[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 476
1. Thatipelli MR, Uber PA, Mehra MR: Isolated tricuspid stenosis and heart failure: a focus on carcinoid heart disease. Congest Heart Fail; 2003 Sep-Oct;9(5):294-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Isolated tricuspid stenosis and heart failure: a focus on carcinoid heart disease.
  • A rare clinical occurrence, heart failure in the setting of tricuspid stenosis should immediately trigger a search for underlying systemic carcinoid disease.
  • Carcinoid tumor cells can secrete a variety of vasoactive substances that result in skin erythema, excretory diarrhea, bronchospasm, and hemodynamic instability, but these manifestations are noted only in a few patients.
  • Right heart valvular disease is common since the vasoactive noxious substances pass through the right heart unaffected and undergo metabolism in the pulmonary circulation, thereby decreasing involvement of the left-sided valves.
  • Localization of the carcinoid tumor followed by surgically directed valvular treatment is mandatory for relief of symptoms.
  • In nonoperative candidates, cytotoxic chemotherapy or long-term symptomatic drug treatment with somatostatin is indicated.
  • [MeSH-major] Carcinoid Heart Disease / complications. Heart Failure / etiology. Tricuspid Valve Insufficiency / etiology

  • Genetic Alliance. consumer health - Heart Disease.
  • MedlinePlus Health Information. consumer health - Heart Failure.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14564150.001).
  • [ISSN] 1527-5299
  • [Journal-full-title] Congestive heart failure (Greenwich, Conn.)
  • [ISO-abbreviation] Congest Heart Fail
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


2. Ono M, Sato H, Kazumori H, Yuki M, Rumi MA, Ortega-Cava CF, Ishihara Y, Ishihara S, Adachi K, Kinoshita Y: Effect of a gastrin/cholecystokinin B receptor antagonist, S-0509, on the omeprazole-induced proliferation of gastric mucosa in rats. J Lab Clin Med; 2003 Dec;142(6):364-71
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In some clinical conditions causing hypergastrinemia, such as long-term gastric-acid inhibition and gastric-mucosa atrophy, hyperplastic ECL cells may develop into gastric carcinoid tumors.
  • [MeSH-major] Benzophenones / pharmacology. Gastric Mucosa / drug effects. Membrane Transport Proteins. Neuropeptides. Omeprazole / pharmacology. Phenylurea Compounds / pharmacology. Receptors, Cholecystokinin / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Division / drug effects. Enterochromaffin Cells / drug effects. Gastrins / blood. Histidine Decarboxylase / genetics. Male. Membrane Glycoproteins / genetics. Proliferating Cell Nuclear Antigen / analysis. RNA, Messenger / analysis. Rats. Rats, Sprague-Dawley. Vesicular Biogenic Amine Transport Proteins

  • Hazardous Substances Data Bank. OMEPRAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14713888.001).
  • [ISSN] 0022-2143
  • [Journal-full-title] The Journal of laboratory and clinical medicine
  • [ISO-abbreviation] J. Lab. Clin. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzophenones; 0 / Gastrins; 0 / Membrane Glycoproteins; 0 / Membrane Transport Proteins; 0 / Neuropeptides; 0 / Phenylurea Compounds; 0 / Proliferating Cell Nuclear Antigen; 0 / RNA, Messenger; 0 / Receptors, Cholecystokinin; 0 / S 0509; 0 / Vesicular Biogenic Amine Transport Proteins; EC 4.1.1.22 / Histidine Decarboxylase; KG60484QX9 / Omeprazole
  •  go-up   go-down


3. Klibanski A, Melmed S, Clemmons DR, Colao A, Cunningham RS, Molitch ME, Vinik AI, Adelman DT, Liebert KJ: The endocrine tumor summit 2008: appraising therapeutic approaches for acromegaly and carcinoid syndrome. Pituitary; 2010 Sep;13(3):266-86
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The endocrine tumor summit 2008: appraising therapeutic approaches for acromegaly and carcinoid syndrome.
  • The Endocrine Tumor Summit convened in December 2008 to address 6 statements prepared by panel members that reflect important questions in the treatment of acromegaly and carcinoid syndrome.
  • Three statements addressed the validity of serum growth hormone (GH) and insulin-like growth factor-I (IGF-I) concentrations as indicators or predictors of disease in acromegaly.
  • Statements regarding the effects of preoperative somatostatin analog use on pituitary surgical outcomes, their effects on hormone and symptom control in carcinoid syndrome, and the efficacy of extended dosing intervals were reviewed.
  • [MeSH-major] Acromegaly / diagnosis. Malignant Carcinoid Syndrome / diagnosis
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Female. Human Growth Hormone / metabolism. Humans. Insulin-Like Growth Factor I / metabolism. Male. Neuroendocrine Tumors / diagnosis. Neuroendocrine Tumors / drug therapy. Neuroendocrine Tumors / metabolism. Neuroendocrine Tumors / pathology. Octreotide / therapeutic use. Peptides, Cyclic / therapeutic use. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use

  • Genetic Alliance. consumer health - Carcinoid Syndrome.
  • Genetic Alliance. consumer health - Carcinoid Tumor.
  • Genetic Alliance. consumer health - Acromegaly.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Endocrinol Metab. 2004 Jun;89(6):2789-96 [15181059.001]
  • [Cites] Clin Endocrinol (Oxf). 2004 Aug;61(2):224-31 [15272918.001]
  • [Cites] Eur J Endocrinol. 2004 Oct;151(4):439-46 [15476442.001]
  • [Cites] N Engl J Med. 1979 Nov 22;301(21):1138-42 [492275.001]
  • [Cites] Clin Endocrinol (Oxf). 1980 Jan;12(1):71-9 [7379316.001]
  • [Cites] J Clin Endocrinol Metab. 1988 Nov;67(5):1040-8 [2903168.001]
  • [Cites] Horm Metab Res. 1990 Jun;22(6):313-8 [2199362.001]
  • [Cites] Q J Med. 1993 May;86(5):293-9 [8327647.001]
  • [Cites] Acta Endocrinol (Copenh). 1993 Jul;129 Suppl 1:18-20 [8372606.001]
  • [Cites] Gut. 1996 Aug;39(2):279-83 [8977344.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Oct;82(10):3308-14 [9329359.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Aug;83(8):2730-4 [9709939.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Oct;83(10):3411-8 [9768640.001]
  • [Cites] J Clin Oncol. 1999 Feb;17(2):600-6 [10080605.001]
  • [Cites] Acta Neurochir (Wien). 1999;141(4):399-405 [10352750.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Oct;84(10):3551-5 [10522994.001]
  • [Cites] Eur J Endocrinol. 2005 Mar;152(3):379-87 [15757854.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1377-82 [15585548.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Apr;62(4):410-7 [15807870.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Apr;90(4):1972-8 [15634715.001]
  • [Cites] Acta Neurochir (Wien). 2005 May;147(5):485-93; discussion 493 [15806331.001]
  • [Cites] Acta Neurochir (Wien). 2005 Mar;147(3):243-51; discussion 250-1 [15627919.001]
  • [Cites] J Clin Pharmacol. 2005 Jul;45(7):836-44 [15951474.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Jul;63(1):103-10 [15963069.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Jul;90(7):4405-10 [15827109.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Jul;90(7):4081-6 [15886256.001]
  • [Cites] Eur J Endocrinol. 2005 Aug;153(2):231-8 [16061829.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Sep;63(3):342-9 [16117824.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Mar;64(3):342-51 [16487447.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Apr;91(4):1239-45 [16403824.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Apr;91(4):1397-403 [16449332.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Jun;91(6):2112-8 [16537687.001]
  • [Cites] J Neurosurg. 2006 Jun;104(6):899-906 [16776333.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Aug;65(2):250-6 [16886969.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Sep;65(3):320-6 [16918950.001]
  • [Cites] Clin Chim Acta. 2006 Nov;373(1-2):176-9 [16815351.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Oct;91(10):3891-6 [16849407.001]
  • [Cites] Gut. 2006 Nov;55(11):1586-91 [16556667.001]
  • [Cites] Cancer. 2006 Nov 15;107(10):2474-81 [17054107.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Feb;92(2):476-82 [17105844.001]
  • [Cites] J Gastrointest Surg. 2007 Mar;11(3):264-71 [17458596.001]
  • [Cites] Pituitary. 2007;10(2):115-9 [17429592.001]
  • [Cites] Clin Endocrinol (Oxf). 2007 Jun;66(6):859-68 [17465997.001]
  • [Cites] Am J Gastroenterol. 2007 Jul;102(7):1464-73 [17391319.001]
  • [Cites] Endocr Relat Cancer. 2007 Jun;14(2):473-82 [17639060.001]
  • [Cites] Clin Endocrinol (Oxf). 2007 Sep;67(3):358-62 [17555502.001]
  • [Cites] Clin Endocrinol (Oxf). 2007 Oct;67(4):512-9 [17555511.001]
  • [Cites] J Clin Oncol. 2009 Oct 1;27(28):4656-63 [19704057.001]
  • [Cites] Eur J Endocrinol. 2007 Nov;157(5):571-7 [17984236.001]
  • [Cites] Horm Res. 2007;68 Suppl 5:166-72 [18174739.001]
  • [Cites] J Clin Oncol. 2008 Mar 10;26(8):1316-23 [18323556.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Apr;93(4):1254-62 [18171702.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Apr;93(4):1324-30 [18230660.001]
  • [Cites] Pancreas. 2008 Jul;37(1):94-100 [18580450.001]
  • [Cites] J Clin Oncol. 2008 Jul 10;26(20):3403-10 [18612155.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Jul;93(7):2639-46 [18445662.001]
  • [Cites] Eur J Endocrinol. 2008 Aug;159(2):89-95 [18524797.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Aug;93(8):2957-68 [18477663.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Aug;93(8):2984-90 [18492760.001]
  • [Cites] J Natl Cancer Inst. 2008 Sep 17;100(18):1282-9 [18780869.001]
  • [Cites] Eur J Endocrinol. 2008 Oct;159(4):475-82 [18662970.001]
  • [Cites] Ann Clin Biochem. 2008 Nov;45(Pt 6):560-6 [18782815.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Feb;94(2):523-7 [19033371.001]
  • [Cites] Pancreas. 2009 Apr;38(3):e87-95 [19276865.001]
  • [Cites] Clin Endocrinol (Oxf). 2009 Aug;71(2):237-45 [19094074.001]
  • [Cites] Cancer. 2000 Feb 15;88(4):770-6 [10679645.001]
  • [Cites] Am J Clin Oncol. 2000 Aug;23(4):412-5 [10955874.001]
  • [Cites] Ann Oncol. 2000 Sep;11(9):1127-30 [11061606.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Nov;85(11):4099-103 [11095439.001]
  • [Cites] Clin Endocrinol (Oxf). 2000 Dec;53(6):719-24 [11155094.001]
  • [Cites] Eur J Endocrinol. 2001 Aug;145(2):137-45 [11454508.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Nov;86(11):5240-4 [11701684.001]
  • [Cites] Eur J Endocrinol. 2002 May;146(5):707-16 [11980628.001]
  • [Cites] Clin Endocrinol (Oxf). 2002 Jul;57(1):59-64 [12100070.001]
  • [Cites] Pituitary. 2001 Aug;4(3):163-71 [12138989.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Aug;87(8):3537-42 [12161471.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Oct;87(10):4554-63 [12364434.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Jan;58(1):86-91 [12519417.001]
  • [Cites] Metabolism. 2003 Feb;52(2):181-5 [12601629.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Mar;58(3):288-95 [12608933.001]
  • [Cites] Endocr J. 2003 Apr;50(2):163-72 [12803236.001]
  • [Cites] Growth Horm IGF Res. 2003 Aug;13(4):185-92 [12914751.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Feb;89(2):667-74 [14764779.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Apr;89(4):1613-7 [15070920.001]
  • [Cites] Eur J Endocrinol. 2004 Apr;150(4):489-95 [15080778.001]
  • (PMID = 20012914.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Peptides, Cyclic; 118992-92-0 / lanreotide; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I; RWM8CCW8GP / Octreotide
  • [Other-IDs] NLM/ PMC2913001
  •  go-up   go-down


Advertisement
4. Engelbach M, Heusel CP, Kriegsmann J, Both S, Walgenbach S: [Drug therapy of carcinoids of the gastrointestinal tract]. Zentralbl Chir; 2001 Sep;126(9):682-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Drug therapy of carcinoids of the gastrointestinal tract].
  • [Transliterated title] Medikamentöse Therapie bei Karzinoiden des Gastrointestinaltraktes.
  • Carcinoid tumors are rare and slowly growing neuroendocrine tumors of the foregut, midgut and hindgut.
  • Drug therapy is of special importance in patients with inoperable metastasising disease.
  • This palliative therapy is aimed at reduction of the hormone-dependent symptoms and inhibition of tumor growth.
  • Somatostatin analogues, alpha-interferon and various chemotherapeutic agents are used for this purpose.
  • Drug therapy can be supplemented by surgical and radiological intervention through interdisciplinary cooperation of the surgeon, radiologist, endocrinologist and gastroenterologist.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoid Tumor / drug therapy. Gastrointestinal Neoplasms / drug therapy. Interferon-alpha / therapeutic use. Somatostatin / analogs & derivatives
  • [MeSH-minor] Humans. Neoplasm Staging. Prognosis

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11699283.001).
  • [ISSN] 0044-409X
  • [Journal-full-title] Zentralblatt für Chirurgie
  • [ISO-abbreviation] Zentralbl Chir
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Interferon-alpha; 51110-01-1 / Somatostatin
  •  go-up   go-down


5. Larsson G, Janson ET: Anemia in patients with midgut carcinoid, treated with alpha interferon: effects by erythropoietin treatment on the perceived quality of life. Eur J Cancer Care (Engl); 2008 Mar;17(2):200-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anemia in patients with midgut carcinoid, treated with alpha interferon: effects by erythropoietin treatment on the perceived quality of life.
  • One important side effect from alpha interferon is depression of bone marrow function and studies have shown that patients with carcinoid tumours treated with alpha interferon suffers from fatigue and impaired physical functions.
  • Eighteen patients with midgut carcinoid treated with alpha interferon were included in the study.
  • There were statistical significant increases in haemoglobin (Hb) levels between baseline and 4 months, between baseline and 8 months as well as between baseline and 2-year follow-up.
  • Even though the analysis did not reveal any statistically significant relation between the observed increase in Hb levels and self-rated QoL, this pilot study has increased the knowledge about benefits, doses and frequency of EPO treatment in patients with midgut carcinoid suffering from interferon related anaemia.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Carcinoid Tumor / drug therapy. Erythropoietin / therapeutic use. Gastrointestinal Neoplasms / drug therapy. Interferon-alpha / adverse effects. Quality of Life
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Anemia / drug therapy. Anemia / etiology. Fatigue / etiology. Female. Follow-Up Studies. Hemoglobins / metabolism. Humans. Male. Middle Aged. Pilot Projects. Treatment Outcome

  • Genetic Alliance. consumer health - Anemia.
  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18302658.001).
  • [ISSN] 1365-2354
  • [Journal-full-title] European journal of cancer care
  • [ISO-abbreviation] Eur J Cancer Care (Engl)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hemoglobins; 0 / Interferon-alpha; 11096-26-7 / Erythropoietin
  •  go-up   go-down


6. Pinchot SN, Adler JT, Luo Y, Ju J, Li W, Shen B, Kunnimalaiyaan M, Chen H: Tautomycin suppresses growth and neuroendocrine hormone markers in carcinoid cells through activation of the Raf-1 pathway. Am J Surg; 2009 Mar;197(3):313-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tautomycin suppresses growth and neuroendocrine hormone markers in carcinoid cells through activation of the Raf-1 pathway.
  • BACKGROUND: Carcinoids are neuroendocrine (NE) tumors with limited treatment options.
  • Raf-1 pathway activation has been shown to suppress hormone production in carcinoid cells.
  • We investigated a novel treatment for carcinoid cell growth based on pharmacologic Raf-1 activation using the compound tautomycin (TTY).
  • METHODS: Human carcinoid cells were treated with TTY for 48 hours.
  • Western blot analysis was used to demonstrate Raf-1 pathway activation by phosphorylation of ERK1/2 and to determine the effect on NE tumor markers.
  • Furthermore, a significant decrease in NE tumor markers was seen.
  • Importantly, TTY inhibited carcinoid cellular growth and induced the cell-cycle inhibitors p21 and p27.
  • CONCLUSION: TTY activates the Raf-1 pathway, limits carcinoid cell growth, and suppresses NE marker production in vitro.
  • This new compound warrants further investigation in animal models of carcinoid cancer.

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cancer Ther. 2006 Dec;5(12):3222-31 [17172426.001]
  • [Cites] Surg Oncol Clin N Am. 2006 Jul;15(3):463-78 [16882492.001]
  • [Cites] J Surg Res. 2007 Oct;142(2):219-26 [17612559.001]
  • [Cites] Curr Opin Investig Drugs. 2008 Jun;9(6):576-82 [18516757.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Sep 21;287(2):328-31 [11554729.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Aug 6;99(16):10617-22 [12149481.001]
  • [Cites] N Engl J Med. 2003 Mar 13;348(11):1005-15 [12637610.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2003 Aug;285(2):G245-54 [12851216.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2003 Dec;285(6):G1181-8 [12816758.001]
  • [Cites] Am J Gastroenterol. 2004 Jan;99(1):23-32 [14687136.001]
  • [Cites] Cancer. 1975 Aug;36(2):560-9 [1157019.001]
  • [Cites] J Antibiot (Tokyo). 1989 Jan;42(1):141-4 [2921220.001]
  • [Cites] Surgery. 1993 Oct;114(4):758-63; discussion 763-4 [8211691.001]
  • [Cites] Cancer. 1997 May 1;79(9):1804-8 [9128999.001]
  • [Cites] Mol Cell Biol. 1997 Sep;17(9):5588-97 [9271434.001]
  • [Cites] Mol Cell Biol. 1997 Sep;17(9):5598-611 [9271435.001]
  • [Cites] J Am Coll Surg. 1998 Jul;187(1):88-92; discussion 92-3 [9660030.001]
  • [Cites] Oncogene. 1998 Sep 17;17(11 Reviews):1457-62 [9779991.001]
  • [Cites] N Engl J Med. 1999 Mar 18;340(11):858-68 [10080850.001]
  • [Cites] Chem Biol. 1999 Aug;6(8):559-68 [10421767.001]
  • [Cites] Pathol Oncol Res. 1999;5(3):205-10 [10491018.001]
  • [Cites] J Surg Res. 2005 Jun 1;126(1):102-5 [15916982.001]
  • [Cites] Mol Cancer Ther. 2005 Jun;4(6):910-7 [15956248.001]
  • [Cites] Thyroid. 2005 Jun;15(6):511-21 [16029117.001]
  • [Cites] Curr Opin Oncol. 2006 Jan;18(1):9-15 [16357558.001]
  • [Cites] J Bacteriol. 2006 Jun;188(11):4148-52 [16707708.001]
  • [Cites] Mol Cancer Ther. 2007 Mar;6(3):1151-8 [17363508.001]
  • (PMID = 19245907.001).
  • [ISSN] 1879-1883
  • [Journal-full-title] American journal of surgery
  • [ISO-abbreviation] Am. J. Surg.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA117117-01A2; United States / NCI NIH HHS / CA / CA109053-03; United States / NIDDK NIH HHS / DK / R21 DK066169; United States / NCI NIH HHS / CA / R21 CA117117-02; United States / NCI NIH HHS / CA / R01 CA109053-03; United States / NIDDK NIH HHS / DK / DK066169; United States / NCI NIH HHS / CA / R01 CA109053-01A2; United States / NCI NIH HHS / CA / R01 CA109053; United States / NCI NIH HHS / CA / CA117117-02; United States / NCI NIH HHS / CA / R21 CA117117-01A2; United States / NCI NIH HHS / CA / CA109053; United States / NCI NIH HHS / CA / CA109053-01A2; United States / NCI NIH HHS / CA / CA113297; United States / NCI NIH HHS / CA / CA109053-02; United States / NIDDK NIH HHS / DK / DK064735; United States / NCI NIH HHS / CA / R21 CA117117; United States / NCI NIH HHS / CA / R01 CA109053-02; United States / NIDDK NIH HHS / DK / R21 DK064735
  • [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 / Biomarkers, Tumor; 0 / Enzyme Inhibitors; 0 / Pyrans; 0 / Spiro Compounds; 109946-35-2 / tautomycin; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf
  • [Other-IDs] NLM/ NIHMS98904; NLM/ PMC2664746
  •  go-up   go-down


7. Marini F, Falchetti A, Del Monte F, Carbonell Sala S, Gozzini A, Luzi E, Brandi ML: Multiple endocrine neoplasia type 1. Orphanet J Rare Dis; 2006;1:38
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multiple endocrine neoplasia type 1.
  • Multiple Endocrine Neoplasia type 1 (MEN1) is a rare autosomal dominant hereditary cancer syndrome presented mostly by tumours of the parathyroids, endocrine pancreas and anterior pituitary, and characterised by a very high penetrance and an equal sex distribution.
  • The sporadic form presents with two of the three principal MEN1-related endocrine tumours (parathyroid adenomas, entero-pancreatic tumours and pituitary tumours) within a single patient, while the familial form consists of a MEN1 case with at least one first degree relative showing one of the endocrine characterising tumours.
  • Other endocrine and non-endocrine lesions, such as adrenal cortical tumours, carcinoids of the bronchi, gastrointestinal tract and thymus, lipomas, angiofibromas, collagenomas have been described.
  • The responsible gene, MEN1, maps on chromosome 11q13 and encodes a 610 aminoacid nuclear protein, menin, with no sequence homology to other known human proteins.
  • MEN1 syndrome is caused by inactivating mutations of the MEN1 tumour suppressor gene.
  • Treatment consists of surgery and/or drug therapy, often in association with radiotherapy or chemotherapy.
  • Currently, DNA testing allows the early identification of germline mutations in asymptomatic gene carriers, to whom routine surveillance (regular biochemical and/or radiological screenings to detect the development of MEN1-associated tumours and lesions) is recommended.
  • [MeSH-major] Multiple Endocrine Neoplasia Type 1 / diagnosis. Multiple Endocrine Neoplasia Type 1 / therapy. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / therapy. Parathyroid Neoplasms / diagnosis. Parathyroid Neoplasms / therapy. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / therapy
  • [MeSH-minor] Adolescent. Adrenal Cortex Neoplasms / diagnosis. Adult. Aged. Aged, 80 and over. Angiofibroma / diagnosis. Carcinoid Tumor / diagnosis. Child. Facial Neoplasms / diagnosis. Female. Gastrinoma / diagnosis. Genetic Testing / methods. Humans. Insulinoma / diagnosis. Lipoma / diagnosis. Male. Meningioma / diagnosis. Middle Aged. Prolactinoma / diagnosis. Proto-Oncogene Proteins / genetics. Thyroid Neoplasms / diagnosis. Vasoactive Intestinal Peptide / blood. Vasoactive Intestinal Peptide / secretion. Young Adult

  • Genetic Alliance. consumer health - Multiple Endocrine Neoplasia.
  • Genetic Alliance. consumer health - Multiple endocrine neoplasia type 1.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Oncogene. 1999 Oct 21;18(43):5936-42 [10557080.001]
  • [Cites] Cell. 1999 Jan 8;96(1):143-52 [9989505.001]
  • [Cites] Eur J Endocrinol. 2000 Feb;142(2):131-7 [10664520.001]
  • [Cites] Endocr Relat Cancer. 1999 Dec;6(4):449-73 [10730900.001]
  • [Cites] Mamm Genome. 2000 Jun;11(6):448-54 [10818209.001]
  • [Cites] Mol Cell Endocrinol. 2000 Oct 25;168(1-2):135-40 [11064160.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Aug 17;286(2):426-31 [11500056.001]
  • [Cites] Oncogene. 2001 Aug 16;20(36):4917-25 [11526476.001]
  • [Cites] Ann Surg. 2001 Oct;234(4):495-505; discussion 505-6 [11573043.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Dec;86(12):5658-71 [11739416.001]
  • [Cites] J Biol Chem. 2002 Oct 11;277(41):38197-204 [12145286.001]
  • [Cites] Ann N Y Acad Sci. 2004 Apr;1014:189-98 [15153434.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Aug;89(8):3776-84 [15292304.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Aug;89(8):4124-9 [15292357.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Oct 22;264(2):404-8 [10529376.001]
  • [Cites] Gastroenterology. 1967 Apr;52(4):695-708 [4290095.001]
  • [Cites] N Engl J Med. 1987 Nov 5;317(19):1200-9 [3309661.001]
  • [Cites] Nature. 1988 Mar 3;332(6159):85-7 [2894610.001]
  • [Cites] N Engl J Med. 1989 Jul 27;321(4):213-8 [2568586.001]
  • [Cites] N Engl J Med. 1989 Jul 27;321(4):218-24 [2568587.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Mar;87(5):1968-72 [1968641.001]
  • [Cites] Cancer Genet Cytogenet. 1991 Mar;52(1):85-92 [1672620.001]
  • [Cites] N Engl J Med. 1992 Jun 25;326(26):1721-6 [1317506.001]
  • [Cites] Endocr Rev. 1992 May;13(2):220-40 [1352243.001]
  • [Cites] J Clin Endocrinol Metab. 1992 Jul;75(1):76-81 [1352309.001]
  • [Cites] Cancer Genet Cytogenet. 1992 Oct 1;63(1):17-21 [1358429.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Dec 1;90(23):10914-21 [7902574.001]
  • [Cites] Am J Med. 1994 Nov;97(5):436-44 [7977432.001]
  • [Cites] Cancer Genet Cytogenet. 1995 Feb;79(2):123-6 [7889502.001]
  • [Cites] Arch Surg. 1996 Jul;131(7):699-702 [8678766.001]
  • [Cites] QJM. 1996 Sep;89(9):653-69 [8917740.001]
  • [Cites] Gut. 1996 Oct;39(4):562-8 [8944566.001]
  • [Cites] Medicine (Baltimore). 1997 Jan;76(1):21-9 [9064485.001]
  • [Cites] Science. 1997 Apr 18;276(5311):404-7 [9103196.001]
  • [Cites] Hum Mol Genet. 1997 Jul;6(7):1169-75 [9215689.001]
  • [Cites] Hum Mol Genet. 1997 Jul;6(7):1177-83 [9215690.001]
  • [Cites] Arch Dermatol. 1997 Jul;133(7):853-7 [9236523.001]
  • [Cites] Gastroenterology. 1997 Sep;113(3):773-81 [9287968.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Oct;82(10):3487-92 [9329390.001]
  • [Cites] Hum Mol Genet. 1997 Dec;6(13):2285-90 [9361035.001]
  • [Cites] Eur J Endocrinol. 1997 Dec;137(6):684-7 [9437237.001]
  • [Cites] Jpn J Cancer Res. 1997 Nov;88(11):1029-32 [9439676.001]
  • [Cites] Am J Hum Genet. 1998 Feb;62(2):232-44 [9463336.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1630-4 [9465067.001]
  • [Cites] Cancer Genet Cytogenet. 1999 Mar;109(2):138-40 [10087948.001]
  • [Cites] Mamm Genome. 1999 Jun;10(6):592-6 [10341092.001]
  • [Cites] Biochim Biophys Acta. 1999 Oct 6;1447(1):51-6 [10500243.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Oct;84(10):3775-80 [10523029.001]
  • [Cites] Biochim Biophys Acta. 1999 Sep 3;1446(3):286-94 [10524203.001]
  • [Cites] J Surg Oncol. 2005 Mar 1;89(3):143-50 [15719382.001]
  • [Cites] Nat Rev Cancer. 2005 May;5(5):367-75 [15864278.001]
  • [Cites] J Clin Endocrinol Metab. 2005 May;90(5):2603-9 [15713725.001]
  • [Cites] J Invest Dermatol. 1998 Apr;110(4):438-40 [9540988.001]
  • [Cites] Genes Chromosomes Cancer. 1998 Jun;22(2):130-7 [9598800.001]
  • [Cites] Lancet. 1997 Oct 25;350(9086):1223 [9652567.001]
  • [Cites] J Intern Med. 1998 Jun;243(6):501-4 [9681849.001]
  • [Cites] Am J Hum Genet. 1998 Aug;63(2):455-67 [9683585.001]
  • [Cites] Anticancer Res. 1998 Jul-Aug;18(4A):2685-9 [9703929.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Aug;83(8):2621-6 [9709921.001]
  • [Cites] N Engl J Med. 1998 Oct 8;339(15):1063-72 [9761809.001]
  • [Cites] J Med Genet. 1998 Nov;35(11):915-9 [9832038.001]
  • [Cites] Surgery. 1998 Dec;124(6):1106-13; discussion 1113-4 [9854591.001]
  • [Cites] Hum Mutat. 1999;13(1):54-60 [9888389.001]
  • [Cites] Eur J Endocrinol. 1999 Nov;141(5):475-80 [10576763.001]
  • (PMID = 17014705.001).
  • [ISSN] 1750-1172
  • [Journal-full-title] Orphanet journal of rare diseases
  • [ISO-abbreviation] Orphanet J Rare Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 37221-79-7 / Vasoactive Intestinal Peptide
  • [Number-of-references] 64
  • [Other-IDs] NLM/ PMC1594566
  • [General-notes] NLM/ Original DateCompleted: 20070618
  •  go-up   go-down


8. Waldum HL, Brenna E: Personal review: is profound acid inhibition safe? Aliment Pharmacol Ther; 2000 Jan;14(1):15-22
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Inhibitors of gastric acid secretion, particular proton pump inhibitors, are effective drugs in the treatment and prophylaxis of acid-related diseases.
  • Gastric acidity kills swallowed microorganisms, and acid secretion must be of biological importance because it is maintained in phylogenesis.
  • ECL cell derived tumours in man were previously regarded as rare, and also as rather benign.
  • Moreover, ECL cell carcinoids secondary to hypergastrinaemia may develop into highly malignant tumours.
  • Treatment with a proton pump inhibitor is followed by rebound acid hypersecretion and decreased efficiency of H2-blockers, thus such treatment may induce a type of physical dependence.

