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1. Schneider C, Schmidt T, Ziske C, Tiemann K, Lee KM, Uhlinsky V, Behrens P, Sauerbruch T, Schmidt-Wolf IG, Mühlradt PF, Schmidt J, Märten A: Tumour suppression induced by the macrophage activating lipopeptide MALP-2 in an ultrasound guided pancreatic carcinoma mouse model. Gut; 2004 Mar;53(3):355-61
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  • [Title] Tumour suppression induced by the macrophage activating lipopeptide MALP-2 in an ultrasound guided pancreatic carcinoma mouse model.
  • BACKGROUND AND AIM: Carcinoma of the exocrine pancreas has a particularly poor prognosis.
  • Therefore, novel therapeutic strategies such as immunotherapy are required.
  • METHODS: MALP-2 was tested in a new orthotopic ultrasound guided pancreatic cancer mouse model.
  • MALP-2 was administered intratumorally or intraperitoneally and tumour growth, immune status, and leucocyte infiltration at the tumour site were determined.
  • RESULTS: We showed a tumour suppressive effect induced by a single injection of MALP-2.
  • Combining chemotherapy (gemcitabine) with MALP-2 treatment caused further prolonged survival (median survival 27 days with chemotherapy alone v 37 days for combined treatment; p<0.0002).
  • CONCLUSIONS: In conclusion, in a model of orthotopic pancreatic cancer in mice, we induced a tumour suppressive effect by treatment with a synthetic lipopeptide.
  • Treatment with MALP-2 could be an option for immunotherapy in pancreatic cancer.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / therapeutic use. Deoxycytidine / analogs & derivatives. Oligopeptides / therapeutic use. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antimetabolites, Antineoplastic / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease Models, Animal. Female. Flow Cytometry. Lipopeptides. Macrophage Activation. Male. Mice. Mice, Inbred C57BL. Neoplasm Transplantation / methods. Pancreas / ultrasonography. Spleen / immunology. Survival Analysis

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  • (PMID = 14960515.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Lipopeptides; 0 / Oligopeptides; 0 / macrophage stimulatory lipopeptide 2; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
  • [Other-IDs] NLM/ PMC1773953
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2. 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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3. Boeck S, Vehling-Kaiser U, Waldschmidt D, Kettner E, Märten A, Winkelmann C, Klein S, Kojouharoff G, Gauler T, Fischer von Weikersthal L, Clemens MR, Geissler M, Greten TF, Hegewisch-Becker S, Neugebauer S, Heinemann V: Erlotinib 150 mg daily plus chemotherapy in advanced pancreatic cancer: an interim safety analysis of a multicenter, randomized, cross-over phase III trial of the 'Arbeitsgemeinschaft Internistische Onkologie'. Anticancer Drugs; 2010 Jan;21(1):94-100
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  • [Title] Erlotinib 150 mg daily plus chemotherapy in advanced pancreatic cancer: an interim safety analysis of a multicenter, randomized, cross-over phase III trial of the 'Arbeitsgemeinschaft Internistische Onkologie'.
  • To date, only limited toxicity data are available for the combination of erlotinib with either capecitabine or gemcitabine as front-line therapy for advanced pancreatic cancer.
  • Within a randomized phase III trial, 281 treatment-naive patients were randomly assigned between capecitabine (2000 mg/m/day, for 14 days, once every 3 weeks) plus erlotinib (150 mg/day, arm A) and gemcitabine (1000 mg/m as a 30-min infusion) plus erlotinib (150 mg/day, arm B).
  • In case of treatment failure, patients were crossed over to a second-line treatment with the comparator cytostatic drug without erlotinib.
  • The primary study endpoint was the time to treatment failure of second-line therapy (TTF2).
  • During first-line therapy, patients received a median number of three treatment cycles (range 0-13) in both the arms.
  • Regarding chemotherapy, a treatment delay was observed in 12% of the cycles in arm A and in 22% of the cycles in arm B.
  • Dose reductions of the cytostatic drug were performed in 18 and 27% of treatment cycles, respectively.
  • No treatment-related death was observed.
  • In conclusion, this interim safety analysis suggests that treatment with erlotinib 150 mg/day is feasible in combination with capecitabine or gemcitabine.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Capecitabine. Cross-Over Studies. Deoxycytidine / administration & dosage. Deoxycytidine / adverse effects. Deoxycytidine / analogs & derivatives. Deoxycytidine / therapeutic use. Drug Administration Schedule. Erlotinib Hydrochloride. Female. Fluorouracil / administration & dosage. Fluorouracil / adverse effects. Fluorouracil / analogs & derivatives. Fluorouracil / therapeutic use. Germany. Humans. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Pancreas, Exocrine / pathology. Prospective Studies. Quinazolines / administration & dosage. Quinazolines / adverse effects. Quinazolines / therapeutic use

