Article Data

  • Views 1077
  • Dowloads 217

Reviews

Open Access Special Issue

Treatment Progress in Triple Negative Breast Cancer

  • Stefan Krämer1
  • Christoph Rogmans2
  • Dilek Saylan1
  • Dominique Friedrich1
  • Clayton Kraft1
  • Gunther Rogmans1
  • Marina Wirtz1
  • Michael Friedrich1,*,

1Department of Obstetrics and Gynecology, Helios Hospital, 47805 Krefeld, Germany

2Department of Obstetrics and Gynecology, University Hospital Schleswig-Holstein, Campus Kiel, 24105 Kiel, Germany

DOI: 10.31083/j.ejgo4302040 Vol.43,Issue 2,April 2022 pp.341-352

Submitted: 22 November 2021 Accepted: 18 February 2022

Published: 15 April 2022

(This article belongs to the Special Issue Breast Cancer)

*Corresponding Author(s): Michael Friedrich E-mail: michael.friedrich@helios-gesundheit.de

Abstract

Triple-negative breast cancer (TNBC) lacks expression of the three biomarkers (the estrogen receptor (ER), progesterone receptor (PR), and the human epidermal growth factor receptor 2 (HER2) protein) and are typically higher grade. While the triple-negative clinical phenotype is heterogeneous, the basal-like molecular subtype comprises a large proportion, particularly for breast cancer susceptibility gene 1 (BRCA1)-associated breast cancer. New treatment options are checkpoint inhibitors like inhibition of PD-L1 pathway with pembrolizumab and atezolizumab, parp-inhibition with olaparib or talozoparib and treatment with the an antibody drug conjugate sacituzumab-govitecan.


Keywords

breast cancer; triple negative; chemotherapy; immunoncology; PD -L1; Parp; pembrolizumab; atezolizumab; olaparib; talozoparib; sacituzumab-govitecan

Cite and Share

Stefan Krämer,Christoph Rogmans,Dilek Saylan,Dominique Friedrich,Clayton Kraft,Gunther Rogmans,Marina Wirtz,Michael Friedrich. Treatment Progress in Triple Negative Breast Cancer. European Journal of Gynaecological Oncology. 2022. 43(2);341-352.

References

[1] Hammond ME, Hayes DF, Dowsett M, Allred DC, Hagerty KL, Badve S, et al. American Society of Clinical Oncology/College of American Pathologists guideline recommendations for immunohistochemical testing of estrogen and progesterone receptors in breast cancer (unabridged version). Archives of Pathology & Laboratory Medicine. 2010; 134: e48–e72.

[2] Hammond MEH, Hayes DF, Dowsett M, Allred DC, Hagerty KL, Badve S, et al. American Society of Clinical Oncology/College of American Pathologists guideline recommendations for immunohistochemical testing of estrogen and progesterone receptors in breast cancer. Journal of Clinical Oncology. 2010; 28: 2784–2795.

[3] Wolff AC, Hammond MEH, Hicks DG, Dowsett M, McShane LM, Allison KH, et al. Recommendations for human epidermal growth factor receptor 2 testing in breast cancer: American Society of Clinical Oncology/College of American Pathologists clinical practice guideline update. Journal of Clinical Oncology. 2013; 31: 3997–4013.

[4] Swain SM. Triple-Negative Breast Cancer: One Size Does Not Fit All. The Cancer Journal. 2021; 27: 1.

[5] Trivers KF, Lund MJ, Porter PL, Liff JM, Flagg EW, Coates RJ, et al. The epidemiology of triple-negative breast cancer, including race. Cancer Causes & Control. 2009; 20: 1071–1082.

[6] Lehmann BD, Bauer JA, Chen X, Sanders ME, Chakravarthy AB, Shyr Y, et al. Identification of human triple-negative breast cancer subtypes and preclinical models for selection of targeted therapies. The Journal of Clinical Investigation. 2011; 121: 2750–2767.

[7] Gonzalez-Angulo AM, Timms KM, Liu S, Chen H, Litton JK, Potter J, et al. Incidence and Outcome of BRCA Mutations in Unselected Patients with Triple Receptor-Negative Breast Cancer. Clinical Cancer Research. 2011; 17: 1082–1089.

