Surviving Mesothelioma

All too often, a diagnosis of mesothelioma has meant a death sentence. Treatments like radiation or chemotherapy have been found to extend a patient's life perhaps five years. It's a form of cancer most associated with asbestos exposure.

Now consider the case of Paul Kraus. In 1997 Kraus was diagnosed with the disease and his mesothelioma prognosis was just a few months to live. Today, 12 years later, Kraus is alive and said to have a good quality of life.

How was it done? Click on these links to learn more about surviving pleural mesothelioma and related disease. In fact, right now through these web links, you can request a free copy of the book Surviving Mesothelioma, available for newly diagnosed mesothelioma patients.

If mesothlioma is now part of your life, you owe it to yourself to get the facts. Don't give up.

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Researchers Study New Drug Combinations to Treat Childhood Leukemia

Scientists from the Barbara Ann Karmanos Cancer Institute in Detroit presented data today at the American Association for Cancer Research's 100th Annual Meeting 2009 that could potentially provide a brighter future for children who suffer from a more deadly form of acute leukemia.

Yubin Ge and Chengzhi Xie presented work at the conference revealing that a combination of FDA-approved drugs works synergistically to help children with acute myeloid leukemia (AML). Ge is an assistant professor at the Karmanos Cancer Institute and at the Wayne State University School of Medicine's Department of Pediatrics. Xie is a postdoctoral fellow with the Developmental Therapeutics Program at Karmanos Cancer Institute and Wayne State University School of Medicine. He also is a lecturer with the College of Life Science at Jilin University in Changchun, China.

AML, which originates in bone marrow, accounts for one-fourth of acute leukemia in children and is responsible for more than half of the leukemia deaths in this population. Approximately 600 children are diagnosed with AML each year, according to Ge and presently there is no effective drug treatment for those children should they relapse.

"Right now, we are at a bottleneck," Ge says. "We really want to find a better treatment for those relapsed cases."

Ge and fellow researchers considered drugs that are already FDA-approved to help fight AML. Resistance among patients to FDA-approved cytarabine is a major cause of treatment failure in AML. Scientists considered clofarabine, approved by the FDA in 2004, and paired it with valproic acid (VPA), typically used to treat epilepsy. They found the two drugs worked together to dramatically stimulate cell death.

"We considered an old drug for a new use," Ge says. "It looks like the increased drug activity or synergy is not due to the transport or delivery of clofarabine, but to enhanced cell death. We were so pleased with the results."

AML afflicts mostly adults -- about 10,000 new cases each year -- and strikes older children. Acute lymphoblastic leukemia usually affects children between the ages of 2 to 5 and is generally easier to treat. Treatment advancements for AML, however, have been less successful.

Ge says that researchers at Karmanos discovered the synergy between VPA and clofarabine only a few months ago, though departmental research has spanned some 15 years in the field of treating childhood leukemias. The current research represents a unique partnership between Ge, his Karmanos colleagues, and Dr. Jeffrey Taub, M.D., a pediatric oncologist at Children's Hospital of Michigan, also in Detroit.

Ge expects that their findings will move into the clinical phase in the next few years. St. Jude Children's Research Hospital in Memphis, Tenn. Is now conducting its own clinical drug trial studying the combined effects of VPA and cytarabine to treat newly diagnosed AML patients 21 years old and younger.

"This is truly translational research," Ge says. "We really want to translate what we do in the laboratory to the clinic and hopefully save more lives."

Located in mid-town Detroit, Mich., the Barbara Ann Karmanos Cancer Institute is one of 40 National Cancer Institute-designated comprehensive cancer centers in the United States. Caring for more than 6,000 new patients annually on a budget of $216 million, conducting more than 700 cancer-specific scientific investigation programs and clinical trials, the Karmanos Cancer Institute is among the nation's best cancer centers.

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Book Chronicles the Journeys of Women Physicians, Scientists to the Front Lines of Fighting Cancer

Just more than one year after it was created, the office of Women Faculty Programs at The University of Texas M. D. Anderson Cancer Center has introduced a collection of essays by leading women faculty aimed at inspiring generations of women scientists to come.

Legends and Legacies: Personal Journeys of Women Physicians and Scientists at M. D. Anderson Cancer Center presents the reflections of 26 current faculty women on their formative years and influences, their hurdles and opportunities as they pursued rewarding careers -- and leadership roles -- in science and academic medicine.

Anecdotes and insight shared throughout the book reveal personal struggles and bias based on gender, race or social/economic background, as the women sought to balance personal and professional lives, including the often competing demands of motherhood and the tenure track. The women profiled represent diverse ages, backgrounds and cultures and various professional roles, from clinicians and physician scientists to basic scientists and veterinarians. (Please see sidebar.)

In his foreword, Dr. John Mendelsohn, M.D., president of M. D. Anderson Cancer Center, noted "I was struck by how diverse -- and often difficult -- their pilgrimages have been, yet all share the common bond of growing up knowing they wanted to make a difference."

