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1. Ziske C, Schlie C, Gorschlüter M, Glasmacher A, Mey U, Strehl J, Sauerbruch T, Schmidt-Wolf IG: Prognostic value of CA 19-9 levels in patients with inoperable adenocarcinoma of the pancreas treated with gemcitabine. Br J Cancer; 2003 Oct 20;89(8):1413-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic value of CA 19-9 levels in patients with inoperable adenocarcinoma of the pancreas treated with gemcitabine.
  • Serum carbohydrate antigen 19-9 (CA 19-9) has been identified as a useful tumour marker for diagnosis of exocrine pancreatic carcinoma, but its value for evaluating the response to chemotherapy with gemcitabine is not clear.
  • Tumour regression in pancreatic carcinoma is hard to determine due to massive desmoplastic tissue.
  • Furthermore, objective tumour response does not automatically transcribe into better survival.
  • Therefore, clinical benefit response, a composed parameter consisting of factors like performance status, pain, and body weight was integrated in evaluating tumour response.
  • The aim of this prospective study was to evaluate the usefulness of serial CA 19-9 measurements as a biochemical response marker and an outcome prognostic parameter in patients with advanced pancreatic cancer receiving gemcitabine treatment.
  • A total of 46 consecutive patients (median age 66 years) suffering from histologically proven locally advanced or metastatic adenocarcinoma of the exocrine pancreas were analysed.
  • Patients with a decrease of >20% of the baseline CA 19-9 level after 8 weeks of chemotherapy had a significantly better median survival than patients with a rise or a decline <20%.
  • The response of CA 19-9 >20% during chemotherapy was the only independent predictor of survival in a multivariate analyses.
  • In contrast, neither objective tumour response nor clinical benefit response showed this level of significance.
  • In conclusion, kinetics of CA19-9 serum concentration serves as an early indicator of response to gemcitabine chemotherapy in advanced pancreatic cancer.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antimetabolites, Antineoplastic / pharmacology. Biomarkers, Tumor / analysis. CA-19-9 Antigen / analysis. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Kinetics. Male. Middle Aged. Predictive Value of Tests. Prognosis. Survival Analysis. Treatment Outcome

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  • (PMID = 14562009.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Biomarkers, Tumor; 0 / CA-19-9 Antigen; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
  • [Other-IDs] NLM/ PMC2394360
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2. Freda F, Procaccini E, Ruggiero R, Antropoli M, Manganiello A, Nunziata L, Petronella P, Lo Schiavo F: Solid-cystic pseudopapillary tumor of pancreas: description of two cases and literature review. Tumori; 2007 Sep-Oct;93(5):522-5
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  • [Title] Solid-cystic pseudopapillary tumor of pancreas: description of two cases and literature review.
  • The authors report the cases of two young female patients aged 17 and 27 years who underwent surgery for a rare tumor of the pancreas, Frantz's tumor or solid-cystic pseudopapillary tumor.
  • Solid-cystic pseudopapillary tumor of the pancreas is a rare tumor, accounting for 2.7% of pancreatic exocrine tumors.
  • Due to their rareness and behavior, they are often associated with diagnostic and therapeutic problems.
  • In most cases surgical treatment is curative and neither chemotherapy nor radiotherapy should be added.
  • [MeSH-major] Carcinoma, Papillary / diagnosis. Pancreatic Neoplasms / diagnosis. Pancreatic Pseudocyst / diagnosis

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  • (PMID = 18038892.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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3. Ehehalt F, Saeger HD, Schmidt CM, Grützmann R: Neuroendocrine tumors of the pancreas. Oncologist; 2009 May;14(5):456-67
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  • [Title] Neuroendocrine tumors of the pancreas.
  • This literature review briefly summarizes the epidemiology, pathophysiology, clinical management, and outcomes of patients with pancreatic neuroendocrine tumors (PNETs) and highlights recent advances in PNET research.
  • PNETs are rare neoplasms, compared with carcinomas arising from pancreatic exocrine tissue.
  • They, like other neuroendocrine tumor types, display variable malignant potential, hormone-related syndromes (functionality), localization, and genetic background.
  • Although tumor origin and molecular pathogenesis remain poorly understood, recently established grading and staging systems facilitate patient risk stratification, and thereby directly impact clinical decision making.
  • Although the optimal clinical management of PNETs involves a multidisciplinary approach, surgery remains the only curative treatment for early-stage disease.
  • Alternative therapeutic approaches applied to PNETs, including chemotherapy, radiofrequency ablation, transarterial chemoembolization, biotherapy, polypeptide radionuclide receptor therapy, antiangiogenic therapy, and selective internal radiotherapy, have failed to demonstrate a long-term survival benefit.
  • Surgery remains the primary therapeutic option for patients with PNETs.
  • Research on PNETs is desperately needed to improve the therapeutic options for patients with this disease.
  • [MeSH-major] Neuroendocrine Tumors. Pancreatic Neoplasms
  • [MeSH-minor] Gastrinoma / diagnosis. Gastrinoma / therapy. Humans. Incidence. Insulinoma / diagnosis. Insulinoma / therapy. Neoplasm Staging. Prognosis

