p53 gene therapy brings clinical benefits to lung cancer patients (pages 985-991).
References
Harris, C.C. p53 Tumor suppressor gene: From the basic research laboratory to the clinic — an abridged historical perspective. Carcinogenesis 17, 1187–1198 (1996).
Roth, J.A. et al. Retroviral-mediated wild-type p53 gene transfer to tumors of patients with lung cancer. Nature Med. 2, 985–991 (1996).
Cai, D.W., Mukhopadhyay, T., Liu, Y., Fujiwara, T. & Roth, J.A. Stable expression of the wild-type p53 gene in human lung cancer cells after retro-virus-mediated gene transfer. Hum. Gene Ther. 4, 617–624 (1993).
Takahashi, T. et al. Wild-type but not mutant p53 suppresses the growth of human lung cancer cells bearing multiple genetic lesions. Cancer Res 52, 2340–2343 (1992).
Takahashi, T. et al p53: A frequent target for genetic abnormalities in lung cancer. Science 246, 491–494 (1989).
Fujiwara, T. et al. Therapeutic effect of a retro viral wild-type p53 expression vector in an ortho-topic lung cancer model. j. Natl. Cancer Inst. 86, 1458–1462 (1994).
Jacks, T. & Weinberg, R.A. Cell-cycle control and its watchman. Naure 381, 643–644 (1996).
Sozzi, G. et al. Deletions of 17p and p53 mutations in preneoplastic lesions of the lung. Cancer Res. 52, 6079–6082 (1992).
Sundaresan, V. et al. p53 and chromosome 3 abnormalities, characteristic of malignant lung tumours, are detectable in preinvasive lesions of the bronchus. Oncogene 7, 1989–1997 (1992).
Hayashi, N., Sugimoto, Y., Tsuchiya, E., Ogawa, M. & Nakamura, Y. Somatic mutations of the MTS (Multiple tumor suppressor) 1/CDK4I (cyclin-dependent kinase-4 inhibitor) gene in human primary non-small cell lung carcinomas. Biochem. Biophys. Res. Commun. 202, 1426–1430 (1994).
Gerwin, B.I. et al. Mutant p53 can induce tumorigenic conversion of human bronchial epithelial cells and reduce their responsiveness to a negative growth factor, transforming growth factor beta 1. Proc. Natl. Acad. Sci. USA 89, 2759–2763 (1992).
Winter, S.F. et al. Development of antibodies against p53 in lung cancer patients appears to be dependent on the type of p53 mutation. Cancer Res. 52, 4168–4174(1992).
Fujiwara, T. et al. A retroviral wild-type p53 expression vector penetrates human lung cancer spheroids and inhibits growth by inducing apoptosis. Cancer Res. 53, 4129–4133 (1993).
Takeshima, Y. et al. p53 mutations in lung cancers from non-smoking atomic-bomb survivors. Lancet 342, 1520–1521 (1993).
Mao, L., Hruban, R.H., Boyle, J.O., Tockman, M. & Sidransky, D. Detection of oncogene mutations in sputum precedes diagnosis of lung cancer. Cancer Res. 54, 1634–1637 (1994).
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Minna, J., Gazdar, A. Translational research comes of age. Nat Med 2, 974–975 (1996). https://doi.org/10.1038/nm0996-974
Issue Date:
DOI: https://doi.org/10.1038/nm0996-974
- Springer Nature America, Inc.
This article is cited by
-
Beyond Bench and Bedside: Disentangling the Concept of Translational Research
Health Care Analysis (2015)
-
Respiratory diseases call for special attention from clinical and translational science
Translational Respiratory Medicine (2013)
-
Clinical and translational medicine: Integrative and practical science
Clinical and Translational Medicine (2012)