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Like horses running down the long stretch of a quality track, two different artery-opening treatments appear to be running neck-and-neck when it comes to preventing stroke among people with clogged neck arteries and other health problems.

After three years, patients who had a minimally-invasive procedure were just as convenient to suffer a stroke or will attack, or to die, as those who had open-neck surgery.

The findings should help guide the management of patients who need to have one of the two carotid arteries in their necks un-clogged to reduce their risk of a stroke - but who face a high risk of complications during surgery because of other health issues. Such patients may do better with the minimally invasive option, called carotid stenting.

But the study, called SAPPHIRE, doesn’t settle the question in the place of many other patients, with respect to whom the open surgery - carotid endarterectomy - is a tried-and-true option.

The results, from 260 patients who were randomly assigned to single of the two treatments at 29 hospitals, are published in the April 10 issue of the New England Journal of Medicine by means of researchers from the University of Michigan Cardiovascular Center, Harvard University and others. The study was funded by Cordis, a Johnson & Johnson company, which had no role in the analysis of ponder data.

“Patients who are undergoing a procedure want to know that they’ll be protected long-term from stroke, and that the procedure is safe,” says Hitinder Gurm, M.D., the U-M interventional cardiologist who is the study’s first author. “This is the first research to suggest that stents produce just as well long-term as surgery, in high-risk patients.”

The study’s senior and corresponding author is Donald Cutlip, M.D., executive director of clinical investigations at Harvard University’s Clinical Research Institute. SAPPHIRE was led by Jay Yadav, M.D., in days of yore at the Cleveland Clinic and now at Piedmont Hospital in Atlanta.

In all, 41 of the 143 patients who received carotid stents, and 45 of the 117 patients who had open surgery, suffered a heart attack or a stroke, or died, within the first three years. The two rates are statistically equivalent, showing nay discrimination between the two treatments. About a third of those events were strokes, most of them minor.

The two procedures both aim to do the same thing: to reduce the chance that a patient will suffer a stroke for a blood clot forms in a narrowed, plaque-clogged carotid artery, and soon afterward travels to the brain.

greatest number numerous people are familiar with the idea that clogged arteries near the heart can lead to a heart attack. But far fewer people know the risks related to carotid artery disease.

This is despite the fact that both heart (coronary) artery disease and carotid artery disease are caused by the same plaque-forming processes involving inflammation, cholesterol and genetics. Just as in the heart, most patients experience not any symptoms from clogged carotids. As a result, many people don’t realize they have the disease until they be punished a stroke or mini-stroke.

As many as one in four American adults consider some narrowing of the carotid arteries. About 5 percent of women over age 65 and a slightly higher percentage of men in the same age group be with less than the necessity at least one carotid blockage that cuts off 50 percent of the opening through which blood can flow.

The greater the blockage, the higher the risk of stroke. People who have already had a stroke or mini-stroke that originated in their carotid arteries are at an extremely high risk of suffering another stroke, while those who have severe carotid blockages but no history of stroke have less risk.

Both groups of patients are often considered the best candidates for some sort of treatment, though Medicare will only covering stents for patients who have experienced symptoms of carotid artery disease. But the debate over whether surgery or stenting is best or safest has raged for years.

Stents, which are tiny wire-mesh tubes that can hold open a blocked carotid, have been seen as a less-invasive option, because they have power to be threaded up into the neck from a tiny incision in the arm or groin. But the stent procedure carries its own risk of stroke, if not a debris-catching device is deployed to intercept anything that breaks off from the wall of the artery while the procedure is under way. Such filters, called emboli protection devices, were used in the SAPPHIRE study.

Meanwhile, carotid endarterectomy operations have been performed tens of thousands of spells each year for decades. The operation opens an incision in the neck below the jaw, allowing a surgeon to divert the blood flow temporarily while he or she opens the carotid and clears lacking the plaque. Sometimes a stretch of new blood vessel is sewn into place.

But as tried-and-true as the operation is, it can lead to complications among people who have heart failure, lung disease, a history of neck surgery or radiation therapy - or who are excessively age 80 or have had previous carotid artery treatment but have developed new blockages.

Such patients are called high-risk, and stents have been seen as a lower-risk option for them. But until now, it was not known whether they would get the same stroke-preventing benefit from a stent.

In the SAPPHIRE study, patients who had symptoms of their carotid disease - such as a mini-stroke, stroke or dizziness - could participate if one of their carotids had a blockage of 50 percent or greater. end those without symptoms could only participate if they had a blockage of 80 percent or more that had been discovered through an exam such as an ultrasound scan of the neck.

In all, three-year given conditions was available on 260 of the 334 patients who were randomly assigned to one of the two treatments at the beginning of the study. Previous analyses of SAPPHIRE data have shown none difference between the couple treatment groups after 30 days and united year. The main measure to compare the two treatments was a combination of stroke, heart attack or death from any cause, though each type of incident was also analyzed.

