WASHINGTON (AP) ? Healthy men shouldn't get routine prostate cancer screenings, says updated advice from a government panel that found the PSA blood tests do more harm than good.
Despite strenuous protests from urologists, the U.S. Preventive Services Task Force is sticking by a contentious proposal it made last fall. A final guideline published Monday says there's little if any evidence that PSA testing saves lives ? while too many men suffer impotence, incontinence, heart attacks, occasionally even death from treatment of tiny tumors that never would have killed them.
The guideline isn't a mandate. The task force stresses that men who want a PSA test still can get one, but only after the doctor explains the uncertainties. That's in part because the panel found PSA testing hasn't been studied adequately in black men and those with prostate cancer in the family, who are at highest risk of the disease.
The Obama administration said Monday that Medicare will continue to pay for PSA screenings, a simple blood test. Other insurers tend to follow Medicare's lead.
"This is important information for the public and men to have, and they should talk with their doctors about the risks and benefits of prostate cancer screening and make the decision that's best for them," said Mark Weber, a spokesman for the Department of Health and Human Services.
The task force advice goes a step further than major health groups including the American Cancer Society, which has long urged that men decide the issue for themselves after being told of PSA's pros and cons. But it's not likely to end an annual ritual for many men 50 and older. After all, the same task force has long urged men over 75 to skip PSA screening, and research suggests almost half of them still get tested.
The controversy will end only with development of better tests ? to finally tell which men's tumors really will threaten their lives, and who will die with prostate cancer rather than from it, said Dr. Virginia Moyer of the Baylor College of Medicine, who heads the task force.
"We have been told for decades to be terrified of cancer and that the only hope is early detection and treatment," she said. The reality: "You don't need to detect all cancers."
"We don't want this to be the answer," Moyer added. "We want to screen for the ones that are going to be aggressive, manage those early ? and leave everyone else alone."
In an editorial published with the guideline in Annals of Internal Medicine, some urologists argue the panel underestimated PSA's value and overestimated its harms.
"What PSA screening offers the men is a substantial opportunity to avoid dying a particularly unpleasant death from prostate cancer," said editorial co-author Dr. William Catalona of Northwestern University, who pioneered the testing.
He spoke Monday from a meeting of the American Urological Association, where doctors debated the guideline's impact. The urology association advises that men be informed of the potential risks and benefits before screening.
But Dr. Otis Brawley, the American Cancer Society's chief medical officer, welcomed the task force's recommendation. He hoped it would help deter mass screenings, where men are given free PSAs at shopping malls and sports arenas without being told of the controversy, screenings that Brawley calls big business when health centers profit from the follow-up care.
"The question is, are we actually curing anybody who needs to be cured right now?" Brawley asked.
Too much PSA, or prostate-specific antigen, in the blood only sometimes signals prostate cancer is brewing. It also can mean a benign enlarged prostate or an infection. Only a biopsy can tell. Most men will get prostate cancer if they live long enough. Some 240,000 U.S. men a year are diagnosed with it, most with slow-growing tumors that carry a very low risk of morphing into the kind that can kill.
To evaluate whether routine screening saves lives, the task force analyzed previous research, focusing in particular on two huge studies in the U.S. and Europe. The panel's conclusion:
?Without screening, about 5 in every 1,000 men die of prostate cancer over 10 years. The European study found PSA testing might prevent one of those deaths, while the U.S. study found no difference.
?Of every 1,000 men screened, two will have a heart attack or stroke from resulting cancer treatment, and 30 to 40 will experience treatment-caused impotence or incontinence.
?Of every 3,000 men screened, one will die from complications of surgery.
Both the U.S. and European studies have flaws, and task force critics argue over which are most believable. And while U.S. death rates from prostate cancer have dropped over 20 years, the cancer society's Brawley says the drop began before PSA testing became widespread. Moreover, the risk of death is the same in Europe and the U.S. even though many more American men are screened, diagnosed and treated, he said.
