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中华乳腺病杂志(电子版) ›› 2017, Vol. 11 ›› Issue (03) : 171 -174. doi: 10.3877/cma.j.issn.1674-0807.2017.03.010

综述

芳香化酶抑制剂耐药机制研究进展
李焱1, 鲁海玲1, 霍明鸣1, 庞慧1, 蔡莉1,()   
  1. 1.150081 哈尔滨医科大学附属肿瘤医院乳腺内四科
  • 收稿日期:2016-10-13 出版日期:2017-06-01
  • 通信作者: 蔡莉

Drug resistance mechanism of aromatase inhibitors

Yan Li, Hailing Lu, Mingming Huo, Hui Pang, Li Cai()   

  • Received:2016-10-13 Published:2017-06-01
  • Corresponding author: Li Cai
引用本文:

李焱, 鲁海玲, 霍明鸣, 庞慧, 蔡莉. 芳香化酶抑制剂耐药机制研究进展[J/OL]. 中华乳腺病杂志(电子版), 2017, 11(03): 171-174.

Yan Li, Hailing Lu, Mingming Huo, Hui Pang, Li Cai. Drug resistance mechanism of aromatase inhibitors[J/OL]. Chinese Journal of Breast Disease(Electronic Edition), 2017, 11(03): 171-174.

芳香化酶抑制剂(AI)在乳腺癌内分泌治疗中发挥重要作用。 然而,随着药物治疗研究的不断深入,AI 耐药(原发性和获得性)现象也逐渐显现,针对AI 耐药的治疗策略是当前亟待解决的临床问题。 研究证实,ER 通路及其他相关信号通路的异常激活是AI 耐药的主要机制。 笔者就AI 的原发与继发耐药机制及逆转耐药的策略进行综述,以期为激素受体阳性乳腺癌的治疗提供新思路。