“Clinical trials are now under determined course to determine the relative risks and benefits of stenting and endarterect-omy in average-surgical-risk patients, and to compare different stent procedures,” says Gurm, an assistant professor of internal medicine at the U-M Medical School and the VA Ann Arbor Healthcare Center. He notes that two such trials are under way at U-M. “Outside of trials, I do not think a person with average surgical risk should suffer stenting. But for high-risk patients, we can very lately be certain that they will have a similar long-term outcome from stenting as they would have had from surgery.”

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Article adapted by Medical News Today from original press release.
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Reference: New England Journal of Medicine, Volume 358, Number 15, April 10, 2008

Source: Kara Gavin
University of Michigan Health System

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Researchers from the University of Pittsburgh and the University of Chicago were apt to control heart muscle function in a new way after discovering the previously unknown role of two enzymes in heart muscle contraction, as detailed in the April 11 cover story of the Journal of Biological Chemistry. Although in the soon stages, the research provides fresh knowledge of how heart muscle functions and also holds in good time potential as a treatment for various heart diseases - including congestive heart failure - that is possibly less taxing on the heart than current regimens.

Experiments on slivers of heart muscle revealed that heart muscle contractions can be regulated by the enzymes histone acetyltransferases (HATs) and histone deacetylases (HDACs), explained Pitt professor Sanjeev Shroff, the Gerald McGinnis Chair of Bioengineering in the Swanson School of Engineering. Shroff and Pitt exploration associate Stephen Smith collaborated through Mahesh Gupta, an compeer professor of surgery at the University of Chicago, and his research associate Sadhana Samant. The project was funded by a grant from the National Institutes of Health.

The team found that HATs and HDACs influence acetylation of certain heart muscle proteins, a process wherein a radical cluster of atoms called an acetyl group attach to a protein and change its function. HATs facilitate acetylation, and HDACs remove the acetyl group. The team discovered that acetylation renders the muscle fiber more sensitive to calcium, what one. causes the muscle to abridge.

“This is a completely new process in the realm of heart muscle contraction,” Shroff said. “Acetylation is widely known to regulate of that kind events inside the cell nucleus as gene regulation, but it’s never before been associated with heart muscle contraction.”

Furthermore, Shroff and his colleagues could intervene in this microscopic process to control heart muscle contraction. By inhibiting HDACs, they increased the calcium sensitivity of the muscle fibers and strengthened contraction.

As a possible manipulation for such conditions as congestive heart failure, this technique could present an alternative to current therapies that counteract heart muscle weakness by boosting cellular calcium content, Shroff said. The heightened calcium improves muscle contraction but also results in more energy consumption in hearts that often are energy-starved to begin with.

In contrast, inhibiting HDAC alters a natural process to make heart muscle more sensitive to the prevailing level of calcium, he said.

“We did not create this process - we are just manipulating what is already in that place,” Shroff explained. “The physiology to block HDAC is even now there, and we just took advantage of that. This trepidation does not require greater mobilization of calcium, so we won’t extreme point up with increased cardiac energy consumption. That’s been the Achilles heel of treatment so far.”

The team’s nearest step involves examining HAT- and HDAC-driven regulation of cardiac contraction in the whole animal rather than just muscle samples. Then it can better determine the overall significance of the newly discovered process to the intact heart function and its therapeutic potential.

“We want to see how much protein acetylation matters when operating alongside all the other processes in the heart and the body,” Shroff said. “If this process is shown to be significant under these stipulations, it will be an exciting finding.”

For the entire paper, visit the Journal of Biological Chemistry Web site

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Article adapted by Medical News Today from commencement press release.
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4/9/08/tmw

Source: Morgan Kelly
University of Pittsburgh

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Individuals with hemophilia lack either factor VIII or factor IX, proteins crucial for the cascade of events that leads to disposition clotting. Although individuals with hemophilia can be treated by intravenous infusion of the factor that they miss, over time, some individuals develop antibodies that prevent the infused factor from acting. Intravenous infusion of an activated form of a factor that works earlier in the blood clotting cascade, factor VII (FVIIa), has been used for over a decade to treat individuals who develop antibodies that target factor VIII or factor IX. However, some researchers and clinicians hope that FVIIa gene therapy might provide a simplified way to get ready FVIIa to individuals with hemophilia. In a new study, Katherine High and colleagues, at The Children’s Hospital of Philadelphia, gain determined a safe and forcible level of mouse FVIIa that can be continuously expressed in hemophilia B mice through gene therapy.

The authors observed that continuous expression for up to 16 months of up to 1.5 micrograms per milliliter of mouse FVIIa, either by engineering hemophilia B mice to express this factor throughout life or by treating hemophilia B mice through gene therapy, was safe and corrected the divergent bleeding of the mice. By contrast, continuous expression of 2 micrograms per milliliter (or more) of mouse FVIIa was associated with early subjection to death and with inner part and lung problems. These given conditions should provide useful information for researchers and clinicians developing gene therapy approaches for the treatment of individuals with hemophilia.

