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Items 1 to 43 of about 43
1. Klapdor R, Bahlo M, Babinsky A, Brenzinger ML: Reflections on treatment strategies for palliative chemotherapy of pancreatic cancer. Anticancer Res; 2007 Jul-Aug;27(4A):1789-94
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  • [Title] Reflections on treatment strategies for palliative chemotherapy of pancreatic cancer.
  • Following our concept of efficacy-orientated sequential polychemotherapy, we report on the results of palliative chemotherapy in 69 patients suffering from exocrine pancreatic cancer, admitted to our unit in 2004.
  • Evaluation of tumor response was mainly based on the serum courses of the tumor markers CA 19-9 and CEA; in addition, the modern imaging methods CT or MRT, including MRCP and MR-angiography, were performed bi-monthly.
  • The median survival increased with the number of effective treatment sequences, for the whole group from 5 to 10 and 23 months in relation to 0, 1 and > 1 effective sequences respectively.
  • The results support our concept of EOSPC in pancreatic cancer patients, compared to clinical studies following protocols with only 1 treatment sequence and median survival rates of no more than 6-9 months.
  • Compared to the efficacy-orientated sequential polychemotherapy (EOSPC) concept, which does not exclude but also allows the inclusion of clinical trials for further evaluation of new drugs or drug combinations, the common practice looking for survival in studies following protocols with only 1 treatment sequence might represent a negative predictive factor with respect to overall survival, as can be demonstrated by a comparison of our data with relevant recent literature.
  • Our results further indicate that the interest of the clinicians and companies should not be focused only on first-line therapies, but also on 2nd- and 3rd-line strategies, as in our patients a second- and third-line therapy could be started in 73% and 68% of the patients respectively.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Adult. CA-19-9 Antigen / blood. Carcinoembryonic Antigen / blood. Female. Humans. Magnetic Resonance Angiography. Male. Middle Aged. Palliative Care. Survival Analysis. Tomography, X-Ray Computed

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  • (PMID = 17649774.001).
  • [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 / CA-19-9 Antigen; 0 / Carcinoembryonic Antigen
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2. Burch PA, Block M, Schroeder G, Kugler JW, Sargent DJ, Braich TA, Mailliard JA, Michalak JC, Hatfield AK, Wright K, Kuross SA: Phase III evaluation of octreotide versus chemotherapy with 5-fluorouracil or 5-fluorouracil plus leucovorin in advanced exocrine pancreatic cancer: a North Central Cancer Treatment Group study. Clin Cancer Res; 2000 Sep;6(9):3486-92
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  • [Title] Phase III evaluation of octreotide versus chemotherapy with 5-fluorouracil or 5-fluorouracil plus leucovorin in advanced exocrine pancreatic cancer: a North Central Cancer Treatment Group study.
  • There continues to be a need for new systemic approaches for the treatment of advanced pancreatic cancer.
  • The purpose of this study was to compare the antitumor activity of the somatostatin analogue octreotide to 5-fluorouracil chemotherapy in a Phase III setting.
  • Eighty-four patients with an Eastern Cooperative Oncology Group performance status of 0 or 1 and limited tumor volume were randomized to receive octreotide 200 microg three times daily or 5-fluorouracil with or without leucovorin.
  • After the first 12 patients had been randomized to octreotide, we increased the dose in the remaining patients to 500 microg three times daily.
  • A planned interim analysis performed after 84 patients were enrolled demonstrated inferior time to progression and survival for the patients randomized to octreotide.
  • Octreotide in doses of 200-500 microg three times daily does not delay progression or extend survival in patients with advanced pancreatic cancer compared with treatment with 5-fluorouracil with or without leucovorin.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Pancreatic Ductal / drug therapy. Fluorouracil / therapeutic use. Octreotide / therapeutic use. Pancreatic Neoplasms / drug therapy

