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1. 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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  • [Title] Inhibition of PC-3 human prostate cancers by analogs of growth hormone-releasing hormone (GH-RH) endowed with vasoactive intestinal peptide (VIP) antagonistic activity.
  • Vasoactive intestinal peptide (VIP) stimulates the proliferation and invasiveness of malignant prostatic cells.
  • Receptors for VIP and the closely related growth hormone-releasing hormone (GH-RH) show considerable homology and are found in prostatic and other carcinomas.
  • Among various analogs of GH-RH synthesized, JV-1-52 is a non-selective VIP/GH-RH antagonist, whereas JV-1-53 is a VIP antagonist devoid of GH-RH antagonistic effect.
  • In our study, nude mice bearing PC-3 human androgen-independent prostate carcinomas were treated with JV-1-52 or JV-1-53 (20 microg/day, s.c.) for 28 days.
  • 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).
  • 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.
  • Our results suggest that VIP/GH-RH antagonists can inhibit the growth of androgen-independent prostate cancer by abrogating the autocrine/paracrine mitogenic stimuli of VIP.
  • 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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2. Foey AD, Field S, Ahmed S, Jain A, Feldmann M, Brennan FM, Williams R: Impact of VIP and cAMP on the regulation of TNF-alpha and IL-10 production: implications for rheumatoid arthritis. Arthritis Res Ther; 2003;5(6):R317-28
Hazardous Substances Data Bank. 12-O-TETRADECANOYLPHORBOL-13-ACETATE .

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  • [Title] Impact of VIP and cAMP on the regulation of TNF-alpha and IL-10 production: implications for rheumatoid arthritis.
  • Vasoactive intestinal peptide (VIP) is an anti-inflammatory immunomodulatory neuropeptide with therapeutic potential demonstrated for collagen-induced arthritis.
  • The aim of this study was to characterise its potential anti-arthritic effect on human monocytes, macrophages, T cells, and rheumatoid arthritis synovial membrane cells.
  • Monocytes, macrophages, and T cells derived from human peripheral blood were treated with VIP and compared with other cAMP-elevating drugs for a range of activating stimuli.
  • Cytokine production was assessed for cell cultures and, in addition, the ability of VIPs to activate cAMP response element binding protein.
  • VIP partially suppressed monocyte- and macrophage-derived tumour necrosis factor alpha (TNF-alpha) with no effect on IL-10, whereas VIP fails to regulate IL-10 and TNF-alpha production by T lymphocytes.
  • Elevation of intracellular cAMP, on the other hand, potently suppressed macrophage TNF-alpha production and modulated T-cell response by inhibiting TNF-alpha and IFN-gamma.
  • VIP's lack of effect on IL-10 and its slight effect on TNF-alpha results from cAMP being rapidly degraded as the phosphodiesterase IV inhibitor, rolipram, rescues cAMP-dependent activation of cAMP response element binding protein.
  • Interestingly, macrophages stimulated with phorbol 12-myristate 13-acetate/ionomycin displayed an augmented IL-10 response upon addition of dibutyryl cAMP, with corresponding downregulation in TNF-alpha, suggesting a complex interaction between protein kinase C and protein kinase A in cytokine regulation.
  • In conclusion, VIP may represent an efficaceous anti-arthritic treatment modulating macrophage and T-cell cytokine profiles when used alongside a phosphodiesterase inhibitor.
  • [MeSH-major] Arthritis, Rheumatoid / metabolism. Cyclic AMP / pharmacology. Interleukin-10 / biosynthesis. Macrophages / drug effects. Monocytes / drug effects. Synovial Membrane / drug effects. T-Lymphocytes / drug effects. Tumor Necrosis Factor-alpha / biosynthesis. Vasoactive Intestinal Peptide / pharmacology
  • [MeSH-minor] 3',5'-Cyclic-AMP Phosphodiesterases / antagonists & inhibitors. 3',5'-Cyclic-AMP Phosphodiesterases / metabolism. Bucladesine / pharmacology. Cells, Cultured / drug effects. Cells, Cultured / metabolism. Colforsin / pharmacology. Cyclic AMP-Dependent Protein Kinase Type II. Cyclic AMP-Dependent Protein Kinases / metabolism. Cyclic Nucleotide Phosphodiesterases, Type 4. Gene Expression Regulation / drug effects. Humans. Interferon-gamma / biosynthesis. Interferon-gamma / genetics. Ionomycin / pharmacology. Lipopolysaccharides / pharmacology. Phosphodiesterase Inhibitors / pharmacology. Protein Kinase C / metabolism. Rolipram / pharmacology. Tetradecanoylphorbol Acetate / pharmacology

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  • (PMID = 14680506.001).
  • [ISSN] 1478-6362
  • [Journal-full-title] Arthritis research & therapy
  • [ISO-abbreviation] Arthritis Res. Ther.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Lipopolysaccharides; 0 / Phosphodiesterase Inhibitors; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 1F7A44V6OU / Colforsin; 37221-79-7 / Vasoactive Intestinal Peptide; 56092-81-0 / Ionomycin; 63X7MBT2LQ / Bucladesine; 82115-62-6 / Interferon-gamma; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinase Type II; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.13 / Protein Kinase C; EC 3.1.4.17 / 3',5'-Cyclic-AMP Phosphodiesterases; EC 3.1.4.17 / Cyclic Nucleotide Phosphodiesterases, Type 4; K676NL63N7 / Rolipram; NI40JAQ945 / Tetradecanoylphorbol Acetate
  • [Other-IDs] NLM/ PMC333423
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3. Chen L, Li T, Li R, Wei B, Peng Z: Alphastatin downregulates vascular endothelial cells sphingosine kinase activity and suppresses tumor growth in nude mice bearing human gastric cancer xenografts. World J Gastroenterol; 2006 Jul 14;12(26):4130-6
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  • [Title] Alphastatin downregulates vascular endothelial cells sphingosine kinase activity and suppresses tumor growth in nude mice bearing human gastric cancer xenografts.
  • AIM: To investigate whether alphastatin could inhibit human gastric cancer growth and furthermore whether sphingosine kinase (SPK) activity is involved in this process.
  • SPK and endothelial differentiation gene (EDG)-1, -3, -5 mRNAs were detected by reverse transcription-polymerase chain reaction (RT-PCR).
  • Female nude mice were subcutaneously implanted with human gastric cancer cells (BGC823) for the tumor xenografts studies.
  • Micro vessel density was analyzed in Factor VIII-stained tumor sections by the immunohistochemical SP method.
  • In vivo, alphastatin sufficiently suppressed neovascularization of the tumor in the nude mice.
  • Daily administration of alphastatin produced significant tumor growth suppression.
  • Immunohistochemical studies of tumor tissues revealed decreased micro vessel density in alphastatin-treated animals as compared with controls.
  • Alphastatin might be a useful and relatively nontoxic adjuvant therapy in the treatment of gastric cancer.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Proliferation / drug effects. Endothelium, Vascular / enzymology. Fibrinogen / pharmacology. Gene Expression Regulation, Enzymologic / drug effects. Phosphotransferases (Alcohol Group Acceptor) / metabolism. Stomach Neoplasms / pathology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Movement / drug effects. Cells, Cultured. Drug Screening Assays, Antitumor. Female. Humans. Mice. Mice, Nude. Neovascularization, Pathologic / prevention & control. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, Lysosphingolipid / genetics. Receptors, Lysosphingolipid / metabolism

