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Can the balance of therapeutic benefits and reversible side effects be struck in combinatorial treatments consisting of multiple antimitotics targeting different stages of mitosis?
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Some predicted targets were likely to be targeted by multiple miRNAs at multiple targeting sites.
Although it is valid to reason that the current antimitotics are targeting only a limited fraction of cells within a tumor population, it still does not explain how taxanes achieved considerable clinical efficacy by similarly affecting the propagation of mitosis.
Antimitotic agents targeting tubulin, including the vinca alkaloids and taxanes, are arguably the most successful anticancer drugs developed to date.
Microtubules and their dynamic behaviour are essential for multiple steps in mitosis and as such represent good antimitotic targets.
Polo-like kinase 1 (Plk1) is a regulator of cell cycle progression during mitosis; it is overexpressed in many different tumors and has been implicated as a potential antimitotic target.
It would be important to corroborate these and other novel candidates and establish if they are promising antimitotic targets.
These results establish the importance of SIK3 as a mitotic regulator and underscore the potential of SIK3 as a druggable antimitotic target.
Mcl1 is gaining traction as an antimitotic target with increasing evidences associating its degradation in mitosis to the timely induction of cell death.
The possible numbers and permutations of antimitotic targets that can be selected are theoretically endless (limited only to the tolerance level of a patient); the challenge would then be to find combinations that work synergistically and complement one another.
By contrast, in cells with normal centrosome complement, KIFC1 is dispensable for bipolar spindle formation, and thus represents an antimitotic target specific for tumour types with a high incidence of centrosome amplification.
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CEO of Professional Science Editing for Scientists @ prosciediting.com