S
Steven M. Frisch
Researcher at National Foundation for Cancer Research
Publications - 10
Citations - 3502
Steven M. Frisch is an academic researcher from National Foundation for Cancer Research. The author has contributed to research in topics: Cell & Anoikis. The author has an hindex of 7, co-authored 10 publications receiving 3393 citations.
Papers
More filters
Journal ArticleDOI
Disruption of epithelial cell-matrix interactions induces apoptosis
Steven M. Frisch,Hunter Francis +1 more
TL;DR: It is demonstrated that apoptosis was induced by disruption of the interactions between normal epithelial cells and extracellular matrix, and the circumvention of anoikis accompanies the acquisition of anchorage independence or cell motility.
Journal ArticleDOI
E1a induces the expression of epithelial characteristics.
TL;DR: It is demonstrated that adenovirus E1a expression caused diverse human tumor cells and fibroblasts to assume at least two of the following epithelial characteristics: epithelioid morphology; epithelial-type intercellular adhesion proteins localized to newly formed junctional complexes; and keratin-containing intermediate filaments.
Journal ArticleDOI
Expression of the integrin α5 subunit in HT29 colon carcinoma cells suppresses apoptosis triggered by serum deprivation
TL;DR: It is observed that apoptosis can be triggered in HT29 cells by removal of serum and that this process can be suppressed by the stable expression of full-length integrin alpha 5 subunits.
Journal Article
Adenovirus E1a-mediated tumor suppression by a c-erbB-2/neu-independent mechanism.
Steven M. Frisch,Karen E. Dolter +1 more
TL;DR: It is demonstrated here that the expression of E1a severely reduced the anchorage-independent and tumorigenic growth of these cell lines without affecting their growth under normal culture conditions, suggesting that E 1a could prove useful for the gene therapy of a wide variety of human cancers.
Patent
Method of sensitizing tumor cells with adenovirus E1A
TL;DR: In this paper, a method for sensitizing a human tumor cell with adenovirus E1A was proposed, which can enhance the subject's response to chemotherapy or irradiation by introducing into a subject's tumor cells nucleic acid encoding a polypeptide having E 1A activity.