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Article adapted by Medical News Today from original press release.
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TITLE: Long-term expression of murine activated factor VII is safe, but elevated levels cause premature mortality

AUTHOR CONTACT:

Katherine A. High
The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USA.
http://www.chop.edu

View the PDF of this article at: http://www.the-jci.org/article.php?id=32878

Source:
Karen Honey
Journal of Clinical Investigation

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Many Swedish men have no one to turn to for emotional support other than their partners, not divisible by two in particularly traumatic situations, such as when suffering from cancer. However, according to new research, the partners of cancer patients also often lack support outside the relationship.

Previous scrutiny has shown that many Swedish men over 50 with cancer confide their feelings and fears about the ail to few other people, if any. For 80 per cent of men who have prostate cancer and who wide-awake simultaneously through someone else, the partner is the only head of emotional support they have. Seventy per cent of single men by prostate cancer do not share their feelings with another human frame.

The same group of researchers at Karolinska Institutet has now examined the extent to which women in the same age group who have lost their husbands to cancer confide in other people. Their results show that one third of these women have no person else with whom to certain quantity their feelings.

“We’re surprised that so many women are emotionally isolated, by which we mean that they lack low, emotional contacts,” says study leader Asgeir Helgason, associate professor at Karolinska Institutet. “There’s a general sense that the problem only applies to men, but this isn’t the subject of discussion.”

“We’ve decided to enhance this at a conference on men’s health in some measure on this account that of the very important role the member of a partnership plays in giving psychosocial support to men with cancer,” says Dr Helgason. “Our findings suggest that the care of masculine cancer patients should also be directed at their partners.”

KAROLINSKA INSTITUTET
SE-171 77 Stockholm
http://ki.se

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According to data presented today at the 48th Annual Scientific Meeting of the British Society for Haematology (BSH), patients taking Revlimid® (lenalidomide) plus high dose dexamethasone for treatment of multiple myeloma experience a significant survival gain. without ceasing average, patients experienced nearly three extra years of life whenever treated with lenalidomide plus high dose dexamethasone (4.7 life years) compared with dexamethasone alone (1.9 life-years).1

Myeloma is a type of line cancer that develops in the bone marrow’s plasma cells. There are nearly 3,800 cases of myeloma in the UK per year with more than 2,400 people dying from the disease annually. 2

“The data presented today further substantiates previous outstanding trial results,” specified Dr Steve Schey, Clinical Lead for Myeloma, King’s College Hospital, London and Chair of the UK Myeloma Forum. “Lenalidomide will bestow patients the opportunity to live with their cancer for years rather than months. It represents a major step forward towards turning myeloma into a of long duration ailment rather than the death sentence it has been until now.”

In trials evaluating lenalidomide plus high dose dexamethasone versus dexamethasone alone, many patients receiving dexamethasone alone were switched to lenalidomide combination at disease progression given the significantly better efficacy of the lenalidomide combination. As a result, the true survival gain for the dexamethasone alone group was previously overestimated. Today’s premises revealed a more accurate lifetime simulated survival rate in spite of patients taking dexamethasone alone to account notwithstanding the cross over of treatment in trials, based put on pooled data from the UK Medical Research Council (MRC).1

Dr Schey continued, “These projected figures give us a more realistic picture of the real benefits we can hope to see in patients with lenalidomide, versus the older standard of treatment.”

Additional data also presented at the BSH demonstrated that lenalidomide is a costeffective treatment. The results show that the incremental cost-effectiveness ratio is £28,980 per kind adjusted life year (QALY) for patients taking lenalidomide when compared with the older standard treatment. This cost is lower than the threshold of £30,000 per QALY that is widely considered to be an agreeable value for an additional QALY.3

“The licensing of lenalidomide in the UK represented a major advance for patients with myeloma,” stated Eric Low Chief Executive of Myeloma UK. “We are publicly working with HTA authorities to ensure that patients have wider access to new handling options such as this.”

Lenalidomide is currently undergoing a review by the Scottish Medical Consortium (SMC), with a decision anticipated in May 2008.

About myeloma

Myeloma is a type of blood cancer that develops in the bone marrow’s plasma cells. Since myeloma can develop wherever there are plasma cells, it can arise in several places in the body and so is often called multiple myeloma. In myeloma, too many plasma cells are made and the body is impotent to make normal white blood cells, red blood cells and platelets. The be wanting of white and red blood cells and platelets means that people with myeloma are more prone to infections, feel tired and breathless, and prone to bleeding problems.4

About quality-adjusted life years (QALYs)

Quality-adjusted life years, or QALYs, is a way of measuring disease burden, including both the quality and the quantity of life lived, as a means of quantifying in benefit of a medical intervention.

About Revlimid®

Revlimid® (lenalidomide) (which is the active substance in the treatment) is the first of the IMiDs®, to be licensed, a proprietary group of novel immunomodulatory agents developed by dint of. the biopharmaceutical company Celgene. Immunomodulatory agents enhance or keep secret the immune system. It is an oral treatment, which means that patients no longer need to go to hospital for all their manipulation courses.

