For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
23
views
112
references
 Top references
cited by
13
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
1 collections
    0
    shares
      1,111
      similar
       All similar
      OncoTargets and Therapy (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on the pathological basis of cancers, potential targets for therapy and treatment protocols to improve the management of cancer patients. Publishing high-quality, original research on molecular aspects of cancer, including the molecular diagnosis, since 2008. Sign up for email alerts here. 50,877 Monthly downloads/views I 4.345 Impact Factor I 7.0 CiteScore I 0.81 Source Normalized Impact per Paper (SNIP) I 0.811 Scimago Journal & Country Rank (SJR)

      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Immunocompromised and immunocompetent mouse models for head and neck squamous cell carcinoma

      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

          Mouse models can closely mimic human oral squamous epithelial carcinogenesis, greatly expand the in vivo research possibilities, and play a critical role in the development of diagnosis, monitoring, and treatment of head and neck squamous cell carcinoma. With the development of the recent research on the contribution of immunity/inflammation to cancer initiation and progression, mouse models have been divided into two categories, namely, immunocompromised and immunocompetent mouse models. And thus, this paper will review these two kinds of models applied in head and neck squamous cell carcinoma to provide a platform to understand the complicated histological, molecular, and genetic changes of oral squamous epithelial tumorigenesis.

          Most cited references112

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

          Why don't we get more cancer? A proposed role of the microenvironment in restraining cancer progression.

          Mina Bissell, William C. Hines (2011)
          Tumors are like new organs and are made of multiple cell types and components. The tumor competes with the normal microenvironment to overcome antitumorigenic pressures. Before that battle is won, the tumor may exist within the organ unnoticed by the host, referred to as 'occult cancer'. We review how normal tissue homeostasis and architecture inhibit progression of cancer and how changes in the microenvironment can shift the balance of these signals to the procancerous state. We also include a discussion of how this information is being tailored for clinical use.
          Article 0 comments Cited 557 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            TGFβ2 dictates disseminated tumour cell fate in target organs through TGFβ-RIII and p38α/β signalling

            Paloma Bragado, Yeriel Estrada, Falguni Parikh … (2013)
            In patients non-proliferative disseminated tumour cells (DTCs) can persist in the bone marrow (BM) while other organs (i.e. lung) present growing metastasis. This suggested that the BM might be a metastasis “restrictive soil” by encoding dormancy-inducing cues in DTCs. Here we show in a HNSCC model that strong and specific TGFβ2 signalling in the BM activates p38α/β, inducing a [ERK/p38]low signalling ratio. This results in induction of DEC2/SHARP1 and p27, downregulation of CDK4 and dormancy of malignant DTCs. TGFβ2-induced dormancy required TGFβ-receptor-I, TGFβ-receptor-III and SMAD1/5 activation to induce p27. In lungs, a metastasis “permissive soil” with low TGFβ2 levels, DTC dormancy was short lived and followed by metastatic growth. Importantly, systemic inhibition of TGFβ-receptor-I or p38α/β activities awakened dormant DTCs fueling multi-organ metastasis. Our work reveals a “seed and soil” mechanism where TGFβ2 and TGFβRIII signalling through p38α/β regulates DTC dormancy and defines restrictive (BM) and -permissive (lung) microenvironments for HNSCC metastasis.
            Article 0 comments Cited 218 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Multiple defects in innate and adaptive immunologic function in NOD/LtSz-scid mice.

