Archive for the ‘Brain’ Category

Nanoparticles home in on brain tumors, boost accuracy of surgical removal

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Posted 15 Apr 2012 — by James Street
Category Brain, Clinical Trials, NanoTechnology
Posted: Apr 15th, 2012
(Nanowerk News) Like special-forces troops laser-tagging targets for a bomber pilot, tiny particles that can be imaged three different ways at once have enabled Stanford University School of Medicine scientists to remove brain tumors from mice with unprecedented accuracy.
In a study to be published online April 15 in Nature Medicine, a team led by Sam Gambhir, MD, PhD, professor and chair of radiology, showed that the minuscule nanoparticles engineered in his lab homed in on and highlighted brain tumors, precisely delineating their boundaries and greatly easing their complete removal. The new technique could someday help improve the prognosis of patients with deadly brain cancers.
About 14,000 people are diagnosed annually with brain cancer in the United States. Of those cases, about 3,000 are glioblastomas, the most aggressive form of brain tumor. The prognosis for glioblastoma is bleak: the median survival time without treatment is three months. Surgical removal of such tumors — a virtual imperative whenever possible — prolongs the typical patient’s survival by less than a year. One big reason for this is that it is almost impossible for even the most skilled neurosurgeon to remove the entire tumor while sparing normal brain.
“With brain tumors, surgeons don’t have the luxury of removing large amounts of surrounding normal brain tissue to be sure no cancer cells are left,” said Gambhir, who is the Virginia and D.K. Ludwig Professor for Clinical Investigation in Cancer Research and director of the Molecular Imaging Program at Stanford. “You clearly have to leave as much of the healthy brain intact as you possibly can.”
This is a real problem for glioblastomas, which are particularly rough-edged tumors. In these tumors, tiny fingerlike projections commonly infiltrate healthy tissues, following the paths of blood vessels and nerve tracts. An additional challenge is posed by micrometastases: minuscule tumor patches caused by the migration and replication of cells from the primary tumor. Micrometastases dotting otherwise healthy nearby tissue but invisible to the surgeon’s naked eye can burgeon into new tumors.
Although brain surgery today tends to be guided by the surgeon’s naked eye, new molecular imaging methods could change that, and this study demonstrates the potential of using high-technology nanoparticles to highlight tumor tissue before and during brain surgery.
The nanoparticles used in the study are essentially tiny gold balls coated with imaging reagents. Each nanoparticle measures less than five one-millionths of an inch in diameter — about one-sixtieth that of a human red blood cell.
“We hypothesized that these particles, injected intravenously, would preferentially home in on tumors but not healthy brain tissue,” said Gambhir, who is also a member of the Stanford Cancer Institute. “The tiny blood vessels that feed a brain tumor are leaky, so we hoped that the spheres would bleed out of these vessels and lodge in nearby tumor material.” The particles’ gold cores, enhanced as they are by specialized coatings, would then render the particles simultaneously visible to three distinct methods of imaging, each contributing uniquely to an improved surgical outcome.
One of those methods, magnetic resonance imaging, is already frequently used to give surgeons an idea of where in the brain the tumor resides before they operate. MRI is well-equipped to determine a tumor’s boundaries, but when used preoperatively it can’t perfectly describe an aggressively growing tumor’s position within a subtly dynamic brain at the time the operation itself takes place.
The Gambhir team’s nanoparticles are coated with gadolinium, an MRI contrast agent, in a way that keeps them stably attached to the relatively inert spheres in a blood-like environment. (In a 2011 study published in Science Translational Medicine, Gambhir and his colleagues showed in small animal models that nanoparticles similar to those used in this new study, but not containing gadolinium, were nontoxic.)
A second, newer method is photoacoustic imaging, in which pulses of light are absorbed by materials such as the nanoparticles’ gold cores. The particles heat up slightly, producing detectable ultrasound signals from which a three-dimensional image of the tumor can be computed. Because this mode of imaging has high depth penetration and is highly sensitive to the presence of the gold particles, it can be useful in guiding removal of the bulk of a tumor during surgery.
The third method, called Raman imaging, leverages the capacity of certain materials (included in a layer coating the gold spheres) to give off almost undetectable amounts of light in a signature pattern consisting of several distinct wavelengths. The gold cores’ surfaces amplify the feeble Raman signals so they can be captured by a special microscope.
To demonstrate the utility of their approach, the investigators first showed via various methods that the lab’s nanoparticles specifically targeted tumor tissue, and only tumor tissue.
Next, they implanted several different types of human glioblastoma cells deep into the brains of laboratory mice. After injecting the imaging-enhancing nanoparticles into the mice’s tail veins, they were able to visualize, with all three imaging modes, the tumors that the glioblastoma cells had spawned.
The MRI scans provided good preoperative images of tumors’ general shapes and locations. And during the operation itself, photoacoustic imaging permitted accurate, real-time visualization of tumors’ edges, enhancing surgical precision.
But neither MRI nor photoacoustic imaging by themselves can distinguish healthy from cancerous tissue at a sufficiently minute level to identify every last bit of a tumor. Here, the third method, Raman imaging, proved crucial. In the study, Raman signals emanated only from tumor-ensconced nanoparticles, never from nanoparticle-free healthy tissue. So, after the bulk of an animal’s tumor had been cleared, the highly sensitive Raman-imaging technique was extremely accurate in flagging residual micrometastases and tiny fingerlike tumor projections still holed up in adjacent normal tissue that had been missed on visual inspection. This, in turn, enabled these dangerous remnants’ removal.
“Now we can learn the tumor’s extent before we go into the operating room, be guided with molecular precision during the excision procedure itself and then immediately afterward be able to ‘see’ once-invisible residual tumor material and take that out, too,” said Gambhir, who suggested that the nanoparticles’ propensity to heat up on photoacoustic stimulation, combined with their tumor specificity, might also make it possible for them to be used to selectively destroy tumors. He also expressed optimism that this kind of precision could eventually be brought to bear on other tumor types.