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  • (PMID = 16830360.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Messenger; 0 / Receptors, Lysosphingolipid; 0 / alphastatin; 9001-32-5 / Fibrinogen; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.- / sphingosine kinase
  • [Other-IDs] NLM/ PMC4087359
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4. Kobayashi H, Sawamura Y, Ikeda J: A tumor in the medulla oblongata producing beta-HCG and AFP. J Clin Neurosci; 2005 Aug;12(6):709-11
Hazardous Substances Data Bank. LINDANE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A tumor in the medulla oblongata producing beta-HCG and AFP.
  • MRI showed a mass of heterogeneous intensity at the dorsal medulla oblongata.
  • Laboratory studies revealed high serum alpha-fetoprotein (AFP) and beta-subunit human chorionic gonadotropin (beta-HCG) levels.
  • No other tumours were found on systemic investigation.
  • An intracranial non-germinomatous germ cell tumour (NGGCT) was strongly suspected.
  • The patient received combination chemotherapy using ifosfamide, cisplatin, and etoposide and local irradiation to a total of 52 Gy.
  • Serum AFP and beta-HCG levels normalized after four cycles of chemotherapy and she became asymptomatic apart from mild postural hypotension.
  • Surgical resection should be carefully considered in patients with brainstem tumours with elevation of serum tumour markers as chemo- and radiotherapy may be effective for brainstem NGGCT.
  • [MeSH-major] Brain Stem Neoplasms / blood. Lindane / blood. Medulla Oblongata / pathology. Neoplasms / blood. alpha-Fetoproteins / metabolism

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  • (PMID = 16098752.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / alpha-Fetoproteins; 319-85-7 / beta-hexachlorocyclohexane; 59NEE7PCAB / Lindane
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5. Kiaris H, Schally AV, Busto R, Halmos G, Artavanis-Tsakonas S, Varga JL: Expression of a splice variant of the receptor for GHRH in 3T3 fibroblasts activates cell proliferation responses to GHRH analogs. Proc Natl Acad Sci U S A; 2002 Jan 8;99(1):196-200
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  • The stimulatory effects of growth hormone-releasing hormone (GHRH) and the antiproliferative action of GHRH antagonists have been demonstrated in various cancers, but the receptors that mediate these responses are not clearly identified.
  • Recently, we reported that human cancer cell lines express splice variants (SVs) of the receptors for GHRH.
  • To ascertain whether SV1 mediates mitogenic effects on nonpituitary tissues, we expressed SV1 in 3T3 mouse fibroblasts and studied the properties of the transfected cells.
  • Radioligand binding assays with (125)I-labeled GHRH antagonist JV-1-42 detected high affinity (K(d) = 0.58 +/- 0.17 nM) binding sites for GHRH with a maximal binding capacity (B(max)) of 103 +/- 17.4 fmol/mg of membrane protein in 3T3 cells transfected with pcDNA3-SV1, whereas the control cells transfected with the empty vector did not show any GHRH binding.
  • The stimulation of SV1-expressing cells by GHRH or JI-38 is followed by an increase in cAMP production, but no GH release occurs.
  • Vasoactive intestinal peptide had no effect, and its antagonist JV-1-53 did not inhibit the proliferation of SV1-expressing cells stimulated by GHRH.
  • Our results suggest that SV1 could mediate responses of nonpituitary cells and various tumors to GHRH and GHRH antagonists.
  • The presence of SV1 in several human cancer cell lines provides a rationale for antitumor therapy based on the blockade of this receptor by specific GHRH antagonists.

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  • (PMID = 11773624.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS2608412
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ligands; 0 / Peptides; 0 / Receptors, Neuropeptide; 0 / Receptors, Pituitary Hormone-Regulating Hormone; 0 / somatotropin releasing hormone receptor; 37221-79-7 / Vasoactive Intestinal Peptide; 9002-72-6 / Growth Hormone; E0399OZS9N / Cyclic AMP
  • [Other-IDs] NLM/ PMC117538
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6. Jiang H, Ma Y, Chen X, Pan S, Sun B, Krissansen GW, Sun X: Genistein synergizes with arsenic trioxide to suppress human hepatocellular carcinoma. Cancer Sci; 2010 Apr;101(4):975-83
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  • [Title] Genistein synergizes with arsenic trioxide to suppress human hepatocellular carcinoma.
  • Arsenic trioxide (ATO) is of limited therapeutic benefit for the treatment of solid tumors.
  • Three human HCC cell lines, namely HepG2, Hep3B, and SK-Hep-1, were incubated with ATO, genistein, or ATO + genistein.
  • The combination therapy down-regulated Bcl-2 expression, up-regulated Bax expression, enhanced the activation of caspase-9 and -3, and increased the release of cytochrome c.
  • Genistein increased the production of intracellular ROS, while ATO had little effect.
  • Genistein synergized with a low dose of ATO (2.5 mg/kg) to significantly inhibit the growth of HepG2 tumors, and suppress cell proliferation and induce apoptosis in situ.
  • There were no obvious side effects, as seen with a high dose of ATO (5 mg/kg).
  • Combining genistein with ATO warrants investigation as a therapeutic strategy to combat HCC.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Arsenicals / therapeutic use. Carcinoma, Hepatocellular / drug therapy. Genistein / therapeutic use. Liver Neoplasms / drug therapy. Oxides / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Caspase 9 / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Drug Synergism. Humans. Male. Mice. Mice, Nude. Reactive Oxygen Species / metabolism. Reactive Oxygen Species / pharmacology. Xenograft Model Antitumor Assays