[8] NCCN Clinical Practice Guidelines in Oncology: Genetic/Familial High-Risk assessment: Breast and Ovarian. Version 4. 2013. Available at: http://www.nccn.org/professio nals/physician_gls/pdf/genetics_screening.pdf (Accessed: 26 November 2013).

[9] Millikan RC, Newman B, Tse C, Moorman PG, Conway K, Dressler LG, et al. Epidemiology of basal-like breast cancer. Breast Cancer Research and Treatment. 2008; 109: 123–139.

[10] Parise CA, Bauer KR, Brown MM, Caggiano V. Breast Cancer Subtypes as Defined by the Estrogen Receptor (ER), Proges-terone Receptor (PR), and the Human Epidermal Growth Factor Receptor 2 (her2) among Women with Invasive Breast Cancer in California, 1999-2004. The Breast Journal. 2009; 15: 593–602.

[11] Carey LA, Perou CM, Livasy CA, Dressler LG, Cowan D, Conway K, et al. Race, breast cancer subtypes, and survival in the Carolina Breast Cancer Study. Journal of the American Medical Association. 2006; 295: 2492–2502.

[12] Phipps AI, Chlebowski RT, Prentice R, McTiernan A, Wactawski-Wende J, Kuller LH, et al. Reproductive history and oral contraceptive use in relation to risk of triple-negative breast cancer. Journal of the National Cancer Institute. 2011; 103: 470–477.

[13] Palmer JR, Viscidi E, Troester MA, Hong C, Schedin P, Bethea TN, et al. Parity, Lactation, and Breast Cancer Subtypes in African American Women: Results from the AMBER Consortium. Journal of the National Cancer Institute. 2014; 106: dju237.

[14] Pierobon M, Frankenfeld CL. Obesity as a risk factor for triple-negative breast cancers: a systematic review and meta-analysis. Breast Cancer Research and Treatment. 2013; 137: 307–314.

[15] Dent R, Trudeau M, Pritchard KI, Hanna WM, Kahn HK, Sawka CA, et al. Triple-negative breast cancer: clinical features and patterns of recurrence. Clinical Cancer Research. 2007; 13: 4429–4434.

[16] Collett K, Stefansson IM, Eide J, Braaten A, Wang H, Eide GE, et al. A basal epithelial phenotype is more frequent in interval breast cancers compared with screen detected tumors. Cancer Epidemiology, Biomarkers & Prevention. 2005; 14: 1108–1112.

[17] Livasy CA, Karaca G, Nanda R, Tretiakova MS, Olopade OI, Moore DT, et al. Phenotypic evaluation of the basal-like sub-type of invasive breast carcinoma. Modern Pathology. 2006; 19: 264–271.

[18] Burstein MD, Tsimelzon A, Poage GM, Covington KR, Contreras A, Fuqua SAW, et al. Comprehensive genomic analysis identifies novel subtypes and targets of triple-negative breast cancer. Clinical Cancer Research. 2015; 21: 1688–1698.

[19] Bertucci F, Finetti P, Cervera N, Esterni B, Hermitte F, Viens P, et al. How basal are triple-negative breast cancers? International Journal of Cancer. 2008; 123: 236–240.

[20] Shah SP, Roth A, Goya R, Oloumi A, Ha G, Zhao Y, et al. The clonal and mutational evolution spectrum of primary triple-negative breast cancers. Nature. 2012; 486: 395–399.

[21] Carey LA, Rugo HS, Marcom PK, Irvin W, Ferraro M, Burrows E, et al. TBCRC 001: EGFR inhibition with cetuximab added to carboplatin in metastatic triple-negative (basal-like) breast cancer. Journal of Clinical Oncology. 2008; 26: 1009–1009.

[22] Korsching E, Packeisen J, Agelopoulos K, Eisenacher M, Voss R, Isola J, et al. Cytogenetic alterations and cytokeratin expression patterns in breast cancer: integrating a new model of breast differentiation into cytogenetic pathways of breast carcinogenesis. Laboratory Investigation. 2002; 82: 1525–1533.