Source: Stanford University Medical Center

Yale study: Recipients of frequent dental X-rays at greater risk of developing non-cancerous brain tumor

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Posted 14 Apr 2012 — by James Street
Category Brain, Carcinogens, Radiation

Published: Friday, April 13, 2012

By Jim Shelton, Register Staff
jshelton@nhregister.com / Twitter: @jimboshelton

People who received frequent dental X-rays a generation ago, before stricter radiation dosages were put in place, are at greater risk for developing a type of non-cancerous brain tumor, according to Yale University researchers.

The findings are being published today in the American Cancer Society’s online journal, Cancer.

“We know people will be very concerned, but we are not telling people they should stop going to see their dentist,” said the study’s lead author, Dr. Elizabeth Claus, a professor at Yale’s School of Public Health and an attending neurosurgeon at Brigham and Women’s Hospital in Boston.

The Yale study looked at more than 1,400 people from Connecticut, Massachusetts, North Carolina, California and Texas who were diagnosed with a meningioma, a non-cancerous tumor that can cause a range of medical problems with vision, speech and motor control, as well as causing headaches. The study also looked at a similar group of people who did not have a meningioma.

The average age of the patients was 57, according to Claus.

Researchers found that patients with meningioma were twice as likely to have had dental X-ray exams since childhood in which they bit down on a tab of X-ray film at least once a year. That type of test is known as a bitewing exam.

There was an even stronger link between meningioma and the panorex dental exam, in which a single X-ray picture of teeth is taken outside of the mouth. Patients who had this exam when they were younger than 10 years old had a nearly five times greater risk for meningioma.

Claus pointed out that today’s dental X-ray technology and practices use significantly lower radiation dosages than in the past. She estimated there has been at least a 50 percent reduction in dosage since the 1980s.

Meningioma occurs in eight out of every 100,000 people, according to the National Institutes of Health. This makes it a rare disease, even though it is the most commonly diagnosed brain tumor.

In a statement released to the media, the Chicago-based American Dental Association says it has a long-standing position that “dentists should order dental X-rays for patients only when necessary for diagnosis and treatment,” but called certain aspects of the Yale study into question.

The association faulted the study for relying on “individuals’ memories of having dental X-rays taken years earlier,” and that “results of studies that use this design can be unreliable because they are affected by what scientists call ‘recall bias.’”

The ADA stresses it encourages use of protective aprons and thyroid collars on all patients to minimize radiation exposure. It also says X-rays are needed to detect oral diseases that can’t be found through visual and physical examination.

