Agent orange chemical, dioxin, attacks the mitochondria to cause cancer, says Penn research team

Contact: Jordan Reese
jreese@upenn.edu
215-573-6604
University of Pennsylvania

PHILADELPHIA— Researchers with the University of Pennsylvania School of Veterinary Medicine have demonstrated the process by which the cancer-causing chemical dioxin attacks the cellular machinery, disrupts normal cellular function and ultimately promotes tumor progression.

The team identified for the first time that mitochondria, the cellular sub-units that convert oxygen and nutrients into cellular fuel, are the target of tetrachlorodibenzodioxin, or TCDD. The study showed that TCDD induces mitochondria-to-nucleus stress signaling, which in turn induces the expression of cell nucleus genes associated with tumor promotion and metastasis.

The mechanism the research team has described is directly relevant to understanding incidences of breast and other cancers in human populations exposed to these chemicals. With a better understanding of this underlying cellular mechanism, researchers hope to improve their understanding of tumor growth and promotion.

“Now that we have identified this signaling mechanism we can look at ways to disrupt this complex chain of events,” said Narayah Avadhani, chair of the Department of Animal Biology at Penn’s School of Veterinary Medicine and the study’s lead investigator. “Our ultimate goal is to block the propagation of this mitochondrial stress signaling and inhibit the expression of the proteins that combine to assist cancer growth.”

A well-characterized mechanism of TCDD action occurs through activation of arylhydrocarbon receptors, AhR, by directly binding to the protein subunits. Activated AhR mediates the transcriptional activation of many genes including those involved in fatty acid metabolism, cell cycle regulation and immune response. The present study, however, shows that TCDD starts the chain of events that promote tumor progression in vivo by directly targeting mitochondrial transcription and induction of mitochondrial stress signaling. A unique feature of this TCDD-induced signaling is that it does not involve the action of AhR but occurs through increased calcium levels in cells and activation of calcium responsive factors. A net result of signaling cascade is slowing down of cellular apoptosis, increased cell proliferation and tumor cell metastasis. Taken together, this study describes a novel mechanism of TCDD-induced tumor progression and emergence of metastatic cancer cells.

TCDD is the most toxic compound in the dioxin family. Formed as a by-product during waste incineration, paper, chemical and pesticide manufacturing, it was the toxic ingredient in Agent Orange and closed the Love Canal in Niagara Falls. The public health impact of dioxin, according to the Environmental Protection Agency, compares to that of the pesticide DDT.

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The study appears online and in the Dec. 17 issue of the Proceedings of the National Academy of Sciences and was performed by Avadhani, Gopa Biswas, Satish Srinivasan and Hindupur Anandatheerthavarada of the Penn School of Veterinary Medicine.

The research was supported by a grant from the National Cancer Institute and the National Institutes of Health.

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ESF EURYI award winner aims to stop cancer cells reading their own DNA

A promising new line in anti-cancer therapy by blocking the molecular motors involved in copying genetic information during cell division is being pursued by young Dutch researcher Dr. Nynke Dekker in one of this year’s EURYI award winning projects sponsored by the European Science Foundation (ESF) and the European Heads of Research Councils (EuroHORCS). Dekker and her team are trying to stop tumor development by interfering with the molecular motors that copy DNA during cell division. This will cut off the genetic information flow that tumours need to grow, and could complement existing cancer therapies, while in the longer term bringing the promise of improved outcomes with greatly reduced side effects.

There are three primary ways of treating cancer at present, and these have fundamentally changed little in 30 years. In the case of solid tumours, surgery can be used to cut out the cancerous tissue, while radiation therapy can kill the malignant cells, and chemotherapy stops them dividing. Dekker’s work is aiming towards a new generation of drugs that target cancer cells much more specifically than traditional chemotherapy, avoiding side effects such as temporary hair loss.

