Brain Tumour Survivor

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PostPosted: Tue Mar 26, 2013 2:01 pm 
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Mifepristone improves chemo-radiation response in glioblastoma xenografts

We have investigated the ability of Mifepristone, an anti-progestin and anti-glucocorticoid drug, to modulate the antitumor effect of current standard clinical treatment in glioblastoma xenografts.

Methods: The effect of radiation alone or combined with Mifepristone and Temozolamide was evaluated on tumor growth in glioblastoma xenografts, both in terms of preferentially triggering tumor cell death and inhibiting angiogenesis. Tumor size was measured once a week using a caliper and tumor metabolic-activity was carried out by molecular imaging using a microPET/CT scanner.

The effect of Mifepristone on the expression of angiogenic factors after concomitant radio-chemotherapy was determined using a quantitative real-time PCR analysis of VEGF gene expression.

Results: The analysis of the data shows a significant antitumoral effect by the simultaneous administration of radiation-Mifepristone-Temozolamide in comparison with radiation alone or radiation-Temozolamide.

Conclusion: Our results suggest that Mifepristone could improve the efficacy of chemo-radiotherapy in Glioblastoma. The addition of Mifepristone to standard radiation-Temozolamide therapy represents a potential approach as a chemo-radio-sensitizer in treating GBMs, which have very limited treatment options.

http://7thspace.com/headlines/434809/mi ... rafts.html


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PostPosted: Thu Mar 28, 2013 1:00 pm 
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5-ALA fluorescence guide improves resection of glioblastoma multiforme

Fluorescence form 5-aminolevulinic acid (5-ALA) has been used to guide resection of recurrent glioblastoma multiforme (GBM). Before surgery, the patient ingests 5-ALA, then the tumor cells fluoresce intraoperatively in response to certain wavelengths of light. This can provide information not necessarily available through magnetic resonance imaging (MRI), which is the standard mode of imaging used to detect primary and recurrent GBMs. The additional information provided by 5-ALA fluorescence can guide surgeons in the treatment of individual cases.

GBM is the most common primary tumor of the brain. It is extremely aggressive and is usually treated with resection followed by chemotherapy and radiotherapy. Even using this regimen, patient survival is not long: on average 1 to 2 years. The best way to lengthen survival is to remove as much tumor as possible. This holds for recurrent GBMs as well as for the initial tumor.

A 56-year-old man presented with frequent transient vision disturbances. Seven years earlier, he had undergone gross-total (maximum) resection of a GBM located in the right occipital lobe. A new MRI study was performed, and the images showed three distinct, new sites of tumor in the man's right temporal lobe. No evidence of recurrent tumor was seen at the site where the original tumor had been located.

The patient in this case was scheduled for surgery to remove the three new lesions. To aid intraoperative visualization of the lesions, the neurosurgical team, led by Mitchel S. Berger, MD, chairman of the Department of Neurological Surgery at the University of California at San Francisco, administered 5-ALA to the patient 4 hours prior to surgery.

During surgery, a blue light was used to activate 5-ALA fluorescence of tumor cells, thus differentiating the tumor from other brain tissue. Using the blue light, the surgeons were also able to detect tumor cells along the lining of the right lateral ventricle, in the ependymal and subependymal regions.

Although the appearance of the three lesions on preoperative MRI had indicated distinct sites of recurrent disease (multicentric tumor recurrence), the fluorescence of tumor cells during surgery mapped out the spread of disease from the original GBM site in the right occipital lobe to three sites in the right temporal lobe through a pathway along the wall of the right ventricle. This showed that the GBM recurrence was not multicentric at all. The fluorescence also made it possible for the surgeons to identify and resect additional tumor tissue along the pathway between the original and recurrent lesions.

According to the authors, MRI is unable to clearly delineate diffuse tumor infiltrating the ependyma and subependymal zone lining the lateral ventricle. However, adding 5-ALA fluorescence during surgery revealed the pathway of tumor spread through these regions. This case study was published in the Journal of Neurosurgery (2013; doi:10.3171/2013.1.JNS121537.).

http://www.oncologynurseadvisor.com/5-a ... e/281996/#


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PostPosted: Sat Mar 30, 2013 8:35 am 
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Stem cells from fat may aid glioblastoma treatment

Adipose tissue may provide a more efficient source of mesenchymal stem cells (MSCs) than bone marrow, and the cell-harvesting process would be less invasive and less expensive.

This finding emerged from research led by Alfredo Quinones-Hinojosa, MD, who is a professor of neurosurgery, oncology, and neuroscience at the Johns Hopkins University School of Medicine in Baltimore, Maryland. The work focused on glioblastoma, the most common primary malignant brain tumor.