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  • (PMID = 19770635.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Quinazolines; 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; B76N6SBZ8R / gemcitabine; DA87705X9K / Erlotinib Hydrochloride; U3P01618RT / Fluorouracil
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4. Klapdor R, Bahlo M, Babinski A, Broemel T, Müller C, Seutter R: Sequential polychemotherapy in exocrine pancreatic cancer. Anticancer Res; 2003 Mar-Apr;23(2A):841-4
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  • [Title] Sequential polychemotherapy in exocrine pancreatic cancer.
  • The results of palliative chemotherapy in 162 patients suffering from exocrine pancreatic cancer are presented.
  • They are mainly discussed with respect to the possibility of improving survival of exocrine pancreatic cancer patients by an efficacy-orientated sequential polychemotherapy (EOSP).
  • In about 40% of the patients treated between 1998 and 2001, sequential chemotherapy induced more than one effective treatment in the case that SD after a progressive prephase as well as MR, PR and CR are considered as antitumoral efficacy.
  • Especially in the case of metastasized tumor disease (M1), sequential polychemotherapy seems to be able to prolong survival: 45% of the metastasized tumor patients survived more than 1 year, 12% more than 2 years.
  • The results should stimulate clinicians to try palliative chemotherapy for pancreatic cancer more actively than before and to rediscuss the actual concepts of prospective therapeutical trials mainly based on analysing the effects of single agents or drug combinations on survival.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Drug Administration Schedule. Follow-Up Studies. Humans. Middle Aged. Neoplasm Staging. Palliative Care. Retrospective Studies. Survival Analysis. Time Factors

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  • (PMID = 12820310.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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5. 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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6. Huguier M, Barrier A, Valinas R, Flahault A, Adloff M, Pezet D, Jaeck D, Millat B, French University Association for Surgical Research: Randomized trial of 5-fluorouracil, leucovorin and cisplatin in advanced pancreatic cancer. Hepatogastroenterology; 2001 May-Jun;48(39):875-8
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  • [Title] Randomized trial of 5-fluorouracil, leucovorin and cisplatin in advanced pancreatic cancer.
  • BACKGROUND/AIMS: Phase II trials of combined 5 fluorouracil, leucovorin and cisplatin have demonstrated an 18-28% response rate in advanced pancreatic carcinomas.
  • We investigated the effect of this chemotherapy regime on patients' survival.
  • They had an advanced and proven pancreatic adenocarcinoma.
  • The main end points were survival time (Kaplan-Meier and log-rank methods) a[not readable: see text]side effects of chemotherapy.
  • Median survival times were 8.6 months (SD +/- 1.8) and 7.0 months (SD +/- 0.6), respectively.
  • CONCLUSIONS: This multicentric trial failed to demonstrate any advantage of the evaluated chemotherapy regime in the palliative treatment of cancer of the exocrine pancreas.
  • Other trials including gemcitabine and/or radiotherapy are needed in advanced pancreatic adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / administration & dosage. Fluorouracil / administration & dosage. Leucovorin / administration & dosage. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Humans. Male. Middle Aged. Neoplasm Staging. Palliative Care. Prospective Studies

