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1. Poggi G, Villani L, Bernardo G: Multimodality treatment of unresectable hepatic metastases from pancreatic glucagonoma. Rare Tumors; 2009;1(1):e6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multimodality treatment of unresectable hepatic metastases from pancreatic glucagonoma.
  • Glucagonomas are pancreatic islet cell tumors arising from the alpha cells which belong to neuroendocrine tumors.
  • We report the case of a 52- year old man with a pancreatic glucagonoma with synchronous multiple liver metastases treated by surgery, transarterial chemoembolization, percutaneous radiofrequency thermal ablation and long-acting octreotide.
  • Our report confirms that a multimodal approach is very effective in patients with unresectable liver metastases from pancreatic endocrine tumors providing long-lasting palliation and probably prolonging survival.

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  • [Cites] Cancer. 1993 Jul 1;72(1):244-8 [8389666.001]
  • [Cites] Cancer. 1993 Apr 15;71(8):2624-30 [8384072.001]
  • [Cites] Ann Intern Med. 1994 Feb 15;120(4):302-9 [8291824.001]
  • [Cites] Anticancer Res. 2008 Nov-Dec;28(6B):3835-42 [19192637.001]
  • [Cites] J Vasc Interv Radiol. 2008 Jun;19(6):855-61 [18503899.001]
  • [Cites] J Hepatol. 2008 Aug;49(2):217-22 [18486261.001]
  • [Cites] J Vasc Interv Radiol. 2006 Aug;17(8):1335-43 [16923981.001]
  • [Cites] World J Gastroenterol. 2005 Dec 28;11(48):7676-83 [16437698.001]
  • [Cites] J Am Coll Surg. 2000 Apr;190(4):432-45 [10757381.001]
  • [Cites] N Engl J Med. 1982 Mar 11;306(10):580-90 [6120456.001]
  • [Cites] Eur J Radiol. 2009 Dec;72(3):517-28 [18829195.001]
  • [Cites] J Hepatol. 2007 Mar;46(3):474-81 [17239480.001]
  • [Cites] Neuroendocrinology. 2004;80(6):394-424 [15838182.001]
  • [Cites] Cancer. 1990 May 15;65(10):2227-32 [2161278.001]
  • [Cites] Dig Surg. 1999;16(1):32-8 [9949265.001]
  • [Cites] Lancet. 1974 Jul 6;2(7871):1-5 [4134714.001]
  • [Cites] Abdom Imaging. 2005 Jul-Aug;30(4):435-41 [15759207.001]
  • [Cites] Surg Oncol Clin N Am. 2003 Jan;12(1):231-42 [12735141.001]
  • [Cites] Eur Radiol. 2003 Jan;13(1):136-40 [12541121.001]
  • [Cites] Radiology. 2000 Oct;217(1):119-26 [11012432.001]
  • (PMID = 21139900.001).
  • [ISSN] 2036-3613
  • [Journal-full-title] Rare tumors
  • [ISO-abbreviation] Rare Tumors
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2994425
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2. Okauchi Y, Nammo T, Iwahashi H, Kizu T, Hayashi I, Okita K, Yamagata K, Uno S, Katsube F, Matsuhisa M, Kato K, Aozasa K, Kim T, Osuga K, Nakamori S, Tamaki Y, Funahashi T, Miyagawa J, Shimomura I: Glucagonoma diagnosed by arterial stimulation and venous sampling (ASVS). Intern Med; 2009;48(12):1025-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glucagonoma diagnosed by arterial stimulation and venous sampling (ASVS).
  • To identify the location of pancreatic endocrine tumors, arterial stimulation and venous sampling (ASVS) is known to be useful for insulinoma and gastrinoma, but its usefulness for glucagonoma has not been verified to date.
  • Here we report a case of glucagonoma that was diagnosed by ASVS with calcium loading, in which an approximately 6-fold increase of glucagon was observed in the splenic artery territory.
  • MEN1 gene analysis verified the presence of a mutation and the glucagonoma was confirmed after operation.
  • In conclusion, ASVS could be useful for the diagnosis of glucagonoma.
  • [MeSH-major] Glucagon / blood. Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 19525592.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 9007-92-5 / Glucagon; SY7Q814VUP / Calcium
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3. Zhou C, Dhall D, Nissen NN, Chen CR, Yu R: Homozygous P86S mutation of the human glucagon receptor is associated with hyperglucagonemia, alpha cell hyperplasia, and islet cell tumor. Pancreas; 2009 Nov;38(8):941-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Homozygous P86S mutation of the human glucagon receptor is associated with hyperglucagonemia, alpha cell hyperplasia, and islet cell tumor.
  • OBJECTIVE: The goal of the study was to investigate the genetic and molecular basis of a novel syndrome of marked hyperglucagonemia and pancreatic alpha cell hyperplasia without glucagonoma syndrome.
  • METHODS: The glucagon receptor (GCGR) gene and the glucagon gene were sequenced in a patient with hyperglucagonemia and pancreatic alpha cell hyperplasia without glucagonoma syndrome.
  • RESULTS: The glucagon gene sequence was normal, but the GCGR sequencing uncovered a homozygous missense mutation, c.256C>T, p.P86S in the extracellular domain of GCGR.
  • When expressed in human embryonic kidney 293 cells, GCGR P86S localized to the plasma membrane but bound 96% less radiolabeled glucagon than WT GCGR.
  • The median effective concentration of glucagon-induced cyclic adenosine monophosphate production was 24 nmol/L for GCGR P86S but 2.4 nmol/L for WT GCGR.
  • The patient's alpha cells also express glucagonlike peptide 1 and pancreatic polypeptide.
  • CONCLUSIONS: We hereby report the first homozygous missense mutation in the human GCGR, which is associated with alpha cell hyperplasia and hyperglucagonemia.
  • This mutation lowers the receptor's affinity to glucagon and decreases cyclic adenosine monophosphate production with physiological concentrations of glucagon.
  • Thus, the P86S mutation in GCGR likely causes alpha cell hyperplasia and hyperglucagonemia.

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  • [Cites] Mech Dev. 2002 Jul;115(1-2):171-6 [12049785.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Jan;94(1):213-7 [18957496.001]
  • [Cites] Pharmacol Rev. 2003 Mar;55(1):167-94 [12615957.001]
  • [Cites] Pancreas. 2003 May;26(4):402-5 [12717275.001]
  • [Cites] Annu Rev Med. 2004;55:27-39 [14746508.001]
  • [Cites] N Engl J Med. 1977 Mar 10;296(10):534-8 [189188.001]
  • [Cites] World J Surg. 1984 Aug;8(4):561-74 [6207668.001]
  • [Cites] Nat Genet. 1995 Mar;9(3):299-304 [7773293.001]
  • [Cites] J Biol Chem. 1995 Nov 17;270(46):27720-7 [7499239.001]
  • [Cites] Diabetes. 1996 Jun;45(6):725-30 [8635644.001]
  • [Cites] Hum Genet. 1996 Dec;98(6):636-9 [8931690.001]
  • [Cites] Am J Pathol. 1998 Jul;153(1):223-31 [9665483.001]
  • [Cites] Endocrinology. 2006 May;147(5):2346-56 [16484329.001]
  • [Cites] Endocrinology. 2006 Sep;147(9):3995-4006 [16627579.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Dec 19;103(51):19541-5 [17159157.001]
  • [Cites] Am J Med Sci. 2001 May;321(5):306-20 [11370794.001]
  • [Cites] Endocr Rev. 2007 Feb;28(1):84-116 [17261637.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Aug 28;104(35):13942-7 [17715056.001]
  • [Cites] J Biol Chem. 2008 Apr 25;283(17):11340-7 [18287102.001]
  • [Cites] Pancreas. 2008 May;36(4):428-31 [18437091.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):1438-43 [12552113.001]
  • (PMID = 19657311.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK071870-04; United States / NIDDK NIH HHS / DK / K08 DK071870; United States / NIDDK NIH HHS / DK / DK071870; United States / NIDDK NIH HHS / DK / K08 DK071870-04
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Glucagon; 147336-22-9 / Green Fluorescent Proteins; 9007-92-5 / Glucagon
  • [Other-IDs] NLM/ NIHMS139678; NLM/ PMC2767399
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4. Williams LE, DeNardo GL, Meredith RF: Targeted radionuclide therapy. Med Phys; 2008 Jul;35(7Part1):3062-3068

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Targeted radionuclide therapy (TRT) seeks molecular and functional targets within patient tumor sites.
  • A number of agents have been constructed and labeled with beta, alpha, and Auger emitters.
  • Lymphoma (B-cell) has been the primary clinical application.
  • Extension to solid tumors will require raising the macroscopic absorbed dose by several-fold over values found in present technology.

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  • [Copyright] © 2008 American Association of Physicists in Medicine.
  • (PMID = 28513035.001).
  • [ISSN] 2473-4209
  • [Journal-full-title] Medical physics
  • [ISO-abbreviation] Med Phys
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Anatomy / Auger effect / Cancer / Computed tomography / Conformal radiation treatment / Dosimetry / Medical imaging / Positron emission tomography / Positron emission tomography (PET) / Proteins / Single photon emission computed tomography / Single photon emission computed tomography (SPECT) / Tissue engineering / Tissues / absorbed dose / alpha-particle sources / antibodies / beta-ray sources / blood / cellular biophysics / positron emission tomography / radiation therapy / radioisotopes / radionuclide therapy / single photon emission computed tomography / tumours
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5. Zhu X, Palmer MR, Makrigiorgos GM, Kassis AI: Solid-tumor radionuclide therapy dosimetry: New paradigms in view of tumor microenvironment and angiogenesis. Med Phys; 2010 Jun;37(6Part1):2974-2984

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Solid-tumor radionuclide therapy dosimetry: New paradigms in view of tumor microenvironment and angiogenesis.
  • PURPOSE: The objective of this study is to evaluate requirements for radionuclide-based solid tumor therapy by assessing the radial dose distribution of beta-particle-emitting and alpha-particle-emitting molecules localized either solely within endothelial cells of tumor vasculature or diffusing from the vasculature throughout the adjacent viable tumor cells.
  • METHODS: Tumor blood vessels were modeled as a group of microcylindrical layers comprising endothelial cells (one-cell thick, 10μm diameter), viable tumor cells (25-cell thick, 250μm radius), and necrotic tumor region (>250μm from any blood vessel).
  • Sources of radioactivity were assumed to distribute uniformly in either endothelial cells or in concentric cylindrical 10μm shells within the viable tumor-cell region.
  • The EGSnrc Monte Carlo simulation code system was used for beta particle dosimetry and a dose-point kernel method for alpha particle dosimetry.
  • The radioactive decays required to deposit cytocidal doses (≥100Gy) in the vascular endothelial cells (endothelial cell mean dose) or, alternatively, at the tumor edge [tumor-edge mean dose (TEMD)] of adjacent viable tumor cells were then determined for six beta (P32, P33, C67u, Y90, I131, and R188e) and two alpha (A211t and B213i) particle emitters.
  • RESULTS: Contrary to previous modeling in targeted radionuclide therapy dosimetry of solid tumors, the present work restricts the region of tumor viability to 250μm around tumor blood vessels for consistency with biological observations.
  • For delivering ≥100Gy at the viable tumor edge (TEMD) rather than throughout a solid tumor, energetic beta emitters Y90, P32, and R188e can be effective even when the radionuclide is confined to the blood vessel (i.e., no diffusion into the tumor).
  • Furthermore, the increase in tumor-edge dose consequent to beta emitter diffusion is dependent on the energy of the emitted beta particles, being much greater for lower-energy emitters I131, C67u, and P33 relative to higher-energy emitters Y90, P32, and R188e.
  • Compared to alpha particle emitters, a ∼150-400 times higher number of beta-particle-emitting radioactive atoms is required to deposit the same dose in tumor neovasculature.
  • However, for the alpha particle emitters A211t and B213i to be effective in irradiating viable tumor-cell regions in addition to the vasculature, the carrier molecules must diffuse substantially from the vasculature into the viable tumor.
  • CONCLUSION: The presented data enable comparison of radionuclides used for antiangiogenic therapy on the basis of their radioactive decay properties, tumor neovasculature geometry, and tumor-cell viability.
  • For alpha particle emitters or low-energy beta particle emitters, the targeting carrier molecule should be chosen to permit the radiopharmaceutical to diffuse from the endothelial wall of the blood vessel, while for long-range energetic beta particle emitters that target neovasculature, a radiopharmaceutical that binds to newly formed endothelial cells and does not diffuse is preferable.
  • The work is a first approximation to modeling of tumor neovasculature that ignores factors such as pharmacokinetics and targeting capability of carrier molecules.
  • The calculations quantify the interplay between irradiation of neovasculature, the surrounding viable tumor cells, and the physical properties of commonly used radionuclides and can be used to assist estimation of radioactivity to be administered for neovasculature-targeted tumor therapy.

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  • [Copyright] © 2010 American Association of Physicists in Medicine.
  • (PMID = 28512969.001).
  • [ISSN] 2473-4209
  • [Journal-full-title] Medical physics
  • [ISO-abbreviation] Med Phys
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Alpha particles / Beta particles / Cancer / Cell growth / Cell processes / Diffusion / Dose-volume analysis / Dosimetry / Monte Carlo methods / Nutrients / Radiation treatment / Radioactivity / Radiopharmaceuticals / alpha particle emitter / blood vessels / cellular biophysics / dosimetry / electron emitter / neovasculature targeting / radiation therapy / targeted radionuclide therapy / tumor targeting / tumor vascularity / tumours
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6. Marko PB, Miljković J, Zemljic TG: Necrolytic migratory erythema associated with hyperglucagonemia and neuroendocrine hepatic tumors. Acta Dermatovenerol Alp Pannonica Adriat; 2005 Dec;14(4):161-4, 166
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Necrolytic migratory erythema associated with hyperglucagonemia and neuroendocrine hepatic tumors.
  • The computed tomographic scan of the abdomen revealed multiple hepatic tumors.
  • Histopathological examination of ultrasound-guided needle biopsy from a hepatic lesion demonstrated a neuroendocrine tumor.
  • Somatostatin-receptor scintigraphy with radio-labelled octreotide confirmed the likelihood of the neuroendocrine nature of the hepatic tumors and excluded the presence of other such lesions throughout the rest of the body, including the pancreas.
  • The serum glucagon level was markedly increased.
  • The diagnosis of necrolytic migratory erythema associated with hyperglucagonemia and neuroendocrine hepatic tumors was made and therapy with the long-acting somatostatin analogue octreotide was started.
  • Having reached the final stage of the disease, which was further complicated by congestive heart failure, the patient died one year later.
  • As no autopsy was performed, we were unable to establish whether the hepatic tumors represented a metastatic process of previously undetected pancreatic glucagonoma or if they were extra-pancreatic glucagon-secreting tumors.
  • The correct diagnosis of necrolytic migratory erythema is important, since it might be the clue for early detection of glucagonoma or of extra-pancreatic glucagon-secreting tumors.
  • [MeSH-major] Dermatitis / etiology. Erythema / etiology. Liver Neoplasms / diagnosis. Neuroendocrine Tumors / diagnosis. Paraneoplastic Syndromes / diagnosis
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Glucagon / blood. Humans. Male. Middle Aged. Octreotide / therapeutic use

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  • (PMID = 16435046.001).
  • [ISSN] 1318-4458
  • [Journal-full-title] Acta dermatovenerologica Alpina, Pannonica, et Adriatica
  • [ISO-abbreviation] Acta Dermatovenerol Alp Pannonica Adriat
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Slovenia
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 9007-92-5 / Glucagon; RWM8CCW8GP / Octreotide
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7. Paula LC, Zen VL, Czepielewski MA: [Granulosa-stromal tumor of the ovary: a case of mixed germ cell-cord stromal tumor of the ovary with endocrinological considerations]. Arq Bras Endocrinol Metabol; 2005 Oct;49(5):776-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Granulosa-stromal tumor of the ovary: a case of mixed germ cell-cord stromal tumor of the ovary with endocrinological considerations].
  • [Transliterated title] Puberdade precoce associada a tumor misto ovariano (células germinativas- estroma-cordão sexual): aspectos clínicos, diagnósticos e manejo de um caso.
  • Granulosa-stromal tumors comprise 5 to 8% of all primary ovarian neoplasms.
  • We report a case of mixed germ cell-cord stromal tumor of ovary in a 7.2 years old girl, who presented with isosexual pseudo-precocious puberty of progressive outcome.
  • Unilateral salpingo-oophorectomy was performed with complete resection of the tumor.
  • The patient is well 7 years after surgery with normal pubertal and growth development and no signs of tumor relapse.
  • We review the clinical manifestations of ovarian tumors, classification and staging of sex cord-stromal tumors, follow-up, tumor markers, treatment and prognosis.
  • [MeSH-major] Granulosa Cell Tumor / complications. Mixed Tumor, Malignant / complications. Ovarian Neoplasms / complications. Puberty, Precocious / etiology
  • [MeSH-minor] 17-alpha-Hydroxyprogesterone / blood. Biomarkers, Tumor / blood. Child. Estradiol / blood. Female. Humans. Ovariectomy / methods. Testosterone / blood. Treatment Outcome

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  • (PMID = 16444360.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol; 68-96-2 / 17-alpha-Hydroxyprogesterone
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8. DeBusk LM, Massion PP, Lin PC: IkappaB kinase-alpha regulates endothelial cell motility and tumor angiogenesis. Cancer Res; 2008 Dec 15;68(24):10223-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IkappaB kinase-alpha regulates endothelial cell motility and tumor angiogenesis.
  • The transcription factor nuclear factor-kappaB (NF-kappaB) is constitutively activated in many types of cancers and has been implicated in gene expression important for angiogenesis, tumor growth, progression, and metastasis.
  • Here, we show that the NF-kappaB activator, IkappaB kinase-alpha (IKKalpha), but not IKKbeta, promotes endothelial cell motility and tumor angiogenesis.
  • IKKalpha is elevated in tumor vasculature compared with normal endothelium.
  • Overexpression of IKKalpha in endothelial cells promoted cell motility and vascular tubule formation in a three-dimensional culture assay, and conversely, knockdown of IKKalpha in endothelial cells inhibited cell motility, compared with controls.
  • Furthermore, using a tumor and endothelial cell cotransplantation model, we show that overexpression of IKKalpha in endothelial cells significantly increased tumor vascular formation compared with controls, which contributed to increased tumor growth and tumor cell proliferation, and decreased tumor cell apoptosis.
  • Collectively, these findings have identified a new function for IKKalpha through the canonical NF-kappaB pathway in tumor angiogenesis.
  • [MeSH-major] Carcinoma, Lewis Lung / enzymology. Cell Movement / physiology. I-kappa B Kinase / physiology
  • [MeSH-minor] Animals. Cells, Cultured. Endothelial Cells / enzymology. Endothelial Cells / pathology. Female. Humans. Mice. Neovascularization, Pathologic / enzymology. Neovascularization, Pathologic / genetics. Up-Regulation

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  • (PMID = 19074890.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / AR053718; United States / NCI NIH HHS / CA / CA108856; United States / NINDS NIH HHS / NS / NS45888; United States / NCI NIH HHS / CA / T32CA009592
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.11.10 / I-kappa B Kinase
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9. Lobo I, Carvalho A, Amaral C, Machado S, Carvalho R: Glucagonoma syndrome and necrolytic migratory erythema. Int J Dermatol; 2010 Jan;49(1):24-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glucagonoma syndrome and necrolytic migratory erythema.
  • The glucagonoma syndrome is a rare disorder, characterized by necrolytic migratory erythema, elevated serum glucagon levels, abnormal glucose tolerance, weight loss, and anemia in association with a glucagon-secreting alpha-cell tumor of the pancreas.
  • The clinical investigation revealed a pancreatic glucagonoma with resolution of the cutaneous and systemic features after surgical removal.
  • The dermatologic and endocrine approach to this syndrome is discussed here.
  • Early recognition and treatment may prevent metastatic disease and ensure its cure with resolution of the cutaneous and catabolic manifestations.
  • [MeSH-major] Erythema / etiology. Erythema / pathology. Glucagonoma / complications. Pancreatic Neoplasms / complications. Skin / pathology
  • [MeSH-minor] Aged. Biopsy. Glucagon / blood. Humans. Male. Necrosis. Pancreatectomy. Tomography, X-Ray Computed

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  • (PMID = 20465606.001).
  • [ISSN] 1365-4632
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-92-5 / Glucagon
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10. Yoshida M, Hayashi K, Ohara H, Miyabe K, Okumura F, Naitoh I, Tanaka H, Ando T, Nakazawa T, Takahashi S, Joh T: A case of pancreatic glucagonoma with erythema. Nihon Shokakibyo Gakkai Zasshi; 2010 Jun;107(6):930-6
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  • [Title] A case of pancreatic glucagonoma with erythema.
  • Full-body computed tomography (CT) scanning revealed a tumor mass in the tail of the pancreas; CT and magnetic resonance imaging (MRI) scans confirmed the presence of a spherical mass.
  • In contrast CT scans, although the contrast was gradually increased, no strong contrast differences were observed between the tumor and the surrounding tissue.
  • Blood test results revealed that the patient had a high glucagon level.
  • We diagnosed glucagonoma syndrome on the basis of the above results and resected the tail of the pancreas.
  • Pathological analysis revealed that the tumor cells had proliferated in ribbon-like, cord-like structures.
  • Immunostaining results were positive for glucagon, which confirmed our diagnosis.
  • [MeSH-major] Erythema / etiology. Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 20530930.001).
  • [ISSN] 0446-6586
  • [Journal-full-title] Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology
  • [ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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11. Simonenko VB, Dulin PA, Beliaev LB, Makanin MA, Dem'ianenko AV, Zykova AA, Zhuravleva SI, Kolesnikova VN: [A case of pancreatic glucagonoma]. Klin Med (Mosk); 2007;85(8):67-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A case of pancreatic glucagonoma].
  • Neuroendocrine tumor consisting of pancreatic alpha-cells -- glucagonoma -- is a very rare finding (one case per two million people a year).
  • This functionally active, usually malignant tumor has typical clinical manifestations.
  • Glucagonoma syndrome is a disease that has an original clinical picture that includes necrolytic migrating erythema with secondary bullous dermatitis, glucose tolerance disorder or diabetes mellitus, weight loss, anemia, hypoaminoacidemia, venous thrombosis, and alimentary and mental disturbances.
  • By the time diagnosis is made, 60 to 70% of glucagonomas already give metastases, and even small glucagonomas should be considered tumors with unknown malignant potential or malignant tumors.
  • Glucagonomas grow slowly, and patients live long (the survival median is approximately 15 years).
  • [MeSH-major] Glucagonoma / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 17926496.001).
  • [ISSN] 0023-2149
  • [Journal-full-title] Klinicheskaia meditsina
  • [ISO-abbreviation] Klin Med (Mosk)
  • [Language] rus
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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12. Technau K, Renkl A, Norgauer J, Ziemer M: Necrolytic migratory erythema with myelodysplastic syndrome without glucagonoma. Eur J Dermatol; 2005 Mar-Apr;15(2):110-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Necrolytic migratory erythema with myelodysplastic syndrome without glucagonoma.
  • Necrolytic migratory erythema is a cutaneous paraneoplastic manifestation, which is usually associated with a glucagon-secreting pancreatic tumor.
  • However, it also may occur in other circumstances in which serum glucagon is elevated, as in hepatic cirrhosis.
  • Rarely, necrolytic migratory erythema is reported in association with a jejunal and rectal adenocarcinoma or villous atrophy of the small intestine without any evidence for increased serum glucagon levels.
  • In this context we report the case of an 85-year-old male with myelodysplastic syndrome who developed typical necrolytic migratory erythema without glucagonoma syndrome or evidence for other pancreatic or liver disease.
  • We suggest that, in addition to the diseases listed, myelodysplastic syndrome might be able to cause necrolytic migratory erythema.
  • [MeSH-major] Erythema / complications. Glucagonoma / complications. Myelodysplastic Syndromes / complications. Pancreatic Neoplasms / complications. Paraneoplastic Syndromes / complications


13. Werther M, Schmelz HU, Schwerer M, Sparwasser C: [Sclerosing Sertoli cell tumor of the testis: a rare tumor. Case report and review of the literature on the subtypes of Sertoli-cell tumor]. Urologe A; 2007 Nov;46(11):1551-6
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  • [Title] [Sclerosing Sertoli cell tumor of the testis: a rare tumor. Case report and review of the literature on the subtypes of Sertoli-cell tumor].
  • [Transliterated title] Sklerosierender Sertoli-Zell-Tumor des Hodens - ein seltener Tumor : Fallvorstellung und Literaturübersicht über die Subtypen des Sertoli-Zell-Tumors.
  • Sertoli cell tumors of the testis are extremely rare (0.4-1.5% of all testicular neoplasms) and have a heterogeneous pathology.
  • Histopathologically classic, large cell calcifying and sclerosing subtypes are differentiated.Up to now, 14 cases of sclerosing Sertoli cell tumor are known.
  • While no cases of sclerosing Sertoli cell tumor with a malignant course have been reported, both other subtypes have been found to be potentially malignant.
  • In the case of malignancy the prognosis is very poor, and it is difficult to select the best treatment because there is so little experience with this type of tumor.
  • Once the diagnosis of a Sertoli cell tumor has been confirmed, exact determination of the histological subtype is essential to allow appropriate risk-adapted therapy.
  • [MeSH-major] Sertoli Cell Tumor / diagnosis. Testicular Neoplasms / diagnosis
  • [MeSH-minor] Adult. Biomarkers, Tumor / blood. Biopsy. Diagnosis, Differential. Fatty Liver, Alcoholic / blood. Humans. Male. Neoplasm Staging. Sclerosis. Testis / pathology. Ultrasonography. alpha-Fetoproteins