[23] Nielsen TO, Hsu FD, Jensen K, Cheang M, Karaca G, Hu Z, et al. Immunohistochemical and clinical characterization of the basal-like subtype of invasive breast carcinoma. Clinical Cancer Research. 2004; 10: 5367–5374.

[24] Teschendorff AE, Miremadi A, Pinder SE, Ellis IO, Caldas C. An immune response gene expression module identifies a good prognosis subtype in estrogen receptor negative breast cancer. Genome Biology. 2008; 8: R157.

[25] Prat A, Parker JS, Karginova O, Fan C, Livasy C, Herschkowitz JI, et al. Phenotypic and molecular characterization of the claudin-low intrinsic subtype of breast cancer. Breast Cancer Research. 2010; 12: R68.

[26] Sørlie T, Perou CM, Tibshirani R, Aas T, Geisler S, Johnsen H, et al. Gene expression patterns of breast carcinomas distinguish tumor subclasses with clinical implications. Proceedings of the National Academy of Sciences of the United States of America. 2001; 98: 10869–10874.

[27] Troester MA, Herschkowitz JI, Oh DS, He X, Hoadley KA, Barbier CS, et al. Gene expression patterns associated with p53 status in breast cancer. BMC Cancer. 2007; 6: 276.

[28] Cheang MCU, Martin M, Nielsen TO, Prat A, Rodriguez-Lescure A, Ruiz A, et al. Quantitative hormone receptors, triple-negative breast cancer (TNBC), and molecular subtypes: a collaborative effort of the BIGNCI NABCG. Journal of Clinical Oncology. 2012; 30: 1008–1008.

[29] Iwamoto T, Booser D, Valero V, Murray JL, Koenig K, Esteva FJ, et al. Estrogen receptor (ER) mRNA and ER-related gene expression in breast cancers that are 1% to 10% ER-positive by immunohistochemistry. Journal of Clinical Oncology. 2012; 30: 729–734.

[30] Pilewskie M, Morrow M. Axillary Nodal Management Follow-ing Neoadjuvant Chemotherapy: a Review. JAMA Oncology. 2017; 3: 549–555.

[31] Liedtke C, Mazouni C, Hess KR, André F, Tordai A, Mejia JA, et al. Response to neoadjuvant therapy and long-term survival in patients with triple-negative breast cancer. Journal of Clinical Oncology. 2008; 26: 1275–1281

[32] von Minckwitz G, Untch M, Blohmer J, Costa SD, Eidtmann H, Fasching PA, et al. Definition and impact of pathologic complete response on prognosis after neoadjuvant chemotherapy in various intrinsic breast cancer subtypes. Journal of Clinical Oncology. 2012; 30: 1796–1804.

[33] Berry DA, Cirrincione C, Henderson IC, Citron ML, Budman DR, Goldstein LJ, et al. Estrogen-receptor status and outcomes of modern chemotherapy for patients with node-positive breast cancer. Journal of the American Medical Association. 2006; 295: 1658–1667.

[34] Hayes DF, Thor AD, Dressler LG, Weaver D, Edgerton S, Cowan D, et al. Her2 and Response to Paclitaxel in Node-Positive Breast Cancer. New England Journal of Medicine. 2007; 357: 1496–1506.

[35] Hugh J, Hanson J, Cheang MCU, Nielsen TO, Perou CM, Dumontet C, et al. Breast Cancer Subtypes and Response to Docetaxel in Node-Positive Breast Cancer: Use of an Immunohistochemical Definition in the BCIRG 001 Trial. Journal of Clinical Oncology. 2009; 27: 1168–1176.

[36] Martín M, Rodríguez-Lescure A, Ruiz A, Alba E, Calvo L, Ruiz-Borrego M, et al. Molecular predictors of efficacy of adjuvant weekly paclitaxel in early breast cancer. Breast Cancer Research and Treatment. 2010; 123: 149–157.

