Gene therapy target tumor blood vessels.

Working with mice, St. Louis （ Alvin j. Siteman Cancer Center home) of long gene delivery method is required in the field of gene therapy, Washington University School of Medicine researchers reported development: carry a gene of interest can be deactivated virus to inject into the blood stream, making its way to the cell the. You can target the tumor blood vessels in mice without affecting healthy tissue they are scientists in this early concept study, shows.

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Personalized for the most deadly type of brain tumor vaccine shows promise

History showed itself from the patients with treatment of patients with recurrent glioblastoma made an experimental vaccine (GBM) resection tumor survival rates improve, alone, received the standard care patients compared to this vaccine has been published in the journal of neuro-oncology, accompanied by an editorial to emphasize the importance of the trial phase 2 according to the analysis of the test. Phase 2 trials, Northwestern Feinberg School and the Robert H. Lurie Comprehensive Cancer Center enrolled 41 conducted by adult recurrent tumor cases 2007-2011, from the researchers.

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Change elevated circulating tumor cell metastasis BC before patients not beneficial chemotherapy.

Women with metastatic breast cancer, after first line chemotherapy in the amount of their blood circulating tumor cell (Ctc) were higher in the immediately switch to another chemotherapy did not improve overall survival or phase III clinical trials, 2013 at the San Antonio Breast Cancer Symposium University of Michigan comprehensive cancer time to progress, according to results announced by researchers in the Center, held 10-14 December.

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Scientists find 'missing link' in important tumor suppression mechanism

Nov. 12, 2013 — RUNX3, a gene that is intensively studied for its function as a tumor suppressor, is likely to be a key and critical component of the body's first line of defense against lung cancer development, according to a recent study by scientists from the Cancer Science Institute of Singapore (CSI Singapore) at the National University of Singapore (NUS), together with their collaborators from Chungbuk National University in Korea.

The team, led by Professor Yoshiaki Ito of CSI Singapore, showed that RUNX3 is a major component in a well-established tumor suppression mechanism involving p53, a tumor suppressor protein that regulates cell proliferation and prevent cancer. In addition, the research team also demonstrated that RUNX3 plays a pivotal role in preventing early tumor formation.

Although the current study focused on lung cancer, the results help to explain the development of other types of human cancers.

These novel findings were published in leading scientific journal Cancer Cell on 11 November 2013.

Implications on early cancer detection and prevention

Mutations of the p53 gene occur in 50 per cent of virtually all cancer types, indicating that p53 inactivation constitutes one of the main drivers of cancer development. p53 has since been shown to exert multiple effects -- be it enhancing DNA repair, arresting cell proliferation or promoting cell death -- to inhibit cancer growth.

"This study uncovered an important missing component of the tumor suppressor pathway that regulates p53 function. The identification of RUNX3 as the key component throws light on why RUNX3 gene inactivation, particularly via epigenetic mechanisms, is so prevalent in cancer," Prof Ito explained.

"From a clinical viewpoint, this finding has applications in early cancer detection and prevention. Cancer-specific epigenetic inactivation of RUNX3 is marked by DNA methylation, which can be readily screened for early detection or prognosis of a wide variety of cancer. It also suggests the exciting possibility that RUNX3 inactivation, if reversed by therapeutic means, may restrain cancer growth. It is therefore likely that many new approaches of cancer treatment or prevention will be generated," he added.

Role of RUNX3 in suppressing tumor formation

Lung cancer is the most frequently occurring cancer worldwide, and it is also the No. 1 killer cancer for both men and women in Asia-Pacific and Singapore. The prevalent type of lung cancer, called adenocarcinoma, is frequently observed to harbour genetic alterations in the oncogene K-Ras.

In normal cells, K-Ras is activated by a short-lived signal to promote cell growth and then rapidly deactivated. However, in lung cancer, a mutated version of K-Ras gene -- K-Ras^G12D -- is expressed. Instead of responding to the growth signal, the mutant K-Ras^G12D constantly stimulates cell growth, causing the uncontrolled and rapid growth of the cancer cells. Confronted with the activation of such oncogenes, normal cells would turn on tumor suppressor pathways to stop cell growth or kill abnormal cells.