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  • [Cites] J Surg Oncol. 1990 Jun;44(2):129-31 [2355742.001]
  • [Cites] Cancer. 2003 Aug 15;98(4):753-7 [12910519.001]
  • [Cites] J Coll Physicians Surg Pak. 2005 Jul;15(7):437-8 [16197877.001]
  • [Cites] AJR Am J Roentgenol. 1994 Aug;163(2):373-5 [8037034.001]
  • [Cites] Medicine (Baltimore). 1985 Jul;64(4):270-83 [4010501.001]
  • [Cites] Am J Surg Pathol. 1998 Jun;22(6):709-21 [9630178.001]
  • [Cites] Urol Int. 2005;75(4):365-7 [16327308.001]
  • [Cites] Am J Surg Pathol. 1995 Jan;19(1):50-8 [7802138.001]
  • [Cites] Int Urol Nephrol. 2003;35(4):515-6 [15198158.001]
  • [Cites] Scand J Urol Nephrol. 1999 Jun;33(3):197-9 [10452297.001]
  • [Cites] J Am Osteopath Assoc. 1996 Oct;96(10):612-4 [8936931.001]
  • [Cites] Am J Surg Pathol. 1997 Nov;21(11):1271-80 [9351565.001]
  • [Cites] Br J Urol. 1988 May;61(5):456-7 [3134972.001]
  • [Cites] J Urol. 1995 Nov;154(5):1756-8 [7563340.001]
  • [Cites] Urol Int. 2003;70(3):205-10 [12660458.001]
  • [Cites] Acta Oncol. 1990;29(7):946-9 [2261213.001]
  • [Cites] Am J Surg Pathol. 1991 Sep;15(9):829-34 [1719830.001]
  • [Cites] Histopathology. 1995 Mar;26(3):255-9 [7541015.001]
  • (PMID = 17898983.001).
  • [ISSN] 0340-2592
  • [Journal-full-title] Der Urologe. Ausg. A
  • [ISO-abbreviation] Urologe A
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / alpha-Fetoproteins
  • [Number-of-references] 20
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14. Székelyhidi Z, Pató J, Hegymegi-Barakonyi B, Bánhegyi P, Mészáros G, Kéri G, Orfi L: [Synthesis of thiophene and alpha-terthiophene derivatives with antiproliferative activity]. Acta Pharm Hung; 2005;75(4):185-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Synthesis of thiophene and alpha-terthiophene derivatives with antiproliferative activity].
  • [Transliterated title] Antiproliferatív hatású tiofén es alpha-tertiofénszármazékok eloállítása.
  • We have synthesised a series of known alpha-terthiophene lead molecules with PKC (protein kinase C) inhibitory activity and the compounds were tested in cell proliferation assay on EGF-RTK (epidermal growth factor receptor protein tyrosine kinase) over-expressing tumour cell line (A431).
  • We prepared a focused molecule library around the thiophene and the terthiophene scaffold and examined these compounds in cell proliferation assay on A431.
  • [MeSH-major] Anti-Infective Agents / pharmacology. Cell Division / drug effects. Thiophenes / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Humans. Protein Kinase C / antagonists & inhibitors. Receptor, Epidermal Growth Factor / antagonists & inhibitors

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  • (PMID = 16711395.001).
  • [ISSN] 0001-6659
  • [Journal-full-title] Acta pharmaceutica Hungarica
  • [ISO-abbreviation] Acta Pharm Hung
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Enzyme Inhibitors; 0 / Thiophenes; 0P77RAU2RR / alpha-terthienyl; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.13 / Protein Kinase C
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15. Heinrich MC, Carden R, Griffith D, Liang C, Marino-Enriquez A, McKinley A, Presnell A, Fletcher JA: In vitro activity of sorafenib against imatinib- and sunitinib-resistant kinase mutations associated with drug-resistant GI stromal tumors. J Clin Oncol; 2009 May 20;27(15_suppl):10500

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro activity of sorafenib against imatinib- and sunitinib-resistant kinase mutations associated with drug-resistant GI stromal tumors.
  • : 10500 Background: Most gastrointestinal stromal tumors (GISTs) harbor mutant KIT or platelet-derived growth factor receptor alpha (PDGFRA) kinases, which are targets of imatinib (front-line therapy) or sunitinib (second-line therapy).
  • METHODS: Kinase mutants were biochemically profiled for SOR, SU, and IM sensitivity by measuring inhibition of kinase phosphorylation after drug treatment in mutant-expressing CHO cells.
  • We also tested the biochemical and cellular activity of SOR and IM against GIST cells derived from IM-resistant tumor clones.
  • To confirm these observations in a GIST cellular context, we tested the relative potency of IM and SU against two previously described IM-resistant GIST cell lines (GIST430: exon 11 + V654A, GIST48: exon 11 + D820A).
  • SOR was significantly more potent than IM against KIT in these cell lines.

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  • (PMID = 27963686.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Seto T, Yamanaka T, Masuda N, Eguchi K, Takiguchi Y, Okamoto H, Ogura T, Yokoyama A, Ichinose Y, Watanabe K, Thoracic Oncology Research Group: Topoisomerase II, carbonyl reductase I, and chemosensitivity for amrubicin in the treatment of patients with small-cell lung cancer. J Clin Oncol; 2009 May 20;27(15_suppl):8104

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Topoisomerase II, carbonyl reductase I, and chemosensitivity for amrubicin in the treatment of patients with small-cell lung cancer.
  • : 8104 Background: Amrubicin (AMR) has been suggested to provide a new effective therapeutic option for small-cell lung cancer (SCLC).
  • We previously reported the promising result of a prospective phase II trial for AMR monotherapy in patients with second-line SCLC (Thoracic Oncology Research Group Study 0301).
  • Quantification of target cDNA (Top-II alpha, CBR-I and beta-actin gene) was conducted using an ABI PRISM 7700 Sequence Detection System (Applied Biosystems Inc.).
  • Patients with tumor response had a significantly lower Topo-II level than those without (p=0.0465, Wilcoxon test), although there was no association between tumor response and the level of CBR-I (p=0.3229, Wilcoxon test).

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  • (PMID = 27964278.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Phuphanich S, Rudnick J, Chu R, Mazer M, Wang H, Serrano N, Francisco M, Wheeler C, Singh M, Yu JS: A phase I trial of tumor-associated antigen-pulsed dendritic cell immunotherapy for patients with brain stem glioma and glioblastoma. J Clin Oncol; 2009 May 20;27(15_suppl):2032

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I trial of tumor-associated antigen-pulsed dendritic cell immunotherapy for patients with brain stem glioma and glioblastoma.
  • 2001;61:842-7 and 2004;64;4973-9) have demonstrated efficacy in generating a tumor specific immune response.
  • METHODS: The goal of this study is to use tumor associated antigens (TAA) known to be expressed on gliomas and pulse dendritic cells with these antigens in an MHC compatible fashion using epitopes of HER-2, TRP-2, gp100, MAGE-1, IL13R alpha, and AIM-3.
  • Leukapheresis was used to isolate mononuclear cells which were differentiated into dendritic cells in culture, pulsed with tumor peptide, and then administered intradermally three times at 2-week intervals.
  • Our data on 19 patients and 54 courses of dendritic cell vaccines demonstrate zero grade 3 /4 toxicities that were attributable to the vaccination.
  • Thirteen patients continue to have stable disease (ranging from 15 to 115 weeks), six patients have demonstrated tumor progression.
  • Of 15 patients tested to date, six patients demonstrated an antigen-specific cytotoxic T-cell response to at least one antigen after vaccination.
  • Only 17% of CTL responders (1/6) demonstrated tumor progression compared to 56% (5/9) of nonresponders to date.
  • CONCLUSIONS: This phase I study demonstrated the feasibility, safety, and bioactivity of a TAA-pulsed dendritic cell vaccine for patients with glioblastoma progression free survival correlated with CTL response.

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  • (PMID = 27964632.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Jha MN, Bedford JS, Jha S, Prasad K: Effect of caffeine treatment on low-dose γ- irradiation-induced chromatid-type aberrations in human leukemia cells and human normal fibroblast cells in culture. J Clin Oncol; 2009 May 20;27(15_suppl):e22113

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of caffeine treatment on low-dose γ- irradiation-induced chromatid-type aberrations in human leukemia cells and human normal fibroblast cells in culture.
  • We investigated the effects of caffeine on low dose- gamma-radiation-induced chromosomal damage in human T leukemia cells (Jurket T-cells) and two normal human fibroblast cell lines (AG1522 and GM 2149).
  • METHOD: Jurkat cells were maintained in RPMI 1640 medium and fibroblast in alpha-minimal essential medium (MEM) All cells were incubated at 37o C in a humidified atmosphere of 5% CO2 in air.
  • Cells from the exponential phase were treated with 1 mg/ml caffeine ( control cells received same amount of solvent) and irradiated with low doses (3, 5, 10, 20 and 40 cGy,), using a 137 Cs-gamma radiation source.
  • Cells were fixed in methanol: acetic acid solution and stained with Giemsa.
  • 100 irradiated and un-irradiated metaphase- like cells were scored for chromatid-type aberrations.
  • RESULTS: Low dose gamma-radiation increased the levels of chromatid breaks(dose dependent) in both normal and cancer cells; however, cancer cells appeared to be more sensitive than the normal cells.
  • Caffeine treatment markedly increased chromatid aberrations in Jurkat T-cells at all radiation doses but not in normal cells.
  • Previously, we reported that caffeine eliminates gamma-ray-induced G2 delay in other human tumor cells but not normal cells (Jha, et.al., Radiat. Res.
  • CONCLUSIONS: The mechanisms that may underlie this differential effect of caffeine in cancer and normal cells are unknown, but if one result of a G2 delay is to allow more time for chromosome breakage rejoining processes to occur, then elimination of this delay by caffeine in tumor cells but not normal cells might account for the difference.
  • To the extent these observations are generally true for tumor vs normal cells, the differential sensitization could have an impact in improving the efficacy of radiation therapy.

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  • (PMID = 27963510.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Wagner AJ, Von Hoff DH, LoRusso PM, Tibes R, Mazina KE, Ware JA, Yan Y, Derynck MK, Demetri GD: A first-in-human phase I study to evaluate the pan-PI3K inhibitor GDC-0941 administered QD or BID in patients with advanced solid tumors. J Clin Oncol; 2009 May 20;27(15_suppl):3501

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A first-in-human phase I study to evaluate the pan-PI3K inhibitor GDC-0941 administered QD or BID in patients with advanced solid tumors.
  • GDC-0941 is a potent and selective oral inhibitor of the class I PI3K with 3 nM IC50 for the p110-alpha subunit in vitro and 28 nM IC50 in a cell-based pAKT assay and demonstrates broad activity in breast, ovarian, lung, and prostate cancer models.
  • METHODS: A Phase I dose escalation study using a 3+3 design was initiated in patients (pts) with solid tumors.
  • Potential signs of anti-tumor activity have been observed with a soft tissue sarcoma pt on-study for >176 days with stable disease (30 mg qd), an ovarian cancer pt with an on-study 2.8-fold decrease in CA-125 response to normal levels (30 mg bid) and a pt with endometrial cancer with a decrease in tumor FDG-PET uptake (80 mg qd).
  • CONCLUSIONS: GDC-0941 is generally well-tolerated with potential signs of anti-tumor activity.

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  • (PMID = 27961289.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Boyle H, You B, Fronton L, Ribba B, Girard P, Tranchand B, Tod M, Coquelin H, Droz J, Flechon A: Major prognostic value of modeled AUC<sub>hCG-AFP</sub>, a dynamic kinetic marker characterizing tumor marker decline of nonseminomatous germ cell tumors (NSGCT) intermediate-poor-risk patients according to the IGCCCG. J Clin Oncol; 2009 May 20;27(15_suppl):5085

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Major prognostic value of modeled AUC<sub>hCG-AFP</sub>, a dynamic kinetic marker characterizing tumor marker decline of nonseminomatous germ cell tumors (NSGCT) intermediate-poor-risk patients according to the IGCCCG.
  • : 5085 Background: The level of human chorionic gonadotrophin (hCG) and alpha-foetoprotein (AFP) serum tumor marker is well established in NSGCT as prognostic factor, the relevance of marker kinetic analysis under treatment is still unclear.
  • AUC<sub>hCG-AFP</sub> was a significant prognostic factor in the univariate analysis on the 2 year PFS (100% vs 73.8% vs 67.7%, p = 0.035) as well as IGCCCG score (poor/intermediate risk groups), primary site (mediastinal/other) and HL<sub>hCG-AFP</sub>.

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  • (PMID = 27964275.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Ung Y, Sun A, MacRae R, Gu C, Wright J, Yu E, Darling G, Leighl N, Evans W, Levine M: Impact of positron emission tomography (PET) in stage III non-small cell lung cancer (NSCLC): A prospective randomized trial (PET START). J Clin Oncol; 2009 May 20;27(15_suppl):7548

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of positron emission tomography (PET) in stage III non-small cell lung cancer (NSCLC): A prospective randomized trial (PET START).
  • The use of PET-CT rather than conventional imaging (CI) may better identify patients for CMT by enhanced tumor staging and improved definition of RT treatment volumes.
  • The primary outcome was the proportion of patients who did not receive CMT because their tumor was upstaged to Stage 4 or their intrathoracic tumor was too extensive for radical RT.
  • Target sample size was 400 patients based on a hazard rate reduction of 30% in OS at 2 years in favor of PET-CT with 2-sided alpha = 0.05 and 80% power.

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  • (PMID = 27963324.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Kamai T, Tomosugi N, Abe H, Yoshida K: Protein profiling of tumor tissues by surface-enhanced laser desorption/ionization time-of-flight mass spectrometry to discriminate between localized and metastatic renal cell carcinoma. J Clin Oncol; 2009 May 20;27(15_suppl):e16098

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Protein profiling of tumor tissues by surface-enhanced laser desorption/ionization time-of-flight mass spectrometry to discriminate between localized and metastatic renal cell carcinoma.
  • : e16098 Background: We previously reported that mRNA of interferon-alpha receptor type 2 (IFNAR2) was upregulated in metastatic and IFN-a resistant renal cell carcinoma (RCC) in comparison to localized RCC or metastatic tumors with good response to IFN-a (BMC Cancer, 2007).
  • Protein profiling using human tumor tissues may give insight into cellular pathways leading to carcinogenesis and metastasis in RCC.
  • METHODS: We examined mRNAs expression for IFNAR2 in paired tumor and non-tumor samples from the surgical specimens of Japanese patients with RCC using a real-time reverse transcription polymerase chain reaction.
  • Then we selected representative five IFNAR2 upregulated clear cell carcinomas cases with metastatic tumor, five IFNAR2 upregulated metastatic sarcomatoid carcinomas, and five normal expression clear cell carcinomas with localized tumor.
  • We investigated protein profiling in the tumor tissues of above three groups using surface-enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF MS) coupled with IMAC-Cu chips.
  • The heat map analysis based on the clustering distinguished completely metastatic tumors with IFNAR2 upregulated groups from localized tumors with IFNAR2 normal expression group.
  • Furthermore, the heat map discriminated metastatic sarcomatoid carcinomas from metastatic clear cell carcinomas with a sensitivity of 100% and a specificity of 80%.
  • CONCLUSIONS: SELDI-TOF MS profiling of tumor tissues can be applied to differentiate patients with three types of RCCs.

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  • (PMID = 27963090.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Nortier JW, Ogilvie A: A phase II study of early up-front red blood cell transfusion followed by maintenance epoetin-alpha subcutaneously support during chemotherapy. J Clin Oncol; 2009 May 20;27(15_suppl):e20719

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study of early up-front red blood cell transfusion followed by maintenance epoetin-alpha subcutaneously support during chemotherapy.
  • : e20719 Background: To determine in patients with cancer related anaemia (Hb<11,3 g/d) starting with their chemotherapy the efficacy and safety of up-front red blood cell transfusion and subsequently maintenance epoetin-alpha (Epo) administration.
  • The study target was the range of low-normal Hb levels of 11,3 to 12,9 g/dL aiming at improving tumor oxygenation.
  • An intention-to-treatment analysis was performed for the primary objectives in 16 patients (8 with breast-, 4 with colorectal-, 1 with ovarian- and 1 with pancreatic cancer) and reported here.
  • Grade 3/4 adverse events and serious adverse events that occurred were found to be all chemotherapy or progressive disease related.
  • This was presumably related to the lesser than projected yield of the red blood cell transfusion.

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  • (PMID = 27962027.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Lopez R, Gallardo E, Ruibal A, Leon L, Sanchez-Salmon A, Abdulkader I, Gude F, Curiel T, Barandela J, Gayoso L: HIF expression and Max-SUV-18F-FDG-PET in non-small cell lung cancer (NSCLC) patients. J Clin Oncol; 2009 May 20;27(15_suppl):e22010

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HIF expression and Max-SUV-18F-FDG-PET in non-small cell lung cancer (NSCLC) patients.
  • : e22010 Background: Tumor hipoxia induces the up-regulation of several genes via the hipoxia-inducible transcription factors (HIF) 1 and 2.
  • HIF-2 alpha (HIF-2 α) and HIF-1 alpha (HIF-1α) are associated with the prognosis of operable NSCLC patients.
  • Sections were scored as positive if >10% of cells stained positively.
  • RESULTS: HIF- 1α expression was observed in 84/96 patients (34/39 adenocarcinomas and 50/57 squamous cell carcinomas), however it did not correlate with clinical stage (I-II: 41/45 vs III-IV: 44/51).
  • The maxSUV values of 18F-FDG-PET were higher (p:0,039) in HIF-1α -positive (17,1±8,6) than in negative tumors (11,8±4,4).
  • HIF-2 α expression was observed in 60/103 cases (27/42 adenocarcinomas and 33/61 squamous cell carcinomas) and it did not correlate with clinical stage ((I-II: 28/45 vs III-IV: 32/57).

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  • (PMID = 27963184.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Schwandt A, Garcia JA, Elson P, Wyckhouse J, Finke JH, Ireland J, Triozzi P, Zhou M, Dreicer R, Rini BI: A translational phase II trial of celecoxib plus interferon-alpha (IFN-α2b) in metastatic renal cell carcinoma (RCC) patients (pts) with 3+ COX-2 tumor immunostaining. J Clin Oncol; 2009 May 20;27(15_suppl):5116

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A translational phase II trial of celecoxib plus interferon-alpha (IFN-α2b) in metastatic renal cell carcinoma (RCC) patients (pts) with 3+ COX-2 tumor immunostaining.
  • : 5116 Background: Cyclooxygenase-2 (COX-2) has been correlated with RCC stage and grade, and overexpression can lead to dysregulation of dendritic cells (DC) and CD4+/CD25+/FOXP3+ regulatory T cells (Treg).
  • 2006) demonstrated an association between more intense COX-2 RCC tumor staining and clinical response.
  • METHODS: Pts with cytokine-naïve mRCC with at least 10% maximal COX-2 tumor staining received IFNα2b MU five times/week plus celecoxib 400 mg BID continuously.
  • Baseline tumor tissue was stained for COX-2, CD4+ and CD8+ T cells, Treg and DC (s100 and CD208).
  • Peripheral blood prostaglandin E2 (PGE2), DC and Treg number/function and intracellular T cell cytokine production were measured at baseline, at the end of cycles 2 and 4 and at end of treatment.
  • The trial tested a null hypothesis of ORR <20% vs. alternative hypothesis of ORR >40%; beta = 0.8 and alpha = 0.05 (n = 34).
  • The ORR was 21% and 69% of pts experienced tumor shrinkage.
  • Baseline 3+ COX-2 staining was associated with elevated peripheral blood PGE2 levels (p = 0.02), reduced DC IL-12 expression (p = 0.04) and reduction in IFN gamma-producing CD3+CD4+ T-cells (p = 0.04) compared to a control group of RCC pts with <10% 3+ COX-2 staining (n = 21).
  • No significant changes in immunomodulatory cells were observed with therapy.
  • COX-2 RCC tumor expression promotes an immunosuppressive phenotype.

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  • (PMID = 27964389.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Sumiyoshi Y, Hashine K, Niwakawa M, Yamaguchi R, Fujii H, Hamamoto Y, Fukino K: Phase I trial of sorafenib in combination with interferon-alpha in Japanese patients with unresectable or metastatic renal cell carcinoma. J Clin Oncol; 2009 May 20;27(15_suppl):e16107

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trial of sorafenib in combination with interferon-alpha in Japanese patients with unresectable or metastatic renal cell carcinoma.
  • Interferon-α (IFN) is most commonly used for metastatic renal cell carcinoma (RCC) in Japan.
  • In this phase I study, we investigated the safety profile, pharmacokinetics (PK), and tumor response of SOR/(recombinant)IFN combination in Japanese patients (pts) with RCC.
  • Objectives were safety/tolerability and recommended dose of SOR/IFN as primary, and tumor response and PK as secondary.

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  • (PMID = 27963330.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Warren GW, Kudrimoti M, McGarry R, Arnold S, Rangnekar V: Mechanisms of nicotine-induced resistance to treatment with chemotherapy and radiotherapy. J Clin Oncol; 2009 May 20;27(15_suppl):e22008

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e22008 Background: Nicotine (NIC), used for smoking cessation in cancer patients, is associated with increased tumor growth, angiogenesis, migration, invasion, growth factor production, and inhibition of apoptosis.
  • METHODS: A review of the literature produced a construct demonstrating that NIC generates more than 100 interactions with 40 proteins involved in tumor promotion and progression.
  • The effect of NIC on cell proliferation, cell survival, and protein activation was analyzed following CT, XRT, or chemoradiotherapy (CRT) in FaDu, A549, and H460 human cancer cell lines.
  • NIC administration increased cell survival (colony survival) following XRT and following CT (cisplatin, doxorubicin, or etoposide) regimens in all cell lines. nAChR expression was verified in each cell line using Western blot.
  • Non-specific inhibition of nAChR demonstrated no consistent effect on preventing NIC induced resistance to CT, XRT, or CRT; however, specific inhibition of the alpha-3- or alpha-7-nAChR had variable cell specific ability to prevent NIC induced resistance.
  • Inhibition of MAPK activity (using PD98059) produced marked reduction in proliferation of all cell lines, but generally had no effect on NIC induced resistance.

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  • (PMID = 27963179.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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28. Overgaard J Sr, Hoff CM, Hansen HS, Specht L, Overgaard M, Grau C, Andersen E, Johansen J, Andersen LJ, Evensen JF, Danish Head and Neck Cancer Group (DAHANCA): Randomized study of darbepoetin alfa as modifier of radiotherapy in patients with primary squamous cell carcinoma of the head and neck (HNSCC): Final outcome of the DAHANCA 10 trial. J Clin Oncol; 2009 May 20;27(15_suppl):6007

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Randomized study of darbepoetin alfa as modifier of radiotherapy in patients with primary squamous cell carcinoma of the head and neck (HNSCC): Final outcome of the DAHANCA 10 trial.
  • : 6007 Background: The study aimed to evaluate if correction of low hemoglobin (Hb) levels by means of the erythropoietin stimulating agent: darbepoetin alpha (Aranesp) during radiotherapy (RT) improves outcome in patients with HNSCC.
  • METHODS: Pts with HNSCC eligible for primary RT alone and with Hb values below 14.0 g/dl were randomized to receive Aranesp together with accelerated fractionated RT. Pts. were stratified according to gender, T and N staging, tumor site, and institution.
  • RESULTS: In total, 522 patients (of a planned intake of 600) were included at the time of the interim analysis.
  • The patients were evenly distributed according to the stratification parameters (gender, T and N staging, tumor site, institution).Aranesp resulted in the expected increase in Hb in more than 81% of the patients.
  • This was also seen for the endpoint of disease-free survival (37% vs. 47%, p = 0.02, RR: 1.32 [1.04-1.68]), whereas there was no significant difference in overall survival (40% vs. 51%, p = 0.16, RR: 1.20 [0.93-1.55]).
  • CONCLUSIONS: Correction of the Hb level with Aranesp in patients with HNSCC resulted in a significantly poorer tumor control after radiotherapy.

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  • (PMID = 27962413.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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29. Amato R, Hernandez-McClain J, Harrop R, Cen P, Doshi G: Vaccination of renal cell cancer (RCC) patients with modified vaccinia Ankara (MVA) delivering tumor antigen 5T4 administered alone or with interleukin 2 (IL-2) or interferon-alpha (IFN). J Clin Oncol; 2009 May 20;27(15_suppl):3026

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vaccination of renal cell cancer (RCC) patients with modified vaccinia Ankara (MVA) delivering tumor antigen 5T4 administered alone or with interleukin 2 (IL-2) or interferon-alpha (IFN).
  • : 3026 Background: The attenuated vaccinia virus (MVA) has been engineered to deliver the tumor antigen 5T4 (TroVax).
  • METHODS: Eligibility: Pathologic diagnosis of clear cell or papillary RCC, progressive measurable metastases, any prior therapy, adequate physiological parameters, Karnofsky performance status ≥ 80%, and no active CNS involvement.
  • Clinical responses were assessed by measuring changes in tumor burden via computed tomography or magnetic resonance imaging scan.
  • 20 pts demonstrated disease stabilization for ≥ 3 months.

