promise technology

Monday, October 31, 2011

Key driver of metastasis identified

Public release date: 31-Oct-2011
[ | E-mail |

Share ]

Contact: Jeremy Moore
Jeremy.Moore@aacr.org
267-646-0557
American Association for Cancer Research

PHILADELPHIA -- Scientists at Dalhousie University in Nova Scotia have identified a key mechanism of metastasis that could lead to blocking tumor growth if their findings are confirmed.

In a recent issue of Cancer Research, a journal of the American Association for Cancer Research, lead researcher David Waisman, Ph.D., professor in the Departments of Biochemistry and Molecular Biology and Pathology, and Canada Research Chair in Cancer Research at Dalhousie University, detailed the key role the macrophage cell surface protein S100A10 plays in allowing macrophages to move to the site of tumor growth a process that is essential to tumor development.

Waisman said the findings are an example of the complicated biology of cancer.

"We used to think that the only cells that mattered in a tumor were the cancer cells, and that's it, but now we are beginning to see that other cells must collaborate with cancer cells to drive tumor growth and permit an evolution of the cancer cells into metastatic cells. This change is what causes poor prognosis and ultimately what kills the patient," he said.

Waisman and colleagues discovered that tumors will not grow without macrophage assistance. These macrophages must come from the blood or from other locations in the tissues. How they are able to move through the tissues or from the blood supply into the tumor had always been a mystery.

These macrophages need to chew their way through the tissue that forms a barrier around the growing tumor in order to move into the tumor site and combine with the cancer cells. The researchers found on the outside surface of the macrophage is a protein called S100A10, which enables the macrophage to remove the tissue barriers retarding migration to the tumor site.

Theoretically, blocking either the macrophages or S100A10 chemically could slow, or even stop, tumor growth.

"We found that the protein, S100A10, acts like a pair of scissors on the outside of the macrophages that empowers the macrophages with the ability to chew their way through tissues and enter the tumor site where they release substances that stimulate cancer cell growth and metastatic evolution," said Waisman.

He said the next step is to figure out exactly how S100A10 functions as a molecular scissor and also to identify pharmaceutical agents that can block the action of S100A10, thereby preventing the movement of macrophages to the tumor site. By understanding exactly how S100A10 works at the molecular level, it may even be possible to design agents which block its activity.

###

The study was funded by a grant from the Canadian Cancer Society Research Institute and the Canadian Institutes of Health Research.

Follow the AACR on Twitter: @aacr #aacr
Follow the AACR on Facebook: http://www.facebook.com/aacr.org

The mission of the American Association for Cancer Research is to prevent and cure cancer. Founded in 1907, the AACR is the world's oldest and largest professional organization dedicated to advancing cancer research. The membership includes 33,000 laboratory, translational and clinical researchers; health care professionals; and cancer survivors and advocates in the United States and more than 90 other countries. The AACR marshals the full spectrum of expertise from the cancer community to accelerate progress in the prevention, diagnosis and treatment of cancer through high-quality scientific and educational programs. It funds innovative, meritorious research grants, research fellowships and career development awards to young investigators, and it also funds cutting-edge research projects conducted by senior researchers.
The AACR has numerous fruitful collaborations with organizations and foundations in the U.S. and abroad, and functions as the Scientific Partner of Stand Up To Cancer, a charitable initiative that supports groundbreaking research aimed at getting new cancer treatments to patients in an accelerated time frame. The AACR Annual Meeting attracts more than 17,000 participants who share the latest discoveries and developments in the field. Special Conferences throughout the year present novel data across a wide variety of topics in cancer research, treatment and patient care, and Educational Workshops are held for the training of young cancer investigators. The AACR publishes seven major peer-reviewed journals: Cancer Discovery; Cancer Research; Clinical Cancer Research; Cancer Epidemiology, Biomarkers & Prevention; Molecular Cancer Therapeutics; Molecular Cancer Research; and Cancer Prevention Research. In 2010, AACR journals received 20 percent of the total number of citations given to oncology journals. The AACR also publishes Cancer Today, a magazine for cancer patients, survivors and their caregivers, which provides practical knowledge and new hope for cancer survivors.
A major goal of the AACR is to educate the general public and policymakers about the value of cancer research in improving public health, the vital importance of increases in sustained funding for cancer research and biomedical science, and the need for national policies that foster innovation and the acceleration of progress against the 200 diseases we call cancer.

[ | 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.

