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Archive - Oct 28, 2014

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Exosomes Used by Male Fruit Flies to Improve Their Mating Odds

There are many biological tools that help animals ensure reproductive success. A new study published in the August 25, 2014 issue of The Journal of Cell Biology provides further detail into how one such mechanism enables male fruit flies to improve their odds by stopping females from mating with other flies. In addition to sperm, semen carries products that foster sperm survival, promote egg fertilization, and serve other functions that optimize a male's chances of passing along his genes. In male fruit flies, for example, reproductive accessory glands (thought to be equivalent to the prostate gland in humans) secrete signaling factors into the seminal fluid that make the recipient females less inclined to remate. But it's unclear how some of these signaling factors are produced and delivered in order to reprogram a female's behavior against her own self-interest. Researchers from the University of Oxford identified tiny, membrane-bound vesicles called exosomes that are secreted into the seminal fluid by the so-called "secondary cells" of male accessory glands. The authors showed that, after mating, the exosomes fuse with sperm and interact with cells along the female reproductive tract. "Exosomes not only carry ligands that will bind to target cells, but they also carry receptors and intracellular signaling molecules inside them," explains senior author Dr. Clive Wilson, "so they potentially have a lot of possibilities in terms of their ability to reprogram cells." When the researchers reduced the number of exosomes produced by secondary cells, the female flies were more inclined to remate. This indicates that the exosomes are responsible for the behavioral changes, by interacting with the targeted female cells to overpower normal signaling pathways.

New 'Lab-on-a-Chip' for Exosome Analysis Could Revolutionize Early Diagnosis of Cancer

Scientists have been laboring to detect cancer and a host of other diseases in people using promising new biomarkers contained in vesicles called "exosomes." Indeed, Popular Science magazine named exosome-based cancer diagnostics one of the 20 breakthroughs that will shape the world this year. Exosomes could lead to less invasive, earlier detection of cancer, and sharply boost patients' odds of survival. "Exosomes are minuscule membrane vesicles — or sacs — released from most, if not all, cell types, including cancer cells," said Dr. Yong Zeng, assistant professor of chemistry at the University of Kansas. "First described in the mid-'80s, they were once thought to be 'cell dust,' or trash bags containing unwanted cellular contents. However, in the past decade scientists realized that exosomes play important roles in many biological functions through capsuling and delivering molecular messages in the form of nucleic acids and proteins from the donor cells to affect the functions of nearby or distant cells. In other words, this forms a crucial pathway in which cells talk to others." While the average piece of paper is about 100,000 nanometers thick, exosomes run just 30 to 150 nanometers in size. Because of this, exosomes are hard to separate out and test, typically requiring multiple-step ultracentrifugation — a tedious and inefficient process requires long stretches in the lab, according to scientists. "There aren't many technologies out there that are suitable for efficient isolation and sensitive molecular profiling of exosomes," said Dr. Zeng. "First, current exosome isolation protocols are time-consuming and difficult to standardize. Second, conventional downstream analyses on collected exosomes are slow and require large samples, which is a key setback in clinical development of exosomal biomarkers." Now, Dr.

Tiny Exosomes Show Huge Potential in Clinical Medicine; ASEMV Holds Annual Meeting

Over two hundred visionary scientists, pragmatic physicians, and savvy biotech sales reps from the United States and around the world gathered from October 10-13, 2014, to discuss the latest advances in research and technology related to exosomes, a new and extremely hot area of science with possibly huge potential for game-changing applications in clinical medicine. The occasion was the fourth annual meeting of the American Society for Exosomes and Microvesicles (ASEMV). The site was the magnificently beautiful Asilomar Conference Grounds bordering the Pacific Ocean on Northern California’s Monterey Peninsula. This meeting was organized by Stephen Gould, M.D., President of the ASEMV, Professor of Biological Chemistry at The Johns Hopkins University School of Medicine, and an expert on exosome biogenesis; and by Douglas Taylor, Ph.D., Secretary-General of the ASEMV, formerly a professor at the University of Louisville, an exosome pioneer, and now the chief scientific officer (CSO) of a year-old start-up company called Exosome Sciences, Inc., located just outside Princeton, New Jersey, and a majority-owned subsidiary of Aethlon Medical, Inc. There was also notable organizational assistance from Sasha Vlassov, Ph.D., from Life Technologies (Thermo Fisher Scientific, Inc.), from Travis Antes of System Biosciences, Inc. (SBI), and from many of the graduate students in Dr. Gould’s lab.

Salk Findings Point to an "Off Switch" for Drug Resistance in Cancer

Like a colony of bacteria or species of animal, cancer cells within a tumor must evolve to survive. A dose of chemotherapy may kill hundreds of thousands of cancer cells, for example, but a single cell with a unique mutation can survive and quickly generate a new batch of drug-resistant cells, making cancer hard to combat. Now, scientists at the Salk Institute have uncovered details about how cancer is able to become drug-resistant over time, a phenomenon that occurs because cancer cells within the same tumor are not identical–the cells have slight genetic variation, or diversity. The new work, published online on October 22, 2014 in PNAS, shows how variations in breast cancer cells’ RNA, the molecule that decodes genes and produces proteins, helps the cancer to evolve more quickly than previously thought. These new findings may potentially point to a “switch” to turn off this diversity–and thereby drug resistance–in cancer cells. “It’s an inherent property of nature that in a community–whether it is people, bacteria, or cells–a small number of members will likely survive different types of unanticipated environmental stress by maintaining diversity among its members,” says the senior author of the new work, Dr. Beverly Emerson, professor of Salk’s Regulatory Biology Laboratory and holder of the Edwin K. Hunter Chair. “Cancer co-opts this diversification strategy to foster drug resistance.” Instead of looking at a single gene or pathway to target with cancer therapies, lead author Fernando Lopez-Diaz, Ph.D., Salk staff scientist, and the team aim to uncover the diversification “switch” by which cancer cells replicate, but vary slightly from one another. Turning off this cellular process would strip cancer’s ability to survive drug treatment. “Cancer isn’t one cell but it’s an ecosystem, a community of cells,” says Dr. Emerson.