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1. Rivera F, Carrato A, Grávalos C, Pericay C, Sastre J, Aranda E: Recommendations on current approach to gastric cancer. Clin Transl Oncol; 2009 Aug;11(8):518-25
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  • [Title] Recommendations on current approach to gastric cancer.
  • The management of gastric cancer has been updated by the Grupo Español de Tratamiento de Tumores Digestivos (TTD).
  • A multidisciplinary approach is essential in these patients including a precise diagnosis and staging and correct nutritional evaluation.
  • Recently a phase III trial has shown a significant improvement in overall survival when trastuzumab is added to cisplatin-capecitabine or cisplatin-5-fluorouracil in patients with HER2+ advanced gastric cancer.
  • Currently, there are several ongoing clinical trials evaluating the role of other new drugs against cellular targets.
  • [MeSH-major] Stomach Neoplasms / drug therapy

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  • [Cites] Ann Oncol. 2008 Sep;19(9):1523-9 [18441328.001]
  • [Cites] Ann Oncol. 2000 Jul;11(7):837-43 [10997811.001]
  • [Cites] J Clin Oncol. 2006 Jun 20;24(18):2903-9 [16782930.001]
  • [Cites] J Clin Oncol. 2005 Aug 20;23(24):5660-7 [16110025.001]
  • [Cites] J Clin Oncol. 2006 Nov 1;24(31):4991-7 [17075117.001]
  • [Cites] N Engl J Med. 2008 Jan 3;358(1):36-46 [18172173.001]
  • [Cites] JPEN J Parenter Enteral Nutr. 2002 Sep-Oct;26(5 Suppl):S63-71 [12216725.001]
  • [Cites] Lancet. 1996 Apr 13;347(9007):995-9 [8606613.001]
  • [Cites] J Clin Oncol. 2007 Aug 1;25(22):3217-23 [17664469.001]
  • [Cites] Ann Oncol. 2005;16 Suppl 1:i22-3 [15888740.001]
  • [Cites] Ann Oncol. 2008 Aug;19(8):1450-7 [18558665.001]
  • [Cites] Ann Oncol. 2005 Feb;16(2):273-8 [15668283.001]
  • [Cites] Am J Clin Oncol. 2005 Apr;28(2):188-94 [15803015.001]
  • [Cites] Oncology. 2005;68(2-3):190-5 [16006756.001]
  • [Cites] Ann Oncol. 2006 Apr;17(4):652-6 [16497828.001]
  • [Cites] J Clin Oncol. 2000 Jul;18(14):2648-57 [10894863.001]
  • [Cites] Semin Oncol. 1996 Jun;23(3):352-9 [8658219.001]
  • [Cites] Ann Surg. 1994 Aug;220(2):176-82 [8053740.001]
  • [Cites] Lancet. 1995 Mar 25;345(8952):745-8 [7891484.001]
  • [Cites] Eur J Surg. 2002;168(11):597-608 [12699095.001]
  • [Cites] World J Gastroenterol. 2006 Jan 14;12(2):204-13 [16482619.001]
  • [Cites] Cancer Treat Rev. 2007 Jun;33(4):315-24 [17376598.001]
  • [Cites] Am J Clin Nutr. 2005 Nov;82(5):1082-9 [16280442.001]
  • [Cites] Ann Surg. 1999 Aug;230(2):170-8 [10450730.001]
  • [Cites] N Engl J Med. 2007 Nov 1;357(18):1810-20 [17978289.001]
  • [Cites] Ann Oncol. 2009 Apr;20(4):666-73 [19153121.001]
  • [Cites] J Clin Oncol. 2005 Jul 10;23(20):4509-17 [16002841.001]
  • [Cites] J Clin Oncol. 1993 Aug;11(8):1441-7 [8336183.001]
  • [Cites] Proc Nutr Soc. 1999 Nov;58(4):821-9 [10817149.001]
  • [Cites] Ann Oncol. 2007 Mar;18(3):581-92 [17287242.001]
  • [Cites] N Engl J Med. 2001 Sep 6;345(10):725-30 [11547741.001]
  • [Cites] J Clin Oncol. 2006 Nov 20;24(33):5201-6 [17114652.001]
  • [Cites] Nutrition. 2002 Nov-Dec;18(11-12):953-9 [12431717.001]
  • [Cites] Eur J Cancer. 1999 Jul;35(7):1059-64 [10533448.001]
  • [Cites] Tumori. 2002 Jan-Feb;88(1):21-7 [12004845.001]
  • [Cites] N Engl J Med. 2006 Jul 6;355(1):11-20 [16822992.001]
  • [Cites] J Clin Oncol. 1997 Jan;15(1):261-7 [8996151.001]
  • [Cites] Ann Surg. 1989 Feb;209(2):162-6 [2644898.001]
  • [Cites] Ann Oncol. 2007 Mar;18(3):510-7 [17164226.001]
  • (PMID = 19661026.001).