Editor Elizabeth Travis, a professor in the departments of Radiation Oncology and Pulmonary Medicine and the first associate vice president for Women Faculty Programs at M. D. Anderson, conceived the book project to recognize the accomplishments of M. D. Anderson's women faculty while spotlighting advocacy efforts intended to improve opportunities for women already in the field, as well as inspire others to choose and then stay in the field.

"Legends and Legacies is about seeing dreams through in the face of adversity," says Travis. "I hope it serves as a source of inspiration for young women dreaming of careers in science and medicine - and as a reminder to those women and men who are mentoring the next generation."

Mendelsohn also credited the women's "innate tenacity to succeed," commending Travis and the faculty women for their efforts to make M. D. Anderson a top destination for women physicians and scientists. "We are proud to be the home of so many remarkable women physicians and scientists who continue to be leaders in cancer patient care, research, education and prevention."

Through its Women Faculty Programs, M. D. Anderson promotes workplace initiatives for women physicians and scientists, such as creating a better work-life environment; nominating women faculty for prizes and awards; increasing the number of women leaders; providing career development and mentoring programs; reviewing faculty salaries annually; hosting women physicians and scientists to give scientific and women-in-science talks; promoting institution-wide gender-balanced participation; and reviewing status of women faculty annually.

Offering the book's final note, Dr. Raymond Dubois, provost and executive vice president of M. D. Anderson, says, "We must discard past gender stereotypes and do everything possible to attract, train and support the best and brightest minds to meet the challenges of conquering such relentless and stubborn problems as cancer. Future generations are counting on all of us."

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Is Smaller Better? Minimally Invasive Oncologic Surgery Options Discussed

Cutting-edge surgery with less cutting is appealing for many, but how do minimally invasive surgical offerings rate in terms of outcomes for people with cancer? At the National Comprehensive Cancer Network's (NCCN) 14th Annual Conference, Dr. Thomas D'Amico, MD, of Duke Comprehensive Cancer Center discussed the pros and the cons of minimally invasive oncologic surgery alternatives.

D'Amico acknowledges the tremendous technological advances that have resulted in minimally invasive offerings, but emphasized three guidelines that physicians need to be aware of when presenting the option to patients; the minimally invasive option must be oncologically equivalent or superior to the open procedure, the procedure should offer quality of life outcome advantages, and cost effectiveness needs to be considered, according to a statement from the NCCN, a not-for-profit alliance of 21 of the world's leading cancer centers.

Five minimally invasive procedures for oncologic surgery including robotic prostatectomy, laparoscopic colectomy, laparoscopic adrenalectory, minimally invasive esophagectomy, and thoracoscopic lobectomy were presented by D'Amico. In each procedure, he provided a comparison of the minimally invasive option versus the traditional open approach to surgery noting operating time, cost, recovery rates, length of stay, and oncologic outcomes.

Overall, the benefits to the minimally invasive options were a shorter hospital stay, faster recovery, and less pain. However, except for the thoracoscopic lobectomy, there is no data from randomized controlled clinical trials on minimally invasive options to provide any insight into oncologic outcomes or survival rates.

"The lack of evidence-based data for the majority of minimally invasive surgical options is one of the current shortcomings in the field," says D'Amico.

Another cause of debate includes the training and credentialing of physicians who perform minimally invasive procedures. D'Amico says that the learning curve for physicians being trained needs to be addressed. Lastly, D'Amico touched upon the controversy of using minimally invasive surgery as a marketing tool particularly in the field of robotics, which can lend itself to eye-catching publicity.

The future of minimally invasive surgery will likely see an expanded use of robotics as well as an increased interest in a new technique called natural orifice surgery. D'Amico explains that natural orifice surgery is when surgeons conduct surgery through the natural orifices in the body such as the mouth, nose, or rectum. Since there are no incisions made on the body, the benefits are a reduced risk of infection and a quicker recovery, says D'Amico.

In conclusion, D'Amico emphasizes that improved outcomes should drive the utilization of minimally invasive procedures and that oncologic principles must be preserved.

"There is continued progress of minimally invasive oncology surgery," says D'Amico, "but also the need for further evolution to optimize morbidity and oncologic outcomes. The question we need to ask ourselves is not 'what can be done', but 'what should be done'."

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Researchers Find Physics, Math Provide Clues to Unraveling Cancer

Biology exists in a physical world. That's a fact cancer researchers are beginning to recognize as they look to include concepts of physics and mathematics in their efforts to understand how cancer develops -- and how to stop it.

The movement, led by researchers at the University of Michigan Comprehensive Cancer Center, has come to a head with a new section in one of the top cancer research journals and a new grant program from the National Cancer Institute.

Traditional cancer biology involves taking a sample of cells and holding them in time so they can be studied. Then the researchers look at that slice of cells to understand what signals and pathways are involved. But that doesn't capture the full picture, says Dr. Sofia Merajver, M.D., co-director of the Breast Oncology Program at the Comprehensive Cancer Center.

"The living cell is really a dynamic process. We need to consider the properties of physics to help us understand these data. In order to develop a drug directed against a given molecule that has real hope of treating cancer, we need to understand how that molecule is sitting in the cell, interacting with other molecules," says Merajver, professor of internal medicine at the U-M Medical School.