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  • (PMID = 19411317.001).
  • [ISSN] 1549-490X
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 130
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4. Knaebel HP, Märten A, Schmidt J, Hoffmann K, Seiler C, Lindel K, Schmitz-Winnenthal H, Fritz S, Herrmann T, Goldschmidt H, Krempien R, Mansmann U, Debus J, Diehl V, Büchler MW: Phase III trial of postoperative cisplatin, interferon alpha-2b, and 5-FU combined with external radiation treatment versus 5-FU alone for patients with resected pancreatic adenocarcinoma -- CapRI: study protocol [ISRCTN62866759]. BMC Cancer; 2005;5:37
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  • [Title] Phase III trial of postoperative cisplatin, interferon alpha-2b, and 5-FU combined with external radiation treatment versus 5-FU alone for patients with resected pancreatic adenocarcinoma -- CapRI: study protocol [ISRCTN62866759].
  • After surgical intervention with curative intention in specialised centres the five-year survival of patients with carcinoma of the exocrine pancreas is only 15%.
  • The ESPAC-1 trial showed an increased five-year survival of 21% achieved with adjuvant chemotherapy.
  • Investigators from the Virginia Mason Clinic have reported a 5-year survival rate of 55% in a phase II trial evaluating adjuvant chemotherapy, immunotherapy and external-beam radiation.
  • A total of 110 patients with specimen-proven R0 or R1 resected pancreatic adenocarcinoma will be enrolled.
  • DISCUSSION: The aim of this study is to evaluate the overall survival period attained by chemo-radiotherapy including interferon alpha 2b administration with adjuvant chemotherapy.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / administration & dosage. Fluorouracil / administration & dosage. Interferon-alpha / administration & dosage. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / radiotherapy. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Biomarkers, Tumor. Clinical Trials as Topic. Combined Modality Therapy. Follow-Up Studies. Humans. Models, Statistical. Monte Carlo Method. Prospective Studies. Quality of Life. Recombinant Proteins. Sample Size. Time Factors

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  • (PMID = 15826316.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Databank-accession-numbers] ISRCTN/ ISRCTN62866759
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Interferon-alpha; 0 / Recombinant Proteins; 99210-65-8 / interferon alfa-2b; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC1087479
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5. Petropavlovskaia M, Makhlin J, Sampalis J, Rosenberg L: Development of an in vitro pancreatic tissue model to study regulation of islet neogenesis associated protein expression. J Endocrinol; 2006 Oct;191(1):65-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of an in vitro pancreatic tissue model to study regulation of islet neogenesis associated protein expression.
  • Here, we report the establishment of the first in vitro tissue model of INGAP expression that consists of epithelial cystic structures derived from hamster pancreatic acinar tissue cultured in collagen matrix.
  • We also demonstrate for the first time that INGAP gene expression was significantly induced by treatment with interleukin (IL)-6 and further enhanced by a combination of IL-6 with dexamethazone and nicotinamide.
  • In summary, the in vitro model of INGAP expression described here represents an important step in the development of strategies for the use of INGAP and related proteins as islet neogenic agents in the pharmacotherapy of both type-1 and type-2 diabetes.
  • [MeSH-major] Cytokines / pharmacology. Gene Expression Regulation. Lectins, C-Type / genetics. Models, Animal. Pancreas, Exocrine / metabolism. Pancreas, Exocrine / pathology. Regeneration
  • [MeSH-minor] Animals. Blotting, Western / methods. Cell Differentiation. Collagen. Cricetinae. DNA Primers. Dactinomycin / pharmacology. Genetic Engineering. Interferon-gamma / pharmacology. Interleukin-1beta / pharmacology. Interleukin-6 / pharmacology. Male. Mesocricetus. Microscopy, Confocal. Pancreatic Ducts / physiology. Pancreatic Ducts / ultrastructure. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Tissue Culture Techniques. Transcription, Genetic / drug effects. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 17065390.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / DNA Primers; 0 / Interleukin-1beta; 0 / Interleukin-6; 0 / Lectins, C-Type; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 1CC1JFE158 / Dactinomycin; 82115-62-6 / Interferon-gamma; 9007-34-5 / Collagen
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6. Grozinsky-Glasberg S, Shimon I, Korbonits M, Grossman AB: Somatostatin analogues in the control of neuroendocrine tumours: efficacy and mechanisms. Endocr Relat Cancer; 2008 Sep;15(3):701-20
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  • Neuroendocrine tumours (NETs) represent a heterogeneous family of neoplasms, which may develop from different endocrine glands (such as the pituitary, the parathyroid or the neuroendocrine adrenal glands), endocrine islets (within the thyroid or pancreas) as well as from endocrine cells dispersed between exocrine cells throughout the digestive and respiratory tracts.
  • The development of somatostatin analogues (SSA) as important diagnostic and treatment tools has revolutionised the clinical management of patients with NETs.
  • However, although symptomatic relief and stabilisation of tumour growth for various periods of time are observed in many patients treated with SSA, tumour regression is rare.
  • The development of new SSA, new drug combination therapies and chimaeric molecules should further improve the clinical management of these patients, as should a more complete understanding of their mode of action.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Endocrine Gland Neoplasms / drug therapy. Neuroendocrine Tumors / drug therapy. Somatostatin / analogs & derivatives
  • [MeSH-minor] Angiogenesis Inhibitors / pharmacology. Angiogenesis Inhibitors / therapeutic use. Animals. Apoptosis / drug effects. Cell Proliferation / drug effects. Clinical Trials as Topic. Drug Evaluation, Preclinical. Humans. Models, Biological. Tumor Burden / drug effects