  • [ISSN] 1699-3055
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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2. Becker KF, Höfler H: Mutant cell surface receptors as targets for individualized cancer diagnosis and therapy. Curr Cancer Drug Targets; 2001 Aug;1(2):121-8
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  • [Title] Mutant cell surface receptors as targets for individualized cancer diagnosis and therapy.
  • The catalogue of gene alterations in human cancer is growing rapidly.
  • Alterations in specific genes that play important roles in diverse cellular functions such as cell adhesion, signal transduction, differentiation, development or DNA-repair have been identified.
  • Cancer-associated mutant cell surface molecules are very attractive candidates to target tumor cells because they offer the possibility of minimizing toxic effects to non-tumor cells.
  • The cell adhesion molecule E-cadherin has been shown to play a major role in determining which of the two subtypes of gastric cancer, diffuse or intestinal type, develops.
  • E-cadherin gene mutations typically affect the extracellular portion of the homophilic receptor and are frequently found in patients with diffuse-type tumors.
  • Cancer-specific monoclonal antibodies against the E-cadherin mutational hot spot region are now available.
  • After linking to toxins, drugs or radiolabeled mutation-specific antibodies could serve as very specific agents to treat small tumor deposits.
  • Patients for this novel individualized cancer therapy can be identified within a day using routine immunohistochemistry of biopsies.
  • [MeSH-major] Cadherins / genetics. Mutation / genetics. Receptors, Cell Surface / genetics. Stomach Neoplasms / diagnosis. Stomach Neoplasms / therapy

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  • (PMID = 12188885.001).
  • [ISSN] 1568-0096
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cadherins; 0 / Receptors, Cell Surface
  • [Number-of-references] 53
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3. Liang S, Lin T, Ding J, Pan Y, Dang D, Guo C, Zhi M, Zhao P, Sun L, Hong L, Shi Y, Yao L, Liu J, Wu K, Fan D: Screening and identification of vascular-endothelial-cell-specific binding peptide in gastric cancer. J Mol Med (Berl); 2006 Sep;84(9):764-73
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  • [Title] Screening and identification of vascular-endothelial-cell-specific binding peptide in gastric cancer.
  • Antiangiogenesis therapy has become a hot field in cancer research.
  • In this study, we established an in vitro co-culture model of human umbilical vein endothelial cells (HUVECs) and gastric adenocarcinoma cell line SGC7901, screened the peptides binding specifically to the HUVECs co-cultured with gastric cancer cells (Co-HUVECs) using phage display peptides library, and studied the affinity of these peptides to gastric cancer vascular endothelial cells.
  • Five phage clones (M6, M3, M9, IN12, IN11), which could strongly bind to Co-HUVECs instead of wild-type HUVECs, were characterized by ELISA.
  • In vitro cellular binding assay showed that phage IN11 preferably bound to Co-HUVECs rather than control HUVECs, and the number of the phage IN11 recovered from Co-HUVECs was 5.7- and 16.9-folds, respectively, as much as those from control HUVECs and GES cells.
  • Immunocytochemical and immunohistochemical staining confirmed that phage IN11 could specifically bind to Co-HUVECs as well as vascular endothelial cells in gastric cancer tissue sections.
  • Meanwhile, GEBP11 was found to be able to target the gastric cancer vascular endothelial cells.
  • Therefore, GEBP11 may be a potential candidate for targeted drug delivery in antivascular therapy and diagnosis of gastric cancer.