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  • (PMID = 11462946.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] Greece
  • [Chemical-registry-number] Q20Q21Q62J / Cisplatin; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil
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7. Elliott MJ, Farmer MR, Atienza C Jr, Stilwell A, Dong YB, Yang HL, Wong SL, McMasters KM: E2F-1 gene therapy induces apoptosis and increases chemosensitivity in human pancreatic carcinoma cells. Tumour Biol; 2002 Mar-Apr;23(2):76-86
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  • [Title] E2F-1 gene therapy induces apoptosis and increases chemosensitivity in human pancreatic carcinoma cells.
  • Pancreatic cancer is often resistant to conventional chemotherapy.
  • In this study, we examined the role of adenovirus-mediated overexpression of E2F-1 in inducing apoptosis and increasing the sensitivity of pancreatic cancer cells to chemotherapeutic agents.
  • MIA PaCa-2 pancreatic head exocrine adenocarcinoma cells (mutant p53) were treated by mock infection or adenoviruses expressing beta-galactosidase or E2F-1 (Ad-E2F-1) alone or in combination with sublethal concentrations of each chemotherapeutic drug.
  • Cell growth and viability were assessed at selected time points.
  • By 3 days after infection, Ad-E2F-1 treatment at an MOI of 70 resulted in approximately a 20-fold reduction in cell growth and 60% reduction in cell viability as compared to mock-infected cells.
  • In order to test the efficacy of treatment with a combination of gene therapy and chemotherapy, we utilized concentrations of Ad-E2F-1 which reduced viability to 50% in combination with each chemotherapeutic agent.
  • Interestingly, 5-fluorouracil did not cooperate with Ad-E2F-1 in the mediation of tumor death or inhibition of cell growth.
  • Immunoblotting for Bcl-2 family members revealed no significant changes in the expression levels of Bcl-2, Bcl X(L), Bax or Bak following gene or 'chemogene' therapy with E2F-1.
  • E2F-1 overexpression initiates apoptosis and suppresses growth in pancreatic MIA PaCa-2 cells in vitro.
  • E2F-1-mediated apoptosis was not associated with significant changes in the expression of Bcl-2 family member proteins in these pancreatic cancer cells.
  • This chemogene combination may provide a potentially useful therapeutic strategy for advanced pancreatic cancer.
  • [MeSH-major] Apoptosis. Cell Cycle Proteins. DNA-Binding Proteins. Drug Resistance, Neoplasm. Genetic Therapy. Pancreatic Neoplasms / pathology. Transcription Factors / physiology
  • [MeSH-minor] Adenoviruses, Human / genetics. Antimetabolites, Antineoplastic / pharmacology. Cell Cycle. Cell Division / drug effects. Cyclin-Dependent Kinases / antagonists & inhibitors. DNA Replication / drug effects. Drug Synergism. E2F Transcription Factors. E2F1 Transcription Factor. Enzyme Inhibitors / pharmacology. Etoposide / pharmacology. Fluorouracil / pharmacology. Genetic Vectors / genetics. Humans. Neoplasm Proteins / antagonists & inhibitors. Poly(ADP-ribose) Polymerases / metabolism. Purines / pharmacology. Recombinant Fusion Proteins / physiology. Topoisomerase II Inhibitors. Transfection. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / pathology

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  • [Copyright] Copyright 2002 S. Karger AG, Basel
  • (PMID = 12065845.001).
  • [ISSN] 1010-4283
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / E2F Transcription Factors; 0 / E2F1 Transcription Factor; 0 / E2F1 protein, human; 0 / Enzyme Inhibitors; 0 / Neoplasm Proteins; 0 / Purines; 0 / Recombinant Fusion Proteins; 0 / Topoisomerase II Inhibitors; 0 / Transcription Factors; 0ES1C2KQ94 / roscovitine; 6PLQ3CP4P3 / Etoposide; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.11.22 / Cyclin-Dependent Kinases; U3P01618RT / Fluorouracil
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8. Haas M, Laubender RP, Stieber P, Holdenrieder S, Bruns CJ, Wilkowski R, Mansmann U, Heinemann V, Boeck S: Prognostic relevance of CA 19-9, CEA, CRP, and LDH kinetics in patients treated with palliative second-line therapy for advanced pancreatic cancer. Tumour Biol; 2010 Aug;31(4):351-7
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  • [Title] Prognostic relevance of CA 19-9, CEA, CRP, and LDH kinetics in patients treated with palliative second-line therapy for advanced pancreatic cancer.
  • The objective of this study was to define prognostic serum biomarkers that could serve as surrogate survival endpoints during second-line treatment for advanced pancreatic cancer.
  • This retrospective single-center study included patients treated with second-line therapy for advanced exocrine pancreatic cancer.
  • A pretreatment value and at least one serial measurement during the first two cycles of second-line chemotherapy for CA 19-9, CEA, CRP, and LDH had to be available in order to evaluate the prognostic role of kinetics on overall survival.
  • A cutoff of a >20% increase from baseline during treatment was defined in order to form groups with suspected different outcomes.
  • Overall, 70 patients treated with second-line therapy for advanced disease were included; 94% had distant metastases at treatment initiation.
  • Median time to progression was 2.7 months and median survival 5.4 months.
  • Univariate analysis found that an increase of >20% during treatment was significantly associated with a worse overall survival for CA 19-9 (HR 2.00, p = 0.018), CEA (HR 2.38, p = 0.004), and CRP (HR 3.06, p < 0.001).
  • Serum biomarker kinetics might serve as useful prognostic tools during second-line chemotherapy in advanced pancreatic cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. C-Reactive Protein / metabolism. CA-19-9 Antigen / blood. Carcinoembryonic Antigen / blood. L-Lactate Dehydrogenase / blood. Palliative Care. Pancreatic Neoplasms / blood
  • [MeSH-minor] Adenocarcinoma / blood. Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adult. Aged. Biomarkers, Tumor / blood. Bone Neoplasms / blood. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Carcinoma, Acinar Cell / blood. Carcinoma, Acinar Cell / drug therapy. Carcinoma, Acinar Cell / pathology. Female. Humans. Kinetics. Liver Neoplasms / drug therapy. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Lung Neoplasms / blood. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Male. Middle Aged. Neoplasm Staging. Peritoneal Neoplasms / blood. Peritoneal Neoplasms / drug therapy. Peritoneal Neoplasms / secondary. Prognosis. Retrospective Studies. Survival Rate

