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Michael A. Tainsky

Researcher at Wayne State University

Publications -  143
Citations -  15365

Michael A. Tainsky is an academic researcher from Wayne State University. The author has contributed to research in topics: Cancer & Gene. The author has an hindex of 50, co-authored 140 publications receiving 14860 citations. Previous affiliations of Michael A. Tainsky include University of Texas MD Anderson Cancer Center & Howard Hughes Medical Institute.

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Germ line p53 mutations in a familial syndrome of breast cancer, sarcomas, and other neoplasms

TL;DR: Germ line p53 mutations have been detected in all five LFS families analyzed and can now be examined in additional families with LFS, and in other cancer patients and families with clinical features that might be attributed to the mutation.
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Control of angiogenesis in fibroblasts by p53 regulation of thrombospondin-1

TL;DR: Transfection assays indicate that, in fibroblasts, wild-type p53 inhibits angiogenesis through regulation of TSP-1 synthesis.
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Wild-type p53 restores cell cycle control and inhibits gene amplification in cells with mutant p53 alleles

TL;DR: It is shown that the wild-type p53 allele is lost when fibroblasts from patients with the Li-Fraumeni syndrome are passaged in vitro, and p53 contributes to a metabolically regulated G1 check-point, and they provide a model for understanding how abnormal cell cycle progression leads to the genetic rearrangements involved in tumor progression.
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Molecular cloning of a new transforming gene from a chemically transformed human cell line

TL;DR: Molecular cloning of the transforming gene from a chemically transformed human osteosarcoma-derived cell line enables the gene to be mapped to chromosome 7 (7p11.4–7qter) and by direct hybridization to be shown to be unrelated to known oncogenes.
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In vitro growth characteristics of embryo fibroblasts isolated from p53-deficient mice.

TL;DR: It is concluded that the loss of p53 by itself is insufficient to confer immortality on a cell, but does confer a growth advantage, confirming that the absence of p 53 promotes genomic instability, which in turn may result in genetic alterations which directly produce immortality.