Claus says the Yale study looked into a connection between meningioma and dental X-rays because ionizing radiation is the “most consistent environmental factor” known to be a risk factor for the tumor.

Claus also says the study should serve as a starting point to examine how often dental X-rays are necessary even with today’s practices and technology. She says the American Dental Association suggests that children have one dental X-ray every one to two years, that teens have one every one and a half to three years, and that adults have one every two to three years.

“It is worthwhile to have a discussion as to whether they are needed in every instance,” Claus says. “That is probably our biggest message.”

Cancer cells send out the alarm on tumor-killing virus

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Posted 18 Mar 2012 — by James Street
Category Brain, CCN1, Virus, virus studies

March 15, 2012 in Cancer

Brain-tumor cells that are infected with a cancer-killing virus release a protein “alarm bell” that warns other tumor cells of the impending infection and enables them to mount a defense against the virus, according to a study led by researchers at The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC – James).

The infected release a protein called CCN1 into the narrow space between where it initiates an antiviral response. The response limits the spread of the oncolytic virus through the tumor, reducing its ability to kill cancer cells and limiting the efficacy of the therapy.

The study suggests that cells in general might use this mechanism to help control viral infections, and that blocking the response might improve oncolytic viral therapy for glioblastoma and perhaps future gene therapy treatments.

Oncolytic viruses replicate in tumor cells and kill them. They have shown promise for the treatment of glioblastoma, the most common and deadly form of brain cancer. Patients with glioblastoma survive about 15 months after diagnosis on average, so there is great need for new treatments.

The study was published in a recent issue of the journal Research.

“We found that, in the extracellular matrix, this orchestrates a striking cellular antiviral response that reduces viral replication and limits its cytolytic efficacy,” says researcher and principal investigator Balveen Kaur, associate professor of Neurological Surgery at the OSUCCC – James.

“These findings are significant because they reveal a novel mechanism used by infected cells to fight viral infections and alert adjacent uninfected cells to prepare their defenses to fight off forthcoming viral attacks,” Kaur says.

Kaur notes that CCN1 helps regulate cellular functions that include adhesion, migration, and proliferation, and that it is overexpressed in 68 percent of glioblastoma specimens.

Previous research led by Kaur found that oncolytic virus therapy induced the release of CCN1 into the tumor microenvironment. For this study, Kaur and her colleagues used glioma cell lines, oncolytic viruses derived from human herpesvirus type 1 (HSV-1), and glioblastoma animal models. Key findings include:

  • CNN1 expression is upregulated by the oncolytic but not by chemotherapy or radiation treatment. Thus, it may be a general response of glioma cells to viral infection.
  • In the extracellular space, CCN1 reduces viral replication and the killing of glioma cells.
  • CCN1 induces a type-I interferon antiviral response using an integrin cell-surface receptor.

“Overall, this finding reveals how extracellular signaling can contribute to viral clearance,” Kaur says. “We can now utilize this knowledge to improve future viral gene therapy.”

Provided by Ohio State University Medical Center

Brain Cancer Blood Vessels Not Substantially Tumor-Derived

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Posted 11 Mar 2012 — by James Street
Category antiangiogenesis, Avastin, Brain, Stem Cell Research

ScienceDaily (Mar. 8, 2012) — Johns Hopkins scientists have published laboratory data refuting studies that suggest blood vessels that form within brain cancers are largely made up of cancer cells. The theory of cancer-based blood vessels calls into question the use and value of anticancer drugs that target these blood vessels, including bevacizumab (Avastin).

“We don’t question whether brain cancer cells have the potential to express blood vessel markers and may occasionally find their way into blood vessels, but we do question the extent to which this happens,” says Charles Eberhart, M.D., Ph.D., chief of neuropathology at the Johns Hopkins University School of Medicine. “In general, we find no evidence in our study that these vessels contain substantial amounts of cancer cells.”

Eberhart, professor of pathology, ophthalmology and oncology at Johns Hopkins, said he first encountered claims about the cancerous nature of tumor blood vessels about a year ago when he was invited to join students at a journal club meeting, a forum for discussing studies published in medical journals. “My first reaction to this research was ‘How could this be true?’” says Eberhart. “Our clinical experience examining tissue from brain cancers does not support it.”

Studies have long demonstrated that malignant brain tumors contain large numbers of blood vessels to feed their growing demand for nutrients. The blood vessels are formed when tumors pump out growth factors that increase vessel production. Such studies opened the door to treatment strategies that specifically targeted blood-vessel growth and the vessel cells themselves.

More recently, scientists in Italy and the Memorial Sloan Kettering Cancer Center in New York published results of studies suggesting that these tumor blood vessels are made by primitive types of brain cancer cells that are a form of stem cells. In their studies, they found tumor markers on blood vessel cells in 20 to 90 percent of their brain cancer samples. The U.S./Italian research teams said their findings also suggested that the cancerlike blood vessels were more prone to drug resistance, potentially explaining why drugs like bevacizumab yield tumor-shrinking responses, but only for short periods. Bevacizumab is currently approved by the U.S. Food and Drug Administration for use in patients with colorectal, lung, kidney and brain cancers.

Eberhart said pathologists, including those who work on brain tissue, use certain tissue-based techniques to distinguish cancer cells from normal ones. When evaluating specimens of brain tissue removed during surgery for suspected cancer, he said, most pathologists agree that blood vessel cells in these specimens consistently lack the molecular changes associated with cancer cells, according to Eberhart. In fact, they often use these blood vessel cells as “normal controls” to compare with potentially cancerous ones.

After the journal club experience, Eberhart teamed up with fellow neuropathologist Fausto Rodriguez, M.D., and colleagues at the Dana Farber Cancer Institute and Harvard Medical School in Boston to look more closely at the molecular features of blood vessel cells in brain cancer samples. They tested more than 100 samples from patients at Johns Hopkins and Dana Farber for EGFR and IDH1 markers, two common genes altered in brain cancer.

“We also used a marker called CD34 to differentiate vascular [blood vessel] cells from other types of cells,” says Rodriguez, assistant professor of pathology at Johns Hopkins. The research teams found no more than 10 percent of their samples contained vascular cells with EGFR or IDH1 cancer markers, and in those rare tumor samples, only a few cells exhibited those markers. The Johns Hopkins-Dana Farber-Harvard team tested all parts of the vessel walls for presence of the cancer markers.

Results of the team’s laboratory experiments were published in the online journal Oncotarget in January.

Although the two groups used different markers to identify vessel cells, Rodriguez says “there is no marker that is absolute for each cell.”

Eberhart and Rodriguez noted that the U.S./Italian research teams focused mainly on cell-by-cell research techniques in dissociated specimens to evaluate cancer markers, losing associations that can be made by looking at a cell’s shape and physical relationship within clusters of cells. The Johns Hopkins and Dana Farber researchers conducted studies examining cells in intact tissue.

“Pathologists with extensive experience in examining cells become accustomed to quickly identifying a blood vessel cell from a normal cell, and we can gain a lot of information when we look at how cells connect with other cells in real-life examples,” notes Rodriguez, who says that his team’s findings could potentially apply to any cancer thought to contain stem cells.

In addition to Eberhart and Rodriguez, the research team included Brent Orr from Johns Hopkins and Keith Ligon from the Dana Farber Cancer Institute/Harvard Medical School.

Funding for the study was provided by a National Institutes of Health postdoctoral fellowship (T32CA067751) to Orr and a grant (5R01NS055089) to Eberhart.

Robert Gibbs, founder of Miles For Hope, Inc., loses his seven-year battle with brain cancer – Boston Globe

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Posted 18 Dec 2011 — by James Street
Category Brain, Finance and Politics of cancer research and treatment

Publication Date 17 December 2011

Read this interesting article here: Robert Gibbs, founder of Miles For Hope, Inc., loses his seven-year battle with brain cancer – Boston Globe

Robert Gibbs, founder of Miles For Hope, Inc., loses his seven-year battle with brain cancer

(PR NewsChannel) / CLEARWATER, Fla. / Robert (Bob) Gibbs, co-founder of Miles For Hope, Inc., a nonprofit organization, passed away Saturday December 10th, 2011 at 2:05 a.m., after a seven-year battle with brain cancer. Gibbs, 42, died peacefully with family by his side. Gibbs was a leader in the brain tumor community. His focus through Miles For Hope was to raise awareness and funding for cutting-edge brain tumor research and clinical trials. In July 2011, Miles For Hope partnered with two other brain tumor organizations, in awarding a $100,000 research grant to University of California Los Angeles (UCLA) neurosurgeon Linda Liau, M.D., PhD to begin the clinical trial, Optimizing Dendritic Cell Vaccination for Low Grade Glioma Patients. This is the first trial of its kind for patients that have been diagnosed with low grade gliomas, a common form of brain cancer, which has the potential to improve the lives of brain cancer patients.