  • [MeSH-major] Endothelial Cells / metabolism. Peptides / analysis. Peptides / metabolism. Stomach Neoplasms / pathology
  • [MeSH-minor] Amino Acid Sequence. Bacteriophages. Binding, Competitive. Clone Cells. Coculture Techniques. Databases, Protein. Drug Evaluation, Preclinical. Enzyme-Linked Immunosorbent Assay. Humans. Molecular Sequence Data. Peptide Library. Protein Binding. Sequence Alignment. Sequence Homology, Amino Acid

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  • [Cites] Zhonghua Zhong Liu Za Zhi. 1994 Jan;16(1):7-10 [8033753.001]
  • [Cites] Cancer Cell. 2003 Nov;4(5):383-91 [14667505.001]
  • [Cites] Cell. 1996 Aug 9;86(3):353-64 [8756718.001]
  • [Cites] J Mol Biol. 1991 Dec 5;222(3):581-97 [1748994.001]
  • [Cites] Carcinogenesis. 2004 Nov;25(11):2115-23 [15297368.001]
  • [Cites] Cancer Biol Ther. 2004 Dec;3(12):1232-5 [15492500.001]
  • [Cites] Int J Biochem Cell Biol. 2001 Apr;33(4):325-35 [11312103.001]
  • [Cites] Semin Cancer Biol. 2003 Apr;13(2):159-67 [12654259.001]
  • [Cites] J Clin Invest. 1973 Nov;52(11):2745-56 [4355998.001]
  • [Cites] J Cell Sci. 2003 Mar 15;116(Pt 6):1013-22 [12584245.001]
  • [Cites] J Mol Biol. 2000 Sep 1;301(5):1149-61 [10966812.001]
  • [Cites] N Engl J Med. 1971 Nov 18;285(21):1182-6 [4938153.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Sep 16;100(19):10623-8 [12963823.001]
  • [Cites] Cell Res. 2003 Dec;13(6):473-9 [14728804.001]
  • [Cites] Nat Med. 2002 Jul;8(7):751-5 [12053175.001]
  • [Cites] Cancer Lett. 2004 Dec 8;216(1):63-71 [15575081.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Feb 5;99(3):1527-31 [11830668.001]
  • [Cites] Am J Pathol. 2003 May;162(5):1591-601 [12707043.001]
  • [Cites] Cancer Res. 1999 Jun 1;59(11):2718-23 [10363997.001]
  • [Cites] Am J Physiol Cell Physiol. 2002 May;282(5):C947-70 [11940508.001]
  • [Cites] Cancer Cell. 2003 Nov;4(5):331-3 [14667498.001]
  • [Cites] Genome Biol. 2004;5(2):207 [14759250.001]
  • [Cites] Microvasc Res. 2002 May;63(3):316-26 [11969308.001]
  • [Cites] Nat Rev Cancer. 2002 Feb;2(2):83-90 [12635171.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Nov 21;97(24):13003-8 [11087855.001]
  • [Cites] Nature. 1996 Mar 28;380(6572):364-6 [8598934.001]
  • [Cites] J Control Release. 2003 Aug 28;91(1-2):183-6 [12932650.001]
  • [Cites] Curr Opin Chem Biol. 2000 Feb;4(1):16-21 [10679380.001]
  • [Cites] Semin Oncol. 2002 Dec;29(6 Suppl 16):15-8 [12516034.001]
  • [Cites] Semin Cancer Biol. 2000 Dec;10(6):435-42 [11170865.001]
  • [Cites] Cancer Res. 2004 Aug 1;64(15):5390-7 [15289347.001]
  • [Cites] Am J Pathol. 2002 Mar;160(3):985-1000 [11891196.001]
  • [Cites] Carcinogenesis. 2004 Nov;25(11):2075-81 [15205362.001]
  • [Cites] Science. 1985 Jun 14;228(4705):1315-7 [4001944.001]
  • [Cites] Int J Cancer. 2005 Aug 10;116(1):155-60 [15756676.001]
  • (PMID = 16763842.001).
  • [ISSN] 0946-2716
  • [Journal-full-title] Journal of molecular medicine (Berlin, Germany)
  • [ISO-abbreviation] J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Peptide Library; 0 / Peptides
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4. Nakao M, Yoshida S, Tanaka S, Takemura Y, Oka S, Yoshihara M, Chayama K: Optical biopsy of early gastroesophageal cancer by catheter-based reflectance-type laser-scanning confocal microscopy. J Biomed Opt; 2008 Sep-Oct;13(5):054043
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  • [Title] Optical biopsy of early gastroesophageal cancer by catheter-based reflectance-type laser-scanning confocal microscopy.
