Oslo Cancer Cluster today signed a groundbreaking strategic agreement with the Toulouse Cancéropole and Cancer-Bio-Santé Cluster which will lead to an integrated effort to become the leading cancer centers in Europe for developing new cancer therapies. The signatories were Philippe Douste-Blazy, President of Cancéropole Toulouse Association, former mayor of Toulouse and former French foreign minister, Jean-Pierre Saintouil, CEO of Toulouse Cancer-Bio-Santé Cluster and Bjarte Reve, CEO of Oslo Cancer Cluster NCE. It also contained an initial series of key initiatives to be implemented over the next two years, including a joint response to the next cancer calls of the EU -Innovative Medicines Initiative.

According to Bjarte Reve, the agreement stems from growing recognition that combined research and industry-based clusters focusing on a particular therapeutic area are the way forward: “Oslo and Toulouse are pioneers in this area. Through partnership between the life science industry, research institutions, university hospitals, government and the Norwegian Cancer Society, we have been able to rapidly develop the Oslo Cancer Cluster. Having developed links with like-minded centres in the US, such as MD Anderson, when we turned to Europe, Toulouse stood out as a potential partner. We are therefore delighted to have signed this agreement and to share our vision of ensuring that patients have access to the latest cancer diagnostics and therapeutics as quickly and cost-effectively as possible.”

Philippe Douste-Blazy , initiator of the Toulouse project, congratulated the creators of this collaboration and stressed the similarities between Oslo and Toulouse: “This is especially evident in their ethical approach that cannot be categorized as a purely economic approach but instead places the patient at the heart of the concept.”
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When mice are exposed to arsenic at federally-approved levels for drinking water, pores in liver blood vessels close, potentially leading to cardiovascular disease, say University of Pittsburgh researchers in the Dec. 1 issue of the Journal of Clinical Investigation, available online Nov. 13. The study, while preliminary, also reveals how an enzyme linked to hypertension and atherosclerosis alters cells, and may call into question current Environmental Protection Agency standards that are based solely on risks for cancer.

In the study, Aaron Barchowsky, Ph.D., associate professor of environmental and occupational health at the University of Pittsburgh Graduate School of Public Health, and his research team looked at specialized cells in the liver called sinusoidal endothelial cells, which are tasked with removing wastes from blood and enabling nutrients to regulate metabolism. After exposing mice to 10 to 100 parts per billion (ppb) of arsenic over a two-week period, the cells were less able to remove damaged proteins from the blood and lost their characteristic pores or “windows,” severely compromising the cells’ ability to effectively exchange nutrients and waste. Dr. Barchowsky notes that despite their small size, mice are usually less sensitive to the effects of arsenic than people  Read the rest of this entry »

The finding: Researchers at the University of Michigan Comprehensive Cancer Center have found a genetic marker that controls an enzyme present in aggressive and metastatic cancer. The study suggests an absence of microRNA-101 is related to high expression of the protein EZH2, which was previously shown to be active in metastatic cancers. MicroRNA’s are molecules that help regulate gene expression. miR-101 is one of few miRNA’s shown to play such an important role in the development of cancer.
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Using a new approach that combines scientific technologies to hunt down genetic changes involved in cancer, researchers have discovered 13 tumor suppressor genes that, when mutated, can lead to liver cancers. Twelve of those genes had never been linked to cancer before, according to the report published online in the journal Cell, a Cell Press publication, on November 13th.

” It’s important to understand all the genetic alterations that can give rise to cancer,” said Howard Hughes Medical Institute Investigator Scott Lowe of Cold Spring Harbor Laboratory. “If we understand cancer, we can treat it better by going after the molecular causes or by categorizing cancers to better predict their behavior.”

One of the challenges in identifying those mutations that are responsible for causing cancer is that, as Lowe puts it, cancers are often a mess. In other words, a given cancer may contain many mutations, some that drive the cancer and others that are just along for the ride. The challenge then is to sift through all the changes found in cancer to identify those that are functionally relevant to the disease.

Recent efforts to catalogue the cancer genome - all the genes that can play a role in cancer - have been stimulated by advances in genomics, Lowe said. But a genomic approach on its own can only identify genes that are, statistically speaking, more often altered, lost or amplified, in cancer than they are in non-cancer. It doesn’t tell you what those genes do.

