Corrigendum to: Enhanced brain delivery and therapeutic activity of trastuzumab after blood-brain barrier opening by NEO100 in mouse models of brain-metastatic breast cancer

Symptomatic central nervous system (CNS) metastases are diagnosed in 10–16% of patients with metastatic breast cancer (BC). Half of all these cases are HER2-positive. At present, there are no generally accepted algorithms regarding the combination and sequence of local and systemic treatment options for these patients. According to current guidelines, different local management options remain one of the main treatment methods of brain metastases control. When local treatment is limited, patients with HER2-positive BC with СNS metastases can receive anti-HER2 therapy in combination with chemo- or hormonal therapy (for luminal tumors) or as single option. Trastuzumab poorly penetrates the blood-brain barrier, but trastuzumab-based treatment schedules increase the life expectancy in patients with HER2-positive BC with CNS metastases mainly due to control of extracranial metastases. Lapatinib, by contrast, penetrates the blood-brain barrier well, and its combination with capecitabine achieves response in heavily pretreated patients, especially in those who have central nervous system metastases as the only site of disease progression.

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Targeting metastatic breast cancer with ANG1005, a novel peptide-paclitaxel conjugate that crosses the blood-brain-barrier (BBB)

Genes & Diseases ◽

10.1016/j.gendis.2017.01.004 ◽

2017 ◽

Vol 4 (1) ◽

pp. 1-3 ◽

Cited By ~ 9

Author(s):

Fei Li ◽

Shou-Ching Tang

Keyword(s):

Breast Cancer ◽

Metastatic Breast Cancer ◽

Blood Brain Barrier ◽

Metastatic Breast ◽

Brain Barrier ◽

Blood Brain

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Challenging metastatic breast cancer with the natural defensinPvD1

Nanoscale ◽

10.1039/c7nr05872a ◽

2017 ◽

Vol 9 (43) ◽

pp. 16887-16899 ◽

Cited By ~ 7

Author(s):

Tiago N. Figueira ◽

Filipa D. Oliveira ◽

Inês Almeida ◽

Érica O. Mello ◽

Valdirene M. Gomes ◽

...

Keyword(s):

Breast Cancer ◽

Metastatic Breast Cancer ◽

Brain Metastasis ◽

Tumor Cells ◽

Blood Brain Barrier ◽

Metastatic Breast ◽

Biomechanical Properties ◽

Brain Barrier ◽

Blood Brain ◽

Metastasis Development

PvD1 hampers brain metastasis development by manipulating the biomechanical properties of tumor cells and preventing their adhesion to the blood–brain-barrier.

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Systemic HER3 ligand-mimicking bioparticles cross the blood–brain barrier reducing intracranial triple-negative breast cancer growth

10.21203/rs.3.rs-1139650/v1 ◽

2022 ◽

Author(s):

Felix Alonso-Valenteen ◽

Sam Sances ◽

HongQiang Wang ◽

Simoun Mikhael ◽

Jessica Sims ◽

...

Keyword(s):

Breast Cancer ◽

Blood Brain Barrier ◽

Triple Negative Breast Cancer ◽

Triple Negative ◽

Growth Factor Receptor ◽

Metastatic Breast ◽

Induced Pluripotent Stem Cell ◽

Brain Barrier ◽

Blood Brain ◽

The Brain

Abstract Triple-negative breast cancer (TNBC) lacks selective biomarkers targeted by current clinical therapies and often metastasizes to the brain. Crossing the blood-brain barrier (BBB) and reaching intracranial tumors is a clinical challenge contributing to poor prognoses for patients. The human epidermal growth factor receptor HER3 has emerged as a biomarker of metastasis and may provide a means of therapeutically targeting TNBC. We have developed HER3-targeted biological particles (bioparticles) that exhibit systemic homing to resistant and metastatic breast tumors. Here we show that HER3 is expressed on the brain endothelium and can mediate the passage of bioparticles across the BBB and into intracranial TNBC. Our findings show that the extravasation of systemic bioparticles in mice and in human induced pluripotent stem cell-based BBB chips corresponds to HER3 levels. Furthermore, systemically delivered bioparticles carrying tumoricidal agents reduced the growth of intracranial TNBC in mice and exhibited improved therapeutic profile compared to current therapies.

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The treatment of brain metastasis from breast cancer, role of blood-brain barrier disruption and early experience with trastuzumab

Therapy ◽

10.1586/14750708.3.1.97 ◽

2006 ◽

Vol 3 (1) ◽

pp. 97-112 ◽

Cited By ~ 2

Author(s):

Rose Marie Tyson ◽

Dale F Kraemer ◽

Matthew A Hunt ◽

Leslie L Muldoon ◽

Peter Orbay ◽

...

Keyword(s):

Breast Cancer ◽

Brain Metastasis ◽

Blood Brain Barrier ◽

Early Experience ◽

Brain Barrier ◽

Barrier Disruption ◽

Blood Brain Barrier Disruption ◽

Blood Brain ◽

Brain Barrier Disruption

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Bisphenol A Inhibits the Transporter Function of the Blood-Brain Barrier by Directly Interacting with the ABC Transporter Breast Cancer Resistance Protein (BCRP)

International Journal of Molecular Sciences ◽

10.3390/ijms22115534 ◽

2021 ◽

Vol 22 (11) ◽

pp. 5534

Author(s):

Elin Engdahl ◽

Maarten van Schijndel ◽

Dimitrios Voulgaris ◽

Michela Di Criscio ◽

Kerry Ramsbottom ◽

...

Keyword(s):

Breast Cancer ◽

Bisphenol A ◽

Blood Brain Barrier ◽

Breast Cancer Resistance Protein ◽

Brain Barrier ◽

Production Volume ◽

Cancer Resistance ◽

Blood Brain ◽

Resistance Protein

The breast cancer resistance protein (BCRP) is an important efflux transporter in the blood-brain barrier (BBB), protecting the brain from a wide range of substances. In this study, we investigated if BCRP function is affected by bisphenol A (BPA), a high production volume chemical used in common consumer products, as well as by bisphenol F (BPF) and bisphenol S (BPS), which are used to substitute BPA. We employed a transwell-based in vitro cell model of iPSC-derived brain microvascular endothelial cells, where BCRP function was assessed by measuring the intracellular accumulation of its substrate Hoechst 33342. Additionally, we used in silico modelling to predict if the bisphenols could directly interact with BCRP. Our results showed that BPA significantly inhibits the transport function of BCRP. Additionally, BPA was predicted to bind to the cavity that is targeted by known BCRP inhibitors. Taken together, our findings demonstrate that BPA inhibits BCRP function in vitro, probably by direct interaction with the transporter. This effect might contribute to BPA’s known impact on neurodevelopment.

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