Being obese increases the risk of breast cancer in post-menopausal women, shortens the time between return of the disease and lowers overall survival rates. Italian researchers speaking at Experimental Biology 2007 in Washington, DC, now report evidence on how leptin, a hormone found in fat cells, significantly influences breast cancer development and progression in mice. This new understanding, says Dr. Sebastiano Ando, establishes a new mechanism for the link between obesity and breast cancer and suggests new targets for drugs that could intervene in that mechanism.
Dr. Ando's presentation on Sunday, April 29 is part of the scientific program of the American Society of Investigative Pathology.
Leptin, an adipocyte-derived hormone, is best known for its efforts to send messages to the body that no more food is needed, a process that may go awry in many people with obesity. But it also is involved in many other processes, from reproduction and lactation to cell differentiation and proliferation. Leptin is activated by signals from the leptin receptor ObR, and it is this partnership that has previously been found to be involved in the development of breast cancer. It was recently reported, for example, that leptin was detected in 86.4 percent of primary breast tumors and that its expression was highly correlated with ObR.
In previous studies in Dr. Ando's laboratory, leptin was demonstrated to play a significant role in promoting breast cancer in obese women by increasing the amount of estrogen (estradiol) in breast tissue. In the current study, the researchers found that leptin also upregulated or increases the production of E-cadherin, an intercellular adhesion molecule generally viewed as a tumor suppressor. The researchers grafted human breast cancer tissue in "nude" mice (genetically bred to be unable to reject tumors and therefore a frequently used animal in cancer research) and also in a three dimensional tissue culture which
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Federation of American Societies for Experimental Biology
29-Apr-2007