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Aliment Pharmacol Ther. 2001 Apr;15(4):559-60 [11284786.001]
  • [CommentIn] Aliment Pharmacol Ther. 2001 May;15(5):729-30 [11328270.001]
  • [CommentIn] Aliment Pharmacol Ther. 2000 Nov;14(11):1537-8 [11069327.001]
  • (PMID = 10632641.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Antacids; 0 / Gastrins; 0 / Histamine H2 Antagonists; 0 / Proton Pump Inhibitors
  • [Number-of-references] 94
  •  go-up   go-down


9. Seibyl JP, Chen W, Silverman DH: 3,4-dihydroxy-6-[18f]-fluoro-L-phenylalanine positron emission tomography in patients with central motor disorders and in evaluation of brain and other tumors. Semin Nucl Med; 2007 Nov;37(6):440-50
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 3,4-dihydroxy-6-[18f]-fluoro-L-phenylalanine positron emission tomography in patients with central motor disorders and in evaluation of brain and other tumors.
  • The roles of this tracer have since expanded to include monitoring disease progression, potentially contributing to drug development, and even questioning the current gold standard for making the diagnosis of Parkinson's disease.
  • As with some other amino acids, (18)F-FDOPA has also been effective for visualizing brain tumors, either at time of diagnosis or when monitoring for recurrence, with high sensitivity and overall accuracy. (18)F-FDOPA may be especially useful for imaging patients with low-grade gliomas, as well in the evaluation of patients with neuroendocrine tumors such as carcinoid and pheochromocytoma, in which its role as a precursor for amine neurotransmitter/neurohormones serves as a basis for its differential uptake.
  • [MeSH-minor] Adrenal Gland Neoplasms / radionuclide imaging. Amino Acids / metabolism. Caudate Nucleus / radionuclide imaging. Fluorine Radioisotopes. Glioma / radionuclide imaging. Humans. Neuroendocrine Tumors / radionuclide imaging. Parkinsonian Disorders / radionuclide imaging. Putamen / radionuclide imaging

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Movement Disorders.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17920351.001).
  • [ISSN] 0001-2998
  • [Journal-full-title] Seminars in nuclear medicine
  • [ISO-abbreviation] Semin Nucl Med
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acids; 0 / Fluorine Radioisotopes; 0 / Radiopharmaceuticals; 2C598205QX / fluorodopa F 18; 63-84-3 / Dihydroxyphenylalanine
  • [Number-of-references] 96
  •  go-up   go-down


10. Davies H, Hunter C, Smith R, Stephens P, Greenman C, Bignell G, Teague J, Butler A, Edkins S, Stevens C, Parker A, O'Meara S, Avis T, Barthorpe S, Brackenbury L, Buck G, Clements J, Cole J, Dicks E, Edwards K, Forbes S, Gorton M, Gray K, Halliday K, Harrison R, Hills K, Hinton J, Jones D, Kosmidou V, Laman R, Lugg R, Menzies A, Perry J, Petty R, Raine K, Shepherd R, Small A, Solomon H, Stephens Y, Tofts C, Varian J, Webb A, West S, Widaa S, Yates A, Brasseur F, Cooper CS, Flanagan AM, Green A, Knowles M, Leung SY, Looijenga LH, Malkowicz B, Pierotti MA, Teh BT, Yuen ST, Lakhani SR, Easton DF, Weber BL, Goldstraw P, Nicholson AG, Wooster R, Stratton MR, Futreal PA: Somatic mutations of the protein kinase gene family in human lung cancer. Cancer Res; 2005 Sep 1;65(17):7591-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Protein kinases are frequently mutated in human cancer and inhibitors of mutant protein kinases have proven to be effective anticancer drugs.
  • There was considerable variation between individual lung cancers in the number of mutations observed and no mutations were found in lung carcinoids.
  • [MeSH-minor] Adenocarcinoma / enzymology. Adenocarcinoma / genetics. Carcinoid Tumor / enzymology. Carcinoid Tumor / genetics. Carcinoma, Large Cell / enzymology. Carcinoma, Large Cell / genetics. Carcinoma, Squamous Cell / enzymology. Carcinoma, Squamous Cell / genetics. Cell Line, Tumor. DNA Mutational Analysis. Humans

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16140923.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.- / Protein Kinases
  •  go-up   go-down


11. Molenaar JP, Baten A, Blokx WA, Hoogendam A: Development of carcinoid tumour in hormonally treated adenocarcinoma of the prostate. Eur Urol; 2009 Nov;56(5):874-7; quiz 876
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of carcinoid tumour in hormonally treated adenocarcinoma of the prostate.
  • We present the case of an 81-yr-old man with a prostatic adenocarcinoma and a metastatic carcinoid.
  • Simultaneous occurrence of hormonally treated adenocarcinoma of the prostate and a carcinoid has been described before.
  • Early recognition of the carcinoid syndrome is crucial, as surgical cure is not possible after metastasis.
  • [MeSH-major] Adenocarcinoma / drug therapy. Androgen Antagonists / therapeutic use. Anilides / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Carcinoid Tumor / pathology. Liver Neoplasms / pathology. Neoplasms, Multiple Primary. Nitriles / therapeutic use. Prostatic Neoplasms / drug therapy. Tosyl Compounds / therapeutic use
  • [MeSH-minor] Aged, 80 and over. Biopsy. Humans. Male. Malignant Carcinoid Syndrome / drug therapy. Positron-Emission Tomography. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. BICALUTAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19171417.001).
  • [ISSN] 1873-7560
  • [Journal-full-title] European urology
  • [ISO-abbreviation] Eur. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Antineoplastic Agents, Hormonal; 0 / Nitriles; 0 / Tosyl Compounds; 51110-01-1 / Somatostatin; A0Z3NAU9DP / bicalutamide
  •  go-up   go-down


12. Bushnell DL Jr, O'Dorisio TM, O'Dorisio MS, Menda Y, Hicks RJ, Van Cutsem E, Baulieu JL, Borson-Chazot F, Anthony L, Benson AB, Oberg K, Grossman AB, Connolly M, Bouterfa H, Li Y, Kacena KA, LaFrance N, Pauwels SA: 90Y-edotreotide for metastatic carcinoid refractory to octreotide. J Clin Oncol; 2010 Apr 01;28(10):1652-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 90Y-edotreotide for metastatic carcinoid refractory to octreotide.
  • PURPOSE: Metastatic carcinoid is an incurable malignancy whose symptoms, such as diarrhea and flushing, can be debilitating and occasionally life-threatening.
  • Although symptom relief is available with octreotide, the disease eventually becomes refractory to octreotide, leaving no proven treatment options.
  • The goal of this study was to evaluate the clinical effect of using (90)Y-edotreotide to treat symptomatic patients with carcinoid tumors.
  • PATIENTS AND METHODS: Patients enrolled had metastatic carcinoid, at least one sign/symptom refractory to octreotide, and at least one measurable lesion.
  • Using Southwest Oncology Group tumor response criteria, 67 (74.
  • CONCLUSION: (90)Y-edotreotide treatment improved symptoms associated with malignant carcinoid among subjects with no treatment alternatives.
  • Treatment was well-tolerated and had an acceptable expected AE profile.
  • [MeSH-major] Carcinoid Tumor / drug therapy. Carcinoid Tumor / secondary. Octreotide / analogs & derivatives
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Disease-Free Survival. Drug Resistance, Neoplasm. Female. Humans. Male. Middle Aged. Yttrium Radioisotopes

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20194865.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / R01 CA167632
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 90Y-octreotide, DOTA-Tyr(3)-; 0 / Yttrium Radioisotopes; RWM8CCW8GP / Octreotide
  • [Other-IDs] NLM/ PMC4872330
  •  go-up   go-down


13. Schmid HA, Schoeffter P: Functional activity of the multiligand analog SOM230 at human recombinant somatostatin receptor subtypes supports its usefulness in neuroendocrine tumors. Neuroendocrinology; 2004;80 Suppl 1:47-50
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Functional activity of the multiligand analog SOM230 at human recombinant somatostatin receptor subtypes supports its usefulness in neuroendocrine tumors.
  • Functional gastroenteropancreatic tumors express all 5 somatostatin receptor subtypes (sst) in different quantities.
  • Octreotide and lanreotide treat patients with these tumors by binding preferentially to sst2 and, to a lesser extent, to sst3 and sst5 receptors, thereby controlling prominent symptoms caused by hormone hypersecretion (diarrhea and flushing).
  • The multiligand activity profile of SOM230, together with its nondesensitizing inhibitory effect on growth hormone and insulin-like growth factor-I secretion in rats, may underlie its successful use in clinical trials and its potential for use in refractory patients with carcinoid tumors.
  • [MeSH-major] Neuroectodermal Tumors / metabolism. Receptors, Somatostatin / metabolism. Somatostatin / analogs & derivatives. Somatostatin / pharmacology
  • [MeSH-minor] Animals. Antineoplastic Agents, Hormonal / therapeutic use. Cell Line, Tumor. Colforsin / pharmacology. Cricetinae. Cricetulus. Cyclic AMP / metabolism. Dose-Response Relationship, Drug. Drug Interactions. Humans. Octreotide / therapeutic use. Recombinant Proteins / metabolism. Transfection / methods


14. van Gerven MA, Taal BG, Lucas PJ: Dynamic Bayesian networks as prognostic models for clinical patient management. J Biomed Inform; 2008 Aug;41(4):515-29
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Prognostic models in medicine are usually been built using simple decision rules, proportional hazards models, or Markov models.
  • To this end, we focus on the construction of a DBN for prognosis of carcinoid patients, compare performance with that of a proportional hazards model, and describe predictions for three individual patients.
  • We show that the DBN can make detailed predictions, about not only patient survival, but also other variables of interest, such as disease progression, the effect of treatment, and the development of complications.
  • [MeSH-major] Carcinoid Tumor / diagnosis. Carcinoid Tumor / mortality. Decision Support Systems, Clinical. Diagnosis, Computer-Assisted / methods. Neural Networks (Computer). Risk Assessment / methods

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18337188.001).
  • [ISSN] 1532-0480
  • [Journal-full-title] Journal of biomedical informatics
  • [ISO-abbreviation] J Biomed Inform
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


15. Erlandsen SE, Fykse V, Waldum HL, Sandvik AK: Octreotide induces apoptosis in the oxyntic mucosa. Mol Cell Endocrinol; 2007 Jan 29;264(1-2):188-96
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Previous studies show that octreotide LAR causes regression of gastric ECL-cell carcinoids, reducing both number and size of tumours.
  • [MeSH-major] Apoptosis / drug effects. Cell Proliferation / drug effects. Gastric Mucosa / metabolism. Gastrointestinal Agents / pharmacology. Gene Expression Regulation / drug effects. Octreotide / pharmacology
  • [MeSH-minor] Animals. Carcinoid Tumor / drug therapy. Carcinoid Tumor / metabolism. Female. Gene Expression Profiling. Oligonucleotide Array Sequence Analysis. Rats. Rats, Sprague-Dawley. Stomach Neoplasms / drug therapy. Stomach Neoplasms / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17210224.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Gastrointestinal Agents; RWM8CCW8GP / Octreotide
  •  go-up   go-down


16. Kowalski J, Henze M, Schuhmacher J, Mäcke HR, Hofmann M, Haberkorn U: Evaluation of positron emission tomography imaging using [68Ga]-DOTA-D Phe(1)-Tyr(3)-Octreotide in comparison to [111In]-DTPAOC SPECT. First results in patients with neuroendocrine tumors. Mol Imaging Biol; 2003 Jan-Feb;5(1):42-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of positron emission tomography imaging using [68Ga]-DOTA-D Phe(1)-Tyr(3)-Octreotide in comparison to [111In]-DTPAOC SPECT. First results in patients with neuroendocrine tumors.
  • PURPOSE: [111In]-DTPAOC (Octreoscan(R)) has been shown to be very useful in the detection of somatostatin receptor (SSTR) positive tumors and their metastases using either conventional scintigraphy or single photon emission computed tomography (SPECT).
  • Due to the increased spatial resolution and the ability of quantification, an agent for positron emission tomography (PET) imaging of SSTR is desirable.
  • This communication shows our initial experience using [68Ga]-DOTA-D-Phe(1)-Tyr(3)-Octreotide (DOTATOC) in comparison to [111In]-DTPAOC-SPECT in patients with neuroendocrine tumors.
  • All of them suffered from neuroendocrine tumors and/or their metastases.
  • In two patients with previously known localization of tumor, dynamic PET scans after intravenous bolus-injection of 181+/-17 MBq [68Ga]-DOTATOC until 120 minutes post-injection were acquired.
  • Due to the fast tracer accumulation in the tumor and the rapid clearance of the compound, resulting in high tumor to background ratios even 40 minutes after injection, the short half life of 68Ga is reasonable.
  • Both [111In]-DTPAOC-SPECT and [68Ga]-DOTATOC-PET were less sensitive in the detection of liver metastases of neuroendocrine tumors compared to computerized tomography CT because they showed a lower uptake than the surrounding liver tissue.
  • CONCLUSIONS: According to our initial experiences in a limited number of patients, [68Ga]-DOTATOC is a promising PET tracer for imaging neuroendocrine tumors and their metastases.
  • In comparison to the [111In]-DTPAOC-scan it seems to be superior especially in detecting small tumors or tumors bearing only a low density of SSTRs.
  • It offers excellent imaging properties and very high tumor to background ratios.
  • [MeSH-minor] Carcinoid Tumor / diagnosis. Carcinoid Tumor / radionuclide imaging. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Time Factors. Tissue Distribution

  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14499161.001).
  • [ISSN] 1536-1632
  • [Journal-full-title] Molecular imaging and biology : MIB : the official publication of the Academy of Molecular Imaging
  • [ISO-abbreviation] Mol Imaging Biol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 51110-01-1 / Somatostatin; G083B71P98 / pentetreotide; RWM8CCW8GP / Octreotide; U194AS08HZ / Edotreotide
  •  go-up   go-down


17. Dolezal J, Vizd'a J, Bures J: Detection of acute gastrointestinal bleeding by means of technetium-99m in vivo labelled red blood cells. Nucl Med Rev Cent East Eur; 2002;5(2):151-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Scintigraphy with red blood cells (RBCs) in vivo labelled by means of technetium-99m hastened detection of source of GI bleeding and improved management of the particular disease.
  • MATERIAL AND METHODS: 31 patients (13 men, 18 women, aged 20-91, mean 56 years) underwent this investigation from 1998 till 2001 at the Department of Nuclear Medicine.
  • Final diagnoses of our 16 patients with positive scintigraphy with autological labelled RBCs were: bleeding small bowel arteriovenous malformation (6 patients), uraemic enteritis with bleeding erosions in ileum and jejunum (2 patients), Osler-Rendu- Weber disease (1 patient), pseudocyst of the pancreas with bleeding vessel communicating to the transverse colon (1 patient), bleeding submucose varix in jejunum (1 patient), carcinoid of the ileum (1 patient), bleeding from the ileosigmoideoanastomosis six days after hemicolectomy for Crohn's disease (1 patient), bleeding from an ulcer close to the papilla of Vater (1 patient), bleeding from ulcer at jejunum after previous NSAIDs treatment (1 patient), bleeding inflammatory polyp at ileotransversoanastomosis (1 patient).
  • CONCLUSIONS: Scintigraphy with RBCs in vivo labelled technetium- 99m hastened detection of the source of GI bleeding and improved management of the source of GI bleeding and improved management of disease.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14600875.001).
  • [ISSN] 1506-9680
  • [Journal-full-title] Nuclear medicine review. Central & Eastern Europe
  • [ISO-abbreviation] Nucl Med Rev Cent East Eur
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  •  go-up   go-down


18. Yao JC, Kvols LK: Octreotide LAR in carcinoid: how to dose? Pancreas; 2008 Oct;37(3):337-8; author reply 338-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Octreotide LAR in carcinoid: how to dose?
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Carcinoid Tumor / drug therapy. Neuroendocrine Tumors / drug therapy. Octreotide / therapeutic use
  • [MeSH-minor] Dose-Response Relationship, Drug. Drug Monitoring. Humans. Receptors, Somatostatin / metabolism. Research Design. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Pancreas. 2008 Jul;37(1):94-100 [18580450.001]
  • (PMID = 18815562.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; RWM8CCW8GP / Octreotide
  •  go-up   go-down


19. Murali D, Flores LG, Roberts AD, Nickles RJ, DeJesus OT: Aromatic L-amino acid decarboxylase (AAAD) inhibitors as carcinoid tumor-imaging agents: synthesis of 18F-labeled alpha-fluoromethyl-6-fluoro-m-tyrosine (FM-6-FmT). Appl Radiat Isot; 2003 Oct;59(4):237-43
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aromatic L-amino acid decarboxylase (AAAD) inhibitors as carcinoid tumor-imaging agents: synthesis of 18F-labeled alpha-fluoromethyl-6-fluoro-m-tyrosine (FM-6-FmT).
  • The aromatic L-amino acid decarboxylase (AAAD) enzyme is significantly upregulated in neuroendocrine tumors and, thus, would be a good target for PET imaging agents.
  • Alpha-fluoromethyl-DOPA (FMDOPA) is one of the most potent irreversible AAAD inhibitor and its non-catechol derivative, alpha-fluoromethyl-m-tyrosine (FMmT), is a promising AAAD imaging agent.
  • We synthesized FMmT and its direct electrophilic fluorination provided a mixture of products identified by NMR analysis after HPLC purification as 6-fluoro-, 2-fluoro- and 2,6-difluoro-derivatives of FMmT.
  • Based on its proposed mechanism of inhibition, FM-6-[18F]FmT is expected to irreversibly bind to AAAD and, hence, could be used as a PET agent to image tumors of endocrine origin containing high concentrations of AAAD.
  • [MeSH-major] Aromatic Amino Acid Decarboxylase Inhibitors. Fluorine Radioisotopes / chemistry. Isotope Labeling / methods. Neuroendocrine Tumors / radionuclide imaging. Radioligand Assay / methods. Radiopharmaceuticals / chemistry. Tyrosine / analogs & derivatives. Tyrosine / chemistry
  • [MeSH-minor] Aromatic-L-Amino-Acid Decarboxylases / chemistry. Aromatic-L-Amino-Acid Decarboxylases / metabolism. Carcinoid Tumor / metabolism. Carcinoid Tumor / radionuclide imaging. Humans. Protein Binding. Tomography, Emission-Computed / methods

  • Genetic Alliance. consumer health - Carcinoid Tumor.
  • Hazardous Substances Data Bank. L-TYROSINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14522231.001).
  • [ISSN] 0969-8043
  • [Journal-full-title] Applied radiation and isotopes : including data, instrumentation and methods for use in agriculture, industry and medicine
  • [ISO-abbreviation] Appl Radiat Isot
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / 5R01NS26621
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aromatic Amino Acid Decarboxylase Inhibitors; 0 / Fluorine Radioisotopes; 0 / Radiopharmaceuticals; 42HK56048U / Tyrosine; 97123-83-6 / beta-fluoromethylene-3-tyrosine; EC 4.1.1.28 / Aromatic-L-Amino-Acid Decarboxylases
  •  go-up   go-down


20. Hoegerle S, Altehoefer C, Ghanem N, Koehler G, Waller CF, Scheruebl H, Moser E, Nitzsche E: Whole-body 18F dopa PET for detection of gastrointestinal carcinoid tumors. Radiology; 2001 Aug;220(2):373-80
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Whole-body 18F dopa PET for detection of gastrointestinal carcinoid tumors.
  • PURPOSE: To evaluate fluorine 18 (18F) dopa positron emission tomography (PET) in comparison with established imaging procedures in gastrointestinal carcinoid tumors.
  • MATERIALS AND METHODS: After evaluation of the normal distribution of 18F dopa, 17 patients with histologically confirmed tumors were examined with 18F dopa PET.
  • Results of 2-[fluorine 18]fluoro-2-deoxy-D-glucose (FDG) PET, somatostatin-receptor scintigraphy, and morphologic imaging (computed tomography and/or magnetic resonance imaging) were available for all patients.
  • Results of the procedures were evaluated by two radiologists and two nuclear medicine specialists, whose consensus based on all available histologic, imaging, and follow-up findings was used as the reference standard.
  • RESULTS: Ninety-two tumors were diagnosed: eight primary tumors, 47 lymph node metastases, and 37 organ metastases.
  • 18F dopa PET led to 60 true-positive findings (seven primary tumors, 41 lymph node metastases, 12 organ metastases); FDG PET, 27 (two primary tumors, 14 lymph node metastases, 11 organ metastases); somatostatin-receptor scintigraphy, 52 (four primary tumors, 27 lymph node metastases, 21 organ metastases); and morphologic imaging, 67 (two primary tumors, 29 lymph node metastases, 36 organ metastases).
  • This resulted in the following overall sensitivities: 18F dopa PET, 65% (60 of 92); FDG PET, 29% (27 of 92); somatostatin-receptor scintigraphy, 57% (52 of 92); morphologic procedures, 73% (67 of 92).
  • Although the morphologic procedures were most sensitive for organ metastases, 18F dopa PET enabled best localization of primary tumors and lymph node staging.
  • CONCLUSION: 18F dopa PET is a promising procedure and useful supplement to morphologic methods in diagnostic imaging of gastrointestinal carcinoid tumors.
  • [MeSH-major] Carcinoid Tumor / radionuclide imaging. Dihydroxyphenylalanine. Fluorine Radioisotopes. Gastrointestinal Neoplasms / radionuclide imaging. Tomography, Emission-Computed

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11477239.001).
  • [ISSN] 0033-8419
  • [Journal-full-title] Radiology
  • [ISO-abbreviation] Radiology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fluorine Radioisotopes; 0 / Receptors, Somatostatin; 0Z5B2CJX4D / Fluorodeoxyglucose F18; 63-84-3 / Dihydroxyphenylalanine
  •  go-up   go-down


21. Shah MH, Young D, Kindler HL, Webb I, Kleiber B, Wright J, Grever M: Phase II study of the proteasome inhibitor bortezomib (PS-341) in patients with metastatic neuroendocrine tumors. Clin Cancer Res; 2004 Sep 15;10(18 Pt 1):6111-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of the proteasome inhibitor bortezomib (PS-341) in patients with metastatic neuroendocrine tumors.
  • PURPOSE: This phase II study was undertaken to assess objective response, toxicity, tumor marker response, and pharmacodynamics of bortezomib in patients with metastatic neuroendocrine (carcinoid and islet cell) tumors.
  • EXPERIMENTAL DESIGN: A total of 16 patients with measurable metastatic carcinoid (n=12) or islet cell (n=4) tumors received i.v. bolus of single agent bortezomib at a dose of 1.5 mg/m2 on days 1, 4, 8, and 11 every 21 days.
  • Tumor response was assessed at 12-week intervals using Response Evaluation Criteria in Solid Tumors (RECIST) criteria.
  • RESULTS: No patient achieved a partial or a complete remission.
  • Changes in tumor marker levels did not correlate with tumor response.
  • CONCLUSIONS: Despite achieving the surrogate biologic end point, single-agent bortezomib did not induce any objective responses in patients with metastatic carcinoid or islet cell tumors.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Boronic Acids / therapeutic use. Carcinoid Tumor / drug therapy. Neuroendocrine Tumors / drug therapy. Pancreatic Neoplasms / drug therapy. Protease Inhibitors / therapeutic use. Pyrazines / therapeutic use
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor. Bortezomib. Female. Humans. Male. Maximum Tolerated Dose. Middle Aged. Neoplasm Metastasis. Proteasome Inhibitors. Time Factors. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15447997.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA63185
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
  •  go-up   go-down


22. Detjen KM, Welzel M, Wiedenmann B, Rosewicz S: Nonsteroidal anti-inflammatory drugs inhibit growth of human neuroendocrine tumor cells via G1 cell-cycle arrest. Int J Cancer; 2003 Dec 10;107(5):844-53
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nonsteroidal anti-inflammatory drugs inhibit growth of human neuroendocrine tumor cells via G1 cell-cycle arrest.
  • Therapeutic options to inhibit growth of human NETs of the GEP system are limited.
  • Since NSAIDs might provide an antiproliferative treatment alternative with acceptable toxicity, we examined the effects of different NSAIDs on growth and survival in a representative set of human GEP NET cell lines.
  • Depending on the drug and cell line investigated, NSAID treatment resulted in profound growth inhibition of GEP NET cells.
  • Cell-cycle analyses documented a G1 arrest in NSAID-treated GEP NET populations.
  • At therapeutically relevant concentrations, sulindac significantly reduced GEP NET cell numbers, whereas IFN-alpha and octreotide remained ineffective.
  • The extent of growth inhibition in GEP NETs was comparable to the antiproliferative effects of sulindac in established NSAID-sensitive cell models.
  • NSAIDs acted as potent antiproliferative agents in GEP NET cells via G1 cell-cycle arrest and might therefore offer a therapeutic alternative to current treatment modalities.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Cell Cycle / drug effects. Cell Division / drug effects. Cyclooxygenase Inhibitors / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Carcinoma, Neuroendocrine. DNA Fragmentation. Flow Cytometry. G1 Phase / drug effects. Humans. Indomethacin / pharmacology. Sulindac / pharmacology. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Pancreatic islet cell tumors.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. INDOMETHACIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2003 Wiley-Liss, Inc.
  • (PMID = 14566837.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase Inhibitors; 184SNS8VUH / Sulindac; XXE1CET956 / Indomethacin
  •  go-up   go-down


23. Hofland LJ, Lamberts SW: The pathophysiological consequences of somatostatin receptor internalization and resistance. Endocr Rev; 2003 Feb;24(1):28-47
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Somatostatin receptors expressed on tumor cells form the rationale for somatostatin analog treatment of patients with somatostatin receptor-positive neuroendocrine tumors.
  • Nevertheless, although somatostatin analogs effectively control hormonal hypersecretion by GH-secreting pituitary adenomas, islet cell tumors, and carcinoid tumors, significant differences are observed among patients with respect to the efficacy of treatment.
  • This may be related to a differential expression of somatostatin receptor subtypes among tumors.
  • In addition, the property of somatostatin receptor subtypes to undergo agonist-induced internalization has important consequences for visualizing, as well as for therapy, of receptor-positive tumors using radioisotope- or chemotherapeutic-compound-coupled somatostatin analogs.
  • This review covers the pathophysiological role of somatostatin receptor subtypes in determining the efficacy of treatment of patients with somatostatin receptor-positive tumors using somatostatin analogs, as well as the preclinical and clinical consequences of agonist-induced receptor internalization for somatostatin receptor-targeted radio- and chemotherapy.
  • [MeSH-minor] Animals. Drug Resistance. Gene Expression. Humans. Neoplasms / drug therapy. Neoplasms / metabolism. Neoplasms / radiotherapy. Radiopharmaceuticals / therapeutic use. Somatostatin / pharmacology. Tachyphylaxis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12588807.001).
  • [ISSN] 0163-769X
  • [Journal-full-title] Endocrine reviews
  • [ISO-abbreviation] Endocr. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin
  • [Number-of-references] 199
  •  go-up   go-down


24. Greenblatt DY, Vaccaro AM, Jaskula-Sztul R, Ning L, Haymart M, Kunnimalaiyaan M, Chen H: Valproic acid activates notch-1 signaling and regulates the neuroendocrine phenotype in carcinoid cancer cells. Oncologist; 2007 Aug;12(8):942-51
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Valproic acid activates notch-1 signaling and regulates the neuroendocrine phenotype in carcinoid cancer cells.
  • Carcinoid tumors are neuroendocrine malignancies that frequently metastasize and secrete hormones that cause debilitating symptoms in patients.
  • In this study we report the effects of valproic acid (VPA), a drug long used for the treatment of epilepsy, on the growth and neuroendocrine phenotype of human carcinoid cancer cells.
  • VPA treatment of gastrointestinal and pulmonary carcinoid cells resulted in a dose-dependent inhibition of cancer cell growth.
  • Furthermore, VPA suppressed expression of the neuroendocrine tumor marker chromogranin A.
  • Transfection of Notch-1 small-interfering RNA into carcinoid tumor cells blocked the effects of VPA on Notch-1 activation, ASCL-1 suppression, p21 induction, and cell growth inhibition.
  • VPA also suppressed growth of carcinoid tumors in vivo in a mouse tumor xenograft experiment.
  • These findings confirm the important role of Notch-1 in regulating the growth and neuroendocrine phenotype of carcinoid tumor cells.
  • On the basis of this study, a clinical trial of VPA for patients with advanced carcinoid cancer will be conducted.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoid Tumor / metabolism. Gastrointestinal Neoplasms / metabolism. Lung Neoplasms / metabolism. Receptor, Notch1 / metabolism. Valproic Acid / pharmacology
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation. Chromogranin A / antagonists & inhibitors. Chromogranin A / metabolism. Cyclin D1 / metabolism. Genes, Reporter. Humans. Luciferases / analysis. Luciferases / genetics. Male. Mice. Mice, Nude. Phenotype. RNA Interference. Signal Transduction / drug effects. Xenograft Model Antitumor Assays

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. VALPROIC ACID .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17766653.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA109053; United States / NIDDK NIH HHS / DK / DK064735; United States / NIDDK NIH HHS / DK / DK066169
  • [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 / Antineoplastic Agents; 0 / Chromogranin A; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 136601-57-5 / Cyclin D1; 614OI1Z5WI / Valproic Acid; EC 1.13.12.- / Luciferases
  •  go-up   go-down


25. Zomerhuis MT, Hussain SM, Feelders RA, van der Lely AJ, de Herder WW: Octreotide exerts only acute, but no sustained, effects on MRI enhancement of liver metastases in carcinoid syndrome. Neuroendocrinology; 2005;82(1):41-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Octreotide exerts only acute, but no sustained, effects on MRI enhancement of liver metastases in carcinoid syndrome.
  • We have investigated the acute and sustained hemodynamic effects of octreotide on hepatic metastases of midgut carcinoids using contrast-enhanced dynamic magnetic resonance imaging (MRI).
  • Seven patients with the carcinoid syndrome and metastasized midgut carcinoid tumors underwent functional dynamic multi-phase gadolinium-enhanced MRI of selected liver metastases at baseline and 60 min after the subcutaneous (s.c.) administration of 100 microg octreotide, and also after 3 months with three times daily (t.i.d.
  • Baseline MRIs showed the typical aspect of carcinoid liver metastases with a very bright signal on the T2-weighted sequences and intense enhancement in the arterial phase after injection of gadolinium-diethylenetriaminepentaacetate.
  • This study further shows that contrast-enhanced dynamic MRI can be a very useful tool for studying hemodynamic effects of medical therapies on liver metastases in patients with metastatic midgut carcinoids.
  • [MeSH-major] Antineoplastic Agents, Hormonal / pharmacology. Carcinoid Tumor / drug therapy. Carcinoid Tumor / pathology. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Octreotide / pharmacology. Splanchnic Circulation / drug effects
  • [MeSH-minor] Aged. Female. Gastrointestinal Neoplasms / drug therapy. Gastrointestinal Neoplasms / pathology. Humans. Image Enhancement. Magnetic Resonance Imaging. Male. Middle Aged. Regional Blood Flow / drug effects

  • Genetic Alliance. consumer health - Carcinoid Syndrome.
  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2005 S. Karger AG, Basel.
  • (PMID = 16391492.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; RWM8CCW8GP / Octreotide
  •  go-up   go-down


26. Adler JT, Hottinger DG, Kunnimalaiyaan M, Chen H: Combination therapy with histone deacetylase inhibitors and lithium chloride: a novel treatment for carcinoid tumors. Ann Surg Oncol; 2009 Feb;16(2):481-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combination therapy with histone deacetylase inhibitors and lithium chloride: a novel treatment for carcinoid tumors.
  • In carcinoid cell lines, the histone deacetylase (HDAC) inhibitors valproic acid (VPA) and suberoyl bis-hydroxamic acid (SBHA) activate the Notch1 pathway, whereas lithium inhibits glycogen synthase kinase-3beta (GSK-3beta).
  • We hypothesized that lower-dose combination therapy of HDAC inhibitors and lithium chloride could achieve similar growth inhibition to that of the drugs alone.
  • Gastrointestinal and pulmonary carcinoid cells were treated with either VPA or SBHA and lithium chloride for up to 48 hours.
  • Western blot analysis was used to measure the effects on the Notch1 and GSK-3beta pathways and the neuroendocrine tumor marker chromogranin A (CgA).
  • Treatment of carcinoid cells with either VPA or SBHA and lithium chloride suppresses the neuroendocrine marker CgA while upregulating Notch1 and inhibiting GSK-3beta.
  • Thus, lower-dose combination therapy may be a viable therapeutic approach for carcinoid tumors.