  • However, such observation at the cellular level remains difficult.
  • We compare prototype catheter-based reflectance-type LCM images in vivo and histologic images of early gastroesophageal cancer to assess the usefulness of LCM in diagnosing such cancer.
  • 20 sites in the esophagus and 40 sites in the stomach are examined by LCM under endoscopy prior to endoscopic or surgical resection.
  • A prototype catheter LCM system, equipped with a semiconductor laser that oscillates at 685 nm and analyzes reflected light (Mauna Kea Technologies, Paris, France; Fujinon, Saitama, Japan) is used in vivo without fluorescent agent.
  • In all normal gastric mucosa, nuclei and cell membranes are not visualized, but in ten of the 20 gastric cancers, nuclei are visualized.
  • This novel method will aid in immediate diagnosis under endoscopy without the need for biopsy.
  • [MeSH-major] Biopsy / instrumentation. Catheterization. Esophageal Neoplasms / pathology. Microscopy, Confocal / instrumentation. Optical Devices. Stomach Neoplasms / pathology

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  • (PMID = 19021423.001).
  • [ISSN] 1083-3668
  • [Journal-full-title] Journal of biomedical optics
  • [ISO-abbreviation] J Biomed Opt
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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5. Chikama T, Takahashi N, Wakuta M, Nishida T: Noninvasive direct detection of ocular mucositis by in vivo confocal microscopy in patients treated with S-1. Mol Vis; 2009;15:2896-904
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  • PURPOSE: S-1 is an oral antineoplastic agent that contains a prodrug of 5-fluorouracil and has adverse effects on skin, alimentary tract mucosa, and the ocular surface.
  • METHODS: Twelve patients with eye problems related to S-1 treatment participated in the study.
  • Corneal epithelial debridement as a diagnostic therapy and histopathologic analysis were performed for five eyes of three subjects affected in the pupillary zone of the cornea.
  • One of five specimens subjected to cytologic diagnosis showed moderate dysplasia.
  • CONCLUSIONS: S-1 can induce ocular mucositis with dysplasia, likely affecting cellular functions, including differentiation, of the corneal epithelium.
  • In vivo confocal microscopy allowed the noninvasive detection of cellular changes in the cornea as an adverse effect of S-1 administration.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Eye Diseases / chemically induced. Eye Diseases / diagnosis. Microscopy, Confocal / methods. Mucositis / chemically induced. Mucositis / diagnosis. Oxonic Acid / adverse effects. Tegafur / adverse effects
  • [MeSH-minor] Aged. Drug Combinations. Female. Humans. Inflammation / pathology. Male. Middle Aged

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  • [Cites] Anticancer Drugs. 1996 Jul;7(5):548-57 [8862723.001]
  • [Cites] Doc Ophthalmol. 1995;90(1):1-6 [8549238.001]
  • [Cites] Toxicol Lett. 1998 Dec 28;102-103:19-27 [10022227.001]
  • [Cites] Mod Rheumatol. 2006;16(4):197-205 [16906368.001]
  • [Cites] Cancer Treat Rev. 2007 Aug;33(5):448-60 [17507164.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2008 Jun;49(6):2432-7 [18362114.001]
  • [Cites] Eur J Ophthalmol. 2008 Sep-Oct;18(5):703-7 [18850546.001]
  • [Cites] Mol Vis. 2008;14:2333-9 [19093010.001]
  • [Cites] Biomed Tech (Berl). 2009 Feb;54(1):23-8 [19182870.001]
  • [Cites] Cornea. 2000 Sep;19(5):712-22 [11009323.001]
  • [Cites] Prog Retin Eye Res. 2001 Sep;20(5):639-73 [11470454.001]
  • [Cites] Ophthalmologe. 2002 Apr;99(4):276-80 [12058503.001]
  • [Cites] J Cataract Refract Surg. 2002 Aug;28(8):1390-9 [12160809.001]
  • [Cites] Ophthalmology. 2002 Dec;109(12):2359-61 [12466185.001]
  • [Cites] Gastric Cancer. 2003;6 Suppl 1:2-8 [12775012.001]
  • [Cites] Ophthal Plast Reconstr Surg. 2003 May;19(3):216-24 [12918558.001]
  • [Cites] Cancer. 2004 May 1;100(9 Suppl):1995-2025 [15108222.001]
  • [Cites] Cancer. 2004 May 1;100(9 Suppl):2026-46 [15108223.001]
  • [Cites] Br J Dermatol. 2004 Sep;151(3):698-700 [15377362.001]
  • [Cites] Gan. 1977 Oct;68(5):553-60 [22472.001]
  • [Cites] Aust N Z J Med. 1979 Apr;9(2):143-4 [287454.001]
  • [Cites] J Dermatol. 1988 Aug;15(4):342-6 [3058765.001]
  • [Cites] Cancer Invest. 1990;8(5):459-65 [2124943.001]
  • [Cites] Neurosci Biobehav Rev. 1993 Winter;17(4):483-98 [8309657.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1994 Feb;35(2):730-43 [8113024.001]
  • [Cites] Curr Eye Res. 1994 Nov;13(11):805-14 [7531631.001]
  • [Cites] Prostate. 1995 Sep;27(3):129-40 [7567691.001]
  • [Cites] Ophthalmology. 1995 Sep;102(9):1338-44 [9097771.001]
  • (PMID = 20057904.001).
