Figure 3.

(A) Clinical course of a pancreatic ductal adenocarcinoma patient who underwent prior pancreatic tumor resection, and subsequently progressed while on Parp-1 inhibitor therapy. ExoDNA enrichment led to capture of tumor derived material which was not previously detectable. (B) Relevant mutations found in the metastatic tissue and liquid biopsies 6 months (lbx_02) and 9 months (lbx_03) after tissue biopsy. Of note is the presence of a stopgain BRCA mutation (L583*) that was correlated to her prolonged response to PARP1 inhibitor therapy. (C) A subsequent mechanism of resistance was detected in the liquid biopsies and confirmed in the tissue in the form of a BRCA2 splice site variant which splices out the aberrant stopgain mutation. SLD sum of the largest dimension; exoDNA MAF represent the KRAS mutant allele fraction. ABR, abraxane (nab-paclitaxel); CIS, cisplatin; GEM, gemcitabine.