“Nektar Therapeutics to Present at the UBS 2009 Global Life Sciences ... - MSN Money” plus 4 more

Nektar Therapeutics to Present at the UBS 2009 Global Life Sciences ... - MSN Money
Column: The skinny on the Fat Tax - U-Wire.com
Medications effective in reducing risks for breast cancer can also ... - PhysOrg
Diabetes drug kills cancer stem cells in combination treatment in mice - Harvard Medical School
High School Extra /News and notes - Buffalo News

Nektar Therapeutics to Present at the UBS 2009 Global Life Sciences ... - MSN Money

Posted: 18 Sep 2009 12:19 PM PDT

SAN CARLOS, Calif., Sept. 18 /PRNewswire-FirstCall/ -- Nektar Therapeutics NKTR is scheduled to present at the upcoming UBS 2009 Global Life Sciences Conference in New York at the Grand Hyatt Hotel on Tuesday, September 22, 2009 at 10:30 a.m. Eastern time.

The presentation will be accessible via a Webcast through a link posted on the Investor Relations, Events Calendar section of the Nektar website: http://www.nektar.com. This Webcast will be available for replay until October 25, 2009.

About Nektar

Nektar Therapeutics is a biopharmaceutical company developing novel therapeutics based on its PEGylation and advanced polymer conjugation technology platforms. Nektar's technology and drug development expertise have enabled nine approved products in the U.S. or Europe for partners, which include leading biopharmaceutical companies, including UCB's Cimzia(R), Roche's PEGASYS(R) for hepatitis C and Amgen's Neulasta(R) for neutropenia. Nektar has created a robust pipeline of potentially high-value therapeutics to address unmet medical needs by leveraging and expanding its technology platforms to improve and enable molecules. Nektar is currently conducting clinical and preclinical programs in oncology, pain and other therapeutic areas. NKTR-102, PEGylated irinotecan, is currently in Phase 2 clinical studies in ovarian, breast and colorectal cancer. NKTR-105, PEGylated docetaxel, is currently in a Phase 1 clinical study in patients with refractory solid tumors.

Nektar is headquartered in San Carlos, California, with additional R&D operations in Huntsville, Alabama and Hyderabad, India. Further information about the company and its drug development programs and capabilities may be found online at http://www.nektar.com.

 Nektar Contacts:  Jennifer Ruddock Nektar Therapeutics 650-631-4954 jruddock@nektar.com

 Susan Noonan The SAN Group 212-966-3650 susan@sanoonan.com

SOURCE Nektar Therapeutics

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Column: The skinny on the Fat Tax - U-Wire.com

Posted: 18 Sep 2009 12:34 PM PDT

This past year I picked up a mild smoking habit. I say mild because it's laughable to call it a habit: I went from being a soap-box anti-smoker to becoming an occasional social/stress smoker (replete with a really personally embarrassing/toolish situation in which I mooched a cigarette from a friend … and proceeded to smoke it backwards).

As I mentioned, my parents are cancer doctors. While the perils of smoking were never drilled into my head by my parents — Truth.org did that for them — the perils of eating meat, dairy, sugar and anything with a high cholesterol or fat content were. Yet while I've been consuming French fries, donuts and all manners of artery-clogging greasy goodness since I could toddle, my silly flirtation with cigarettes was short lived, thanks in most part to the recently imposed smokers' tax. It's a lot easier to rationalize slowly killing yourself at 80 cents a carton than it is when a carton costs about four times as much as a cup of coffee.

Arguably, it's not just cost keeping people away: junk food is much yummier than cigarettes, and there have never been any lengthy campaigns telling you not to eat it. While junk food has taken the hit, and being fat is definitely not fashionable, obesity is still too touchy a subject to be vilified in the same way that smoking is. We have yet to have a War on Hamburgers.

But that might finally change, hallelujah. Behold the Fat Tax.

I apologize if I come off as offensive. It's definitely not the most P.C. of tax names, although it definitely has a nice ring to it. We could call it the curb-the-obesity-epidemic tax, the think-twice-before-you-eat-another-quarter-pounder tax, or the stop-practically-breast-feeding-your-children-so-that-they-grow-addicted-to-carbonated-liquidated-sugar-and-get-type-II-diabetes-which-everyone-else-will-then-have-to-pay-for tax. But even if those are more accurate, they are way too many words to fit in one mouth — even a supersized one.