Key driver of metastasis identified Public release date: 31-Oct-2011
[ | E-mail | Share ]
Contact: Jeremy Moore
Jeremy.Moore@aacr.org
267-646-0557
American Association for Cancer Research

PHILADELPHIA -- Scientists at Dalhousie University in Nova Scotia have identified a key mechanism of metastasis that could lead to blocking tumor growth if their findings are confirmed.

In a recent issue of Cancer Research, a journal of the American Association for Cancer Research, lead researcher David Waisman, Ph.D., professor in the Departments of Biochemistry and Molecular Biology and Pathology, and Canada Research Chair in Cancer Research at Dalhousie University, detailed the key role the macrophage cell surface protein S100A10 plays in allowing macrophages to move to the site of tumor growth a process that is essential to tumor development.

Waisman said the findings are an example of the complicated biology of cancer.

"We used to think that the only cells that mattered in a tumor were the cancer cells, and that's it, but now we are beginning to see that other cells must collaborate with cancer cells to drive tumor growth and permit an evolution of the cancer cells into metastatic cells. This change is what causes poor prognosis and ultimately what kills the patient," he said.

Waisman and colleagues discovered that tumors will not grow without macrophage assistance. These macrophages must come from the blood or from other locations in the tissues. How they are able to move through the tissues or from the blood supply into the tumor had always been a mystery.

These macrophages need to chew their way through the tissue that forms a barrier around the growing tumor in order to move into the tumor site and combine with the cancer cells. The researchers found on the outside surface of the macrophage is a protein called S100A10, which enables the macrophage to remove the tissue barriers retarding migration to the tumor site.

Theoretically, blocking either the macrophages or S100A10 chemically could slow, or even stop, tumor growth.

"We found that the protein, S100A10, acts like a pair of scissors on the outside of the macrophages that empowers the macrophages with the ability to chew their way through tissues and enter the tumor site where they release substances that stimulate cancer cell growth and metastatic evolution," said Waisman.

He said the next step is to figure out exactly how S100A10 functions as a molecular scissor and also to identify pharmaceutical agents that can block the action of S100A10, thereby preventing the movement of macrophages to the tumor site. By understanding exactly how S100A10 works at the molecular level, it may even be possible to design agents which block its activity.

###

The study was funded by a grant from the Canadian Cancer Society Research Institute and the Canadian Institutes of Health Research.

Follow the AACR on Twitter: @aacr #aacr
Follow the AACR on Facebook: http://www.facebook.com/aacr.org

The mission of the American Association for Cancer Research is to prevent and cure cancer. Founded in 1907, the AACR is the world's oldest and largest professional organization dedicated to advancing cancer research. The membership includes 33,000 laboratory, translational and clinical researchers; health care professionals; and cancer survivors and advocates in the United States and more than 90 other countries. The AACR marshals the full spectrum of expertise from the cancer community to accelerate progress in the prevention, diagnosis and treatment of cancer through high-quality scientific and educational programs. It funds innovative, meritorious research grants, research fellowships and career development awards to young investigators, and it also funds cutting-edge research projects conducted by senior researchers.
The AACR has numerous fruitful collaborations with organizations and foundations in the U.S. and abroad, and functions as the Scientific Partner of Stand Up To Cancer, a charitable initiative that supports groundbreaking research aimed at getting new cancer treatments to patients in an accelerated time frame. The AACR Annual Meeting attracts more than 17,000 participants who share the latest discoveries and developments in the field. Special Conferences throughout the year present novel data across a wide variety of topics in cancer research, treatment and patient care, and Educational Workshops are held for the training of young cancer investigators. The AACR publishes seven major peer-reviewed journals: Cancer Discovery; Cancer Research; Clinical Cancer Research; Cancer Epidemiology, Biomarkers & Prevention; Molecular Cancer Therapeutics; Molecular Cancer Research; and Cancer Prevention Research. In 2010, AACR journals received 20 percent of the total number of citations given to oncology journals. The AACR also publishes Cancer Today, a magazine for cancer patients, survivors and their caregivers, which provides practical knowledge and new hope for cancer survivors.
A major goal of the AACR is to educate the general public and policymakers about the value of cancer research in improving public health, the vital importance of increases in sustained funding for cancer research and biomedical science, and the need for national policies that foster innovation and the acceleration of progress against the 200 diseases we call cancer.

[ | 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.

Source: http://www.eurekalert.org/pub_releases/2011-10/aafc-kdo102411.php
bush ellie goulding ginger aron ralston aron ralston grandparents day 911

Expert resumes testifying for Jackson doctor (AP)

LOS ANGELES ? An anesthesia expert testifying for the doctor charged in Michael Jackson's death on Friday challenged some of the prosecution's theories about the events leading up to the singer's death.