  • [ISSN] 1090-0535
  • [Journal-full-title] Molecular vision
  • [ISO-abbreviation] Mol. Vis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drug Combinations; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid
  • [Other-IDs] NLM/ PMC2802292
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6. Santini D, Vincenzi B, Fratto ME, Perrone G, Lai R, Catalano V, Cass C, Ruffini PA, Spoto C, Muretto P, Rizzo S, Muda AO, Mackey JR, Russo A, Tonini G, Graziano F: Prognostic role of human equilibrative transporter 1 (hENT1) in patients with resected gastric cancer. J Cell Physiol; 2010 May;223(2):384-8
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  • [Title] Prognostic role of human equilibrative transporter 1 (hENT1) in patients with resected gastric cancer.
  • Nucleoside transporter proteins are specialized proteins that mediate the transport of nucleosides and nucleoside analog drugs across the plasma membrane.
  • The human equilibrative nucleoside transporter 1 (hENT1) is a member of these proteins and mediates cellular entry of gemcitabine, cytarabine, and fludarabine.
  • The hENT1 expression has been demonstrated to be related with prognosis and activity of gemcitabine-based therapy in breast, ampullary, lung, and pancreatic cancer.
  • We investigated the immunohistochemical expression of hENT in tumor samples from 111 patients with resected gastric adenocarcinoma, correlating these data with clinical parameters and disease outcomes.
  • Immunohistochemistry for the hENT1 protein carries prognostic information in patients with resected gastric cancer and holds promise as a predictive factor in chemotherapy decisions.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Equilibrative Nucleoside Transporter 1 / metabolism. Gastric Mucosa / metabolism. Stomach Neoplasms / diagnosis. Stomach Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / metabolism. Antineoplastic Agents / pharmacokinetics. Cohort Studies. Disease Progression. Disease-Free Survival. Drug Resistance, Neoplasm / physiology. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Metastasis / physiopathology. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / prevention & control. Predictive Value of Tests. Prognosis. Retrospective Studies. Survival Rate

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  • (PMID = 20082300.001).
  • [ISSN] 1097-4652
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Equilibrative Nucleoside Transporter 1; 0 / SLC29A1 protein, human
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7. Feng WH, Cohen JI, Fischer S, Li L, Sneller M, Goldbach-Mansky R, Raab-Traub N, Delecluse HJ, Kenney SC: Reactivation of latent Epstein-Barr virus by methotrexate: a potential contributor to methotrexate-associated lymphomas. J Natl Cancer Inst; 2004 Nov 17;96(22):1691-702
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  • Here we determined whether MTX, in contrast to other commonly used medications for rheumatoid arthritis or polymyositis, is unique in its ability to induce the release of infectious EBV from latently infected cells.
  • METHODS: The effect of MTX and other immunosuppressant drugs on EBV replication in vitro was assessed using latently infected EBV-positive lymphoblastoid and gastric carcinoma cell lines.