Dekker is focusing on an enzyme called Topoisomerase IB that plays a key role in some of the molecular motors involved in the processes of DNA and RNA copying during cell division. These are responsible for reading the genetic code and making sure it is encoded correctly in the daughter cell. In healthy cells it is important that this process works normally, but in cancer cells it is a natural target for disruptive therapy. “Specifically targeting these molecular motors in cancer cells would then prevent the cancer cells from growing into a larger tumor,” said Dekker. This molecular copying machinery, constructed mostly out of proteins, in effect walks along the DNA double helix reading the genetic code so that it can be copied accurately into new DNA during division. Other components of the machinery are responsible for slicing and assembling the DNA itself. All of these are potential targets for anti-cancer therapy, providing it is possible to single out the tumor cells. Most existing chemotherapy targets all dividing cells, and the aim to find more sensitive techniques.

However Dekker’s work is not just confined to cancer, having the broader goal within the ESF EURYI project of unraveling the underlying physical principles behind these molecular motors that operate at the nanometer scale to process and manipulate the information stored within the DNA and RNA of our cells. Dekker is exploiting a variety of new highly sensitive manipulation and imaging techniques capable of resolving single molecules. These include force spectroscopy, new forms of optical microscopy with greatly improved resolving power and field depth, as well as nanotechnologies. The research involves cross-disciplinary work among scientists in different fields with the long term goal of developing more precisely targeted molecular medicines for a variety of diseases involving disruption to normal cellular functions and not just cancer.

Dekker’s work has already shown great promise, and she has been able to predict what effect certain antitumor drugs would have on the basis of her molecular insights, confirming her hypotheses in yeast cells. “Indeed the work with antitumor drugs is, as far as I know, the first experiment in which single-molecule experiments have resulted in a prediction for a cellular effect,” said Dekker.

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Dekker, a 36-year-old Dutch associate professor at the Technische Universiteit Delft in the Netherlands, is currently undertaking single-molecule studies of DNA and RNA and their interactions with proteins, integrated with nanotechnology where appropriate. She gained her PhD in physics at Harvard University, having graduated from Yale.

As well as being awarded multiple grants and fellowship programmes, Dr. Dekker is a member of the Council of the Biophysical Society, and of the Young Academy of the Royal Academy of Arts and Sciences. She is actively involved in conference organization at the interface of biology and physics. Her group’s research has appeared in Nature and in The Proceedings of the National Academy, USA, among others.

The EURYI awards scheme, entering its fourth and final year, is designed to attract outstanding young scientists from around the world to create their own research teams at European research centres and launch potential world-leading research careers. Most awards are between €1,000,000 and €1,250,000, comparable in size to the Nobel Prize. Dekker will receive his award in Helsinki, Finland on 27 September 2007 with other 19 young researchers.

More on Dekker’s work http://www.esf.org/activities/euryi/awards/2007/nynke-hester-dekker.html

More on EURYI: http://www.esf.org/ext-ceo-news-singleview/article/2007-euryi-20-young-researchers-to-receive-nobel-prize-sized-awards-for-breakthrough-ideas-294.html

Contact: Thomas Lau
tlau@esf.org
33-388-762-158
European Science Foundation

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Multicenter study nets new lung tumor-suppressor gene

BOSTON–Collaborating scientists in Boston and North Carolina have found that a particular gene can block key steps of the lung cancer process in mice. The researchers report in the journal Nature that LKB1 is not only a “tumor-suppressor” gene for non-small cell lung cancer in mice, it also may be more powerful than other, better-known suppressors. The study will be published on the journal’s Web site on Aug. 5 and later in a print version.

If further research shows LKB1 has a similar effect in human lung cells, it could influence the way non-small cell lung cancer is diagnosed and treated, says the study’s senior author, Kwok-Kin Wong, MD, PhD, of Dana-Farber, one of three institutions, along with Massachusetts General Hospital and the University of North Carolina School of Medicine, leading the work. If tumors with LKB1 mutations are found to be especially fast-growing, for example, patients with such tumors might be candidates for more aggressive therapy.