This grant reflected Gibbs commitment to increase awareness and funding for potentially life-saving brain tumor research. The next step in carrying out Gibbs vision is to fund a vaccine trial for Pediatric Brain Tumor Patients.

In addition to supporting the latest research, advancements and clinical trials, Gibbs was also dedicated to offering patients and their families much needed support through his organization. This includes providing information about up-to-date treatment options and providing medically necessary flight assistance to patients so they can get the treatment they desperately need.

According to his wife Barb, Bobs mission was not only to find a cure for this devastating disease, but to offer his own brain cancer experiences to others to assist them during their battle. He always put others before himself. He touched many lives while battling his own illness. He always found time to speak with other brain tumor patients or their families, providing hope, information, comfort and support. Although his own treatments exhausted him, he never tired from helping others or turned anyone away. His strength, determination and drive touched and helped so many.

Gibbs, married and father of four, was diagnosed in 2004 with brain cancer at the age of 34. He is survived by his wife, Barb, their four sons Christopher, Justin, Matthew, and Dylan, his parents Clayton and JoAnne Gibbs, and his sister Jackie (Jeff) Tonkel.

A public memorial service will be held Saturday, December 17th, at 3 p.m., at Sylvan Abbey Memorial Park, 2860 Sunset Point Road, Clearwater, FL 33759. In lieu of flowers, the family requests donations to Miles For Hope, Inc., www.MilesForHope.org, to continue Gibbs dedication in Moving Towards a Cure for brain tumors.

About Mile for Hope, Inc: Miles for Hope, Inc. is a 501(3) nonprofit organization dedicated to funding cutting-edge Brain Tumor research, raising awareness and providing medically necessary travel assistance to Brain Tumor patients.

MEDIA CONTACT Barb Gibbs 1684 North Belcher Road Clearwater, FL 33765 (727) 781-4673 Barb@milesforhope.org

Direct link: http://www.prnewschannel.com/2011/12/15/robert-gibbs-founder-of-miles-for-hope-inc-loses-his-seven-year-battle-with-brain-cancer/

SOURCE: Miles for Hope, Inc.

This press release is distributed by PR NewsChannel. Your News. Everywhere

Novocure brings brain cancer therapeutic device to U.S. sites

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Posted 05 Dec 2011 — by James Street
Category Brain, electromagnetic, Radiation

By Michelle Lang

Novocure Ltd., a medical device company in Portsmouth, N.H., has announced that its new brain tumor therapeutic device is going to be used at four clinical sites in the U.S., including Beth Israel Deaconess Medical Center in Boston.

The Tumor Treating Fields (TTFields) device,  NovoTTF-110A System, is designed to block tumor growth and prompt tumor cell death before the cells divide in patients with recurrent glioblastoma multiforme, a deadly form of brain cancer. FDA-approved in April, the TTFields device is made to produce an artificial electric field in the tumor that inhibits the cell division. The device may be used after surgery and radiation treatments have been attempted.

In the U.S., the TTFields device will see use at the four initial clinical sites by the following doctors: Dr. Eric T. Wong, Beth Israel Deaconess Medical Center in Boston; Dr. Jay-Jiguang Zhu, Mischer Neuroscience Institute in the Memorial Hermann Hospital and The University of Texas Health Science Center, Houston; Dr. Joseph Landolfi, New Jersey Neuroscience Institute at JFK, Edison, N.J.; and Dr. Herbert Engelhard, University of Illinois Hospital in Chicago.

