Review Article

BRCA突变状态是三阴性乳腺癌中铂类化疗的有前途的预测生物标志物

卷 21, 期 10, 2020

页: [962 - 973] 页: 12

弟呕挨: 10.2174/1389450121666200203162541

价格: $65

摘要

三阴性乳腺癌(TNBC)可通过缺乏雌激素受体(ER),孕激素受体(PR)以及人类表皮生长因子受体2(HER2)的表达而与其他乳腺恶性肿瘤区分开。 TNBC与不良的临床结果和高转移风险相关。当前,一些临床和转化报告集中在针对这种侵袭性癌症开发靶向疗法。除了批准的靶向药物(例如聚(ADP-核糖)聚合酶抑制剂(PARPi)和免疫检查点抑制剂)外,基于铂的化学疗法仍是TNBC的基础治疗选择。但是,尽管在TNBC中观察到铂类化学疗法的预后有所改善,但是仍然有很大一部分患者对该治疗无反应,因此,仍需要预测性生物标志物对TNBC患者进行分层,从而避免这些药物的不良毒性代理商。随着基因检测的出现,最近的一些研究表明,TNBC患者的乳腺癌易感基因(BRCA)突变是重要的预后指标。这些突变改变了导致基因组不稳定的同源重组修复(HRR)机制。因此,这些强抗癌药诱导的脱氧核糖核酸(DNA)损伤可增强细胞死亡,从而可以解释TNBC患者亚群对铂类治疗的敏感性。通过本文,我们回顾了有关该主题的最新研究,以更好地了解其机制,并讨论了BRCA突变状态作为TNBC中铂类化学疗法的预测生物标志物的潜力。

关键词: 三阴性乳腺癌,BRCA1,BRCA2,铂类,化疗,预测生物标志物。

图形摘要

[1]
Bray F, Ferlay J, Soerjomataram I, Siegel RL, Torre LA, Jemal A. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin 2018; 68(6): 394-424.
[http://dx.doi.org/10.3322/caac.21492] [PMID: 30207593]
[2]
Palma G, Frasci G, Chirico A, et al. Triple negative breast cancer: looking for the missing link between biology and treatments. Oncotarget 2015; 6(29): 26560-74.
[http://dx.doi.org/10.18632/oncotarget.5306] [PMID: 26387133]
[3]
Yuan N, Meng M, Liu C, et al. Clinical characteristics and prognostic analysis of triple-negative breast cancer patients. Mol Clin Oncol 2014; 2(2): 245-51.
[http://dx.doi.org/10.3892/mco.2013.230] [PMID: 24649341]
[4]
Plasilova ML, Hayse B, Killelea BK, Horowitz NR, Chagpar AB, Lannin DR. Features of triple-negative breast cancer: Analysis of 38,813 cases from the national cancer database. Medicine (Baltimore) 2016; 95(35) e4614
[http://dx.doi.org/10.1097/MD.0000000000004614] [PMID: 27583878]
[5]
Dent R, Trudeau M, Pritchard KI, et al. Triple-negative breast cancer: clinical features and patterns of recurrence. Clin Cancer Res 2007; 13(15 Pt 1): 4429-34.
[http://dx.doi.org/10.1158/1078-0432.CCR-06-3045] [PMID: 17671126]
[6]
Freedman GM, Anderson PR, Li T, Nicolaou N. Locoregional recurrence of triple-negative breast cancer after breast-conserving surgery and radiation. Cancer 2009; 115(5): 946-51.
[http://dx.doi.org/10.1002/cncr.24094] [PMID: 19156929]
[7]
Lowery AJ, Kell MR, Glynn RW, Kerin MJ, Sweeney KJ. Locoregional recurrence after breast cancer surgery: a systematic review by receptor phenotype. Breast Cancer Res Treat 2012; 133(3): 831-41.
[http://dx.doi.org/10.1007/s10549-011-1891-6] [PMID: 22147079]
[8]
Jhan JR, Andrechek ER. Triple-negative breast cancer and the potential for targeted therapy. Pharmacogenomics 2017; 18(17): 1595-609.
[http://dx.doi.org/10.2217/pgs-2017-0117] [PMID: 29095114]
[9]
McCann KE. Advances in the use of PARP inhibitors for BRCA1/2-associated breast cancer: talazoparib. Future Oncol 2019; 15(15): 1707-15.
[http://dx.doi.org/10.2217/fon-2018-0751] [PMID: 30912451]
[10]
Cyprian FS, Akhtar S, Gatalica Z, Vranic S. Targeted immunotherapy with a checkpoint inhibitor in combination with chemotherapy: A new clinical paradigm in the treatment of triple-negative breast cancer. Bosn J Basic Med Sci 2019; 19(3): 227-33.
