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  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
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We are analyzing https://link.springer.com/article/10.1007/s00268-009-0070-y.

Title:
Overexpression and Interactions of Interleukin-10, Transforming Growth Factor β, and Vascular Endothelial Growth Factor in Esophageal Squamous Cell Carcinoma | World Journal of Surgery
Description:
Sharing the role of immune suppression, interleukin-10 (IL-10), transforming growth factor β (TGF-β), and vascular endothelial growth factor (VEGF) are critical genes in several aspects of tumorigenesis. To elucidate the role of these cytokines in esophageal squamous cell carcinoma (ESCC), their relative mRNA expression in tumoral tissue compared with corresponding tumor-free tissue was evaluated. A total of 49 patients with histologically confirmed ESCC were included in the study prior to any therapeutic interventions. Quantitative analysis of the mRNA expression was performed by real-time reverse transcription-polymerase chain reaction and the clinicopathologic associations were assessed. The mRNA of IL-10, VEGF, and TGF-β was frequently overexpressed in 53.2%, 44.9%, and 37.5% of ESCC patients, respectively. TGF-β was significantly co-expressed with IL-10 and with VEGF. Although VEGF was not independently associated with increased tumor size (p = 0.065), concomitant overexpression of VEGF with TGF-β was significantly correlated with increased size of the tumor (p < 0.05). Overexpression of IL-10, TGF-β, and VEGF plays an important role in ESCC and consequently leads to the frequent event of immune evasion in ESCC. TGF-β is concomitantly overexpressed with IL-10 and with VEGF in ESCC. A stimulatory signal from TGF-β to VEGF is necessary for VEGF to promote tumor progression.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Science
  • Social Networks

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,643,078 visitors per month in the current month.

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How Does Link.springer.com Make Money? {💸}

We find it hard to spot revenue streams.

Some websites aren't about earning revenue; they're built to connect communities or raise awareness. There are numerous motivations behind creating websites. This might be one of them. Link.springer.com could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {🔍}

google, scholar, article, pubmed, cas, growth, factor, cancer, transforming, cell, vegf, expression, endothelial, esophageal, vascular, carcinoma, tgfβ, cells, human, tgfbeta, interleukin, squamous, immune, tumor, res, research, mohammad, mrna, role, escc, access, beta, iran, factorbeta, mashhad, privacy, cookies, content, journal, overexpression, reza, int, rev, immunol, analysis, data, publish, search, world, surgery,

Topics {✒️}

mohammad taghi rajabi-mashhadi transforming growth factor-beta transforming growth factor anti-tumour activity mohammad naser forghani month download article/chapter quantitative real-time pcr mohammad reza abbaszadegan tumor-induced immune suppression esophageal carcinoma human esophageal cancer related subjects immunology research center injury endothelial cells mhc class unfavorable prognostic factor promote tumor progression full article pdf tumor-free tissue article world journal privacy choices/manage cookies hossein naseh tumoral tissue compared esophageal cancer avicenna research institute check access instant access dendritic cell induction endothelial cells human melanoma cells mesenchymal stem cells vegf-targeted therapy tumor growth increased tumor size tgf-beta1 expression tgf-beta stimulation tumor–host interaction tumor-infiltrating lymphocytes important immune mediators bahram memar lymph node metastasis cell proliferation messenger rna expression true immunoregulatory cytokine european economic area isolated perfused microvessels emerging immunotherapeutic targets synthetic peptide homologous elevates nitric oxide relative mrna expression

