WASHINGTON (AP) ? A small comet survived what astronomers figured would be a sure death when it danced uncomfortably close to the broiling sun Thursday night.
Comet Lovejoy was only discovered a couple of weeks ago. It was supposed to melt as it came so close to the sun that the temperatures would hit several million degrees.
But astronomers watching live with NASA telescopes were shocked when a bright spot emerged on the sun's other side. Lovejoy lived.
The comet came within 75,000 miles (121,000 kilometers) of the sun. For a small object often described as a dirty snowball, that brush with the sun should have been fatal.
Astronomers say it probably was not deadly because the comet was larger than they thought.
MicroRNAs or miRNAs are tiny RNA molecules that have only about 20 nucleotides and do not code for proteins. They regulate many important processes in cells by binding to target messenger RNAs ? the instructions for protein production ?, thus blocking production of the respective protein. In cancer, the production of some miRNAs is often reduced or amplified. This particularly affects miRNAs that regulate the activity of cancer-promoting genes.
A key molecule in the development of cancer is a transcription factor called NFkappaB, which is an important switch for many genes with inflammation-promoting effects. At DKFZ, Professor Dr. Stefan Wiemann and collaborators have now investigated whether microRNAs that affect NFkappaB production are deregulated in breast cancer. Jointly with colleagues at Heidelberg and Tuebingen University Hospitals, the DKFZ team studied over 800 miRNAs and discovered a family of RNA molecules known as miR-520, which particularly strongly reduce the production of NFkappaB. "If the cells produce less NFkappaB, the production of inflammation-promoting signaling molecules is reduced. This puts a brake on cancer growth, because these signaling molecules promote invasive capacity, formation of new vessels and metastasis," says Ioanna Keklikoglou, a doctoral student Wiemann's department, explaining this mechanism.
However, miR-520 does not only act like a cancer brake by suppressing NFkappaB. In addition, Wiemann's team discovered that this microRNA also blocks another cancer-promoting signaling pathway that is triggered by growth factor TGF-beta. TGF-beta signals cause malignant cells to be less firmly anchored in the tissue and, thus, better able to invade surrounding organs ? a characteristic feature of cancer cells.
Subsequently, the DKFZ researchers studied the question of whether the findings obtained in cancer cells in the culture dish are also involved in breast cancer. Studying tumor tissue samples of 76 patients, the team discovered that tumors which have already spread to the lymph nodes produce less miR-520 than those which have not yet spread. However, this connection was only found in tumors that do not produce receptors for the female sexual hormone, estrogen (ER-negative tumors).
"Our findings clearly demonstrate that miR-520 is a genuine cancer brake that suppresses the malignant behavior of tumor cells in two different ways at once," said Stefan Wiemann, commenting on the findings reported in his now published work. "This cancer brake appears to fail in many ER-negative breast tumors ? and also in cells of other types of cancer, as colleagues have now demonstrated." ER-negative breast cancer is particularly difficult to treat in many cases. Developing a microRNA therapy that blocks several cancer-promoting signaling pathways at once may therefore be an interesting option.
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I Keklikoglou, C Koerner, C Schmidt, JD Zhang, D Heckmann, A Shavinskaya, H Allgayer, B G?ckel, T Fehm, A Schneeweiss, ? Sahin, S Wiemann and U Tschulena: MicroRNA-520/373 family functions as a tumor suppressor in estrogen receptor negative breast cancer by targeting NF-kappaB and TGF-b signaling pathways. Oncogene 2011, DOI: 10.1038/onc.2011.571
Helmholtz Association of German Research Centres: http://www.helmholtz.de/en/index.html
Thanks to Helmholtz Association of German Research Centres for this article.
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Some of the Republican presidential candidates are squeezing in campaign events before participating in a televised debate in Sioux City, Iowa. It's their last debate before the Iowa caucuses on Jan. 3.
The debate, scheduled for 9 p.m. EST Thursday, is sponsored by Fox News and the Iowa Republican Party.
Earlier Thursday, Rick Santorum is set to meet with voters in Rockwell City, Sac City and Holstein, Iowa.
Newt Gingrich will be in Fort Dodge, Iowa, and Rick Perry will be in the Iowa town of Le Mars.
Congolese President Joseph Kabila and opposition leader Etienne Tshisekedi both claim to have won the Nov. 28 elections. Tshisekedi is now calling for street protests.
Congo could be at risk of another round of violence, as the two men who both claim to be president of the country draw up strategies of confrontation.
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President Joseph Kabila and opposition leader Etienne Tshisekedi each claim to have won the Nov. 28 ballot, the second in the country?s history since the fall of the dictator Mobutu Sese Seko in 1998. Election observers have called the recent elections ?seriously flawed,? and ?lacking credibility.? Even President Kabila admits that ?mistakes? were made, but says that the number of disputed ballots would still not deny him a victory.
