Downs Tracy M, Bailey Howard H, Lozar Taja, Schmitz Natalie S, Green Heather, Scarlett Cameron O, Havighurst Thomas C, Twaroski Kyleigh, DeShong Katina, Wollmer Barbara, Bivalacqua Trinity J, Saltzstein Daniel R, Shore Neal, Kim KyungMann, Huang Wei, Ricke William A, Barroilhet Lisa, House Margaret, Parnes Howard L, Messing Edward
University of Wisconsin Carbone Cancer Center, Madison, Wisconsin.
University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Cancer Prev Res (Phila). 2025 Jan 6;18(1):31-39. doi: 10.1158/1940-6207.CAPR-24-0194.
We performed a clinical trial in patients with non-muscle-invasive (NMI) urothelial cancer randomized (2:1) to the EGFR tyrosine kinase inhibitor erlotinib or placebo (either orally once weekly × 3 doses prior to scheduled surgery) to assess for a difference in EGFR phosphorylation in tumor-adjacent normal urothelium <24 hours post-study dose and tolerance of weekly erlotinib therapy. Thirty-seven volunteers (6 female/31 male; mean age 70; 35 White/2 non-White) with confirmed or suspected NMI urothelial cancer were enrolled into either erlotinib (n = 24; 900 mg-13, 600 mg-11) or placebo (n = 13). IHC assessment of phosphorylated and total EGFR in tumor-adjacent normal urothelium (20 erlotinib and 9 placebo subjects) or tumor (21 erlotinib and 11 placebo subjects) at study end showed no significant difference between those receiving erlotinib or placebo. This was also true for other assessed tissue biomarkers (phosphorylated ERK, ERK, E-cadherin, p53, and Ki67). Adverse events were more common, in a dose-related fashion, in participants receiving erlotinib, e.g., 38% experienced grade 1 with rare grade 2 diarrhea and skin toxicity versus 8% in placebo. Clinically insignificant but statistically significant (P = 0.001) elevations in serum total bilirubin and creatinine were observed in participants receiving erlotinib. Serum erlotinib and metabolite concentrations (OSI-420) confirmed compliance in all subjects receiving erlotinib and did not significantly differ between the 600 and 900 mg doses. Despite compelling preclinical and clinical data for targeted EGFR inhibition in bladder cancer prevention, these data do not support the use of weekly erlotinib therapy to prevent progression of NMI bladder cancer. Prevention Relevance: We evaluated the potential of erlotinib in preventing cancer by performing a randomized, double-blind, placebo-controlled trial of weekly erlotinib therapy in participants undergoing surgical removal of suspected noninvasive bladder neoplasia. Weekly erlotinib therapy was tolerated with common grade 1 to 2 toxicities but without evidence of beneficial effect upon urothelial tissue. See related Spotlight, p. 7.
我们对非肌肉浸润性(NMI)尿路上皮癌患者进行了一项临床试验,将患者随机(2:1)分为表皮生长因子受体(EGFR)酪氨酸激酶抑制剂厄洛替尼组或安慰剂组(在计划手术前均口服给药,每周一次,共3剂),以评估研究用药后<24小时肿瘤相邻正常尿路上皮中EGFR磷酸化情况的差异以及厄洛替尼每周治疗的耐受性。37名确诊或疑似NMI尿路上皮癌的志愿者(6名女性/31名男性;平均年龄70岁;35名白人/2名非白人)被纳入厄洛替尼组(n = 24;900 mg剂量组13人,600 mg剂量组11人)或安慰剂组(n = 13)。研究结束时,对肿瘤相邻正常尿路上皮(20名厄洛替尼组受试者和9名安慰剂组受试者)或肿瘤组织(21名厄洛替尼组受试者和11名安慰剂组受试者)进行免疫组化评估,结果显示接受厄洛替尼或安慰剂治疗的患者之间无显著差异。其他评估的组织生物标志物(磷酸化细胞外信号调节激酶、细胞外信号调节激酶、E-钙黏蛋白、p53和Ki67)也是如此。接受厄洛替尼治疗的参与者中不良事件更为常见,呈剂量相关,例如,38%的患者出现1级不良事件,罕见2级腹泻和皮肤毒性,而安慰剂组为8%。接受厄洛替尼治疗的参与者血清总胆红素和肌酐出现临床上无显著意义但具有统计学意义(P = 0.001)的升高。血清厄洛替尼和代谢物浓度(OSI-420)证实所有接受厄洛替尼治疗的受试者均依从用药,600 mg和900 mg剂量组之间无显著差异。尽管在膀胱癌预防中靶向EGFR抑制有令人信服的临床前和临床数据,但这些数据并不支持使用厄洛替尼每周治疗来预防NMI膀胱癌的进展。预防相关性:我们通过对接受疑似非侵袭性膀胱肿瘤手术切除的参与者进行每周一次厄洛替尼治疗的随机、双盲、安慰剂对照试验,评估了厄洛替尼在预防癌症方面的潜力。每周一次的厄洛替尼治疗耐受性良好,常见1至2级毒性,但对尿路上皮组织无有益作用证据。见相关聚焦文章,第7页。