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It has been found that patients with ER+ (Estrogen receptor positive)/HER2+ compared with ER-/HER2+ breast cancers may actually benefit more from drugs that inhibit the PI3K/AKT molecular pathway. [37] Over-expression of HER2 can also be suppressed by the amplification of other genes.
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]
The ErbB family of proteins contains four receptor tyrosine kinases, structurally related to the epidermal growth factor receptor (EGFR), its first discovered member. In humans, the family includes Her1 (EGFR, ErbB1), Her2 , Her3 , and Her4 . The gene symbol, ErbB, is derived from the name of a viral oncogene to which these receptors are ...
The HER2 gene (also known as HER2/neu and ErbB2 gene) is amplified in 20–30% of early-stage breast cancers. [44] 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. [58]
TNBC is hard to treat because, unlike many other breast cancers, the tumor cells do not have estrogen or progesterone receptors, and do not make a protein called HER2. They, therefore, do not ...
HER2-positive tumors have a kind of receptor that allows the tumor to spread more quickly — or better respond to treatment. In all cases, the receptors can serve as clear targets for treatments.
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