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  • (PMID = 10999733.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-15083; United States / NCI NIH HHS / CA / CA-25224; United States / NCI NIH HHS / CA / CA-37404; etc
  • [Publication-type] Clinical Trial; Clinical Trial, Phase III; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Hormonal; Q573I9DVLP / Leucovorin; RWM8CCW8GP / Octreotide; U3P01618RT / Fluorouracil
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3. Klapdor R, Bahlo M, Babinsky A: Further evidence for prolongation of survival of pancreatic cancer patients by efficacy orientated sequential polychemotherapy (EOSPC) based on serial tumor marker determinations (CA 19-9/CEA). Anticancer Res; 2005 May-Jun;25(3A):1687-91
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  • [Title] Further evidence for prolongation of survival of pancreatic cancer patients by efficacy orientated sequential polychemotherapy (EOSPC) based on serial tumor marker determinations (CA 19-9/CEA).
  • The results of palliative chemotherapy in 55 patients suffering from exocrine pancreatic cancer are reported, following our concept of efficacy orientated sequential polychemotherapy (EOSPC).
  • Tumor answer/regression was mainly analyzed on the basis of the serum courses of the tumor markers CA 19-9 and CEA.
  • Up to four different treatment trials were tried in the individual patients.
  • The results confirm previously published data: a prolongation of survival in relation to the number of effective treatments (CR/PR/MR/SD vs. PD).
  • The results support our concept of EOSPC in pancreatic cancer patients in order to improve survival.
  • Furthermore, the data should stimulate attention not only on new and potentially more effective 1st- line regimens, but also to effective 2nd- and/or 3rd-line treatments.
  • Moreover, the results should encourage clinicians to rediscuss the actual concepts of prospective therapeutical trails mainly based on analyzing the effects of single agents or drug combinations on survival.
  • Furthermore, a comparison of 1st-line treatments with gemcitabine as monotherapy, and in combination with mitomycin-C, confirms that the combination of gemcitabine + mitomycin-C seems to be more active than gemcitabine monotherapy and that this combination might also be of value as 2nd-line therapy after gemcitabine monotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / blood. CA-19-9 Antigen / blood. Carcinoembryonic Antigen / blood. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / pathology. Survival Analysis

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  • (PMID = 16033083.001).
  • [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; 0 / CA-19-9 Antigen; 0 / Carcinoembryonic Antigen
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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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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. Klapdor R, Müller C, Seutter R, Bahlo M, Peters W, Fenner C: Improvement of survival by efficacy orientated sequential polychemotherapy of exocrine pancreatic cancer. Anticancer Res; 2000 Nov-Dec;20(6D):5201-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Improvement of survival by efficacy orientated sequential polychemotherapy of exocrine pancreatic cancer.
  • Results of palliative chemotherapy in 104 patients suffering from exocrine pancreatic carcinomas are presented.
  • First-line therapy included intraarterial approaches with gemcitabine + mitomycin-C and intravenous systemic treatments with gemcitabine, gemcitabine + mitomycin-C and oxaliplatin, respectively.
  • Follow-up included clinical investigations, imaging methods and determination of tumor markers.
  • The results indicated the intraarterial locoregional treatment of exocrine pancreatic cancer with a combination of mitomycin-C + gemcitabine as a highly effective treatment modality with PR + CR of 40% measured by imaging methods and 81% analysed by tumor marker determinations.
  • The survival analyses suggested relevant prolongation of survival in relation to the number of effective second- and/or third-line therapies (0/1/> 1) with median survival--based on the imaging data--of 7, 11 and 20 months for Mo tumors and 3, 8 and 14 months for tumor diseases with liver metastases at time of admission, respectively.
  • Relevant preconditions for second- and/or third-line therapies of pancreatic carcinomas are given by more or less effective first-line treatment modalities of this cancer disease on the one hand and by the actual diagnostic aids allowing the beginning of first-line therapy as well as the detection of recurrence early enough to try a second- or third-line therapy before clinical/ethical aspects prevent further antitumoral treatment trials in the individual patient.
  • [MeSH-major] Drug Therapy, Combination. Palliative Care. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Infusions, Intravenous. Male. Middle Aged. Pain / drug therapy. Pain / etiology. Survival Rate

