Lisa Arendt

Position title: Associate Professor, Comparative Biosciences


Phone: Obesity; Breast cancer; Mammary gland; Inflammation; Stromal/epithelial interactions


BS 1996 University of Wisconsin-Madison, Madison, WI
DVM 2002 University of Wisconsin-Madison, Madison, WI
PhD 2007 University of Wisconsin-Madison, Madison, WI
Postdoc 2014 Tufts University, Boston, MA

Lisa Arendt. Assistant Professor, Comparative Biosciences. Obesity; Breast cancer; Mammary gland; Inflammation; Stromal/epithelial interactions.

NIH Biosketch
PubMed Publications

Research Focus

Obesity is a world-wide problem, and two-thirds of the population in the United States is currently considered to be either overweight or obese. Obesity increases the risk for multiple different types of cancer. In particular, obesity significantly increases the risk for postmenopausal breast cancer. Obesity also enhances other risk factors, such as in women with a family history of breast cancer. Postmenopausal women are most commonly diagnosed with breast tumors that have a marker called estrogen receptor alpha (ERa). However in women with a higher body mass index, these ERa positive tumors are larger at the time of diagnosis and are more clinically aggressive. Both pre- and postmenopausal women who develop breast cancer also have an increased incidence of triple negative breast tumors. These tumors, which lack the markers ERa, progesterone receptor, and Her-2, are more difficult to treat clinically. Obese women also have an increased risk for the development of metastases and a shorter time before tumors may recur.

Obesity is a complex disorder, with metabolic changes that occur systemically. In addition, breast tissue is a reservoir of fat that exhibits inflammatory changes and has been largely ignored in the study of breast cancer. In the obese state, changes in the breast fat may have profound effects on breast cancer development and progression. In order to understand how obesity alters breast cancer risk and tumor progression, we utilize high fat diet and transgenic mouse models of obesity, a novel xenograft model of obesity, and complementary cell culture models. Using these systems, we hope to understand the how changes in the breasts of obese women promote tumor development and identify potential targets for therapeutics to treat obese women with breast cancer.

Program Activities

  • Joined ERP Program: 2015
  • ERP T32 Training Partner


No past or current ERP students