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  • (PMID = 20480409.001).
  • [ISSN] 1423-0380
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-19-9 Antigen; 0 / Carcinoembryonic Antigen; 9007-41-4 / C-Reactive Protein; EC 1.1.1.27 / L-Lactate Dehydrogenase
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9. Araneo M, Bruckner HW, Grossbard ML, Frager D, Homel P, Marino J, DeGregorio P, Mortazabi F, Firoozi K, Jindal K, Kozuch P: Biweekly low-dose sequential gemcitabine, 5-fluorouracil, leucovorin, and cisplatin (GFP): a highly active novel therapy for metastatic adenocarcinoma of the exocrine pancreas. Cancer Invest; 2003;21(4):489-96
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  • [Title] Biweekly low-dose sequential gemcitabine, 5-fluorouracil, leucovorin, and cisplatin (GFP): a highly active novel therapy for metastatic adenocarcinoma of the exocrine pancreas.
  • Phase II studies have suggested an improved response rate and acceptable toxicity profile associated with gemcitabine combinations compared to gemcitabine alone for treatment of metastatic adenocarcinoma of the pancreas.
  • The GFP regimen (gemcitabine, 5-fluorouracil, leucovorin, and cisplatin) is based on laboratory evidence of disease-specific chemotherapy interaction.
  • This retrospective analysis examined the outcome of 49 consecutive patients with histologically confirmed metastatic pancreatic adenocarcinoma treated between July 1998 and September 2000.
  • Day 1 treatment consisted of gemcitabine 500 mg/m2 over 30 minutes and then leucovorin 300 mg bolus, 5-fluorouracil (5-FU) 400 mg/m2 bolus, followed by infusional 5-FU 600 mg/m2 over 8 hours.
  • Treatment was administered every 2 weeks.
  • Median patient age was 61.5 years, 74% were men, and 20 patients had refractory disease (11 patients had disease progression upon gemcitabine-based therapy).
  • Two patients attaining PR and two attaining SD had progressive disease with prior gemcitabine-based therapy.
  • The median time to disease progression (TTP) from GFP start was 9 weeks.
  • This experience also demonstrates that adding a single new drug such as irinotecan to the same first-line chemotherapy combination upon disease progression may be an important alternative for the treatment of relapsed/resistant cancer.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Deoxycytidine / analogs & derivatives. Fluorouracil / analogs & derivatives. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Cisplatin / administration & dosage. Drug Administration Schedule. Female. Humans. Infusions, Intravenous. Injections, Intravenous. Leucovorin / administration & dosage. Male. Middle Aged. Neoplasm Metastasis. Retrospective Studies. Survival Analysis. Treatment Outcome

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  • (PMID = 14533437.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; Q20Q21Q62J / Cisplatin; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil
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10. 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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11. Klapdor R, Fenner C: Irinotecan(Campto R): efficacy as third/forth line therapy in advanced pancreatic cancer. Anticancer Res; 2000 Nov-Dec;20(6D):5209-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Irinotecan(Campto R): efficacy as third/forth line therapy in advanced pancreatic cancer.
  • Following the concept that the actual survival of pancreatic cancer patients can only be significantly improved by sequential poly-chemotherapy (EOSPC) in order to add one or two further progression free-survival times (PFST), in addition to the potential antitumoral effects of a first- or second-line therapy we studied the therapeutic efficacy of a third- or fourth-line chemotherapy with irinotecan alone, or in combination with oxaliplatin and high dose 5-FU/FA respectively, in a pilot study in 17 patients.
  • Follow-up was performed on the basis of clinical investigations, imaging methods and the course of tumor markers, mainly CT and CA 19-9.
  • The overall response rate in these cases of third/fourth-line therapies was 1 PR, 4 MR, 6 SD in the imaging methods compared to 5 PR, 2 MR and 5 SD on the basis of the tumor marker courses in the serum.
  • Only in 1 patient did treatment have to be stopped due to irinotecan-induced gastrointestinal symptoms.
  • The results suggested that irinotecan alone or in combination might also be used as third- and fourth-line therapeutical trials in exocrine pancreatic cancer in order to improve the survival time of these patients based on efficacy orientated sequential poly-chemotherapy (EOSPC).
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Camptothecin / analogs & derivatives. Camptothecin / therapeutic use. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Female. Humans. Male. Middle Aged. Neoplasm Staging. Pilot Projects. Treatment Outcome

