNA, Messenger / metabolism. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / pharmacokinetics. Recombinant Fusion Proteins / pharmacology. Regeneration / drug effects

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  • (PMID = 17198191.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Lectins, C-Type; 0 / RNA, Messenger; 0 / Recombinant Fusion Proteins; 0 / pancreatitis-associated protein
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6. Kitami CE, Shimizu T, Sato O, Kurosaki I, Mori S, Yanagisawa Y, Ajioka Y, Hatakeyama K: Malignant islet cell tumor projecting into the main pancreatic duct. J Hepatobiliary Pancreat Surg; 2000;7(5):529-33
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  • [Title] Malignant islet cell tumor projecting into the main pancreatic duct.
  • We report herein a rare case of islet cell tumor showing a unique growth pattern in a patient who developed repeated acute pancreatitis as the tumor's initial symptom.
  • Preoperative imaging examinations showed dilatation of the main pancreatic duct (MPD) and cysts around the pancreatic tail.
  • A distal pancreatectomy with splenectomy was performed because the pancreatitis was localized in the distal pancreas and was not controlled by various drug therapies.
  • Grossly, the tumor consisted of two component parts: a markedly infiltrative part in the pancreatic parenchyma, and a papillary elevated part in the MPD.
  • The MPD was obstructed by the tumor spreading widely along the distal MPD.
  • Microscopically, the tumor was composed entirely of islet cell tumors (nonfunctioning), with several foci of venous and lymphatic involvement.
  • Based on its growth behavior, we assumed that the tumor may have arisen from the MPD or from islet cells closely adjacent to the MPD.
  • [MeSH-major] Carcinoma, Islet Cell / pathology. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Acute Disease. Humans. Male. Middle Aged. Neoplasm Invasiveness. Pancreatectomy. Pancreatitis / etiology

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  • (PMID = 11180883.001).
  • [ISSN] 0944-1166
  • [Journal-full-title] Journal of hepato-biliary-pancreatic surgery
  • [ISO-abbreviation] J Hepatobiliary Pancreat Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 22
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7. Pittenger GL, Taylor-Fishwick D, Vinik AI: The role of islet neogeneis-associated protein (INGAP) in pancreatic islet neogenesis. Curr Protein Pept Sci; 2009 Feb;10(1):37-45
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  • [Title] The role of islet neogeneis-associated protein (INGAP) in pancreatic islet neogenesis.
  • Islet neogenesis, the regeneration of pancreatic islets from pancreatic stem cells, is arguably the least fraught with barriers to widespread use as a therapy for diabetes.
  • These animal models have led to the description of the reg family of proteins that appear to be related to islet regeneration.
  • Islet neogenesis-associated protein (INGAP) is an initiator of islet neogenesis in animal models and a peptide sequence from INGAP carries the biological activity.
  • INGAP is also found in the pancreas in human pathological states involving islet neogenesis.
  • The evidence points to INGAP as a major factor in stimulating islet neogenesis, and, therefore, may play a significant therapeutic role in diabetes.
  • [MeSH-major] Antigens, Neoplasm / physiology. Biomarkers, Tumor / physiology. Cytokines / therapeutic use. Diabetes Mellitus / drug therapy. Hypoglycemic Agents / therapeutic use. Islets of Langerhans / physiology. Lectins, C-Type / physiology. Peptide Fragments / therapeutic use. Regeneration / drug effects
  • [MeSH-minor] Animals. Clinical Trials as Topic. Disease Models, Animal. Humans. Pancreas / drug effects. Pancreas / physiology