"We need to do a better job of using PSA wisely," said Dr. Scott Eggener, a University of Chicago prostate cancer specialist who was disappointed the task force went so far. "Most people would agree that a well-informed, young, healthy patient should have the opportunity to talk about it with their physician."
But he's studying a way beyond the screen-or-not controversy: Having men with small, low-risk tumors postpone treatment in favor of "active surveillance," keeping close watch on their tumors and treating only if they grow. More than 100,000 men a year are candidates, concluded a recent meeting at the National Institutes of Health.
That approach could "maximize the benefits of screening," Eggener said.
___
Online:
Task force information: http://www.uspreventiveservicestaskforce.org/recommendations.htm
In today?s world where almost everything can be performed online ? from feeding to fornication and everything else in between ? jobs search using the Internet is a natural progression for professionals. You have to thank business social networking sites like Facebook, LinkedIn, Plaxo and Ryze for making your jobs search easier after the PMP exam by expanding your network of contacts at the click of a mouse.
It is this social networking feature of the Internet that you should explore and exploit if you desire to transform your success in the PMP exam into juicier jobs. Here is how.
Right Target, Right Groups
First, you have to set the target/criteria of your jobs search ? location, expertise needed, educational attainment, industry, and current position, among others. With the plethora of groups in these social networking sites, you will find one that perfectly fits your jobs search criteria. On the other hand, you can always join many groups to expand your network. Eventually, you will have many referrals that will enable you to apply for jobs that are not advertised on the classified ads as well as the positive recommendations from your network of online contacts.
In fact, you can even start establishing your online social network on the day of the PMP exam itself! If you can be your charming self, you can ask for business cards and request for your inclusion in existing groups. You have to set aside your competitive instincts because the PMP exam is not a competition against other project managers ? it is a competition against yourself.
Be Professional, Be Sociable
Unless you are in a social networking site to find your soul mate, posting too informal and too casual messages will not do the trick of finding your dream job. You have to treat virtual networking like it is a face-to-face interaction ? with a sense of professionalism and responsibility. You can look back into the Professional and Social Responsibility portion of the PMP exam. Some tips:
* Comment and post to industry links in a professional manner, which shows you are an expert in the field
* Start a conversation within the group, which reflects your initiative and expertise
* Continue the conversation others have started in a clear and concise manner, which attests to your willingness to participate in discussions
With online social skills such as these, you will not fail to get your dream job soon after passing the PMP exam!
Link Up, Link to Many
Don?t forget to provide a link back to your Facebook, LinkedIn, Plaxo and Ryze profiles, even your personal webpage. Not only will you be inviting hiring managers trawling for project managers, you will also be providing an ingenious way to have your profile rank higher in Yahoo and Google searches.
Besides, it never did hurt anyone to have as many contacts as possible. Nowadays, finding your dream job is often who you know, not what you know simply because there are many other individuals as bright, as talented, as credentialed as you are. Maybe even more than you are!
So, what are you waiting for? Sign up and link up now!
Jessica Parklanes
~John Sotruo
? Business Networking Sites- Your Career Pulley LeverAre You not Into Social Networking Yet? ?
This entry was posted by John Sotruo at 2:51 pm and is filed under LinkedIn Networking.
You can follow any responses to this entry through the RSS 2.0 feed.
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The National Association for Business Economics said the country's "subpar" recovery will continue over the next year and a half. Employment, housing and spending metrics will continue to improve, albeit at a sluggish pace, the group forecasted, with unemployment only ticking down to 8 percent by the end of this year, before falling to 7.5 percent at the end of 2013.
The 54 economists who participated in the survey predicted an average of 188,000 jobs added monthly for 2012, compared to the 170,000 forecasted in NABE's last survey.
This is a considerably brighter outlook than the group's September report, in which surveyed economists predicted an 8.5 unemployment rate at the end of this year.?A recovery in housing also appears to be inching forward. NABE revised an earlier projection of no price increases for this year to a positive but meager 0.5 percent increase, followed by a 2 percent increase next year.?
Still, the new survey's modest expectations for the next year and a half show that economists think the nation's financial recovery has a long way to go.?