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  • (PMID = 18524947.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents, Hormonal; 51110-01-1 / Somatostatin
  • [Number-of-references] 180
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7. Shimizu K, Shiratori K, Hayashi N, Fujiwara T, Horikoshi H: Effect of troglitazone on exocrine pancreas in rats with streptozotocin-induced diabetes mellitus. Pancreas; 2000 Nov;21(4):421-6
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  • [Title] Effect of troglitazone on exocrine pancreas in rats with streptozotocin-induced diabetes mellitus.
  • Abnormality of pancreatic exocrine secretion has been observed in patients with diabetes mellitus.
  • We investigated the effect of troglitazone on exocrine pancreas in streptozotocin (STZ)-induced diabetic rats.
  • Pancreas weight, enzyme, protein, and insulin contents in the pancreas were measured.
  • For the exocrine secretory study, pure pancreatic juice was collected hourly.
  • Pancreas weight in diabetic rats was less than that in normal rats.
  • Administration of troglitazone resulted in a significant increase in pancreas weight and amylase and trypsin output.
  • However, protein and insulin contents were not affected by the treatment with troglitazone.
  • Both basal and cholecystokinin (CCK-8; 26 pmol/kg/h) stimulated exocrine secretion in juice volume, amylase, and trypsin output were markedly decreased in diabetic rats, compared with those in normal rats.
  • Impaired basal and CCK-stimulated pancreatic exocrine secretion in diabetic rats recovered to the normal levels when troglitazone was given.
  • In conclusion, troglitazone might be effective to restore exocrine pancreatic insufficiency in STZ-diabetic rats.
  • [MeSH-major] Chromans / pharmacology. Diabetes Mellitus, Experimental / drug therapy. Hypoglycemic Agents / pharmacology. Pancreas / drug effects. Thiazoles / pharmacology. Thiazolidinediones
  • [MeSH-minor] Animals. Cholecystokinin / pharmacology. Glucose Tolerance Test. Insulin / analysis. Male. Rats. Rats, Wistar. Streptozocin. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 11075998.001).
  • [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 / Chromans; 0 / Hypoglycemic Agents; 0 / Insulin; 0 / Thiazoles; 0 / Thiazolidinediones; 0 / Tumor Necrosis Factor-alpha; 5W494URQ81 / Streptozocin; 9011-97-6 / Cholecystokinin; I66ZZ0ZN0E / troglitazone
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8. Holen KD, Klimstra DS, Hummer A, Gonen M, Conlon K, Brennan M, Saltz LB: Clinical characteristics and outcomes from an institutional series of acinar cell carcinoma of the pancreas and related tumors. J Clin Oncol; 2002 Dec 15;20(24):4673-8
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  • [Title] Clinical characteristics and outcomes from an institutional series of acinar cell carcinoma of the pancreas and related tumors.
  • PURPOSE: Acinar cell carcinoma is a rare tumor of the exocrine pancreas.
  • Clinical features such as prognostic information, survival, and treatment outcomes are unknown.
  • PATIENTS AND METHODS: Thirty-nine patients with pathologically confirmed acinar neoplasms of the pancreas were identified between August 1981 and January 2001.
  • Demographic data, tumor characteristics, and treatment information were obtained by chart review.
  • Patients who could be treated with surgery as first-line therapy had a longer survival time (36 months) compared with those who did not have surgery (14 months).
  • Two of 18 patients who received chemotherapy and three of eight patients who received radiation had a major response.
  • CONCLUSION: The survival curves suggest a more aggressive cancer than pancreatic endocrine neoplasms but one that is less aggressive than ductal adenocarcinoma of the pancreas.
  • There is a high recurrence rate after complete surgical resection, suggesting that micrometastases are present even in localized disease and that adjuvant therapies may be indicated.
  • Chemotherapy and radiation afford disappointing results, however, and novel therapies are needed.
  • [MeSH-major] Carcinoma, Acinar Cell / therapy. Pancreatic Neoplasms / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Combined Modality Therapy. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Staging. Retrospective Studies. Survival Rate. Treatment Outcome

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  • (PMID = 12488412.001).
  • [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] Journal Article
  • [Publication-country] United States
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9. Wiernik PH: Current status of and future prospects for the medical management of adenocarcinoma of the exocrine pancreas. J Clin Gastroenterol; 2000 Jun;30(4):357-63
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  • [Title] Current status of and future prospects for the medical management of adenocarcinoma of the exocrine pancreas.
  • Adenocarcinoma of the exocrine pancreas is one of the most refractory neoplasms to medical treatment.
  • Although of marginal value, 5-fluorouracil (5-FU) alone or in combination with other agents or modalities has been the standard surgical adjuvant approach to localized unresectable tumor as well as the standard treatment for disseminated pancreatic cancer.
  • Recently, a new chemotherapeutic agent, gemcitabine, has been shown to be somewhat more effective than 5-FU against metastatic pancreatic cancer.
  • Treatment with gemcitabine usually results in a greater likelihood of objective response and better symptom control than treatment with 5-FU or drug combinations that include 5-FU.
  • However, treatment with gemcitabine does not improve overall survival of patients with disseminated neoplasm.
  • Newer promising agents such as 9-nitrocamptothecin have recently entered clinical trials, and novel modalities (e.g., gene therapy) are nearing full-scale clinical trial.
  • There are reasons to believe that these and other new initiatives may soon significantly improve the medical management of adenocarcinoma of the exocrine pancreas.
  • [MeSH-major] Adenocarcinoma / therapy. Pancreatic Neoplasms / therapy
  • [MeSH-minor] Antimetabolites, Antineoplastic / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Fluorouracil / therapeutic use. Genetic Therapy. Humans. Pancreatectomy. Radiotherapy, Adjuvant

