About 600 million people around the world live with whipworms (image). Most are children in the developing world, whose physical and mental development is stunted by these gastrointestinal parasites. The whipworms affect the children’s ability to learn and therefore have a long-term impact on the social and economic situations of some of the world's poorest people. Although the whipworm species Trichuris trichiura is known to inhabit both non-human primates and humans, little is known about the parasite. Indeed, until a recent study by Ria Ghai, a doctoral student in biology at McGill University in Canada, it was widely assumed that a single species was capable of infecting both primates and humans. But Ghai has discovered that there are three genetically distinct groups of whipworms - and only one of the three appears to be transmissible between humans and non-human primates. It is important information for public health officers around the world. Ghai's research, published on October 23, 2014 in the open-access journal PLoS Neglected Tropical Diseases, was done in the rainforest of Kibale National Park in southwestern Uganda, which has one of the largest concentrations of primates in the world. The trees are alive with monkeys, and include endangered species such as the red colobus monkey, the eastern chimpanzee, and the rare l'hoest's monkey, as well as more common species, like baboons. In all, there are 13 different species of primates within the park. But the park is an island of forest within one of the most densely populated agricultural regions in East Africa, with a population of 300-600 people per square kilometer. And there is increasing human pressure on limited land and growing interaction between the humans and the non-human primates.
A team led by Professor Mike Berridge from the Malaghan Institute of Medical Research in Wellington, New Zealand, and Professor Jiri Neuzil from the Griffith University, Queensland, Australia, has become the first in the world to demonstrate mitochondrial DNA movement between cells in an animal tumor. Their paper was published in the January 6, 2015 issue of the biological journal Cell Metabolism. The research lays important groundwork for understanding human diseases other than cancer, because defective mitochondrial DNA is known to account for approximately 200 diseases and is implicated in many more. It could also usher in a new field where synthetic mitochondrial DNA is custom-designed to replace defective genes. In mouse models of breast cancer and melanoma that had had their mitochondrial DNA removed, replacement DNA was acquired from surrounding normal mouse tissue. After adopting this new DNA, the cancer cells went on to form tumors that spread to other parts of the body. Professor Berridge says the landmark discovery could open up whole new areas of research. “Our findings overturn the dogma that genes of higher organisms are usually constrained within cells except during reproduction. It may be that mitochondrial gene transfer between different cells is actually quite a common biological occurrence.” Although other research groups have seen mitochondrial DNA move between cells in the laboratory, the Malaghan team is the first to demonstrate the transfer in an animal tumor model. Professor Berridge says the research wouldn’t have happened without the extraordinary patience of his research colleague, An Tan. “A normal person would have terminated the experiment after a week, before this effect was observed, thinking that the tumor cells without mitochondrial DNA weren’t going to grow.
Researchers at Oregon State University (OSU) have developed a new way to selectively insert compounds into cancer cells - a system that will help surgeons identify malignant tissues and then, in combination with phototherapy, kill any remaining cancer cells after a tumor is removed. It's about as simple as, "If it glows, cut it out." And if a few malignant cells remain, they'll soon die. The findings, published online on November 14, 2014 in the journal Nanoscale, describe remarkable success in laboratory animals. The technique should allow more accurate surgical removal of solid tumors at the same time as it eradicates any remaining cancer cells. In laboratory tests, it completely prevented cancer recurrence after phototherapy. Technology such as this, scientists said, may have a promising future in the identification and surgical removal of malignant tumors, as well as using near-infrared light therapies that can kill remaining cancer cells, both by mild heating of them and by generating reactive oxygen species that can also kill them. "This is kind of a double attack that could significantly improve the success of cancer surgeries," said Dr. Oleh Taratula, an assistant professor in the OSU College of Pharmacy. "With this approach, cancerous cells and tumors will literally glow and fluoresce when exposed to near-infrared light, giving the surgeon a precise guide about what to remove," Dr. Taratula said. "That same light will activate compounds in the cancer cells that will kill any malignant cells that remain. It's an exciting new approach to help surgery succeed." The work is based on the use of a known compound called naphthalocyanine, which has some unusual properties when exposed to near-infrared light.
A large whale that can live over 200 years with little evidence of age-related disease may provide untapped insights into how to live a long and healthy life. In an open-access report published as the cover story of the January 6, 2015 issue of the Cell Press journal Cell Reports, researchers present the complete bowhead whale genome sequence and identify key differences compared to other mammals. Alterations in bowhead genes related to cell division, DNA repair, cancer, and aging may have helped increase this whale’s longevity (it is the longest-lived mammal) and its resistance to cancer. "Our understanding of species' differences in longevity is very poor, and thus our findings provide novel candidate genes for future studies," says senior author Dr. João Pedro de Magalhães, of the University of Liverpool, in the UK. "My view is that species evolved different 'tricks' to have a longer lifespan, and by discovering the 'tricks' used by the bowhead we may be able to apply those findings to humans in order to fight age-related diseases." Also, large whales with over 1,000 times more cells than humans do not seem to have an increased risk of cancer, suggesting the existence of natural mechanisms that can suppress cancer more effectively than cancer suppression mechanisms in other animals. Dr. Magalhães and his team would next like to breed mice that will express various bowhead genes, with the hopes of determining the importance of different genes for longevity and resistance to diseases. The researches also note that because the bowhead's genome is the first among large whales to be sequenced, the new information may help reveal physiological adaptations related to size.
