OAKLAND, Calif. (AP) ? All-Star forward David Lee made a surprising return for the Golden State Warriors in Game 6 against the Denver Nuggets on Thursday night after not dressing the previous four games with what the team had called a season-ending hip injury.
Lee didn't participate in early pregame warm-ups, then sprinted out of the tunnel second behind Stephen Curry about 15 minutes before tipoff, ripping off his jacket and getting a rousing ovation from fans when he was shown on the videoboard.
With 6:05 remaining in the first quarter, Lee took off the shirt over his uniform and began to check in at the scorer's table. As fans started to roar to its feet, Nuggets coach George Karl quickly called timeout and quieted the crowd.
Lee didn't come in following the timeout, then went back to the scorer's table once played resumed. He finally entered the game with 2:23 to play following a timeout by Warriors coach Mark Jackson, getting a standing ovation from fans as he jogged to center court and pointed to the sky with both hands.
Lee had one rebound and missed his only shot in 87 seconds of play in the first quarter.
Lee was hurt in the fourth quarter of Game 1, when he banged into Denver's JaVale McGee on a drive and landed on his side. The Warriors said April 21 he had a season-ending tear of his right hip flexor.
Carl Landry started at power forward alongside point guard Stephen Curry, shooting guard Klay Thompson, small forward Harrison Barnes and center Andrew Bogut.
Lee gave Jackson a hug and the two spoke for a few seconds while the lights dimmed during player introductions. Lee led the pep talk in the huddle after starters were announced.
The Republican establishment breathed a sigh of relief when Boston businessman Gabriel Gomez won Tuesday's GOP primary in the Massachusetts special Senate race, believing he represents the party's best chance at an unlikely pick-up in liberal Massachusetts.
In a study using mice, researchers from the University of North Carolina at Chapel Hill found that a hormone, adrenomedullin, plays a crucial role in preventing the pregnancy complication preeclampsia. Surprisingly, this hormone protects women from preeclampsia when emitted by the fetus, not the mother, during the most critical times in pregnancy.
"We've identified the fact that the baby is important in protecting the mom from preeclampsia," said the study's senior author, Kathleen M. Caron, Ph.D., Assistant Dean for Research at the UNC School of Medicine and an associate professor in the Department of Cell Biology and Physiology. "If the baby's cells are not secreting this hormone, the mother's blood vessels don't undergo the dilation that they should."
Preeclampsia affects roughly one in fifteen pregnancies. An important characteristic of the condition is that blood vessels in the placenta fail to enlarge, or dilate, to accommodate increased blood flow to the fetus. Untreated, it can threaten the life of both mother and baby.
"We really don't know that a pregnant woman is going to get preeclampsia until she has it," said Caron. Because the condition has numerous risk factors and causes, it's difficult for doctors to know which patients are at highest risk. "Identifying molecules that could predict preeclampsia would be really important."
The researchers studied mice that were genetically programmed to produce either reduced or increased levels of adrenomedullin. The study revealed that in a normal pregnancy, the fetus secretes adrenomedullin into the placenta during the second trimester, signaling special cells called "natural killer cells" to help dilate the mother's blood vessels and allow more blood to flow to the growing fetus.
The study is one of the first to identify an important chemical message sent from fetus to mother in the womb. Scientists understand more about the mom's side of the 'chemical conversation' that goes on between mother and baby, but much of the hormonal signaling in the placenta remains a mystery.
By identifying the key role of adrenomedullin, the research could pave the way to new methods for detecting and preventing preeclampsia. For example, adrenomedullin levels could potentially be used as a biomarker, or early indicator, to identify which patients might be predisposed to the condition. "Having a biomarker would be wonderful?it could allow the physician to manage a woman differently in the early part of her pregnancy," said Caron.
As a next step, the researchers plan to build upon their mouse studies to examine patterns of adrenomedullin levels and preeclampsia in pregnant women.
###
This paper was published online ahead of print on May 1, 2013 in the Journal of Clinical Investigation (JCI). The paper will appear in the June 2013 print edition.