[http://dx.doi.org/10.17305/bjbms.2019.4204] [PMID: 30915922]
[11]
Perou CM, Sørlie T, Eisen MB, et al. Molecular portraits of human breast tumours. Nature 2000; 406(6797): 747-52.
[http://dx.doi.org/10.1038/35021093] [PMID: 10963602]
[12]
Sørlie T, Wang Y, Xiao C, et al. Distinct molecular mechanisms underlying clinically relevant subtypes of breast cancer: gene expression analyses across three different platforms. BMC Genomics 2006; 7: 127.
[http://dx.doi.org/10.1186/1471-2164-7-127] [PMID: 16729877]
[13]
Hubalek M, Czech T, Müller H. Biological subtypes of triple-negative breast cancer. Breast Care (Basel) 2017; 12(1): 8-14.
[http://dx.doi.org/10.1159/000455820] [PMID: 28611535]
[14]
Perou CM. Molecular stratification of triple-negative breast cancers. Oncologist 2010; 15(Suppl. 5): 39-48.
[http://dx.doi.org/10.1634/theoncologist.2010-S5-39] [PMID: 21138954]
[15]
Prat A, Adamo B, Cheang MC, Anders CK, Carey LA, Perou CM. Molecular characterization of basal-like and non-basal-like triple-negative breast cancer. Oncologist 2013; 18(2): 123-33.
[http://dx.doi.org/10.1634/theoncologist.2012-0397] [PMID: 23404817]
[16]
Yersal O, Barutca S. Biological subtypes of breast cancer: Prognostic and therapeutic implications. World J Clin Oncol 2014; 5(3): 412-24.
[http://dx.doi.org/10.5306/wjco.v5.i3.412] [PMID: 25114856]
[17]
Rouzier R, Perou CM, Symmans WF, et al. Breast cancer molecular subtypes respond differently to preoperative chemotherapy. Clin Cancer Res 2005; 11(16): 5678-85.
[http://dx.doi.org/10.1158/1078-0432.CCR-04-2421] [PMID: 16115903]
[18]
Subbiah S, Gopu G, Senthilkumar P, Muniasamy P. Molecular subtypes as a predictor of response to neoadjuvant chemotherapy in breast cancer patients. Indian J Cancer 2017; 54(4): 652-7.
[http://dx.doi.org/10.4103/ijc.IJC_238_17] [PMID: 30082552]
[19]
Symmans WF, Wei C, Gould R, et al. Long-Term Prognostic Risk After Neoadjuvant Chemotherapy Associated With Residual Cancer Burden and Breast Cancer Subtype. J Clin Oncol 2017; 35(10): 1049-60.
[http://dx.doi.org/10.1200/JCO.2015.63.1010] [PMID: 28135148]
[20]
Cortazar P, Zhang L, Untch M, et al. Pathological complete response and long-term clinical benefit in breast cancer: the CTNeoBC pooled analysis. Lancet 2014; 384(9938): 164-72.
[http://dx.doi.org/10.1016/S0140-6736(13)62422-8] [PMID: 24529560]
[21]
Poggio F, Bruzzone M, Ceppi M, et al. Platinum-based neoadjuvant chemotherapy in triple-negative breast cancer: a systematic review and meta-analysis. Ann Oncol 2018; 29(7): 1497-508.
[http://dx.doi.org/10.1093/annonc/mdy127] [PMID: 29873695]
[22]
Lehmann BD, Bauer JA, Chen X, et al. Identification of human triple-negative breast cancer subtypes and preclinical models for selection of targeted therapies. J Clin Invest 2011; 121(7): 2750-67.
[http://dx.doi.org/10.1172/JCI45014] [PMID: 21633166]
[23]
Masuda H, Baggerly KA, Wang Y, et al. Differential response to neoadjuvant chemotherapy among 7 triple-negative breast cancer molecular subtypes. Clin Cancer Res 2013; 19(19): 5533-40.
[http://dx.doi.org/10.1158/1078-0432.CCR-13-0799] [PMID: 23948975]
[24]
Burstein MD, Tsimelzon A, Poage GM, et al. Comprehensive genomic analysis identifies novel subtypes and targets of triple-negative breast cancer. Clin Cancer Res 2015; 21(7): 1688-98.
[http://dx.doi.org/10.1158/1078-0432.CCR-14-0432] [PMID: 25208879]
[25]
Jézéquel P, Loussouarn D, Guérin-Charbonnel C, et al. Gene-expression molecular subtyping of triple-negative breast cancer tumours: importance of immune response. Breast Cancer Res 2015; 17: 43.
[http://dx.doi.org/10.1186/s13058-015-0550-y] [PMID: 25887482]
[26]
Milioli HH, Tishchenko I, Riveros C, Berretta R, Moscato P. Basal-like breast cancer: molecular profiles, clinical features and survival outcomes. BMC Med Genomics 2017; 10(1): 19.