The results of trials using Revlimid® (lenalidomide) have shown better results in patients with multiple myeloma than ever seen before.5

- In nearly two thirds (60.2%) of patients taking lenalidomide plus dexamethasone the signs and symptoms of their myeloma either disappeared or were substantially reduced compared by a quarter (24%) for those on dexamethasone more a dummy drug called a placebo. (Dexamethasone is a corticosteroid used to treat inflammatory and autoimmune conditions as well as some cancers.)

- Overall survival was significantly improved in the lenalidomide arrange.

- In this same trial, the patients taking lenalidomide were free of the signs and symptoms of cancer for longer than those who had received dexamethasone and placebo, at 16.5 months.

- Patients in the trial treated by lenalidomide also experienced the longest disease-free stretch of time ever reported in clinical trials. In the trial the median time until the disease came end for the patients taking lenalidomide plus dexamethasone, was 11.3 months - more than knavish the time for patients taking dexamethasone and placebo, 4.7 months.

The most common side effects associated with lenalidomide are low platelets (atomic cell fragments in the blood essential for clotting), low white blood cells, and diarrhoea. Other reported harmful events include constipation, rash, itchiness, weakness, dizziness and fatigue. Lenalidomide has also demonstrated a risk of deep vein thrombosis in some patients with certain of the healing art conditions. Many of these serious adverse events are consistent with the patients’ disease state, age, and other health problems.5

About Celgene UK

Celgene UK is a wholly-owned subsidiary of Celgene Corporation. Celgene Corporation, with its worldwide headquarters in Summit, New Jersey, is an integrated global pharmaceutical company engaged in a primary manner in the discovery, development and commercialization of innovative therapies for the treatment of cancer and seditious diseases through gene and protein regulation. For more information, please visit the Company’s website at http://www.celgene.com.

This dispensation contains forward-looking statements which are subject to known and unknown risks, delays, uncertainties and other factors not under the Company’s control, which may cause actual results, performance or achievements of the Company to be materially different from the results, performance or other expectations expressed or implied by these forward-looking statements. These factors include results of current or pending research and development activities, actions by the FDA and other regulatory authorities, and other factors described in the Company’s filings with the Securities and Exchange Commission such as our 10K, 10Q and 8K reports.

References

1. J. Ishak, et al., “Modeling overall survival in the event of patient cross-over from dexamethasome to lenalidomide in phase III multiple myeloma trials” presented at the British Society for Haematology (BSH) meeting in April 2007 in Glasgow.

2. Cancer Research UK. UK Multiple myeloma incidence statistics. Accessed February 2008.

3. B. Deniz, et al., “Economic evaluation of lenalidomide for the treatment of multiple myeloma in Scotland in patients who have received one prior therapy” presented at the British Society in the place of Haematology (BSH) meeting in April 2007 in Glasgow.

4. Cancer Research UK. What is myeloma? accessed February 2008

5. Dimopoulos M, Spencer A, Attal M, et al. Lenalidomide plus dexamethasone for relapsed or refractory multiple myeloma. N Engl J Med 2007; 357: 2123-32

Celgene UK

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Abraxis BioScience, Inc. (NASDAQ:ABII), a fully integrated biotechnology company, announced that the Korean FDA (KFDA) has granted marketing approval for ABRAXANE® (paclitaxel protein-bound particles for injectable suspension) (albumin-bound) for the treatment of breast cancer after failure of standard chemotherapy for metastatic disease. The Phase III clinical trial results on which this approval was based demonstrated that ABRAXANE doubled the response rate and significantly prolonged progression-free survival and overall survival versus Taxol® in the approved indication. ABRAXANE is now approved for marketing in 34 countries.

As previously announced, Abraxis granted an snobbish license to Green Cross Corporation for the commercialization of ABRAXANE in Korea. Green Cross made an upfront payment and will recompense a royalty on net sales of ABRAXANE in Korea as well as milestone payments. In a separate agreement, Green Cross has granted an exclusive license to Abraxis for the future commercialization of the following biosimilars in the U.S. and Canada: erythropoetin, pegylated G-CSF (granulocyte-colony stimulating factor), Interferon-Alpha, recombinant Factor VIII, and etanercept. Interferon Alpha has been launched in Korea by Green Cross. Green Cross filed for regulatory approval with the KFDA for recombinant Factor VIII in the second quarter of 2008 and Green Cross has completed Phase III studies for erythropoetin. Pegylated GCSF and etanercept are in early stages of development. Once approval has been received, Abraxis will pay Green Cross a milestone on each product in addition to royalties on net sales.

Green Cross popularly expects to launch ABRAXANE in Korea in the first quarter of 2009 following pricing approval. Green Cross plans to establish a dedicated sales force for ABRAXANE and implement various marketing campaigns to support a successful launch. Abraxis has two extra global partnerships for the commercialization of ABRAXANE with Taiho Pharmaceuticals in Japan and Biocon Limited in India.

