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ScienceDaily (Jan. 15, 2012) — Scientists working at the Medical Research Council have identified changes in the patterns of sugar molecules that line pre-cancerous cells in the esophagus, a condition called Barrett’s dysplasia, making it much easier to detect and remove these cells before they develop into esophageal cancer. These findings, reported in the journal Nature Medicine, have important implications for patients and may help to monitor their condition and prevent the development of cancer.
Esophageal cancer is the fifth biggest cause of cancer death in the United Kingdom and the eighth leading cause of cancer deaths for men in the United States. Moreover, the number of people diagnosed with this disease is increasing rapidly. Individuals with a pre-cancerous condition known as Barrett’s esophagus are at an increased risk of developing esophageal cancer, and need to be closely monitored to make sure that the disease is not progressing.
Dysplasia offers a stage at which cancer can be prevented by removing these cells. However correctly identifying these areas has proved to be problematic, as they can easily be missed during endoscopy and biopsy, which only take samples from a small part of the esophagus. This can result in false reassurance for patients in whom their dysplasia has been missed, and conversely those without dysplasia having to undergo further unnecessary treatments.
The team, based at the MRC Cancer Cell Unit in Cambridge, was led by Dr. Rebecca Fitzgerald and included New York University’s Lara Mahal, an associate professor of chemistry, and William Eng, a laboratory technician.
The researchers discovered a new mechanism for identifying Barrett’s dysplasia cells by spraying on a fluorescent probe that sticks to sugars and lights up any abnormal areas during endoscopy. By analyzing the sugars present in human tissue samples taken from different stages on the pathway to cancer — using microarray technology developed by NYU’s Mahal — they found that there were different sugar molecules present on the surface of the pre-cancerous cells. This technology uses sugar binding proteins, known as lectins, to identify changes in sugars and pinpointed carbohydrate binding wheat germ proteins as a potential diagnostic. When the wheat germ proteins, attached to a fluorescent tag that glows under a specific type of light, were sprayed onto tissue samples, it showed decreased binding in areas of dysplasia, and these cells were clearly marked compared with the glowing green background.
“The rise in cases of esophageal cancer both in the UK and throughout the Western world means that it is increasingly important to find ways of detecting it as early as possible,” Fitzgerald said. “Our work has many potential benefits for those with Barrett’s esophagus who have an increased risk of developing esophageal cancer.”
“We have demonstrated that binding of a wheat germ protein, which is cheap and non-toxic, can identify differences in surface sugars on pre-cancerous cells,” she added. “And when coupled with fluorescence imaging using an endoscopic camera, this technique offers a promising new way of finding and then treating patients with the highest risk of developing esophageal cancer, at the earliest stage.”
ScienceDaily (Jan. 13, 2012) — In a typical working week, people spend on average 5 hours and 41 minutes per day sitting at their desk and 7 hours sleeping at night. Prolonged sitting at your desk is not only bad for your physical health, but potentially your mental well-being.
These are some of the key findings of research being presented the 13th of January, by Dr Myanna Duncan, Mr. Aadil Kazi and Professor Cheryl Haslam from the Work & Health Research Centre, Loughborough University, to delegates at the British Psychological Society’s Annual Occupational Conference, at the Crowne Plaza, Chester.
Nearly 70% of employees surveyed did not meet recommended guidelines for physical activity; interestingly 50% of people surveyed aged 50 years and under, failed to meet these guidelines.
The findings also showed:
- That those who sit for longer at work are more likely to sit outside of work.
- A correlation between BMI scores and sitting time at work, as one would expect
- That more time spent sitting at work was associated with a decrease in mental well-being.
The findings were a subset of a larger study looking at employee’s experiences of Occupational Health provision, over an 18 month period during 2009-2011. The psychologists conducted an on-line and paper based survey with over 1000 employees measuring employee’s use and experiences of occupational health services and their physical activity levels.
Specific measures included Lifestyle and physical activity, Domain Specific Sitting Time Questionnaire, Work Ability Index, General Health Questionnaire and Job Attitudes (job satisfaction, organisational commitment, job motivation, intention to quit). Interviews and focus groups with Occupational Health professionals were also conducted.
In the UK, as elsewhere in Europe, there are now twice as many workers aged 50 and over as there are aged 25 or younger. Health, work and well-being have been identified by Dame Carol Black as a key Government priority in order to maintain the health of all workers across their lifespan so as they are able to continue working healthily and productively into their 70s.
Dr Duncan says “People don’t need a psychologist to tell them to get up and walk around. But if it helps, I’d tell them to put a post-it note on their computer to remind them. Anyway go and talk to your colleagues face to face, it’s a lot more sociable and better for you than emailing them.”
ScienceDaily (Jan. 13, 2012) — Researchers have discovered that a subtype of leukemia characterized by a poor prognosis is fueled by mutations in pathways distinctly different from a seemingly similar leukemia associated with a much better outcome. The findings from the St. Jude Children’s Research Hospital — Washington University Pediatric Cancer Genome Project (PCGP) highlight a possible new strategy for treating patients with this more aggressive cancer.
The work provides the first details of the genetic alterations fueling a subtype of acute lymphoblastic leukemia (ALL) known as early T-cell precursor ALL (ETP-ALL). The results suggest ETP-ALL has more in common with acute myeloid leukemia (AML) than with other subtypes of ALL. The study appears in the January 12 edition of the journal Nature.
ALL is the most common childhood cancer and about 12 percent of patients have T-ALL. T-ALL arises from T-lineage white blood cells that make up one branch of the immune system. ETP-ALL was discovered by St. Jude researchers and accounts for about 12 percent of T-cell ALL. Many ETP-ALL patients fail to respond to current therapy and never enter remission. Only 30 to 40 percent of these patients become long-term survivors, compared to about 80 percent of children battling other T-ALL subtypes.
“The mutations and gene expression profile we identified in this study suggest that patients with ETP-ALL might benefit from treatment that includes drugs developed for treatment of acute myeloid leukemia,” said Charles Mullighan, M.D., Ph.D., an associate member of the St. Jude Department of Pathology and one of the study’s corresponding authors.
Mullighan said ETP-ALL was selected for inclusion in the pediatric cancer genome project due to the poor outcome and the lack of information on the genetic lesions that underlie this aggressive subtype of leukemia. “St. Jude is a pioneer in increasing overall ALL survival rates, which today exceed 90 percent for St. Jude patients. Now we are working toward similar progress against this rare form of the disease,” he said.
The human genome is the complete set of instructions needed to assemble and sustain human life. Leukemia and other cancers develop when normal cells accumulate mutations in the genome that cause the unchecked cell growth that is a hallmark of cancer. The three-year Pediatric Cancer Genome Project is sequencing the genomes of tumor cells and matched normal DNA samples of 600 children with some of the most poorly understood and aggressive cancers. Investigators believe the findings will be the foundation for the next generation of clinical tools.
For this study, researchers sequenced and analyzed the normal and cancer genomes of 12 St. Jude patients with ETP-ALL. Investigators then checked for some of the same mutations in an additional 94 young leukemia patients with either ETP-ALL or other types of T-cell ALL.
“We found mutations unique to ETP-ALL that are not seen in other forms of ALL,” said co-author Richard Wilson, Ph.D., director of The Genome Institute at Washington University. “The results provide new targets for therapy and a way to use genetic tests to identify ETP-ALL patients early and earmark them for more aggressive therapy.” The pattern of mutations identified in ETP-ALL was reminiscent of changes associated with AML, Mullighan said. The alterations were concentrated in genes in the cytokine receptor and RAS signaling pathways that are involved in the type of cell regulation disrupted in cancer. The mutations, which included NRAS, FLT3, JAK3, IL7R and other genes, were found in about 67 percent of patients with ETP-ALL, but in only 19 percent of other T-ALL patients.
In addition, mutations in genes known or predicted to disrupt normal development of blood stem cells or lymphocytes were identified in 58 percent of ETP-ALL patients, but in just 17 percent of other T-ALL patients. The affected genes included ETV6, RUNX1, IKZF1 and GATA3. GATA3 helps regulate the early stages of T cell development, and mutations in the gene were found exclusively in ETP-ALL patients.
Epigenetic mutations, which are alterations affecting genes that indirectly influence the activity of other genes, were also more common in ETP-ALL patients. These genes, including EZH2 and SUZ12, were mutated or deleted in 45 percent of ETP-ALL patients, but in just 11 percent of the comparison group. The targeted genes modify proteins known as histones, which control gene activity through DNA binding.
Researchers also showed that ETP-ALL includes recurring mutations in about a half-dozen genes not previously linked to blood cancers. The list includes the genes RELN and DNM2. “The pattern of mutations we found in those genes suggests they function as tumor suppressors and their loss contributes to the malignant transformation of developing blood cells,” Mullighan said.
Mullighan said work is under way to develop laboratory models of human ETP-ALL and to use these models to identify AML drugs that are most likely to benefit ETP-ALL patients. The list of possible drugs includes high-dose cytarabine and targeted chemotherapy agents that inhibit activity in the cytokine receptor and JAK signaling pathways found in this study to be disrupted in ETP-ALL patients, researchers said. Those pathways help regulate cell division and normal development of the blood system.
“This is the first of a series of important discoveries on the genomic basis of childhood cancers that are emerging from the Pediatric Cancer Genome Project, which is on schedule to fully sequence 600 pediatric cancer genomes by 2013,” said Dr. William E. Evans, St. Jude director and CEO. James Downing, M.D., St. Jude scientific director, St. Jude PCGP site leader and a corresponding author of the study, added: “This study highlights how the genome project is generating new insights into the genetic alterations that underlie some of the most aggressive childhood cancers and in turn is pointing us toward new therapeutic options that may increase the survival rates for children with these cancers.”
ScienceDaily (Jan. 13, 2012) — A Loyola University Chicago Stritch School of Medicine study includes some unexpected findings about the immune systems of smoke-inhalation patients.
Contrary to expectations, patients who died from their injuries had lower inflammatory responses in their lungs than patients who survived.
“Perhaps a better understanding of this early pulmonary immune dysfunction will allow for therapies that further improve outcomes in burn care,” researchers reported.
The study is published in the January/February issue of the Journal of Burn Care & Research. First author of the study is Christopher S. Davis, MD, MPH, a research resident in Loyola’s Burn & Shock Trauma Institute. Corresponding author is Elizabeth J. Kovacs, PhD, director of research of the Burn & Shock Trauma Institute.
Researchers followed 60 burn patients in Loyola’s Burn Center. As expected, patients with the worst combined burn and smoke-inhalation injuries required more time on the ventilator, in the intensive care unit and in the hospital. They also were more likely to die, although this finding fell just short of being statistically significant.
Also according to expectations, patients who died were older and had larger injuries than patients who survived.
But the immune system findings were unexpected. Researchers measured concentrations of 28 immune system modulators in fluid collected from the lungs of patients within 14 hours of burn and smoke-inhalation injuries.
These modulators are proteins produced by leukocytes (white blood cells) and other cells, including those that line the airway. Some of the modulators recruit leukocytes to areas of tissue damage or activate them to begin the repair process that follows tissue injury.
Based on studies conducted at Loyola and other centers, researchers had expected to find higher concentrations of modulators in patients who died, because sicker patients tend to have more active inflammatory responses. But researchers found just the opposite: patients who died had lower concentrations of these modulators in their lungs.
Why do some patients mount robust immune responses in the lungs while others do not? The reason may be due to age, genetics, differences in patients’ underlying health conditions or anything that might disrupt the balance between too much and too little inflammation, Davis said.
Survival of burn patients has significantly improved since the 1950s, due to advancements such as better wound care and improved prevention and treatment of infections. But progress has somewhat stalled in the last 10 years.
The immune response to injury “remains incompletely understood and additional effort is required to further improve survival of the burn-injured patient,” researchers wrote.
The study was presented at the 2011 meeting of the American Burn Association, where it won the 2011 Carl A. Moyer Resident Award for the best study submitted by a resident physician.
Other co-authors of the study are Richard L. Gamelli, MD, FACS, director of the Burn & Shock Trauma Institute; Joslyn M. Albright, MD, chief resident in the Department of Surgery; Stewart R. Carter, MD, research resident; Luis Ramirez, BA, laboratory technician; and Hajwa Kim, MA, MS. All are from Loyola except Kim, who is at the University of Illinois at Chicago.
The study was funded by grants from the National Institutes of Health, Department of Defense, International Association of Fire Fighters and the Dr. Ralph and Marian C. Falk Medical Research Trust.
Loyola’s Burn Center is one of the busiest in the Midwest, treating more than 600 patients annually in the hospital, and another 3,500 patients each year in its clinic. It is one of only two centers in Illinois that have received verification by the American Burn Association.
The study is among the results of research over the last several years conducted in Loyola’s Burn Center and Burn & Shock Trauma Institute, which is investigating the lung’s response to burn and inhalation injuries.
ScienceDaily (Jan. 13, 2012) — A constellation of defective proteins suspected in causing a malfunction in the body’s ability to repair its own DNA could be the link scientists need to prove a new class of drugs will be effective in treating a broad range of ovarian cancer patients, an Oregon Health & Science University Knight Cancer Institute study found.
These research results, published this week in PLoS ONE, have prompted additional exploration into whether the patient population included in clinical trials for drugs that target the enzyme poly ADP ribose polymerase (PARP) should be expanded. Several forms of cancer are more dependent on PARP for their growth than regular cells, which means that targeting these enzymes when they go haywire is a potentially effective way to treat ovarian cancer. Currently PARP inhibitors are being tested with patients who have two types of malfunctioning proteins, BRCA1 or BRCA2. But, the OHSU Knight Cancer Institute study of additional proteins, beyond BRCA proteins, suggests that they too are playing a role in driving ovarian cancer.
Tapping into the potential of PARP inhibitors could change the dynamics of ovarian cancer treatment. There has not been a substantial increase in treatment options for ovarian cancer in the past two decades, said Tanja Pejovic, M.D., Ph.D., gynecologic oncologist at the OHSU Knight Cancer Institute. Pejovic, who led the study of these additional defective proteins, added that the results provide evidence that further research into the role of multiple proteins is warranted.
Only about 10 to 15 percent of women with ovarian cancer have BRCA 1 or BRCA 2 mutations. Pejovic’s study of 186 patients with nonhereditary cancer found that 41 percent who had an early recurrence of the disease also had abnormal levels of the other proteins tracked. In contrast, only 19.5 percent of patients who hadn’t yet had a recurrence of the disease in three years had abnormal levels of these proteins.
“If we are able to identify the proteins that differentiate these patients at risk for early recurrence, this would open up a new direction in ovarian cancer treatment,” Pejovic said.
The study — which was supported by the Sherie Hildreth Ovarian Cancer (SHOC) Foundation — focused on proteins that are supposed to assist cells in repairing harmful breaks in DNA strands, a process called homologous recombination (HR). The malfunctioning of HR is not well understood in ovarian cancers where there is no family history of the disease. However, there is evidence that these proteins influence a patient’s ability to respond to drugs and their survival rates after treatment.
Ovarian cancer is the second most common gynecologic cancer and the most common cause of death among women with a gynecologic cancer. About 21,000 ovarian cancer cases are diagnosed annually and about 14,000 deaths occur each year from the disease.
The OHSU Knight Cancer Institute, which helped pioneer the field of personalized cancer medicine, is committed to research that identifies the specific mutations driving each individual patient’s cancer. Other researchers at the Knight Cancer Institute who contributed to the study are: Weiya Z. Wysham, M.D.; Hong Li, M.S., M.D.; Laura Hays, Ph.D.; Jay Wright; Nupur Pande, Ph.D.; and Maureen Hoatlin, Ph.D
ScienceDaily (Jan. 6, 2012) — Two related studies from Northwestern University offer new strategies for tackling the challenges of preventing and treating diseases of protein folding, such as Alzheimer’s, Parkinson’s and Huntington’s diseases, amyotrophic lateral sclerosis (ALS), cancer, cystic fibrosis and type 2 diabetes.
To do its job properly within the cell, a protein first must fold itself into the proper shape. If it doesn’t, trouble can result. More than 300 diseases have at their root proteins that misfold, aggregate and eventually cause cellular dysfunction and death.
The new Northwestern research identifies new genes and pathways that prevent protein misfolding and toxic aggregation, keeping cells healthy, and also identifies small molecules with therapeutic potential that restore health to damaged cells, providing new targets for drug development.
The genetic screening study is published by the journal PLoS Genetics. The small molecule study is published by the journal Nature Chemical Biology.
“These discoveries are exciting because we have identified genes that keep us healthy and small molecules that keep us healthy,” said Richard I. Morimoto, who led the research. “Future research should explain how these two important areas interact.”
Morimoto is the Bill and Gayle Cook Professor of Biology in the department of molecular biosciences and the Rice Institute for Biomedical Research in Northwestern’s Weinberg College of Arts and Sciences. He also is a scientific director of the Chicago Biomedical Consortium.
The genetic study reported in PLoS Genetics was conducted in the transparent roundworm C. elegans, which shares much of the same biology with humans. The small animal is a valued research tool because of this and also because its genome, or complete genetic sequence, is known.
In the work, Morimoto and his team tested all of the approximately 19,000 genes in C. elegans. They reduced expression of each gene one at a time and looked to see if the gene suppressed protein aggregation in the cell. Did the gene increase aggregation or lessen it or have no effect at all?
The researchers found 150 genes that did have an effect. They then conducted a series of tests and zeroed in on nine genes that made all proteins in the cell healthier. (These genes had a positive effect on a number of different proteins associated with different diseases.)
These nine genes define a core homeostastis network that protects the animal’s proteome (the entire set of proteins expressed by the organism) from protein damage. “These are the most important genes,” Morimoto said. “Figuring out how nine genes — as opposed to 150 — work is a manageable task.”
In the Nature Chemical Biology study, Morimoto and his colleagues screened nearly one million small molecules in human tissue culture cells to identify those that restore the cell’s ability to protect itself from protein damage.
They identified seven classes of compounds (based on chemical structure) that all enhance the cell’s ability to make more protective molecular chaperones, which restore proper protein folding. The researchers call these compounds proteostasis regulators. They found that the compounds restored the health of the cell and resulted in reduction of protein aggregation and protection against misfolding. Consequently, health was restored when diseased animals were treated with the small molecules.
Morimoto and his team then conducted detailed molecular analyses of 30 promising small molecules, representing all seven classes. They discovered some compounds were much more effective than others.
“We don’t yet know the detailed mechanisms of these small molecules, but we have identified some good drug targets for further development,” Morimoto said.
The PLoS Genetics paper is titled “A Genetic Screening Strategy Identifies Novel Regulators of the Proteostasis Network.” M. Catarina Silva, a joint-doctoral student at Northwestern in the Morimoto lab and the University of Lisbon is the first author. The National Institutes of Health, the Huntington’s Disease Society of America Coalition for the Cure and the Daniel F. and Ada L. Rice Foundation supported the research.
The Nature Chemical Biology paper is titled “Small-Molecule Proteostasis Regulators for Protein Conformational Diseases.” Barbara Calamini, a former postdoctoral fellow at Northwestern who is now a research scientist at Duke University, is the first author. The National Institutes of Health and the Daniel F. and Ada L. Rice Foundation supported the research