Glioblastoma is refractory to surgical resection, radiation, and chemotherapy. MSCs, which can be harvested from bone marrow as well as from adipose tissue, are a promising avenue of investigation for the delivery of adjuvant therapies, wrote the researchers in PLOS ONE (2013;8[3]:e58198).

“The biggest challenge in brain cancer is the migration of cancer cells,” explained Quinones-Hinojosa in a statement issued by Johns Hopkins Medicine. “Even when we remove the tumor, some of the cells have already slipped away and are causing damage somewhere else.”

However, MSCs have an unexplained ability to seek out damaged cells and may be able to act as a vehicle to bring drugs, nanoparticles, or some other treatment directly to cells. Moreover, the investigators discovered in test-tube experiments that whether derived from fat or bone marrow, MSCs proliferated, migrated, survived, and maintained their potential as stem cells equally well.

Although human trials of MSC delivery systems are still years away, it is possible that eventually, adipose tissue could be removed from any number of sites in a patient's body shortly before glioblastoma surgery. The MSCs from that tissue would be engineered to carry treatments, and would be deposited into the brain after tumor removal to seek out and destroy remaining cancer cells.

As Quinones-Hinojosa and his colleagues noted in their report, the ability to harvest larger numbers of adipose MSCs than bone marrow MSCs under local anesthesia is well-documented, and patient morbidity may be minimized during the harvesting of the adipose MSCs.

http://www.oncologynurseadvisor.com/ste ... le/285728/


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PostPosted: Wed Apr 03, 2013 1:48 pm 
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Brain tumor, prayers, stuffed doggie bring love, friendship

A young woman who has been diagnosed with brain tumor has received a lot of encouragement, but the kind and thoughtful deed of an 8-year-old boy who did not even know her has touched her more than anything.

Tonette Cox, who lives in the Williamsons Crossroads area with her husband Joe was diagnosed with glioblastoma at Duke Hospital on March 4 after suffering a seizure a few days earlier. She underwent an “awake craniotomy” at Duke to remove the tumors from the right side of her brain and will soon begin taking chemo pills and radiation. She explained that doctors got all of the tumors but there are what they call “fingers” that cannot be seen, therefore chemo and radiation are recommended.

“I have been given a good chance by all of my wonderful doctors and nurses at Duke,” Tonette said. “I have been very open on Facebook about what is wrong with me, so everyone pretty much knows what is going on with me. I call them my prayer people and we have started a prayer chain and pray for people on Facebook. It has grown so big and means the world to me. I can’t do much right now but I can pray for others and I can bring attention to this cancer and the warning signs.”

Eight-year-old Elijah Bullard heard about Tonette and her illness through prayer requests at his church, The Refuge at Five Points in Cerro Gordo where his father Archie Paul Bullard is pastor. While at Build-A-Bear at Myrtle Beach on March 23, he told his mother Amanda that he wanted to make the lady who was sick a doggie, and he named the doggie Hope because he hoped Miss Tonette would get well. Among the doggie’s stuffing he put a mechanical beating heart and prayed that Miss Tonette would get better.

His mother said Elijah had people in the Build-A-Bear store in tears, “but to him it was no big deal. He said, ‘She’s gonna like this, won’t she?’ He has a big heart, he’s tender-hearted and he can be rambunctious, too,” she added.

Elijah wanted to take the doggie to Tonette that day, “and it really touched her,” Amanda Bullard said.

“He said he wanted to take the bear to me that very day,” Tonette said. “I was made aware of this on Facebook and was in pure tears for nearly an hour. It touched my heart in a way it has never been touched or ever will be. This little boy who did not even know me but knew I was sick decided he wanted to make me a doggie and give it to me. He also made himself a military monkey that was pretty cool.”

Tears in the Build-A-Bear store couldn’t compare to those at the Cox home when Elijah delivered the doggie to Tonette.

“It made Elijah so happy that she was happy,” Amanda said.

Elijah didn’t understand why so much was made over him making a doggie for Tonette and his mother explained that people don’t always do nice things for people.

“He didn’t understand why everyone can’t do nice things for people,” she said.

Elijah said he wanted to make Tonette a doggie to make her feel better.

“I prayed over it when I put the heart in it,” he said. “She told me she could hug my head off and I told her no, I need my head. It made me happy because it made her happy.”

Days later Elijah still didn’t understand the big deal about the doggie and why everyone can’t be kind to people.

“I gave my toys to people who don’t have any toys,” he said.

Elijah said Tonette told him that her daughter, Aubrey Hardin, was pregnant and Elijah is one of the names considered if the baby is a boy.

“She told me that now, if the baby is a boy, it would be named Elijah,” he said.

Tonette confirmed that, stating that the Hardins would name their baby Elijah if it’s a boy, and would call him Eli.