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  • (PMID = 11326696.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Controlled Clinical Trial; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
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12. Traverso LW: Pancreatic cancer: surgery alone is not sufficient. Surg Endosc; 2006 Apr;20 Suppl 2:S446-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic cancer: surgery alone is not sufficient.
  • For a patient with resected pancreatic cancer at the head of the pancreas, the goal of the medical community in the new millennium is a long-term survival rate exceeding 50% at 5 years.
  • This goal can best be achieved with the following formula: accurate staging by improved imaging that includes laparoscopy for selected patients with locally extensive disease using computed tomography; a balanced resection, not too extensive and not too limited; centralized treatment in high-volume centers, which includes not just the surgeons and hospitals, but also the chemotherapy infusion units; and use of an effective adjuvant or neoadjuvant treatment in which toxicity is associated with efficacy.
  • The ideal outcome for the surgeon is delivery of a patient who has been accurately staged to receive the most appropriate treatment in a timely fashion for an effective chemoradiotherapy protocol.
  • To do this, the surgeon should use objective benchmarks of safe pancreatic resection, which involves resecting only enough, achieving low blood loss, and achieving a minimal length of hospital stay.
  • The outcome is a patient who has optimized his or her gastrointestinal, endocrine, and exocrine functions and is ready for adjuvant treatment 6 weeks after resection.
  • [MeSH-major] Chemotherapy, Adjuvant. Pancreatectomy. Pancreatic Neoplasms / therapy. Radiotherapy, Adjuvant
  • [MeSH-minor] Adenocarcinoma / mortality. Adenocarcinoma / pathology. Adenocarcinoma / secondary. Adenocarcinoma / therapy. Combined Modality Therapy. Female. Humans. Life Tables. Liver Neoplasms / secondary. Male. Neoplasm Staging. Neoplasm, Residual. Peritoneal Neoplasms / secondary. Survival Analysis. Survival Rate. Treatment Outcome

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  • (PMID = 16557419.001).
  • [ISSN] 1432-2218
  • [Journal-full-title] Surgical endoscopy
  • [ISO-abbreviation] Surg Endosc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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13. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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14. 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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15. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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16. Nikou GC, Marinou K, Thomakos P, Papageorgiou D, Sanzanidis V, Nikolaou P, Kosmidis C, Moulakakis A, Mallas E: Chromogranin a levels in diagnosis, treatment and follow-up of 42 patients with non-functioning pancreatic endocrine tumours. Pancreatology; 2008;8(4-5):510-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chromogranin a levels in diagnosis, treatment and follow-up of 42 patients with non-functioning pancreatic endocrine tumours.
  • BACKGROUND/AIMS: Non-functioning pancreatic endocrine tumours (NFPET) constitute the largest component (35-50%) of pancreatic endocrine tumours.
  • They are characterized by the absence of symptoms of hormone hypersecretion and frequently have clinical manifestations similar to the more common exocrine pancreatic adenocarcinoma.
  • The present studyaims toevaluate the clinical features, diagnostic approach and, in particular, the significance of serum chromogranin A levels (CgA) in the management and outcome of 42 patients with NFPET (from a series of 121 patients with pancreatic endocrine tumours).
  • METHODS: Twenty-five males and 17 females were included, and the mean age at diagnosis was 52.3 years (range: 26-68 years).
  • The diagnosis for each patient was established by histopathological examination and immunohistochemistry.
  • After the histopathological confirmation of diagnosis and during the follow-up period, patients were evaluated clinically and radiologically (including OctreoScan), whilst fasting gut hormones (including CgA) were also estimated.
  • At diagnosis, all patients were checked for the presence of multiple endocrine neoplasia type I syndrome.
  • RESULTS: Dyspepsia (66.5%) and weight loss (47.6%) were the most common symptoms at diagnosis, while in 21.4% of patients tumour lesions were revealed incidentally.
  • Plasma CgA levels were significantly or moderately elevated in all patients with liver metastases at diagnosis (64.3%).
  • The levels also reflected tumour progression or response to treatment during the follow-up period.
  • CONCLUSIONS:. (1) NFPET may present with clinical manifestations similar to those of an exocrine pancreatic tumour;.
  • (2) plasma CgA levels reflect tumour load, and also seem to correlate with tumour progression or response to treatment;.
  • (3) surgeryin patients with localized disease at presentation can be curative, while it can also reduce tumour burden in patients with metastases;.
  • (5) systemic chemotherapy or chemoembolization seem to be beneficial in high-grade and progressive tumours.
  • [MeSH-major] Biomarkers, Tumor / blood. Chemoembolization, Therapeutic. Chromogranin A / blood. Multiple Endocrine Neoplasia Type 1 / blood. Neuroendocrine Tumors / blood. Pancreatic Neoplasms / blood
  • [MeSH-minor] Adult. Aged. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Staging