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  • (PMID = 10875462.001).
  • [ISSN] 0192-0790
  • [Journal-full-title] Journal of clinical gastroenterology
  • [ISO-abbreviation] J. Clin. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; U3P01618RT / Fluorouracil
  • [Number-of-references] 79
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10. Sylla A, Hervieu V, Lombard-Bohas C, Tanière P, Elbaz N, Scoazec JY: [Amphicrine carcinoma of the pancreas. Report of two cases]. Ann Pathol; 2003 Oct;23(5):424-9
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  • [Title] [Amphicrine carcinoma of the pancreas. Report of two cases].
  • Amphicrine carcinomas are rare tumors defined by the presence of tumor cells showing evidence of both exocrine and endocrine differentiation.
  • We here report two cases of amphicrine carcinomas of the pancreas, an exceedingly rare localization for this type of tumors.
  • Diagnosis was made in respectively, a 32-year-old woman and a 66-year-old man; tumors measured 7 and 3 cm in diameter; metastatic dissemination was present in both cases.
  • The first patient, treated by surgery and chemotherapy, is alive, without disease progression, after 26 months; the second patient deceased early after the diagnosis.
  • In both cases, the first diagnosis considered at cytological and histological examination was endocrine carcinoma.
  • In one case, the amphicrine nature of tumor cells was confirmed by the ultrastructural examination.
  • The identification of the amphicrine nature of an apparently endocrine tumor is of relevance, because of the poor prognosis of amphicrine carcinomas as compared to endocrine carcinomas and the requirement for aggressive therapy.
  • [MeSH-major] Carcinoma / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Fatal Outcome. Female. Humans. Male. Neoplasm Metastasis

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  • (PMID = 14752385.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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11. Trikudanathan G, Dasanu CA: Adenosquamous carcinoma of the pancreas: a distinct clinicopathologic entity. South Med J; 2010 Sep;103(9):903-10
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  • [Title] Adenosquamous carcinoma of the pancreas: a distinct clinicopathologic entity.
  • Among exocrine pancreatic tumors, adenosquamous carcinoma (ASC) is a rare, aggressive subtype with a worse prognosis and a higher potential for metastases compared to its more conventional glandular counterpart, adenocarcinoma.
  • Although such features as central necrosis and hypervascularity are suggestive of pancreatic ASC, more research is necessary to identify other, more specific markers for this tumor subtype.
  • Humoral hypercalcemia of malignancy has also been described with ASC of the pancreas, likely as a result of PTHrP production by the squamous component of the tumor.
  • Similar to the therapeutics of pancreatic adenocarcinoma, adjuvant chemotherapy or chemoradiotherapy is currently indicated for resectable ASC of the pancreas, while gemcitabine or gemcitabine combinations are used for a more advanced disease.
  • Both pathologic and molecular features of pancreatic ASC characterize it as a distinct subtype of pancreatic cancer.
  • As a result, its molecular and genetic makeup could be exploited for both diagnostic and therapeutic quests in the future.
  • [MeSH-major] Carcinoma, Adenosquamous / diagnosis. Carcinoma, Adenosquamous / therapy. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / therapy
  • [MeSH-minor] Abdominal Pain / etiology. Biomarkers, Tumor. Chemotherapy, Adjuvant. Diagnostic Imaging. Genetic Predisposition to Disease. Humans. Jaundice / etiology. Mutation. Necrosis. Palliative Care. Pancreas / pathology. Pancreatectomy. Risk Factors. Survival Analysis. Weight Loss

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  • (PMID = 20697320.001).
  • [ISSN] 1541-8243
  • [Journal-full-title] Southern medical journal
  • [ISO-abbreviation] South. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 43
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12. Morales-Miranda A, Robles-Díaz G, Díaz-Sánchez V: [Steroid hormones and pancreas: a new paradigm]. Rev Invest Clin; 2007 Mar-Apr;59(2):124-9
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  • [Title] [Steroid hormones and pancreas: a new paradigm].
  • The relation between steroid hormones and pancreatic function has been poorly discussed and not very well understood.
  • In general, there is a lack of recognition among the scientific community about the importance of steroids in pancreatic function (current paradigm).
  • In the present article we present basic, as well as clinic and epidemiologic data that demonstrate steroid synthesis and steroid biotransformation by pancreatic tissue, how exocrine and endocrine functions are modulated by steroids, the gender specific frequency and behavior of some tumors and the use of synthetic steroids and steroid action antagonists as therapeutic agents.
  • Pancreatic tissue synthesize and transform steroid hormones.
  • 2. Pancreatic tissue respond to steroid hormones and express steroid specific receptor molecules.
  • 4. Tumor growth is modulated by steroids and anti-steroid drugs.
  • This set of data creates a new paradigm for the holistic study of pancreas and opens new research fields.
  • The application of this new paradigm might result in an increase in the knowledge of pancreatic physiology, in the design of new and better diagnostic methods and eventually in the design of more effective medical treatments for the pancreatic cancers.
  • [MeSH-major] Hormones / physiology. Models, Biological. Pancreas / physiology. Steroids / physiology
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / epidemiology. Adenocarcinoma / physiopathology. Animals. Antineoplastic Agents, Hormonal / therapeutic use. Female. Gonadal Steroid Hormones / physiology. Humans. Insulin / secretion. Male. Mammals / physiology. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / epidemiology. Pancreatic Neoplasms / physiopathology. Rats

