[1]BIANCHINI G,DE ANGELIS C,LICATA L,et al.Treatment landscape of triple-negative breast cancer-expanded options,evolving needs[J].Nat Rev Clin Oncol,2022,19(2):91-113.
[2]PODO F,BUYDENS LM,DEGANI H,et al.Triple-negative breast cancer:Present challenges and new perspectives[J].Mol Oncol,2010,4(3):209-229.
[3]PLANA D,PALMER AC,SORGER PK.Independent drug action in combination therapy:Implications for precision oncology[J].Cancer Discov,2022,12(3):606-624.
[4]刘佳静,黄桂春,王文艺,等.化疗联合PD-(L)1单抗治疗晚期三阴性乳腺癌的研究进展[J].现代肿瘤医学,2023,31(6):1156-1161.LIU JJ,HUANG GC,WANG WY,et al.Research progress of chemotherapy combined with anti-PD-(L)1 treatment in advanced triple-negative breast cancer[J].Modern Oncology,2023,31(6):1156-1161.
[5]OU Y,WANG M,XU Q,et al.Small molecule agents for triple negative breast cancer:Current status and future prospects[J].Transl Oncol,2024,41:101893.
[6]YANG H,LI S,LI W,et al.Actinomycin D synergizes with Doxorubicin in triple-negative breast cancer by inducing P53-dependent cell apoptosis[J].Carcinogenesis,2024,45(4):262-273.
[7]FARBER S,D’ANGIO G,EVANS A,et al.Clinical studies on actinomycin D with special reference to Wilms’ tumor in children[J].Ann N Y Acad Sci,1960,89:421-425.
[8]FOSTER SA,DEMERS GW,ETSCHEID BG,et al.The ability of human papillomavirus E6 proteins to target p53 for degradation in vivo correlates with their ability to abrogate actinomycin D-induced growth arrest[J].J Virol,1994,68(9):5698-5705.
[9]CHOONG ML,YANG H,LEE MA,et al.Specific activation of the p53 pathway by low dose actinomycin D:a new route to p53 based cyclotherapy[J].Cell Cycle,2009,8(17):2810-2818.
[10]YANG K,YANG J,YI J.Nucleolar stress:Hallmarks,sensing mechanism and diseases[J].Cell Stress,2018,2(6):125-140.
[11]SOLLNER-WEBB B,TOWER J.Transcription of cloned eukaryotic ribosomal RNA genes[J].Annu Rev Biochem,1986,55:801-830.
[12]GONZALEZ-ARZOLA K.The nucleolus:Coordinating stress response and genomic stability[J].Biochim Biophys Acta Gene Regul Mech,2024,1867(2):195029.
[13]SIROZH O,SAEZ-MAS A,JUNG B,et al.Nucleolar stress caused by arginine-rich peptides triggers a ribosomopathy and accelerates aging in mice[J].Mol Cell,2024,84(8):1527-1540.
[14]ZENGER K,AGNOLET S,SCHNEIDER B,et al.Biotransformation of Flavokawains A,B,and C,Chalcones from Kava (Piper methysticum),by human liver microsomes[J].J Agric Food Chem,2015,63(28):6376-6385.
[15]MALAMI I,ABDUL AB,ABDULLAH R,et al.Crude extracts,Flavokawain B and Alpinetin compounds from the rhizome of alpinia mutica induce cell death via UCK2 enzyme inhibition and in turn reduce 18S rRNA biosynthesis in HT-29 cells[J].PLoS One,2017,12(1):e0170233.
[16]RAO B,LAIN S,THOMPSON AM.p53-based cyclotherapy:Exploiting the ’guardian of the genome’ to protect normal cells from cytotoxic therapy[J].Br J Cancer,2013,109(12):2954-2958.
[17]DERAKHSHAN F,REIS-FILHO JS.Pathogenesis of triple-negative breast cancer[J].Annu Rev Pathol,2022,17:181-204.
[18]LI Y,ZHANG H,MERKHER Y,et al.Recent advances in therapeutic strategies for triple-negative breast cancer[J].J Hematol Oncol,2022,15(1):121.