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  • (PMID = 11326695.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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6. 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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  • [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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7. 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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8. 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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9. Bădulescu F, Bădulescu A, Rogoz S, Mustaţă R: Immunological approach in the diagnosis, therapy and prognosis of the exocrine pancreatic cancer. Roum Arch Microbiol Immunol; 2001 Jan-Mar;60(1):5-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunological approach in the diagnosis, therapy and prognosis of the exocrine pancreatic cancer.
  • The aim of the paper is to outline the most important up-to-date methods regarding the immunological approach in the diagnosis, treatment and prognosis of the exocrine pancreatic cancer, keeping in mind that this localisation of neoplastic disease represents the 5th cause of cancer-related death and especially, an important cause of morbidity.
  • This disease, diagnosed in the past in later stages, being therefore associated with poor results, has turned to be characterized by increasing survival rates due to the improvements in diagnostic and therapeutic methods.
  • Regarding the diagnosis strategy, progress was made in imagistic sphera, aiming: 1. an early diagnosis of pancreatic cancer and, implicitly, a high resectability rate of tumor, and 2. an evaluation of the timing for palliative therapeutic methods.
  • So that, if in the past the diagnostic algorithm meant endoscopic retrograde-cholangio-pancreatography, computed tomography and angiography, at present it means nuclear magnetic resonance and helicoidal tomography.
  • Concerning the treatment, it has to be multidisciplinary (surgery, radiotherapy, chemotherapy, immunotherapy), complex, because, after a resection for cure (R0), the main stay of the treatment, the mean survival at 5 years is 3%-28% and the rate of recurrences is 33%-80%.
  • Biological therapy (sometimes called immunotherapy, biotherapy or biological response modifier therapy) is a relatively new addition to the family of cancer treatments that also includes surgery, chemotherapy and radiation therapy.
  • Biological therapies are designed to repair, stimulate or enhance the immune system responses.
  • We shall try to point out how the exocrine pancreatic cancers, the same stages and undergoing the same approaches, have had different responses due to a different biological behavior and how the biological response modifiers (interferons, interleukins, colony-stimulating factors, monoclonal antibodies and vaccines) can improve the results in pancreatic cancer.
  • [MeSH-major] Immunologic Factors / therapeutic use. Pancreatic Neoplasms

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  • (PMID = 11850897.001).
  • [ISSN] 1222-3891
  • [Journal-full-title] Roumanian archives of microbiology and immunology
  • [ISO-abbreviation] Roum Arch Microbiol Immunol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Immunologic Factors
  • [Number-of-references] 17
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10. 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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11. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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12. 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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13. Ridwelski K, Meyer F: Current options for palliative treatment in patients with pancreatic cancer. Dig Dis; 2001;19(1):63-75
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  • [Title] Current options for palliative treatment in patients with pancreatic cancer.
  • Palliative treatment is often the only remaining option in the management of pancreatic carcinoma, but its efficacy is poor due to low tumor sensitivity and inadequate treatment protocols.
  • There are several options of palliative treatment with antitumor or supportive intention.
  • Classical end points of palliative treatment are survival, tumor response, and quality of life.
  • A decade ago, palliative chemotherapy consisted mainly of 5-fluorouracil as the standard agent in combination with either other agents and/or radiotherapy.
  • Only the new antineoplastic drug gemcitabine, which was introduced simultaneously with the definition of novel end points of chemotherapy such as clinical benefit, allowed to achieve some progress.
  • A novel concept, therefore, is to improve this beneficial cytostatic response in pancreatic carcinoma using a gemcitabine-based protocol by combining it with antineoplastic drugs such as taxanes or platin analogs.
  • This strategy may have the potential to improve the outcome in palliative chemotherapy of pancreatic carcinoma patients with advanced tumor growth or metastases.
  • Best supportive care in pancreatic cancer consists of the treatment of symptoms, such as pain, jaundice, duodenal obstruction, weight loss, exocrine pancreatic insufficiency, and tumor-associated depression.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma / drug therapy. Deoxycytidine / therapeutic use. Palliative Care. Pancreatic Neoplasms / drug therapy

