WASHINGTON ? Rick Santorum says he's under no pressure to quit the GOP presidential race so conservative voters can coalesce around Newt Gingrich.
The former Pennsylvania senator tells CNN's "State of the Union" that his campaign is building momentum even after a third-place finish in South Carolina. He says he expects to run well in Florida's Jan. 31 primary.
Santorum says the suggestion that conservatives will have to coalesce to beat former Massachusetts Gov. Mitt Romney is "objectively false."
Santorum points out that he beat Romney in Iowa and says Gingrich "smoked him here in South Carolina."
Santorum says that while Romney has more campaign money, he has the better ideas and message to inspire voters.
A study published this week in the journal Leukemia identifies a mechanism that acute myeloid leukemia (AML) cells use to evade chemotherapy ? and details how to close this escape route.
"Introducing chemotherapy to cells is like putting a curve in front of a speeding car," says Christopher Porter, MD, investigator at the University of Colorado Cancer Center and assistant professor of pediatrics at the University of Colorado School of Medicine. "Cells that can put on the brakes make it around the corner and cells that can't speed off the track."
Porter and colleagues collaborated with James DeGregori, PhD, CU Cancer Center investigator and professor of biochemistry and molecular genetics at the CU School of Medicine to define a molecular braking process that AML cells use to survive the curves of chemotherapy. They also showed that when this molecular brake is removed, AML cells (but not their healthy neighbors) die on the corners.
The discovery of this escape route and how to plug it provides hope for survival for a greater proportion of the estimated 12,950 people diagnosed with AML every year in the United States.
The group's findings rely on the relatively new technique of functional genomic screening of AML cells, accomplished by the CU Cancer Center Functional Genomics Shared Resource at the University of Colorado Boulder.
Using techniques they developed, the group turned off a different gene in each of a population of AML cells all at once. Then they hit all cells with chemotherapy traditionally used for AML. The goal: to see which genes, when turned off, would make the cells especially susceptible to chemo.
In this study, which generated over 30 million data points, cells that lacked a gene to make something called WEE1 died in disproportionate numbers. When you turn off WEE1, cancer cells die.
"WEE1 is the brakes," Porter says. "With chemotherapy we introduce DNA damage in cancer cells ? we push them toward the curve hopefully at a greater rate than healthy cells. If WEE1 is there, cancer cells can round the curve. Without it, they flip."
Hidden in Porter's words is an element that makes this an especially exciting finding: AML cells may be more dependent than are healthy cells on WEE1. And so when you inhibit WEE1, you strip the brakes from cancer cells but not their healthy neighbors, killing AML cells but leaving healthy cells able to corner on rails.
"I'm optimistic that this will eventually lead to a therapeutic regimen that allows us to target AML cells that have escaped conventional therapies," Porter says.
Porter calls the team's initial results combining a drug that inhibits WEE1 with chemotherapy in mouse models of AML, "extremely promising."
"In light of these data, we are already early in the clinical trial planning process," Porter says.
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University of Colorado Denver: http://www.ucdenver.edu
Thanks to University of Colorado Denver for this article.
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[unable to retrieve full-text content]Changes to the way autism is diagnosed may make it harder for many people who would no longer meet the criteria to get health, educational and social services, researchers say.
In this film image released by Sundance Film Festival, Melanie Lynskey is shown in a scene from "Hello I Must Be Going," a love story between a 19-year-old man and a 35-year-old divorcee that will be featured at the Sundance Film Festival, opening Thursday, Jan. 19, 2012. (AP Photo/Sundance Film Festival)
In this film image released by Sundance Film Festival, Melanie Lynskey is shown in a scene from "Hello I Must Be Going," a love story between a 19-year-old man and a 35-year-old divorcee that will be featured at the Sundance Film Festival, opening Thursday, Jan. 19, 2012. (AP Photo/Sundance Film Festival)
In this image released by Sundance Film Festival, Jackie Siegel is shown with her children during the filming of a documentary, "The Queen of Versailles," being shown at the Sundance Film Festival. The festival begins Thursday, Jan. 19, 2012. (AP Photo/Sundance Film Festival, Lauren Greenfield)
PARK CITY, Utah (AP) ? A fresh dusting of snow over Park City heralded the opening of the Sundance Film Festival on Thursday.
For 11 days every January, Sundance becomes the focal point of the independent film world as established directors and stars mix with up-and-coming talent, while theatrical distributors prowl the festival looking for the next indie hit and film lovers have a good time being the first audiences to see new movies.
"You can't make a film with a festival in mind, and it's not something I would have expected or taken for granted. But it's always kind of the dream in the back of your mind," said Lauren Greenfield, who premiered her debut documentary "Thin" at Sundance in 2006 and returns this time with one of the opening-night films, "The Queen of Versailles." It chronicles the housing-bust story of a couple that tried to build a palatial mansion.
