[1] |
Sung H, Ferlay J, Siegel RL, et al. Global cancer statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries[J]. CA Cancer J Clin,2021,71(3):209-249.
|
[2] |
Rizzolo P, Silvestri V, Falchetti M, et al. Inherited and acquired alterations in development of breast cancer [J]. Appl Clin Genet, 2011, 4: 145-158.
|
[3] |
Claus EB, Risch N, Thompson WD. Autosomal dominant inheritance of early-onset breast cancer. Implications for risk prediction [J]. Cancer, 1994, 73(3): 643-651.
|
[4] |
Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer and hormone replacement therapy: collaborative reanalysis of data from 51 epidemiological studies of 52,705 women with breast cancer and 108,411 women without breast cancer[J]. Lancet, 1997, 350(9084): 1047-1059.
|
[5] |
Lewin R, Sulkes A, Shochat T, et al. Oncotype-dx recurrence score distribution in breast cancer patients with BRCA1/2 mutations [J]. Breast Cancer Res Treat, 2016, 157(3): 511-516.
|
[6] |
Kuchenbaecker KB, Hopper JL, Barnes DR, et al. Risks of breast, ovarian, and contralateral breast cancer for BRCA1 and BRCA2 mutation carriers [J]. JAMA, 2017, 317(23): 2402-2016.
|
[7] |
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]. J Clin Oncol, 2015, 33(4): 304-311.
|
[8] |
Aleskandarany M, Caracappa D, Nolan CC, et al. DNA damage response markers are differentially expressed in BRCA-mutated breast cancers [J]. Breast Cancer Res Treat, 2015, 150(1): 81-90.
|
[9] |
Cardoso F, Senkus E, Costa A, et al. 4th ESO-ESMO international consensus guidelines for advanced breast cancer (ABC 4)[J]. Ann Oncol, 2018, 29(8): 1634-1657.
|
[10] |
Dent R, Valentini A, Hanna W, et al. Factors associated with breast cancer mortality after local recurrence [J]. Curr Oncol, 2014, 21(3): e418-e425.
|
[11] |
D’Andrea AD. Mechanisms of PARP inhibitor sensitivity and resistance [J]. DNA Repair (Amst), 2018, 71: 172-176.
|
[12] |
Majidinia M, Yousefi B. DNA damage response regulation by microRNAs as a therapeutic target in cancer [J]. DNA Repair (Amst), 2016, 47: 1-11.
|
[13] |
Falck J, Coates J, Jackson SP. Conserved modes of recruitment of ATM, ATR and DNA-PKcs to sites of DNA damage [J]. Nature, 2005, 434(7033): 605-611.
|
[14] |
Zhou BB, Elledge SJ. The DNA damage response: putting checkpoints in perspective [J]. Nature, 2000, 408(6811): 433-439.
|
[15] |
Solyom S, Aressy B, Pylkäs K, et al. Breast cancer-associated abraxas mutation disrupts nuclear localization and DNA damage response functions [J]. Sci Transl Med, 2012, 4(122): 122ra23.
|
[16] |
Muñoz-Galván S, López-Saavedra A, Jackson SP, et al. Competing roles of DNA end resection and non-homologous end joining functions in the repair of replication-born double-strand breaks by sister-chromatid recombination [J]. Nucleic Acids Res, 2013, 41(3): 1669-1683.
|
[17] |
Aymard F, Bugler B, Schmidt CK, et al. Transcriptionally active chromatin recruits homologous recombination at DNA double-strand breaks [J]. Nat Struct Mol Biol, 2014, 21(4): 366-374.
|
[18] |
Kato M, Yano K, Matsuo F, et al. Identification of rad51 alteration in patients with bilateral breast cancer [J]. J Hum Genet, 2000, 45(3): 133-137.
|
[19] |
Maacke H, Opitz S, Jost K, et al. Over-expression of wild-type rad51 correlates with histological grading of invasive ductal breast cancer [J]. Int J Cancer, 2000, 88(6): 907-913.
|
[20] |
Gasparini P, Lovat F, Fassan M, et al. Protective role of mir-155 in breast cancer through rad51 targeting impairs homologous recombination after irradiation [J]. Proc Natl Acad Sci U S A, 2014, 111(12): 4536-4541.
|
[21] |
Yousefi B, Samadi N, Baradaran B, et al. Peroxisome proliferator-activated receptor ligands and their role in chronic myeloid leukemia: therapeutic strategies [J]. Chem Biol Drug Des, 2016, 88(1): 17-25.
|
[22] |
Thomas G, Jacobs KB, Kraft P, et al. A multistage genome-wide association study in breast cancer identifies two new risk alleles at 1p11.2 and 14q24.1 (rad51l1) [J]. Nat Genet, 2009, 41(5): 579-584.