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  • [ErratumIn] Cancer Sci. 2010 Jun;101(6):1574
  • (PMID = 20219070.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; 0 / Reactive Oxygen Species; DH2M523P0H / Genistein; EC 3.4.22.- / Caspase 9; S7V92P67HO / arsenic trioxide
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7. Raney RB, Maurer HM, Anderson JR, Andrassy RJ, Donaldson SS, Qualman SJ, Wharam MD, Wiener ES, Crist WM: The Intergroup Rhabdomyosarcoma Study Group (IRSG): Major Lessons From the IRS-I Through IRS-IV Studies as Background for the Current IRS-V Treatment Protocols. Sarcoma; 2001;5(1):9-15
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  • [Title] The Intergroup Rhabdomyosarcoma Study Group (IRSG): Major Lessons From the IRS-I Through IRS-IV Studies as Background for the Current IRS-V Treatment Protocols.
  • Untreated patients < 21 years of age at diagnosis received systemic chemotherapy, with or without irradiation (XRT) and/or surgical removal of the tumor.Methods.
  • Pathologic materials and treatment were reviewed to ascertain compliance and to confirm response and relapse status.Results.
  • Important lessons include the fact that extent of disease at diagnosis affects prognosis.
  • Re-excising an incompletely removed tumor is worthwhile if acceptable form and function can be preserved.
  • Hyperfractionated XRT has thus far not produced superior local control rates compared with conventional, once-daily XRT.
  • Patients with non-metastatic cranial parameningeal sarcoma can usually be cured with localized XRT and systemic chemotherapy, without whole-brain XRT and intrathecal drugs.
  • Adding doxorubicin, cisplatin, etoposide, and ifosfamide has not significantly improved survival of patients with gross residual or metastatic disease beyond that achieved with VAC (vincristine, actinomycin D, cyclophosphamide) and XRT.
  • Most patients with alveolar RMS have a tumor-specific translocation.
  • Mature rhabdomyoblasts after treatment of patients with bladder rhabdomyosarcoma are not necessarily malignant, provided that the tumor has shrunk and malignant cells have disappeared.Discussion.
  • Two new agents, topotecan and irinotecan, are under investigation for patients who have an intermediate or high risk of recurrence.

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  • (PMID = 18521303.001).
  • [ISSN] 1357-714X
  • [Journal-full-title] Sarcoma
  • [ISO-abbreviation] Sarcoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2395450
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8. Kojima M, Ito T, Oono T, Hisano T, Igarashi H, Arita Y, Kawabe K, Coy DH, Jensen RT, Nawata H: VIP attenuation of the severity of experimental pancreatitis is due to VPAC1 receptor-mediated inhibition of cytokine production. Pancreas; 2005 Jan;30(1):62-70
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  • [Title] VIP attenuation of the severity of experimental pancreatitis is due to VPAC1 receptor-mediated inhibition of cytokine production.
  • OBJECTIVES: VIP receptor has been clarified to exist on immune cells, indicating its possible involvement in immunity and inflammatory response.
  • Therefore, we investigated the effects of VIP and selective agonists for 2 subtypes of VIP receptor (VPAC1-R and VPAC2-R agonist) on acute pancreatitis.
  • VIP, VPAC1-R agonist, VPAC2-R agonist, or secretin (5 nmol/body) was administered 30 minutes before and after the administration of LPS.
  • In vitro, IL-6 and TNF-alpha production by monocytes from the spleen was determined under the stimulation of LPS with VIP, VPAC1-R agonist, or VPAC2-R agonist, and the expression of VPAC1-R and VPAC2-R mRNA in monocytes was examined.
  • RESULTS: VPAC1-R agonist significantly decreased serum amylase, IL-6, and TNF-alpha, whereas VPAC2-R agonist markedly increased serum amylase.
  • Histologically, VIP and VPAC1-R agonist attenuated the severity of pancreatitis, although VPAC2-R agonist or secretin showed no significant effect.
  • Under the stimulation with LPS, VIP presented a biphasic pattern that once decreased IL-6 production from monocytes and then enhanced at high concentration.
  • VPAC1-R agonist reduced TNF-alpha levels in a dose-dependent manner.
  • CONCLUSION: VIP attenuated the experimental acute pancreatitis enzymatically and morphologically by inhibiting proinflammatory cytokine production from monocytes mainly through the VPAC1-R.
  • [MeSH-major] Cytokines / blood. Pancreatitis / drug therapy. Pancreatitis / immunology. Receptors, Vasoactive Intestinal Polypeptide, Type I / metabolism. Vasoactive Intestinal Peptide / pharmacology
  • [MeSH-minor] Acute Disease. Amylases / blood. Animals. Ceruletide. Interleukin-10 / blood. Interleukin-6 / blood. Lipopolysaccharides / pharmacology. Male. Mice. Mice, Inbred BALB C. Monocytes / metabolism. Pancreas / immunology. Pancreas / pathology. RNA, Messenger / analysis. Receptors, Vasoactive Intestinal Peptide, Type II / agonists. Receptors, Vasoactive Intestinal Peptide, Type II / genetics. Receptors, Vasoactive Intestinal Peptide, Type II / metabolism. Severity of Illness Index. Spleen / cytology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 15632701.001).
  • [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 / Cytokines; 0 / Interleukin-6; 0 / Lipopolysaccharides; 0 / RNA, Messenger; 0 / Receptors, Vasoactive Intestinal Peptide, Type II; 0 / Receptors, Vasoactive Intestinal Polypeptide, Type I; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 37221-79-7 / Vasoactive Intestinal Peptide; 888Y08971B / Ceruletide; EC 3.2.1.- / Amylases
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9. Halászlaki C, Horváth H, Kiss L, Takács I, Speer G, Nagy Z, Winternitz T, Dabasi G, Zalatnai A, Patócs A, Lakatos P: [Verner-Morrison syndrome: a case study]. Orv Hetil; 2010 Jul 4;151(27):1111-4
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  • [Title] [Verner-Morrison syndrome: a case study].
  • Verner and Morrison described a syndrome of watery diarrhea, hypokalemia, and achlorhydria (WDHA) in 1958.
  • VIPomas producing high amounts of vasoactive intestinal peptide (VIP) commonly originate from the pancreas.
  • Morbidity from untreated WDHA syndrome is associated with long-standing dehydration and with electrolyte and acid-base metabolism disorders, which may cause chronic renal failure.
  • Assessment of specific marker (VIP) offers high sensitivity in establishing the diagnosis.
  • Imaging modalities include endoscopic ultrasonography, computed tomography and magnetic resonance imaging, and particularly, scintigraphy with somatostatin analogues.
  • Treatment options include resection of the tumor, chemotherapy or the reduction of symptoms with somatostatin analogues.
  • VIPoma cases may be associated with multiple endocrine neoplasia type 1.
  • [MeSH-major] Pancreatic Neoplasms. Vipoma
  • [MeSH-minor] Achlorhydria / etiology. Aged. Biomarkers, Tumor / metabolism. Diarrhea / etiology. Endosonography. Female. Humans. Hypokalemia / etiology. Immunohistochemistry. Magnetic Resonance Imaging. Multiple Endocrine Neoplasia Type 1 / complications. Tomography, X-Ray Computed. Vasoactive Intestinal Peptide / metabolism

