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HER2. Receptor tyrosine-protein kinase erbB-2 is a protein that normally resides in the membranes of cells and is encoded by the ERBB2 gene. ERBB is abbreviated from erythroblastic oncogene B, a gene originally isolated from the avian genome.
The HER2 gene (also known as HER2/neu and ErbB2 gene) is amplified in 20–30% of early-stage breast cancers. [34] Trastuzumab is a monoclonal antibody targeting HER2, inducing an immune-mediated response that causes internalization and recycling of HER2. It may also upregulate cell cycle inhibitors such as p21 Waf1 and p27 Kip1. [47]
HER2-low has some HER2 proteins on the cell surface, but not enough to be classified as HER2-positive. [4] Trastuzumab deruxtecan is the first approved therapy by the US Food and Drug Administration (FDA) targeted to people with the HER2-low breast cancer subtype. [4] DNA-based classification.
The epidermal growth factor receptor is a member of the ErbB family of receptors, a subfamily of four closely related receptor tyrosine kinases: EGFR (ErbB-1), HER2/neu (ErbB-2), Her 3 (ErbB-3) and Her 4 (ErbB-4). In many cancer types, mutations affecting EGFR expression or activity could result in cancer. [ 6]
Gene target examples HER2. HER2 is an established therapeutic target within breast cancer, and the activation of HER2 is observed in approximately 20% of breast cancers as a result of overexpression. Trastuzumab, the first HER2-targeted drug developed
Triple-negative breast cancer. Triple-negative breast cancer ( TNBC) is any breast cancer that either lacks or shows low levels of estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2) overexpression and/or gene amplification (i.e. the tumor is negative on all three tests giving the name triple ...
HERC2. HERC2 is a giant E3 ubiquitin protein ligase, implicated in DNA repair regulation, pigmentation and neurological disorders. It is encoded by a gene of the same name belonging to the HERC family, which typically encodes large protein products with C-terminal HECT domains and one or more RCC1 -like (RLD) domains. [1] [2]
In 1982, Palmiter and Brinster implanted a foreign gene into fertilized egg, finally generating the first transgenic mice genetically engineered to express dominant oncogenes. [20] In 1982, the stimulation of expression from the MMTV-LTR (Mouse mammary tumor virus-Long terminal repeat) was done by multiple rounds of pregnancy and lactation to ...
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