University of North Carolina Health Care: http://www.med.unc.edu
Thanks to University of North Carolina Health Care for this article.
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There's are kinds of asteroids and other debris cruising through space, but a lot of the really dangerous stuff is stuff we put there ourselves. NASA's cosmic bubble-spotting Fermi telescope almost had an intergalactic fender bender, but not with some epoch-old rock floating through the cosmos. No, it almost got crushed by some Cold War-era trash.
BARCELONA, Spain (AP) ? The Champions League final will feature two German teams for the first time after Bayern Munich completed surprising 7-0 rout of Barcelona.
Playing with a big cushion after a 4-0 win in the first leg at home last week, Bayern beat Barcelona 3-0 in the second leg Wednesday night on goals by Arjen Robben in the 48th minute and Thomas Mueller in the 76th around Gerard Pique's own goal in the 72nd.
Bayern, which relaxed when it saw injured Lionel Messi wasn't in Barcelona's starting lineup, is in the final for the third time in four years and will play Borussia Dortmund at London's Wembley Stadium on May 25.
"I think it is a terrific performance, it is a little bit of history," Robben said. "If we perform like this, against a team who have dominated Europe for the past five years, who have so much quality, it is amazing."
This final wll be just the fourth single-nation championship match in Europe. Real Madrid beat Valencia in 2000, AC Milan defeated Juventus in 2003 and Manchester United edged Chelsea in 2008.
Bayern will be seeking its fifth title, and first since 2001, while Dortmund won its only championship in 1997. Bayern, which clinched the Bundesliga title on April 6 with six games to spare, travels to Dortmund for a league match Saturday night.
"I'm sure we'll celebrate with a few beers tonight," Bayern captain Philipp Lahm said. "I've always said we have special characters in our squad, and that we are capable of great things."
Bayern lost last year's final at home to Chelsea on penalty kicks, two years after it was defeated 2-0 by Inter Milan.
While many expected Barcelona to meet Real Madrid in the final, Dortmund defeated Madrid 4-1 in Germany last week and hung on Tuesday for a 4-3 aggregate win.
Bayern had no such scare. Missing Messi, the four-time world player of the year who has hampered by a hamstring injury for the past month, Barcelona showed little offensive spark.
"When we saw his name wasn't in the starting lineup, we breathed a sigh of relief," Bayern midfielder Javi Martinez said.
Messi started in the first leg but was largely ineffective, and didn't get off the substitutes bench for the second.
"We trained today but he wasn't comfortable, and we decided that if we were going to risk him it would be at the end," Barcelona coach Tito Vilanova said.
Bayern made sure the final minutes didn't mattter.
"I do not think his participation tonight would have changed things all that much," Pique said. "It isn't pleasant living through a situation like this. In the first half we really tried but when they scored the first, we were left feeling down. We have to congratulate Bayern, who were superior."
When Xavi Hernandez and Andres Iniesta were substituted in the second half, it left Barcelona without its three biggest stars on the field. Barcelona also was missing defenders Carles Puyol and Javier Mascherano and midfielder Sergio Busquets because of injuries, and left back Jordi Alba because of a suspension for yellow-card accumulation.
While Barcelona has an 11-point lead in the Spanish league with five games left, its first season since Vilanova replaced Pep Guardiola as coach will be considered a disappointment because it failed to win the Champions League following titles in 2006, 2009 and 2011.
Guardiola was hired by Bayern in January to replace Jupp Heynckes as coach at the end of the season.
"When the draw came out and we were paired with Barcelona, I would never have imagined that we would win 4-0 and then 3-0 at the Camp Nou," Heynckes said "Barcelona is a fantastic team. Today it had personnel problems, when Messi plays it is very different."
NOTES: Barcelona had gone unbeaten in 21 Champions League home matches since its 2-1 loss to Rubin Kazan on Oct. 20, 2009. ... Barcelona goalkeeper Victor Valdes became the 17th player to make 100 Champions League appearances.
