Immune Checkpoint Blockade in Patients with Triple-Negative Breast Cancer

Michel, Laura L.; Au, Alexandra von; Mavratzas, Athanasios; Smetanay, Katharina; Schütz, Florian; Schneeweiß, Andreas

doi:10.1007/s11523-020-00730-0

Cited by 24 publications

(18 citation statements)

References 78 publications

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“…However, recent studies demonstrated that the tumors of TNBC are more immunogenic (showing a higher degree of lymphocyteinfiltrating and higher PD-L1 expression) than the other BC subtypes 71 . Currently, several clinical trials are investigating immune checkpoint programmed death 1/PD-L1 inhibitors as monotherapy or in combination with other therapies, such as chemotherapy, radiotherapy, poly adenosine ribose polymerase inhibitors, or angiogenesis inhibitors in patients with metastatic TNBC 72 . Based on the results of the IMpassion 130 study, anti-PD-L1 drug atezolizumab plus nab-paclitaxel received accelerated approval on March 8, 2019 from the Food and Drug Administration for unresectable locally advanced or metastatic TNBC with PD-L1 expression 3 .…”

Section: Exosome and Immunotherapeutic Resistance In Bcmentioning

confidence: 99%

Exosomes and breast cancer drug resistance

et al. 2020

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Drug resistance is a daunting challenge in the treatment of breast cancer (BC). Exosomes, as intercellular communicative vectors in the tumor microenvironment, play an important role in BC progression. With the in-depth understanding of tumor heterogeneity, an emerging role of exosomes in drug resistance has attracted extensive attention. The functional proteins or non-coding RNAs contained in exosomes secreted from tumor and stromal cells mediate drug resistance by regulating drug efflux and metabolism, pro-survival signaling, epithelial–mesenchymal transition, stem-like property, and tumor microenvironmental remodeling. In this review, we summarize the underlying associations between exosomes and drug resistance of BC and discuss the unique biogenesis of exosomes, the change of exosome cargo, and the pattern of release by BC cells in response to drug treatment. Moreover, we propose exosome as a candidate biomarker in predicting and monitoring the therapeutic drug response of BC and as a potential target or carrier to reverse the drug resistance of BC.

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Section: Exosome and Immunotherapeutic Resistance In Bcmentioning

confidence: 99%

Exosomes and breast cancer drug resistance

et al. 2020

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“…The presence or absence of ER in the breast cancer cell is a valuable prognostic factor that provides predictive value to the potential benefits of target-based therapies [ 47 ]. Approximately 70% of metastatic breast cancers are ER-positive, and the patients tend to have a greater chance of effective tumor response and longer survival than patients with ER-negative cancers [ 48 , 49 , 50 ].…”

Section: Introductionmentioning

confidence: 99%

Induction of Redox-Mediated Cell Death in ER-Positive and ER-Negative Breast Cancer Cells by a Copper(II)-Phenolate Complex: An In Vitro and In Silico Study

et al. 2020

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This research was aimed at finding the cytotoxic potential of the mixed ligand copper(II) complex [Cu(tdp)(phen)](ClO4)—where H(tdp) is the tetradentate ligand 2-[(2-(2-hydroxyethylamino)-ethylimino)methyl]phenol, and phen is 1,10-phenanthroline—to two genotypically different breast cancer cells, MCF-7 (p53+ and ER+) and MDA-MB-231 (p53- and ER-). The complex has been already shown to be cytotoxic to ME180 cervical carcinoma cells. The special focus in this study was the induction of cell death by apoptosis and necrosis, and its link with ROS. The treatment brought about nuclear fragmentation, phosphatidylserine externalization, disruption of mitochondrial trans-membrane potential, DNA damage, cell cycle arrest at sub-G1 phase, and increase of ROS generation, followed by apoptotic death of cells during early hours and a late onset of necrosis in the cells surviving the apoptosis. The efficacy of the complex against genotypically different breast cancer cells is attributed to a strong association through p53-mitochondrial redox—cell cycle junction. The ADMET properties and docking of the complex at the active site of Top1 are desirable attributes of a lead molecule for development into a therapeutic. Thus, it is shown that the copper(II)–phenolate complex[Cu(tdp)(phen)]+ offers potential to be developed into a therapeutic for breast cancers in general and ER-negative ones in particular.

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“…Immune system blends with every step of tumor progression, and cancer immune therapy have made drastically progress in past several years. As a highly immune infiltrated malignancy neoplasm [47,51], breast cancer is promised beautiful landscape by immunotherapy [52]. Immune gene signature is one of independent response predictors associating with Bev-containing regimen, making immune combining with vascular-targeted a hopeful therapy for BC.…”

Section: Discussionmentioning

confidence: 99%

Bevacizumab Plays a double-edged role in Neoadjuvant Therapy for Non-metastatic Breast Cancer: A Systemic Review and Meta-Analysis

Chen¹,

Gao²,

Zhang³

et al. 2021

J. Cancer

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The anti-angiogenic drug Bevacizumab (Bev) is engaged in neoadjuvant therapy for non-metastatic breast cancer (NMBC). However, whether neoadjuvant Bev providing a greater benefit to patients is debatable. Our study aimed to review Bev's role in Neoadjuvant therapy (NAT) in NMBC and identify predictive markers associated with its efficacy by systemic review and meta-analysis. Eligible trials were retrieved from the Pubmed, Embase, and Cochrane Library, and random or fixed effects models were applied to synthesize data. Power of pCR to predict DFS or OS was evaluated by nonlinear mixed effect model. In NMBC, Bev significantly improved the rate of patients achieving pCR, but this benefit discontinued in DFS or OS. Biomarkers such as PAM50 intrinsic subtype, VEGF overexpression, regulation of VEGF signaling pathway, hypoxia-related genes, BRCA1/2 mutation, P53 mutation and immune phenotype can be used to predict Bev-inducing pCR and/or DFS/OS. Unfortunately, although patients with pCR survived longer than those without pCR when ignoring the use of Bev, but patients achieving pCR with Bev might survive shorter than those achieving pCR without Bev. Subgroup analyses found Bev prolonged patients' OS when given pre-and post-surgery. Lastly, adding Bev increased adverse effects. Overall, Bev offered limited effect for patients with NMBC in an unscreened population. However, in biomarkers-identified subgroup, Bev could be promising to ameliorate the prognosis of specific patients with NMBC.

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Immune Checkpoint Blockade in Patients with Triple-Negative Breast Cancer

Cited by 24 publications

References 78 publications

Exosomes and breast cancer drug resistance

Exosomes and breast cancer drug resistance

Induction of Redox-Mediated Cell Death in ER-Positive and ER-Negative Breast Cancer Cells by a Copper(II)-Phenolate Complex: An In Vitro and In Silico Study

Bevacizumab Plays a double-edged role in Neoadjuvant Therapy for Non-metastatic Breast Cancer: A Systemic Review and Meta-Analysis

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