Syndicate content

Archive - Apr 20, 2015

Discovery of Gene Involved in Determining Melting Point of Cocoa Butter May Have Major Economic Impact; Current Global Cocoa Production Valued at $11.8 Billion; New Specialty Chocolates, Cosmetics, and Pharmaceuticals Envisioned

The discovery of a gene involved in determining the melting point of cocoa butter -- a critical attribute of the substance widely used in foods and pharmaceuticals -- will likely lead to new and improved products, according to researchers in Penn State's College of Agricultural Sciences. The finding by plant geneticists also should lead to new varieties of the cocoa plant that could extend the climate and soil-nutrient range for growing the crop and increase the value of its yield, they said, providing a boost to farmers' incomes in the cocoa-growing regions of the world. Cacao, Theobroma cacao L., is an understory tropical tree domesticated in the Amazon basin and today widely cultivated in West Africa, Central and South America, and Southeast Asia. Around the world, more than five million cocoa farmers -- and more than 40 million people total -- depend on cocoa for their livelihood, according to the World Cocoa Foundation, which puts annual cocoa production worldwide at 3.8 million tons, valued at $11.8 billion. Cacao pods, each containing around 40 seeds, are harvested approximately 20 weeks after pollination. The seeds contain about 50 percent total lipids (cocoa butter), which provides a main raw ingredient for chocolate manufacturing, as well as ingredients for pharmaceutical and cosmetic products. Cocoa butter with altered melting points may find new uses in specialty chocolates, cosmeticsm and pharmaceuticals, said lead researcher Dr. Mark Guiltinan, Professor of Plant Molecular Biology, who has been conducting research on the cacao tree for three decades. For example, a chocolate with a higher or lower melting point would be useful for production of chocolate with specific textures and specialty applications.

Draft Genome for Upland Cotton—Which Accounts for More Than 90% of the World’s Cultivated Cotton and $500 Billion in Economic Impact—Is Established; Should Prove Resource for Engineering Superior Cotton Lines and Fiber Improvement

In a groundbreaking achievement led by an international team that includes Clemson (South Carolina) scientist Dr. Chris Saski, the intricately woven genetic makeup of Upland cotton has been decoded for the first time in the ancient plant's history. Dr. Saski participated in sequencing the genome, which is a crucial stepping-stone toward further advancements of understanding the inner workings of one of the most complex and treasured plants on the planet. The future implications of Dr. Saski's and his colleagues’ research, in the short and long terms, are both financial and holistic. Upland cotton, which accounts for more than 90 percent of cultivated cotton worldwide and has a global economic impact of $500 billion, is the main source of renewable textile fibers. The draft genome sequence, unveiled April 20, 2015 in an online, open-access article in Nature Biotechnology, will provide the know-how to engineer superior lines that will help clothe, feed, and fuel the ever-expanding human population. The Nature Biotechnology article is titled “Sequencing of Allotetraploid Cotton (Gossypium hirsutum L. acc. TM-1) Provides a Resource for Fiber Improvement.” "From the discovery standpoint - having a solid foundation to begin measuring genetic diversity and how the genes are organized - this is a game-changer," said Dr. Saski, Director of Clemson's Genomics and Computational Biology Laboratory. "With a genome map and genetically diverse populations, you can reveal the biology and DNA signature underlying cotton fiber development. Then you can use this information to breed cotton lines with advanced fiber elongation and fiber strength, which are crucial to the industry.

With Systemic Administration in Animal Models, Common Topical Drugs for Athlete’s Foot and Eczema Both Stimulate Body's Own Stem Cells to Replace Brain Cells Lost in Multiple Sclerosis and Enhance Remyelination

A pair of topical medicines already alleviating skin conditions each may prove to have another, even more compelling use: instructing stem cells in the brain to reverse damage caused by multiple sclerosis. Led by researchers at Case Western Reserve School of Medicine, a multi-institutional team used a new discovery approach to identify drugs that could activate mouse and human brain stem cells in the laboratory. The two most potent drugs - one that currently treats athlete's foot (miconazole), and the other (clobetasol), eczema - were capable of stimulating the regeneration of damaged brain cells and reversing paralysis when administered systemically to animal models of multiple sclerosis. The results were published online on Monday, April 20, in Nature. The article is titled “Drug-Based Modulation of Endogenous Stem Cells Promotes Functional Remyelination in Vivo.” "We know that there are stem cells throughout the adult nervous system that are capable of repairing the damage caused by multiple sclerosis, but until now, we had no way to direct them to act," said Paul Tesar, Ph.D., the Dr. Donald and Ruth Weber Goodman Professor of Innovative Therapeutics, and Associate Professor in the Department of Genetics & Genome Sciences at the Case Western Reserve School of Medicine. "Our approach was to find drugs that could catalyze the body's own stem cells to replace the cells lost in multiple sclerosis." The findings mark the most promising developments to date in efforts to help the millions of people around the world who suffer from multiple sclerosis. The disease is the most common chronic neurological disorder among young adults, and results from aberrant immune cells destroying the protective coating, called myelin, around nerve cells in the brain and spinal cord.