[http://dx.doi.org/10.1186/s12920-017-0250-9] [PMID: 28351365]
[27]
Lehmann BD, Jovanović B, Chen X, et al. refinement of triple-negative breast cancer molecular subtypes: implications for neoadjuvant chemotherapy selection. PLoS One 2016; 11(6) e0157368
[http://dx.doi.org/10.1371/journal.pone.0157368] [PMID: 27310713]
[28]
Santonja A, Sánchez-Muñoz A, Lluch A, et al. Triple negative breast cancer subtypes and pathologic complete response rate to neoadjuvant chemotherapy. Oncotarget 2018; 9(41): 26406-16.
[http://dx.doi.org/10.18632/oncotarget.25413] [PMID: 29899867]
[29]
Banerji S, Cibulskis K, Rangel-Escareno C, et al. Sequence analysis of mutations and translocations across breast cancer subtypes. Nature 2012; 486(7403): 405-9.
[http://dx.doi.org/10.1038/nature11154] [PMID: 22722202]
[30]
Lips EH, Michaut M, Hoogstraat M, et al. Next generation sequencing of triple negative breast cancer to find predictors for chemotherapy response. Breast Cancer Res 2015; 17(1): 134.
[http://dx.doi.org/10.1186/s13058-015-0642-8] [PMID: 26433948]
[31]
Shah SP, Roth A, Goya R, et al. The clonal and mutational evolution spectrum of primary triple-negative breast cancers. Nature 2012; 486(7403): 395-9.
[http://dx.doi.org/10.1038/nature10933] [PMID: 22495314]
[32]
Bareche Y, Venet D, Ignatiadis M, et al. Unravelling triple-negative breast cancer molecular heterogeneity using an integrative multiomic analysis. Ann Oncol 2018; 29(4): 895-902.
[http://dx.doi.org/10.1093/annonc/mdy024] [PMID: 29365031]
[33]
Jiang YZ, Ma D, Suo C, et al. Genomic and transcriptomic landscape of triple-negative breast cancers: subtypes and treatment strategies. Cancer Cell 2019; 35(3): 428-440.e5.
[http://dx.doi.org/10.1016/j.ccell.2019.02.001] [PMID: 30853353]
[34]
Mills MN, Yang GQ, Oliver DE, et al. Histologic heterogeneity of triple negative breast cancer: A National Cancer Centre Database analysis. Eur J Cancer 2018; 98: 48-58.
[http://dx.doi.org/10.1016/j.ejca.2018.04.011] [PMID: 29870876]
[35]
Cardoso F, Kyriakides S, Ohno S, et al. Early breast cancer: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up. Ann Oncol 2019; 30(10): 1674.
[http://dx.doi.org/10.1093/annonc/mdz189] [PMID: 31236598]
[36]
Cardoso F, Senkus E, Costa A, et al. 4th ESO-ESMO international consensus guidelines for advanced breast cancer (abc 4). Ann Oncol 2018; 29(8): 1634-57.
[http://dx.doi.org/10.1093/annonc/mdy192] [PMID: 30032243]
[37]
Wu K, Yang Q, Liu Y, Wu A, Yang Z. Meta-analysis on the association between pathologic complete response and triple-negative breast cancer after neoadjuvant chemotherapy. World J Surg Oncol 2014; 12: 95.
[http://dx.doi.org/10.1186/1477-7819-12-95] [PMID: 24731479]
[38]
Spring LM, Fell G, Arfe A, et al. Pathological complete response after neoadjuvant chemotherapy and impact on breast cancer recurrence and mortality, stratified by breast cancer subtypes and adjuvant chemotherapy usage: Individual patient-level meta-analyses of over 27,000 patients [abstract]. Proceedings of the 2018 San Antonio Breast Cancer Symposium. 2018 Dec 4-8; San Antonio, TX. 2019; pp. GS2-03.
[http://dx.doi.org/10.1158/1538-7445.SABCS18-GS2-03]
[39]
von Minckwitz G, Schneeweiss A, Loibl S, et al. Neoadjuvant carboplatin in patients with triple-negative and HER2-positive early breast cancer (GeparSixto; GBG 66): a randomised phase 2 trial. Lancet Oncol 2014; 15(7): 747-56.
[http://dx.doi.org/10.1016/S1470-2045(14)70160-3] [PMID: 24794243]
[40]
Sikov WM, Berry DA, Perou CM, et al. Impact of the addition of carboplatin and/or bevacizumab to neoadjuvant once-per-week paclitaxel followed by dose-dense doxorubicin and cyclophosphamide on pathologic complete response rates in stage II to III triple-negative breast cancer: CALGB 40603 (Alliance). J Clin Oncol 2015; 33(1): 13-21.