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. LITHIUM CHLORIDE .
  • Hazardous Substances Data Bank. VALPROIC ACID .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] World J Surg. 2004 Apr;28(4):387-92 [14994141.001]
  • [Cites] Curr Opin Genet Dev. 2004 Oct;14(5):506-12 [15380241.001]
  • [Cites] Nature. 1995 Mar 9;374(6518):131-4 [7877684.001]
  • [Cites] Mol Cancer Ther. 2005 Jun;4(6):910-7 [15956248.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Jul;90(7):4350-6 [15870121.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2005 Oct;289(4):G636-42 [16160079.001]
  • [Cites] Curr Opin Oncol. 2006 Jan;18(1):9-15 [16357558.001]
  • [Cites] Surg Oncol Clin N Am. 2006 Jul;15(3):463-78 [16882492.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2003 Aug;285(2):G245-54 [12851216.001]
  • [Cites] Cancer Cell. 2003 Mar;3(3):203-5 [12676578.001]
  • [Cites] Cancer. 2003 Feb 15;97(4):934-59 [12569593.001]
  • [Cites] J Biol Chem. 2006 Dec 29;281(52):39819-30 [17090547.001]
  • [Cites] Surgery. 2008 Dec;144(6):956-61; discussion 961-2 [19041003.001]
  • [Cites] J Surg Res. 2008 Jul;148(1):31-7 [18570928.001]
  • [Cites] Ann Surg. 2008 Jun;247(6):1036-40 [18520232.001]
  • [Cites] Surgery. 2007 Feb;141(2):161-5; discussion 165 [17263970.001]
  • [Cites] Mol Cancer Ther. 2007 Mar;6(3):1151-8 [17363508.001]
  • [Cites] Oncologist. 2007 May;12(5):535-42 [17522241.001]
  • [Cites] Oncologist. 2007 Aug;12(8):942-51 [17766653.001]
  • [Cites] J Gastrointest Surg. 2007 Nov;11(11):1515-20; discussion 1520 [17874277.001]
  • [Cites] Lancet Oncol. 2008 Jan;9(1):61-72 [18177818.001]
  • [Cites] Oncologist. 2008 Feb;13(2):98-104 [18305053.001]
  • (PMID = 19030935.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA117117-01A2; United States / NCI NIH HHS / CA / CA109053-03; United States / NCI NIH HHS / CA / R21 CA117117-02; United States / NCI NIH HHS / CA / CA117117; United States / NCI NIH HHS / CA / R01 CA109053-03; United States / NCI NIH HHS / CA / R01 CA109053-01A2; United States / NCI NIH HHS / CA / R01 CA109053; United States / NCI NIH HHS / CA / CA117117-02; United States / NCI NIH HHS / CA / R21 CA117117-01A2; United States / NCI NIH HHS / CA / CA109053; United States / NCI NIH HHS / CA / CA109053-01A2; United States / NCI NIH HHS / CA / CA109053-02; United States / NCI NIH HHS / CA / R21 CA117117; United States / NCI NIH HHS / CA / R01 CA109053-02
  • [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 / Adjuvants, Immunologic; 0 / Chromogranin A; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Immunoglobulin J Recombination Signal Sequence-Binding Protein; 0 / RBPJ protein, human; 0 / Receptor, Notch1; 0 / suberoyl bis-hydroxamic acid; 614OI1Z5WI / Valproic Acid; EC 1.13.12.- / Luciferases; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 3.5.1.98 / Histone Deacetylases; G4962QA067 / Lithium Chloride
  • [Other-IDs] NLM/ NIHMS127901; NLM/ PMC2740795
  •  go-up   go-down


27. Friedman S: Cancer in Crohn's disease. Gastroenterol Clin North Am; 2006 Sep;35(3):621-39
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cancer in Crohn's disease.
  • When each of these studies is scrutinized, however, there is only enough evidence to support a link between colorectal adenocarcinoma, SBA, and squamous and adenocarcinomas that are associated with perianal fistulizing disease.
  • All of the studies of large bowel adenocarcinoma or SBA follow patients in an era during which there were far fewer effective medicines to treat CD and surgery was more commonplace.
  • Overall results from this study and the multitude of the other studies show that the risk for cancer in Crohn's colitis is equal to that in UC given equal extent and duration of disease.
  • Patients who have Crohn's colitis that affects at least one third of the colon and with at least 8 years of disease should undergo screening and surveillance, just as in UC.
  • Although the absolute risk for SBA in CD is low (2.2% at 25 years in one study), we should not rule out screening and surveying for this complication that is associated with significant morbidity and mortality in patients who have long-standing, extensive, small bowel disease.
  • The evidence that links carcinoid tumors to CD is weak, and population-based studies need to be done.
  • [MeSH-major] Crohn Disease / complications. Intestinal Neoplasms / etiology

  • Genetic Alliance. consumer health - Crohn Disease.
  • MedlinePlus Health Information. consumer health - Crohn's Disease.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16952744.001).
  • [ISSN] 0889-8553
  • [Journal-full-title] Gastroenterology clinics of North America
  • [ISO-abbreviation] Gastroenterol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 102
  •  go-up   go-down


28. Wong M, Kong A, Constantine S, Pathi R, Parrish FJ, Verma R, Lim C, Steer C: Radiopathological review of small bowel carcinoid tumours. J Med Imaging Radiat Oncol; 2009 Feb;53(1):1-12
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radiopathological review of small bowel carcinoid tumours.
  • Small bowel carcinoid tumours are endocrine tumours of the gastrointestinal tract.
  • This pictorial essay will review the pathology, clinical features, treatment and prognosis and illustrate the radiographic, computed tomographic, sonographic, magnetic resonance and nuclear medicine appearances of small bowel carcinoid tumours.
  • [MeSH-major] Carcinoid Tumor / diagnosis. Intestinal Neoplasms / diagnosis. Intestine, Small / pathology. Intestine, Small / radiography. Magnetic Resonance Imaging / methods. Tomography, X-Ray Computed / methods

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • MedlinePlus Health Information. consumer health - CT Scans.
  • MedlinePlus Health Information. consumer health - MRI Scans.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19453523.001).
  • [ISSN] 1754-9485
  • [Journal-full-title] Journal of medical imaging and radiation oncology
  • [ISO-abbreviation] J Med Imaging Radiat Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Australia
  • [Number-of-references] 42
  •  go-up   go-down


29. Lyons JM 3rd, Abergel J, Thomson JL, Anthony CT, Wang YZ, Anthony LB, Boudreaux JP, Strauchen J, Idrees M, Warner RR, Woltering EA: In vitro chemoresistance testing in well-differentiated carcinoid tumors. Ann Surg Oncol; 2009 Mar;16(3):649-55
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro chemoresistance testing in well-differentiated carcinoid tumors.
  • BACKGROUND: Well-differentiated, "typical" carcinoid tumors traditionally have a very poor response to chemotherapy.
  • We hypothesized that tumor specimens from well-differentiated carcinoid tumors would be highly resistant to the effects of chemotherapy when tested against a variety of antineoplastic agents in vitro.
  • METHODS: Ninety-eight typical carcinoid specimens were surgically harvested, cultured, and tested against antineoplastics in vitro. (3)H-Thymidine incorporation was used to assess the percentage of cell-growth inhibition (PCI) of tested specimens.
  • PCI was used to determine if specimens had extreme drug resistance (EDR), intermediate drug resistance (IDR), or low drug resistance (LDR) to each reagent against which they were tested.
  • Each was tested with an average of six drugs.
  • The mean proportions of drugs classified as LDR, IDR, and EDR were 0.48 (range 0-1), 0.34 (range 0-1), and 0.18 (range 0-0.80), respectively.
  • The mean numbers of drugs per specimen exhibiting LDR, IDR, and EDR chemoresistance were 2.7, 2.1, and 1.2, respectively.
  • 57 of 70 specimens (81%) had LDR to at least two drugs.
  • Low in vitro resistance to chemotherapeutics was prevalent among typical carcinoids, while EDR was comparatively infrequent.
  • CONCLUSIONS: This implies that there may be less clinical chemoresistance and more chemosensitivity among typical carcinoid tumors than clinical trials have previously revealed.
  • These findings warrant additional investigations assessing the response of carcinoid tumors to assay-guided chemotherapy regimens.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoid Tumor / drug therapy. Carcinoma, Neuroendocrine / drug therapy. Cell Differentiation. Drug Resistance, Neoplasm
  • [MeSH-minor] Drug Screening Assays, Antitumor. Female. Humans. Male. Prognosis

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19130141.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


30. Zuetenhorst JM, Valdes Olmos RA, Muller M, Hoefnagel CA, Taal BG: Interferon and meta-iodobenzylguanidin combinations in the treatment of metastatic carcinoid tumours. Endocr Relat Cancer; 2004 Sep;11(3):553-61
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interferon and meta-iodobenzylguanidin combinations in the treatment of metastatic carcinoid tumours.
  • Interferon (IFN) and meta-iodobenzylguanidin (MIBG) are active in metastatic carcinoids.
  • In a phase II study, we evaluated the effect upon diagnostic 131I-MIBG uptake and the clinical response of the combination.
  • The tumour over non-tumour (T/NT) ratios were quantitatively determined by comparing counts in the centre of the tumour (liver metastases) with those in an adjacent area of normal liver uptake (T/NT1) and with abdominal background area (T/NT2).
  • The absolute uptake in tumour deposits was also increased if compared with the abdominal background (T/NT2: 23% increase after IFN and 83% increase after unlabelled MIBG).
  • The combination produced 91% of patients with stable disease (using World Health Organisation criteria) at computed tomography scan and a biochemical response (a reduction of at least 50% in urinary 5-hydroxyindolacetic acid excretion) in 39%.
  • IFN-alpha did not significantly improve tumour retention of 131I-MIBG.
  • In contrast, unlabelled MIBG significantly improved biodistribution and tumour uptake in 83%.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoid Tumor / drug therapy. Carcinoid Tumor / secondary. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary
  • [MeSH-minor] 3-Iodobenzylguanidine / administration & dosage. Adult. Aged. Disease Progression. Female. Humans. Hydroxyindoleacetic Acid / urine. Interferon-alpha / administration & dosage. Intestinal Neoplasms / drug therapy. Intestinal Neoplasms / pathology. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology. Male. Middle Aged. Recombinant Proteins. Stomach Neoplasms / drug therapy. Stomach Neoplasms / pathology. Survival Rate. Tomography, Emission-Computed

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15369454.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Recombinant Proteins; 35MRW7B4AD / 3-Iodobenzylguanidine; 54-16-0 / Hydroxyindoleacetic Acid; 99210-65-8 / interferon alfa-2b
  •  go-up   go-down


31. Davì MV, Bodei L, Francia G, Bartolomei M, Oliani C, Scilanga L, Reghellin D, Falconi M, Paganelli G, Lo Cascio V, Ferdeghini M: Carcinoid crisis induced by receptor radionuclide therapy with 90Y-DOTATOC in a case of liver metastases from bronchial neuroendocrine tumor (atypical carcinoid). J Endocrinol Invest; 2006 Jun;29(6):563-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Carcinoid crisis induced by receptor radionuclide therapy with 90Y-DOTATOC in a case of liver metastases from bronchial neuroendocrine tumor (atypical carcinoid).
  • SS receptors are overexpressed in many tumors, mainly of neuroendocrine origin, thus enabling the treatment with SS analogs.
  • The clinical experience of receptor radionuclide therapy with the new analog [90Y-DOTA0-Tyr3 ]-octreotide [90Y-DOTATOC] has been developed over the last decade and is gaining a pivotal role in the therapeutic workout of these tumors.
  • It is well known that some procedures performed in diagnostic and therapeutic management of endocrine tumors, such as agobiopsy and hepatic chemoembolization, can be associated with the occurrence of symptoms related to the release of vasoactive amines and/or hormonal peptides from tumor cell lysis.
  • This is the first report of a severe carcinoid crisis developed after receptor radionuclide therapy with 90Y-DOTATOC administered in a patient affected by liver metastases from bronchial neuroendocrine tumor (atypical carcinoid).
  • The patient received iv infusion of octreotide associated with H1 and H2 receptor antagonists and corticosteroid therapy, which induced symptom remission within few days.
  • The case here reported confirms that radionuclide therapy is highly effective in determining early rupture of metastatic tissue and also suggests that pre-medication should be implemented before the radiopeptide administration associated with a close monitoring of the patient in the following days.
  • [MeSH-major] Bronchial Neoplasms / pathology. Liver Neoplasms / secondary. Malignant Carcinoid Syndrome / chemically induced. Octreotide / analogs & derivatives
  • [MeSH-minor] Aged. Bone Neoplasms / secondary. Carcinoid Tumor / drug therapy. Carcinoid Tumor / radiotherapy. Humans. Male. Yttrium Radioisotopes / adverse effects

  • Genetic Alliance. consumer health - Carcinoid Tumor.
  • Genetic Alliance. consumer health - Pancreatic islet cell tumors.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Nucl Med. 2002 May;43(5):610-6 [11994522.001]
  • [Cites] Endocr Rev. 2004 Jun;25(3):458-511 [15180952.001]
  • [Cites] Surg Oncol Clin N Am. 2003 Jan;12(1):231-42 [12735141.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2004 Jul;31(7):1038-46 [15150675.001]
  • [Cites] Br J Anaesth. 2001 Sep;87(3):447-52 [11517130.001]
  • [Cites] Semin Nucl Med. 2002 Apr;32(2):133-40 [11965608.001]
  • [Cites] N Engl J Med. 1996 Jan 25;334(4):246-54 [8532003.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2003 Feb;30(2):207-16 [12552338.001]
  • [Cites] N Engl J Med. 1999 Mar 18;340(11):858-68 [10080850.001]
  • [Cites] Aliment Pharmacol Ther. 2003 Feb;17(3):437-44 [12562458.001]
  • [Cites] Ann Oncol. 2004 Jun;15(6):966-73 [15151956.001]
  • [Cites] Am J Clin Oncol. 2000 Aug;23 (4):412-5 [10955874.001]
  • [Cites] Semin Nucl Med. 2002 Apr;32(2):141-7 [11965609.001]
  • [Cites] Eur J Nucl Med. 2001 Apr;28(4):426-34 [11357492.001]
  • (PMID = 16840837.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / 90Y-octreotide, DOTA-Tyr(3)-; 0 / Yttrium Radioisotopes; RWM8CCW8GP / Octreotide
  •  go-up   go-down


32. Tanvetyanon T, Choudhury AM: Hypocalcemia and azotemia associated with zoledronic acid and interferon alfa. Ann Pharmacother; 2004 Mar;38(3):418-21
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: To describe severe hypocalcemia and acute renal failure associated with zoledronic acid and interferon alfa in a patient with metastatic carcinoid tumors.
  • CASE SUMMARY: A 39-year-old white man with metastatic carcinoid tumor tolerated treatment with subcutaneous long-acting octreotide monthly and interferon alfa 6 million units 3 times weekly for 6 months.
  • Although the first infusion went well, the patient developed severe hypocalcemia and acute renal failure after the second zoledronic infusion.
  • CONCLUSIONS: In our patient with metastatic carcinoid tumor, treatment with zoledronic acid and interferon alfa was associated with symptomatic hypocalcemia and acute renal failure.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Diphosphonates / adverse effects. Hypocalcemia / chemically induced. Imidazoles / adverse effects. Interferon-alpha / adverse effects. Uremia / chemically induced
  • [MeSH-minor] Adult. Carcinoid Tumor / drug therapy. Humans. Male

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14970365.001).
  • [ISSN] 1060-0280
  • [Journal-full-title] The Annals of pharmacotherapy
  • [ISO-abbreviation] Ann Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diphosphonates; 0 / Imidazoles; 0 / Interferon-alpha; 6XC1PAD3KF / zoledronic acid
  •  go-up   go-down


33. Schran HF, Hager DF: Comments on "Clinical value of monitoring plasma octreotide levels during chronic octreotide long-acting repeatable therapy in carcinoid patients". Pancreas; 2008 Oct;37(3):334-5; author reply 336-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comments on "Clinical value of monitoring plasma octreotide levels during chronic octreotide long-acting repeatable therapy in carcinoid patients".
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Carcinoid Tumor / drug therapy. Neuroendocrine Tumors / drug therapy. Octreotide / therapeutic use
  • [MeSH-minor] Biological Availability. Drug Monitoring. Humans. Research Design. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Pancreas. 2008 Jul;37(1):94-100 [18580450.001]
  • (PMID = 18815560.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; RWM8CCW8GP / Octreotide
  •  go-up   go-down


34. Zatelli MC, Maffei P, Piccin D, Martini C, Rea F, Rubello D, Margutti A, Culler MD, Sicolo N, degli Uberti EC: Somatostatin analogs in vitro effects in a growth hormone-releasing hormone-secreting bronchial carcinoid. J Clin Endocrinol Metab; 2005 Apr;90(4):2104-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatostatin analogs in vitro effects in a growth hormone-releasing hormone-secreting bronchial carcinoid.
  • The patient underwent left lung upper lobectomy, and histopathology disclosed a bronchial atypical carcinoid.
  • Cultured tumor cells were treated with SRIH, lanreotide (BIM-23014), or SRIH analogs selective for SSTR2 (BIM-23120), SSTR5 (BIM-23206), or SSTR1 (BIM-23926).
  • GHRH secretion was significantly reduced by SRIH (-50%), Lan (-35%), as well as by the SSTR2, SSTR5, and SSTR1 selective agonists (-55, -75, and -20%, respectively), whereas cell viability was not affected.
  • Our data show SSTR expression in a GHRH-secreting bronchial carcinoid and provide evidence that, in vitro, selective SSTR activation differently inhibit ectopic GHRH secretion.
  • These findings suggest that SSTR-specific SRIH analogs may be useful in the medical therapy of GHRH-secreting bronchial carcinoids.
  • [MeSH-major] Bronchial Neoplasms / drug therapy. Carcinoid Tumor / drug therapy. Growth Hormone-Releasing Hormone / secretion. Receptors, Somatostatin / agonists
  • [MeSH-minor] Adult. Cell Survival / drug effects. Female. Humans

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15671091.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Somatostatin; 9034-39-3 / Growth Hormone-Releasing Hormone
  •  go-up   go-down


35. Chen JY, Cook MR, Pinchot SN, Kunnimalaiyaan M, Chen H: MG-132 inhibits carcinoid growth and alters the neuroendocrine phenotype. J Surg Res; 2010 Jan;158(1):15-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MG-132 inhibits carcinoid growth and alters the neuroendocrine phenotype.
  • BACKGROUND: Carcinoid cancers are the most common neuroendocrine (NE) tumors, and limited treatment options exist.
  • The inhibition of glycogen synthase kinase-3beta (GSK-3beta) has been shown to be a potential therapeutic target for the treatment of carcinoid disease.
  • In this study, we investigate the ability of MG-132, a proteasome inhibitor, to inhibit carcinoid growth, the neuroendocrine phenotype, and its association with GSK-3beta.
  • MATERIALS AND METHODS: Human pulmonary (NCI-H727) and gastrointestinal (BON) carcinoid cells were treated with MG-132 (0-4microM).
  • Levels of total and phosphorylated GSK-3beta and the NE markers chromogranin A (CgA), Achaete-Scute complex-like 1 (ASCL1), as well as the apoptotic markers poly (ADP-ribose), polymerase (PARP), and cleaved caspase-3 were determined by Western blot.
  • RESULTS: Treating carcinoid cells with MG-132 resulted in growth inhibition, a dose-dependent inhibition of CgA and ASCL1, as well as an increase in the levels of cleaved PARP and cleaved caspase-3.
  • This proteasome inhibitor warrants further preclinical investigation as a possible therapeutic strategy for intractable carcinoid disease.

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cancer Ther. 2005 Jun;4(6):910-7 [15956248.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Sep 9;334(4):1365-73 [16043125.001]
  • [Cites] Cell Biol Int. 2005 Jul;29(7):489-96 [15939633.001]
  • [Cites] Cancer Res. 2005 Mar 15;65(6):2076-81 [15781615.001]
  • [Cites] J Am Coll Surg. 1998 Jul;187(1):88-92; discussion 92-3 [9660030.001]
  • [Cites] Endocrinology. 2004 Jun;145(6):2941-9 [14988390.001]
  • [Cites] Nat Rev Cancer. 2004 May;4(5):349-60 [15122206.001]
  • [Cites] Cell Cycle. 2003 Sep-Oct;2(5):438-41 [12963837.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2003 Aug;285(2):G245-54 [12851216.001]
  • [Cites] Curr Opin Oncol. 2002 Nov;14(6):628-34 [12409653.001]
  • [Cites] J Biol Chem. 2002 Sep 27;277(39):36602-10 [12140294.001]
  • [Cites] Circ Res. 2002 May 31;90(10):1055-63 [12039794.001]
  • [Cites] Leukemia. 2002 Apr;16(4):433-43 [11960320.001]
  • [Cites] Surg Oncol. 2001 Jul-Aug;10(1-2):43-52 [11719028.001]
  • [Cites] Clin Exp Immunol. 2009 Apr;156(1):172-82 [19220323.001]
  • [Cites] Oncologist. 2008 Dec;13(12):1255-69 [19091780.001]
  • [Cites] Br J Pharmacol. 2008 Jun;154(3):632-8 [18414391.001]
  • [Cites] Surgery. 2007 Dec;142(6):959-64; discussion 959-64 [18063082.001]
  • [Cites] Cell Biol Int. 2007 Oct;31(10):1136-43 [17493842.001]
  • [Cites] Mol Cancer Ther. 2007 Mar;6(3):1151-8 [17363508.001]
  • [Cites] Surgery. 2007 Feb;141(2):161-5; discussion 165 [17263970.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Jun 23;345(1):38-42 [16674919.001]
  • [Cites] J Surg Res. 2006 Jun 1;133(1):42-5 [16603190.001]
  • [Cites] Mol Cancer Ther. 2006 Mar;5(3):665-75 [16546981.001]
  • [Cites] Annu Rev Med. 2006;57:33-47 [16409135.001]
  • [Cites] Curr Opin Oncol. 2006 Jan;18(1):9-15 [16357558.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2005 Oct;289(4):G636-42 [16160079.001]
  • (PMID = 19765735.001).
  • [ISSN] 1095-8673
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA117117-01A2; United States / NCI NIH HHS / CA / R01 CA121115-01A2; United States / NCI NIH HHS / CA / CA109053-03; United States / NCI NIH HHS / CA / R01 CA109053-03; United States / NCI NIH HHS / CA / R01 CA121115; United States / NCI NIH HHS / CA / R01 CA109053-01A2; United States / NCI NIH HHS / CA / R01 CA109053; United States / NCI NIH HHS / CA / R21 CA117117-01A2; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / CA109053; United States / NCI NIH HHS / CA / CA109053-01A2; United States / NCI NIH HHS / CA / CA109053-02; United States / NCI NIH HHS / CA / T32 CA090217; United States / NCI NIH HHS / CA / R21 CA117117; United States / NCI NIH HHS / CA / R01 CA109053-02
  • [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 / ASCL1 protein, human; 0 / Antineoplastic Agents; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Chromogranin A; 0 / Cysteine Proteinase Inhibitors; 0 / Leupeptins; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3
  • [Other-IDs] NLM/ NIHMS119777; NLM/ PMC2795050
  •  go-up   go-down


36. Fykse V, Sandvik AK, Qvigstad G, Falkmer SE, Syversen U, Waldum HL: Treatment of ECL cell carcinoids with octreotide LAR. Scand J Gastroenterol; 2004 Jul;39(7):621-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of ECL cell carcinoids with octreotide LAR.
  • BACKGROUND: Patients with chronic atrophic gastritis (CAG) and hypergastrinaemia are at risk of developing hyperplasia of the enterochromaffin-like (ECL) cells and ECL-cell-derived tumours.
  • The effect of the somatostatin analogue octreotide on ECL cell carcinoids is examined.
  • METHODS: Five patients with hypergastrinaemia and ECL cell carcinoids were enrolled in a 1-year study of octreotide LAR (long-acting release) 20 mg given at monthly intervals.
  • Biopsies from tumours and from flat oxyntic mucosa were done at the start and 3, 6 and 12 months thereafter.
  • RESULTS: The number of visible tumours was reduced by more than 50 %.
  • Sections from both tumours and flat mucosa showed a reduced number of CgA immunoreactive cells.
  • A diminished tumour load and reduced ECL cell density were found, indicating an antiproliferative effect of octreotide directly on the ECL cells.
  • [MeSH-major] Antineoplastic Agents, Hormonal / administration & dosage. Carcinoid Tumor / drug therapy. Enterochromaffin-like Cells / drug effects. Octreotide / administration & dosage. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Aged. Cell Proliferation / drug effects. Chromogranin A. Chromogranins / blood. Chromogranins / drug effects. Delayed-Action Preparations. Female. Gastric Mucosa / drug effects. Gastric Mucosa / pathology. Gastrins / blood. Gastrins / drug effects. Gastroscopy. Humans. Male. Middle Aged. Time Factors

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15370681.001).
  • [ISSN] 0036-5521
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Chromogranin A; 0 / Chromogranins; 0 / Delayed-Action Preparations; 0 / Gastrins; RWM8CCW8GP / Octreotide
  •  go-up   go-down


37. Duques P, Araújo RS, de Amorim WP: [Esophagus-enteric anastomosis ulceration caused by alendronate]. Arq Gastroenterol; 2001 Apr-Jun;38(2):129-31
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Transliterated title] Ulceração de anastomose esôfago-entérica causada por alendronato.
  • OBJECTIVE: Report a case of a patient who underwent total gastrectomy with Y-en-Roux anastomosis for a gastric carcinoid tumor and developed an esophagus-enteric anastomosis ulceration after the use of alendronate.
  • After a period of one month of medical treatment with this drug she began to complain of dysphagic symptoms and abdominal pain.
  • She improved in her general state and nowadays she is free of symptoms.
  • Special attention must be given to gastrectomized patients that use this drug because of the possibility to develop mucosal lesions in the enteric anastomosed part and its fearful complications as stenosis.
  • [MeSH-major] Alendronate / adverse effects. Esophageal Diseases / chemically induced. Intestinal Diseases / chemically induced. Osteoporosis / drug therapy. Stomach Neoplasms / surgery. Ulcer / chemically induced

  • MedlinePlus Health Information. consumer health - Esophagus Disorders.
  • MedlinePlus Health Information. consumer health - Osteoporosis.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • Hazardous Substances Data Bank. Alendronic acid .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11793943.001).
  • [ISSN] 0004-2803
  • [Journal-full-title] Arquivos de gastroenterologia
  • [ISO-abbreviation] Arq Gastroenterol
  • [Language] por
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] X1J18R4W8P / Alendronate
  •  go-up   go-down


38. Schmid HA: Pasireotide (SOM230): development, mechanism of action and potential applications. Mol Cell Endocrinol; 2008 May 14;286(1-2):69-74
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Pasireotide potently suppresses GH, IGF-I and ACTH secretion, indicating potential efficacy in acromegaly and Cushing's disease.
  • The prolonged inhibition of hormone secretion by pasireotide in animal models and expression of multiple sst receptors in carcinoid tumors suggests that pasireotide may have clinical advantages over octreotide in patients with carcinoid tumors.
  • In summary, preclinical evidence, as well as preliminary results from clinical studies suggests that pasireotide is a promising new treatment for patients with symptoms of metastatic carcinoid tumors refractory or resistant to octreotide, de novo or persistent acromegaly, and that pasireotide has the potential to be the first directed medical therapy for Cushing's disease.
  • [MeSH-minor] Acromegaly / drug therapy. Adrenocorticotropic Hormone / antagonists & inhibitors. Adrenocorticotropic Hormone / metabolism. Animals. Antineoplastic Agents, Hormonal / chemistry. Antineoplastic Agents, Hormonal / therapeutic use. Carcinoid Tumor / drug therapy. Carcinoid Tumor / metabolism. Drug Resistance, Neoplasm. Growth Hormone / antagonists & inhibitors. Growth Hormone / metabolism. Humans. Insulin-Like Growth Factor I / antagonists & inhibitors. Insulin-Like Growth Factor I / metabolism. Octreotide / therapeutic use. Pituitary ACTH Hypersecretion / drug therapy. Structure-Activity Relationship

  • Hazardous Substances Data Bank. Corticotropin .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17977644.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I; 9002-60-2 / Adrenocorticotropic Hormone; 9002-72-6 / Growth Hormone; 98H1T17066 / pasireotide; RWM8CCW8GP / Octreotide
  • [Number-of-references] 36
  •  go-up   go-down


39. Burkitt MD, Pritchard DM: Review article: Pathogenesis and management of gastric carcinoid tumours. Aliment Pharmacol Ther; 2006 Nov 1;24(9):1305-20
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Review article: Pathogenesis and management of gastric carcinoid tumours.
  • BACKGROUND: Gastric carcinoid tumours are rare, but are increasing in incidence.
  • AIM: To discuss tumour pathogenesis and outline current approaches to patient management.
  • RESULTS: Although interest in gastric carcinoids has increased since it was recognized that they are associated with achlorhydria, to date there is no definite evidence that humans taking long-term acid suppressing medication are at increased risk.
  • Type I tumours are associated with autoimmune atrophic gastritis and hypergastrinaemia, type II are associated with Zollinger-Ellison syndrome, multiple endocrine neoplasia-1 and hypergastrinaemia and sporadic type III carcinoids are gastrin-independent and carry the worst prognosis.
  • Careful investigation of these patients is required, particularly to identify the tumour type, the source of hypergastrinaemia and the presence of metastases.
  • Treatment can be directed at the source of hypergastrinaemia if type I or II tumours are still gastrin responsive and not growing autonomously.
  • Type III tumours should be treated surgically.
  • CONCLUSIONS: Advances in our understanding of the pathogenesis of gastric carcinoids have led to recent improvements in investigation and management.
  • Challenges remain in identifying the genetic and environmental factors, in addition to hypergastrinaemia, that are responsible for tumour development in susceptible patients.
  • [MeSH-major] Carcinoid Tumor / physiopathology. Carcinoid Tumor / therapy. Stomach Neoplasms / physiopathology. Stomach Neoplasms / therapy

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17059512.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 108
  •  go-up   go-down


40. Modlin IM, Kidd M, Drozdov I, Siddique ZL, Gustafsson BI: Pharmacotherapy of neuroendocrine cancers. Expert Opin Pharmacother; 2008 Oct;9(15):2617-26
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Neuroendocrine tumors (NETs) of the diffuse neuroendocrine cell system often present a considerable diagnostic and therapeutic challenge.
  • METHODS: We have reviewed the literature on NET treatment between 1979 and 2008 (PubMed search: carcinoid or neuroendocrine tumor/tumour + treatment or management), and summarized current therapeutic options and recommendations.
  • RESULTS: The majority of tumors are diagnosed at a stage that the only curative treatment, radical surgical intervention, is no longer an option.
  • The interferon class of agents may have a role in selected individuals but substantial adverse events often limit their use.
  • Peptide receptor targeted radiotherapy may lead to reduction in tumor size but in most circumstances has a tumor-stabilizing effect.
  • A variety of antiangiogenesis and growth factor-targeted agents have been evaluated but to date the results have failed to meet expectations.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Neuroendocrine Tumors / drug therapy

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18803449.001).
  • [ISSN] 1744-7666
  • [Journal-full-title] Expert opinion on pharmacotherapy
  • [ISO-abbreviation] Expert Opin Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunologic Factors
  • [Number-of-references] 115
  •  go-up   go-down


41. Mathieu N: [Risk of long-term treatment with proton pump inhibitors]. Rev Prat; 2008 Sep 15;58(13):1451-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Transliterated title] Risques des traitements prolongés par les inhibiteurs de la pompe a protons.
  • Proton pump inhibitors (PPIs) have become the mainstay of therapy in acid-related upper gastrointestinal disorders including gastroesophageal reflux disease and peptic ulcer disease.
  • Alltough these medications are generally accepted as safe, the long-term clinical consequences of the inducing hypochlorhydria are not completely clear.
  • Gastric endocrine cell hyperplasia can occur in 10 to 30% of patients without carcinoid tumors.
  • Proton pump inhibitor-associated gastric polyps are totally benign tumors that should not be followed.
  • [MeSH-minor] Bacterial Infections / chemically induced. Colonic Neoplasms / chemically induced. Gastric Acid / secretion. Gastrins / blood. Gastrins / drug effects. Humans. Polyps / chemically induced. Vitamin B 12 Deficiency / chemically induced

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18924330.001).
  • [ISSN] 0035-2640
  • [Journal-full-title] La Revue du praticien
  • [ISO-abbreviation] Rev Prat
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Gastrins; 0 / Proton Pump Inhibitors
  •  go-up   go-down


42. Ozyurt E, Oğuzoğlu SA, Kaya AH, Tanriverdi T, Enar R, Uçak D: [Surgical treatment of essential hypertension resistant to medical treatment: Report of two cases]. Anadolu Kardiyol Derg; 2002 Mar;2(1):40-4, AXVII
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Causes such as renal diseases, carcinoid syndrome, pheochromocytoma were ruled out before surgery.
  • Indications for surgery included mainly systolic blood pressures greater than 180 mm Hg or uncontrolled blood pressures under three or more medications.
  • RESULTS: Both patients experienced more than 20 mm Hg reduction in systolic blood pressure although the number of medications was decreased after surgery.

