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Items 1 to 25 of about 25
1. Hemminki A, Belousova N, Zinn KR, Liu B, Wang M, Chaudhuri TR, Rogers BE, Buchsbaum DJ, Siegal GP, Barnes MN, Gomez-Navarro J, Curiel DT, Alvarez RD: An adenovirus with enhanced infectivity mediates molecular chemotherapy of ovarian cancer cells and allows imaging of gene expression. Mol Ther; 2001 Sep;4(3):223-31
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  • [Title] An adenovirus with enhanced infectivity mediates molecular chemotherapy of ovarian cancer cells and allows imaging of gene expression.
  • The adenovirus (Ad) is a useful vector for cancer gene therapy due to its unparalleled gene transfer efficiency to dividing and quiescent cells.
  • We describe here two novel bicistronic adenoviral (Ad) vectors, AdTKSSTR and RGDTKSSTR, which contain the herpes simplex virus thymidine kinase gene (TK) for molecular chemotherapy and bystander effect.
  • In addition, the viruses contain the human somatostatin receptor subtype-2 gene (SSTR2), the expression of which can be noninvasively imaged.
  • The expanded tropism of RGDTKSSTR results in increased infectivity of purified primary ovarian cancer cells and allows enhanced gene transfer in the presence of malignant ascites containing anti-Ad antibodies.
  • [MeSH-major] Adenoviridae / genetics. Adenoviridae / physiology. Diagnostic Imaging / methods. Gene Expression. Genetic Therapy / methods. Ovarian Neoplasms / genetics. Ovarian Neoplasms / therapy
  • [MeSH-minor] Ascites / genetics. Ascites / metabolism. Ascites / pathology. Ascites / virology. Cell Survival / drug effects. Coxsackie and Adenovirus Receptor-Like Membrane Protein. DNA, Recombinant / genetics. Female. Ganciclovir / pharmacology. Genetic Vectors / genetics. Gentian Violet. HeLa Cells. Humans. Mutagenesis, Insertional. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, Somatostatin / genetics. Receptors, Virus / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Thymidine Kinase / genetics. Tumor Cells, Cultured

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  • (PMID = 11545613.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5P30-CA13148; United States / NCI NIH HHS / CA / CA68245; United States / NCI NIH HHS / CA / CA74242; United States / NCI NIH HHS / CA / CA83591; United States / NCI NIH HHS / CO / CO97110
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CLMP protein, human; 0 / Coxsackie and Adenovirus Receptor-Like Membrane Protein; 0 / DNA, Recombinant; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 0 / Receptors, Virus; 0 / somatostatin receptor 2; EC 2.7.1.21 / Thymidine Kinase; J4Z741D6O5 / Gentian Violet; P9G3CKZ4P5 / Ganciclovir
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2. Fueger BJ, Hamilton G, Raderer M, Pangerl T, Traub T, Angelberger P, Baumgartner G, Dudczak R, Virgolini I: Effects of chemotherapeutic agents on expression of somatostatin receptors in pancreatic tumor cells. J Nucl Med; 2001 Dec;42(12):1856-62
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  • [Title] Effects of chemotherapeutic agents on expression of somatostatin receptors in pancreatic tumor cells.
  • Specific tumors express high amounts of receptors for somatostatin (SST), providing the basis for imaging and treatment using radiolabeled SST analogs.
  • However, little is known about the potential influence of cytotoxic drugs on SST receptor (SSTR) expression in malignant cells.
  • METHODS: To study the interaction between cytotoxic drugs and SSTR expression, the pancreatic cancer-derived tumor cell lines BxPC-3, Panc-1, Capan-1, and ASPC-1 were exposed to a range of cytotoxic drugs in vitro: Gemcitabine, 5-fluorouracil, cisplatin (cis-diaminedichloroplatinum [II]), camptothecin, mitomycin C, and doxorubicin were checked for changes in binding characteristics of the SSTR ligand (111)In-1,4,7,10-tetraazacyclododecane- N,N',N",N"'-tetraacetic acid-lanreotide (DOTA-LAN).
  • Chemosensitivity was quantitated by measurements of reduction in cell numbers, changes in cell cycle distribution, and appearance of apoptotic subG1 (subG1/0 cell DNA content) cells.
  • For gemcitabine, these effects were reversed after 4 d of recovery of the cell lines, eventually revealing overexpression of low- and high-affinity sites for BxPC-3 and Panc-1 cells and low-affinity sites for ASPC-1 cells.
  • CONCLUSION: Our results clearly show that the pancreatic tumor lines reduce the expression of high-affinity DOTA-LAN binding sites during application of chemotherapeutic drugs, which is accompanied by variable overexpression of low-affinity binding sites.
  • In the case of gemcitabine, SSTRs are overexpressed during recovery from drug exposure within 4 d.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / pharmacology. Pancreatic Neoplasms / drug therapy. Receptors, Somatostatin / drug effects
  • [MeSH-minor] Heterocyclic Compounds, 1-Ring. Humans. Indium Radioisotopes. Peptides, Cyclic. Radiopharmaceuticals. Tumor Cells, Cultured

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  • (PMID = 11752085.001).
  • [ISSN] 0161-5505
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DOTALAN; 0 / Heterocyclic Compounds, 1-Ring; 0 / Indium Radioisotopes; 0 / Peptides, Cyclic; 0 / Radiopharmaceuticals; 0 / Receptors, Somatostatin
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3. Kaltsas G, Rockall A, Papadogias D, Reznek R, Grossman AB: Recent advances in radiological and radionuclide imaging and therapy of neuroendocrine tumours. Eur J Endocrinol; 2004 Jul;151(1):15-27
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  • [Title] Recent advances in radiological and radionuclide imaging and therapy of neuroendocrine tumours.
  • Neuroendocrine tumours (NETs) constitute a heterogeneous group of tumours that are able to express cell membrane neuroamine uptake mechanisms and/or specific receptors, such as somatostatin receptors, which can be of great value in the localization and treatment of these tumours.
  • Scintigraphy with (111)In-pentetreotide has become one of the most important imaging investigations in the initial identification and staging of gastro-enteropancreatic (GEP) tumours, whereas helical computed tomography (CT), magnetic resonance imaging (MRI), endoscopic and/or peri-operative ultrasonography are used for the precise localization of GEPs and in monitoring their response to treatment.
  • Scintigraphy with (123)I-MIBG (meta-iodobenzylguanidine) is sensitive in the identification of chromaffin cell tumours, although scintigraphy with (111)In-pentetreotide may also have a role in the localization of malignant chromaffin cell tumours and medullary thyroid carcinoma; for further localization and monitoring of the response to treatment both CT and MRI are used with high diagnostic accuracy.
  • More recently, positron emission tomography (PET) scanning is being increasingly used for the localization of NETs, particularly when other imaging modalities have failed, although its precise role and utility remain to be defined.
  • Surgery is still the usual initial therapeutic, and only curative, modality of choice; however, the majority of NETs will require further treatment with somatostatin analogues and/or interferon; chemotherapy may be used for progressive and highly aggressive NETs, but its role has not been clearly defined.
  • For those NETs that demonstrate uptake to a diagnostic scan with (123)I-MIBG or (111)In-octreotide, therapy with radionuclides such as (131)I-MIBG or (111)In/(90)Y-octreotide or other isotopes, presents a further evolving therapeutic modality.