"Expectations for housing, vehicle sales, employment, and industrial production all improved in the current survey. However, expectations for overall economic growth as measured by inflation-adjusted gross domestic product, business investment, and consumer spending remain below historical norms,? survey chair Shawn DuBravac wrote.
Economists surveyed by NABE projected GDP growth for this year and next year of 2.4 percent and 2.8 percent, respectively. These figures are at the low end of the Federal Reserve's recent estimates last month. The Fed predicted a range of 2.4 percent to 2.9 percent GDP growth for this year, and 2.7 percent to 3.1 percent growth in 2013.?
On the positive side, economists continue to think that inflation and interest rates will remain low through the end of 2013.
JERUSALEM (AP) ? The U.S. has plans in place to attack Iran if necessary to prevent it from developing nuclear weapons, Washington's envoy to Israel said, days ahead of a crucial round of nuclear talks with Tehran.
Dan Shapiro's message resonated Thursday far beyond the closed forum in which it was made: Iran should not test Washington's resolve to act on its promise to strike if diplomacy and sanctions fail to pressure Tehran to abandon its disputed nuclear program.
Shapiro told the Israel Bar Association the U.S. hopes it will not have to resort to military force.
"But that doesn't mean that option is not fully available. Not just available, but it's ready," he said. "The necessary planning has been done to ensure that it's ready."
Iran says its nuclear program is for peaceful purposes, like energy production. The U.S. and Israel suspect Iran is pursuing nuclear weapons, but differences have emerged in how to persuade Tehran to curb its program.
Washington says diplomacy and economic sanctions must be given a chance to run its course, and is taking the lead in the ongoing talks between six global powers and Iran.
Israel, while saying it would prefer a diplomatic solution, has expressed skepticism about these talks and says time is running out for military action to be effective.
President Barack Obama has assured Israel that the U.S. is prepared to take military action if necessary, and it is standard procedure for armies to draw up plans for a broad range of possible scenarios. But Shapiro's comments were the most explicit sign yet that preparations have been stepped up.
In his speech, Shapiro acknowledged the clock is ticking.
"We do believe there is time. Some time, not an unlimited amount of time," Shapiro said. "But at a certain point, we may have to make a judgment that the diplomacy will not work."
The U.S. envoy spoke on Tuesday. The Associated Press obtained a recording of his remarks on Thursday.
The five permanent members of the U.N. Security Council and Germany are gearing up to for a May 23 meeting with Iran in Baghdad. Shortly after the meeting, the U.N. atomic agency is to release its latest report card on Iran's nuclear efforts.
In Tehran on Thursday, top nuclear negotiator Saeed Jalili warned against Western pressure at next week's talks, which are a follow-up to negotiations in Istanbul last month that all sides praised as positive.
"Cooperation is what we can talk about in Baghdad," Jalili said in comments broadcast on Iranian state TV.
"Some say time is running out for the talks," he added. "I say time for the (West's) pressure strategy is running out."
Four rounds of U.N. sanctions have failed to persuade Iran to halt its uranium enrichment, a process that has civilian uses but is also key to bomb-making. But recent U.S. and European measures, including an oil embargo and financial and banking sanctions, have bludgeoned Iran's economy by curtailing its ability to carry on economic transactions with the international community.
Israel says a nuclear weapon in the hands of Iran would threaten the Jewish state's survival and has waged a fierce diplomatic campaign against the Iranian nuclear program for years. Israel cites Iranian calls for Israel's destruction, Iran's arsenal of missiles, and its support for anti-Israel militant groups.
Senior officials have expressed skepticism about the sanctions' effectiveness, and believe Tehran is using the talks to stall the international community as Iran moves ever closer to a nuclear bomb.
The United States has urged Israel to refrain from attacking, at least at this point. Tough new economic sanctions are to go into effect over the summer, and American officials fear an Israeli strike could set off a regional war without significantly setting back the Iranian program.
Prime Minister Benjamin Netanyahu argues the negotiations will fail unless Iran agrees to halt all uranium enrichment, ship its current stockpile of enriched uranium out of the country and dismantle an underground enrichment facility near the city of Qom.