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  • [Copyright] Copyright 2001 S. Karger AG, Basel
  • (PMID = 11385253.001).
  • [ISSN] 0257-2753
  • [Journal-full-title] Digestive diseases (Basel, Switzerland)
  • [ISO-abbreviation] Dig Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
  • [Number-of-references] 70
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14. Varadhachary GR, Tamm EP, Crane C, Evans DB, Wolff RA: Borderline resectable pancreatic cancer. Curr Treat Options Gastroenterol; 2005 Oct;8(5):377-84

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Borderline resectable pancreatic cancer.
  • Rigorous criteria to define "borderline resectable" pancreatic cancer are required for appropriate patient accrual into clinical trials that examine the utility of chemotherapy and/or chemoradiation that will be delivered prior to pancreatic resection for exocrine cancer.
  • At our institution, tumor abutment of less than or equal to 180 degrees (< or = 50% of the vessel circumference) of the superior mesenteric artery, short segment abutment or encasement (> or = 50% of the vessel circumference) of the common hepatic artery (typically at the gastroduodenal artery origin), or segmental venous occlusion are used to categorize a pancreatic tumor as borderline resectable.
  • These patients are at a high risk for margin positive resection with initial surgery; therefore, we favor a treatment schema that incorporates preoperative (neoadjuvant) therapy with systemic chemotherapy and chemoradiation.
  • Patients whose tumors show radiographic stability or regression that are often accompanied by an improvement in serum tumor markers are candidates for pancreaticoduodenectomy.
  • A prospective multicenter clinical trial with well-defined eligibility criteria may help decide the best overall treatment strategy for these patients.
  • Vascular resection and reconstruction may be required in patients with borderline resectable tumors, and surgery should be performed at centers with expertise in such complex pancreatic resections.

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  • (PMID = 16162303.001).
  • [ISSN] 1092-8472
  • [Journal-full-title] Current treatment options in gastroenterology
  • [ISO-abbreviation] Curr Treat Options Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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16. 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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17. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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18. Klapdor R, Bahlo M, Babinski A, Klapdor S: CA19-9 serum concentrations--analysis of the serum kinetics during first-line therapy of pancreatic cancer in relation to overall survival. Anticancer Res; 2010 May;30(5):1869-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CA19-9 serum concentrations--analysis of the serum kinetics during first-line therapy of pancreatic cancer in relation to overall survival.
  • In order to investigate the use of CA19-9 serum concentration kinetics during first-line chemotherapy of pancreatic cancer as a potential predictive prognostic factor for overall survival, we retrospectively analysed the data of 47 patients suffering from proven exocrine pancreatic cancer.
  • The patients were treated following our concept of efficacy-orientated sequential palliative chemotherapy (EOSPC), on the basis of a short-term follow-up including CA19-9 determinations at least monthly and imaging methods CT and/or MR every 2 months.
  • The results are in agreement with our previous reports suggesting an increase of survival of pancreatic cancer patients in relation to the number of effective treatment regimens applied.
  • However, apart from a weak correlation between the lowest CA19-9 levels induced by the first-line therapy (as a % of the initial pretherapeutical CA19-9 levels) and progression-free survival there was no correlation between the various parameters of serum kinetics of CA19-9 in the course of the first-line therapy and overall survival of the patients.
  • A potential correlation as reported by others seems to be confirmed in our patient group by the potential antitumoral and life-prolonging effects of the second- and third-line therapies.
  • [MeSH-major] Biomarkers, Tumor / blood. CA-19-9 Antigen / blood. Pancreatic Neoplasms / blood. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / therapeutic use. Disease-Free Survival. Humans. Kinetics. Middle Aged. Palliative Care. Prognosis. Retrospective Studies. Treatment Outcome

