Please use this identifier to cite or link to this item: http://cmuir.cmu.ac.th/jspui/handle/6653943832/49712
Full metadata record
DC FieldValueLanguage
dc.contributor.authorY. Liuen_US
dc.contributor.authorS. Tuveen_US
dc.contributor.authorJ. Perssonen_US
dc.contributor.authorI. Beyeren_US
dc.contributor.authorR. Yumulen_US
dc.contributor.authorZ. Y. Lien_US
dc.contributor.authorK. Tragoolpuaen_US
dc.contributor.authorK. E. Hellströmen_US
dc.contributor.authorS. Roffleren_US
dc.contributor.authorA. Lieberen_US
dc.date.accessioned2018-09-04T04:05:51Z-
dc.date.available2018-09-04T04:05:51Z-
dc.date.issued2011-06-01en_US
dc.identifier.issn14765500en_US
dc.identifier.issn09291903en_US
dc.identifier.other2-s2.0-79956110698en_US
dc.identifier.other10.1038/cgt.2011.8en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=79956110698&origin=inwarden_US
dc.identifier.urihttp://cmuir.cmu.ac.th/jspui/handle/6653943832/49712-
dc.description.abstractTumor-associated antigens (TAAs) include overexpressed self-antigens (for example, Her2/neu) and tumor virus antigens (for example, HPV-16 E6/E7). Although in cancer patients, TAA-specific CD4+ and CD8+ cells are often present, they are not able to control tumor growth. In recent studies, it became apparent that tumor site-located immune evasion mechanisms contribute to this phenomenon and that regulatory T cells have a major role. We tested in Her2/neu breast cancer and HPV-16 E6/E7 cervical cancer mouse models, whether intratumoral expression of immunostimulatory proteins (ISPs), for example, recombinant antibodies (αCTLA-4, αCD137, αCD3), cyto/chemokines (IL-15, LIGHT, mda-7) and costimulatory ligands (CD80), through adenovirus(Ad)-mediated gene transfer would overcome resistance. In both the breast and cervical cancer model, none of the Ad.ISP vectors displayed a significant therapeutic effect when compared with an Ad vector that lacked a transgene (Ad.zero). However, the combination of Ad.ISP vectors with systemic T regulatory (Treg) depletion, using anti-CD25 mAb (breast cancer model) or low-dose cyclophosphamide (cervical cancer model) resulted in a significant delay of tumor growth in mice treated with Ad.αCTLA4. In the cervical cancer model, we also demonstrated the induction of a systemic antitumor immune response that was able to delay the growth of distant tumors. Ad.αCTLA4-mediated tumor-destructive immune responses involved NKT and CD8 T cells. In both models no autoimmune reactions were observed. This study shows that Ad.αCTLA4 in combination with systemic Treg depletion has potentials in the immunotherapy of cancer. © 2011 Nature America, Inc. All rights reserved.en_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleAdenovirus-mediated intratumoral expression of immunostimulatory proteins in combination with systemic Treg inactivation induces tumor-destructive immune responses in mouse modelsen_US
dc.typeJournalen_US
article.title.sourcetitleCancer Gene Therapyen_US
article.volume18en_US
article.stream.affiliationsUniversity of Washington, Seattleen_US
article.stream.affiliationsChiang Mai Universityen_US
article.stream.affiliationsInstitute of Biomedical Sciences Academia Sinica Taiwanen_US
article.stream.affiliationsDresden University Faculty of Medicine and University Hospital Carl Gustav Carusen_US
Appears in Collections:CMUL: Journal Articles

Files in This Item:
There are no files associated with this item.


Items in CMUIR are protected by copyright, with all rights reserved, unless otherwise indicated.