Maj. Gen. Ido Nehushtan, who until a few days ago commanded Israel's air force, said in a Jerusalem Post interview Thursday that the air force is prepared for any scenario, including striking Iranian nuclear facilities.
Israel's military chief told the Associated Press last month that other countries as well as Israel have readied their armed forces for a potential strike against Iran's nuclear sites.
[unable to retrieve full-text content]With the growing availability of tools to modify organisms, a creature like the bird imagined in the ?Hunger Games? series is not an impossible fantasy.
FILE - In this May 10, 2012 file photo released by Fox, Jessica Sanchez poses in Los Angeles. The Philippines' leader is rooting for Sanchez, the 16-year-old American Idol finalist of Filipino and Latino heritage. (AP Photo/Fox, Michael Becker, File)
FILE - In this May 10, 2012 file photo released by Fox, Jessica Sanchez poses in Los Angeles. The Philippines' leader is rooting for Sanchez, the 16-year-old American Idol finalist of Filipino and Latino heritage. (AP Photo/Fox, Michael Becker, File)
MANILA, Philippines (AP) ? Philippine President Benigno Aquino III has picked his "American Idol."
The Philippines' leader says he is happy Jessica Sanchez is one of the singing contest's top three finalists and "hopefully she really reaches the top."
The 16-year-old Sanchez is from Chula Vista, California, and has Filipino and Latino heritage. She is being cheered by many in the Philippines and by the Filipino and Mexican communities in the U.S.
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Scientists discover marker to identify, attack breast cancer stem cellsPublic release date: 15-May-2012 [ | E-mail | Share ]
Contact: Scott Merville smerville@mdanderson.org 713-792-0661 University of Texas M. D. Anderson Cancer Center
Cell surface protein blows potent cells' cover; targeted drug works in preclinical tests
HOUSTON Breast cancer stem cells wear a cell surface protein that is part nametag and part bull's eye, identifying them as potent tumor-generating cells and flagging their vulnerability to a drug, researchers at The University of Texas MD Anderson Cancer Center report online in Journal of Clinical Investigation.
"We've discovered a single marker for breast cancer stem cells and also found that it's targetable with a small molecule drug that inhibits an enzyme crucial to its synthesis," said co-senior author Michael Andreeff, M.D., Ph.D., professor in MD Anderson's Departments of Leukemia and Stem Cell Transplantation and Cellular Therapy.
Andreeff and colleagues are refining the drug as a potential targeted therapy for breast cancer stem cells, which are thought to be crucial to therapy resistance, disease progression and spread to other organs.
"It's been difficult to identify cancer stem cells in solid tumors," Andreeff said. "And nobody has managed to target these cells very well."
The marker is the cell surface protein ganglioside GD2. The drug is triptolide, an experimental drug that Andreeff has used in preclinical leukemia research. The team found triptolide blocks expression of GD3 synthase, which is essential to GD2production.
Triptolide stymied cancer growth in cell line experiments and resulted in smaller tumors and prolonged survival in mouse experiments. Drug development for human trials probably will take several years.
Cancer stem cells are similar to normal stem cells
Research in several types of cancer has shown cancer stem cells are a small subpopulation of cancer cells that are capable of long-term self-renewal and generation of new tumors. More recent research shows they resist treatment and promote metastasis.
Cancer stem cells are similar to normal stem cells that renew specialized tissues. The breast cancer findings grew out of Andreeff's long-term research in mesenchymal stem cells, which can divide into one copy of themselves and one differentiated copy of a bone, muscle, fat or cartilage cell.
Andreeff has shown these mobile mesenchymal stem cells home to wounds, including tumors, making them potential carriers of cancer therapy.
An important cellular transition also comes into play.
Co-senior author Sendurai Mani, Ph.D., assistant professor in MD Anderson's Department of Molecular Pathology and Co-Director of the Metastasis Research Center, is an expert on epithelial-to-mesenchymal transition (EMT). About 85 percent of all solid tumors start in the lining of an organ, called the epithelium. Mani and colleagues at MIT showed that epithelial cells can be induced to take on stem cell properties by forcing them to undergo EMT.