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  • (PMID = 20592394.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / CA-19-9 Antigen
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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. 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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21. 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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22. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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23. Saif MW, Larson H, Kaley K, Shaib W: Chronic octreotide therapy can induce pancreatic insufficiency: a common but under-recognized adverse effect. Expert Opin Drug Saf; 2010 Nov;9(6):867-73

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic octreotide therapy can induce pancreatic insufficiency: a common but under-recognized adverse effect.
  • Octreotide analogs are used in the treatment of neuroendocrine tumors and are investigated as treatment options in many diseases.
  • These agents mimic somatostatin effect which is inhibitory to pancreatic hormones.
  • Pancreatic insufficiency is a common adverse effect of this medication which is explained by the direct inhibition of pancreatic hormones responsible for stimulating the production and excretion of pancreatic enzymes.
  • This side effect is misdiagnosed leading to increasing octreotide analog dosage, and eventually more pancreatic insufficiency and cost of treatment.
  • We report our experience with pancreatic insufficiency developing in neuroendocrine tumor patients treated with octreotide analogs, reviewing the pathogenesis of this side effect.
  • [MeSH-major] Exocrine Pancreatic Insufficiency / chemically induced. Gastrointestinal Agents / adverse effects. Gastrointestinal Agents / therapeutic use. Octreotide / adverse effects. Octreotide / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Diagnostic Errors. Diarrhea / chemically induced. Female. Humans. Male. Middle Aged. Receptors, Serotonin / metabolism. Time Factors

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  • (PMID = 20662741.001).
  • [ISSN] 1744-764X
  • [Journal-full-title] Expert opinion on drug safety
  • [ISO-abbreviation] Expert Opin Drug Saf
  • [Language] eng
  • [Publication-type] Case Reports; Editorial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gastrointestinal Agents; 0 / Receptors, Serotonin; RWM8CCW8GP / Octreotide
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24. Kaltsas GA, Besser GM, Grossman AB: The diagnosis and medical management of advanced neuroendocrine tumors. Endocr Rev; 2004 Jun;25(3):458-511
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The diagnosis and medical management of advanced neuroendocrine tumors.
  • Neuroendocrine tumors (NETs) constitute a heterogeneous group of neoplasms that originate from endocrine glands such as the pituitary, the parathyroids, and the (neuroendocrine) adrenal, as well as endocrine islets within glandular tissue (thyroid or pancreatic) and cells dispersed between exocrine cells, such as endocrine cells of the digestive (gastroenteropancreatic) and respiratory tracts.
  • Assessment of specific or general tumor markers offers high sensitivity in establishing the diagnosis and can also have prognostic significance.
  • Imaging modalities include endoscopic ultrasonography, computed tomography and magnetic resonance imaging, and particularly, scintigraphy with somatostatin analogs and metaiodobenzylguanidine.
  • Successful treatment of disseminated NETs requires a multimodal approach; radical tumor surgery may be curative but is rarely possible.
  • Well-differentiated and slow-growing gastroenteropancreatic tumors should be treated with somatostatin analogs or alpha-interferon, with chemotherapy being reserved for poorly differentiated and progressive tumors.
  • Therapy with radionuclides may be used for tumors exhibiting uptake to a diagnostic scan, either after surgery to eradicate microscopic residual disease or later if conventional treatment or biotherapy fails.
  • [MeSH-major] Interferon-alpha / therapeutic use. Neuroendocrine Tumors / diagnosis. Neuroendocrine Tumors / drug therapy. Somatostatin / therapeutic use
  • [MeSH-minor] Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / therapy. Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Carcinoma, Neuroendocrine / diagnosis. Carcinoma, Neuroendocrine / drug therapy. Gastrointestinal Neoplasms / diagnosis. Gastrointestinal Neoplasms / therapy. Humans. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / therapy. Parathyroid Neoplasms / diagnosis. Parathyroid Neoplasms / therapy. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / therapy. Prognosis. Quality of Life. Sensitivity and Specificity. Thyroid Neoplasms / diagnosis. Thyroid Neoplasms / therapy. Tomography, X-Ray Computed