But Dr. Paul White has yet to address the crux of the defense's case ? its theory that the pop superstar gave himself a lethal dose of a powerful anesthetic.

Instead, White spent much of his early testimony challenging a prosecution expert's estimation of how much of the sedative lorazepam Jackson received.

The drug, along with another sedative, was cited as a contributing factor in Jackson's June 2009 death, which was blamed on propofol intoxication. White is an expert in the anesthetic propofol and is expected to be the final defense witness.

Dr. Conrad Murray has acknowledged he was giving the singer propofol as a sleep aid.

White showed jurors a model he helped create that contends Jackson took some oral lorazepam in addition to an injection of the medication that Murray acknowledged giving the singer. In opening statements, Murray's attorneys claimed Jackson may have taken several lorazepam pills without his doctor's knowledge.

White's testimony disputes a theory presented by prosecution expert Dr. Steven Shafer that Jackson would have had to receive several injections of the sedative to reach the level of lorazepam found in his blood after his death.

White has not yet challenged Shafer's theory that Murray must have given Jackson more propofol than he acknowledged in an interview with police two days after the singer's death.

White's testimony will likely be vigorously challenged by prosecutors, who spent four weeks laying out their case that Murray is a greedy, inept and reckless doctor who was giving Jackson propofol as a sleep aid in the singer's bedroom.

The anesthetic is not intended as a sleep aid and, medical groups say, should be administered only in a hospital or surgical setting with advanced monitoring equipment.

Cross-examination of White will be delayed until Monday to give prosecutors more time to review a new analysis prepared by the defense based on recently conducted tests of samples taken during Jackson's autopsy.

The judge hearing the case, which ends its fifth week Friday, reluctantly agreed to delay the cross examination and said he is concerned about losing jurors. Superior Court Judge Michael Pastor, however, noted the panel has remained rapt throughout the trial.

"Every single member of that jury and all the alternates are paying extraordinary attention to every witness," Pastor said.

Murray has pleaded not guilty to involuntary manslaughter.

White will likely challenge Shafer's theory that the only scenario he believes explains Jackson's death is that Murray placed Jackson on an IV drip and left the room after he thought the singer was sleeping peacefully.

Murray told police he left Jackson's bedside but claims he gave the singer only a small dose of propofol the morning of Jackson's death. He said he left the room and returned after two minutes to find the pop superstar unresponsive.

Murray's defense attorneys have repeatedly claimed that Jackson somehow gave himself the fatal dose, but it will be up to White to explain how that would be possible.

White is a retired researcher and professor who performed clinical studies of propofol for years before it was approved for usage by the Food and Drug Administration in 1989. He said he was initially reluctant to become involved in the case, but after reading through more than a dozen expert reports, he couldn't figure out how others came to the conclusion that Murray would have had to leave Jackson on a propofol IV drip for the singer to have died with the anesthetic still coursing through his body.

He said the others' theories didn't make sense based on Murray's statement to police.

"I thought that there were questions if in fact Murray had administered the drugs that he described in his conversations with the police department in the doses he described, I would not have expected Michael Jackson to have died," White said.

___

AP Special Correspondent Linda Deutsch contributed to this report.

___

McCartney can be reached at http://twitter.com/mccartneyAP

Source: http://us.rd.yahoo.com/dailynews/rss/celebrity/*http%3A//news.yahoo.com/s/ap/20111028/ap_en_mu/us_michael_jackson_doctor

wes welker the music man the music man new england patriots jerry brown zsa zsa gabor ny giants

Sunday, October 30, 2011

Dragonflies Are Literally Scared to Death of Fish (LiveScience.com)

Just the mere presence of a predator can stress out dragonfly larvae enough to kill them ? even if the dragonflies are out of the predator's reach and completely safe, a new study shows.

Biologists at the University of Toronto placed juvenile dragonfly (Leucorrhinia intacta) larvae and their predatory fish together in aquarium tanks. The two were separated so that although the dragonflies could see and smell their predators, the fish could not actually reach or eat the dragonflies.

"What we found was unexpected ? more of the dragonflies died when predators shared their habitat," study researcher Locke Rowe, chairman of the Department of Ecology and Evolutionary Biology at the university, said in a statement.