  • Genetic Alliance. consumer health - Essential hypertension.
  • MedlinePlus Health Information. consumer health - High Blood Pressure.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12101793.001).
  • [ISSN] 1302-8723
  • [Journal-full-title] Anadolu kardiyoloji dergisi : AKD = the Anatolian journal of cardiology
  • [ISO-abbreviation] Anadolu Kardiyol Derg
  • [Language] tur
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Turkey
  •  go-up   go-down


43. Townsend A, Price T, Yeend S, Pittman K, Patterson K, Luke C: Metastatic carcinoid tumor: changing patterns of care over two decades. J Clin Gastroenterol; 2010 Mar;44(3):195-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metastatic carcinoid tumor: changing patterns of care over two decades.
  • BACKGROUND: Metastatic carcinoid tumors (MCTs), an important subgroup of neuroendocrine tumors, occur infrequently and often have an indolent course, limiting data on long-term treatment outcomes.
  • STUDY: Patients diagnosed with carcinoid tumors in the North West Adelaide Health Service between January 1, 1985 and March 1, 2007 were identified from the South Australian Cancer Registry.
  • RESULTS: We identified 92 patients with carcinoid tumors; 49 had MCT.
  • CONCLUSIONS: This single center experience has provided insight into current treatment options for MCT, and suggests the use of long-acting somatostatin analogs may impact on disease control and survival.
  • However, the uptake of other treatment options seems limited and there is a need for agents that target tumor progression.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Carcinoid Tumor / therapy. Octreotide / therapeutic use
  • [MeSH-minor] Aged. Databases, Factual. Disease Progression. Female. Humans. Male. Neoplasm Metastasis. Registries. Retrospective Studies. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use. South Australia. Survival Rate. Time Factors. Treatment Outcome

  • Genetic Alliance. consumer health - Carcinoid Tumor.
  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19609217.001).
  • [ISSN] 1539-2031
  • [Journal-full-title] Journal of clinical gastroenterology
  • [ISO-abbreviation] J. Clin. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide
  •  go-up   go-down


44. Fehmann HC, Wulbrand U, Arnold R: Treatment of endocrine gastroenteropancreatic tumors with somatostatin analogues. Recent Results Cancer Res; 2000;153:15-22
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of endocrine gastroenteropancreatic tumors with somatostatin analogues.
  • Somatostatin is a hormone that regulates the function of several exocrine and endocrine glands.
  • These proteins are expressed in a tissue-specific manner.
  • Somatostatin receptors are also present in neuroendocrine gastroenteropancreatic tumors.
  • Excessive hormone secretion in carcinoid syndrome can be controlled by these drugs.
  • In addition, at least a subgroup of patients with carcinoid syndromes respond with delayed tumor growth during octreotide therapy.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Endocrine Gland Neoplasms / drug therapy. Gastrointestinal Neoplasms / drug therapy. Pancreatic Neoplasms / drug therapy. Somatostatin / analogs & derivatives
  • [MeSH-minor] Animals. Humans

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10626286.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] GERMANY
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 51110-01-1 / Somatostatin
  • [Number-of-references] 34
  •  go-up   go-down


45. Druce M, Rockall A, Grossman AB: Fibrosis and carcinoid syndrome: from causation to future therapy. Nat Rev Endocrinol; 2009 May;5(5):276-83
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fibrosis and carcinoid syndrome: from causation to future therapy.
  • Carcinoid tumors are part of a heterogeneous group of gastrointestinal and pancreatic endocrine tumors that are characterized by their capacity to produce and secrete hormones, 5-hydroxytryptamine, tachykinins and other mediators.
  • These substances are thought to be responsible for the collection of symptoms, which include diarrhea, flushing and wheezing, that is known as carcinoid syndrome.
  • Fibrosis that occurs either local to or distant from the primary tumor is one of the hallmarks of carcinoid tumors that originate from the midgut.
  • One or more products that are secreted by the tumor and enter into the circulation are likely to have a role in this process.
  • This Review discusses the incidence and prevalence of fibrosis in carcinoid syndrome and explores evidence to date for causative agents, in particular the roles of 5-hydroxytryptamine and elements of the downstream signaling pathway.
  • Improved understanding of the etiology of carcinoid-tumor-related fibrosis may lead to better treatments for this condition than those we currently have.
  • [MeSH-major] Carcinoid Tumor / complications. Carcinoid Tumor / pathology. Fibrosis / pathology

  • Genetic Alliance. consumer health - Carcinoid Syndrome.
  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19444261.001).
  • [ISSN] 1759-5037
  • [Journal-full-title] Nature reviews. Endocrinology
  • [ISO-abbreviation] Nat Rev Endocrinol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Transforming Growth Factor beta; 333DO1RDJY / Serotonin
  • [Number-of-references] 72
  •  go-up   go-down


46. Gilbert JA, Frederick LM, Pobst LJ, Ames MM: Hydrogen peroxide degradation and selective carbidopa-induced cytotoxicity against human tumor lines. Biochem Pharmacol; 2005 Apr 15;69(8):1159-66
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hydrogen peroxide degradation and selective carbidopa-induced cytotoxicity against human tumor lines.
  • The carcinoid tumor, an uncommon neuroendocrine neoplasm, is associated with serotonin overproduction as is more common small cell lung carcinoma (SCLC).
  • alpha-Methyl-dopahydrazine (carbidopa), an inhibitor of the serotonin synthetic enzyme aromatic-L-amino acid decarboxylase, proved lethal to NCI-H727 lung carcinoid cells as well as NCI-H146 and NCI-H209 SCLC cells, but not to five other human tumor cell lines of differing origins [Gilbert JA, Frederick LM, Ames MM.
  • The aromatic-L-amino acid decarboxylase inhibitor carbidopa is selectively cytotoxic to human pulmonary carcinoid and small cell lung carcinoma cells. Clin.
  • Alkaline elution studies revealed carbidopa-dependent single-strand DNA breaks in sensitive carcinoid cells comparable to those induced by similar concentrations of H2O2.
  • Furthermore, when carbidopa was incubated with a variety of tumor cell types, not only were decreased media H2O2 concentrations detected in the presence of cells, but cell lines least sensitive to carbidopa degraded exogenous H2O2 more rapidly than did sensitive cells.
  • Implicated in these studies, pyruvate degraded H2O2 in RPMI in a dose- and time-dependent manner and reversed carbidopa-induced cytotoxicity to carcinoid cells.
  • Extracellular pyruvate levels produced per h by resistant large cell lung carcinoma cells averaged four-fold that of sensitive carcinoid cells plated at equal density (24 h time course).
  • Finally, carbidopa exposure (100 microM, 24 h) depleted extracellular pyruvate from sensitive carcinoid cells, but reduced pyruvate levels from resistant NCI-H460 cells less than 17%.
  • [MeSH-major] Aromatic Amino Acid Decarboxylase Inhibitors. Carbidopa / toxicity. Carcinoid Tumor / drug therapy. Carcinoma, Small Cell / drug therapy. Hydrogen Peroxide / metabolism. Lung Neoplasms / drug therapy
  • [MeSH-minor] Cell Survival / drug effects. Culture Media / chemistry. Culture Media / metabolism. Dose-Response Relationship, Drug. Humans. Kinetics. Oxidation-Reduction. Pyruvic Acid / metabolism. Pyruvic Acid / pharmacology. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. HYDROGEN PEROXIDE .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15794936.001).
  • [ISSN] 0006-2952
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aromatic Amino Acid Decarboxylase Inhibitors; 0 / Culture Media; 8558G7RUTR / Pyruvic Acid; BBX060AN9V / Hydrogen Peroxide; MNX7R8C5VO / Carbidopa
  •  go-up   go-down


47. Miquel C, Sabourin JC, Elias D, Grandjouan S, Viguier J, Ducreux M, Duvillard P, Praz F: An appendix carcinoid tumor in a patient with hereditary nonpolyposis colorectal cancer. Hum Pathol; 2004 Dec;35(12):1564-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An appendix carcinoid tumor in a patient with hereditary nonpolyposis colorectal cancer.
  • Gastrointestinal carcinoid tumors are often associated with other tumors, particularly colon adenocarcinomas; but the association between carcinoid tumors and hereditary nonpolyposis colorectal cancer (HNPCC) syndrome has not yet been explored.
  • We report an unusual case of a 28-year-old woman with HNPCC who underwent surgery for a transverse colon adenocarcinoma in whom an appendix carcinoid tumor was incidentally found.
  • To assess whether the carcinoid tumor displayed the characteristic molecular features of HNPCC tumors, we investigated the expression of mismatch-repair (MMR) proteins and microsatellite instability (MSI) status in both tumors.
  • Both tumors demonstrated normal expression of the MMR proteins hMLH1, hMSH2, hMSH6, and hPMS2.
  • Interestingly, the adenocarcinoma exhibited an MSI phenotype but the carcinoid tumor did not, indicating that these 2 tumors arose through different molecular pathways.
  • [MeSH-major] Appendiceal Neoplasms / pathology. Carcinoid Tumor / pathology. Colonic Neoplasms / pathology. Colorectal Neoplasms, Hereditary Nonpolyposis / pathology
  • [MeSH-minor] Adult. Antimetabolites, Antineoplastic / therapeutic use. Chemotherapy, Adjuvant. DNA, Neoplasm / analysis. DNA-Binding Proteins / analysis. Drug Therapy, Combination. Female. Fluorouracil / therapeutic use. Humans. Leucovorin / therapeutic use. Microsatellite Repeats / genetics. Treatment Outcome

  • Genetic Alliance. consumer health - Carcinoid Tumor.
  • Genetic Alliance. consumer health - Colorectal Cancer.
  • Genetic Alliance. consumer health - Hereditary Cancer.
  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • Hazardous Substances Data Bank. LEUCOVORIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15619218.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / MSH3 protein, human; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil
  •  go-up   go-down


48. Paix AD, Runciman WB, Horan BF, Chapman MJ, Currie M: Crisis management during anaesthesia: hypertension. Qual Saf Health Care; 2005 Jun;14(3):e12
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Drug related causes accounted for 59% of all incidents.
  • It was considered that, properly applied, this structured approach would have led to a quicker and/or better resolution of the problem in 21% of the cases.
  • CONCLUSION: Once hypertension is identified and confirmed, its rapid control by the careful use of a volatile anaesthetic agent, intravenous opioids, or rapidly acting antihypertensives will usually avoid serious morbidity.
  • If hypertension is unresponsive to the treatment recommended in the relevant sub-algorithm, an unusual cause such as phaeochromocytoma, carcinoid syndrome, or thyroid storm should be considered.

  • MedlinePlus Health Information. consumer health - Anesthesia.
  • MedlinePlus Health Information. consumer health - High Blood Pressure.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Anesth Analg. 2002 Aug;95(2):273-7, table of contents [12145033.001]
  • [Cites] Anaesth Intensive Care. 2003 Dec;31(6):619-28 [14719422.001]
  • [Cites] Anesthesiology. 1979 Apr;50(4):281-4 [434529.001]
  • [Cites] Anaesth Intensive Care. 1993 Oct;21(5):579-92 [8273879.001]
  • [Cites] Am J Public Health. 1988 Jun;78(6):676-9 [3259405.001]
  • [Cites] Anaesth Intensive Care. 1993 Oct;21(5):520-8 [8273871.001]
  • [Cites] Anaesth Intensive Care. 1993 Oct;21(5):529-42 [8273872.001]
  • [Cites] Ann Thorac Surg. 1986 Jan;41(1):42-50 [3484621.001]
  • (PMID = 15933285.001).
  • [ISSN] 1475-3901
  • [Journal-full-title] Quality & safety in health care
  • [ISO-abbreviation] Qual Saf Health Care
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1744002
  •  go-up   go-down


49. Christante D, Pommier S, Givi B, Pommier R: Hepatic artery chemoinfusion with chemoembolization for neuroendocrine cancer with progressive hepatic metastases despite octreotide therapy. Surgery; 2008 Dec;144(6):885-93; discussion 893-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Patients with neuroendocrine cancer and diffuse hepatic metastases were treated with hepatic artery chemoinfusion and chemoembolization when they demonstrated disease progression despite octreotide therapy.
  • The overall response rate was 80% for patients with carcinoid or islet cell neoplasms.
  • Median disease-specific survival was 39 months from the first treatment; 1- and 5-year survival rates were 78% and 27%, respectively.
  • CONCLUSION: Survival after initiating this regimen was over 3 years for the majority of patients exhibiting progression of extensive, unresectable hepatic disease despite octreotide therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Fluorouracil / administration & dosage. Liver Neoplasms / drug therapy. Neuroendocrine Tumors / drug therapy. Octreotide / therapeutic use
  • [MeSH-minor] Adenoma, Islet Cell / drug therapy. Adult. Aged. Carcinoid Tumor / drug therapy. Carcinoid Tumor / secondary. Chemoembolization, Therapeutic. Digestive System Neoplasms / pathology. Disease Progression. Female. Hepatic Artery. Humans. Infusions, Intra-Arterial. Male. Middle Aged. Retrospective Studies. Survival Analysis. Young Adult

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Surgery. 2008 Dec;144(6):895-8 [19040994.001]
  • (PMID = 19040993.001).
  • [ISSN] 1532-7361
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; RWM8CCW8GP / Octreotide; U3P01618RT / Fluorouracil
  •  go-up   go-down


50. Wester HJ, Schottelius M, Scheidhauer K, Meisetschläger G, Herz M, Rau FC, Reubi JC, Schwaiger M: PET imaging of somatostatin receptors: design, synthesis and preclinical evaluation of a novel 18F-labelled, carbohydrated analogue of octreotide. Eur J Nucl Med Mol Imaging; 2003 Jan;30(1):117-22
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [(19)F]FP-Gluc-TOCA showed no affinity to hsst1 and hsst3, moderate affinity to hsst4 (IC(50): 437+/-84 n M) and hsst5 (IC(50): 123+/-8.8 n M) and very high affinity to hsst2 (IC(50): 2.8+/-0.4 n M).
  • In mice, the tracer was rapidly cleared via renal excretion (kidneys: 8.69%+/-1.09%ID/g) and showed low uptake in liver (0.72%+/-0.14%ID/g) and intestine (1.88%+/-0.52%ID/g) and high tumour uptake (13.54%+/-1.47%ID/g) (all data at 1 h p.i.).
  • Tumour to non-tumour ratios at 60 min p.i. reached 25, 19, 7, 1.6 and 56 for blood, liver, intestine, kidney and muscle, respectively.
  • A similar biodistribution pattern was observed in pancreatic tumour-bearing rats.
  • Tumour uptake in rats was reduced to 36% and 18% of control (30 and 60 min) by co-injection of 500 microg Tyr(3)-octreotide, demonstrating sst-specific uptake.
  • In a first [(18)F]FP-Gluc-TOCA-PET study of a patient with a metastatic carcinoid in the liver the tracer showed superior pharmacokinetics, e.g. rapid urinary excretion and low uptake in liver, kidney and spleen.
  • This is the first report on PET imaging using an (18)F-labelled sst binding peptide; it indicates that [(18)F]FP-Gluc-TOCA offers excellent imaging characteristics and allows sst imaging with high tumour to non-tumour contrast.
  • [MeSH-minor] Aged. Animals. Carcinoid Tumor / metabolism. Carcinoid Tumor / radionuclide imaging. Carcinoid Tumor / secondary. Cells, Cultured. Drug Design. Drug Evaluation, Preclinical / methods. Female. Humans. Isotope Labeling / methods. Male. Metabolic Clearance Rate. Mice. Mice, Nude. Neoplasm Transplantation. Neoplasms, Unknown Primary / metabolism. Neoplasms, Unknown Primary / radionuclide imaging. Organ Specificity. Radiopharmaceuticals / pharmacokinetics. Rats. Rats, Inbred Lew. Somatostatin / pharmacokinetics. Somatostatin-28. Tissue Distribution

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12483418.001).
  • [ISSN] 1619-7070
  • [Journal-full-title] European journal of nuclear medicine and molecular imaging
  • [ISO-abbreviation] Eur. J. Nucl. Med. Mol. Imaging
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / N(alpha)-(1-deoxy- D-fructosyl)- N(epsilon)-(2-fluoropropionyl)-Lys(0)-Tyr(3)-octreotate; 0 / Peptides, Cyclic; 0 / Radiopharmaceuticals; 0 / Receptors, Somatostatin; 178181-50-5 / SDZ 223228; 30237-26-4 / Fructose; 51110-01-1 / Somatostatin; 75037-27-3 / Somatostatin-28; RWM8CCW8GP / Octreotide
  •  go-up   go-down


51. Zimmer C, Günnicker M, Peters J: [Anaesthetic management for hemihepatectomy in a patient with carcinoid-syndrome]. Anasthesiol Intensivmed Notfallmed Schmerzther; 2001 Dec;36(12):763-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Anaesthetic management for hemihepatectomy in a patient with carcinoid-syndrome].
  • [Transliterated title] Anästhesiologisches Vorgehen bei Hemihepatektomie bei einem Patienten mit Karzinoid-Syndrom.
  • Carcinoids are rare tumors of enterochromaffin cells.
  • The carcinoid-syndrome most often occurs with hepatic metastases of carcinoids and is evoked by release of serotonin and other vasoactive substances, leading to typical symptoms such as hyper- or hypotension, bronchospasm, tachycardia, diarrhoe, and flushing.
  • A lethal perioperative "carcinoid-crisis" may occur.
  • We report on a patient with carcinoid-syndrome due to liver metastases undergoing hemihepatectomy.
  • [MeSH-major] Anesthesia. Hepatectomy. Intraoperative Complications / prevention & control. Malignant Carcinoid Syndrome / surgery
  • [MeSH-minor] Anti-Inflammatory Agents / therapeutic use. Hemodynamics / drug effects. Hemodynamics / physiology. Histamine Antagonists / therapeutic use. Humans. Male. Middle Aged. Serotonin / metabolism. Steroids

  • Genetic Alliance. consumer health - Carcinoid Syndrome.
  • MedlinePlus Health Information. consumer health - Anesthesia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11743674.001).
  • [ISSN] 0939-2661
  • [Journal-full-title] Anästhesiologie, Intensivmedizin, Notfallmedizin, Schmerztherapie : AINS
  • [ISO-abbreviation] Anasthesiol Intensivmed Notfallmed Schmerzther
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Histamine Antagonists; 0 / Steroids; 333DO1RDJY / Serotonin
  •  go-up   go-down


52. Feng XD, Huang SG, Shou JY, Liao BR, Yingling JM, Ye X, Lin X, Gelbert LM, Su EW, Onyia JE, Li SY: Analysis of pathway activity in primary tumors and NCI60 cell lines using gene expression profiling data. Genomics Proteomics Bioinformatics; 2007 Feb;5(1):15-24
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of pathway activity in primary tumors and NCI60 cell lines using gene expression profiling data.
  • To determine cancer pathway activities in nine types of primary tumors and NCI60 cell lines, we applied an in silica approach by examining gene signatures reflective of consequent pathway activation using gene expression data.
  • Supervised learning approaches predicted that the Ras pathway is active in approximately 70% of lung adenocarcinomas but inactive in most squamous cell carcinomas, pulmonary carcinoids, and small cell lung carcinomas.
  • To our knowledge, this is the first comprehensive survey of cancer pathway activities in nine major tumor types and the most widely used NCI60 cell lines.
  • The "gene expression pathway signatures" we have defined could facilitate the understanding of molecular mechanisms in cancer development and provide guidance to the selection of appropriate cell lines for cancer research and pharmaceutical compound screening.
  • [MeSH-minor] Cell Line, Tumor. Computational Biology. Humans. Models, Genetic

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17572360.001).
  • [ISSN] 1672-0229
  • [Journal-full-title] Genomics, proteomics & bioinformatics
  • [ISO-abbreviation] Genomics Proteomics Bioinformatics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  •  go-up   go-down


53. Seghatol FF, Rigolin VH: Appetite suppressants and valvular heart disease. Curr Opin Cardiol; 2002 Sep;17(5):486-92
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Appetite suppressants and valvular heart disease.
  • This therapy was halted in 1997 after reports of valvular lesions affecting almost one third of patients treated with these drugs.
  • Fortunately, most cases of appetite suppressant-related valve disease are mild or moderate and rarely required valve repair or replacement.
  • The mechanism of valve disease induced by these drugs is speculative and may be related to their serotonergic effects.
  • Echocardiographic features are similar to carcinoid heart disease and valvulopathy associated with ergot use.
  • [MeSH-minor] Carcinoid Heart Disease / ultrasonography. Dexfenfluramine / adverse effects. Fenfluramine / adverse effects. Humans. Hypertension, Pulmonary / chemically induced. Phentermine / adverse effects

  • Genetic Alliance. consumer health - Heart Disease.
  • MedlinePlus Health Information. consumer health - Heart Valve Diseases.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. PHENTERMINE .
  • Hazardous Substances Data Bank. DEXFENFLURAMINE .
  • Hazardous Substances Data Bank. FENFLURAMINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12357124.001).
  • [ISSN] 0268-4705
  • [Journal-full-title] Current opinion in cardiology
  • [ISO-abbreviation] Curr. Opin. Cardiol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Appetite Depressants; 2DS058H2CF / Fenfluramine; C045TQL4WP / Phentermine; E35R3G56OV / Dexfenfluramine
  • [Number-of-references] 31
  •  go-up   go-down


54. Arnold C: [Neuroendocrine tumors of the gastrointestinal tract]. Praxis (Bern 1994); 2007 Jan 10;96(1-2):19-28
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Neuroendocrine tumors of the gastrointestinal tract].
  • [Transliterated title] Neuroendokrine Tumoren des Gastrointestinaltraktes.
  • Neuroendocrine tumors (NET) of the gastrointestinal tract are rare and constitute 0.5-1% of all human malignancies.
  • Based on their endocrine secretion, they are functional active or inactive.
  • They are further classified into fore-, mid-, or hindgut tumors.
  • The recently published WHO-classification grouped the tumors according to their tumor size, angioinvasion and Ki-67 index.
  • NET are mainly diagnosed in an advanced tumor stadium because of the paucity of symptoms or when symptoms occur due to endocrine hypersecretion.
  • NET are diagnosed serologically by their hormone secretion and by measuring Chromogranin A levels.
  • Many NET have somatostatin receptors on their surface and can be diagnosed by somatostatin receptor scintigrafy with high sensitivity and specificity.
  • Only by surgery NET can be cured.
  • Because many tumors are diagnosed late, medical options are of utmost importance.
  • Net of the gastrointestinal tract should be treated in a multidisciplinary approach with gastroenterologists, surgeons and experts in nuclear medicine.
  • An overview about epidemiology, clinical features, diagnostic methods and therapy of NET of the gastrointestinal tract will is provided in this article.
  • [MeSH-major] Gastrointestinal Neoplasms. Neuroendocrine Tumors. Pancreatic Neoplasms
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Biological Therapy. Chromogranin A / analysis. Clinical Trials as Topic. Clinical Trials, Phase II as Topic. Clinical Trials, Phase III as Topic. Diagnosis, Differential. Gastrinoma / diagnosis. Gastrinoma / therapy. Gastrointestinal Agents / therapeutic use. Glucagonoma / diagnosis. Glucagonoma / therapy. Humans. Incidence. Insulinoma / diagnosis. Insulinoma / therapy. Malignant Carcinoid Syndrome / diagnosis. Malignant Carcinoid Syndrome / therapy. Multiple Endocrine Neoplasia Type 1 / diagnosis. Octreotide / therapeutic use. Prevalence. Proton Pump Inhibitors. Receptors, Somatostatin / analysis. Vipoma / diagnosis. Vipoma / therapy. World Health Organization. Zollinger-Ellison Syndrome / diagnosis. Zollinger-Ellison Syndrome / therapy. von Hippel-Lindau Disease / diagnosis

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17256557.001).
  • [ISSN] 1661-8157
  • [Journal-full-title] Praxis
  • [ISO-abbreviation] Praxis (Bern 1994)
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Chromogranin A; 0 / Gastrointestinal Agents; 0 / Proton Pump Inhibitors; 0 / Receptors, Somatostatin; RWM8CCW8GP / Octreotide
  • [Number-of-references] 26
  •  go-up   go-down


55. Manger WM: The protean manifestations of pheochromocytoma. Horm Metab Res; 2009 Sep;41(9):658-63
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Hypertension attacks may be precipitated by physical activity, postural changes, anxiety, certain foods or wine, some drugs, operative procedures, etc.
  • Baro-reflex failure, postural tachycardia syndrome, sleep apnea, carcinoid, renal failure, and pseudopheochromocytoma may be diagnostic challenges.
  • The history, physical examination, biochemical testing (after eliminating interfering drugs, when possible) for plasma and urinary metanephrines can usually establish or exclude presence of pheochromocytomas.