Questions {❓}

  • Wakkach A, Cottrez F, Groux H (2000) Can interleukin-10 be used as a true immunoregulatory cytokine?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Overexpression and Interactions of Interleukin-10, Transforming Growth Factor β, and Vascular Endothelial Growth Factor in Esophageal Squamous Cell Carcinoma
         description:Sharing the role of immune suppression, interleukin-10 (IL-10), transforming growth factor β (TGF-β), and vascular endothelial growth factor (VEGF) are critical genes in several aspects of tumorigenesis. To elucidate the role of these cytokines in esophageal squamous cell carcinoma (ESCC), their relative mRNA expression in tumoral tissue compared with corresponding tumor-free tissue was evaluated. A total of 49 patients with histologically confirmed ESCC were included in the study prior to any therapeutic interventions. Quantitative analysis of the mRNA expression was performed by real-time reverse transcription-polymerase chain reaction and the clinicopathologic associations were assessed. The mRNA of IL-10, VEGF, and TGF-β was frequently overexpressed in 53.2%, 44.9%, and 37.5% of ESCC patients, respectively. TGF-β was significantly co-expressed with IL-10 and with VEGF. Although VEGF was not independently associated with increased tumor size (p = 0.065), concomitant overexpression of VEGF with TGF-β was significantly correlated with increased size of the tumor (p < 0.05). Overexpression of IL-10, TGF-β, and VEGF plays an important role in ESCC and consequently leads to the frequent event of immune evasion in ESCC. TGF-β is concomitantly overexpressed with IL-10 and with VEGF in ESCC. A stimulatory signal from TGF-β to VEGF is necessary for VEGF to promote tumor progression.
         datePublished:2009-05-14T00:00:00Z
         dateModified:2009-05-14T00:00:00Z
         pageStart:1439
         pageEnd:1445
         sameAs:https://doi.org/10.1007/s00268-009-0070-y
         keywords:
            Vascular Endothelial Growth Factor
            Esophageal Cancer
            Esophageal Squamous Cell Carcinoma
            Major Histocompatibility Complex Class
            Esophageal Squamous Cell Carcinoma Patient
            Surgery
            Abdominal Surgery
            Cardiac Surgery
            General Surgery
            Thoracic Surgery
            Vascular Surgery
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                        name:Division of Human Genetics, Immunology Research Center, Avicenna Research Institute, Mashhad University of Medical Sciences (MUMS), Mashhad, Iran
                        type:PostalAddress
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                        type:PostalAddress
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                        type:PostalAddress
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               name:Mohammad Taghi Rajabi-Mashhadi
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                     name:Omid Hospital, MUMS
                     address:
                        name:Department of Surgery, Omid Hospital, MUMS, Mashhad, Iran
                        type:PostalAddress
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                        name:Department of Pathology, Razavi Hospital, Mashhad, Iran
                        type:PostalAddress
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               name:Mohammad Reza Abbaszadegan
               affiliation:
                     name:Mashhad University of Medical Sciences (MUMS)
                     address:
                        name:Division of Human Genetics, Immunology Research Center, Avicenna Research Institute, Mashhad University of Medical Sciences (MUMS), Mashhad, Iran
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ScholarlyArticle:
      headline:Overexpression and Interactions of Interleukin-10, Transforming Growth Factor β, and Vascular Endothelial Growth Factor in Esophageal Squamous Cell Carcinoma
      description:Sharing the role of immune suppression, interleukin-10 (IL-10), transforming growth factor β (TGF-β), and vascular endothelial growth factor (VEGF) are critical genes in several aspects of tumorigenesis. To elucidate the role of these cytokines in esophageal squamous cell carcinoma (ESCC), their relative mRNA expression in tumoral tissue compared with corresponding tumor-free tissue was evaluated. A total of 49 patients with histologically confirmed ESCC were included in the study prior to any therapeutic interventions. Quantitative analysis of the mRNA expression was performed by real-time reverse transcription-polymerase chain reaction and the clinicopathologic associations were assessed. The mRNA of IL-10, VEGF, and TGF-β was frequently overexpressed in 53.2%, 44.9%, and 37.5% of ESCC patients, respectively. TGF-β was significantly co-expressed with IL-10 and with VEGF. Although VEGF was not independently associated with increased tumor size (p = 0.065), concomitant overexpression of VEGF with TGF-β was significantly correlated with increased size of the tumor (p < 0.05). Overexpression of IL-10, TGF-β, and VEGF plays an important role in ESCC and consequently leads to the frequent event of immune evasion in ESCC. TGF-β is concomitantly overexpressed with IL-10 and with VEGF in ESCC. A stimulatory signal from TGF-β to VEGF is necessary for VEGF to promote tumor progression.