[http://dx.doi.org/10.1200/JCO.2014.57.0572] [PMID: 25092775]
[41]
Sharma P, López-Tarruella S, García-Saenz JA, et al. Pathological response and survival in triple-negative breast cancer following neoadjuvant carboplatin plus docetaxel. Clin Cancer Res 2018; 24(23): 5820-9.
[http://dx.doi.org/10.1158/1078-0432.CCR-18-0585] [PMID: 30061361]
[42]
Su YW, Hung CY, Lam HB, Chang YC, Yang PS. A single institution experience of incorporation of cisplatin into adjuvant chemotherapy for patients with triple-negative breast cancer of unknown BRCA mutation status. Clin Med Insights Oncol 2018; 12 1179554918794672
[http://dx.doi.org/10.1177/1179554918794672] [PMID: 30150877]
[43]
Vetter M, Fokas S, Biskup E, et al. Efficacy of adjuvant chemotherapy with carboplatin for early triple negative breast cancer: a single center experience. Oncotarget 2017; 8(43): 75617-26.
[http://dx.doi.org/10.18632/oncotarget.18118] [PMID: 29088896]
[44]
Kaya V, Yildirim M, Yazici G, Gunduz S, Bozcuk H, Paydas S. Effectiveness of platinum-based treatment for triple negative metastatic breast cancer: a meta-analysis. Asian Pac J Cancer Prev 2018; 19(5): 1169-73.
[PMID: 29801396]
[45]
Zhang J, Lin Y, Sun XJ, et al. Biomarker assessment of the CBCSG006 trial: a randomized phase III trial of cisplatin plus gemcitabine compared with paclitaxel plus gemcitabine as first-line therapy for patients with metastatic triple-negative breast cancer. Ann Oncol 2018; 29(8): 1741-7.
[http://dx.doi.org/10.1093/annonc/mdy209] [PMID: 29905759]
[46]
Pandy JGP, Balolong-Garcia JC, Cruz-Ordinario MVB, Que FVF. Triple negative breast cancer and platinum-based systemic treatment: a meta-analysis and systematic review. BMC Cancer 2019; 19(1): 1065.
[http://dx.doi.org/10.1186/s12885-019-6253-5] [PMID: 31703646]
[47]
Sharma P, Klemp JR, Kimler BF, et al. Germline BRCA mutation evaluation in a prospective triple-negative breast cancer registry: implications for hereditary breast and/or ovarian cancer syndrome testing. Breast Cancer Res Treat 2014; 145(3): 707-14.
[http://dx.doi.org/10.1007/s10549-014-2980-0] [PMID: 24807107]
[48]
Couch FJ, Hart SN, Sharma P, et al. Inherited mutations in 17 breast cancer susceptibility genes among a large triple-negative breast cancer cohort unselected for family history of breast cancer. J Clin Oncol 2015; 33(4): 304-11.
[http://dx.doi.org/10.1200/JCO.2014.57.1414] [PMID: 25452441]
[49]
Xie Y, Gou Q, Wang Q, Zhong X, Zheng H. The role of BRCA status on prognosis in patients with triple-negative breast cancer. Oncotarget 2017; 8(50): 87151-62.
[http://dx.doi.org/10.18632/oncotarget.19895] [PMID: 29152070]
[50]
Wunderle M, Gass P, Häberle L, et al. BRCA mutations and their influence on pathological complete response and prognosis in a clinical cohort of neoadjuvantly treated breast cancer patients. Breast Cancer Res Treat 2018; 171(1): 85-94.
[http://dx.doi.org/10.1007/s10549-018-4797-8] [PMID: 29725888]
[51]
Chen H, Wu J, Zhang Z, et al. Association between BRCA Status and triple-negative breast cancer: A meta-analysis. Front Pharmacol 2018; 9: 909.
[http://dx.doi.org/10.3389/fphar.2018.00909] [PMID: 30186165]
[52]
Venkitaraman AR. Cancer suppression by the chromosome custodians, BRCA1 and BRCA2. Science 2014; 343(6178): 1470-5.
[http://dx.doi.org/10.1126/science.1252230] [PMID: 24675954]
[53]
Peng L, Xu T, Long T, Zuo H. Association between BRCA status and P53 status in breast cancer: a meta-analysis. Med Sci Monit 2016; 22: 1939-45.
[http://dx.doi.org/10.12659/MSM.896260] [PMID: 27272763]
[54]
Kuchenbaecker KB, Hopper JL, Barnes DR, et al. Risks of breast, ovarian, and contralateral breast cancer for BRCA1 and BRCA2 Mutation Carriers. JAMA 2017; 317(23): 2402-16.
[http://dx.doi.org/10.1001/jama.2017.7112] [PMID: 28632866]
[56]
Gorodetska I, Kozeretska I, Dubrovska A. BRCA Genes: The Role in Genome Stability, Cancer Stemness and Therapy Resistance. J Cancer 2019; 10(9): 2109-27.