[1]
Ewertz M,Gray KP,Regan MM,et al.Obesity and risk of recurrence or death after adjuvant endocrine therapy with letrozole or tamoxifen in the breast international group 1-98 trial[J]. J Clin Oncol,2012,30(32):3967-3975.
[2]
Early Breast Cancer Trialists' Collaborative Group (EBCTCG).Aromatase inhibitors versus tamoxife in early breast cancer:patient-level meta-analysis of the randomized trials[J]. Lancet,2015,386(10001):1341-1352.
[3]
Ferraldeschi R,Arnedos M,Hadfield KD. Polymorphisms of CYP19A1 and response to aromatase inhibitors in metastatic breast cancer patients[J].Breast Cancer Res Treat,2012,133(3):1191-1198.
[4]
Fuqua SA, Wiltschke C,Zhang QX,et al. A hypersensitive estrogen receptor - alpha mutation in premalignant breast lesions [J]. Cancer Res,2000,60(15):4026-4029.
[5]
Lundberg AS,Weinberg RA.Control of the cell cycle and apoptosis[J].Eur J Cancer,1999,35(14):1886-1894.
[6]
Toy W,Shen Y,Won H,et al. ESR1 ligand-blinding domain mutations in hormone-resistant breast cancer[J]. Nat Genet, 2013,45(12):1439-1445.
[7]
Li S, Shen D, Shao J,et al. Endocrine-therapy-resistant ESR1 variants revealed by genomic characterization of breast-cancer-derived xenografts[J]. Cell Rep,2013,4(6):1116-1130.
[8]
Visvanathan K, Hurley P, Bantug E, et al. Use of pharmacologic interventions for breast cancer risk reduction: American Society of Clinical Oncology clinical practice guideline[J]. J Clin Oncol, 2013,31(23):2942-2962.
[9]
Chumsri S, Howes T, Bao T, et al. Aromatase,aromatase inhibitors,and breast cancer[J]. J Steroid Biochem Mol Biol,2011,125(1/2):13-22.
[10]
Burstein HJ, Cirrincione CT, Barry WT,et al. Endocrine therapy with or without inhibition of epidermal growth factor receptor and human epidermal growth factor receptor 2[J]. J Clin Oncol,2014,32(35):3959-3966.
[11]
Roop RP, Ma CX. Endocrine resistance in breast cancer: molecular pathways and rational development of targeted therapies[J]. Future Oncol,2012,8(3):273-292.
[12]
Bose R, Kavuri SM, Searleman AC,et al. Activating HER2 mutations in HER2 gene amplification negative breast cancer[J]. Cancer Discov,2013,3(2):224-237.
[13]
Cancer Genome Atlas Network. Comprehensive molecular portraits of human breast tumours[J]. Nature,2012,490(7418):61-70.
[14]
Cizkova M, Susini A, Vacher S, et al. PIK3CA mutation impact on survival in breast cancer patients and in ERα, PR and ERBB2- based subgroups[J]. Breast Cancer Res,2012,14(1):R28.
[15]
Sanchez CG, Ma CX, Crowder RJ,et al. Preclinical modeling of combined phosphatidylinositol-3-kinase inhibition with endocrine therapy for estrogen receptor-positive breast cancer[J]. Breast Cancer Res,2011,13(2): R21.
[16]
Dobashi Y, Watanabe Y, Miwa C, et al. Mammalian target of rapamycin: acentral node of complex signaling cascades[J].Int J Clin Exp Pathol,2011,4(5):476-495.
[17]
Jelovac D, Sabnis G, Long BJ, et al. Activation of mitogen-activated protein kinase in xenografts and cells during prolonged treatment with aromatase inhibitor letrozole [J]. Cancer Res, 2005, 65 (12):5380-5389.
[18]
Hiscox S, Barrett-Lee P, Borley AC, et al. Combining Src inhibitors and aromatase inhibitors: a novel strategy for overcoming endocrine resistance and bone loss[J].Eur J Cancer,2010,46(12):2187-2195.
[19]
Fan P, Agboke FA, McDaniel RE,et al. Inhibition of Src blocks oestrogen-induced apoptosis and restores oestrogen-stimulated growth in long-term oestrogen-deprived breast cancer cells[J]. Eur J Cancer,2014(50):457-468.
[20]
Mcbryan J, Theissen SM, Byrne C, et al. Metastatic progression with resistance to aromatase inhibitors is driven by the steroid receptor coactivator SRC-1[J]. Cancer Res,2012,72(2):548-559.
[21]
Tran B, Bedard PL. Luminal-B breast cancer and novel therapeutic targets[J]. Breast Cancer Res,2011,13(6):221.
[22]
Choi YJ, Anders L.Signaling through cyclin D-dependent kinases [J].Oncogene,2014,33(15):1890-1903.
[23]
Bertelli G,Garrone O,Merlano M,et al. Sequential treatment with exemestane and non-steroidal aromatase inhibitors in advanced breast cancer[J].Oncology,2005,69(6):471-477.
[24]
Chia S, Gradishar W, Mauriac L, et al. Double-blind, randomized placebo controlled trial of fulvestrant compared with exemestane after prior nonsteroidal aromatase inhibitor theray in postmenopausal women with hormone receptor-positive,advanced breast cancer:results from EFECT[J]. J Clin Oncol,2008,26(10):1664-1670.
[25]
Johnston SR,Kilburn LS, Ellis P, et al. Fulvestrant plus anastrozole or placebo versus exemestane alone after progression on non-steroidal aromatase inhibition in postmenopausal patients with hormone-receptorpositive locally advanced or metastatic breast cancer (SoFEA): a composite, multicentre, phase 3 rand omised trial[J]. Lancet Oncol,2013,14(10):989-998.
[26]
Finn RS,Dering J,Conklin D,et al. PD0332991,a selective cyclin D kinase 4/6 inhibitor, preferentially inhibits proliferation of luminal estrogen receptor-positive human breast cancer cell lines in vitro[J].Breast Cancer Res,2009,11(5):R77.
[27]
Finn R, Crown J, Lang I, et al. The cyclin-dependent kinase (CDK)4/6 inhibitor palbociclib in combination with letrozole versus letrozole alone as first-line treatment of ER+/HER2- advanced breast cancer(PALOMA-1/TRIO-18) [J].Lancet Oncol,2015,16(1):25-35.
[28]
Cristofanilli M, Turner NC, Bondarenko I, et al. Fulvestrant plus palbociclib versus fulvestrant plus placebo for treatment of hormonereceptor-positive, HER2-negative metastatic breast cancer that progressed on previous endocrine therapy(PALOMA-3):Final analysis of the multicentre,double-blind,phase 3 randomised controlled trial[J].Lancet Oncol,2016,17(4):425-439.
[29]
Ma CX, Luo J,Naughton M, et al. A phase I trial of BKM120(buparlisib) in combination with fulvestrant in postmenopausal women with estrogen receptor-positive metastatic breast cancer [J]. Clin Cancer Res,2016,22(7):1583-1591.
[30]
Villarreal-Garza C,Cortes J,Andre F,et al. mTOR inhibitors in the management of hormone receptor-positive breast cancer: the latest evidence and future directions[J]. Ann Oncol, 2012, 23 (10):2526-2535.
[31]
Alexander W. San antonio breast cancer symposium[J]. P T, 2011,36(3):156-158.
[32]
Benjamin D,Colombi M,Moroni C,et al. Rapamycin passes the torch:a new generation of mTOR inhibitors[J]. Nat Rev Drug Discov,2011,10(11):868-880.
[33]
Martin LA, Farmer I, Johnston SR,et al. Enhanced estrogen receptor(ER) α,ERBB2, and MAPK signal transduction pathways operate during the adaptation of MCF-7 cells to longterm estrogen deprivation[J].J Biol Chem,2003,278(33):30 458-30 468.
[34]
Chumsri S, Schech A, Chakkabat C,et al.Advances in mechanisms of resistance to aromatase inhibitors[J]. Expert Rev Anticancer Ther,2014,14(4):381-393.
[35]
Sabnis GJ, Goloubeva OG, Kazi AA,et al. HDAC inhibitor entinostat restores responsiveness of letrozole resistant MCF-7Ca xenografts to AIs through modulation of Her-2[J]. Mol Cancer Ther, 2013,12(12):2804-2816.
[36]
Yardley DA, Ismail-Khan RR, Melichar B, et al. Randomized phaseⅡ, double-blind, placebo-controlled study of exemestane with or without entinostat in postmenopausal women with locally recurrent or metastatic estrogen receptor-positive breast cancer progressing on treatment with a nonsteroidal aromatase inhibitor[J]. J Clin Oncol,2013,31(17):2128-2135.
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