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Alloantigen gene therapy for head and neck cancer: evaluation of animal models
Lyon L Gleich1, Ya-Qin Li, Shunan Li
1Department of Otolaryngology-Head and Neck Surgery, University of Cincinnati Medical Center, P.O. Box 670528, 213 Albert Sabin Way, Cincinnati, Ohio 45267-0528, USA. lyon.gleich@uc.edu
Background:
Human trials of alloantigen gene therapy, using the class I major histocompatibility complex (MHC) HLA-B7, have demonstrated the potential efficacy of this treatment for head and neck cancer. Its mechanism remains unclear. An immune-competent mouse model of MHC gene therapy to test factors potentially important to the tumor response is needed.
Methods:
Two cell lines were used, B4B8 cells that grow in Balb/c mice and SCC-VII cells that grow in C3H mice. The mouse MHC H2-K(b) was used as the therapeutic gene, because it is an alloantigen to both mice strains. Plasmids that encode the H2-K(b) cDNA were prepared, and the cell lines were transfected. Mice were injected subcutaneously with naive cells to determine the tumor kinetics and serve as controls. Mice were injected with H2-K(b) transfected cells and tumor growth was compared with controls. Mice that did not grow tumor were rechallenged with naive cells to assess for tumor immunity. Mice were injected with transfected and naive cells admixed to determine whether the concentration of the alloantigen is important.
Results:
B4B8 tumors grew slowly, whereas SCC-VII tumors grew rapidly. Transfection with H2-K(b) plasmid prevented or inhibited tumor growth of both the B4B8 and SCC-VII tumors. This growth inhibition was independent of the number of cells injected. In the mice that did not grow tumor, tumor immunity was demonstrated after challenge with naive cells in both models. There was no relationship between induction of immunity and the timing of the challenge or initial cell quantity. The mice injected with a mixture of naive and transfected cells grew tumor, although growth was delayed in the B4B8 model.
Conclusions:
The results demonstrate that the two mouse models can serve as a rapid and slow growing tumor model of alloantigen gene therapy. In addition, it was noted that initial tumor cell number is not a significant factor for predicting tumor response and demonstrated that in both of these models alloantigen gene therapy results in significant antitumor immunity.
Insights
Alloantigen gene therapy using mouse MHC H2-K(b) inhibited tumor growth in two mouse models. This therapy also induced significant antitumor immunity, independent of initial cell number.
Area of Science:
- Immunology
- Cancer Therapy
- Gene Therapy
Background:
- Human trials of alloantigen gene therapy for head and neck cancer show promise.
- The precise mechanism of action for MHC gene therapy remains unclear.
- An immune-competent mouse model is needed to study MHC gene therapy's impact on tumor response.
Purpose of the Study:
- To establish and utilize immune-competent mouse models for studying MHC gene therapy.
- To investigate the efficacy of H2-K(b) gene therapy in inhibiting tumor growth.
- To assess the induction of antitumor immunity following MHC gene therapy.
Main Methods:
- Utilized B4B8 (slow-growing) and SCC-VII (rapid-growing) mouse tumor models.
- Transfected tumor cell lines with the mouse MHC H2-K(b) gene.
- Evaluated tumor growth kinetics, tumor immunity induction, and the effect of cell concentration.
Main Results:
- H2-K(b) gene therapy significantly inhibited or prevented tumor growth in both models.
- Tumor growth inhibition was independent of the initial number of transfected cells.
- Mice that rejected tumors developed significant antitumor immunity upon rechallenge.
Conclusions:
- Established rapid and slow-growing mouse models for studying alloantigen gene therapy.
- Demonstrated that initial tumor cell number is not a critical factor for predicting therapeutic response.
- Confirmed that alloantigen gene therapy effectively induces significant antitumor immunity in these models.
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