[http://dx.doi.org/10.7150/jca.30410] [PMID: 31205572]
[57]
Lord CJ, Ashworth A. The DNA damage response and cancer therapy. Nature 2012; 481(7381): 287-94.
[http://dx.doi.org/10.1038/nature10760] [PMID: 22258607]
[58]
Bhattacharyya A, Ear US, Koller BH, Weichselbaum RR, Bishop DK. The breast cancer susceptibility gene BRCA1 is required for subnuclear assembly of Rad51 and survival following treatment with the DNA cross-linking agent cisplatin. J Biol Chem 2000; 275(31): 23899-903.
[http://dx.doi.org/10.1074/jbc.C000276200] [PMID: 10843985]
[59]
Suchánková T, Kubíček K, Kašpárková J, Brabec V, Kozelka J. Platinum-DNA interstrand crosslinks: molecular determinants of bending and unwinding of the double helix. J Inorg Biochem 2012; 108: 69-79.
[http://dx.doi.org/10.1016/j.jinorgbio.2011.09.025] [PMID: 22019433]
[60]
Basourakos SP, Li L, Aparicio AM, Corn PG, Kim J, Thompson TC. Combination platinum-based and DNA damage response-targeting cancer therapy: evolution and future directions. Curr Med Chem 2017; 24(15): 1586-606.
[http://dx.doi.org/10.2174/0929867323666161214114948] [PMID: 27978798]
[61]
Caramelo O, Silva C, Caramelo F, Frutuoso C, Almeida-Santos T. The effect of neoadjuvant platinum-based chemotherapy in BRCA mutated triple negative breast cancers -systematic review and meta-analysis. Hered Cancer Clin Pract 2019; 17: 11.
[http://dx.doi.org/10.1186/s13053-019-0111-y] [PMID: 30962858]
[62]
Sharma P, López-Tarruella S, García-Saenz JA, et al. Efficacy of neoadjuvant carboplatin plus docetaxel in triple-negative breast cancer: Combined analysis of two cohorts. Clin Cancer Res 2017; 23(3): 649-57.
[http://dx.doi.org/10.1158/1078-0432.CCR-16-0162] [PMID: 27301700]
[63]
Wang C, Zhang J, Wang Y, et al. Prevalence of BRCA1 mutations and responses to neoadjuvant chemotherapy among BRCA1 carriers and non-carriers with triple-negative breast cancer. Ann Oncol 2015; 26(3): 523-8.
[http://dx.doi.org/10.1093/annonc/mdu559] [PMID: 25480878]
[64]
Isakoff SJ, Mayer EL, He L, et al. TBCRC009: A multicenter phase II clinical trial of platinum monotherapy with biomarker assessment in metastatic triple-negative breast cancer. J Clin Oncol 2015; 33(17): 1902-9.
[http://dx.doi.org/10.1200/JCO.2014.57.6660] [PMID: 25847936]
[65]
Tutt A, Tovey H, Cheang MCU, et al. Carboplatin in BRCA1/2-mutated and triple-negative breast cancer BRCAness subgroups: the TNT Trial. Nat Med 2018; 24(5): 628-37.
[http://dx.doi.org/10.1038/s41591-018-0009-7] [PMID: 29713086]
[66]
Kaklamani VG, Jeruss JS, Hughes E, et al. Phase II neoadjuvant clinical trial of carboplatin and eribulin in women with triple negative early-stage breast cancer (NCT01372579). Breast Cancer Res Treat 2015; 151(3): 629-38.
[http://dx.doi.org/10.1007/s10549-015-3435-y] [PMID: 26006067]
[67]
Hahnen E, Lederer B, Hauke J, et al. Germline mutation status, pathological complete response, and disease-free survival in triple-negative breast cancer: secondary analysis of the GeparSixto randomized clinical trial. JAMA Oncol 2017; 3(10): 1378-85.
[http://dx.doi.org/10.1001/jamaoncol.2017.1007] [PMID: 28715532]
[68]
Sella T, Gal Yam EN, Levanon K, et al. Evaluation of tolerability and efficacy of incorporating carboplatin in neoadjuvant anthracycline and taxane based therapy in a BRCA1 enriched triple-negative breast cancer cohort. Breast 2018; 40: 141-6.
[http://dx.doi.org/10.1016/j.breast.2018.05.007] [PMID: 29800932]
[69]
Lord CJ, Ashworth A. BRCAness revisited. Nat Rev Cancer 2016; 16(2): 110-20.
[http://dx.doi.org/10.1038/nrc.2015.21] [PMID: 26775620]
[70]
Lim D, Ngeow J. Evaluation of the methods to identify patients who may benefit from PARP inhibitor use. Endocr Relat Cancer 2016; 23(6): R267-85.