  • Genetic Alliance. consumer health - Pheochromocytoma.
  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • MedlinePlus Health Information. consumer health - Pheochromocytoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19242899.001).
  • [ISSN] 1439-4286
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 20
  •  go-up   go-down


56. Panzuto F, Nasoni S, Delle Fave G: [Medical treatment of digestive neuroendocrine tumours]. Minerva Endocrinol; 2001 Sep;26(3):145-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Medical treatment of digestive neuroendocrine tumours].
  • [Transliterated title] Terapia medica dei tumori neuroendocrini digestivi.
  • Surgery is the only therapy able to cure patients with digestive neuroendocrine tumor.
  • In these cases, medical treatment plays a critical role, because of its ability to control symptoms in functioning tumors and to inhibit tumor growth.
  • Different therapeutic approaches, such as chemotherapy, hepatic artery chemoembolization and targeted radio-nuclide therapy can be used alone or combined to the biologic treatment with somatostatin analogues and interferon.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Digestive System Neoplasms / drug therapy. Neuroendocrine Tumors / drug therapy. Octreotide / analogs & derivatives. Pentetic Acid / analogs & derivatives
  • [MeSH-minor] Algorithms. Carcinoid Tumor / drug therapy. Carcinoid Tumor / pathology. Carcinoid Tumor / radiotherapy. Cell Differentiation. Combined Modality Therapy. Embolization, Therapeutic. Humans. Indium Radioisotopes / therapeutic use. Neoplasm Proteins / drug effects. Neoplasm Staging. Peptides, Cyclic / therapeutic use. Receptors, Somatostatin / drug effects. Retrospective Studies. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11753237.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Indium Radioisotopes; 0 / Neoplasm Proteins; 0 / Peptides, Cyclic; 0 / Receptors, Somatostatin; 118992-92-0 / lanreotide; 142694-57-3 / SDZ 215-811; 51110-01-1 / Somatostatin; 7A314HQM0I / Pentetic Acid; RWM8CCW8GP / Octreotide
  • [Number-of-references] 16
  •  go-up   go-down


57. Kaltsas GA, Papadogias D, Makras P, Grossman AB: Treatment of advanced neuroendocrine tumours with radiolabelled somatostatin analogues. Endocr Relat Cancer; 2005 Dec;12(4):683-99
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of advanced neuroendocrine tumours with radiolabelled somatostatin analogues.
  • Neuroendocrine tumours (NETs) constitute a heterogeneous group of tumours that frequently express cell membrane-specific peptide receptors, such as somatostatin receptors (SSTRs), and of which gastroenteropancreatic (GEP), carcinoid and pancreatic islet cell tumours exhibit the highest expression of SSTRs.
  • The administration of high doses of the Auger electron and gamma-emitter (111)In-diethylenetriaminepenta-acetic acid (DTPA)(0),octreotide in patients with metastatic tumours has been associated with considerable symptomatic improvement but relatively few and short-lived objective tumour responses.
  • The use of another radiolabelled somatostatin analogue coupled with (90)Y, a pure beta-emitter, (90)Y-1,4,7,10-tetraazacyclododecane-N,N',N'',N'''-tetraacetic acid (DOTA)(0),Tyr(3),octreotide ((90)Y-DOTATOC, OctreoTher), was associated with 10-30% objective tumour response rates, and appears to be particularly effective in larger tumours. (111)In- and (90)Y-DOTA-lanreotide has also been used for the treatment of NETs although its therapeutic efficacy is probably inferior to that of octreotide-based radiopharmaceuticals.
  • More recently, treatment with (177)Lu-DOTA(0),Tyr(3)octreotate ((177)Lu-DOTATATE), which has a higher affinity for the SSTR subtype 2, resulted in approximately 30% complete or partial tumour responses; this radiopharmaceutical is particularly effective in smaller tumours.
  • Furthermore, treatment using both (90)Y-DOTATOC and (177)Lu-DOTA(0),Tyr(3)octreotate seems promising, as the combination of these radiopharmaceuticals could be effective in tumours bearing both small and large lesions.
  • Tumour regression is positively correlated with a high level of uptake on (111)In-octreotide scintigraphy, limited tumour mass and good performance status.
  • In general, better responses have been obtained in GEP tumours than other NETs.
  • The side effects of this form of therapy are relatively few and mild, particularly when kidney-protective agents are used.
  • Treatment with radiolabelled somatostatin analogues presents a promising tool for the management of patients with inoperable or disseminated NETs, and particularly GEP tumours.
  • [MeSH-major] Neuroendocrine Tumors / radiotherapy. Radiopharmaceuticals / therapeutic use. Somatostatin / analogs & derivatives

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16322317.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Peptides, Cyclic; 0 / Radiopharmaceuticals; 0 / Receptors, Somatostatin; 118992-92-0 / lanreotide; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide
  • [Number-of-references] 63
  •  go-up   go-down


58. Larsson DE, Hassan S, Larsson R, Oberg K, Granberg D: Combination analyses of anti-cancer drugs on human neuroendocrine tumor cell lines. Cancer Chemother Pharmacol; 2009 Dec;65(1):5-12
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combination analyses of anti-cancer drugs on human neuroendocrine tumor cell lines.
  • PURPOSE: There is a large need for better pharmacological treatment of neuroendocrine tumors.
  • The aim of this study was to investigate and quantify the cytotoxic potentiating effects resulting from a combination of five substances, NSC 95397, emetine, CGP-74514A hydrochloride, Brefeldin A and sanguinarine chloride, chosen from a previous screening of 1,280 pharmacologically active agents on neuroendocrine tumor cells, with standard cytotoxic agents currently used in the treatment of neuroendocrine tumors.
  • METHOD: The human pancreatic carcinoid cell line BON-1, human typical bronchial carcinoid cell line NCI-H727 and the human atypical bronchial carcinoid cell line NCI-H720 were used.
  • Combinations between doxorubicin, etoposide, oxaliplatin, docetaxel, and each one of the five agents were studied and simultaneous exposures were explored using the median-effect method.
  • Almost all of the CGP-74514A hydrochloride interactions were additive, while brefeldin A and sanguinarine displayed less synergy but more additive and antagonistic interactions in combination with the standard drugs.
  • CONCLUSION: The synergistic and additive interactions make NSC-95397, emetine, and CGP-74514A hydrochloride potential candidates for incorporation into combination chemotherapy regimens and these drugs might be the suitable candidates for further clinical studies in patients with bronchial carcinoids and pancreatic endocrine tumors.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Carcinoid Tumor / drug therapy. Neuroendocrine Tumors / drug therapy
  • [MeSH-minor] 2-Aminopurine / administration & dosage. 2-Aminopurine / analogs & derivatives. Bronchial Neoplasms / drug therapy. Bronchial Neoplasms / pathology. Cell Line, Tumor. Drug Screening Assays, Antitumor. Drug Synergism. Emetine / administration & dosage. Humans. Naphthoquinones / administration & dosage. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / pathology

  • Genetic Alliance. consumer health - Pancreatic islet cell tumors.
  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. EMETINE .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19381631.001).
  • [ISSN] 1432-0843
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 2,3-bis(2-hydroxyethylsulfanyl)-(1,4)naphthoquinone; 0 / N(2)-(2-aminocyclohexyl)-N(6)-(3-chlorophenyl)-9-ethyl-9H-purine-2,6-diamine; 0 / Naphthoquinones; 452-06-2 / 2-Aminopurine; X8D5EPO80M / Emetine
  •  go-up   go-down


59. Simsek I, Pay S, Dinc A, Erdem H, Kurt B: Atypical carcinoid tumor of the thymus with ectopic ACTH production developed during the course of etanercept treatment--case report. Clin Rheumatol; 2007 Sep;26(9):1561-2
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atypical carcinoid tumor of the thymus with ectopic ACTH production developed during the course of etanercept treatment--case report.
  • Ever since the introduction of anti-tumor necrosis factor (TNF) agents, concerns have been raised regarding their potential for developing malignancy.
  • We report the development of thymic atypical carcinoid tumor 9 months after the initiation of etanercept therapy in a patient having refractory spondylarthritis.
  • This case indicates the need for following large cohorts of patients receiving anti-TNF agents to address the long-term effect of these agents on malignancies.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Carcinoid Tumor / chemically induced. Immunoglobulin G / adverse effects. Thymus Neoplasms / chemically induced. Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • [MeSH-minor] Adult. Etanercept. Humans. Male. Pituitary ACTH Hypersecretion / etiology. Receptors, Tumor Necrosis Factor. Spondylarthritis / drug therapy

  • Genetic Alliance. consumer health - Carcinoid Tumor.
  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • MedlinePlus Health Information. consumer health - Thymus Cancer.
  • Hazardous Substances Data Bank. Etanercept .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Chest. 2003 Jul;124(1):141-6 [12853516.001]
  • [Cites] Ann Rheum Dis. 2005 May;64(5):699-703 [15695534.001]
  • [Cites] Drug Saf. 2004;27(5):307-24 [15061685.001]
  • [Cites] Dis Colon Rectum. 2005 Aug;48(8):1651-5 [15933793.001]
  • [Cites] J Am Acad Dermatol. 2004 May;50(5 Suppl):S75-7 [15097933.001]
  • [Cites] Rheumatology (Oxford). 2003 Jul;42(7):900-1 [12826706.001]
  • [Cites] J Rheumatol. 2002 Jan;29(1):118-22 [11824947.001]
  • [Cites] Arthritis Rheum. 2002 Dec;46(12):3151-8 [12483718.001]
  • (PMID = 17061154.001).
  • [ISSN] 0770-3198
  • [Journal-full-title] Clinical rheumatology
  • [ISO-abbreviation] Clin. Rheumatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunoglobulin G; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; OP401G7OJC / Etanercept
  •  go-up   go-down


60. Rothermel J, Wartmann M, Chen T, Hohneker J: EPO906 (epothilone B): a promising novel microtubule stabilizer. Semin Oncol; 2003 Jun;30(3 Suppl 6):51-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • EPO906 (epothilone B) is a potent member of a new class of microtubule-stabilizing cytotoxic agents known as epothilones.
  • Tumor responses were seen in colorectal cancer as well as a variety of other tumor types, such as breast, ovarian, lung, and carcinoid in these two phase I trials.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Epothilones / pharmacology. Microtubules / drug effects
  • [MeSH-minor] Animals. Clinical Trials as Topic. Colorectal Neoplasms / drug therapy. Drug Screening Assays, Antitumor. Humans

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2003 Elsevier Inc. All rights reserved.
  • (PMID = 12802795.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Epothilones; UEC0H0URSE / epothilone B
  • [Number-of-references] 22
  •  go-up   go-down


61. Barbaro B, Caputo F, Tebala C, Di Stasi C, Vellone M, Giuliante F, Nuzzo G, Bonomo L: Preoperative right portal vein embolisation: indications and results. Radiol Med; 2009 Jun;114(4):553-70
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • MATERIALS AND METHODS: Twenty-six consecutive patients, 14 with liver metastases (ten from colorectal cancer; four from carcinoid tumours) and 12 with biliary cancers (ten Klatskin tumours; one gallbladder tumour; one intrahepatic cholangiocarcinoma) with insufficient predicted future remnant liver (FRL) underwent right PVE to induce hypertrophy of the contralateral hemiliver prior to surgical resection.
  • Total liver volume, tumour volume and FRL volume were calculated on a 3D workstation.
  • [MeSH-major] Biliary Tract Neoplasms / drug therapy. Biliary Tract Neoplasms / surgery. Embolization, Therapeutic. Hepatectomy / methods. Liver Neoplasms / drug therapy. Liver Neoplasms / surgery. Portal Vein. Preoperative Care / methods
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bile Duct Neoplasms / drug therapy. Bile Duct Neoplasms / surgery. Bile Ducts, Intrahepatic. Cholangiocarcinoma / drug therapy. Cholangiocarcinoma / surgery. Female. Gallbladder Neoplasms / drug therapy. Gallbladder Neoplasms / surgery. Humans. Klatskin Tumor / drug therapy. Klatskin Tumor / surgery. Male. Middle Aged. Practice Guidelines as Topic. Retrospective Studies. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] World J Surg. 2007 Feb;31(2):367-74 [17219273.001]
  • [Cites] Surgery. 1997 Feb;121(2):135-41 [9037224.001]
  • [Cites] Hepatogastroenterology. 2002 Mar-Apr;49(44):472-7 [11995476.001]
  • [Cites] Radiographics. 2008 Jan-Feb;28(1):119-34 [18203934.001]
  • [Cites] N Engl J Med. 2007 Apr 12;356(15):1545-59 [17429086.001]
  • [Cites] Arch Surg. 2005 Nov;140(11):1100-3 [16301448.001]
  • [Cites] Ann Surg. 2003 Feb;237(2):208-17 [12560779.001]
  • [Cites] Hepatogastroenterology. 2000 Jul-Aug;47(34):1077-81 [11020883.001]
  • [Cites] Hepatology. 2001 Aug;34(2):267-72 [11481611.001]
  • [Cites] Br J Surg. 1997 Jul;84(7):977-80 [9240140.001]
  • [Cites] J Am Coll Surg. 2005 Jun;200(6):845-53 [15922194.001]
  • [Cites] Br J Surg. 2001 Feb;88(2):165-75 [11167863.001]
  • [Cites] Br J Surg. 1999 Jun;86(6):784-8 [10383579.001]
  • [Cites] World J Surg. 1993 Jan-Feb;17(1):109-15 [8383379.001]
  • [Cites] Ann Surg. 2000 Apr;231(4):480-6 [10749607.001]
  • [Cites] Acta Radiol. 2003 Jan;44(1):98-102 [12631007.001]
  • [Cites] Eur Radiol. 2000;10 (11):1703-7 [11097391.001]
  • [Cites] Surgery. 2008 Mar;143(3):384-93 [18291260.001]
  • [Cites] Arch Surg. 2002 Jun;137(6):675-80; discussion 680-1 [12049538.001]
  • [Cites] Ann Surg. 2006 Mar;243(3):364-72 [16495702.001]
  • [Cites] Hepatology. 1995 Feb;21(2):434-9 [7843717.001]
  • [Cites] Colorectal Dis. 2003 Jan;5(1):2-23 [12780921.001]
  • [Cites] Br J Surg. 2007 Nov;94(11):1386-94 [17583900.001]
  • [Cites] J Clin Oncol. 2006 May 1;24(13):2065-72 [16648507.001]
  • [Cites] Radiology. 1993 Jul;188(1):73-7 [8511321.001]
  • [Cites] Ann Oncol. 2004 Mar;15(3):460-6 [14998849.001]
  • [Cites] Surg Gynecol Obstet. 1973 Aug;137(2):179-99 [4353133.001]
  • [Cites] J Surg Oncol. 2008 Mar 1;97(3):253-8 [18264984.001]
  • [Cites] Surgery. 1990 May;107(5):521-7 [2333592.001]
  • [Cites] Br J Surg. 2006 May;93(5):587-92 [16523448.001]
  • [Cites] Surgery. 2002 Mar;131(3):294-9 [11894034.001]
  • [Cites] Hepatology. 1997 Nov;26(5):1176-81 [9362359.001]
  • [Cites] Hepatology. 1993 Jul;18(1):79-85 [8392029.001]
  • [Cites] Ann Surg. 2004 Dec;240(6):1037-49; discussion 1049-51 [15570209.001]
  • [Cites] Radiology. 2003 Apr;227(1):251-60 [12616006.001]
  • [Cites] Br J Radiol. 2001 Nov;74(887):983-6 [11709461.001]
  • [Cites] Transplantation. 2004 Nov 27;78(10):1501-5 [15599315.001]
  • [Cites] Ann Surg. 2004 Oct;240(4):644-57; discussion 657-8 [15383792.001]
  • [Cites] World J Surg. 1995 Jan-Feb;19(1):59-71 [7740812.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9073-8 [16361615.001]
  • [Cites] J Am Coll Surg. 2003 Jul;197(1):164-70 [12831938.001]
  • [Cites] J Exp Med. 1920 Apr 30;31(5):609-32 [19868417.001]
  • (PMID = 19367466.001).
  • [ISSN] 0033-8362
  • [Journal-full-title] La Radiologia medica
  • [ISO-abbreviation] Radiol Med
  • [Language] eng; ita
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Italy
  •  go-up   go-down


62. Massironi S, Sciola V, Peracchi M, Ciafardini C, Spampatti MP, Conte D: Neuroendocrine tumors of the gastro-entero-pancreatic system. World J Gastroenterol; 2008 Sep 21;14(35):5377-84
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neuroendocrine tumors of the gastro-entero-pancreatic system.
  • Gastro-entero-pancreatic (GEP) neuroendocrine tumors (NETs) are rare neoplasms, although their prevalence has increased substantially over the past three decades.
  • They show extremely variable biological behavior and clinical course.
  • Most NETs have endocrine function and secrete peptides and neuroamines that cause distinct clinical syndromes, including carcinoid syndrome; however, many are clinically silent until late presentation with mass effects.
  • Investigation and management should be individualized for each patient, taking into account the likely natural history of the tumor and general health of the patient.
  • Management strategies include surgery for cure or palliation, and a variety of other cytoreductive techniques, and medical treatment including chemotherapy, and biotherapy to control symptoms due to hormone release and tumor growth, with somatostatin analogues (SSAs) and alpha-interferon.
  • New biological agents and somatostatin-tagged radionuclides are under investigation.
  • Advances in the therapy and development of centers of excellence which coordinate multicenter studies, are needed to improve diagnosis, treatment and therefore survival of patients with GEP NETs.
  • [MeSH-major] Digestive System Neoplasms / diagnosis. Neuroendocrine Tumors / diagnosis

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Cancer. 1999 Dec;81(8):1351-5 [10604732.001]
  • [Cites] Lancet Oncol. 2008 Jan;9(1):61-72 [18177818.001]
  • [Cites] J Surg Oncol. 2000 Dec;75(4):310-6 [11135275.001]
  • [Cites] Cancer. 2001 Oct 15;92(8):2204-10 [11596039.001]
  • [Cites] Dis Colon Rectum. 2002 Jan;45(1):91-7 [11786770.001]
  • [Cites] Semin Nucl Med. 2002 Apr;32(2):110-22 [11965606.001]
  • [Cites] Semin Nucl Med. 2002 Apr;32(2):123-32 [11965607.001]
  • [Cites] Eur J Endocrinol. 2003 Jan;148(1):39-43 [12534356.001]
  • [Cites] Cancer. 2003 Feb 15;97(4):934-59 [12569593.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2003 Mar;30(3):417-22 [12634971.001]
  • [Cites] N Engl J Med. 2003 Mar 20;348(12):1134-49 [12646671.001]
  • [Cites] Br J Surg. 2003 Nov;90(11):1317-22 [14598408.001]
  • [Cites] Eur J Cancer. 2004 Mar;40(4):515-20 [14962717.001]
  • [Cites] Ann Oncol. 2004 Jun;15(6):966-73 [15151956.001]
  • [Cites] Clin Cancer Res. 2004 Sep 15;10(18 Pt 1):6111-8 [15447997.001]
  • [Cites] Am J Gastroenterol. 2008 Feb;103(2):475-83; quiz 484 [18028508.001]
  • [Cites] J Clin Oncol. 2008 Mar 10;26(8):1316-23 [18323556.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2008;22(1):183-205 [18206821.001]
  • [Cites] Am J Gastroenterol. 2008 Mar;103(3):729-32 [18341492.001]
  • [Cites] J Clin Oncol. 2008 May 1;26(13):2124-30 [18445841.001]
  • [Cites] N Engl J Med. 1983 Jul 21;309(3):129-33 [6191217.001]
  • [Cites] N Engl J Med. 1987 Dec 31;317(27):1699-701 [3696178.001]
  • [Cites] Cancer. 1991 Jul 15;68(2):227-32 [1712661.001]
  • [Cites] N Engl J Med. 1992 Feb 20;326(8):519-23 [1310159.001]
  • [Cites] Ann Intern Med. 1996 Jul 1;125(1):26-34 [8644985.001]
  • [Cites] Eur J Clin Invest. 1998 Jun;28(6):431-40 [9693933.001]
  • [Cites] Lancet. 1998 Sep 5;352(9130):799-805 [9737302.001]
  • [Cites] Physiol Rev. 1998 Oct;78(4):1087-108 [9790570.001]
  • [Cites] Am J Gastroenterol. 1999 May;94(5):1381-7 [10235222.001]
  • [Cites] Lancet. 1963 Feb 2;1(7275):238-9 [14000847.001]
  • [Cites] Eur J Endocrinol. 2005 Mar;152(3):443-8 [15757862.001]
  • [Cites] J Clin Gastroenterol. 2005 May-Jun;39(5):376-80 [15815204.001]
  • [Cites] Ann Surg. 2005 May;241(5):776-83; discussion 783-5 [15849513.001]
  • [Cites] Gastroenterology. 2005 May;128(6):1668-84 [15887158.001]
  • [Cites] Gastroenterology. 2005 May;128(6):1717-51 [15887161.001]
  • [Cites] Gut. 2005 Jun;54 Suppl 4:iv1-16 [15888809.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2005 Oct;19(5):675-97 [16253893.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2005 Oct;19(5):729-38 [16253897.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2005 Oct;19(5):753-81 [16253899.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2005 Oct;19(5):783-98 [16253900.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2005 Oct;19(5):807-17 [16253902.001]
  • [Cites] Virchows Arch. 2006 Oct;449(4):395-401 [16967267.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2006 Nov;33(11):1346-51 [16847654.001]
  • [Cites] Br J Cancer. 2006 Nov 6;95(9):1148-54 [17031397.001]
  • [Cites] Medicine (Baltimore). 2006 Nov;85(6):331-64 [17108779.001]
  • [Cites] Clin Cancer Res. 2007 Jan 1;13(1):234-40 [17200360.001]
  • [Cites] Best Pract Res Clin Endocrinol Metab. 2007 Mar;21(1):1-14 [17382262.001]
  • [Cites] Best Pract Res Clin Endocrinol Metab. 2007 Mar;21(1):33-41 [17382264.001]
  • [Cites] Best Pract Res Clin Endocrinol Metab. 2007 Mar;21(1):43-68 [17382265.001]
  • [Cites] Best Pract Res Clin Endocrinol Metab. 2007 Mar;21(1):69-85 [17382266.001]
  • [Cites] Best Pract Res Clin Endocrinol Metab. 2007 Mar;21(1):111-29 [17382268.001]
  • [Cites] Best Pract Res Clin Endocrinol Metab. 2007 Mar;21(1):145-62 [17382270.001]
  • [Cites] Best Pract Res Clin Endocrinol Metab. 2007 Mar;21(1):163-72 [17382271.001]
  • [Cites] J Clin Oncol. 2007 May 20;25(15):1967-73 [17513802.001]
  • [Cites] Hematol Oncol Clin North Am. 2007 Jun;21(3):575-81; x [17548041.001]
  • [Cites] Virchows Arch. 2007 Oct;451(4):757-62 [17674042.001]
  • [Cites] Am J Gastroenterol. 2007 Dec;102(12):2648-54 [17764495.001]
  • [Cites] IDrugs. 2007 Dec;10(12):885-95 [18041687.001]
  • [Cites] Endocr Pathol. 2007 Fall;18(3):145-9 [18058263.001]
  • [Cites] Neuroendocrinology. 2008;87(1):8-19 [18097129.001]
  • [Cites] Neuroendocrinology. 2008;87(1):31-9 [18097130.001]
  • [Cites] Neuroendocrinology. 2008;87(1):47-62 [18097131.001]
  • [Cites] Br J Cancer. 2000 Oct;83(7):952-5 [10970700.001]
  • (PMID = 18803349.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
  • [Number-of-references] 65
  • [Other-IDs] NLM/ PMC2744160
  •  go-up   go-down


63. Lafaras CT, Mandala EM, Platogiannis DN, Saratzis AN, Barbetakis NG, Paraskevopoulos PP, Ilonidis GC, Bischiniotis TS: Evaluation of treatment with bosentan in patients with carcinoid heart disease: single center study. Onkologie; 2010;33(6):300-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of treatment with bosentan in patients with carcinoid heart disease: single center study.
  • BACKGROUND: The primary aim of this study was to evaluate a combined therapeutic intervention, including the dual endothelin receptor antagonist bosentan, in patients with carcinoid heart disease (CaHD).
  • PATIENTS AND METHODS: Since 2003, 40 patients with neuroendocrine tumours were identified; 14 had echocardiographic findings consistent with CaHD.
  • Further clarification of the CaHD fibrosis pathogenesis is needed to facilitate development of targeted antifibrotic therapeutic agents.
  • [MeSH-major] Antihypertensive Agents / therapeutic use. Carcinoid Heart Disease / drug therapy. Endothelin Receptor Antagonists. Gastrointestinal Neoplasms / drug therapy. Lung Neoplasms / drug therapy. Ovarian Neoplasms / drug therapy. Sulfonamides / therapeutic use
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Echocardiography, Doppler. Exercise Test / drug effects. Female. Follow-Up Studies. Humans. Male. Middle Aged. Natriuretic Peptide, Brain / blood. Peptide Fragments / blood

  • Genetic Alliance. consumer health - Heart Disease.
  • MedlinePlus Health Information. consumer health - Blood Pressure Medicines.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Ovarian Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20523093.001).
  • [ISSN] 1423-0240
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antihypertensive Agents; 0 / Endothelin Receptor Antagonists; 0 / Peptide Fragments; 0 / Sulfonamides; 0 / pro-brain natriuretic peptide (1-76); 114471-18-0 / Natriuretic Peptide, Brain; Q326023R30 / bosentan
  •  go-up   go-down


64. Nørsett KG, Laegreid A, Langaas M, Wörlund S, Fossmark R, Waldum HL, Sandvik AK: Molecular characterization of rat gastric mucosal response to potent acid inhibition. Physiol Genomics; 2005 Jun 16;22(1):24-32
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Potent acid inhibition with proton pump inhibitors (PPIs) is widely used in clinical medicine, especially for gastroesophageal reflux disease.
  • Long-term hypergastrinemia increases mucosal thickness and enterochromaffin-like cell density in gastric corpus mucosa and results in development of gastric carcinoids in experimental animals.
  • Many genes are identified that were not previously known to be affected by inhibition of gastric acid secretion or that have unknown biological functions.
  • [MeSH-major] Gastric Acid / metabolism. Gastric Mucosa / drug effects. Gastric Mucosa / metabolism. Gene Expression Regulation / drug effects. Omeprazole / pharmacology
  • [MeSH-minor] Animals. Blotting, Northern. Humans. Immunohistochemistry. Male. Microarray Analysis. Parietal Cells, Gastric / cytology. Quality Control. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Rats, Sprague-Dawley. Receptors, CXCR4 / metabolism. Reproducibility of Results. Reverse Transcriptase Polymerase Chain Reaction. Sequence Analysis, DNA

  • Hazardous Substances Data Bank. OMEPRAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15827235.001).
  • [ISSN] 1531-2267
  • [Journal-full-title] Physiological genomics
  • [ISO-abbreviation] Physiol. Genomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cxcr4 protein, rat; 0 / RNA, Messenger; 0 / Receptors, CXCR4; KG60484QX9 / Omeprazole
  •  go-up   go-down


65. Ameri P, Gatto F, Arvigo M, Villa G, Resmini E, Minuto F, Murialdo G, Ferone D: Somatostatin receptor scintigraphy in thoracic diseases. J Endocrinol Invest; 2007 Nov;30(10):889-902
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Somatostatin (SS) receptor scintigraphy is useful for the diagnosis of lesions with high density of SS receptors, and above all neuroendocrine tumors.
  • Radiolabeled octreotide became the gold standard for the detection of neuroendocrine tumors.
  • Indeed, in the management of SS receptor-positive lesions, the contribution of nuclear medicine is essential in several clinical settings, such as initial diagnosis, disease staging, follow-up, treatment planning, and treatment monitoring.
  • In the chest, apart in (neuro)endocrine tumors, SS receptors have been demonstrated in granulomatous diseases, like sarcoidosis and other immune-mediated disorders, such as anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis.
  • [MeSH-major] Positron-Emission Tomography / methods. Receptors, Somatostatin / metabolism. Thoracic Diseases / diagnostic imaging. Tomography, Emission-Computed, Single-Photon / methods
  • [MeSH-minor] Carcinoid Tumor / diagnostic imaging. Carcinoma, Small Cell / diagnostic imaging. Humans. Lung Neoplasms / diagnostic imaging

