Abstract:
:Although docetaxel significantly improves survival in a variety of malignancies, its clinical utility is severely restricted by acquired chemoresistance and disease relapse. To uncover the mechanisms underlying these all too common occurrences, an abundance of research has focused on mutations and gene expression patterns; however, these findings are yet to translate into improved outcomes for patients being administered this drug. These analyses have overlooked a promising lead in the quest to discern key mediators of resistance and relapse following docetaxel therapy: polyploidization. This process is manifested following docetaxel-mediated mitotic arrest by the appearance of giant, multinucleated cells, which slipped from mitosis without undergoing cytokinesis. Polyploid cells generally possess supernumerary centrosomes, are chromosomally instable, and resist chemotherapy. We thus suspect that chemoresistance and relapse following treatment with docetaxel might be combatted by co-administration of centrosome declustering drugs, which could selectively destroy polyploid cells given that normal cells do not possess amplified centrosomes, an intriguing paradigm that warrants further investigation.
journal_name
Cancer Lettjournal_title
Cancer lettersauthors
Ogden A,Rida PC,Knudsen BS,Kucuk O,Aneja Rdoi
10.1016/j.canlet.2015.06.025subject
Has Abstractpub_date
2015-10-28 00:00:00pages
89-92issue
2eissn
0304-3835issn
1872-7980pii
S0304-3835(15)00447-4journal_volume
367pub_type
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