Breast MRI Scan Could Determine Need For Radiation Therapy

For women whose breast cancer has spread to their lymph nodes, a magnetic resonance imaging (MRI) scan could replace exploratory surgery as the method for determining whether those women need radiation therapy to treat their disease, according to a study to be presented during the annual meeting of the American Society for Therapeutic Radiology and Oncology (ASTRO) in Boston.

In a retrospective study of 167 patients who underwent radiation therapy for invasive breast cancer after surgical staging of their tumors, physician researchers at the Seattle Cancer Care Alliance and University of Washington Medical Center found that the tumors' physiological information shown on MRI scans correlated with surgically based findings of cancer having spread to lymph nodes. This suggests that breast MRI could help determine if women scheduled to undergo surgery will later need radiation therapy and how much.

The findings are significant because the standard of care for women with breast cancer has evolved during the past five years. In the past, decisions regarding radiation therapy were made after surgery and before chemotherapy, according to lead author Christopher Loiselle, M.D., a resident in the Department of Radiation Oncology at UW Medical Center. Today, increasing numbers of women may be treated with chemotherapy before surgery.

"When you give chemotherapy first, and then perform the surgery to remove the cancer and sample the lymph nodes, you reduce your ability to know whether there was cancer in the axillary (underarm) lymph nodes before the patient was treated with chemotherapy," Loiselle said. "This raises the question: is there another way to stage those lymph nodes? Our study showed that tumor characteristics as seen on an MRI scan may be the answer."

The ultimate benefit is that some women can be spared radiation therapy, especially those with smaller tumors and tumors that have not spread to the lymph nodes, he said..

A contrast dye used routinely in MRI scans not only highlights the size and location of the tumor but also details the blood vessels feeding the tumor. The kinetics or activity of the contrast dye in the tumor provided some key parameters for comparing MRI to traditional surgical tumor staging, he said.

"MRI is evolving rapidly as a diagnostic tool for breast cancer, particularly among women with high risk for the disease, because not only does it give us traditional anatomic information about tumors but information about the biology of the tumor as well," Loiselle said.

Prospective studies will need to be done to confirm the value of MRI scans in staging tumors for radiation therapy,

Immune System Can Hurt As Well As Help Fight Cancer, Study Shows

University of Pennsylvania School of Medicine have found that some proteins of the immune system can promote tumor growth. Investigators found that instead of fighting tumors, the protein C5a, which is produced during an immune response to a developing tumor, helps tumors build molecular shields against T-cell attack. These findings appeared online this week in Nature Immunology.

C5a is part of the complement system, one of the body’s immune defenses against pathogens. When activated, the system’s proteins rid the body of microbes and foreign cells. Many cancer treatments are aimed at boosting the immune system to kill tumors.

“Until now, everyone thought that the complement system was there to eliminate tumor cells. We found that in some conditions, the complement system can promote tumor growth, depending on the specific tumor and the specific environment in which the tumors are developing,” says John Lambris, PhD, the Dr. Ralph and Sallie Weaver Professor of Research Medicine.

However, Penn researchers found that in a mouse model, activation of the complement system in tumor tissue leads to the generation of C5a, which recruits myeloid-derived suppressor cells (MDSC) to tumors. These MDSCs block the function of CD8+ T cells, which would normally dismantle a tumor.

Researchers also found that blocking the C5a receptor on cell surfaces impairs tumor growth at the same rate of Paclitaxel, a chemotherapy drug. This discovery could lead to new cancer treatments with far fewer side effects than chemotherapy, surmise the investigators.

“Researchers are trying to introduce immune therapies and anti-tumor vaccines, but most of these vaccines fail,” says Lambris. “We show in this study a possible mechanism how to overcome this problem.” Lambris and his team are conducting studies that apply the approaches outlined in this paper to five models of cancer.

In addition to Lambris, Penn co-authors are Maciej M. Markiewski, Robert A. DeAngelis, Salome K Ricklin-Lichtsteiner, Anna Koutoulaki, Fabian Benencia (now at the University of Ohio), and George Coukos, as well as Craig Gerard, Children’s Hospital, Boston. The National Institutes of Health provided funding for this research.