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  • (PMID = 19275671.001).
  • [ISSN] 1389-2037
  • [Journal-full-title] Current protein & peptide science
  • [ISO-abbreviation] Curr. Protein Pept. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Cytokines; 0 / Hypoglycemic Agents; 0 / INGAP peptide; 0 / Lectins, C-Type; 0 / Peptide Fragments; 0 / pancreatitis-associated protein
  • [Number-of-references] 66
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8. McKenzie S, Lee W, Artinyan A, Mailey B, Pigazzi A, Ellenhorn J, Kim J: Surgical resection and multidisciplinary care for primary and metastatic pancreatic islet cell carcinomas. J Gastrointest Surg; 2010 Nov;14(11):1796-803
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  • [Title] Surgical resection and multidisciplinary care for primary and metastatic pancreatic islet cell carcinomas.
  • INTRODUCTION: The role of multidisciplinary management of islet cell cancers (ICC) has not been fully investigated in a population-based setting.
  • Patients were stratified by treatment received and clinicopathologic characteristics and survival were compared.
  • To determine whether adjuvant chemotherapy was associated with improved survival, we compared patients who underwent surgery alone compared to patients who underwent surgery followed by adjuvant chemotherapy.
  • Although patients with metastatic disease had 3-year longer survival with adjuvant chemotherapy, these improvements in survival were not statistically significant.
  • Furthermore, adjuvant chemotherapy was not associated with survival but does warrant further examination in patients with metastatic disease.
  • [MeSH-major] Carcinoma, Islet Cell / therapy. Pancreatectomy. Pancreatic Neoplasms / therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Survival Rate

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  • (PMID = 20480251.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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9. O'Grady HL, Conlon KC: Pancreatic neuroendocrine tumours. Eur J Surg Oncol; 2008 Mar;34(3):324-32
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  • [Title] Pancreatic neuroendocrine tumours.
  • Pancreatic neuroendocrine tumours (PET) are rare neoplasms of the pancreas accounting for less than 5% of all primary pancreatic malignancies.
  • Non-functioning PETs are pancreatic tumours with endocrine differentiation but lack a clinical syndrome of hormone hypersecretion.
  • Treatment is surgical excision with chemotherapy and hormonal therapy is controversial.
  • For functioning PETs, surgery remains the optimal therapy, however, long-term survival can be expected even in the presence of metastases.
  • With advances in medical management, radiolabelled somatostatin therapy, hepatic arterial chemoembolisation and radiofrequency ablation, symptoms may be controlled to optimize quality of life.
  • [MeSH-major] Adenoma, Islet Cell. Carcinoma, Islet Cell. Pancreatic Neoplasms
  • [MeSH-minor] Algorithms. Biomarkers, Tumor. Diagnostic Imaging. Humans. Neoplasm Metastasis. Prognosis

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  • (PMID = 17967523.001).
  • [ISSN] 1532-2157
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 74
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10. Ramanathan RK, Cnaan A, Hahn RG, Carbone PP, Haller DG: Phase II trial of dacarbazine (DTIC) in advanced pancreatic islet cell carcinoma. Study of the Eastern Cooperative Oncology Group-E6282. Ann Oncol; 2001 Aug;12(8):1139-43
Hazardous Substances Data Bank. DACARBAZINE .

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  • [Title] Phase II trial of dacarbazine (DTIC) in advanced pancreatic islet cell carcinoma. Study of the Eastern Cooperative Oncology Group-E6282.
  • BACKGROUND: A phase II study of dacarbazine (DTIC), was conducted to determine the response rate, duration of response, toxicity and overall survival of patients with advanced pancreatic islet cell tumors.
  • PATIENTS AND METHODS: Fifty patients with advanced pancreatic islet cell tumors, having progressive symptoms or evidence of rapidly advancing disease were entered on this study.
  • The majority of the responses were seen in patients without prior chemotherapy.
  • CONCLUSIONS: DTIC has activity in advanced previously untreated pancreatic islet cell tumors.

