Prostaglandin E2, Inflammatory Mediators and Epigenetic Modulation of Cancer Progression

Date/Time
Date(s) - 4 Jun 2012 until 4 Jun 2012
11:00 AM - 12:00 PM

Location
The Biodesign Institute at ASU


Prostaglandin E2, Inflammatory Mediators and Epigenetic Modulation of Cancer Progression

 Time and Date

11:00am -12:00pm, Jun 04, 2012

Location

The Biodesign Institute Auditorium, B105

Address:   727 E. Tyler St. Tempe AZ 85287

Description

Presentation by Dr. Raymond N. DuBois, Jr., University of Texas MD Anderson Cancer Center. Sponsored by ASU’s Office of Knowledge Enterprise Development.

Dr. Raymond N. DuBois, Jr.

Provost & Executive Vice President, The University of Texas MD Anderson Cancer Center, Houston, TX

Professor of Cancer Biology & Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX

About the DuBois Laboratory

The DuBois Laboratory goals are to advance the understanding, diagnosis, treatment and prevention of colorectal cancer. We actively seek to understand the molecular mechanisms and biology that drive the development and progression of colon cancer. We have learned that bioactive lipids and inflammation play central roles in this process. We were among the first labs to recognize that cyclooxygenase (COX) plays a key role in the formation of adenomatous polyps and colorectal cancer. We were also among the first to appreciate that prostaglandin E2 (PGE2) exhibits most of the cancer promoting activity of the PGs. These exciting discoveries led to successful clinical translational studies applying the use of non-steroidal anti-inflammatory drugs (NSAIDs) that include cyclooxygenase-2 selective inhibitors (COXIBs) in the treatment of high-risk colorectal cancer patients.

We are heavily engaged in identifying important molecular targets downstream of COX-2 to improve the treatment and prevention of colorectal cancer. This is to eliminate the cardiovascular risk associated with the long-term use of COXIBs. These efforts include identifying the molecules involved in tissue inflammation that cause the progression of colorectal cancer. They also involve uncovering the role of nuclear receptor signaling through peroxisome proliferator activated receptors in colorectal cancer. Furthermore, we are learning about other arachidonic acid based molecules such as endocannabinoids that act through cannabinoid receptors to inhibit colon cancer.

These are very exciting times to be involved in the basic and clinical translational research of cancer. We have pioneered many concepts regarding the role of eicosanoids in cancer through the development of robust collaborations that integrate our extensive clinical and basic science expertise. The ultimate goal of our work is to meet the long-term objective of reducing the local and global cancer burden.

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