Immune checkpoint inhibitors plus targeted therapy for advanced triple negative breast cancer

doi:10.3877/cma.j.issn.1674-0807.2020.05.001

Abstract

Abstract:

With the in-depth exploration in mechanisms of tumor proliferation, invasion and metastasis, immunotherapy and targeted therapy have gradually used for advanced triple negative breast cancer. Preclinical studies showed that targeted therapy could remodel tumor microenvironment and enhance the anti-tumor immune response in combination with immunotherapy. Currently, several clinical trials on the efficacy of the combination of both are ongoing, including immune checkpoint inhibitors plus poly(ADP-ribose) polymerase (PARP) inhibitors, angiogenesis inhibitors and epigenetic modification inhibitors. In this paper, we demonstrated the mechanism, clinical efficacy and safety of combination treatment of immune checkpoint inhibitors and targeted therapy drugs for advanced triple negative breast cancer.

Key words: Triple negative breast neoplasms, Molecular targeted therapy, Immune checkpoint inhibitors

Yiqun Han, Jiayu Wang, Binghe Xu. Immune checkpoint inhibitors plus targeted therapy for advanced triple negative breast cancer[J]. Chinese Journal of Breast Disease(Electronic Edition), 2020, 14(05): 261-265.

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https://zhrxbzz.cma-cmc.com.cn/EN/Y2020/V14/I05/261

