Chemistry: molecular biology and microbiology – Measuring or testing process involving enzymes or... – Involving antigen-antibody binding – specific binding protein...
Patent
1995-03-31
1998-12-01
Scheiner, Toni R.
Chemistry: molecular biology and microbiology
Measuring or testing process involving enzymes or...
Involving antigen-antibody binding, specific binding protein...
435 6, 435326, 436 64, 436813, 5303888, 53038885, 5303877, G01N 33574, C07K 1630
Patent
active
058436847
DESCRIPTION:
BRIEF SUMMARY
BACKGROUND OF THE INVENTION
Mutations of proto-oncogenes in somatic cells are increasingly being recognized as significant in the induction of human cancers. Some examples of oncogenes formed by such mutations include: neu, fes, fos, myc, myb, fms, Ha-ras, and Ki-ras. The mutations that convert proto-oncogenes to oncogenes are often point mutations. Much needs to be learned in order to understand how oncogenes and their expression products function to transform normal cells to cancer cells.
Oncogenes are generally believed to act in a dominant fashion. This is generally considered to mean that the conversion of a proto-oncogene to an oncogene results in the acquisition of a new function, i.e., enhancing transformation.
A different type of mutation associated with cancer occurs when a tumor suppressor gene is altered in a way that causes the product of the gene to lose its tumor suppressor function. An example of such a tumor suppressor gene is the retinoblastoma susceptibility gene, Rb. Tumor suppressor genes are sometimes called recessive oncogenes, although, strictly speaking, the products of tumor suppressor genes do not contribute to tumor formation. The phenotype is recessive since, when both alleles are mutated, the absence of a tumor suppressor gene results in an enhancement of tumorigenesis.
A gene product that exhibits some properties of both a dominant and a recessive oncogene is the 53 kd phosphoprotein, p53. Evidence is growing that mutations in the p53 gene is associated with a large number of many types of cancers. For example, Iggo et al., Lancet 335, 675-679 (1990) has expressed the opinion that p53 is the most common proto-oncogene to undergo mutation in lung cancers.
Much of what is known about p53 has been derived from studying the effect of transfecting wild-type and mutant murine p53 in rat embryo fibroblast cells. This work has been reviewed by Levine et al., "The P53 Proto-Oncogene And Its Product," in Common Mechanisms of Transformation By Small DNA Tumor Viruses, L. Villarreal, ed., American Society for Microbiology, Chapter 2 (1989); Hinds et al., ibid, Chapter 7; and Levine, BioEssays 12, 60-66 (1990).
The p53 gene appears to be involved in transcriptional control (Fields, S. & Jang, S. K. (1990) Science 249, 1046-1049; Raycroft, L., Wu, H. & Lozano, G. (1990) Science 249, 1049-1051; and Levine, A. J., Momand, J. & Finlay, C. A. (1991) Nature 351, 453-456) and may act as a regulatory check point in the cell cycle, arresting cells in the G-1 phase (Martinez, J., Georgoff, I. & Levine, A. J. (1991) Genes Dev. 5, 151-159; Hupp, T. R., Meek, D. W., Midgley, C. A. & Lane, D. P. (1992) Cell 71, 875-886; and Yin, Y., Tainsky, M. A., Bischoff, F. Z., Strong, C. C. & Wahl, E. M. (1992) Cell 70, 937-948). Genetic alterations of the p53 gene, such as intragenic mutations, homozygous deletions, and structural rearrangements, are frequent events in human cancer (Vogelstein, B. & Kinzler, K. (1992) Cell 70, 523-526; Baker, S. J. et al. (1990) Cancer Res 50, 7717-7722; Mori, N. et al. (1989) Cancer Res 49, 5130-5135; Lee, J. H. et al. (1990) Cancer Res 50, 2724-2728; Varley, J. M. et al. (1991) Oncogene 6, 413-421; Presti, J. C. et al. (1991) Cancer Res 51, 5405; Dalbagni, G., et al. (1993) Diagnostic Molecular Pathology 2, 4-13). These altered patterns of p53 either reduce or inhibit the activity of functional homotetramer units (Stenger, J. E., et al. (1992) Mol Carcinog 5, 102-106; Sturzbecher, H. W., et al. (1992) Oncogene 7, 1513-1523). Mutant p53 proteins have a prolonged half-life and retarded degradation, yielding accumulation of inactive complexes and self-aggregatory molecules in the nuclei of tumor cells (Sturzbecher, H. W. et al. (1987) Oncogene 1, 201-211; Halevy, O. et al. (1989) Mol Cell Biol 9, 3385-3392),
In humans, germ-line mutations of the p53 gene have been characterized in members of families affected with the Li-Fraumeni syndrome, a rare autosomal dominant trait that predisposes these individuals to develop a variety of tumors, including soft tissue sarcomas (Li, F. P. &
REFERENCES:
patent: 4762706 (1988-08-01), McCormick et al.
Cahilly-Snyder, L. et al., Somatic Cell and Molecular Genetics, vol. 13, No. 3, pp. 235-244, 1987.
Fakharzadeh, et al., EMBO Journal, vol. 10, No. 6, pp. 1565-1569, 1991.
Hinds, et al., Cell Growth & Differentiation, vol. 1,pp. 571-580, Dec. 1990.
Werness et al., Science, vol. 248, pp. 76-79, 6 Apr. 1990.
Cordon-Cardo Carlos
Finlay Cathy A.
Levine Arnold J.
Feit Irving N.
Gallagher Thomas C.
Scheiner Toni R.
The Trustees of Princeton University
Weiss Laura S.
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