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Peers elect MD Anderson's Hung and Lozano as Fellows of AAAS

HOUSTON - Innovative insights into a vital tumor-suppressing mechanism that is often broken in malignant cells and a type of receptor protein that frequently goes haywire to stimulate cancer growth have earned two scientists at The University of Texas MD Anderson Cancer Center membership in a distinguished association of scholars.

Mien-Chie Hung, Ph.D., vice president for basic research, professor and chair of MD Anderson's Department of Molecular and Cellular Oncology, and Guillermina Lozano, Ph.D., professor and chair of the Department of Genetics, have been elected fellows in the American Association for the Advancement of Science.

"Outstanding basic science research provides the foundation for improving cancer treatment and prevention," said Raymond DuBois, M.D., Ph.D., executive vice president and provost at MD Anderson. "Election as AAAS Fellows recognizes Mien-Chie Hung and Guillermina Lozano for their leadership in uncovering the molecular details that reveal how cancer develops, grows and might be eliminated."

Both scientists, DuBois noted, also work closely with clinicians to translate their findings to clinical applications.

New fellows will be inducted in a ceremony on Feb. 19 at the AAAS annual meeting in Washington, D.C. Founded in 1848, the AAAS is the world's largest general scientific society. Nominations are offered by at least three existing fellows in one of the association's 24 sections, or by the section's steering group, or by the AAAS chief executive officer. The steering groups review nominations and send a final list to the AAAS Council for a vote.

After Hung and Lozano are inducted, MD Anderson will have 11 AAAS members on its faculty.

In its announcement, the AAAS cited Hung for "distinguished contributions to novel findings about how receptor tyrosine kinases operate, which have generated a paradigm-shift on receptor biology with important clinical implications."

Lozano is recognized "for distinguished contributions to the field of cancer genetics and molecular biology increasing the understanding of the p53 tumor suppressor pathway and its physiologic significance."

Discovering secrets of receptor tyrosine kinases

Tyrosine kinases are enzymes that regulate many cell functions by attaching phosphate groups to other proteins. They carry signals from growth factors outside of the cell that connect with these receptors on the cell surface. Cancer cells are often overloaded with receptor tyrosine kinases.

Hung was one of a trio of scientists who cloned the functional human epidermal growth factor receptor 2 (HER2/neu) oncogene, which is now known as a marker for poor prognosis for many human cancers and as a successful therapeutic target. The drug Herceptin targets the receptor in HER2-positive breast cancer.

Hung also showed that the receptor tyrosine kinase EGFR also makes its way from the cell surface to inside its nucleus, where it promotes cancer growth in an entirely different way, a discovery that opened a new avenue for receptor biology and cancer drug development. Additionally, Hung and colleagues found that EGFR on the cell surface helps another surface protein channel glucose to cancer cells.

Understanding p53, the protector

The p53 protein is central to regulation of the cell division cycle. It can halt the process, initiate repair of defective DNA and if repair fails, order the cell to kill itself, a process called apoptosis. This frontline defense against cancer is mutated, deleted or otherwise inactivated in more than half of human cancers.

Lozano was first to establish p53 as a transcriptional activator of other genes. Transcription is the first step in a gene's expression of its protein. She also showed that common p53 mutants fail to launch transcription. Lozano also discovered that another protein, Mdm2, plays a critical role in regulating p53 activity.

She also demonstrated that p53's ability to halt the cell cycle and protect chromosomal stability through DNA repair are as important as its ability to initiate apoptosis in preventing tumor development.


Contact: Scott Merville
University of Texas M. D. Anderson Cancer Center

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