References 58

[1]	Bray F, Ferlay J, Soerjomataram I, et al. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries[J]. CA Cancer J Clin, 2018, 68 (6): 394-424.
[2]	Goldhirsch A, Wood WC, Coates AS, et al. Strategies for subtypes--dealing with the diversity of breast cancer: highlights of the St. Gallen International Expert Consensus on the primary therapy of early breast cancer 2011[J]. Ann Oncol, 2011, 22 (8): 1736-1747.
[3]	Waks AG, Winer EP. Breast cancer treatment: a review[J]. JAMA, 2019, 321 (3): 288-300.
[4]	Foulkes WD, Smith IE, Reis-Filho JS. Triple-negative breast cancer[J]. N Engl J Med, 2010, 363 (20): 1938-1948.
[5]	Bonotto M, Gerratana L, Poletto E, et al. Measures of outcome in metastatic breast cancer: insights from a real-world scenario[J]. Oncologist, 2014, 19 (6): 608-615. URL
[6]	Goetz MP, Gradishar WJ, Anderson BO, et al. NCCN guidelines insights: breast cancer, version 3.2018[J]. J Natl Compr Canc Netw: NCCN, 2019, 17 (2): 118-126.
[7]	Marra A, Viale G, Curigliano G. Recent advances in triple negative breast cancer: the immunotherapy era[J]. BMC Med, 2019, 17 (1): 90.
[8]	Brown SD, Warren RL, Gibb EA, et al. Neo-antigens predicted by tumor genome meta-analysis correlate with increased patient survival[J]. Genome Res, 2014, 24 (5): 743-750. URL
[9]	Loi S, Sirtaine N, Piette F, et al. Prognostic and predictive value of tumor-infiltrating lymphocytes in a phase Ⅲ randomized adjuvant breast cancer trial in node-positive breast cancer comparing the addition of docetaxel to doxorubicin with doxorubicin-based chemotherapy: BIG 02-98[J]. J Clin Oncol, 2013, 31 (7): 860-867. URL
[10]	Wimberly H, Brown JR, Schalper K, et al. PD-L1 Expression correlates with tumor-infiltrating lymphocytes and response to neoadjuvant chemotherapy in breast cancer[J]. Cancer Immunol Res, 2015, 3 (4): 326-332.
[11]	Schmid P, Adams S, Rugo HS, et al. Atezolizumab and nab-paclitaxel in advanced triple-negative breast cancer[J]. N Engl J Med, 2018, 379 (22): 2108-2121.
[12]	Jia H, Truica CI, Wang B, et al. Immunotherapy for triple-negative breast cancer: existing challenges and exciting prospects[J]. Drug Resist Updat, 2017, 32: 1-15.
[13]	Adams S, Loi S, Toppmeyer D, et al. Pembrolizumab monotherapy for previously untreated, PD-L1-positive, metastatic triple-negative breast cancer: cohort B of the phase Ⅱ KEYNOTE-086 study[J]. Ann Oncol, 2019, 30 (3): 405-411.
[14]	Adams S, Schmid P, Rugo HS, et al. Pembrolizumab monotherapy for previously treated metastatic triple-negative breast cancer: cohort A of the phase Ⅱ KEYNOTE-086 study [J]. Ann Oncol, 2019, 30 (3): 397-404.
[15]	Gallyas F Jr, Sumegi B. Mitochondrial protection by PARP inhibition[J]. Int J Mol Sci, 2020, 21 (8): 2767.
[16]	Byrum AK, Vindigni A, Mosammaparast N. Defining and modulating 'BRCAness’[J]. Trends Cell Biol, 2019, 29 (9): 740-751.
[17]	Dobzhansky T. Genetics of natural populations; recombination and variability in populations of Drosophila pseudoobscura[J]. Genetics, 1946, 31(3): 269-290.
[18]	Dobzhansky T. Genetics of natural populations; recombination and variability in populations of Drosophila pseudoobscura[J]. Genetics, 1946, 31 (3): 269-290.
[19]	Mavaddat N, Barrowdale D, Andrulis IL, et al. Pathology of breast and ovarian cancers among BRCA1 and BRCA2 mutation carriers: results from the consortium of investigators of modifiers of BRCA1/2 (CIMBA)[J]. Cancer Epidemiol Biomarkers Prev, 2012, 21 (1): 134-147.
[20]	Robson M, Im SA, Senkus E, et al. Olaparib for metastatic breast cancer in patients with a germline BRCA mutation[J]. N Engl J Med, 2017, 377 (6): 523-533.
[21]	Jiao S, Xia W, Yamaguchi H, et al. PARP inhibitor upregulates PD-L1 expression and enhances cancer-associated immunosuppression[J]. Clin Cancer Res, 2017, 23 (14): 3711-3720.
[22]	Prasanna T, Wu F, Khanna KK, et al. Optimizing poly (ADP-ribose) polymerase inhibition through combined epigenetic and immunotherapy[J]. Cancer Sci, 2018, 109 (11): 3383-3392.
[23]	Mella M, Kauppila JH, Karihtala P, et al. Tumor infiltrating CD8(＋) T lymphocyte count is independent of tumor TLR9 status in treatment naive triple negative breast cancer and renal cell carcinoma[J]. Oncoimmunology, 2015, 4 (6): e1002726.
[24]	Huang J, Wang L, Cong Z, et al. The PARP1 inhibitor BMN 673 exhibits immunoregulatory effects in a Brca1(-/-) murine model of ovarian cancer[J]. Biochem Biophys Res Commun, 2015, 463 (4): 551-556.
[25]	Konstantinopoulos PA, Waggoner S, Vidal GA, et al. Single-arm phases 1 and 2 trial of niraparib in combination with pembrolizumab in patients with recurrent platinum-resistant ovarian carcinoma[J]. JAMA Oncol, 2019, 5 (8): 1141-1149.
[26]	Fridman WH, Zitvogel L, Sautès-Fridman C, et al. The immune contexture in cancer prognosis and treatment[J]. Nat Rev Clin Oncol, 2017, 14 (12): 717-734.
[27]	Ovais M, Mukherjee S, Pramanik A, et al. Designing stimuli-responsive upconversion nanoparticles that exploit the tumor microenvironment[J]. Adv Mater, 2020, 32 (22): e2000055.
[28]	Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation[J]. Cell, 2011, 144 (5): 646-674. URL
[29]	Yi M, Jiao D, Qin S, et al. Synergistic effect of immune checkpoint blockade and anti-angiogenesis in cancer treatment[J]. Mol Cancer, 2019, 18 (1): 60.