Cell biologists at the University of Texas (UT) Southwestern Medical Center have targeted telomeres (see image) with a small molecule called 6-thiodG that takes advantage of the cell's “biological clock” to kill cancer cells and shrink tumor growth. Dr. Jerry W. Shay, Professor and Vice Chairman of Cell Biology at UT Southwestern, and colleague, Dr. Woodring E. Wright, Professor of Cell Biology and Internal Medicine, found that 6-thio-2'-deoxyguanosine (6-thiodG) could stop the growth of cancer cells in culture and decrease the growth of tumors in mice. "We observed broad efficacy against a range of cancer cell lines with very low concentrations of 6-thiodG, as well as tumor burden shrinkage in mice," said Dr. Shay, Associate Director of the Harold C. Simmons Comprehensive Cancer Center. Dr. Shay and Dr. Wright, who hold The Southland Financial Corporation Distinguished Chair in Geriatrics, are co-senior authors of the paper published online on December 16, 2014 in Cancer Discovery. 6-thiodG acts by targeting a unique mechanism that is thought to regulate how long cells can stay alive, a type of aging clock. This biological clock is defined by DNA structures known as telomeres, which cap the ends of the cell's chromosomes to protect them from damage, and which become shorter every time the cell divides. Once telomeres have shortened to a critical length, the cell can no longer divide and dies though a process known as apoptosis. Cancer cells are protected from this death by an RNA protein complex called telomerase, an enzyme that ensures that telomeres do not shorten with every division. Telomerase has therefore been the subject of intense research as a target for cancer therapy.
Cholera is caused when the bacterium Vibrio cholerae infects the small intestine. The disease is characterized by acute watery diarrhea resulting in severe dehydration. EPFL (École Polytechnique Fédérale de Lausanne ) scientists in Switzerland have now demonstrated that V. cholerae uses a tiny spear to stab and kill neighboring bacteria - even of its own kind - and then steal their DNA. This mechanism, known as "horizontal gene transfer," allows the cholera bacterium to become more virulent by absorbing the traits of its prey. The study is published in the January 2, 2015 issue of Science. The laboratory of Dr. Melanie Blokesch at EPFL has uncovered how V. cholerae uses a predatory killing device to compete with surrounding bacteria and steal their DNA. This molecular killing device is essentially a spring-loaded spear that is constantly shooting out. This weapon is called the "type VI secretion system" (T6SS) and is known to exist in many types of bacteria. When V. cholerae comes close to other bacteria, the spear punches a hole into them, leaving them to die and release their genetic material, which the predator pulls into itself. This spear-killing, predatory behavior is triggered by the bacterium's environment. The cholera bacterium naturally lives in water, such as the sea, where it attaches onto small planktonic crustaceans. There, it feeds on the main component of their shells: a sugar polymer called chitin. When chitin is available, V. cholerae goes into an aggressive survival mode called "natural competence." When in this mode, V. cholerae attacks neighboring bacteria with its spear - even if they are of the same species. Dr. Blokesch set out to explore how V. cholerae uses this behavior to compete for survival in nature.
Scientists from the Johns Hopkins Kimmel Cancer Center have created a statistical model that measures the proportion of cancer incidence, across many tissue types, caused mainly by random mutations that occur when stem cells divide. By their measure, two-thirds of adult cancer incidence across tissues can be explained primarily by “bad luck,” when these random mutations occur in genes that can drive cancer growth, while the remaining third are due to environmental factors and inherited genes. “All cancers are caused by a combination of bad luck, the environment, and heredity, and we’ve created a model that may help quantify how much of these three factors contribute to cancer development,” says Bert Vogelstein, M.D., the Clayton Professor of Oncology at the Johns Hopkins University School of Medicine, Co-Director of the Ludwig Center at Johns Hopkins, and an Investigator at the Howard Hughes Medical Institute. Dr. Vogelstein is an acknowledged giant in the field of cancer genetics and among his myriad accomplishments over many years of stellar work were, with colleagues, the determination that the TP53 gene coding for the p53 tumor suppressor protein, the so-called "Guardian of the Genome," is the most frequently mutated gene in cancers and the discovery of the genes responsible for hereditary non-polyposis colorectal cancer (HNPCC). “Cancer-free longevity in people exposed to cancer-causing agents, such as tobacco, is often attributed to their ‘good genes,’ but the truth is that most of them simply had good luck,” adds Dr. Vogelstein, who cautions that poor lifestyles can add to the bad luck factor in the development of cancer. The implications of the new model range from altering public perception about cancer risk factors to the funding of cancer research, the authors say.
