Yuval Shaked, PhD
Assistant Professor of Molecular Pharmacology
PhD, 2004 - Hebrew University, Israel
The double-edged sword of cancer therapy
Anti-cancer therapies, including chemotherapy, radiation, surgery and targeted drugs, often generate host responses that contribute to tumor outgrowth and relapse despite an initial successful therapy outcome. Tumor relapse due to host effects is attributed to angiogenesis, tumor cell repopulation, dissemination from the primary location, and seeding at metastatic sites. The therapy triggers host cell colonization at the primary tumor site and secretion of cytokines and growth factors that, in turn, promote tumor relapse and resistance to therapy. In my laboratory we study the host responses generated by a variety of anti-cancer drug therapies and their attendant clinical implications.
Beyar-Katz O and Shaked Y. 2014. Host effects contributing to cancer therapy resistance. Drug Resistance Updates. S1368-7646(14)00080-6.
Voloshin T, Voest EE, and Shaked, Y. 2013. The host immunological response to cancer therapy: an emerging concept in tumor biology. Experimental Cell Research S0014-4827(13)00115-8. (Cover).
Benayoun L, Gingis-Velitski S, Voloshin T, Segal E, Segev R, Munster M, Bril R, Satchi-Fainaro R, Scherer SJ, and Shaked Y. 2012. Tumor initiating cells of various tumor types exhibit differential angiogenic properties and react differently to antiangiogenic drugs. Stem Cells. 30, 1831-41.
Gingis-Velitski S, Loven D, Benayoun L, Munster M, Bril R, Voloshin T, Alishekevitz D, Bertolini F, and Shaked Y. 2011. Host response to short-term, single-agent chemotherapy induces matrix metalloproteinase-9 expression and accelerates metastasis in mice. Cancer Research. 71, 6986-96.
Voloshin T, Gingis-Veltski S, Milsom C, Man S, Munster M, Kerbel RS, and Shaked Y. 2011. G-CSF supplementation with chemotherapy can promote revascularization and subsequent tumor regrowth: prevention by a CXCR4 antagonist. Blood. 118, 3426-35.
Studying aspects of tumor-host interactions