  • MedlinePlus Health Information. consumer health - Chest Injuries and Disorders.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Chest. 2004 Feb;125(2):494-501 [14769730.001]
  • [Cites] Semin Surg Oncol. 1998 Dec;15(4):220-2 [9829375.001]
  • [Cites] J Nucl Med. 2001 Jul;42(7):1134-8 [11438641.001]
  • [Cites] Endocrinology. 1999 Nov;140(11):5136-48 [10537142.001]
  • [Cites] Blood. 1993 Oct 1;82(7):2143-51 [8400264.001]
  • [Cites] J Nucl Med. 2000 Oct;41(10 ):1704-13 [11038002.001]
  • [Cites] Ann Surg. 1998 Jul;228(1):99-105 [9671073.001]
  • [Cites] Acta Radiol. 2004 Dec;45(8):833-9 [15690613.001]
  • [Cites] J Clin Endocrinol Metab. 2004 May;89(5):2214-21 [15126544.001]
  • [Cites] Peptides. 2000 Dec;21(12):1941-64 [11150654.001]
  • [Cites] Clin Cancer Res. 1999 Nov;5(11):3483-7 [10589762.001]
  • [Cites] Eur J Cancer. 2001 Mar;37(5):620-8 [11290438.001]
  • [Cites] Radiology. 2005 Nov;237(2):718-26 [16192318.001]
  • [Cites] Cancer Biother Radiopharm. 2004 Apr;19(2):253-9 [15186606.001]
  • [Cites] Eur J Nucl Med. 1993 Aug;20(8):716-31 [8404961.001]
  • [Cites] J Nucl Med. 2000 Nov;41(11):1808-12 [11079487.001]
  • [Cites] Cancer. 2002 Mar 1;94(5):1414-20 [11920496.001]
  • [Cites] J Nucl Med. 2006 Oct;47(10):1599-606 [17015894.001]
  • [Cites] Oncol Rep. 1998 Jan-Feb;5(1):177-80 [9458317.001]
  • [Cites] Cancer Biother Radiopharm. 2006 Feb;21(1):61-7 [16480332.001]
  • [Cites] Chest. 2002 Oct;122(4):1493; author reply 1493-4 [12377888.001]
  • [Cites] J Nucl Med. 2002 Jul;43(7):889-95 [12097458.001]
  • [Cites] J Nucl Med. 1998 Feb;39(2):224-7 [9476922.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2006 Sep;33(9):1041-7 [16715455.001]
  • [Cites] Eur J Endocrinol. 2000 Oct;143 Suppl 1:S27-34 [11068937.001]
  • [Cites] J Cardiovasc Surg (Torino). 2005 Jun;46(3):318-9 [15956934.001]
  • [Cites] J Nucl Med. 2003 Aug;44(8):1315-21 [12902423.001]
  • [Cites] N Engl J Med. 1996 Jan 25;334(4):246-54 [8532003.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Mar;88(3):1066-81 [12629087.001]
  • [Cites] N Engl J Med. 2005 Jun 9;352(23 ):2457-8 [15944436.001]
  • [Cites] J Clin Endocrinol Metab. 2005 May;90(5):2603-9 [15713725.001]
  • [Cites] J Endocrinol Invest. 2005;28(11 Suppl International):36-42 [16625843.001]
  • [Cites] J Nucl Med. 2006 Aug;47(8):1281-7 [16883006.001]
  • [Cites] Scand Cardiovasc J. 1999;33(1):49-53 [10093860.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2007 Aug;34(8):1219-27 [17260141.001]
  • [Cites] Br J Cancer. 1998 Feb;77(4):632-7 [9484822.001]
  • [Cites] Clin Nucl Med. 1999 May;24(5):343-5 [10232474.001]
  • [Cites] Eur J Nucl Med. 1994 Jun;21(6):497-502 [8082663.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2004 Jul;31(7):1005-10 [15029463.001]
  • [Cites] Clin Nucl Med. 1994 Feb;19(2):129-32 [7910542.001]
  • [Cites] Ann Oncol. 2005;16 Suppl 2:ii235-9 [15958464.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Oct;88(10 ):4754-8 [14557451.001]
  • [Cites] Ann Oncol. 2001;12 Suppl 2:S31-6 [11762349.001]
  • [Cites] J Endocrinol Invest. 2005 Jan;28(1):72-8 [15816375.001]
  • [Cites] Eur J Nucl Med. 1998 Jun;25(6):639-58 [9618580.001]
  • [Cites] Clin Nucl Med. 1997 Dec;22(12 ):811-6 [9408640.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Nov;88(11):5150-7 [14602742.001]
  • [Cites] N Engl J Med. 1997 Apr 24;336(17):1224-34 [9110911.001]
  • [Cites] Cancer. 2002 Feb 1;94(3):633-40 [11857294.001]
  • [Cites] Lung Cancer. 2004 Sep;45(3):365-71 [15301877.001]
  • [Cites] Ann N Y Acad Sci. 2006 Jun;1069:129-44 [16855140.001]
  • [Cites] J Cardiovasc Surg (Torino). 1997 Jun;38(3):313-5 [9219485.001]
  • [Cites] J Nucl Med. 1998 Apr;39(4):634-9 [9544670.001]
  • [Cites] Cancer. 1999 Jan 1;85(1):188-98 [9921992.001]
  • [Cites] Clin Nucl Med. 1998 Dec;23 (12 ):847-8 [9858303.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Apr;85(4):1719-26 [10770220.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2004 Oct;31(10 ):1399-404 [15221296.001]
  • [Cites] Eur J Pharmacol. 1994 Dec 27;271(2-3):371-8 [7705437.001]
  • [Cites] Klin Oczna. 2002;104(3-4):266-9 [12608317.001]
  • [Cites] Ann Med. 1999 Oct;31 Suppl 2:63-9 [10574158.001]
  • [Cites] Cancer Res. 1998 May 1;58(9):1850-9 [9581824.001]
  • [Cites] Trends Endocrinol Metab. 2002 Dec;13(10 ):451-7 [12431842.001]
  • [Cites] Eur J Cardiothorac Surg. 2002 May;21(5):913-7 [12062286.001]
  • [Cites] Chest. 2002 Mar;121(3):985-8 [11888987.001]
  • [Cites] J Nucl Med. 2003 May;44(5):708-16 [12732671.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2005 Aug;19(4):595-616 [16183530.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Apr;84(4):1193-202 [10199752.001]
  • [Cites] J Endocrinol Invest. 2001 Jul-Aug;24(7):522-8 [11508787.001]
  • [Cites] Clin Nucl Med. 2000 Jan;25(1):24-8 [10634526.001]
  • [Cites] Chest. 1999 Jan;115(1):224-32 [9925088.001]
  • [Cites] J Endocrinol Invest. 2005;28(11 Suppl International):10-4 [16625839.001]
  • [Cites] Eur J Nucl Med. 1994 Oct;21(10 ):1106-13 [7828621.001]
  • [Cites] Cancer Biother Radiopharm. 2004 Oct;19(5):613-20 [15650454.001]
  • [Cites] Eur J Clin Invest. 1999 Jul;29(7):630-6 [10411670.001]
  • [Cites] Semin Nucl Med. 2004 Jan;34(1):32-46 [14735457.001]
  • [Cites] Endocr Rev. 2003 Aug;24(4):389-427 [12920149.001]
  • [Cites] Nucl Med Biol. 2006 Oct;33(7):841-6 [17045163.001]
  • [Cites] Postgrad Med J. 1999 Feb;75(880):65-6 [10448463.001]
  • [Cites] J Biol Chem. 2001 Apr 27;276(17):14027-36 [11134004.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Dec;59(6):793-9 [14974924.001]
  • [Cites] Eur J Cancer. 1994;30A(11):1682-7 [7833144.001]
  • [Cites] Cancer. 2003 Feb 15;97(4):934-59 [12569593.001]
  • [Cites] N Engl J Med. 1983 Dec 15;309(24):1495-501 [6139753.001]
  • [Cites] Ann Surg Oncol. 2003 Jul;10(6):697-704 [12839856.001]
  • [Cites] Nat Rev Drug Discov. 2003 Dec;2(12):999-1017 [14654798.001]
  • [Cites] Q J Nucl Med Mol Imaging. 2006 Dec;50(4):272-87 [17043625.001]
  • [Cites] Chest. 2004 Oct;126(4):1337-43 [15486401.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 Nov;55(5):689-93 [11894982.001]
  • [Cites] J Nucl Med. 1996 Jun;37(6):886-92 [8683305.001]
  • [Cites] Eur J Endocrinol. 1997 Dec;137(6):688-90 [9437238.001]
  • [Cites] Eur J Nucl Med. 2001 Sep;28(9):1421-9 [11585303.001]
  • [Cites] Clin Nucl Med. 2003 Dec;28(12 ):994-5 [14663328.001]
  • [Cites] N Engl J Med. 1997 Jan 23;336(4):263-5 [8995089.001]
  • [Cites] J Nucl Med. 2004 Sep;45(9):1542-8 [15347722.001]
  • [Cites] Rheumatology (Oxford). 2004 Feb;43(2):195-201 [12949255.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Apr;84(4):1186-92 [10199751.001]
  • [Cites] J Endocrinol Invest. 2002 Jul-Aug;25(7):650-62 [12150344.001]
  • [Cites] Clin Nucl Med. 1999 Jan;24(1):24-8 [9890489.001]
  • [Cites] Clin Nucl Med. 1996 Jun;21(6):487-8 [8744192.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2005 Sep;32(9):1026-32 [15877227.001]
  • [Cites] J Rheumatol. 1999 Mar;26(3):532-5 [10090157.001]
  • [Cites] Ann Oncol. 2004 Jun;15(6):966-73 [15151956.001]
  • [Cites] Eur J Nucl Med. 1998 Sep;25(9):1284-92 [9724378.001]
  • [Cites] Biochim Biophys Acta. 2003 Sep 22;1616(1):1-84 [14507421.001]
  • [Cites] Lung Cancer. 1998 Nov;22(2):97-102 [10022217.001]
  • [Cites] Australas Radiol. 2006 Jun;50(3):218-21 [16732817.001]
  • [Cites] Eur J Nucl Med. 2000 Mar;27(3):273-82 [10774879.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2005 Aug;32(8):925-31 [15841374.001]
  • [Cites] Nucl Med Commun. 2006 Jun;27(6):507-14 [16710105.001]
  • [Cites] Allergy. 2005 May;60(5):565-82 [15813801.001]
  • [Cites] Clin Nucl Med. 2003 Jul;28(7):548-52 [12819406.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2003 Oct;30(10 ):1402-6 [12845490.001]
  • [Cites] J Nucl Med. 2001 Jan;42(1):21-6 [11197973.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2003 Aug;285(2):E344-53 [12684217.001]
  • [Cites] Lancet. 2005 Oct 15-21;366(9494):1385-96 [16226617.001]
  • [Cites] Semin Nucl Med. 2002 Apr;32(2):148-55 [11965610.001]
  • [Cites] Ann Oncol. 2002 May;13(5):653-68 [12075733.001]
  • [Cites] Virchows Arch. 2001 Dec;439(6):787-97 [11787852.001]
  • [Cites] Semin Nucl Med. 2002 Apr;32(2):92-6 [11965604.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jan;88(1):270-6 [12519865.001]
  • [Cites] Metabolism. 1996 Aug;45(8 Suppl 1):86-7 [8769392.001]
  • [Cites] Chemotherapy. 2001;47 Suppl 2:78-108 [11275704.001]
  • [Cites] J Nucl Med. 2005 Jan;46 Suppl 1:172S-8S [15653666.001]
  • [Cites] Endocr Rev. 2003 Feb;24(1):28-47 [12588807.001]
  • [Cites] Sarcoidosis Vasc Diffuse Lung Dis. 1997 Sep;14 (2):146-51 [9306505.001]
  • [Cites] Chest. 2000 May;117(5):1232-8 [10807805.001]
  • [Cites] Eur Rev Med Pharmacol Sci. 2003 Jul-Aug;7(4):97-105 [15068232.001]
  • [Cites] Urol Oncol. 2002 May-Jun;7(3):91-8 [12474541.001]
  • [Cites] J Endocrinol Invest. 2003;26(8 Suppl):103-8 [15233223.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Aug;90(8):4955-62 [15914534.001]
  • [Cites] Ann Med. 1999 Oct;31 Suppl 2:80-5 [10574161.001]
  • [Cites] Nucl Med Rev Cent East Eur. 2006;9(1):24-9 [16791800.001]
  • [Cites] J Nucl Med. 2001 Sep;42(9):1309-15 [11535718.001]
  • (PMID = 18075294.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Receptors, Somatostatin
  • [Number-of-references] 134
  •  go-up   go-down


66. Woltering EA, Salvo VA, O'Dorisio TM, Lyons J 3rd, Li G, Zhou Y, Seward JR, Go VL, Vinik AI, Mamikunian P, Mamikunian G: Clinical value of monitoring plasma octreotide levels during chronic octreotide long-acting repeatable therapy in carcinoid patients. Pancreas; 2008 Jul;37(1):94-100
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical value of monitoring plasma octreotide levels during chronic octreotide long-acting repeatable therapy in carcinoid patients.
  • OBJECTIVE: Octreotide is used to treat patients with neuroendocrine tumors.
  • Changes in plasma drug levels were analyzed over time using random effects models.
  • Serial plasma octreotide value measurements should be used to determine if increasing symptoms or tumor growth are associated with suboptimal octreotide levels.

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Endocrinol Metab. 1993 Dec;77(6):1577-83 [7903312.001]
  • [Cites] Cell Growth Differ. 1994 Jan;5(1):1-8 [8123588.001]
  • [Cites] Cancer Res. 1992 Sep 15;52(18):4973-8 [1325289.001]
  • [Cites] Dig Dis Sci. 1995 Jul;40(7):1464-73 [7628270.001]
  • [Cites] Pancreas. 2005 Nov;31(4):392-400 [16258376.001]
  • [Cites] J Clin Oncol. 1999 Feb;17(2):600-6 [10080605.001]
  • [CommentIn] Pancreas. 2008 Oct;37(3):334-5; author reply 336-7 [18815560.001]
  • [CommentIn] Pancreas. 2008 Oct;37(3):337-8; author reply 338-9 [18815562.001]
  • (PMID = 18580450.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016042-25; United States / NCCIH NIH HHS / AT / AT003960-01A1; United States / NCI NIH HHS / CA / P30 CA016042; United States / NCCIH NIH HHS / AT / P01 AT003960; United States / NCI NIH HHS / CA / CA016042-25; United States / NCCIH NIH HHS / AT / P01 AT003960-01A1
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Delayed-Action Preparations; RWM8CCW8GP / Octreotide
  • [Other-IDs] NLM/ NIHMS63368; NLM/ PMC2698789
  •  go-up   go-down


67. Ricci S, Antonuzzo A, Galli L, Orlandini C, Ferdeghini M, Boni G, Roncella M, Mosca F, Conte PF: Long-acting depot lanreotide in the treatment of patients with advanced neuroendocrine tumors. Am J Clin Oncol; 2000 Aug;23(4):412-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-acting depot lanreotide in the treatment of patients with advanced neuroendocrine tumors.
  • Long-acting depot forms of somatostatin analogs administered by intramuscular injections are now available for the treatment of neuroendocrine tumors (NETs).
  • From July 1996 to January 1999, 25 patients with advanced NETs (12 carcinoids, 13 endocrine pancreatic tumors) were enrolled in the study.
  • All the patients had measurable disease.
  • Lanreotide was administered as intramuscular injections at the dose of 30 mg every 2 weeks until there was objective, biochemical, or symptomatic tumor progression.
  • Objective partial responses (PRs) were documented in 2 patients (8%), whereas 10 patients (40%) had tumor stabilization.
  • The PRs were observed in patients with midgut carcinoids, of whom one was pretreated with subcutaneous octreotide.
  • The response duration was 21+ and 24+ months in responding patients; the median duration of disease stabilization was 8.5 months (range, 4-21+).
  • The overall biochemical response rate was 42%, including 2 complete responses (CRs) (10.5%) and 6 PRs (31.5%); all biochemical responses were observed mostly in patients with carcinoid tumors; the duration of response was 18+ and 30+ months for CRs; the median duration of biochemical response was 7 months (range, 4-18+) for PRs.
  • Depot lanreotide 30 mg shows significant efficacy in terms of objective response rate and in biochemical and symptomatic control, in pretreated patients as well as nonpretreated patients with advanced NETs.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Neuroendocrine Tumors / drug therapy. Peptides, Cyclic / therapeutic use. Somatostatin / analogs & derivatives
  • [MeSH-minor] Abdominal Pain / chemically induced. Adult. Aged. Biomarkers, Tumor / analysis. Carcinoid Tumor / drug therapy. Delayed-Action Preparations. Diarrhea / chemically induced. Disease Progression. Female. Flushing / chemically induced. Gastrinoma / drug therapy. Humans. Injections, Intramuscular. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Male. Middle Aged. Pancreatic Neoplasms / drug therapy. Patient Compliance. Remission Induction

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10955874.001).
  • [ISSN] 0277-3732
  • [Journal-full-title] American journal of clinical oncology
  • [ISO-abbreviation] Am. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Delayed-Action Preparations; 0 / Peptides, Cyclic; 118992-92-0 / lanreotide; 51110-01-1 / Somatostatin
  •  go-up   go-down


68. Chandra SA, Nolan MW, Malarkey DE: Chemical carcinogenesis of the gastrointestinal tract in rodents: an overview with emphasis on NTP carcinogenesis bioassays. Toxicol Pathol; 2010 Jan;38(1):188-97
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Within the GIT, epithelial tumors of the forestomach in mice and rats and LI of the rat are most common.
  • Generally, there is a high species concordance for forestomach with at least 26 chemicals inducing tumors in both species.
  • Glandular stomach tumors are rare, and the few reported are usually neuroendocrine tumors (carcinoids) originating from the enterochromaffin-like (ECL) cells.
  • Of 290 carcinogenic agents identified by the NTP, 19 (7%) caused intestinal neoplasia, 14 in the rat and 5 in the mouse.
  • In conclusion, the most common induced GIT tumors are squamous neoplasms of the forestomach, glandular neoplasms of the stomach are rare, and rats appear more prone to developing LI (colorectal) cancer compared to mice.
  • [MeSH-minor] Animals. Female. Humans. Intestinal Neoplasms / chemically induced. Male. Mice. Rats. Stomach Neoplasms / chemically induced

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Carcinogenesis. 2000 Jan;21(1):23-7 [10607729.001]
  • [Cites] Gastroenterology. 2009 Mar;136(3):780-98 [19263594.001]
  • [Cites] Natl Toxicol Program Tech Rep Ser. 2002 May;(498):1-277 [12118261.001]
  • [Cites] Carcinogenesis. 2002 Oct;23(10):1729-35 [12376483.001]
  • [Cites] Toxicology. 2003 Feb 1;183(1-3):221-34 [12504353.001]
  • [Cites] BMC Cancer. 2002 Dec 26;2:37 [12502432.001]
  • [Cites] Carcinogenesis. 2004 Apr;25(4):605-12 [14688030.001]
  • [Cites] Semin Oncol. 2004 Aug;31(4):450-64 [15297938.001]
  • [Cites] Gan. 1979 Oct;70(5):653-62 [520756.001]
  • [Cites] Scand J Gastroenterol Suppl. 1985;108:53-69 [3858976.001]
  • [Cites] Br Med J (Clin Res Ed). 1985 Oct 19;291(6502):1084-8 [3931805.001]
  • [Cites] Gastroenterology. 1986 Feb;90(2):391-9 [3510144.001]
  • [Cites] Toxicology. 1986 Jan;38(1):103-17 [3942006.001]
  • [Cites] Digestion. 1986;35 Suppl 1:84-97 [3792674.001]
  • [Cites] Toxicol Pathol. 1988;16(2):267-72 [3187355.001]
  • [Cites] Toxicol Pathol. 1988;16(2):288-98 [2903544.001]
  • [Cites] Toxicol Pathol. 1989;17(1 Pt 1):7-15 [2501865.001]
  • [Cites] Cancer Res. 1989 Sep 15;49(18):5143-7 [2766283.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1989;416(2):141-51 [2512742.001]
  • [Cites] Digestion. 1990;45(4):189-95 [2401393.001]
  • [Cites] Eur J Clin Invest. 1990 Oct;20 Suppl 1:S65-71 [2125000.001]
  • [Cites] Digestion. 1990;47 Suppl 1:17-23; discussion 49-52 [2093010.001]
  • [Cites] Cancer Res. 1992 May 15;52(10):2995-8 [1316233.001]
  • [Cites] Toxicol Pathol. 1992;20(2):141-5 [1335613.001]
  • [Cites] Jpn J Cancer Res. 1993 Nov;84(11):1120-9 [8276717.001]
  • [Cites] Environ Health Perspect. 1993 Dec;101 Suppl 5:107-10 [8013396.001]
  • [Cites] Environ Health Perspect. 1993 Dec;101 Suppl 5:277-9 [8013421.001]
  • [Cites] Fundam Appl Toxicol. 1994 Apr;22(3):411-21 [7519572.001]
  • [Cites] Toxicol Pathol. 1994 Sep-Oct;22(5):497-509 [7899778.001]
  • [Cites] Carcinogenesis. 1995 Sep;16(9):2135-41 [7554066.001]
  • [Cites] Toxicol Pathol. 1998 May-Jun;26(3):403-10 [9608647.001]
  • [Cites] Lab Anim Sci. 1999 Jun;49(3):241-7 [10403437.001]
  • [Cites] Eur J Cancer. 2005 Sep;41(13):1911-22 [16084718.001]
  • [Cites] Toxicol Sci. 2007 Aug;98(2):313-26 [17426108.001]
  • [Cites] Toxicol Pathol. 2007 Aug;35(5):636-48 [17654405.001]
  • [Cites] Carcinogenesis. 2009 Feb;30(2):183-96 [19037092.001]
  • [Cites] Int J Toxicol. 2002 May-Jun;21(3):219-30 [12055023.001]
  • (PMID = 20019352.001).
  • [ISSN] 1533-1601
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 ES999999
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] United States
  • [Number-of-references] 48
  • [Other-IDs] NLM/ NIHMS226604; NLM/ PMC3166531
  •  go-up   go-down


69. Vilar E, Salazar R, Pérez-García J, Cortes J, Oberg K, Tabernero J: Chemotherapy and role of the proliferation marker Ki-67 in digestive neuroendocrine tumors. Endocr Relat Cancer; 2007 Jun;14(2):221-32
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemotherapy and role of the proliferation marker Ki-67 in digestive neuroendocrine tumors.
  • Neuroendocrine tumors (NETs) of the digestive tract are a heterogeneous group of rare malignancies.
  • Three major subgroups can be defined: pancreatic endocrine tumors, carcinoid tumors, and poorly differentiated gastroenteropancreatic NETs.
  • Retrospective studies have identified several clinicopathological and immunohistochemical factors as angioinvasion and proliferative index assessed by Ki-67 expression, which predict biological behavior and correlate with survival.
  • Chemotherapy regimens based on the combination of several active drugs such as streptozocin, doxorubicin, 5-fluorouracil, dacarbazine, and temozolomide show low response rates, which sets the need to improve the results of the medical treatment of these malignancies.
  • [MeSH-major] Biomarkers, Tumor / analysis. Digestive System Neoplasms / diagnosis. Digestive System Neoplasms / drug therapy. Ki-67 Antigen / analysis. Neuroendocrine Tumors / diagnosis. Neuroendocrine Tumors / drug therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17639039.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen
  • [Number-of-references] 67
  •  go-up   go-down


70. Katai M, Sakurai A, Inaba H, Ikeo Y, Yamauchi K, Hashizume K: Octreotide as a rapid and effective painkiller for metastatic carcinoid tumor. Endocr J; 2005 Apr;52(2):277-80
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Octreotide as a rapid and effective painkiller for metastatic carcinoid tumor.
  • Octreotide is one of the somatostatin analogue used for the treatment of endocrine tumors principally to suppress hormone secretion and to inhibit tumor growth.
  • We experienced a case with multiple endocrine neoplasia type 1 who small amount of octreotide dramatically relieved the lumber pain caused by metastatic bone tumor.
  • He had recurrent bronchial carcinoid tumors that metastasized to liver and bones.
  • The spontaneous and radiated pain by bone tumors subsided within a few minutes after the initial injection of octreotide and the effect persisted for several hours.
  • Combination therapy of octreotide and interferon alpha-2b significantly reduced the size of metastatic liver tumors and inhibited further growth of metastatic bone tumors for the last 27 months.
  • The use of octreotide may be a good option for controlling pain by metastatic bone disease and combination therapy of octreotide and interferon alpha-2b is worth to try for patients with inoperable metastatic carcinoid tumor.
  • [MeSH-major] Analgesics / therapeutic use. Bronchial Neoplasms / physiopathology. Carcinoid Tumor / secondary. Octreotide / therapeutic use
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Back Pain / drug therapy. Bone Neoplasms / drug therapy. Bone Neoplasms / physiopathology. Bone Neoplasms / secondary. Humans. Interferon-alpha / therapeutic use. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Male. Middle Aged. Multiple Endocrine Neoplasia Type 1. Recombinant Proteins

  • Genetic Alliance. consumer health - Carcinoid Tumor.
  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15863961.001).
  • [ISSN] 0918-8959
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Analgesics; 0 / Interferon-alpha; 0 / Recombinant Proteins; 99210-65-8 / interferon alfa-2b; RWM8CCW8GP / Octreotide
  •  go-up   go-down


71. Ihtiyar E, Paşaoğlu O, Erkasap S, Karakaş BR, Yaşar FN: Perforated mixed carcinoid-adenocarcinoma in transverse colon and at gastroenterostomy site: case report. World J Surg Oncol; 2010;8:110
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Perforated mixed carcinoid-adenocarcinoma in transverse colon and at gastroenterostomy site: case report.
  • Goblet cell carcinoid of the large intestine is a rare neoplasm, usually located in ascending colon and rectum.
  • Histopathological investigation of the biopsies, taken from the gastroenterostomy site and the tumor, revealed mixed carcinoid-adenocarcinoma with carcinoid component, predominantly composed of goblet cells.
  • Our aim with this paper is to point out that more cases should be reported for more effective diagnosis, histopathological study, clinical investigation, treatment and prognosis of this specific neoplasm.
  • [MeSH-major] Carcinoid Tumor / pathology. Colonic Neoplasms / pathology. Gastroenterostomy. Intestinal Perforation / pathology
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adenocarcinoma / surgery. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colon, Transverse / pathology. Combined Modality Therapy. Fluorouracil / therapeutic use. Humans. Laparotomy. Leucovorin / therapeutic use. Male. Middle Aged. Organoplatinum Compounds / therapeutic use. Prognosis

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • Hazardous Substances Data Bank. LEUCOVORIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pathol Int. 2003 Jul;53(7):457-62 [12828611.001]
  • [Cites] Am J Surg Pathol. 1988 Aug;12(8):607-11 [3400791.001]
  • [Cites] Cancer. 1974 Aug;34(2):338-44 [4852178.001]
  • (PMID = 21176192.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Organoplatinum Compounds; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil; Adenocarcinoid tumor; Folfox protocol
  • [Other-IDs] NLM/ PMC3014938
  •  go-up   go-down


72. Tomao S, Romiti A, Spigone B, Oliveti A, Campisi C, Zullo A: [Chemotherapy in gastroenterologic neuroendocrine tumors]. Recenti Prog Med; 2001 Jun;92(6):395-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Chemotherapy in gastroenterologic neuroendocrine tumors].
  • [Transliterated title] Chemioterapia nei tumori neuroendocrini gastroenterici.
  • Gastrointestinal neuroendocrine tumors (carcinoids tumors and endocrine islet cell tumors) are a family of rare malignancies with many typical characteristics by a biologic, epidemiologic and clinical point of view.
  • In this category of neoplasia an integrated clinical and therapeutic approach is mandatory, whereas for too many years these tumors were investigated and treated in an empirical way without considering an integrated approach.
  • Chemotherapy has a marginal role in gastrointestinal neuroendocrine tumors mostly because it is used in patients with advanced disease not suitable for other therapeutic approach (surgery, thermoablation, chemoembolization, biotherapy).
  • Unfortunately in the past it was not possible to establish the efficacy of chemotherapy in these malignancies because most of the studies pooled without distinction carcinoids, pancreatic tumors and hepatic metastases from unknown primary.
  • The most extensively studied drugs have been streptozotocin, doxorubicin, mitoxantrone, dacarbazine, used alone or in combination; the gold standard today is considered the association of streptozotocin with doxorubicin or 5-fluorouracil, but there is strong evidence that the disappointing results in the treatment of these rare malignancies could be improved in a multidisciplinary fashion; in this field the combination of new drugs with aggressive surgery, radionuclide therapy, biotherapy and local therapeutic approach will give new opportunities to better control the symptoms and the clinical course of gastrointestinal neuroendocrine tumors.
  • [MeSH-major] Gastrointestinal Neoplasms / drug therapy. Neuroendocrine Tumors / drug therapy

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11433719.001).
  • [ISSN] 0034-1193
  • [Journal-full-title] Recenti progressi in medicina
  • [ISO-abbreviation] Recenti Prog Med
  • [Language] ita
  • [Publication-type] Editorial; English Abstract; Review
  • [Publication-country] Italy
  • [Number-of-references] 27
  •  go-up   go-down


73. Konturek SJ, Konturek PC, Bielański W, Lorens K, Sito E, Konturek JW, Kwiecień S, Bobrzyński A, Pawlik T, Karcz D, Areny H, Stachura T: Case presentation of gastrinoma combined with gastric carcinoid with the longest survival record -- Zollinger-Ellison syndrome: pathophysiology, diagnosis and therapy. Med Sci Monit; 2002 Jun;8(6):CS43-59
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Case presentation of gastrinoma combined with gastric carcinoid with the longest survival record -- Zollinger-Ellison syndrome: pathophysiology, diagnosis and therapy.
  • BACKGROUND: Zollinger-Ellison syndrome is a very rare disease caused by tumor with gastrin producing cells accompanied by hypergastrinemia leading to gastric hypersecretion and peptic ulcers and their complications.
  • She was also treated with many H2-receptor (R) antagonists and proton-pump inhibitors (PPI), each new drug being initially highly effective but then showing declining efficacy except when PPI, lansoprazole was used.
  • The gastrin level rose in the course of disease from initial high value of 2000 pg/mL to the extreme 4500 ng/mL at present.
  • Biopsy taken from liver metastasis showed the presence of typical gastrinoma cells with gastrin and chromogranin, while that from oxyntic mucosa revealed the ECL-cell hyperplasia with carcinoid tumors and unexpected gastric atrophy.
  • [MeSH-major] Carcinoid Tumor / complications. Gastrinoma / complications. Stomach Neoplasms / complications. Survivors. Zollinger-Ellison Syndrome / complications
  • [MeSH-minor] Adult. Anti-Ulcer Agents / therapeutic use. Female. Histamine H2 Antagonists / pharmacology. Humans

  • Genetic Alliance. consumer health - Carcinoid Syndrome.
  • Genetic Alliance. consumer health - Zollinger-Ellison syndrome.
  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Med Sci Monit. 2003 Sep;9(9):LE23 [14598848.001]
  • (PMID = 12070442.001).
  • [ISSN] 1234-1010
  • [Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research
  • [ISO-abbreviation] Med. Sci. Monit.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Anti-Ulcer Agents; 0 / Histamine H2 Antagonists
  • [Number-of-references] 129
  •  go-up   go-down


74. Toumpanakis C, Garland J, Marelli L, Srirajaskanthan R, Soh J, Davies P, Buscombe J, Caplin ME: Long-term results of patients with malignant carcinoid syndrome receiving octreotide LAR. Aliment Pharmacol Ther; 2009 Oct;30(7):733-40
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term results of patients with malignant carcinoid syndrome receiving octreotide LAR.
  • BACKGROUND: Octreotide LAR is an established treatment for malignant carcinoid syndrome.
  • AIM: To present long-terms results with octreotide LAR, assessing duration of clinical and objective response and treatment tolerance, in a large, homogeneous cohort of patients with malignant carcinoid syndrome.
  • METHODS: A total of 108 patients with metastatic midgut neuroendocrine tumours were included in this 8-year study.
  • Radiological assessment was based on RECIST (Response Evaluation Criteria In Solid Tumours) criteria.
  • Overall, in 45.3% of patients, symptoms were well controlled during the study period with only octreotide LAR, and no additional treatment was required.
  • CONCLUSIONS: Octreotide LAR treatment provides a sustained symptomatic response in about half of the patients with malignant carcinoid syndrome and contributes to disease stabilization for a longer period than previously described.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Gastrointestinal Agents / therapeutic use. Malignant Carcinoid Syndrome / drug therapy. Neuroendocrine Tumors / drug therapy. Octreotide / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Dose-Response Relationship, Drug. Epidemiologic Methods. Female. Humans. Male. Middle Aged. Time Factors. Treatment Outcome. Young Adult

  • Genetic Alliance. consumer health - Carcinoid Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19573169.001).
  • [ISSN] 1365-2036
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Gastrointestinal Agents; RWM8CCW8GP / Octreotide
  •  go-up   go-down


75. Höpfner M, Sutter AP, Gerst B, Zeitz M, Scherübl H: A novel approach in the treatment of neuroendocrine gastrointestinal tumours. Targeting the epidermal growth factor receptor by gefitinib (ZD1839). Br J Cancer; 2003 Nov 3;89(9):1766-75
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel approach in the treatment of neuroendocrine gastrointestinal tumours. Targeting the epidermal growth factor receptor by gefitinib (ZD1839).
  • Therapeutic options to inhibit the growth and spread of neuroendocrine (NE) gastrointestinal tumours are still limited.
  • Since gefitinib (4-(3-chloro-4-fluoroanilino)-7-methoxy-6-(3-morpholinopropoxy)quinazoline), an inhibitor of epidermal growth factor receptor-sensitive tyrosine kinase (EGFR-TK), had been shown to suppress potently the growth of various non-NE tumour entities, we studied the antineoplastic potency of gefitinib in NE gastrointestinal tumour cells.
  • In human insulinoma (CM) cells, in human pancreatic carcinoid (BON) cells and in NE tumour cells of the gut (STC-1), gefitinib induced a time- and dose-dependent growth inhibition by almost 100%.
  • The antiproliferative potency of gefitinib correlated with the proliferation rate of the tumour cells.
  • Our data demonstrate that the inhibition of EGFR-TK by gefitinib induces growth inhibition, apoptosis and cell-cycle arrest in NE gastrointestinal tumour cells.
  • Thus, EGFR-TK inhibition appears to be a promising novel approach for the treatment of NE tumour disease.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Carcinoma, Neuroendocrine / drug therapy. Gastrointestinal Neoplasms / drug therapy. Quinazolines / pharmacology. Receptor, Epidermal Growth Factor / drug effects
  • [MeSH-minor] Blotting, Western. Carcinoid Tumor / drug therapy. Carcinoid Tumor / genetics. Cell Cycle / drug effects. Cell Line, Tumor. Dose-Response Relationship, Drug. Fluorescent Antibody Technique. Gene Expression Regulation, Neoplastic / drug effects. Humans. Insulinoma / drug therapy. Insulinoma / genetics. Oligonucleotide Array Sequence Analysis. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / genetics. Reverse Transcriptase Polymerase Chain Reaction