      datePublished:2009-05-14T00:00:00Z
      dateModified:2009-05-14T00:00:00Z
      pageStart:1439
      pageEnd:1445
      sameAs:https://doi.org/10.1007/s00268-009-0070-y
      keywords:
         Vascular Endothelial Growth Factor
         Esophageal Cancer
         Esophageal Squamous Cell Carcinoma
         Major Histocompatibility Complex Class
         Esophageal Squamous Cell Carcinoma Patient
         Surgery
         Abdominal Surgery
         Cardiac Surgery
         General Surgery
         Thoracic Surgery
         Vascular Surgery
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            1432-2323
            0364-2313
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         name:Springer-Verlag
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            name:Mehran Gholamin
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                     name:Division of Human Genetics, Immunology Research Center, Avicenna Research Institute, Mashhad University of Medical Sciences (MUMS), Mashhad, Iran
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Omeed Moaven
            affiliation:
                  name:Mashhad University of Medical Sciences (MUMS)
                  address:
                     name:Division of Human Genetics, Immunology Research Center, Avicenna Research Institute, Mashhad University of Medical Sciences (MUMS), Mashhad, Iran
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Bahram Memar
            affiliation:
                  name:Omid Hospital, MUMS
                  address:
                     name:Department of Pathology, Omid Hospital, MUMS, Mashhad, Iran
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Moein Farshchian
            affiliation:
                  name:Mashhad University of Medical Sciences (MUMS)
                  address:
                     name:Division of Human Genetics, Immunology Research Center, Avicenna Research Institute, Mashhad University of Medical Sciences (MUMS), Mashhad, Iran
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Hossein Naseh
            affiliation:
                  name:Omid Hospital, MUMS
                  address:
                     name:Department of Pathology, Omid Hospital, MUMS, Mashhad, Iran
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Reza Malekzadeh
            affiliation:
                  name:University of Tehran
                  address:
                     name:Digestive Disease Research Center, University of Tehran, Tehran, Iran
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Masoud Sotoudeh
            affiliation:
                  name:University of Tehran
                  address:
                     name:Digestive Disease Research Center, University of Tehran, Tehran, Iran
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Mohammad Taghi Rajabi-Mashhadi
            affiliation:
                  name:Omid Hospital, MUMS
                  address:
                     name:Department of Surgery, Omid Hospital, MUMS, Mashhad, Iran
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Mohammad Naser Forghani
            affiliation:
                  name:Omid Hospital, MUMS
                  address:
                     name:Department of Surgery, Omid Hospital, MUMS, Mashhad, Iran
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Farid Farrokhi
            affiliation:
                  name:Razavi Hospital
                  address:
                     name:Department of Pathology, Razavi Hospital, Mashhad, Iran
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Mohammad Reza Abbaszadegan
            affiliation:
                  name:Mashhad University of Medical Sciences (MUMS)
                  address:
                     name:Division of Human Genetics, Immunology Research Center, Avicenna Research Institute, Mashhad University of Medical Sciences (MUMS), Mashhad, Iran
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      name:University of Tehran
      address:
         name:Digestive Disease Research Center, University of Tehran, Tehran, Iran
         type:PostalAddress
