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Modeling human lung cancer in mice: similarities and shortcomings

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Abstract

Lung cancer kills more Americans yearly than any other neoplastic process. Mortality rates have changed little over the past several decades, despite improvements in surgical techniques, radiation therapy and chemotherapy. The identification of mutations in oncogenes and tumor suppressor genes in human lung tumor specimens, including K-ras, p53, p16INK4a and Rb, offers molecular explanations for tumor development and resistance to therapy. Mouse models of human lung cancer may advance our understanding of this disease. The examination of mice which develop lung cancer either spontaneously or due to carcinogen exposure, and the creation of mouse strains harboring the specific genetic mutations found in human lung cancer are among strategies being pursued.

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Acknowledgements

We thank Drs Sunil Hingorani and Julien Sage for reviewing this manuscript. DA Tuveson is supported by an NCI oncology fellowship training grant (T32CA71345). T Jacks is an Associate Investigator of the Howard Hughes Medical Institute.

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  1. Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, Massachusetts, USA

    David A Tuveson

  2. MIT Center for Cancer Research, E17-518, 40 Ames Street, Cambridge, MA 02139, Massachusetts, USA

    David A Tuveson & Tyler Jacks

  3. Howard Hughes Medical Institute, MIT, Cambridge, MA 02139, Massachusetts, USA

    Tyler Jacks

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Tuveson, D., Jacks, T. Modeling human lung cancer in mice: similarities and shortcomings. Oncogene 18, 5318–5324 (1999). https://doi.org/10.1038/sj.onc.1203107

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