Ph.D., St. Petersburg State University, 1986
Cancer; cell fusion; apoptosis
Our laboratory seeks to understand how cells become cancerous, how cancer cells evolve, and how they can be killed selectively.
To understand how cells become cancerous and how they evolve, we explore a model that cell fusion is a co-factor in carcinogenesis and tumor progression. This model argues that fusion of cells whose cell cycle is deregulated produces unstable hybrids that by chance may acquire carcinogenic properties. The cancer cells may further evolve by fusing to normal cells, thereby producing hybrids with additional properties, including the ability to form metastases. We focus on common viruses, many of which are fusogenic, as a cause of cell fusion in the body.
To understand how to kill cancer cells selectively, we explore a model that oncogenic transformation induces apoptosis, but that this link is disabled in cancer cells. The idea is that by learning how to restore this link we may understand how to kill cancer cells selectively.
Duelli, D.M., Padilla-Nash, H.M., Berman, D., Murphy, K.M., Ried, T., and Lazebnik. Y. 2007. A virus causes cancer by inducing massive chromosomal instability through cell fusion. Curr. Biol. 17: 431-437.
Duelli, D.M., Hearn, S., Myers, M.P., and Lazebnik, Y. 2005. A primate virus generates transformed human cells by fusion. J. Cell Biol. 171: 493–503.
Duelli, D., and Lazebnik, Y. 2003. Cell fusion: a hidden enemy? Cancer Cell 3: 445–448.
Lazebnik, Y. 2002. Can a biologist fix a radio?—Or what I learned while studying apoptosis. Cancer Cell 2: 179–182.
Rodriguez, J., and Lazebnik, Y. 1999. Caspase-9 and APAF-1 form an active holoenzyme. Genes Dev. 13: 3179–3184.