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  • (PMID = 11583197.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA13650; United States / NCI NIH HHS / CA / CA15488; United States / NCI NIH HHS / CA / CA21076; United States / NCI NIH HHS / CA / CA2111; United States / NCI NIH HHS / CA / CA23318; United States / NCI NIH HHS / CA / CA39229; United States / NCI NIH HHS / CA / CA66636
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 7GR28W0FJI / Dacarbazine
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11. Ekeblad S: Islet cell tumours. Adv Exp Med Biol; 2010;654:771-89
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  • [Title] Islet cell tumours.
  • Pancreatic endocrine tumours can cause hormonal symptoms by over-secretion of hormones.
  • They are less aggressive than exocrine pancreatic cancer, but carry a variable prognosis.
  • The tumours are either sporadic or hereditary, as part of the multiple endocrine neoplasia type 1 syndrome.
  • Hereditary forms of pancreatic endocrine tumours are caused by mutations in the MEN1 gene.
  • It is hoped that the tumour-node-metastasis system and other prognostic markers will be adopted in clinical routine and improve prognostication and treatment choices.
  • Surgery is still the only cure, but several new palliative drugs and interventions are in use or under investigation.
  • Radiofrequency ablation is increasingly used for liver metastases, and a number of new chemotherapy drugs are being tested.
  • Despite improvements in treatment, no clear improvement in survival has been demonstrated.
  • [MeSH-major] Adenoma, Islet Cell / therapy. Multiple Endocrine Neoplasia Type 1 / therapy
  • [MeSH-minor] Animals. Hormones / metabolism. Humans. Insulinoma / metabolism. Medical Oncology / methods. Neoplasm Metastasis. Time Factors. Treatment Outcome

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  • (PMID = 20217524.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hormones
  • [Number-of-references] 81
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12. Varker KA, Campbell J, Shah MH: Phase II study of thalidomide in patients with metastatic carcinoid and islet cell tumors. Cancer Chemother Pharmacol; 2008 Apr;61(4):661-8
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  • [Title] Phase II study of thalidomide in patients with metastatic carcinoid and islet cell tumors.
  • PURPOSE: Carcinoid and islet cell tumors are known to be highly vascular.
  • There is no effective systemic therapy currently available for metastatic disease.
  • Planned treatment duration was 24 weeks unless unacceptable toxicity or disease progression was observed.
  • CONCLUSIONS: Thalidomide was fairly well tolerated in patients with metastatic carcinoid/islet cell tumors, but failed to reveal any objective responses.
  • [MeSH-major] Adenoma, Islet Cell / drug therapy. Angiogenesis Inhibitors / therapeutic use. Carcinoid Tumor / drug therapy. Carcinoid Tumor / secondary. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / secondary. Thalidomide / therapeutic use
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Pancreatic Hormones / blood. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17589846.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Biomarkers, Tumor; 0 / Pancreatic Hormones; 106477-83-2 / pancreastatin; 4Z8R6ORS6L / Thalidomide
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13. Wang L, Zhao YP, Lee CI, Liao Q: Diagnosis and treatment of malignant pancreatic endocrine tumour. Chin Med Sci J; 2004 Jun;19(2):130-3
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  • [Title] Diagnosis and treatment of malignant pancreatic endocrine tumour.
  • OBJECTIVE: To summarize our experience in the diagnosis and treatment of malignant pancreatic endocrine tumour.
  • METHODS: We retrospectively reviewed 36 cases of malignant pancreatic endocrine tumours in our hospital from July 1987 to April 2002, and summarized its clinical features.
  • RESULTS: Liver metastasis was the main malignant manifestation of malignant pancreatic endocrine tumours (incidence rate 72.2%).
  • Removals of primary lesion and isolated hepatic metastatic lesion were means of curative therapy.
  • Interventional chemotherapy was an important adjuvant treatment.
  • CONCLUSION: Comprehensive therapy plays an important role in improving the prognosis of malignant pancreatic endocrine tumour.