“I hope she gets better,” Elijah said of Tonette.

The Coxes have another daughter, Holly Williams.

Elijah is a third grader at Cerro Gordo Elementary School. His teacher is Stephanie Hammond and his favorite subject is math.

“This little boy is an inspiration to me and I know he will be one to others when they read about him. I can never thank him or his parents enough or explain how what he did helped me and made me feel. I slept with that little doggie all night like a kid. God truly has brought some wonderful people into my life with this… pure strangers praying for me and sending me cards. It’s our God bringing us together in His love.

“Our little community is just full of good Christian people, people who want to help and who care,” she continued. “And I am so thankful for them all. I thank God for this little boy and his family and that He brought them into my life. Elijah is a sweet, loving, good little Christian boy who deserves all this attention for being so kind to me. He inspires me to be a better Christian.”

http://www.whiteville.com/lifestyles/br ... 963f4.html


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PostPosted: Sat Apr 06, 2013 4:10 pm 
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Radiation therapy new cancer cure

WASHINGTON: Scientists have developed a new form of radiation therapy that successfully put cancer into remission in mice, without producing harmful side-effects of conventional chemo and radiation cancer therapies. Scientists from the University of Missouri found that mice treated with the radiation therapy showed no signs of cancer afterwards.

"Since the 1930s, scientists have sought success with a cancer treatment known as boron neutron capture therapy (BNCT)," said lead researcher professor M Frederick Hawthorne.

"Our team at MU's International Institute of Nano and Molecular Medicine finally found the way to make BNCT work by taking advantage of a cancer cell's biology with nanochemistry," Hawthorne said.

Cancer cells grow faster than normal cells and in the process absorb more materials than normal cells. Hawthorne's team took advantage of that fact by getting cancer cells to take in and store a boron chemical designed by Hawthorne.

When those boron-infused cancer cells were exposed to neutrons, a subatomic particle, the boron atom shattered and selectively tore apart the cancer cells, sparing neighbouring healthy cells. The physical properties of boron made Hawthorne's technique possible. A particular form of boron will split when it captures a neutron and release lithium, helium and energy. Like pool balls careening around a billiards table, the helium and lithium atoms penetrate the cancer cell and destroy it from the inside without harming surrounding tissues.

"The technique worked excellently in mice. We are ready to move on to trials in larger animals, then people. However, before we can start treating humans, we will need to build suitable equipment and facilities. When it is built, MU will have the first radiation therapy of this kind in the world," Hawthorne said.

http://articles.timesofindia.indiatimes ... rmal-cells


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PostPosted: Thu Aug 15, 2013 12:23 pm 
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Sydney team develop new cancer drug

Sydney researchers have developed a new class of cancer drugs, the first to target the internal structure of tumour cells.

The new drugs, which have been trialled in rodents, destroy one of the fundamental building blocks of cancer cells - the molecules that form the struts and cables of their interior scaffold.

Tests in cell cultures show the drugs, the culmination of 30 years of research, are effective against every cancer type tested, including difficult-to-treat childhood cancers such as neuroblastomas.

"Our drug causes the structure of the cancer cell to collapse - and it happens relatively quickly,'' said lead researcher Peter Gunning of the University of NSW. "It is much like what happens when you see a building collapse on the TV news.''

Professor Gunning hopes the drugs, called anti-tropomyosins, will soon be added to the few other chemotherapy drug classes. ''This is a long sought-after big target.''

Scientists have tried to attack the architecture of cancer cells for decades, but until now they had been unable to develop a drug that would only destroy tumour cells and not other tissues in the body.

''Nobody has ever made a drug like these,'' he said.

The new drugs target a protein called tropomyosin, a molecule that pairs with another protein called actin to organise the internal structure of all cells in the body including cancer cells.

The protein pairs also form the smallest contracting units inside muscles such as the heart.

Most other research groups have focused on finding drugs that worked against actin. The problem with targeting this protein is that the actin found in the heart and other muscles is almost identical to the actin found in cancer cells.

''The issue [with those drugs] is the heart stops beating,'' he said.

When Professor Gunning and others discovered that tropomyosin in heart and other muscle cells was different to the tropomyosin in cancer cells, they saw a way around the problem. His group developed a computer model of tropomyosin and screened thousands of potential pharmaceutical targets for an appropriate drug candidate.

Out of 25,000 targets, most simple molecules, only one killed tumour cells in the lab.

When the group refined its computer models they identified another five drugs that are now being tested in animals in the US to establish which molecule will be trialled as a chemotherapy treatment in humans.