"I think it's this really magical environment, a place that's such a nurturing, supportive influence for independent films. Even when you're out there making your film, I think that you think about Sundance, and it just kind of gives you motivation."
Also opening Thursday is "Hello I Must Be Going," actor-turned-director Todd Louiso's U.S. dramatic entry, which centers on a love story between a 19-year-old man and a 35-year-old divorcee that stars Melanie Lynskey.; the world-cinema drama "Wish You Were Here," a dark story of a vacation gone wrong from Australian filmmaker Kieran Darcy-Smith that stars Joel Edgerton and Teresa Palmer; and Swedish director Malik Bendjelloul's world-cinema documentary "Searching for Sugar Man," a portrait of promising 1970s singer-songwriter Rodriguez and his fade into obscurity.
Sundance also is a launch place for films that already have distributors, who show off their films hoping to build buzz among audiences and the legions of cinema journalists and bloggers who attend the festival.
"All the film press in North America is at Sundance to discover films," said Michael Barker, co-president of Sony Pictures Classics, which is showing director Nadine Labaki's Lebanese drama "Where Do We Go Now?" and Gareth Huw Evans' Indonesian action tale "The Raid" at the festival. "
Among the more established filmmakers showcasing their work at the festival are Spike Lee with his urban drama "Red Hook Summer," in which he reprises the character he played in "Do the Right Thing"; Stephen Frears with his sports-wagering caper "Lay the Favorite," starring Bruce Willis, Catherine Zeta-Jones and Rebecca Hall; documentary veteran Joe Berlinger with his Paul Simon portrait "Under African Skies"; and Julie Delpy with her relationship comedy "2 Days in New York," in which she stars with Chris Rock.
The Sundance Film Festival continues through Jan. 29.
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AP Movie Writer David Germain contributed to this report.
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AP Entertainment Writer Sandy Cohen is on Twitter: www.twitter.com/APSandy .
ScienceDaily (Jan. 17, 2012) ? A natural enzyme derived from human blood plasma showed potential in significantly reducing the effects of graft-vs.-host disease, a common and deadly side effect of lifesaving bone marrow transplants.
Researchers from the University of Michigan Comprehensive Cancer Center looked at the drug alpha-1-antitrypsin, which is approved by the U.S. Food and Drug Administration for use in people who have a genetic mutation that makes them deficient in a certain enzyme. This drug has been used in many of these patients over extended periods of time and is known to cause minimal side effects.
More important, there are no known reports of increased susceptibility to infections. This is key for people with graft-vs.-host disease, where existing treatment options tend to suppress the immune system, putting patients at risk of infection. Graft-vs.-host disease is a major complication of bone marrow transplants using marrow from a donor, called an allogeneic transplant. This often-deadly side effect is what makes the procedure so risky.
"If we can get graft-vs.-host disease under control, we can more effectively use allogeneic bone marrow transplant to treat people with leukemia and lymphoma as well as other blood disorders. It would be a curative therapy for people who otherwise have no hope," says senior study author Pavan Reddy, M.D., associate professor of hematology/oncology at the U-M Medical School.
In this study, which appears in the Proceedings of the National Academy of Sciences, researchers used alpha-1-antitrypsin in mice that received allogeneic bone marrow transplants. The drug significantly reduced mortality from graft-vs.-host disease, compared to control mice who did not receive the drug.
In addition, alpha-1-antitrypsin reduced the number of inflammatory cells called T Effector cells that are known to be present in graft-vs.-host disease. It also increased the number of T-regulatory cells, which immunologists believe play a positive role in immune responses.
"It's likely the balance between the T-regulatory cells and the T Effector cells that leads to graft-vs.-host disease. Alpha-1-antitrypsin appears to have tipped that balance favorably," says lead study author Isao Tawara, M.D., Ph.D., a research investigator at the U-M Medical School.
The U-M researchers collaborated on this work with researchers from the University of Colorado and from Ben Gurion University of the Negev in Israel. The researchers are beginning to discuss a possible clinical trial using alpha-1-antitrypsin in post-transplant patients with graft-vs.-host disease for whom conventional therapies are no longer working.
Additional authors include Yaping Sun, Tomomi Toubai, Rebecca Evers and Evelyn Nieves, all from U-M; Eli C. Lewis, from Ben-Gurion University of the Negev in Israel; Tania Azam and Charles A. Dinarello, from the University of Colorado.