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  • (PMID = 15248818.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 127
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4. Plonowski A, Varga JL, Schally AV, Krupa M, Groot K, Halmos G: Inhibition of PC-3 human prostate cancers by analogs of growth hormone-releasing hormone (GH-RH) endowed with vasoactive intestinal peptide (VIP) antagonistic activity. Int J Cancer; 2002 Apr 1;98(4):624-9
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  • Vasoactive intestinal peptide (VIP) stimulates the proliferation and invasiveness of malignant prostatic cells.
  • Both antagonists produced a similar reduction in tumor volume (62-67%, p < 0.01) and tumor weight (59-62%; p < 0.05) vs. controls and extended tumor doubling-time from 9.1 to about 16 days (p < 0.05).
  • To investigate the mechanisms involved, in another study we compared the effects of JV-1-53 with those of somatostatin analog RC-160.
  • VIP antagonist JV-1-53 reduced tumor weight by 67% (p < 0.01) and suppressed the expression of mRNA for c-fos and c-jun oncogenes by about 34% (p < 0.05), without affecting serum levels of insulin-like growth factor-I (IGF-I).
  • In contrast, RC-160 (50 microg/day) reduced serum IGF-I by 19% (p < 0.05), but did not significantly decrease tumor weight. mRNA for VIP and high affinity receptors for VIP were detected on PC-3 tumors.
  • The ability of GH-RH antagonists to block tumoral VIP receptors, in addition to GH-RH receptors, could be potentially beneficial for prostate cancer therapy.
  • [MeSH-major] Growth Hormone-Releasing Hormone / antagonists & inhibitors. Growth Hormone-Releasing Hormone / pharmacology. Peptide Fragments / pharmacology. Prostatic Neoplasms / drug therapy. Vasoactive Intestinal Peptide / antagonists & inhibitors
  • [MeSH-minor] Animals. Binding, Competitive. Cell Division / drug effects. Humans. Insulin-Like Growth Factor I / drug effects. Insulin-Like Growth Factor I / metabolism. Male. Mice. Mice, Nude. Proto-Oncogene Proteins c-fos / genetics. Proto-Oncogene Proteins c-jun / genetics. RNA, Messenger / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, Vasoactive Intestinal Peptide / metabolism. Time Factors. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 11920625.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / JV 1-52; 0 / JV 1-53; 0 / Peptide Fragments; 0 / Proto-Oncogene Proteins c-fos; 0 / Proto-Oncogene Proteins c-jun; 0 / RNA, Messenger; 0 / Receptors, Vasoactive Intestinal Peptide; 37221-79-7 / Vasoactive Intestinal Peptide; 67763-96-6 / Insulin-Like Growth Factor I; 9034-39-3 / Growth Hormone-Releasing Hormone
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5. Ferone D, Resmini E, Boschetti M, Arvigo M, Albanese V, Ceresola E, Pivonello R, Albertelli M, Bianchi F, Giusti M, Minuto F: Potential indications for somatostatin analogues: immune system and limphoproliferative disorders. J Endocrinol Invest; 2005;28(11 Suppl International):111-7
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  • [Title] Potential indications for somatostatin analogues: immune system and limphoproliferative disorders.
  • Among hormones and neuropeptides influencing the immune system, somatostatin seems to play a key role not only in inhibiting specific immune cell activities, but also in promoting selected functions of particular immune cell subsets.
  • Indeed, controversial effects have been observed in experimental conditions where somatostatin seems to stimulate certain cell functions, such as secretion of specific products (immunoglobulin, cytokines), cell migration and adhesion to extracellular matrix components.
  • However, interestingly, cortistatin (CST), a neuropeptide that strongly resembles somatostatin, from both the structural and functional points of view, seems to have potential roles in regulating immune responses, as well as other lymphoid cell functions.
  • The actions of somatostatin and its synthetic analogs (SSA) are mediated by five membrane G protein-coupled receptors subtypes (SSTR1-5), displaying a tissue specific distribution.
  • The majority of somatostatin-target tissues, including lymphoid tissues, may co-express multiple somatostatin receptor (SSTR).
  • The number of SSTRs in lymphoid cells is significantly lower compared to neuroendocrine tissues.
  • In specific cases, this technique may contribute to establishing the diagnosis and staging the disease.
  • Moreover, since lymphomas are highly radiosensitive malignancies, a promising approach in refractory patients with malignant lymphomas may be represented by radionuclide-targeted therapy with radioactive-coupled SSAs combined with gene therapy.
  • This latter technique seems effective in inducing the expression or increasing the number of given SSTR in order to ameliorate the impact of radionuclide-targeted therapy.
  • Medical treatment of lymphoproliferative diseases with currently available synthetic analogs have produced unsatisfactory and conflicting results.
  • The application of receptor-based localization and anti-tumor strategies should also be taking into account the new knowledge recently emerged on the physiopathology of neuropeptide receptors: firstly, neuropeptide receptor homo- and heterodimerization, which may involve different subtypes of SSTRs, as well as other neuropetide receptors, and secondly, the role of endogenous SSTR ligands, such as CST.
  • [MeSH-major] Immunity / drug effects. Lymphoproliferative Disorders / drug therapy. Somatostatin / analogs & derivatives
  • [MeSH-minor] Humans. Immune System / chemistry. Immune System / drug effects. Immune System / physiopathology. Neuropeptides / physiology. Receptors, Somatostatin / analysis. Receptors, Somatostatin / physiology