Turning Cancer Friend Into Cancer Foe

created a peptide that binds to Bcl-2, a protein that protects cancer cells from programmed cell death, and converts it into a cancer cell killer.

The Bcl-2 protein has long been implicated in protecting cancer cells from apoptosis (programmed cell death), the process that usually keeps cancer cells in check. This peptide (called NuBCP-9) and its enantiomer (mirror-image molecule) work on Bcl-2 like a molecular switch, converting it into a pro-apoptotic protein, and inducing cell death in cancer cells.

“Our results provide insight into Bcl-2 conversion and identify a new direction for Bcl-2-based drug leads and cancer drug development,” said Xiao-kun Zhang, Ph.D. of the Burnham Institute for Medical Research, who co-authored the paper with Arnold Satterthwait, Ph.D. and others.

The NuBCP-9 peptide was created from Nur77, a potent pro-apoptotic protein. Nur77 often moves from the nucleus to mitochondria, in response to different death signals, where it binds to Bcl-2, changing its shape and function.

The research, which was published in the October 7 edition of Cancer Cell, may lead to new cancer treatments.

New Findings May Improve Treatment Of Inherited Breast Cancer

identified some of the elusive downstream molecules that play a critical role in the development and progression of familial breast cancer. The research, published by Cell Press in the October 10th issue of the journal Molecular Cell, also identifies a compound found in grapes and red wine as an excellent candidate for treatment of some forms of breast cancer.identified some of the elusive downstream molecules that play a critical role in the development and progression of familial breast cancer. The research, published by Cell Press in the October 10th issue of the journal Molecular Cell, also identifies a compound found in grapes and red wine as an excellent candidate for treatment of some forms of breast cancer.

About 8% of breast cancer cases are caused by mutations in tumor suppressor genes, such as breast cancer associated gene-1 (BRCA1). BRCA1 is the most frequently mutated tumor suppressor gene found in inherited breast cancers and BRCA1 mutation carriers have a 50-80% risk of developing breast cancer by age 70. "Although work with animal models of BRCA1 mutation has provided some insight into the many biological processes linked with BRCA1, very little is known about the downstream mediators of BRCA1 function in tumor suppression," says lead study author Dr. Chu-Xia Deng from the Genetics of Development and Diseases Branch at the National Institutes of Health.

Dr. Deng and colleagues were interested in investigating the relationship among BRCA1, SIRT1 and Survivin. SIRT1 is a protein and histone deacetylase involved in numerous critical cell processes including metabolism, DNA repair and programmed cell death, known as apoptosis. Although SIRT1 has been implicated in tumorigenesis, no concrete role in cancer initiation or progression has been identified. Survivin is an apoptosis inhibitor that is dramatically elevated in many types of tumors. Research has suggested that Survivin may serve to maintain the tumor and promote growth.

The researchers found that BRCA1 functioned as a tumor suppressor by maintaining SIRT1 expression, which in turn inhibited Survivin expression. When BRCA1 was not functioning properly, SIRT levels decreased and Survivin levels increased, allowing BRCA1-deficient cells to overcome apoptosis and undergo malignant transformation.

They went on to show that the compound resveratrol strongly inhibited BRCA1-mutant tumor growth in cultured cells and animal models. Resveratrol is an important constituent of traditional Japanese and Chinese medicine that has recently been shown to inhibit some types of cancer by inducing apoptosis with very little associated toxicity. In the current paper, resveratrol enhanced SIRT1 activity, this leading to reduced Survivin expression and subsequent apoptosis of BRCA1 deficient cancer cells.

These findings identify SIRT1 and Survivin as downstream mediators of BRCA1-regulated tumor suppression and identify resveratrol as a potent inhibitor of BRCA1-mutant cancer cells. "Resveratrol may serve as an excellent compound for targeted therapy for BRCA1 associated breast cancers," says Dr. Deng.