[30]	Hendry SA, Farnsworth RH, Solomon B, et al. The role of the tumor vasculature in the host immune response: implications for therapeutic strategies targeting the tumor microenvironment[J]. Front Immunol, 2016, 7: 621.
[31]	Schmittnaegel M, Rigamonti N, Kadioglu E, et al. Dual angiopoietin-2 and VEGFA inhibition elicits antitumor immunity that is enhanced by PD-1 checkpoint blockade[J]. Sci Transl Med, 2017, 9 (385): eaak9670.
[32]	Raman D, Baugher PJ, Thu YM, et al. Role of chemokines in tumor growth[J]. Cancer Lett, 2007, 256 (2): 137-165.
[33]	Chang AL, Miska J, Wainwright DA, et al. CCL2 produced by the glioma microenvironment is essential for the recruitment of regulatory T cells and myeloid-derived suppressor cells[J]. Cancer Res, 2016, 76 (19): 5671-5682.
[34]	Jain RK. Antiangiogenesis strategies revisited: from starving tumors to alleviating hypoxia[J]. Cancer Cell, 2014, 26 (5): 605-622. URL
[35]	Vitale I, Manic G, Coussens LM, et al. Macrophages and metabolism in the tumor microenvironment[J]. Cell Metab, 2019, 30 (1): 36-50.
[36]	Teleanu RI, Chircov C, Grumezescu AM, et al. Tumor angiogenesis and anti-Angiogenic strategies for cancer treatment[J]. J Clin Med, 2019, 9 (1): 84.
[37]	Wallin JJ, Bendell JC, Funke R, et al. Atezolizumab in combination with bevacizumab enhances antigen-specific T-cell migration in metastatic renal cell carcinoma[J]. Nat Commun, 2016, 7: 12 624.
[38]	Carter T, Shaw H, Mulholland P. Combining ipilimumab and bevacizumab in glioblastoma: is it really safe and effective? Author response[J]. Clin Oncol (R Coll Radiol), 2016, 28 (10): 664.
[39]	Hodi FS, Lawrence D, Lezcano C, et al. Bevacizumab plus ipilimumab in patients with metastatic melanoma[J]. Cancer Immunol Res, 2014, 2 (7): 632-642. URL
[40]	Miles DW, Chan A, Dirix LY, 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 [J]. J Clin Oncol, 2010, 28 (20): 3239-3247.
[41]	Curigliano G, Pivot X, Cortes J, et al. Randomized phase Ⅱ study of sunitinib versus standard of care for patients with previously treated advanced triple-negative breast cancer[J]. Breast, 2013, 22 (5): 650-656.
[42]	Baselga J, Zamagni C, Gómez P, et al. RESILIENCE: Phase Ⅲ randomized, double-blind trial comparing sorafenib with capecitabine versus placebo with capecitabine in locally advanced or metastatic HER-2-negative breast cancer[J]. Clin Breast Cancer, 2017, 17 (8): 585-594.
[43]	Hu X, Zhang J, Xu B, et al. Multicenter phase Ⅱ study of apatinib, a novel VEGFR inhibitor in heavily pretreated patients with metastatic triple-negative breast cancer[J]. Int J Cancer, 2014, 135 (8): 1961-1969.
[44]	Liu J, Liu Q, Li Y, et al. Efficacy and safety of camrelizumab combined with apatinib in advanced triple-negative breast cancer: an open-label phase Ⅱ trial[J]. J Immunother Cancer, 2020, 8 (1): e000696.
[45]	Li Q, Wang Y, Jia W, et al. Low-dose anti-angiogenic therapy sensitizes breast cancer to PD-1 blockade[J]. Clin Cancer Res, 2019, 26 (7): 1712-1724.
[46]	Carlson RD, Flickinger JC Jr, Snook AE. Talkin’ toxins: from Coley’s to modern cancer immunotherapy[J]. Toxins (Basel), 2020, 12(4): 241.
[47]	Godfrey DI, Le Nours J, Andrews DM, et al. Unconventional T cell targets for cancer immunotherapy[J]. Immunity, 2018, 48 (3): 453-473.
[48]	Nagarsheth N, Wicha MS, Zou W. Chemokines in the cancer microenvironment and their relevance in cancer immunotherapy[J]. Nat Rev Immunol, 2017, 17 (9): 559-572.
[49]	Hodi FS, Chiarion-Sileni V, Gonzalez R, et al. Nivolumab plus ipilimumab or nivolumab alone versus ipilimumab alone in advanced melanoma (CheckMate 067): 4-year outcomes of a multicentre, randomised, phase 3 trial[J]. Lancet Oncol, 2018, 19 (11): 1480-1492.
[50]	Motzer RJ, Tannir NM, McDermott DF, et al. Nivolumab plus ipilimumab versus sunitinib in advanced renal-cell carcinoma[J]. N Engl J Med, 2018, 378 (14): 1277-1290.
[51]	Hellmann MD, Ciuleanu TE, Pluzanski A, et al. Nivolumab plus ipilimumab in lung cancer with a high tumor mutational burden[J]. N Engl J Med, 2018, 378 (22): 2093-2104.
[52]	Santa-Maria CA, Kato T, Park JH, et al. A pilot study of durvalumab and tremelimumab and immunogenomic dynamics in metastatic breast cancer[J]. Oncotarget, 2018, 9 (27): 18 985-18 996.
[53]	Allis CD, Jenuwein T. The molecular hallmarks of epigenetic control[J]. Nat Rev Genet, 2016, 17 (8): 487-500.
[54]	张競文，续倩，李国亮. 癌症发生发展中的表观遗传学研究[J]. 遗传，2019, 41 (7): 567-581.
[55]	Huang M, Zhang J, Yan C, et al. Small molecule HDAC inhibitors: promising agents for breast cancer treatment[J]. Bioorg Chem, 2019, 91: 103 184.
[56]	Chao MW, Chu PC, Chuang HC, et al. Non-epigenetic function of HDAC8 in regulating breast cancer stem cells by maintaining Notch1 protein stability[J]. Oncotarget, 2016, 7 (2): 1796-1807.
[57]	Gameiro SR, Malamas AS, Tsang KY, et al. Inhibitors of histone deacetylase 1 reverse the immune evasion phenotype to enhance T-cell mediated lysis of prostate and breast carcinoma cells[J]. Oncotarget, 2016, 7 (7): 7390-7402.
[58]	Guerriero JL, Sotayo A, Ponichtera HE, et al. Class Ⅱa HDAC inhibition reduces breast tumors and metastases through anti-tumor macrophages[J]. Nature, 2017, 543 (7645): 428-432.

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