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  • (PMID = 15250251.001).
  • [ISSN] 1001-9294
  • [Journal-full-title] Chinese medical sciences journal = Chung-kuo i hsueh k'o hsueh tsa chih
  • [ISO-abbreviation] Chin. Med. Sci. J.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] China
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14. Lipsett M, Hanley S, Castellarin M, Austin E, Suarez-Pinzon WL, Rabinovitch A, Rosenberg L: The role of islet neogenesis-associated protein (INGAP) in islet neogenesis. Cell Biochem Biophys; 2007;48(2-3):127-37

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  • [Title] The role of islet neogenesis-associated protein (INGAP) in islet neogenesis.
  • Islet Neogenesis-Associated Protein (INGAP) is a member of the Reg family of proteins implicated in various settings of endogenous pancreatic regeneration.
  • The expression of INGAP and other RegIII proteins has also been linked temporally and spatially with the induction of islet neogenesis in animal models of disease and regeneration.
  • Furthermore, administration of a peptide fragment of INGAP (INGAP peptide) has been demonstrated to reverse chemically induced diabetes as well as improve glycemic control and survival in an animal model of type 1 diabetes.
  • Cultured human pancreatic tissue has also been shown to be responsive to INGAP peptide, producing islet-like structures with function, architecture and gene expression matching that of freshly isolated islets.
  • Likewise, studies in normoglycemic animals show evidence of islet neogenesis.
  • Finally, recent clinical studies suggest an effect of INGAP peptide to improve insulin production in type 1 diabetes and glycemic control in type 2 diabetes.
  • [MeSH-major] Antigens, Neoplasm / physiology. Biomarkers, Tumor / physiology. Islets of Langerhans / physiology. Lectins, C-Type / physiology. Regeneration / physiology
  • [MeSH-minor] Animals. Clinical Trials, Phase II as Topic. Diabetes Mellitus / drug therapy. Diabetes Mellitus / metabolism. Drug Evaluation, Preclinical. Humans. Hypoglycemic Agents / pharmacology. Hypoglycemic Agents / therapeutic use. Pancreas / drug effects. Pancreas / metabolism. Pancreas / physiology

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  • (PMID = 17709882.001).
  • [ISSN] 1085-9195
  • [Journal-full-title] Cell biochemistry and biophysics
  • [ISO-abbreviation] Cell Biochem. Biophys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Hypoglycemic Agents; 0 / Lectins, C-Type; 0 / pancreatitis-associated protein
  • [Number-of-references] 104
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15. Kouvaraki MA, Ajani JA, Hoff P, Wolff R, Evans DB, Lozano R, Yao JC: Fluorouracil, doxorubicin, and streptozocin in the treatment of patients with locally advanced and metastatic pancreatic endocrine carcinomas. J Clin Oncol; 2004 Dec 1;22(23):4762-71
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  • [Title] Fluorouracil, doxorubicin, and streptozocin in the treatment of patients with locally advanced and metastatic pancreatic endocrine carcinomas.
  • PURPOSE: The role of systemic chemotherapy in the management of pancreatic endocrine carcinoma (islet cell carcinoma;.
  • Response rates ranging from 6% to 69% have been reported for streptozocin-based chemotherapy.
  • PATIENTS AND METHODS: Eligible patients had histologic or cytologic confirmation of their tumor and measurable disease on computed tomography or magnetic resonance imaging scans.
  • Response to treatment was evaluated in this study using the new international criteria proposed by the Response Evaluation Criteria in Solid Tumors Committee.
  • Analyses showed that metastatic replacement of more than 75% of the liver and prior chemotherapy were independently associated with inferior PFS.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Carcinoma, Islet Cell / drug therapy. Carcinoma, Islet Cell / secondary. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Dose-Response Relationship, Drug. Doxorubicin / administration & dosage. Drug Administration Schedule. Female. Fluorouracil / administration & dosage. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Pulse Therapy, Drug. Retrospective Studies. Risk Assessment. Sampling Studies. Streptozocin / administration & dosage. Survival Analysis. Treatment Outcome