''The aim is to be able to initiate a trial for neuroblastoma at the end of 2014,'' said Professor Gunning, whose findings are published in journal Cancer Research

http://www.smh.com.au/national/health/s ... 2rwte.html


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PostPosted: Wed Oct 09, 2013 1:20 pm 
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Surgery, radiation and chemo didn’t stop the tumor, but an experimental treatment did

The results were terrible. I had a glioblastoma multiforme (commonly called a GBM) grade IV. This is the most malignant brain tumor; no grade II or III exist. A glioblastoma is what killed Sen. Edward M. Kennedy (D-Mass.) in 2009. While rare, it is the most common of the brain tumors. The prognosis is dismal; on average, patients survive only 14 months after diagnosis even with chemotherapy and radiation. After five years, only 5 percent of patients are still alive.

The life of a patient with a brain tumor has its ups and downs. I decided to have all my white hair cut off, since it was going to fall out in any case. Radiation to the brain starts with a plastic mask (like an Olympic fencing mask) molded to the face and then placed over it and locked to the stretcher. The radiation treatment is not painful, though the mask induces a bit of claustrophobia; luckily, the treatment lasts only 10 to 20 minutes each session. The chemotherapy, though, is another story: It gave me nausea, lethargy, fatigue, general weakness, muscle aches and tingling in my extremities. It also dropped my platelets and white blood counts, requiring weekly blood studies and leaving me vulnerable to bacterial and viral infections.

From mice to men

The Preston Robert Tisch Brain Cancer Center at Duke University has the largest experience on the East Coast with my sort of tumor, so I went there for further consultation and treatment.

After thinking about this, reviewing the animal studies and discussing it with my wife and children, I decided to do it, becoming the second patient enrolled in the study. I was, of course, worried; during my youth I had seen a lot of polio in Argentina and knew well the ravages of this virus on the neurological system. Now I was having this virus implanted into me.

The procedure

I was given the Salk polio vaccine to prevent a systemic polio infection. Three weeks later, in May 2012, I was ready for my operation.

At Duke, my skull was opened under local anesthesia and I had the viral infusion dripped through a small catheter directly into the tumor in my brain for six hours.

It is difficult not to get depressed when you are a cancer patient, confronting such things as writing a will or even one’s obituary, all the while dealing with the emotional response of family and friends.

I returned to Duke a month after the infusion, and though an MRI showed some expected swelling, the more significant fact was that the tumor had stopped growing. I have gone back to Duke every two months since then, and the tumor, initially the size of a grape, is now a scar, the size of a small pea. It’s been two years since the initial biopsy and radiation, and one year since the experimental polio viral treatment, and I have no evidence of recurrence nor tumor regrowth.

http://articles.washingtonpost.com/2013 ... emotherapy


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PostPosted: Sat Nov 23, 2013 7:07 am 
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Michael Weiner, MLBPA executive director, dies after cancer battle

Michael Weiner, executive director of the Major League Baseball Players Association, died Thursday after a lengthy battle with brain cancer. He was 51.

The union said Weiner died at his home in Mansfield Township, N.J. Weiner was diagnosed with an inoperable tumor 15 months ago.

Weiner was a plain-speaking labor lawyer known for his casual dress and easygoing manner. He helped maintain labor peace in the sport after succeeding Donald Fehr as executive director in 2009. He joined the union as a staff attorney in 1988.

"Here you had an individual who came to me as a kid for his first private sector job," Fehr told The Associated Press in a telephone interview. "He impressed me at the time and ever after with his intelligence, his dedication, his innate sense of fairness, his focus on finding what the right thing was to do and then doing it. This was an extraordinary individual all the way around."

Players were universal in their praise of Weiner and expressed gratitude for what did on their behalf. A sampling:

Pittsburgh Pirates center fielder and National League MVP Andrew McCutchen:

Michael Weiner worked even thru his sickness. He didn't look at it as an excuse to quit. He never gave up on us even when at his worst...

"Our strong professional relationship was built on a foundation of respect and a shared commitment to finding fair solutions for our industry. I appreciated Michael's tireless, thoughtful leadership of the players and his pivotal role in the prosperous state of baseball today," Selig said in a statement. "Michael was a courageous human being, and the final year of his remarkable life inspired so many people in our profession."

A succession plan was put in place last summer that will lead to former big league All-Star Tony Clark taking over Weiner's role.

"Words cannot describe the love and affection that the players have for Michael, nor can they describe the level of sadness we feel today," Clark said in a statement. "Not only has the game lost one of its most important and influential leaders in this generation, all involved in the game have lost a true friend."

At Weiner's last public speaking engagement, a 25-minute meeting with baseball writers on the day of the All-Star game in July, he was confined to a wheelchair and unable to move his right side. Yet, he wanted to respond to questions about his illness and issues in the game, and did so with the grace and humor he was known for throughout his life.