Undergoing training on the devices so they can be ready to use it by the end of 2011 are: Dr. Andrew Lassman, Columbia University Medical Center at New York – Presbyterian Hospital, New York City; Dr. Lisa DeAngelis, Memorial Sloan Kettering Cancer Center, New York City; and Dr. Santosh Kesari, University of California San Diego Moores Cancer Center, San Diego.

Novocure was founded in 2000 and has a research facility in Haifa, Israel. The privately held company is backed by WFD Ventures, Index Ventures, Johnson & Johnson Development Corp. and Pfizer Ventures.

A twist on epigenetic therapy vs cancer

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Posted 01 Dec 2011 — by James Street
Category BAI1, Brain, Epigenetics, genetic research, Methylation

November 30, 2011

Epigenetic therapies against cancer have attracted considerable attention in recent years. But many of the drugs currently being studied as epigenetic anticancer therapies may have indiscriminate effects. A recent paper in Cancer Research from brain cancer researcher Erwin Van Meir’s laboratory highlights a different type of target within cancer cells that may be more selective. Postdoctoral fellow Dan Zhu is the first author of the paper.

Erwin Van Meir, PhD

The basic idea for epigenetic therapy is to focus on how cancer cells’ DNA is wrapped instead of the mutations in the DNA. Cancer cells often have aberrant patterns of methylation or chromatin modifications. Methylation is a punctuation-like modification of DNA that usually shuts genes off, and chromatin is the term describing DNA when it is clothed by proteins such as histones, a form of packaging that determines whether a gene is on or off.

In contrast to mutations that are hard-wired in the DNA, changes in cancer cells’ methylation or chromatin may be reversible with certain drug treatments. But a puzzle remains: if a drug wipes away methylation indiscriminately, that might turn on an oncogene just as much as it might restore a tumor suppressor gene.

The ability of an inhibitor of methylation to treat cancer may depend on cell type and context, explains chromatin/methylation expert and co-author Paula Vertino. She points out that one well-known methylation inhibitor, azacytidine (Vidaza), is a standard treatment for myelodysplastic syndrome, but the strategy of blanket-inhibition of methylation can’t be expected to work for all cancers. A similar challenge exists for agents that target histone acetylation in a global fashion.

Epigenetic therapies seek to modify how DNA is packaged in the cell.

Van Meir’s laboratory has been studying a tumor suppressor protein called BAI1 (brain angiogenesis inhibitor 1), which prevents tumor and blood vessel growth. BAI1 is produced by brain cells naturally, but is often silenced epigenetically in glioblastoma cells. His team found that azacytidine de-represses the BAI1 gene.

Methylation won’t turn a gene off without the help of a set of proteins that bind preferentially to methylated DNA. These proteins are what recognize the methylation state of a given gene and recruit repressive chromatin. Zhu and colleagues in Van Meir’s group found that one particular methyl-binding protein, MBD2, is overproduced in glioblastoma and is enriched on the BAI1 gene.

“Taken together, our results suggest that MBD2 overexpression during gliomagenesis may drive tumor growth by suppressing the anti-angiogenic activity of a key tumor suppressor. These findings have therapeutic implications since inhibiting MBD2 could offer a strategy to reactivate BAI1 and suppress glioma pathobiology,” the authors write.

By itself, MBD2 appears to be dispensable, since mice seem to be able to develop and survive without it. Not having it even seems to push back against tumor formation in the intestine, for example. Targeting MBD2 may represent an alternative way to steer away from cancer cells’ altered state.

Van Meir cautions: “We need to have a better understanding of all the genes that are turned on or off by silencing MBD2 in a given cancer before we can envision to use this approach for therapy.”

Vertino, Shaoman Yin and Steven Hunter, all at Emory, are co-authors on the paper. The work was supported by grants from the NIH and the Southeastern Brain Tumor Foundation and the Emory University Research Council.

Brain cancer vaccine might turn fatal disease into a chronic condition

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Posted 24 Nov 2011 — by James Street
Category Brain, Vaccine
Nov, 23, 2011

Fred Tasker / The Miami Herald

When U.S. Sen. Edward Kennedy was diagnosed with a glioblastoma of the brain in May 2009, doctors understood there was little chance he could survive it. He died that August.

“That’s a malignant tumor. The current five-year survival rate is 1 percent,” says Ricardo Komotar, a neurooncologist at Sylvester Comprehensive Cancer Center.