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  • (PMID = 20558361.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 37221-79-7 / Vasoactive Intestinal Peptide
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10. Prasse A, Zissel G, Lützen N, Schupp J, Schmiedlin R, Gonzalez-Rey E, Rensing-Ehl A, Bacher G, Cavalli V, Bevec D, Delgado M, Müller-Quernheim J: Inhaled vasoactive intestinal peptide exerts immunoregulatory effects in sarcoidosis. Am J Respir Crit Care Med; 2010 Aug 15;182(4):540-8
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  • [Title] Inhaled vasoactive intestinal peptide exerts immunoregulatory effects in sarcoidosis.
  • RATIONALE: Previous studies suggest an important immunoregulatory role of vasoactive intestinal peptide (VIP) in experimental models of chronic noninfectious inflammation.
  • Sarcoidosis is characterized by noncaseating epitheloid cell granulomas, where excessive tumor necrosis factor-alpha production by pulmonary macrophages plays a critical role in granuloma formation and disease progression, which may lead to fatal organ dysfunction.
  • OBJECTIVES: To test whether inhaled VIP has an immunoregulatory role.
  • METHODS: In an open clinical phase II study, we treated 20 patients with histologically proved sarcoidosis and active disease with nebulized VIP for 4 weeks.
  • MEASUREMENTS AND MAIN RESULTS: VIP inhalation was safe, well-tolerated, and significantly reduced the production of tumor necrosis factor-alpha by cells isolated from bronchoalveolar lavage fluids of these patients.
  • VIP treatment significantly increased the numbers of bronchoalveolar lavage CD4(+)CD127(-)CD25(+) T cells, which showed regulatory activities on conventional effector T cells.
  • In vitro experiments demonstrated the capacity of VIP to convert naive CD4(+)CD25(-) T cells into CD4(+)CD25(+)FoxP3(+) regulatory T cells, suggesting the generation of peripheral regulatory T cells by VIP treatment.
  • CONCLUSIONS: This study is the first to show the immunoregulatory effect of VIP in humans, and supports the notion of inhaled VIP as an attractive future therapy to dampen exaggerated immune responses in lung disorders.
  • Thus, the inhalation of neuropeptides may be developed into a new therapeutic principle for chronic inflammatory lung disorders in humans.
  • [MeSH-major] Sarcoidosis, Pulmonary / drug therapy. Sarcoidosis, Pulmonary / immunology. Vasoactive Intestinal Peptide / immunology. Vasoactive Intestinal Peptide / pharmacology. Vasodilator Agents / immunology. Vasodilator Agents / pharmacology
  • [MeSH-minor] Administration, Inhalation. Bronchoalveolar Lavage Fluid / immunology. Cells, Cultured. Enzyme-Linked Immunosorbent Assay. Female. Flow Cytometry / methods. Follow-Up Studies. Humans. Male. Middle Aged. T-Lymphocytes, Regulatory / drug effects. T-Lymphocytes, Regulatory / immunology. Tumor Necrosis Factor-alpha / drug effects. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 20442436.001).
  • [ISSN] 1535-4970
  • [Journal-full-title] American journal of respiratory and critical care medicine
  • [ISO-abbreviation] Am. J. Respir. Crit. Care Med.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 0 / Vasodilator Agents; 37221-79-7 / Vasoactive Intestinal Peptide
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11. Oberg K: Chemotherapy and biotherapy in the treatment of neuroendocrine tumours. Ann Oncol; 2001;12 Suppl 2:S111-4
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  • [Title] Chemotherapy and biotherapy in the treatment of neuroendocrine tumours.
  • The medical treatment of neuroendocrine GEP tumours must be based on the growth properties of the tumour.
  • Medical treatment includes chemotherapy, somatostatin analogues and alpha interferons.
  • Chemotherapy has been particularly active in patients with high proliferating neuroendocrine tumours such as endocrine pancreatic tumours and lung carcinoids.
  • Streptozotocin-based combinations including 5-flourouracil and doxorubicin have generated partial remissions in 40%-60% of the patients giving a median survival of about two years in patients with advanced disease.
  • Cisplatinum plus etoposide have demonstrated significant antitumour effects in anaplastic endocrine pancreatic tumours and lung carcinoids.
  • However, in low proliferating tumours such as classical midgut carcinoids the response rates with the same combinations of cytotoxic agents have only generated short lasting responses in less than 10% of patients.
  • In these patients, biological treatment has been of benefit.
  • Alpha interferon at doses of 3-9 million units three to seven times per week subcutaneously, has given biochemical response rates of 50% and significant tumour reduction in about 15% of patients with long duration, up to three years.
  • Somatostatin analogues have been widely used in the treatment of neuroendocrine gut and pancreatic tumours.
  • The currently available somatostatin analogues particularly bind somatostatin receptor 2 and 5 and with low affinity also receptor subtype 3.
  • Octreotide is registered in most countries for the treatment of patients with carcinoid syndrome and also VIP and glucagon producing tumours.
  • Significant tumour responses are rare, less than 5%.

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  • (PMID = 11762335.001).
  • [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; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 0 / Interferon-alpha; 0 / Peptides, Cyclic; 0 / Receptors, Somatostatin; 118992-92-0 / lanreotide; 51110-01-1 / Somatostatin; 5W494URQ81 / Streptozocin; Q20Q21Q62J / Cisplatin; RWM8CCW8GP / Octreotide
  • [Number-of-references] 23
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12. Allam G: Vasoactive intestinal peptide inhibits liver pathology in acute murine schistosomiasis mansoni and modulates IL-10, IL-12 and TNF-alpha production. Immunobiology; 2007;212(8):603-12
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  • [Title] Vasoactive intestinal peptide inhibits liver pathology in acute murine schistosomiasis mansoni and modulates IL-10, IL-12 and TNF-alpha production.
  • Vasoactive intestinal peptide (VIP) exerts a broad range of biologic actions that may include modulation of hepatic granuloma formation.
  • This study aimed to investigate the effect of VIP administration on the course of acute murine schistosomiasis mansoni.
  • Mice were infected each with 40 Schistosoma (S.) mansoni cercariae and injected intraperitoneally with VIP at a total dose of 1mug/kg body weight.
  • VIP treatment was very effective in diminishing worm fecundity, hepatic granuloma size and number by about 54%, 75% and 51%, respectively, and reducing liver collagen content.
  • Serum level of interleukin (IL)-10 was increased, while level of IL-12 and tumor necrosis factor (TNF)-alpha were decreased as a result of VIP administration.
  • Carbohydrate antigen 19.9 (CA 19.9) induced by S. mansoni infection was decreased with VIP treatment.
  • Activities of hepatic gamma-glutamyl transferase (gamma-GT), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) in liver tissue homogenate of infected treated mice were increased.
  • These results indicate that suitable administration of exogenous VIP can be effective in ameliorating immunopathologic damage associated with schistosomiasis.
  • [MeSH-major] Interleukin-10 / blood. Interleukin-12 / blood. Liver Diseases, Parasitic / drug therapy. Schistosomiasis mansoni / drug therapy. Tumor Necrosis Factor-alpha / biosynthesis. Vasoactive Intestinal Peptide / pharmacology
  • [MeSH-minor] Acute Disease. Alanine Transaminase / metabolism. Animals. Aspartate Aminotransferases / metabolism. Liver / enzymology. Liver / immunology. Liver / parasitology. Liver / pathology. Liver Extracts / metabolism. Male. Mice. Schistosoma mansoni / growth & development. Schistosoma mansoni / immunology. Swine. Vasodilator Agents / pharmacology. gamma-Glutamyltransferase / metabolism