“The approval for ABRAXANE in Korea provides an effective new treatment option to physicians and patients in Korea in the fight against metastatic breast cancer. We look forward to expanding the global market presence of ABRAXANE,” said Patrick Soon-Shiong, M.D., chairman and most important executive officer of Abraxis BioScience.

“This approval represents an exciting new direction for Green Cross’s oncology business and we are very pleased to bring this unique and efficacious drug to cancer patients in Korea,” said B.G. Rhee, Ph.D., executory vice president of Green Cross.

In Korea, there are approximately 20,000 cases of metastatic breast cancer. The Korean oncology market for 2007 is estimated at US$533 million of what one. the chemotherapy market and its taxanes component are estimated at US$400 million and US$77 million, respectively, per IMS.

In addition to the approval in Korea, ABRAXANE is approved for marketing in the U.S. and is popularly co-promoted in collaboration with AstraZeneca Pharmaceuticals LP. ABRAXANE is the fastest growing taxane in the U.S.

ABRAXANE was approved in Canada in 2006 for the treatment of metastatic breast cancer including first-line disease. ABRAXANE was approved in India in November 2007 for the second-line treatment of breast cancer after failure of combination chemotherapy for metastatic disease or relapse within 6 months of adjuvant chemotherapy. Most recently, ABRAXANE was approved in the European Union in January 2008 for the treatment of metastatic breast cancer. ABRAXANE is currently under active review in Australia, Russia and China by their respective regulatory agencies.

About ABRAXANE

ABRAXANE, the first in a new rank of protein-bound nanoparticle drugs utilizing the company’s proprietary nanoparticle albumin-bound (catch™) technology, is currently in various stages of expanding for the treatment of the following cancers: first-line metastatic breast, non-small cell lung, malignant melanoma, pancreatic, gastric, and head and neck.

The U.S. Food and Drug Administration (FDA) approved ABRAXANE for Injectable Suspension (paclitaxel protein-bound particles for injectable delay) (albumin-bound) in 2005 for the treatment of breast cancer after failure of combination chemotherapy for metastatic disease or relapse within six months of adjuvant chemotherapy. Prior therapy should have included an anthracycline unless clinically contraindicated.

ABRAXANE uses albumin, a like a man protein, to deliver the assiduous ingredient paclitaxel. Unlike more other chemotherapy treatments, ABRAXANE does not contain chemical solvents, that eliminates the need for pre-medication with steroids or antihistamines often needed to prevent the toxic side effects associated with solvents. ABRAXANE is administered in 30 minutes in the manner that compared to three hours for solvent-based paclitaxel.

The most serious adverse events associated with ABRAXANE in the randomized metastatic breast cancer study for which FDA approval was based included neutropenia, anemia, infections, sensory neuropathy, nausea, vomiting and myalgia/arthralgia. Other common adverse reactions included anemia, prostration, diarrhea, ocular/visual disturbances, fluid retention, alopecia, hepatic dysfunction, mucositis and renal dysfunction. For the full prescribing information for ABRAXANE, please visit http://www.abraxane.com.

ABRAXANE was developed by Abraxis BioScience, Inc. ABRAXANE is marketed in the United States under a co-promotion agreement between Abraxis and AstraZeneca Pharmaceuticals LP.

About Green Cross

Green Cross, a leader in the Korean biotechnology and pharmaceutical industries, is a fully integrated, internationally recognized biotechnology company dedicated to the research, development and marketing of products such as vaccines and biopharmaceuticals. Green Cross has successfully developed vaccines conducive to Hepatitis B (Hepavax), Epidemic Hemorrhagic Fever (Hantavax) and chicken pox. The company manufactures the only seasonal influenza vaccine in Korea and is developing an avian influenza vaccine as well as recombinant Factor VIII and IX for hemophilia, and recombinant PTH for severe osteoporosis. In oncology, Green Cross is developing Greenstatin (anti-angiogenic peptide) and modified PEG-G-CSF for neutropenia.

http://www.greencross.com

About Abraxis BioScience

Abraxis BioScience is a fully integrated global biotechnology company dedicated to the discovery, unravelling and delivery of next-generation therapeutics and core technologies that offer patients safer and more effective treatments for cancer and other critical illnesses. The social meeting’s portfolio includes the universe’s first and simply protein-based nanoparticle chemotherapeutic compound (ABRAXANE®) which is based on the company’s proprietary swelling targeting technology known as the nab™ platform. The first FDA approved product to use this nab platform, ABRAXANE®, was launched in 2005 for the treatment of metastatic breast cancer. Abraxis trades on the Nasdaq Global Market under the symbol ABII. For more information about the company and its products, please visit http://www.abraxisbio.com.

