For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
47
views
Article has an altmetric score of 2
122
references
 Top references
cited by
25
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      1,119
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Dendritic cell defects in the colorectal cancer

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Colorectal cancer (CRC) results from the accumulation of both genetic and epigenetic alterations of the genome. However, also the formation of an inflammatory milieu plays a pivotal role in tumor development and progression. Dendritic cells (DCs) play a relevant role in tumor by exerting differential pro-tumorigenic and anti-tumorigenic functions, depending on the local milieu. Quantitative and functional impairments of DCs have been widely observed in several types of cancer, including CRC, representing a tumor-escape mechanism employed by cancer cells to elude host immunosurveillance.

          Understanding the interactions between DCs and tumors is important for comprehending the mechanisms of tumor immune surveillance and escape, and provides novel approaches to therapy of cancer. This review summarizes updated information on the role of the DCs in colon cancer development and/or progression.

          Related collections

          Most cited references122

          • Record: found
          • Abstract: found
          • Article: not found

          Myeloid-derived suppressor cells: linking inflammation and cancer.

          Suzanne Ostrand-Rosenberg, Pratima Sinha (2009)
          Many cancer immunotherapies developed in experimental animals have been tested in clinical trials. Although some have shown modest clinical effects, most have not been effective. Recent studies have identified myeloid-origin cells that are potent suppressors of tumor immunity and therefore a significant impediment to cancer immunotherapy. "Myeloid-derived suppressor cells" (MDSC) accumulate in the blood, lymph nodes, and bone marrow and at tumor sites in most patients and experimental animals with cancer and inhibit both adaptive and innate immunity. MDSC are induced by tumor-secreted and host-secreted factors, many of which are proinflammatory molecules. The induction of MDSC by proinflammatory mediators led to the hypothesis that inflammation promotes the accumulation of MDSC that down-regulate immune surveillance and antitumor immunity, thereby facilitating tumor growth. This article reviews the characterization and suppressive mechanisms used by MDSC to block tumor immunity and describes the mechanisms by which inflammation promotes tumor progression through the induction of MDSC.
          Article 0 comments Cited 546 times – based on 0 reviews     Review now
          Article has an altmetric score of 15
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Normalizing tumor microenvironment to treat cancer: bench to bedside to biomarkers.

            Rakesh K Jain (2013)
            For almost four decades, my work has focused on one challenge: improving the delivery and efficacy of anticancer therapeutics. Working on the hypothesis that the abnormal tumor microenvironment-characterized by hypoxia and high interstitial fluid pressure--fuels tumor progression and treatment resistance, we developed an array of sophisticated imaging technologies and animal models as well as mathematic models to unravel the complex biology of tumors. Using these tools, we demonstrated that the blood and lymphatic vasculature, fibroblasts, immune cells, and extracellular matrix associated with tumors are abnormal, which together create a hostile tumor microenvironment. We next hypothesized that agents that induce normalization of the microenvironment can improve treatment outcome. Indeed, we demonstrated that judicious use of antiangiogenic agents--originally designed to starve tumors--could transiently normalize tumor vasculature, alleviate hypoxia, increase delivery of drugs and antitumor immune cells, and improve the outcome of various therapies. Our trials of antiangiogenics in patients with newly diagnosed and recurrent glioblastoma supported this concept. They revealed that patients whose tumor blood perfusion increased in response to cediranib survived 6 to 9 months longer than those whose blood perfusion did not increase. The normalization hypothesis also opened doors to treating various nonmalignant diseases characterized by abnormal vasculature, such as neurofibromatosis type 2. More recently, we discovered that antifibrosis drugs capable of normalizing the tumor microenvironment can improve the delivery and efficacy of nano- and molecular medicines. Our current efforts are directed at identifying predictive biomarkers and more-effective strategies to normalize the tumor microenvironment for enhancing anticancer therapies.
            Article 0 comments Cited 445 times – based on 0 reviews     Review now
            Article has an altmetric score of 27
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Quantitative expression of toll-like receptor 1-10 mRNA in cellular subsets of human peripheral blood mononuclear cells and sensitivity to CpG oligodeoxynucleotides.