In the new study, the researchers first identified genes that were recurrently deleted in 100 human liver cancers. The notion was that genes frequently lost in cancer likely include tumor suppressors that normally keep cancer at bay. That effort turned up 58 deletions, each including one to 46 genes, for a total of 362 genes.
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There has been much speculation over the last few years about whether cell phones increase the risk of developing a brain tumor. Research has not conclusively answered this question, which has left consumers confused. The majority of studies that have been published in scientific journals do not have sufficient evidence to show that cell phones increase the risk of brain tumors. The problem is that cell phone technology is in its infancy, so none of these studies could analyze long-term risks. This unknown is a particular issue for children, who will face a lifetime of cell phone usage. While the cell phone/brain tumor connection remains inconclusive, the American Association of Neurological Surgeons (AANS) cautions that cell phones present plenty of other risks to people’s neurological health, as illustrated by these few real-life scenarios:

~A 29-year-old male was talking on his cell phone while on an escalator, fell backwards, and lacerated his head.

~A 25-year-old male was talking on his cell phone and walked into a street sign, lacerating his head.

~A 43-year-old female fell down 13-14 steps while talking on her cell phone, after drinking alcohol. She suffered a neck sprain and contusions to her head, back, shoulder, and leg.

~A 50-year-old female suffered nerve damage which was related to extensive cell phone usage. She felt pain in her fingers and the length of her arm while holding her cell phone, and was diagnosed with cervical radiculopathy.

~A 39-year-old man suffered a head injury after crashing into a tree on his bicycle while texting

~A 16-year-old boy suffered a concussion because he was texting and walked into a telephone pole.

Several studies show cell phones are a leading cause of automobile crashes. It is estimated that drivers distracted by cell phones are four times more likely to be in a motor vehicle accident. The following are some sobering statistics:

~According to a Harvard University study, an estimated 2,600 people die and 12,000 suffer serious to moderate injuries each year in cell phone-related accidents.

~A Canadian study analysis of 26,798 cell phone calls made during the 14-month study period showed that the risk of an automobile accident was four times higher when using a cell phone.

~National statistics indicate that an estimated 50,000 traumatic brain injury-related deaths occur annually in the United States, 25,000-35,000 of which are attributed to motor vehicle accidents.

Cell Phone Injury Prevention Tips

~Talk hands free by using an earpiece or on speaker mode whenever possible.

~Follow all cell phone laws applicable to your city and state these vary greatly.

~Use your cell phone only when safely parked, or have a passenger use it.

~Do not dial the phone or take notes while driving, cycling, skateboarding, rollerblading, etc.

~Never text message while driving, walking, cycling, skateboarding, rollerblading, etc.

~Never text message or use a cell phone while performing any physical activities that require attention.

~If your phone rings while driving, let the call go into voice mail and respond later when you are safely parked.

For more information on injury prevention, visit the AANS Web site at: http://www.neurosurgerytoday.org/what/patient_safety.
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An intra cellular pathway not previously linked to breast cancer is driving a sub-type of the disease that is highly lethal and disproportionately over-represented in African American women. The pathway regulates how cells identify and destroy proteins and represents a class of genes called proteasome targeting complexes. The work shows that basal cancer cells degrade the tumor suppressor gene p27 by making a new type of proteasome targeting complex. The gene p27 is one of a handful of proteins that are expressed in normal cells and act to prevent rapid cell growth, which is indicative of cancer. Beyond chemotherapy, no specific therapeutic target has been identified for this sub-type of cancer, found in between 12 to 15 percent of breast cancers in the general population and up to 25 percent of cases in African American women.

“The mortality rates in this subgroup of cancer are very high,” said Tim Lane, senior author of the paper and a researcher at UCLA’s Jonsson Comprehensive Cancer Center. “The possibility that this new proteasome targeting complex might provide targets for therapeutic intervention is a completely new area for breast cancer research.”

The research, done in animal models and human breast cancer cell lines, is published in the Nov. 15 issue of the journal Genes and Development.