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  • [ErratumIn] J Clin Oncol. 2005 Jan 1;23(1):248
  • (PMID = 15570077.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5W494URQ81 / Streptozocin; 80168379AG / Doxorubicin; U3P01618RT / Fluorouracil
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16. Didolkar MS, Coleman CW, Brenner MJ, Chu KU, Olexa N, Stanwyck E, Yu A, Neerchal N, Rabinowitz S: Image-guided stereotactic radiosurgery for locally advanced pancreatic adenocarcinoma results of first 85 patients. J Gastrointest Surg; 2010 Oct;14(10):1547-59
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  • [Title] Image-guided stereotactic radiosurgery for locally advanced pancreatic adenocarcinoma results of first 85 patients.
  • BACKGROUND: Locally advanced unresectable pancreatic adenocarcinoma is characterized by poor survival despite chemotherapy and conventional radiation therapy (RT).
  • Recent advances in real-time image-guided stereotactic radiosurgery (SRS) have made it possible to treat these cancers in two to four fractions followed by systemic chemotherapy.
  • METHODS: Pancreatic SRS involves delivery of high doses of accurately targeted radiation given non-invasively in two to four fractions.
  • We treated 85 consecutive patients with locally advanced and recurrent pancreatic adenocarcinoma from February 2004 to November 2009.
  • Age range: 36-88 years, median 66 years; sex: 50 males, 35 females; race: 79 Caucasian, five African American, one Asian; histology: 80 adenocarcinoma, three islet cell, two other.
  • All patients were unresectable at the time of SRS.
  • Pre-SRS chemotherapy was given in 48 patients.
  • All patients received gemcitabine-based chemotherapy regimen after SRS.
  • SRS doses ranged from 15 to 30 Gy with a mean dose of 25.5 Gy delivered in 3 days divided in equal fractions.
  • TOXICITY: A total of 19 (22.37%) patients developed grades III/IV GI toxicity including duodenitis, 12 (14.1%); gastritis, 11 (12.9%); diarrhea, three (3.5%); and renal failure was noted in one (1.2%).
  • CONCLUSIONS: SRS for unresectable pancreatic carcinoma can be delivered in three fractions with minimal morbidity and a local tumor control rate of 91.7%.
  • The survival is comparable or better than the reported results for advanced pancreatic cancer, specifically for the group of previously untreated patients with unresectable tumors.
  • [MeSH-major] Adenocarcinoma / therapy. Pancreatic Neoplasms / therapy. Radiosurgery
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged. Neoplasm Staging. Surgery, Computer-Assisted. Survival Analysis

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  • (PMID = 20839073.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Ding XZ, Fehsenfeld DM, Murphy LO, Permert J, Adrian TE: Physiological concentrations of insulin augment pancreatic cancer cell proliferation and glucose utilization by activating MAP kinase, PI3 kinase and enhancing GLUT-1 expression. Pancreas; 2000 Oct;21(3):310-20
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  • [Title] Physiological concentrations of insulin augment pancreatic cancer cell proliferation and glucose utilization by activating MAP kinase, PI3 kinase and enhancing GLUT-1 expression.
  • Pancreatic carcinoma is characterized by poor prognosis and lack of response to conventional therapy for reasons that are not clear.
  • Because of the structural relationship between the exocrine and endocrine pancreas and high concentrations of islet hormones bathing pancreatic tissue, we hypothesized that pancreatic cancer cell proliferation and glucose utilization are regulated by pancreatic islet hormones, particularly insulin.
  • Based on this, the effect of islet hormones on pancreatic cancer cells in vitro was investigated.
  • Five pancreatic cancer cell lines, CD11, CD18, HPAF, PANC-1, and MiaPaCa2 were used to investigate the effect of islet hormones on cell proliferation, glucose utilization, and GLUT-1 expression.
  • Insulin, but not somatostatin and glucagon, induced pancreatic cancer cell growth in a concentration- and time-dependent manner.
  • Insulin significantly enhanced glucose utilization of pancreatic cancer cells before it enhanced cell proliferation.
  • Furthermore, after 24-hour treatment with insulin, GLUT-I expression in pancreatic cancer cells was markedly increased, indicating that insulin enhances glucose utilization partly through increasing glucose transport.
  • These findings suggest that insulin stimulates proliferation and glucose utilization in pancreatic cancer cells by two distinct pathways.
  • High intrapancreatic concentrations of insulin are likely to play an important role in stimulating pancreatic cancer growth indirectly by increasing substrate availability as well as by direct action as a trophic factor.
  • [MeSH-major] Glucose / metabolism. Insulin / administration & dosage. Monosaccharide Transport Proteins / analysis. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. Protein Kinases / metabolism
  • [MeSH-minor] Androstadienes / pharmacology. Cell Division / drug effects. DNA, Neoplasm / biosynthesis. Enzyme Activation / drug effects. Enzyme Inhibitors / pharmacology. Flavonoids / pharmacology. Glucagon / pharmacology. Glucose Transporter Type 1. Humans. Mitogen-Activated Protein Kinases / antagonists & inhibitors. Mitogen-Activated Protein Kinases / metabolism. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / metabolism. Somatostatin / pharmacology. Tumor Cells, Cultured