The dragonfly larvae that were exposed to predatory fish or aquatic insects whose presence may have also caused the larvae stress had survival rates 2.5 to 4.3 times lower than those that had not been exposed to either stressor.

Rowe and colleagues then conducted another experiment to determine whether stressful conditions influence dragonfly metamorphosis. "We allowed the juvenile dragonflies to go through metamorphosis to become adult dragonflies, and found those that had grown up around predators were more likely to fail to complete metamorphosis successfully, more often dying in the process," Rowe said.

The results showed that 11 percent of the larvae that were exposed to fish died before reaching adulthood, compared with only 2 percent of larvae that went through metamorphosis in a predator-free environment.

"As we learn more about how animals respond to stressful conditions ? whether it's the presence of predators or stresses from other natural or human-caused disruptions ? we increasingly find that stress brings a greater risk of death, presumably from things such as infections that normally wouldn't kill them," Rowe said.

The findings can be used as a model for future studies on the harmful and potentially lethal effects of stress on living organisms, the researchers suggested.

The study was recently published in the journal Ecology and is highlighted in the journal Nature this week.

You can follow LiveScience writer Remy Melina on Twitter @remymelina. Follow LiveScience for the latest in science news and discoveries on Twitter @livescience? and on Facebook.

Source: http://us.rd.yahoo.com/dailynews/rss/science/*http%3A//news.yahoo.com/s/livescience/20111028/sc_livescience/dragonfliesareliterallyscaredtodeathoffish

nina dobrev michael turner tom brady emmy nominations desean jackson monsters vs aliens jeremy maclin

ToyotaEquipment: RT @deepgreendesign: World Clock is #fun! http://t.co/C6QROesz Clock of #energy, #population, #food, #US Crime & More! #Science #Statist ...

Passer la navigation
Twitter sur votre mobile ? Cliquez ici m.twitter.com!
Passer cette ?tape
Connexion

World Clock is #fun! goo.gl/bQof6 Clock of #energy, #population, #food, #US Crime & More! #Science #Statistics #Math #CdnPoli Il y a 31 minutes via web Retweeted by 1 person

deepgreendesign

Graham Chivers

Pied de page

Source: http://twitter.com/ToyotaEquipment/statuses/130430366644322304

david blaine iowa state evan rachel wood i don t know how she does it katamari roatan new planet

22 wounded Libyan rebel fighters arrive in Mass.

A wounded Libyan fighter is helped off of a U.S. Air Force plane at Logan International Airport in Boston Saturday, Oct. 29, 2011. The fighters will be treated at Spaulding Hospital for Continuing Medical Care North Shore in Salem, Mass. (AP Photo/Winslow Townson)

A wounded Libyan fighter is taken of a U.S. Air Force plane at Logan International Airport in Boston Saturday, Oct. 29, 2011. The fighters will be treated at Spaulding Hospital for Continuing Medical Care North Shore in Salem, Mass. (AP Photo/Winslow Townson)

A wounded Libyan is assisted as he prepares to board a U.S. military aircraft along with more than 20 others bound for the US for medical care in Tripoli, Libya, Saturday, Oct. 29, 2011. A U.S. military plane is flying more than 20 Libyans wounded in the country's eight-month civil war to the United States for treatment. Thousands have been wounded in the fight to topple Moammar Gadhafi, and Libya's new leaders say caring for them is a critical need. (AP Photo/Abdel Magid al-Fergany)

A wounded Libyan lies on a stretcher as he is readied to be loaded onto a U.S. military aircraft along with more than 20 others bound for the US for medical care in Tripoli, Libya, Saturday, Oct. 29, 2011. A U.S. military plane is flying more than 20 Libyans wounded in the country's eight-month civil war to the United States for treatment. Thousands have been wounded in the fight to topple Moammar Gadhafi, and Libya's new leaders say caring for them is a critical need. (AP Photo/Abdel Magid al-Fergany)

U.S. Ambassador to Libya Gene Kretz makes remarks in front of a U.S. military aircraft bound for the United States to transport more then 20 wounded Libyans for medical care in Tripoli, Libya, Saturday, Oct. 29, 2011. A U.S. military plane is flying more than 20 Libyans wounded in the country's eight-month civil war to the United States for treatment. Thousands have been wounded in the fight to topple Moammar Gadhafi, and Libya's new leaders say caring for them is a critical need. (AP Photo/Abdel Magid al-Fergany)

BOSTON (AP) ? Nearly two dozen former Libyan rebel fighters were carried in stretchers or limped and hobbled out of a U.S. Air Force medical evacuation jet in Massachusetts on Saturday at the end of a 13-hour flight for treatment of wounds sustained in the war that ousted slain longtime leader Moammar Gadhafi.

