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Accelerated tumor development in interferon-treated B6.C-Hyal-1 a mice
J De Maeyer-Guignard1, E Lauret, L Eusèbe
1Centre National de la Recherche Scientifique, Unité de Recherche Associée 1343, Institut Curie, Orsay, France.
Summary
Host genes influence interferon's (IFN) anti-tumor effects. In certain mice, IFN treatment unexpectedly accelerated tumor growth, unlike typical results showing tumor inhibition.
Area of Science:
- Immunology
- Genetics
- Oncology
Background:
- The Hyal-1 locus on mouse chromosome 9 affects hyaluronidase levels and influences the growth of 3LL carcinoma and B16F10 melanoma tumors.
- Tumor growth is typically slower in B6.C-Hyal-1a mice compared to C57BL/6 mice.
Purpose of the Study:
- To investigate the effect of alpha/beta interferon (IFN-alpha/beta) on tumor development in mice with different Hyal-1 alleles.
- To determine if host genetic background modulates the anti-tumor activity of IFN.
Main Methods:
- Transplantable 3LL carcinoma and B16F10 melanoma cells were grafted into B6.C-Hyal-1a and C57BL/6 mice.
- Mice were treated with IFN-alpha/beta or IFN-beta.
- Tumor development, mortality, and IFN treatment effects were monitored and compared between mouse strains.
Main Results:
- IFN-alpha/beta treatment stimulated tumor growth and accelerated mortality in B6.C-Hyal-1a mice with 3LL carcinoma.
- Conversely, IFN treatment inhibited 3LL tumor growth in C57BL/6 mice.
- IFN-alpha/beta treatment also stimulated B16F10 melanoma growth in B6.C-Hyal-1a mice, while inhibiting it in C57BL/6 mice.
Conclusions:
- Host genes, specifically the Hyal-1 locus, can up-regulate or down-regulate the anti-tumor activity of IFN.
- On certain genetic backgrounds, IFN treatment can enhance tumor development, contradicting established findings.
- These results may explain discrepancies between mouse model studies and clinical trials regarding IFN efficacy.