People born with defective versions of LKB1 often develop Peutz-Jeghers syndrome, which is marked by intestinal growths and an increased risk for certain cancers. Non-inherited mutations of the gene have been found in some lung cancers. This suggested that LKB1 normally thwarts tumors from forming. Mutated versions may be unable to act as a brake on cancer.

To find out, the investigators ran a series of experiments in mice with a defective form of a gene called Kras, which drives the formation and growth of lung cancer. They tracked the development of lung cancer in animals with mutated LKB1 and compared it to the experience of animals with abnormalities in either of two well-known tumor-suppressor genes.

They found that while Kras “cooperated” with the mutated tumor-suppressor genes to produce lung cancer, it cooperated even more strongly with mutated LKB1. “The LKB1-deficient tumors grew more rapidly and spread more frequently than the others, and comprised all three types of non-small cell lung cancer — squamous cell carcinoma, large-cell carcinoma, and adenocarcinoma — rather than just one or two,” Wong says. “This suggests that LKB1 plays a role at major stages of the tumors’ development: initiation, differentiation of normal lung cells into cancer cells, and metastasis.”

An examination of human non-small-cell lung tissue suggests LKB1 mutations play a role there as well. Of 144 samples analyzed, 34 percent of the lung adenocarcinomas and 19 percent of the squamous cell carcinomas contained abnormal versions of the gene, researchers report.

“We were surprised at how significant a role LKB1 mutations play in non-small cell lung cancer development in mice,” say Wong, who is also an assistant professor of medicine at Harvard Medical School. “This suggests there may be additional lung tumor-suppressor genes yet to be discovered. We’re currently examining whether these results apply to human lung cancers as well and, if so, how such information can improve treatment.”

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The lead author of the study was Hongbin Ji, PhD, of Dana-Farber. Other Dana-Farber co-authors include Dongpo Cai, PhD, Liang Chen, PhD, Pasi Janne, MD, PhD, Bruce Johnson, MD, Jussi Koivunen, MD, PhD, Danan Li, Mei-Chih Liang, PhD, Kate McNamara, Matthew Meyerson, MD, PhD, Samanthi Perera, PhD, Geoffrey Shapiro, MD, PhD, and Takeshi Shimamura, PhD. Other authors were based at Children’s Hospital Boston, Brigham and Women’s Hospital, Broad Institute of Harvard University and Massachusetts Institute of Technology, University of Tennessee Health Science Center, and the University of Texas Southwestern Medical Center.

The research was supported by the National Institutes of Health, the Sidney Kimmel Foundation for Cancer Research, the American Federation of Aging, the Joan Scarangello Foundation to Conquer Lung Cancer, the Flight Attendant Medical Research Institute, the Waxman Foundation, the Harvard Stem Cell Institute, and the Linda Verville Foundation.

Dana-Farber Cancer Institute (www.dana-farber.org) is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute.

Contact: Bill Schaller
william_schaller@dfci.harvard.edu
617-632-5357
Dana-Farber Cancer Institute

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U-M researchers find family of ‘on switches’ that cause prostate cancer

Gene fusions trigger cancer growth, could impact treatment choices

ANN ARBOR, Mich. — Researchers at the University of Michigan Comprehensive Cancer Center have discovered how genes turn on the switch that leads to prostate cancer.

The team discovered that pieces of two chromosomes can trade places with each other and cause two genes to fuse together. The fused genes then override the “off” switch that keeps cells from growing uncontrollably, causing prostate cancer to develop.

By testing these gene fusions in mice and in cell cultures, the researchers showed that the fusions are what cause prostate cancer to develop. But it’s not just one set of genes that fuse. The researchers found that any one of several in a family of genes can become scrambled and fuse. Results of the study appear in the Aug. 2 issue of Nature.

“Each of these switches, or gene fusions, represent different molecular subtypes. This tells us there’s not just one type of prostate cancer. It’s a more complex disease and potentially needs to be treated differently in each patient,” says lead study author Arul Chinnaiyan, M.D., Ph.D., director of the Michigan Center for Translational Pathology, a new U-M center whose goal is to translate research into real world practice.