"I don't know if I look at things differently. Maybe they just became more important to me and more conscious to me going forward," he said. "As corny as this sounds, I get up in the morning and I feel I'm going to live each day as it comes. I don't take any day for granted. I don't take the next morning for granted. What I look for each day is beauty, meaning and joy, and if I can find beauty, meaning and joy, that's a good day."

Weiner is survived by his wife, the former Diane Margolin, and daughters Margie, Grace and Sally.

http://www.sportingnews.com/mlb/story/2 ... tony-clark


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PostPosted: Fri Dec 20, 2013 1:29 pm 
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Novogen, Cornell seek brain cancer cure

Drug developer Novogen and Cornell University in the US have agreed to collaborate on seeking a treatment for brain cancer.

It is the second collaborative deal for Novogen with a high-profile US University.

Novogen has a joint-venture with Yale University seeking to develop personalised chemotherapy for patients with ovarian cancer.

Shares in Novogen were 0.5 cents higher at 20 cents at 1110 AEDT.

http://finance.ninemsn.com.au/newsbusin ... ancer-cure


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PostPosted: Sun Jan 12, 2014 7:35 am 
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Major donation for cancer research

Six U.S. scientific and medical institutions will split a $540 million donation to study cancer immunotherapy and other related areas.

Six U.S. medical centers will each receive $90 million to pursue cancer research thanks to a donation from the trust fund of late billionaire Daniel Ludwig. The money comes with no strings attached, other than the money must be used for cancer research.

Daniel Ludwig was a U.S. shipping magnate who died in 1992. In 1971, he established the Ludwig Institute for Cancer Research and funded the institution. The Ludwig Institute for Cancer Research is an international not-for-profit organization committed to improving the understanding and control of cancer. The institute conducts its own research and translates discoveries into applications for patient benefit. It fosters collaborative research and supports six scientific initiatives across basic and translational research: brain cancer, breast cancer, cancer prevention, colon cancer, immunotherapy and melanoma.

Since his death, much of Ludwig's wealth was placed in trust with the stipulation that it is used to fund medical research. The latest issue of $540 million is part of that legacy.

The money will go to: Harvard Medical School, Johns Hopkins University, Massachusetts Institute of Technology, Memorial Sloan-Kettering Cancer Center in New York City, Stanford University, and the University of Chicago.

http://www.digitaljournal.com/tech/scie ... cle/365491


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PostPosted: Thu Mar 20, 2014 10:20 am 
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IBM's Watson to help in brain cancer research

NEW YORK (AP) — IBM is teaming up with the New York Genome Center to help fight brain cancer.

The company said Wednesday that its Watson cloud computing system will be used in partnership with a New York-based genetic research center to help develop treatments for glioblastoma, the most common type of brain cancer in U.S. adults.

"Time definitely is not on your side when you have glioblastoma and that's where Watson comes in," Dr. Robert Darnell, New York Genome's president, CEO and scientific director, said at a Wednesday event announcing the deal.

Glioblastoma is an extremely aggressive form of cancer. The median survival rate is 12 to 14 months and the disease kills about 13,000 people each year.

As part of the clinical trial, New York Genome Center, a nonprofit consortium of academic, medical and industry officials, will sequence the DNA of glioblastoma patients, then use Watson to combine that data with clinical information to help determine the best way to treat each patient.

What makes Watson unique is that it isn't programed like most computers. Instead of relying on the information that's put into it, Watson learns by "reading" vast amounts of information and combining it with the results of previous work to find answers to problems. Those characteristics make Watson ideal for extremely data-heavy work in fields such as health care and finance.

The partnership also comes at a time when IBM is increasing its focus on Watson and other cloud-based software services, as it moves further away from its computer hardware roots. Earlier this year, IBM announced it would invest $1 billion to give Watson its own business division and headquarters in New York City.

John Kelly, a senior vice president and director of IBM Research, says there's a vast amount of data involved in DNA sequencing, which then must be combined with all of the clinical data involved in a particular patient's case. The resulting pool of information is so big that it's impossible for people to deal with.

"This is sort of big data on steroids," Kelly says.

Darnell says the hope is that Watson will speed up the time it takes for physicians to determine a patient's treatment plan.

For instance, if Watson determines that a child's leukemia has genetic traits similar to melanoma, a melanoma drug might be successful in shrinking that child's tumor, he says.

In addition, while a team of top physicians and researchers could do the same work, though at a slower pace, there aren't enough resources to help everyone. But Watson has the potential to be scalable and help many more people, Darnell says.

"This is the proverbial needle in the haystack and the haystack is enormous," Kelly says. "Watson can do in seconds what would take people years. And we can get it down to a really personal level."

The doctors working on the project hope to start with 20 brain cancer patients, sequence their DNA and then run the information through Watson to figure out the best ways to treat them, Darnell says.