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  • (PMID = 27962068.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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30. Massard C, Huguet H, Kramar A, Beyer J, Hartmann JT, Lorch A, Pico J, Rosti G, Droz J, Fizazi K: Cross-validation of a new prognostic index integrating tumor marker decline in patients with relapsed disseminated germ cell tumors. J Clin Oncol; 2009 May 20;27(15_suppl):5086

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cross-validation of a new prognostic index integrating tumor marker decline in patients with relapsed disseminated germ cell tumors.
  • : 5086 Background: Early serum tumor marker decline during chemotherapy was previously shown to be prognostic for progression-free survival (PFS) and overall survival (OS) in patients with relapsed GCT in an analysis of the IT94 phase III trial, which compared conventional chemotherapy versus high dose chemotherapy (Massard C, ASCO 2008.
  • METHODS: Data on tumor site, response to first line chemotherapy, serum tumor markers at baseline and after two cycles of chemotherapy were obtained from 235 patients accrued in the IT94 trial (training set) and from 181 patients included in phase III prospective trials of high-dose chemotherapy conducted by the German GCT group (Lorch et al, J Clin Oncol.
  • The change from baseline of serum alpha-fetoprotein (AFP) and human chorionic gonadotropin (hCG) was assessed and classified into 'favorable marker decline' and 'unfavorable marker decline' group, as previously described (ASCO 2008.
  • In multivariate analysis of the IT94 trial, an unfavorable AFP decline and a mediastinal primary site were adverse prognostic factors for both PFS and OS, and this was confirmed in the validation set.
  • Among patients from the good prognostic group (favorable AFP decline and non-mediastinal primary site), those who were treated with high-dose chemotherapy had a better PFS (2-year PFS rate: 54% vs 37%; HR = 0.62; p = 0.017), and a trend for a better OS (2-year OS rate: 68% vs. 58%; HR = 0.77; p = 0.29) as compared to patients who were treated with conventional chemotherapy.
  • In contrast, there was no difference in outcome in patients from the poor prognostic group (unfavourable AFP decline and/or mediastinal primary site), whether they received conventional chemotherapy or high-dose chemotherapy.
  • CONCLUSIONS: AFP decline during the first 6 weeks of salvage chemotherapy and a mediastinal primary tumor site predict for PFS and OS in patients with relapsed disseminated GCT.

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  • (PMID = 27964274.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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31. Kuhberg M Sr, Skowronek P, Chen F, Oskay-Oezcelik G, Oskay-Oezcelik G, Lichtenegger W, Lichtenegger W, Sehouli J: Prediction of nutritional status and intestinal tumor involvement in patients with primary or recurrent ovarian cancer: Results of a prospective study. J Clin Oncol; 2009 May 20;27(15_suppl):5570

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prediction of nutritional status and intestinal tumor involvement in patients with primary or recurrent ovarian cancer: Results of a prospective study.
  • 79 (52%) of them had primary and 73 (48%) recurrent disease.
  • At the time of admission for surgical therapy, the body composition was analysed with Bioelectrical Impedance Analysis (BIA) using phase angle alpha and ratio of extra-cellular mass and body cell mass (ECM/BCM).
  • During operation a standardised and validated tumor documentation tool (IMO) was performed.
  • FIGO stage and NRS correlated negatively with phase angle alpha and positively with ECM/BCM in patients with primary diagnosis (p < 0.05).
  • Patients with primary or recurrent disease who required surgical resection of small or large intestine, phase angle alpha and serum albumin level were significantly lower than in patients with no intestinal involvement (p < 0.05).
  • CONCLUSIONS: Independent of tumor stage, the preoperative evaluation of BIA, especially phase angle α, is a valid method to predict surgical outcome in patients with ovarian and peritoneal cancer.

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  • (PMID = 27962572.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Pollak MN, Blouin M, Zakikhani M, Zhao Y, Algire C: Dependence of malignant proliferation associated with loss of PTEN on glucose concentration in the hyperglycemic range: Relevance to population studies linking hyperglycemia to unfavorable cancer prognosis. J Clin Oncol; 2009 May 20;27(15_suppl):11113

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 11113 Background: Loss of function of the tumor suppressor PTEN enhances malignant proliferation, but effects on cellular energy metabolism are less well characterized.
  • Population studies show that the metabolic syndrome (characterized by hyperglycemia, hyperinsulinism, and obesity) is increasingly prevalent in affluent societies and is associated with adverse outcome of many cancers, but the molecular basis for this is poorly understood.
  • METHODS: We used a tetracycline-inducible PTEN expression vector in the PTEN-null U251 glioma cell line to characterize effects of PTEN on cellular energy metabolism.
  • RESULTS: Forced expression of PTEN led to decreased phospho-AKT<sup>Ser473</sup>, decreased hexokinase II and HIF-1 alpha levels, and increased p53 levels.
  • While proliferation of PTEN-positive cells was insensitive to variation in glucose concentration at levels higher than 2.5 mM, PTEN-null cells significantly increased proliferation with increasing glucose concentration across normal physiologic range to ∼10 mM.
  • PTEN-null cells consumed more glucose than PTEN-positive cells (17.2 ± 2.0 vs. 8.8 ± 1.5 mM/million cells/48 hrs) and produced more lactate (35.9 ± 4.8 vs. 10.7 ± 2.3 mM/million cells/48 hrs).
  • When cells were incubated in presence of 2-deoxy-glucose (2-DG), growth inhibition was greater for PTEN-null cells (47.4% inhibition relative to control without 2-DG) compared with PTEN-positive cells (10.8% inhibition relative to control without 2-DG).
  • The data also suggest that PTEN status is relevant to selection of tumors likely to respond to experimental therapies that exploit glucose dependency.

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  • (PMID = 27963493.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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33. Irigoyen A, Olmedo C, Valdivia J, Comino A, Cano C, Luque R, Conde V, Delgado J, Blanco A, Bueno P: Microarray study of gene expression profiles in peripheral blood samples from lung cancer patients before and after erlotinib treatment. J Clin Oncol; 2009 May 20;27(15_suppl):e19072

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Before treatment (T0) when patients were compared to healthy volunteers there was an increase in the expression of: histone 1 H4c, transforming growth factor beta 2, endothelial cell growth factor 1 (platelet-derived), glucose-6-phosphatase catalytic 2, Relaxin 3 receptor 1, Insulin-like growth factor binding protein 2, RAS-like family 11 member B, and ELK4.
  • After treatment (T15d), when each lung cancer patient's results were compared to their own before treatment results (T0), there was an increase in the expression of: Bcl2, myosin light polypeptide 4; interferon alpha-inducible protein 27; interferon gamma receptor 1; RASSF5, ARHGEF6, IGFBP5, tumor protein p53 inducible nuclear protein 1, peroxisome proliferative activated receptor gamma.

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  • (PMID = 27962211.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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34. Olszanecka-Glinianowicz M, Zahorska-Markiewicz B, Zurakowski A, Glinianowicz M: [The role of tumor necrosis factor (TNF-alpha) in control of metabolism]. Wiad Lek; 2005;58(11-12):670-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The role of tumor necrosis factor (TNF-alpha) in control of metabolism].
  • [Transliterated title] Rola czynnika martwicy nowotworów (TNF-alpha) w kontroli metabolizmu.
  • Tumor necrosis factor is multifunctional cytokine involved in various cell functions, such as differentiation, mitosis, angiogenesis, inflammation and immune controls.
  • TNF-alpha plays also an important role in the control of metabolism.
  • The review of the current literature on the TNF-alpha role in metabolism is presented in this paper.
  • [MeSH-major] Tumor Necrosis Factor-alpha / physiology

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  • (PMID = 16594480.001).
  • [ISSN] 0043-5147
  • [Journal-full-title] Wiadomości lekarskie (Warsaw, Poland : 1960)
  • [ISO-abbreviation] Wiad. Lek.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Fatty Acids, Nonesterified; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 35
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35. Cruz-Bautista I, Lerman I, Perez-Enriquez B, Padilla LS, Torres CL, Lopez A, Cabrera T, Mehta RP, Gómez-Pérez FJ, Rull JA, Orozco-Topete R: Diagnostic challenge of glucagonoma: case report and literature review. Endocr Pract; 2006 Jul-Aug;12(4):422-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnostic challenge of glucagonoma: case report and literature review.
  • OBJECTIVE: To report the diagnostic difficulties encountered in a case of glucagonoma.
  • METHODS: We provide a literature review and present the clinical findings, pertinent laboratory data, and results of related studies in a patient with a glucagonoma.
  • The patient was hospitalized, and because of the dermatologic findings suggestive of necrolytic migratory erythema, the presence of a glucagonoma was suspected.
  • Glucagon levels were found to be elevated, and imaging studies confirmed the presence of an enlarged mass in the pancreatic tail, without evidence of extension to surrounding structures.
  • After surgical removal of the tumor, the skin and oral mucosal lesions disappeared spontaneously.
  • The histologic appearance and immunohistochemical staining results confirmed the diagnosis of a glucagonoma.
  • Subsequently, all related symptoms resolved, and the glucagon levels normalized.
  • CONCLUSION: The diagnosis of glucagonoma is often delayed.
  • Clinicians should be aware of the unusual initial manifestations of this tumor and the potential for less than a full spectrum of the characteristic features of the glucagonoma syndrome.
  • [MeSH-major] Glucagonoma / diagnosis
  • [MeSH-minor] Erythema / etiology. Humans. Hyperpigmentation / etiology. Male. Middle Aged. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / ultrasonography. Pancreatic Neoplasms / ultrastructure. Regional Blood Flow. Tomography, X-Ray Computed. Wound Healing

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  • (PMID = 16901799.001).
  • [ISSN] 1530-891X
  • [Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
  • [ISO-abbreviation] Endocr Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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36. Mutschler J, Steinbach G, Bunjes D, Reske SN, Buchmann I: [Myeloablative radioimmunotherapy with 188Re-CD66mAb before stem cell transplantation. No increase of proinflammatory cytokine levels of TNF-alpha]. Nuklearmedizin; 2009;48(1):30-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Myeloablative radioimmunotherapy with 188Re-CD66mAb before stem cell transplantation. No increase of proinflammatory cytokine levels of TNF-alpha].
  • [Transliterated title] Myeloablative Radioimmuntherapie mit 188Re-CD66mAb vor Stammzelltransplantation: Kein Anstieg proinflammatorischer Zytokinspiegel von TNF-alpha.
  • AIM: Tumour necrosis factor-alpha (TNF-alpha) serum levels may increase due to intensive conditioning regimes with high-dose-chemotherapy and total body irradiation (TBI) before stem cell transplantation.
  • This increases the risk for developing acute graft versus host disease (aGvHD) after stem cell transplantation.
  • In this prospective study we investigated the influence of radioimmunotherapy with 188Re-CD-66-mAb on changes on TNF-alpha serum levels.
  • PATIENTS, METHODS: In 18 patients we measured TNF-alpha before and up to 96 hours after radioimmunotherapy, in 2 patients in addition following TBI, in 9 patients also following chemotherapy.
  • For measuring TNF-alpha we used an automated immunochemiluminescence assay (Immulite 1000 DPC Biermann, Bad Nauheim).
  • The mean follow up period to record incidence of aGVHD was 100 days after stem cell transplantation.
  • RESULTS: Compared to the basal levels before, the levels of TNF-alpha after conditioning with 188Re-CD-66-mAb did not increase significantly and remained in the physiological range.
  • CONCLUSION: These results demonstrate that additional conditioning therapy with 188Re-CD-66-mAb does not increase proinflammatory cytokine levels of TNF-alpha.
  • This finding may indicate that additive radioimmunotherapy may not be a significant factor for increasing the rate of conditioning-associated aGvHD.
  • [MeSH-major] Leukemia, Myeloid, Acute / radiotherapy. Myelodysplastic Syndromes / radiotherapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy. Radioimmunotherapy / methods. Radioisotopes / therapeutic use. Rhenium / therapeutic use. Stem Cell Transplantation / methods. Tumor Necrosis Factor-alpha / blood
  • [MeSH-minor] Adult. Antibodies, Monoclonal / therapeutic use. Antigens, CD / immunology. Cell Adhesion Molecules / immunology. Child. Female. Humans. Male. Middle Aged. Young Adult

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  • (PMID = 19212609.001).
  • [ISSN] 0029-5566
  • [Journal-full-title] Nuklearmedizin. Nuclear medicine
  • [ISO-abbreviation] Nuklearmedizin
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / CD66 antigens; 0 / Cell Adhesion Molecules; 0 / Radioisotopes; 0 / Tumor Necrosis Factor-alpha; 7440-15-5 / Rhenium
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37. Gogacz M, Bogusiewicz M, Putowski L, Adamiak A, Wertel I, Jakowicki JA, Rechberger T: [Expression of tumor necrosis factor-alpha (TNF-alpha) on peritoneal fluid mononuclear cells in women with endometriosis]. Ginekol Pol; 2008 Jan;79(1):31-5
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of tumor necrosis factor-alpha (TNF-alpha) on peritoneal fluid mononuclear cells in women with endometriosis].
  • [Transliterated title] Ekspresja receptorów dla czynnika martwicy guza-alpha (TNF-alpha) na jednojadrzastych komórkach immunokompetentnych płynu otrzewnowego u kobiet z endometrioza.
  • OBJECTIVES: Tumor necrosis factor-alpha (TNF-alpha) plays a key role in the processes underlying the development of pelvic endometriosis.
  • TNF-alpha acts on target cells via two receptors: TNFR1(p55) and TNFR2(p75).
  • Depending on cell type and its activation state, ligand binding to TNF-alpha may induce activation and proliferation of the cells or promote apoptosis.
  • 14 patients with benign, non-inflammatory ovarian tumors composed the reference group.
  • Mononuclear cells have been isolated from peritoneal fluid, obtained during laparoscopy.
  • CONCLUSION: Higher percentage of peritoneal fluid macrophages expressing TNFR1 and TNFR2 proteins in endometriosis suggests dependence of these cells on TNF-alpha stimulation.
  • [MeSH-major] Ascitic Fluid / metabolism. Endometriosis / metabolism. Macrophages, Peritoneal / metabolism. Receptors, Tumor Necrosis Factor, Type I / metabolism. Receptors, Tumor Necrosis Factor, Type II / metabolism. T-Lymphocytes / metabolism

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  • (PMID = 18510047.001).
  • [ISSN] 0017-0011
  • [Journal-full-title] Ginekologia polska
  • [ISO-abbreviation] Ginekol. Pol.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II
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38. Oberkirchner U, Linder KE, Zadrozny L, Olivry T: Successful treatment of canine necrolytic migratory erythema (superficial necrolytic dermatitis) due to metastatic glucagonoma with octreotide. Vet Dermatol; 2010 Oct;21(5):510-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment of canine necrolytic migratory erythema (superficial necrolytic dermatitis) due to metastatic glucagonoma with octreotide.
  • Necrolytic migratory erythema (NME; also known as superficial necrolytic dermatitis) is a syndrome most often associated with certain chronic liver diseases or pancreatic glucagonomas.
  • In humans with glucagonoma-associated NME, skin lesions usually respond to octreotide, a somatostatin analogue that inhibits glucagon release.
  • In this report an 11-year-old golden retriever dog with pancreatic glucagonoma and metastasis to the regional lymph nodes, spleen and liver was diagnosed with NME.
  • The dog was later euthanized because of progressive metastatic disease.
  • In conclusion, subcutaneous octreotide injections were beneficial in this dog with glucagonoma-associated NME.
  • This somatostatin analogue could be a valuable option to treat canine patients with non-resectable or relapsing pancreatic glucagonoma-associated NME.
  • [MeSH-major] Dog Diseases / drug therapy. Glucagonoma / veterinary. Necrolytic Migratory Erythema / veterinary. Octreotide / therapeutic use. Pancreatic Neoplasms / veterinary
  • [MeSH-minor] Animals. Anorexia / chemically induced. Anorexia / veterinary. Antineoplastic Agents, Hormonal / administration & dosage. Antineoplastic Agents, Hormonal / adverse effects. Antineoplastic Agents, Hormonal / therapeutic use. Dogs. Dose-Response Relationship, Drug. Lymph Nodes / pathology. Male. Paraneoplastic Syndromes / pathology. Paraneoplastic Syndromes / veterinary

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  • [Copyright] © 2010 The Authors. Journal compilation © 2010 ESVD and ACVD.
  • (PMID = 20500495.001).
  • [ISSN] 1365-3164
  • [Journal-full-title] Veterinary dermatology
  • [ISO-abbreviation] Vet. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; RWM8CCW8GP / Octreotide
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39. Yu R, Nissen NN, Dhall D, Heaney AP: Nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas: review of the literature. Pancreas; 2008 May;36(4):428-31
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  • [Title] Nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas: review of the literature.
  • We report a rare case of nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas.
  • The patient's clinical presentation, diagnosis, treatment, pancreas pathology, and follow-up are reviewed.
  • A 60-year-old patient was incidentally found to harbor a pancreatic mass with markedly elevated glucagon levels but without glucagonoma syndrome.
  • She was initially diagnosed with glucagonoma, and the tumor was resected.
  • Pathological examination demonstrated that the tumor was a nonfunctioning islet cell tumor and revealed nesidioblastosis and hyperplasia of alpha cells and microglucagonoma in the apparently normal surgical margin.
  • No pancreatic tumors recurred 36 months after surgery.
  • This is the third case of alpha-cell nesidioblastosis reported in the English literature.
  • Nesidioblastosis and hyperplasia of alpha cells should be considered in the differential diagnosis of hyperglucagonemia.
  • Somatostatin analog may be used to suppress glucagon secretion in alpha-cell hyperplasia.
  • [MeSH-major] Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / pathology. Glucagonoma / pathology. Islets of Langerhans / pathology. Nesidioblastosis / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 18437091.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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40. Kovács RK, Korom I, Dobozy A, Farkas G, Ormos J, Kemény L: Necrolytic migratory erythema. J Cutan Pathol; 2006 Mar;33(3):242-5
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  • The classical symptoms are associated with alpha-cell pancreatic islet cell tumor or 'glucagonoma'.
  • Generally, extracutaneous hallmarks of this disease include weight loss, diabetes, anaemia and diarrhoea.
  • OBSERVATION: We report a case of a 39-year-old woman with a 3-year history of recalcitrant psoriasiform eruption, who had no other associated symptoms on routine examination.
  • Abdominal computer tomography was performed, which revealed a tumor in the tail of the pancreas.
  • After distal resection of the pancreas her skin symptoms resolved in a few days time.
  • Histology was consistent with glucagonoma.
  • CONCLUSIONS: It is infrequent to have only necrolytic migratory erythema, hyperglucagonaemia and islet-cell tumor but no other extracutaneous symptoms in glucagonoma syndrome.
  • Skin symptoms are important, often they are the clue to the diagnosis of glucagonoma syndrome.
  • [MeSH-major] Erythema / etiology. Erythema / pathology. Glucagonoma / complications. Glucagonoma / pathology. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Female. Humans. Necrosis. Paraneoplastic Syndromes. Treatment Outcome

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  • (PMID = 16466513.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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41. Peros G, Sakorafas GH, Konstantoudakis G, Giannopoulos GA, Petropoulou K, Parasi A: Duodeno-pancreatic neuroendocrine tumours. Eur J Cancer Care (Engl); 2010 May;19(3):393-402
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  • [Title] Duodeno-pancreatic neuroendocrine tumours.
  • Duodeno-pancreatic neuroendocrine tumours (DP-ETs) are increasingly diagnosed today due to the widespread use of modern imaging methods.
  • Duodeno-pancreatic endocrine tumours should be treated by radical surgical resection, which offers a high chance for cure when the disease is localized.
  • A high index of suspicion is required in these patients for the presence of a multiple endocrine neoplasia type syndrome.
  • Histological/immunohistochemical diagnosis was somatostatin-producing tumour in the first patient, oncocytic endocrine tumour positive for neurone-specific enolase and focally for chromogranin in the second patient, glucagonoma and pancreatic polypeptide-producing endocrine pancreatic tumour in the third patient, and gastrin, somatostatin, calcitonin, insulin and adrenocorticotropic hormone (ACTH)-producing tumour in the fourth.
  • The second patient died 6.5 years following surgery due to disseminated disease.
  • [MeSH-major] Duodenal Neoplasms / diagnosis. Neuroendocrine Tumors / diagnosis. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / analysis. Biopsy. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Proteins / metabolism. Treatment Outcome

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  • (PMID = 19708940.001).
  • [ISSN] 1365-2354
  • [Journal-full-title] European journal of cancer care
  • [ISO-abbreviation] Eur J Cancer Care (Engl)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
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42. Szczepański M, Kamianowska M, Wnuczko K, Pietruczuk M, Wołczyński S: [The influence of erythropoietin (Epo) on intercellular adhesion molecule-1 (ICAM-1, CD54) and platelet-endothelial cell adhesion molecule-1 (PECAM-1, CD31) expression on human umbilical vein endothelial cells (HUVEC) induced by tumor necrosis factor-alpha (TNF-alpha)]. Wiad Lek; 2007;60(1-2):22-7

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  • [Title] [The influence of erythropoietin (Epo) on intercellular adhesion molecule-1 (ICAM-1, CD54) and platelet-endothelial cell adhesion molecule-1 (PECAM-1, CD31) expression on human umbilical vein endothelial cells (HUVEC) induced by tumor necrosis factor-alpha (TNF-alpha)].
  • [Transliterated title] Wpływ erytropoetyny (Epo) na indukowana czynnikiem martwicy nowotworów-alpa (tnf-alpha) ekspresje czasteczek adhezji miedzykomórkowej-1 (ICAM-1, CD54) i czasteczek adhezji komórkowej płytek i śródbłonka-1 (PECAM-1, CD31) na powierzchni komórek śródbłonka ludzkiej zyły pepowinowej (HUVEC).
  • The aim of the study was to examine the influence of Epo on intercellular adhesion molecule-1 (ICAM-1) and platelet-endothelial cell adhesion molecule-1 (PECAM--1) expression on human umbilical vein endothelial cells (HUVEC) induced by tumor necrosis factor-a (TNF-alpha).
  • MATERIAL AND METHODS: Human umbilical vein endothelial cells were cultured in a standard medium (M 199).
  • For stimulation TNF-alpha was used in concentrations: 10, 20, 40 ng/ml (6 hours) and Epo in concentrations: 10, 20, 40 IU/ml (24 hours).
  • CONCLUSIONS: Erythropoietin statistically significantly decreases ICAM-1 and PECAM-1 expression on HUVEC stimulated by TNF-alpha.
  • [MeSH-major] Antigens, CD31 / biosynthesis. Endothelium, Vascular / metabolism. Erythropoietin / pharmacology. Gene Expression / drug effects. Intercellular Adhesion Molecule-1 / biosynthesis. Tumor Necrosis Factor-alpha / pharmacology. Umbilical Veins / drug effects
  • [MeSH-minor] Cell Adhesion / drug effects. Cells, Cultured. Flow Cytometry. Humans. Metabolic Networks and Pathways

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  • (PMID = 17607964.001).
  • [ISSN] 0043-5147
  • [Journal-full-title] Wiadomości lekarskie (Warsaw, Poland : 1960)
  • [ISO-abbreviation] Wiad. Lek.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Tumor Necrosis Factor-alpha; 11096-26-7 / Erythropoietin; 126547-89-5 / Intercellular Adhesion Molecule-1
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43. Walker UA, Hasler P: [Safety and efficacy of biologics directed against TNF-alpha and CD20 in the therapy of vasculitis and systemic lupus erythematosus]. Ther Umsch; 2008 May;65(5):303-10
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  • [Title] [Safety and efficacy of biologics directed against TNF-alpha and CD20 in the therapy of vasculitis and systemic lupus erythematosus].
  • [Transliterated title] Stellenwert von gegen TNF-alpha und CD20 gerichteten Biologika in der Therapie der Vaskulitis und des systemischen Lupus erythematodes.
  • While the inhibition of TNF-alpha has been shown to improve vasculitis in vitro and in animal models, the clinical evidence for the efficacy of TNF-alpha blockade in most forms of vasculitis is mainly based on case reports and case series.
  • Randomised controlled studies have so far not shown superiority of anti-TNF-alpha agents for Wegener's granulomatosis and giant cell arteritis.
  • In refractory cases of Behçet's disease therapy of uveitis and other organ manifestations is promising.
  • The increased frequency of severe infections under TNF-alpha blockade requires a stringent benefit and risk assessment in addition to a multidisciplinary analysis of follow-up parameters.
  • A detailed information of the patient regarding symptoms and signs of a possible infection are a prerequisite.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal / adverse effects. Antigens, CD20 / immunology. Lupus Erythematosus, Systemic / drug therapy. Lupus Erythematosus, Systemic / immunology. Tumor Necrosis Factor-alpha / immunology. Vasculitis / drug therapy. Vasculitis / immunology

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  • (PMID = 18622936.001).
  • [ISSN] 0040-5930
  • [Journal-full-title] Therapeutische Umschau. Revue thérapeutique
  • [ISO-abbreviation] Ther Umsch
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD20; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 42
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44. Grzelewska-Rzymowska I, Pietrzkowicz M, Kroczyńska-Bednarek J: [Correlation of serum concentration of tumor necrosis factor alpha, clinical course, ventilation and nonspecific bronchial hyperresponsiveness in patients with isolated seasonal rhinitis and seasonal asthma]. Pol Merkur Lekarski; 2005 May;18(107):530-5
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  • [Title] [Correlation of serum concentration of tumor necrosis factor alpha, clinical course, ventilation and nonspecific bronchial hyperresponsiveness in patients with isolated seasonal rhinitis and seasonal asthma].
  • [Transliterated title] Zalezności miedzy stezeniem czynnika martwicy nowotworu alpha w surowicy a przebiegiem klinicznym, wentylacja i nieswoista nadreaktywnościa oskrzeli u chorych na izolowany sezonowy niezyt nosa i sezonowa astme.
  • Tumor necrosis factor alpha (TNF-alpha) plays a central role in pathogenesis of many inflammatory diseases including asthma and allergic rhinitis.
  • Its capability for cell activation, chemotaxis and upregulation of adhesion molecule expression on surface of inflammatory cells suggests that TNF-alpha may be responsible for bronchial hyperresponsiveness (BHR) and clinical symptoms of atopic diseases.
  • THE AIM: Relationships between serum concentration of TNF-alpha and clinical course as well as nonspecific BHR in patients with isolated seasonal rhinitis (SR) and seasonal bronchial asthma (SA) were assessed.
  • MATERIAL AND METHODS: The study was performed in 19 subjects with SR and 26 subjects with asthma sensitized to pollens, with measurable BHR during symptomatic phase of disease.
  • Serum concentration of TNF-alpha, ventilatory parameters, BHR to methacholine, asthma and seasonal rhinitis score were assessed two times--during and outside pollen season.
  • TNF-alpha concentration in serum in both groups of patients was significant higher than in healthy subjects.
  • There was no correlation between serum concentration of TNF-alpha, BHR and symptom score.
  • There is increased serum concentration of TNF-alpha in patients with seasonal airway allergy even in asymptomatic period of disease.
  • CONCLUSIONS: Natural exposure to allergens causes significant increase of TNF-alpha concentration in patients with rhinitis and asthma.
  • Although level of BHR and intensification of clinical symptoms coexist with changes in TNF-alpha concentration there is no correlation between them.
  • [MeSH-major] Asthma / blood. Bronchial Hyperreactivity / blood. Rhinitis, Allergic, Seasonal / blood. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16161949.001).
  • [ISSN] 1426-9686
  • [Journal-full-title] Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego
  • [ISO-abbreviation] Pol. Merkur. Lekarski
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha
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45. Mendoza-Guil F, Hernández-Jurado I, Burkhardt P, Linares J, Naranjo R: [Necrolytic migratory erythema associated with glucagonoma]. Actas Dermosifiliogr; 2005 Apr;96(3):175-8
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  • [Title] [Necrolytic migratory erythema associated with glucagonoma].
  • [Transliterated title] Eritema necrolítico migratorio asociado a glucagonoma.
  • Glucagonoma is a rare pancreatic tumor that is usually associated with a syndrome that includes diabetes, anemia, weight loss and skin lesions in the form of necrolytic migratory erythema.
  • We present the case of a patient with malignant glucagonoma treated with surgery and octreotide, which manifested with skin lesions.
  • The discussion will review the physiopathology, other causes of necrolytic erythema, diagnosis and differential diagnosis and treatment.
  • [MeSH-major] Erythema / complications. Erythema / pathology. Glucagonoma / complications. Pancreatic Neoplasms / complications