Genomics to reshape endometrial cancer treatmentPublic release date: 1-May-2013 [ | E-mail | Share ]
Contact: Caroline Arbanas arbanasc@wustl.edu 314-286-0109 Washington University School of Medicine
The most in-depth look yet at endometrial cancer shows that adding genomics-based testing to the standard diagnostic workup could change the recommended course of treatment for some women.
The new research, involving nearly 400 women with endometrial cancer, is published May 2 in the journal Nature. The endeavor is part of The Cancer Genome Atlas project, funded by the National Institutes of Health (NIH).
The study also indicates that some endometrial tumors are genetically similar to subtypes of ovarian cancer and deadly basal-like breast cancer. Future clinical trials should evaluate whether some endometrial cancers could be treated with drugs typically used for the other cancers, says project co-leader Elaine Mardis, PhD, co-director of The Genome Institute at Washington University School of Medicine in St. Louis. The other co-leader is Douglas A. Levine, MD, of the Memorial Sloan-Kettering Cancer Center.
A second Cancer Genome Atlas paper will be published May 1 in the New England Journal of Medicine. That research, also led by Washington University, describes finding virtually all the major mutations involved in acute myeloid leukemia.
While gynecologic oncologists have long recognized two subtypes of endometrial cancer, one more aggressive than the other, the new data reveal four novel subtypes and also suggest that the frequency of mutations in a tumor could be used to help guide treatment decisions.
"We are entering an era when tumors can be evaluated from a genomics standpoint, not just by looking at cancer cells under a microscope," Mardis says. "This more comprehensive approach provides a clearer picture of the way particular endometrial cancers will behave and will be important to gynecological oncologists who treat this disease."
As part of the new research, a consortium of researchers analyzed tumors from 373 women with endometrial cancer using different technologies to look for defects in DNA, RNA (a close chemical cousin of DNA) and proteins.
Their analysis indicates that about 25 percent of women with endometrial cancer who are thought to have a favorable prognosis based on pathology reports instead have a more formidable form of the disease, based on underlying genetic changes, and should be treated aggressively.
Clinically, endometrial cancers fall into two categories: endometrioid and serous. Endometrioid cancers generally are associated with excess estrogen, obesity and a favorable prognosis. In contrast, serous endometrial cancers are more common in older women and generally have poorer outcomes.
After surgery to remove endometrial cancer, women with the endometrioid subtype typically are treated with radiation therapy to kill remaining cancer cells, while those with serous tumors receive a more aggressive treatment chemotherapy.
Doctors distinguish between the two tumor subtypes by evaluating cancer cells under a microscope. But categorizing some tumors is difficult, and pathologists don't always agree.
Looking closely at endometrioid tumors classified as high-grade, meaning they are more likely to grow quickly and spread, the investigators showed that many share genetic features with serous tumors. These include frequent mutations in TP53, a tumor suppressor gene, as well as extensive copy number alterations, which refer to a cell having too many or too few copies of a gene.
"This highlights the benefit of digging deeper to find the genetic drivers of cancer growth," Mardis says. "Even though high-grade endometrioid and serous endometrial cancer are different from a pathological standpoint, they are genetically very similar and may require a similar course of treatment."
With a complete analysis of the tumor samples, the investigators identified four novel genomic-based subtypes of endometrial cancer, which set the stage for developing new ways to diagnose and treat the disease. The subtypes are based, in part, on the frequency of mutations in the tumors.
"The Cancer Genome Atlas' multidimensional approach to collecting genomic data, including clinical and pathology information, have made these findings possible," says Harold Varmus, MD, director on the National Cancer Institute. "Without the integrated characterization of so many tumor samples, correlations between histology and genomic data may not have been observed or potential clinical outcomes identified."
Interestingly, one subtype features an exceedingly high mutation rate in the POLE gene and, in this respect, is similar to an "ultramutated" subtype of colorectal cancer. But, surprisingly, patients with these kinds of tumors generally have good outcomes.
