<h3>Objectives:</h3> To evaluate the potential of DNA damage response protein expression and foci formation to serve as biomarkers of resistance to platinum chemotherpay or Poly-(ADP)-Ribose Polymerase Inhibitors (PARPi) using immunohistochemistry (IHC). <h3>Methods:</h3> A collection of four patient-derived xenografts (PDX) mouse models with <i>BRCA1</i> mutations in exon 11, a <i>BRCA1</i> exon 13 mutant, and a <i>BRCA1</i> wild-type tumor were analyzed. <i>BRCA1</i> exon 11 mutants included: PDX196, mutation: c1961delA; PDX124, mutation: c196delA; PDX017, mutation: c1105_1106insTC; PDX056, mutation: c895_896delGT; <i>BRCA1</i> WT control: PDX036 and <i>BRCA1</i> exon 13 mutant: PDX1126, mutation: c4327C>T. Mice harboring PDX tumors were subjected to vehicle, PARPi (rucaparib), or platinum (cisplatin) treatment. Passaging and re-treatment of tumors was performed until minimal therapy response. Formalin-fixed paraffin embedded tumor samples was prepared for IHC analyses. IHC protocols were optimized to evaluate expression and foci formation for the following proteins: phosphorylated-RPA32, Rad51, phosphorylated-53BP1, 53BP1, <i>BRCA1,</i> Ki67. <h3>Results:</h3> <i>BRCA1</i> foci formation was observed by IHC in PARPi and cisplatin resistant tumors. Reversion mutations were not detected and <i>BRCA1</i> protein expression was due to increased levels of <i>BRCA1</i>-D11q. Increased RPA32 and RAD51 foci were also observed in several therapy resistant PDX models, which indicate active HR repair. Interestingly, acquired resistance to cisplatin and PARPi was associated with a reduction in 53BP1 and phosphorylated-53BP1. Finally, PARPi and cisplatin resistant tumors exhibited similar levels of <i>BRCA1</i> and RAD51 foci. <h3>Conclusions:</h3> <i>BRCA1</i>-D11q protein expression correlates with platinum and PARPi response in several <i>BRCA1</i> exon 11 mutant PDX models. We predict that increased <i>BRCA1</i>-D11q in combination with decreased 53BP1 expression drives RPA and RAD51 foci, resulting in active homologous recombination and therapy resistance. Our results suggest that IHC can be utilized for detection of DNA damage repair protein expression as well as foci formation, and could lead to the development of biomarkers that are predictive of therapy response.