Armonk, N.Y.-based IBM Corp. already has a partnership with Memorial Sloan-Kettering Cancer Center, where Watson is also used to help treat cancer.

http://www.utsandiego.com/news/2014/mar ... -research/


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PostPosted: Tue Apr 01, 2014 3:36 pm 
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Adding Bevacizumab To Initial Glioblastoma Treatment Doesn't Improve Overall Survival

Glioblastoma is the most common primary malignant adult brain tumor and, despite treatment advances in recent years, the average survival of patients enrolled in clinical trials is less than 16 months.

Few patients live beyond five years.

Glioblastoma tumors are characterized by angiogenesis — the formation of new blood vessels that support tumor growth stimulated by the GBM-produced vascular endothelial growth factor A (VEGF-A).

Bevacizumab is a monoclonal antibody that targets VEGF-A production to block the growth of tumor-derived blood vessels.

"Clinical trials evaluating the addition of bevacizumab to standard treatment for recurrent glioblastoma demonstrated clinical benefit and led to the drug's U.S. Food and Drug Administration approval for this indication," says Mark Gilbert, M.D., Radiation Therapy Oncology Group 0825 principal investigator and professor of neuro-oncology at The University of Texas MD Anderson Cancer Center in Houston. "Additionally, compelling preclinical data suggest that anti-angiogenic targeted therapies may normalize the tumor's rapidly forming and underdeveloped blood vessels, resulting in improved oxygen and chemotherapy delivery to the tumor and potentially enhanced radiotherapy (RT) and chemotherapy treatment."

The Radiation Therapy Oncology Group (RTOG) 0825 study tested this hypothesis.

Six hundred and twenty-one adult study participants included in the study's final analysis were enrolled in the multicenter trial and randomized into one of two study arms, with treating physicians blinded to treatment assignment. All participants were treated with standard-of-care (60 Gy RT and daily temozolomide chemotherapy). Bevacizumab (experimental arm) or a placebo (standard treatment arm) was administered starting at week 4 of RT and continued every 2 weeks until 1) disease progression, or 2) severe treatment-related toxicity, or 3) completion of adjuvant therapy. At the time of disease progression, the treatment arm was unblinded allowing for follow on treatment with or without bevacizumab.

The authors reported data at a median follow-up time of 20.5 months, which revealed no statistical difference in overall survival between the two study arms (median 16.1 months for the standard-treatment arm vs. 15.7 months for the bevacizumab arm). Although there was a difference in progression-free survival (PFS) (7.3 months for the placebo arm vs. 10.7 months for the bevacizumab arm), the pre-established level of benefit for PFS was not reached.

"The relevant result is that the upfront use of bevacizumab is not indicated," says Gilbert. "It's important to emphasize that the question we sought to answer was whether administering bevacizumab as first-line treatment improved survival; the cross-over component allowed comparison of risk and benefit of early versus late treatment We now know by giving it late you delay the risk of toxicity, and that may be relevant."

Study participants were stratified equally across study arms by prognostic molecular markers of tumor O6-methylguanine–DNA methyltransferase (MGMT) methylation status and a tumor-based 9-gene assay. Investigators, however, did not find a subgroup of patients based on the molecular marker analysis who survived longer from first-line bevacizumab administration. "We postulated that patients with worse prognosis, determined by their tumor markers, would do better if they received bevacizumab as first-line treatment because they may not survive to take advantage of, or do well enough to be considered for, second-line treatment, but we didn't find that result" says Gilbert.

Because bevacizumab is known to confound magnetic resonance imaging (MRI) examination results used to assess GBM tumor progression, RTOG 0825 investigators incorporated a "net clinical benefit" component in the trial design to determine if quality of life, symptom burden and neurocognitive function test results corroborate MRI-reported stable or improved disease status. More than 80 percent of study participants agreed to take part in the net clinical benefits component, which demonstrated a greater decline of cognitive function for patients in the bevacizumab arm compared with those in the placebo arm.

"While we found a difference in progression-free survival in the bevacizumab arm, there was an overall increase in symptom burden and decline in neurocognitive function and some measures of quality of life over time comparing the patients receiving bevacizumab with those on placebo," says Gilbert.

"Study participants' consent allowing the collection of tumor tissue and blood samples, as well as imaging examination, longitudinal symptom, QOL, and neurocognitive function data provides RTOG investigators a rich archive of data to support ongoing investigations of potential molecular markers to identify subgroups of patients who may benefit from early bevacizumab," says study co-principal investigator Minesh Mehta, M.D., chair of the Radiation Therapy Oncology Group Brain Tumor Committee and a professor of radiation oncology at the University of Maryland School of Medicine.