Potential New Tool For Brain Surgeons

ways of treating brain cancer is surgically removing the tumors. The risk of this sort of procedure is obvious -- it involves cutting away tissue from the brain, potentially severing nerve fibers and causing neurological damage. MRI and CT scans can reveal the extent of tumors, but only prior to surgery.

These techniques rely on large instruments that cannot be used in the operating room, and during the operation the brain may relax and move, forcing surgeons to adjust where they are cutting to minimize the damage to the brain tissue.

During surgery, doctors make these adjustments by asking their patients to perform certain tasks while electrically stimulating parts of the brain bordering where they plan to cut. The electrical stimulation inhibits brain function in that region, revealing whether losing that tissue would cause permanent damage. Although slow, this is a good way to detect and protect critical areas of the brain.

Now Paul Hoy and his colleagues at the University of Southampton in England are developing a rapid and highly sensitive method for measuring brain function across the entire area during surgery. The method is based on observing blood flow in the brain. Active brain regions have increased blood flow, and this change can be observed by looking at light reflected off the brain because hemoglobin, the protein that ferries oxygen within the bloodstream, will absorb light differently depending on whether it carries oxygen or not.

Recently Hoy and his colleagues measured this signal on four people undergoing brain surgery and showed that their results agreed with the electrical stimulation. They hope that the technique will one day provide information quickly for neurosurgeons, and they are now collecting data that will lead to a clinical trial designed to test how effective the technique is.

Medical research is a cornerstone of Frontiers in Optics 2008 (FiO), the 92nd Annual Meeting of the Optical Society (OSA), being held Oct. 19-23 at the Riverside Convention Center in Rochester, N.Y. FiO 2008 will take place alongside Laser Science XXIV, the annual meeting of the American Physical Society’s Division of Laser Science. Presentation FTuD3, “Optical Intraoperative Measurement of Function in the Human Brain,” takes place on Oct. 21.

Mechanism In Cells That Generate Malignant Brain Tumors May Offer Target For Gene Therapy

Cedars-Sinai Medical Center's Maxine Dunitz Neurosurgical Institute who first isolated cancer stem cells in adult brain tumors in 2004 have now identified a molecular mechanism that is involved in the development of these cells from which malignant brain tumors may originate. This could offer a target for scientists seeking treatments that would kill malignant brain tumors at their source and prevent them from recurring.

Normal stem cells are "immature" cells that have the potential to become any of several types of cells. Cancer stem cells have the same multi-potent and self-renewing properties, but instead of producing healthy cells, they propagate cancer cells. Theoretically, if these "mother cells" can be destroyed, the tumor will not be able to sustain itself. On the other hand, if these cells are not removed or destroyed, the tumor will continue to return despite the use of existing cancer-killing therapies.

Glioblastoma multiforme is the most malignant form of tumor that develops in the brain, but not all glioblastomas are identical. Subgroups are comprised of cells originating from different brain tumor stem cells with unique genetic characteristics that use different signaling pathways in their development and growth. The Cedars-Sinai researchers are building genetic "profiles" of these cancer stem cells and the tumors they appear to produce.

In this study, published in the journal Stem Cells (Stem Cells Express online Sept 11., ahead of print), the researchers identified a subset of brain tumor stem cells that is dependent on a protein called Sonic Hedgehog and another subset that is not Hedgehog dependent. The brain tumors resulting from each subset retained the "signaling dependency" characteristics of the mother cells, and in laboratory experiments and studies in laboratory mice, pathway-specific blocking interventions prevented the brain tumor stem cells from being able to renew themselves.

Although cancer stem cell involvement in the genesis of brain tumors is hypothetical and in the early stages of scientific discovery, the Sonic Hedgehog signaling mechanism appears to be one of the molecular mechanisms regulating both normal stem cell growth and cancer stem cell growth.

"According to our analysis, patients who have malignant brain tumors produced from cancer stem cells that rely on this mechanism have a shorter survival than those who don't," said John S. Yu, M.D., director of Surgical Neuro-oncology at Cedars-Sinai and senior author of the Stem Cells article.