Currently, the best studied tumor suppressor is p53, which is frequently inactivated in various human cancers. The activity of p53 is tightly regulated by a gene called MDM2 (which acts to limit the p53 growth-suppressive function) and its inhibitor p14^ARF. While scientists have found that p14^ARF inhibits MDM2 and thus promotes p53 activity, it is unclear how p14^ARF is induced.

To fill this gap in knowledge, the research team studied the molecular mechanism underlying K-Ras-induced lung adenocarcinoma. They found that p14^ARF is induced by the RUNX3 in collaboration with another protein called BRD2, in response to K-Ras^G12D. This suggests that RUNX3 is one of the major components of the well-established tumor suppressor pathway involving p53.

The discovery of the link between RUNX3 and BRD2 will also initiate new directions in studies on complex mechanisms that regulate gene expression, the impairment of which is often associated with cancer development.

RUNX3 as first line of defense against cancer formation

Another important breakthrough achieved by Prof Ito and the team was the discovery of different roles of RUNX3 and p53 in tumor suppression.

Since 2010, it has been known that while p53 can effectively destroy well-developed cancer cells, but it cannot respond to low levels of oncogenic stimuli and prevent the early stages of cancer development.

The research team showed that the sole inactivation of RUNX3 results in the rapid development of pre-cancerous adenoma (a benign tumor that may become malignant over time) in less than four months. On the other hand, inactivation of p53 alone has not been shown to induce adenoma. By showing that RUNX3 prevents adenoma formation, the team contributes to a better understanding of an important aspect of tumor suppression mechanism.

Commenting on the findings, Prof Ito said, "It is very likely that our body is protected by two lines of defense mechanisms against lung cancer development -- RUNX3 forms the first line which protects against adenoma formation while p53 forms the second line in protecting against adenocarcinoma formation. It will be important to examine whether other types of cancer also show two lines of defense mechanisms, since p53 is frequently inactivated in various cancer types."

The next step

p53 is often mutated and it is practically impossible to revert this mutation for the purpose of treatment. By contrast, RUNX3 is inactivated by DNA methylation (ie. epigenetic inactivation), a chemical event that silences the gene without altering its coding information.

"Clinical trials have shown that reactivation of epigenetically inactivated genes is feasible. Indeed, RUNX3 gene can be reactivated by chemicals in cancer cells in laboratory. Therefore, the team's immediate task is to find a way to effectively re-ignite RUNX3 gene activity. Since RUNX3 functions at early stages of cancer, reversal of RUNX3 inactivation could halt cancer development by timely prevention of permanent neoplastic changes," said Prof Ito.

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May predict response to Imaging Research anti new crude tumor

Advanced image processing technology for patients with tumor responds to angiogenesis drug therapy, able to distinguish which one might be. Patient's brain tumor glioma risk, Massachusetts General Hospital (Dana Farber Cancer Institute component) of researchers report, for those whose treatment anti angiogenesis drug cediranib and rapidly of their tumors around of abnormal blood vessels that "normalize" and who cediranib did not increase blood flow of patients significantly the longer survival tumor in a blood flow increases and newly diagnosed. Displays the report in PNAS Early Edition.

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To determine risk of Microbiology tumor in the intestines

University of Michigan published mBio prone to these mouse intestinal bacteria are transferred from the mouse with the germ-free mice Colorectal tumor （ University of Michigan Comprehensive Cancer Center home ） getting tumors as well, according to results of a study from R, online open access journal of the American Society of microbiology. Indicate the microbiological components there is a risk for human health implications colorectal cancer work.

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Pan-cancer studies find common patterns shared by different tumor types

Sep. 26, 2013 — Cancer encompasses a complex group of diseases traditionally defined by where in the body it originates, as in lung cancer or colon cancer. This framework for studying and treating cancer has made sense for generations, but molecular analysis now shows that cancers of different organs have many shared features, while cancers from the same organ or tissue are often quite distinct.

