Sylvia S Gayle's research while affiliated with Emory University and other places

What is this page?
This page lists the scientific contributions of an author, who either does not have a ResearchGate profile, or has not yet added these contributions to their profile.

It was automatically created by ResearchGate to create a record of this author's body of work. We create such pages to advance our goal of creating and maintaining the most comprehensive scientific repository possible. In doing so, we process publicly available (personal) data relating to the author as a member of the scientific community.

If you're a ResearchGate member, you can follow this page to keep up with this author's work.

If you are this author, and you don't want us to display this page anymore, please let us know.

Publications (3)

Figure 1. 
Figure 2. Sustained MEK Signaling in lapatinib-resistant cells 
Figure 3. MEK inhibition by PD0325901 (P) increases lapatinib (L) response 
Figure 4. MEK inhibition by selumetinib (S) increases lapatinib (L)...
+4 Figure 5. MEK knockdown increases lapatinib (L) response 
MEK Inhibition Increases Lapatinib Sensitivity Via Modulation of FOXM1
Article
Full-text available
  • Mar 2013
The standard targeted therapy for HER2-overexpressing breast cancer is the HER2 monoclonal antibody, trastuzumab. Although effective, many patients eventually develop trastuzumab resistance. The dual EGFR/HER2 small molecule tyrosine kinase inhibitor lapatinib is approved for use in trastuzumab-refractory metastatic HER2-positive breast cancer. How...
Abstract A6: Sustained MAPK signaling contributes to reduced sensitivity to lapatinib
Article
  • Mar 2013
Background: Approximately 20% to 30% of metastatic breast cancers overexpress the HER2 receptor tyrosine kinase. The standard front-line therapy for HER2-overexpressing breast cancer is the HER2 monoclonal antibody trastuzumab. However, for patients whose disease progresses on trastuzumab-based therapy, the dual EGFR/HER2 small-molecule tyrosine ki...
Pharmacologic Inhibition of mTOR Improves Lapatinib Sensitivity in HER2-Overexpressing Breast Cancer Cells with Primary Trastuzumab Resistance
Article
  • Oct 2011
Lapatinib, a dual EGFR/HER2 kinase inhibitor, is approved for use in patients with trastuzumab-refractory HER2- overexpressing breast cancer. Increased PI3K signaling has been associated with resistance to trastuzumab, although its role in lapatinib resistance remains unclear. The purpose of the current study was to determine if PI3K/mTOR activity...

Citations

... The reduction in growth rate as an apparent additional feature of MEK inhibition in nonsmall cell lung cancer tumour initiating cells was already mentioned in (Lundholm et al. 2014), but there we did not have any tool to measure it quantitatively. Another example of reduced colony size was reported after combined MEK and EGFR/HER2 inhibition in breast cancer cells (Gayle et al. 2013). The quantitative description was possible to perform when using the software presented here. ...
Reference: Freeware tool for analysing numbers and sizes of cell colonies
... However, MK-2206 has not yet been developed further. AKT/mTOR is highly activated in lapatinib-resistant HER2+ breast cancer cells [131]. The mTOR inhibitor INK-128 can restore the sensitivity of lapatinibresistant HER2+ breast cancer cells to TKIs [127]. ...
Reference: PI3K/AKT/mTOR-Targeted Therapy for Breast Cancer