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  • (PMID = 16476361.001).
  • [ISSN] 0001-7310
  • [Journal-full-title] Actas dermo-sifiliográficas
  • [ISO-abbreviation] Actas Dermosifiliogr
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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46. Kindmark H, Sundin A, Granberg D, Dunder K, Skogseid B, Janson ET, Welin S, Oberg K, Eriksson B: Endocrine pancreatic tumors with glucagon hypersecretion: a retrospective study of 23 cases during 20 years. Med Oncol; 2007;24(3):330-7
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  • [Title] Endocrine pancreatic tumors with glucagon hypersecretion: a retrospective study of 23 cases during 20 years.
  • BACKGROUND: Glucagon-secreting endocrine pancreatic tumor is a rare disease, hence controlled studies on clinical management are lacking.
  • In an attempt to assess the efficacy of diagnostic and therapeutic measures in patients with glucagonoma, a retrospective study was performed using the archives of a tertiary care center.
  • PATIENTS AND METHODS: Records from 340 patients with endocrine pancreatic tumors were reassessed and 23 patients with malignant endocrine pancreatic tumor and elevated plasma glucagon levels were identified.
  • RESULTS: About 7% of patients with histologically verified tumors fullfilled our criteria for glucagonoma.
  • Only 22% of these patients had developed diabetes prior to the diagnosis of glucagonoma.
  • Seventy eight percent had metastatic disease to the liver at diagnosis.
  • During the study period, 11 patients died at a median of 80 months from diagnosis whereas 11 patients are still alive after a median follow up of 52 months.
  • CONCLUSIONS: Glucagonomas represent 7% of our comprehensive referral material of endocrine pancreatic tumors.
  • Necrolytic migratory erythema was a common finding (52%) and diabetes less frequent at presentation than previously reported.
  • Tumors were positive on somatostatin receptor scintigraphy and objective responses were seen to chemotherapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Erythema / complications. Glucagonoma / therapy. Pancreatic Neoplasms / therapy
  • [MeSH-minor] Adult. Aged. Combined Modality Therapy. Female. Glucagon / blood. Humans. Interferons. Liver Neoplasms / secondary. Male. Middle Aged. Receptors, Somatostatin / metabolism. Retrospective Studies. Sex Factors. Survival Analysis. Treatment Outcome

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  • [Cites] J Natl Cancer Inst. 2000 Feb 2;92 (3):205-16 [10655437.001]
  • [Cites] J Nucl Med. 2005 Jan;46 Suppl 1:13S-7S [15653647.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2005 Aug;19(4):649-56 [16183533.001]
  • [Cites] Endocr Pathol. 1997 Autumn;8(3):181-187 [12114721.001]
  • [Cites] Acta Oncol. 1993;32(2):203-8 [8391832.001]
  • [Cites] N Engl J Med. 1966 Jun 23;274(25):1408-13 [4286757.001]
  • [Cites] Lancet. 1986 Dec 6;2(8519):1307-9 [2878177.001]
  • [Cites] Cancer. 1990 May 1;65(9):1883-90 [1695540.001]
  • [Cites] Medicine (Baltimore). 1996 Mar;75(2):53-63 [8606627.001]
  • [Cites] Curr Probl Surg. 1990 Jun;27(6):301-86 [1973365.001]
  • [Cites] Cancer. 1998 Dec 1;83(11):2293-301 [9840528.001]
  • [Cites] Endocr Rev. 1981 Summer;2(3):347-61 [6268399.001]
  • [Cites] Lancet. 1974 Jul 6;2(7871):1-5 [4134714.001]
  • [Cites] Eur J Endocrinol. 2004 Jul;151(1):107-12 [15248829.001]
  • [Cites] Digestion. 1989;42(2):116-20 [2548911.001]
  • [Cites] Bull Cancer. 2004 Jul-Aug;91(7-8):637-40 [15381454.001]
  • [Cites] Int J Dermatol. 1979 Jan-Feb;18(1):17-22 [216645.001]
  • [Cites] Endocrinol Metab Clin North Am. 1989 Jun;18(2):483-518 [2663483.001]
  • [Cites] J Clin Invest. 1970 Apr;49(4):837-48 [4986215.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2005 Oct;19(5):753-81 [16253899.001]
  • [Cites] Endocr Pract. 2003 Jan-Feb;9(1):22-5 [12917088.001]
  • [Cites] Semin Oncol. 1987 Sep;14(3):253-62 [2888194.001]
  • [Cites] J Clin Oncol. 2005 Apr 20;23(12):2754-62 [15837990.001]
  • (PMID = 17873310.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Somatostatin; 9007-92-5 / Glucagon; 9008-11-1 / Interferons
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47. Kiersnowska-Rogowska B, Izycka A, Jabłońska E, Rogowski F, Parfieńczyk A: [Estimation of level of soluble form PECAM-1, ICAM-2 and TNF-alpha, IL-18 in serum patients with chronic myelogenic leukemia]. Przegl Lek; 2005;62(8):772-4
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  • [Title] [Estimation of level of soluble form PECAM-1, ICAM-2 and TNF-alpha, IL-18 in serum patients with chronic myelogenic leukemia].
  • [Transliterated title] Ocena stezenia rozpuszczalnych form PECAM-1 i ICAM-2 i stezenia TNF-alpha i IL-18 w surowicy krwi pacjentów z przewlekła białaczka, szpikowa.
  • The aim of this study was to estimate sPECAM-1, sICAM-2 and TNF-alpha and IL-18 concentrations in serum patients with chronic myelogenic leukemia.
  • The results indicate of increased level sPECAM-1, sICAM-2 and TNF-alpha, IL-18 concentrations in serum patients with chronic myelogenic leukemia.
  • Elevation levels of sPECAM-1 and sICAM-2 may lead to inhibit of making myelogenic leukemia cells infiltrations through the block of surface their receptors in patients with CML.
  • High concentration of TNF-alpha and 11-18 in blood serum may indicate high expression of sPECAM-1 by activated specific enzymes responsible for releasing sPECAM-1.
  • [MeSH-major] Antigens, CD / blood. Antigens, CD31 / blood. Cell Adhesion Molecules / blood. Interleukin-18 / blood. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / blood. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16521495.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD31; 0 / Cell Adhesion Molecules; 0 / ICAM2 protein, human; 0 / Interleukin-18; 0 / Tumor Necrosis Factor-alpha
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48. Wnuczko K, Szczepański M: [Influence of insulin-like growth factor 1 on PECAM-1 and ICAM-1 adhesion molecules expression in tumor necrosis factor alpha and hyperglycemia induced umbilical vein endothelial cells]. Wiad Lek; 2008;61(4-6):119-25
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  • [Title] [Influence of insulin-like growth factor 1 on PECAM-1 and ICAM-1 adhesion molecules expression in tumor necrosis factor alpha and hyperglycemia induced umbilical vein endothelial cells].
  • [Transliterated title] Wpływ insulinopodobnego czynnika wzrostu 1 na ekspresji czasteczek adhezyjnych PECAM-1 i ICAM-1 na powierzchni komórek sródbłonka naczyń zylnych pepowiny indukowanych czynnikiem martwicy nowotworu alpha oraz hiperglikemia.
  • Interactions between endothelial cells and growth factors are complex and environment dependent.
  • Cytokines, including tumor necrosis factor alpha (TNF-alpha) activate endothelium cells during inflammatory process.
  • Aim of the study was to assess the influence of IGF-1 on platelet/endothelial cell adhesion molecule 1 (PECAM-1;.
  • CD54) expression on human umbilical vein endothelial cells (HUVECs) stimulated by hyperglycemia and TNF-alpha.
  • Cell cultures were incubated with IGF-1 concentrations of 50 ng/ml and 200 ng/ml, glucose concentrations of 11.1 mmol/l and 22.2 mmol/l, TNF-alpha concentrations of 10 ng/ml and 20 ng/ml, as well as combinations of above.
  • Ratio of PECAM-1 and ICAM-1 expression revealing cells was obtained using flow cytometry method.
  • RESULTS: It was demonstrated, that IGF-1 concentrations of 50 ng/ml, 200 ng/ml enhance PECAM-1 and ICAM-1 endothelial cells expression (respectively to 57.2 +/- 4.8%, 76.1 +/- 1.5% and 91.7 +/- 5.0%, 86.8 +/- 4.7%) compared to control group (respectively: 20.9 +/- 0.5% and 26.6 +/- 0.5%).
  • Expression under influence of 10 ng/ml and 20 ng/ml TNF-alpha increases up to respectively: 78.4 +/- 0.9% and 86.5 +/- 0.7% for CD31 and respectively: 65.1 +/- 3.8% and 70.8 +/- 1.4% for CD54.
  • Combination of 20 ng/ml TNF-alpha with 50 ng/ml IGF-1 enhances expression of CD54 to 96.8 +/- 1.2%, with 200 ng/ml IGF-1 enhances CD31 and CD54 expression respectively to 90.5 +/- 2.3% and 96.6 +/- 0.6%.
  • It was concluded, that IGF-1, hyperglycemia and TNF-alpha enhance PECAM-1 and ICAM-1 adhesion molecules expression on HUVEC cells, activating the endothelium.
  • 2. Combination of IGF-1, TNF-alpha and hyperglycemia influence synergistically enhances PECAM-1 and ICAM-1 expression on endothelial cells surface.
  • [MeSH-major] Antigens, CD31 / metabolism. Endothelium, Vascular / metabolism. Hyperglycemia / metabolism. Insulin-Like Growth Factor Binding Protein 1 / metabolism. Intercellular Adhesion Molecule-1 / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Cells, Cultured. Humans. Umbilical Veins

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  • (PMID = 18939362.001).
  • [ISSN] 0043-5147
  • [Journal-full-title] Wiadomości lekarskie (Warsaw, Poland : 1960)
  • [ISO-abbreviation] Wiad. Lek.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Insulin-Like Growth Factor Binding Protein 1; 0 / Tumor Necrosis Factor-alpha; 126547-89-5 / Intercellular Adhesion Molecule-1
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49. Izycka A, Jabłońska E, Izycki T, Chyczewska E: [Expression of L-selectin on the surface of neutrophils stimulated by TNF-alpha and level of sL-selectin in serum of patients with lung cancer]. Pol Merkur Lekarski; 2005 Jan;18(103):62-5
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  • [Title] [Expression of L-selectin on the surface of neutrophils stimulated by TNF-alpha and level of sL-selectin in serum of patients with lung cancer].
  • [Transliterated title] Ocena ekspresji czasteczki adhezyjnej L-selektyny na powierzchni neutrofilów krwi obwodowej stymulowanych TNF-alpha oraz stezenia rozpuszczalnej formy selektyny w surowicy u chorych na raka płuca.
  • The aim of the study was to estimate L-selectin expression on peripheral blood PMN stimulated by TNF-alpha and concentration of a soluble form of L-selectin in serum of patients with small cell and non-small cell lung cancer.
  • The results showed an increased expression of L-selectin on PMN isolated from peripheral blood and an elevated concentration of sL-selectin in serum of patients with small cell and non-small cell lung cancer.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / blood. Carcinoma, Small Cell / blood. L-Selectin / blood. Lung Neoplasms / blood. Neutrophils / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 15859550.001).
  • [ISSN] 1426-9686
  • [Journal-full-title] Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego
  • [ISO-abbreviation] Pol. Merkur. Lekarski
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 126880-86-2 / L-Selectin
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50. Jmal A, Ghanem A, Boussen H, Gara Y, Abaza H, Gara S, Harzallah L, Ladgham A, Guemira F: [Seric soluble interleukin-2 receptor alpha in nasopharyngeal carcinoma in Tunisia. Prospective study about 45 cases]. Tunis Med; 2007 Aug;85(8):651-4
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  • [Title] [Seric soluble interleukin-2 receptor alpha in nasopharyngeal carcinoma in Tunisia. Prospective study about 45 cases].
  • [Transliterated title] Taux serique du recepteur alpha soluble de l'interleukine 2 dans le carcinome du nasopharynx en Tunisie. Etude prospective sur 45 cas.
  • BACKGROUND: Soluble interleukin-2 receptor alpha (slL-2Ralpha) is a well-known indicator of T-cell activation noted to be increasing in nasopharyngeal cancer.
  • According to the disease status after a period of follow-up ranging from three to 22 months (median 12 months), patients were divided into two groups: The remission group (n=28) represented those with favourable evolution and a second group of 15 patients with unfavourable evolution (2 death, 4 cases of persistent primary disease and 9 patients with distance metastasis).
  • CONCLUSION: Measurement of serum sIL-2Ralpha provides a good estimation of the nasopharyngeal tumor burden.
  • [MeSH-major] Carcinoma / blood. Interleukin-2 Receptor alpha Subunit / blood. Nasopharyngeal Neoplasms / blood

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  • (PMID = 18254285.001).
  • [ISSN] 0041-4131
  • [Journal-full-title] La Tunisie médicale
  • [ISO-abbreviation] Tunis Med
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Tunisia
  • [Chemical-registry-number] 0 / Interleukin-2 Receptor alpha Subunit
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51. Abreu Velez AM, Howard MS: Diagnosis and treatment of cutaneous paraneoplastic disorders. Dermatol Ther; 2010 Nov-Dec;23(6):662-75
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  • [Title] Diagnosis and treatment of cutaneous paraneoplastic disorders.
  • Cutaneous signs of these disorders afford clinicians opportunities for early diagnosis and treatment.
  • We aim to succinctly review the recognition, diagnosis, and treatment of selected cutaneous paraneoplastic diseases.
  • Skin disorders that may be associated with paraneoplastic syndromes include: cutaneous metastases, tripe palms, Sweet's syndrome, glucagonoma, Paget's disease and extramammary Paget's disease, acanthosis nigricans, Birt-Hogg-Dube syndrome, basal cell nevus syndrome, Bazex syndrome (acrokeratosis paraneoplastica), carcinoid syndrome, Cowden's disease(multiple hamartoma syndrome), dermatomyositis, erythema gyratum repens, ichthyosis aquisita, von Recklinghausen's disease, pityriasis rotunda, pyoderma gangrenosum, Quincke's edema (angioedema and paraneoplastic uricaria), paraneoplastic pemphigus, Degos' disease, superior vena cava syndrome, Werner's syndrome, diffuse normolipemic plane xanthomas, and yellow nail syndrome.
  • [MeSH-major] Paraneoplastic Syndromes / diagnosis. Paraneoplastic Syndromes / therapy. Skin Diseases / diagnosis. Skin Diseases / therapy

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  • [Copyright] © 2010 Wiley Periodicals, Inc.
  • (PMID = 21054710.001).
  • [ISSN] 1529-8019
  • [Journal-full-title] Dermatologic therapy
  • [ISO-abbreviation] Dermatol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
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52. Lu J, Herrera PL, Carreira C, Bonnavion R, Seigne C, Calender A, Bertolino P, Zhang CX: Alpha cell-specific Men1 ablation triggers the transdifferentiation of glucagon-expressing cells and insulinoma development. Gastroenterology; 2010 May;138(5):1954-65
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  • [Title] Alpha cell-specific Men1 ablation triggers the transdifferentiation of glucagon-expressing cells and insulinoma development.
  • BACKGROUND & AIMS: The tumor suppressor menin is recognized as a key regulator of pancreatic islet development, proliferation, and beta-cell function, whereas its role in alpha cells remains poorly understood.
  • The purpose of the current study was to address this issue in relation to islet tumor histogenesis.
  • METHODS: We generated alpha cell-specific Men1 mutant mice with Cre/loxP technology and carried out analyses of pancreatic lesions developed in the mutant mice during aging.
  • RESULTS: We showed that, despite the alpha-cell specificity of the GluCre transgene, both glucagonomas and a large amount of insulinomas developed in mutant mice older than 6 months, accompanied by mixed islet tumors.
  • Interestingly, the cells sharing characteristics of both alpha and beta cells were identified shortly after the appearance of menin-deficient alpha cells but well before the tumor onset.
  • Using a genetic cell lineage tracing analysis, we demonstrated that insulinoma cells were directly derived from transdifferentiating glucagon-expressing cells.
  • CONCLUSIONS: Our work shows cell transdifferentiation as a novel mechanism involved in islet tumor development and provides evidence showing that menin regulates the plasticity of differentiated pancreatic alpha cells in vivo, shedding new light on the mechanisms of islet tumorigenesis.
  • [MeSH-major] Cell Transdifferentiation. Cell Transformation, Neoplastic / metabolism. Glucagon / metabolism. Glucagon-Secreting Cells / metabolism. Glucagonoma / metabolism. Insulinoma / metabolism. Pancreatic Neoplasms / metabolism. Proto-Oncogene Proteins / deficiency
  • [MeSH-minor] Age Factors. Aging / metabolism. Aging / pathology. Animals. Biomarkers / metabolism. Cell Fusion. Cell Lineage. Cell Proliferation. Gene Deletion. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Genotype. Insulin / metabolism. Insulin-Secreting Cells / metabolism. Insulin-Secreting Cells / pathology. Mice. Mice, Knockout. Phenotype. Transcription Factors / metabolism


53. Shimizu K, Goto A, Fukui M, Taniguchi M, Fujii S: Tumor cells loaded with alpha-galactosylceramide induce innate NKT and NK cell-dependent resistance to tumor implantation in mice. J Immunol; 2007 Mar 1;178(5):2853-61
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  • [Title] Tumor cells loaded with alpha-galactosylceramide induce innate NKT and NK cell-dependent resistance to tumor implantation in mice.
  • Dendritic cells (DCs) loaded with alpha-galactosylceramide (alpha-GalCer) are known to be active APCs for the stimulation of innate NKT and NK cell responses in vivo.
  • In this study, we evaluated the capacity of non-DCs to present alpha-GalCer in vitro and in vivo, particularly tumor cells loaded with alpha-GalCer (tumor/Gal).
  • Even though the tumor cells lacked expression of CD40, CD80, and CD86 costimulatory molecules, the i.v. injection of tumor/Gal resulted in IFN-gamma secretion by NKT and NK cells.
  • These innate responses to tumor/Gal, including the induction of IL-12p70, were comparable to or better than alpha-GalCer-loaded DCs.
  • B16 melanoma cells that were stably transduced to express higher levels of CD1d showed an increased capacity relative to wild-type B16 cells to present alpha-GalCer in vivo.
  • Three different tumor cell lines, when loaded with alpha-GalCer, failed to establish tumors upon i.v. injection, and the mice survived for at least 6 mo.
  • The resistance against tumor cells was independent of CD4 and CD8 T cells but dependent upon NKT and NK cells.
  • Mice were protected from the development of metastases if the administration of live B16 tumor cells was followed 3 h or 3 days later by the injection of CD1d(high)-alpha-GalCer-loaded B16 tumor cells with or without irradiation.
  • Taken together, these results indicate that tumor/Gal are effective APCs for innate NKT and NK cell responses, and that these innate immune responses are able to resist the establishment of metastases in vivo.
  • [MeSH-major] Dendritic Cells / immunology. Galactosylceramides / immunology. Immunity, Innate. Killer Cells, Natural / immunology. Neoplasms, Experimental / immunology. T-Lymphocytes / immunology
  • [MeSH-minor] Animals. Antigens, CD / immunology. Cell Line, Tumor. Female. Graft Rejection / immunology. Interferon-gamma / immunology. Interleukin-12 / immunology. Mice. Mice, Inbred BALB C. Mice, Knockout. Neoplasm Transplantation / immunology

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  • (PMID = 17312129.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Galactosylceramides; 0 / alpha-galactosylceramide; 187348-17-0 / Interleukin-12; 82115-62-6 / Interferon-gamma
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54. Gómez-Mateo C, Avalos-Peralta SP, Ríos-Martín JJ, Carrizosa-Esquivel AM, González-Cámpora R, Camacho-Martínez F: [Sequential histological and immunohistochemical assessment of proliferation and apoptotic markers during treatment of psoriasis with antitumor necrosis factor alpha (infliximab)]. Actas Dermosifiliogr; 2009 Jun;100(5):420-4
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  • [Title] [Sequential histological and immunohistochemical assessment of proliferation and apoptotic markers during treatment of psoriasis with antitumor necrosis factor alpha (infliximab)].
  • [Transliterated title] Evaluación histológica e inmunohistoquímica secuencial de marcadores de proliferación y apoptosis durante el tratamiento de la psoriasis con anti-factor de necrosis tumoral alpha (infliximab).
  • BACKGROUND AND OBJECTIVES: Psoriasis is an inflammatory skin disease of immunologic nature that is mediated by T-helper-1 cytokines.
  • Clinical response to treatment with antitumor necrosis factor (TNF) alpha antibodies (infliximab) has been significant; however, the mechanisms for clearance of lesions have not been elucidated.
  • The apoptotic markers used were TP53, B-cell lymphoma 2 protein, anticaspase 3, and anticaspase 8.
  • The cell proliferation marker used was Ki67.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Apoptosis / drug effects. Cell Proliferation / drug effects. Psoriasis / drug therapy. Psoriasis / pathology. Tumor Necrosis Factor-alpha / antagonists & inhibitors

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  • (PMID = 19558920.001).
  • [ISSN] 0001-7310
  • [Journal-full-title] Actas dermo-sifiliográficas
  • [ISO-abbreviation] Actas Dermosifiliogr
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Biomarkers; 0 / Tumor Necrosis Factor-alpha; B72HH48FLU / Infliximab
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55. Tandle A, Hanna E, Lorang D, Hajitou A, Moya CA, Pasqualini R, Arap W, Adem A, Starker E, Hewitt S, Libutti SK: Tumor vasculature-targeted delivery of tumor necrosis factor-alpha. Cancer; 2009 Jan 01;115(1):128-39
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  • [Title] Tumor vasculature-targeted delivery of tumor necrosis factor-alpha.
  • However, targeting a therapeutic gene of interest to the tumor vasculature with minimal toxicity to other tissues remains the objective of antivascular gene therapy.
  • Tumor necrosis factor-alpha (TNF-alpha) is a potent antivascular agent but has limited clinical utility because of significant systemic toxicity.
  • At the maximum tolerated doses of systemic TNF-alpha, there is no meaningful antitumor activity.
  • Hence, the objective of this study was to deliver TNF-alpha targeted to tumor vasculature by systemic delivery to examine its antitumor activity.
  • METHODS: A hybrid adeno-associated virus phage vector (AAVP) was used that targets tumor endothelium to express TNF-alpha (AAVP-TNF-alpha).
  • The activity of AAVP-TNF-alpha was analyzed in various in vitro and in vivo settings using a human melanoma tumor model.
  • RESULTS: In vitro, AAVP-TNF-alpha infection of human melanoma cells resulted in high levels of TNF-alpha expression.
  • Systemic administration of targeted AAVP-TNF-alpha to melanoma xenografts in mice produced the specific delivery of virus to tumor vasculature.
  • In contrast, the nontargeted vector did not target to tumor vasculature.
  • Targeted AAVP delivery resulted in expression of TNF-alpha, induction of apoptosis in tumor vessels, and significant inhibition of tumor growth.
  • CONCLUSIONS: Targeted AAVP vectors can be used to deliver TNF-alpha specifically to tumor vasculature, potentially reducing its systemic toxicity.
  • Because TNF-alpha is a promising antivascular agent that currently is limited by its toxicity, the current results suggest the potential for clinical translation of this strategy.
  • [MeSH-major] Melanoma / blood supply. Melanoma / therapy. Skin Neoplasms / blood supply. Skin Neoplasms / therapy. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Dependovirus / genetics. Gene Expression. Genetic Therapy / methods. Genetic Vectors. Humans. Melanoma, Experimental / blood supply. Melanoma, Experimental / therapy. Mice. Mice, Nude. Neoplasm Transplantation. Transduction, Genetic

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  • (PMID = 19090007.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0701159; United States / Intramural NIH HHS / /
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha
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56. Wang M, Pan JY: [Prothymosin alpha and tumor: current status and perspective]. Ai Zheng; 2007 Mar;26(3):333-6

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  • [Title] [Prothymosin alpha and tumor: current status and perspective].
  • Prothymosin alpha (ProTalpha) is a small molecule of natively unstructured acidic protein, and widely exists in mammalian tissues.
  • We reviewed current reports on the potential roles of ProTalpha in cell proliferation, carcinogenesis, apoptosis, and immunomodulatory, discussed the regulation of ProTalpha gene expression and possible molecular mechanisms underlying its internal and external actions in cells, and explored its significance in tumor diagnosis and treatment.
  • [MeSH-major] Apoptosis. Biomarkers, Tumor / analysis. Cell Proliferation. Neoplasms / pathology. Protein Precursors. Thymosin / analogs & derivatives