University of California (Berkeley) herpetologist Dr. Jim McGuire was slogging through the rain forests of Indonesia's Sulawesi Island one night this past summer when he grabbed what he thought was a male frog and found himself juggling not only a frog but also dozens of slippery, newborn tadpoles. He had found what he was looking for: direct proof that the female of a new species of frog does what no other frog does. It gives birth to live tadpoles instead of laying eggs. A member of the Asian group of fanged frogs, the new species was discovered a few decades ago by Indonesian researcher Dr. Djoko Iskandar, McGuire's colleague, and was thought to give direct birth to tadpoles, though the frog's mating and an actual birth had never been observed before. "Almost all frogs in the world - more than 6,000 species - have external fertilization, where the male grips the female in amplexus and releases sperm as the eggs are released by the female," Dr. McGuire said. "But there are lots of weird modifications to this standard mode of mating. This new frog is one of only 10 or 12 species that has evolved internal fertilization, and of those, it is the only one that gives birth to tadpoles as opposed to froglets or laying fertilized eggs." Dr. Iskander, Dr. McGuire and Dr. Ben Evans of McMaster University in Ontario, Canada, named the species Limnonectes larvaepartus and fully described it in an article published online on December 31, 2014 in the open-access journal PLOS ONE. Frogs have evolved an amazing variety of reproductive methods, says Dr. McGuire, an associate professor of integrative biology and curator of herpetology at UC Berkeley's Museum of Vertebrate Zoology. Most male frogs fertilize eggs after the female lays them.
Women with atypical hyperplasia of the breast have a higher risk of developing breast cancer than previously thought, a Mayo Clinic study has found. The authors note that measures to prevent the progression of atypical hyperplasia to cancer are available but underutilized. Results of the Mayo study, including work from colleagues at Vanderbilt University and the University of Virginia, appear in a special report on breast cancer published online on January 1, 2015 in the New England Journal of Medicine. Atypical hyperplasia of the breast is a precancerous condition found in about one-tenth of the over 1 million breast biopsies with benign findings performed annually in the United States. Viewed under a microscope, atypia contains breast cells that are beginning to grow out of control (hyperplasia) and cluster into abnormal patterns (atypical). Atypia lesions are considered benign, but by its risk and appearance and genetic changes, these lesions exhibit some of the early features of cancer. Data from hundreds of women with these benign lesions indicate that their absolute risk of developing breast cancer grows by over 1 percent a year. The study found that after five years, 7 percent of these women had developed the disease; after 10 years, that number had increased to 13 percent; and after 25 years, 30 percent had breast cancer. The finding places the more than 100,000 women diagnosed each year with atypical hyperplasia -- also known as atypia -- into a high-risk category, where they are more likely to benefit from intense screening and use of medications to reduce risk. "By providing better risk prediction for this group, we can tailor a woman's clinical care to her individual level of risk," says Lynn Hartmann, M.D., an oncologist at the Mayo Clinic and lead author of the study.
In a press release issued on December 31, 2014, the American Cancer Society announced that its annual cancer statistics report finds that there has been a 22% drop in cancer mortality in the United States over two decades, leading to the avoidance of more than 1.5 million cancer deaths that would have occurred if peak rates had persisted. And while cancer death rates have declined in every state, the report finds substantial variation in the magnitude of these declines, generally with the states in the South showing the smallest decline and in the Northeast the largest decline. Each year, the American Cancer Society compiles the most recent data on cancer incidence, mortality, and survival based on incidence data from the National Cancer Institute and the Centers for Disease Control and Prevention, and mortality data from the National Center for Health Statistics. The data are disseminated in two reports: Cancer Statistics 2015, that will be published online in CA: A Cancer Journal for Clinicians on January 5, 2015, and also in its companion, consumer-friendly publication, Cancer Facts & Figures 2015 on January 5, 2015. The reports also estimate the number of new cancer cases and deaths expected in the United States in the current year. Largely driven by rapid increases in lung cancer deaths among men as a consequence of the tobacco epidemic, the overall cancer death rate rose during most of the 20th century, peaking in 1991. The subsequent steady decline in the cancer death rate is the result of fewer Americans smoking, as well as advances in cancer prevention, early detection, and treatment. During the most recent five years for which data are available (2007-2011), the average annual decline in cancer death rates was slightly larger among men (1.8%) than women (1.4%).