But cancer specialists from the University of Miami Medical School and nine other U.S. institutions are well into clinical experiments aimed at ending the tumor’s fatal reputation.

“We’re not going to cure it,” says Komotar, who is also director of surgical neurooncology at UM Hospital. “Our goal is to convert it into a chronic condition like high blood pressure or diabetes that you can live the rest of your life with and live a very normal life.”

Their weapon: a brain cancer vaccine. It’s not a preventive vaccine like a flu or polio shot, given to ward off disease. Instead, it’s a “therapeutic” vaccine given after the patient already has the tumor. It’s still called a vaccine because, unlike most cancer medicines, it doesn’t attack the disease directly. Instead, it marshals the body’s own immune system to attack it.

“This is the future of cancer therapy,” Komotar says. “Radiation and chemotherapy fight the cancer but they also kill normal cells, and they’re toxic. This kills the cancer without harming normal tissue.”

Sheryl Shetsky, president of the Florida Brain Tumor Association, said the research is important because “glioblastomas are 30 percent of all brain tumors, and they’re the most devastating tumor. You’re still going to want radiation and chemo for others cells you can’t see. But this can buy the patient a lot more time.”

The new vaccine is given quickly after a patient’s glioblastoma is diagnosed, Komotar says —before surgery, chemotherapy or radiation — because doctors need to use the excised tumor to make the vaccine.

In the treatment, surgeons remove the malignant tumor, then isolate and concentrate essential proteins from it and inject them back into the patient’s arm six to eight weeks later. The patient’s immune system recognizes the proteins as invaders, and produces billions of T-cells, its natural attack system, to fight it.

“It really sparks the immune system; it gives it a target,” Komotar says. “Lots of work remains to be done, but it is a step in the right direction.”

Developed about five years ago at the University of California at San Francisco, the vaccine did so well in Phase I clinical trials for safety that it now has U.S Food and Drug Administration approval to begin Phase II trials for efficacy.

Even in the Phase I trials, it greatly extended the life expectancy of volunteers, Komotar says.

To read the complete article, visit www.miamiherald.com.

ImmunoCellular (IMUC) to Present at the 16th Annual Meeting of the Society for Oncology

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Posted 19 Nov 2011 — by James Street
Category Brain, ICT-107, Immune System, vaccination, Vaccine

November 18, 2011

ImmunoCellular Therapeutics Ltd. (OTCBB: IMUC), a biopharmaceutical company developing new therapeutics to fight cancer using the immune system, is taking a different approach than companies like ImmunoGen Inc. (NASDAQ: IMGN) and Immunomedics Inc. (NASDAQ: IMMU) by targeting cancer stem cells (CSCs) to prevent instances of recurrence.

Recently, the company announced that it would be presenting at the 16th annual meeting of the Society for Oncology. The company will give a presentation entitled, “A cancer vaccine targeting cancer stem cell antigens (ICT-107) demonstrates correlated tumor antigen expression and progression free survival and may reduce the cancer stem cell population in recurrent tumors.”

Here’s a copy of the complete press release from ImmunoCellular:

ImmunoCellular Therapeutics, Ltd. (“ImmunoCellular” or the “Company”) (OTCBB: IMUC.OB), a biotechnology company focused on the development of novel immune-based therapies, today announced that John Yu, MD, Chairman of ImmunoCellular Therapeutics, will take part in the 16th Annual Meeting and Education Day of the Society for Neuro-Oncology (SNO) to be held at the Hyatt Regency, Orange County, California from November 17-20, 2011. SNO is the premier professional society comprising neuro-oncologists from across the U.S. and abroad.

The Company’s presentation titled, “A cancer vaccine targeting cancer stem cell antigens (ICT-107) demonstrates correlated tumor antigen expression and progression free survival and may reduce the cancer stem cell population in recurrent tumors,” will be presented at 7:30 p.m. on Friday, November 18, 2011 at the Hyatt Hotel in Orange County, California. It discusses updated data on antigen expression and immune response referencing correlations of increased progression-free survival (PFS) and overall survival (OS) from the Company’s Phase I clinical trial of ICT-107. Of the 16 patients in the study, 6 showed no signs of tumor recurrence, with 3 experiencing no disease progression over 4 years after vaccination, while the other three have been disease free for at least 3 years. The expression of four out of six ICT-107 antigens in the pre-vaccine tumors correlates with prolonged PFS and OS in newly diagnosed GBM patients. The goal of targeting tumor antigens highly expressed on glioblastoma cancer stem cells is supported by the observation of decreased or absent CD133 expression in patients with recurrent tumors. ICT-107 may thus immunologically target the cancer stem cell population of glioblastoma.