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  • (PMID = 17355803.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Protein Precursors; 0 / prothymosin alpha; 61512-21-8 / Thymosin
  • [Number-of-references] 41
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57. Shen XX, Li HL, Hong J, Xiao J, Pan L, Li GW: [The role of syntaxin1A/synaptosome-associated protein-25 in reversing hyperglycemia-induced alpha cell toxicity]. Zhonghua Yi Xue Za Zhi; 2009 Mar 31;89(12):851-4
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  • [Title] [The role of syntaxin1A/synaptosome-associated protein-25 in reversing hyperglycemia-induced alpha cell toxicity].
  • OBJECTIVE: To investigate the effects of reversal of hyperglycemic toxicity on the synthesis and secretion of glucagon by the alpha cells and the possible mechanisms thereof.
  • METHODS: Mouse glucagonoma cells of the line TC1-6 were cultured in medium containing 5.5 mmol/L glucose for 10 days (low glucose group, LG), in medium containing 25 mmol/L glucose for 10 days (high glucose group, HG), in medium with 25 mmol/L glucose for 5 days and then in medium with 5.5 mmol/L glucose for 5 days (high-low glucose group, HL group), or in medium with 5.5 mmol/L glucose for 5 days and then in medium with 25 mmol/L glucose for 5 days (LH group), Radioimmunoassay was used to detect the glucagon concentration in the supernatant.
  • RT-PCR was used to detect the mRNA expression of glucagon in the TC1-6 cells.
  • (1) The glucagon level of the HG/LG group was lower than that of the HG group by 29% (P < 0.05). (2) The glucagon mRNA expression level in the TC1-6 cells of the HG/HL group was significantly lower than that of the HG group by (52.6 +/- 2.8)% (P < 0.05). (3) The syntaxin1A and SNAP-25 expression levels in the TC1-6 cells of the HG group were significantly higher than those of the LG group by 36% and 69% respectively (both P < 0.05), and the syntaxin1A and SNAP-25 expression levels in the TC1-6 cells of the HG/LG group were significantly lower than those of the HG group by 49% and 56% respectively (both P < 0.05).
  • CONCLUSION: After removing the high glucose toxicity the abnormal glucagon secretion by the alpha-cells can be ameliorated obviously, and the expression levels of syntaxin1A and SNAP-25 proteins that promote the secretion of glucagon are reduced accordingly.
  • [MeSH-major] Glucagon / secretion. Hyperglycemia / metabolism. Islets of Langerhans / cytology. Synaptosomal-Associated Protein 25 / metabolism. Syntaxin 1 / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival. Gene Expression. Mice. Signal Transduction

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  • (PMID = 19595128.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Snap25 protein, mouse; 0 / Stx1a protein, mouse; 0 / Synaptosomal-Associated Protein 25; 0 / Syntaxin 1; 9007-92-5 / Glucagon
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58. Docherty HM, Hay CW, Ferguson LA, Barrow J, Durward E, Docherty K: Relative contribution of PDX-1, MafA and E47/beta2 to the regulation of the human insulin promoter. Biochem J; 2005 Aug 1;389(Pt 3):813-20
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  • Of these, the homoeodomain protein PDX-1 (pancreatic duodenal homeobox factor-1), the basic leucine zipper protein MafA and the basic helix-loop-helix heterodimer E47/BETA2 (beta-cell E box transactivator 2; referred to here as beta2) bind to important regulatory sites.
  • Mutagenesis of the PDX-1, MafA and E47/beta2 binding sites reduced promoter activity by 60, 74 and 94% respectively, in INS-1 beta-cells.
  • In the islet glucagonoma cell line alphaTC1.6, overexpression of PDX-1 and MafA separately increased promoter activity approx.
  • In HeLa cells, PDX-1 stimulated the basal promoter by approx.
  • PDX-1 was shown further to activate the endogenous insulin 1 gene in alphaTC1.6 cells, whereas MafA activated the insulin 2 gene.

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  • [Cites] Mol Endocrinol. 1994 Dec;8(12):1798-806 [7708065.001]
  • [Cites] J Biol Chem. 2005 Mar 25;280(12):11887-94 [15665000.001]
  • [Cites] Diabetes. 1990 Apr;39(4):406-14 [2156740.001]
  • [Cites] J Biol Chem. 1990 May 15;265(14):8285-96 [2186040.001]
  • [Cites] Mol Endocrinol. 1991 Jun;5(6):836-43 [1922098.001]
  • [Cites] Endocrinology. 1992 Jan;130(1):167-78 [1370150.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Feb 1;89(3):1045-9 [1310538.001]
  • [Cites] Mol Cell Biol. 1992 Apr;12(4):1777-88 [1549125.001]
  • [Cites] EMBO J. 1993 Nov;12(11):4251-9 [7901001.001]
  • [Cites] Mol Endocrinol. 1993 Oct;7(10):1275-83 [7505393.001]
  • [Cites] EMBO J. 1994 Mar 1;13(5):1145-56 [7907546.001]
  • [Cites] Nature. 1994 Oct 13;371(6498):606-9 [7935793.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Dec 6;91(25):12203-7 [7991607.001]
  • [Cites] Genes Dev. 1995 Apr 15;9(8):1009-19 [7774807.001]
  • [Cites] Diabetes. 1995 Aug;44(8):1002-4 [7621988.001]
  • [Cites] Development. 1996 Mar;122(3):983-95 [8631275.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Aug 20;93(17):9015-20 [8799146.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Dec 24;93(26):15057-62 [8986763.001]
  • [Cites] Mol Cell Biol. 1997 Jul;17(7):3987-96 [9199333.001]
  • [Cites] Mol Cell Biol. 2000 Feb;20(3):900-11 [10629047.001]
  • [Cites] J Biol Chem. 2000 Jan 21;275(3):2199-204 [10636926.001]
  • [Cites] J Biol Chem. 2001 Jan 5;276(1):104-13 [11024035.001]
  • [Cites] Mol Cell Biol. 2001 May;21(9):3234-43 [11287626.001]
  • [Cites] J Biol Chem. 2001 Sep 21;276(38):35751-60 [11457839.001]
  • [Cites] Diabetologia. 2001 Oct;44(10):1203-14 [11692168.001]
  • [Cites] Mol Cell Biol. 2002 Jan;22(2):412-20 [11756538.001]
  • [Cites] J Endocrinol. 2002 Mar;172(3):653-72 [11874714.001]
  • [Cites] Diabetologia. 2002 Mar;45(3):309-26 [11914736.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6737-42 [12011435.001]
  • [Cites] Mol Biol Evol. 2002 Jul;19(7):1114-21 [12082130.001]
  • [Cites] J Biol Chem. 2002 Dec 20;277(51):49903-10 [12368292.001]
  • [Cites] Curr Biol. 2003 Jan 21;13(2):105-15 [12546783.001]
  • [Cites] J Biol Chem. 2003 Jun 27;278(26):23617-23 [12711597.001]
  • [Cites] Mol Cell Biol. 2003 Sep;23(17):6049-62 [12917329.001]
  • [Cites] Mol Biol Evol. 2003 Sep;20(9):1377-419 [12777501.001]
  • [Cites] Mol Cell Biol. 2003 Oct;23(19):6713-24 [12972592.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Dec 19;312(3):831-42 [14680841.001]
  • [Cites] J Mol Endocrinol. 2004 Feb;32(1):9-20 [14765989.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):2930-3 [14973194.001]
  • [Cites] J Biol Chem. 2004 May 21;279(21):22228-35 [15028719.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 1;101(22):8319-24 [15148392.001]
  • [Cites] Nature. 1980 Mar 6;284(5751):26-32 [6243748.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Dec;84(24):8819-23 [3321054.001]
  • [Cites] Nature. 1988 Mar 3;332(6159):87-90 [2831456.001]
  • [Cites] Mol Cell Biol. 1989 Aug;9(8):3253-9 [2552288.001]
  • [Cites] Genes Dev. 1997 Sep 15;11(18):2323-34 [9308961.001]
  • [Cites] J Biol Chem. 1999 Jul 23;274(30):21095-103 [10409662.001]
  • [Cites] Biochem J. 1989 Nov 15;264(1):233-9 [2690822.001]
  • (PMID = 15862113.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / HMGB Proteins; 0 / Homeodomain Proteins; 0 / Insulin; 0 / MAFA protein, human; 0 / Maf Transcription Factors, Large; 0 / NEUROD1 protein, human; 0 / TCF Transcription Factors; 0 / TCF7L1 protein, human; 0 / Tcf7l1 protein, rat; 0 / Trans-Activators; 0 / Transcription Factor 7-Like 1 Protein; 0 / Transcription Factors; 0 / pancreatic and duodenal homeobox 1 protein
  • [Other-IDs] NLM/ PMC1180732
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59. Bhattacharyya S, Mandal D, Sen GS, Pal S, Banerjee S, Lahiry L, Finke JH, Tannenbaum CS, Das T, Sa G: Tumor-induced oxidative stress perturbs nuclear factor-kappaB activity-augmenting tumor necrosis factor-alpha-mediated T-cell death: protection by curcumin. Cancer Res; 2007 Jan 1;67(1):362-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor-induced oxidative stress perturbs nuclear factor-kappaB activity-augmenting tumor necrosis factor-alpha-mediated T-cell death: protection by curcumin.
  • Cancer patients often exhibit loss of proper cell-mediated immunity and reduced effector T-cell population in the circulation.
  • Thymus is a major site of T-cell maturation, and tumors induce thymic atrophy to evade cellular immune response.
  • Here, we report severe thymic hypocellularity along with decreased thymic integrity in tumor bearer.
  • In an effort to delineate the mechanisms behind such thymic atrophy, we observed that tumor-induced oxidative stress played a critical role, as it perturbed nuclear factor-kappaB (NF-kappaB) activity.
  • Tumor-induced oxidative stress increased cytosolic IkappaBalpha retention and inhibited NF-kappaB nuclear translocation in thymic T cells.
  • These NF-kappaB-perturbed cells became vulnerable to tumor-secreted tumor necrosis factor (TNF)-alpha (TNF-alpha)-mediated apoptosis through the activation of TNF receptor-associated protein death domain-associated Fas-associated protein death domain and caspase-8.
  • Interestingly, TNF-alpha-depleted tumor supernatants, either by antibody neutralization or by TNF-alpha-small interfering RNA transfection of tumor cells, were unable to kill T cell effectively.
  • When T cells were overexpressed with NF-kappaB, the cells became resistant to tumor-induced apoptosis.
  • In contrast, when degradation-defective IkappaBalpha (IkappaBalpha super-repressor) was introduced into T cells, the cells became more vulnerable, indicating that inhibition of NF-kappaB is the reason behind such tumor/TNF-alpha-mediated apoptosis.
  • Curcumin could prevent tumor-induced thymic atrophy by restoring the activity of NF-kappaB.
  • Further investigations suggest that neutralization of tumor-induced oxidative stress and restoration of NF-kappaB activity along with the reeducation of the TNF-alpha signaling pathway can be the mechanism behind curcumin-mediated thymic protection.
  • Thus, our results suggest that unlike many other anticancer agents, curcumin is not only devoid of immunosuppressive effects but also acts as immunorestorer in tumor-bearing host.
  • [MeSH-major] Curcumin / pharmacology. NF-kappa B / immunology. Neoplasms, Experimental / immunology. T-Lymphocytes / immunology. Tumor Necrosis Factor-alpha / immunology
  • [MeSH-minor] Animals. Atrophy. Cell Death / immunology. Cell Line, Tumor. Humans. Mice. Oxidative Stress / immunology. Receptors, Tumor Necrosis Factor, Type I / immunology. Thymus Gland / drug effects. Thymus Gland / immunology. Thymus Gland / pathology

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  • (PMID = 17210719.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Tumor Necrosis Factor-alpha; IT942ZTH98 / Curcumin
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60. Sundstedt A, Celander M, Hedlund G: Combining tumor-targeted superantigens with interferon-alpha results in synergistic anti-tumor effects. Int Immunopharmacol; 2008 Mar;8(3):442-52

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combining tumor-targeted superantigens with interferon-alpha results in synergistic anti-tumor effects.
  • In this study we explored the possibility of improving the anti-tumor potency of tumor-targeted superantigens (TTS) by combination treatment with interferon-alpha (IFN-alpha).
  • TTS utilizes the powerful T cell activating property of the superantigen staphylococcal enterotoxin A (SEA) in fusion with an anti-tumor Fab-fragment to target this T cell activity against tumor cells.
  • TTS fusion proteins have shown anti-tumor efficacy in a number of experimental tumor models including the B16 mouse melanoma transfected with a human tumor-associated antigen recognized by the C215 monoclonal antibody.
  • IFN-alpha is approved for the treatment of solid tumors such as renal cell carcinoma and malignant melanoma and exerts immunomodulatory effects, which make it an appropriate candidate to combine with immunotherapy against cancer.
  • Here we report that daily administration of IFN-alpha (20 000 U i.p.) enhances and sustains CD8+ T cell activation induced by the TTS C215Fab-SEA (10 microg i.v.) in C57Bl/6 mice, as reflected by increased and prolonged cell-mediated cytotoxicity against tumor cells ex vivo as well as by augmented serum IFN-gamma levels.
  • C215Fab-SEA synergized with IFN-alpha in reducing the number of lung tumors in B16-C215 melanoma bearing mice as compared to mono therapy.
  • In a long term tumor survival experiment, the prolonged median survival time of the combination treatment was 3.5 and 7.7 times the prolonged median survival times of C215Fab-SEA and IFN-alpha monotherapies, respectively.
  • Hence, the combination treatment provoked synergistic anti-tumor effects as measured by the number of lung tumors and markedly prolonged survival.
  • The enhanced therapeutic efficacy correlated with a striking and sustained increase of CD8- and perforin-expressing tumor-infiltrating cells.
  • These results suggest significant potential of combining TTS with IFN-alpha for human cancer therapy.
  • [MeSH-major] Enterotoxins / administration & dosage. Immunoglobulin Fab Fragments / administration & dosage. Interferon-alpha / administration & dosage. Melanoma, Experimental / therapy. Superantigens / administration & dosage
  • [MeSH-minor] Animals. Cell Line, Tumor. Cytotoxicity, Immunologic. Female. Interferon-gamma / biosynthesis. Lymphocytes, Tumor-Infiltrating / immunology. Mice. Mice, Inbred C57BL. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 18279798.001).
  • [ISSN] 1567-5769
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Enterotoxins; 0 / Immunoglobulin Fab Fragments; 0 / Interferon-alpha; 0 / Superantigens; 37337-57-8 / enterotoxin A, Staphylococcal; 82115-62-6 / Interferon-gamma
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61. Stübgen JP: Tumor necrosis factor-alpha antagonists and neuropathy. Muscle Nerve; 2008 Mar;37(3):281-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor necrosis factor-alpha antagonists and neuropathy.
  • Tumor necrosis factor (TNF)-alpha plays an important role in many aspects of immune system development, immune-response regulation, and T-cell-mediated tissue injury.
  • The evidence that TNF-alpha, released by autoreactive T cells and macrophages, may contribute to the pathogenesis of immune-mediated demyelinating neuropathies is reviewed.
  • TNF-alpha antagonists (infliximab, etanercept, adalimumab) are indicated for the treatment of advanced inflammatory rheumatic and bowel disease, but these drugs can induce a range of autoimmune diseases that also attack the central and peripheral nervous systems.
  • Case histories and series report on the association between anti-TNF-alpha treatment and various disorders of peripheral nerve such as Guillain-Barré syndrome, Miller Fisher syndrome, chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathy with conduction block, mononeuropathy multiplex, and axonal sensorimotor polyneuropathies.
  • The proposed pathogeneses of TNF-alpha-associated neuropathies include both a T-cell and humoral immune attack against peripheral nerve myelin, vasculitis-induced nerve ischemia, and inhibition of signaling support for axons.
  • Most neuropathies improve over a period of months by withdrawal of the TNF-alpha antagonist, with or without additional immune-modulating treatment.
  • Preliminary observations suggest that TNF-alpha antagonists may be useful as an antigen-nonspecific treatment approach to immune-mediated neuropathies in patients with a poor response to, or intolerance of, standard therapies, but further studies are required.
  • [MeSH-major] Anti-Infective Agents / therapeutic use. Polyneuropathies / drug therapy. Tumor Necrosis Factor-alpha / antagonists & inhibitors. Tumor Necrosis Factor-alpha / metabolism

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  • [CommentIn] Muscle Nerve. 2009 Sep;40(3):488-9 [19623630.001]
  • (PMID = 18041052.001).
  • [ISSN] 0148-639X
  • [Journal-full-title] Muscle & nerve
  • [ISO-abbreviation] Muscle Nerve
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 91
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62. da Silva AP, Martini MV, de Oliveira CM, Cunha S, de Carvalho JE, Ruiz AL, da Silva CC: Antitumor activity of (-)-alpha-bisabolol-based thiosemicarbazones against human tumor cell lines. Eur J Med Chem; 2010 Jul;45(7):2987-93

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antitumor activity of (-)-alpha-bisabolol-based thiosemicarbazones against human tumor cell lines.
  • A series of thiosemicarbazones deriving from the natural sesquiterpene (-)-alpha-bisabolol were synthesized and tested against a panel of eight human tumor cell lines to evaluate their anti-tumor potential.
  • Some of the compounds exhibited inhibitory effects on the growth of a wide range of cancer cell lines, but myeloid leukemia cells (K-562) were especially sensitive to all tested thiosemicarbazones (GI(50) 0.01-4.22 microM).
  • Among the analogues, the ketone derivative 3l was the most active, exhibiting potent antitumoral activity (GI(50) 0.01 microM) and high selectivity for K-562 cells (deltaTGI 505).
  • It also demonstrated high cytotoxicity, with an LC(50) of 1.55 microM for the K-562 cells, but it showed only moderate selectivity (deltaLC(50) 38.5 microM).
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. Humans

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  • [Copyright] Copyright 2010 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20413188.001).
  • [ISSN] 1768-3254
  • [Journal-full-title] European journal of medicinal chemistry
  • [ISO-abbreviation] Eur J Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Sesquiterpenes; 0 / Thiosemicarbazones; 24WE03BX2T / bisabolol
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63. Aits S, Gustafsson L, Hallgren O, Brest P, Gustafsson M, Trulsson M, Mossberg AK, Simon HU, Mograbi B, Svanborg C: HAMLET (human alpha-lactalbumin made lethal to tumor cells) triggers autophagic tumor cell death. Int J Cancer; 2009 Mar 1;124(5):1008-19
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HAMLET (human alpha-lactalbumin made lethal to tumor cells) triggers autophagic tumor cell death.
  • HAMLET, a complex of partially unfolded alpha-lactalbumin and oleic acid, kills a wide range of tumor cells.
  • Here we propose that HAMLET causes macroautophagy in tumor cells and that this contributes to their death.
  • Cell death was accompanied by mitochondrial damage and a reduction in the level of active mTOR and HAMLET triggered extensive cytoplasmic vacuolization and the formation of double-membrane-enclosed vesicles typical of macroautophagy.
  • In addition, HAMLET caused a change from uniform (LC3-I) to granular (LC3-II) staining in LC3-GFP-transfected cells reflecting LC3 translocation during macroautophagy, and this was blocked by the macroautophagy inhibitor 3-methyladenine.
  • To determine if macroautophagy contributed to cell death, we used RNA interference against Beclin-1 and Atg5.
  • Suppression of Beclin-1 and Atg5 improved the survival of HAMLET-treated tumor cells and inhibited the increase in granular LC3-GFP staining.
  • The results show that HAMLET triggers macroautophagy in tumor cells and suggest that macroautophagy contributes to HAMLET-induced tumor cell death.
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis Regulatory Proteins / analysis. Apoptosis Regulatory Proteins / genetics. Apoptosis Regulatory Proteins / physiology. Cell Line, Tumor. Humans. Membrane Proteins / analysis. Membrane Proteins / genetics. Membrane Proteins / physiology. Microtubule-Associated Proteins / genetics. Microtubule-Associated Proteins / metabolism. Microtubule-Associated Proteins / physiology. Mitochondria / drug effects. Protein Kinases / analysis. RNA, Messenger / analysis. TOR Serine-Threonine Kinases

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  • (PMID = 19048621.001).
  • [ISSN] 1097-0215
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATG5 protein, human; 0 / Apoptosis Regulatory Proteins; 0 / BECN1 protein, human; 0 / HAMLET complex, human; 0 / Membrane Proteins; 0 / Microtubule-Associated Proteins; 0 / Oleic Acids; 0 / RNA, Messenger; 0 / light chain 3, human; 9013-90-5 / Lactalbumin; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases
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64. Luo JC, Cho CH, Ng KM, Hsiang KW, Lu CL, Chen TS, Chang FY, Lin HC, Perng CL, Lee SD: Dexamethasone inhibits tumor necrosis factor-alpha-stimulated gastric epithelial cell migration. J Chin Med Assoc; 2009 Oct;72(10):509-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dexamethasone inhibits tumor necrosis factor-alpha-stimulated gastric epithelial cell migration.
  • BACKGROUND: Cell migration (restitution) occurs in the early phase of gastric ulcer healing.
  • Tumor necrosis factor (TNF)-alpha is overexpressed at the ulcer margin and plays a physiologic role in gastric ulcer healing.
  • We evaluated whether dexamethasone inhibited TNF-alpha-stimulated gastric epithelial cell migration using a rat normal gastric epithelial cell line (RGM-1).
  • METHODS: An artificial wound model was employed to measure cell migration.
  • RESULTS: TNF-alpha treatment (10 ng/mL) for 12-48 hours significantly increased RGM-1 cell migration, and TNF-alpha treatment increased cyclooxygenase (COX)-2 protein expression 8 hours later and prostaglandin E2 (PGE2) synthesis 12 hours later compared with control (p < 0.05).
  • Dexamethasone (10(-6) M) significantly inhibited the stimulatory effect of TNF-alpha on RGM-1 cell migration, which was associated with a significant decrease in COX-2 expression and PGE2 level in cells (p < 0.05).
  • CONCLUSION: TNF-alpha plays a regulatory role in rat gastric epithelial cell migration and dexamethasone inhibited TNF-alpha-stimulated cell migration, which was associated with a decrease in COX-2 expression and PGE2 formation.
  • [MeSH-major] Dexamethasone / pharmacology. Gastric Mucosa / drug effects. Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Movement / drug effects. Cells, Cultured. Dinoprostone / analysis. Fibroblast Growth Factor 2 / analysis. Prostaglandin-Endoperoxide Synthases / analysis. Rats. Rats, Wistar

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  • (PMID = 19837644.001).
  • [ISSN] 1728-7731
  • [Journal-full-title] Journal of the Chinese Medical Association : JCMA
  • [ISO-abbreviation] J Chin Med Assoc
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China (Republic : 1949- )
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 103107-01-3 / Fibroblast Growth Factor 2; 7S5I7G3JQL / Dexamethasone; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; K7Q1JQR04M / Dinoprostone
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65. Colović R, Matić S, Micev M, Grubor N, Latincić S: [Glucagonoma without glucagonoma syndrome]. Srp Arh Celok Lek; 2010 Mar-Apr;138(3-4):244-7
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  • [Title] [Glucagonoma without glucagonoma syndrome].
  • INTRODUCTION: Glucagonomas are rare, frequently malignant tumours, arising from the Langerhans' islets of the pancreas.
  • They usually secrete large amounts of glucagon that can cause a characteristic "glucagonoma syndrome", which includes necrolytic migratory erythema, glucose intolerance or diabetes, weight loss and sometimes, normochromic normocytic anaemia, stomatitis or cheilitis, diarrhoea or other digestive symptoms, thoromboembolism, hepatosplenomegaly, depression or other psychiatric and paraneoplastic symptoms.
  • In certain cases, some or all glucagonoma symptoms may appear late, or even may be completely absent.
  • CASE OUTLINE: The authors present a 43-year-old woman in whom an investigation for abdominal pain revealed a tumour of the body of the pancreas.
  • During operation, the tumour of the body of the pancreas extending to the mesentery measuring 85 x 55 x 55 mm was excised.
  • Histology and immunohistochemistry showed malignant glucagonoma, with co-expression of somatostatin in about 5% and pancreatic polypeptide in a few tumour cells.
  • CONCLUSION: Glucagonoma syndrome may be absent in glucagonoma tumour patients so that in unclear pancreatic tumours the clinician should frequently request the serum hormone level (including glucagon) measurement by radioimmunoassay and the pathologist should perform immunohistochemistry investigation.
  • Those two would probably result in discovery of more glucagonomas and other neuroendocrine tumours without characteristic clinical syndromes.
  • [MeSH-major] Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 20499510.001).
  • [ISSN] 0370-8179
  • [Journal-full-title] Srpski arhiv za celokupno lekarstvo
  • [ISO-abbreviation] Srp Arh Celok Lek
  • [Language] srp
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Serbia
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66. Indraccolo S: Interferon-alpha as angiogenesis inhibitor: learning from tumor models. Autoimmunity; 2010 Apr;43(3):244-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interferon-alpha as angiogenesis inhibitor: learning from tumor models.
  • Interferon-alpha (IFN-alpha), a cytokine with marked therapeutic activity in transplantable tumor models, has been identified as powerful angiogenesis inhibitor.
  • The effects of IFN-alpha on the vasculature have been mainly attributed to inhibition of basic fibroblast growth factor production by tumor cells or downregulation of IL-8 and vascular endothelial growth factor gene expression.
  • Moreover, IFN-alpha has direct effects on endothelial cells (EC), including impairment of their proliferation and migration.
  • The gene expression profile induced by IFN-alpha in EC has recently been defined, and it was found that several genes encoding negative regulators of angiogenesis are upmodulated, thus providing a potential amplification mechanism for this biological activity.
  • The anti-angiogenic effects of IFN-alpha appear to be associated with increased hypoxia and ischemic necrosis in subcutaneous xenograft models, whereas in transgenic mouse models, IFN-alpha may simultaneously interfere with both blood vessels and tumor cell proliferation, leading to regression of tumors without necrosis.
  • The consequences of IFN-alpha therapy on the invasive and metastatic behavior of tumor cells are currently unknown.
  • Finally, as effective anti-angiogenic therapy with IFN-alpha demands sustained localized production of this cytokine, innovative strategies of targeted delivery of the IFN-alpha gene into tumors are discussed.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Interferon-alpha / pharmacology. Neoplasms, Experimental / blood supply. Neoplasms, Experimental / therapy

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  • (PMID = 20166871.001).
  • [ISSN] 1607-842X
  • [Journal-full-title] Autoimmunity
  • [ISO-abbreviation] Autoimmunity
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Interferon-alpha
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67. Singh Jaggi J, Henke E, Seshan SV, Kappel BJ, Chattopadhyay D, May C, McDevitt MR, Nolan D, Mittal V, Benezra R, Scheinberg DA: Selective alpha-particle mediated depletion of tumor vasculature with vascular normalization. PLoS One; 2007 Mar 07;2(3):e267
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selective alpha-particle mediated depletion of tumor vasculature with vascular normalization.
  • BACKGROUND: Abnormal regulation of angiogenesis in tumors results in the formation of vessels that are necessary for tumor growth, but compromised in structure and function.
  • Abnormal tumor vasculature impairs oxygen and drug delivery and results in radiotherapy and chemotherapy resistance, respectively.
  • Alpha particles are extraordinarily potent, short-ranged radiations with geometry uniquely suitable for selectively killing neovasculature.
  • METHODOLOGY AND PRINCIPAL FINDINGS: Actinium-225 ((225)Ac)-E4G10, an alpha-emitting antibody construct reactive with the unengaged form of vascular endothelial cadherin, is capable of potent, selective killing of tumor neovascular endothelium and late endothelial progenitors in bone-marrow and blood.
  • In a mouse-model of prostatic carcinoma, (225)Ac-E4G10 treatment resulted in inhibition of tumor growth, lower serum prostate specific antigen level and markedly prolonged survival, which was further enhanced by subsequent administration of paclitaxel.
  • Immunohistochemistry revealed lower vessel density and enhanced tumor cell apoptosis in (225)Ac-E4G10 treated tumors.
  • Additionally, the residual tumor vasculature appeared normalized as evident by enhanced pericyte coverage following (225)Ac-E4G10 therapy.
  • CONCLUSIONS: The data suggest that alpha-particle immunotherapy to neovasculature, alone or in combination with sequential chemotherapy, is an effective approach to cancer therapy.