The Pan-Cancer Initiative, a major effort to analyze the molecular aberrations in cancer cells across a range of tumor types, has yielded an abundance of new findings reported in 18 forthcoming papers, including four published in the October issue of Nature Genetics. The initiative, launched in October 2012 at a meeting in Santa Cruz, California, is part of the Cancer Genome Atlas (TCGA) project led by the National Cancer Institute and the National Human Genome Research Institute.

Josh Stuart, professor of biomolecular engineering at the University of California, Santa Cruz, helped organize the Pan-Cancer Initiative and is lead author of a commentary in Nature Genetics giving an overview of the project and its initial findings.

"For years we've been looking at one tumor type at a time, but there are patterns you can only spot by making connections across different tissues and tumor types. Finding these similarities across tissues can have important implications for treatment," Stuart said.

For example, some types of bladder cancer look very similar to certain lung and head-and-neck cancers, and recognizing those similarities may open up new therapeutic options. "This could allow oncologists to apply all they know about treating head-and-neck squamous cell tumors to the ten percent of bladder cancers that have the same characteristics," Stuart said.

TCGA is generating comprehensive maps of the key genomic changes in major types and subtypes of cancer, eventually covering at least 20 different cancer types. TCGA researchers are profiling thousands of tumors to discover molecular aberrations at the DNA, RNA, protein, and epigenetic levels. The Pan-Cancer Initiative has done comparative analyses of the first 12 tumor types profiled by TCGA.

The analyses show that the tissue of origin is an important factor, producing a dominant signal that groups tumors mostly according to their tissue of origin. But the data also reveal a number of interesting signals that cut across tumor types and suggest new ways of categorizing tumors, Stuart said. In addition, the statistical power gained by combining all of the data available from different tumor types has enabled researchers to see new patterns of genomic aberrations.

"In ovarian cancer, for example, we were able to identify mutations that correlate with the response to treatment, but only by using data from other types of cancer," Stuart said.

A persistent problem in cancer genomics has been distinguishing "driver" mutations from "passenger" mutations. Cancer cells often accumulate large numbers of genetic mutations that do not play a role in driving the uncontrolled cell growth that is a hallmark of cancer. These passenger mutations greatly complicate efforts to identify the genomic drivers of cancer. Aggregating data from the 12 tumor types gave Pan-Cancer researchers enough statistical power to see patterns that weren't apparent before. One of the forthcoming papers identifies with high confidence many new genomic drivers of cancer, Stuart said.

The Pan-Cancer analyses have also revealed the importance of new classes of mutations, such as those that affect how a cell's DNA is packaged in the chromosomes. As cells differentiate into specialized cell types during an organism's development, some genes are turned off and others are turned on depending on how the DNA is packaged together with specialized proteins to make "chromatin." Genomic changes (gene amplification, deletion or mutation) affecting genes that control the packaging of DNA can disrupt this key regulatory mechanism. One of the Nature Genetics papers (Zack et al.) analyzed amplifications and deletions and found 104 novel regions that had not been associated with cancer previously, and these regions contain a rich supply of genes involved in "epigenetic" modifications of chromatin.

"There are so many different ways to mess up the packaging of DNA that the mutations look random in any one tumor type, but now we have enough data to see that chromatin remodeling is a big factor in a lot of these tumors," Stuart said.

Stuart played a central role in creating the organizational framework that made the Pan-Cancer analyses possible. The project started as an informal collaboration among members of the TCGA research network, but then quickly expanded to include many other interested researchers. Coordinating all these efforts was a major task. Stuart worked with the bioinformatics company Sage Bionetworks to create a data repository called Synapse for the project. To ensure that everyone was working from the same data set, a data "freeze" was established in December 2012. But Stuart realized that many important analyses would depend on the results of other analyses carried out by different research groups.

"The interdependencies are so complicated that everybody had to abide by a schedule in order to play the game," Stuart said. "The system worked really well, and the project has ballooned because there are so many interesting things to look at. We have 18 papers coming out in this first release, and there are 60 more Pan-Cancer papers coming that I'm currently tracking."