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  • [Copyright] Copyright 2008 S. Karger AG, Basel.
  • (PMID = 18765956.001).
  • [ISSN] 1424-3911
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chromogranin A
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17. Chen S, Bartick T: Resection and use of a cyclooxygenase-2 inhibitor for treatment of pancreatic adenocarcinoma in a cockatiel. J Am Vet Med Assoc; 2006 Jan 1;228(1):69-73
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  • [Title] Resection and use of a cyclooxygenase-2 inhibitor for treatment of pancreatic adenocarcinoma in a cockatiel.
  • Radiography (with and without contrast medium) and ultrasonography revealed a soft tissue mass in the caudoventral portion of the coelom.
  • TREATMENT AND OUTCOME: Exploratory surgery of the coelomic cavity was performed and the neoplasm was excised.
  • Histologic examination of the neoplasm was consistent with a high-grade pancreatic exocrine adenocarcinoma.
  • Necropsy findings indicated that the pancreatic adenocarcinoma had metastasized to surrounding tissues and vessels, which was not unexpected given the high grade assigned to the neoplasm during histologic analysis.
  • CLINICAL RELEVANCE: Pancreatic neoplasms are associated with a poor prognosis, regardless of treatment modality.
  • Celecoxib can be administered as palliative treatment to affected birds, but as with any nonsteroidal anti-inflammatory drug, COX-2 inhibitors should be used cautiously because they can adversely affect renal function by decreasing renal prostaglandin synthesis.
  • [MeSH-major] Adenocarcinoma / veterinary. Bird Diseases / drug therapy. Cockatoos. Cyclooxygenase Inhibitors / therapeutic use. Pancreatic Neoplasms / veterinary. Pyrazoles / therapeutic use. Sulfonamides / therapeutic use
  • [MeSH-minor] Animals. Anticarcinogenic Agents / adverse effects. Anticarcinogenic Agents / therapeutic use. Celecoxib. Cyclooxygenase 2 Inhibitors / adverse effects. Cyclooxygenase 2 Inhibitors / therapeutic use. Fatal Outcome. Male. Neoplasm Metastasis

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  • (PMID = 16426169.001).
  • [ISSN] 0003-1488
  • [Journal-full-title] Journal of the American Veterinary Medical Association
  • [ISO-abbreviation] J. Am. Vet. Med. Assoc.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; JCX84Q7J1L / Celecoxib
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18. Shimada K, Sano T, Sakamoto Y, Kosuge T: Safe management of the pancreatic remnant with prolamine duct occlusion after extended pancreaticoduodenectomy. Hepatogastroenterology; 2005 Nov-Dec;52(66):1874-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Safe management of the pancreatic remnant with prolamine duct occlusion after extended pancreaticoduodenectomy.
  • BACKGROUND/AIMS: Occlusion of the pancreatic duct system has been used to prevent pancreatic leakage by abolishing pancreatic exocrine secretion in pancreatic surgery.
  • However, ductal occlusion has not proved satisfactory for preventing pancreatic fistulas in pancreaticoduodenectomy (PD).
  • METHODOLOGY: Pancreatic duct occlusion with a watertight drainage system around the pancreatic stump was performed following extended PD in 17 patients with (n=12) or without (n=5) a dilated pancreatic duct.
  • RESULTS: Transient pancreatitis during the early postoperative period occurred in all patients with a nondilated pancreatic duct.
  • No patient developed pancreatic fistula or any other serious complication in both groups.
  • CONCLUSIONS: Pancreatic duct occlusion may minimize the risk of pancreatic leakage in patients with a nondilated pancreatic duct and a normal pancreas as well as in those with a dilated, obstructed pancreatic duct without compromising the postoperative quality of life.
  • This is a safe and reliable technique for managing the pancreatic remnant in patients undergoing extended PD for advanced pancreaticobiliary malignancy.
  • [MeSH-major] Neoplasm, Residual / drug therapy. Pancreatic Ducts / drug effects. Pancreatic Fistula / prevention & control. Pancreaticoduodenectomy / adverse effects. Phenylpropanolamine / therapeutic use
  • [MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / surgery. Adult. Aged. Anastomosis, Surgical / adverse effects. Anastomosis, Surgical / methods. Combined Modality Therapy. Female. Follow-Up Studies. Humans. Injections, Intralesional. Male. Middle Aged. Neoplasm Staging. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery. Postoperative Care / methods. Probability. Retrospective Studies. Risk Assessment. Safety Management. Treatment Outcome