[http://dx.doi.org/10.1530/ERC-16-0116] [PMID: 27226207]
[71]
Akashi-Tanaka S, Watanabe C, Takamaru T, et al. BRCAness predicts resistance to taxane-containing regimens in triple negative breast cancer during neoadjuvant chemotherapy. Clin Breast Cancer 2015; 15(1): 80-5.
[http://dx.doi.org/10.1016/j.clbc.2014.08.003] [PMID: 25445419]
[72]
Domagala P, Hybiak J, Cybulski C, Lubinski J. BRCA1/2-negative hereditary triple-negative breast cancers exhibit BRCAness. Int J Cancer 2017; 140(7): 1545-50.
[http://dx.doi.org/10.1002/ijc.30570] [PMID: 27943282]
[73]
Timms KM, Abkevich V, Hughes E, et al. Association of BRCA1/2 defects with genomic scores predictive of DNA damage repair deficiency among breast cancer subtypes. Breast Cancer Res 2014; 16(6): 475.
[http://dx.doi.org/10.1186/s13058-014-0475-x] [PMID: 25475740]
[74]
von Minckwitz G, Timms K, Untch M, et al. Prediction of pathological complete response (pcr) by homologous recombination deficiency (hrd) after carboplatin-containing neoadjuvant chemotherapy in patients with tnbc: results from geparsixto. J Clin Oncol 2015; 33: abstr 1004.
[75]
Telli ML, Jensen KC, Vinayak S, et al. Phase II study of gemcitabine, carboplatin, and iniparib as neoadjuvant therapy for triple-negative and BRCA1/2 mutation-associated breast cancer with assessment of a tumor-based measure of genomic instability: PrECOG 0105. J Clin Oncol 2015; 33(17): 1895-901.
[http://dx.doi.org/10.1200/JCO.2014.57.0085] [PMID: 25847929]
[76]
Telli ML, Timms KM, Reid J, et al. Homologous Recombination Deficiency (HRD) Score Predicts Response to Platinum-Containing Neoadjuvant Chemotherapy in Patients with Triple-Negative Breast Cancer. Clin Cancer Res 2016; 22(15): 3764-73.
[http://dx.doi.org/10.1158/1078-0432.CCR-15-2477] [PMID: 26957554]
[77]
Davies H, Glodzik D, Morganella S, et al. HRDetect is a predictor of BRCA1 and BRCA2 deficiency based on mutational signatures. Nat Med 2017; 23(4): 517-25.
[http://dx.doi.org/10.1038/nm.4292] [PMID: 28288110]
[78]
Zhao EY, Shen Y, Pleasance E, et al. Homologous Recombination Deficiency and Platinum-Based Therapy Outcomes in Advanced Breast Cancer. Clin Cancer Res 2017; 23(24): 7521-30.
[http://dx.doi.org/10.1158/1078-0432.CCR-17-1941] [PMID: 29246904]
[79]
Brianese RC, Nakamura KDM, Almeida FGDSR, et al. BRCA1 deficiency is a recurrent event in early-onset triple-negative breast cancer: a comprehensive analysis of germline mutations and somatic promoter methylation. Breast Cancer Res Treat 2018; 167(3): 803-14.
[http://dx.doi.org/10.1007/s10549-017-4552-6] [PMID: 29116469]
[80]
Sharma P, Stecklein SR, Kimler BF, et al. The prognostic value of BRCA1 promoter methylation in early stage triple negative breast cancer. J Cancer Ther Res 2014; 3(2): 1-11.
[http://dx.doi.org/10.7243/2049-7962-3-2] [PMID: 25177489]
[81]
Tian T, Shan L, Yang W, Zhou X, Shui R. Evaluation of the BRCAness phenotype and its correlations with clinicopathological features in triple-negative breast cancers. Hum Pathol 2019; 84: 231-8.
[http://dx.doi.org/10.1016/j.humpath.2018.10.004] [PMID: 30339969]
[82]
Stefansson OA, Villanueva A, Vidal A, Martí L, Esteller M. BRCA1 epigenetic inactivation predicts sensitivity to platinum-based chemotherapy in breast and ovarian cancer. Epigenetics 2012; 7(11): 1225-9.
[http://dx.doi.org/10.4161/epi.22561] [PMID: 23069641]
[83]
Silver DP, Richardson AL, Eklund AC, et al. Efficacy of neoadjuvant Cisplatin in triple-negative breast cancer. J Clin Oncol 2010; 28(7): 1145-53.
[http://dx.doi.org/10.1200/JCO.2009.22.4725] [PMID: 20100965]
[84]
Clark CC, Weitzel JN, O’Connor TR. Enhancement of synthetic lethality via combinations of ABT-888, a PARP inhibitor, and carboplatin in vitro and in vivo using BRCA1 and BRCA2 isogenic models. Mol Cancer Ther 2012; 11(9): 1948-58.