The Synapse system created by Sage Bionetworks is described in one of the Nature Genetics papers (Omberg et al.). "This beautifully organized data repository is now available for scientists around the world to use to go beyond these initial analyses and discover even more about cancer," Stuart said.

Researchers will continue to use the framework and procedures Stuart established as they integrate new tumor types and new data from TCGA, as well as data from other cancer genomics projects. Stuart has just been named, along with Gad Getz of the Broad Institute of MIT and Harvard, to lead an international pan-cancer initiative that will combine TCGA data with data from other cancer genomics efforts around the world.

The hope is that these cross-tumor investigations will lead to new and improved cancer treatments. One goal is to identify biomarkers that can be used across a range of tumor types to indicate which therapies are likely to be most effective. The results of these studies may also point toward targets for novel therapeutic agents that can be tested clinically.

"These initial papers are just the first step, and we expect much more to come from the Pan-Cancer Initiative," Stuart said. "With the infrastructure now in place, we can scale up to look at more types of data, especially whole genome sequencing data, and to include many more tumor types, including rare tumors."

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Human brain tumor cells erased in mice

Sep. 23, 2013 — Working with mice, Johns Hopkins researchers have discovered that weeks of treatment with a repurposed FDA-approved drug halted the growth of -- and ultimately left no detectable trace of -- brain tumor cells taken from adult human patients.

The scientists targeted a mutation in the IDH1 gene first identified in human brain tumors called gliomas by a team of Johns Hopkins cancer researchers in 2008. This mutation was found in 70 to 80 percent of lower-grade and progressive forms of the brain cancer. The change occurs within a single spot along a string of thousands of genetic coding letters, and is disruptive enough to keep the seemingly innocuous protein from playing its role in converting glucose into energy. Instead, the mutation hijacks the protein to make a new molecule not normally found in the cell, which is apparently a linchpin in the process of forming and maintaining cancer cells.

Encouraged by the new findings, described online Sept. 16 in the open-access journal Oncotarget, the Johns Hopkins researchers say they want to work quickly to design a clinical trial to bring what they learned in mice to humans with gliomas. Despite the growing understanding of IDH1 mutant gliomas, the development of effective therapies has proven challenging, they say.

"Usually in the lab, we're happy to see a drug slow down tumor growth," says Alexandra Borodovsky, a graduate student in the Cellular and Molecular Medicine Program at the Johns Hopkins University School of Medicine who performed the experiments. "We never expect tumors to regress, but that is exactly what happened here."

"This therapy has worked amazingly well in these mice," says study leader Gregory J. Riggins, M.D., Ph.D., a professor of neurosurgery and oncology at the Johns Hopkins University School of Medicine. "We have spoken with neurosurgeons here, and as soon as possible, we want to start discussing the parameters of a clinical trial to see if this will work in our patients as a follow-up to surgery."

The researchers caution that many treatments have cured cancers in mice, and then failed in humans.

The IDH1 gene, whose name stands for isocitrate dehydrogenase 1, produces an enzyme that regulates cell metabolism. Mutations, or changes in the DNA code, force the IDH1 gene to increase production of a flawed version of the enzyme. The flawed enzyme produces large amounts of an entirely new molecule, called 2-hydroxyglutarate. This molecule is believed to cause groups of atoms called methyl groups to latch onto the DNA strand.

Although methylation is a normal cellular process, when too many methyl groups glom onto the DNA, Riggins says, this can interfere with normal cell biology and eventually contribute to cancer formation and growth.

Borodovsky, Riggins and their colleagues -- including Timothy A. Chan, M.D., Ph.D., of Memorial Sloan-Kettering Cancer Center in New York -- thought that a drug that could strip those methyl groups might be able to reverse the cancer process in those cancers with IDH1 mutations. They chose 5-azacytidine, which is approved to treat a pre-leukemia condition called myelodysplastic syndrome and is being tested on lung and other cancers at Johns Hopkins and elsewhere.

