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. 2019 Jun 4;1(1):vdz005. doi: 10.1093/noajnl/vdz005

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© The Author(s) 2019. Published by Oxford University Press, the Society for Neuro-Oncology and the European Association of Neuro-Oncology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. 2 — Niraparib accumulates in intracranial tissues and in some models inhibits PARP. (A) Niraparib concentration as nanogram per gram of tissue detected in tumor, peri-tumor, and contralateral normal brain tissues from mice with intracranial SUM149 and MDA-MB-231Br treated for 2 weeks with daily 50 mg/kg niraparib. *Tumor levels being significantly higher than levels in the peri-tumor (P = .021) and contralateral (P = 0.018) tissues. (B) PAR levels in intracranial (IC) tumors of mice injected with MDA-MB-231Br, SUM149, or MDA-MB-436 TNBC cells, or MDA-MB-436 in vitro, and treated with vehicle or niraparib. PAR levels as pg PAR/ml per 100-µg tissue. *PAR levels being significantly lower in niraparib treated tissue (P = .0027) or cells (P = .035) relative to vehicle treatment.