Let's look at the facts: The number of obese Americans now outweighs the number of fat Americans. This is going to put an even bigger strain on health care, Medicare and Medicade costs, which fluctuate between 127 and a trillion dollars, depending on whom you ask. According to John Ridley in The Huffington Post last Friday, that's an added $1,250 in taxes per year … a fairly hefty sum, especially if the family in question isn't benefiting. Eric Finkelstein, the health economist, argues an additional indirect cost to companies, both through "presenteeism" — reduced productivity while at work, caused by obesity-triggered slothfulness — or "absenteeism," missing work due to obesity-related diseases, depression or lethargy. In other words: calling in fat.

Are my fat puns inappropriate? Perhaps. But isn't that our major problem with curbing obesity in the first place? In a society where smoking is appropriately bedeviled and preaching to smokers is, if somewhat self-righteous, still tolerated, why is no one pointing the finger at the actually frighteningly obese?

After the movie "Supersize Me" came out, it finally seemed like this attitude might change, and it did in small but important ways: McDonalds changed its menu to include carrots and apple slices, schools finally started educating their students on healthy eating choices and, overall, people became more health conscious. But while I still see about four anti-smoking ads a day, I have never seen an infomercial with lots of obese people in body bags while teenagers on loudspeakers yell at fast food executives. In fact, the only people on my TV telling me to eat healthier are trying to sell me food.

To me, government-based initiatives to curb obesity sound just peachy. But to many, taxing fat — either the food or the people directly — makes you a bully, a communist or both. However, families with smaller incomes — below the upper-middle-class but above the poverty line — are more likely to be obese. This is unsurprising, given that a healthy lifestyle costs much more than an unhealthy one. Aside from gym costs, diets and the always expanding get-thin-quick industry, healthy food costs more than unhealthy food. Taxing unhealthy food levels the playing field — giving public schools and families incentives to buy whole grains and vegetables will slim the socioeconomic obesity gap even more.

Slate writer Daniel Engber — and others of kindred ilk — argue that by imposing these legislations, we're just making the overweight feel worse about themselves in a society where they are already made to feel unattractive. But there's a difference between idolizing anorexic supermodels and encouraging a healthy lifestyle. Besides, haven't we been making smokers feel bad about themselves for years? Do we really assume that smokers are less sensitive than fat people?

Tax the fat. Tax the food. Tax the freaky Chicken McNugget mascot at McDonalds who looks, honestly, more like a big blob of fat than anything else. I don't care whom or which — just tax them. Not only will it save us a load of money, it may finally encourage people to think before they a big gulp.

Medications effective in reducing risks for breast cancer can also ... - PhysOrg

Posted: 18 Sep 2009 12:27 PM PDT

Medications effective in reducing risks for breast cancer can also cause serious side effects

September 18th, 2009

Three drugs that reduce a woman's chance of getting breast cancer also have been shown to cause adverse effects, according to a new report from the Agency for Healthcare Research and Quality (AHRQ), U.S. Department of Health & Human Services.

The report is based on a study led by Heidi D. Nelson, M.D., M.P.H., research professor in the Oregon Evidence-Based Practice Center at Oregon Health & Science University and medical director of the Women and Children's Program and Research Center at Providence Health & Services. It is published online in the Sept. 15 issue of the Annals of Internal Medicine.

The study is the first to make a direct, comprehensive comparison of drugs that reduce the risk of breast cancer so that women and their health care providers can assess their potential effectiveness and adverse effects. It compares the use of tamoxifen, raloxifene and tibolone to reduce the risks of getting breast cancer in women without pre-existing cancer.

Tamoxifen, raloxifene and tibolone can be prescribed to women with a family history of breast cancer or other risk factors, but prescribing practices vary widely. According to the study, all three drugs significantly reduce invasive breast cancer in midlife and older women, but benefits and adverse effects can vary depending on the drug and the patient.