Possible Cure for Hepatitis B Virus (HBV) Infection; 2 Billion People Infected Worldwide; 400 Million Have Chronic Infections; 780,000 Deaths Annually; Human Clinical Trials Underway in Australia

Australian scientists have found a potential cure for hepatitis B virus (HBV) infections, with a promising new treatment proving 100 per cent successful in eliminating the infection in preclinical models. Australian patients are now the first in the world to have access to the potential treatment - a combination of an antiviral drug and an anti-cancer drug - which is in phase 1/2a clinical trials in Melbourne, Perth, and Adelaide. Scientists from Melbourne's Walter and Eliza Hall Institute developed the combination treatment using birinapant, a drug developed by U.S. biotech company TetraLogic Pharmaceuticals ( for treating cancer. Hepatitis B is a chronic viral disease that is currently incurable. Dr. Marc Pellegrini (photo), Dr. Greg Ebert, and colleagues at the Institute used their studies of the behavior of hepatitis B virus in infected cells as a basis for the treatment. The research was published online on April 20, 2015 in two papers in PNAS. Dr. Pellegrini said the treatment was successful in curing infections in preclinical models, leading to a human trial that began in December 2014. "We were 100 per cent successful in curing HBV infection in hundreds of tests in preclinical models," Dr. Pellegrini said. "Birinapant enabled the destruction of hepatitis B-infected liver cells while leaving normal cells unharmed. Excitingly, when birinapant was administered in combination with current antiviral drug entecavir, the infection was cleared twice as fast compared with birinapant alone.

AACR ANNUAL MEETING: Gene Signatures (COXEN Model) Can Predict Doxorubicin Response in Canine Osteosarcoma; Similar Approach May Also Prove Useful in Human Cancers

There are two chemotherapies commonly used to treat bone cancer in dogs: doxorubicin and carboplatin. Some dogs respond better to one drug than to the other. But until now, the choice has been left largely to chance. New work by University of Colorado (CU) Cancer Center members at Colorado State University Flint Animal Cancer Center and presented on April 19, 2015 at the American Association for Cancer Research (AACR) Annual Meeting 2015 (April 18-22, 2015, in Philadelphia) demonstrates a gene expression model that predicts canine osteosarcoma response to doxorubicin, potentially allowing veterinary oncologists to better choose which drug to use with their canine patients. The approach is adopted from, and further validates, a model known as COXEN (CO-eXpression gEne aNalysis), developed at the CU Cancer Center by Center Director Dan Theodorescu, M.D., Ph.D., and which is currently in clinical trials to predict the response of human tumors to drugs. "This is a cool thing for us, showing that we can use human models in canine cancer, and hinting that the reverse might also be true: the lessons we learn from canine osteosarcoma may help us better understand the human disease," says Daniel L. Gustafson, Ph.D., CU Cancer Center Investigator and Director for Basic Research at the Flint Animal Cancer Center. The COXEN model depends on the idea that cancer can be defined as the sum of its genetic alterations. Rather than looking at a cancer by its site in the body - say lung cancer or prostate cancer or breast cancer - the COXEN model evaluates a panel of genes known to be important to the development of cancer and uses gene expression to label the cancer with a genetic signature.

AACR ANNUAL MEETING: Oral Milk Thistle Extract (Silibinin) Stops Colorectal Cancer Stem Cells from Growing Tumors; University of Colorado Cancer Group Sees Future Human Clinical Trial As Likely

In results presented at the American Association for Cancer Research (AACR) Annual Meeting 2015 (April 18-22, 2015, in Philadelphia), a University of Colorado (CU) Cancer Center study shows that orally administering the chemical silibinin, purified from milk thistle, slows the ability of colorectal cancer stem cells to grow the disease. When stem cells from tumors grown in silibinin-fed conditions were re-injected into new models, the cells failed to develop equally aggressive tumors even in the absence of silibinin. "It's very simple: tumors from mice that were initially fed silibinin had fewer cancer stem cells, were smaller, had lower metabolisms and showed decreased growth of new blood vessels. Importantly, when these cancer stem cells from tumors in mice fed silibinin were re-injected into new mice, we found these stem cells had lost their potential to repopulate even in the absence of silibinin exposure," says Rajesh Agarwal, Ph.D., Co-Program Leader of Cancer Prevention and Control at the CU Cancer Center and Professor at the Skaggs School of Pharmacy and Pharmaceutical Sciences. Silibinin is a non-toxic, potentially chemopreventive agent derived from milk thistle seeds. Results presented by Dr. Agarwal and colleagues at last year's AACR Annual Meeting showed that, in cell cultures, silibinin affects cell signaling associated with the formation and survival of colorectal cancer stem cells. The current study extends this promising line of research into mouse models. Specifically, the group used sorted colorectal cancer stem cells to grow tumors in mice that were either fed or not fed with silibinin. Tumor growth was measured by visible size, MRI scan, and measurement of tumor metabolism (glucose use).