[37] Blum JL, Flynn PJ, Yothers G, Asmar L, Geyer CE, Jacobs SA, et al. Anthracyclines in Early Breast Cancer: the ABC Trials-USOR 06-090, NSABP B-46-i/USOR 07132, and NSABP B-49 (NRG Oncology). Journal of Clinical Oncology. 2017; 35: 2647–2655.

[38] Yu KD, Ye FG, He M, Fan L, Ma D, Mo M, et al. Effect of Adjuvant Paclitaxel and Carboplatin on Survival in Women With Triple-Negative Breast Cancer: A Phase 3 Randomized Clinical Trial. JAMA Oncology. 2020; 6:1390–1396.

[39] Masuda N, Lee S, Ohtani S, Im Y, Lee E, Yokota I, et al. Adjuvant Capecitabine for Breast Cancer after Preoperative Chemotherapy. The New England Journal of Medicine. 2017; 376: 2147–2159.

[40] Lluch A, Barrios CH, Torrecillas L, Ruiz-Borrego M, Bines J, Segalla J, et al. Phase III Trial of Adjuvant Capecitabine After Standard Neo-/Adjuvant Chemotherapy in Patients With Early Triple-Negative Breast Cancer (GEICAM/2003-11_CIBOMA/2004-01). Journal of clinical oncology. 2020; 38: 203–213.

[41] Li J, Yu K, Pang D, Wang C, Jiang J, Yang S, et al. Adjuvant Capecitabine With Docetaxel and Cyclophosphamide Plus Epirubicin for Triple-Negative Breast Cancer (CBCSG010): An Open-Label, Randomized, Multicenter, Phase III Trial. Journal of Clinical Oncology. 2020; 38:1774–1784.

[42] Wang X, Wang S, Huang H, Cai L, Zhao L, Peng R, et al. Effect of Capecitabine Maintenance Therapy Using Lower Dosage and Higher Frequency vs Observation on Disease-Free Survival among Patients with Early-Stage Triple-Negative Breast Cancer who had Received Standard Treatment: The SYSUCC-001 Ran-domized Clinical Trial. Journal of the American Medical Association. 2021; 325: 50–58.

[43] von Minckwitz G, Schneeweiss A, Loibl S, Salat C, Denkert C, Rezai M, et al. Neoadjuvant carboplatin in patients with triple-negative and her2-positive early breast cancer (Gepar-Sixto; GBG 66): a randomised phase 2 trial. The Lancet. Oncology. 2014; 15: 747–756.

[44] Sikov WM, Berry DA, Perou CM, Singh B, Cirrincione CT, Tolaney SM, 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). Journal of Clinical Oncology. 2015; 33: 13–21.

[45] Steenbruggen TG, van Werkhoven E, van Ramshorst MS, Dezentjé VO, Kok M, Linn SC, et al. Adjuvant chemotherapy in small node-negative triple-negative breast cancer. European Journal of Cancer. 2020; 135: 66–74.

[46] Theriault RL, Litton JK, Mittendorf EA, Chen H, Meric-Bernstam F, Chavez-Macgregor M, et al. Age and survival estimates in patients who have node-negative T1ab breast cancer by breast cancer subtype. Clinical Breast Cancer. 2011; 11: 325–331.

[47] Vaz-Luis I, Ottesen RA, Hughes ME, Mamet R, Burstein HJ, Edge SB, et al. Outcomes by tumor subtype and treatment pattern in women with small, node-negative breast cancer: a multi-institutional study. Journal of Clinical Oncology. 2014; 32: 2142–2150.

[48] Smid M, Wang Y, Zhang Y, Sieuwerts AM, Yu J, Klijn JGM, et al. Subtypes of Breast Cancer Show Preferential Site of Relapse. Cancer Research. 2008; 68: 3108–3114.

[49] Lin NU, Claus E, Sohl J, Razzak AR, Arnaout A, Winer EP. Sites of distant recurrence and clinical outcomes in patients with metastatic triple-negative breast cancer: high incidence of central nervous system metastases. Cancer. 2008; 113: 2638–2645.