Official results from the Independent National Electoral Commission (CENI), gave Kabila the victory, with 49 percent of the vote, compared with Mr. Tshisekedi?s 32 percent.
It all comes down to mathematics: If the opposition can come up with enough disputed or missing votes, 1.5 million, it can claim victory.
Opposition leader Tshisekedi, whose party the Union for Democracy and Social Progress is conducting its own vote tally from polling station results, has meanwhile called for ?peaceful and democratic demonstrations.? Neither Tshisekedi nor Kabila appear to be reaching out to each other for a negotiated solution, and diplomats are working behind the scenes to prevent a clash that could cost civilian lives.
In Kinshasa, US Amb. James Entwistle cast doubt on the official CENI final results, telling the Reuters news agency, "The United States believes that the management and technical execution of these elections were seriously flawed." The elections, he said, ?lacked transparency and did not measure up to the positive democratic gains we have seen in recent African elections."?
While Africa has witnessed a kind of democratic renaissance in recent years with the end of authoritarian regimes such as Zimbabwe, Sudan, and Uganda, disputed elections still have the potential for horrific violence. In Kenya, after the disputed Dec. 27, 2007, elections, more than 1,300 people were killed and 300,000 displaced before the two main parties agreed to sit down and negotiate their way into a power-sharing agreement. In Cote D?Ivoire, the Nov. 2010 election gave a clear victory to opposition Alessane Ouattara, but President Laurent Gbagbo?s refusal to step down pushed the country dangerously close to civil war.
A police officer, right, stands in front of children holding a banner that reads in Greek, "Accuracy is killing us every day," as they gather Wednesday outside parliament to protest a proposed two-year public-sector wage freeze and other deficit-fighting austerity measures, in Nicosia, Cyprus.
By The Associated Press
NICOSIA, Cyprus -- Airports and government offices will shut down Thursday in a daylong strike to protest a public-sector wage freeze and other Cypriot austerity measures.
The island's two airports will close after air traffic controllers said Wednesday they will stage a 12-hour work stoppage to protest what they regard as the government's broken promise not to freeze their salaries as well.
The airport shutdown will affect more than 70 flights and 5,000 passengers, airports spokesman Adamos Aspris said.
Separately, the government worker union PASYDY said state-run hospitals will operate on a skeleton staff.
Municipal elections in the eurozone country are slated for Sunday and could be thrown into disarray after PASYDY urged members not to work then and to avoid voting.
Cyprus' communist-rooted President Dimitris Christofias publicly appealed to union leaders to let the elections run problem-free. "With all due respect to the unions and especially PASYDY, that's too much," he said.
PASYDY called for the stepped-up strike action a day after government workers briefly walked off the job to demonstrate against not being consulted on the austerity measures.
The union's boss, Glafcos Hadjipetrou, said government workers have already seen their incomes shrink by a tenth because of earlier salary rollbacks and suggested that more cuts are being discussed behind their backs.
"Today the numbers don't add up, tomorrow the numbers won't add up, and they're asking workers to cover the shortfall. This won't pass," Hadjipetrou said.
Finance Minister Kikis Kazamias dismissed what he called a "suspicious and dishonorable whispering campaign" that the government would move to cut government workers' Christmas bonus and tax their retirement bonus.
"I consider this action as a deliberate crime against the public interest," he told reporters.
Salaries and other benefits to the 70,000-strong public sector represented by powerful unions in the country of 800,000 take up a third of all government spending.
Dozens of union members on Wednesday descended on Parliament where lawmakers approved the two-year wage freeze and other deficit-fighting measures, including a sales tax hike from 15 to 17 percent and a levy on private sector salaries above ?2,500 ($3,250), also valid for two years.
Other measures include a tax increase on company dividends from 17 to 20 percent and slashing social handouts by ?200 million ($260 million).
Bills setting up a bank stability fund and enabling the government to backstop troubled financial institutions also were approved.
The sales tax increase will take effect in March. Lawmakers postponed a vote on raising the retirement age by a year to 64. A vote on the budget will take place Thursday.
The government is struggling to restore investor confidence following a string of credit rating downgrades this year ? mainly due to its banks heavy exposure to debt-shackled Greece ? that have taken Cyprus to the brink of junk status.
Kazamias earlier this month struck a deal with opposition parties ? which hold a majority in Parliament ? on the measures aimed at shrinking the deficit from around 6.5 percent of gross domestic product this year to 2.4 percent in 2012.
Without these measures, he warned that the country would likely need a bailout.
Kazamias said trade unions weren't consulted because he needed a swift agreement to avoid sanctions the island faces under EU rules if it doesn't agree on deficit-cutting measures by mid-December.
