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Cancer-obesity Link Could Aid Prevention Efforts

Date:
May 7, 2009
Source:
Michigan State University
Summary:
A new link between body fat and cancer underscores obesity's health risk and could lead to new cancer treatment and prevention strategies. Scientists identified the connection between obesity and colon cancer, the third-leading killer of Americans, in part by examining tissue hormones.

A new link between body fat and cancer identified by a Michigan State University researcher underscores obesity’s health risk and could lead to new cancer treatment and prevention strategies.

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Jenifer Fenton, an MSU food science and human nutrition researcher with the Michigan Agricultural Experiment Station, identified the connection between obesity and colon cancer, the third-leading killer of Americans, in part by examining tissue hormones.

Working with MSU/MAES physiologist Julia Busik and biologist Fay Hansen-Smith of Oakland University in Rochester, Mich., Fenton examined a key hormone found in fat tissue and thought to promote cancer. Her conclusions are published in a study today in the journal Carcinogenesis.

Leptin – a fat cell-derived hormone regulating body energy – is higher in obese individuals. Fenton’s study is the first to demonstrate that, at higher levels, leptin induces precancerous colon cells to produce more of a growth factor that can increase blood supply to early cancer cells – promoting tumor growth and cancer progression.

“Adipose tissue, or fat, is recognized as a significant risk factor for diabetes and heart disease, but the role of adipose tissue in cancer risk is less understood,” Fenton said. “Abdominal fat in particular seems to be associated with the greatest risk for cancer. As your waist-to-hip ratio increases, so does your risk for cancer, especially breast, colon and endometrial cancers.”

Some 149,000 Americans will be diagnosed with colon cancer and 50,000 will die from it this year, according to the American Cancer Society. More than a million have been diagnosed with colon or rectal cancer in the U.S. as of 2006, the National Cancer Institute reported.

Fenton and her team focused on colon cancer because, unlike breast or prostate cancer, colon cancer affects both genders equally, allowing them broader reach and a larger impact on cancer prevention.

“Trying to address the problem when someone already has a late-stage tumor is not primary prevention,” Fenton said. “Our goal is to understand the active signals and mechanisms involved so we can create opportunities to prevent or interrupt cancer progression early in the process.

“The impact of obesity and cancer are a priority for the health of the nation,” Fenton added. “Although weight loss is the ideal prevention strategy for reducing obesity as a risk factor for colon cancer, 95 percent of all people who lose weight will gain it back – and often more – within a year, so behavior modification as a prevention strategy is difficult and challenging. For this reason, continuing research also will include the identification of dietary compounds that may prevent or reduce colon cancer risk associated with obesity in the absence of weight loss.”

The research is supported by the Michigan Agricultural Experiment Station and the National Cancer Institute.


Story Source:

The above story is based on materials provided by Michigan State University. Note: Materials may be edited for content and length.


Journal Reference:

  1. Birmingham et al. Novel mechanism for obesity-induced colon cancer progression. Carcinogenesis, 2009; 30 (4): 690 DOI: 10.1093/carcin/bgp041

Cite This Page:

Michigan State University. "Cancer-obesity Link Could Aid Prevention Efforts." ScienceDaily. ScienceDaily, 7 May 2009. <www.sciencedaily.com/releases/2009/04/090430161240.htm>.
Michigan State University. (2009, May 7). Cancer-obesity Link Could Aid Prevention Efforts. ScienceDaily. Retrieved December 17, 2014 from www.sciencedaily.com/releases/2009/04/090430161240.htm
Michigan State University. "Cancer-obesity Link Could Aid Prevention Efforts." ScienceDaily. www.sciencedaily.com/releases/2009/04/090430161240.htm (accessed December 17, 2014).

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