Riggins notes that one of the difficulties in developing treatments for IDH1 mutant brain cancers is finding a model in which to study them. Cell lines containing the IDH1 mutation are difficult to grow in the laboratory, for example. Borodovsky worked with Johns Hopkins neurosurgeons to obtain tumor cells from glioma patients likely to have IDH1 mutations and injected them under the skins of mice. She did this for months, before finally getting the tumor cells to grow.

Once the tumors grew, the researchers injected the mice with 5-azacytidine for 14 weeks and saw a dramatic reduction in growth and what appeared to be complete regression. Then they withdrew therapy. Seven weeks later, the tumors had not regrown. The researchers, however, said they do expect the tumors to regrow at some point, and are still monitoring the mice.

The type of tumor targeted by the researchers eventually progresses to a subtype of glioblastoma multiform -- the deadliest form of brain cancer -- known as progressive or secondary glioblastoma. They arise as a lower-grade glioma and are initially treated with surgery alone, but eventually they progress to the more lethal form of tumor. Survival is longer than with glioblastoma, but it is found in younger patients, those under the age of 50. While both types of tumor look the same at the end, they look very different at the molecular level, Riggins says, leading researchers to believe they may have a better chance at targeting the progressive tumors, which are more likely to have the IDH1 mutation.

Chan's team at Sloan-Kettering simultaneously published a paper in Oncotarget, along with Borodovsky and Riggins, which describes similar results in a different animal model using a similar drug. This is further evidence that the strategy is a sound one, Riggins says.

Other Johns Hopkins researchers involved in the Borodovsky paper include Charles G. Eberhart, M.D., Ph.D.; Jon D. Weingart, M.D.; Gary L. Gallia, M.D., Ph.D.; and Stephen B. Baylin, M.D.

The work was supported by the Conrad N. Hilton Foundation, the Virginia and D.K. Ludwig Fund for Cancer Research, Margaret H. Riggins, and the Irving J. Sherman Research Professorship in Neurosurgery. Funding also came from grants from the National Institutes of Health's National Cancer Institute (P30 CA006973) and the National Center for Research Resources (UL1 RR025005 and 1S10RR026824-01).

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Proton therapy is cost effective for patients with pediatric brain tumor treatment.

Research affecting mainly children when healthy organs and tissues, spare the Proton line treatment cost effectiveness, external beam radiation therapy were compared with spinal cord and a standard photon radiation therapy, providing accurate tumor dose Proton, announced that the fast-growing brain tumor treatments in the 55 annual general meeting of the American Society of radiation therapy (Astro Boy) by researchers from the Mount Auburn hospital, according to Harvard Medical School (Dana Farber Cancer Institute component) of is a teaching hospital.

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Researchers identify switch that controls growth of most aggressive brain tumor cells

Sep. 20, 2013 — Researchers at UT Southwestern Medical Center have identified a cellular switch that potentially can be turned off and on to slow down, and eventually inhibit the growth of the most commonly diagnosed and aggressive malignant brain tumor.

Findings of their investigation show that the protein RIP1 acts as a mediator of brain tumor cell survival, either protecting or destroying cells. Researchers believe that the protein, found in most glioblastomas, can be targeted to develop a drug treatment for these highly malignant brain tumors. The study was published online Aug. 22 in Cell Reports.

"Our study identifies a new mechanism involving RIP1that regulates cell division and death in glioblastomas," said senior author Dr. Amyn Habib, associate professor of neurology and neurotherapeutics at UT Southwestern, and staff neurologist at VA North Texas Health Care System. "For individuals with glioblastomas, this finding identified a target for the development of a drug treatment option that currently does not exist."

In the study, researchers used animal models to examine the interactions of the cell receptor EGFRvIII and RIP1. Both are used to activate NFκB, a family of proteins that is important to the growth of cancerous tumor cells. When RIP1 is switched off in the experimental model, NFκB and the signaling that promotes tumor growth is also inhibited. Furthermore, the findings show that RIP1 can be activated to divert cancer cells into a death mode so that they self-destruct.