  • Drug effects on transcription of the two EBV immediate-early promoters (BRLF1 and BZLF1) and on promoter constructs lacking cis-acting sequences required for activation by other effectors was examined using reporter gene assays.
  • EBV viral load in rheumatoid arthritis and polymyositis patients receiving MTX was compared with that in patients receiving other immunosuppressive medications.
  • Patients treated with MTX-containing regimens had statistically significantly higher mean EBV loads in their blood than patients treated with immunosuppressing regimens that did not include MTX (40 EBV copies per 10(6) cellular genomes versus 5.1 copies; geometric mean fold difference in copies = 10.8, 95%, confidence interval = 3.0 to 38; P = .011).
  • [MeSH-major] DNA, Viral / drug effects. Gene Expression Regulation, Viral / drug effects. Herpesvirus 4, Human / drug effects. Immunosuppressive Agents / adverse effects. Lymphoma / virology. Methotrexate / adverse effects
  • [MeSH-minor] Arthritis, Rheumatoid / drug therapy. Cell Line, Tumor. Epstein-Barr Virus Infections / complications. Epstein-Barr Virus Infections / diagnosis. Gene Expression Regulation, Neoplastic. Humans. MAP Kinase Kinase Kinases / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Polymerase Chain Reaction. Polymyositis / drug therapy. Promoter Regions, Genetic. Signal Transduction / drug effects. Viral Load. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 15547182.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01-CA19014; United States / NHLBI NIH HHS / HL / R01 HL 64851; United States / NCI NIH HHS / CA / R01-CA 66519; United States / NCI NIH HHS / CA / R01-CA58853
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / Immunosuppressive Agents; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinases; YL5FZ2Y5U1 / Methotrexate
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8. Takaishi S, Okumura T, Tu S, Wang SS, Shibata W, Vigneshwaran R, Gordon SA, Shimada Y, Wang TC: Identification of gastric cancer stem cells using the cell surface marker CD44. Stem Cells; 2009 May;27(5):1006-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of gastric cancer stem cells using the cell surface marker CD44.
  • Cancer stem cells (CSCs) have been defined as a unique subpopulation in tumors that possess the ability to initiate tumor growth and sustain tumor self-renewal.
  • Although the evidence has been provided to support the existence of CSCs in various solid tumors, the identity of gastric CSCs has not been reported.
  • In this study, we have identified gastric cancer-initiating cells from a panel of human gastric cancer cell lines using cell surface marker CD44.
  • Among six gastric cancer cell lines, three lines MKN-45, MKN-74, and NCI-N87 had a sizeable subpopulation of CD44(+) cells, and these cells showed spheroid colony formation in serum-free media in vitro as well as tumorigenic ability when injected into stomach and skin of severe combined immunodeficient (SCID) mice in vivo.
  • The CD44(+) gastric cancer cells showed the stem cell properties of self-renewal and the ability to form differentiated progeny and gave rise to CD44(-) cells.
  • The CD44(+) gastric cancer cells showed increased resistance for chemotherapy- or radiation-induced cell death.
  • These results support the existence of gastric CSCs and may provide novel approaches to the diagnosis and treatment of gastric cancer.


9. Kakeji Y, Yamaguchi S, Yoshida D, Tanoue K, Ueda M, Masunari A, Utsunomiya T, Imamura M, Honda H, Maehara Y, Hashizume M: Development and assessment of morphologic criteria for diagnosing gastric cancer using confocal endomicroscopy: an ex vivo and in vivo study. Endoscopy; 2006 Sep;38(9):886-90
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  • [Title] Development and assessment of morphologic criteria for diagnosing gastric cancer using confocal endomicroscopy: an ex vivo and in vivo study.
  • BACKGROUND AND STUDY AIMS: The Confocal Endomicroscopy System (Optiscan Pty Ltd. and Pentax Corp.) is a newly developed imaging tool that uses laser light and optical technology to visualize living tissue at the cellular level.
  • Digital images of cells magnified 1000-fold appear in real time on a computer screen, which enables immediate detection of changes in cellular structure without the need for a biopsy.
  • The aim of this study was to assess the features of the cellular architecture of cancerous tissue that can be used in the differential diagnosis of cancerous tissue and normal mucosa using this system's image-processing software.
  • PATIENTS AND METHODS: A total of 27 gastric cancers were examined ex vivo using confocal endomicroscopy.