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  • (PMID = 16625859.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Neuropeptides; 0 / Receptors, Somatostatin; 0 / cortistatin; 51110-01-1 / Somatostatin
  • [Number-of-references] 65
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6. Keller G, Schally AV, Nagy A, Baker B, Halmos G, Engel JB: Effective therapy of experimental human malignant melanomas with a targeted cytotoxic somatostatin analogue without induction of multi-drug resistance proteins. Int J Oncol; 2006 Jun;28(6):1507-13
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  • [Title] Effective therapy of experimental human malignant melanomas with a targeted cytotoxic somatostatin analogue without induction of multi-drug resistance proteins.
  • Malignant melanomas are characterized by a high intrinsic resistance to chemotherapy.
  • Multiple drug resistance (MDR) can be mediated by transport proteins such as MDR-1, multidrug resistance-associated protein (MRP) or lung resistance protein (LRP).
  • The cytotoxic analogue of somatostatin AN-238 consisting of 2-pyrrolinodoxorubicin (AN-201) linked to a somatostatin analogue RC-121 binds to receptors for somatostatin and is targeted to tumors expressing these receptors.
  • We evaluated the expression of somatostatin receptors on human malignant melanoma tumor lines MRI-H255 and MRI-H187 and examined the effects of the targeted analogue AN-238 and its cytotoxic radical AN-201 on growth of these tumors in nude mice.
  • We also studied the effects of AN-238 and AN-201 on the expression of MDR-1, MRP-1 and LRP by real-time PCR.
  • Blockade of somatostatin receptors by somatostatin analogue RC-121 abolished the effects of AN-238.
  • Targeted therapy with AN-238 did not produce an induction of mRNA of MDR-1, MRP-1 or LRP.
  • Our findings show that targeted chemotherapy with cytotoxic somatostatin analogue AN-238 inhibits the growth of malignant melanomas.
  • AN-238 could provide a novel treatment approach for advanced malignant melanomas.
  • [MeSH-major] Melanoma / drug therapy. Octreotide / analogs & derivatives
  • [MeSH-minor] Amino Acid Sequence. Animals. Base Sequence. Cell Line, Tumor. Cell Survival / drug effects. DNA Primers. Drug Resistance, Multiple. Humans. Kinetics. Mice. Mice, Nude. P-Glycoprotein / drug effects. P-Glycoprotein / genetics. Polymerase Chain Reaction. Transplantation, Heterologous

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  • (PMID = 16685451.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA Primers; 0 / P-Glycoprotein; 99660-13-6 / RC 121; RWM8CCW8GP / Octreotide
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7. Cattaneo MG, Gentilini D, Vicentini LM: Deregulated human glioma cell motility: inhibitory effect of somatostatin. Mol Cell Endocrinol; 2006 Aug 15;256(1-2):34-9
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  • [Title] Deregulated human glioma cell motility: inhibitory effect of somatostatin.
  • Malignant gliomas are highly invasive tumors which are lethal despite aggressive therapy.
  • The motility behavior of two human glioma cell lines i.e.
  • The two cell lines responded equally well to platelet-derived growth factor (PDGF) as chemoattractant factor.
  • The phosphatidylinositol 3-kinase (PI3-K) signaling, but not the extracellular signal-related kinase (ERK) signaling, was strongly involved in the PDGF-stimulated glioma cell motility.
  • Somatostatin was capable of inhibiting the migration in both glioma cell lines without affecting crucial targets for motility control like PI3-K and Rac activity.
  • These data suggest that somatostatin, by interfering with a target further downstream to Rac, negatively affects glioma cell motility, and may thus offer a pharmacological approach to controlling the deregulated motility of these aggressive tumoral cells.
  • [MeSH-major] Cell Movement / drug effects. Glioma / metabolism. Hormones / pharmacology. Somatostatin / pharmacology
  • [MeSH-minor] Butadienes / metabolism. Cell Line, Tumor. Chemotactic Factors / pharmacology. Chromones / metabolism. Enzyme Inhibitors / metabolism. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. Morpholines / metabolism. Neoplasm Metastasis. Nitriles / metabolism. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / metabolism. Platelet-Derived Growth Factor / pharmacology. Proto-Oncogene Proteins c-akt / metabolism. rac GTP-Binding Proteins / metabolism

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  • (PMID = 16828967.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Butadienes; 0 / Chemotactic Factors; 0 / Chromones; 0 / Enzyme Inhibitors; 0 / Hormones; 0 / Morpholines; 0 / Nitriles; 0 / Platelet-Derived Growth Factor; 0 / U 0126; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 51110-01-1 / Somatostatin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.6.5.2 / rac GTP-Binding Proteins
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8. Rougier P, Mitry E: Chemotherapy in the treatment of neuroendocrine malignant tumors. Digestion; 2000;62 Suppl 1:73-8
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  • [Title] Chemotherapy in the treatment of neuroendocrine malignant tumors.
  • The efficacy of chemotherapy in digestive neuroendocrine tumors (NET) depends on primary site and histological differentiation.
  • Many reports have suggested a superior activity of chemotherapy for pancreatic NET than for metastatic carcinoid tumors with response rates ranging from 40 to 60% compared to 20%.
  • The standard chemotherapy for pancreatic NET is a combination of adriamycin and streptozocin and to a lesser extent a combination of 5FU and streptozocin.
  • In contrast, there is no clear standard chemotherapy for carcinoid tumors and if most oncologists use a combination of 5FU and streptozocin in the case of advanced, progressive and nonresectable carcinoid tumors, the results are mostly poor and the benefit seldom counterbalances its toxicity.
  • In these carcinoid tumors the combination of hepatic artery ischemia alternating with chemotherapy has given impressive results in one study, which, however, have never been confirmed.
  • Tumor cell differentiation is a major prognostic factor and some reports have suggested a higher chemosensitivity for undifferentiated or poorly differentiated NET with tumor response rates ranging from 41 to 69% when a VP16-CDDP combination is used.
  • This chemosensitivity is, unfortunately, as in small cell lung carcinomas, of short duration.
  • Related to this special problem and the number of other active treatments in NET, the place of chemotherapy always has to be discussed in a multidisciplinary fashion.
  • Surgical excision, chemoembolization, interferons and somatostatin analogues have to be emphasized and eventually combined with chemotherapy, especially in slowly growing tumors.
  • New active chemotherapy regimens have to be tested clearly in this orphan group of tumors which does not hold much interest to the pharmaceutical companies.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Gastrointestinal Neoplasms / drug therapy. Neuroendocrine Tumors / drug therapy. Pancreatic Neoplasms / drug therapy

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  • [Copyright] Copyright 2000 S. Karger AG, Basel
  • (PMID = 10940691.001).
  • [ISSN] 0012-2823
  • [Journal-full-title] Digestion
  • [ISO-abbreviation] Digestion
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 5W494URQ81 / Streptozocin; 6PLQ3CP4P3 / Etoposide; 7GR28W0FJI / Dacarbazine; 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
  • [Number-of-references] 23
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9. Ahlman H: Malignant pheochromocytoma: state of the field with future projections. Ann N Y Acad Sci; 2006 Aug;1073:449-64
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  • [Title] Malignant pheochromocytoma: state of the field with future projections.
  • The prevalence of malignant pheochromocytoma is about 10%, and is somewhat higher for paraganglioma.
  • The discussion related to future strategies for better clinical/histopathologic diagnosis and understanding of different geno- and phenotypes.
  • The main therapeutic goal is therefore often tumor reduction and control of hypertension.
  • To date the best adjunct to surgery is radionuclide therapy using 131I-MIBG, but the background information for optimal treatment is still incomplete.
  • Certain patients may benefit from 131I-MIBG combined with radiotherapy via somatostatin receptors expressed by the tumor, or the combination with chemotherapy.
  • Ongoing microarray studies will reveal novel intracellular pathways of importance for proliferation/cell cycle control, which can be inhibited by pharmacologic tools.
  • [MeSH-minor] Animals. Combined Modality Therapy. Disease Models, Animal. Humans. Prevalence


