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Inhibition of aberrantly overexpressed Polo-like kinase 4 is a potential effective treatment for DNA damage repair-deficient uterine leiomyosarcoma.

Horace H Y LeeKin Long ChowHo Shing WongTsz Yan ChongAlice Sze Tsai WongGrace H W ChengJasmine M K KoHoi Cheong SiuMaximus C F YeungMichael Shing Yan HuenKa-Yu TseMark R BrayTak Wah MakSuet Yi LeungPhilip Pun-Ching Ip
Published in: Clinical cancer research : an official journal of the American Association for Cancer Research (2024)
Uterine LMS with DNA repair defects is sensitive to PLK4 inhibition because of the effects of chromosome missegregation and increased DNA damage. Loss-of-function BRCA2 alterations or pharmacological inhibition of ATM enhanced the efficacy of PLK4 inhibitor. Genomic profiling of an advanced-stage or recurrent uterine LMS may guide therapy.
Keyphrases
  • dna damage
  • dna repair
  • oxidative stress
  • dna damage response
  • copy number
  • stem cells
  • gene expression
  • single cell
  • bone marrow
  • genome wide
  • mesenchymal stem cells
  • wild type