? 2011 The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.
Key genetic error found in family of blood cancersPublic release date: 15-Dec-2011 [ | E-mail | Share ]
Contact: Caroline Arbanas arbanasc@wustl.edu 314-286-0109 Washington University School of Medicine
Scientists have uncovered a critical genetic mutation in some patients with myelodysplastic syndromes a group of blood cancers that can progress to a fatal form of leukemia.
The research team at Washington University School of Medicine in St. Louis also found evidence that patients with the mutation are more likely to develop acute leukemia. While this finding needs to be confirmed in additional patients, the study raises the prospect that a genetic test could one day more accurately diagnose the disorder and predict the course of the disease.
The research is available online in Nature Genetics.
The scientists discovered the mutation in a gene known as U2AF1 when they sequenced the entire genome of a 65-year old man with myelodysplastic syndrome that had progressed to leukemia and compared it with the genome of his tumor cells. They also found the genetic error in other patients with myelodysplastic syndromes, an indication of the mutation's significance.
"The mutation in this gene was not on anyone's radar screen," says senior author and hematologist/oncologist Matthew Walter, MD, assistant professor of medicine. "In many cases, the diagnosis of myelodysplastic syndromes is unclear because there isn't a straightforward diagnostic test. By understanding at the genetic level what is contributing to this disease, we hope to eventually improve the diagnosis and treatment of this disorder."
Myelodysplastic syndromes are a difficult-to-treat family of blood cancers that occur when blood cells in the bone marrow don't mature properly. About 28,000 Americans are diagnosed with the disorder each year, most of them over age 60. Drugs are available to treat the disease, but none can cure it.
In about 30 percent of cases, the disorder progresses to a form of acute myeloid leukemia that usually is fatal because chemotherapy drugs are not effective in these patients. Doctors currently assess the likelihood that a patient with myelodysplastic syndrome will develop leukemia by looking at the chromosomes in the tumor cells to determine the extent to which they have broken apart and rearranged themselves, an indicator of the severity of the disease.
"There are chromosomal patterns that indicate high risk and low risk, but the current methods to determine prognosis aren't perfect," says first author Timothy Graubert, MD, associate professor of medicine, who specializes in treating patients with myelodysplastic syndromes.
After identifying the U2AF1 mutation in three patients through whole-genome sequencing, the researchers scoured the gene for the mutation in another 150 patients with myelodysplastic syndromes. They identified the mutation in 13, or nearly 9 percent. The mutations were acquired during development of myelodysplastic syndromes because they were not present in normal cells obtained from each patient.
Patients were almost three times as likely to develop leukemia if they had a mutation in the U2AF1 gene. The disorder progressed to leukemia in 15.2 percent of patients with the mutation, compared with 5.8 percent of those without the genetic error.
The most common mutation results in a single letter change in the DNA at a precise location in the U2AF1 gene. Patients with the genetic error were most likely to have the amino acids phenylalanine or tyrosine substituted for a serine. The researchers say that the mutation by itself does not cause myelodysplastic syndromes but appears to be an early event in the course of the disease.
Normally, the U2AF1 gene makes a protein involved in splicing RNA, a sister molecule of DNA that carries the instructions for building proteins. Splicing brings together different sections of RNA necessary to make a protein and discards those sections that are not needed. The mutated version of the gene still produces a protein, but its splicing activity is altered, which may be important for the development of some cancers.
The new research, funded in part by a federal stimulus grant, adds to a flurry of new findings about the genetic basis of myelodysplastic syndromes. Recent studies in Nature and the New England Journal of Medicine, along with the current study, have identified mutations in a total of eight genes involved in RNA splicing in patients with the disorder.
"Together, these findings are a real game-changer," Graubert says. "A mutation in any one of these eight genes occurs in up to 50 percent of patients with myelodysplastic syndromes. Because these changes are so common, we think there are likely to be implications for improving the diagnosis of the disorder and finding new therapeutic options."
Whole-genome sequencing for cancer was pioneered by scientists at Washington University School of Medicine and the university's Genome Institute, including Richard Wilson, PhD; Elaine Mardis, PhD; Timothy Ley, MD; and Li Ding, PhD, all of whom are co-authors of the study. The new research builds on their work to find novel mutations in cancer by looking across a patient's entire genome.
###
The research was supported by the National Institutes of Health (NIH) and a Howard Hughes Medical Institute Physician-Scientist Early Career Award.
Graubert, TA et al. Recurrent mutations in the U2AF1 splicing factor in myelodysplastic syndromes. Nature Genetics. Advance online publication, Dec. 11, 2011.
Washington University School of Medicine's 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children's hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked fourth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children's hospitals, the School of Medicine is linked to BJC HealthCare.