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  • (PMID = 15180952.001).
  • [ISSN] 0163-769X
  • [Journal-full-title] Endocrine reviews
  • [ISO-abbreviation] Endocr. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Interferon-alpha; 51110-01-1 / Somatostatin
  • [Number-of-references] 620
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25. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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26. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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27. 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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28. 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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29. 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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30. 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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31. Kamisawa T, Yoshiike M, Egawa N, Nakajima H, Tsuruta K, Okamoto A: Treating patients with autoimmune pancreatitis: results from a long-term follow-up study. Pancreatology; 2005;5(2-3):234-8; discussion 238-40
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  • BACKGROUND: Steroid therapy is currently common treatment for autoimmune pancreatitis (AIP); however, indications of steroid therapy have yet to be established, and the clinical course after steroid therapy is unknown.
  • METHODS: A total of 23 patients with AIP were subdivided into 4 groups according to the initial treatments undertaken.
  • They were treated with pancreatoduodenectomy on suspicion of pancreatic tumor in 6 patients, choledochoduodenostomy with pancreatic biopsy in 4 patients, supportive therapy in 3 patients, and steroid therapy in 10 patients.
  • RESULTS: Prognosis of the AIP patients is almost good except for the 2 patients who progressed to pancreatic insufficiency after resection.
  • Steroid therapy was effective in all patients treated, but pancreatic atrophy developed in 5 of these patients.
  • Steroid therapy improved insulin secretion and glycemic control in 4 of 7 diabetes mellitus (DM) patients.
  • CONCLUSION: To avoid futile surgery, in relatively elderly male patients with obstructive jaundice suggestive of pancreatic carcinoma, preoperative clinical suspicion of AIP is mandatory.
  • Indications of steroid therapy for AIP are thought to be obstructive jaundice due to stenosis of the bile duct, other associated systemic autoimmune, and DM coincidental with AIP.
  • [MeSH-major] Autoimmune Diseases / drug therapy. Pancreatitis / drug therapy. Pancreatitis / immunology. Steroids / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Choledochostomy. Chronic Disease. Exocrine Pancreatic Insufficiency / drug therapy. Exocrine Pancreatic Insufficiency / prevention & control. Female. Follow-Up Studies. Humans. Jaundice, Obstructive / drug therapy. Jaundice, Obstructive / surgery. Male. Middle Aged. Pancreaticoduodenectomy. Treatment Outcome

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  • (PMID = 15855821.001).
  • [ISSN] 1424-3903
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Steroids
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32. Fehmann HC, Wulbrand U, Arnold R: Treatment of endocrine gastroenteropancreatic tumors with somatostatin analogues. Recent Results Cancer Res; 2000;153:15-22
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  • [Title] Treatment of endocrine gastroenteropancreatic tumors with somatostatin analogues.
  • Somatostatin is a hormone that regulates the function of several exocrine and endocrine glands.
  • These proteins are expressed in a tissue-specific manner.
  • Excessive hormone secretion in carcinoid syndrome can be controlled by these drugs.
  • In addition, at least a subgroup of patients with carcinoid syndromes respond with delayed tumor growth during octreotide therapy.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Endocrine Gland Neoplasms / drug therapy. Gastrointestinal Neoplasms / drug therapy. Pancreatic Neoplasms / drug therapy. Somatostatin / analogs & derivatives

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  • (PMID = 10626286.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] GERMANY
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 51110-01-1 / Somatostatin
  • [Number-of-references] 34
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33. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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34. 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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35. 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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36. 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