Breast cancer is the second most commonly diagnosed cancer among women (after skin cancer), with more than 190,000 new cases diagnosed each year in the United States. It is estimated to cause more than 40,000 deaths per year. The National Cancer Institute estimates that nearly 15 percent of women born today will develop breast cancer in their lifetimes. Most cases of breast cancer occur in women with no specific risk factors other than age and gender, although family history of breast and ovarian cancer is associated with higher risk.

Tamoxifen, a selective estrogen receptor modulator (SERM), was approved by the Food and Drug Administration in 1998 to reduce risk for breast cancer in women at high risk of developing the disease. Its use to reduce the risk of breast cancer is accepted clinical practice, although it is primarily used for treatment rather than risk reduction.

The study compared tamoxifen with another SERM, raloxifene, which is primarily used to prevent and treat osteoporosis and was approved by the FDA for breast cancer risk reduction in 2007. A third drug, tibolone, which has not been approved by the FDA for use in the United States but is commonly used in other countries to treat menopausal symptoms and osteoporosis, also was included in the study.

The study found that all three drugs reduce the occurrence of breast cancer but have various side effects. The most common side effects for tamoxifen are flushing and other vasomotor symptoms (e.g., night sweats, hot flashes), vaginal discharge and other vaginal symptoms such as itching or dryness; for raloxifene, side effects include vasomotor symptoms and leg cramps; and for tibolone, side effects include vaginal bleeding.

The study also found that each drug carried risks of adverse effects. Tamoxifen increases risks of endometrial cancer, hysterectomies and cataracts compared with the other drugs. Tamoxifen and raloxifene increase risk of blood clots, although tamoxifen's risk is greater. Tibolone carries an increased risk of stroke, according to the study.

The study also examined the drugs' effectiveness and harms based on age, menopausal status, estrogen use and family history of breast cancer, and sought to identify the kinds of women who might be good candidates for therapy, although the evidence is limited in this area. The investigators called for more research to more clearly identify characteristics of patients who would benefit from these drugs while suffering the least harm.

"Before applying the findings of the report to practice, clinicians must ensure that women understand their individual risks for breast cancer and can favorably balance these with the unwanted effects of risk-reducing medications," explained Nelson.

Source: Oregon Health & Science University (news : web)

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Diabetes drug kills cancer stem cells in combination treatment in mice - Harvard Medical School

Posted: 18 Sep 2009 12:12 PM PDT

NEWS ALERT
Harvard Medical School Office of Communications and External Relations

Diabetes drug kills cancer stem cells in combination treatment in mice

FINDINGS:
In tumors formed by human breast cancer cells in mice, a diabetes drug was more effective than chemotherapy alone in prolonging remission. Mice appeared tumor-free for the two months after treatment before the end of the experiment. The drug, metformin, appears to selectively kill cancer stem cells in culture dishes and in mice.

RELEVANCE:
The findings provide additional rationale for testing metformin in combination with chemotherapy in people with breast cancer and perhaps other cancers. The study supports the cancer stem cell hypothesis, an intense area of research that tackles the small subset of cancer cells able to initiate tumors, resist conventional chemotherapies, and promote recurrence.

BOSTON,

Boston, Mass. (Sept. 14, 2009) — In a one-two punch, a familiar diabetes drug reduced tumors faster and prolonged remission in mice longer than chemotherapy alone, apparently by targeting cancer stem cells, report Harvard Medical School researchers in the Sept. 14 advance online Cancer Research.

"We have found a compound selective for cancer stem cells," said senior author Kevin Struhl, the David Wesley Gaiser professor of biological chemistry and molecular pharmacology at HMS. "What's different is that ours is a first-line diabetes drug."

The findings add to a growing body of preliminary evidence in cells, mice, and people that metformin may improve breast cancer outcomes in people. In this study, the diabetes drug seemed to work independently of its ability to improve insulin sensitivity and lower blood sugar and insulin levels, all of which are also associated with better breast cancer outcomes.

The results fit within the cancer stem cell hypothesis, an intensely studied idea that a small subset of cancer cells has a special power to initiate tumors, fuel tumor growth, and promote recurrence of cancer. Cancer stem cells appear to resist conventional chemotherapies, which kill the bulk of the tumor.