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  • (PMID = 17633800.001).
  • [ISSN] 0034-8376
  • [Journal-full-title] Revista de investigación clínica; organo del Hospital de Enfermedades de la Nutrición
  • [ISO-abbreviation] Rev. Invest. Clin.
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Gonadal Steroid Hormones; 0 / Hormones; 0 / Insulin; 0 / Steroids
  • [Number-of-references] 40
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13. Jia D, Otsuki M: Bezafibrate, a peroxisome proliferator-activated receptor (PPAR)-alpha activator, prevents pancreatic degeneration in obese and diabetic rats. Pancreas; 2003 Apr;26(3):286-91
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  • [Title] Bezafibrate, a peroxisome proliferator-activated receptor (PPAR)-alpha activator, prevents pancreatic degeneration in obese and diabetic rats.
  • INTRODUCTION: Damage to the exocrine pancreas has been observed in patients and animals with hyperlipidemia and hyperglycemia.
  • AIM: To examine the effects of bezafibrate on exocrine pancreas in hyperlipidemic obese and diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats that have no cholecystokinin-1 receptor gene expression.
  • RESULTS: Bezafibrate treatment significantly reduced serum triglyceride, total cholesterol, and free fatty acids levels and significantly increased the pancreatic wet weight (1,145 +/- 54 vs 874 +/- 33 mg/rat, p < 0.01), and protein (169 +/- 7 vs 128 +/- 11 mg/pancreas p < 0.01) and enzyme contents in the pancreas compared with those in untreated control rats.
  • Immunohistochemical studies of the pancreas showed that expression of proinflammatory cytokines such as tumor necrosis factor-alpha, interleukin-1beta and interleukin-6, and alpha-smooth muscle actin in bezafibrate-treated rats was greatly suppressed compared with that in the untreated control rats.
  • The histopathologic changes such as vacuolar degeneration and tubular complexes observed in the control rat pancreas were markedly improved in bezafibrate-treated rats.
  • CONCLUSIONS: Our results suggest that bezafibrate reduces hyperlipidemia, inhibits pancreatic inflammation, and prevents pancreatic degeneration in obese and diabetic OLETF rats.
  • [MeSH-major] Bezafibrate / therapeutic use. Diabetes Mellitus, Type 2 / drug therapy. Hypolipidemic Agents / therapeutic use. Obesity / drug therapy. Receptors, Cytoplasmic and Nuclear / agonists. Transcription Factors / agonists
  • [MeSH-minor] Actins / metabolism. Animals. Blood Glucose / analysis. Cytokines / metabolism. Insulin / blood. Lipids / blood. Organ Size. Pancreas / drug effects. Pancreas / pathology. Rats. Rats, Inbred OLETF

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  • (PMID = 12657956.001).
  • [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 / Actins; 0 / Blood Glucose; 0 / Cytokines; 0 / Hypolipidemic Agents; 0 / Insulin; 0 / Lipids; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Transcription Factors; Y9449Q51XH / Bezafibrate
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14. Salvia R, Festa L, Butturini G, Tonsi A, Sartori N, Biasutti C, Capelli P, Pederzoli P: Pancreatic cystic tumors. Minerva Chir; 2004 Apr;59(2):185-207
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  • [Title] Pancreatic cystic tumors.
  • Cystic tumors of the pancreas are less frequent than other tumors in neoplastic pancreatic pathology, but in recent years the literature has reported an increasing number.
  • After the first report by Becourt in 1830, cystic tumors were classified into 2 different types by Compagno and Oertel in 1978: benign tumors with glycogen-rich cells and mucinous cystic neoplasms with overt and latent malignancy.
  • The WHO classification of exocrine tumors of the pancreas, published in 1996, is based on the histopathological features of the epithelial wall, which are the main factor in differential diagnosis with cystic lesions of the pancreas.
  • Thanks to the knowledge acquired up to now, a surgical procedure is not always required because the therapeutic choice is conditioned by the correct classification of this heterogeneous group of tumors.
  • Clinical signs are not really useful in the clinical work up, most patients have no symptoms and when clinical signs are present, they may help us to pinpoint the organ of origin but never to identify the type of pathology.
  • More invasive diagnostic procedures such as fine needle aspiration and intracystic fluid tumor marker level are not really useful because they are not sensitive and the cystic wall can show different degrees of dysplasia and de-epithelialization.
  • Good cooperation between surgeons, pathologists, radiologists and gastroenterologists is mandatory to increase the chances of making a proper diagnosis.
  • Therefore, we must analyze all the information we have, such as age, sex, clinical history, location of the tumor and radiological features, in order to avoid the mistake of treating a cystic neoplasm as a benign lesion or as a pseudocyst, as described in the literature.
  • Except for inoperable cases due to the critical condition of the patient or non-resectable lesions, surgical treatment differs with the diagnosis.
  • Cystic tumors of the pancreas, therefore, are a heterogeneous group of tumors, with a real problem regarding differential diagnosis between neoplastic and inflammatory lesions.
  • Even with a proper work up, some perplexity may remain about the nature of the lesion and in these cases the surgical procedure has a therapeutic value as well as playing a diagnostic role.
  • The role of surgery is central in the treatment of these tumors because it could be curative when complete resection is possible.
  • In this way, the lack of good therapeutic results with chemotherapy and radiotherapy force the surgeon to go ahead with the procedure.
  • In the last few years the therapeutic approach has changed thanks to new knowledge of the biological behavior of these tumors.
  • A follow-up could be planned even for solid pseudopapillary tumors but it seems risky to leave untreated big tumors in young patients without a certain diagnosis and with so few studies reported in the literature.
  • [MeSH-major] Pancreatic Cyst. Pancreatic Neoplasms
  • [MeSH-minor] Cystadenocarcinoma, Serous / diagnosis. Cystadenocarcinoma, Serous / surgery. Cystadenoma, Serous / diagnosis. Cystadenoma, Serous / surgery. Humans

