Scipher Medicine Corporation, Waltham MA.
Center for Research and Interdisciplinarity (CRI), University Paris Descartes, Paris, France.
Transl Res. 2022 Aug;246:78-86. doi: 10.1016/j.trsl.2022.03.006. Epub 2022 Mar 16.
This cross-cohort study aimed to (1) determine a network-based molecular signature that predicts the likelihood of inadequate response to the tumor necrosis factor-ɑ inhibitor (TNFi) therapy, infliximab, in ulcerative colitis (UC) patients, and (2) address biomarker irreproducibility across different cohort studies. Whole-transcriptome microarray data were derived from biopsies of affected colon tissue from 2 cohorts of infliximab-treated UC patients (training N = 24 and validation N = 22). Response was defined as endoscopic and histologic healing at 4-6 weeks and 8 weeks, respectively. From the training cohort, genes with RNA expression that significantly correlated with clinical response outcomes were mapped onto the Human Interactome network map of protein-protein interactions to identify a largest connected component (LCC) of proteins indicative of infliximab response status in UC. Expression levels of transcripts within the LCC were fed into a probabilistic neural network model to generate a classifier that predicts inadequate response to infliximab. A classifier predictive of inadequate response to infliximab was generated and tested in a cross-cohort, blinded fashion; the AUC was 0.83 and inadequate response was predicted with a 100% positive predictive value and 64% sensitivity. Genes separately identified from the 2 cohorts that correlated with response to infliximab appeared distinct but mapped onto the same network region of the Human Interactome, reflecting a common underlying biology of response among UC patients. Cross-cohort validation of a classifier predictive of infliximab response status in UC patients indicates that a molecular signature of non-response to TNFi therapies is present in patients' baseline gene expression data. The goal is to develop a diagnostic test that predicts which patients will have an inadequate response to targeted therapies and define new targets and pathways for therapeutic development.
本跨队列研究旨在:(1) 确定一种基于网络的分子特征,预测肿瘤坏死因子-α 抑制剂(TNFi)治疗溃疡性结肠炎(UC)患者时反应不足的可能性,该抑制剂为英夫利昔单抗;(2) 解决不同队列研究中生物标志物不可重现的问题。从接受英夫利昔单抗治疗的 UC 患者的病变结肠组织活检中获取全转录组微阵列数据(训练队列 N=24,验证队列 N=22)。分别在 4-6 周和 8 周时,将内镜和组织学缓解定义为反应。从训练队列中,将与临床反应结果显著相关的 RNA 表达基因映射到蛋白质-蛋白质相互作用的人类互作网络图谱上,以确定反映 UC 中英夫利昔单抗反应状态的最大连通组件(LCC)中的蛋白质。将 LCC 内转录本的表达水平输入概率神经网络模型,生成一个预测英夫利昔单抗反应不足的分类器。以交叉队列、盲法的方式生成并测试预测英夫利昔单抗反应不足的分类器;AUC 为 0.83,对英夫利昔单抗反应不足的预测具有 100%的阳性预测值和 64%的灵敏度。从两个队列中分别鉴定出与英夫利昔单抗反应相关的基因似乎不同,但映射到人类互作网络的同一区域,反映出 UC 患者的反应具有共同的潜在生物学机制。UC 患者预测英夫利昔单抗反应状态的分类器的跨队列验证表明,TNFi 治疗反应不足的分子特征存在于患者的基线基因表达数据中。目标是开发一种诊断测试,预测哪些患者对靶向治疗反应不足,并定义新的治疗靶点和途径。
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