10. Romeo S, Milione M, Gatti A, Fallarino M, Corleto V, Morano S, Baroni MG: Complete clinical remission and disappearance of liver metastases after treatment with somatostatin analogue in a 40-year-old woman with a malignant insulinoma positive for somatostatin receptors type 2. Horm Res; 2006;65(3):120-5
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  • [Title] Complete clinical remission and disappearance of liver metastases after treatment with somatostatin analogue in a 40-year-old woman with a malignant insulinoma positive for somatostatin receptors type 2.
  • Insulinoma is the most common pancreatic endocrine tumor, accounting for 40% of all pancreatic functional neoplasm, and is characterized by hypersecretion of insulin and hypoglycemia.
  • Elective treatment for insulinomas is surgical enucleation.
  • Medical therapy with diazoxide, followed by somatostatin analogues in some cases, may be necessary to treat the hypoglycemic symptoms.
  • After surgery, histopathology confirmed the presence of a malignant insulinoma with multiple metastases in the liver.
  • Due to the persistence of hypoglycemia, the patient was started on octreotide LAR treatment, which determined a complete clinical remission with regression of the metastatic lesions in the liver after one year.
  • To our knowledge, the complete regression of the disease in insulinomas treated with long-standing somatostatin analogue therapy has never been reported.
  • Immunohistochemical analysis in tissue specimens showed a strong membrane immunoreactivity for somatostatin receptors type 2 (SSTR2) in both the primary nodule and the metastases.
  • The capacity of somatostatin analogues to negatively regulate cell proliferation through indirect and direct mechanisms has been experimentally demonstrated.
  • This case underlies the potential impact of the treatment of pancreatic insulinomas with somatostatin analogues, and, if confirmed, the usefulness of SSTR determination in these neoplastic specimens.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Insulinoma / secondary. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Octreotide / therapeutic use. Pancreatic Neoplasms / chemistry. Receptors, Somatostatin / analysis
  • [MeSH-minor] Adult. Apoptosis. Cell Proliferation. Female. Humans. Immunohistochemistry. Remission Induction. Tomography, X-Ray Computed

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  • [Copyright] Copyright (c) 2006 S. Karger AG, Basel.
  • (PMID = 16479142.001).
  • [ISSN] 0301-0163
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; RWM8CCW8GP / Octreotide
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11. Ludvigsen E, Stridsberg M, Taylor JE, Culler MD, Oberg K, Janson ET: Subtype selective interactions of somatostatin and somatostatin analogs with sst1, sst2, and sst5 in BON-1 cells. Med Oncol; 2004;21(3):285-95
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  • [Title] Subtype selective interactions of somatostatin and somatostatin analogs with sst1, sst2, and sst5 in BON-1 cells.
  • Somatostatin is a polypeptide hormone acting as an inhibitor of pituitary, pancreatic, and gastrointestinal secretion through specific membrane receptors of which five subtypes have been cloned (sst(1-5)).
  • Somatostatin analogs are used in the clinic to treat patients with excessive hormone production due to a neuroendocrine tumor.
  • The aim of this study was to investigate the biological activity of three new somatostatin receptor subtype selective analogs (BIM-23926, sst(1)-selective; BIM-23120, sst(2)-selective; and BIM-23206, sst(5)-selective) in the human neuroendocrine tumor cell line, BON-1, which expresses sst(1), sst(2), and sst(5) natively.
  • Somatostatin-14 and octreotide were used as reference substances.
  • Forskolin-induced cAMP accumulation and chromogranin A (CgA) secretion were inhibited by BIM-23120, BIM-23206, and somatostatin-14 in a dose-dependent manner.
  • We conclude that increasing knowledge about sst physiology and expression in malignant disease indicates a need for new analogs that can be incorporated into the therapeutic arsenal.
  • [MeSH-major] Neuroendocrine Tumors / drug therapy. Neuroendocrine Tumors / metabolism. Receptors, Somatostatin / metabolism. Somatostatin / analogs & derivatives. Somatostatin / pharmacology
  • [MeSH-minor] Antineoplastic Agents, Hormonal / pharmacology. Cell Line, Tumor / drug effects. Cell Line, Tumor / enzymology. Cholecystokinin / pharmacology. Chromogranin A. Chromogranins / secretion. Colforsin / pharmacology. Cyclic AMP / metabolism. Enzyme Activation. Humans. Mitogens / pharmacology. Octreotide / pharmacology. Protein Kinases / drug effects. Protein Kinases / metabolism

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  • (PMID = 15456957.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Chromogranin A; 0 / Chromogranins; 0 / Mitogens; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 0 / somatostatin receptor type 1; 1F7A44V6OU / Colforsin; 51110-01-1 / Somatostatin; 9011-97-6 / Cholecystokinin; E0399OZS9N / Cyclic AMP; EC 2.7.- / Protein Kinases; RWM8CCW8GP / Octreotide
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12. Pasquali D, Rossi V, Conzo G, Pannone G, Bufo P, De Bellis A, Renzullo A, Bellastella G, Colao A, Vallone G, Bellastella A, Sinisi AA: Effects of somatostatin analog SOM230 on cell proliferation, apoptosis, and catecholamine levels in cultured pheochromocytoma cells. J Mol Endocrinol; 2008 Jun;40(6):263-71
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  • [Title] Effects of somatostatin analog SOM230 on cell proliferation, apoptosis, and catecholamine levels in cultured pheochromocytoma cells.
  • Surgery is the primary therapy for pheochromocytoma (PHEO), a catecholamine-producing tumor.
  • Benign and malignant PHEO could develop recurrences, and the intraoperative risk of recurrent PHEO is an important unresolved issue.
  • Non-surgical treatments of PHEO recurrence would therefore better prepare patients for reintervention as well as provide them with palliative management.
  • We investigated the effects of the new somatostatin analog (pasireotide) SOM230 versus octreotide (OCT) in primary PHEO cell cultures (Pheo-c).
  • Real-time PCR, using both PHEO tissues and Pheo-c, showed different levels of somatostatin receptor(1-5) mRNA expression.
  • Cells treated with various doses of OCT or SOM230 for 48 and 72 h were analyzed to assess their effects on cell proliferation and apoptosis and catecholamine levels.
  • Even if reduction of cell viability was observed in Pheo-c treated for 48 h with either OCT or SOM230 and this effect increased after 72 h, a more significant inhibition of cell growth as well as a significantly higher induction of apoptosis was seen in Pheo-c treated with SOM230 versus OCT.
  • Our results indicate that while both OCT and SOM230 modulate cell growth and apoptosis and catecholamine levels in Pheo-c through specific receptors, SOM230 is more effective.
  • This improves our knowledge on the mechanism of SOM230 action in PHEO and supports a possible therapeutic use in benign PHEO recurrence.
  • [MeSH-major] Apoptosis / drug effects. Catecholamines / metabolism. Pheochromocytoma / pathology. Somatostatin / analogs & derivatives
  • [MeSH-minor] Adult. Caspase 3 / metabolism. Cell Proliferation / drug effects. Cell Survival / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Immunohistochemistry. Intracellular Space / drug effects. Intracellular Space / metabolism. Middle Aged. Octreotide / pharmacology. Poly(ADP-ribose) Polymerases / metabolism. Receptors, Somatostatin / genetics. Receptors, Somatostatin / metabolism. Tumor Cells, Cultured