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  • (PMID = 17869638.001).
  • [ISSN] 0171-2985
  • [Journal-full-title] Immunobiology
  • [ISO-abbreviation] Immunobiology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Liver Extracts; 0 / Tumor Necrosis Factor-alpha; 0 / Vasodilator Agents; 130068-27-8 / Interleukin-10; 187348-17-0 / Interleukin-12; 37221-79-7 / Vasoactive Intestinal Peptide; EC 2.3.2.2 / gamma-Glutamyltransferase; EC 2.6.1.1 / Aspartate Aminotransferases; EC 2.6.1.2 / Alanine Transaminase
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13. Delgado M, Ganea D: Vasoactive intestinal peptide prevents activated microglia-induced neurodegeneration under inflammatory conditions: potential therapeutic role in brain trauma. FASEB J; 2003 Oct;17(13):1922-4
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  • [Title] Vasoactive intestinal peptide prevents activated microglia-induced neurodegeneration under inflammatory conditions: potential therapeutic role in brain trauma.
  • In most neurodegenerative disorders, including multiple sclerosis, Parkinson's disease, and Alzheimer's disease, a massive neuronal cell death occurs as a consequence of an uncontrolled inflammatory response, where activated microglia and its cytotoxic agents play a crucial pathologic role.
  • Because current treatments for these diseases are not effective, several regulatory molecules termed "microglia-deactivating factors" recently have been the focus of considerable research.
  • Vasoactive intestinal peptide (VIP) is a neuropeptide with a potent anti-inflammatory effect, which has been found to protect from other inflammatory disorders, such as endotoxic shock and rheumatoid arthritis.
  • In the present study, we investigate the effect of VIP on inflammation-mediated neurodegeneration in vitro and in vivo as well as on the putative neuroprotective effect of VIP on experimental pathological conditions in which central nervous system (CNS) inflammation is involved, such as brain trauma.
  • VIP has a clear neuroprotective effect on inflammatory conditions by inhibiting the production of microglia-derived proinflammatory factors (tumor necrosis factor alpha, interleukin-1beta, nitric oxide).
  • In this sense, VIP prevents neuronal cell death following brain trauma by reducing the inflammatory response of neighboring microglia.
  • Therefore, VIP emerges as a valuable neuroprotective agent for the treatment of pathologic conditions of the CNS where inflammation-induced neurodegeneration occurs.
  • [MeSH-major] Encephalitis / drug therapy. Microglia / drug effects. Neurodegenerative Diseases / prevention & control. Neuroprotective Agents / therapeutic use. Vasoactive Intestinal Peptide / therapeutic use

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  • (PMID = 12923064.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neuroprotective Agents; 37221-79-7 / Vasoactive Intestinal Peptide
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14. Chatzistamou I, Schally AV, Varga JL, Groot K, Armatis P, Bajo AM: Inhibition of growth and reduction in tumorigenicity of UCI-107 ovarian cancer by antagonists of growth hormone-releasing hormone and vasoactive intestinal peptide. J Cancer Res Clin Oncol; 2001 Nov;127(11):645-52
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  • [Title] Inhibition of growth and reduction in tumorigenicity of UCI-107 ovarian cancer by antagonists of growth hormone-releasing hormone and vasoactive intestinal peptide.
  • PURPOSE: To evaluate the tumor inhibitory activities of antagonists of growth hormone-releasing hormone (GH-RH) and vasoactive intestinal peptide (VIP) in UCI-107 human ovarian cancer model, and to investigate the role of the insulin-like growth factor (IGF) system in the response.
  • METHODS: In the present study we investigated the effects of GH-RH antagonist JV-1-36 and VIP antagonist JV-1-52, on the growth and tumorigenicity of UCI-107 ovarian cell carcinoma xenografted into nude mice.
  • RESULTS: After 22 days of therapy with JV-1-36 or JV-1-52 at the dose of 20 microg/day, the final volume of UCI-107 tumors was significantly (P<0.05) decreased by 50.5% and 56%, respectively, compared to controls.
  • The concentration of IGF-II in tumors was reduced by 66% in the JV-1-36-treated group and by 62% in the group given JV-1-52 (both P < 0.05).
  • All ten mice injected with cells treated with medium alone developed tumors within 23 days after cell inoculation, while only eight of ten and four of ten mice injected with cells exposed to JV-1-36 or JV-1-52, respectively, had tumors.
  • In vitro exposure of UCI-107 cells to 5-35 ng/ml IGF-II produced a significant suppression in the rate of cell proliferation (P < 0.01).
  • CONCLUSION: Our results suggest that GH-RH and VIP antagonists inhibit the growth of UCI-107 ovarian cell carcinoma by mechanisms that appear to involve direct effects on the cancer cells.
  • [MeSH-major] Growth Hormone-Releasing Hormone / antagonists & inhibitors. Ovarian Neoplasms / drug therapy. Vasoactive Intestinal Peptide / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Division / drug effects. Dose-Response Relationship, Drug. Female. Human Growth Hormone / metabolism. Humans. Insulin-Like Growth Factor I / metabolism. Insulin-Like Growth Factor II / metabolism. Mice. Mice, Nude. Neoplasm Transplantation. Protein Binding. RNA, Messenger / metabolism. Radioimmunoassay. Receptor, IGF Type 1 / metabolism. Receptor, IGF Type 2 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Tumor Cells, Cultured