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  • [Cites] Cancer Biother Radiopharm. 2000 Feb;15(1):71-9 [10740655.001]
  • [Cites] Blood. 2005 Jun 1;105(11):4337-44 [15701713.001]
  • [Cites] Nature. 2000 Sep 14;407(6801):249-57 [11001068.001]
  • [Cites] J Biol Chem. 2001 Aug 24;276(34):31959-68 [11399763.001]
  • [Cites] Nat Med. 2001 Sep;7(9):987-9 [11533692.001]
  • [Cites] Curr Opin Pharmacol. 2001 Aug;1(4):378-84 [11710736.001]
  • [Cites] Science. 2001 Nov 16;294(5546):1537-40 [11711678.001]
  • [Cites] Cancer Res. 2002 May 1;62(9):2567-75 [11980651.001]
  • [Cites] Radiat Res. 2002 Jun;157(6):633-41 [12005541.001]
  • [Cites] Cell Death Differ. 2002 Jun;9(6):593-4 [12032666.001]
  • [Cites] Cancer Res. 2002 Jun 1;62(11):3298-307 [12036948.001]
  • [Cites] Appl Radiat Isot. 2002 Dec;57(6):841-7 [12406626.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2002 Nov 15;54(4):1259-75 [12419456.001]
  • [Cites] Cancer Res. 2003 Aug 15;63(16):5084-90 [12941838.001]
  • [Cites] Mol Cancer Res. 2004 Jan;2(1):36-42 [14757844.001]
  • [Cites] Clin Cancer Res. 2004 Jan 15;10(2):415-27 [14760060.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2004 Mar 15;58(4):1215-27 [15001266.001]
  • [Cites] Cancer Res. 2004 Jun 1;64(11):3731-6 [15172975.001]
  • [Cites] Clin Cancer Res. 2004 Oct 15;10(20):6985-92 [15501978.001]
  • [Cites] Radiat Res. 1991 Nov;128(2):204-9 [1947017.001]
  • [Cites] Cancer Res. 1992 Mar 15;52(6):1598-605 [1371718.001]
  • [Cites] Cancer Res. 2005 Jun 1;65(11):4888-95 [15930310.001]
  • [Cites] Nature. 2005 Jul 28;436(7050):568-72 [16049491.001]
  • [Cites] J Am Soc Nephrol. 2005 Sep;16(9):2677-89 [15987754.001]
  • [Cites] Oncology. 2005;69(2):159-66 [16127287.001]
  • [Cites] Cancer Cell. 2005 Oct;8(4):299-309 [16226705.001]
  • [Cites] J Clin Invest. 2006 Mar;116(3):642-51 [16470244.001]
  • [Cites] Curr Med Chem. 2006;13(8):849-62 [16611071.001]
  • [Cites] J Nucl Med. 2006 Jul;47(7):1127-35 [16818947.001]
  • [Cites] Clin Cancer Res. 2006 Jul 15;12(14 Pt 1):4331-8 [16857808.001]
  • [Cites] Nat Rev Cancer. 2006 Aug;6(8):626-35 [16837971.001]
  • [Cites] Science. 2006 Sep 22;313(5794):1785-7 [16990548.001]
  • [Cites] J Clin Invest. 2006 Oct;116(10):2610-21 [17016557.001]
  • [Cites] Cell. 1996 Aug 9;86(3):353-64 [8756718.001]
  • [Cites] Anat Rec. 1997 Sep;249(1):63-73 [9294650.001]
  • [Cites] AJR Am J Roentgenol. 1998 Oct;171(4):941-9 [9762973.001]
  • [Cites] Clin Cancer Res. 1996 Nov;2(11):1843-9 [9816139.001]
  • [Cites] Cancer Cell. 2004 Dec;6(6):553-63 [15607960.001]
  • [Cites] Am J Pathol. 2000 Apr;156(4):1363-80 [10751361.001]
  • (PMID = 17342201.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA055349; United States / PHS HHS / / P01-33049; United States / NCI NIH HHS / CA / R01-CA 55349
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Indium Radioisotopes; NIK1K0956U / Actinium
  • [Other-IDs] NLM/ PMC1801076
  • [General-notes] NLM/ Original DateCompleted: 20070725
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68. Kobayashi T, Kawakita M, Terachi T, Habuchi T, Ogawa O, Kamoto T: Significance of elevated preoperative alpha-fetoprotein in postchemotherapy residual tumor resection for the disseminated germ cell tumors. J Surg Oncol; 2006 Dec 1;94(7):619-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Significance of elevated preoperative alpha-fetoprotein in postchemotherapy residual tumor resection for the disseminated germ cell tumors.
  • BACKGROUND AND OBJECTIVES: The purpose of the study is to determine the significance of elevated serum alpha-fetoprotein (AFP) in the setting prior to residual tumor resection (RTR) following chemotherapy for metastatic germ cell tumor in terms of the prediction of histology of the specimen and postoperative survival.
  • METHODS: We conducted a retrospective review of 68 patients undergoing RTR for metastatic nonseminomatous germ cell tumor or extragonadal germ cell tumor after at least a first-line chemotherapy.
  • Rates of presence of residual malignant cell in RTR specimen were similar between patients with normal AFP (7/28 or 25%) and with mildly elevated (10-30 ng/ml) AFP (3/11 or 27%).
  • [MeSH-major] Biomarkers, Tumor / blood. Chorionic Gonadotropin, beta Subunit, Human / blood. Neoplasms, Germ Cell and Embryonal / surgery. Testicular Neoplasms / surgery. alpha-Fetoproteins / metabolism

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 17111392.001).
  • [ISSN] 0022-4790
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / alpha-Fetoproteins
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69. Lisková K, Kelly AL, O'Brien N, Brodkorb A: Effect of denaturation of alpha-lactalbumin on the formation of BAMLET (bovine alpha-lactalbumin made lethal to tumor cells). J Agric Food Chem; 2010 Apr 14;58(7):4421-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of denaturation of alpha-lactalbumin on the formation of BAMLET (bovine alpha-lactalbumin made lethal to tumor cells).
  • A complex of alpha-lactalbumin with oleic acid, also known as HAMLET/BAMLET (human/bovine alpha-lactalbumin made lethal to tumor cells), causes apoptosis-like death in tumor cells but has little effect on healthy differentiated cells.
  • The aim of this study was to examine whether irreversible denaturation of alpha-lactalbumin is detrimental to the formation and cytotoxicity of BAMLET.
  • Commercial bovine holo alpha-lactalbumin (1-4% w/v) was heated at 80 degrees C for up to 100 min.
  • With an increasing concentration of protein, the denaturation of alpha-lactalbumin proceeded faster, and aggregation became more extensive.
  • BAMLET was prepared from native and heat-treated alpha-lactalbumin according to a previously described chromatographic method.
  • Despite the high content of denatured and aggregated alpha-lactalbumin in the heat-treated samples, their conversion into BAMLET was not negatively affected, resulting in BAMLET complexes partly composed of covalently linked aggregates of alpha-lactalbumin.
  • The cytotoxicity of all prepared BAMLET samples was comparable to that of the control sample prepared from native alpha-lactalbumin (LD(50) = 34.6 +/- 2.7 mumol L(-1)).
  • It was concluded that alpha-lactalbumin is not required to be in its native conformation for the conversion into its biologically active BAMLET complex.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cattle. Cell Line, Tumor. Humans. Protein Conformation. Protein Denaturation. Protein Folding. Structure-Activity Relationship

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  • (PMID = 20232795.001).
  • [ISSN] 1520-5118
  • [Journal-full-title] Journal of agricultural and food chemistry
  • [ISO-abbreviation] J. Agric. Food Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 9013-90-5 / Lactalbumin
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70. Yang X, Chu Y, Wang Y, Guo Q, Xiong S: Vaccination with IFN-inducible T cell alpha chemoattractant (ITAC) gene-modified tumor cell attenuates disseminated metastases of circulating tumor cells. Vaccine; 2006 Apr 5;24(15):2966-74

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vaccination with IFN-inducible T cell alpha chemoattractant (ITAC) gene-modified tumor cell attenuates disseminated metastases of circulating tumor cells.
  • IFN-inducible T cell alpha chemoattractant (ITAC) has been demonstrated to be able to induce Th1-type immune response.
  • However, the effects of ITAC on the tumor metastasis have not been fully understood.
  • In the present study, the ITAC-modified tumor cell vaccine in inhibiting the disseminated pulmonary metastasis was evaluated.
  • ITAC-modified tumor cell vaccine 4T1-ITAC was developed by stably transfecting 4T1 cells with pcDNA3-ITAC plasmid.
  • The number of clonogenic metastatic tumor cells and metastatic forci on the surface of lung were counted by histological examination.
  • Results showed that a significant enhancement of proliferative and cytotoxic activities accompanied with increased IFN-gamma and TNF-alpha production as well as decreased IL-4 production were obtained from the mice vaccinated with 4T1-ITAC.
  • The number of clonogenic metastatic tumor cells in the mice vaccinated with 4T1-ITAC cells reduced markedly and no visible metastasis was found in the lungs of the 4T1-ITAC vaccinated mice.
  • Taken together, our results demonstrated that ITAC-modified tumor cell vaccine can enhance the anti-tumor immunity and reduce the incidence of disseminated metastasis.
  • [MeSH-minor] Animals. Cell Line, Tumor. Chemokine CXCL11. Colon / pathology. Cytokines / biosynthesis. Cytotoxicity Tests, Immunologic. Female. Histocytochemistry. Lung / pathology. Mice. Mice, Inbred BALB C. T-Lymphocytes / immunology. Vaccines, Synthetic / genetics. Vaccines, Synthetic / immunology

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  • (PMID = 16503368.001).
  • [ISSN] 0264-410X
  • [Journal-full-title] Vaccine
  • [ISO-abbreviation] Vaccine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Chemokine CXCL11; 0 / Chemokines, CXC; 0 / Cxcl11 protein, mouse; 0 / Cytokines; 0 / Vaccines, Synthetic
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71. Niu JX, Zhang WJ, Ye LY, Wu LQ, Zhu GJ, Yang ZH, Grau GE, Lou JN: The role of adhesion molecules, alpha v beta 3, alpha v beta 5 and their ligands in the tumor cell and endothelial cell adhesion. Eur J Cancer Prev; 2007 Dec;16(6):517-27
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of adhesion molecules, alpha v beta 3, alpha v beta 5 and their ligands in the tumor cell and endothelial cell adhesion.
  • Tumor metastasis is a complex process involving the interaction between tumor cells and endothelial cells in which some adhesion molecules play an important role.
  • It was our aim to investigate the role of the adhesion molecules, alpha v beta 3 and alpha v beta 5 and their ligands, developmental endothelial locus-1 (Del-1) and L1, in tumor cell adhesion to endothelial cells in vitro.
  • In this study, the expression and regulation of alpha v beta 3, alpha v beta 5 and intercellular adhesion molecule -1 on liver sinusoidal endothelial cells and liver cancer endothelial cells (T3A) were analyzed by real-time PCR and fluorescent-activated cell sorter.
  • The expression and regulation of the integrin ligands, Del-1 and L1, in six tumor cell lines were analyzed by real-time PCR and western blot.
  • We found the expressions of alpha v beta 3 and alpha v beta 5 were higher on T3A than that on liver sinusoidal endothelial cells, whereas expression of intercellular adhesion molecule-1 was lower on T3A than that on liver sinusoidal endothelial cells.
  • After 24 h hypoxia, the expressions of alpha v beta 3 and alpha v beta 5 were upregulated on T3A and liver sinusoidal endothelial cells; the expression of intercellular adhesion molecule-1 was increased on liver sinusoidal endothelial cells, but remained unchanged on T3A.
  • Del-1 and L1 expression levels were obviously diverse in various tumor cell lines and differentially modulated after 12 h hypoxia.
  • The adhesion of tumor cells with Del-1 and L1 expression was higher in T3A than that in liver sinusoidal endothelial cells, and was significantly increased under hypoxic conditions.
  • Interestingly, the tumor cell adherence could be inhibited by antibodies against alpha v beta 5 and alpha v beta 5, but not by an antibody against intercellular adhesion molecule-1.
  • The adhesion of tumor cells without Del-1 and L1 expression was also higher on T3A than that on liver sinusoidal endothelial cells, but the adhesion could not be inhibited by antibodies against alpha v beta 5, alpha v beta 5 or intercellular adhesion molecule-1, suggesting that other receptors are involved.
  • In conclusion, alpha v beta 5, alpha v beta 5 and their ligands Del-1 and L1 play an important role in the process of tumor cells moving from the original place.
  • [MeSH-major] Carrier Proteins / physiology. Endothelial Cells / physiology. Integrin alphaVbeta3 / physiology. Integrin beta Chains / physiology. Neoplasms / pathology. Neural Cell Adhesion Molecule L1 / physiology
  • [MeSH-minor] Cell Adhesion. Cell Adhesion Molecules / metabolism. Cell Adhesion Molecules / physiology. Cell Hypoxia / physiology. Cell Line, Tumor. Cell Movement / physiology. Cells, Cultured. Humans. Ligands. RNA Interference / physiology

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  • (PMID = 18090124.001).
  • [ISSN] 0959-8278
  • [Journal-full-title] European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)
  • [ISO-abbreviation] Eur. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Cell Adhesion Molecules; 0 / EDIL3 protein, human; 0 / Integrin alphaVbeta3; 0 / Integrin beta Chains; 0 / Ligands; 0 / Neural Cell Adhesion Molecule L1; 0 / integrin beta5
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72. Kesik V, Ozcan A, Sari E, Guven A, Kismet E, Koseoglu V: Alpha-fetoprotein producing tumor cells in children with Wilms' tumor. Fetal Pediatr Pathol; 2010;29(3):127-32
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  • [Title] Alpha-fetoprotein producing tumor cells in children with Wilms' tumor.
  • Alpha fetoprotein (AFP) is generally used as a marker in diagnosis and follow-up of germ cell tumors and hepatoblastomas.
  • However, serum AFP levels were elevated in our three patients with Wilms tumor.
  • Histopathologically, the tumors consisted of blastemal, stromal, and epithelial cells.
  • Chemotherapy was only effective on stromal and epithelial components of the tumors.
  • In AFP staining, the source of AFP production was identified as blastemal tumor cells.
  • Because the increased AFP levels were decreased after surgery, AFP levels may be used in the follow-up of the patients with Wilms tumor.
  • Herein, we report three patients with Wilms tumor whose serum AFP levels were elevated and who had diffuse WT-1 and focal AFP expression in all tumors, immunohistochemically.
  • [MeSH-major] Kidney Neoplasms / metabolism. Wilms Tumor / metabolism. alpha-Fetoproteins / metabolism
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Chemotherapy, Adjuvant. Child, Preschool. Female. Humans. Infant. Neoplasm Staging. Nephrectomy. Prognosis. Remission Induction

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  • (PMID = 20450265.001).
  • [ISSN] 1551-3823
  • [Journal-full-title] Fetal and pediatric pathology
  • [ISO-abbreviation] Fetal Pediatr Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / alpha-Fetoproteins
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73. Hwang SM, Lee YJ, Yoon JJ, Lee SM, Kang DG, Lee HS: Gardenia jasminoides inhibits tumor necrosis factor-alpha-induced vascular inflammation in endothelial cells. Phytother Res; 2010 Jun;24 Suppl 2:S214-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gardenia jasminoides inhibits tumor necrosis factor-alpha-induced vascular inflammation in endothelial cells.
  • Inflammatory mediators such as tumor necrosis factor-alpha (TNF-alpha) enhance binding of low-density lipoprotein to endothelium and upregulate the expression of endothelial leukocyte adhesion molecules during atherogenesis.
  • The present study examined the effect of ethanol extract of Gardenia jasminoides (EGJ) on vascular inflammation in primary cultured human umbilical vein endothelial cells (HUVEC).
  • TNF-alpha-induced the expression of vascular cell adhesion molecule-1 (VCAM-1) and endothelial cell-selectin (E-selectin) expression was inhibited in HUVEC pretreated with EGJ.
  • A further analysis indicated that EGJ attenuated TNF-alpha-induced nuclear p65 nuclear factor-kappa B (NF-kappaB) translocation, suggesting that EGJ primarily affects the TNF-alpha-induced NF-kappaB signaling pathway.
  • Taken together, we provided here the first evidence showing that EGJ is able to inhibit TNF-alpha-induced NF-kappaB activation, adhesion molecule expression, and monocyte-endothelial interaction, suggesting an anti-inflammatory role of EGJ, which may be useful in preventing vascular diseases, such as atherosclerosis.
  • [MeSH-major] Endothelial Cells / drug effects. Gardenia / chemistry. Plant Extracts / pharmacology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Cell Adhesion. Cells, Cultured. E-Selectin / metabolism. Humans. I-kappa B Proteins / metabolism. Monocytes / cytology. NF-kappa B / metabolism. Umbilical Veins / cytology. Vascular Cell Adhesion Molecule-1 / metabolism

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  • [ErratumIn] Phytother Res. 2010 Jun;24 Suppl 2:S233-4
  • (PMID = 20104512.001).
  • [ISSN] 1099-1573
  • [Journal-full-title] Phytotherapy research : PTR
  • [ISO-abbreviation] Phytother Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / E-Selectin; 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / Plant Extracts; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Cell Adhesion Molecule-1; 139874-52-5 / NF-kappaB inhibitor alpha
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74. Lee J, Lee SH, Shin N, Jeong M, Kim MS, Kim MJ, Yoon SR, Chung JW, Kim TD, Choi I: Tumor necrosis factor-alpha enhances IL-15-induced natural killer cell differentiation. Biochem Biophys Res Commun; 2009 Sep 4;386(4):718-23
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  • [Title] Tumor necrosis factor-alpha enhances IL-15-induced natural killer cell differentiation.
  • The differentiation of natural killer (NK) cells is regulated by various factors including soluble growth factors and transcription factors.
  • Here, we have demonstrated that tumor necrosis factor-alpha (TNF-alpha) is a positive regulator of NK cell differentiation.
  • TNF-alpha augmented the IL-15-induced expression of NK1.1 and CD122 in mature NK cells, and TNF-alpha alone also induced NK cell maturation as well as IL-15.
  • TNF-alpha also increased IFN-gamma production in NK cells in the presence of IL-15.
  • Meanwhile, mRNA expression of several transcription factors, including T-bet and GATA-3, was increased by the addition of TNF-alpha and IL-15.
  • In addition, TNF-alpha increased nuclear factor-kappa B (NF-kappaB) activity in NK cells and inhibition of NF-kappaB impeded TNF-alpha-enhanced NK cell maturation.
  • Overall, these data suggest that TNF-alpha significantly increased IL-15-driven NK cell differentiation by increasing the expression of transcription factors that play crucial roles in NK cell maturation and inducing the NF-kappaB activity.
  • [MeSH-major] Cell Differentiation. Interleukin-15 / physiology. Killer Cells, Natural / cytology. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Animals. Antigens, Ly / biosynthesis. Interleukin-2 Receptor beta Subunit / biosynthesis. Mice. Mice, Inbred C57BL. NK Cell Lectin-Like Receptor Subfamily B / biosynthesis

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  • (PMID = 19559672.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Ly; 0 / Il2rb protein, mouse; 0 / Interleukin-15; 0 / Interleukin-2 Receptor beta Subunit; 0 / Klrb1c protein, mouse; 0 / NK Cell Lectin-Like Receptor Subfamily B; 0 / Tumor Necrosis Factor-alpha
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75. Chen Q, Zhao Y, Cheng Z, Xu Y, Yu C: Establishment of a cell-based assay for examining the expression of tumor necrosis factor alpha (TNF-alpha) gene. Appl Microbiol Biotechnol; 2008 Aug;80(2):357-63

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Establishment of a cell-based assay for examining the expression of tumor necrosis factor alpha (TNF-alpha) gene.
  • Tumor necrosis factor alpha (TNF-alpha) is a proinflammatory cytokine produced by activated macrophages and lymphocytes and involved in many inflammatory diseases.
  • Preventing the production or action of TNF-alpha is a potent therapeutic strategy for these inflammatory diseases.
  • Since there is a lack of rapid and effective assay for examining the expression TNF-alpha in macrophages, we attempt to establish a reporter system to assess TNF-alpha gene expression through measuring luciferase activity.
  • In this study, mouse macrophage cell line RAW 264.7 was stably transfected with a luciferase reporter pGL3-TNFPro-UTR, which contains TNF-alpha promoter and 3'-untranslated region (3'-UTR).
  • The TNF-alpha-luciferase reporter cell line is used for assessing the expression of TNF-alpha gene induced by LPS in the presence or absence of chemicals that inhibit the biosynthesis of TNF-alpha such as dexamethasone and emodin, and also for measuring change of expression of TNF-alpha gene under downregulation of the expression of steroid receptor coactivator-3, a modulator for TNF-alpha.
  • The luciferase activity correlated well with the ELISA results for TNF-alpha production, therefore, the TNF-alpha-luciferase reporter cell line is a sensitive, effective tool for studying the expression of TNF-alpha gene.
  • [MeSH-major] Gene Expression. Luminescent Measurements / methods. Macrophages / immunology. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Cell Line. Enzyme-Linked Immunosorbent Assay. Genes, Reporter. Luciferases / genetics. Luciferases / metabolism. Mice

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  • (PMID = 18560829.001).
  • [ISSN] 0175-7598
  • [Journal-full-title] Applied microbiology and biotechnology
  • [ISO-abbreviation] Appl. Microbiol. Biotechnol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; EC 1.13.12.- / Luciferases
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76. Visaria RK, Griffin RJ, Williams BW, Ebbini ES, Paciotti GF, Song CW, Bischof JC: Enhancement of tumor thermal therapy using gold nanoparticle-assisted tumor necrosis factor-alpha delivery. Mol Cancer Ther; 2006 Apr;5(4):1014-20
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  • [Title] Enhancement of tumor thermal therapy using gold nanoparticle-assisted tumor necrosis factor-alpha delivery.
  • Tumor necrosis factor-alpha (TNF-alpha) is a potent cytokine with anticancer efficacy that can significantly enhance hyperthermic injury.
  • However, TNF-alpha is systemically toxic, thereby creating a need for its selective tumor delivery.
  • We used a newly developed nanoparticle delivery system consisting of 33-nm polyethylene glycol-coated colloidal gold nanoparticles (PT-cAu-TNF-alpha) with incorporated TNF-alpha payload (several hundred TNF-alpha molecules per nanoparticle) to maximize tumor damage and minimize systemic exposure to TNF-alpha.
  • SCK mammary carcinomas grown in A/J mice were treated with 125 or 250 microg/kg PT-cAu-TNF-alpha alone or followed by local heating at 42.5 degrees C using a water bath for 60 minutes, 4 hours after nanoparticle injection.
  • Increases in tumor growth delay were observed for both PT-cAu-TNF-alpha alone and heat alone, although the most dramatic effect was found in the combination treatment.
  • Tumor blood flow was significantly suppressed 4 hours after an i.v. injection of free TNF-alpha or PT-cAu-TNF-alpha.
  • Tumor perfusion, imaged by contrast enhanced ultrasonography, on days 1 and 5 after treatment revealed perfusion defects after the injection of PT-cAu-TNF-alpha alone and, in many regions, complete flow inhibition in tumors treated with combination treatment.
  • The combination treatment of SCK tumors in vivo reduced the in vivo/in vitro tumor cell survival to 0.05% immediately following heating and to 0.005% at 18 hours after heating, suggesting vascular damage-mediated tumor cell killing.
  • Thermally induced tumor growth delay was enhanced by pretreatment with TNF-alpha-coated gold nanoparticles when given i.v. at the proper dosage and timing.
  • [MeSH-major] Gold. Mammary Neoplasms, Experimental / therapy. Tumor Necrosis Factor-alpha / pharmacokinetics. Tumor Necrosis Factor-alpha / therapeutic use
  • [MeSH-minor] Animals. Biological Transport. Cell Survival / drug effects. Cell Survival / physiology. Hyperthermia, Induced. Mice. Nanostructures. Rubidium / pharmacokinetics