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  • (PMID = 18502819.001).
  • [ISSN] 1479-6813
  • [Journal-full-title] Journal of molecular endocrinology
  • [ISO-abbreviation] J. Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Catecholamines; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin; 98H1T17066 / pasireotide; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspase 3; RWM8CCW8GP / Octreotide
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13. Kondo H, Takino H, Akino K, Yamasaki H, Yamaguchi Y, Ito M, Eguchi K: Octreotide treatment suppresses malignant somatotrophic pituitary tumor cell growth in rats. Oncol Rep; 2000 Sep-Oct;7(5):965-9
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  • [Title] Octreotide treatment suppresses malignant somatotrophic pituitary tumor cell growth in rats.
  • We have recently established an in vitro cell line (metastatic mGH3) derived from lymph node metastases of the rat pituitary somatotroph.
  • Here we examined the in vivo effects of octreotide, a somatostatin analog, against malignant pituitary tumors.
  • Four rats were treated with octreotide three times daily while another group of four rats were treated with saline only.
  • After 6 weeks of treatment, histopathological and immunohistological analyses were performed.
  • The tumor weights of rats treated with octreotide were significantly lighter than those of untreated rats.
  • All rats implanted mGH3, but not administered treatment, developed inguinal lymph node metastases, whereas none of those implanted mGH3 and treated with octreotide developed such metastases.
  • The proportion of PCNA-stained tumor cells was higher in tumors of untreated rats than in those of octreotide-treated rats.
  • However, the proportion of apoptotic cells in the tumor was not different between treated and untreated rats.
  • Our results suggest that octreotide might be potentially effective for invasive and malignant human pituitary tumors by regulating the tumor cell cycle.
  • [MeSH-major] Antineoplastic Agents, Hormonal / pharmacology. Growth Hormone / blood. Octreotide / pharmacology. Pituitary Neoplasms / drug therapy
  • [MeSH-minor] Animals. Body Weight / drug effects. Cell Division / drug effects. Female. Immunohistochemistry. Neoplasm Transplantation. Rats. Rats, Inbred WF. Tumor Cells, Cultured

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  • (PMID = 10948323.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] GREECE
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 9002-72-6 / Growth Hormone; RWM8CCW8GP / Octreotide
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14. Louthan O: [Goblet cell carcinoid of the appendix]. Vnitr Lek; 2009 Nov;55(11):1056-9
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  • [Title] [Goblet cell carcinoid of the appendix].
  • Appendiceal goblet cell carcinoids are mixed tumors including neuroendocrine cells and intestinal type of goblet cells.
  • Compared to typical carcinoids, goblet cell carcinoids are malignant tumors with degree of malignity differing from case to case.
  • There is limited experience with chemotherapy in metastasizing tumors and sporadic with somatostatin analogues.
  • [MeSH-major] Appendiceal Neoplasms. Carcinoid Tumor

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  • (PMID = 20017437.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Czech Republic
  • [Number-of-references] 18
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15. Meier G, Waldherr C, Herrmann R, Maecke H, Mueller-Brand J, Pless M: Successful targeted radiotherapy with 90Y-DOTATOC in a patient with Merkel cell carcinoma. A Case Report. Oncology; 2004;66(2):160-3
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  • [Title] Successful targeted radiotherapy with 90Y-DOTATOC in a patient with Merkel cell carcinoma. A Case Report.
  • Merkel cell carcinomas (MCC) belong to the family of neuroendocrine tumors.
  • In addition to other markers, they express somatostatin receptors.
  • They are uncommon, highly malignant skin tumors with an aggressive clinical course.
  • Treatment is stage dependent and consists of operation and chemo- and/or radiotherapy, respectively.
  • The advanced age of patients often impedes adequate therapy. (90)Y-DOTATOC is a novel radiolabeled somatostatin analogue containing the active octapeptide of somatostatin.
  • It is very well tolerated and offers the option of treating somatostatin receptor-positive tumors by targeted radiotherapy.
  • The primary tumor and several relapses were treated with surgery and locoregional radiotherapy.
  • After the 3rd relapse, she was treated 4 times with (90)Y-DOTATOC and two complete remissions were achieved.
  • The fourth administration after the 2nd relapse was ineffective and conventional chemotherapy was started.
  • We conclude that due to its good tolerability, (90)Y-DOTATOC therapy should be evaluated further as a new therapy for somatostatin receptor-positive MCC.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Merkel Cell / drug therapy. Facial Neoplasms / drug therapy. Octreotide / analogs & derivatives. Octreotide / therapeutic use. Skin Neoplasms / drug therapy. Yttrium Radioisotopes / therapeutic use
  • [MeSH-minor] Aged. Aged, 80 and over. Cheek. Fatal Outcome. Female. Humans. Radiopharmaceuticals / therapeutic use

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  • [Copyright] Copyright 2004 S. Karger AG, Basel
  • (PMID = 15138369.001).
  • [ISSN] 0030-2414
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Radiopharmaceuticals; 0 / Yttrium Radioisotopes; RWM8CCW8GP / Octreotide; U194AS08HZ / Edotreotide
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16. Campana D, Piscitelli L, Mazzotta E, Bonora M, Serra C, Salomone L, Corinaldesi R, Tomassetti P: Zollinger-Ellison syndrome. Diagnosis and therapy. Minerva Med; 2005 Jun;96(3):187-206
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  • [Title] Zollinger-Ellison syndrome. Diagnosis and therapy.
  • Zollinger-Ellison syndrome (ZES) is characterised by refractory peptic ulcer disease, severe diarrhoea and gastric acid hypersecretion associated with an islet-cell tumor of the pancreas (gastrinoma).
  • ZES is sporadic in 62-80% of cases and in 20-38% of cases is associated with multiple endocrine neoplasia type 1 (MEN 1).
  • The diagnosis of ZES is certain when the plasma gastrin is >1000 pg/mL and the basal acid output is >15 mEq/h in patients with an intact stomach, >5 mEq/h in gastrectomised patients, or when the hypergastrinemia is associated with a pH <2.
  • Treatment is based on the control of gastric acid hypersecretion and of the malignant tumor and its possible metastases.
  • Proton pump inhibitors are the most effective antisecretory drugs and can be administered at high dosages without drug-related adverse effects.
  • When liver metastases are also present, their debulking may improve symptoms and survival, and facilitate medical treatment.
  • Somatostatin analogues can be useful in reducing gastric acid hypersecretion, serum gastrin and gastric enterochromaffin-like cells, and can thus contribute to treating the disease more effectively.
  • Chemotherapy and/or interferon are indicated only in patients with malignant progressive disease.
  • [MeSH-major] Zollinger-Ellison Syndrome / diagnosis. Zollinger-Ellison Syndrome / therapy