According to the American Cancer Society, about 30 percent of brain tumors are gliomas, a fast-growing, treatment-resistant type of tumor that includes glioblastomas, astrocytomas, oligodendrogliomas, and ependymomas. In many cases, survival is tied to novel clinical trial treatments and research that will lead to drug development.

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First randomized trial of targeted cancer medicine in all tumor types

Sep. 11, 2013 — A further step along the road to the personalisation of cancer medicine, where treatment is based on the individual molecular characteristics of tumours rather than their primary site, will be presented at the 2013 European Cancer Congress (ECC2013), which starts on Friday 27 September in Amsterdam, The Netherlands.

Dr Christophe Le Tourneau, Head of the Phase I Programme at the Institut Curie, Paris, France, will tell the congress that the SHIVA trial is the first randomised trial to look at patient outcomes after treatments were chosen according to the individual molecular profiles of each person's tumour. It is also the first trial to do this for all tumour types. About 40% of all those taking part in the trial have molecular abnormalities that can be targeted by existing drugs, he will say.

To date, 320 patients from seven comprehensive cancer centres across France have been included in this phase II trial, of whom 60 have been randomised. In the standard arm, the patients received the chemotherapy they would have received if they had not been participating in the trial. All patients had recurrent or metastatic cancer that was unresponsive to standard treatment for their disease.

"Our goal is to have 200 randomised patients," says Dr Le Tourneau. "Although 40% of the 320 patients have a tumour for which targeted drugs are available, some are still on the chemotherapy that was started at the time of the biopsy and therefore we will have to randomise them later. Because we are looking for an effect in different kinds of tumours, we have ruled out the inclusion of any particular type of tumour if this brings the number of randomised patients with this type to over 20% of the total. We have also allowed the inclusion of patients with rare tumours."

Preliminary results of the feasibility study, to be presented at the congress, show that this approach works, the researchers say. The ultimate goal of the phase II trial is to see whether the selection of drugs that target the specific molecular profiles of tumours will improve outcomes for patients.

Once the first 100 patients were included, the researchers looked at the feasibility of a biopsy of a metastasis, since the molecular profile of the primary tumour, if tissue is available, may not be the same as that found in a metastasis. They also investigated the quality of available tumour samples, the proportion of the patients for which the necessary analyses could be undertaken, the proportion for which a molecular abnormality can be identified and for which a targeted therapy exists, and the timeframe needed to establish the tumour profile.

"Recent advances in diagnostics have enabled us to ascertain the molecular profile of tumours in a timeframe which is compatible with good clinical care, but we needed to verify this in our study," says Dr Le Tourneau.

Unlike conventional chemotherapy, molecular targeted agents only work in the presence of their targets. Side-effects are lessened and, in principle, efficacy heightened. One of the problems to date, however, is that such drugs have principally been developed based on the primary location and histology (cellular make-up) of the tumour. This has meant that many potentially promising targeted drugs have failed in early clinical trials simply because they have not induced a response in a sufficient number of patients.

"The history of breast cancer changed beyond recognition with the discovery of the role played by the ErB2/HER2 gene, which is amplified in up to 20% of breast cancers. And we now know that trastuzumab (Herceptin), one of the most widely-used targeted cancer therapies, which targets that gene, is effective in several tumour types and not just in breast when the ERBB2/HER2 gene is amplified or even mutated," says Dr Le Tourneau. "We also know that patient outcomes in the few trials to date where the choice of treatment is based on a molecular abnormality are better than those where the treatment is not matched to the abnormality. What was missing to date is a histology-independent randomised trial comparing molecular targeted treatment with conventional therapy, and this is why I decided to set up the SHIVA trial."

Even today, the researchers say, molecularly targeted therapy for cancer patients is initially prescribed according to the location of the primary tumour. At the end of the trial, analysis of progression-free survival will show whether this practice needs to be changed.

A positive finding would imply the need to make major changes in the way cancer drugs are developed and tested in patients. But this would represent a new and difficult challenge.