[http://dx.doi.org/10.1158/1535-7163.MCT-11-0597] [PMID: 22778154]
[85]
Balmaña J, Tung NM, Isakoff SJ, et al. Phase I trial of olaparib in combination with cisplatin for the treatment of patients with advanced breast, ovarian and other solid tumors. Ann Oncol 2014; 25(8): 1656-63.
[http://dx.doi.org/10.1093/annonc/mdu187] [PMID: 24827126]
[86]
Kaelin WG Jr. The concept of synthetic lethality in the context of anticancer therapy. Nat Rev Cancer 2005; 5(9): 689-98.
[http://dx.doi.org/10.1038/nrc1691] [PMID: 16110319]
[87]
Miller K, Tong Y, Jones DR, et al. Cisplatin with or without rucaparib after preoperative chemotherapy in with triple negative breast cancer: final efficacy results of Hoosier Oncology Group BRE09-146. J Clin Oncol 2015; 33(15): 1082.
[http://dx.doi.org/10.1200/jco.2015.33.15_suppl.1082]
[88]
Rugo HS, Olopade OI, DeMichele A, et al. Adaptive Randomization of Veliparib-Carboplatin Treatment in Breast Cancer. N Engl J Med 2016; 375(1): 23-34.
[http://dx.doi.org/10.1056/NEJMoa1513749] [PMID: 27406347]
[89]
Bartelink IH, Prideaux B, Krings G, et al. Heterogeneous drug penetrance of veliparib and carboplatin measured in triple negative breast tumors. Breast Cancer Res 2017; 19(1): 107.
[http://dx.doi.org/10.1186/s13058-017-0896-4] [PMID: 28893315]
[90]
Loibl S, O’Shaughnessy J, Untch M, et al. Addition of the PARP inhibitor veliparib plus carboplatin or carboplatin alone to standard neoadjuvant chemotherapy in triple-negative breast cancer (BrighTNess): a randomised, phase 3 trial. Lancet Oncol 2018; 19(4): 497-509.
[http://dx.doi.org/10.1016/S1470-2045(18)30111-6] [PMID: 29501363]
[91]
Han HS, Diéras V, Robson M, et al. Veliparib with temozolomide or carboplatin/paclitaxel versus placebo with carboplatin/paclitaxel in patients with BRCA1/2 locally recurrent/metastatic breast cancer: randomized phase II study. Ann Oncol 2018; 29(1): 154-61.
[http://dx.doi.org/10.1093/annonc/mdx505] [PMID: 29045554]
[92]
Mader S, Pantel K. Liquid Biopsy: Current Status and Future Perspectives. Oncol Res Treat 2017; 40(7-8): 404-8.
[http://dx.doi.org/10.1159/000478018] [PMID: 28693023]
[93]
Thierry AR, El Messaoudi S, Gahan PB, Anker P, Stroun M. Origins, structures, and functions of circulating DNA in oncology. Cancer Metastasis Rev 2016; 35(3): 347-76.
[http://dx.doi.org/10.1007/s10555-016-9629-x] [PMID: 27392603]
[94]
Pantel K, Speicher MR. The biology of circulating tumor cells. Oncogene 2016; 35(10): 1216-24.
[http://dx.doi.org/10.1038/onc.2015.192] [PMID: 26050619]
[95]
Alimirzaie S, Bagherzadeh M, Akbari MR. Liquid biopsy in breast cancer: A comprehensive review. Clin Genet 2019; 95(6): 643-60.
[http://dx.doi.org/10.1111/cge.13514] [PMID: 30671931]
[96]
Mandel P, Metais P. Les acides nucléiques du plasma sanguin chez l’homme. C R Seances Soc Biol Fil 1948; 142(3-4): 241-3.
[PMID: 18875018]
[97]
Stroun M, Anker P, Lyautey J, Lederrey C, Maurice PA. Isolation and characterization of DNA from the plasma of cancer patients. Eur J Cancer Clin Oncol 1987; 23(6): 707-12.
[http://dx.doi.org/10.1016/0277-5379(87)90266-5] [PMID: 3653190]
[98]
Garcia-Murillas I, Chopra N, Comino-Méndez I, et al. Assessment of molecular relapse detection in early-stage breast cancer. JAMA Oncol 2019; 5(10): 1473-8.
[http://dx.doi.org/10.1001/jamaoncol.2019.1838] [PMID: 31369045]
[99]
Riva F, Bidard FC, Houy A, et al. Patient-specific circulating tumor dna detection during neoadjuvant chemotherapy in triple-negative breast cancer. Clin Chem 2017; 63(3): 691-9.
[http://dx.doi.org/10.1373/clinchem.2016.262337] [PMID: 28073896]
[100]
Chen YH, Hancock BA, Solzak JP, et al. Next-generation sequencing of circulating tumor DNA to predict recurrence in triple-negative breast cancer patients with residual disease after neoadjuvant chemotherapy. NPJ Breast Cancer 2017; 3: 24.