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Semin Oncol. 2003 Feb;30(1 Suppl 1):3-11 [12644979.001]
  • [Cites] Acta Oncol. 1997;36(4):407-11 [9247102.001]
  • [Cites] Cancer Immunol Immunother. 2003 May;52(5):342-6 [12700950.001]
  • [Cites] J Cell Biochem. 1988 Oct;38(2):87-97 [2464605.001]
  • [Cites] Acta Oncol. 1993;32(2):115-24 [8323752.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Aug 2;91(16):7727-31 [8052651.001]
  • [Cites] Ann N Y Acad Sci. 1994 Sep 15;733:46-55 [7978895.001]
  • [Cites] Int J Cancer. 1995 Mar 3;60(5):645-51 [7860139.001]
  • [Cites] Cancer Res. 1995 Jul 15;55(14):3140-8 [7606735.001]
  • [Cites] Cancer Res. 1995 Dec 1;55(23):5536-9 [7585629.001]
  • [Cites] Gastroenterology. 1996 May;110(5):1595-604 [8613067.001]
  • [Cites] Science. 1996 May 31;272(5266):1347-9 [8650547.001]
  • [Cites] J Clin Oncol. 1996 Jun;14(6):1829-38 [8656251.001]
  • [Cites] J Exp Med. 1996 Apr 1;183(4):1533-44 [8666911.001]
  • [Cites] Recent Results Cancer Res. 1996;142:193-207 [8893342.001]
  • [Cites] Oncogene. 1997 Jul 17;15(3):285-90 [9233763.001]
  • [Cites] Clin Cancer Res. 2000 May;6(5):2053-63 [10815932.001]
  • [Cites] Cancer. 2000 Jul 1;89(1):74-82 [10897003.001]
  • [Cites] Eur J Clin Invest. 2000 Aug;30(8):729-39 [10964166.001]
  • [Cites] Oncology. 2000 Sep;59(3):229-37 [11053991.001]
  • [Cites] Clin Cancer Res. 2000 Dec;6(12):4885-92 [11156248.001]
  • [Cites] Free Radic Biol Med. 2001 Jan 15;30(2):213-21 [11163539.001]
  • [Cites] Br J Surg. 2001 Mar;88(3):412-8 [11260109.001]
  • [Cites] Brain Pathol. 2001 Jul;11(3):356-70 [11414477.001]
  • [Cites] Clin Cancer Res. 2001 Jul;7(7):1850-5 [11448895.001]
  • [Cites] J Biol Chem. 1998 May 29;273(22):13645-51 [9593703.001]
  • [Cites] J Physiol. 1998 Aug 1;510 ( Pt 3):805-14 [9660895.001]
  • [Cites] Eur J Clin Invest. 1998 Dec;28(12):1038-49 [9893017.001]
  • [Cites] Clin Cancer Res. 1997 Dec;3(12 Pt 1):2405-14 [9815641.001]
  • [Cites] J Endocrinol. 1999 Apr;161(1):59-68 [10194529.001]
  • [Cites] Curr Opin Cell Biol. 1999 Apr;11(2):190-6 [10209155.001]
  • [Cites] Pharmacol Ther. 1999 May-Jun;82(2-3):241-50 [10454201.001]
  • [Cites] Int J Colorectal Dis. 2001 Jun;16(3):154-66 [11459289.001]
  • [Cites] Cancer Res. 2001 Sep 1;61(17):6500-10 [11522647.001]
  • [Cites] Clin Cancer Res. 2001 Oct;7(10):2958-70 [11595683.001]
  • [Cites] Ann Oncol. 2001;12 Suppl 2:S111-4 [11762335.001]
  • [Cites] Br J Cancer. 2001 Nov 30;85(11):1771-80 [11742501.001]
  • [Cites] Ann Oncol. 2002 Jan;13(1):65-72 [11863114.001]
  • [Cites] Br J Cancer. 2002 Feb 12;86(4):636-44 [11870549.001]
  • [Cites] Br J Cancer. 2002 Feb 1;86(3):456-62 [11875715.001]
  • [Cites] Expert Opin Investig Drugs. 2002 Jun;11(6):837-49 [12036427.001]
  • [Cites] Life Sci. 2002 Jun 28;71(6):667-78 [12072155.001]
  • [Cites] Clin Cancer Res. 2002 Jul;8(7):2273-85 [12114431.001]
  • [Cites] J Biol Chem. 2002 Aug 2;277(31):27643-50 [12011069.001]
  • [Cites] Cancer Res. 2002 Aug 1;62(15):4300-6 [12154033.001]
  • [Cites] Oncologist. 2002;7 Suppl 4:2-8 [12202782.001]
  • [Cites] Oncologist. 2002;7 Suppl 4:31-9 [12202786.001]
  • [Cites] Int J Cancer. 2002 Sep 20;101(3):210-6 [12209970.001]
  • [Cites] Cancer Res. 2002 Sep 15;62(18):5242-7 [12234991.001]
  • [Cites] J Clin Oncol. 2002 Sep 15;20(18 Suppl):1S-13S [12235219.001]
  • [Cites] Int J Cancer. 2002 Dec 1;102(4):318-27 [12402299.001]
  • [Cites] J Clin Oncol. 2002 Nov 1;20(21):4292-302 [12409327.001]
  • [Cites] Clin Cancer Res. 2002 Nov;8(11):3438-44 [12429632.001]
  • [Cites] Int J Colorectal Dis. 2003 May;18(3):239-47 [12673490.001]
  • (PMID = 14583782.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
  • [Other-IDs] NLM/ PMC2394425
  •  go-up   go-down


76. Keltner JR, Donegan E, Hynson JM, Shapiro WA: Acute renal failure after radiofrequency liver ablation of metastatic carcinoid tumor. Anesth Analg; 2001 Sep;93(3):587-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute renal failure after radiofrequency liver ablation of metastatic carcinoid tumor.
  • IMPLICATIONS: We report a case of prolonged radiofrequency liver ablation for metastatic carcinoid tumor complicated by hemolysis, rhabdomyolysis, and transient acute renal failure.
  • Brief radiofrequency liver ablation procedures or those for a small number of tumor sites are not associated with these complications.
  • [MeSH-major] Acute Kidney Injury / etiology. Carcinoid Tumor / secondary. Carcinoid Tumor / surgery. Catheter Ablation / adverse effects. Kidney Neoplasms / secondary. Kidney Neoplasms / surgery
  • [MeSH-minor] Blood Pressure / drug effects. Electrocardiography. Humans. Laparoscopy. Male. Middle Aged. Neoplasm Metastasis

  • Genetic Alliance. consumer health - Carcinoid Tumor.
  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11524322.001).
  • [ISSN] 0003-2999
  • [Journal-full-title] Anesthesia and analgesia
  • [ISO-abbreviation] Anesth. Analg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


77. Izikson L, English JC 3rd, Zirwas MJ: The flushing patient: differential diagnosis, workup, and treatment. J Am Acad Dermatol; 2006 Aug;55(2):193-208
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In particular, the serious diagnoses of carcinoid syndrome, pheochromocytoma, mastocytosis, and anaphylaxis need to be excluded by laboratory studies.
  • If this work-up is unrevealing, rare causes, such as medullary carcinoma of the thyroid, pancreatic cell tumor, renal carcinoma, and others, should be considered.
  • [MeSH-minor] Alcohol Drinking. Diagnosis, Differential. Drug Eruptions. Humans. Menopause. Mental Disorders / complications. Nervous System Diseases / complications. Nervous System Diseases / diagnosis

  • MedlinePlus Health Information. consumer health - Rosacea.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16844500.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 101
  •  go-up   go-down


78. Merola E, Capurso G, Campana D, Panzuto F, Monarca B, Tomassetti P, Delle Fave G: Acute leukaemia following low dose peptide receptor radionuclide therapy for an intestinal carcinoid. Dig Liver Dis; 2010 Jun;42(6):457-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute leukaemia following low dose peptide receptor radionuclide therapy for an intestinal carcinoid.
  • [MeSH-major] Carcinoid Tumor / radiotherapy. Ileal Neoplasms / radiotherapy. Octreotide / analogs & derivatives. Precursor Cell Lymphoblastic Leukemia-Lymphoma / chemically induced. Receptors, Peptide
  • [MeSH-minor] Aged. Dose-Response Relationship, Drug. Follow-Up Studies. Humans. Male. Tomography, X-Ray Computed. Yttrium Radioisotopes

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • MedlinePlus Health Information. consumer health - Intestinal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19783489.001).
  • [ISSN] 1878-3562
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / 90Y-octreotide, DOTA-Tyr(3)-; 0 / Receptors, Peptide; 0 / Yttrium Radioisotopes; RWM8CCW8GP / Octreotide
  •  go-up   go-down


79. Savelli G, Lucignani G, Seregni E, Marchianò A, Serafini G, Aliberti G, Villano C, Maccauro M, Bombardieri E: Feasibility of somatostatin receptor scintigraphy in the detection of occult primary gastro-entero-pancreatic (GEP) neuroendocrine tumours. Nucl Med Commun; 2004 May;25(5):445-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Feasibility of somatostatin receptor scintigraphy in the detection of occult primary gastro-entero-pancreatic (GEP) neuroendocrine tumours.
  • From 1996 to 2000, 36 patients were referred with gastro-entero-pancreatic (GEP) neuroendocrine tumours.
  • In these patients, no clinical, radiological or endoscopic diagnostic modalities had been able to identify the primary tumour.
  • Of the others, one had skin and one had lymph node metastases, three had diffuse metastatic involvement and two had carcinoid syndrome.
  • In the remaining six patients, the final diagnosis was reached after at least 2 years of follow-up by means of clinical, radiological and/or nuclear medicine findings.
  • However, the most important finding was that SRS prompted surgical management in 17% of cases.
  • [MeSH-major] Digestive System Neoplasms / radionuclide imaging. Neoplasms, Unknown Primary / radionuclide imaging. Neuroendocrine Tumors / radionuclide imaging. Receptors, Somatostatin / metabolism. Somatostatin / analogs & derivatives

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15100502.001).
  • [ISSN] 0143-3636
  • [Journal-full-title] Nuclear medicine communications
  • [ISO-abbreviation] Nucl Med Commun
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin; G083B71P98 / pentetreotide
  •  go-up   go-down


80. Pittock SJ, Lennon VA: Aquaporin-4 autoantibodies in a paraneoplastic context. Arch Neurol; 2008 May;65(5):629-32
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • SETTING: Neuroimmunology Laboratory and Neurology Clinical Practice, Mayo Clinic College of Medicine.
  • (1) 31 patients (88% female) identified incidentally among 180 000 patients evaluated for paraneoplastic autoantibodies and (2) 141 patients identified through physician-requested serological evaluation for a suspected NMO-spectrum disorder.
  • An NMO-spectrum disorder was diagnosed in 26 patients (93%), of whom 6 had a neoplasm (5 carcinomas [2 breast, 1 lung, 1 thymic, and 1 uterine cervical] and 1 B-cell lymphoma) and 1 had monoclonal gammopathy.
  • Two patients had carcinoma (1 breast and 1 lung) without neurological evidence of an NMO-spectrum disorder.
  • In the second group, neoplasms were recorded in 7 seropositive patients (5.0%) with a clinically diagnosed NMO-spectrum disorder: 3 carcinomas (all breast), 1 thyroid Hürthle cell, 1 carcinoid, 1 pituitary somatotropinoma, and 1 B-cell lymphoma.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Arch Neurol. 2008 Oct;65(10):1394
  • (PMID = 18474738.001).
  • [ISSN] 1538-3687
  • [Journal-full-title] Archives of neurology
  • [ISO-abbreviation] Arch. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aquaporin 4; 0 / Autoantibodies; 0 / Biomarkers; 0 / Immunoglobulin G
  •  go-up   go-down


81. Turan M, Karadayi K, Duman M, Ozer H, Arici S, Yildirir C, Koçak O, Sen M: Small bowel tumors in emergency surgery. Ulus Travma Acil Cerrahi Derg; 2010 Jul;16(4):327-33
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Small bowel tumors in emergency surgery.
  • BACKGROUND: The aim of the present study was to describe the clinical presentation, diagnostic work-up, surgical therapy, and prognosis of 13 patients with small bowel tumor admitted for surgical procedures in an emergency setting.
  • METHODS: From 1996 to 2008, 13 consecutive surgical cases of small bowel tumors were treated at the Cumhuriyet University Faculty of Medicine, Department of General Surgery, and Kütahya State Hospital, Department of General Surgery.
  • Adenocarcinoma was the most frequent histologic type (4 cases), while small bowel sarcoma was seen in three cases and non-Hodgkin lymphoma in two cases.
  • The remaining cases had carcinoid tumor, small bowel angioleiomyoma, Brunner's gland adenoma, and inflammatory pseudotumor of the small intestine.
  • CONCLUSION: Small bowel tumors are rare, the symptoms often non-specific, and the accuracy of different diagnostic tests remains to be improved.
  • Timing and type of the intervention to the process and biological behavior of the pathological cells predict the prognosis.

  • MedlinePlus Health Information. consumer health - Surgery.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20849049.001).
  • [ISSN] 1306-696X
  • [Journal-full-title] Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES
  • [ISO-abbreviation] Ulus Travma Acil Cerrahi Derg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
  •  go-up   go-down


82. Coleman RE, Stubbs JB, Barrett JA, de la Guardia M, Lafrance N, Babich JW: Radiation dosimetry, pharmacokinetics, and safety of ultratrace Iobenguane I-131 in patients with malignant pheochromocytoma/paraganglioma or metastatic carcinoid. Cancer Biother Radiopharm; 2009 Aug;24(4):469-75
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radiation dosimetry, pharmacokinetics, and safety of ultratrace Iobenguane I-131 in patients with malignant pheochromocytoma/paraganglioma or metastatic carcinoid.
  • This is a first of many phase 1 study of Ultratrace Iobenguane I-131 (Ultratrace 131I-MIBG; Molecular Insight Pharmaceuticals, Inc., Cambridge, MA).
  • We investigated the pharmacokinetics (PK), radiation dosimetry, and clinical safety in 11 patients with confirmed pheochromocytoma/paraganglioma (Pheo) or carcinoid tumors.
  • For a therapeutic administration of 500 mCi (18.5 GBq), our estimate of the projected dose is 1.4 Gy for marrow and 10.4 Gy for kidneys.
  • Safety results showed 12 mild adverse events, all considered unrelated to study drug, in 8 of 11 patients.
  • These findings support the further development of Ultratrace 131I-MIBG for the treatment of neuroendocrine tumors, such as metastatic Pheo and carcinoid.

  • Genetic Alliance. consumer health - Pheochromocytoma.
  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • MedlinePlus Health Information. consumer health - Pheochromocytoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19694582.001).
  • [ISSN] 1557-8852
  • [Journal-full-title] Cancer biotherapy & radiopharmaceuticals
  • [ISO-abbreviation] Cancer Biother. Radiopharm.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Iodine Radioisotopes; 0 / Radiopharmaceuticals; 35MRW7B4AD / 3-Iodobenzylguanidine
  •  go-up   go-down


83. Strosberg JR, Coppola D, Klimstra DS, Phan AT, Kulke MH, Wiseman GA, Kvols LK, North American Neuroendocrine Tumor Society (NANETS): The NANETS consensus guidelines for the diagnosis and management of poorly differentiated (high-grade) extrapulmonary neuroendocrine carcinomas. Pancreas; 2010 Aug;39(6):799-800
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The NANETS consensus guidelines for the diagnosis and management of poorly differentiated (high-grade) extrapulmonary neuroendocrine carcinomas.
  • Extrapulmonary poorly differentiated neuroendocrine carcinomas can originate in the gastrointestinal tract, bladder, cervix, and prostate.
  • They are infrequently associated with secretory hormonal syndromes (such as the carcinoid syndrome) and rarely express somatostatin receptors.Most poorly differentiated neuroendocrine carcinomas are locally advanced or metastatic at presentation.
  • First-line systemic chemotherapy with a platinum agent (cisplatin or carboplatin) and etoposide is recommended for most patients with metastatic-stage disease; however, response durations are often short.
  • Sequential or concurrent chemoradiation is recommended for patients with loco-regional disease.
  • In patients with localized tumors undergoing surgical resection, adjuvant treatment (chemotherapy with or without radiation) is warranted in most cases.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2002 Jul 15;20(14):3054-60 [12118018.001]
  • [Cites] Br J Cancer. 1999 Dec;81(8):1351-5 [10604732.001]
  • [Cites] Br J Cancer. 2004 May 4;90(9):1720-6 [15150595.001]
  • [Cites] Cancer. 1991 Jul 15;68(2):227-32 [1712661.001]
  • [Cites] Virchows Arch. 1995;425(6):547-60 [7697211.001]
  • [Cites] World J Surg. 1996 Feb;20(2):132-41 [8661808.001]
  • [Cites] Ann Oncol. 1996 Apr;7(4):365-71 [8805928.001]
  • [Cites] Cancer. 1997 Oct 15;80(8):1366-72 [9338459.001]
  • [Cites] J Clin Oncol. 2006 May 1;24(13):2038-43 [16648503.001]
  • [Cites] J Clin Oncol. 2006 Dec 1;24(34):5441-7 [17135646.001]
  • [Cites] Cancer. 2007 Sep 1;110(5):1068-76 [17614337.001]
  • [Cites] Am J Surg Pathol. 2008 May;32(5):719-31 [18360283.001]
  • [Cites] J Clin Oncol. 2008 Jun 20;26(18):3063-72 [18565894.001]
  • [Cites] Cancer Treat Rev. 2009 May;35(3):228-36 [19068273.001]
  • [Cites] Hum Pathol. 2009 Sep;40(9):1262-8 [19368957.001]
  • [Cites] BMC Cancer. 2001;1:5 [11432756.001]
  • (PMID = 20664477.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA093401-05; United States / NCI NIH HHS / CA / CA093401-01A2; United States / NCI NIH HHS / CA / K23 CA093401-01A2; United States / NCI NIH HHS / CA / K23 CA093401-04; United States / NCI NIH HHS / CA / CA093401-03; United States / NCI NIH HHS / CA / K23 CA093401-02; United States / NCI NIH HHS / CA / CA093401-02; United States / NCI NIH HHS / CA / CA093401-04; United States / NCI NIH HHS / CA / K23 CA093401; United States / NCI NIH HHS / CA / K23 CA093401-03; United States / NCI NIH HHS / CA / K23 CA093401-05
  • [Publication-type] Consensus Development Conference; Journal Article; Practice Guideline
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS286321; NLM/ PMC3100733
  •  go-up   go-down


84. Filosso PL, Ruffini E, Oliaro A, Papalia E, Donati G, Rena O: Long-term survival of atypical bronchial carcinoids with liver metastases, treated with octreotide. Eur J Cardiothorac Surg; 2002 May;21(5):913-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term survival of atypical bronchial carcinoids with liver metastases, treated with octreotide.
  • OBJECTIVE: To demonstrate that liver metastases by radically resected atypical carcinoids of the lung can be effectively treated by new somatostatin analogs.
  • METHODS: Between January 1977 and December 1999, 126 patients affected by bronchial carcinoids were submitted to a radical resection of the lung.
  • Seven of them (5.5%) presented liver metastases 27, 22, 14, 18, 16, 12 and 9 months after surgery: carcinoid syndrome (CS) was ever present.
  • The patients are alive and well at 51, 36, 24, 24, 23, 19, and 16 months after the diagnosis of the metastases, respectively.
  • CONCLUSIONS: Octreotide is effective in controlling symptoms of CS of patients with liver metastases of resected atypical bronchial carcinoid.
  • The efficacy of the drug is due to the presence of sst2 somatostatin receptors in the pathologic tissue, as demonstrated by PCR method.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Bronchial Neoplasms / pathology. Carcinoid Tumor / drug therapy. Liver Neoplasms / drug therapy. Octreotide / therapeutic use

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12062286.001).
  • [ISSN] 1010-7940
  • [Journal-full-title] European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery
  • [ISO-abbreviation] Eur J Cardiothorac Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 51110-01-1 / Somatostatin; G083B71P98 / pentetreotide; RWM8CCW8GP / Octreotide
  •  go-up   go-down


85. Kim BW, Lee BI, Kim HK, Cho YS, Chae HS, Lee HK, Kim HJ, Han SW: [Influence of long-term gastric acid suppression therapy on the expression of serum gastrin, chromogranin A, and ghrelin]. Korean J Gastroenterol; 2009 Feb;53(2):84-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Hypergastrinemia causes enterochromaffin-like (ECL) cell hyperplasia, which is a predisposing factor of carcinoid tumor of stomach.
  • METHODS: Control group included patients who had no medication over six months.
  • Both H(2)RA (H(2) receptor antagonist) and PPI groups had medication at least for six months.
  • [MeSH-major] Anti-Ulcer Agents / therapeutic use. Chromogranin A / blood. Gastrins / blood. Ghrelin / blood. Histamine H2 Antagonists / therapeutic use. Proton Pump Inhibitors / therapeutic use

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Korean J Gastroenterol. 2009 Feb;53(2):126-8 [19237840.001]
  • (PMID = 19237833.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] Controlled Clinical Trial; English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Anti-Ulcer Agents; 0 / Chromogranin A; 0 / Gastrins; 0 / Ghrelin; 0 / Histamine H2 Antagonists; 0 / Proton Pump Inhibitors
  •  go-up   go-down


86. Karhoff D, Sauer S, Schrader J, Arnold R, Fendrich V, Bartsch DK, Hörsch D: Rap1/B-Raf signaling is activated in neuroendocrine tumors of the digestive tract and Raf kinase inhibition constitutes a putative therapeutic target. Neuroendocrinology; 2007;85(1):45-53
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rap1/B-Raf signaling is activated in neuroendocrine tumors of the digestive tract and Raf kinase inhibition constitutes a putative therapeutic target.
  • OBJECTIVE: Molecular pathogenesis of digestive neuroendocrine tumors (dNETs) is largely unknown.
  • Recently, the serine-threonine kinase B-Raf was identified as an oncogene in endocrine cancer such as thyroid carcinoma.
  • In endocrine cells, the small G-protein Rap1 stimulates mitogen-activated protein kinase (MAPK) signaling by activating B-Raf.
  • METHODS AND RESULTS: Expression of Rap1 and B-Raf in dNETs (19 insulinomas, 15 carcinoid tumors and 10 gastrinomas) was examined by immunohistochemistry, which revealed that Rap1 and B-Raf were highly prevalent in the majority of dNETs.
  • [MeSH-major] Digestive System Neoplasms / metabolism. Neuroendocrine Tumors / metabolism. Proto-Oncogene Proteins B-raf / metabolism. Signal Transduction / physiology. raf Kinases / physiology. rap1 GTP-Binding Proteins / metabolism
  • [MeSH-minor] Benzenesulfonates / pharmacology. Dose-Response Relationship, Drug. Enzyme Activation / drug effects. Enzyme Activation / physiology. Enzyme Inhibitors / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / physiology. Humans. Immunohistochemistry. Niacinamide / analogs & derivatives. Phenylurea Compounds. Pyridines / pharmacology. Tetrazolium Salts. Thiazoles


87. Watanabe T, Ohshima N, Shirai T, Someya T: [Surgical treatment of carcinoid heart disease]. Kyobu Geka; 2010 Oct;63(11):999-1003
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Surgical treatment of carcinoid heart disease].
  • The liver biopsy revealed metastatic carcinoid disease, which was thought as an etiology in severe tricuspid regurgitation and stenosis.
  • We administered long acting somatostatin analog, octreotide to control carcinoid symptoms.
  • After improvement of general condition, she successfully underwent bioprosthetic valve replacement with concomitant octreotide administration.
  • Cardiac surgery for carcinoid heart disease is complicated by hemodynamic instability secondary to carcinoid crises which can be provoked pharmacologically by administration of vasoactive medications.
  • Octreotide is an effective tool to manage manifestation of carcinoid activity.
  • We could performed surgical treatment of carcinoid heart disease safely in the perioperative presence of octreotide.
  • [MeSH-major] Carcinoid Heart Disease / surgery

  • Genetic Alliance. consumer health - Heart Disease.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20954358.001).
  • [ISSN] 0021-5252
  • [Journal-full-title] Kyobu geka. The Japanese journal of thoracic surgery
  • [ISO-abbreviation] Kyobu Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


88. Namasivayam S, Martin DR, Saini S: Imaging of liver metastases: MRI. Cancer Imaging; 2007;7:2-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Specific characterization of liver metastases in patients with primary non-hepatic tumors is crucial to avoid unnecessary diagnostic work-up for incidental benign liver lesions.
  • MR contrast agents provide critical tumor characterization and can be safely used in patients with iodine contrast allergy and renal failure.
  • Other agents, including newly developing gadolinium-chelates or iron oxide agents may provide additional benefits in selected applications.
  • The degree and nature of tumor vascularity form the basis for liver lesion characterization based on enhancement properties.
  • Colon, lung, breast and gastric carcinomas are the most common tumors causing hypovascular liver metastases, and typically show perilesional enhancement.
  • Neuroendocrine tumors including carcinoid and islet cell tumors, renal cell carcinoma, breast, melanoma, and thyroid carcinoma are tumors most commonly causing hypervascular hepatic metastases, which may develop early enhancement with variable degrees of washout and peripheral rim enhancement.

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • MedlinePlus Health Information. consumer health - MRI Scans.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] AJR Am J Roentgenol. 1995 Dec;165(6):1407-13 [7484575.001]
  • [Cites] Radiology. 1995 Aug;196(2):471-8 [7617863.001]
  • [Cites] Radiology. 1996 Mar;198(3):881-7 [8628887.001]
  • [Cites] Radiology. 1996 May;199(2):513-20 [8668804.001]
  • [Cites] Radiology. 1996 Jul;200(1):59-67 [8657946.001]
  • [Cites] Radiology. 1996 Sep;200(3):785-92 [8756932.001]
  • [Cites] J Magn Reson Imaging. 1996 Mar-Apr;6(2):291-4 [9132092.001]
  • [Cites] Eur Radiol. 1997;7(2):275-80 [9038130.001]
  • [Cites] Radiology. 1997 May;203(2):449-56 [9114103.001]
  • [Cites] Acta Radiol. 1997 Jul;38(4 Pt 2):626-30 [9245955.001]
  • [Cites] Acta Radiol. 1997 Jul;38(4 Pt 2):631-7 [9245956.001]
  • [Cites] Radiol Clin North Am. 1998 Mar;36(2):287-97 [9520982.001]
  • [Cites] Magn Reson Imaging Clin N Am. 2005 May;13(2):241-54, v-vi [15935310.001]
  • [Cites] Radiol Clin North Am. 2005 Sep;43(5):861-86, viii [16098344.001]
  • [Cites] Cancer Imaging. 2005;5 Spec No A:S149-56 [16361131.001]
  • [Cites] AJR Am J Roentgenol. 2006 Apr;186(4):1051-8 [16554578.001]
  • [Cites] Radiology. 2006 Apr;239(1):122-30 [16493012.001]
  • [Cites] Eur Radiol. 2006 Jun;16(6):1337-45 [16453115.001]
  • [Cites] Cancer Imaging. 2006;6:33-42 [16766267.001]
  • [Cites] Eur Radiol. 2006 Sep;16(9):1898-905 [16691378.001]
  • [Cites] Radiology. 1999 Oct;213(1):86-91 [10540645.001]
  • [Cites] Radiology. 2000 Apr;215(1):89-94 [10751472.001]
  • [Cites] Magn Reson Imaging Clin N Am. 2000 Nov;8(4):741-56 [11149677.001]
  • [Cites] Clin Liver Dis. 2002 Feb;6(1):73-90 [11933597.001]
  • [Cites] Clin Liver Dis. 2002 Feb;6(1):165-79, vii [11933587.001]
  • [Cites] AJR Am J Roentgenol. 1988 Jul;151(1):79-84 [3259825.001]
  • [Cites] Radiology. 1992 Jan;182(1):167-74 [1309218.001]
  • [Cites] J Comput Assist Tomogr. 1993 Jan-Feb;17(1):67-74 [8419443.001]
  • [Cites] Radiology. 1994 Dec;193(3):657-63 [7972804.001]
  • [Cites] Radiology. 1995 Dec;197(3):575-7 [7480718.001]
  • (PMID = 17293303.001).
  • [ISSN] 1470-7330
  • [Journal-full-title] Cancer imaging : the official publication of the International Cancer Imaging Society
  • [ISO-abbreviation] Cancer Imaging
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Contrast Media
  • [Number-of-references] 31
  • [Other-IDs] NLM/ PMC1804118
  •  go-up   go-down


89. Craige H, Cohen JB: Symptomatic treatment of idiopathic and rosacea-associated cutaneous flushing with propranolol. J Am Acad Dermatol; 2005 Nov;53(5):881-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Flushing has been associated with medications, rosacea, menopause, carcinoid syndrome, pheochromocytoma, polycythemia, and mastocytosis, although it can occur without known cause.
  • [MeSH-major] Adrenergic beta-Antagonists / therapeutic use. Flushing / drug therapy. Propranolol / therapeutic use. Rosacea / complications

  • MedlinePlus Health Information. consumer health - Rosacea.
  • Hazardous Substances Data Bank. PROPRANOLOL HYDROCHLORIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16243148.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic beta-Antagonists; 9Y8NXQ24VQ / Propranolol
  •  go-up   go-down


90. Ketai L, Hartshorne M: Potential uses of computed tomography-SPECT and computed tomography-coincidence fusion images of the chest. Clin Nucl Med; 2001 May;26(5):433-41
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The ability to fuse (or merge) data sets from SPECT and coincidence nuclear medicine scans with computed tomographic images combines physiologic information from the former method with the superior anatomic resolution of the latter technique.
  • In many cases, this allows more definitive diagnosis than can be obtained by simple visual comparison of nuclear medicine images and conventional cross-sectional imaging.
  • The technique may be used in the staging and follow-up of lung carcinoma, pulmonary carcinoid, and lymphoma.
  • In this nuclear medicine atlas, the method used to create fusion images in the chest is described, and examples of fusion imaging with radiopharmaceuticals are given that may be of clinical use in chest disease.