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  • (PMID = 16175161.001).
  • [ISSN] 0026-4806
  • [Journal-full-title] Minerva medica
  • [ISO-abbreviation] Minerva Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Gastrins
  • [Number-of-references] 0
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17. Helmbold P, Schröter S, Holzhausen HJ, Hartschuh W, Marsch WC: [Merkel cell carcinoma: a diagnostic and therapeutic challenge]. Chirurg; 2001 Apr;72(4):396-401
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  • [Title] [Merkel cell carcinoma: a diagnostic and therapeutic challenge].
  • Merkel cell carcinoma (cutaneous neuroendocrine carcinoma) is a highly malignant, neuroendocrine skin tumor.
  • Merkel cell carcinomas develop as fast-growing dermal tumors.
  • Histology reveals uniform, round cells with a small cytoplasmic rim expressing cytokeratin 20, neurofilament, synaptophysin, chromogranin, and neuron-specific enolase.
  • Wide surgical excision, followed by radiotherapy, is the treatment of choice.
  • In advanced metastatic Merkel cell carcinoma, a remission can be achieved by different chemotherapy schedules or the somatostatin analogue octreotide.
  • The current knowledge about this disease and guidelines for effective diagnosis and treatment are given.
  • [MeSH-major] Carcinoma, Merkel Cell / surgery. Skin Neoplasms / surgery
  • [MeSH-minor] Biomarkers, Tumor / analysis. Dermatologic Surgical Procedures. Humans. Microscopy, Electron. Prognosis. Skin / pathology

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  • (PMID = 11357530.001).
  • [ISSN] 0009-4722
  • [Journal-full-title] Der Chirurg; Zeitschrift für alle Gebiete der operativen Medizen
  • [ISO-abbreviation] Chirurg
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 38
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18. De Dosso S, Bajetta E, Procopio G, Cortinovis D, Buzzoni R, Catena L, Platania M, Verzoni E: Pulmonary carcinoid tumours: indolent but not benign. Oncology; 2007;73(3-4):162-8
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  • BACKGROUND: The aim of this retrospective study was to analyse the malignant behaviour of low-grade pulmonary neuroendocrine tumours (NETs) treated at our institution.
  • RESULTS: At diagnosis, there were 37 metastatic and 11 non-metastatic patients.
  • Medical treatments used were somatostatin analogues, combined chemotherapy, within study protocols, 5-fluorouracil/dacarbazine/epiadriamycin (FDE), and oxaliplatin plus capecitabine (XELOX).
  • CONCLUSION: Cell type is the strongest determinant of prognosis, and the degree of malignancy increases from TCs to ACs.
  • Our analysis suggests that patients with advanced disease should receive first-line therapy with a somatostatin analogue, with chemotherapy regimens (FDE, XELOX) used in progressing cases.
  • [MeSH-major] Carcinoid Tumor / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease Progression. Disease-Free Survival. Female. Humans. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Recurrence, Local / diagnosis. Neoplasm Staging. Prognosis. Retrospective Studies. Survival Rate

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  • [Copyright] (c) 2008 S. Karger AG, Basel
  • (PMID = 18418008.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
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19. Berruti A, Dogliotti L, Mosca A, Gorzegno G, Bollito E, Mari M, Tarabuzzi R, Poggio M, Torta M, Fontana D, Angeli A: Potential clinical value of circulating chromogranin A in patients with prostate carcinoma. Ann Oncol; 2001;12 Suppl 2:S153-7
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  • [Title] Potential clinical value of circulating chromogranin A in patients with prostate carcinoma.
  • BACKGROUND: Neuroendocrine (NE) differentiation of prostate adenocarcinoma has received increasing attention in recent years as a result of possible implications for prognosis and therapy.
  • The presence of NE tumor subpopulation can be gauged non invasively by measuring circulating levels of secretory products, primarily chromogranin A (CgA).
  • RESULTS: Circulating CgA levels were found to be higher in prostate cancer patients than in patients with benign or pre-malignant prostatic diseases.
  • CgA values were not substantially affected by either endocrine therapy or chemotherapy.
  • The administration of a somatostatin analog in hormone refractory cases was able to reduce plasma CgA values consistently.
  • Serial evaluation of circulating CgA could provide information on changes in the NE phenotype expression as a consequence of tumor progression and/or treatment administration.

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  • (PMID = 11762344.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Biomarkers, Tumor; 0 / CHGA protein, human; 0 / Chromogranin A; 0 / Chromogranins; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Number-of-references] 42
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20. Ercan MT, Caglar M: Therapeutic radiopharmaceuticals. Curr Pharm Des; 2000 Jul;6(11):1085-121
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  • [Title] Therapeutic radiopharmaceuticals.
  • A variety of radiopharmaceuticals have been introduced for the internal therapy of malignant and inflammatory lesions in nuclear medicine.
  • In order to destroy the diseased tissues radionuclides with high linear energy transfer (LET) such as beta, alpha, Auger or low energy conversion electron emitters are needed.
  • The range of alpha particles is short, only a few cell diameters.
  • Thus, they are effective in treating circulating malignant cells and micrometastases.
  • They are very effective in cell killing when they are carried across cell membrane into the nucleus to damage DNA.
  • Monoclonal antibodies to specific antigens expressed on tumor cells have been developed to increase the uptake by malignant tissues by specific accumulation.
  • Radiolabelled peptides such as somatostatin, small molecules such as metaiodo-benzylguanidine (MIBG) and many different nano-and micro-particles have been investigated.
  • The effectiveness of therapy can be increased by direct locoregional administration of the radiopharmaceutical.
  • This way the radiation effects are confined locally and the normal tissues are spared from radiation effects.
  • In this review article selection criteria and characteristics of radionuclides and carrier ions, molecules and particles for various therapeutic applications will be discussed, including mainly the recent developments.
  • [MeSH-major] Radiopharmaceuticals / therapeutic use. Radiotherapy
  • [MeSH-minor] Animals. Drug Carriers. Humans. Radioisotopes / therapeutic use

