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HER2 is a member of the human epidermal growth factor receptor (HER/EGFR/ERBB) family. But contrary to other members of the ERBB family, HER2 does not directly bind ligand. HER2 activation results from heterodimerization with another ERBB member or by homodimerization when HER2 concentration are high, for instance in cancer. [8]
These downstream signaling proteins initiate several signal transduction cascades, principally the MAPK, Akt and JNK pathways, leading to DNA synthesis and cell proliferation. [12] Such proteins modulate phenotypes such as cell migration, adhesion, and proliferation. Activation of the receptor is important for the innate immune response in ...
The Ras-Raf-MAPK pathway is a major signalling route for the ErbB family, as is the PI3-K/AKT pathway, both of which lead to increased cell proliferation and inhibition of apoptosis. [ 25 ] Genetic Ras mutations are infrequent in breast cancer but Ras may be pathologically activated in breast cancer by overexpression of ErbB receptors. [ 26 ]
3815 16590 Ensembl ENSG00000157404 ENSMUSG00000005672 UniProt P10721 P05532 RefSeq (mRNA) NM_000222 NM_001093772 NM_001122733 NM_021099 RefSeq (protein) NP_000213 NP_001087241 NP_001116205 NP_066922 Location (UCSC) Chr 4: 54.66 – 54.74 Mb Chr 5: 75.74 – 75.82 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Proto-oncogene c-KIT is the gene encoding the receptor tyrosine kinase ...
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. [ 19 ] [ 20 ] Trastuzumab , the first HER2-targeted drug developed in 1990, interferes with HER2 signalling.
The main approach in overcoming endocrine resistance in those breast cancers that are both ER+ and HER2+ is by using a combination of endocrine and HER2-targeting agents. [22] In trials conducted with a combination of anti-HER2 agents and an aromatase inhibitor, significant clinical benefit and improved progression-free survival have been observed.
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When one of the proteins in the pathway is mutated, it can become stuck in the "on" or "off" position, a necessary step in the development of many cancers. In fact, components of the MAPK/ERK pathway were first discovered in cancer cells, and drugs that reverse the "on" or "off" switch are being investigated as cancer treatments. [1]
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