Abstract S6-07: Detrimental effects of sequential compared to concurrent treatment of pertuzumab plus T-DM1 in HER2+ breast cancer cell lines

2015 ◽  
Author(s):  
James E Korkola ◽  
Moqing Liu ◽  
Tiera Liby ◽  
Laura Heiser ◽  
Heidi Feiler ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Concurrent Treatment ◽  
Her2 Breast Cancer

Crosstalk between PARP-1 and NF-κB signaling pathways as a potential determinant of PARPi sensitivity in trastuzumab resistant HER2+ breast cancer cell lines.

2015 ◽  
Vol 33 (15_suppl) ◽  
pp. 606-606
Author(s):  
Monicka Wielgos ◽  
Tiffiny Cooper ◽  
Andres Forero-Torres ◽  
Francisco J. Esteva ◽  
Rachel Schiff ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Signaling Pathways ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Her2 Breast Cancer ◽  
Parp 1 ◽  
Potential Determinant

scholarly journals Combination treatment with a PI3K/Akt/mTOR pathway inhibitor overcomes resistance to anti-HER2 therapy in PIK3CA-mutant HER2-positive breast cancer cells

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yumi Fujimoto ◽  
Tomoko Yamamori Morita ◽  
Akihiro Ohashi ◽  
Hiroshi Haeno ◽  
Yumi Hakozaki ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Combination Therapy ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Single Agent ◽  
Cancer Cell Lines ◽  
Pi3k Pathway ◽  
Breast Cancer Cell Lines ◽  
Her2 Breast Cancer

AbstractAmplification and/or overexpression of human epidermal growth factor receptor 2 (HER2) are observed in 15–20% of breast cancers (HER2+ breast cancers), and anti-HER2 therapies have significantly improved prognosis of patients with HER2+ breast cancer. One resistance mechanism to anti-HER2 therapies is constitutive activation of the phosphoinositide 3-kinase (PI3K) pathway. Combination therapy with small-molecule inhibitors of AKT and HER2 was conducted in HER2+ breast cancer cell lines with or without PIK3CA mutations, which lead to constitutive activation of the PI3K pathway. PIK3CA mutations played important roles in resistance to single-agent anti-HER2 therapy in breast cancer cell lines. Combination therapy of a HER2 inhibitor and an AKT inhibitor, as well as other PI3K pathway inhibitors, could overcome the therapeutic limitations associated with single-agent anti-HER2 treatment in PIK3CA-mutant HER2+ breast cancer cell lines. Furthermore, expression of phosphorylated 4E-binding protein 1 (p4EBP1) following the treatment correlated with the antiproliferative activities of the combination, suggesting that p4EBP1 may have potential as a prognostic and/or efficacy-linking biomarkers for these combination therapies in patients with HER2+ breast cancer. These findings highlight potential clinical strategies using combination therapy to overcome the limitations associated with single-agent anti-HER2 therapies in patients with HER2+ breast cancer.

Abstract PD2-10: Predicting sensitivity to CDK4/6 inhibition in ER+/HER2- breast cancer cell lines

2020 ◽  
Author(s):  
Lauren Bathurst ◽  
Linda Liao ◽  
Cheryl Crozier ◽  
Jane Bayani ◽  
John Bartlett ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Her2 Breast Cancer

scholarly journals Alpelisib Exhibits a Synergistic Effect with Pyrotinib and Reverses Acquired Pyrotinib Resistance in HER2+ Breast Cancer

2022 ◽  
Author(s):  
Hao Chen ◽  
Yuhao Si ◽  
Jialiang Wen ◽  
Chunlei Hu ◽  
Erjie Xia ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Synergistic Effect ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Quantitative Polymerase Chain Reaction ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Her2 Breast Cancer ◽  
Resistant Cells

Abstract Background: Human epidermal growth factor receptor 2 (HER2) plays a vital role in breast cancer progression in patients who overexpress HER2, thus promoting the rapid progress of targeted drugs development and therapy strategies advancement targeting this gene. Pyrotinib, approved in clinical by the Chinese State Drug Administration, is a novel pan-ErbB kinase inhibitor and exhibits better efficacy than lapatinib. Alpelisib is a selective PI3K p110α inhibitor approved for application in HR+, HER2-, PIK3CA mutated breast cancers. We assumed that combining pyrotinib with alpelisib worked better than single-drug treatment.Methods: We performed the drug combination assay to evaluate the combination index (CI) of pyrotinib and alpelisib in HER2+ breast cancer cell lines. Cell functional assays, RT-qPCR (Real Time-Quantitative Polymerase Chain Reaction) and western blotting were performed to elucidate the combined efficacy of two drugs and explore the underlying mechanism. Then we established the acquired pyrotinib resistant HER2+ breast cancer cell lines and evaluate the combined efficacy of two drugs in pyrotinib resistant cells and explore the potential mechanisms.Results: Our data exhibited that a combination of alpelisib and pyrotinib showed a synergistic effect in HER2+ breast cancer by enhancing cell proliferation and migration decrease, G0-G1 cell cycle arrest, and apoptosis rate increase. Additionally, alpelisib combined with pyrotinib showed a tremendous synergistic effect in acquired pyrotinib resistant cells.Conclusions: Our results provided the preclinical evidence that a combination of pyrotinib and alpelisib as an effective therapeutic strategy in treating HER2+ breast cancer, whether patients were sensitive or resistant to pyrotinib treatment.

Sign in / Sign up

Export Citation Format

Share Document