Laura Bowers Works to Sever the Link Between Obesity and Cancer
Laura Bowers Works to Sever the Link Between Obesity and Cancer

Laura Bowers Works to Sever the Link Between Obesity and Cancer

The Purdue University nutrition researcher delves into the details of how fat tissue affects tumors.

Jul 15, 2019
Shawna Williams

ABOVE: © Harold Lee
Miller Photography

After graduating from Swarthmore College, Laura Bowers considered going to law school—until she worked in a law firm and realized it wasn’t for her. Instead, she earned her dietitian license and worked as a clinical dietitian for four years. But Bowers found herself increasingly interested in “understanding how different nutrients and diet patterns affected disease risk,” she says. She started a PhD in nutritional sciences at the University of Texas at Austin in 2009.

Something clicked soon after Bowers started a rotation in the lab of oncology researcher Linda deGraffenried. There, she says, she “fell in love” with deGraffenried’s research on the influence of obesity on breast and prostate cancers. “I just found that very fascinating, that nutrition can really play a big role in cancer risk as well as response to treatment.” To study obesity’s effects, Bowers validated and started using an in vitro model system that treated cultured estrogen receptor–positive breast cancer cells, together with macrophages and adipose stromal cells, with pooled serum from either obese or lean postmenopausal patients with breast cancer. The serum of the obese women fostered the growth of cancer cells by stimulating an inflammatory pathway involving estrogen receptor α (ERα), Bowers and her colleagues found.1 The researchers then analyzed retrospective data on obese women whose ERα-positive tumors had gone into remission. Individuals who took nonsteroidal anti-inflammatory drugs daily had lower cancer recurrence rates. Based on results from in vitro experiments, Bowers and her colleagues suggested that the drugs lowered cancer recurrence because they inhibit a pro-inflammatory enzyme released from adipose cells. Without the drugs, the enzyme would stimulate estrogen production.2

“From the beginning, [Bowers] was very much more demanding of herself than anyone else was,” deGraffenried tells The Scientist. “She has probably to this day been my most productive, and one of the brightest, graduate students that I’ve interacted with.”

In addition to deGraffenried, Bowers also worked closely with another professor in the same department, Stephen Hursting. As the end of Bowers’s PhD work neared, Hursting, who also studies links between nutrition, obesity, and cancer, accepted a position at the University of North Carolina, and Bowers joined his lab as a postdoc. In experiments on mice, she found that the hormone leptin, which fat cells release to tamp down hunger, is an essential factor linking diet-induced obesity with the development and progression of triple-negative breast cancer; the hormone promotes the growth of cancer stem cells and the transition of epithelial cells into mesenchymal cells.3

At Purdue University, where Bowers started her own lab last summer, she is continuing to study leptin, and whether it affects patients’ responses to chemotherapy by expanding the population of cancer stem cells. She’s also studying the microbiome, transferring fecal matter from obese mice to lean mice treated with a chemical carcinogen to develop colon tumors to see if the microbes influence colon cancer progression independently of other effects of obesity.

“She is a very creative scientist—she’s very well versed in state-of-the-art techniques, and she uses them to address . . . emerging problems that we have identified as forefront issues right now in science,” says Dorothy Teegarden, who studies nutrition and cancer at Purdue and led the search committee that recruited Bowers. “She is going to be a star.”

References

  1. L.W. Bowers et al., “Obesity enhances nongenomic estrogen receptor crosstalk with the PI3K/Akt and MAPK pathways to promote in vitro measures of breast cancer progression,” Breast Cancer Res, 15:R59, 2013. (Cited 32 times)
  2. L.W. Bowers et al., “NSAID use reduces breast cancer recurrence in overweight and obese women: role of prostaglandin–aromatase interactions,” Cancer Res, 74:4446–57, 2014. (Cited 65 times)
  3. L.W. Bowers et al., “Leptin signaling mediates obesity-associated CSC enrichment and ETM in preclinical TNBC models,” Mol Cancer Res, 16:869–79, 2018. (Cited 8 times)