Science Park in the News
UT MD Anderson preclinical research boosts case for new drug approach
A small slice of RNA inhibits prostate cancer metastasis by suppressing a surface protein commonly found on prostate cancer stem cells. A research team led by scientists at The University of Texas MD Anderson Cancer Center reported today in an advance online publication at Nature Medicine. “Our findings are the first to profile a microRNA expression pattern in prostate cancer stem cells and also establish a strong rationale for developing the microRNA miR-34a as a new treatment option for prostate cancer,” said senior author Dean Tang, Ph.D., professor in MD Anderson’s Department of Molecular Carcinogenesis. MicroRNAs, or miRNAs, are short, single-stranded bits of RNA that regulate the messenger RNA expressed by genes to create a protein. Cancer stem cells are capable of self-renewal, have enhanced tumor-initiating ability and are generally more resistant to treatment than other cancer cells. They are associated with tumor recurrence and metastasis, the lethal spreading of cancer to other organs. These capacities are more prevalent in cancer cells that feature a specific cell surface protein called CD44, Tang said. “CD44 has long been linked to promotion of tumor development and, especially, to cancer metastasis,” Tang said. “Many cancer stem cells overexpress this surface adhesion molecule. Another significant finding from our study is identifying CD44 itself as a direct and functional target of miR-34a.”
Researchers Find Melanoma Not Caused by Early UVA Light Exposure
Early life exposure to ultraviolet A light does not cause melanoma in a fish model that previously made that connection, scientists from The University of Texas MD Anderson Cancer Center reported in the online Early Edition of the Proceedings of the National Academy of Sciences. UVA exposure is unlikely to have contributed to the rise in the incidence of melanoma over the past 30 years, the researchers conclude, because the fish model had been the only animal model to indicate a connection between exposure to UVA at a young age and later development of melanoma. “Our data refute the only direct evidence that UVA causes melanoma, which is not to say that UVA is harmless,” said the study’s lead author David Mitchell, Ph.D., professor in MD Anderson’s Department of Molecular Carcinogenesis located at its Science Park – Research Division in Smithville, Texas. “UVA is just not as dangerous as we thought because it doesn’t cause melanoma.” (May 2010)
Researchers Discover Second Protective Role for Tumor-Suppressor
ATM, a protein that reacts to DNA damage by ordering repairs or the suicide of the defective cell, plays a similar, previously unknown role in response to oxidative damage outside of the nucleus, researchers report this week in the online version of the Proceedings of the National Academy of Sciences. "This tumor-suppressor that works in the nucleus to prevent replication of defective cells also has a second life out in the cytoplasm, which was totally unexpected," said senior author Cheryl Walker, Ph.D., professor in The University of Texas MD Anderson Cancer Center Department of Molecular Carcinogenesis. (Feb 2010)
MD Anderson Science Park – Research Division Garners 10 Research Grants from Stimulus Funds
Bastrop Advertiser Article
Smithville Times Article
Smithville, TX ― The University of Texas MD Anderson Cancer Center was awarded 84 stimulus grants from the American Recovery and Reinvestment Act of 2009 totaling more than $53.8 million over a two-year period. Seven investigators at the MD Anderson Science Park – Research Division garnered 10 of these grants totaling more than $4 million.
A list of all Recovery Act grants funded by the National Institutes of Health can be found at: http://report.nih.gov/recovery/arragrants.cfm/. These grants will fund projects investigating the origins of cancer.
The Science Park – Research Division is located in Smithville, 45 miles southeast of Austin, and has been a part of the Central Texas community since 1977. Research at the Science Park – Research Division focuses on Molecular Carcinogenesis (the origins of cancer); DNA damage, repair and mutagenesis; molecular and biochemical genetics, and cancer prevention. Basic science research at the Science Park focuses on cancers of the skin, breast, prostate, gallbladder, pancreas, female reproductive tract and thymus.
“ARRA funds provide a great boost for cancer research during the difficult economic times that have followed a period of decreased research funding,” said Raymond DuBois, M.D., Ph.D., MD Anderson executive vice president and provost. “Our faculty successfully built the innovative and collaborative proposals that were necessary to compete for these grants. Two specialized programs, the Grand Opportunity grants and Challenge grants, offer scientists new avenues to explore areas of great potential that could benefit from a two-year jump-start in funding.”