"The RTOG 0825 results provide important insight about the use of anti-angiogenic therapies with standard first-line treatment," says Walter J. Curran Jr., M.D., Radiation Therapy Oncology Group chairman, co-author and executive director of the Winship Cancer Center at Emory University in Atlanta. "The unprecedented collection of specimens and associated outcome data will provide significant future information as we investigate new treatment strategies for these patients within NRG Oncology. I thank our ECOG and NCCTG colleagues for their significant trial support."

http://www.science20.com/news_articles/ ... val-130099


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PostPosted: Mon Apr 07, 2014 1:17 pm 
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Gene sequencing project discovers mutations tied to deadly brain tumors in young children

St. Jude Children’s Research Hospital-Washington University Pediatric Cancer Genome Project offers new leads to improved outcomes for children with high-grade glioma brain tumors; particularly youngest patients

Memphis, Tennessee - The St. Jude Children’s Research Hospital-Washington University Pediatric Cancer Genome Project has identified new mutations in pediatric brain tumors known as high-grade gliomas (HGGs), which most often occur in the youngest patients. The research appears today as an advance online publication in the scientific journal Nature Genetics.

The discoveries stem from the most comprehensive effort yet to identify the genetic missteps driving these deadly tumors. The results provide desperately needed drug development leads, particularly for agents that target the underlying mutations. This and other studies show these mutations often differ based on patient age. HGGs represent 15 to 20 percent of brain and spinal tumors in children. Despite aggressive therapy with surgery, radiation and chemotherapy, long-term survival for HGG patients remains less than 20 percent.

The study is one of four being published simultaneously in the same issue of Nature Genetics that link recurring mutations in ACVR1 to cancer for the first time. Pediatric Cancer Genome Project researchers found that ACVR1 was mutated in 32 percent of 57 patients diagnosed with a subtype of HGG called diffuse intrinsic pontine glioma (DIPG). While DIPGs are usually found in children ages 5 to 10, ACVR1 mutations occurred most frequently in younger-than-average patients. DIPG occurs in the brainstem, which controls vital functions and cannot be surgically removed.

The investigators also identified alteration in NTRK genes that drove tumor development in young HGG patients whose tumors developed outside the brainstem. This study included 10 patients who were age 3 or younger when they were diagnosed with such non-brainstem HGGs. Of those, 40 percent had tumors with alterations in one of three NTRK genes and few other changes. The alterations occurred when a segment of the NTRK genes involved in regulating cell division fused with part of another gene.

“These results indicate the NTRK fusion genes might be very potent drivers of cancer development that have the ability to generate tumors with few other mutations,” said co-corresponding author Suzanne Baker, Ph.D., a member of the St. Jude Department of Developmental Neurobiology. The other corresponding author is Jinghui Zhang, Ph.D., a member of the St. Jude Department of Computational Biology. “We want to see if these tumors might be selectively sensitive to therapies that target the pathways that are disrupted as a result of these fusion genes,” Baker said.

Added co-author Richard K. Wilson, Ph.D., director of The Genome Institute at Washington University School of Medicine in St. Louis: "We’ve made some very exciting discoveries that likely will result in more effective diagnosis and treatment of these particularly nasty tumors.”

In this study, researchers analyzed 127 HGGs from 118 pediatric patients, including whole genome sequencing of the complete tumor and normal DNA from 42 patients. More targeted sequencing of additional tumors was conducted to track how instructions encoded in DNA were translated into the proteins that do the work of cells.

The recurring presence of ACVR1 mutations in a subset of DIPG patients was one of the biggest surprises, Baker said. ACVR1 carries instructions for making a protein receptor on the cell membrane. The receptor functions as an on-off switch for a biochemical pathway named bone morphogenetic protein, or BMP. The pathway helps regulate growth and development of bone and other tissue. Working in zebra fish and mouse brain cells, researchers found evidence that ACVR1 mutations from DIPG resulted in the BMP pathway being inappropriately and permanently switched on.

In individuals with an inherited disorder called fibrodysplasia ossificans progressiva (FOP), the same ACVR1 mutations lead not to cancer, but to a different mechanism resulting in abnormal growth of bone in other tissues. Patients with FOP carry the ACVR1 mutation in every cell, while the gene is mutated only in the tumor cells of DIPG patients. “The same mutations are doing something very different in these two terrible and rare diseases. We are working to understand not only how the mutations contribute to cancer, but also whether blocking the BMP pathway offers a new way to treat the tumor,” Baker said.

The ACVR1 mutations often occurred with mutations in a gene that carries instructions for making the histone H3.1 protein. That protein influences gene activity through its role in packaging DNA in the nucleus. Mutations in the histone H3 family of proteins were first reported in an earlier Pediatric Cancer Genome Project study. Baker said the new findings suggest the two mutations work together to give tumor cells a selective advantage in the developing brainstem.

