Advances in EGFR/HER2-directed clinical research on breast cancer

Chow, Louis W C; Lie, Erich Ferdiansyah; Toi, Masakazu

doi:10.1016/bs.acr.2020.04.009

Cited by 8 publications

(10 citation statements)

References 98 publications

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“…The fact that it is superior to the first line monotherapy with trastuzumab suggests that members of the HER family may have at least partially redundant functions. This underlines the need for a dual or multipoint therapy strategy, which is also supported by recently published reports (reviewed in [3]). Triple inhibition with antibody mixtures against EGFR, HER2 and HER3 were effective in blocking the growth of cancer cells in vitro and in vivo [66].…”

Section: Discussionsupporting

confidence: 71%

“…The tyrosine kinase human epidermal growth factor receptor 2 (HER2, also ErbB2) belongs to the epidermal growth factor receptor (EGFR) family, consisting of EGFR, HER2, HER3 and HER4 [1]. HER2 represents an overexpressed oncoprotein responsible for approximately 20% of all breast cancer cases [2,3]. HER2 signaling promotes cell survival and cell growth, and is initiated by receptor dimerization [4].…”

Section: Introductionmentioning

confidence: 99%

“…This will in turn phosphorylate and activate the "receiver" kinase of the dimerization partner, leading to full activation of downstream signaling pathways. Preventing dimerization of kinases and inhibiting their kinase activity is a therapeutic strategy to block HER2 signaling in breast cancer [3]. When combined with chemotherapy, current therapeutic strategies for HER2 driven breast cancer include I) blocking receptor dimerization with antibodies, such as trastuzumab and pertuzumab, designed to bind to the extracellular domain of HER2 or II) blocking the kinase activity of the receptors with small molecule compounds like lapatinib and neratinib [6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

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EGFR Expression in HER2-Driven Breast Cancer Cells

Weinberg

Peckys

Jonge

2020

IJMS

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The epidermal growth factor receptor HER2 is overexpressed in 20% of breast cancer cases. HER2 is an orphan receptor that is activated ligand-independently by homodimerization. In addition, HER2 is able to heterodimerize with EGFR, HER3, and HER4. Heterodimerization has been proposed as a mechanism of resistance to therapy for HER2 overexpressing breast cancer. Here, a method is presented for the simultaneous detection of individual EGFR and HER2 receptors in the plasma membrane of breast cancer cells via specific labeling with quantum dot nanoparticles (QDs). Correlative fluorescence microscopy and liquid phase electron microscopy were used to analyze the plasma membrane expression levels of both receptors in individual intact cells. Fluorescent single-cell analysis of SKBR3 breast cancer cells dual-labeled for EGFR and HER2 revealed a heterogeneous expression for receptors within both the cell population as well as within individual cells. Subsequent electron microscopy of individual cells allowed the determination of individual receptors label distributions. QD-labeled EGFR was observed with a surface density of (0.5–5) × 101 QDs/µm2, whereas labeled HER2 expression was higher ranging from (2–10) × 102 QDs/µm2. Although most SKBR3 cells expressed low levels of EGFR, an enrichment was observed at large plasma membrane protrusions, and amongst a newly discovered cellular subpopulation termed EGFR-enriched cells.

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Section: Discussionsupporting

confidence: 71%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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EGFR Expression in HER2-Driven Breast Cancer Cells

Weinberg

Peckys

Jonge

2020

IJMS

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“…In this study, we quanti ed the expression of these indicators and found that the stronger the expression of epithelial markers, the higher the probability of sentinel lymph node metastasis. EGFR is a transmembrane protein directly related to the proliferation, metastasis and apoptosis of tumor cells, and therefore can affect the metastasis of sentinel lymph nodes, which is consistent with the results of previous studies (27) .…”

Section: Discussionsupporting

confidence: 91%

Analysis on factors behind sentinel lymph node metastasis in breast cancer by color ultrasonography, molybdenum target and pathological detection