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  • (PMID = 16334797.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 33RU150WUN / Phenylpropanolamine
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19. Alexandrescu DT, O'Boyle K, Feliz A, Fueg A, Wiernik PH: Metastatic solid-pseudopapillary tumour of the pancreas: clinico-biological correlates and management. Clin Oncol (R Coll Radiol); 2005 Aug;17(5):358-63
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  • [Title] Metastatic solid-pseudopapillary tumour of the pancreas: clinico-biological correlates and management.
  • Solid-pseudopapillary tumour of the pancreas is a rare neoplasm of young women, currently categorised in the World Health Organization classification under exocrine pancreatic tumours.
  • We describe two patients with solid-pseudopapillary tumour of the pancreas.
  • A smaller, localised tumour in an unusually young white man was surgically excised with no evidence of recurrence after 2 years.
  • A literature review was carried out, and the main clinico-pathological features and strategies of treatment of solid-pseudopapillary tumour of the pancreas are presented.
  • Pathological, genetic and molecular features distinguish solid-pseudopapillary tumours from pancreatic ductal adenocarcinoma.
  • Furthermore, neuroendocrine differentiation can be found focally in occasional cases of solid-pseudopapillary tumour.
  • Chemotherapy and radiation therapy are used in rare cases when resection is not possible.
  • No current chemotherapy regimens are considered standard in the treatment of this tumour.
  • A rational chemotherapy protocol for such a rare tumour needs to consider its origin and clinical behaviour.
  • However, the indolent clinical progression of solid-pseudopapillary tumours is similar to that of pancreatic neuroendocrine tumour.
  • [MeSH-major] Carcinoma, Papillary / surgery. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Adult. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 16097567.001).
  • [ISSN] 0936-6555
  • [Journal-full-title] Clinical oncology (Royal College of Radiologists (Great Britain))
  • [ISO-abbreviation] Clin Oncol (R Coll Radiol)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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20. Micke O, Bruns F, Schäfer U, Kurowski R, Horst E, Willich N: CA 19-9 in the therapy monitoring and follow-up of locally advanced cancer of the exocrine pancreas treated with radiochemotherapy. Anticancer Res; 2003 Mar-Apr;23(2A):835-40
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  • [Title] CA 19-9 in the therapy monitoring and follow-up of locally advanced cancer of the exocrine pancreas treated with radiochemotherapy.
  • PURPOSE: The aim of this study was to determine the value of CA 19-9 in therapy monitoring and follow-up of locally advanced pancreatic cancer treated by radiochemotherapy.
  • MATERIALS AND METHODS: Ninety-five patients with locally advanced irresectable adenocarcinoma of the pancreas were treated with hyperfractionated accelerated radiotherapy, with 44.8 Gy and 5-fluorouracil and folinic acid, January 1994 between and June 2001.
  • CA 19-9 was measured before therapy, each week under therapy and every 4 weeks in the follow-up.
  • RESULTS: Median CA 19-9 before treatment was 420 U/ml.
  • Patients with a level below the median had significantly better prognosis and a better treatment response than those above the median.
  • In the follow-up CA 19-9 had a sensitivity of 100% in detection of recurrent disease with a specificity of 88.
  • CONCLUSION: CA 19-9 has a high prognostic value and may serve as an in vivo marker for treatment sensitivity.
  • For detection of recurrent disease it shows a high sensitivity and specificity.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / radiography. CA-19-9 Antigen / blood. Fluorouracil / therapeutic use. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / radiography
  • [MeSH-minor] Adult. Aged. Combined Modality Therapy. Disease-Free Survival. Dose Fractionation. Female. Follow-Up Studies. Humans. Leucovorin / administration & dosage. Male. Middle Aged. Monitoring, Physiologic / methods. Neoplasm Staging. Prognosis. Survival Analysis. Time Factors