The envoy of Libya's National Transitional Council said the 22 fighters are the first of an estimated 200 combatants who will be flown to the United States for treatment. But Mark Ward, senior adviser on Arab transitions for the U.S. Department of State, later said several European nations have offered to treat some fighters, and the number of those who could come to this country has not been determined.

The fighters were brought to the country following a request to Secretary of State Hillary Clinton during her trip to the Libyan capital of Tripoli last week, Ward said shortly before their flight landed at Boston's Logan International Airport in the midst of a wintry storm.

"The United States was very proud to help the Libyan people in eight months of struggle against Gadhafi and his regime," Ward said. "We know the struggle will now continue as they rebuild their country and, in particular, we wanted to help with some of the war wounded, some of those brave, young men that fought the regime's forces and brought it to its knees."

"Libya's new freedom has come at a price in human life and suffering. Just as the United States and the international community stood with the Libyan people during the revolution, we continue to work with them now to address urgent needs," Ward said.

The wounded fighters will be treated at the Spaulding Hospital for Continuing Medical Care North Shore in Salem, Mass., a long-term care facility.

An internationally established fund used by Libya's transitional government says it will pay the fighters' hospital bills.

The fighters were met at the airport by Ward and Ali Aujali, Libya's ambassador to the U.S. The combatants did not speak to reporters. Firefighters stationed at the airport, Massachusetts state troopers and Emergency Medical Services technicians immediately helped them get into ambulances that were waiting on the tarmac in the freezing rain.

Still, Ward said the former rebel fighters had mixed reaction on arrival in the United States.

"We were just on the plane with them ... they look very excited, but also a little bit apprehensive," Ward said. "Many of them have never been on an airplane before, this is a new country, it's very cold for them. ... Tripoli was warm when they left 13 hours ago, so this is going to be quite an experience for them, but also for the wonderful staff at Spaulding Hospital."

Associated Press

Source: http://hosted2.ap.org/APDEFAULT/386c25518f464186bf7a2ac026580ce7/Article_2011-10-29-Wounded%20Libyans-Boston/id-664b969da07f4c6a9f15ea2bc3e84655

portia de rossi portia de rossi herman cain for president herman cain for president pumpkin bread pumpkin bread linus pauling

Saturday, October 29, 2011

Mobb Deep Up For Jay-Z Collabo, Despite Past Beef

'It's just hip-hop, man,' Prodigy tells MTV News' 'RapFix Live.'
By Rob Markman, with reporting by Sway Calloway

Havoc and Prodigy of Mobb Deep
Photo: Natasha Chandel/ MTV News

Time heals all wounds. After Jay-Z and Mobb Deep squared off lyrically in 2001, it was hard to imagine that the rap titans would ever get to a place where they would even consider a collaboration.

Nothing is in the works, but after working with Roc Nation's Jay Electronica, Mobb Deep told MTV News correspondent Sway Calloway that they'd be open to the idea of working with Hov.

"Tell [Jay-Z] to get in the studio," Prodigy said when he and his partner Havoc appeared on Wednesday's "RapFix Live." "He gotta come to Infamous Studios in Queens, though."

Though the two acts threw quite a few barbs at each other, most notably on Jay-Z's "Takeover" and Mobb Deep's "Crawlin' " 10 years ago, Prodigy was recently featured on a track with Hov's signee Jay Electronica on his "Call of Duty" track.

On the song's hook, Prodigy even spits, "Put your diamonds in the sky, wave 'em side to side/ Get juxed for your shine," a double-sided lyric that evokes the spirit of a robbery and makes a play on Jay's diamond-shaped hand gesture that he throws up at all his shows.

Mobb Deep even recorded the song at Jigga's Roc Da Mic studios in Manhattan; they clearly harbor no ill will. After Electronica attempted to reach Prodigy on Twitter, the Queens MC got the word that the Hov protégé wanted to work alongside him. "I just got mad phone calls. I woke up late that morning, and everybody was blowin' me up like, 'Yo, Jay Electronica is trying to get in the studio right now,' " Prodigy recalled. "So we just went and knocked it out."

Mobb Deep also plan to get together with J. Cole, another Jay-Z signee. "I was on the phone with J. Cole like the next day, congratulating him on his album and all that," Prodigy said of his conversation with the Cole World MC. "We're supposed to be doing some work together too."

