By Regina H. DeFrina
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Additional resources for Aggressive Breast Cancer
Although these data provide a rational explanation for the lower response of HER2-overexpressing tumors to endocrine therapy seen in several clinical studies, most were retrospective and nonrandomized. In the largest, retrospective, series derived from the Gruppo Universitario Napoletano 1 (GUN-1) cooperative trial, HER2 expression, by IHC was evaluated in 145 of 308 (47 %) patients with nodenegative breast cancer who were randomly assigned to two years of tamoxifen or observation . 09) in women with HER2negative tumors.
Trastuzumab was approved in 1998 for the treatment of metatastic breast cancer and in 2006 for the adjuvant treatment of HER2 overexpressing breast cancer . The exact mechanisms by which trastuzumab causes regression of HER2overexpressing tumors are still being clarified, but several effects have been reported in the literature . They include antibody-dependent cellular cytotoxicity, angiogenesis inhibition, and reduced downstream signaling through PI3K and MAPK, ultimately resulting in cell-cycle arrest and apoptosis [92, 94, 95].
Increased Signaling from other Receptors Activating the MAPK and PI3K Pathways Overexpression of insulin-like growth factor-1 receptor (IGF1R) is also associated with trastuzumab resistance, as this receptor physically interacts with and phosphorylates HER2. Breast cancer cells with overexpression of both HER2 and IGF1R are resistant to trastuzumab . In vitro, inhibition of IGF1R signaling has been shown to restore trastuzumab resistance, demonstrating the importance of this pathway as potential therapeutic target .
Aggressive Breast Cancer by Regina H. DeFrina
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