Herceptin-induced inhibition of phosphatidylinositol-3 kinase and Akt Is required for antibody-mediated effects on p27, cyclin D1, and antitumor action.

By F. Yakes, W. Chinratanalab, C. Ritter, W. King, S. Seelig, Carlos L. Arteaga. Cancer Research, 2002

674 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/742c107afa3e3b86c6cda5c3f984d601658ecffd

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

1. Carlos L. Arteaga
2. H. Horlings
3. Gwen Macdonald
4. T. Junttila
5. Y. Ogitani
6. R. Akita
7. Gail D Lewis Phillips
8. Kathryn L. Parsons

Citations in the corpus

• ErbB receptors: directing key signaling networks throughout life. (2004, background): “Treatment of a range of cancer cell lines with the antibody resulted in growth inhibition through upregulation of the cell cycle inhibitor p27Kip1 (113, 114) and induction of apoptosis (115).”
• Ligand-independent HER2/HER3/PI3K complex is disrupted by trastuzumab and is effectively inhibited by the PI3K inhibitor GDC-0941. (2009, background): “Several reports suggest that the cytostatic effect of trastuzumab correlates with a downregulation of AKT activity, which ultimately leads to an increase in the CDK2 inhibitor p27 (Lane et al., 2000; Lee et al., 2001; Yakes et al., 2002).”
• DS-8201a, A Novel HER2-Targeting ADC with a Novel DNA Topoisomerase I Inhibitor, Demonstrates a Promising Antitumor Efficacy with Differentiation from T-DM1 (2016, background): “The major mechanisms of action of trastuzumab are thought to involve an ADCC activity by binding to FcgRIII on immune effector cells (38, 39), and a downregulation of phosphorylated Akt (pAkt), which upregulates p27 expression and inhibits cell proliferation (40).”
• Improved classification of breast cancer by analysis of genetic alterations and gene expression profiling (2011, background): “, 2001), or inhibit PI3K/ AKT survival signaling, either by downregulating HER2 signaling (Yakes et al., 2002) or by increasing PTEN membrane localization and phosphatase activity, leading to a decline in PI3K/AKT pathway activation and inhibition of proliferation (Nagata et al.”
• PTEN activation contributes to tumor inhibition by trastuzumab, and loss of PTEN predicts trastuzumab resistance in patients. (2004, background): “Unfortunately, information that is dependent on ErbB2 downregulation or PI3K inhibition (Hudziak et al., 1989; Yakes et al., 2002), the rapid Akt dephoson the mechanisms of trastuzumab resistance in breast cancer cells is limited.”
• AKT inhibition relieves feedback suppression of receptor tyrosine kinase expression and activity (2011, unknown): “In these tumors, PI3K-AKT signaling is HER2 dependent and predominantly driven by HER2-HER3 heterodimers (Holbro et al., 2003; Yakes et al., 2002).”
• Antitumor Activity of HKI-272, an Orally Active, Irreversible Inhibitor of the HER-2 Tyrosine Kinase (2004, background): “This process is antagonized by p27kip1, a cyclin-dependent kinase inhibitor (31) the transcription and stability of which are negatively regulated by both pathways ( 32 ).”
• ERBB receptors: From oncogene discovery to basic science to mechanism-based cancer therapeutics (2014, background): “…uncouples ligand-independent HER2-containing dimers leading to partial inhibition of downstream signaling, and triggers antibodydependent, cell-mediated cytotoxicity (ADCC) (Clynes et al., 2000; Ghosh et al., 2011; Junttila et al., 2009; Molina et al., 2001; Yakes et al., 2002) (Table 2).”
• ErbB receptors and signaling pathways in cancer. (2009, background): “correlates with downregulation of multiple signaling pathways [25,30–33].”
• Activation of the PI3K/Akt pathway and chemotherapeutic resistance. (2002, background): “(2002), Yakes et al. (2002)”