"Having many, many mutations sounds like a bad thing," Mardis explains. "But these patients can't fix the mistakes in their tumor DNA, so their cancer cells mutate themselves into oblivion before they have the opportunity to spread to other locations in the body. The good news for these patients is that their outcomes are excellent, and they don't need aggressive treatment."
Women with serous tumors frequently had mutations in one of two genes that potentially could be targeted with existing targeted therapies. Those with ERBB2 alterations, for example, may be effectively treated with Herceptin, a drug typically used in women with breast cancer who have the same mutation. Additionally, women whose endometrial tumors have PIK3CA mutations may benefit from drugs that inhibit the gene. Those drugs are now in phase II clinical trials.
According to the authors, the new findings provide a roadmap for future clinical trials for endometrial cancer.
"Each tumor subtype may warrant separate clinical trials because of marked genomic differences, which are indicative of different drivers of endometrial cancer," Mardis says. "Developing therapies for each subtype may improve outcomes for many women with endometrial cancer and parallel what has been accomplished in breast cancer."
Endometrial cancer is the fourth most commonly diagnosed cancer among U.S. women. About 50,000 cases will be diagnosed in 2013, and an estimated 8,000 women will die from the disease. For a majority of patients diagnosed with aggressive, high-grade tumors that have spread, the five-year survival rate is about 16 percent, though chemotherapy has been associated with improved survival, and new targeted agents are being tested.
###
Levine DA, Mardis ER and The Cancer Genome Atlas Research Network. Integrated genomic characterization of endometrial carcinoma. Nature. May 2, 2013.
The research is funded by the National Institutes of Health (NIH) as part of The Cancer Genome Atlas Project. Grant numbers: 5U24CA143799-04, 5U24CA143835-04, 5U24CA143840-04, 5U24CA143843-04, 5U24CA143845-04, 5U24CA143848-04, 5U24CA143858-04, 5U24CA143866-04, 5U24CA143867-04, 5U24CA143882-04, 5U24CA143883-04, 5U24CA144025-04, U54HG003067-11, U54HG003079-10 and U54HG003273-10.
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 sixth 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.
Genomics to reshape endometrial cancer treatmentPublic release date: 1-May-2013 [ | E-mail | Share ]
Contact: Caroline Arbanas arbanasc@wustl.edu 314-286-0109 Washington University School of Medicine
The most in-depth look yet at endometrial cancer shows that adding genomics-based testing to the standard diagnostic workup could change the recommended course of treatment for some women.
The new research, involving nearly 400 women with endometrial cancer, is published May 2 in the journal Nature. The endeavor is part of The Cancer Genome Atlas project, funded by the National Institutes of Health (NIH).
The study also indicates that some endometrial tumors are genetically similar to subtypes of ovarian cancer and deadly basal-like breast cancer. Future clinical trials should evaluate whether some endometrial cancers could be treated with drugs typically used for the other cancers, says project co-leader Elaine Mardis, PhD, co-director of The Genome Institute at Washington University School of Medicine in St. Louis. The other co-leader is Douglas A. Levine, MD, of the Memorial Sloan-Kettering Cancer Center.
A second Cancer Genome Atlas paper will be published May 1 in the New England Journal of Medicine. That research, also led by Washington University, describes finding virtually all the major mutations involved in acute myeloid leukemia.
While gynecologic oncologists have long recognized two subtypes of endometrial cancer, one more aggressive than the other, the new data reveal four novel subtypes and also suggest that the frequency of mutations in a tumor could be used to help guide treatment decisions.
"We are entering an era when tumors can be evaluated from a genomics standpoint, not just by looking at cancer cells under a microscope," Mardis says. "This more comprehensive approach provides a clearer picture of the way particular endometrial cancers will behave and will be important to gynecological oncologists who treat this disease."
As part of the new research, a consortium of researchers analyzed tumors from 373 women with endometrial cancer using different technologies to look for defects in DNA, RNA (a close chemical cousin of DNA) and proteins.
Their analysis indicates that about 25 percent of women with endometrial cancer who are thought to have a favorable prognosis based on pathology reports instead have a more formidable form of the disease, based on underlying genetic changes, and should be treated aggressively.