"There is a big desire to find drugs specific to cancer stem cells," Struhl says. "The cancer stem cell hypothesis says you cannot cure cancer unless you also get rid of the cancer stem cells. From a purely practical point of view, this could be tested in humans. Its already used as a first-line diabetes drug."

The possible usefulness of a diabetes drug against cancer lends credence to an emerging idea that, in the vast and complex alphabet soup of molecular interactions within cells, relatively few biological pathways will turn out to be most important for many different diseases, Struhl suggested.

In experiments led by postdoctoral fellows Heather Hirsch and Dimitrios Iliopoulos, the combination of metformin and the cancer drug doxorubicin killed human cancer stem cells and non-stem cancer cells in culture. The researchers used four genetically distinct breast cancer cell lines.

In mice, pretreatment with the diabetes drug prevented the otherwise dramatic ability of human breast cancer stem cells to form tumors. In other mice where tumors were allowed to take hold for 10 days, the dual therapy also reduced tumor mass more quickly and prevented relapse for longer than doxorubicin alone. In the two months between the end of treatment and the end of the experiment, tumors regrew in mice treated with chemotherapy alone, but not in mice that had received both drugs. By itself, metformin was ineffective in treating tumors.

"This is an exciting study," said Jennifer Ligibel, a medical oncologist at Dana-Farber Cancer Institute and an HMS instructor in medicine, who was not involved in the study. Ligibel and colleagues at the National Cancer Institute of Canada Clinical Trials Group are developing a large-scale phase II trial to study metformins impact on recurrence in women treated for early stage breast cancer.

"There is a lot of interest in studying metformin in breast cancer, but so far we do not have direct evidence that metformin will improve outcomes in patients," Ligibel said. "Thats what this trial is for."

So far, observational studies have suggested a lower risk of cancers, including breast cancer, and better response to chemotherapy in diabetics taking metformin, she said. Basic science studies also have suggested plausible biological mechanisms. The study from the Struhl lab suggests a potential new pathway through which metformin could have an effect on breast cancer cells, she said.

In their search for compounds that selectively destroy cancer stem cells, scientists hope to improve cancer outcomes. But the story is never as simple in human cancers, said Kornelia Polyak, a breast cancer researcher at Dana-Farber Cancer Institute and HMS associate professor of medicine, who was not involved in the study.

Cancer stem cells are a shifty target, Polyak said. For example, any cancer cell can acquire the properties of a cancer stem cell, and cancer stem cells can change into non-stem cancer cells, which can be just as deadly. Clinical trials in people are needed to test these ideas, Polyak said.

The Struhl paper is an offshoot of a larger project in his lab to systematically track how gene activity changes when cells transform into cancer. These changes were remarkably similar to gene dynamics in diabetes and other inflammatory conditions.

The researchers reasoned that if a common genetic pathway underlies different diseases, drugs that work against one disease might work against another. In a screen, the most effective drug inhibiting the transformation of cells into cancer was metformin, which led to the experiments in this paper.

The team was further encouraged by the low dose of metformin needed for the effect in the laboratory, compared to the amount needed for analogous molecular experiments in basic diabetes research. The relative dosage in people for treating or preventing cancer is unknown and untested.

HMS has applied for a patent for a combined therapy of metformin and a lower dose of chemotherapy, which is being tested in animals. The research was funded by the National Institutes of Health and the American Cancer Society.

Written by Carol Cruzan Morton

CITATION:

Cancer Research, Sept. 14 advance online publication

"Metformin Selectively Targets Cancer Stem Cells, and Acts Together with Chemotherapy to Block Tumor Growth Q2 and Prolong Remission"

Heather A. Hirsch (1), Dimitrios Iliopoulos (1), Philip N. Tsichlis (2), and Kevin Struhl (1)

CONTACT:
Carol Morton
communications@hms.harvard.edu
617.432.0442

Harvard Medical School has more than 7,500 full-time faculty working in 11 academic departments located at the Schools Boston campus or in one of 47 hospital-based clinical departments at 17 Harvard-affiliated teaching hospitals and research institutes. Those affiliates include Beth Israel Deaconess Medical Center, Brigham and Womens Hospital, Cambridge Health Alliance, Childrens Hospital Boston, Dana-Farber Cancer Institute, Forsyth Institute, Harvard Pilgrim Health Care, Hebrew SeniorLife, Joslin Diabetes Center, Judge Baker Childrens Center, Massachusetts Eye and Ear Infirmary, Massachusetts General Hospital, McLean Hospital, Mount Auburn Hospital, Schepens Eye Research Institute, Spaulding Rehabilitation Hospital, and VA Boston Healthcare System.

