Targeting the Human Epidermal Growth Factor Receptor Family in Breast Cancer beyond HER2

Kerstin Riecke; Isabell Witzel

doi:10.1159/000510998

Targeting the Human Epidermal Growth Factor Receptor Family in Breast Cancer beyond HER2

Standard

Targeting the Human Epidermal Growth Factor Receptor Family in Breast Cancer beyond HER2. / Riecke, Kerstin; Witzel, Isabell.

In: BREAST CARE, Vol. 15, No. 6, 12.2020, p. 579-585.

Research output: SCORING: Contribution to journal › SCORING: Review article › Research

Harvard

Riecke, K & Witzel, I 2020, 'Targeting the Human Epidermal Growth Factor Receptor Family in Breast Cancer beyond HER2', BREAST CARE, vol. 15, no. 6, pp. 579-585. https://doi.org/10.1159/000510998

APA

Riecke, K., & Witzel, I. (2020). Targeting the Human Epidermal Growth Factor Receptor Family in Breast Cancer beyond HER2. BREAST CARE, 15(6), 579-585. https://doi.org/10.1159/000510998

Vancouver

Riecke K, Witzel I. Targeting the Human Epidermal Growth Factor Receptor Family in Breast Cancer beyond HER2. BREAST CARE. 2020 Dec;15(6):579-585. https://doi.org/10.1159/000510998

Bibtex

@article{6ffe3c45f43f474ab2ce816f35a9906b,

title = "Targeting the Human Epidermal Growth Factor Receptor Family in Breast Cancer beyond HER2",

abstract = "Currently, the dichotomous definition of human epidermal growth factor receptor 2 (HER2)-positive versus HER2-negative disease undergoing a change through inclusion of the identification of the {"}HER2-low{"} category, for which new therapeutic compounds in the form of potent antibody drug conjugates (ADC) may be effective. In addition, resistance to HER2-directed targets has become a clinical challenge and, therefore, strategies to bypass the HER2 receptor are of high interest. These are new HER2 ADCs and tyrosine kinase inhibitors, such as tucatinib or neratinib. The underlying mechanisms of resistance to anti-HER2 therapies and compensatory pathways are complex and a wide range of mechanisms of resistance may coexist in the same cell. Therefore, the combined treatment with agents that interact with HER2-associated downstream signaling pathways like the phosphoinositide-3-kinase (PI3K) and the serine/threonine kinases AKT and mTOR might overcome HER2 resistance. In addition, targeting other members of the HER family is a promising approach to improve outcomes in breast cancer patients. This review gives an overview of treatment strategies in targeting HER2 and other members of the HER family, not only in HER2-positive breast cancer, but also in HER2-low expressing tumors, and of approaches to overcome HER2 resistance.",

author = "Kerstin Riecke and Isabell Witzel",

note = "Copyright {\textcopyright} 2020 by S. Karger AG, Basel.",

year = "2020",

month = dec,

doi = "10.1159/000510998",

language = "English",

volume = "15",

pages = "579--585",

journal = "BREAST CARE",

issn = "1661-3791",

publisher = "S. Karger AG",

number = "6",

}

RIS

TY - JOUR

T1 - Targeting the Human Epidermal Growth Factor Receptor Family in Breast Cancer beyond HER2

AU - Riecke, Kerstin

AU - Witzel, Isabell

PY - 2020/12

Y1 - 2020/12

N2 - Currently, the dichotomous definition of human epidermal growth factor receptor 2 (HER2)-positive versus HER2-negative disease undergoing a change through inclusion of the identification of the "HER2-low" category, for which new therapeutic compounds in the form of potent antibody drug conjugates (ADC) may be effective. In addition, resistance to HER2-directed targets has become a clinical challenge and, therefore, strategies to bypass the HER2 receptor are of high interest. These are new HER2 ADCs and tyrosine kinase inhibitors, such as tucatinib or neratinib. The underlying mechanisms of resistance to anti-HER2 therapies and compensatory pathways are complex and a wide range of mechanisms of resistance may coexist in the same cell. Therefore, the combined treatment with agents that interact with HER2-associated downstream signaling pathways like the phosphoinositide-3-kinase (PI3K) and the serine/threonine kinases AKT and mTOR might overcome HER2 resistance. In addition, targeting other members of the HER family is a promising approach to improve outcomes in breast cancer patients. This review gives an overview of treatment strategies in targeting HER2 and other members of the HER family, not only in HER2-positive breast cancer, but also in HER2-low expressing tumors, and of approaches to overcome HER2 resistance.

AB - Currently, the dichotomous definition of human epidermal growth factor receptor 2 (HER2)-positive versus HER2-negative disease undergoing a change through inclusion of the identification of the "HER2-low" category, for which new therapeutic compounds in the form of potent antibody drug conjugates (ADC) may be effective. In addition, resistance to HER2-directed targets has become a clinical challenge and, therefore, strategies to bypass the HER2 receptor are of high interest. These are new HER2 ADCs and tyrosine kinase inhibitors, such as tucatinib or neratinib. The underlying mechanisms of resistance to anti-HER2 therapies and compensatory pathways are complex and a wide range of mechanisms of resistance may coexist in the same cell. Therefore, the combined treatment with agents that interact with HER2-associated downstream signaling pathways like the phosphoinositide-3-kinase (PI3K) and the serine/threonine kinases AKT and mTOR might overcome HER2 resistance. In addition, targeting other members of the HER family is a promising approach to improve outcomes in breast cancer patients. This review gives an overview of treatment strategies in targeting HER2 and other members of the HER family, not only in HER2-positive breast cancer, but also in HER2-low expressing tumors, and of approaches to overcome HER2 resistance.

U2 - 10.1159/000510998

DO - 10.1159/000510998

M3 - SCORING: Review article

C2 - 33447231

VL - 15

SP - 579

EP - 585

JO - BREAST CARE

JF - BREAST CARE

SN - 1661-3791

IS - 6

ER -