DEC 13, 2018 09:00 AM PST

Optimizing Treatment Options for HER2+/ ER+ Breast Cancer using Models of Endocrine Resistance

Speakers
  • Postdoctoral Fellow, Georgetown University Lombardi Comprehensive Cancer Center
    Biography
      Dr. Hillary Stires is a postdoctoral fellow training in the Tumor Biology program funded through a T32 Ruth L. Kirschstein National Research Service Award at Georgetown University Lombardi Comprehensive Cancer Center under the mentorship of Dr. Rebecca Riggins. Dr. Stires received her PhD from Rutgers University in Endocrinology and Animal Biosciences and has always been interested in how steroid hormones (specifically estrogen) influence breast cancer development. In Dr. Riggins lab, Hillary's work focuses on the endocrine resistance in breast cancer. She uses cell culture models of endocrine resistance to compare resistant and parental cell lines, which are then compared with clinical data to ensure clinical relevance. At Georgetown, Hillary initiated the re-establishment of the Georgetown Postdoc Association to foster camaraderie and organize career development activities specifically geared towards postdocs. During the summer of 2019, Dr. Stires will Chair the Hormone-Dependent Cancers Gordon Research Conference. Additionally, Dr. Stires interacts with other scientists, medical oncologists, and patient advocates to improve science communication. She tweets weekly with the group #BCSM (breast cancer social media) to help provide evidence-based education and support for people affected by breast cancer.

    Abstract:
    DATE:   December 13, 2018
    TIME:    09:00am PST, 12:00pm EST
     
    Breast cancers are classified into three main subtypes according to their receptor status: estrogen receptor-positive (ER+), human epidermal growth factor receptor 2-positive (HER2+), and triple negative. These classifications provide information about the biology of the disease and help clinicians determine which treatments to use for patients. Targeted therapy for HER2+ breast cancer, including trastuzamab and pertuzamab, and for ER+ breast cancer, including Tamoxifen and aromatase inhibitors, have drastically improved survival outcomes for patients with these disease subtypes. However, when tumors are both HER2+ and ER+, treatment decisions and outcomes are less clear. HER2+/ER+ breast cancers treated with HER2 targeted therapies do not respond as well as HER2+/ER-negative tumors. Our lab is interested in understanding the biology behind these differences in response as well as better defining treatment options for HER2+/ER+ breast cancer. We have established long-term estrogen deprived (LTED) cell models of HER2+/ER+ breast cancer utilizing phenol-red free media as a surrogate for aromatase inhibitor treatment and Fulvestrant (a selective estrogen receptor degrader) resistant cell lines using increasing doses of Fulvestrant over time. We are testing combination therapy over different time courses then measure proliferation and targets of downstream signaling including protein phosphorylation by western blot and gene transcription by qRTPCR. Ultimately, these results will help inform clinicians about the most effective treatment for patients with HER2+/ER+ breast cancer.
     
    Learning Objectives:
    • Understand how scientists use cell culture to model endocrine resistance in breast cancer
    • Decipher differences between breast cancer subtypes and treatment options
    • Describe changes in signaling pathways that occur during endocrine resistance 

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