  • A fluorescent contrast agent, acriflavine, was applied topically to normal and to cancerous mucosa.
  • In vivo imaging of the gastric mucosa after intravenous injection of fluorescein sodium was also performed in nine patients with gastritis or gastric cancer.
  • The mean nuclear area of cancer cells was found to be significantly larger than that of normal cells in 18/27 gastric cancers (67 %).
  • [MeSH-major] Adenocarcinoma / pathology. Endoscopy, Gastrointestinal / methods. Microscopy, Confocal / methods. Stomach Neoplasms / pathology
  • [MeSH-minor] Cell Differentiation. Diagnosis, Differential. Endothelial Cells / pathology. Gastric Mucosa / pathology. Humans. Image Processing, Computer-Assisted. Sensitivity and Specificity

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  • (PMID = 16981104.001).
  • [ISSN] 0013-726X
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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10. Gold JS, Dematteo RP: Combined surgical and molecular therapy: the gastrointestinal stromal tumor model. Ann Surg; 2006 Aug;244(2):176-84
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  • The integration of surgery and treatment with targeted molecular agents in the treatment of GIST is highlighted.
  • Its cellular origin from the interstitial cell of Cajal and distinctness from smooth muscles tumors were only recently appreciated.
  • The pathology, epidemiology, diagnosis, and treatment of this tumor are summarized with particular emphasis on recent developments in the field.
  • RESULTS: GIST is a rare tumor that usually arises from the stomach or small intestine.
  • CONCLUSIONS: The treatment paradigm for GIST has required the integration of surgery and molecular therapy and this will likely serve as a paradigm for the treatment of other solid tumors as targeted agents are developed.

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  • [Cites] Gastroenterology. 2005 Feb;128(2):270-9 [15685537.001]
  • [Cites] AJR Am J Roentgenol. 2004 Dec;183(6):1619-28 [15547201.001]
  • [Cites] World J Gastroenterol. 2005 Feb 21;11(7):1052-5 [15742414.001]
  • [Cites] Ann Oncol. 2005 Apr;16(4):566-78 [15781488.001]
  • [Cites] Lancet Oncol. 2005 Apr;6(4):249-51 [15811621.001]
  • [Cites] Clin Cancer Res. 2005 Jun 1;11(11):4182-90 [15930355.001]
  • [Cites] J Natl Compr Canc Netw. 2004 May;2 Suppl 1:S-1-26; quiz 27-30 [23573667.001]
  • [Cites] Cancer. 2000 Jan 1;88(1):66-74 [10618607.001]
  • [Cites] Ann Surg. 2000 Jan;231(1):51-8 [10636102.001]
  • [Cites] J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437.001]
  • [Cites] Ann Surg Oncol. 2001 Jan-Feb;8(1):50-9 [11206225.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1052-6 [11287975.001]
  • [Cites] Arch Surg. 2001 Apr;136(4):383-9 [11296107.001]
  • [Cites] Science. 2001 Aug 3;293(5531):876-80 [11423618.001]
  • [Cites] Ann Surg. 2001 Oct;234(4):540-7; discussion 547-8 [11573047.001]
  • [Cites] Lancet. 2001 Oct 27;358(9291):1421-3 [11705489.001]
  • [Cites] Cancer Res. 2001 Dec 15;61(24):8624-8 [11751374.001]
  • [Cites] Lancet. 2002 Apr 13;359(9314):1301-7 [11965276.001]
  • [Cites] Hum Pathol. 2002 May;33(5):459-65 [12094370.001]
  • [Cites] Hum Pathol. 2002 May;33(5):478-83 [12094372.001]
  • [Cites] Hum Pathol. 2002 May;33(5):484-95 [12094373.001]
  • [Cites] N Engl J Med. 2002 Aug 15;347(7):472-80 [12181401.001]
  • [Cites] Cancer Cell. 2002 Aug;2(2):117-25 [12204532.001]
  • [Cites] J Clin Oncol. 2002 Sep 15;20(18):3898-905 [12228211.001]
  • [Cites] Eur J Cancer. 2002 Sep;38 Suppl 5:S83-7 [12528778.001]
  • [Cites] Science. 2003 Jan 31;299(5607):708-10 [12522257.001]
  • [Cites] Curr Probl Surg. 2003 Mar;40(3):144-93 [12571542.001]
  • [Cites] Br J Surg. 2003 Mar;90(3):332-9 [12594669.001]