|
[23] |
Fu YP, Yu JC, Cheng TC, et al. Breast cancer risk associated with genotypic polymorphism of the nonhomologous end-joining genes: a multigenic study on cancer susceptibility [J]. Cancer Res, 2003, 63(10): 2440-2446.
|
[24] |
Kuschel B, Auranen A, McBride S, et al. Variants in DNA double-strand break repair genes and breast cancer susceptibility [J]. Hum Mol Genet, 2002, 11(12): 1399-1407.
|
[25] |
Willems P, Claes K, Baeyens A, et al. Polymorphisms in nonhomologous end-joining genes associated with breast cancer risk and chromosomal radiosensitivity [J]. Genes Chromosomes Cancer, 2008, 47(2): 137-148.
|
[26] |
Ming-Shiean H, Yu JC, Wang HW, et al. Synergistic effects of polymorphisms in DNA repair genes and endogenous estrogen exposure on female breast cancer risk [J]. Ann Surg Oncol, 2010, 17(3): 760-771.
|
[27] |
Latimer JJ, Johnson JM, Kelly CM, et al. Nucleotide excision repair deficiency is intrinsic in sporadic stage I breast cancer [J]. Proc Natl Acad Sci U S A, 2010, 107(50): 21 725-21 730.
|
[28] |
Moinfar F, Beham A, Friedrich G, et al. Macro-environment of breast carcinoma: frequent genetic alterations in the normal appearing skins of patients with breast cancer [J]. Mod Pathol, 2008, 21(5): 639-646.
|
[29] |
O’Donovan PJ, Livingston DM. BRCA1 and BRCA2: breast/ovarian cancer susceptibility gene products and participants in DNA double-strand break repair [J]. Carcinogenesis, 2010, 31(6): 961-967.
|
[30] |
Fridlich R, Annamalai D, Roy R, et al. BRCA1 and BRCA2 protect against oxidative DNA damage converted into double-strand breaks during DNA replication [J]. DNA Repair (Amst), 2015, 30: 11-20.
|
[31] |
Antoniou AC, Pharoah PD, McMullan G, et al. A comprehensive model for familial breast cancer incorporating BRCA1, BRCA2 and other genes [J]. Br J Cancer, 2002, 86(1): 76-83.
|
[32] |
Swift M, Reitnauer PJ, Morrell D, et al. Breast and other cancers in families with ataxia-telangiectasia [J]. N Engl J Med, 1987, 316(21): 1289-1294.
|
[33] |
O’Neil NJ, Bailey ML, Hieter P. Synthetic lethality and cancer [J]. Nat Rev Genet, 2017, 18(10): 613-623.
|
[34] |
Turk AA, Wisinski KB. PARP inhibitors in breast cancer: bringing synthetic lethality to the bedside [J]. Cancer, 2018, 124(12): 2498-2506.
|
[35] |
Kraus M, Alimzhanov MB, Rajewsky N, et al. Survival of resting mature B lymphocytes depends on BCR signaling via the Igalpha/beta heterodimer [J]. Cell, 2004, 117(6): 787-800.
|
[36] |
Chambon P, Weill JD, Mandel P. Nicotinamide mononucleotide activation of new DNA-dependent polyadenylic acid synthesizing nuclear enzyme [J]. Biochem Biophys Res Commun, 1963, 11: 39-43.
|
[37] |
Slade D. PARP and PARG inhibitors in cancer treatment [J]. Genes Dev, 2020, 34(5-6): 360-394.
|
[38] |
Amé JC, Rolli V, Schreiber V, et al. PARP-2, a novel mammalian DNA damage-dependent poly(adp-ribose) polymerase [J]. J Biol Chem, 1999, 274(25): 17 860-17 868.
|
[39] |
Ménissier de Murcia J, Ricoul M, Tartier L, et al. Functional interaction between PARP-1 and PARP-2 in chromosome stability and embryonic development in mouse [J]. EMBO J, 2003, 22(9): 2255-2263.
|
[40] |
Schreiber V, Amé JC, Dollé P, et al. Poly(adp-ribose) polymerase-2 (PARP-2) is required for efficient base excision DNA repair in association with PARP-1 and XRCC1 [J]. J Biol Chem, 2002, 277(25): 23 028-23 036.
|
[41] |
Bryant HE, Petermann E, Schultz N, et al. PARP is activated at stalled forks to mediate mre11-dependent replication restart and recombination [J]. EMBO J, 2009, 28(17): 2601-2615.
|
[42] |
Murai J, Huang SY, Renaud A, et al. Stereospecific PARP trapping by BMN 673 and comparison with olaparib and rucaparib [J]. Mol Cancer Ther, 2014, 13(2): 433-443.
|
[43] |
Ashworth A. A synthetic lethal therapeutic approach: poly(ADP) ribose polymerase inhibitors for the treatment of cancers deficient in DNA double-strand break repair [J]. J Clin Oncol, 2008, 26(22): 3785-3790.
