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Marcin P. Iwanicki

Researcher at Stevens Institute of Technology

Publications -  38
Citations -  4110

Marcin P. Iwanicki is an academic researcher from Stevens Institute of Technology. The author has contributed to research in topics: Ovarian cancer & Integrin. The author has an hindex of 21, co-authored 33 publications receiving 3421 citations. Previous affiliations of Marcin P. Iwanicki include Harvard University & University of Virginia Health System.

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Rethinking ovarian cancer II: Reducing mortality from high-grade serous ovarian cancer

TL;DR: This 'roadmap' for HGSOC was determined after extensive discussions at an Ovarian Cancer Action meeting in January 2015 and aims to reduce incidence and improve outcomes for women with this disease.
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Mutant p53 Drives Invasion by Promoting Integrin Recycling

TL;DR: It is shown that Mutant p53 expression can promote invasion, loss of directionality of migration, and metastatic behavior, and the possibility that blocking alpha5/beta1-integrin and/or the EGF receptor will have therapeutic benefit in mutant p53-expressing cancers is opened.
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Cellular characterization of a novel focal adhesion kinase inhibitor.

TL;DR: P perturbation of adhesion-mediated signaling with a FAK inhibitor, PF-573,228, serves as a useful tool to dissect the functions of FAK in integrin-dependent signaling pathways in normal and cancer cells and forms the basis for the generation of compounds amenable for preclinical and patient trials.
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Inhibition of PI3K/mTOR Leads to Adaptive Resistance in Matrix-Attached Cancer Cells

TL;DR: It is shown that dual inhibition of PI3K/mTOR in ovarian cancer-spheroids leads to death of inner matrix-deprived cells, whereas matrix-attached cells are resistant.
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Ovarian cancer spheroids use myosin-generated force to clear the mesothelium

TL;DR: Evidence is provided that ovarian cancer spheroids utilize integrin- and talin- dependent activation of myosin and traction force to promote mesothelial cells displacement from underneath a tumor cell spheroid, suggesting that ovarian tumor cell clusters gain access to the sub-mesothelial environment by exerting force.