37. 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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38. 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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39. 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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40. Voutetakis A, Cotrim AP, Rowzee A, Zheng C, Rathod T, Yanik T, Loh YP, Baum BJ, Cawley NX: Systemic delivery of bioactive glucagon-like peptide 1 after adenoviral-mediated gene transfer in the murine salivary gland. Endocrinology; 2010 Sep;151(9):4566-72
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  • When expressed in Neuro2A and COS7 cells, an active form of GLP-1 was specifically detected by RIA in the conditioned medium of transduced cells, showed resistance to degradation by dipeptidyl-peptidase IV, and induced the secretion of insulin from NIT1 pancreatic beta-cells in vitro.
  • In vivo studies demonstrated that healthy mice transduced with Ad-GLP-1 in both submandibular glands had serum GLP-1 levels approximately 3 times higher than mice transduced with the control Ad-luciferase vector.
  • These studies demonstrate that the bioactive peptide hormone, GLP-1, normally secreted from endocrine cells in the gut through the regulated secretory pathway, can be engineered for secretion into the circulatory system from exocrine cells of the salivary gland to affect glucose homeostasis.

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  • (PMID = 20610567.001).
  • [ISSN] 1945-7170
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin; 6SW5YHA5NG / Alloxan; 89750-14-1 / Glucagon-Like Peptide 1; EC 3.4.14.5 / Dipeptidyl Peptidase 4; IY9XDZ35W2 / Glucose
  • [Other-IDs] NLM/ PMC2940489
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41. 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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42. Hofsli E: [The somatostatin receptor family--a window against new diagnosis and therapy of cancer]. Tidsskr Nor Laegeforen; 2002 Feb 20;122(5):487-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The somatostatin receptor family--a window against new diagnosis and therapy of cancer].
  • [Transliterated title] Somatostatinreseptorfamilien--et vindu mot ny kreftdiagnostikk og behandling.
  • BACKGROUND: The peptide hormone somatostatin (SST) inhibits secretion from a wide variety of both endocrine and exocrine cells.
  • MATERIAL AND METHODS: The article presents a literature-based review of the somatostatin receptor (SSTR) family, and diagnostic and therapeutic strategies based upon SSTR expression in neuroendocrine (NE) gastroenteropancreatic (GEP) tumours.
  • Many tumour cell lines as well as the majority of human tumours express SSTR mRNAs, usually more than one subtype.
  • SSTR scintigraphy has become an important diagnostic tool for staging of NE GEP tumours and it may also predict sensitivity to treatment with somatostatin analogues.
  • These are regarded as the main choice for symptomatic treatment of hormone related syndromes related to NE GEP tumours.
  • Gene therapy has shown promising results in animal studies.
  • INTERPRETATION: Increased molecular understanding of the SSTR family and especially how the receptors are being regulated will probably lead to the development of new diagnostic and therapeutic strategies against cancer.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Gastrointestinal Neoplasms. Neuroendocrine Tumors. Pancreatic Neoplasms. Receptors, Somatostatin / metabolism. Somatostatin / therapeutic use
  • [MeSH-minor] Gene Expression Regulation. Genetic Therapy. Humans. Signal Transduction. Tumor Cells, Cultured / cytology. Tumor Cells, Cultured / drug effects

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  • (PMID = 11961977.001).
  • [ISSN] 0029-2001
  • [Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række
  • [ISO-abbreviation] Tidsskr. Nor. Laegeforen.
  • [Language] nor
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin
  • [Number-of-references] 30
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43. Talukdar R, Saikia N, Singal DK, Tandon R: Chronic pancreatitis: evolving paradigms. Pancreatology; 2006;6(5):440-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Chronic pancreatitis (CP) is characterized by progressive fibrosis, pain and/or loss of exocrine and endocrine functions.
  • With the identification and characterization of pancreatic stellate cells (PSCs), the pathogenesis of CP and pancreatic fibrosis is now better understood.
  • Molecular mediators shown to regulate the pathogenesis include transforming growth factor-beta, platelet-derived growth factor, and proinflammatory cytokines such as interleukin (IL)-1, IL-6 and tumor necrosis factor-alpha.
  • Understanding the pathogenesis has led to the identification of novel molecular targets and the development of newer potential therapeutic agents.
  • [MeSH-major] Pancreatitis, Chronic / diagnosis. Pancreatitis, Chronic / drug therapy






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