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  • (PMID = 11710593.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [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] Germany
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptor, IGF Type 2; 12629-01-5 / Human Growth Hormone; 37221-79-7 / Vasoactive Intestinal Peptide; 67763-96-6 / Insulin-Like Growth Factor I; 67763-97-7 / Insulin-Like Growth Factor II; 9034-39-3 / Growth Hormone-Releasing Hormone; EC 2.7.10.1 / Receptor, IGF Type 1
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15. Gelber E, Granoth R, Fridkin M, Dreznik Z, Brenneman DE, Moody TW, Gozes I: A lipophilic vasoactive intestinal peptide analog enhances the antiproliferative effect of chemotherapeutic agents on cancer cell lines. Cancer; 2001 Oct 15;92(8):2172-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A lipophilic vasoactive intestinal peptide analog enhances the antiproliferative effect of chemotherapeutic agents on cancer cell lines.
  • BACKGROUND: Vasoactive intestinal peptide (VIP) is one of several small neuropeptides that affect cancer growth.
  • A lipophilic VIP analog, stearyl-Nle(17)-neuroten-sin(6-11)VIP(7-28) (SNH) that inhibited lung carcinoma growth has been described previously.
  • The experiments performed were clonogenic assays in vitro and tumor xenografts in nude mice in vivo.
  • These studies were now extended to colon carcinoma and to combination therapy with chemotherapeutic agents.
  • METHODS: Assays were performed with cell lines, and tumor proliferation was assessed using the (3-[4,5-dimethylthiazol-2-yl-5]-[3-carboxymethoxyphenyl]-2-[4-sulfophenyl]-2H tetrazolium) (MTS) colorimetric assay for mitochondrial function of living cells.
  • RESULTS: The lipophilic analog (SNH) enhanced the antiproliferative activity of diverse chemotherapeutic agents: doxorubicine (antibiotic); vinorelbine (vinca alkaloid, antimicrotubule formation); paclitaxel (antimicrotubule agent); gemcitabine (antimetabolite); irinotecan (topoisomerase I inhibitor); and cisplatin (platinum compound acting as an alkylating agent).
  • For example, 2 microM of the antagonist that produced a 15-20% growth inhibition in the nonsmall cell lung carcinoma cell line reduced the IC(50) by 2-4-fold for most of the chemotherapeutic agents tested.
  • CONCLUSIONS: Chemotherapeutic treatment of advanced solid tumors, such as nonsmall cell lung carcinoma, colon carcinoma, or prostate carcinoma, achieves a response rate of between 10% and 30% with significant toxicity.
  • Combination therapy with the lipophilic VIP analog SNH and the preferred chemotherapeutic agent may greatly enhance the response rate, and by permitting a dose reduction, should significantly reduce side effects.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Growth Inhibitors / pharmacology. Neurotensin / pharmacology. Recombinant Fusion Proteins / pharmacology. Vasoactive Intestinal Peptide / pharmacology
  • [MeSH-minor] Animals. Carcinoma, Non-Small-Cell Lung / metabolism. Drug Synergism. Humans. Lung Neoplasms. Receptors, Vasoactive Intestinal Peptide / metabolism. Receptors, Vasoactive Intestinal Peptide, Type II. Receptors, Vasoactive Intestinal Polypeptide, Type I. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured. Tumor Stem Cell Assay. Xenograft Model Antitumor Assays

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  • [Copyright] Copyright 2001 American Cancer Society.
  • (PMID = 11596035.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Growth Inhibitors; 0 / Receptors, Vasoactive Intestinal Peptide; 0 / Receptors, Vasoactive Intestinal Peptide, Type II; 0 / Receptors, Vasoactive Intestinal Polypeptide, Type I; 0 / Recombinant Fusion Proteins; 0 / stearyl-Nle(17)-neurotensin(6-11)VIP(7-28); 0 / stearyl-norleucine(17)-vasoactive intestinal peptide; 125093-93-8 / (VIP-neurotensin) hybrid antagonist; 37221-79-7 / Vasoactive Intestinal Peptide; 39379-15-2 / Neurotensin
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16. Zhang YC, Yang LP, Tang DH, Zhang YM: [Protective effects of vasoactive intestinal peptide on intestinal lesions induced by endotoxic shock in rat]. Zhonghua Er Ke Za Zhi; 2006 May;44(5):369-73

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Protective effects of vasoactive intestinal peptide on intestinal lesions induced by endotoxic shock in rat].
  • OBJECTIVE: Vasoactive intestinal peptide (VIP) is a neuro-peptide that can modulate immunity in several aspects.
  • Previous reports showed that VIP attenuates the deleterious consequences of severe infection and septic shock by regulating production of inflammatory cytokines in immune activated cells.
  • Intestine is one of the major organ of immune system and it may trigger multiple organ dysfunction syndrome in sepsis.
  • The present study was planned to study the change of serum TNF-alpha, IL-1beta, IL-10 level and histopathological alteration of intestinal tract, and protective effects of VIP on endotoxic shock in rat.
  • METHODS: Twenty eight SD rats were randomly divided into 3 groups, including control group (8 rats), LPS shock group (10 rats), and LPS + VIP group (10 rats).
  • Endotoxic shock model was established by administration of a single dose of 10 mg/kg LPS in LPS shock group, a bolus of 5 nmol VIP intravenous injection following LPS in LPS + VIP group.
  • Blood samples were taken at time points of 1, 2, 4, and 6 hours after intervention from each group for measuring the level of TNF-alpha, IL-1beta and IL-10 by ELISA.
  • RESULTS: Serum TNF-alpha, IL-1beta and IL-10 levels elevated at each time point in LPS shock group and LPS + VIP group (P < 0.05 or P < 0.01).
  • TNF-alpha concentration reached the peak level 2 h after LPS injection; IL-1beta and IL-10 increased continuously till the end of the experiment.
  • In LPS + VIP group, TNF-alpha and IL-1beta elevated slightly and IL-10 increased significantly as compared with LPS shock group (P < 0.01).
  • However, pathological changes in LPS + VIP group were milder than those in LPS group.
  • CONCLUSIONS: VIP improved endotoxic shock-associated histopathological alteration of intestine, down-regulated pro-inflammatory cytokines production and up-regulated anti-inflammatory cytokines.
  • These effects may suggest a protective mechanism of VIP in septic shock.
  • VIP is a potential immunoregulatory substance in treatment of septic shock.
  • [MeSH-major] Intestines / drug effects. Shock, Septic / drug therapy. Shock, Septic / immunology. Vasoactive Intestinal Peptide / immunology. Vasoactive Intestinal Peptide / pharmacology
  • [MeSH-minor] Animals. Biomarkers / blood. Disease Models, Animal. Enzyme-Linked Immunosorbent Assay. Female. Interleukin-10 / blood. Interleukin-1beta / blood. Lipopolysaccharides / toxicity. Male. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 16780716.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Interleukin-1beta; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 37221-79-7 / Vasoactive Intestinal Peptide
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17. Juarranz MG, Santiago B, Torroba M, Gutierrez-Cañas I, Palao G, Galindo M, Abad C, Martinez C, Leceta J, Pablos JL, Gomariz RP: Vasoactive intestinal peptide modulates proinflammatory mediator synthesis in osteoarthritic and rheumatoid synovial cells. Rheumatology (Oxford); 2004 Apr;43(4):416-22
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vasoactive intestinal peptide modulates proinflammatory mediator synthesis in osteoarthritic and rheumatoid synovial cells.
  • OBJECTIVE: Vasoactive intestinal peptide (VIP) has demonstrated beneficial effects in several murine models of immune-mediated inflammation by inhibiting both the inflammatory and the autoimmune components of the disease.
  • We investigate its potential to modulate the release of proinflammatory cytokines and chemokines by human synovial cells from patients with rheumatoid arthritis (RA).
  • METHODS: Fresh suspensions of synovial tissue cells (STC) or cultured fibroblast-like synoviocytes (FLS) were obtained from patients with RA or osteoarthritis (OA).
  • The effects of VIP on basal or tumour necrosis factor alpha (TNF-alpha)-stimulated production of CCL2 (MCP-1, monocyte chemotactic protein 1), CXCL8 [interleukin (IL)-8], IL-6 and TNF-alpha were studied by specific ELISAs (enzyme-linked immunosorbent assays).
  • The mRNAs for CCL2, CXCL8 and IL-6 in FLS were analysed by real-time reverse transcription-polymerase chain reaction.
  • RESULTS: VIP at 10 nm down-regulated chemokine production by STC and FLS from RA and OA patients.
  • VIP also down-regulated the expression of mRNAs for CCL2, CXCL8 and IL-6.
  • The effects of VIP were more clearly detected in RA samples and after stimulation with TNF-alpha.
  • CONCLUSION: Our observations confirm that the proposed anti-inflammatory actions of VIP in murine models also apply to human synovial cells ex vivo.
  • Further studies are encouraged to evaluate the use of VIP as a potential therapy for chronic inflammatory joint diseases.
  • [MeSH-major] Arthritis, Rheumatoid / pathology. Inflammation Mediators / metabolism. Osteoarthritis, Knee / pathology. Synovial Membrane / drug effects. Vasoactive Intestinal Peptide / pharmacology
  • [MeSH-minor] Cells, Cultured. Chemokines / biosynthesis. Chemokines / genetics. Cytokines / biosynthesis. Cytokines / genetics. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Humans. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction


18. Janson ET: Treatment of neuroendocrine tumors with somatostatin analogs. Pituitary; 2006;9(3):249-56
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of neuroendocrine tumors with somatostatin analogs.
  • Neuroendocrine tumors constitute a group of hormone producing tumors originating from neuroendocrine cells in different organs.
  • Most tumors have a low proliferation index measured by Ki67 and the progression of the tumor is slow.
  • However, many patients suffer from endocrine symptoms induced by the hormones produced and released by the tumor cells.
  • For some patients these symptoms can be life- threatening as in midgut carcinoid patients suffering from carcinoid crises with extensive flushes and hypotension or in patients with severe diarrhea induced by tumors producing vasointestinal polypeptide.
  • The introduction of somatostatin analogs in the treatment of these hormone related symptoms has made it possible to control most of them and has added significantly to the quality of life for this group of patients.
  • Unfortunately, the clinical inhibitory effect on tumor growth has not been very good with only 5-10% of the patients showing an objective response.
  • However, stabilization of tumor growth may be achieved in a significant number of patients.
  • In the future, the hope is that development of new somatostatin analogs with broader receptor-binding profiles will give us new analogs which are more efficient with regard to their antiproliferative effect.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Neuroendocrine Tumors / drug therapy. Somatostatin / therapeutic use
  • [MeSH-minor] Activities of Daily Living. Animals. Cell Proliferation / drug effects. Humans. Quality of Life. Receptors, Somatostatin / drug effects. Receptors, Somatostatin / metabolism. Treatment Outcome

  • COS Scholar Universe. author profiles.
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  • (PMID = 17001461.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin
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19. Ferone D, Lombardi G, Colao A: [Somatostatin receptors in immune system cells]. Minerva Endocrinol; 2001 Sep;26(3):165-73
MedlinePlus Health Information. consumer health - Immune System and Disorders.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In particular, somatostatin (ss), substance P (sp) and vasoactive intestinal polypeptide (vip) appear to be involved in numerous regulating mechanisms of cell activities in the immune system under both physiological and pathological conditions. ss may be produced by lymphoid cells and accessories as part of the immune system.
  • The distribution of somatostatin receptors (ssr) in the normal human thymus has prompted the hypothesis that ss, and probably other neuropeptides, may play an important role in cell homeostasis in this organ, as well as being one of the processes that regulates the maturation of T lymphocytes.
  • The advent of molecular biology has showed a variable expression of ssr on the various T and B cell lines or lines deriving from lymphoma/ leukemia and human myeloma.
  • Using autoradiographic studies, ssr have been predominantly found in lymphoblastic areas of lymphoma, which represent the active part of the tumour.
  • The expression of ssR has been found in vivo and in vitro, also in pathological sites in patients with autoimmune and granulomatous diseases like rheumatoid arthritis and sarcoidosis.
  • [MeSH-minor] Animals. Antineoplastic Agents, Hormonal / therapeutic use. Autoimmune Diseases / metabolism. Cell Differentiation. Cell Division. Gene Expression Regulation. Granuloma / metabolism. Hematologic Neoplasms / metabolism. Homeostasis. Humans. Lymphocyte Subsets / metabolism. Lymphocytes / metabolism. Lymphoproliferative Disorders / metabolism. Mice. Models, Animal. Neoplasm Proteins / physiology. Neoplasms / drug therapy. Neoplasms / metabolism. Neoplastic Stem Cells / metabolism. Neuropeptides / physiology. Octreotide / pharmacology. Octreotide / therapeutic use. Organ Specificity. Rats. Signal Transduction. Thymus Gland / metabolism

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  • (PMID = 11753240.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Neoplasm Proteins; 0 / Neuropeptides; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide
  • [Number-of-references] 68
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20. Okarvi SM: Peptide-based radiopharmaceuticals and cytotoxic conjugates: potential tools against cancer. Cancer Treat Rev; 2008 Feb;34(1):13-26
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Peptide-based radiopharmaceuticals and cytotoxic conjugates: potential tools against cancer.
  • A hope for the diagnosis and treatment of cancer is the development of new tumor-specific peptide-based radiopharmaceuticals.
  • The overexpression of many peptide receptors on human tumors makes such receptors an attractive potential target for diagnostic imaging and radiotherapy with specifically designed radiolabeled peptides.
  • The use of solid-phase peptide synthesis, and the availability of a wide range of bifunctional chelating agents for the convenient radiolabeling of bioactive peptides with different radionuclides have produced a wide variety of medicinally useful peptide radiopharmaceuticals.
  • A few of these peptides, such as somatostatin, bombesin, cholecystokinin/gastrin, neurotensin and vasoactive intestinal peptide are currently under investigation for their possible clinical applications in nuclear oncology.
  • This article presents the recent development in radiolabeled small peptides, with major emphasis on somatostatin and bombesin analogs.
  • [MeSH-major] Bombesin / therapeutic use. Neoplasms / diagnosis. Neoplasms / therapy. Peptides / therapeutic use. Radiopharmaceuticals / therapeutic use. Somatostatin / therapeutic use
  • [MeSH-minor] Amino Acid Sequence. Antineoplastic Agents / therapeutic use. Drug Delivery Systems. Humans