Forward-Looking Statements

The statements contained in this press release that are not purely historical are forward-looking statements within the meaning of Section 21E of the Securities Exchange Act of 1934, as amended. Forward-looking statements in this hasten release include statements regarding our expectations, beliefs, hopes, goals, intentions, initiatives or strategies, including statements regarding the launch of ABRAXANE in Korea. Because these forward-looking statements involve risks and uncertainties, in that place are important factors that could cause actual results to differ materially from those in the forward-looking statements. These factors include, without limitation, the market launch of ABRAXANE in Korea, the impact of pharmaceutical endeavors regulation, the impact of competitive products and pricing, the acceptance and demand of new pharmaceutical products, the impact of patents and other proprietary rights held by competitors and other third parties. Additional relevant information concerning risks can be found in Abraxis BioScience’s Form 10-K for the year ended December 31, 2007 and other filings by the Securities and Exchange Commission. The information contained in this press release is as of the date of this release. Abraxis assumes no obligations to update any forward-looking statements contained in this press release as the result of new information or what may occur hereafter events or developments.

Taxol® is a registered trademark of Bristol-Myers Squibb Company.

Abraxis BioScience

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The United Mitochondrial Disease Foundation released the following statement from its executive director and CEO, Chuck Mohan, in light of the National Vaccine Advisory Committee’s (NVAC) meeting of its Vaccine Safety Working Group and recent published reports of possible links between mitochondrial disorders and autism.

“Recent published reports about the potential links between mitochondrial disorders and autism demonstrate the urgent need for more research into mitochondrial illness, a devastating and often fatal complaint.

“Mitochondrial dysfunction has also been implicated in Alzheimer’s Dementia, Parkinson’s disease, Huntington’s disease, heart disease and diabetes.

“Mitochondrial disease is not rare. Researchers estimate that every 15 minutes a child is born with mitochondrial disease or will subsist diagnosed with mitochondrial disease by the age of 10. Most artificial children do not brilliant beyond their teenage years.

“The National Institutes of Health currently spends about $11.8 million on research into mitochondrial-related research — with only about one third of that earmarked for primary mitochondrial disease research. That is less amount than 1/1000 of individual percent of NIH’s $29B yearly report budget. That is why the United Mitochondrial Disease Foundation supports the effort by the National Institutes of Health to standing mitochondrial disease research on an NIH roadmap.

“Mitochondrial disease deprives the visible form of energy making it arduous to function properly. It can concern any organ of the visible form and at any age. The brain may be impaired, vision may be dim, muscles may twitch or may be too vulnerable to allow the body to walk or write, the heart may be weakened, and the ability to eat and digest food can be compromised.

“Finding the cause of and cure because mitochondrial disease would not solitary alleviate the suffering of families around the nature, it would also unlock the door to a world of scientific information and could help lead the way to practicable treatments for many other diseases.”

United Mitochondrial Disease Foundation
http://www.umdf.org

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By revealing the inner workings of a common cell-to-cell signaling system, University of Michigan biologists have uncovered new clues about mysterious and contentious creatures called cancer stalk cells.

The findings also have implications for a high-profile breast-cancer mix with drugs cause getting underway at the U-M Medical School and two other institutions.

In the groundbreaking trial, researchers are combining chemotherapy with a medicine that blocks the Notch signaling pathway, which helps regulate fetal development and is active in most organ systems throughout a person’s life.

The aim is to use so-called Notch inhibitors to attack cancer stem cells, the small fraction of stem cells inside a tumor that help it survive and that fuel its increase.

But a big concern is that the Notch inhibitors, while helping to destroy cancer stem cells, puissance also kill or harm the normal, healthy stem cells critical to a patient’s survival such as blood-forming shoot cells in the bone essential part.

New results from the U-M’s Dr. Ivan Maillard and his colleagues may allay some of those fears. The researchers showed that blood-forming bear up against cells in mice survive just fine when the Notch signaling pathway is experimentally blocked.

“Our facts indicate that normal blood-forming stem cells should not be damaged by the Notch inhibitor drug being used in these patients,” said Maillard, a hematologist and a Life Sciences Institute researcher.

“That’s important, because these patients typically need good blood stem cells to maintain their blood counts and recover from the effects of chemotherapy,” he said.

The Notch tools and materials will be published Thursday in the journal Cell Stem Cell. Maillard’s team includes researchers from the University of Pennsylvania School of Medicine, the Swiss Institute for Experimental Cancer Research, and Harvard Medical School.

Dr. Max Wicha, director of the U-M Comprehensive Cancer Center, said Maillard’s results are welcome news for cancer stem cell researchers, and for the 30-patient metastatic breast-cancer drug trial that launched last month at his center, at the Baylor College of Medicine in Houston, and at the Dana-Farber Cancer Institute in Boston.

“It’s really important, because a lot of what we’re thinking about now, therapeutically, is trying to find ways to attack these cancer stem cells, because we think that’s actually what drives the malignancies,” said Wicha, who was not involved in the Notch study.

“Ivan’s paper, combined with our own work, shows that there may have existence differences between normal stem cells and cancer stem cells, and perhaps those differences can be exploited therapeutically,” Wicha said.

The cancer stem cell theory is polemical. more researchers are not convinced that cancer pedicel cells exist.