[http://dx.doi.org/10.1038/s41523-017-0028-4] [PMID: 28685160]
[101]
Rodriguez BJ, Córdoba GD, Aranda AG, et al. detection of tp53 and pik3ca mutations in circulating tumor dna using next-generation sequencing in the screening process for early breast cancer diagnosis. J Clin Med 2019; 8(8) E1183
[http://dx.doi.org/10.3390/jcm8081183] [PMID: 31394872]
[102]
Cavallone L, Aguilar A, Aldamry M, et al. Circulating tumor DNA (ctDNA) during and after neoadjuvant chemotherapy and prior to surgery is a powerful prognostic factor in triple-negative breast cancer (TNBC). J Clin Oncol 2019; 37(15): 594-4.
[http://dx.doi.org/10.1200/JCO.2019.37.15_suppl.594]
[103]
Stover DG, Parsons HA, Ha G, et al. Association of cell-free DNA tumor fraction and somatic copy number alterations with survival in metastatic triple-negative breast cancer. J Clin Oncol 2018; 36(6): 543-53.
[http://dx.doi.org/10.1200/JCO.2017.76.0033] [PMID: 29298117]
[104]
Parsons HA, Beaver JA, Cimino-Mathews A, et al. Individualized Molecular Analyses Guide Efforts (IMAGE): A Prospective Study of Molecular Profiling of Tissue and Blood in Metastatic Triple-Negative Breast Cancer. Clin Cancer Res 2017; 23(2): 379-86.
[http://dx.doi.org/10.1158/1078-0432.CCR-16-1543] [PMID: 27489289]
[105]
Kim SB, Dent R, Wongchenko MJ, Singel SM, Baselga J. Concordance between plasma-based and tissue-based next-generation sequencing in LOTUS. Lancet Oncol 2017; 18(11) e638
[http://dx.doi.org/10.1016/S1470-2045(17)30785-4] [PMID: 29208392]
[106]
Hu ZY, Xie N, Tian C, et al. Identifying circulating tumor DNA mutation profiles in metastatic breast cancer patients with multiline resistance. EBioMedicine 2018; 32: 111-8.
[http://dx.doi.org/10.1016/j.ebiom.2018.05.015] [PMID: 29807833]
[107]
Madic J, Kiialainen A, Bidard FC, et al. Circulating tumor DNA and circulating tumor cells in metastatic triple negative breast cancer patients. Int J Cancer 2015; 136(9): 2158-65.
[http://dx.doi.org/10.1002/ijc.29265] [PMID: 25307450]
[108]
Vidula N. Somatic BRCA mutation detection by circulating tumor DNA analysis in patients with metastatic breast cancer: Incidence and association with tumor genotyping results, germline BRCA mutation status, and clinical outcomes. Cancer Res 2018; 78(4): Abstract nr PD1-..
[109]
Nedeljković M, Damjanović A. Mechanisms of chemotherapy resistance in triple-negative breast cancer-how we can rise to the challenge. Cells 2019; 8(9) E957
[http://dx.doi.org/10.3390/cells8090957] [PMID: 31443516]
[110]
Wang Y, Krais JJ, Bernhardy AJ, et al. RING domain-deficient BRCA1 promotes PARP inhibitor and platinum resistance. J Clin Invest 2016; 126(8): 3145-57.
[http://dx.doi.org/10.1172/JCI87033] [PMID: 27454289]
[111]
Ganesan S. Tumor suppressor tolerance: reversion mutations in BRCA1 and BRCA2 and resistance to PARP inhibitors and platinum. JCO-Precis Oncol 2018; p. 2.
[112]
Weigelt B, Comino-Méndez I, de Bruijn I, et al. Diverse BRCA1 and BRCA2 Reversion Mutations in Circulating Cell-Free DNA of Therapy-Resistant Breast or Ovarian Cancer. Clin Cancer Res 2017; 23(21): 6708-20.
[http://dx.doi.org/10.1158/1078-0432.CCR-17-0544] [PMID: 28765325]
[113]
Gornstein EL, Sandefur S, Chung JH, et al. BRCA2 reversion mutation associated with acquired resistance to olaparib in estrogen receptor-positive breast cancer detected by genomic profiling of tissue and liquid biopsy. Clin Breast Cancer 2018; 18(2): 184-8.
[http://dx.doi.org/10.1016/j.clbc.2017.12.010] [PMID: 29325860]
[114]
Afghahi A, Timms KM, Vinayak S, et al. tumor brca1 reversion mutation arising during neoadjuvant platinum-based chemotherapy in triple-negative breast cancer is associated with therapy resistance. Clin Cancer Res 2017; 23(13): 3365-70.
[http://dx.doi.org/10.1158/1078-0432.CCR-16-2174] [PMID: 28087643]

Rights & Permissions Print Cite
© 2024 Bentham Science Publishers | Privacy Policy