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  • (PMID = 16648573.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA44114
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; 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 / Tumor Necrosis Factor-alpha; 7440-57-5 / Gold; MLT4718TJW / Rubidium
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77. Wacnik PW, Eikmeier LJ, Simone DA, Wilcox GL, Beitz AJ: Nociceptive characteristics of tumor necrosis factor-alpha in naive and tumor-bearing mice. Neuroscience; 2005;132(2):479-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nociceptive characteristics of tumor necrosis factor-alpha in naive and tumor-bearing mice.
  • A nociceptive role for tumor necrosis factor-alpha (TNF-alpha) in naive mice and in mice with fibrosarcoma tumor-induced primary hyperalgesia was investigated.
  • The presence of TNF-alpha mRNA was confirmed in tumor site homogenates by reverse transcription-polymerase chain reaction (RT-PCR), and examination of TNF-alpha protein levels in tumor-bearing mice indicated a significantly higher concentration of this cytokine in tumor microperfusates and tumor site homogenates compared with that obtained from a similar site on the contralateral limb or in naive mice.
  • Intraplantar injection of TNF-alpha into naive or fibrosarcoma tumor-bearing mice induced mechanical hypersensitivity, as measured by withdrawal responses evoked by von Frey monofilaments.
  • This hypersensitivity suggests that TNF-alpha can excite or sensitize primary afferent fibers to mechanical stimulation in both naive and tumor-bearing mice.
  • In addition, the hyperalgesia produced by TNF-alpha was completely eliminated when the injected TNF-alpha was pre-incubated with the soluble receptor antagonist TNFR:Fc.
  • Importantly, pre-implantation systemic as well as post-implantation intra-tumor injection of TNFR:Fc partially blocked the mechanical hyperalgesia, indicating that local production of TNF-alpha may contribute to tumor-induced nociception.
  • [MeSH-major] Fibrosarcoma / metabolism. Neoplasms, Experimental / metabolism. Pain / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Behavior, Animal. Cell Line, Tumor. Gene Expression Regulation, Neoplastic / physiology. Immunohistochemistry / methods. Male. Mice. Mice, Inbred C3H. Neoplasm Transplantation. Pain Measurement / methods. RNA, Messenger / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 15802198.001).
  • [ISSN] 0306-4522
  • [Journal-full-title] Neuroscience
  • [ISO-abbreviation] Neuroscience
  • [Language] eng
  • [Grant] United States / NIDCR NIH HHS / DE / 5T 32-DEO 7288-02; United States / NIDA NIH HHS / DA / DA07239; United States / NCI NIH HHS / CA / R01-CA72669; United States / NCI NIH HHS / CA / R01-CA84233; United States / NCI NIH HHS / CA / R01-CA91007; United States / NCI NIH HHS / CA / R21-CA86330
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha
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78. Luo JC, Shin VY, Yang YH, Wu WK, Ye YN, So WH, Chang FY, Cho CH: Tumor necrosis factor-alpha stimulates gastric epithelial cell proliferation. Am J Physiol Gastrointest Liver Physiol; 2005 Jan;288(1):G32-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor necrosis factor-alpha stimulates gastric epithelial cell proliferation.
  • TNF-alpha is a cytokine produced during gastric mucosal injury.
  • We examined whether TNF-alpha could promote mucosal repair by stimulation of epithelial cell proliferation and explored further the underlying mechanisms in a rat gastric mucosal epithelial cell line (RGM-1).
  • TNF-alpha treatment (1-10 ng/ml) for 12 or 24 h significantly increased cell proliferation but did not induce apoptosis in RGM-1 cells.
  • TNF-alpha treatment significantly increased cytosolic phospholipase A(2) and cyclooxygenase-2 (COX-2) protein expression and PGE(2) level but did not affect the protein levels of EGF, basic fibroblast growth factor, and COX-1 in RGM-1 cells.
  • Dexamethasone dose dependently inhibited the stimulatory effect of TNF-alpha on cell proliferation, which was associated with a significant decrease in cellular COX-2 expression and PGE(2) level.
  • A selective COX-2 inhibitor 3-(3-fluorophenyl)-4-[4-(methylsulfonyl)phenyl]-5,5-dimethyl-(5)H-furan-2-one (DFU) by itself had no effect on basal cell proliferation but significantly reduced the stimulatory effect of TNF-alpha on RMG-1 cells.
  • PGE(2) significantly reversed the depressive action of dexamethasone on cell proliferation.
  • These results suggest that TNF-alpha plays a regulatory role in epithelial cell repair in the gastric mucosa via the TNF-alpha receptor and activation of the arachidonic acid/PG pathway.
  • [MeSH-major] Cell Proliferation. Gastric Mucosa / cytology. Gastric Mucosa / pathology. Stomach / cytology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Apoptosis. Arachidonic Acid / pharmacology. Cell Survival. Cyclooxygenase 2. Dinoprostone / pharmacology. Epithelial Cells / physiology. Gene Expression Regulation. Prostaglandin-Endoperoxide Synthases / biosynthesis. Rats

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  • (PMID = 15256360.001).
  • [ISSN] 0193-1857
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 27YG812J1I / Arachidonic Acid; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; K7Q1JQR04M / Dinoprostone
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79. de Vries-van Leeuwen IJ, Kortekaas-Thijssen C, Nzigou Mandouckou JA, Kas S, Evidente A, de Boer AH: Fusicoccin-A selectively induces apoptosis in tumor cells after interferon-alpha priming. Cancer Lett; 2010 Jul 28;293(2):198-206

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fusicoccin-A selectively induces apoptosis in tumor cells after interferon-alpha priming.
  • Here we analysed the effect of the natural occurring fusicoccanes, Fusicoccin-A (FC), Ophiobolin-A (OPH-A) and Ophiobolin-I (OPH-I) on various tumor cell lines.
  • Both FC and OPH-A inhibit tumor cell growth efficiently, in contrast to OPH-I.
  • Further analysis showed that FC is tumor specific, and that its efficacy can be enhanced by combining it with the cytokine interferon-alpha (IFN-alpha).
  • In this, IFN-alpha primes the tumor cells for apoptosis induction by FC, in which DR4 and the TRAIL pathway plays an important role.
  • Healthy cells (HUVECs, Human Umbilical Vein Endothelial Cells) are far less sensitive to IFN-alpha/FC treatment and need the continuous presence of both compounds in order to achieve a growth reduction.
  • This differential response between healthy and tumor cells indicates that the IFN-alpha/FC treatment is a promising new cancer treatment, especially when IFN-alpha and FC are used sequentially.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Glycosides / pharmacology. Interferon-alpha / pharmacology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Cell Line. Cell Line, Tumor. Humans. Sesterterpenes / pharmacology. TNF-Related Apoptosis-Inducing Ligand / metabolism

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  • [Copyright] Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20153922.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Glycosides; 0 / Interferon-alpha; 0 / Sesterterpenes; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / ophiobolins; 20108-30-9 / fusicoccin
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80. Hara H, Kobayashi A, Narumi K, Kondoh A, Yoshida K, Nishimoto T, Ohashi M, Higashihara E, Ohnami S, Yoshida T, Aoki K: Intratumoral interferon-alpha gene transfer enhances tumor immunity after allogeneic hematopoietic stem cell transplantation. Cancer Immunol Immunother; 2009 Jul;58(7):1007-21
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  • [Title] Intratumoral interferon-alpha gene transfer enhances tumor immunity after allogeneic hematopoietic stem cell transplantation.
  • One of the major challenges in the treatment of solid cancers by allogenic hematopoietic stem cell transfer (alloHSCT) is the specific enhancement of antitumor immunity.
  • Interferon (IFN) is a cytokine with pleiotropic biological functions including an immunomoduration, and our preclinical studies have shown that an intratumoral IFN-alpha gene transfer induced strong local tumor control and systemic tumor-specific immunity.
  • In the present study, we examined whether the IFN-alpha gene transfer could enhance recognition of tumor-associated antigens by donor T cells and augment the antitumor activity of alloHSCT.
  • First, when a mouse IFN-alpha adenovirus vector (Ad-mIFN) was injected into subcutaneous xenografts of syngeneic renal and colon cancer cells, tumor growth was significantly suppressed in a dose-dependent manner.
  • A significant tumor cell death and infiltration of immune cells was recognized in the Ad-mIFN-injected tumors, and the dendritic cells isolated from the tumors showed a strong Th1-oriented response.
  • The antitumor effect of Ad-mIFN was then examined in a murine model of minor histocompatibility antigen-mismatched alloHSCT.
  • The intratumoral IFN-alpha gene transfer caused significant tumor suppression in the alloHSCT recipients, and this suppression was evident not only in the gene-transduced tumors but also in simultaneously inoculated distant tumors which did not receive the vector injection.
  • A cytotoxicity assay showed specific tumor cell lysis by donor T cells responding to IFN-alpha.
  • Graft-versus-host disease was not exacerbated serologically or clinically in the mice treated with IFN-alpha.
  • [MeSH-major] Colonic Neoplasms / immunology. Hematopoietic Stem Cell Transplantation. Hematopoietic Stem Cells / immunology. Interferon-alpha / genetics. Kidney Neoplasms / immunology
  • [MeSH-minor] Animals. CD8-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / metabolism. Cell Line, Tumor. Dendritic Cells / immunology. Dendritic Cells / metabolism. Female. Gene Transfer Techniques. Genetic Therapy. Genetic Vectors. Graft vs Host Disease / immunology. Killer Cells, Natural / immunology. Killer Cells, Natural / metabolism. Lymphoma / immunology. Mice. Mice, Inbred BALB C. Mice, Inbred DBA

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  • (PMID = 18998126.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Interferon-alpha
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81. Tong AL, Zeng ZP, Li HZ, Yang D, Lu L, Li M: Expression and effect of transforming growth factor-alpha and tumor necrosis factor-alpha in human pheochromocytoma. Ann N Y Acad Sci; 2006 Aug;1073:277-83
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  • [Title] Expression and effect of transforming growth factor-alpha and tumor necrosis factor-alpha in human pheochromocytoma.
  • This study observed the expression of transforming growth factor-alpha (TGF-alpha) and tumor necrosis factor-alpha (TNF-alpha) in pheochromocytoma (PHEO) tissue and examined their effects on the proliferation and apoptosis of human PHEO cells.
  • The mRNA and protein expressions of TGF-alpha and TNF-alpha were higher in PHEO tissues than in normal adrenal medullary tissues, and their expressions varied with pathological features.
  • TGF-alpha and TNF-alpha stimulated the proliferation of primary human PHEO cells, but had no effect on the cell apoptosis.
  • Both TGF-alpha and TNF-alpha might be involved in the pathogenesis of human PHEO.
  • TNF-alpha needs to be further investigated before its treatment of PHEO can be realized in clinical practice.
  • [MeSH-major] Adrenal Gland Neoplasms / metabolism. Pheochromocytoma / metabolism. Transforming Growth Factor alpha / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Apoptosis. Cell Proliferation. Humans. Immunohistochemistry. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17102096.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Transforming Growth Factor alpha; 0 / Tumor Necrosis Factor-alpha
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82. Liu CJ, Wong YK, Chang KW, Chang HC, Liu HF, Lee YJ: Tumor necrosis factor-alpha promoter polymorphism is associated with susceptibility to oral squamous cell carcinoma. J Oral Pathol Med; 2005 Nov;34(10):608-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor necrosis factor-alpha promoter polymorphism is associated with susceptibility to oral squamous cell carcinoma.
  • BACKGROUND: Oral squamous cell carcinoma (OSCC) is one of the leading cancers in most Asian countries.
  • The pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) is a central mediator of the immune response involved in a wide range of immuno-inflammatory and infectious diseases.
  • Polymorphism of the TNF-alpha gene has been intensively studied as a potential determinant of susceptibility to numerous cancers.
  • METHODS: We genotyped 192 patients with OSCC and 146 healthy case controls by using polymerase chain reaction-double restriction fragment length polymorphism with amplification-created restriction sites to assess allelic determinants at the TNF-alpha polymorphic sites -308 and -238 in the promoter region.
  • RESULTS: The -308 TNFG (tumor necrosis factor G) allele genotype was higher in patients with OSCC (91.2% vs. 82.2%; P = 0.02) and TNFG/A was lower (8.3% vs. 11.8%; P = 0.02); the -238 TNFG/A allele genotype was lower in patient with OSCC (2.1% vs. 6.9%; P = 0.02).
  • CONCLUSION: This is the first report that the TNF-alpha polymorphism is associated with the risk for OSCC in Taiwan.
  • [MeSH-major] Carcinoma, Squamous Cell / genetics. Genetic Predisposition to Disease / genetics. Mouth Neoplasms / genetics. Polymorphism, Genetic / genetics. Promoter Regions, Genetic / genetics. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 16202081.001).
  • [ISSN] 0904-2512
  • [Journal-full-title] Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
  • [ISO-abbreviation] J. Oral Pathol. Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 5Z93L87A1R / Guanine; JAC85A2161 / Adenine
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83. Lee HO, Lee JH, Kim TY, Lee H: Regulation of DeltaNp63alpha by tumor necrosis factor-alpha in epithelial homeostasis. FEBS J; 2007 Dec;274(24):6511-22
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  • [Title] Regulation of DeltaNp63alpha by tumor necrosis factor-alpha in epithelial homeostasis.
  • A dominant negative form of p63, DeltaNp63alpha, is critical for maintaining the proliferative potential of epidermal stem cells and progenitor cells.
  • The expression of DeltaNp63alpha also confers a selective advantage for cancer cell survival, underscoring the importance of DeltaNp63alpha in both normal and neoplastic stratified epithelia.
  • In this study, we have found that tumor necrosis factor-alpha (TNF-alpha), a multifunctional cytokine that has been implicated in epidermal homeostasis during normal and pathophysiologic conditions, also triggers the degradation of DeltaNp63alpha in immortalized keratinocytes and cervical cancer cells.
  • Conversely, downregulation of DeltaNp63alpha sensitized cancer cells to TNF-alpha-induced apoptosis, suggesting a counteractive interaction between TNF-alpha and DeltaNp63alpha in the regulation of epithelial cell death.
  • The degradation of DeltaNp63alpha by TNF-alpha was delayed when cells were treated with nuclear factor-kappaB inhibitors, whereas the induction of apoptosis by TNF-alpha was accompanied by the dramatic upregulation of the proapoptotic gene Puma.
  • These observations further elucidate the relationship between TNF-alpha and DeltaNp63alpha, two well-known mediators of epidermal homeostasis, and further suggest crosstalk between the two molecules in normal and pathophysiologic epidermis.
  • [MeSH-major] Epithelial Cells / drug effects. Tumor Necrosis Factor-alpha / pharmacology. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Cell Line. Cell Line, Tumor. Flow Cytometry. Gene Expression Regulation / drug effects. Homeostasis / drug effects. Humans. NF-kappa B / antagonists & inhibitors. NF-kappa B / metabolism. Proteasome Endopeptidase Complex / metabolism. RNA, Small Interfering / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transfection. Ubiquitin / metabolism

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  • (PMID = 18028447.001).
  • [ISSN] 1742-464X
  • [Journal-full-title] The FEBS journal
  • [ISO-abbreviation] FEBS J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / RNA, Small Interfering; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Proteins; 0 / Ubiquitin; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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84. Bessis A, Bernard D, Triller A: Tumor necrosis factor-alpha and neuronal development. Neuroscientist; 2005 Aug;11(4):277-81
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  • [Title] Tumor necrosis factor-alpha and neuronal development.
  • Tumor necrosis factor-alpha (TNFalpha) is a prototypic inflammatory cytokine up-regulated in most if not all neurodegenerative diseases.
  • In contrast, the implication of TNFalpha in developmental neuronal cell death has been well documented in few studies.
  • In sympathetic and trigeminal neurons, TNFalpha acts in an autocrine manner to induce immediate cell death on neurotrophic factor deprivation.
  • [MeSH-major] Neurons / physiology. Peripheral Nerves / cytology. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Animals. Cell Death / physiology. Models, Neurological

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  • (PMID = 16061514.001).
  • [ISSN] 1073-8584
  • [Journal-full-title] The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry
  • [ISO-abbreviation] Neuroscientist
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 29
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85. Hallgren O, Aits S, Brest P, Gustafsson L, Mossberg AK, Wullt B, Svanborg C: Apoptosis and tumor cell death in response to HAMLET (human alpha-lactalbumin made lethal to tumor cells). Adv Exp Med Biol; 2008;606:217-40
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  • [Title] Apoptosis and tumor cell death in response to HAMLET (human alpha-lactalbumin made lethal to tumor cells).
  • HAMLET (human alpha-lactalbumin made lethal to tumor cells) is a molecular complex derived from human milk that kills tumor cells by a process resembling programmed cell death.
  • The complex consists of partially unfolded alpha-lactalbumin and oleic acid, and both the protein and the fatty acid are required for cell death.
  • The mechanisms of tumor cell death remain unclear, however.
  • Immediately after the encounter with tumor cells, HAMLET invades the cells and causes mitochondrial membrane depolarization, cytochrome c release, phosphatidyl serine exposure, and a low caspase response.
  • A fraction of the cells undergoes morphological changes characteristic of apoptosis, but caspase inhibition does not rescue the cells and Bcl-2 overexpression or altered p53 status does not influence the sensitivity of tumor cells to HAMLET.
  • HAMLET also creates a state of unfolded protein overload and activates 20S proteasomes, which contributes to cell death.
  • In parallel, HAMLET translocates to tumor cell nuclei, where high-affinity interactions with histones cause chromatin disruption, loss of transcription, and nuclear condensation.
  • The dying cells also show morphological changes compatible with macroautophagy, and recent studies indicate that macroautophagy is involved in the cell death response to HAMLET.
  • The results suggest that HAMLET, like a hydra with many heads, may interact with several crucial cellular organelles, thereby activating several forms of cell death, in parallel.
  • This complexity might underlie the rapid death response of tumor cells and the broad antitumor activity of HAMLET.

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  • (PMID = 18183931.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HAMLET complex, human; 0 / Oleic Acids; 9013-90-5 / Lactalbumin
  • [Number-of-references] 122
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86. De Palma M, Mazzieri R, Politi LS, Pucci F, Zonari E, Sitia G, Mazzoleni S, Moi D, Venneri MA, Indraccolo S, Falini A, Guidotti LG, Galli R, Naldini L: Tumor-targeted interferon-alpha delivery by Tie2-expressing monocytes inhibits tumor growth and metastasis. Cancer Cell; 2008 Oct 07;14(4):299-311
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  • [Title] Tumor-targeted interferon-alpha delivery by Tie2-expressing monocytes inhibits tumor growth and metastasis.
  • Here, we exploited the tumor-homing ability of proangiogenic Tie2-expressing monocytes (TEMs) to deliver IFN-alpha to tumors.
  • By transplanting hematopoietic progenitors transduced with a Tie2 promoter/enhancer-driven Ifna1 gene, we turned TEMs into IFN-alpha cell vehicles that efficiently targeted the IFN response to orthotopic human gliomas and spontaneous mouse mammary carcinomas and obtained significant antitumor responses and near complete abrogation of metastasis.
  • TEM-mediated IFN-alpha delivery inhibited tumor angiogenesis and activated innate and adaptive immune cells but did not impair myelopoiesis and wound healing detectably.
  • These results illustrate the therapeutic potential of gene- and cell-based IFN-alpha delivery and should allow the development of IFN treatments that more effectively treat cancer.
  • [MeSH-major] Cell Proliferation. Genetic Therapy / methods. Glioma / therapy. Hematopoietic Stem Cell Transplantation. Hematopoietic Stem Cells / metabolism. Interferon-alpha / metabolism. Mammary Neoplasms, Experimental / prevention & control. Monocytes / metabolism. Receptor, TIE-2 / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cells, Cultured. Female. Hematopoiesis. Humans. Immunity, Innate. Mice. Mice, Nude. Mice, Transgenic. Neoplasm Metastasis. Neovascularization, Pathologic / immunology. Neovascularization, Pathologic / metabolism. Neovascularization, Pathologic / prevention & control. Promoter Regions, Genetic. Recombinant Fusion Proteins / metabolism. Time Factors. Transduction, Genetic. Wound Healing

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  • (PMID = 18835032.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Grant] Italy / Telethon / / TGT06S01
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Recombinant Fusion Proteins; EC 2.7.10.1 / Receptor, TIE-2
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87. Pettersson J, Mossberg AK, Svanborg C: alpha-Lactalbumin species variation, HAMLET formation, and tumor cell death. Biochem Biophys Res Commun; 2006 Jun 23;345(1):260-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] alpha-Lactalbumin species variation, HAMLET formation, and tumor cell death.
  • HAMLET (human alpha-lactalbumin made lethal to tumor cells) is a tumoricidal complex of apo alpha-lactalbumin and oleic acid, formed in casein after low pH treatment of human milk.
  • This study examined if HAMLET-like complexes are present in casein from different species and if isolated alpha-lactalbumin from those species can form such complexes with oleic acid.
  • This was not explained by alpha-lactalbumin sequence variation, as purified bovine, equine, porcine, and caprine alpha-lactalbumins formed complexes with oleic acid with biological activity similar to HAMLET.
  • We conclude that structural variation of alpha-lactalbumins does not preclude the formation of HAMLET-like complexes and that natural HAMLET formation in casein was unique to human milk, which also showed the highest oleic acid content.
  • [MeSH-minor] Amino Acid Sequence. Animals. Apoptosis / drug effects. Cattle. Cell Line, Tumor. Dose-Response Relationship, Drug. Horses. Humans. Mice. Molecular Sequence Data. Sequence Homology, Amino Acid. Species Specificity. Swine

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  • (PMID = 16678133.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Caseins; 0 / HAMLET complex, human; 0 / Oleic Acids; 2UMI9U37CP / Oleic Acid; 9013-90-5 / Lactalbumin
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88. Bernardino L, Agasse F, Silva B, Ferreira R, Grade S, Malva JO: Tumor necrosis factor-alpha modulates survival, proliferation, and neuronal differentiation in neonatal subventricular zone cell cultures. Stem Cells; 2008 Sep;26(9):2361-71
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  • [Title] Tumor necrosis factor-alpha modulates survival, proliferation, and neuronal differentiation in neonatal subventricular zone cell cultures.
  • Tumor necrosis factor (TNF)-alpha has been reported to modulate brain injury, but remarkably, little is known about its effects on neurogenesis.
  • We report that TNF-alpha strongly influences survival, proliferation, and neuronal differentiation in cultured subventricular zone (SVZ) neural stem/progenitor cells derived from the neonatal P1-3 C57BL/6 mice.
  • By using single-cell calcium imaging, we developed a method, based on cellular response to KCl and/or histamine, that allows the functional evaluation of neuronal differentiation.
  • Exposure of SVZ cultures to 1 and 10 ng/ml mouse or 1 ng/ml human recombinant TNF-alpha resulted in increased differentiation of cells displaying a neuronal-like profile of [Ca2+](i) responses, compared with the predominant profile of immature cells observed in control, nontreated cultures.
  • Moreover, by using neutralizing antibodies for each TNF-alpha receptor, we found that the proneurogenic effect of 1 ng/ml TNF-alpha is mediated via tumor necrosis factor receptor 1 activation.
  • Accordingly, the percentage of neuronal nuclear protein-positive neurons was increased following exposure to mouse TNF-alpha.
  • Interestingly, exposure of SVZ cultures to 1 ng/ml TNF-alpha induced cell proliferation, whereas 10 and 100 ng/ml TNF-alpha induced apoptotic cell death.
  • Moreover, we found that exposure of SVZ cells to TNF-alpha for 15 minutes or 6 hours caused an increase in the phospho-stress-activated protein kinase/c-Jun N-terminal kinase immunoreactivity initially in the nucleus and then in growing axons, colocalizing with tau, consistent with axonogenesis.
  • Taken together, these results show that TNF-alpha induces neurogenesis in neonatal SVZ cell cultures of mice.
  • TNF-alpha, a proinflammatory cytokine and a proneurogenic factor, may play a central role in promoting neurogenesis and brain repair in response to brain injury and infection.
  • [MeSH-major] Cell Differentiation / drug effects. Cell Proliferation / drug effects. Neurons / cytology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Animals, Newborn. Brain / cytology. Cell Survival / drug effects. Cells, Cultured. Humans. JNK Mitogen-Activated Protein Kinases / metabolism. Mice. Mice, Inbred C57BL. Neurogenesis. Recombinant Proteins / pharmacology. Stem Cells / cytology. Stem Cells / drug effects


89. Takauji SR, Watanabe M, Uyama R, Nakagawa T, Miyajima N, Mochizuki M, Nishimura R, Sugano S, Sasaki N: Expression and subcellular localization of E-cadherin, alpha-catenin, and beta-catenin in 8 feline mammary tumor cell lines. J Vet Med Sci; 2007 Aug;69(8):831-4
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  • [Title] Expression and subcellular localization of E-cadherin, alpha-catenin, and beta-catenin in 8 feline mammary tumor cell lines.
  • Protein expression and subcellular localization of E-cadherin, alpha-catenin, and beta-catenin in 8 feline mammary tumor cell lines were examined by western blot analysis and fluorescence immunocytochemistry.
  • A low E-cadherin expression was observed in FNN-m cells.
  • Furthermore, compared to other cell lines, two E-cadherin bands existed in FMC-p1 cells and were localized in the perinuclear region; distinct radial lines were observed in the cytoplasm.
  • A low alpha-catenin expression was observed in FON-m cells, but there were no apparent abnormalities in its localization.
  • In contrast, similar levels of beta-catenin expression and cytoplasmic localization were observed in all cell lines.