  • Guide to Pharmacology. gene/protein/disease-specific - Bombesin receptors - overview and references .
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  • (PMID = 17870245.001).
  • [ISSN] 0305-7372
  • [Journal-full-title] Cancer treatment reviews
  • [ISO-abbreviation] Cancer Treat. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Peptides; 0 / Radiopharmaceuticals; 51110-01-1 / Somatostatin; PX9AZU7QPK / Bombesin
  • [Number-of-references] 99
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21. Bodei L, Ferone D, Grana CM, Cremonesi M, Signore A, Dierckx RA, Paganelli G: Peptide receptor therapies in neuroendocrine tumors. J Endocrinol Invest; 2009 Apr;32(4):360-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Peptide receptor therapies in neuroendocrine tumors.
  • Neuroendocrine tumors (NETs) are relatively rare tumors, mainly originating from the digestive system, able to produce bioactive amines and hormones.
  • The localization of a NETs and the assessment of the extent of disease are crucial for management.
  • Commonly used diagnostic techniques include morphological imaging (ultrasound, computerized tomography, magnetic resonance), and functional imaging (somatostatin receptor scintigraphy, positron emission tomography techniques).
  • Treatment is multidisciplinary and should be individualized according to the tumor type, burden, and symptoms.
  • Therapeutic tools include surgery, interventional radiology, and medical treatments such as somatostatin analogues, interferon, chemotherapy, new targeted drugs and peptide receptor radionuclide therapy (PRRT) with radiolabeled somatostatin analogues.
  • NETs usually over-express somatostatin receptors, thus enabling the therapeutic use of somatostatin analogues, one of the basic tools, able to reduce signs and symptoms of hormone hypersecretion, improve quality of life, and slow tumor growth.
  • Present knowledge and clinical studies indicate that it is possible to deliver high-absorbed doses to tumors expressing sst2 receptors, with partial and complete objective responses in up to 30% of patients.
  • As NETs may also express cholecystokinin 2, bombesin, neuropeptide Y or vasoactive intestinal peptide receptors even simultaneously, the potential availability and biological stability of radio-analogues will improve the multireceptor targeting of NETs.
  • [MeSH-major] Neuroendocrine Tumors / therapy. Octreotide / therapeutic use. Radiopharmaceuticals / therapeutic use. Receptors, Somatostatin / metabolism. Somatostatin / therapeutic use

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  • (PMID = 19636207.001).
  • [ISSN] 1720-8386
  • [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 / Radiopharmaceuticals; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide
  • [Number-of-references] 85
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22. Berdjis N, Baldauf A, Kittner T, Manseck A, Wirth M: [Paraneoplastic hyperthyroidism in a patient with metastasizing teratocarcinoma and excessively high HCG]. Aktuelle Urol; 2003 Oct;34(6):407-9
MedlinePlus Health Information. consumer health - Testicular Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Transliterated title] Paraneoplastische Hyperthyreose bei metastasiertem Teratokarzinom mit exzessiver HCG-Erhöhung.
  • Clinically manifest hyperthyroidism is a rare paraneoplastic syndrome in patients with excessive HCG production due to testicular cancer.
  • The patient received immediately thyrostatic therapy and 4 cycles of PEI chemotherapy (Cisplatin, Etoposide, Ifosfamide).
  • Thyroid function had returned to normal by the beginning of the second course of chemotherapy.
  • After right orchiectomy and resection of residual pulmonary masses which revealed vital tumor cells, two additional courses of chemotherapy were performed.
  • The patient is well and without evidence of disease 11 months after therapy.
  • All patients with testicular cancer and excessive HCG production should be evaluated for biochemical and clinical signs of hyperthyroidism and treated accordingly with antithyroidal medication and immediate cytoreductive chemotherapy.
  • [MeSH-major] Chorionic Gonadotropin / blood. Hyperthyroidism / diagnosis. Lung Neoplasms / secondary. Paraneoplastic Syndromes / diagnosis. Teratocarcinoma / secondary. Testicular Neoplasms / diagnosis
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Antithyroid Agents / therapeutic use. Combined Modality Therapy. Humans. Lymphatic Metastasis. Male. Neoadjuvant Therapy. Orchiectomy. Pneumonectomy. Tomography, X-Ray Computed

  • MedlinePlus Health Information. consumer health - Hyperthyroidism.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
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  • (PMID = 14579189.001).
  • [ISSN] 0001-7868
  • [Journal-full-title] Aktuelle Urologie
  • [ISO-abbreviation] Aktuelle Urol
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antithyroid Agents; 0 / Chorionic Gonadotropin
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23. Zhang Q, Wan L, Guo Y, Cheng N, Cheng W, Sun Q, Zhu J: Radiosensitization effect of luteolin on human gastric cancer SGC-7901 cells. J Biol Regul Homeost Agents; 2009 Apr-Jun;23(2):71-8
MedlinePlus Health Information. consumer health - Stomach Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radiosensitization effect of luteolin on human gastric cancer SGC-7901 cells.
  • In order to study the underlying mechanism, the levels of apoptosis-related proteins, the activities of caspase-3 and -9, and the production of PGE2 were measured.
  • The results showed that luteolin could enhance irradiation-induced colonogenic inhibition and the activities of Caspase-3 and -9.
  • The remarkable down-regulation of Bcl-2 and release of cytochrome C were also observed.
  • In addition, significantly reduced production of PGE(2) was observed in luteolin plus radiation treatment by ELISA, as well as decreased expression levels of VEGF and HIF-1 alpha.
  • Finally, luteolin significantly enhances the radioresponse of human tumors transplanted into nude mice.
  • Our results indicate that luteolin may be a promising radiosensitizer for use in the treatment of gastric cancer.
  • [MeSH-major] Luteolin / therapeutic use. Radiation-Sensitizing Agents / therapeutic use. Stomach Neoplasms / drug therapy. Stomach Neoplasms / radiotherapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / radiation effects. Caspase 3 / metabolism. Caspase 9 / metabolism. Cell Line, Tumor. Combined Modality Therapy. Dinoprostone / biosynthesis. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Mice. Mice, Inbred BALB C. Mice, Nude. Tumor Stem Cell Assay. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 19589287.001).
  • [ISSN] 0393-974X
  • [Journal-full-title] Journal of biological regulators and homeostatic agents
  • [ISO-abbreviation] J. Biol. Regul. Homeost. Agents
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Radiation-Sensitizing Agents; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9; K7Q1JQR04M / Dinoprostone; KUX1ZNC9J2 / Luteolin
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