Further investigation of these and other pathways may allow scientists to devise therapies to block the underlying cancer-causing mechanisms with genes or small molecules, according to the research team.

"Understanding the mechanisms behind cancer stem cells, which may be the root and cause of cancers, may allow us to determine how these cancers start and, more importantly, how best to target them to prevent their growth and spread," said Keith L. Black, M.D., chairman of the Department of Neurosurgery, director of the Maxine Dunitz Neurosurgical Institute, and one of the paper's authors.

After isolating cancer stem cells in adult brain tumors in 2004, the Cedars-Sinai researchers in 2006 reported that these cells are highly resistant to chemotherapy and other treatments. Even if a tumor is almost completely obliterated, it will regenerate from the surviving cancer stem cells and be even more resistant to treatment than before.

This study was supported in part by grants from the National Institutes of Health.

Novel Marker Of Colon Cancer

second of all gastrointestinal malignant tumors, it is one of the leading causes of cancer-related deaths worldwide. Until now, several molecules have been reported to play an important role in gastroenterological tumorigenesis and tumor metastasis, but the molecular mechanisms involved tumor development and progression still remain unclear in colon cancer.

A research article to be published on October 14, 2008 in the World Journal of Gastroenterology addresses this question. In this research, by using the combined methods of laser microdissection (LMD), P27-based RNA amplification, and polypeptide, They evaluated differentially expressed genes between early carcinoma and lymph node metastatic patients. Moreover, They further identified four differentially expressed genes in the progression of colon cancer in another group of 15 patients by means of semiquantitative reverse transcribed polymerase chain.

Their result indicated that the five gene expressions were changed in colon carcinoma cells compared with that of controls. Of the five genes, three genes were downregulated and two were upregulated in invasive submucosal colon carcinoma compared with non-invasive cases. The results were confirmed at the level of RNA and gene expression. Five genes were further identified as differentially expressed genes in the majority of cases (> 50%, 25/40) in progression of colon cancer, and their expression patterns of which were similar to tumor suppressor genes or oncogenes.

These results not only reveal the differentially expressed genes in progression of colon cancer, but also provide information that may prove useful for identifying novel diagnostic and therapeutic targets.

Double-barreled Immune Cell Approach For Neuroblastoma

tumor-specific receptor to immune system cells called T-lymphocytes that target a particular virus extended and improved the cells' ability to fight a form of childhood cancer called neuroblastoma, said researchers form Baylor College of Medicine and Texas Children's Hospital in a report that appears online today in the journal Nature Medicine.

"This is a way to convert a naturally occurring problem into a benefit in treating cancer," said Dr. Malcolm Brenner, director of the Center for Cell and Gene Therapy at BCM, TCH and The Methodist Hospital, and professor of pediatrics and medicine at BCM. He and his colleagues reported on using the new treatment in 11 patients with recurring neuroblastoma. "For the first time, we started to see tumor responses. We have one complete remission and others who have had stable disease for more than a year," said Brenner.

The patients responded after only the one infusion of cells because they last a long time in the body and their numbers can increase, said Brenner.

Previous attempted to use T-lymphocytes with an artificial receptor directed to tumor cells proved disappointing because they disappeared from the body too quickly to have an anti-cancer effect. However, cytotoxic T cells that already have a natural receptor for the Epstein-Barr virus are continually activated by the presence of the virus, which is never eliminated from the body.

Brenner and his group added to these T-lymphocytes a particular receptor for a protein called diasialoganglioside GD2, which is found in human neuroblastoma cells.

"We took the T-lymphocytes' with specificity for Epstein-Barr and added another receptor," said Brenner. "In effect they trampoline off the virus and onto the tumor."

Thus these cytotoxic T-lymphocytes remain in the body because they are constantly stimulated by the virus. Their artificial antigen receptor enables them to latch onto and kill the cancer cells.

When the researchers put the artificial receptor into both ordinary T-lymphocytes and those that are stimulated by the virus into the 11 patients, they found that the cancer directed cells stimulated by the Epstein-Barr virus lasted as long as 18 months and at higher levels than the other cells.