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  • (PMID = 11039477.001).
  • [ISSN] 0885-3177
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Androstadienes; 0 / DNA, Neoplasm; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Glucose Transporter Type 1; 0 / Insulin; 0 / Monosaccharide Transport Proteins; 0 / SLC2A1 protein, human; 51110-01-1 / Somatostatin; 9007-92-5 / Glucagon; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; IY9XDZ35W2 / Glucose; XVA4O219QW / wortmannin
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18. Kaubisch A, Kaleya R, Haynes H, Rozenblit A, Wadler S: Phase II clinical trial of parenteral hydroxyurea in combination with fluorouracil, interferon and filgrastim in the treatment of advanced pancreatic, gastric and neuroendocrine tumors. Cancer Chemother Pharmacol; 2004 Apr;53(4):337-40
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  • [Title] Phase II clinical trial of parenteral hydroxyurea in combination with fluorouracil, interferon and filgrastim in the treatment of advanced pancreatic, gastric and neuroendocrine tumors.
  • In the clinic, prolonged infusion of the RR inhibitor, hydroxyurea (HU), may be more effective than bolus or oral administration of drug.
  • METHODS: A clinical trial of parenteral, weekly, high-dose HU in combination with weekly, high-dose infusional fluorouracil (5FU) was initiated in patients with advanced pancreatic and gastric cancer.
  • Patients also received the biologic agent interferon alfa-2a 9 MU subcutaneously (s.c.) three times per week and filgrastim 480 microg s.c. on days 3 (starting after midday), 4, 5, and 6 each week.
  • Each cycle required treatment on days 1 and 8 every 22 days.
  • Primary sites included pancreas (18), gastric (13) and islet cell (1).
  • Of the 30 patients, 4 developed grade 3/4 diarrhea.
  • Of 12 evaluable patients with gastric cancer, 1 had a partial response, and there were no responders among patients with pancreatic cancer.
  • CONCLUSIONS: Combined inhibition of RR and TS using this high-dose, weekly, 48-h infusional regimen is not an improvement over single-agent therapy in these tumor types.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neuroendocrine Tumors / drug therapy. Pancreatic Neoplasms / drug therapy. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Drug Administration Schedule. Female. Filgrastim. Fluorouracil / administration & dosage. Fluorouracil / adverse effects. Granulocyte Colony-Stimulating Factor / administration & dosage. Granulocyte Colony-Stimulating Factor / adverse effects. Humans. Hydroxyurea / administration & dosage. Hydroxyurea / adverse effects. Infusions, Intravenous. Injections, Subcutaneous. Interferons / administration & dosage. Interferons / adverse effects. Male. Middle Aged. Neoplasm Metastasis. Recombinant Proteins. Treatment Outcome