The gene fusion research is the centerpiece project of the new center. In the current study, researchers found one of several abnormal gene fusions in the prostate cancer tissue samples they tested. In 2005, the researchers identified a prostate-specific gene called TMPRSS2, which fuses with either ERG or ETV1, two genes known to be involved in several types of cancer.

The Nature paper reports on five additional genes that fuse with ERG or ETV1 to cause prostate cancer. Gene fusions were involved in 60 percent to 70 percent of the prostate cancer cell lines the researchers looked at. The genes involved are all controlled by a different mechanism. For example, four of the genes are regulated by androgen, a male sex hormone known to fuel prostate cancer. Androgen deprivation is a common therapy for prostate cancer.

Knowing which gene fusion is involved in an individual patient’s tumor could impact treatment options. If an androgen-regulated gene is involved, androgen therapy would be appropriate. But if the gene fusion involves a gene that represses androgen, the anti-androgen therapy could encourage the cancer’s growth. This may also explain why androgen treatment is not effective for some prostate cancers.

“Typing someone’s prostate cancer by gene fusion can affect the treatment given. We would not want to give androgen to someone whose prostate cancer gene fusion is not regulated by androgen,” says Chinnaiyan, who is the S.P. Hicks Collegiate Professor of Pathology at the U-M Medical School.

Rearrangements in chromosomes and fused genes are known to play a role in blood cell cancers like leukemia and lymphoma, and in Ewing’s sarcoma. A fused gene combination that plays a role in chronic myelogenous leukemia led researchers to develop the drug Gleevec, which has dramatically improved survival rates for that disease.

Chinnaiyan believes the prostate gene fusions will eventually lead to similar treatments for prostate cancer.

“More immediately, we hope to develop tests for diagnosis or prognosis. But long-term, we hope this will lead to better therapies to treat prostate cancer. The key challenge is to find a drug that would go after this gene fusion,” Chinnaiyan says.

The gene fusion technology has been licensed to San Diego-based Gen-Probe Inc., which is working on a screening tool to detect gene fusions in urine. The tool could one day supplement or replace the prostate specific antigen, or PSA, test currently used to screen for prostate cancer.

The idea of translating laboratory research findings into a test or treatment that will impact patients is central to the new Michigan Center for Translational Pathology. The center brings together experts in genomics, proteomics and bioinformatics to look at common patterns and potential targets in cancer and other diseases. This is the first center of its kind in the nation in that it is associated with one of 39 National Cancer Institute-designated “comprehensive” cancer centers, a premier medical school and a large health system with both clinicians and patients.

The center’s goal is to study the genes, proteins and other markers on cells to develop new diagnostic tests or screening tools as well as targeted treatments for cancer and other diseases, with the key being to translate these laboratory discoveries into clinical applications.

Chinnaiyan and his team have received numerous awards and honors, including the American Association for Cancer Research Team Science Award for their previously published work on gene fusions, and the Specialized Program of Research Excellence Outstanding Investigator award. The new Center for Translational Pathology supported in part by the Prostate Cancer Foundation, which has offered to match up to $1 million dollars in donations to support work related to developing therapies against prostate cancer gene fusions at the university.

“Mapping of the human genome was only the beginning. Equipped with the comprehensive analysis of the human genome, we can now systematically examine the blueprint of disease at the molecular level. This essential knowledge may lead to better diagnostic tests and promising new treatments for cancer, cardiovascular disease, diabetes and other illnesses,” Chinnaiyan says.

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For information about the Michigan Center for Translational Pathology, go to http://www.med.umich.edu/mctp.

About 218,890 men will be diagnosed with prostate cancer this year, and 27,050 will die from the disease, according to the American Cancer Society. The gene fusion work is not currently available for treatment or diagnosis, and no clinical trials are currently recruiting. For information about prostate cancer and currently available treatments, go to http://www.mcancer.org or call the U-M Cancer AnswerLine at 800-865-1125.