Neuroblastoma is a tumor of primitive cells that go on to form the sympathetic nervous system. Apart from brain tumors, it is the most common solid cancer of children, and accounts for 7 percent of the total. In two-thirds of cases, it is not diagnosed until it has already spread to other parts of the body.

He and his colleagues hope to improve the treatment to make the T-lymphocytes more potent cancer killers, he said. One way would be to add specific receptors for proteins that allow the T-lymphocytes to avoid the immune-dampening effects of the cancers. Another might be to give the treatment right after the patients receive a stem cell transplant. At that time, the number of tumor cells would be at its lowest and there would be a lot of signals telling the T-lymphocytes to increase in number.

Within the next year, they plan to add receptors for other cancers to the virus-specific T-cells and see if they get the same cancer-fighting effect.

Others who took part in this research include Martin A. Pule, Barbara Savoldo, G. Doug Myers, Claudia Rossig, Heidi V. Russell, Gianpietro Dotti,M. Helen Huls, Enli Liu, Adrian P. Gee, Zhuyong Mei, Eric Yvon, Heidi L. Weiss, Cliona M. Rooney and Helen E. Heslop, all of BCM.

Funding for this work came from the National Institutes of Health, the General Clinical Research Centers at BCM and the Doris Duke Charitable Foundation.

Tumors Grow Faster Without Blood-supply Promoting Molecule

blood vessels thought to spur cancer’s growth could actually hinder rather than promote tumor progression, according to a new study at the University of California, San Diego.

The findings partly explain why drugs designed to treat cancer by strangling its blood supply have been disappointing when used alone and why those treatments are more effective when combined with traditional chemotherapy.

Despite their rapid progression, tumors fed by more normal vascular were also more vulnerable to the effects of standard chemotherapy drugs, the team reports in this week’s early online edition of the journal Nature.

Nascent tumors take off as new blood vessels invade, an event called angiogenesis that many see as key to the development of malignancy. But those pathological vessels form tangled structures that are far from normal.

“Tumor blood vessels become more chaotic, disorganized and leaky,” said Randall S. Johnson, professor of molecular biology at UC San Diego who led the study. “They become dysfunctional in many ways as a blood vessel network.”

Cellular secretions within tumors promote the invasion. The first drugs designed to curtail cancer’s blood supply targeted one of these, called VEGF for vascular endothelial growth factor. Inflammatory cells, which infiltrate many types of tumors, provide one source of VEGF.

Johnson’s team created a strain of mice in which most inflammatory cells were missing the gene for VEGF, then cross-bred them with a strain that reliably develops mammary tumors and is commonly used to study breast cancer.

“The blood vessels look more organized and less leaky in the engineered mice,” said Christian Stockmann, a molecular biology postdoctoral fellow and the first author of the paper.

The blood supply to tumors in these mice was also sparse compared to mice with intact VEGF genes.

“A lot of these classic hallmarks of tumor blood vessels disappeared when the inflammatory cells couldn’t make VEGF,” Johnson said.

But the cancer grew faster.

All of the mice developed tumors, but at 20 weeks of age, those with low levels of VEGF from inflammatory cells had larger growths that were more likely to have progressed to a later stage of cancer.

“The tumors seemed much happier when they didn’t have this chaotic vasculature,” Johnson said.

The scientists also injected a cancerous cell line into normal and engineered mice and found that the introduced cells invaded normal tissues more readily without VEGF from inflammatory cells and developed more normal blood supplies.

The tumors that formed were also more susceptible to two different chemotherapy drugs in the mice lacking VEGF from inflammatory cells.

By identifying the cellular source of the critical factor for one pathology associated with cancer, the researchers say their findings may open new avenues for treatment.

The National Institutes of Health funded the research.

Relative Risk Of Brain Cancer: Tell Your Doctor If Tumors Run In The Family

you’re at a higher risk for breast, colon and prostate cancers if they’ve been found in your family. Brain cancer can now be placed on that same list, says a new study by Tel Aviv University and the University of Utah.