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  • (PMID = 15238892.001).
  • [ISSN] 0026-4733
  • [Journal-full-title] Minerva chirurgica
  • [ISO-abbreviation] Minerva Chir
  • [Language] eng; ita
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 45
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15. Matsubayashi H, Takagaki S, Otsubo T, Iiri T, Kobayashi Y, Yokota T, Shichijo K, Iwafuchi M, Kijima H: Pancreatic T-cell lymphoma with high level of soluble interleukin-2 receptor. J Gastroenterol; 2002;37(10):863-7
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  • [Title] Pancreatic T-cell lymphoma with high level of soluble interleukin-2 receptor.
  • Abdominal computed tomography (CT) scan and ultrasonography showed enlargement of the whole pancreas with para-aortic lymphadenopathy.
  • Endoscopic retrograde pancreatography (ERP) showed diffuse narrowing of the main pancreatic duct (MPD), and brushing cytology from the MPD was non-neoplastic.
  • Differential diagnosis between lymphoma and other exocrine and endocrine pancreatic malignancies was needed, and the level of serum soluble interleukin-2 receptor (17 751 U/ml) was revealed to be significantly high, which was strongly suggestive of pancreatic lymphoma.
  • Chemotherapy was refused by the patient's family and the patient succumbed after 2 months of conservative follow-up.
  • Autopsy revealed diffuse, mixed cell-type, non-Hodgkin's lymphoma of T-cell subtype.
  • [MeSH-major] Biomarkers, Tumor / blood. Lymphoma, T-Cell / diagnosis. Pancreatic Neoplasms / diagnosis. Receptors, Interleukin-2 / blood

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  • (PMID = 12424573.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, Interleukin-2
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16. Honoré B, Baandrup U, Vorum H: Heterogeneous nuclear ribonucleoproteins F and H/H' show differential expression in normal and selected cancer tissues. Exp Cell Res; 2004 Mar 10;294(1):199-209
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  • [Title] Heterogeneous nuclear ribonucleoproteins F and H/H' show differential expression in normal and selected cancer tissues.
  • We have compared a set of tissues and found striking differences in their levels of expression as well as in the nuclear versus the cytoplasmic distribution.
  • Generally, hnRNP F is broadly expressed in many tissues with extremely strong expression in the prostate gland while hnRNP H/H' shows a more restricted degree of expression with low expression in some tissues, for example, liver, exocrine acini of the pancreas, thyroid gland and heart.
  • A quite pronounced heterogeneous expression pattern is seen in the proximal tubules of the kidney where hnRNP F is present at moderate cytoplasmic levels while hnRNP H/H' is undetectable, whereas both proteins are more evenly expressed in distal tubules and collecting ducts.
  • Generally, tumor tissues reveal a broad expression of hnRNP F in the nuclei as well as in the cytoplasm while hnRNP H/H' is expressed at higher levels in the nuclei than in the cytoplasm.
  • Up-regulation of hnRNP H/H' is found in a few tissues that normally express low cytoplasmic levels of hnRNP H/H', for example, adenocarcinoma of the pancreas, hepatocellular carcinoma and gastric carcinoma. hnRNP F is down-regulated in hepatocellular carcinoma and up-regulated in gastric carcinoma.
  • The present study indicates the important potential role of this subset of hnRNPs on the gene expression in many tissues.
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology. Humans. Immunohistochemistry. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. Tissue Distribution. Tumor Cells, Cultured

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  • (PMID = 14980514.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Heterogeneous-Nuclear Ribonucleoprotein Group F-H
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17. Chun SG, Zhou W, Yee NS: Combined targeting of histone deacetylases and hedgehog signaling enhances cytoxicity in pancreatic cancer. Cancer Biol Ther; 2009 Jul;8(14):1328-39
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  • [Title] Combined targeting of histone deacetylases and hedgehog signaling enhances cytoxicity in pancreatic cancer.
  • Combined targeting of distinct cellular signaling mechanisms may improve the efficacy and reduce the toxicity of therapy in pancreatic cancer.
  • Histone deacetylases (HDACs) control cellular functions through epigenetic modulation, and HDACs inhibitors suppress cell growth in pancreatic adenocarcinoma.
  • The Hedgehog (Hh) pathway regulates the development of the pancreas, and aberrant Hh signaling promotes the initiation and progression of pancreatic neoplasia.
  • We hypothesize that HDACs and the Hh pathway cooperatively interact to regulate cellular proliferation of the exocrine pancreas.
  • A combination of the HDAC inhibitor SAHA and the Smoothened antagonist SANT-1 was evaluated for their ability to suppress growth of the Gemcitabine-resistant pancreatic adenocarcinoma cell lines Panc-1 and BxPC-3.
  • In summary, we have developed a molecular target-based therapeutic approach that overcomes chemoresistance in pancreatic cancer cells by chemically inhibiting HDACs and Hh signaling in combination.
  • [MeSH-major] Adenocarcinoma / pathology. Antineoplastic Agents / pharmacology. Drug Delivery Systems. Epigenesis, Genetic / drug effects. Hedgehog Proteins / antagonists & inhibitors. Histone Deacetylase Inhibitors / pharmacology. Hydroxamic Acids / pharmacology. Neoplasm Proteins / antagonists & inhibitors. Pancreatic Neoplasms / pathology. Piperazines / pharmacology. Pyrazoles / pharmacology. Signal Transduction / drug effects
  • [MeSH-minor] Antimetabolites, Antineoplastic / pharmacology. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Differentiation / drug effects. Cell Division / drug effects. Cell Line, Tumor / drug effects. Cell Line, Tumor / pathology. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Drug Resistance, Neoplasm / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Tumor Stem Cell Assay