              L Shultz, P Schweitzer, S Christianson … (1995)
              The scid mutation was backcrossed ten generations onto the NOD/Lt strain background, resulting in an immunodeficient stock (NOD/LtSz-scid/scid) with multiple defects in adaptive as well as nonadaptive immunologic function. NOD/LtSz-scid/scid mice lack functional lymphoid cells and show little or no serum Ig with age. Although NOD/(Lt-)+/+ mice develop T cell-mediated autoimmune, insulin-dependent diabetes mellitus, NOD/LtSz-scid/scid mice are both insulitis- and diabetes-free throughout life. However, because of a high incidence of thymic lymphomas, the mean lifespan of this congenic stock is only 8.5 mo under specific pathogen-free conditions. After i.v. injection of human CEM T-lymphoblastoid cells, splenic engraftment of these cells was fourfold greater in NOD/LtSz-scid/scid mice than in C.B17/Sz-scid/scid mice. Although C.B-17Sz-scid/scid mice exhibit robust NK cell activity, this activity is markedly reduced in both NOD/(Lt-)+/+ and NOD/LtSz-scid/scid mice. Presence of a functionally less mature macrophage population in NOD/LtSz-scid/scid vs C.B-17Sz-scid/scid mice is indicated by persistence in the former of the NOD/Lt strain-specific defect in LPS-stimulated IL-1 secretion by marrow-derived macrophages. Although C.B-17Sz-scid/scid and C57BL/6Sz-scid/scid mice have elevated serum hemolytic complement activity compared with their respective +/+ controls, both NOD/(LtSz-)+/+ and NOD/LtSz-scid/scid mice lack this activity. Age-dependent increases in serum Ig levels (> 1 micrograms/ml) were observed in only 2 of 30 NOD/LtSz-scid/scid mice vs 21 of 29 C.B-17/Sz-scid/scid animals. The multiple defects in innate and adaptive immunity unique to the NOD/LtSz-scid/scid mouse provide an excellent in vivo environment for reconstitution with human hematopoietic cells.
              Article 0 comments Cited 214 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Onco Targets Ther
                Journal ID (iso-abbrev): Onco Targets Ther
                Journal ID (publisher-id): OncoTargets and Therapy
                Title: OncoTargets and therapy
                Publisher: Dove Medical Press
                ISSN (Electronic): 1178-6930
                Publication date Collection: 2016
                Publication date (Electronic): 27 January 2016
                Volume: 9
                Pages: 545-555
                Affiliations
                [1 ]Department of Oral and Maxillofacial Surgery, Stomatological Hospital Affiliated to Nanchang University, Nanchang, Jiangxi, People’s Republic of China
                [2 ]Department of Stomatology, Sichuan Medical Science Academy and Sichuan Provincial People’s Hospital, Chengdu, Sichuan, People’s Republic of China
                [3 ]State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, People’s Republic of China
                [4 ]Department of Oral and Maxillofacial Surgery, West China College of Stomatology, Sichuan University, Chengdu, Sichuan, People’s Republic of China
                [5 ]Department of Oral Pathology, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, People’s Republic of China
                Author notes
                Correspondence: Ya-ling Tang, State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, No 14, Section 3, Renminnan Road, Chengdu 610041, Sichuan, People’s Republic of China, Tel +86 150 0845 8098, Email tangyaling@ 123456scu.edu.cn
                Xin-hua Liang, Department of Oral and Maxillofacial Surgery, West China College of Stomatology, Sichuan University, No 14, Section 3, Renminnan Road, Chengdu 610041, Sichuan, People’s Republic of China, Tel +86 158 8448 3965, Email lxh88866@ 123456scu.edu.cn
                [*]

                These authors contributed equally to this work

                Article
                Publisher ID: ott-9-545
                DOI: 10.2147/OTT.S95633
                PMC ID: 4734789
                PubMed ID: 26869799
                SO-VID: 9dca7122-4c6f-4c65-ab37-bbe00a519548
                Copyright © © 2016 Lei et al. This work is published and licensed by Dove Medical Press Limited
                License:

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Subject: Review

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: head and neck squamous cell carcinoma,hnscc,mouse models,immunocompromised models,immunocompetent models,transgenic models
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: head and neck squamous cell carcinoma, hnscc, mouse models, immunocompromised models, immunocompetent models, transgenic models

                Comments

                Comment on this article

                scite_

                Similar content1,111

                See all similar

                Cited by13

                See all cited by

                Most referenced authors1,402

                See all reference authors