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  • (PMID = 14704829.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 13330
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 9008-11-1 / Interferons; PVI5M0M1GW / Filgrastim; U3P01618RT / Fluorouracil; X6Q56QN5QC / Hydroxyurea
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19. Raymond E, Faivre S, Hammel P, Ruszniewski P: Sunitinib paves the way for targeted therapies in neuroendocrine tumors. Target Oncol; 2009 Dec;4(4):253-4
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  • [Title] Sunitinib paves the way for targeted therapies in neuroendocrine tumors.
  • Sunitinib demonstrating efficacy in pancreatic islet cell carcinomas will pave the way for further trials in other neuroendocrine tumor types such as carcinoid, poorly differentiated neuroendocrine disease, and several other endocrine tumors that are dependent on VEGF/VEGFR for angiogenesis.
  • In addition, other drugs with distinct mechanisms of action, such as mTOR inhibitors, currently investigated in phase III trials, may also supply novel options in those diseases to control tumor growth and metastasis.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Indoles / therapeutic use. Lung Neoplasms / drug therapy. Neovascularization, Pathologic / prevention & control. Neuroendocrine Tumors / drug therapy. Pyrroles / therapeutic use
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor. Carcinoid Tumor / drug therapy. Cell Line, Tumor. Clinical Trials as Topic. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Humans. Kidney Neoplasms / drug therapy. Melphalan / therapeutic use. Pancreatic Neoplasms / drug therapy. Procarbazine / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Proto-Oncogene Proteins c-kit. Receptor, Epidermal Growth Factor / therapeutic use. Vinblastine / therapeutic use. Xenograft Model Antitumor Assays

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  • (PMID = 19911111.001).
  • [ISSN] 1776-260X
  • [Journal-full-title] Targeted oncology
  • [ISO-abbreviation] Target Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Biomarkers, Tumor; 0 / Indoles; 0 / Protein Kinase Inhibitors; 0 / Pyrroles; 35S93Y190K / Procarbazine; 5V9KLZ54CY / Vinblastine; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; Q41OR9510P / Melphalan; V99T50803M / sunitinib; PAVe protocol 1
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20. Case CC, Vassilopoulou-Sellin R: Reproduction of features of the glucagonoma syndrome with continuous intravenous glucagon infusion as therapy for tumor-induced hypoglycemia. Endocr Pract; 2003 Jan-Feb;9(1):22-5
Hazardous Substances Data Bank. GLUCAGON .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reproduction of features of the glucagonoma syndrome with continuous intravenous glucagon infusion as therapy for tumor-induced hypoglycemia.
  • OBJECTIVE: To describe the adverse effects of continuous intravenous infusion of glucagon as therapy for tumor-induced hypoglycemia and to correlate these treatment-related effects with symptoms of endogenous hyper-glucagonemia.
  • METHODS: We reviewed three cases in which patients received continuous glucagon therapy for tumor-induced hypoglycemia and experienced adverse side effects to the treatment.
  • RESULTS: Continuous intravenous glucagon infusion has evolved as a reliable and efficacious modality for the treatment of tumor-induced hypoglycemia.
  • We report the adverse events of venous thromboembolism, necrolytic migratory erythema, and angular cheilitis in conjunction with continuous intravenous glucagon treatment.
  • These complications resemble symptoms that characterize the human model of hyperglucagonemia--the glucagonoma syndrome--which is associated with hyperglucagonemia and alpha-islet cell neoplasms of the pancreas.
  • CONCLUSION: Symptoms that characterize the islet cell neoplasm-related glucagonoma syndrome may develop in patients receiving an infusion of exogenous glucagon.
  • [MeSH-major] Glucagon / therapeutic use. Glucagonoma / metabolism. Hypoglycemia / drug therapy. Hypoglycemia / etiology. Insulinoma / metabolism. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Drug Eruptions / pathology. Female. Hemangioma / complications. Humans. Infusions, Intravenous. Lung Neoplasms / complications. Male. Meningeal Neoplasms / complications. Middle Aged. Pleural Neoplasms / complications. Sarcoma / complications






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