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  • (PMID = 10903384.001).
  • [ISSN] 1381-6128
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] NETHERLANDS
  • [Chemical-registry-number] 0 / Drug Carriers; 0 / Radioisotopes; 0 / Radiopharmaceuticals
  • [Number-of-references] 351
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21. Tomassetti P, Salomone T, Migliori M, Campana D, Corinaldesi R: Optimal treatment of Zollinger-Ellison syndrome and related conditions in elderly patients. Drugs Aging; 2003;20(14):1019-34
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  • [Title] Optimal treatment of Zollinger-Ellison syndrome and related conditions in elderly patients.
  • Zollinger-Ellison syndrome is characterised by refractory peptic ulcer disease, severe diarrhoea and gastric acid hypersecretion associated with an islet-cell tumour of the pancreas (gastrinoma).
  • Zollinger-Ellison syndrome is sporadic in 62-80% of cases and in 20-38% of cases is associated with multiple endocrine neoplasia type 1 (MEN 1).
  • The diagnosis of Zollinger-Ellison syndrome is certain when the plasma gastrin is >1000 pg/mL and the basal acid output is >15 mEq/h in patients with an intact stomach, >5 mEq/h in gastrectomised patients, or when this hypergastrinemia is associated with a pH <2.
  • The treatment is based on control of gastric acid hypersecretion and of the malignant tumour and its possible metastases.
  • Proton pump inhibitors are the most effective antisecretory drugs and can be administered in the elderly at high dosages without drug-related adverse effects.
  • As an initial therapy, daily dosages of omeprazole 80-100 mg or pantoprazole 40-160 mg are employed.
  • In long-term treatment the doses can be greatly reduced once effective control of the gastric output has been established.
  • Intravenous proton pump inhibitors may be administered when patients cannot take oral therapy, particularly in acute conditions.
  • When liver metastases are also present, their debulking may improve symptoms and survival, and facilitate medical treatment.
  • Somatostatin analogues can be useful in reducing gastric acid hypersecretion, serum gastrin and gastric enterochromaffin-like (ECL) cells and can thus contribute to treating the disease more effectively.
  • Chemotherapy is not the therapy of choice in patients with gastrinomas and is indicated only in those with malignant progressive disease; interferon alpha, embolisation and chemoembolisation are not advisable for the elderly.
  • The treatment of elderly Zollinger-Ellison syndrome patients, similarly to all elderly oncological patients, should be based on the use of comprehensive geriatric assessment.
  • This will enable the clinician to define the functional status of the elderly person, to decide whether the patient can tolerate surgery and/or the stress of antineoplastic therapy, and finally, to determine whether this patient can tolerate an aggressive treatment for Zollinger-Ellison syndrome or whether the only possible choice is palliative relief of symptoms.
  • [MeSH-major] Geriatrics. Helicobacter pylori. Histamine H2 Antagonists / therapeutic use. Proton Pump Inhibitors. Zollinger-Ellison Syndrome
  • [MeSH-minor] Aged. Carcinoid Tumor / complications. Helicobacter Infections / complications. Humans. Multiple Endocrine Neoplasia Type 1 / complications

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  • (PMID = 14651442.001).
  • [ISSN] 1170-229X
  • [Journal-full-title] Drugs & aging
  • [ISO-abbreviation] Drugs Aging
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Histamine H2 Antagonists; 0 / Proton Pump Inhibitors
  • [Number-of-references] 143
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22. Caplin ME, Mielcarek W, Buscombe JR, Jones AL, Croasdale PL, Cooper MS, Burroughs AK, Hilson AW: Toxicity of high-activity 111In-Octreotide therapy in patients with disseminated neuroendocrine tumours. Nucl Med Commun; 2000 Jan;21(1):97-102
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  • [Title] Toxicity of high-activity 111In-Octreotide therapy in patients with disseminated neuroendocrine tumours.
  • Disseminated neuroendocrine tumours are difficult to treat and are generally not responsive to radiotherapy or chemotherapy.
  • Nuclear medicine techniques using a radiolabelled somatostatin analogue, 111In-Octreotide, have been used for the diagnosis of neuroendocrine tumours.
  • It has been suggested that high activities of such an agent may have a therapeutic effect.
  • Eight patients with known disseminated neuroendocrine tumours were enrolled in the study; six had carcinoid tumours, one had a medullary cell carcinoma of the thyroid and one patient had a malignant gastrinoma.
  • Tests of vital signs, renal, liver and endocrine function as well as haematological markers were taken before and after treatment.
  • The treatment was well tolerated with only one patient suffering from a sensation of flushing during the infusion but no changes in vital sings.
  • There was a transient (up to 48 h) drop in circulating lymphocytes in four patients and platelets in two patients; no supportive therapy was needed.
  • [MeSH-major] Carcinoid Tumor / radiotherapy. Gastrinoma / radiotherapy. Multiple Endocrine Neoplasia / radiotherapy. Neuroendocrine Tumors / radiotherapy. Octreotide / analogs & derivatives. Pentetic Acid / analogs & derivatives. Radiopharmaceuticals / adverse effects

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  • (PMID = 10717909.001).
  • [ISSN] 0143-3636
  • [Journal-full-title] Nuclear medicine communications
  • [ISO-abbreviation] Nucl Med Commun
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 142694-57-3 / SDZ 215-811; 7A314HQM0I / Pentetic Acid; RWM8CCW8GP / Octreotide
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23. Georgieva I, Koychev D, Wang Y, Holstein J, Hopfenmüller W, Zeitz M, Grabowski P: ZM447439, a novel promising aurora kinase inhibitor, provokes antiproliferative and proapoptotic effects alone and in combination with bio- and chemotherapeutic agents in gastroenteropancreatic neuroendocrine tumor cell lines. Neuroendocrinology; 2010;91(2):121-30
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  • [Title] ZM447439, a novel promising aurora kinase inhibitor, provokes antiproliferative and proapoptotic effects alone and in combination with bio- and chemotherapeutic agents in gastroenteropancreatic neuroendocrine tumor cell lines.
  • BACKGROUND: Therapeutic approaches to gastroenteropancreatic neuroendocrine tumors (GEP-NETs) are still not satisfactory.
  • A new direction in treatment options could be the novel aurora kinase inhibitor ZM447439, which was previously reported to interfere with the mitotic spindle integrity checkpoint and chromosome segregation, but does not interfere with other kinases when used up to 5 muM.
  • METHODS: We evaluated the antineoplastic effects of ZM447439 on growth and apoptosis of the GEP-NET cell lines BON, QGP-1 and MIP-101, representing the different malignant tumor types, using standard cell biological tests as crystal violet assays, caspase activation, DNA fragmentation and cell cycle analysis.
  • RESULTS: ZM447439 dose-dependently inhibited proliferation of all three cell lines with IC(50) values in the nanomolar to low micromolar range.
  • Furthermore, we observed cell cycle arrest at G(0)/G(1) phase as well as a block in G(2)/M transition.
  • In addition, combined treatment with the chemotherapeutic agents streptozocin and cisplatin augmented significantly the antiproliferative effects of those agents.
  • CONCLUSION: Aurora kinase inhibition by ZM447439 seems to be a promising new therapeutic approach in GEP-NETs, which should be evaluated in further clinical trials.
  • [MeSH-major] Benzamides / pharmacology. Carcinoid Tumor / drug therapy. Carcinoma, Neuroendocrine / drug therapy. Pancreatic Neoplasms / drug therapy. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Quinazolines / pharmacology
  • [MeSH-minor] Antibiotics, Antineoplastic / pharmacology. Antimetabolites, Antineoplastic / pharmacology. Antineoplastic Agents, Hormonal / pharmacology. Apoptosis / drug effects. Aurora Kinases. Cell Division / drug effects. Cell Line, Tumor. Cisplatin / pharmacology. Doxorubicin / pharmacology. Drug Interactions. Drug Therapy, Combination. Fluorouracil / pharmacology. Humans. Inhibitor of Apoptosis Proteins. Microtubule-Associated Proteins / metabolism. Octreotide / pharmacology. Somatostatin / analogs & derivatives. Somatostatin / pharmacology. Streptozocin / pharmacology. Synaptophysin / metabolism