"This change from stationary epithelial cells to the mobile mesenchymal stem cells is an important step in metastasis," Mani said.
Andreeff and Mani in 2010 discovered that human mammary epithelial cells that undergo epithelial-to-mesenchymal transition act similarly to human bone-marrow-derived mesenchymal stem cells. They can home in to wounds and differentiate into the same cell types.
GD2 separates cancer stem cells from other tumor cells
In the current project, the researchers hypothesized that the cell markers expressed on the surface of mesenchymal stem cells would also be expressed on the surface of breast cancer stem cells.
They found that GD2 expression, one such mesenchymal stem cell marker, divided the breast cancer cell lines into two distinct groups: about 4.5 percent of cells were GD2-positive and about 92.7 percent were GD2-negative.
GD2-positive breast cancer cells:
Form twice as many mammospheres, a clumping of cells considered an indicator of tumor-forming capacity, as compared to GD2-negative cells. And the spheres were three times as large.
Migrate four times as fast as GD2-negative cells.
Form five times as many tumors when 10 cells of each type are transplanted into mice.
GD2-positive cells also have general cancer stem cell marker
A known combination marker of cancer stem cells is high expression of CD44 and low expression of CD24 surface proteins. The researchers found 85 percent of GD2-positive breast cancer cells were CD44 high/CD24 low, while only 1 percent of GD2-negative cells shared that characteristic.
An analysis of 12 human breast cancer tumors found an even higher correlation of 95.5 percent between GD2+ cells and CD44 high/CD24 low status.
Comparing gene expression between GD2+ cells and CD44 high/CD24 low cells revealed 100 percent correlation in the expression of 231 genes.
GD2+ cells had greater expression of genes involved in migration, invasion and epithelial-mesenchymal transition than GD2- cells. They also had a nine-fold increase in GD3 synthase, a key enzyme in the eventual synthesis of GD2.
Further experiments showed that:
Inducing EMT raised the percentage of GD2+ cells in two breast cancer cell lines.
Knocking down GD3 synthase cut the percentage of GD2+ cells by more than half.
Mice injected with 1 million breast cancer cells having a small interfering RNA that blocked GD3 synthase never developed tumors even after eight weeks, while all of the control mice with active GD3S developed tumors.
Triptolide stymies tumor growth, extends survival
The researchers then used triptolide, a known inhibitor of GD3 synthase, to treat immune-deficient mice injected with breast cancer cells. Of the mice treated, 50 percent did not develop breast cancer and the other half had smaller tumors than the control mice. The treated mice also lived longer than the controls.
GD2's function in cancer stem cells remains unclear. "As GD2 is an immune suppressant, it would be needed by cancer stem cells to counter immune cells during metastases," said first author Venkata Lokesh Battula, Ph.D., of MD Anderson's Department of Leukemia. "Inhibition of GD2 expression in cancer cells may enhance the inherent ability of immune cells to kill cancer cells."
###
Co-authors with Andreeff, Mani and Battula are Yuexi Shi, Rui-Yu Wang, M.D., Ph.D., Erika Spaeth, Ph.D., Rodrigo Jacamo, and Frank Marini, Ph.D., all of MD Anderson's Department of Leukemia, Section of Molecular Hematology and Therapy; Kurt Evans, of the Department of Molecular Pathology; Aysegul Sahin, M.D., of the Department of Pathology; and Gabriel Hortobagyi, M.D., of the Department of Breast Medical Oncology; and Rudy Guerra, Ph.D., Rice University Department of Statistics.
This project was funded by grants from the National Cancer Institute of the National Institutes of Health, including MD Anderson's Specialized Program of Research Excellence in Breast Cancer, the MD Anderson Research Trust Fellow Award, which is funded by the George and Barbara Bush Endowment for Innovative Cancer Research, for Mani and by the Paul and Mary Haas Chair in Genetics in Honor of Amanda Marie Whittle held by Andreeff.