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  • [CommentIn] Cancer Biol Ther. 2009 Jul;8(14):1340-2 [19440037.001]
  • (PMID = 19421011.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA 086862
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Hedgehog Proteins; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Neoplasm Proteins; 0 / Piperazines; 0 / Pyrazoles; 0 / SANT-1 compound; 0W860991D6 / Deoxycytidine; 58IFB293JI / vorinostat; B76N6SBZ8R / gemcitabine
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18. Bang UC, Semb S, Nojgaard C, Bendtsen F: Pharmacological approach to acute pancreatitis. World J Gastroenterol; 2008 May 21;14(19):2968-76
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  • [Title] Pharmacological approach to acute pancreatitis.
  • The aim of the present review is to summarize the current knowledge regarding pharmacological prevention and treatment of acute pancreatitis (AP) based on experimental animal models and clinical trials.
  • Somatostatin (SS) and octreotide inhibit the exocrine production of pancreatic enzymes and may be useful as prophylaxis against post endoscopic retrograde cholangiopancreatography pancreatitis (PEP).
  • The protease inhibitor gabexate mesilate (GM) is used routinely as treatment to AP in some countries, but randomized clinical trials and a meta-analysis do not support this practice.
  • The non-steroidal anti-inflammatory drugs (NSAID) indomethacin and diclofenac have in randomized studies showed potential as prophylaxis against PEP.
  • Antibodies against tumor necrosis factor-alpha (TNF-alpha) have a potential as rescue therapy but no clinical trials are currently being conducted.
  • The antibiotics beta-lactams and quinolones reduce mortality when necrosis is present in pancreas and may also reduce incidence of infected necrosis.
  • Evidence based pharmacological treatment of AP is limited and studies on the effect of potent anti-inflammatory drugs are warranted.
  • [MeSH-major] Pancreatitis / drug therapy
  • [MeSH-minor] Acute Disease. Adrenal Cortex Hormones / therapeutic use. Animals. Anti-Bacterial Agents / therapeutic use. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Antioxidants / therapeutic use. Evidence-Based Medicine. Gabexate / therapeutic use. Humans. Interleukin-10 / therapeutic use. Nitroglycerin / therapeutic use. Octreotide / therapeutic use. Platelet Activating Factor / antagonists & inhibitors. Probiotics / therapeutic use. Serine Proteinase Inhibitors / therapeutic use. Treatment Outcome. Tumor Necrosis Factor-alpha / antagonists & inhibitors

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  • (PMID = 18494044.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Anti-Bacterial Agents; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antioxidants; 0 / Platelet Activating Factor; 0 / Serine Proteinase Inhibitors; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 4V7M9137X9 / Gabexate; G59M7S0WS3 / Nitroglycerin; RWM8CCW8GP / Octreotide
  • [Number-of-references] 125
  • [Other-IDs] NLM/ PMC2712160
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19. Kitasato A, Tajima Y, Kuroki T, Tsutsumi R, Tsuneoka N, Adachi T, Mishima T, Kanematsu T: Limited pancreatectomy for metastatic pancreatic tumors from renal cell carcinoma. Hepatogastroenterology; 2010 Mar-Apr;57(98):354-7
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  • [Title] Limited pancreatectomy for metastatic pancreatic tumors from renal cell carcinoma.
  • BACKGROUND/AIMS: Metastasis of renal cell carcinoma (RCC) to distant organs occurs commonly, even after radical nephrectomy, but metastatic lesions are rarely detected in the pancreas.
  • The present study aim was to improve the postoperative quality of life of a patient with pancreatic metastasis of RCC through limited resection of the pancreas.
  • METHODOLOGY: Since therapeutic modalities including chemotherapy or radiation are ineffective for metastatic tumors, surgical intervention is a treatment of choice in selected patients.
  • In patients with multiple pancreatic metastases, however, near-total or total pancreatectomy may result in a lower quality of life postoperatively due to endocrine and exocrine pancreatic insufficiency.
  • RESULTS: We used limited resection of the pancreas combined with removal of the uncinate process and distal pancreatectomy for a 65-year-old woman with multifocal pancreatic metastases located in the uncinate process, body, and tail of the pancreas, which were detected 6 years after radical nephrectomy for RCC.
  • This surgical procedure allowed preservation of about 40% of the pancreatic parenchyma, with complete excision of metastatic tumors in the pancreas.
  • CONCLUSIONS: The patient has had an excellent quality of life with well-preserved pancreatic function and no evidence of tumor recurrence for 31 months after pancreatic surgery.
  • [MeSH-major] Carcinoma, Renal Cell / secondary. Carcinoma, Renal Cell / surgery. Kidney Neoplasms / pathology. Pancreatectomy / methods. Pancreatic Neoplasms / secondary. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Aged. Female. Humans. Neoplasm Staging. Nephrectomy. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 20583442.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
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20. Deschamps L, Dokmak S, Guedj N, Ruszniewski P, Sauvanet A, Couvelard A: Mixed endocrine somatostatinoma of the ampulla of vater associated with a neurofibromatosis type 1: a case report and review of the literature. JOP; 2010;11(1):64-8
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  • [Title] Mixed endocrine somatostatinoma of the ampulla of vater associated with a neurofibromatosis type 1: a case report and review of the literature.
  • Ampullary somatostatinomas are classically associated with neurofibromatosis type 1.
  • We herein describe the first reported case of a mixed endocrine somatostatinoma of the ampulla of Vater associated with neurofibromatosis type 1; we also present a review of the literature of the 7 mixed endocrine tumors of the ampulla which have been reported so far.
  • Endoscopic examination revealed a tumor involving the ampulla of Vater and a CT scan identified stenoses of both the distal common bile duct and the main pancreatic duct.
  • A pancreaticoduodenectomy was performed and pathological examination revealed two tumor components, exocrine (high grade adenoma with infiltrative adenocarcinoma) and endocrine (expressing somatostatin hormone) with lymph node metastases originating from both types.
  • The patient was treated with adjuvant chemotherapy and has had no recurrence for 3 years.
  • DISCUSSION: In ampullary somatostatinomas, psammoma bodies are pathognomonic and chromogranin A is rarely expressed: these features should alert the pathologist to an association with neurofibromatosis type 1.
  • The treatment of choice is surgery, and adjuvant chemotherapy should be adapted to the most aggressive component, i.e. the exocrine one.
  • CONCLUSION: Because of their rarity, the diagnosis of ampullary mixed endocrine tumors is difficult.
  • Our case points out the characteristic features of these neoplasms and their possible association with neurofibromatosis type 1.
  • [MeSH-major] Ampulla of Vater. Common Bile Duct Neoplasms / diagnosis. Mixed Tumor, Malignant / diagnosis. Neurofibromatosis 1 / diagnosis. Somatostatinoma / diagnosis