  • [Cites] Gastric Cancer. 2003;6(1):39-48 [12673425.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 May 27;100(11):6706-11 [12754375.001]
  • [Cites] Am J Pathol. 2003 Aug;163(2):691-700 [12875988.001]
  • [Cites] J Clin Oncol. 2003 Dec 1;21(23):4342-9 [14645423.001]
  • [Cites] Gastroenterology. 2004 Jan;126(1):318-21 [14699510.001]
  • [Cites] Eur J Cancer. 2004 Mar;40(5):689-95 [15010069.001]
  • [Cites] Clin Cancer Res. 2004 May 1;10(9):3076-81 [15131046.001]
  • [Cites] Clin Cancer Res. 2004 May 15;10(10):3282-90 [15161681.001]
  • [Cites] Lab Invest. 2004 Jul;84(7):874-83 [15146165.001]
  • [Cites] Am J Surg Pathol. 2004 Jul;28(7):889-94 [15223958.001]
  • [Cites] Gastroenterology. 2004 Jul;127(1):294-9 [15236194.001]
  • [Cites] Cancer Res. 2004 Sep 1;64(17):5913-9 [15342366.001]
  • [Cites] Lancet. 2004 Sep 25-Oct 1;364(9440):1127-34 [15451219.001]
  • [Cites] Oncogene. 2004 Oct 14;23(47):7780-90 [15326474.001]
  • [Cites] Cancer. 1981 Jan 1;47(1):207-14 [7459811.001]
  • [Cites] Cancer. 1995 Jan 1;75(1 Suppl):154-70 [8000994.001]
  • [Cites] Nat Med. 1996 May;2(5):561-6 [8616716.001]
  • [Cites] Science. 1998 Jan 23;279(5350):577-80 [9438854.001]
  • [Cites] Nat Genet. 1998 Aug;19(4):323-4 [9697690.001]
  • [Cites] Am J Surg Pathol. 1999 Jan;23(1):82-7 [9888707.001]
  • [Cites] Cancer Res. 1999 Sep 1;59(17):4297-300 [10485475.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2005 Feb;32(2):153-62 [15690223.001]
  • (PMID = 16858179.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102613; United States / NCI NIH HHS / CA / CA102613
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  • [Number-of-references] 61
  • [Other-IDs] NLM/ PMC1602162
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11. Moss SF, Sood S: Helicobacter pylori. Curr Opin Infect Dis; 2003 Oct;16(5):445-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE OF REVIEW: Helicobacter pylori is an important human pathogen, responsible for most peptic ulcer disease, gastritis and gastric malignancies. H. pylori has several unique features: it is highly adapted for gastric colonization, yet it produces clinical consequences in a small minority, its genome is known, and it is the only bacterium strongly associated with cancer. H. pylori is therefore of great interest to clinicians and researchers of many, often disparate, disciplines.
  • RECENT FINDINGS: The major contentious clinical issues relate to the synergistic gastrotoxic interactions of H. pylori with non-steroidal anti-inflammatory drugs, and a possible association of H. pylori with atherosclerotic events.
  • Accumulating evidence implicates genetic variation in the inflammatory response to H. pylori in the etiology of the increased risk of gastric cancer after H. pylori infection.
  • The effects in gastric epithelial cells of two of the major virulence factors (genes within the cag pathogenicity island and the vacuolating cytotoxin, VacA) of H. pylori illustrate the complex network of cellular reactions activated by H. pylori.
  • [MeSH-major] Helicobacter Infections / diagnosis. Helicobacter Infections / drug therapy
  • [MeSH-minor] Animals. Anti-Infective Agents / administration & dosage. Anti-Ulcer Agents / administration & dosage. Disease Models, Animal. Drug Therapy, Combination. Helicobacter pylori / metabolism. Helicobacter pylori / pathogenicity. Humans. Peptic Ulcer / diagnosis. Peptic Ulcer / drug therapy

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  • (PMID = 14501997.001).
  • [ISSN] 0951-7375
  • [Journal-full-title] Current opinion in infectious diseases
  • [ISO-abbreviation] Curr. Opin. Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Anti-Ulcer Agents
  • [Number-of-references] 58
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