Skip to main content

Main menu

  • Home
  • Current Issue
  • Archive
  • Info for
    • Authors
    • Editorial Policies
    • Subscribers
    • Advertisers
    • Editorial Board
  • Other Publications
    • In Vivo
    • Cancer Genomics & Proteomics
    • Cancer Diagnosis & Prognosis
  • More
    • IIAR
    • Conferences
    • 2008 Nobel Laureates
  • About Us
    • General Policy
    • Contact
  • Other Publications
    • Anticancer Research
    • In Vivo
    • Cancer Genomics & Proteomics

User menu

  • Register
  • Subscribe
  • My alerts
  • Log in
  • My Cart

Search

  • Advanced search
Anticancer Research
  • Other Publications
    • Anticancer Research
    • In Vivo
    • Cancer Genomics & Proteomics
  • Register
  • Subscribe
  • My alerts
  • Log in
  • My Cart
Anticancer Research

Advanced Search

  • Home
  • Current Issue
  • Archive
  • Info for
    • Authors
    • Editorial Policies
    • Subscribers
    • Advertisers
    • Editorial Board
  • Other Publications
    • In Vivo
    • Cancer Genomics & Proteomics
    • Cancer Diagnosis & Prognosis
  • More
    • IIAR
    • Conferences
    • 2008 Nobel Laureates
  • About Us
    • General Policy
    • Contact
  • Visit us on Facebook
  • Follow us on Linkedin
Research ArticleExperimental Studies

Endogenous Expression of CD80 Co-stimulatory Molecule Facilitates In Vivo Tumor Regression of Oral Squamous Carcinoma

GIOVANA R. THOMAS and JUDY WEN
Anticancer Research November 2006, 26 (6B) 4093-4101;
GIOVANA R. THOMAS
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • For correspondence: gthomas@med.miami.edu
JUDY WEN
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Info & Metrics
  • PDF
Loading

Abstract

Background: Most tumor tissues, especially those of non-hematopoietic origin, do not express CD80 co-stimulatory molecules, possibly as a mechanism to evade immune surveillance. The objective of this study was to determine whether abundant endogenous CD80 expression on oral squamous cell carcinoma (SCC) early during tumor progression can facilitate immune elimination and reverse immune tolerance. Materials and Methods: The growth of regressor and progressor oral SCC lines with differing endogenous CD80 expression were examined in immunecompetent and -deficient mice. Immune effectors were determined by T-cell depletion experiments and immunohistochemistry. Results: Our studies show regression of early tumor growth when immunocompetent animals are inoculated with oral SCC progressor cell lines expressing abundant endogenous CD80. The CD80-induced antitumor response was due largely to induced T-cell responses. Conclusion: Our findings suggest that inadequate CD80 expression during early oral SCC formation may contribute to the escape of tumors from immune elimination. This information can be useful in the design of new approaches to generate more effective immunotherapy against this disease.

  • CD80
  • head and neck squamous cell carcinoma
  • immune surveillance
  • progressor cell line
  • regressor cell line
  • T-cells
  • CD8+ T-cells
  • costimulatory molecules
  • oral carcinoma
  • tumor regression

Footnotes

  • ↵* Supported by NIH grant: DE015338A.

  • Received September 19, 2006.
  • Accepted September 28, 2006.
  • Copyright© 2006 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved
PreviousNext
Back to top

In this issue

Anticancer Research: 26 (6B)
Anticancer Research
Vol. 26, Issue 6B
November-December 2006
  • Table of Contents
  • Table of Contents (PDF)
  • Index by author
  • Front Matter (PDF)
Download PDF
Article Alerts
Sign In to Email Alerts with your Email Address
Email Article

Thank you for your interest in spreading the word on Anticancer Research.

NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

Enter multiple addresses on separate lines or separate them with commas.
Endogenous Expression of CD80 Co-stimulatory Molecule Facilitates In Vivo Tumor Regression of Oral Squamous Carcinoma
(Your Name) has sent you a message from Anticancer Research
(Your Name) thought you would like to see the Anticancer Research web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
5 + 1 =
Solve this simple math problem and enter the result. E.g. for 1+3, enter 4.
Citation Tools
Endogenous Expression of CD80 Co-stimulatory Molecule Facilitates In Vivo Tumor Regression of Oral Squamous Carcinoma
GIOVANA R. THOMAS, JUDY WEN
Anticancer Research Nov 2006, 26 (6B) 4093-4101;

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Reprints and Permissions
Share
Endogenous Expression of CD80 Co-stimulatory Molecule Facilitates In Vivo Tumor Regression of Oral Squamous Carcinoma
GIOVANA R. THOMAS, JUDY WEN
Anticancer Research Nov 2006, 26 (6B) 4093-4101;
Reddit logo Twitter logo Facebook logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
  • Info & Metrics
  • PDF

Related Articles

  • No related articles found.
  • PubMed
  • Google Scholar

Cited By...

  • PIK3CA in KrasG12D/Trp53R172H Tumor Cells Promotes Immune Evasion by Limiting Infiltration of T Cells in a Model of Pancreatic Cancer
  • Google Scholar

More in this TOC Section

  • Comprehensive Analysis of KREMEN2 as an Immunotherapeutic and Prognostic Biomarker in Pan-Cancer
  • PD-L1 mRNA Detection in Immunohistochemically Negative Patients: A Complementary Method for a Better Treatment Selection?
  • Immune Cell Infiltration and Clinical Significance of Angiogenesis-related Genes in Lung Adenocarcinoma
Show more Experimental Studies

Similar Articles

Anticancer Research

© 2023 Anticancer Research

Powered by HighWire