21. Nishino T, Toki F, Oyama H, Shimizu K, Shiratori K: Long-term outcome of autoimmune pancreatitis after oral prednisolone therapy. Intern Med; 2006;45(8):497-501
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  • [Title] Long-term outcome of autoimmune pancreatitis after oral prednisolone therapy.
  • OBJECTIVE: We investigated the long-term outcome of autoimmune pancreatitis (AIP) including morphological changes in the pancreas, pancreatic duct, biliary tract, pancreatic function, and changes in the clinical manifestations after oral prednisolone (PSL) therapy.
  • The morphological findings consisted of pancreatic enlargement (n=12), an irregularly narrowed main pancreatic duct (n=12), and bile duct stricture (n=10), and salivary gland swelling was observed in six patients.
  • RESULTS: All 12 patients responded to PSL therapy.
  • The enlargement of the pancreas and the irregularly narrowed main pancreatic duct improved to almost normal.
  • Pancreatic atrophy developed in four of them (4/12, 33%), but no pancreatic calcification was observed in any of the patients.
  • The salivary gland swelling also improved after PSL therapy.
  • There was no recurrence of enlargement of the pancreas or irregularly narrowed main pancreatic duct after PSL therapy, but the bile duct stricture recurred in one case, and in three cases there was a relapse of salivary gland swelling that required a temporary increase in PSL dose during tapering.
  • No deterioration of pancreatic exocrine function was detected in any of the patients.
  • A malignant tumor was diagnosed in two patients during PSL therapy: early gastric cancer in one and rectal cancer in the other.
  • CONCLUSIONS: AIP treated with PSL has a favorable long-term outcome based on the morphological findings and assessments of pancreatic function.
  • However, since two of the twelve patients developed a malignancy during PSL therapy, strict follow up should be part of the management of AIP.
  • [MeSH-major] Autoimmune Diseases / drug therapy. Glucocorticoids / administration & dosage. Pancreatitis / drug therapy. Prednisolone / administration & dosage
  • [MeSH-minor] Administration, Oral. Aged. Biliary Tract / pathology. Cholangiopancreatography, Endoscopic Retrograde. Female. Humans. Immunoglobulin G / blood. Male. Middle Aged. Pancreatic Ducts / pathology. Pancreatic Function Tests. Salivary Glands / pathology. Sjogren's Syndrome / diagnosis. Tomography, X-Ray Computed

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  • (PMID = 16702740.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Immunoglobulin G; 9PHQ9Y1OLM / Prednisolone
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22. 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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23. Pyronnet S, Bousquet C, Najib S, Azar R, Laklai H, Susini C: Antitumor effects of somatostatin. Mol Cell Endocrinol; 2008 May 14;286(1-2):230-7
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  • Since its discovery three decades ago as an inhibitor of GH release from the pituitary gland, somatostatin has attracted much attention because of its functional role in the regulation of a wide variety of physiological functions in the brain, pituitary, pancreas, gastrointestinal tract, adrenals, thyroid, kidney and immune system.
  • In addition to its negative role in the control of endocrine and exocrine secretions, somatostatin and analogs also exert inhibitory effects on the proliferation and survival of normal and tumor cells.
  • This review covers the present knowledge in the antitumor effect of somatostatin and analogs and discusses the perspectives of novel clinical strategies based on somatostatin receptor sst2 gene transfer therapy.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Proliferation / drug effects. Human Growth Hormone / metabolism. Humans. Signal Transduction / drug effects

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  • (PMID = 18359151.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Receptors, Somatostatin; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin
  • [Number-of-references] 80
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24. Grise KR, McFadden DW: Peptide YY improves local and systemic parameters and prevents death in lethal necrotizing pancreatitis. Pancreas; 2002 Jan;24(1):90-5
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  • INTRODUCTION: Peptide YY (PYY) is a gastrointestinal hormone with multiple inhibitory effects on the proximal digestive tract, including suppression of secretion by the exocrine pancreas.
  • The prophylactic group received PYY pumps at the onset; the therapeutic group received pumps 24 hours later.
  • Serum interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) values were determined by ELISA.
  • RESULTS: Both prophylactic and therapeutic PYY significantly reduced mortality compared with that seen in controls ( p = 0.05 and p = 0.007).
  • Five-day survival was 33% in controls, 80% in those receiving prophylactic PYY, and 100% in the therapeutic group.
  • Amylasemia was reduced in the therapeutic group by day 3 ( p < 0.02) and in the prophylactic group by day 4 ( p < 0.01).
  • Prophylactic and therapeutic administration of PYY suppressed early circulating levels of IL-6.
  • [MeSH-major] Pancreatitis, Acute Necrotizing / drug therapy. Peptide YY / therapeutic use
  • [MeSH-minor] Amylases / blood. Animals. Interleukin-6 / blood. Mice. Pancreas / drug effects. Pancreas / secretion. Time Factors. Tumor Necrosis Factor-alpha / analysis

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  • (PMID = 11741187.001).
  • [ISSN] 0885-3177
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 106388-42-5 / Peptide YY; EC 3.2.1.- / Amylases
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