In addition to Chinnaiyan, U-M study authors were Scott Tomlins; Saravana Dhanasekaran, Ph.D.; Bharathi Laxman; Qi Cao; Beth Helgeson; Xuhong Cao; David Morris, M.D.; Anjana Menon; Xiaojun Jing; Bo Han; James Montie, M.D.; Kenneth Pienta, M.D.; Diane Roulston; Rajal Shah, M.D.; Sooryanarayana Varambally, Ph.D.; and Rohit Mehra, M.D. Mark Rubin, M.D., from Brigham and Women’s Hospital, Dana-Farber Cancer Institute and Harvard Medical School is also a study author.

Funding for the study came from the U.S. Department of Defense, the National Institutes of Health, the Early Detection Research Network, the Prostate Cancer Foundation and Gen-Probe Inc.

The University of Michigan has filed for a patent on the detection of gene fusions in prostate cancer, on which Tomlins, Mehra, Rubin and Chinnaiyan are co-inventors. The diagnostic field of use has been licensed to Gen-Probe Inc. Chinnaiyan also has a sponsored research agreement with Gen-Probe; however, GenProbe has had no role in the design or experimentation of this study, nor has it participated in the writing of the manuscript.

Reference: Nature, Vol. 448, No. 7153, Aug. 2, 2007

Contact: Nicole Fawcett
nfawcett@umich.edu
734-764-2220
University of Michigan Health System

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Flip of genetic switch causes cancers in mice to self-destruct, Stanford researchers find

STANFORD, Calif. – Killing cancerous tumors isn’t easy, as anyone who has suffered through chemotherapy can attest. But a new study in mice shows that switching off a single malfunctioning gene can halt the limitless division of tumor cells and turn them back to the path of their own planned obsolescence.

The surprising possibility that a cell’s own natural mechanism for ensuring its mortality could be used to vanquish tumors opens the door to a new approach to developing drugs to treat cancer patients, according to Dean Felsher, MD, PhD, associate professor of medicine (oncology) and of pathology at the Stanford University School of Medicine. Felsher is the senior author of the study to be published July 30 in the advance online version of the Proceedings of the National Academy of Sciences.

“Our research implies that by shutting off a critical cancer gene, tumor cells can realize that they are broken and restore this physiologic fail-safe program,” said Felsher.

Cancer can be notoriously resistant to medical treatment. Not only do cancer cells proliferate uncontrollably, they somehow circumvent the mechanism that causes normal cells to die when they get old or malfunction. That makes cancer cells effectively immortal unless doctors manage to squelch them.

The gene Felsher’s team studied produces a protein called Myc (pronounced “mick”), which promotes cell division. A mutation of the gene causes cells to overproduce the protein, prompting perpetual cell division and tumor growth. By turning off the mutated gene, the researchers found that not only did uncontrolled cell division cease, but the cells also reactivated a normal physiological mechanism, called senescence, which makes it possible for a cell to eventually die.

“What was unexpected was just the fact that cancer cells had retained the ability to undergo senescence at all,” said Felsher. Cancer researchers had long thought the senescence process had to be irreversibly disrupted for a tumor to develop.

The researchers worked with a series of mice engineered to have Myc-triggered cancers of either the liver, blood or bones, along with a specially constructed version of the Myc gene that they could switch off by feeding the mice antibiotics. When the mice dined on doses of the drugs, invariably, the tumors ceased growing and then diminished, with some disappearing over the course of just a few days.

Although Felsher’s lab had previously shown that mouse tumors diminished and disappeared when Myc was switched off, they hadn’t been sure how the process actually worked. Historically, most research involving genetic methods of battling cancer cells has focused on reactivating genes called tumor-suppressor genes, which are generally overcome by a proliferating cancer. No one had explored the idea that senescence might play a key role in diminishing tumors.

