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HER2 activation results from heterodimerization with another ERBB member or by homodimerization when HER2 concentration are high, for instance in cancer. [8] Amplification or over-expression of this oncogene has been shown to play an important role in the development and progression of certain aggressive types of breast cancer .
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]
ErbB2 overexpression can occur in breast, ovarian, bladder, non-small-cell lung carcinoma, as well as several other tumor types. [28] Trastuzumab or Herceptin inhibits downstream signal cascades by selectively binding to the extracellular domain of ErbB-2 receptors to inhibit it. [28] This leads to decreased proliferation of tumor cells. [28]
HER2 amplification can be detected by virtual karyotyping of formalin-fixed paraffin embedded tumor. Virtual karyotyping has the added advantage of assessing copy number changes throughout the genome, in addition to detecting HER-2 amplification (but not overexpression). Numerous PCR-based methodologies have also been described in the ...
In the United States, trastuzumab emtansine was approved specifically for treatment of HER2-positive metastatic breast cancer (mBC) in patients who have been treated previously with trastuzumab and a taxane (paclitaxel or docetaxel), and who have already been treated for mBC or developed tumor recurrence within six months of adjuvant therapy.
The dihydropyrimidine dehydrogenase (DPD) protein is responsible for the inactivation of more than 80% of the anticancer drug 5-Fluorouracil (5-FU) in the liver. This drug is commonly used in colorectal cancer treatment, and increased exposure to it can cause myelosuppression, mucositis, neurotoxicity , hand-foot syndrome, and diarrhea. [ 29 ]
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