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| From OncoLog,
January 2006, Vol. 51, No. 1 |
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Weight Could Predict Prostate Cancer Progression
A man’s weight at the time he is diagnosed with prostate cancer, as well as his history of weight gain, appear to play significant roles in how aggressive his cancer may become, say researchers at The University of Texas M. D. Anderson Cancer Center.
While a link between weight and the initial development of prostate cancer already has been made, this report, published in the October 1, 2005 issue of Clinical Cancer Research, is the first to associate a man’s body mass at different ages and his weight gain as an adult with the risk of progression after prostatectomy.
“These findings support the view that the development of aggressive forms of prostate cancer may be influenced by environmental effects that occur early in life,” said the study’s lead researcher Sara Strom, Ph.D., an associate professor in the Department of Epidemiology.
Given further validation of the results, Dr. Strom suggests that a man’s history of body weight should be a factor oncologists consider when designing a treatment plan for patients newly diagnosed with prostate cancer.
The data also suggest that interventions such as diet and exercise could be a way to reduce the risk of prostate cancer progression, Dr. Strom said.
Dr. Strom says that it is currently unclear how excess weight contributes to prostate cancer progression, although leading theories suggest it could be linked to changes in a number of different hormones (such as androgen and growth factors) and/or lifestyle behaviors (such as poor diet and inadequate physical activity). Understanding the mechanisms by which weight gain contributes to prostate cancer progression may lead to the development of rationally designed preventive strategies, she said.
Enzyme Complex Can Promote or Prevent Cancer Development
In a case of basic science detective work, researchers at M. D. Anderson Cancer Center have solved the puzzle of the “inconsistent biomarker” and, in the process, may have discovered an agent that can suppress cancer development.
In the October 14, 2005, issue of Science, researchers report that the biomarker in question—an enzyme known as EZH2—leads a duplicitous life. In its “native” state, the enzyme acts as a suppressor for cancer cell growth that works to inhibit cancer development. But when it is phosphorylated, it turns vicious and acts to promote oncogenesis.
The researchers found the two forms of EZH2 after they identified the “switch” that leads to its phosphorylation—the well-known culprit Akt, an enzyme that has already been associated with cancer development.
The findings explain not only why high levels of EZH2 (when bound to its partner proteins, such as EED) have been shown to identify people who have an aggressive, metastatic form of breast or prostate cancer, but also why elevated levels of EED appear to offer protective effects against virulent lymphoma.
“This has become a big riddle to cancer researchers who want to be able to use EZH2 as a marker upon which to base aggressive treatment,” said the study’s lead author, Mien-Chie Hung, Ph.D., chair of the Department of Molecular and Cellular Oncology. “We now know there are two different forms of EZH2. The phosphorylated one enhances oncogenesis, whereas the nonphosphorylated EZH2 works to inhibit cell growth.”
For
more information on this topic or for questions about M. D. Anderson’s treatments,
programs, or services, call askMDAnderson at (877) MDA-6789.
Other
articles in OncoLog, January 2006 issue:
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