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  • (PMID = 17827890.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cadherins; 0 / Neoplasm Proteins; 0 / alpha Catenin; 0 / beta Catenin
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90. Wieser F, Vigne JL, Wenzl R, Huber J, Taylor RN: Effects of phorbol dibutyrate on cell proliferation, apoptosis, and tumor necrosis factor-alpha expression in human endometrial adenocarcinoma cells. J Soc Gynecol Investig; 2005 Jul;12(5):370-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of phorbol dibutyrate on cell proliferation, apoptosis, and tumor necrosis factor-alpha expression in human endometrial adenocarcinoma cells.
  • OBJECTIVES: Recent evidence suggested that protein kinase C (PKC), a major cell cycle regulator in endometrial models, mimics progesterone withdrawal by inducing downstream signals.
  • In the current study we examined the hypothesis that the PKC activator phorbol 12,13 dibutyrate (PDB) would inhibit cell proliferation and induce apoptosis in two endometrial adenocarcinoma cell (EAC) lines, HEC-1B and Ishikawa cells.
  • We further examined whether the induction of tumor necrosis factor-alpha (TNF-alpha) might mediate these effects.
  • METHODS: EAC lines were cultured under standard and serum-free conditions to study the effects of PDB on cell kinetics.
  • Cell proliferation was determined by cell count using a hemacytometer and by incorporation of (3)H thymidine into 10% trichloracetic acid-precipitable DNA.
  • Conditioned media concentrations of TNF-alpha were measured by a commercially available enzyme-linked immunosorbent assay (ELISA).
  • EACs were transfected with a -125-bp TNF-alpha promoter luciferase construct and treated with PDB to evaluate transcriptional activation.
  • RESULTS: Activation of the PKC system with PDB (10 nM) decreased cell proliferation and mitogenesis in EACs.
  • EACs exhibit basal TNF-alpha gene expression and protein secretion and these were increased potently by PDB.
  • However, neutralization of TNF-alpha by addition of anti-TNF-alpha antibodies did not prevent the suppression of mitogenesis, induction of apoptosis, or activation of TNF-alpha gene expression by PDB.
  • CONCLUSION: Activation of the PKC system leads to inhibition of cell proliferation, induction of apoptosis, and TNF-alpha expression in EACs.
  • However, apoptosis in this setting does not appear to require TNF-alpha action.
  • [MeSH-major] Adenocarcinoma / pathology. Apoptosis / drug effects. Carcinogens / pharmacology. Cell Proliferation / drug effects. Endometrial Neoplasms / pathology. Phorbol 12,13-Dibutyrate / pharmacology
  • [MeSH-minor] Enzyme-Linked Immunosorbent Assay. Female. Gene Expression Profiling. Humans. Protein Kinase C / metabolism. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 15979550.001).
  • [ISSN] 1556-7117
  • [Journal-full-title] Journal of the Society for Gynecologic Investigation
  • [ISO-abbreviation] J. Soc. Gynecol. Investig.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Tumor Necrosis Factor-alpha; 37558-16-0 / Phorbol 12,13-Dibutyrate; EC 2.7.11.13 / Protein Kinase C
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91. Ishii H, Arai T, Mori H, Yamada H, Endo N, Makino K, Fukuda K: Protective effects of intracellular reactive oxygen species generated by 6-formylpterin on tumor necrosis factor-alpha-induced apoptotic cell injury in cultured rat hepatocytes. Life Sci; 2005 Jul 8;77(8):858-68
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  • [Title] Protective effects of intracellular reactive oxygen species generated by 6-formylpterin on tumor necrosis factor-alpha-induced apoptotic cell injury in cultured rat hepatocytes.
  • The effects of 6-formylpterin on tumor necrosis factor (TNF)-alpha-induced apoptotic cell injury were studied in cultured rat hepatocytes.
  • The incubation of the hepatocytes with TNF-alpha and actinomycin D (ActD) induced the apoptotic cell injury.
  • The level of aspartate transaminase (AST) in the culture supernatant increased, and the cell viability, estimated by mitochondrial respiration (MTT assay), decreased.
  • When the hepatocytes were incubated with 100-500 microM 6-formylpterin, the intracellular formation of reactive oxygen species (ROS) was observed, and the ratio of reduced and oxidized glutathione (GSH/GSSG) of whole cell lysate decreased.
  • The co-incubation of the TNF-alpha/ActD-treated hepatocytes with 100-500 microM 6-formylpterin attenuated the TNF-alpha/ActD-induced apoptotic cell injury.
  • The level of AST decreased and the cell viability increased.
  • The caspases, executors of apoptosis, are known to require a reduced cystein in their active site to function, and the intact intracellular GSH/GSSG is essential for the caspase activation.
  • Therefore, our findings suggest that intracellular ROS generated by 6-formylpterin decline the intracellular redox state to an oxidant state, which suppresses the caspase activity and prevents the apoptotic cell injury of hepatocytes.
  • [MeSH-major] Apoptosis / drug effects. Hepatocytes / drug effects. Pterins / pharmacology. Reactive Oxygen Species / metabolism. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Aspartate Aminotransferases / metabolism. Caspase 3. Caspases / metabolism. Cells, Cultured. Dactinomycin / pharmacology. Glutathione / metabolism. Male. Mitochondria, Liver / drug effects. Oxidation-Reduction. Protein Synthesis Inhibitors / pharmacology. Rats. Rats, Wistar

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  • (PMID = 15964307.001).
  • [ISSN] 0024-3205
  • [Journal-full-title] Life sciences
  • [ISO-abbreviation] Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Synthesis Inhibitors; 0 / Pterins; 0 / Reactive Oxygen Species; 0 / Tumor Necrosis Factor-alpha; 1CC1JFE158 / Dactinomycin; 712-30-1 / 2-amino-4-hydroxy-6-formylpteridine; EC 2.6.1.1 / Aspartate Aminotransferases; EC 3.4.22.- / Casp3 protein, rat; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; GAN16C9B8O / Glutathione
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92. Choi YS, Hoory T, Monie A, Wu A, Connolly D, Hung CF: alpha-Galactosylceramide enhances the protective and therapeutic effects of tumor cell based vaccines for ovarian tumors. Vaccine; 2008 Oct 29;26(46):5855-63
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  • [Title] alpha-Galactosylceramide enhances the protective and therapeutic effects of tumor cell based vaccines for ovarian tumors.
  • In the current study, we characterized the therapeutic effect of tumor cell-based vaccines combined with the adjuvant, alpha-galactosylceramide (alpha-GalCer) using two different mouse models.
  • Our data suggests that treatment with alpha-GalCer led to an increase in the IFN-gamma serum levels in the presence or absence of irradiated mouse ovarian surface epithelial tumor cells (MOSEC).
  • Furthermore, administration of irradiated MOSEC tumor cells with adjuvant alpha-GalCer generated significant protective and therapeutic antitumor effects against MOSEC tumors in vaccinated C57BL/6 mice.
  • In addition, immune cells expressing CD4, CD8 or NK1.1 markers were found to be important for the protective antitumor effects generated by irradiated tumor cell-based vaccines combined with adjuvant alpha-GalCer.
  • We also found that treatment of a spontaneous ovarian cancer murine model, the Müllerian inhibiting substance type II receptor T antigen (TgMISIIR-TAg) transgenic mice with ovarian tumor cell-based vaccines combined with adjuvant alpha-GalCer led to prolonged survival as well as increased numbers of tumor-specific CD8+ T cells.
  • Therefore, irradiated tumor cell-based vaccines in combination with alpha-GalCer are capable of breaking immune tolerance and generating significant antitumor effects in two different mouse tumor models.

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  • [Cites] CA Cancer J Clin. 2000 Jan-Feb;50(1):7-33 [10735013.001]
  • [Cites] Blood. 2007 Sep 15;110(6):2013-9 [17581919.001]
  • [Cites] Curr Opin Mol Ther. 1999 Feb;1(1):50-6 [11249684.001]
  • [Cites] Eur J Immunol. 2001 Jun;31(6):1720-7 [11385616.001]
  • [Cites] Nat Immunol. 2002 Sep;3(9):867-74 [12154358.001]
  • [Cites] Immunol Rev. 2002 Oct;188:147-54 [12445288.001]
  • [Cites] Cancer Res. 2003 Mar 15;63(6):1389-97 [12649204.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Sep 16;100(19):10913-8 [12960397.001]
  • [Cites] Oncol Res. 1995;7(10-11):529-34 [8866665.001]
  • [Cites] J Immunol. 1997 Sep 1;159(5):2240-9 [9278312.001]
  • [Cites] Science. 1997 Nov 28;278(5343):1626-9 [9374463.001]
  • [Cites] Cancer Res. 1998 Mar 15;58(6):1202-7 [9515806.001]
  • [Cites] J Immunol. 1998 Oct 1;161(7):3271-81 [9759842.001]
  • [Cites] J Exp Med. 1998 Oct 19;188(8):1529-34 [9782130.001]
  • [Cites] J Clin Invest. 2004 Dec;114(12):1800-11 [15599405.001]
  • [Cites] J Immunol. 2005 Sep 1;175(5):3309-17 [16116223.001]
  • [Cites] Expert Opin Biol Ther. 2005 Sep;5(9):1193-210 [16120050.001]
  • [Cites] Int Immunol. 2006 Aug;18(8):1279-83 [16772371.001]
  • [Cites] Vaccine. 2007 Jan 2;25(1):127-35 [16930783.001]
  • [Cites] J Immunol. 2007 Mar 1;178(5):2853-61 [17312129.001]
  • [Cites] Gene Ther. 2007 Jun;14(12):921-9 [17377599.001]
  • [Cites] Vaccine. 2007 Jul 9;25(28):5189-98 [17548137.001]
  • [Cites] Hum Gene Ther. 2007 Jul;18(7):575-88 [17576157.001]
  • [Cites] Gene Ther. 2007 Aug;14(16):1189-98 [17581599.001]
  • [Cites] Adv Exp Med Biol. 2007;601:345-55 [17713023.001]
  • [Cites] Carcinogenesis. 2000 Apr;21(4):585-91 [10753190.001]
  • (PMID = 18771701.001).
  • [ISSN] 0264-410X
  • [Journal-full-title] Vaccine
  • [ISO-abbreviation] Vaccine
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA113341-04; United States / NCI NIH HHS / CA / U19 CA113341; United States / NCI NIH HHS / CA / 1U19 CA113341-01; United States / NCI NIH HHS / CA / U19 CA113341-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Cancer Vaccines; 0 / Cytokines; 0 / Galactosylceramides; 0 / alpha-galactosylceramide; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ NIHMS77539; NLM/ PMC2597163
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93. Ramanathapuram LV, Hahn T, Graner MW, Katsanis E, Akporiaye ET: Vesiculated alpha-tocopheryl succinate enhances the anti-tumor effect of dendritic cell vaccines. Cancer Immunol Immunother; 2006 Feb;55(2):166-77
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  • [Title] Vesiculated alpha-tocopheryl succinate enhances the anti-tumor effect of dendritic cell vaccines.
  • Alpha tocopheryl succinate (alpha-TOS) is a non-toxic vitamin E analog under study for its anti-cancer properties.
  • In an earlier study, we showed that alpha-TOS, when used in combination with non-matured dendritic cells (nmDC) to treat pre-established tumors, acts as an effective adjuvant.
  • In this study, we have used vesiculated alpha-TOS (Valpha-TOS), a more soluble form of alpha-TOS that is relevant for clinical use, in combination with dendritic cells to treat pre-established murine tumors.
  • We demonstrate that Valpha-TOS kills tumor cells in vitro and inhibits the growth of pre-established murine lung carcinoma (3LLD122) as effectively as alpha-TOS.
  • The combination of Valpha-TOS plus non-matured or TNF-alpha-matured DC is more effective at inhibiting the growth of established tumors than Valpha-TOS alone.
  • We also observed that Valpha-TOS induces expression of heat shock proteins in tumor cells and that co-incubation of non-matured DC with lysate derived from Valpha-TOS-treated tumor cells leads to DC maturation evidenced by up-regulation of co-stimulatory molecules and secretion of IL-12p70.
  • This study therefore demonstrates the immunomodulatory properties of Valpha-TOS that may account for its adjuvant effect when combined with DC vaccines to treat established tumors.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cancer Vaccines / pharmacology. Carcinoma, Lewis Lung / immunology. Dendritic Cells / immunology. Lung Neoplasms / immunology. Vitamin E / analogs & derivatives
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Dosage Forms. Drug Screening Assays, Antitumor. Heat-Shock Proteins / biosynthesis. In Vitro Techniques. Mice. Mice, Inbred C57BL. Tocopherols. Ultrasonics. alpha-Macroglobulins / pharmacology

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  • (PMID = 16041582.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1 R01 CA94111-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cancer Vaccines; 0 / Dosage Forms; 0 / Heat-Shock Proteins; 0 / alpha-Macroglobulins; 1406-18-4 / Vitamin E; 1406-66-2 / Tocopherols
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94. Liu YP, Lin HI, Tzeng SF: Tumor necrosis factor-alpha and interleukin-18 modulate neuronal cell fate in embryonic neural progenitor culture. Brain Res; 2005 Aug 30;1054(2):152-8
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  • [Title] Tumor necrosis factor-alpha and interleukin-18 modulate neuronal cell fate in embryonic neural progenitor culture.
  • Neural progenitor cells (NPCs) in developing and adult CNS are capable of giving rise to various neuronal and glial cell populations.
  • Yet, little is known about the effect of microglia-derived factors on the cell fate of embryonic NPCs.
  • Treatment with pentoxifylline (PTX), an inhibitor for tumor necrosis factor-alpha (TNF-alpha) secretion from LPS-activated microglia, blocked the reduction of betaIII-tubulin+ cells in NPC culture.
  • Furthermore, treatment of NPCs with interleukin-18 (IL-18), a recently discovered proinflammatory cytokine, also decreased the number of betaIII-tubulin+ cells in a dose- and time-dependent manner.
  • Surprisingly, we also observed that the remaining betaIII-tubulin+ cells in the LPS/M-CM-treated culture exhibited more branching neurites.
  • Thus, the activated microglia-derived cytokines, TNF-alpha and IL-18, may either inhibit the neuronal differentiation or induce neuronal cell death in the NPC culture, whereas these cells may also produce factors to improve the neurite branching in the NPC culture.
  • [MeSH-major] Interleukin-18 / metabolism. Neurons / physiology. Stem Cells / physiology. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Animals, Newborn. Blotting, Western / methods. Cell Count / methods. Cell Death / drug effects. Cell Death / physiology. Cell Differentiation / drug effects. Cell Differentiation / physiology. Cells, Cultured. Dose-Response Relationship, Drug. Embryo, Mammalian. Immunohistochemistry / methods. Lipopolysaccharides / pharmacology. Microglia / drug effects. Microglia / physiology. Pertussis Toxin / pharmacology. Rats. Rats, Sprague-Dawley. Tubulin / metabolism

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  • (PMID = 16054598.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Interleukin-18; 0 / Lipopolysaccharides; 0 / Tubb3 protein, rat; 0 / Tubulin; 0 / Tumor Necrosis Factor-alpha; EC 2.4.2.31 / Pertussis Toxin
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95. Hanley S, Liu S, Lipsett M, Castellarin M, Rosenberg L, Tchervenkov J, Paraskevas S: Tumor necrosis factor-alpha production by human islets leads to postisolation cell death. Transplantation; 2006 Sep 27;82(6):813-8
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  • [Title] Tumor necrosis factor-alpha production by human islets leads to postisolation cell death.
  • BACKGROUND: Recent successes in islet transplantation highlight the importance of islet isolation by experienced centers and minimization of cell injury as crucial to the achievement of insulin independence.
  • Islet injury may manifest as cell death by apoptosis, shorter graft survival, and the need for retransplantation.
  • Although an inflammatory cytokine response at the graft site is known to inhibit engraftment, recent evidence indicates that islet cells may contribute to this response.
  • METHODS: Isolated human islets were cultured for up to one week in serum-free CMRL-1066 with 25 microM of tumor necrosis factor (TNF)alpha inhibitor RDP58.
  • Gene expression was measured by reverse transcriptase polymerase chain reaction, apoptosis and TNFalpha secretion by enzyme-linked immunosorbent assay and enzyme-linked immunospot, and islet function by stimulated insulin secretion.
  • CONCLUSIONS: These data demonstrate that intraislet cytokine production should be considered as a factor leading to islet cell death postisolation and postengraftment, and strategies aimed at countering islet cytokine production represent a novel target for improving islet viability and function.
  • [MeSH-major] Cell Death / physiology. Islets of Langerhans / physiology. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Adult. Apoptosis. Cadaver. Cells, Cultured. DNA Primers. Female. Gene Expression Regulation. Humans. Insulin / secretion. Male. Middle Aged. Peptides / pharmacology. Tissue Donors. Transcription, Genetic

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  • (PMID = 17006329.001).
  • [ISSN] 0041-1337
  • [Journal-full-title] Transplantation
  • [ISO-abbreviation] Transplantation
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Insulin; 0 / Peptides; 0 / Tumor Necrosis Factor-alpha; 151232-75-6 / allotrap
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96. Morikawa T, Xie Y, Ninomiya K, Okamoto M, Muraoka O, Yuan D, Yoshikawa M, Hayakawa T: Inhibitory effects of acylated acyclic sesquiterpene oligoglycosides from the pericarps of Sapindus rarak on tumor necrosis factor-alpha-induced cytotoxicity. Chem Pharm Bull (Tokyo); 2010 Sep;58(9):1276-80

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  • [Title] Inhibitory effects of acylated acyclic sesquiterpene oligoglycosides from the pericarps of Sapindus rarak on tumor necrosis factor-alpha-induced cytotoxicity.
  • These newly isolated compounds (1-4) were found to show inhibitory effects on tumor necrosis factor-alpha-induced cytotoxicity in L929 cells at concentrations of 30-100 microM.
  • [MeSH-major] Cytotoxins / pharmacology. Glycosides / pharmacology. Sapindus / chemistry. Sesquiterpenes / pharmacology. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Acylation. Animals. Cell Death / drug effects. Cell Line. Molecular Structure

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  • (PMID = 20823617.001).
  • [ISSN] 1347-5223
  • [Journal-full-title] Chemical & pharmaceutical bulletin
  • [ISO-abbreviation] Chem. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cytotoxins; 0 / Glycosides; 0 / Sesquiterpenes; 0 / Tumor Necrosis Factor-alpha
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97. Reguiaï Z, Grange F: The role of anti-tumor necrosis factor-alpha therapy in Pyoderma gangrenosum associated with inflammatory bowel disease. Am J Clin Dermatol; 2007;8(2):67-77
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  • [Title] The role of anti-tumor necrosis factor-alpha therapy in Pyoderma gangrenosum associated with inflammatory bowel disease.
  • Pyoderma gangrenosum (PG) is an ulcerative neutrophilic dermatosis seen in 1-5% of patients with inflammatory bowel disease (IBD).
  • The pathogenesis of PG remains unclear, but may be related to abnormal T-cell responses and production of tumor necrosis factor (TNF)-alpha, a powerful proinflammatory cytokine.
  • A new era for the management of chronic inflammatory disease began with the advent of biotherapies and particularly anti-TNFalpha therapy, which allows for a specific intervention in the immune cascade.
  • Anti-TNFalpha therapy has improved and broadened the therapeutic options for IBD and, therefore, has brought new perspectives to management of the extra-intestinal manifestations of this disorder, including PG.
  • [MeSH-major] Immunologic Factors / therapeutic use. Inflammatory Bowel Diseases / complications. Pyoderma Gangrenosum / drug therapy. Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • [MeSH-minor] Adalimumab. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Etanercept. Humans. Immunoglobulin G / therapeutic use. Infliximab. Receptors, Tumor Necrosis Factor / therapeutic use

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  • (PMID = 17428111.001).
  • [ISSN] 1175-0561
  • [Journal-full-title] American journal of clinical dermatology
  • [ISO-abbreviation] Am J Clin Dermatol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Immunoglobulin G; 0 / Immunologic Factors; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; B72HH48FLU / Infliximab; FYS6T7F842 / Adalimumab; OP401G7OJC / Etanercept
  • [Number-of-references] 83
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98. Yuan J, Sun N, Wang LJ, Tian W, Zhou XM, Chen DB, Gu HB: [Radiosensitivity of nasopharyngeal carcinoma in relation to cell cycle synchronization effect of tumor necrosis factor alpha]. Nan Fang Yi Ke Da Xue Xue Bao; 2007 Mar;27(3):374-6
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  • [Title] [Radiosensitivity of nasopharyngeal carcinoma in relation to cell cycle synchronization effect of tumor necrosis factor alpha].
  • OBJECTIVE: To investigate the effect of tumor necrosis factor alpha (TNFalpha) on radiosensitivity of nasopharyngeal carcinoma (NPC) in relation to TNFalpha-induced cell cycle synchronization.
  • METHODS: The radio-resistance of a NPC cell line subclone CNE-2Z-S1 was verified by in vivo experiments and flow cytometry was performed to evaluate cell cycle synchronization in TNFalpha-treated CNE-2Z-S1 cells.
  • The radiosensitivity of the cell synchronized CNE-2Z-S1 cells was determined by clone formation in vitro and in vivo experiment in nude mice.
  • RESULTS: TNFalpha was capable of inducing cell cycle arrest and synchronization of CNE-2Z-S1 cells.
  • CONCLUSION: TNFalpha can enhance the radiosensitivity of NPC cells by inducing cell cycle synchronization.
  • [MeSH-major] Cell Cycle / drug effects. Nasopharyngeal Neoplasms / drug therapy. Radiation-Sensitizing Agents / pharmacology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Mice. Mice, Nude. Xenograft Model Antitumor Assays

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  • (PMID = 17425997.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Radiation-Sensitizing Agents; 0 / Tumor Necrosis Factor-alpha
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99. Tang X, Molina M, Amar S: p53 short peptide (p53pep164) regulates lipopolysaccharide-induced tumor necrosis factor-alpha factor/cytokine expression. Cancer Res; 2007 Feb 1;67(3):1308-16
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  • [Title] p53 short peptide (p53pep164) regulates lipopolysaccharide-induced tumor necrosis factor-alpha factor/cytokine expression.
  • By using serial analysis of gene expression technique, p53-induced genes (PIGs) have been identified, one of which was lipopolysaccharide (LPS)-induced tumor necrosis factor-alpha (TNF-alpha) factor (LITAF/PIG7).
  • LITAF regulates the transcription of cytokines such as TNF-alpha.
  • In this study, we found that the element required for transcriptional activity is mainly located in the region from -990 to -500 of the LITAF promoter; the specific site required for p53 protein-DNA binding is located between -550 and -500.
  • We also found that transient transfection of either a p53 short DNA sequence, called p53LFB12, or its corresponding 7-amino-acid synthetic peptide from amino acids 164 to 170 (K164Q165S166Q167H168M169T170), named p53pep164, significantly reduced LITAF promoter activity to 15% in p53-null H1299 cells.
  • Transfection of p53pep164 into H1299 cells significantly down-regulated LPS-induced LITAF expression as well.
  • Furthermore, transfection of p53pep164 into human monocytes resulted in down-regulation of nine proinflammatory cytokines, including TNF-alpha.
  • The present finding proposes a novel link between p53 and the inflammatory processes and highlights potential interventional approaches to control p53-associated inflammatory processes.
  • [MeSH-major] DNA / metabolism. Nuclear Proteins / biosynthesis. Peptide Fragments / metabolism. Transcription Factors / biosynthesis. Tumor Necrosis Factor-alpha / biosynthesis. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Apoptosis / genetics. Base Sequence. Cell Line, Tumor. Gene Expression / drug effects. Humans. Lipopolysaccharides / pharmacology. Molecular Sequence Data. Promoter Regions, Genetic. Protein Binding. Transfection

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  • (PMID = 17283168.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIDCR NIH HHS / DE / DE 14079
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / LITAF protein, human; 0 / Lipopolysaccharides; 0 / Nuclear Proteins; 0 / Peptide Fragments; 0 / TP53 protein, human; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Protein p53; 9007-49-2 / DNA
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100. Sugimoto K, Nomura K, Nishimura T, Kiso T, Sugimoto K, Kuriki T: Syntheses of alpha-arbutin-alpha-glycosides and their inhibitory effects on human tyrosinase. J Biosci Bioeng; 2005 Mar;99(3):272-6
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  • [Title] Syntheses of alpha-arbutin-alpha-glycosides and their inhibitory effects on human tyrosinase.
  • Alpha-arbutin is a tyrosinase inhibitor.
  • We synthesized alpha-arbutin-alpha-glycosides by the transglycosylation reaction of cyclomaltodextrin glucanotransferase from Bacillus macerans using alpha-arbutin and starch as acceptor and donor molecules, respectively.
  • The structural analyses using 13C- and 1H-NMR spectroscopy proved that they were 4-hydroxyphenyl alpha-maltoside (alpha-Ab-alpha-G1) and 4-hydroxyphenyl alpha-maltotrioside (alpha-Ab-alpha-G2).
  • Both alpha-Ab-alpha-G1 and alpha-Ab-alpha-G2 exhibited competitive-type inhibition on human tyrosinase as alpha-arbutin does.
  • Their K(i) values were calculated to be 0.6 mM and 2.8 mM, respectively, which is slightly and significantly higher than that of alpha-arbutin (0.2 mM).
  • [MeSH-minor] Cell Line, Tumor. Enzyme Activation. Enzyme Stability. Glycosides / biosynthesis. Glycosides / chemistry. Humans

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  • (PMID = 16233788.001).
  • [ISSN] 1389-1723
  • [Journal-full-title] Journal of bioscience and bioengineering
  • [ISO-abbreviation] J. Biosci. Bioeng.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Glycosides; 0 / Peptides; C5INA23HXF / Arbutin; EC 1.14.18.1 / Monophenol Monooxygenase
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