The current two-stage drug trial uses a Notch inhibitor originally developed by Merck for Alzheimer’s patients in the late 1990s, followed by chemotherapy. The purview is to use the Notch inhibitor to make cancer stem cells sensitive to the chemotherapy—a one-two punch to strike out tumors.

If the treatment is effective, the results could help sway some cancer-stem-cell skeptics.

The Notch pathway sends signals from a cell’s surface membrane into its nucleus. Those signals activate genes that instruct the cell to make proteins that perform uncertain tasks.

In the lab, Maillard and his colleagues were able to intercept Notch signals from activating mouse target genes using two independent techniques.

Many scientists have spun out assumed that blood-forming stem cells need Notch signals to function properly. But Maillard’s team found that the signals are not required for the maintenance of blood-forming stem cells in adult mice.

In addition to his position as a research assistant professor at the Life Sciences Institute’s Center as being Stem Cell Biology, Maillard is an assistant professor of inward medicine and an assistant professor of cell and developmental biology at the U-M Medical School.

Funding with respect to the Notch study was provided by grants from the National Institutes of Health, The Leukemia & Lymphoma Society, the Swiss National Science Foundation, and the Damon Runyon Cancer Research Foundation.

For more information about stem small cavity research, visit: http://www.umich.edu/stemcell/

U-M Comprehensive Cancer Center: http://www.cancer.med.umich.edu/research/stemcells.shtml

LSI’s Center for Stem Cell Biology: http://lsi.umich.edu/facultyresearch/centers/stemcellbiology

Maillard Lab: http://lsi.umich.edu/facultyresearch/labs/maillard

University of Michigan
412 Maynard St.
Ann Arbor, MI 48109-1399
United States
http://www.umich.edu

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Deadly and difficult to treat, liver cancer has long resisted attempts by researchers to make known ways to prolong life and prevent recurrence. But Mayo Clinic Cancer Center, in collaboration with the National Cancer Institute, reports in the April issue of Hepatology that the protein sulfatase 2 (SULF2) may provide united of the keys needed to begin the design of new therapies.

Mayo Clinic Cancer Center leads the field in researching the impact and effect of SULF1, a protein whose normal role is to degrade heparin sulfate proteoglycans — molecules that are part sugar and part protein. Mayo scientists have found that the protein also helps inhibit tumefaction growth. Now, Mayo researchers are studying a related gene, SULF2. The role of the SULF2 gene and protein has not been fully defined, but in this study, researchers investigated the effect of SULF2 on liver swelling growth in the laboratory. They found that increased expression of SULF2 enhances cancer cell growth and migration, while on the contrary decreased expression reduces both.

“The liver is designed to excrete toxins, and its tumors are no exception,” says Mayo Clinic gastroenterologist Lewis Roberts, M.B.Ch.B., Ph.D., the study’s primary investigator. “Our problem is that the tumors tend to excrete chemotherapeutic agents rather than be affected by them. So we are looking for ways to get around that.”

The researchers sought answers by examining a protein related to person they already knew had a role in suppressing liver tumors. SULF1 and SULF2 are similar proteins, but cause conflicting results. SULF1 removes sulfate groups that allow pullulation factors to bind to cells, thus inhibiting growth. The investigators found that SULF2 did the opposite — it increased binding of a specific growth factor, fibroblast growth factor 2 (FGF2), to tumor cells, and also increased look of the heparan sulfate proteoglycan glypican 3 (GPC3), which plays an important role in solitary abode; squalid division and growth. These findings were confirmed in mouse models.

This discovery indicates if scientists can decrease the levels or activity of SULF2 in a tumor, they might exist able to stop its development. Mayo researchers are exploring use of an agent that mimics heparin and inhibits SULF2. They are also examining whether preventing heparin sulfate synthesis would inhibit tumor growth.

“If something has a exceedingly broad effect on signaling by growth factors, it may lead to an effective treatment,” says Jinping Lai, M.D., Ph.D., a Mayo oncology researcher and the lead author of the study. “SULF2 has a number of characteristics that make it an attractive mark, like as the fact that it is widely present in tumors. We are exploring a count of options by SULF2 as a focal point for treatment not single in liver cancer, but likewise in head and neck, pancreas, heart and other types of cancer.”

The researchers hope to identify drugs that block SULF2, and seek to thoroughly understand the mechanisms involved, including the determination of what other growth signaling pathways are affected by SULF2. They are also looking further at GPC3 as a potential biomarker for liver cancer or as a possible therapeutic target.

In 2007, Dr. Lai presented information at the occurring once a year assembly of the American Association for Cancer Research on the role of SULF2 in survival of patients with head and neck cancer — the first concrete link to survival of patients with a specific tumor type.

Additional Mayo researchers on this study include: Catherine Moser; Ruben Bonilla Guerrero, M.D.; Ileana Aderca, Megan Garrity-Park; Hongzhi Zou, M.D., Ph.D.; Abdirashid Shire, Ph.D.; David Nagorney, M.D.; and Schuyler Sanderson, M.D.; also former fellows: Dalbir Sandhu, M.D.; Tao Han, M.D., Ph.D.; Kenard Jackson; and Hajime Isomoto, M.D.; and former staff member Alex Adjei, M.D., Ph.D., and Chunrong Yu, Ph.D., both currently of Roswell Park Cancer Institute, Buffalo, N.Y. Other collaborators included Ju-Seog Lee, Ph.D., and Snorri Thorgeirsson, M.D., Ph.D., of the National Cancer Institute, Bethesda, Md.

This research was supported by the National Institutes of Health, The Richard M. Schulze Family Foundation, and both Mayo Clinic’s Miles and Shirley Fiterman Center for Digestive Diseases and the Cancer Center. For more information on liver cancer exploration at Mayo Clinic, visit: http://mayoresearch.mayo.edu/mayo/research/gastro_cancer/hepatobiliary.cfm.

Mayo Clinic
200 First St. SW
Rochester, MN 55902
United States
http://www.mayoclinic.com

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Embryonic stem cell therapies have been proposed for regenerative medicine and tissue replacement after injury or indisposition. However, the inability of stem cells to efficiently develop into the desired specific cell type - such as muscle, skin, blood vessels, bone or neurons - now limits the potential clinical utility of this therapy.

New research shows that delivering molecules within aggregates of embryonic stem cells via biodegradable microspheres enhances the efficiency and purity of differentiation, that is the process the cells undergo to become more specialized. Details of the microsphere-mediated delivery method, which is funded by the National Science Foundation, were presented at the 235th American Chemical Society national meeting.

“Directing embryonic stem cells to efficiently differentiate into a specific cell type has been challenging to this point,” said Todd McDevitt, an assistant professor in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University. “In my lab, we’re trying to better define and then control the environmental cues that regulate the fate and function of the stem cells.”

Because physical interactions between stem cells is critical during normal embryonic development, most laboratory growth methods allow the cells to aggregate in three-dimensional clumps called “embryoid bodies” in order to differentiate. hinder individual cells whole together, hollow internal structures begin to develop and the aggregate becomes larger and more complex over time.

“Many researchers add soluble factors to the culture dish medium to direct differentiation, but this does not accurately mimic the time and location of signaling events present in normal development, and may grant to heterogeneous differentiation,” said McDevitt. “Our method focuses on incorporating the differentiation factors directly into the cell aggregates in order to wish a more controlled mechanism of presentation.”

The research team - which also includes graduate students Richard Carpenedo and Andrés Bratt-Leal and undergraduate students Ross Marklein and Scott Seaman - fabricated biodegradable polymer microspheres that could contain growth factors, proteins or other small molecules.

McDevitt’s team tested the impact of the poly(lactic-co-glycolic acid) (PLGA) microspheres on embryonic stock cell differentiation under different conditions by varying the microsphere-to-cell ratio and speed at which the aggregate cells were mixed with the microspheres. They also included a fluorescent dye in the microspheres so the degree of incorporation of the microspheres within the embryoid bodies could subsist assessed using fluorescent microscopy and spectroscopy.

The results revealed that the microspheres were incorporated into embryoid bodies under a multiformity of mixing conditions, but that slower rotary speeds and higher microsphere-to-cell ratios resulted in a greater degree of incorporation.

Next, the researchers compared differentiation of untreated cells, cells mixed with empty microspheres, cells mixed with retinoic acid-loaded microspheres, and cells treated with soluble retinoic acid. Retinoic acid was chosen initially because it is a potent inducer of embryonic oppose cell differentiation.

After ten days, approximately 90 percent of the embryoid bodies mixed with retinoic acid-loaded microspheres began to display the hollow structure signifying differentiation, compared to 6 percent of the untreated bodies, 10 percent of the bodies coated with soluble retinoic acid, and 30 percent of the bodies mixed with empty microspheres. In addition, thirty percent of the embryoid bodies mixed with retinoic acid-loaded microspheres were completely channel in the center, compared to nearly zero percent on the side of the other groups.

“These results suggest that admitting that you can curb the signaling by presenting molecules locally on the inside of the embryoid body from biodegradable microspheres, you can effectively change the course and synchrony of differentiation,” said McDevitt.

To examine the cells in else detail, McDevitt teamed with Georgia Tech School of Biology chair John McDonald and research scientist Nathan Bowen to conduct microarray gene expression studies to determine cell phenotype.

The results revealed enhanced expression of fibroblast increase factor 5 (FGF-5) - a marker for primitive ectoderm - in the embryoid bodies mixed with retinoic acid-loaded microspheres compared to the other treatment groups after 10 days. The researchers also confirmed increased or inhibited expression of many additional markers.

“The importance of these findings is that we’ve shown that biomaterial-based approaches to regulate stem cell microenvironments can significantly improve differentiation methods,” said McDevitt. “Our ultimate goal is to improve the efficiency of this differentiation process into specific cell types for cell replacement therapies.”

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Article adapted by Medical News Today from model press release.
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Source: Abby Vogel
Georgia Institute of Technology Research News

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