[50] Hicks DG, Short SM, Prescott NL, Tarr SM, Coleman KA, Yoder BJ, et al. Breast cancers with brain metastases are more likely to be estrogen receptor negative, express the basal cytokeratin CK5/6, and overexpress her2 or EGFR. The American Journal of Surgical Pathology. 2006; 30: 1097–1104.

[51] Lin NU, Vanderplas A, Hughes ME, Theriault RL, Edge SB, Wong Y, et al. Clinicopathologic features, patterns of recurrence, and survival among women with triple-negative breast cancer in the National Comprehensive Cancer Network. Cancer. 2012; 118: 5463–5472.

[52] Niwińska A, Murawska M, Pogoda K. Breast cancer subtypes and response to systemic treatment after whole-brain radiotherapy in patients with brain metastases. Cancer. 2010; 116: 4238–4247.

[53] Anders CK, Deal AM, Miller CR, Khorram C, Meng H, Burrows E, et al. The prognostic contribution of clinical breast cancer subtype, age, and race among patients with breast cancer brain metastases. Cancer. 2011; 117: 1602–1611.

[54] Sorlie T, Tibshirani R, Parker J, Hastie T, Marron JS, Nobel A, et al. Repeated observation of breast tumor subtypes in independent gene expression data sets. Proceedings of the National Academy of Sciences of the United States of America. 2003; 100: 8418–8423.

[55] Reddy SM, Barcenas CH, Sinha AK, Hsu L, Moulder SL, Tripathy D, et al. Long-term survival outcomes of triple-receptor negative breast cancer survivors who are disease free at 5 years and relationship with low hormone receptor positivity. British Journal of Cancer. 2018; 118: 17–23.

[56] Cossetti RJD, Tyldesley SK, Speers CH, Zheng Y, Gelmon KA. Comparison of Breast Cancer Recurrence and Outcome Patterns between Patients Treated from 1986 to 1992 and from 2004 to 2008. Journal of Clinical Oncology. 2015; 33: 65–73.

[57] Hull DF, Clark GM, Osborne CK, Chamness GC, Knight WA, McGuire WL. Multiple estrogen receptor assays in human breast cancer. Cancer Research. 1983; 43: 413–416.

[58] Amir E, Clemons M, Freedman OC, Miller N, Coleman RE, Purdie C, et al. Tissue confirmation of disease recurrence in patients with breast cancer: Pooled analysis of two large prospective studies. Journal of Clinical Oncology. 2010; 28: 1007–1007.

[59] Simmons C, Miller N, Geddie W, Gianfelice D, Oldfield M, Dranitsaris G, et al. Does confirmatory tumor biopsy alter the management of breast cancer patients with distant metastases?Annals of Oncology. 2009; 20: 1499–1504.

[60] Amir E, Clemons M. Should a biopsy be recommended to confirm metastatic disease in women with breast cancer? The Lancet Oncology. 2009; 10: 933–935.

[61] Khasraw M, Brogi E, Seidman AD. The need to examine metastatic tissue at the time of progression of breast cancer: is rebiopsy a necessity or a luxury? Current Oncology Reports. 2011; 13: 17–25.

[62] Egger SJ, Chan MMK, Luo Q, Wilcken N. Platinum-containing regimens for triple-negative metastatic breast cancer. The Cochrane Database of Systematic Reviews. 2020; 10: CD013750.

[63] Highlights of Prescribing Information for Intravenous Use of Keytruda® (Pembrolizumab) Injection. 2014. Available at: https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/ 125514s088lbl.pdf (Accessed: 13 November 2020).

[64] Schmid P, Adams S, Rugo HS, Schneeweiss A, Barrios CH, Iwata H, et al. Atezolizumab and Nab-Paclitaxel in Advanced Triple-Negative Breast Cancer. The New England Journal of Medicine. 2018; 379: 2108–2121.

[65] Emens LA, Adams S, Barrios CH, Diéras V, Iwata H, Loi S, et al. First-line atezolizumab plus nab-paclitaxel for unresectable, locally advanced, or metastatic triple-negative breast cancer: IMpassion130 final overall survival analysis. Annals of Oncology. 2021; 32: 983–993.

