Regina H. DeFrina's Aggressive Breast Cancer PDF

By Regina H. DeFrina

ISBN-10: 1617618640

ISBN-13: 9781617618642

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Other reports implicating PI3K mutations in HER2 resistance have only been in vitro or are very small cohorts of patients [107]. The proposed main resistance mechanisms related to HER2-directed therapy are given in Table 5. Theoretically, in addition to tumor heterogeneity, resistance to trastuzumab may be caused by altered receptor-antibody interaction, compensatory activation of the downstream pathways by increased signaling from either other members of the HER family or other receptors, or constitutive activation of downstream elements [108, 109].

Lapatinib is an orally administered small molecule inhibitor that targets both EGFR and HER2 [112]. It targets the tyrosine kinase domain of these receptors by reversibly binding to the adenosine triphosphate binding site of the kinase, as illustrated in Figure 2. This interaction prevents the phosphorylation and subsequent signal transduction of both the MAPK and the PIK-3/Akt pathways, leading to an increase in apoptosis and decreased cellular proliferation. In addition to inhibiting wild-type HER receptors, lapatinib is able to inhibit truncated forms of these receptors [113].

Evaluation of amplification and overexpression of the HER2 gene Gene amplification Southern blot/slot blot analysis FISH* PCR analysis Protein expression mRNA expression IHC* Northern blot analysis Western blot analysis ELISA PCR analysis FISH FISH: Fluoroscene in situ hybridization, PCR: polymerase chain reaction, IHC: Immunohistochemistry, ELISA: Enzyme immunoassay *FDA approved The HER2 Oncogene in Breast Cancer No stain observed Weak staining of tumor cells Complete staining that is non-uniform or weak, but with circumferential distribution in atleast 10% of cells.

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Aggressive Breast Cancer by Regina H. DeFrina

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