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  • (PMID = 12820309.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / CA-19-9 Antigen; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil
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21. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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22. Uchida K, Joseph JM, Gapany C, Chardot C: Modified digestive reconstruction with midgut transposition after pylorus-preserving pancreaticoduodenectomy for pancreatic head tumor in childhood. J Pediatr Surg; 2008 Oct;43(10):1932-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modified digestive reconstruction with midgut transposition after pylorus-preserving pancreaticoduodenectomy for pancreatic head tumor in childhood.
  • We describe a new procedure of digestive reconstruction after pylorus-preserving pancreaticoduodenectomy in a 13-year-old girl presenting with a large solid and papillary epithelial neoplasm of the pancreatic head.
  • A midgut transposition (like in a cure of midgut malrotation) was easily performed after tumor removal with minimal additional dissection.
  • Separate biliary and pancreatic conduits prevented both activation of pancreatic enzymes at the pancreatic duct anastomosis and reflux of pancreatic juice in the bile ducts.
  • This technique may be useful after pancreatic head resections in children and adolescents.
  • [MeSH-major] Cystadenoma, Papillary / surgery. Pancreatic Neoplasms / surgery. Pancreaticoduodenectomy / methods
  • [MeSH-minor] Adolescent. Anastomosis, Roux-en-Y. Enzymes / therapeutic use. Exocrine Pancreatic Insufficiency / drug therapy. Exocrine Pancreatic Insufficiency / etiology. Female. Humans. Jejunum / surgery. Pylorus. Remission Induction

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  • (PMID = 18926236.001).
  • [ISSN] 1531-5037
  • [Journal-full-title] Journal of pediatric surgery
  • [ISO-abbreviation] J. Pediatr. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzymes
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23. Ekeblad S: Islet cell tumours. Adv Exp Med Biol; 2010;654:771-89
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  • 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.
  • Several advances have been made in prognostication; a tumour-node-metastasis system has been evaluated and seems to have prognostic value, and several new molecular prognostic markers are under evaluation.
  • 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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24. Pasetto LM, D'Andrea MR, Falci C, Monfardini S: Gemcitabine in advanced biliary tract cancers. Crit Rev Oncol Hematol; 2007 Mar;61(3):230-42

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Despite this increase, it still continues to be a rare neoplasm.
  • Surgical resection is the treatment of choice, but a high percentage of patients are unsuitable for resection.
  • These patients have a very poor prognosis because of the lack of efficacious therapy options.
  • For some time, mitomycin C, doxorubicin and 5-fluorouracil have been considered among the most active chemotherapeutic agents, with a response rate ranging from 10 to 20%.
  • More recently, gemcitabine has become the reference agent for these neoplasias because of the histologically common origin of biliary cancer and exocrine pancreatic cancer.
  • Here we examine clinical trials designed for locally advanced and metastatic biliary tract cancer and review the existing data supporting palliative therapy with gemcitabine alone or in association with other drugs.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Biliary Tract Neoplasms / drug therapy. Deoxycytidine / analogs & derivatives
  • [MeSH-minor] Clinical Trials as Topic. Dose-Response Relationship, Drug. Humans. Neoplasm Staging. Palliative Care. Radiotherapy, Adjuvant

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  • (PMID = 17157524.001).
  • [ISSN] 1040-8428
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
  • [Number-of-references] 62
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25. García-Garayoa E, Maes V, Bläuenstein P, Blanc A, Hohn A, Tourwé D, Schubiger PA: Double-stabilized neurotensin analogues as potential radiopharmaceuticals for NTR-positive tumors. Nucl Med Biol; 2006 May;33(4):495-503
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  • INTRODUCTION: Overexpression of neurotensin (NT) receptors in exocrine pancreatic cancer and other neuroendocrine cancers make them interesting targets for tumor imaging and therapy.
  • NT-XII showed the highest tumor uptake as well as the best tumor to nontumor ratios.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Iodine Radioisotopes / pharmacokinetics. Neurotensin / pharmacokinetics. Receptors, Neurotensin / metabolism
  • [MeSH-minor] Animals. Drug Delivery Systems / methods. Drug Evaluation, Preclinical. Drug Stability. Feasibility Studies. Female. HT29 Cells. Humans. Isotope Labeling / methods. Metabolic Clearance Rate. Mice. Mice, Nude. Neoplasm Proteins / metabolism. Organ Specificity. Radiopharmaceuticals / chemical synthesis. Radiopharmaceuticals / pharmacokinetics. Tissue Distribution

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  • (PMID = 16720241.001).
  • [ISSN] 0969-8051
  • [Journal-full-title] Nuclear medicine and biology
  • [ISO-abbreviation] Nucl. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Iodine Radioisotopes; 0 / Neoplasm Proteins; 0 / Radiopharmaceuticals; 0 / Receptors, Neurotensin; 39379-15-2 / Neurotensin
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26. 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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