For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
7
views
29
references
 Top references
cited by
1
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      317
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      GEFT aberrant expression in soft tissue sarcomas

      research-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

          Background

          Guanine nucleotide exchange factor T (GEFT) exhibits high amplification level using high-resolution array comparative genomic hybridization in rhabdomyosarcoma. The overexpression rate of GEFT protein is higher in rhabdomyosarcoma than in normal striated muscle tissues. This study evaluated the aberrant expression of GEFT in multiple subtypes of soft tissue sarcoma (STS) and compared the differences in clinical pathology, histological feature and expression levels of GEFT protein and mRNA between chromosomal translocation-associated sarcomas (CTAS) and non-chromosomal translocation-associated sarcomas (NCTAS).

          Methods

          GEFT protein expression was detected using immunohistochemistry (IHC) and tissue microarrays. Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) was used to detect the expression of GEFT mRNA.

          Results

          The rates of GEFT positive expression (196/219, 89.50%) and overexpression (113/219, 51.60%) were higher in multiple subtypes of STS than in normal striated muscle tissues. The rates of GEFT positive expression and overexpression in all subtypes of STS detected were significantly higher than that in the controls. No difference of GEFT expression was detected between CTAS and NCTAS.

          Conclusions

          The abnormal expression of GEFT exists in various subtypes of STS, which may play an important role in tumorigenesis of STS.

          Related collections

          Most cited references29

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

          Sarcoma classification: an update based on the 2013 World Health Organization Classification of Tumors of Soft Tissue and Bone.

          Leona Doyle (2014)
          The 2013 World Health Organization Classification of Tumors of Soft Tissue and Bone incorporates changes in tumor classification, as well as new genetic insights into the pathogenesis of many different tumor types that have emerged over the 11 years since the publication of the prior volume. This article reviews changes in the classification of soft tissue and bone sarcomas as well as tumors of intermediate biologic potential in the 2013 World Health Organization volume, new molecular insights into these tumors, and associated surgical and clinical implications.
          Article 0 comments Cited 149 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Rho GTPases: Regulation and roles in cancer cell biology

            Anne J Ridley, Raquel B. Haga (2016)
            Rho GTPases are well known for their roles in regulating cell migration, and also contribute to a variety of other cellular responses. They are subdivided into 2 groups: typical and atypical. The typical Rho family members, including RhoA, Rac1 and Cdc42, cycle between an active GTP-bound and inactive GDP-bound conformation, and are regulated by GEFs, GAPs and GDIs, whereas atypical Rho family members have amino acid substitutions that alter their ability to interact with GTP/GDP and hence are regulated by different mechanisms. Both typical and atypical Rho GTPases contribute to cancer progression. In a few cancers, RhoA or Rac1 are mutated, but in most cancers expression levels and/or activity of Rho GTPases is altered. Rho GTPase signaling could therefore be therapeutically targeted in cancer treatment.
            Article 0 comments Cited 144 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Rho GTPases modulate malignant transformation of tumor cells.

              José Orgaz, Cecilia Herraiz, Victoria Sanz-Moreno (2014)
              Rho GTPases are involved in the acquisition of all the hallmarks of cancer, which comprise 6 biological capabilities acquired during the development of human tumors. The hallmarks include proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis programs, as defined by Hanahan and Weinberg. (1) Controlling these hallmarks are genome instability and inflammation. Emerging hallmarks are reprogramming of energy metabolism and evading immune destruction. To give a different view to the readers, we will not be focusing on invasion, metastasis, or cytoskeletal remodeling, but we will review here how Rho GTPases contribute to other hallmarks of cancer with a special emphasis on malignant transformation.
              Article 0 comments Cited 70 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Transl Cancer Res
                Journal ID (iso-abbrev): Transl Cancer Res
                Journal ID (publisher-id): TCR
                Title: Translational Cancer Research
                Publisher: AME Publishing Company
                ISSN (Print): 2218-676X
                ISSN (Electronic): 2219-6803
                Publication date (Print and electronic): February 2019
                Publication date (Print): February 2019
                Volume: 8
                Issue: 1
                Pages: 141-149
                Affiliations
                [1 ]Department of Pathology, Shihezi University School of Medicine, Shihezi 832002, China, ;
                [2 ]deptDepartment of Pathology, Beijing Chaoyang Hospital , Capital Medical University , Beijing 100020, China
                Author notes

                Contributions: (I) Conception and design: F Li, C Liu, Y Liu, S Qi; (II) Administrative support: None; (III) Provision of study materials or patients: F Li, C Liu; (IV) Collection and assembly of data: C Liu, Y Liu, S Qi, L Meng, L Zhang, Y Pang, W Cui, J Du ; (V) Data analysis and interpretation: Y Liu, S Qi; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

                [#]

                These authors contributed equally to this work.

                Correspondence to: Chunxia Liu, MD. Department of Pathology, Shihezi University School of Medicine, No. 221, North Fourth Road, Shihezi City, Xinjiang Uygur Autonomous Region, Shihezi 832002, China. Email: liuliu2239@ 123456sina.com ; Feng Li, MD. Department of Pathology, Beijing Chaoyang Hospital, Capital Medical University, No. 8, South Workers Stadium, Chaoyang District, Beijing 100020, China. Email: lifeng7855@ 123456126.com .
                Article
                Publisher ID: tcr-08-01-141
                DOI: 10.21037/tcr.2019.01.16
                PMC ID: 8798328
                PubMed ID: 35116743
                SO-VID: 72032f22-7795-494c-ae77-f10c979c5390
                Copyright © 2019 Translational Cancer Research. All rights reserved.
                License:

                Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

                History
                Date received : 15 September 2018
                Date accepted : 07 January 2019
                Funding
                Funded by: National Natural Science Foundation of China
                Award ID: No. 81660441
                Award ID: No. 81460404
                Funded by: Shihezi University Initiative Research Projects for Senior Fellows
                Award ID: No. RCZX201447
                Categories
                Subject: Original Article

                Keywords: guanine nucleotide exchange factor t (geft),soft tissue sarcoma (sts),chromosomal translocation,non-chromosomal translocation-associated,immunohistochemistry
                Data availability:
                Keywords: guanine nucleotide exchange factor t (geft), soft tissue sarcoma (sts), chromosomal translocation, non-chromosomal translocation-associated, immunohistochemistry

                Comments

                Comment on this article