[19]CHATTERJEE N,BIVONA TG.Polytherapy and targeted cancer drug resistance[J].Trends Cancer,2019,5(3):170-182.
[20]JIN H,WANG L,BERNARDS R.Rational combinations of targeted cancer therapies:background,advances and challenges[J].Nat Rev Drug Discov,2023,22(3):213-234.
[21]ZAGIDULLIN B,ALDAHDOOH J,ZHENG S,et al.DrugComb:An integrative cancer drug combination data portal[J].Nucleic Acids Res,2019,47(W1):W43-W51.
[22]陈安莉,沈浩元,王舒.三阴性乳腺癌新辅助治疗的临床研究进展[J].现代肿瘤医学,2023,31(3):566-571.CHEN AL,SHEN HY,WANG S.Neoadjuvant therapy for triple negative breast cancer:Clinical progress[J].Modern Oncology,2023,31(3):566-571.
[23]TONG X,TANG R,XIAO M,et al.Targeting cell death pathways for cancer therapy:Recent developments in necroptosis,pyroptosis,ferroptosis,and cuproptosis research[J].J Hematol Oncol,2022,15(1):174.
[24]CHOI HK,RYU H,SON AR,et al.The novel anthraquinone derivative IMP1338 induces death of human cancer cells by p53-independent S and G2/M cell cycle arrest[J].Biomed Pharmacother,2016,79:308-314.
[25]SUSKI JM,BRAUN M,STRMISKA V,et al.Targeting cell-cycle machinery in cancer[J].Cancer Cell,2021,39(6):759-778.
[26]YUAN J,OFENGEIM D.A guide to cell death pathways[J].Nat Rev Mol Cell Biol,2024,25(5):379-395.
[27]RUBBI CP,MILNER J.Disruption of the nucleolus mediates stabilization of p53 in response to DNA damage and other stresses[J].EMBO J,2003,22(22):6068-6077.
[28]YANG K,WANG M,ZHAO Y,et al.A redox mechanism underlying nucleolar stress sensing by nucleophosmin[J].Nat Commun,2016,7:13599.
[29]DE LA TORRE P,FERNANDEZ-DE LA TORRE M,FLORES AI.Premature senescence of placental decidua cells as a possible cause of miscarriage produced by mycophenolic acid[J].J Biomed Sci,2021,28(1):3.
[30]LIU S,BISHOP WR,LIU M.Differential effects of cell cycle regulatory protein p21(WAF1/Cip1) on apoptosis and sensitivity to cancer chemotherapy[J].Drug Resist Updat,2003,6(4):183-195.
[31]ADAMS CM,MITRA R,XIAO Y,et al.Targeted MDM2 degradation reveals a new vulnerability for p53-inactivated triple-negative breast cancer[J].Cancer Discov,2023,13(5):1210-1229.
[32]TORRISI R,BALDUZZI A,GHISINI R,et al.Tailored preoperative treatment of locally advanced triple negative (hormone receptor negative and HER2 negative) breast cancer with epirubicin,cisplatin,and infusional fluorouracil followed by weekly paclitaxel[J].Cancer Chemother Pharmacol,2008,62(4):667-672.
[33]DUFFY MJ,SYNNOTT NC,CROWN J.Mutant p53 in breast cancer:Potential as a therapeutic target and biomarker[J].Breast Cancer Res Treat,2018,170(2):213-219.
[34]MAEHAMA T,NISHIO M,OTANI J,et al.Nucleolar stress:Molecular mechanisms and related human diseases[J].Cancer Sci,2023,114(5):2078-2086.
[35]IAROVAIA OV,MININA EP,SHEVAL EV,et al.Nucleolus:A central hub for nuclear functions[J].Trends Cell Biol,2019,29(8):647-659.
[36]CHEN J,STARK LA.Insights into the relationship between nucleolar stress and the NF-kappaB pathway[J].Trends Genet,2019,35(10):768-780.
[37]JAMES A,WANG Y,RAJE H,et al.Nucleolar stress with and without p53[J].Nucleus,2014,5(5):402-426.