All faculty at the Science Park are in MD Anderson’s Department of Molecular Carcinogenesis.
Investigating the mechanism of DNA damage repair in response UV radiation The primary cause of skin cancer is chronic exposure to ultraviolet (UV) rays from sunlight. A crucial event in the prevention of UV-induced skin cancer is the repair of DNA damage and/or the removal of the damaged cells. Instructor Thomas Berton, Ph.D., will study how the DNA repair protein E2F1 prevents UV-induced Molecular Carcinogenesis.
Elucidating skin cancer signaling pathways
John DiGiovanni, Ph.D., was awarded two grants to investigate the role of the proteins Akt, mTOR and Stat3 in chemical and UV-induced epithelial Molecular Carcinogenesis. Increased understanding of these proteins may lead to chemoprevention strategies against cancer.
Understanding the link between obesity and pancreatic cancer
Obesity has increased dramatically over the past 30 years in the United States and has been associated with pancreatitis and pancreatic cancer, as well as other cancers. Professor Susan Fischer, Ph.D., has identified insulin-like growth factor-1 (IGF-1) as potential link between obesity and cancer susceptibility. This study will examine the role of IGF-1 in mediating anti-cancer effects.
Recruiting and training the next generation of scientist
Associate Professor Robin Fuchs-Young, Ph.D., is a leader designing and implementing programs to increase access to scientific training and educational opportunities for students in rural and underserved communities. She was awarded two grants to continue her science education initiatives, which include the MENTORS Project: Models of Educational Networking to Optimize Rural Science and the Environmental Health Sciences Summer Undergraduate Research Program. For more information about the programs lead by Fuchs-Young visit: http://sciencepark.mdanderson.org/outreach/index.html
Developing Mouse Models that mimic human cancers
Genetic differences among individuals play a major role in determining the response to environmental exposures and risk for developing disease. Professor David Johnson, Ph.D., is investigating how human DNA sequence variations (polymorphisms) in the p53 tumor suppressor protein influence cancer susceptibility. He has generated mouse models that are the first to mimic naturally occurring human polymorphisms. These mouse models will allow investigators to determine how genetic variation modulates the development of squamous cell carcinoma of the skin and head and neck.
Investigating structural DNA distortions
DNA structures that vary from the classic double helical structure are causative factors in genetic instability and human disease. Associate Professor Karen Vasquez, Ph.D., is studying how these structures can lead to genetic instability and cancer. Discoveries from this research should lead to a better understanding of the pathogenesis of cancers and other diseases that are caused by DNA damage and naturally occurring DNA distortions, and ultimately to the development of new approaches to treatment and prevention.
The role of environmental estrogens in developmental reprogramming and cancer
Developmental reprogramming is an important mechanism by which early life exposures to environmental agents increase susceptibility to adult disease. The xenoestrogen Bisphenol A (BPA), found in consumer plastic products, is a compound that resembles naturally occurring estrogens. Professor Cheryl Walker, Ph.D., was awarded a grant to investigate how neonatal xenoestrogen exposure contributes to the development of uterine leiomyoma, the most common gynecologic tumor in women. Walker was also awarded a Grand Opportunity grant to study how neonatal exposure to BPA leads to increased susceptibility to prostate cancer in adulthood. Grand Opportunity grants were awarded to high impact research projects that will significantly accelerate progress in an established scientific field and/or lay the foundation for new fields of research. These two studies will open opportunities to identify at risk populations for uterine and prostate cancers and will assist governmental agencies in setting regulatory guidelines for their safe use in consumer plastic products.
About MD Anderson
The University of Texas MD Anderson Cancer Center in Houston ranks as one of the world's most respected centers focused on cancer patient care, research, education and prevention. MD Anderson is one of only 40 comprehensive cancer centers designated by the National Cancer Institute. For six of the past eight years, including 2009, MD Anderson has ranked No. 1 in cancer care in “America's Best Hospitals,” a survey published annually in U.S. News & World Report. (Dec 2009)
NIH Awards MD Anderson 84 Research Grants from Stimulus Funds (Ten to the Department of Molecular Carcinogenesis)
Grand Opportunity Grants "GO" grants are designed to support high-impact ideas that lend themselves to short-term funding and may lay the foundation for new fields of investigation.