  • MedlinePlus Health Information. consumer health - Chest Injuries and Disorders.
  • MedlinePlus Health Information. consumer health - CT Scans.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11317024.001).
  • [ISSN] 0363-9762
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals
  • [Number-of-references] 28
  •  go-up   go-down


91. Williams S, Palmer D, Johnson P: New medical options for liver tumours. Clin Med (Lond); 2007 Aug;7(4):351-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New medical options for liver tumours.
  • Significant progress is being made in the prevention of hepatitis B-related hepatocellular carcinoma (HCC) but hepatitis C-related HCC is increasing in the West and therapeutic advances in established disease have been modest.
  • Although ablative therapies, including surgical resection, seem effective in patients with small tumours these only represent a minority of patients.
  • For the majority with advanced disease there is some evidence for survival benefit for transarterial chemoembolisation but only in very carefully selected patients.
  • Survival has increased from around six months to almost two years with the introduction of new cytotoxic agents, irinotecan and oxaliplatin.
  • Somatostatin analogues have had a dramatic impact on the symptomatic control of neuroendocrine tumours, metastatic to the liver that result in the carcinoid syndrome.
  • [MeSH-major] Diffusion of Innovation. Liver Neoplasms / drug therapy
  • [MeSH-minor] Great Britain. Hormones / therapeutic use. Humans. Interferons / therapeutic use. Neoplasm Metastasis. Palliative Care. State Medicine. Survivors

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17882851.001).
  • [ISSN] 1470-2118
  • [Journal-full-title] Clinical medicine (London, England)
  • [ISO-abbreviation] Clin Med (Lond)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hormones; 9008-11-1 / Interferons
  •  go-up   go-down


92. Sathyanarayana UG, Toyooka S, Padar A, Takahashi T, Brambilla E, Minna JD, Gazdar AF: Epigenetic inactivation of laminin-5-encoding genes in lung cancers. Clin Cancer Res; 2003 Jul;9(7):2665-72
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: We investigated the loss of expression of three laminin-5 (LN5)-encoding genes in lung cancer cell lines and elucidated the mechanism of inactivation of the genes in lung cancer cell lines and tumors.
  • To elucidate the mechanism of gene silencing, we treated expression-negative cell lines (two for each gene) with a demethylating agent and examined the restoration of expression by reverse transcription-PCR.
  • We further studied the methylation patterns of primary non-small cell lung cancer [NSCLC (n = 36)], small cell lung cancer [SCLC (n = 26)], and carcinoids (n = 24) tumors.
  • Treatment of expression-negative cell lines with demethylating agent restored expression in all of the cases.
  • Methylation was more frequent in SCLC tumors (58-77%) than in NSCLC tumors (22-42%) and carcinoids (13-33%), and at least one gene was methylated in 92% of SCLC tumors, 47% of NSCLC tumors, and 33% of carcinoids.
  • CONCLUSIONS: Our results demonstrate frequent epigenetic inactivation of LN5-encoding genes in lung cancers, and these findings are of biological interest and are potentially of clinical importance.
  • [MeSH-minor] Carcinoid Tumor / genetics. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Small Cell / genetics. Cell Line, Tumor. CpG Islands. DNA / metabolism. DNA Methylation. Humans. Laminin / biosynthesis. Lymphocytes / metabolism. Methylation. Models, Genetic. Mouth Mucosa / metabolism. Promoter Regions, Genetic. Reverse Transcriptase Polymerase Chain Reaction. Sequence Analysis, DNA. Sulfites / metabolism. Transcription, Genetic. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12855645.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5U01CA8497102
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / LAMC2 protein, human; 0 / Laminin; 0 / Sulfites; 0 / kalinin; 170834-93-2 / laminin alpha 3; 776B62CQ27 / decitabine; 9007-49-2 / DNA; M801H13NRU / Azacitidine
  •  go-up   go-down


93. Adam P, Gernert C, Schmitt S, Haralambieva E, Ott G, Müller-Hermelink HK, Hentschel U: [The spectrum of microbiological agents causing pulmonary MALT-type lymphomas. A 16S rRNA-based analysis of microbial diversity]. Pathologe; 2008 Nov;29 Suppl 2:290-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The spectrum of microbiological agents causing pulmonary MALT-type lymphomas. A 16S rRNA-based analysis of microbial diversity].
  • For several anatomical localisations of extranodal marginal zone B-cell lymphoma of MALT type (eMZBCL), an association with chronic inflammation caused by microbiological agents (e.g.
  • A comprehensive diversity survey using 16S-rDNA library construction followed by restriction fragment length polymorphism (RFLP) analysis, sequencing, and phylogenetic tree construction was employed for nine cases each of BALT lymphoma and control lung tissues (normal foetal lung, pneumonitis, carcinoid).
  • 16S-rDNA library construction in combination with RFLP screening and phylogenetic analyses, hereafter described as SHARP screening, is a cultivation-independent tool for analysing the microbial environment in chronic inflammation processes giving rise to extranodal marginal zone B-cell lymphomas of MALT-type.

  • MedlinePlus Health Information. consumer health - Bacterial Infections.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nucleic Acids Res. 2004 Feb 25;32(4):1363-71 [14985472.001]
  • [Cites] Appl Environ Microbiol. 2002 Sep;68(9):4431-40 [12200297.001]
  • [Cites] J Bacteriol. 1998 Sep;180(18):4765-74 [9733676.001]
  • [Cites] J Cyst Fibros. 2007 Jan;6(1):75-8 [16793350.001]
  • [Cites] J Cutan Pathol. 1997 Sep;24(8):457-61 [9331890.001]
  • [Cites] J Natl Cancer Inst. 2004 Apr 21;96(8):586-94 [15100336.001]
  • [Cites] Nucleic Acids Res. 1997 Dec 15;25(24):4876-82 [9396791.001]
  • [Cites] Microbiol Rev. 1995 Mar;59(1):143-69 [7535888.001]
  • [Cites] N Engl J Med. 2004 Jan 15;350(3):213-5 [14724298.001]
  • [Cites] J Clin Microbiol. 1987 Oct;25(10):1952-5 [3667915.001]
  • [Cites] Science. 1997 May 2;276(5313):734-40 [9115194.001]
  • [Cites] J Pathol. 2006 Jul;209(3):344-51 [16583361.001]
  • [Cites] Important Adv Oncol. 1996;:111-21 [8791131.001]
  • [Cites] Pathologe. 2007 Feb;28(1):6-14 [17211669.001]
  • [Cites] Cancer. 1983 Oct 15;52(8):1410-6 [6193858.001]
  • (PMID = 18854998.001).
  • [ISSN] 1432-1963
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / DNA, Ribosomal; 0 / RNA, Ribosomal, 16S
  •  go-up   go-down


94. Waldum HL, Gustafsson B, Fossmark R, Qvigstad G: Antiulcer drugs and gastric cancer. Dig Dis Sci; 2005 Oct;50 Suppl 1:S39-44
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antiulcer drugs and gastric cancer.
  • Inhibitors of gastric acid secretion are efficient drugs in the treatment of acid-related diseases.
  • Long-term hypergastrinemia in whatever species studied, has been shown to induce tumors originating from the ECL cell.
  • In man, at least 10 years of hypergastrinemia, accompanied by high or reduced gastric acidity is necessary to induce ECL cell carcinoids.
  • There are reports indicating development of ECL cell carcinoids after long-term treatment with proton pump inhibitors.
  • Moreover, the ECL cell may give rise to gastric carcinomas of diffuse type, which have increased during the last decades.
  • [MeSH-major] Anti-Ulcer Agents / adverse effects. Anti-Ulcer Agents / therapeutic use. Carcinoma / chemically induced. Gastrins / adverse effects. Stomach Neoplasms / chemically induced
  • [MeSH-minor] Drug Administration Schedule. Enterochromaffin Cells / physiology. Gastric Acid / secretion. Humans

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Natl Cancer Inst. 1983 Sep;71(3):629-47 [6350677.001]
  • [Cites] APMIS. 2002 Feb;110(2):132-9 [12064868.001]
  • [Cites] J Gastroenterol. 1999 Aug;34(4):450-4 [10452676.001]
  • [Cites] J Natl Cancer Inst. 1972 Oct;49(4):969-88 [4678140.001]
  • [Cites] Carcinogenesis. 1996 Oct;17(10):2153-5 [8895482.001]
  • [Cites] Histochem J. 2000 Sep;32(9):551-6 [11127976.001]
  • [Cites] Aliment Pharmacol Ther. 2000 Jan;14(1):15-22 [10632641.001]
  • [Cites] Arch Pathol Lab Med. 2004 Jul;128(7):765-70 [15214826.001]
  • [Cites] Gastroenterology. 1994 Apr;106(4):907-15 [7848395.001]
  • [Cites] Basic Clin Pharmacol Toxicol. 2005 Feb;96(2):94-102 [15679471.001]
  • [Cites] Aliment Pharmacol Ther. 1998 Jul;12(7):605-12 [9701523.001]
  • [Cites] Acta Pathol Microbiol Scand. 1965;64:31-49 [14320675.001]
  • [Cites] Digestion. 1990;45(4):189-95 [2401393.001]
  • [Cites] Yale J Biol Med. 1998 May-Aug;71(3-4):325-35 [10461363.001]
  • [Cites] Cancer. 1993 Feb 1;71(3):745-50 [8431855.001]
  • [Cites] Gastroenterology. 2000 Jan;118(1):36-47 [10611152.001]
  • [Cites] Scand J Gastroenterol. 1986 Jan;21(1):16-20 [3952447.001]
  • [Cites] Scand J Gastroenterol. 2001 Nov;36(11):1128-33 [11686210.001]
  • [Cites] Surg Oncol. 2003 Aug;12(2):153-72 [12946486.001]
  • [Cites] Gastroenterology. 1999 Jun;116(6):1310-8 [10348814.001]
  • [Cites] Gut. 1992 Sep;33(9):1275-9 [1358767.001]
  • [Cites] Gut. 1994 Feb;35(2):275-7 [8307483.001]
  • [Cites] Cancer Res. 2004 May 15;64(10):3687-93 [15150129.001]
  • [Cites] Dig Dis Sci. 1998 Feb;43(2):253-7 [9512115.001]
  • [Cites] Lancet. 1993 May 29;341(8857):1359-62 [8098787.001]
  • [Cites] Expert Opin Drug Saf. 2002 May;1(1):29-38 [12904157.001]
  • [Cites] N Engl J Med. 1996 Jul 25;335(4):242-9 [8657240.001]
  • [Cites] Gut. 1996 Nov;39(5):649-53 [9026477.001]
  • [Cites] Am J Gastroenterol. 2003 Nov;98(11):2409-14 [14638341.001]
  • [Cites] Dig Dis Sci. 1995 Jun;40(6):1275-8 [7781446.001]
  • [Cites] N Engl J Med. 1971 Feb 25;284(8):408-12 [5540478.001]
  • [Cites] BMJ. 1989 Dec 16;299(6714):1504-5 [2514864.001]
  • [Cites] Acta Physiol Scand. 1976 Aug;97(4):401-14 [184683.001]
  • [Cites] Digestion. 1988;39(2):126-35 [3410169.001]
  • [Cites] N Engl J Med. 1955 Jun 30;252(26):1103-10 [14383972.001]
  • [Cites] Cancer Res. 1992 Dec 15;52(24):6735-40 [1458460.001]
  • [Cites] Aliment Pharmacol Ther. 1990;4 Suppl 1:47-63 [1983346.001]
  • [Cites] Gastroenterology. 1997 Jul;113(1):15-24 [9207257.001]
  • [Cites] Aliment Pharmacol Ther. 1997 Dec;11(6):1013-8 [9663823.001]
  • [Cites] Gastroenterology. 1969 Aug;57(2):147-55 [5799673.001]
  • [Cites] Gut. 1985 Dec;26(12):1284-95 [2867954.001]
  • [Cites] Gastroenterology. 1973 Mar;64(3):421-8 [4691592.001]
  • [Cites] Toxicol Pathol. 1989;17(1 Pt 1):7-15 [2501865.001]
  • [Cites] Lancet. 1978 Feb 25;1(8061):403-7 [75439.001]
  • [Cites] Carcinogenesis. 2003 Dec;24(12):1887-96 [12949047.001]
  • [Cites] Arch Intern Med. 1995 Jul 24;155(14):1465-71 [7605147.001]
  • [Cites] Gut. 1993 Jul;34(7):888-92 [8344574.001]
  • [Cites] Gastroenterology. 1987 Apr;92(4):944-9 [3557000.001]
  • [Cites] Gut. 1993 Aug;34(8):1032-7 [8174948.001]
  • [Cites] Scand J Gastroenterol. 1998 Jan;33(1):88-92 [9489914.001]
  • [Cites] J Natl Cancer Inst. 1995 Dec 6;87(23):1731-2 [7473824.001]
  • [Cites] Gut. 2005 Apr;54(4):566 [15753549.001]
  • [Cites] Aliment Pharmacol Ther. 1987 Jun;1(3):239-51 [2979226.001]
  • [Cites] APMIS. 1999 Dec;107(12):1085-92 [10660138.001]
  • [Cites] J Clin Invest. 1975 Mar;55(3):462-8 [1167869.001]
  • [Cites] Digestion. 1986;35 Suppl 1:42-55 [3792671.001]
  • [Cites] Gastroenterology. 1993 Oct;105(4):1264-6 [8405879.001]
  • [Cites] Epidemiol Rev. 1986;8:1-27 [3533579.001]
  • [Cites] Acta Physiol Scand. 2000 May;169(1):29-37 [10759608.001]
  • [Cites] Aliment Pharmacol Ther. 2001 May;15(5):729-30 [11328270.001]
  • [Cites] Lab Anim Sci. 1999 Jun;49(3):241-7 [10403437.001]
  • [Cites] Gut. 1992 Oct;33(10):1303-6 [1446849.001]
  • [Cites] Am J Surg Pathol. 1990 Jun;14(6):503-13 [1970928.001]
  • [Cites] Gastroenterology. 1985 Mar;88(3):638-48 [2578420.001]
  • [Cites] Cancer. 1998 Aug 1;83(3):435-44 [9690535.001]
  • (PMID = 16184420.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Ulcer Agents; 0 / Gastrins
  • [Number-of-references] 74
  •  go-up   go-down


95. Bergmann F, Breinig M, Höpfner M, Rieker RJ, Fischer L, Köhler C, Esposito I, Kleeff J, Herpel E, Ehemann V, Friess H, Schirmacher P, Kern MA: Expression pattern and functional relevance of epidermal growth factor receptor and cyclooxygenase-2: novel chemotherapeutic targets in pancreatic endocrine tumors? Am J Gastroenterol; 2009 Jan;104(1):171-81
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression pattern and functional relevance of epidermal growth factor receptor and cyclooxygenase-2: novel chemotherapeutic targets in pancreatic endocrine tumors?
  • OBJECTIVES: Pancreatic endocrine tumors represent morphologically and biologically heterogeneous neoplasms.
  • Well-differentiated endocrine tumors (benign or of uncertain behavior) can be distinguished from well-differentiated and poorly differentiated endocrine carcinomas.
  • Although many well-differentiated endocrine carcinomas show rather low rates of tumor growth, more than two-thirds of pancreatic endocrine carcinomas display distant metastases at the time of diagnosis.
  • As the currently applied therapies beyond surgery only achieve partial or complete response rates of approximately 15%, additional chemotherapeutic targets are needed, especially in the therapy of inoperable and progressive pancreatic endocrine carcinomas.
  • METHODS: The expression of epidermal growth factor receptor (EGFR) and cyclooxygenase (COX)-2 were investigated in 110 clinically and pathomorphologically well-characterized pancreatic endocrine tumors, using immunohistochemistry and immunoblot analyses.
  • Functional tests were performed using the human pancreas carcinoid cell line BON and the mouse insulinoma cell line beta-TC-3.
  • RESULTS: The expression of EGFR correlated significantly with the grade of malignancy, increasing from low rates of expression in benign tumors and tumors of uncertain behavior to high rates of expression in well- and poorly differentiated endocrine carcinomas.
  • The expression of COX-2 was independent of the malignant potential, but was more frequently expressed in primary tumors than in metastases.
  • The treatment of the human pancreas carcinoid cell line BON and the mouse insulinoma cell line beta-TC-3 with EGFR and COX-2 inhibitors (monotherapy and combined therapy) resulted in a significant, dose-dependent reduction of cell viability coupled with increased apoptosis.
  • CONCLUSIONS: Our results suggest that EGFR and COX-2 may represent useful additional chemotherapeutic targets in pancreatic endocrine tumors.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Animals. Apoptosis / drug effects. Blotting, Western. Carcinoid Tumor / metabolism. Celecoxib. Cell Line, Tumor. Cell Survival / drug effects. Cyclooxygenase 2 Inhibitors / therapeutic use. Dose-Response Relationship, Drug. Female. Humans. Insulinoma / metabolism. Male. Mice. Mice, Transgenic. Middle Aged. Quinazolines. Tumor Cells, Cultured. Young Adult

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • Hazardous Substances Data Bank. CELECOXIB .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19098866.001).
  • [ISSN] 1572-0241
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Pyrazoles; 0 / Quinazolines; 0 / Sulfonamides; 0 / Tyrphostins; 170449-18-0 / tyrphostin AG 1478; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; JCX84Q7J1L / Celecoxib
  •  go-up   go-down


96. Krysiak R, Okopień B, Herman ZS: [Somatostatin analogs]. Pol Arch Med Wewn; 2006 Oct;116(4):988-97
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Hormones / therapeutic use. Neuroendocrine Tumors / drug therapy. Somatostatin / therapeutic use
  • [MeSH-minor] Acromegaly / drug therapy. Carcinoid Tumor / drug therapy. Gastrointestinal Hemorrhage / drug therapy. Graves Ophthalmopathy / drug therapy. Humans. Octreotide / therapeutic use. Peptides, Cyclic / therapeutic use. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Hormones.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18416302.001).
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] pol
  • [Publication-type] Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Hormones; 0 / Peptides, Cyclic; 0G3DE8943Y / lanreotide; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide
  • [Number-of-references] 43
  •  go-up   go-down


97. Prommer EE: Established and potential therapeutic applications of octreotide in palliative care. Support Care Cancer; 2008 Oct;16(10):1117-23
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Octreotide has proven to be an effective agent for symptoms of carcinoid syndrome.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Octreotide / therapeutic use. Palliative Care
  • [MeSH-minor] Drug Interactions. Humans. Neoplasms / complications

  • MedlinePlus Health Information. consumer health - Palliative Care.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] N Engl J Med. 1989 Mar 9;320(10):671-2 [2918882.001]
  • [Cites] Nihon Rinsho Meneki Gakkai Kaishi. 2005 Feb;28(1):56-61 [15744122.001]
  • [Cites] J Pain Symptom Manage. 2004 Oct;28(4):412-6 [15471659.001]
  • [Cites] AIDS. 1993 Feb;7(2):223-6 [8466684.001]
  • [Cites] Palliat Med. 2003 Apr;17(3):257-62 [12725479.001]
  • [Cites] Intern Med J. 2002 Apr;32(4):191-2 [11951935.001]
  • [Cites] Hematol Oncol. 2003 Jun;21(2):77-81 [12802812.001]
  • [Cites] Am J Med Sci. 2000 Oct;320(4):296-7 [11061359.001]
  • [Cites] Oncology. 1994 Jan-Feb;51(1):70-3 [8265106.001]
  • [Cites] Nephrology (Carlton). 2005 Aug;10(4):344-7 [16109079.001]
  • [Cites] N Engl J Med. 1996 Jan 25;334(4):246-54 [8532003.001]
  • [Cites] Lancet. 1990 Mar 24;335(8691):738 [1969102.001]
  • [Cites] Support Care Cancer. 2001 Jun;9(4):258-60 [11430421.001]
  • [Cites] Aliment Pharmacol Ther. 2002 Apr;16(4):769-77 [11929395.001]
  • [Cites] Gan To Kagaku Ryoho. 1996 Feb;23(3):343-7 [8712828.001]
  • [Cites] Mt Sinai J Med. 1994 Sep;61(4):349-55 [7969229.001]
  • [Cites] Pain. 1995 May;61(2):345-6 [7659445.001]
  • [Cites] J Pain Symptom Manage. 2005 Dec;30(6):563-9 [16376743.001]
  • [Cites] Cancer. 1993 Sep 1;72(5):1543-6 [8348489.001]
  • [Cites] J Physiol. 2003 Jan 1;546(Pt 1):101-17 [12509482.001]
  • [Cites] Curr Opin Oncol. 1998 Jan;10(1):58-65 [9466486.001]
  • [Cites] J Pain Symptom Manage. 2000 Jan;19(1):23-34 [10687323.001]
  • [Cites] Anticancer Drugs. 1993 Aug;4(4):443-5 [8400346.001]
  • [Cites] Anticancer Res. 2002 Mar-Apr;22(2B):1187-92 [12168923.001]
  • [Cites] J Clin Oncol. 1999 Feb;17(2):600-6 [10080605.001]
  • [Cites] Clin Endocrinol (Oxf). 1997 Mar;46(3):373-5 [9156050.001]
  • [Cites] Support Care Cancer. 2000 May;8(3):188-91 [10789958.001]
  • [Cites] Digestion. 1993;54 Suppl 1:30-2 [8395432.001]
  • [Cites] Eur J Cardiothorac Surg. 2002 May;21(5):913-7 [12062286.001]
  • [Cites] Digestion. 1993;54 Suppl 1:88-91 [8359574.001]
  • [Cites] Anticancer Res. 2000 Sep-Oct;20(5C):4039-46 [11268498.001]
  • [Cites] Clin Transplant. 1995 Jun;9(3 Pt 1):205-8 [7549062.001]
  • [Cites] N Engl J Med. 1983 Dec 15;309(24):1495-501 [6139753.001]
  • [Cites] Palliat Med. 1999 Sep;13(5):429-30 [10659116.001]
  • [Cites] Anesth Analg. 2004 Feb;98(2):318-20, table of contents [14742361.001]
  • [Cites] Lancet. 1999 Mar 6;353(9155):846 [10459993.001]
  • [Cites] J Am Coll Surg. 2003 Mar;196(3):365-9 [12648685.001]
  • [Cites] Cancer Invest. 1999;17(5):320-1 [10370359.001]
  • [Cites] J Pain Symptom Manage. 1994 Jan;9(1):34-8 [8169458.001]
  • [Cites] Front Neuroendocrinol. 1999 Jul;20(3):157-98 [10433861.001]
  • [Cites] Eur J Endocrinol. 2004 Jul;151(1):107-12 [15248829.001]
  • [Cites] Am J Clin Oncol. 2000 Aug;23 (4):412-5 [10955874.001]
  • [Cites] Eur J Neurosci. 1998 Dec;10(12):3700-8 [9875349.001]
  • [Cites] J Clin Oncol. 1997 Nov;15(11):3350-4 [9363865.001]
  • [Cites] J Wound Ostomy Continence Nurs. 2002 Sep;29(5):228-33 [12510468.001]
  • [Cites] Oncol Nurs Forum. 1998 Jun;25(5):873-8 [9644703.001]
  • [Cites] Peptides. 1996;17(5):769-73 [8844765.001]
  • [Cites] Pain. 1992 Apr;49(1):13-9 [1594275.001]
  • [Cites] Gut. 2002 May;50 Suppl 3:III15-8 [11953327.001]
  • [Cites] Bone Marrow Transplant. 1997 Nov;20(9):711-4 [9384471.001]
  • [Cites] J Pain Symptom Manage. 1994 Aug;9(6):406-11 [7525789.001]
  • [Cites] South Med J. 1990 Jan;83(1):77 [2300842.001]
  • [Cites] Endocr J. 2005 Apr;52(2):277-80 [15863961.001]
  • [Cites] J Clin Oncol. 1993 Jan;11(1):148-51 [8418225.001]
  • (PMID = 18256859.001).
  • [ISSN] 0941-4355
  • [Journal-full-title] Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer
  • [ISO-abbreviation] Support Care Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; RWM8CCW8GP / Octreotide
  • [Number-of-references] 59
  •  go-up   go-down


98. Höpfner M, Sutter AP, Huether A, Ahnert-Hilger G, Scherübl H: A novel approach in the treatment of neuroendocrine gastrointestinal tumors: additive antiproliferative effects of interferon-gamma and meta-iodobenzylguanidine. BMC Cancer; 2004 May 21;4:23
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel approach in the treatment of neuroendocrine gastrointestinal tumors: additive antiproliferative effects of interferon-gamma and meta-iodobenzylguanidine.
  • BACKGROUND: Therapeutic options to effectively inhibit growth and spread of neuroendocrine gastrointestinal tumors are still limited.
  • As both meta-iodobenzylguanidine (MIBG) and interferon-gamma (IFNgamma) cause antineoplastic effects in neuroendocrine gastrointestinal tumor cells, we investigated the antiproliferative effects of the combination of IFNgamma and non-radiolabeled MIBG in neuroendocrine gut STC-1 and pancreatic carcinoid BON tumor cells.
  • IFNgamma dose- and time-dependently inhibited the growth of both STC-1 and of BON tumor cells with IC50-values of 95 +/- 15 U/ml and 135 +/- 10 U/ml, respectively.
  • Furthermore, IFNgamma induced cytotoxic effects in NE tumor cells.
  • The NE tumor-targeted drug MIBG is selectively taken up via norepinephrine transporters, thereby specifically inhibiting growth in NE tumor cells.
  • Intriguingly, IFNgamma treatment induced an upregulation of norepinephrine transporter expression in neuroendocrine tumors cells, as determined by semi-quantitative RT-PCR.
  • CONCLUSION: Our data show that IFNgamma exerts antiproliferative effects on neuroendocrine gastrointestinal tumor cells by inducing cell cycle arrest, apoptosis and cytotoxicity.
  • The combination of IFNgamma with the NE tumor-targeted agent MIBG leads to effective growth control at reduced doses of either drug.
  • Thus, the administration of IFNgamma alone and more so, in combination with MIBG, is a promising novel approach in the treatment of neuroendocrine gastrointestinal tumors.
  • [MeSH-major] 3-Iodobenzylguanidine / pharmacology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Cell Cycle / drug effects. Gastrointestinal Neoplasms / drug therapy. Interferon-gamma / pharmacology. Neuroendocrine Tumors / drug therapy
  • [MeSH-minor] Apoptosis. Caspase 3. Caspases / analysis. Drug Synergism. G0 Phase / drug effects. G1 Phase / drug effects. Humans. Norepinephrine Plasma Membrane Transport Proteins. Receptors, Interferon. Reverse Transcriptase Polymerase Chain Reaction. S Phase / drug effects. Statistics, Nonparametric. Symporters. Tumor Cells, Cultured / drug effects. Up-Regulation

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Exp Cell Res. 2003 Jan 15;282(2):78-89 [12531694.001]
  • [Cites] Oncogene. 1996 Aug 1;13(3):599-608 [8760301.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2003 Jun;284(6):L1063-71 [12588705.001]
  • [Cites] Cytokines Cell Mol Ther. 2002;7(3):107-16 [12850810.001]
  • [Cites] Br J Cancer. 2003 Aug 4;89(3):564-72 [12888831.001]
  • [Cites] J Interferon Cytokine Res. 2003 Jul;23(7):379-93 [14511464.001]
  • [Cites] Med Oncol. 2003;20(3):271-81 [14514977.001]
  • [Cites] J Interferon Cytokine Res. 2003 Sep;23(9):501-11 [14565859.001]
  • [Cites] Br J Cancer. 2003 Nov 3;89(9):1766-75 [14583782.001]
  • [Cites] J Biol Chem. 2003 Dec 19;278(51):51703-12 [14532292.001]
  • [Cites] J Nucl Med. 1987 Mar;28(3):308-14 [3102701.001]
  • [Cites] Cancer Res. 1987 Jun 1;47(11):2809-13 [3105867.001]
  • [Cites] Cancer Res. 1987 Dec 15;47(24 Pt 1):6710-8 [3479249.001]
  • [Cites] J Immunol Methods. 1988 Nov 25;115(1):61-9 [3192948.001]
  • [Cites] J Interferon Res. 1990 Dec;10(6):579-88 [1707938.001]
  • [Cites] Ann N Y Acad Sci. 1994 Sep 15;733:46-55 [7978895.001]
  • [Cites] Cell. 1996 Feb 9;84(3):431-42 [8608597.001]
  • [Cites] Gastroenterology. 1996 May;110(5):1595-604 [8613067.001]
  • [Cites] J Clin Oncol. 1996 Jun;14(6):1829-38 [8656251.001]
  • [Cites] Br J Cancer. 2000 Mar;82(6):1138-44 [10735496.001]
  • [Cites] Gastroenterology. 2000 Apr;118(4):735-48 [10734025.001]
  • [Cites] Eur J Endocrinol. 2000 Apr;142(4):393-401 [10754482.001]
  • [Cites] Front Biosci. 2000 Apr 1;5:D479-87 [10762599.001]
  • [Cites] Oncogene. 2000 May 15;19(21):2468-73 [10851045.001]
  • [Cites] Cell Growth Differ. 1996 Mar;7(3):289-300 [8838859.001]
  • [Cites] Recent Results Cancer Res. 1996;142:193-207 [8893342.001]
  • [Cites] Biochem Biophys Res Commun. 1996 Dec 4;229(1):21-6 [8954078.001]
  • [Cites] Leukemia. 1997 Apr;11 Suppl 3:439-40 [9209417.001]
  • [Cites] Mol Cell Biol. 1997 Sep;17(9):5328-37 [9271410.001]
  • [Cites] Eur J Cancer. 1997 Oct;33(11):1759-66 [9470829.001]
  • [Cites] Intern Med. 1998 Feb;37(2):179-81 [9550601.001]
  • [Cites] J Physiol. 1998 Aug 1;510 ( Pt 3):805-14 [9660895.001]
  • [Cites] Oncogene. 1998 Dec 10;17(23):2973-9 [9881699.001]
  • [Cites] Hypertension. 1999 Jan;33(1):162-6 [9931097.001]
  • [Cites] Aliment Pharmacol Ther. 1999 Mar;13(3):271-87 [10102959.001]
  • [Cites] Br J Cancer. 1999 Jun;80(8):1236-44 [10376977.001]
  • [Cites] Eur J Gastroenterol Hepatol. 1999 Oct;11(10):1157-64 [10524647.001]
  • [Cites] Digestion. 2000;62 Suppl 1:92-7 [10940694.001]
  • [Cites] Ann Oncol. 2000 Nov;11(11):1437-43 [11142484.001]
  • [Cites] Pflugers Arch. 2000 Dec;441(2-3):294-300 [11211116.001]
  • [Cites] Gut. 2001 Aug;49(2):251-62 [11454803.001]
  • [Cites] Int J Colorectal Dis. 2001 Jun;16(3):154-66 [11459289.001]
  • [Cites] Pharmacol Ther. 2001 Jul;91(1):35-62 [11707293.001]
  • [Cites] Ann Oncol. 2001;12 Suppl 2:S111-4 [11762335.001]
  • [Cites] Br J Cancer. 2001 Nov 30;85(11):1771-80 [11742501.001]
  • [Cites] Br J Cancer. 2002 Feb 12;86(4):636-44 [11870549.001]
  • [Cites] J Cell Biochem. 2002;85(2):369-80 [