Fig. 1: Comparison of DNA damage repair kinetics in bone marrow versus tumour cells. | Nature Communications

Fig. 1: Comparison of DNA damage repair kinetics in bone marrow versus tumour cells.

From: Neoadjuvant PARP inhibitor scheduling in BRCA1 and BRCA2 related breast cancer: PARTNER, a randomized phase II/III trial

Fig. 1

A Examples of γH2AX immunohistochemistry (IHC) staining (brown colour) of sections of rat bone marrow (top panel) with vehicle control treatment or carboplatin (50 mg/kg) at 6 h and 72 h post treatment. The lower panel is a representative image of PDX tumour γH2AX staining. Quantification of γH2AX from both rat bone marrow (B) and PDX tumour (C) is shown using the pathologists’ scoring system of 0–3 from three independent biological replicates (or four independent biological replicates in the case of the PDX 48 h and 72 h data). Individual scores for vehicle control (circles) or platinum treatment (triangles) for the biological replicates are also shown, as is the group mean (orange bars with SD error bars). Source data is provided as a Source Data file. γH2AX staining is indicative of DNA damage induction and repair over time and shows that carboplatin treatment is resolved in rat bone marrow after 48 h, while in the PDX tumour, DNA damage is still increasing at 72 h post treatment.

Back to article page