Synthetic Estrogen and Prostate Cancer Development Understanding the role of early exposure to bisphenol A (BPA), a synthetic estrogen used in the manufacture of plastics, and later development of prostate cancer, is the focus of a $1.9 million grant from the National Institute of Environmental Health Studies. Cheryl Walker, Ph.D., professor in the Department of Molecular Carcinogenesis, and colleagues will expose newborn rats to BPA and follow them into adulthood, correlating their later development of prostate cancer to BPA-induced epigenetic changes affecting the prostate. They also will analyze BPA's interaction with estrogen receptors. The project will provide new data for agencies that set regulatory guidelines for safe use of BPA.
Challenge grants Challenge grants are for novel research in topic areas that address specific scientific and health research challenges that would benefit from two-year jumpstart funding.
Cultivating Future Scientists, Starting in High School Amid growing concerns about future shortages of health-care providers and biomedical researchers, a potential long-term remedy is to engage high school students with enriched science, technology, engineering and math education. That's the premise of the MENTORS program funded by an $892,724 two-year grant from the National Center for Research Resources. The project focuses on rural, underserved and minority school districts where enriched science and career educational programs often are lacking. Led by principal investigator Robin Fuchs-Young, Ph.D., associate professor in the Department of Molecular Carcinogenesis, MENTORS will connect students with scientists in their labs and collaborate with teachers to increase awareness of research and technology careers. (Oct. 2009)
Dream Team Targets Key Driver for Breast, Ovarian, Endometrial Cancers
A Dream Team of leading cancer researchers will accelerate development of drugs to attack the PI3K molecular pathway that fuels endometrial, breast and ovarian cancers. The PI3K network normally promotes cell survival, growth and protein synthesis. When it is abnormally activated by genetic aberrations, it contributes to tumor progression, connects to other cancer-causing pathways and causes resistance to treatment. Dr. Cheryl Lyn Walker, Ph.D., Professor in the Department of Molecular Carcinogenesis is a member of the M.D. Anderson Dream Team. This three-year $15 million grant awarded by Stand Up To Cancer is one of five that bring top researchers from different institutions together to speed new cancer treatments to patients. Stand Up to Cancer, a program of the Entertainment Industry Foundation, is a novel charitable initiative that raised most of its funds during a telecast last September that aired simultaneously on ABC, NBC and CBS. (May 2009)
Protein "Switch" Suppresses Skin Cancer Development - When IKKa fails to keep cell replacement cycle in balance, cancer follows
The protein IKKalpha (IKKa) regulates the cell cycle of keratinocytes and plays a key role in keeping these specialized skin cells from becoming malignant, researchers at The University of Texas MD Anderson Cancer Center, Science Park report in the Sept. 9 issue of Cancer Cell. "We have shown that IKKa acts as a sentry, monitoring and, when necessary, halting proliferation of these important cells. In the first mouse model of its kind, we also found that deleting IKKa spontaneously induced squamous cell carcinomas by activating the epidermal growth factor receptor pathway," said senior author Yinling Hu, Ph.D., assistant professor in MD Anderson's Department of Molecular Carcinogenesis at the Science Park. "These results provide new therapeutic targets for prevention of skin cancer."(Sep. 2008)
Once Suspect Protein Found to Promote DNA Repair, Prevent Cancer
An abundant chromosomal protein that binds to damaged DNA prevents cancer development by enhancing DNA repair. The protein, HMBG1, was previously hypothesized to block DNA repair, says senior author Karen Vasquez, Ph.D. Identification and repair of DNA damage is the frontline defense against the birth and reproduction of mutant cells that cause cancer and other illnesses. Pinpointing HMBG1's role in repair raises a fundamental question about drugs under development to block the protein. The protein also plays a role in inflammation, so it's being targeted in drugs under development for rheumatoid arthritis and sepsis. These finds suggest that depleting this protein may leave patients more vulnerable to developing cancer.(Jul. 2008)
Calorie Restricted Diet Prevents Inflammation and Cancer
Prevention of weight gain with a restricted calorie diet sharply reduced the development of pancreatic lesions that lead to cancer in preclinical research reported by Science Park researchers at the American Association for Cancer Research annual meeting. The research, led by Stephen Hursting, Ph.D. along with post-doctoral fellow Dr. Laura Lashinger, sheds light on the connection between obesity, calorie intake and pancreatic cancer by comparing a calorie restricted diet, an overweight diet and an obesity-inducing diet in a strain of mice that spontaneously develops pancreatic lesions that lead to cancer.(Apr. 2008)