      name:Omid Hospital, MUMS
      address:
         name:Department of Surgery, Omid Hospital, MUMS, Mashhad, Iran
         type:PostalAddress
      name:Omid Hospital, MUMS
      address:
         name:Department of Surgery, Omid Hospital, MUMS, Mashhad, Iran
         type:PostalAddress
      name:Razavi Hospital
      address:
         name:Department of Pathology, Razavi Hospital, Mashhad, Iran
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            name:Mashhad University of Medical Sciences (MUMS)
            address:
               name:Division of Human Genetics, Immunology Research Center, Avicenna Research Institute, Mashhad University of Medical Sciences (MUMS), Mashhad, Iran
               type:PostalAddress
            type:Organization
      name:Omeed Moaven
      affiliation:
            name:Mashhad University of Medical Sciences (MUMS)
            address:
               name:Division of Human Genetics, Immunology Research Center, Avicenna Research Institute, Mashhad University of Medical Sciences (MUMS), Mashhad, Iran
               type:PostalAddress
            type:Organization
      name:Bahram Memar
      affiliation:
            name:Omid Hospital, MUMS
            address:
               name:Department of Pathology, Omid Hospital, MUMS, Mashhad, Iran
               type:PostalAddress
            type:Organization
      name:Moein Farshchian
      affiliation:
            name:Mashhad University of Medical Sciences (MUMS)
            address:
               name:Division of Human Genetics, Immunology Research Center, Avicenna Research Institute, Mashhad University of Medical Sciences (MUMS), Mashhad, Iran
               type:PostalAddress
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            name:Omid Hospital, MUMS
            address:
               name:Department of Pathology, Omid Hospital, MUMS, Mashhad, Iran
               type:PostalAddress
            type:Organization
      name:Reza Malekzadeh
      affiliation:
            name:University of Tehran
            address:
               name:Digestive Disease Research Center, University of Tehran, Tehran, Iran
               type:PostalAddress
            type:Organization
      name:Masoud Sotoudeh
      affiliation:
            name:University of Tehran
            address:
               name:Digestive Disease Research Center, University of Tehran, Tehran, Iran
               type:PostalAddress
            type:Organization
      name:Mohammad Taghi Rajabi-Mashhadi
      affiliation:
            name:Omid Hospital, MUMS
            address:
               name:Department of Surgery, Omid Hospital, MUMS, Mashhad, Iran
               type:PostalAddress
            type:Organization
      name:Mohammad Naser Forghani
      affiliation:
            name:Omid Hospital, MUMS
            address:
               name:Department of Surgery, Omid Hospital, MUMS, Mashhad, Iran
               type:PostalAddress
            type:Organization
      name:Farid Farrokhi
      affiliation:
            name:Razavi Hospital
            address:
               name:Department of Pathology, Razavi Hospital, Mashhad, Iran
               type:PostalAddress
            type:Organization
      name:Mohammad Reza Abbaszadegan
      affiliation:
            name:Mashhad University of Medical Sciences (MUMS)
            address:
               name:Division of Human Genetics, Immunology Research Center, Avicenna Research Institute, Mashhad University of Medical Sciences (MUMS), Mashhad, Iran
               type:PostalAddress
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      name:Division of Human Genetics, Immunology Research Center, Avicenna Research Institute, Mashhad University of Medical Sciences (MUMS), Mashhad, Iran
      name:Department of Pathology, Omid Hospital, MUMS, Mashhad, Iran
      name:Division of Human Genetics, Immunology Research Center, Avicenna Research Institute, Mashhad University of Medical Sciences (MUMS), Mashhad, Iran
      name:Department of Pathology, Omid Hospital, MUMS, Mashhad, Iran
      name:Digestive Disease Research Center, University of Tehran, Tehran, Iran
      name:Digestive Disease Research Center, University of Tehran, Tehran, Iran
      name:Department of Surgery, Omid Hospital, MUMS, Mashhad, Iran
      name:Department of Surgery, Omid Hospital, MUMS, Mashhad, Iran
      name:Department of Pathology, Razavi Hospital, Mashhad, Iran
      name:Division of Human Genetics, Immunology Research Center, Avicenna Research Institute, Mashhad University of Medical Sciences (MUMS), Mashhad, Iran
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External Links {🔗}(152)

Analytics and Tracking {📊}

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