TY - JOUR
T1 - Molecular Targeting Therapy against EGFR Family in Breast Cancer
T2 - Progress and Future Potentials
AU - Maennling, Amaia Eleonora
AU - Tur, Mehmet Kemal
AU - Niebert, Marcus
AU - Klockenbring, Torsten
AU - Zeppernick, Felix
AU - Gattenloehner, Stefan
AU - Meinhold-Heerlein, Ivo
AU - Hussain, Ahmad Fawzi
N1 - Publisher Copyright:
© MDPI AG. All rights reserved.
PY - 2019/12
Y1 - 2019/12
N2 - The epidermal growth factor receptor (EGFR) family contains four transmembrane tyrosine kinases (EGFR1/ErbB1, Her2/ErbB2, Her3/ErbB3 and Her4/ErbB4) and 13 secreted polypeptide ligands. EGFRs are overexpressed in many solid tumors, including breast, pancreas, head-and-neck, prostate, ovarian, renal, colon, and non-small-cell lung cancer. Such overexpression produces strong stimulation of downstream signaling pathways, which induce cell growth, cell differentiation, cell cycle progression, angiogenesis, cell motility and blocking of apoptosis.The high expression and/or functional activation of EGFRs correlates with the pathogenesis and progression of several cancers, which make them attractive targets for both diagnosis and therapy. Several approaches have been developed to target these receptors and/or the EGFR modulated effects in cancer cells. Most approaches include the development of anti-EGFRs antibodies and/or small-molecule EGFR inhibitors. This review presents the state-of-the-art and future prospects of targeting EGFRs to treat breast cancer.
AB - The epidermal growth factor receptor (EGFR) family contains four transmembrane tyrosine kinases (EGFR1/ErbB1, Her2/ErbB2, Her3/ErbB3 and Her4/ErbB4) and 13 secreted polypeptide ligands. EGFRs are overexpressed in many solid tumors, including breast, pancreas, head-and-neck, prostate, ovarian, renal, colon, and non-small-cell lung cancer. Such overexpression produces strong stimulation of downstream signaling pathways, which induce cell growth, cell differentiation, cell cycle progression, angiogenesis, cell motility and blocking of apoptosis.The high expression and/or functional activation of EGFRs correlates with the pathogenesis and progression of several cancers, which make them attractive targets for both diagnosis and therapy. Several approaches have been developed to target these receptors and/or the EGFR modulated effects in cancer cells. Most approaches include the development of anti-EGFRs antibodies and/or small-molecule EGFR inhibitors. This review presents the state-of-the-art and future prospects of targeting EGFRs to treat breast cancer.
KW - epidermal growth factor receptor
KW - antibody
KW - antibody drug conjugate
KW - tyrosine kinase inhibitor
KW - chimeric antigen receptors t cells
KW - GROWTH-FACTOR RECEPTOR
KW - RANDOMIZED PHASE-II
KW - MONOCLONAL-ANTIBODY
KW - CHEMOTHERAPY PLUS
KW - TYROSINE KINASES
KW - ERBB RECEPTORS
KW - TRASTUZUMAB
KW - COMBINATION
KW - HER2
KW - EXPRESSION
U2 - 10.3390/cancers11121826
DO - 10.3390/cancers11121826
M3 - (Systematic) Review article
C2 - 31756933
SN - 2072-6694
VL - 11
JO - Cancers
JF - Cancers
IS - 12
M1 - 1826
ER -