[66] Miles DW, Gligorov J, André F, Cameron D, Schneeweiss A, Barrios C, et al. Primary results from IMpassion131, a double-blind, placebo-controlled, randomised phase III trial of first-line paclitaxel with or without atezolizumab for unresectable locally advanced/metastatic triple-negative breast cancer. Annals of Oncology. 2021; 32: 994–1004.

[67] Cortes J, Cescon DW, Rugo HS, Nowecki Z, Im SA, Yusof MM, et al. Pembrolizumab plus chemotherapy versus placebo plus chemotherapy for previously untreated locally recurrent inoperable or metastatic triple-negative breast cancer (KEYNOTE-355): a randomised, placebo-controlled, double-blind, phase 3 clinical trial. Lancet. 2020; 396: 1817–1828.

[68] Rugo HS, Cortes J, Cescon DW, et al. KEYNOTE 355: Final results from randomized, double blind phase III study of first line Pembrolizumab plus chemotherapy versus placebo plus chemotherapy for metastatic triple-negative breast cancer. ESMO Congress 2021. 16–19 September 2021.

[69] Adams S, Schmid P, Rugo HS, Winer EP, Loirat D, Awada A, et al. Pembrolizumab monotherapy for previously treated metastatic triple-negative breast cancer: cohort a of the phase II KEYNOTE-086 study. Annals of Oncology. 2019; 30: 397–404.

[70] Dirix LY, Takacs I, Jerusalem G, Nikolinakos P, Arkenau H, Forero-Torres A, et al. Avelumab, an anti-PD-L1 antibody, in patients with locally advanced or metastatic breast cancer: a phase 1b JAVELIN Solid Tumor study. Breast Cancer Research and Treatment. 2018; 167: 671–686.

[71] Emens LA. Breast Cancer Immunotherapy: Facts and Hopes. Clinical Cancer Research. 2018; 24: 511–520.

[72] Robson M, Im S, Senkus E, Xu B, Domchek SM, Masuda N, et al. Olaparib for Metastatic Breast Cancer in Patients with a Germline BRCA Mutation. The New England Journal of Medicine. 2017; 377: 523–533.

[73] Tutt A, Robson M, Garber JE, Domchek S, Audeh MW, Weitzel JN, et al. Phase II trial of the oral PARP inhibitor olaparib in BRCA-deficient advanced breast cancer. Journal of Clinical Oncology. 2009; 27: CRA501–CRA501.

[74] Fong PC, Boss DS, Yap TA, Tutt A, Wu P, Mergui-Roelvink M, et al. Inhibition of poly(ADP-ribose) polymerase in tumors from BRCA mutation carriers. The New England Journal of Medicine. 2009; 361:123–134.

[75] Tutt A, Robson M, Garber JE, Domchek SM, Audeh MW, Weitzel JN, et al. Oral poly(ADP-ribose) polymerase inhibitor olaparib in patients with BRCA1 or BRCA2 mutations and advanced breast cancer: a proof-of-concept trial. Lancet. 2010; 376: 235–244.

[76] Gelmon KA, Hirte HW, Robidoux A, Tonkin KS, Tischkowitz M, Swenerton K, et al. Can we define tumors that will respond to PARP inhibitors? A phase II correlative study of olaparib in advanced serous ovarian cancer and triple-negative breast cancer. Journal of Clinical Oncology. 2010; 28: 3002–3002.

[77] O’Shaughnessy J, Osborne C, Pippen JE, Yoffe M, Patt D, Rocha C, et al. Iniparib plus chemotherapy in metastatic triple-negative breast cancer. The New England Journal of Medicine. 2011; 364: 205–214.

[78] Dent RA, Lindeman GJ, Clemons M, Wildiers H, Chan A, McCarthy NJ, et al. Safety and efficacy of the oral PARP inhibitor olaparib (AZD2281) in combination with paclitaxel for the first- or second-line treatment of patients with metastatic triple-negative breast cancer: Results from the safety cohort of a phase I/II multicenter trial. Journal of Clinical Oncology. 2010; 28: 1018–1018.

