医学
危险系数
乳腺癌
内科学
生物标志物
肿瘤科
癌症
无进展生存期
比例危险模型
基因表达
临床终点
转移性乳腺癌
癌症研究
置信区间
基因
临床试验
总体生存率
生物
遗传学
作者
Gabriel N. Hortobágyi,Shani Paluch–Shimon,Katarína Petráková,Cristian Villanueva,Arlene Chan,Arnd Nusch,Yoon Sim Yap,Lowell L. Hart,Anne Favret,Norbert Marschner,Gabe S. Sonke,Hege O. Ohnstad,Carlos L. Arteaga,Fei Su,Wei He,Michelle Kristine Miller,Salomon M. Stemmer
标识
DOI:10.1200/jco.2018.36.15_suppl.1022
摘要
1022 Background: In MONALEESA-2, first-line RIB + LET improved investigator-assessed progression-free survival (PFS; primary endpoint) vs placebo (PBO) + LET in postmenopausal pts with HR+, HER2– ABC. Previous MONALEESA-2 biomarker analyses, involving immunohistochemistry, gene expression, and NGS of ctDNA, showed consistent RIB benefit. Here, we present additional MONALEESA-2 gene expression data. Methods: Tumor samples (n/N, 391/668) were evaluated for gene expression using the NanoString 230-gene nCounter® GX Human Cancer Reference panel. To assess correlations between gene expression level and PFS, pts were classified into low (L) and high (H) messenger RNA expression subgroups using a 10% cut-off for RB1 and median expression as the cut-off for other genes. Cox proportional hazards models were used to estimate hazard ratios and 95% confidence intervals (CI). Results: RIB + LET improved PFS in all pt subgroups (Table). Kaplan–Meier curves will be presented. Clinical trial information: NCT01958021. Conclusions: Benefit of RIB was consistent across gene expression subgroups; H vs L ESR1 and L vs H RTK expression trended towards greater RIB benefit. Genes implicated preclinically in mechanisms of resistance to CDK4/6 inhibitors require further investigation based on metastatic/liquid biopsies, and in larger clinical datasets. Gene(s) Expression level Events, n/N Hazard ratio; 95% CI RIB + LET PBO + LET CDK pathway and breast cancer ESR1 L 51/101 62/95 0.74; 0.51–1.07 H 34/96 58/99 0.39; 0.25–0.60 RB1 L 11/21 14/19 0.52; 0.23–1.16 H 74/176 106/175 0.55; 0.41–0.74 E2F1 L 31/105 45/91 0.56; 0.35–0.89 H 54/92 75/103 0.52; 0.37–0.75 Implicated in CDK4/6 inhibitor resistance CDK2 L 40/103 49/93 0.64; 0.42–0.98 H 45/94 71/101 0.48; 0.33–0.71 CCNE1 L 32/97 51/99 0.53; 0.34–0.83 H 53/100 69/95 0.54; 0.38–0.78 FGFR1 L 32/93 59/103 0.45; 0.29–0.69 H 53/104 61/91 0.63; 0.43–0.91 Involved in alternative pathways Cell cycle control L 32/99 47/97 0.66; 0.42–1.03 H 53/98 73/97 0.45; 0.31–0.64 PI3K pathway L 37/98 54/98 0.57; 0.37–0.86 H 48/99 66/96 0.54; 0.37–0.79 MAPK pathway L 42/99 61/97 0.55; 0.37–0.81 H 43/98 59/97 0.56; 0.37–0.83 RTKs L 39/103 59/93 0.41; 0.27–0.61 H 46/94 61/101 0.74; 0.50–1.08
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