Calorie Restriction Limits and Obesity Fuels Development of Epithelial Cancers
A restricted-calorie diet inhibited the development of precancerous growths in a two-step model of skin cancer, reducing the activation of two signaling pathways known to contribute to cancer growth and development, researchers at The UT MD Anderson Cancer Center, Science Park reported at the American Association for Cancer Research annual meeting. Professor John DiGiovanni and graduate student Tricia Moore found that an obesity-induced diet, by contrast, activated those pathways. "These findings provide the basis for future translational studies targeting Akt/mTOR pathways through combinations of lifestyle and pharmacologic approaches to prevent and control obesity-related epithelial cancers in humans," DiGiovanni said. (Apr. 2008)
Chromatin Remodeling Complex Connected to DNA Damage Control
Xuetong "Snow" Shen, Ph.D., an assistant professor at the Science Park of MD Anderson, discovered that when molecular disaster strikes, causing structural damage to DNA, players in two important pathways talk to each other to help contain the wreckage. This connection between a signaling pathway crucial to DNA damage control and a pathway known as chromatin remodeling "opens up an entirely new category of targets for potentially attacking cancer." (Aug. 2007)
Protein Protects Anti-Cancer Gene from Chemical Shutdown
A protein that is largely absent in one type of skin cancer protects an important gene in a cell's defense against harmful mutations from being silenced, reports Yinling Hu, Ph.D., senior author of a paper in Molecular Cell and assistant professor in MD Anderson's Department of Molecular Carcinogenesis at the Science Park. (Jul. 2007)
Howard Hughes Medical Institute Awards Major Grant to Smithville Researcher
A five-year $750,000 grant has been awarded to Robin Fuchs-Young, Ph.D., Community Outreach and Education director and associate professor of Molecular Carcinogenesis at the Cockrell Cancer Research Center of the Science Park of MD Anderson Cancer Center, to fund a comprehensive program to enhance science and health education in Smithville schools and to promote community interest in science and biomedical research. (Jul. 2007)
MD Anderson Scientist Elected to Lead Society of Toxicology
Cheryl Lyn Walker, Ph.D., a professor at the Science Park of the UT MD Anderson Cancer Center, won a general election of the 5,800-member Society of Toxicology to serve as vice president-elect in 2007, vice president in 2008, and president in 2009. The SOT is the world's premier scientific group for those who work to understand, prevent and better treat the harmful effects of chemical, physical or biological agents on people, other living things and on ecosystems. (May 2007)
MD Anderson Science Park Wins $8.3-million Renewal to Study Environmental Causes of Major Diseases
An $8.3-million federal grant to The University of Texas MD Anderson Science Park addresses the complex interplay between such varied factors as genetics, diet, and environmental exposure to toxins that cause cancer, asthma, diabetes, cardiovascular and other diseases. (Apr. 2007)
Researchers Find Molecular 'Brake' to Cell Death; Discovery Could Yield New Target for Future Therapies
Researchers found that a natural "brake" exists in a cell to prevent it from undergoing apoptosis, or programmed cell death. This finding has direct implications for anti-cancer therapy and can be used to design more targeted chemotherapy drugs. (Jun. 2006)
When Good DNA Goes Bad
When otherwise normal DNA adopts an unusual shape called Z-DNA, it can lead to the kind of genetic instability associated with cancers such as leukemia and lymphoma. (Feb. 2006)
"In Those Genetically Predisposed, 'Developmental Reprogramming' Could Explain Cancer Risk"
Researchers at the Science Park may have uncovered the reason why some people who are genetically predisposed to hormone-dependent cancers develop the disease as an adult, while others who are similarly susceptible don’t. (May 2005)
"MD Anderson Researchers Discover Key Protein in Psoriasis: May be New Target for Treating Common Skin Condition"
Researchers have resolved a controversy over the cause of psoriasis and developed the first mouse model that fully mimics the human disorder. (Apr. 2005)
"Researchers Discover Potential Skin Cancer Prevention Target"
Scientists have identified a protein that serves as a master regulator of skin cancer - a finding that could lead to new ways to prevent skin cancer before it starts. (Nov. 2004)
For specific information regarding each staff member's research programs, please refer to the faculty information page.