Dr. Deborah Blumenthal, co-director of Tel Aviv University’s Neuro-oncology Service at the Tel-Aviv Sourasky Medical Center, says that a family history of brain cancer, like those of other cancers, should be reported to the family doctor during a routine medical checkup.

The new study, using data from the Utah Population Data Base (UPDB) at the University of Utah in Salt Lake City, was unique in the large number of cases examined, which tracked back at least three generations and as far as ten generations in some families. The brain tumors studied by the researchers include glioblastoma, the same tumor afflicting Sen. Edward Kennedy, who has been undergoing treatment since June.

“Until now, brain tumors were not thought to be an inheritable disease,” says Blumenthal. “A few earlier studies did find an increased risk in immediate relatives, but in such cases it is hard to distinguish between the effects of a shared environment and heredity,” she notes.

Genetic Predisposition

Blumenthal, an affiliate associate professor at the University of Utah Huntsman Cancer Institute, and co-author Lisa Cannon-Albright, of the Department of Biomedical Informatics at the University of Utah, found that a family history of cancerous brain tumors does indeed increase one’s odds for succumbing to the disease ― in some cases, a four-fold increase. While the number of primary brain tumors that are inheritable remains low, these cases may provide insight into specific genetic susceptibilities that predispose an individual to primary brain tumors.

Reported in the current issue of Neurology, the study was conducted on medical records of nearly 1,500 people from Utah who had available genealogic material spanning at least three generations. Data dates back to the early 1800s. The study effectively eliminates environmental factors by looking at extended family relations.

“The study is unique in that that we were able to go back so far in tracking genealogy records,” notes Prof. Blumenthal. “Another special aspect of this study is that we’ve been able to identify high-risk pedigree families, in some cases with 5,000 or more descendants.”

Even if brain cancer already appears in your family, the likelihood of it occurring in descendants and relatives is still quite low. There are only about 17,000 primary brain tumors found in Americans every year, of which half are high grade. Less than 5% of these relatively rare brain cancers are hereditary. Consequently, the risk of inheriting the “genes” of a brain tumor from a parent or grandparent is low. What's exciting, she says, is that the scientific community now has a population of high-risk families they may be able to help and utilize to further genetic investigations.

Necessary Steps Before Prevention

With blood and tissue samples, researchers hope to find genes that are associated with brain tumors, and determine those at risk with greater certainty. Though such identification may be years away, this current study is foundational, setting the stage for early screening of people at risk so preventative measures can be taken before any tumor develops.

Prof. Blumenthal emphasizes, “The risks of having such a hereditary tumor are very low. Reporting to your family doctor that brain cancer runs in the family just gives a more comprehensive picture of your medical history. It may provide doctors and family members with useful information.”

Therapy May Block Expansion Of Breast Cancer Cells

stem cells are known to be involved in therapy resistance and the recurrence of cancerous tumors. A new study appearing in Clinical and Translational Science shows the mechanisms governing stem cell expansion in breast cancer (called Notch activity), and finds that therapy targeting a protein called cyclin D1 may block the expansion of cancerous stem cells.

The study, conducted by Dr. Richard Pestell and colleagues at Thomas Jefferson University, was the first to show that cyclin d1 is required for breast cancer growth in mice. As cyclin d1 is known to be over-expressed in human breast cancer, the findings may explain how cyclin d1 contributes to breast tumor growth, and provide the rationale for targeted therapies at cancerous stem cells in humans.

"Breast and other cancers are maintained through a population of cancer stem cells. By specifically targeting cancer stem cells we hope to reduce recurrence and improve therapy responses," says Pestell.

Cancer arises as a result of the accumulation of multiple genetic lesions that ultimately result in unregulated cell cycle, and Notch activity is a key determinant of the cellular development and differentiation related to this process. As Notch signaling is activated in human breast cancer, (and a negative regulator of Notch signaling reduces the disease), the molecular mechanisms regulating Notch activity are of fundamental importance for future therapy.

