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David F. Stern, PhD

Professor of Pathology; Vice Chair for Basic and Translational Sciences, Pathology; Associate Cancer Center Director, Shared Resources

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David F. Stern, PhD

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Research Summary

The HER-2/Neu/ErbB-2 receptor tyrosine kinase is a major human oncogene and a validated therapeutic target in breast cancer. We are investigating the normal and carcinogenic functions of HER2 and other EGF receptor family kinases to understand how they cause cancers and how they can best be treated. An important practical problem with new, targeted cancer therapies is linking patients to therapies that match the specific alterations in their cancers. We are pursuing high throughput genetic and proteomic approaches to this problem.

Specialized Terms: Cancer Biology; Signal transduction by HER2/ErbB2 and other EGF family receptor tyrosine kinases; EGF family receptors in breast cancer and mammary development; DNA damage checkpoint signaling; Functional and genetic analysis of cancer; Melanoma

Extensive Research Description

1. The receptor tyrosine kinase ErbB2/HER2 drives 25% of breast cancers. This receptor is the target for two drugs in use for breast cancer treatment, Herceptin/Trastuzumab and Tykerb/Lapatinib. In order to understand why this receptor is so important in human cancer, and to improve therapeutic targeting of ErbB2/HER2, we investigate normal and pathological functions of this receptor in mammary tissue. Our work spans from fundamental studies on signal transduction to analysis of ERBB2 in human cancer. ERBB2 works in close partnership with other members of the EGF receptor (ERBB family) of tyrosine kinases, so we also study differential signaling by the three related receptors (EGF receptor [HER]), ERBB3 [HER3], ErbB4[HER4).

2. The growing availability of cancer drugs that target receptors and other signaling proteins has created a need to develop integrated methods for best matching of patients to the appropriate target drugs. We are investigating use of DNA-based and functional approaches for predicting response to targeted therapies, in breast cancer, lung cancer, pancreatic cancer, and melanoma.

Coauthors

Research Interests

Breast Neoplasms; DNA Damage; Melanoma; Neoplasms; Pathology; Signal Transduction

Selected Publications