|
[44] |
Bryant HE, Schultz N, Thomas HD, et al. Specific killing of BRCA2-deficient tumours with inhibitors of poly(adp-ribose) polymerase [J]. Nature, 2005, 434(7035): 913-917.
|
[45] |
Rottenberg S, Jaspers JE, Kersbergen A, et al. High sensitivity of BRCA1- deficient mammary tumors to the PARP inhibitor AZD 2281 alone and in combination with platinum drugs [J]. Proc Natl Acad Sci U S A, 2008, 105(44): 17 079-17 084.
|
[46] |
Robson M, Im SA, Senkus E, et al. Olaparib for metastatic breast cancer in patients with a germline BRCA mutation [J]. N Eng J Med, 2017, 377(6): 523-533.
|
[47] |
Gelmon KA, Fasching PA, Couch FJ, et al. Clinical effectiveness of olaparib monotherapy in germline BRCA-mutated, HER2-negative metastatic breast cancer in a real-world setting: phase IIIb LUCY interim analysis[J]. Eur J Cancer,2021,152:68-77.
|
[48] |
Turner NC, Telli ML, Rugo HS, et al. A phase II study of talazoparib after platinum or cytotoxic nonplatinum regimens in patients with advanced breast cancer and germline BRCA1/2 mutations (abrazo) [J]. Clin Cancer Res, 2019, 25(9): 2717-2724.
|
[49] |
Hoy SM. Talazoparib: first global approval [J]. Drugs, 2018, 78(18): 1939-1946.
|
[50] |
Mirza MR, Monk BJ, Herrstedt J, et al. Niraparib maintenance therapy in platinum-sensitive, recurrent ovarian cancer [J]. N Engl J Med, 2016, 375(22): 2154-2164.
|
[51] |
Lorusso D, Guy H, Samyshkin Y, et al. Feasibility study of a network meta-analysis and unanchored population-adjusted indirect treatment comparison of niraparib, olaparib, and bevacizumab as maintenance therapies in patients with newly diagnosed advanced ovarian cancer [J]. Cancers (Basel), 2022, 14(5):1285.
|
[52] |
Keung MYT, Wu Y, Vadgama JV. PARP inhibitors as a therapeutic agent for homologous recombination deficiency in breast cancers [J]. J Clin Med, 2019, 8(4):435.
|
[53] |
Patsouris A, Diop K, Tredan O, et al. Rucaparib in patients presenting a metastatic breast cancer with homologous recombination deficiency, without germline BRCA1/2 mutation [J]. Eur J Cancer, 2021, 159: 283-295.
|
[54] |
Murai J, Huang SY, Das BB, et al. Trapping of PARP1 and PARP2 by clinical PARP inhibitors [J]. Cancer Res, 2012, 72(21): 5588-5599.
|
[55] |
Hopkins TA, Shi Y, Rodriguez LE, et al. Mechanistic dissection of PARP1 trapping and the impact on in vivo tolerability and efficacy of PARP inhibitors [J]. Mol Cancer Res, 2015, 13(11): 1465-1477.
|
[56] |
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 [J]. Ann Oncol, 2018, 29(1): 154-161.
|
[57] |
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 [J]. Lancet Oncol, 2018, 19(4): 497-509.
|
[58] |
Fasching PA, Link T, Hauke J, et al. Neoadjuvant paclitaxel/olaparib in comparison to paclitaxel/carboplatinum in patients with HER2-negative breast cancer and homologous recombination deficiency (geparola study) [J]. Ann Oncol, 2021, 32(1): 49-57.
|
[59] |
Litton JK, Scoggins ME, Hess KR, et al. Neoadjuvant talazoparib for patients with operable breast cancer with a germline BRCA pathogenic variant [J]. J Clin Oncol, 2020, 38(5): 388-394.
|
[60] |
Guney Eskiler G. Talazoparib to treat BRCA-positive breast cancer [J]. Drugs Today (Barc), 2019, 55(7): 459-467.
|
[61] |
Kalra M, Tong Y, Jones DR, et al. Cisplatin +/- rucaparib after preoperative chemotherapy in patients with triple-negative or BRCA mutated breast cancer [J]. NPJ Breast Cancer, 2021, 7(1): 29.
|
[62] |
Tutt ANJ, Garber JE, Kaufman B, et al. Adjuvant olaparib for patients with BRCA1- or BRCA2-mutated breast cancer [J]. N Engl J Med, 2021, 384(25): 2394-2405.
|
[63] |
Rugo HS, Olopade OI, DeMichele A, et al. Adaptive randomization of veliparib-carboplatin treatment in breast cancer [J]. N Engl J Med, 2016, 375(1): 23-34.
|
[64] |
Litton JK, Hurvitz SA, Mina LA, et al. Talazoparib versus chemotherapy in patients with germline BRCA1/2-mutated HER2-negative advanced breast cancer: final overall survival results from the embraca trial [J]. Ann Oncol, 2020, 31(11): 1526-1535.
|