Voulgarelis D, Forment J V, Herencia Ropero A, Polychronopoulos D, Cohen-Setton J, Bender A, Serra V, O'Connor M J, Yates J W T, Bulusu K C
AstraZeneca Postdoc Programme, Cambridge, UK.
DMPK Oncology R&D, AstraZeneca, Cambridge, UK.
NPJ Precis Oncol. 2024 Nov 18;8(1):266. doi: 10.1038/s41698-024-00702-x.
Understanding the mechanisms of resistance to PARP inhibitors (PARPi) is a clinical priority, especially in breast cancer. We developed a novel mathematical framework accounting for intrinsic resistance to olaparib, identified by fitting the model to tumour growth metrics from breast cancer patient-derived xenograft (PDX) data. Pre-treatment transcriptomic profiles were used with the calculated resistance to identify baseline biomarkers of resistance, including potential combination targets. The model provided both a classification of responses, as well as a continuous description of resistance, allowing for more robust biomarker associations and capturing the observed variability. Thirty-six resistance gene markers were identified, including multiple homologous recombination repair (HRR) pathway genes. High WEE1 expression was also linked to resistance, highlighting an opportunity for combining PARP and WEE1 inhibitors. This framework facilitates a fully automated way of capturing intrinsic resistance, and accounts for the pharmacological response variability captured within PDX studies and hence provides a precision medicine approach.
了解对聚(ADP - 核糖)聚合酶抑制剂(PARPi)的耐药机制是临床优先事项,尤其是在乳腺癌中。我们开发了一种新颖的数学框架,用于解释对奥拉帕尼的内在耐药性,该框架通过将模型拟合到来自乳腺癌患者来源异种移植(PDX)数据的肿瘤生长指标来确定。预处理转录组谱与计算出的耐药性一起用于识别耐药的基线生物标志物,包括潜在的联合靶点。该模型不仅提供了反应分类,还提供了对耐药性的连续描述,从而实现更可靠的生物标志物关联,并捕捉观察到的变异性。鉴定出36个耐药基因标志物,包括多个同源重组修复(HRR)途径基因。高WEE1表达也与耐药性相关,这突出了联合使用PARP和WEE1抑制剂的机会。该框架促进了一种完全自动化的方式来捕捉内在耐药性,并解释了PDX研究中捕获的药理反应变异性,因此提供了一种精准医学方法。