Aggressive Breast Cancer by Regina H. DeFrina

By Regina H. DeFrina

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Extra resources for Aggressive Breast Cancer

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Thus, cells with HER1HER3 heterodimers or HER1-HER1 homodimers may initiate MAPK and PI3K signaling even in the presence of trastuzumab [112]. TGF-α is a ligand of the HER family that can lead to formation of heterodimers involving HER2. In vitro, trastuzumab was less efficient in inhibiting cell growth in presence of TGF-α [113]. In addition, increased levels of the HER family ligands heregulin and EGF blocked trastuzumab-mediated growth inhibition in HER2 overexpressing breast cancer cell lines [114].

Axial images of a brain magnetic resonance imaging (MRI) study demonstrating an intracerebral metastasis in a patient with HER2-positive breast cancer. CONCLUSION The abundance of evidence indicates that HER2 gene amplification and protein overexpression are associated with an adverse outcome in breast cancer. HER2 levels strongly correlate with the pathogenesis of prognosis of breast cancer and accurate assessments of HER2 expression are essential. Although controversy exists over the best detection method for measuring abnormalities of HER2, the majority of data favor assays of gene amplification such as the FISH technique and IHC on frozen breast tissue specimens.

Consequently, strategies are being investigated to target HER2 for cancer therapy. To date, targeted therapies include monoclonal antibodies and tyrosine kinase inhibitors. Monoclonal antibodies and small-molecules differ in several pharmacological properties. Antibodies are administrated intravenously and act only on receptors expressed on the cell surface. Tyrosine kinase inhibitors are orally available, small, membrane-permeable compounds that block or compete with ATP binding, thus inhibiting the intracellular, downstream signaling cascade stimulated by a The HER2 Oncogene in Breast Cancer 19 receptor or several receptors [89].

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