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19923785.001).
  • [ISSN] 1423-0194
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / 4-(4-(N-benzoylamino)anilino)-6-methoxy-7-(3-(1-morpholino)propoxy)quinazoline; 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Hormonal; 0 / BIRC5 protein, human; 0 / Benzamides; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Quinazolines; 0 / Synaptophysin; 51110-01-1 / Somatostatin; 5W494URQ81 / Streptozocin; 80168379AG / Doxorubicin; 98H1T17066 / pasireotide; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; Q20Q21Q62J / Cisplatin; RWM8CCW8GP / Octreotide; U3P01618RT / Fluorouracil
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24. Béhé M, Behr TM: Cholecystokinin-B (CCK-B)/gastrin receptor targeting peptides for staging and therapy of medullary thyroid cancer and other CCK-B receptor expressing malignancies. Biopolymers; 2002;66(6):399-418
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  • [Title] Cholecystokinin-B (CCK-B)/gastrin receptor targeting peptides for staging and therapy of medullary thyroid cancer and other CCK-B receptor expressing malignancies.
  • Nuclear medicine is engaged with the detection of pathological processes with the help of radionuclides.
  • An interesting approach is to target antigens, symporters, or receptors with diagnostic and therapeutic radionuclides.
  • Different peptide receptors like somatostatin, bombesin/GRP or VIP are (over)expressed on cancer cells, and are therefore an ideal target for the diagnosis and therapy in nuclear medicine with radiolabeled peptides.
  • The somatostatin analogue OctreoScan [octreotide coupled with diethylene-triamine-pentaacetate (DTPA)] can be labeled with In-111 and is widely used in nuclear oncology for the staging of different tumors (e.g., carcinoids).
  • The high sensitivity of the pentagastrin stimulation test in detecting primary or metastatic MTC indicates the presence of tumor, but its localization is often not possible.
  • This reaction of the tumor cells to the pentagastrin stimulation test suggests a widespread expression of the corresponding receptor type on human MTC.
  • Indeed, autoradiographic studies demonstrated cholecystokinin (CCK)-B/gastrin receptors not only in over 90% of MTCs, but in a high percentage of small cell lung cancers, stromal ovarian, and potentially a variety of other tumors, including gastrointestinal adenocarcinomas, neuroendocrine tumors, and malignant glioma.
  • The aim of our recent work was to develop and systematically optimize suitable radioligands for targeting CCK-B receptors in vivo and to investigate their role in the staging and therapy of MTC and other CCK-B receptor expressing malignancies.
  • Their stability and affinity were studied and optimized in vitro and in vivo; their biodistribution and therapeutic efficacy were tested in preclinical models.
  • Best tumor uptake and tumor-to-nontumor ratios were obtained with members of the gastrin family, due to their superior selectivity and affinity for the CCK-B receptor subtype.
  • Radiometal-labeled derivatives of minigastrin showed excellent targeting of CCK-B receptor expressing tissues in animals and healthy human volunteers.
  • Preclinical therapy experiments in MTC-bearing animals showed significant antitumor efficacy.
  • The normal organ uptake was essentially confined to the stomach (and to a lower extent, to the gallbladder and, in premenopausal women, to normal breast tissue) as a result of CCK-B receptor specific binding, and to the kidneys as excretory organs.
  • All tumor manifestations known from conventional imaging were visualized as early as 1 h p.i., with increasing tumor-to-background ratios over time; at least one lesion was detected in 29/32 patients with occult disease (patient-based sensitivity 91%).
  • Eight patients with advanced metastatic disease were injected in a dose-escalation study with potentially therapeutic activities of a (90)Y-labeled minigastrin derivative at 4-6-weekly intervals (30-50 mCi/m(2) per injection for a maximum of four injections).
  • These data suggest that CCK-B receptor ligands may be a useful new class of receptor binding peptides for diagnosis and therapy of a variety of (CCK-B receptor expressing) tumor types.
  • Initial therapeutic results are promising, but nephrotoxicity is a major concern to be solved.
  • [MeSH-major] Peptides / metabolism. Peptides / therapeutic use. Radiopharmaceuticals. Receptors, Cholecystokinin / metabolism. Thyroid Neoplasms / classification. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Animals. Gastrins / metabolism. Humans. Ligands. Mice. Pentetic Acid / metabolism. Receptor, Cholecystokinin B. Receptors, Somatostatin

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  • [Copyright] Copyright 2003 Wiley Periodicals, Inc.
  • (PMID = 12658727.001).
  • [ISSN] 0006-3525
  • [Journal-full-title] Biopolymers
  • [ISO-abbreviation] Biopolymers
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gastrins; 0 / Ligands; 0 / Peptides; 0 / Radiopharmaceuticals; 0 / Receptor, Cholecystokinin B; 0 / Receptors, Cholecystokinin; 0 / Receptors, Somatostatin; 60748-07-4 / minigastrin; 7A314HQM0I / Pentetic Acid
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25. Hage R, de la Rivière AB, Seldenrijk CA, van den Bosch JM: Update in pulmonary carcinoid tumors: a review article. Ann Surg Oncol; 2003 Jul;10(6):697-704
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  • Pulmonary carcinoid tumors are neuroendocrine malignant tumors that make up 1% to 2% of all lung tumors.
  • Carcinoids can be placed in a spectrum of neuroendocrine tumors, ranging from low-grade malignant TC to intermediate AC to high-grade large-cell neuroendocrine carcinoma and small-cell lung carcinoma.
  • The diagnosis is usually established by flexible bronchoscopy and biopsy, although occasionally this can result in severe hemorrhage.
  • Immunoscintigraphy by somatostatin analogs can also be useful in diagnosis.
  • The treatment of choice is surgical resection, and prognosis is relatively good in TC, although it is worse in AC.
  • The role of radiotherapy and chemotherapy as part of multimodality treatment or palliation is still debated.
  • [MeSH-major] Carcinoid Tumor / pathology. Lung Neoplasms
  • [MeSH-minor] Biopsy. Bronchoscopy. Chemotherapy, Adjuvant. Combined Modality Therapy. Cough / etiology. Fever / etiology. Hemoptysis / etiology. Humans. Neoplasm Staging. Palliative Care. Prognosis. Radioimmunodetection. Radiotherapy, Adjuvant. Respiratory Sounds / etiology. Somatostatin

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
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  • (PMID = 12839856.001).
  • [ISSN] 1068-9265
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 51110-01-1 / Somatostatin
  • [Number-of-references] 65
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