Yiming

Wubulikasimu

Yusuying

2021

Preprint

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Background This study aimed to collect the factors underlying the metastasis of breast cancer and sentinel lymph node, and to screen and analyze the risk factors of sentinel lymph node metastasis, so as to provide reference and basis for clinical work. Methods A total of 100 patients with breast cancer were enrolled in the study. These patients received treatment in our hospital from May 2017 to May 2020. The general information, the characteristics of the color Doppler echocardiography, molybdenum, conventional pathology and molecular pathology of the patients were collected. The influencing factors of sentinel lymph node metastasis in breast cancer patients were retrospectively analyzed. Results In this study, age, tumor diameter and BI-RADS category, pathology type, expression profiles of CK5/6, EGFR, and CK19, and TP53 and BRAC1/2 mutations were independent risk factors for sentinel lymph node metastasis in breast cancer (P<0.05). The number and locations of tumors, the quadrant of tumors, the regularity of tumor margins, the presence of blood flow signals, the presence of posterior echo attenuation, the presence of calcification, histological grade, molecular typing, and mutations of BRAF, ATM and PALB2 were irrelevant factors (P>0.05). Conclusions In conclusion, age, tumor diameter, Bi-rads category, invasive type, expression of CK5/6, EGFR and CK19, and mutations of TP53 and BRAC1/2 were positively correlated with sentinel lymph node metastasis. They are independent risk factors that should be paid more attention in clinical studies, to strengthen the management and control of sentinel lymph node metastasis of high-risk breast cancer, and support early chemotherapy or targeted therapy.

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“…HER2 / ERBB2 amplification has long been known to reduce sensitivity to anti-estrogens in ER + /HER2 + tumors, with the current standard of care for this BC subtype being a combination of ET and HER2 inhibitors. Treatment of HER2-amplified BC will not be explored, as it is out of the scope of this review but has been recently reviewed by Chow et al [ 87 ]. More recently, HER2-activating mutations have been associated with both intrinsic and acquired ET resistance [ 88 , 89 ].…”

Section: A Brief Revisit Of Recognized Mechanisms Of Et Resistancementioning

confidence: 99%

Exploring new pathways in endocrine-resistant breast cancer

Pinho

Abreu

Gomes³

et al. 2022

Exploration of Targeted Anti-Tumor Therapy

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The most common breast cancer (BC) subtypes are hormone-dependent, being either estrogen receptor-positive (ER+), progesterone receptor-positive (PR+), or both, and altogether comprise the luminal subtype. The mainstay of treatment for luminal BC is endocrine therapy (ET), which includes several agents that act either directly targeting ER action or suppressing estrogen production. Over the years, ET has proven efficacy in reducing mortality and improving clinical outcomes in metastatic and nonmetastatic BC. However, the development of ET resistance promotes cancer survival and progression and hinders the use of endocrine agents. Several mechanisms implicated in endocrine resistance have now been extensively studied. Based on the current clinical and pre-clinical data, the present article briefly reviews the well-established pathways of ET resistance and continues by focusing on the three most recently uncovered pathways, which may mediate resistance to ET, namely receptor activator of nuclear factor kappa B ligand (RANKL)/receptor activator of nuclear factor kappa B (RANK), nuclear factor kappa B (NFκB), and Notch. It additionally overviews the evidence underlying the approval of combined therapies to overcome ET resistance in BC, while highlighting the relevance of future studies focusing on putative mediators of ET resistance to uncover new therapeutic options for the disease.

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Advances in EGFR/HER2-directed clinical research on breast cancer

Cited by 8 publications

References 98 publications

EGFR Expression in HER2-Driven Breast Cancer Cells

EGFR Expression in HER2-Driven Breast Cancer Cells

Analysis on factors behind sentinel lymph node metastasis in breast cancer by color ultrasonography, molybdenum target and pathological detection

Exploring new pathways in endocrine-resistant breast cancer

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