In the Company presentation at the symposium, “Current State of the Art: Vaccine Development In The Treatment of GBM,” on Saturday, November 19, 2011, starting at 12:00 p.m., Dr. Yu will discuss the encouraging prior clinical data for ICT-107, and the ongoing Phase-II double-blind, placebo-controlled, 2:1 randomized study designed to evaluate the safety and efficacy of ICT-107 in patients with newly diagnosed GBM. The study will enroll approximately 160 patients at more than 20 clinical trial centers in the U.S. in collaboration with leading experts and opinion leaders in neuro-oncology.

Manish Singh, CEO of ImmunoCellular Therapeutics, said, “We are excited to participate in this premier gathering of medical professionals specializing in neuro-oncology. We believe that it is a great opportunity to update these specialists to the exciting progress being made in our development of ICT-107.”

About ImmunoCellular Therapeutics, Ltd.

ImmunoCellular Therapeutics is a Los Angeles-based clinical-stage company that is developing immune-based therapies for the treatment of brain and other cancers. The Company recently commenced a Phase II trial of its lead product candidate, ICT-107, a dendritic cell-based vaccine targeting multiple tumor associated antigens for glioblastoma. To learn more about the Company, please visit www.imuc.com.

Forward-Looking Statements

This press release contains certain forward-looking statements that are subject to a number of risks and uncertainties, including the risk that the safety and efficacy results obtained in the Phase I trial for ICT-107 will not be confirmed in subsequent trials. Additional risks and uncertainties are described in IMUC’s most recently filed SEC documents, such as its most recent annual report on Form 10-K, all quarterly reports on Form 10-Q and any current reports on Form 8-K. IMUC undertakes no obligation to publicly update or revise any forward-looking statements, whether as a result of new information, future events or otherwise.

Berberine–Containing Herbs (Goldenseal, Barberry, Goldthread, and Oregon Grape)

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Posted 08 Nov 2011 — by James Street
Category Berberine, Bladder Cancer, Brain, Skin

Berberine, strong and bitter in taste and found in various herbs, delivers anti-inflammatory properties via COX-2 inhibition (Fukuda et al. 1999). Kaempferol, a constituent of berberine, is a strikingly active inhibitor of COX-2 activity (Chen et al. 1999; Newmark et al. 2000). Berberine is unique, having the ability to inhibit COX-2 activity without involving the beneficial COX-1 enzyme. Berberine, perhaps by impacting the production of cyclooxygenase, influences the development of cancers at various sites:

  • Berberine is effective against bladder cancers (Chung et al. 1999).
  • Berberine suppressed colon carcinogenesis and inhibited COX-2 without COX-1 inhibition. The COX-2 enzyme is abundantly expressed in colon cancer cells and plays a role in tumorigenesis. The berberine-COX-2 connection appears to best explain the mechanism of berberine’s anti-inflammatory and antitumor-promoting effects (Fukuda et al. 1999, Newmark et al. 2000).
  • Berberine-induced apoptosis in human leukemia cells (Kuo et al. 1995).
  • Berberine inhibited the development of skin tumors (Kitagawa et al. 1986).
  • Berberine has potent antitumor activity against human and rat malignant brain tumors (Zhang et al. 1990). Studies using goldenseal, which contains the alkaloid berberine, showed average cancer kill rate of 91% in rats, over twice that seen in BCNU (a standard chemotherapy agent for brain tumors). Rat studies used 10 mg/kg of berberine.

A suggested dose is three 250-mg capsules of goldenseal each day. The preparation should be standardized to provide 5% hydrastine. Various respected herbalists suggest that goldenseal should be cycled (rotated with other herbals) rather than routinely administered. Goldenseal contains the alkaloids berberine, hydrastine, and canadine.

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