[ | E-mail | Share ]
?
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.
Scientists discover marker to identify, attack breast cancer stem cellsPublic release date: 15-May-2012 [ | E-mail | Share ]
Contact: Scott Merville smerville@mdanderson.org 713-792-0661 University of Texas M. D. Anderson Cancer Center
Cell surface protein blows potent cells' cover; targeted drug works in preclinical tests
HOUSTON Breast cancer stem cells wear a cell surface protein that is part nametag and part bull's eye, identifying them as potent tumor-generating cells and flagging their vulnerability to a drug, researchers at The University of Texas MD Anderson Cancer Center report online in Journal of Clinical Investigation.
"We've discovered a single marker for breast cancer stem cells and also found that it's targetable with a small molecule drug that inhibits an enzyme crucial to its synthesis," said co-senior author Michael Andreeff, M.D., Ph.D., professor in MD Anderson's Departments of Leukemia and Stem Cell Transplantation and Cellular Therapy.
Andreeff and colleagues are refining the drug as a potential targeted therapy for breast cancer stem cells, which are thought to be crucial to therapy resistance, disease progression and spread to other organs.
"It's been difficult to identify cancer stem cells in solid tumors," Andreeff said. "And nobody has managed to target these cells very well."
The marker is the cell surface protein ganglioside GD2. The drug is triptolide, an experimental drug that Andreeff has used in preclinical leukemia research. The team found triptolide blocks expression of GD3 synthase, which is essential to GD2production.
Triptolide stymied cancer growth in cell line experiments and resulted in smaller tumors and prolonged survival in mouse experiments. Drug development for human trials probably will take several years.
Cancer stem cells are similar to normal stem cells
Research in several types of cancer has shown cancer stem cells are a small subpopulation of cancer cells that are capable of long-term self-renewal and generation of new tumors. More recent research shows they resist treatment and promote metastasis.
Cancer stem cells are similar to normal stem cells that renew specialized tissues. The breast cancer findings grew out of Andreeff's long-term research in mesenchymal stem cells, which can divide into one copy of themselves and one differentiated copy of a bone, muscle, fat or cartilage cell.
Andreeff has shown these mobile mesenchymal stem cells home to wounds, including tumors, making them potential carriers of cancer therapy.
An important cellular transition also comes into play.
Co-senior author Sendurai Mani, Ph.D., assistant professor in MD Anderson's Department of Molecular Pathology and Co-Director of the Metastasis Research Center, is an expert on epithelial-to-mesenchymal transition (EMT). About 85 percent of all solid tumors start in the lining of an organ, called the epithelium. Mani and colleagues at MIT showed that epithelial cells can be induced to take on stem cell properties by forcing them to undergo EMT.
"This change from stationary epithelial cells to the mobile mesenchymal stem cells is an important step in metastasis," Mani said.
Andreeff and Mani in 2010 discovered that human mammary epithelial cells that undergo epithelial-to-mesenchymal transition act similarly to human bone-marrow-derived mesenchymal stem cells. They can home in to wounds and differentiate into the same cell types.
GD2 separates cancer stem cells from other tumor cells
In the current project, the researchers hypothesized that the cell markers expressed on the surface of mesenchymal stem cells would also be expressed on the surface of breast cancer stem cells.
They found that GD2 expression, one such mesenchymal stem cell marker, divided the breast cancer cell lines into two distinct groups: about 4.5 percent of cells were GD2-positive and about 92.7 percent were GD2-negative.
GD2-positive breast cancer cells:
Form twice as many mammospheres, a clumping of cells considered an indicator of tumor-forming capacity, as compared to GD2-negative cells. And the spheres were three times as large.
Migrate four times as fast as GD2-negative cells.
Form five times as many tumors when 10 cells of each type are transplanted into mice.
GD2-positive cells also have general cancer stem cell marker
A known combination marker of cancer stem cells is high expression of CD44 and low expression of CD24 surface proteins. The researchers found 85 percent of GD2-positive breast cancer cells were CD44 high/CD24 low, while only 1 percent of GD2-negative cells shared that characteristic.