"At present we have no data on the efficacy of drugs in patients with the same molecular abnormality but different tumour types, and we also suspect that a treatment effect would not depend on the presence of a single molecular abnormality, but, more likely, on several. However, we believe that it is most likely that, in future, tumour location and histology will no longer be the primary criteria for the prescription of molecularly targeted agents; rather, tumour biology will be the deciding factor," says Dr Le Tourneau. "A positive result from our trial would be an important step forward on the road to personalised medicine."

Professor Cornelis van de Velde, President of ECCO, said: "This ground-breaking randomised trial is very exciting since this is the way to individualise therapy. We have already moved from empirical to stratified treatment, and now we can offer patients personalised treatment based on the understanding of the particular molecular profiles of their tumours in order to select drugs that target a specific profile. The means to determine the individual molecular profiles of tumours will be readily available at low cost in the years to come, and the integration of biopsy-based molecular profiles with individual patient characteristics will enable precision diagnosis to be translated into precision personalised therapies. ECCO will have an important role to play in ensuring the incorporation of molecular biology genetics into clinical multidisciplinary meetings."

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Widemann honored by Children’s Tumor Foundation

June 25, 2013, 3:12PM

By Richard Folkers

Posted in: Childhood cancer | cancer

Tags: award, Neurofibromatosis, tumor

Brigitte Widemann, M.D., is flanked by Annette Bakker, chief scientific officer of the Children’s Tumor Foundation, and Kevin Shannon, M.D., from the University of California, San Francisco, after receiving the von Recklinghausen Award at the June 2013 CTF Neurofibromatosis Conference in Monterey, Calif.

Neurofibromatosis type 1, or NF1, is a genetic disorder that usually manifests itself during childhood with a variety of skin conditions and the development of tumors of the peripheral and central nervous system. Although it is not generally considered a fatal condition, people with NF1 can develop tumors called plexiform neurofibromas, which cause substantial morbidity. Those tumors can also become aggressive cancers called malignant peripheral nerve sheath tumors. In addition, NF1 can manifest in every organ system and cause learning problems, high blood pressure, and curvature of the spine. There is currently no cure, although surgery is an option for tumors and some other conditions caused by NF1.

At its Neurofibromatosis Conference in June 2013, the Children’s Tumor Foundation honored NCI’s Brigitte Widemann, M.D., with its von Recklinghausen Award, in recognition of her contributions to neurofibromatosis research and treatment. Widemann, who has been with NCI since 1992, heads the Pharmacology and Experimental Therapeutics Section in the Pediatric Oncology Branch of the Center for Cancer Research. Her contributions include the development of both novel methods of imaging of NF1 tumors and meaningful trial designs and endpoints for NF1 related tumors. In addition, she has built an active clinical trials program of targeted agents for NF1 at the NCI.

The award is named for Friedrich von Recklinghausen, a 19th century German pathologist, who characterized the tumors of NF1, which is still sometimes referred to as “von Recklinghausen syndrome.”

First awarded in 1984, past recipients of the award include NCI Director Francis Collins, M.D., Ph.D., and more recently Nancy Ratner, Ph.D, from Cincinnati Children’s Hospital, and David Gutmann M.D., Ph.D., from the Washington University in St. Louis Alvin J. Siteman Cancer Center.

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New laser-based tool could dramatically improve the accuracy of brain tumor surgery

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A new laser-based technology may make brain tumor surgery much more accurate, allowing surgeons to tell cancer tissue from normal brain at the microscopic level while they are operating, and avoid leaving behind cells that could spawn a new tumor. In a new paper, featured on the cover of the journal Science Translational Medicine, a team of scientists from the University of Michigan Medical School (home of the University of Michigan Comprehensive Cancer Center) and Harvard University (a component of the Dana-Farber Cancer Institute) researchers describes how the technique allows them to “see” the tiniest areas of tumor cells in brain tissue.

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Among the research institutions NCI funds across the United States, it currently designates 68 as Cancer Centers. Largely based in research universities, these facilities are home to many of the NCI-supported scientists who conduct a wide range of intense, laboratory research into cancer’s origins and development. The Cancer Centers Program also focuses on trans-disciplinary research, including population science and clinical research. The centers’ research results are often at the forefront of studies in the cancer field.

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