[79] Isakoff SJ, Overmoyer B, Tung NM, Gelman RS, Giranda VL, Bernhard KM, et al. A phase II trial of the PARP inhibitor veliparib (ABT888) and temozolomide for metastatic breast cancer. Journal of Clinical Oncology. 2010; 28: 1019–1019.

[80] Tentori L, Graziani G. Chemopotentiation by PARP inhibitors in cancer therapy. Pharmacological Research. 2005; 52: 25–33.

[81] Bryant HE, Schultz N, Thomas HD, Parker KM, Flower D, Lopez E, et al. Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase. Nature. 2005; 434: 913–917.

[82] Farmer H, McCabe N, Lord CJ, Tutt ANJ, Johnson DA, Richardson TB, et al. Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy. Nature. 2005; 434: 917–921.

[83] O’Shaughnessy J, Osborne C, Pippen J, Yoffe M, Patt D, Monaghan G, et al. Efficacy of BSI-201, a poly (ADP-ribose) polymerase-1 (PARP1) inhibitor, in combination with gemcitabine/carboplatin (G/C) in patients with metastatic triple-negative breast cancer (TNBC): Results of a randomized phase II trial. Journal of Clinical Oncology. 2009; 27: 3–3.

[84] Tung NM, Boughey JC, Pierce LJ, Robson ME, Bedrosian I, Dietz JR, et al. Management of Hereditary Breast Cancer: Amer-ican Society of Clinical Oncology, American Society for Radiation Oncology, and Society of Surgical Oncology Guideline. Journal of Clinical Oncology. 2020; 38: 2080–2106.

[85] Tutt A, Tovey H, Cheang MCU, Kernaghan S, Kilburn L, Gazinska P, et al. Carboplatin in BRCA1/2-mutated and triple-negative breast cancer BRCAness subgroups: the TNT Trial. Nature Medicine. 2018; 24:628–637.

[86] Sacituzumab govitecan-hziy for injection. United States Prescribing Information. US National Library of Medicine. Available at: https://www.accessdata.fda.gov/drugsatfda_docs/label /2020/761115s000lbl.pdf (Accessed: 28 April 2020).

[87] Bardia A, Mayer IA, Vahdat LT, Tolaney SM, Isakoff SJ, Diamond JR, et al. Sacituzumab Govitecan-hziy in Refractory Metastatic Triple-Negative Breast Cancer. The New England Journal of Medicine. 2019; 380:741–751.

[88] O’Shaughnessy J, Weckstein D, Vukelja S. Preliminary results of a randomized phase II study of weekly irinotecan/carboplatin with or without cetuximab in patients with metastatic breast cancer. Breast Cancer Research and Treatment. 2007; 106: S32.

[89] Carey LA, Rugo HS, Marcom PK, Mayer EL, Esteva FJ, Ma CX, et al. TBCRC 001: randomized phase II study of cetuximab in combination with carboplatin in stage IV triple-negative breast cancer. Journal of Clinical Oncology. 2012; 30: 2615–2623.

[90] Baselga J, Gomez P, Greil R, Braga S, Climent MA, Wardley AM, et al. Randomized phase II study of the anti-epidermal growth factor receptor monoclonal antibody cetuximab with cisplatin versus cisplatin alone in patients with metastatic triple-negative breast cancer. Journal of Clinical Oncology. 2013; 31: 2586-2592.

[91] Cochrane DR, Bernales S, Jacobsen BM, Cittelly DM, Howe EN, D’Amato NC, et al. Role of the androgen receptor in breast cancer and preclinical analysis of enzalutamide. Breast Cancer Research. 2015; 16: R7.

[92] Collins LC, Cole KS, Marotti JD, Hu R, Schnitt SJ, Tamimi RM. Androgen receptor expression in breast cancer in relation to molecular phenotype: results from the Nurses’ Health Study. Modern Pathology. 2011; 24: 924–931.

[93] Gucalp A, Tolaney S, Isakoff SJ, Ingle JN, Liu MC, Carey LA, et al. Phase II trial of bicalutamide in patients with androgen receptor-positive, estrogen receptor-negative metastatic Breast Cancer. Clinical Cancer Research. 2013; 19: 5505–5512.

