File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Myeloid-derived suppressor cells contribute to oral cancer progression in 4NQO-treated mice

TitleMyeloid-derived suppressor cells contribute to oral cancer progression in 4NQO-treated mice
Authors
KeywordsOral cancer
Tumor progression
T cell
MDSC
Issue Date2012
Citation
Oral Diseases, 2012, v. 18, n. 1, p. 67-73 How to Cite?
AbstractObjective: Abnormal myelopoiesis especially the expansion of myeloid-derived suppressor cells (MDSCs) is increasingly recognized as an important reason for the escape of tumor from immune surveillance. This study aims to investigate the role of this specific population of cells in oral cancer progression. Materials and Methods: 4-Nitroquinoline 1-oxide (4NQO) was used to induce oral cancer in C57BL/6 mice. The tongue mucosa was examined by hematoxylin and eosin staining. The distribution of MDSCs in the spleen and peripheral blood and T cell subsets in the spleen was analyzed by flow cytometry. The expression of MDSCs in the tongue tissues was investigated by immunohistochemical staining, and the expression of arginase-1 (ARG-1) and NOS-2 in the tongue tissues was detected by real-time PCR. Results: We found that during tumor progression, significantly increased frequency of MDSCs was observed in the spleens and peripheral blood of 4NQO-treated mice, and the frequency of MDSCs in the spleens was positively correlated with systemic CD3 +CD8 + T cells. Moreover, 4NQO-treated mice showed significantly higher MDSCs infiltration and ARG-1 mRNA level in the tumor site. Conclusions: Myeloid-derived suppressor cells contribute to oral tumor progression and represent a potential target for immunotherapy of oral cancer. © 2011 John Wiley & Sons A/S.
Persistent Identifierhttp://hdl.handle.net/10722/200091
ISSN
2015 Impact Factor: 2.0
2015 SCImago Journal Rankings: 0.828
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChu, Mei-
dc.contributor.authorSu, Yuxiong-
dc.contributor.authorWang, Lin-
dc.contributor.authorZhang, Tonghan-
dc.contributor.authorLiang, Yujie-
dc.contributor.authorLiang, Lizhong-
dc.contributor.authorLiao, Guiqing-
dc.date.accessioned2014-07-26T23:11:07Z-
dc.date.available2014-07-26T23:11:07Z-
dc.date.issued2012-
dc.identifier.citationOral Diseases, 2012, v. 18, n. 1, p. 67-73-
dc.identifier.issn1354-523X-
dc.identifier.urihttp://hdl.handle.net/10722/200091-
dc.description.abstractObjective: Abnormal myelopoiesis especially the expansion of myeloid-derived suppressor cells (MDSCs) is increasingly recognized as an important reason for the escape of tumor from immune surveillance. This study aims to investigate the role of this specific population of cells in oral cancer progression. Materials and Methods: 4-Nitroquinoline 1-oxide (4NQO) was used to induce oral cancer in C57BL/6 mice. The tongue mucosa was examined by hematoxylin and eosin staining. The distribution of MDSCs in the spleen and peripheral blood and T cell subsets in the spleen was analyzed by flow cytometry. The expression of MDSCs in the tongue tissues was investigated by immunohistochemical staining, and the expression of arginase-1 (ARG-1) and NOS-2 in the tongue tissues was detected by real-time PCR. Results: We found that during tumor progression, significantly increased frequency of MDSCs was observed in the spleens and peripheral blood of 4NQO-treated mice, and the frequency of MDSCs in the spleens was positively correlated with systemic CD3 +CD8 + T cells. Moreover, 4NQO-treated mice showed significantly higher MDSCs infiltration and ARG-1 mRNA level in the tumor site. Conclusions: Myeloid-derived suppressor cells contribute to oral tumor progression and represent a potential target for immunotherapy of oral cancer. © 2011 John Wiley & Sons A/S.-
dc.languageeng-
dc.relation.ispartofOral Diseases-
dc.subjectOral cancer-
dc.subjectTumor progression-
dc.subjectT cell-
dc.subjectMDSC-
dc.titleMyeloid-derived suppressor cells contribute to oral cancer progression in 4NQO-treated mice-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1601-0825.2011.01846.x-
dc.identifier.pmid21883708-
dc.identifier.scopuseid_2-s2.0-84155164319-
dc.identifier.volume18-
dc.identifier.issue1-
dc.identifier.spage67-
dc.identifier.epage73-
dc.identifier.eissn1601-0825-
dc.identifier.isiWOS:000298593300008-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats