LOS ANGELES (AP) — The head of the Secret Intelligence Service, where James Bond works, has returned from the dead.
Played by Judi Dench, M was killed off in the most recent Bond adventure, "Skyfall." But Dench resurrected the character in a video released Thursday as part of the Weinstein Co.'s appeal to the Motion Picture Association of America to change the rating of Dench's latest starring vehicle, "Philomena."
The MPAA has given the film an R rating for language, but the Weinstein Co. wants it changed to PG-13. Company co-founder Harvey Weinstein appeared on "CBS This Morning" on Thursday to discuss his fight with the ratings organization.
He previously battled the MPAA over the rating for the 2011 documentary "Bully" and the title of "The Butler" this year, which became "Lee Daniels' The Butler."
Weinstein introduced the Dench video, which shows the actress in M's office, saying, "Just when you thought I was dead." She then appears to send an agent on a mission, asking, "Are you familiar with MPAA?"
NASA's Hubble sees asteroid spouting 6 comet-like tails
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7-Nov-2013
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Contact: Cheryl Gundy gundy@stsci.edu 410-338-4707 NASA/Goddard Space Flight Center
Astronomers viewing our solar system's asteroid belt with NASA's Hubble Space Telescope have seen for the first time an asteroid with six comet-like tails of dust radiating from it like spokes on a wheel.
Unlike all other known asteroids, which appear simply as tiny points of light, this asteroid, designated P/2013 P5, resembles a rotating lawn sprinkler. Astronomers are puzzled over the asteroid's unusual appearance.
"We were literally dumbfounded when we saw it," said lead investigator David Jewitt of the University of California at Los Angeles. "Even more amazing, its tail structures change dramatically in just 13 days as it belches out dust. That also caught us by surprise. It's hard to believe we're looking at an asteroid."
Jewitt leads a team whose research paper appears online in the Nov. 7 issue of the Astrophysical Journal Letters.
P/2013 P5 has been ejecting dust periodically for at least five months. Astronomers believe it is possible the asteroid's rotation rate increased to the point where its surface started flying apart. They do not believe the tails are the result of an impact with another asteroid because they have not seen a large quantity of dust blasted into space all at once.
Scientists using the Pan-STARRS survey telescope in Hawaii announced their discovery of the asteroid Aug. 27. P/2013 P5 appeared as an unusually fuzzy-looking object. The multiple tails were discovered when Hubble was used to take a more detailed image Sept. 10.
When Hubble looked at the asteroid again Sept. 23, its appearance had totally changed. It looked as if the entire structure had swung around.
"We were completely knocked out," Jewitt said.
Careful modeling by team member Jessica Agarwal of the Max Planck Institute for Solar System Research in Lindau, Germany, showed that the tails could have been formed by a series of impulsive dust-ejection events. She calculated that dust-ejection events occurred April 15, July 18, July 24, Aug. 8, Aug. 26 and Sept. 4. Radiation pressure from the sun stretched the dust into streamers.
Radiation pressure could have spun P/2013 P5 up. Jewitt said the spin rate could have increased enough that the asteroid's weak gravity no longer could hold it together. If that happened, dust could slide toward the asteroid's equator, shatter and fall off, and drift into space to make a tail. So far, only about 100 to 1,000 tons of dust, a small fraction of the P/2013 P5's main mass, has been lost. The asteroid's nucleus, which measures 1,400 feet wide, is thousands of times more massive than the observed amount of ejected dust.
Astronomers will continue observing P/2013 P5 to see whether the dust leaves the asteroid in the equatorial plane. If it does, this would be strong evidence for a rotational breakup. Astronomers will also try to measure the asteroid's true spin rate.
Jewitt's interpretation implies that rotational breakup must be a common phenomenon in the asteroid belt; it may even be the main way small asteroids die.
"In astronomy, where you find one, you eventually find a whole bunch more," Jewitt said. "This is just an amazing object to us, and almost certainly the first of many more to come."
Jewitt said it appears P/2013 P5 is a fragment of a larger asteroid that broke apart in a collision roughly 200 million years ago. There are many collision fragments in orbits similar to P/2013 P5's. Meteorites from these bodies show evidence of having been heated to as much as 1,500 degrees Fahrenheit. This means the asteroid likely is composed of metamorphic rocks and does not hold any ice as a comet does.
###
For images and more information about P/2013 P5, visit:
http://hubblesite.org/news/2013/52
For more information about NASA's Hubble Space Telescope, visit:
http://www.nasa.gov/hubble
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NASA's Hubble sees asteroid spouting 6 comet-like tails
PUBLIC RELEASE DATE:
7-Nov-2013
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Contact: Cheryl Gundy gundy@stsci.edu 410-338-4707 NASA/Goddard Space Flight Center
Astronomers viewing our solar system's asteroid belt with NASA's Hubble Space Telescope have seen for the first time an asteroid with six comet-like tails of dust radiating from it like spokes on a wheel.
Unlike all other known asteroids, which appear simply as tiny points of light, this asteroid, designated P/2013 P5, resembles a rotating lawn sprinkler. Astronomers are puzzled over the asteroid's unusual appearance.
"We were literally dumbfounded when we saw it," said lead investigator David Jewitt of the University of California at Los Angeles. "Even more amazing, its tail structures change dramatically in just 13 days as it belches out dust. That also caught us by surprise. It's hard to believe we're looking at an asteroid."
Jewitt leads a team whose research paper appears online in the Nov. 7 issue of the Astrophysical Journal Letters.
P/2013 P5 has been ejecting dust periodically for at least five months. Astronomers believe it is possible the asteroid's rotation rate increased to the point where its surface started flying apart. They do not believe the tails are the result of an impact with another asteroid because they have not seen a large quantity of dust blasted into space all at once.
Scientists using the Pan-STARRS survey telescope in Hawaii announced their discovery of the asteroid Aug. 27. P/2013 P5 appeared as an unusually fuzzy-looking object. The multiple tails were discovered when Hubble was used to take a more detailed image Sept. 10.
When Hubble looked at the asteroid again Sept. 23, its appearance had totally changed. It looked as if the entire structure had swung around.
"We were completely knocked out," Jewitt said.
Careful modeling by team member Jessica Agarwal of the Max Planck Institute for Solar System Research in Lindau, Germany, showed that the tails could have been formed by a series of impulsive dust-ejection events. She calculated that dust-ejection events occurred April 15, July 18, July 24, Aug. 8, Aug. 26 and Sept. 4. Radiation pressure from the sun stretched the dust into streamers.
Radiation pressure could have spun P/2013 P5 up. Jewitt said the spin rate could have increased enough that the asteroid's weak gravity no longer could hold it together. If that happened, dust could slide toward the asteroid's equator, shatter and fall off, and drift into space to make a tail. So far, only about 100 to 1,000 tons of dust, a small fraction of the P/2013 P5's main mass, has been lost. The asteroid's nucleus, which measures 1,400 feet wide, is thousands of times more massive than the observed amount of ejected dust.
Astronomers will continue observing P/2013 P5 to see whether the dust leaves the asteroid in the equatorial plane. If it does, this would be strong evidence for a rotational breakup. Astronomers will also try to measure the asteroid's true spin rate.
Jewitt's interpretation implies that rotational breakup must be a common phenomenon in the asteroid belt; it may even be the main way small asteroids die.
"In astronomy, where you find one, you eventually find a whole bunch more," Jewitt said. "This is just an amazing object to us, and almost certainly the first of many more to come."
Jewitt said it appears P/2013 P5 is a fragment of a larger asteroid that broke apart in a collision roughly 200 million years ago. There are many collision fragments in orbits similar to P/2013 P5's. Meteorites from these bodies show evidence of having been heated to as much as 1,500 degrees Fahrenheit. This means the asteroid likely is composed of metamorphic rocks and does not hold any ice as a comet does.
###
For images and more information about P/2013 P5, visit:
http://hubblesite.org/news/2013/52
For more information about NASA's Hubble Space Telescope, visit:
http://www.nasa.gov/hubble
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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Crisco was the original product made with partially hydrogenated soybean oil, which contains trans fats. Today, Crisco has only small amounts of the fats.
Tony Dejak/ASSOCIATED PRESS
Crisco was the original product made with partially hydrogenated soybean oil, which contains trans fats. Today, Crisco has only small amounts of the fats.
Tony Dejak/ASSOCIATED PRESS
If the Food and Drug Administration has its way, an era of food technology will soon end. The agency announced Thursday it is aiming to ban partially hydrogenated vegetable oils from all food products.
Margaret Hamburg, the FDA commissioner, said at a press conference that her agency has come to the preliminary conclusion that the oils "are not generally recognized as safe for use in food."
If the agency makes this decision final, it will mean a complete ban on this ingredient.
Health concerns about the trans fats in the oil have been mounting for years. The biggest concern? Trans fats raise the risk of heart disease. The Centers for Disease Control and Prevention estimates that an FDA ban on trans fats could prevent an additional 7,000 deaths from heart disease each year and up to 20,000 heart attacks each year.
But it took decades for health officials to arrive at that conclusion.
Partially hydrogenated oil came on the market about a century ago when food scientists figured out how to add hydrogen atoms to a molecule of oil. Typically, it's soybean oil.
Kantha Shelke, a scientist with the Institute of Food Technologists in Chicago, says this makes liquid oil more solid, and stable. Depending on how you add the hydrogen atoms, you can make the oil as solid as you like.
"So we could literally dial the needle to as solid as you wanted, and get the kind of results we were looking for," says Shelke.
These results include cookies or doughnuts that didn't leave a ring of oil behind on a paper towel and don't start tasting rancid after a few weeks.
Also, this oil doesn't have a strong taste of its own so you can use lots of it without ruining the flavor.
"It's really absolutely perfect, and it's also perfect for the American style of shopping: You buy boxes and boxes of crackers, put them in your pantry," says Shelke. "You open this box six months or eight months or a year later, and it would still taste and smell just as good as it was on the day you bought it!"
By the time the government came up with laws regulating food additives, people had been eating this form of oil for decades with no apparent problems.
David Schleifer, a researcher at a nonprofit group called Public Agenda, in New York, says most scientists in the 1980s actually thought this kind of oil was probably safer than lard or palm oil. Schleifer wrote a recent journal article on the history of trans fats.
McDonald's, Schleifer says, previously used beef tallow for frying. "People freaked out about beef tallow because it had saturated fat, and McDonald's responded to that public outcry by replacing beef tallow with trans fat," he says.
Everything changed in the mid-1990s. New studies showed that trans fats raised bad cholesterol and increased the risk of heart disease.
In fact, they were even worse than saturated fats. In 2006, after a campaign by public health advocates, the FDA required food companies to add trans fats to food labels.
Most companies responded by drastically cutting their use of partially hydrogenated oil. That had a big impact on consumption — Americans consumed around 1 gram per day in 2012, down from 4.6 grams per day in 2003.
But not every company has eliminated it from every product.
You can still find trans fats in microwavable popcorn, frozen pies and all kinds of mass-produced baked goods. Often, food companies use just a little bit. If there's less than half a gram of trans fats per serving they can list the amount of trans fats in their products as zero.
A complete ban on trans fats would be a big deal for food manufacturers, says Shelke. She says food companies can drop the trans fats, but their products won't be quite the same.
"They have to go back to re-educating consumers that cookies and consumers don't last forever," says Shelke.
The cookies will have a shorter life, but consumers' lives might be longer.
This combination of Sept. 10 and 23, 2013 photos provided by NASA shows six comet-like tails radiating from a body in the asteroid belt, designated P/2013 P5. The Hubble Space Telescope discovered it in the asteroid belt between the orbits of Mars and Jupiter. A research team led by the University of California at Los Angeles believes the asteroid is rotating so much that its surface is flying apart. It’s believed to be a fragment of a larger asteroid damaged in a collision 200 million years ago. (AP Photo/NASA, ESA, D. Jewitt - UCLA)
CAPE CANAVERAL, Fla. (AP) — This is one strange asteroid.
The Hubble Space Telescope has discovered a six-tailed asteroid in the asteroid belt between the orbits of Mars and Jupiter. Scientists say they've never seen anything like it. Incredibly, the comet-like tails change shape as the asteroid sheds dust. The streams have occurred over several months.
A research team led by the University of California, Los Angeles, believes the asteroid, designated P/2013 P5, is rotating so much that its surface is flying apart. It's believed to be a fragment of a larger asteroid damaged in a collision 200 million years ago.
Scientists using the Pan-STARRS telescope in Hawaii spotted the asteroid in August. Hubble picked out all the tails in September.
The discovery is described in this week's issue of Astrophysical Journal Letters.
Peptide derived from cow's milk kills human stomach cancer cells in culture
PUBLIC RELEASE DATE:
7-Nov-2013
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Contact: Eileen Leahy jdsmedia@elsevier.com 732-238-3628 Elsevier Health Sciences
Findings reported in the Journal of Dairy Science show promise for treatment of gastric cancer
Philadelphia, PA, November 7, 2013 New research from a team of researchers in Taiwan indicates that a peptide fragment derived from cow's milk, known as lactoferricin B25 (LFcinB25), exhibited potent anticancer capability against human stomach cancer cell cultures. The findings, published in the Journal of Dairy Science, provide support for future use of LFcinB25 as a potential therapeutic agent for gastric cancer.
"Gastric cancer is one of the most common causes of cancer-related mortality worldwide, especially in Asian countries," says Wei-Jung Chen, PhD, of the Department of Biotechnology and Animal Science of National Ilan University, Taiwan Republic of China. "In general, the main curative therapies for gastric cancer are surgery and chemotherapy, which are generally only successful if the cancer is diagnosed at an early stage. Novel treatment strategies to improve prognosis are urgently needed."
Investigators evaluated the effects of three peptide fragments derived from lactoferricin B, a peptide in milk that has antimicrobial properties. Only one of the fragments, LFcinB25 reduced the survival of human AGS (Gastric Adenocarcinoma) cells in a dose-dependent and time-dependent manner.
Under a microscope the investigators could see that after an hour of exposure to the gastric cancer cells, LFcinB25 migrated to the cell membrane of the AGS cells, and within 24 hours the cancer cells had shrunken in size and lost their ability to adhere to surfaces. In the early stages of exposure, LFcinB25 reduced cell viability through both apoptosis (programmed cell death) and autophagy (degradation and recycling of obsolete or damaged cell parts). At later stages, apoptosis appeared to dominate, possibly through caspase-dependent mechanisms, and autophagy waned.
"This is the first report describing interplay between apoptosis and autophagy in LFcinB-induced cell death of cancer cells," says Dr. Chen.
The research also suggested a target, Beclin-1, which may enhance LFcinB25's cytotoxic action. Beclin-1 is a protein in humans that plays a central role in autophagy, tumor growth, and degeneration of neurons. In this study, the investigators found that cleaved beclin-1 increased in a time-dependent manner after LFcinB25-exposure, suggesting to the authors a new approach in drug development that may boost the anticancer effects of LFcinB25.
"Optimization of LFcinB using various strategies to enhance further selectivity is expected to yield novel anticancer drugs with chemotherapeutic potential for the treatment of gastric cancer," concludes Dr. Chen.
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Peptide derived from cow's milk kills human stomach cancer cells in culture
PUBLIC RELEASE DATE:
7-Nov-2013
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Contact: Eileen Leahy jdsmedia@elsevier.com 732-238-3628 Elsevier Health Sciences
Findings reported in the Journal of Dairy Science show promise for treatment of gastric cancer
Philadelphia, PA, November 7, 2013 New research from a team of researchers in Taiwan indicates that a peptide fragment derived from cow's milk, known as lactoferricin B25 (LFcinB25), exhibited potent anticancer capability against human stomach cancer cell cultures. The findings, published in the Journal of Dairy Science, provide support for future use of LFcinB25 as a potential therapeutic agent for gastric cancer.
"Gastric cancer is one of the most common causes of cancer-related mortality worldwide, especially in Asian countries," says Wei-Jung Chen, PhD, of the Department of Biotechnology and Animal Science of National Ilan University, Taiwan Republic of China. "In general, the main curative therapies for gastric cancer are surgery and chemotherapy, which are generally only successful if the cancer is diagnosed at an early stage. Novel treatment strategies to improve prognosis are urgently needed."
Investigators evaluated the effects of three peptide fragments derived from lactoferricin B, a peptide in milk that has antimicrobial properties. Only one of the fragments, LFcinB25 reduced the survival of human AGS (Gastric Adenocarcinoma) cells in a dose-dependent and time-dependent manner.
Under a microscope the investigators could see that after an hour of exposure to the gastric cancer cells, LFcinB25 migrated to the cell membrane of the AGS cells, and within 24 hours the cancer cells had shrunken in size and lost their ability to adhere to surfaces. In the early stages of exposure, LFcinB25 reduced cell viability through both apoptosis (programmed cell death) and autophagy (degradation and recycling of obsolete or damaged cell parts). At later stages, apoptosis appeared to dominate, possibly through caspase-dependent mechanisms, and autophagy waned.
"This is the first report describing interplay between apoptosis and autophagy in LFcinB-induced cell death of cancer cells," says Dr. Chen.
The research also suggested a target, Beclin-1, which may enhance LFcinB25's cytotoxic action. Beclin-1 is a protein in humans that plays a central role in autophagy, tumor growth, and degeneration of neurons. In this study, the investigators found that cleaved beclin-1 increased in a time-dependent manner after LFcinB25-exposure, suggesting to the authors a new approach in drug development that may boost the anticancer effects of LFcinB25.
"Optimization of LFcinB using various strategies to enhance further selectivity is expected to yield novel anticancer drugs with chemotherapeutic potential for the treatment of gastric cancer," concludes Dr. Chen.
###
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HPV can damage genes and chromosomes directly, whole-genome sequencing study shows
PUBLIC RELEASE DATE:
7-Nov-2013
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Contact: Darrell E. Ward Darrell.Ward@osumc.edu 614-293-3737 Ohio State University Wexner Medical Center
COLUMBUS, Ohio The virus that causes cervical, head and neck, anal and other cancers can damage chromosomes and genes where it inserts its DNA into human DNA, according to a new study led by researchers at The Ohio State University Comprehensive Cancer Center Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC James).
It's long been known that cancer-causing types of human papillomavirus (HPV) produce two viral proteins, called E6 and E7, which are essential for the development of cancer. However, they are not sufficient to cause cancer. Additional alterations in host-cell genes are necessary for cancer to develop. Here, scientists identified a new mechanism by which HPV may damage host DNA directly and contribute to cancer development.
Published in the journal Genome Research, this laboratory study used whole-genome sequencing to investigate the relationship between the HPV and host genomes in human cancers.
"Our sequencing data showed in vivid detail that HPV can damage host-cell genes and chromosomes at sites of viral insertion," says co-senior author David Symer, MD, PhD, assistant professor of molecular virology, immunology and medical genetics at the OSUCCC James.
"HPV can act like a tornado hitting the genome, disrupting and rearranging nearby host-cell genes," Symer explains. "This can lead to overexpression of cancer-causing genes in some cases, or it can disrupt protective tumor-suppressor genes in others. Both kinds of damage likely promote the development of cancer."
"We observed fragments of the host-cell genome to be removed, rearranged or increased in number at sites of HPV insertion into the genome," says co-senior author Maura Gillison, MD, PhD, professor of medicine, epidemiology and otolaryngology and the Jeg Coughlin Chair of Cancer Research at the OSUCCC James. "These remarkable changes in host genes were accompanied by increases in the number of HPV copies in the host cell, thereby also increasing the expression of viral E6 and E7, the cancer-promoting genes."
HPV causes about 610,000 cancers annually worldwide, including virtually all cervical cancers, and many anogenital and head and neck cancers. How it causes cancer isn't completely understood.
The two cancer-causing proteins, E6 and E7, silence two key tumor-suppressor genes in host cells, contributing to cancer development. "E6 and E7 are critically important for the virus to cause cancer. Our findings shed light on how HPV, and perhaps other viruses, can disrupt the structure of host chromosomes and genes and thereby contribute to cancer development," Gillison explains.
For this study, Symer, Gillison and their colleagues examined 10 cancer-cell lines and two head and neck tumor samples from patients. Along with whole-genome sequencing, the scientists used several molecular assays, including RNA sequencing, spectral karyotyping (SKY) and fluorescence in situ hybridization (FISH).
Key technical findings included:
The genome-wide analysis, at single nucleotide resolution, identified a striking and recurrent association between HPV integrants and adjacent genomic amplifications, deletions and translocations;
The HPV integrants mapped broadly across the human genome, with no evidence of recurrent integration into particular chromosomal hotspots;
The researchers proposed a "looping" model by which abnormal viral replication results in the extraordinary damage that occurs to host chromosomes at the sites of viral DNA insertion.
"Our study reveals new and interesting information about what happens to HPV in the 'end game' in cancers," Symer says. "Overall, our results shed new light on the potentially critical, catastrophic steps in the progression from initial viral infection to development of an HPV-associated cancer."
###
Funding from the Ohio State University Comprehensive Cancer Center Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC James), the Ohio Supercomputer Center, an Ohio Cancer Research Associate grant, the Oral Cancer Foundation and the Intramural Research Program of the National Institutes of Health, National Cancer Institute Center for Cancer Research, supported this research.
Other researchers involved in this study were Keiko Akagi, Jingfeng Li, Tatevik R. Broutian, Weihong Xiao, Bo Jiang, Theodoros N. Teknos, Bhavna Kumar and Dandan He, The Ohio State University; Hesed Padilla-Nash, Danny Wangsa, Thomas Ried, National Cancer Institute; James W. Rocco, Massachusetts General Hospital and Harvard Medical School.
The Ohio State University Comprehensive Cancer Center Arthur G. James Cancer Hospital and Richard J. Solove Research Institute strives to create a cancer-free world by integrating scientific research with excellence in education and patient-centered care, a strategy that leads to better methods of prevention, detection and treatment. Ohio State is one of only 41 National Cancer Institute (NCI)-designated Comprehensive Cancer Centers and one of only four centers funded by the NCI to conduct both phase I and phase II clinical trials. The NCI recently rated Ohio State's cancer program as "exceptional," the highest rating given by NCI survey teams. As the cancer program's 228-bed adult patient-care component, The James is a "Top Hospital" as named by the Leapfrog Group and one of the top cancer hospitals in the nation as ranked by U.S.News & World Report.
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HPV can damage genes and chromosomes directly, whole-genome sequencing study shows
PUBLIC RELEASE DATE:
7-Nov-2013
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Contact: Darrell E. Ward Darrell.Ward@osumc.edu 614-293-3737 Ohio State University Wexner Medical Center
COLUMBUS, Ohio The virus that causes cervical, head and neck, anal and other cancers can damage chromosomes and genes where it inserts its DNA into human DNA, according to a new study led by researchers at The Ohio State University Comprehensive Cancer Center Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC James).
It's long been known that cancer-causing types of human papillomavirus (HPV) produce two viral proteins, called E6 and E7, which are essential for the development of cancer. However, they are not sufficient to cause cancer. Additional alterations in host-cell genes are necessary for cancer to develop. Here, scientists identified a new mechanism by which HPV may damage host DNA directly and contribute to cancer development.
Published in the journal Genome Research, this laboratory study used whole-genome sequencing to investigate the relationship between the HPV and host genomes in human cancers.
"Our sequencing data showed in vivid detail that HPV can damage host-cell genes and chromosomes at sites of viral insertion," says co-senior author David Symer, MD, PhD, assistant professor of molecular virology, immunology and medical genetics at the OSUCCC James.
"HPV can act like a tornado hitting the genome, disrupting and rearranging nearby host-cell genes," Symer explains. "This can lead to overexpression of cancer-causing genes in some cases, or it can disrupt protective tumor-suppressor genes in others. Both kinds of damage likely promote the development of cancer."
"We observed fragments of the host-cell genome to be removed, rearranged or increased in number at sites of HPV insertion into the genome," says co-senior author Maura Gillison, MD, PhD, professor of medicine, epidemiology and otolaryngology and the Jeg Coughlin Chair of Cancer Research at the OSUCCC James. "These remarkable changes in host genes were accompanied by increases in the number of HPV copies in the host cell, thereby also increasing the expression of viral E6 and E7, the cancer-promoting genes."
HPV causes about 610,000 cancers annually worldwide, including virtually all cervical cancers, and many anogenital and head and neck cancers. How it causes cancer isn't completely understood.
The two cancer-causing proteins, E6 and E7, silence two key tumor-suppressor genes in host cells, contributing to cancer development. "E6 and E7 are critically important for the virus to cause cancer. Our findings shed light on how HPV, and perhaps other viruses, can disrupt the structure of host chromosomes and genes and thereby contribute to cancer development," Gillison explains.
For this study, Symer, Gillison and their colleagues examined 10 cancer-cell lines and two head and neck tumor samples from patients. Along with whole-genome sequencing, the scientists used several molecular assays, including RNA sequencing, spectral karyotyping (SKY) and fluorescence in situ hybridization (FISH).
Key technical findings included:
The genome-wide analysis, at single nucleotide resolution, identified a striking and recurrent association between HPV integrants and adjacent genomic amplifications, deletions and translocations;
The HPV integrants mapped broadly across the human genome, with no evidence of recurrent integration into particular chromosomal hotspots;
The researchers proposed a "looping" model by which abnormal viral replication results in the extraordinary damage that occurs to host chromosomes at the sites of viral DNA insertion.
"Our study reveals new and interesting information about what happens to HPV in the 'end game' in cancers," Symer says. "Overall, our results shed new light on the potentially critical, catastrophic steps in the progression from initial viral infection to development of an HPV-associated cancer."
###
Funding from the Ohio State University Comprehensive Cancer Center Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC James), the Ohio Supercomputer Center, an Ohio Cancer Research Associate grant, the Oral Cancer Foundation and the Intramural Research Program of the National Institutes of Health, National Cancer Institute Center for Cancer Research, supported this research.
Other researchers involved in this study were Keiko Akagi, Jingfeng Li, Tatevik R. Broutian, Weihong Xiao, Bo Jiang, Theodoros N. Teknos, Bhavna Kumar and Dandan He, The Ohio State University; Hesed Padilla-Nash, Danny Wangsa, Thomas Ried, National Cancer Institute; James W. Rocco, Massachusetts General Hospital and Harvard Medical School.
The Ohio State University Comprehensive Cancer Center Arthur G. James Cancer Hospital and Richard J. Solove Research Institute strives to create a cancer-free world by integrating scientific research with excellence in education and patient-centered care, a strategy that leads to better methods of prevention, detection and treatment. Ohio State is one of only 41 National Cancer Institute (NCI)-designated Comprehensive Cancer Centers and one of only four centers funded by the NCI to conduct both phase I and phase II clinical trials. The NCI recently rated Ohio State's cancer program as "exceptional," the highest rating given by NCI survey teams. As the cancer program's 228-bed adult patient-care component, The James is a "Top Hospital" as named by the Leapfrog Group and one of the top cancer hospitals in the nation as ranked by U.S.News & World Report.
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Amid the clamor of "bring your own device" (BYOD), a question lurks in the background: "What happens to technical service and support?" Concerns for the tech support function encompass the extremes, from agents being overwhelmed with calls, to their becoming inhabitants of a help desk ghost town.
On the one hand, it’s easy to imagine a flood of calls as employees attempt to access wireless networks or synch their e-mail, especially in companies that permit the use of any device type. At the same time, as more people own smartphones, they are increasingly accustomed to resolving issues independently, through online forums, communities and other means of self-support.
By 2016, says Gartner analyst Jarod Greene, help desks will see a 25% to 30% drop in user-initiated call volume, as BYOD drives a companion trend of BYOS, or “bring your own support.”
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