Jaimee C. Eckers, PhD

Position title: Kimple Laboratory

Email: kubatzke@wisc.edu

Address:
3116 WI Institute Medical Research
1111 Highland Ave
Madison, WI 53705

Research Title. Despite Redundant Expression of Glucose Transporters, Glucose Transporter GLUT8 is Essential for Breast Cancer Cells.

Research Description. Dr. Eckers’ current research focuses on the molecular basis of radiation-induced autophagy as a mechanism of therapeutic resistance in HPV+ and HPV- human head and neck cancer (HNC). HNC is the sixth most common cause of cancer death in the United States, with a five-year survival rate of approximately 50% and high rates of toxicities from traditional treatments. Worldwide there has been a shift in the etiology of HNC. While tobacco/alcohol use remain responsible for the majority of cases, human papillomavirus (HPV) infection causes approximately 1/3 of all HNCs and up to 80% of cancers arising in the oropharynx in this country. Multiple studies have shown that patients with HPV+ HNC have improved outcomes compared to stage-matched patients with HPV- HNC. Over the last few years, the Kimple Lab has shown that HPV+ HNCs are more sensitive to radiation due to the effects of the viral oncogenes E6 and E7. HPV+ HNCs demonstrate impaired DNA repair and increased apoptosis following DNA damage induced by radiation therapy (RT). Disease control rates for patients with locally advanced HPV-positive HNC remain poor: disease progression is seen in 40-50% of patients despite treatment with aggressive chemoradiation. One potential mechanism underlying therapeutic resistance is the upregulation of autophagy, a self-degrading process where cytoplasm, organelles, or membranes are engulfed and digested in lysosomes. Autophagy is classically activated to help cells deal with nutrient deprivation, but recent studies suggest a protective role for autophagy in response to radiation and chemotherapy. Dr. Eckers’ research is aimed at understanding the molecular basis of radiation-induced autophagy as well as how HPV oncogenes modulate autophagic resistance. Her current work suggests that both EGFR and LAPTM4B play a role in the regulation of radiation-induced autophagy. Additionally, her work demonstrates that expression of E6 and E7 significantly lessen the autophagic response in HNC cells. Dr. Eckers’ ongoing work further explores the specific roles of HPV oncogenes in autophagicresponse to radiation as well as whether autophagy inhibition in HPV+ and HPV- cell lines improves tumor response.

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