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Journal Reference:
I. Tawara, Y. Sun, E. C. Lewis, T. Toubai, R. Evers, E. Nieves, T. Azam, C. A. Dinarello, P. Reddy. Alpha-1-antitrypsin monotherapy reduces graft-versus-host disease after experimental allogeneic bone marrow transplantation. Proceedings of the National Academy of Sciences, 2011; 109 (2): 564 DOI: 10.1073/pnas.1117665109
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High risk oesophageal cancer gene discoveredPublic release date: 19-Jan-2012 [ | E-mail | Share ]
Contact: Kerry Noble k.noble@qmul.ac.uk 44-020-788-27943 Queen Mary, University of London
New research from Queen Mary, University of London has uncovered a gene which plays a key role in the development of oesophageal cancer (cancer of the gullet).
The researchers studied families who suffer a rare inherited condition making them highly susceptible to the disease and found that a fault in a single gene was responsible.
Initial studies suggest that the gene could play a role in the more common, non-inherited form of the disease, revealing a new target for treating this aggressive type of cancer.
Oesophageal cancer affects more than 8,000 people each year in the UK and rates are rising. It is more common in the UK than anywhere else in Europe.
Survival rates are poor compared to other types of cancer with only eight per cent of people alive five years after diagnosis. Scientists know little about how oesophageal cancer develops and very few drugs for targeting the disease are currently available.
The new study was led by Professor David Kelsell from Queen Mary, University of London with collaborators from the University of Dundee and the University of Liverpool.
The research concentrated on three families with a hereditary condition called tylosis with oesophageal cancer. This condition affects the skin and mouth and sufferers have a 95 per cent chance of developing oesophageal cancer by the age of 65.
The research revealed that all three families carried a faulty version of a gene called RHBDF2.
Experiments showed that this gene plays an important role in how cells that line the oesophagus, and cells in the skin, respond to injury. When the gene is functioning normally it ensures that cells grow and divide in a controlled fashion to help heal a wound.
However, in tylosis patients' cells, and in cells from oesophageal cancers, the gene malfunctions. This allows cells to divide and grow uncontrollably, causing cancer.
Professor Kelsell explains: "In studying this relatively rare condition, we have made an important dicovery about a cancer that is all too common. Finding a genetic cause for this aggressive cancer, and understanding what that gene is doing, is an enormous step forward.
"By analysing the complex biology which causes a particular type of cancer we begin to understand which treatments might be effective and also which treatments are unlikely to help."
###
The study was funded by Queen Mary Innovations and Cancer Research UK. Professor Kelsell has also received new funding from Barts and The London Charity to continue this research.
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High risk oesophageal cancer gene discoveredPublic release date: 19-Jan-2012 [ | E-mail | Share ]
Contact: Kerry Noble k.noble@qmul.ac.uk 44-020-788-27943 Queen Mary, University of London
New research from Queen Mary, University of London has uncovered a gene which plays a key role in the development of oesophageal cancer (cancer of the gullet).
The researchers studied families who suffer a rare inherited condition making them highly susceptible to the disease and found that a fault in a single gene was responsible.
Initial studies suggest that the gene could play a role in the more common, non-inherited form of the disease, revealing a new target for treating this aggressive type of cancer.
Oesophageal cancer affects more than 8,000 people each year in the UK and rates are rising. It is more common in the UK than anywhere else in Europe.
Survival rates are poor compared to other types of cancer with only eight per cent of people alive five years after diagnosis. Scientists know little about how oesophageal cancer develops and very few drugs for targeting the disease are currently available.
The new study was led by Professor David Kelsell from Queen Mary, University of London with collaborators from the University of Dundee and the University of Liverpool.
The research concentrated on three families with a hereditary condition called tylosis with oesophageal cancer. This condition affects the skin and mouth and sufferers have a 95 per cent chance of developing oesophageal cancer by the age of 65.
The research revealed that all three families carried a faulty version of a gene called RHBDF2.
Experiments showed that this gene plays an important role in how cells that line the oesophagus, and cells in the skin, respond to injury. When the gene is functioning normally it ensures that cells grow and divide in a controlled fashion to help heal a wound.
However, in tylosis patients' cells, and in cells from oesophageal cancers, the gene malfunctions. This allows cells to divide and grow uncontrollably, causing cancer.
Professor Kelsell explains: "In studying this relatively rare condition, we have made an important dicovery about a cancer that is all too common. Finding a genetic cause for this aggressive cancer, and understanding what that gene is doing, is an enormous step forward.
"By analysing the complex biology which causes a particular type of cancer we begin to understand which treatments might be effective and also which treatments are unlikely to help."
###
The study was funded by Queen Mary Innovations and Cancer Research UK. Professor Kelsell has also received new funding from Barts and The London Charity to continue this research.
[ | E-mail | Share ]
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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: 19-Jan-2012
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