For Mobb Deep, it isn't about beef; instead, the duo are at a place in their careers where all they want to do is make quality tunes. "It's just hip-hop, man, making good songs. Everything else is irrelevant, man," Prodigy stated. "All the feelings and dudes wanna act feminine, put that to the side, man."

Do you hope Mobb Deep and Jay-Z team up? Let us know in the comments!

Related Videos

Mobb Deep On 'RapFix Live'

bling ring melissa mccarthy roddy white roddy white vincent jackson green river killer bohemian grove

Moffitt Cancer Center researchers find more clues to causes of breast cancer

Public release date: 27-Oct-2011
[ | E-mail |

Share ]

Contact: Ferdie De Vega
Ferdinand.DeVega@moffitt.org
813-745-7858
H. Lee Moffitt Cancer Center & Research Institute

Hyperactivation of Akt and overexpression of IKBKE observed in 50 percent of human cancers: inhibitors needed

TAMPA, Fla. -- Publishing in the current issue of The Journal of Biological Chemistry (Vol. 286, No 43), researchers at Moffitt Cancer Center in Tampa, Fla., have discovered additional mechanisms of "Akt" activation and suggest a component of that activation mechanism inhibitor of nuclear factor kappa-B kinase subunit epsilon (IKBKE) could be targeted as a therapeutic intervention for treating cancer.

Akt, also known as protein kinase B, is one of about 500 protein kinases in the human genome. Kinases are known to regulate the majority of cellular pathways. Akt modifies other proteins chemically and regulates cell proliferation.

"Recent evidence suggests that IKBKE is an oncogenic kinase that participates in malignant transformation and tumor development," said Moffitt senior researcher and lead author Jin Q. Cheng, Ph.D., M.D. "Our study identified Akt as a bona fide substrate of IKBKE and IKBKE direct activation of Akt independent PI3K and revealed a functional link between IKBKE and Akt activation in breast cancer."

Cheng's lab studies a variety of genetic alterations and their molecular mechanisms in both ovarian and breast cancer, particularly on their effect on the molecules that are regulated by Akt and the small molecule inhibitors of Akt.

"We found that inhibition of Akt suppresses IKBKE's oncogenic transformation," said Cheng. "This is significant because overexpression of IKBKE and activation of Akt has been observed in more than 50 percent of human cancers. Akt inhibitors targeting PH domain do not have inhibitory effect on IKBKE-induced Akt."

The researchers experimented with a variety of inhibitors currently being used in clinical trials.

The laboratory study utilized breast cancer cell lines from received from patient donors at Moffitt and cell lines received from Harvard University and Johns Hopkins University. The work was supported by a National Institutes of Health grant and a grant from the James and Esther King Biomedical Research Program.

###

About Moffitt Cancer Center
Follow Moffitt on Facebook: http://www.facebook.com/MoffittCancerCenter
Follow Moffitt on Twitter: @MoffittNews
Follow Moffitt on YouTube: MoffittNews

Located in Tampa, Moffitt Cancer Center is Florida's only NCI Comprehensive Cancer Center, a designation that recognizes Moffitt's excellence in research and contributions to clinical trials, prevention and cancer control. Moffitt currently has 14 affiliates in Florida, one in Georgia, one in Pennsylvania and two in Puerto Rico. Additionally, Moffitt is a member of the National Comprehensive Cancer Network, a prestigious alliance of the country's leading cancer centers, and is listed in U.S. News & World Report as one of "America's Best Hospitals" for cancer. Moffitt marks a very important anniversary in 2011 - 25 years committed to one mission: to contribute to the prevention and cure of cancer.

[ | 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.

Moffitt Cancer Center researchers find more clues to causes of breast cancer

Public release date: 27-Oct-2011
[ | E-mail |

Share ]

Contact: Ferdie De Vega
Ferdinand.DeVega@moffitt.org
813-745-7858
H. Lee Moffitt Cancer Center & Research Institute

Hyperactivation of Akt and overexpression of IKBKE observed in 50 percent of human cancers: inhibitors needed

The researchers experimented with a variety of inhibitors currently being used in clinical trials.

###

About Moffitt Cancer Center
Follow Moffitt on Facebook: http://www.facebook.com/MoffittCancerCenter
Follow Moffitt on Twitter: @MoffittNews
Follow Moffitt on YouTube: MoffittNews

[ | 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.

Source: http://www.eurekalert.org/pub_releases/2011-10/hlmc-mcc102711.php

oc oc professor professor zanzibar arizona state university nsa