              Veit Hornung, Simon Rothenfusser, Stefanie Britsch … (2002)
              The Toll-like receptor (TLR)9 is critical for the recognition of immunostimulatory CpG motifs but may cooperate with other TLRs. We analyzed TLR1-10 mRNA expression by using quantitative real-time PCR in highly purified subsets of human PBMC and determined the sensitivity of these subsets to CpG oligodeoxynucleotides (ODN). TLR1 and TLR6 were expressed in all cell types examined. TLR10 was highly expressed in B cells and weakly expressed in plasmacytoid dendritic cells (PDC). High expression of TLR2 was characteristic for monocytes. PDC and B cells expressed marked levels of TLR7 and TLR9 and were directly sensitive to CpG ODN. In CpG ODN-stimulated PDC and B cells, TLR9 expression rapidly decreased, as opposed to TLR7, which was up-regulated in PDC and decreased in B cells. In monocytes, NK cells, and T cells, TLR7 was absent. Despite low expression of TLR9, monocytes, NK cells, and T cells did not respond to CpG ODN in the absence of PDC but were activated in the presence of PDC. In conclusion, our studies provide evidence that PDC and B cells, but not monocytes, NK cells, or T cells, are primary targets of CpG ODN in peripheral blood. The characteristic expression pattern of TLR1-10 in cellular subsets of human PBMC is consistent with the concept that TLR9 is essential in the recognition of CpG ODN in PDC and B cells. In addition, selective regulation of TLR7 expression in PDC and B cells by CpG ODN revealed TLR7 as a candidate TLR potentially involved in modulating the recognition of CpG motifs.
              Article 0 comments Cited 434 times – based on 0 reviews     Review now
              Article has an altmetric score of 9
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Hum Vaccin Immunother
                Journal ID (iso-abbrev): Hum Vaccin Immunother
                Journal ID (pmc): KHVI
                Title: Human Vaccines & Immunotherapeutics
                Publisher: Taylor & Francis
                ISSN (Print): 2164-5515
                ISSN (Electronic): 2164-554X
                Publication date (Electronic): 1 November 2014
                Publication date Collection: November 2014
                Volume: 10
                Issue: 11
                Pages: 3224-3235
                Affiliations
                [1 ]Department of Clinical and Experimental Medicine; University of Pisa ; Pisa, Italy
                [2 ]Department of Surgery, Medical, Molecular, and Critical Area Pathology; University of Pisa ; Pisa, Italy
                Author notes
                [†]

                A Legitimo and R Consolini contributed equally to this work.

                [* ]Correspondence to: Rita Consolini; Email: rita.consolini@ 123456med.unipi.it
                Article
                Publisher ID: 974450
                DOI: 10.4161/hv.29857
                PMC ID: 4514061
                PubMed ID: 25483675
                SO-VID: 774829ab-217f-4e7c-a725-0ddf131b63f6
                Copyright © © 2014 The Author(s). Published with license by Taylor & Francis Group, LLC© Annalisa Legitimo, Rita Consolini, Alessandra Failli, Giulia Orsini, and Roberto Spisni
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

                History
                Date received : 16 May 2014
                Date revision received : 26 June 2014
                Date accepted : 8 July 2014
                Page count
                Figures: 4, Tables: 0, References: 150, Pages: 12
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular medicine
                Keywords: colorectal cancer,dendritic cells,immunoescape,immune response,tumor microenvironment
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: colorectal cancer, dendritic cells, immunoescape, immune response, tumor microenvironment

                Comments

                Comment on this article

                scite_
                0
                0
                0
                0
                Smart Citations
                0
                0
                0
                0
                Citing PublicationsSupportingMentioningContrasting
                View Citations

                See how this article has been cited at scite.ai

                scite shows how a scientific paper has been cited by providing the context of the citation, a classification describing whether it supports, mentions, or contrasts the cited claim, and a label indicating in which section the citation was made.

                Similar content1,119

                See all similar

                Cited by49

                See all cited by

                Most referenced authors2,425

                See all reference authors