While the ACVR1 mutations occurred only in tumors in the brainstem, the NTRK fusion genes were found in HGGs that developed throughout the brain. By combining pieces of different genes, fusion genes can lead to production of abnormal proteins that disrupt cell function. Fusion genes were identified in almost half of all pediatric HGGs in this study, but the NTRK fusions were the most common. The NTRK fusions involved a gene segment encoding a tyrosine kinase domain. This domain functions as an on-off switch for several important regulatory mechanisms in cells that often malfunction in cancer cells.

NTRK fusion genes have been identified in other pediatric and adult brain tumors. This study marks the first report of the genes in pediatric HGGs. The NTRK fusion genes were identified in part through targeted sequencing of RNA. RNA molecules help translate the instructions carried in DNA into the proteins that do the work of cells. This study was the first to include RNA sequencing in an analysis of HGGs.

The study was part of the Pediatric Cancer Genome Project, which has sequenced the complete normal and tumor genomes of 700 young cancer patients. The project was launched in 2010 to harness advances in genome sequencing technology to improve understanding and treatment of some of the most aggressive and least understood childhood cancers.

http://www.healthcanal.com/genetics-bir ... ldren.html


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PostPosted: Thu Apr 24, 2014 9:38 am 
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$9 million CyberKnife unveiled at Sir Charles Gairdner Hospital as WA’s new weapon to fight cancer

A SOPHISTICATED new tool to improve tumour treatment was unveiled at Sir Charles Gairdner Hospital today.

The $9 million CyberKnife will be used to treat cancerous tumours – including those previously thought to be inoperable – and is the first of its kind in Australia.

It uses a robotic arm which allows doctors to deliver high-dose radiation in a precise area, meaning fewer treatments for patients.

Health Minister Kim Hames said the instrument would be used to treat up to 450 patients each year.

“The CyberKnife enables doctors to treat tumours with pinpoint accuracy. It is particularly beneficial for the treatment of certain lung, brain, spine, liver and prostate cancers which otherwise may be inoperable, or where other treatment options may compromise other vital organs,” he said.

“Another advantage is its ability to treat tumours that move, such as those in the lungs, to a greater level of accuracy, which is something other technology is not able to do.”

The CyberKnife will be housed at the new State Cancer Centre at Sir Charles Gairdner Hospital in Nedlands.

http://www.news.com.au/national/western ... 6893550924


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PostPosted: Thu May 08, 2014 8:59 pm 
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Curing the 'incurable' — brain cancer doctors welcome new CRUK strategy

A leading group of UK cancer experts has welcomed the announcement by Cancer Research UK that brain tumours will be a focus of their new strategy for the next five years.

The British Neuro-Oncology Society (BNOS) says this new drive for a vitally-needed boost in funds for research could dramatically change the landscape for patients with brain cancer and their families.

Brain tumours are the biggest cancer killer of people under 40 years of age but historically the disease has only attracted around 2% of funding for research into faster diagnosis and new treatments.

President of BNOS, Professor David Walker is a paediatric oncologist who runs The University of Nottingham’s Children’s Brain Tumour Research Centre. He said:

“We cannot be more delighted that CRUK have announced that brain and spinal tumours will be one of the four big ‘hard to treat’ cancers to be the focus of increased research and funding. This development builds upon the successful strategy of a number of patient and family-based, as well as academic charity research initiatives which have been active over the past couple of decades.

“These groups have acted together to raise funds, through community action and through political lobbying to bring about a change in scientific attitude to the challenge of brain tumours across the ages. BNOS has been a sustained partner in this action providing the necessary scientific and clinical knowledge to inform these debates and providing a meeting point for scientific and clinical discussion of new ideas and treatments. BNOS is a major part of the European network of clinicians and scientists who meet regularly to tackle the challenge of brain tumours.”

He added: “CRUK's announcement is most welcome as they are the biggest funder of cancer research in Europe and so can bring substantial resources and cancer expertise to bear upon this subject.”

Brain tumours arise as a product of brain growth during childhood and adolescence and a product of brain degeneration during adulthood to old age. Survival and disability rates vary across the ages, in childhood survival rates are generally higher although some tumours in this age group remain incurable. In adulthood the commonest and most malignant brain tumour, glioblastoma, grade 4 astrocytoma remains resistant to treatment and although drug developments have offered some improvement recently we are still looking for a new treatment which will change the outlook for this disease.

In all ages there are tumours which are curable with surgery and radiotherapy with or without the additional effect of chemotherapy of biological therapy. The challenge is to use the experience of the successful treatments to influence understanding for the tumours which present the greater challenge.

http://www.healthcanal.com/cancers/5059 ... ategy.html


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