An analysis of 12 human breast cancer tumors found an even higher correlation of 95.5 percent between GD2+ cells and CD44 high/CD24 low status.
Comparing gene expression between GD2+ cells and CD44 high/CD24 low cells revealed 100 percent correlation in the expression of 231 genes.
GD2+ cells had greater expression of genes involved in migration, invasion and epithelial-mesenchymal transition than GD2- cells. They also had a nine-fold increase in GD3 synthase, a key enzyme in the eventual synthesis of GD2.
Further experiments showed that:
Inducing EMT raised the percentage of GD2+ cells in two breast cancer cell lines.
Knocking down GD3 synthase cut the percentage of GD2+ cells by more than half.
Mice injected with 1 million breast cancer cells having a small interfering RNA that blocked GD3 synthase never developed tumors even after eight weeks, while all of the control mice with active GD3S developed tumors.
Triptolide stymies tumor growth, extends survival
The researchers then used triptolide, a known inhibitor of GD3 synthase, to treat immune-deficient mice injected with breast cancer cells. Of the mice treated, 50 percent did not develop breast cancer and the other half had smaller tumors than the control mice. The treated mice also lived longer than the controls.
GD2's function in cancer stem cells remains unclear. "As GD2 is an immune suppressant, it would be needed by cancer stem cells to counter immune cells during metastases," said first author Venkata Lokesh Battula, Ph.D., of MD Anderson's Department of Leukemia. "Inhibition of GD2 expression in cancer cells may enhance the inherent ability of immune cells to kill cancer cells."
###
Co-authors with Andreeff, Mani and Battula are Yuexi Shi, Rui-Yu Wang, M.D., Ph.D., Erika Spaeth, Ph.D., Rodrigo Jacamo, and Frank Marini, Ph.D., all of MD Anderson's Department of Leukemia, Section of Molecular Hematology and Therapy; Kurt Evans, of the Department of Molecular Pathology; Aysegul Sahin, M.D., of the Department of Pathology; and Gabriel Hortobagyi, M.D., of the Department of Breast Medical Oncology; and Rudy Guerra, Ph.D., Rice University Department of Statistics.
This project was funded by grants from the National Cancer Institute of the National Institutes of Health, including MD Anderson's Specialized Program of Research Excellence in Breast Cancer, the MD Anderson Research Trust Fellow Award, which is funded by the George and Barbara Bush Endowment for Innovative Cancer Research, for Mani and by the Paul and Mary Haas Chair in Genetics in Honor of Amanda Marie Whittle held by Andreeff.
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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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Numbers of professional moving companies are available in India. They offer wide range of relocation services according to shifting needs and budgets of people. Packing and shipping companies in India are the great help in shifting from one place to another. They offer good quality and affordable packing and goods transportation services in many different areas. Expert packers and movers serve people in simple home relocation, large scale commercial shifting, industry and plant shifting, office and shop relocation, pet shift, vehicle shifting, warehousing and in many other areas according to the situations.
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From the shell leakage present take a look at, the existing values from different details to the shell from the measured devices to the Method Neutral are examined.
7 : Regardless of as part of product structure screening and / or production cable verification
Just in case recent leakage examination, measurement of your latest dimension is placed on item at diverse points about the chassis to the process neutral stage.
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12 : About the class and additionally display about drinking water therapy machines
Drinking water treatment method devices by group is often divided into sewage treatment facilities, raw drinking water treatment method tools
13 : To the distinction and additionally discussion about drinking water therapy equipment
At present, the industry perceived by the public normally contains a water treatment equipment such as drinking water softeners
14 : From a specific rationalization of how a four sewage remedy works
Way of classification of drinking water therapy process, water is definitely authentic and completed drinking water high quality style gap
15 : Is the word for typically the extent associated with application associated with drinking water purification
Tools installation, commissioning from the technicians, set conversion filter cleaning time and time until the addressed water through the inlet to the body,
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