Clue To Stopping Breast-cancer Metastasis Discovered

exactly what a breast cancer cell needs to spread, then they could stop the most deadly part of the disease: metastasis. New research from the University of North Carolina at Chapel Hill School of Medicine takes a step in that direction.

Carol Otey, Ph.D. and UNC colleagues reduced the ability of breast cancer cells to migrate by knocking down the expression of a protein called palladin.

They also found higher levels of palladin in four invasive breast cancer cell lines compared to four non-invasive cell lines.

"This study shows that palladin may play an important role in the metastasis of breast cancer cells as they move out of the tumor and into the blood vessels and lymphatics to spread throughout the body," said Otey, associate professor of cell and molecular physiology.

To conduct the study, the researchers grew breast cancer cells in an "invasion chamber," in which human tumor cells are placed in a plastic well that is inserted into a larger well. Cells will attempt to move to the bottom of the chamber because it's baited with growth factors that cells find attractive. But first the cells have to migrate through a filter coated with a layer of artificial connective tissue. "The cells have to migrate through that and have to degrade it," Otey said. "It's a useful model system that mimics what happens in the body."

The study results appeared in the Nov. 3, 2008, online edition of the journal Oncogene.

Most women would never die from breast cancer if the cancer cells couldn't metastasize to the brain and bone marrow, Otey said. "To really make breast cancer a treatable disease, we have to be able to find a way to prevent or reduce the amount of metastasis."

"Now that we see palladin is expressed mostly in invasive cells, it raises the question as to whether it might be useful as a prognostic marker," Otey said. "Maybe someday doctors could test for the presence of palladin to identify patients who have the most aggressive tumors, then give those patients personalized, more aggressive treatment."

The study benefited from the collaboration between Otey's cell and molecular physiology lab and Dr. Hong Jin ("H.J.") Kim's surgical oncology lab. "I learned a lot from H.J. about the challenges that clinicians face as they try to optimize the treatment of each breast cancer patient," Otey said.

Otey has been investigating palladin's role in cell movement since she discovered and named it in 2000.

Next she will examine a variety of samples of human tumors from a UNC tumor bank, to find out if the tumors from patients who had worse outcomes and more aggressive cancers contain higher levels of palladin.

In addition to Otey and Kim, the study co-authors – all from UNC – are Silvia M Goicoechea, Ph.D., research instructor, and Hannah Prentice-Dunn, undergraduate student, both of the department of cell and molecular physiology; Brian Bednarski M.D., assistant professor of surgery; and Rafael García-Mata, Ph.D., research assistant professor in the department of cell and developmental biology.

The work was funded by the National Institutes of Health.

Understanding Brain Tumor Growth Through Applying Weather Forecasting Technology

students from St. Joseph's Hospital and Medical Center and Arizona State University's Math Department are applying weather forecast technology to model and track the growth patterns of brain tumors.

The technology allows researchers to study various growth patterns of brain tumors and apply treatment parameters to determine the best option for patients. It will forecast how a patient's tumor may grow with different treatment scenarios, help physicians make a much more informed prognosis and be used as a patient consulting tool.

The research study began when Barrow and ASU researchers Mark Preul, Yang Kuang and Eric Kostelich used data from a collection of normal brain images to create a life-like recreation of the brain. They positioned a virtual tumor in the brain image and applied intricate math formulas used in weather forecast technology to predict how the tumor would grow.

Once the virtual tumor began to grow, the researchers determined a way to resect part of the tumor and gave it the effects of radiation and chemotherapy to see how the tumor would respond. A patient study was eventually used to compare the tumor growth and outcome between the patient and virtual model. They closely matched.

"This study has resulted in the most accurate and life-like recreation of the growth of malignant brain tumors," says Mark Preul, MD, Newsome Chair of Neurosurgery Research. "The technology used in the study could pave the way for better treatment plans enabling a greater outcome for patients,"

The study will be published in Cell Proliferation and is the basis for a National Science Foundation grant submission. The Barrow Neurological Foundation funded the initial study.