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The Hemann Laboratory uses high-throughput screening technology, in combination with tractable pre-clinical mouse models, to investigate basic mechanisms of intrinsic and acquired drug resistance. The researchers also use genetic and computational tools to understand how cancer therapies exert their effects and how to best combine drugs to achieve greater efficacy and preempt the evolution of chemoresistance. Their goal is to identify novel cancer drug targets, as well as strategies for tailoring drug regimens to target protective mechanisms used by cancers to evade and escape cancer therapy, which ultimately drives relapse or progression. 

In recent work, the Hemann group found that some of the normal cells, specifically pancreas stellate cells, that surround pancreas tumor cells secrete factors that protect these tumors from front-line therapy. Most notable among these factors are deoxynucleosides, basic building blocks of DNA. Curiously, the key therapy for pancreas cancer—gemcitabine—is itself a modified version of a deoxynucleoside. The net effect of this microenvironmental protection is that deoxynucleosides compete away the chemotherapy used to treat the cancer. This study has two important implications. First, it provides a target pathway that may enhance sensitivity to a standard of care drug in a currently incurable cancer. Second, it highlights what chemotherapy can tell us about basic cancer dependencies. While it was previously thought that gemcitabine was just a generic cancer drug, its effect on pancreas tumors is really quite specific.

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