[94] Traina TA, Miller K, Yardley DA, Eakle J, Schwartzberg LS, O’Shaughnessy J, et al. Enzalutamide for the Treatment of Androgen Receptor-Expressing Triple-Negative Breast Cancer. Journal of Clinical Oncology. 2018; 36: 884–890.

[95] Miller K, Wang M, Gralow J, Dickler M, Cobleigh M, Perez EA, et al. Paclitaxel plus bevacizumab versus paclitaxel alone for metastatic breast cancer. The New England Journal of Medicine. 2007; 357: 2666–2676.

[96] Miles DW, Chan A, Dirix LY, Cortés J, Pivot X, Tomczak P, et al. Phase III Study of Bevacizumab Plus Docetaxel Compared with Placebo Plus Docetaxel for the first-Line Treatment of Human Epidermal Growth Factor Receptor 2-Negative Metastatic Breast Cancer. Journal of Clinical Oncology. 2010; 28: 3239–3247.

[97] Miles DW, Diéras V, Cortés J, Duenne A, Yi J, O’Shaughnessy J. First-line bevacizumab in combination with chemotherapy for her2-negative metastatic breast cancer: pooled and subgroup analyses of data from 2447 patients. Annals of Oncology. 2013; 24: 2773–2780.

[98] Cameron D, Brown J, Dent R, Jackisch C, Mackey J, Pivot X, et al. Adjuvant bevacizumab-containing therapy in triple-negative breast cancer (BEATRICE): primary results of a randomised, phase 3 trial. The Lancet. Oncology. 2013; 14: 933–942.

[99] Brufsky A, Valero V, Tiangco B, Dakhil SR, Brize A, Bousfoul N, et al. Impact of bevacizumab (BEV) on efficacy of second-line chemotherapy (CT) for triple-negative breast cancer (TNBC): Analysis of RIBBON-2. Journal of Clinical Oncology. 2011; 29: 1010–1010.

[100] Nanda R, Liu MC, Yau C, Asare S, Hylton N, Veer LV, et al. Pembrolizumab plus standard neoadjuvant therapy for high-risk breast cancer (BC): Results from I-SPY 2. Journal of Clinical Oncology. 2017; 35S: 506.


Abstracted / indexed in

Science Citation Index Expanded (SciSearch) Created as SCI in 1964, Science Citation Index Expanded now indexes over 9,500 of the world’s most impactful journals across 178 scientific disciplines. More than 53 million records and 1.18 billion cited references date back from 1900 to present.

Biological Abstracts Easily discover critical journal coverage of the life sciences with Biological Abstracts, produced by the Web of Science Group, with topics ranging from botany to microbiology to pharmacology. Including BIOSIS indexing and MeSH terms, specialized indexing in Biological Abstracts helps you to discover more accurate, context-sensitive results.

Google Scholar Google Scholar is a freely accessible web search engine that indexes the full text or metadata of scholarly literature across an array of publishing formats and disciplines.

JournalSeek Genamics JournalSeek is the largest completely categorized database of freely available journal information available on the internet. The database presently contains 39226 titles. Journal information includes the description (aims and scope), journal abbreviation, journal homepage link, subject category and ISSN.

Current Contents - Clinical Medicine Current Contents - Clinical Medicine provides easy access to complete tables of contents, abstracts, bibliographic information and all other significant items in recently published issues from over 1,000 leading journals in clinical medicine.

BIOSIS Previews BIOSIS Previews is an English-language, bibliographic database service, with abstracts and citation indexing. It is part of Clarivate Analytics Web of Science suite. BIOSIS Previews indexes data from 1926 to the present.

Journal Citation Reports/Science Edition Journal Citation Reports/Science Edition aims to evaluate a journal’s value from multiple perspectives including the journal impact factor, descriptive data about a journal’s open access content as well as contributing authors, and provide readers a transparent and publisher-neutral data & statistics information about the journal.

Submission Turnaround Time

Conferences

Top