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To tell the truth, I didn't know synthetic lethality before coming to this lab.
From the point of tumor suppression we study senescence and anoikis.
Recent studies provided some evidences in vivo about tumor suppressive functions of senescence in response to oncogenic stresses.
It has already well known that senescence plays critical roles in preventing tumor progression.
Anoikis, detachment-induced cell death, is an important phenotype from the point of metastasis.
To understand the tumor suppressive mechanism behind senescence and anoikis, we identified genes required for these phenotypes by gain of function or loss of function screen.
Screen is a main strategy of our lab.
Our boss, however, is quite flexible in science.
He tries to apply screens to clinical applications.
Synthetic lethality provides a potential availability of specific cancer therapy.
Two genes are said to be synthetic lethal, if mutation of either gene alone is compatible with viability but simultaneous mutation of both genes causes death.
Let's say, tumor cells carry an oncogenic mutation. If the additional mutation causes cell death, the second mutation is responsible for synthetic lethality.
The inhibitor of synthetic lethal gene will be a specific drug to kill the tumor cells without
fatal effects to normal cells. This is the advantage of synthetic lethality.
I'm always doubtful about clinical applications.
Because I know how difficult it is to apply basic science to hospital.
But some recent studies encourage basic scientists to find genes as a target of effective and specific chemotherapy.
References
Cell 137, 835–848, May 29, 2009
Cell 137, 821–834, May 29, 2009
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