Scientists have identified five to seven different sub-types of breast cancer. Basal-like breast cancers currently are among the most difficult to treat.
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UroToday.com - The molecular mechanisms underlying development of androgen-independent growth of prostate cancer are largely unknown, and no effective therapies for hormone-refractory prostate cancer exist at present. One of the key problems in conducting studies to identify growth factors and signaling pathways that can replace androgens in the growth control of prostate cancer cells is the lack of androgen receptor (AR)-positive human prostate cancer cell lines that are regulated by androgens and tumorigenic in nude mice.

We have established and characterized a new androgen-dependent, highly tumorigenic human prostate cancer cell line, CWR22Pc, from the primary CWR22 human prostate xenograft tumors. The primary CWR22 prostate tumors are highly responsive to androgen deprivation with marked tumor regression after castration, mimicking the course of the human disease.

Comparative genomic hybridization and DNA fingerprinting analysis show that the CWR22Pc cell line genetically originates from the primary CWR22 tumors. The growth of CWR22Pc cells is strictly regulated by androgens, and CWR22Pc cells express high levels of androgen receptor with H874Y mutation but without the exon 3 duplication. Transcription factors Stat5a/b and Stat3, which are highly activated in prostate cancers of high histological grade, are activated by prolactin and IL-6 respectively in CWR22Pc cells and Akt and MAPK signaling pathways are constitutively active in CWR22Pc cells.
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A $3.8 million Innovator Award, from the Department of Defense, is being granted over five years to an internationally renowned cancer researcher at the University of California, Santa Barbara.

Erkki Ruoslahti, recipient of the award, is known for his innovative, interdisciplinary research. “This is a special award because there are only four of them,” said Ruoslahti. “I am very happy at being chosen.” The award is designed to further his current research.

Ruoslahti’s lab made a major advance in the past year. “I think that was part of the reason why the grant was awarded to me, is that we can now make probes, typically peptides,” he said. “These are small pieces of protein that not only bind the particles to the vessels in the tumor, but they also carry the particles into the interior of the tumor, outside the blood vessels.”

He recently showed that targeting a nanoparticle drug into a tumor is more effective than if it isn’t targeted. “What we are working on now, as an additional function, is that we’d like to make the particles respond to a signal so that they would release a drug when we want it to be released,” he said. “But we haven’t solved what would have to be done to get that technology to work.”
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UroToday.com - Can we meaningfully separate inflammatory pseudotumor (a term used since 1937 1 from inflammatory myofibroblastic tumor (IMT, a term introduced in 1990 for lung lesions 2 and from sarcoma?

The oldest large series of 38 such cases in the urinary bladder divided most of them into 17 pseudotumors and 13 sarcomas 3. The 17 patients in the pseudotumor group

1) had no tumor recurrence after resection,
2) histologically had no necrosis even if there was muscularis propria invasion,
3) had less nuclear atypia, and
4) p53 immunoreactivity was minimal to absent 3.

Recently, the term IMT has been used more than pseudotumor, but IMT may include a more aggressive but overlapping set of lesions. Perhaps whether ALK-1 rearrangements are detected in 8% of cases 4 or over half of cases 5, 6, depends on whether the lesions being studied are inflammatory pseudotumors 4 or IMT 5, 6. ALK-1 expression appears to correlate with local recurrence 5 and muscle invasion 6. IMT includes tumors with necrosis in up to 30% 6, and encompasses tumors with recurrence in up to 31% 6, so it is tempting to suggest that of the tumors we classified as sarcoma, at least the 7 low grade ones 3, most may have been considered by others as IMT, and conversely, that IMT is truly a low-grade sarcoma 7.
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Veridex, LLC announced today that the technology used in the CellSearch® System to measure circulating tumor cells (CTCs) was ranked as the top medical innovation for 2009 by the Cleveland Clinic, a leading multispecialty academic medical center. The ranking is based on technologies likely to have a significant impact on health care next year.

The prestigious annual recognition follows a rigorous selection process by a panel of Cleveland Clinic physicians. The list was announced today at the Cleveland Clinic’s 2008 Innovation Summit.

To view the multimedia news release, go to: http://www.nnpkit.com/veridex/cellsearch/.

“We are deeply gratified by this recognition from the Cleveland Clinic,” said Robert McCormack, Ph.D., Vice President of Medical and Scientific Affairs, Veridex. “Our entire team is committed to the research and development of this technology, and our goal with the CellSearch® test is to provide patients and doctors with reliable and timely information about cancer progression.”
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