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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.
Key genetic error found in family of blood cancersPublic release date: 15-Dec-2011 [ | E-mail | Share ]
Contact: Caroline Arbanas arbanasc@wustl.edu 314-286-0109 Washington University School of Medicine
Scientists have uncovered a critical genetic mutation in some patients with myelodysplastic syndromes a group of blood cancers that can progress to a fatal form of leukemia.
The research team at Washington University School of Medicine in St. Louis also found evidence that patients with the mutation are more likely to develop acute leukemia. While this finding needs to be confirmed in additional patients, the study raises the prospect that a genetic test could one day more accurately diagnose the disorder and predict the course of the disease.
The research is available online in Nature Genetics.
The scientists discovered the mutation in a gene known as U2AF1 when they sequenced the entire genome of a 65-year old man with myelodysplastic syndrome that had progressed to leukemia and compared it with the genome of his tumor cells. They also found the genetic error in other patients with myelodysplastic syndromes, an indication of the mutation's significance.
"The mutation in this gene was not on anyone's radar screen," says senior author and hematologist/oncologist Matthew Walter, MD, assistant professor of medicine. "In many cases, the diagnosis of myelodysplastic syndromes is unclear because there isn't a straightforward diagnostic test. By understanding at the genetic level what is contributing to this disease, we hope to eventually improve the diagnosis and treatment of this disorder."
Myelodysplastic syndromes are a difficult-to-treat family of blood cancers that occur when blood cells in the bone marrow don't mature properly. About 28,000 Americans are diagnosed with the disorder each year, most of them over age 60. Drugs are available to treat the disease, but none can cure it.
In about 30 percent of cases, the disorder progresses to a form of acute myeloid leukemia that usually is fatal because chemotherapy drugs are not effective in these patients. Doctors currently assess the likelihood that a patient with myelodysplastic syndrome will develop leukemia by looking at the chromosomes in the tumor cells to determine the extent to which they have broken apart and rearranged themselves, an indicator of the severity of the disease.
"There are chromosomal patterns that indicate high risk and low risk, but the current methods to determine prognosis aren't perfect," says first author Timothy Graubert, MD, associate professor of medicine, who specializes in treating patients with myelodysplastic syndromes.
After identifying the U2AF1 mutation in three patients through whole-genome sequencing, the researchers scoured the gene for the mutation in another 150 patients with myelodysplastic syndromes. They identified the mutation in 13, or nearly 9 percent. The mutations were acquired during development of myelodysplastic syndromes because they were not present in normal cells obtained from each patient.
Patients were almost three times as likely to develop leukemia if they had a mutation in the U2AF1 gene. The disorder progressed to leukemia in 15.2 percent of patients with the mutation, compared with 5.8 percent of those without the genetic error.
The most common mutation results in a single letter change in the DNA at a precise location in the U2AF1 gene. Patients with the genetic error were most likely to have the amino acids phenylalanine or tyrosine substituted for a serine. The researchers say that the mutation by itself does not cause myelodysplastic syndromes but appears to be an early event in the course of the disease.
Normally, the U2AF1 gene makes a protein involved in splicing RNA, a sister molecule of DNA that carries the instructions for building proteins. Splicing brings together different sections of RNA necessary to make a protein and discards those sections that are not needed. The mutated version of the gene still produces a protein, but its splicing activity is altered, which may be important for the development of some cancers.
The new research, funded in part by a federal stimulus grant, adds to a flurry of new findings about the genetic basis of myelodysplastic syndromes. Recent studies in Nature and the New England Journal of Medicine, along with the current study, have identified mutations in a total of eight genes involved in RNA splicing in patients with the disorder.
"Together, these findings are a real game-changer," Graubert says. "A mutation in any one of these eight genes occurs in up to 50 percent of patients with myelodysplastic syndromes. Because these changes are so common, we think there are likely to be implications for improving the diagnosis of the disorder and finding new therapeutic options."
Whole-genome sequencing for cancer was pioneered by scientists at Washington University School of Medicine and the university's Genome Institute, including Richard Wilson, PhD; Elaine Mardis, PhD; Timothy Ley, MD; and Li Ding, PhD, all of whom are co-authors of the study. The new research builds on their work to find novel mutations in cancer by looking across a patient's entire genome.
###
The research was supported by the National Institutes of Health (NIH) and a Howard Hughes Medical Institute Physician-Scientist Early Career Award.
Graubert, TA et al. Recurrent mutations in the U2AF1 splicing factor in myelodysplastic syndromes. Nature Genetics. Advance online publication, Dec. 11, 2011.
Washington University School of Medicine's 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children's hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked fourth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children's hospitals, the School of Medicine is linked to BJC HealthCare.
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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.
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Public release date: 15-Dec-2011
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