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High School Extra /News and notes - Buffalo News

Posted: 18 Sep 2009 12:19 PM PDT

City Honors is still perfect

It's a streak that is not only dear to City Honors' girls volleyball team but one that is respected within its own program. The Centaurs have never lost a set or a match in Buffalo Public Schools league play.

City Honors remained perfect Thursday, as the Centaurs began their 24th season of league play by beating Grover Cleveland, 25-5, 25-16, 25-14.

City Honors has on 778 straight sets. "We certainly take pride in it," coach Deborah Matos said. "We go into every season respecting every team in our league. Buffalo Public Schools teams are getting better. We go in with a little bit of a target on our back. We go in respecting everyone. We take pride in it and it's something you can't take for granted."

Junior Natalie Southard—one of eight returnees— had 11 kills and four aces for last year's Section VI Class C runner-up. Senior Carly Daniel added seven kills for the Centaurs, who finished third last weekend at the Burnt Hills Tournament near Albany. City Honors will be among the local powers participating in Saturday's Sweet Home Tournament. Other tournament participants include defending Section VI Class AA champion Frontier, runner-up Lancaster and Orchard Park— which owns a pair of early- season wins over both Frontier and Lancaster.

Elsewhere, Hutch-Tech— one of the Buffalo schools looking to end City Honors' dominant reign—opened with a convincing three-set win over Lafayette, while Riverside and South Park— other potential threats according to Matos— also opened with straight-set triumphs.

Clarence boys finish tough week

Clarence's boys soccer team earned some much-needed rest and relaxation by earning a 2-1 overtime win over visiting Lancaster.

Joe Stigelmeier scored the game-winner two minutes into overtime off a Derek Maier assist. The Red Devils opened a key week of ECIC I play Tuesday by beating Williamsville North, 2-0, before improving to 6-0 with Thursday's win.

"It's a tough week for us. Coming out 2-0 against those guys is what we were wishing for," Mike Silverstein said.

Maier scored for Clarence in the first half, while Lancaster's P. J. Heist tied it four minutes into the second half. Hunter Hein finished with seven saves for Clarence.

Iroquois was another team that worked overtime to experience that winning feeling as the Chiefs earned an ECIC II triumph over West Seneca East, 2-1. Shawn Colvin's second goal of the game and fourth of the season at seven minutes of the extra period off a goal-mouth scrum was the game-winner.

In ECIC III, Amherst beat Pioneer in overtime, 3-2. Paul Borema scored the game-winner off a rush up the left wing. Ted Tiftickjian scored the tying goal for Amherst, which trailed, 2-1, at halftime.

Etcetera

• In ECIC III girls soccer, Depew earned a measure of revenge against Amherst, beating the Tigers in overtime, 3-2. Kim Obermeier scored three goals for Depew, which lost earlier this season to Amherst, 7-0. Winning goalie Stephanie Peterson finished with 12 saves.

• In ECIC III boys volleyball, Cheektowaga beat East Aurora in four sets, as Sean Walters led the Warriors with eight kills, while Ryan Carr finished with 38 assists in the win.

Kicking it for good cause

Monday's boys soccer matchup of St. Joe's at St. Francis should be a great one on the field —and it should be a great night no matter how the game ends up. The 7 p. m. game is part of St. Francis' dedication of their season to "Kicks Against Breast Cancer." The game is part of an American soccer initiative to raise money to help find a cure for breast cancer and help women living with cancer survive and thrive. Throughout the season, St. Francis players will wear a pink patch on their left shoulder to show support. A pink ball will be used during Monday's game.

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Breast Cancer

Friday, September 18, 2009