Felsher described senescence as acting like a fail-safe mechanism to stop cancer. When a cell detects a deleterious mutation, it launches the senescence process, resulting in the permanent loss of the cell’s ability to proliferate, thus halting any cancer.

“In order to become tumor cells, those cells have to overcome senescence,” said Chi-Hwa Wu, PhD, postdoctoral researcher in Felsher’s lab and first author of the study. Wu had the inspiration to explore whether the sudden diminishment they had observed in the tumors might be due to the reactivation of some latent remnant of the trigger for senescence.

Through a series of experiments looking at enzymes associated with the senescence process, as well as some molecular markers, Wu confirmed her suspicion. And not only was senescence occurring in cells that had been thought to be incapable of it, the process was reactivated in all the different tumors they studied.

Consider it a cell version of the Jekyll-and-Hyde transformation. “It’s sort of like Mr. Hyde realizing that there’s something wrong with him and then being able to put himself back into his normal state as Dr. Jekyll,” Felsher said.

In addition to the deepened understanding of how the process of senescence works, Felsher and Wu see a lot of potential for new approaches to treating cancer, beyond the traditional tactic of trying to kill cancer cells directly. “This work implies that maybe part of the strategy should involve figuring out how to get the cancer cells to just be allowed to do what they originally wanted to do anyway, which is to not be proliferating endlessly and growing uncontrolled,” said Felsher.

The next step for the team is to see how well the approach works in human cancer cells. “And we’re also trying to figure out what the mechanism is,” Felsher said. “What are the molecular mechanisms of this, so that we can figure out how to better treat cancer””

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Other authors on the research paper are Jan van Riggelen, PhD, postdoctoral researcher; Alper Yetil, graduate student in cancer biology; Alice Fan, MD, instructor in medicine (oncology), and medical student Pavan Bachireddy.

The study was funded by the National Cancer Institute, the National Institutes of Health, the Leukemia and Lymphoma Society, the Burroughs Wellcome Fund, the Damon Runyon Lilly Clinical Investigator Award, the Lymphoma Research Foundation and the Howard Hughes Medical Institute.

Stanford University Medical Center integrates research, medical education and patient care at its three institutions – Stanford University School of Medicine, Stanford Hospital & Clinics and Lucile Packard Children’s Hospital at Stanford. For more information, please visit the Web site of the medical center’s Office of Communication & Public Affairs at http://mednews.stanford.edu.

Contact: Lou Bergeron
louisb3@stanford.edu
650-723-3900
Stanford University Medical Center

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New research provides hope for childhood cancer sufferers

Dr Richard Lock, Head of the Leukaemia Biology Program at the Children’s Cancer Institute Australia for Medical Research, Sydney, along with collaborators from the Childrens Hospital Los Angeles and University of Southern California, USA, recently published their findings in the prestigious scientific journal Blood.

ALL is the most common form of childhood cancer. Over the years, improvements in primary therapy have increased the cure rate to approximately 80 percent. However, for the 20 percent of patients who relapse, the majority will die.

“When used in combination with common drugs administered in ALL therapy, ABT-737 has the ability to enhance the combined toxicity of these drugs against the leukaemia cells with minimal effects on the normal cells of the body,” said Dr Lock.

Resistance to common therapeutic drugs is associated with poor long-term outcomes in leukaemia patients. In the study, the effects of ABT-737 in combination with three common chemotherapeutic agents: L-Asparaginase, vincristine and dexamethasone, were tested on a number of ALL cell lines under conditions which were considered clinically relevant for the disease.

ABT-737, developed by Abbott Laboratories, acts by inhibiting the Bcl-2 family of proteins. These proteins are expressed in ALL and inhibit the mechanisms responsible for destroying leukaemia cells. High levels of expression of Bcl-2 is linked with chemoresistance in a variety of cancers.

“There is a critical need for new drugs with novel mechanisms of action that might improve the outcome for relapsed ALL patients,” said Dr Lock.