Clinically, endometrial cancers fall into two categories: endometrioid and serous. Endometrioid cancers generally are associated with excess estrogen, obesity and a favorable prognosis. In contrast, serous endometrial cancers are more common in older women and generally have poorer outcomes.
After surgery to remove endometrial cancer, women with the endometrioid subtype typically are treated with radiation therapy to kill remaining cancer cells, while those with serous tumors receive a more aggressive treatment chemotherapy.
Doctors distinguish between the two tumor subtypes by evaluating cancer cells under a microscope. But categorizing some tumors is difficult, and pathologists don't always agree.
Looking closely at endometrioid tumors classified as high-grade, meaning they are more likely to grow quickly and spread, the investigators showed that many share genetic features with serous tumors. These include frequent mutations in TP53, a tumor suppressor gene, as well as extensive copy number alterations, which refer to a cell having too many or too few copies of a gene.
"This highlights the benefit of digging deeper to find the genetic drivers of cancer growth," Mardis says. "Even though high-grade endometrioid and serous endometrial cancer are different from a pathological standpoint, they are genetically very similar and may require a similar course of treatment."
With a complete analysis of the tumor samples, the investigators identified four novel genomic-based subtypes of endometrial cancer, which set the stage for developing new ways to diagnose and treat the disease. The subtypes are based, in part, on the frequency of mutations in the tumors.
"The Cancer Genome Atlas' multidimensional approach to collecting genomic data, including clinical and pathology information, have made these findings possible," says Harold Varmus, MD, director on the National Cancer Institute. "Without the integrated characterization of so many tumor samples, correlations between histology and genomic data may not have been observed or potential clinical outcomes identified."
Interestingly, one subtype features an exceedingly high mutation rate in the POLE gene and, in this respect, is similar to an "ultramutated" subtype of colorectal cancer. But, surprisingly, patients with these kinds of tumors generally have good outcomes.
"Having many, many mutations sounds like a bad thing," Mardis explains. "But these patients can't fix the mistakes in their tumor DNA, so their cancer cells mutate themselves into oblivion before they have the opportunity to spread to other locations in the body. The good news for these patients is that their outcomes are excellent, and they don't need aggressive treatment."
Women with serous tumors frequently had mutations in one of two genes that potentially could be targeted with existing targeted therapies. Those with ERBB2 alterations, for example, may be effectively treated with Herceptin, a drug typically used in women with breast cancer who have the same mutation. Additionally, women whose endometrial tumors have PIK3CA mutations may benefit from drugs that inhibit the gene. Those drugs are now in phase II clinical trials.
According to the authors, the new findings provide a roadmap for future clinical trials for endometrial cancer.
"Each tumor subtype may warrant separate clinical trials because of marked genomic differences, which are indicative of different drivers of endometrial cancer," Mardis says. "Developing therapies for each subtype may improve outcomes for many women with endometrial cancer and parallel what has been accomplished in breast cancer."
Endometrial cancer is the fourth most commonly diagnosed cancer among U.S. women. About 50,000 cases will be diagnosed in 2013, and an estimated 8,000 women will die from the disease. For a majority of patients diagnosed with aggressive, high-grade tumors that have spread, the five-year survival rate is about 16 percent, though chemotherapy has been associated with improved survival, and new targeted agents are being tested.
###
Levine DA, Mardis ER and The Cancer Genome Atlas Research Network. Integrated genomic characterization of endometrial carcinoma. Nature. May 2, 2013.
The research is funded by the National Institutes of Health (NIH) as part of The Cancer Genome Atlas Project. Grant numbers: 5U24CA143799-04, 5U24CA143835-04, 5U24CA143840-04, 5U24CA143843-04, 5U24CA143845-04, 5U24CA143848-04, 5U24CA143858-04, 5U24CA143866-04, 5U24CA143867-04, 5U24CA143882-04, 5U24CA143883-04, 5U24CA144025-04, U54HG003067-11, U54HG003079-10 and U54HG003273-10.
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 sixth 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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