2008
DOI: 10.1158/0008-5472.can-08-0380
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A Central Role for HER3 in HER2-Amplified Breast Cancer: Implications for Targeted Therapy

Abstract: Epidermal growth factor receptor (EGFR) and HER3 each form heterodimers with HER2 and have independently been implicated as key coreceptors that drive HER2-amplified breast cancer. Some studies suggest a dominant role for EGFR, a notion of renewed interest given the development of dual HER2/EGFR small-molecule inhibitors. Other studies point to HER3 as the primary coreceptor. To clarify the relative contributions of EGFR and HER3 to HER2 signaling, we studied receptor knockdown via small interfering RNA techno… Show more

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Cited by 574 publications
(520 citation statements)
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“…little information on the action or interaction of these agents in ovarian cancer, even though they have shown promise for some patients in the clinic (19,20,24). When combined, trastuzumab and pertuzumab show an enhanced antitumor activity in ovarian cancer xenografts, as they do in breast (38,39) and non-small-cell lung cancer xenografts (39 molecular phenotype and therefore responsiveness to other therapies. ERa was upregulated in response to treatment with trastuzumab (alone or in combination with pertuzumab) but not pertuzumab alone.…”
Section: Discussionmentioning
confidence: 99%
“…little information on the action or interaction of these agents in ovarian cancer, even though they have shown promise for some patients in the clinic (19,20,24). When combined, trastuzumab and pertuzumab show an enhanced antitumor activity in ovarian cancer xenografts, as they do in breast (38,39) and non-small-cell lung cancer xenografts (39 molecular phenotype and therefore responsiveness to other therapies. ERa was upregulated in response to treatment with trastuzumab (alone or in combination with pertuzumab) but not pertuzumab alone.…”
Section: Discussionmentioning
confidence: 99%
“…In contrast, coexpression of erbB3 and erbB2 is frequently observed in breast cancers (Bieche et al, 2003) and cell lines (deFazio et al, 2000). It has been reported that erbB2 requires erbB3 to promote breast cancer cell proliferation (Holbro et al, 2003); and erbB3 has a critical role in erbB2 altered breast cancers (Lee-Hoeflich et al, 2008). These data suggest that the erbB3 receptor, but not EGFR, probably has an important role in erbB2-mediated therapeutic resistance in breast cancer.…”
Section: Introductionmentioning
confidence: 94%
“…In HER2-overexpressing cells, the major mechanism of PI3K activation is the coupling of pHER3 to an N-terminal SH2 domain in p85, the regulatory subunit of PI3K (19,20). In these cells, the main tyrosine phosphorylated protein precipitated with p85 antibodies is pHER3.…”
Section: Knockdown Of Compensatory Feedback To Her3 Sensitizes To Pi3kmentioning
confidence: 99%