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The manuscript is available online at http://bloodjournal.hematologylibrary.org/papbyrecent.dtl Children’s Cancer Institute Australia for Medical Research is associated with the University of NSW and Sydney Children’s Hospital.

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Children and young people show elevated leukaemia rates near nuclear facilities

Review covers 136 countries in US, Canada, UK, France, Germany, Japan and Spain

Leukaemia rates in children and young people are elevated near nuclear facilities, but no clear explanation exists to explain the rise, according to a research review published in the July issue of European Journal of Cancer Care.

Researchers at the Medical University of South Carolina carried out a sophisticated meta-analysis of 17 research papers covering 136 nuclear sites in the UK, Canada, France, the USA, Germany, Japan and Spain.

They found that death rates for children up to the age of nine were elevated by between five and 24 per cent, depending on their proximity to nuclear facilities, and by two to 18 per cent in children and young people up to the age of 25.

Incidence rates were increased by 14 to 21 per cent in zero to nine year olds and seven to ten percent in zero to 25 year-olds.

“Childhood leukaemia is a rare disease and nuclear sites are commonly found in rural areas, which means that sample sizes tend to be small” says lead author Dr Peter J Baker.

“The advantage of carrying out a meta-analysis is that it enables us to draw together a number of studies that have employed common methods and draw wider conclusions.”

Eight separate analyses were performed – including unadjusted, random and fixed effect models – and the figures they produced showed considerable consistency.

But the authors point out that dose-response studies they looked at – which describe how an organism is affected by different levels of exposure – did not show excess rates near nuclear facilities.

“Several difficulties arise when conducting dose-response studies in an epidemiological setting as they rely on a wide range of factors that are often hard to quantify” explains Dr Baker. “It is also possible that there are environmental issues involved that we don’t yet understand.

“If the amount of exposure were too low to cause the excess risk, we would expect leukaemia rates to remain consistent before and after the start-up of a nuclear facility. However, our meta-analysis, consistently showed elevated illness and death rates for children and young people living near nuclear facilities.”

The research review looked at studies carried out between 1984 and 1999, focusing on research that provided statistics for individual sites on children and young people aged from zero to 25.

Four studies covered the UK, with a further three covering just Scotland. Three covered France, two looked at Canada and there was one study each from the USA, Japan, Spain, the former East Germany and the former West Germany.

“Although our meta-analysis found consistently elevated rates of leukaemia near nuclear facilities, it is important to note that there are still many questions to be answered, not least about why these rates increase” concludes Dr Baker.

“Several hypotheses have been proposed to explain the excess of childhood leukaemia in the vicinity of nuclear facilities, including environmental exposure and parental exposure. Professor Kinlen from Oxford University has also put forward a hypothesis that viral transmission, caused by mixing populations in a new rural location, could be responsible.

“It is clear that further research is needed into this important subject.”

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Notes to editors

Meta-analysis of standardized incidence and mortality rates of childhood leukaemia in proximity to nuclear facilities. Baker PJ and Hoel D. European Journal of Cancer Care. 16, pages 355-363. July 2007.

The European Journal of Cancer Care provides a medium for communicating multi-professional cancer care across Europe and internationally. The Journal publishes peer-reviewed papers, reviews, reports, features and news, and provides a means of recording lively debate and an exchange of ideas. It is published six times a year by Blackwell Publishing.
Blackwell Publishing is the world’s leading society publisher, partnering with 665 medical, academic, and professional societies. Blackwell publishes over 800 journals and has over 6,000 books in print. The company employs over 1,000 staff members in offices in the US, UK, Australia, China, Singapore, Denmark, Germany and Japan and officially merged with John Wiley & Sons, Inc’s Scientific, Technical and Medical business in February 2007. Blackwell’s mission as an expert publisher is to create long-term partnerships with our clients that enhance learning, disseminate research, and improve the quality of professional practice. For more information on Blackwell Publishing, please visit http://www.blackwellpublishing.com or http://www.blackwell-synergy.com

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wizard.media@virgin.net
Blackwell Publishing Ltd.

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