Merajver and her team have developed a sophisticated mathematical model to help researchers apply these concepts to cancer. The mathematical model is designed to help give researchers a complete picture of how a cell interacts with its surrounding environment. By understanding the full complexity of signaling pathways, researchers can better target treatments and identify the most promising potential new drugs.

Researchers have learned from this modeling that a well-known and major type of signaling pathway naturally transmits information not just in a forward direction, but also backwards. That implies new considerations for developing drugs to inhibit major growth and metastasis pathways in cancer.

This crosstalk was missed by conventional methods. Typically, when scientists begin to look at a cell, they must make assumptions to simplify the picture of what is happening in cells.

"When you make simplifying assumptions, you always run the risk of eliminating critical aspects of your system, but you have no way of knowing what was discarded. When you simplify, you don't know exactly what you're throwing away because you never looked at the complex case," Merajver says. Mathematical modeling allows researchers to look at the complex case more thoroughly.

"To understand how the laws of physics can be applied to biological systems is a new frontier," she says.

Merajver and her colleagues were successful in getting the journal Cancer Research to add a new regular section to the twice-monthly journal precisely focused on mathematical modeling. The journal has also added new editors to its board who have expertise in this discipline. Merajver and Trachette Jackson, professor of mathematics at U-M, will lead this effort as senior editors.

A review article about mathematical modeling appears in the Jan. 15 issue of Cancer Research, authored by Merajver, Jackson and Alejandra Ventura, a senior postdoctoral fellow in internal medicine at U-M.

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Physicists Receive Patent for Improved Cancer Therapy Device

Four physicists at Brookhaven National Laboratory have been awarded a U.S. patent for the design of a "medical synchrotron" capable of delivering precision doses of proton radiation to cancerous tumors with minimal damage to surrounding healthy tissue. The new device would be more precise and less costly than existing proton-therapy systems, potentially increasing the availability and benefits of this treatment for caner patients worldwide. The Brookhaven scientists are now seeking industrial partners to license and commercialize the technology.

"In the realm of cancer treatment, proton therapy is considered 'surgery without a knife' because proton beams can deliver cell-killing energy with extreme precision, unlike conventional x-ray radiation therapy," says Brookhaven physicist Stephen Peggs, one of the lead scientists on the project. Peggs, while working at the Fermi National Accelerator Laboratory, witnessed the completion of the nation's first hospital-based proton-therapy synchrotron, installed at
California's Loma Linda University Medical Center in 1990.

"Almost as soon as the Loma Linda synchrotron went out the door, we started thinking about ways to build a better machine," Peggs says. The current design -- developed and refined as Peggs and other physicists worked on large-scale accelerators for physics experiments, including the Relativistic Heavy Ion Collider (RHIC) at Brookhaven Lab -- is the culmination of that effort.
"Our new design has improvements in beam-focusing technology to make the smallest possible beam size -- that is, the sharpest possible 'knife,'" says Peggs. Because smaller beams deliver radiation with increased precision, this improvement could have a significant impact by shortening the duration of treatment, increasing its effectiveness, or both. The new design also promises to be less costly and more reliable, which should increase its availability.

How it works

The idea behind radiation therapy is to deliver a lethal dose of radiation to cancerous cells. In conventional x-ray radiation therapy, many healthy surrounding cells are also exposed to the radiation because x-ray beams deposit their energy as they travel through tissue. In fact, most of the dose of x-rays is deposited near the surface of the body. Though cancerous cells tend to be more susceptible to the damaging effects of radiation (or less able to repair it), the collateral damage to healthy tissues limits the dose physicians can use to destroy the tumor.

Proton therapy offers an advance over conventional x-rays because proton beams deposit most of their energy where the beam stops. The original proton therapy synchrotrons were designed to deliver cell-killing doses of radiation to tumors in three dimensions by aiming proton beams from multiple directions to stop at the depth of the tumor tissue. That precision targeting allows doctors to deliver higher doses to the tumor cells while sparing healthy surrounding tissue.

But accelerators are often costly to build and difficult to maintain, explaining why the design principles for hospital-based accelerators must be radically modified, and why relatively few hospitals have them. The new accelerator design developed by the Brookhaven team offers two main advantages: "rapid cycling" and "strong focusing."

Rapid cycling allows proton beams to be injected and extracted from the synchrotron in just one turn around the circular particle accelerator. Unlike the earlier machines, which required multiple turns, this eliminates the need for sensitive feedback systems to control the beam currents, the researchers say.

"This makes the machine more robust and reliable to operate. It's more of a turn-key operation," Peggs says. "Turn it on and it consistently starts up like a transformer, rather than booting up like a PC."

Strong focusing refers to the ability to shape the proton beam and keep it focused to pinpoint dimensions. In contrast to the Loma Linda machine, where beams measure up to a centimeter across, the new design can achieve beams as narrow as one millimeter.

Pinpoint accuracy reduces collateral damage and allows physicians more flexibility in the doses they use. Higher doses could yield more effective therapy, possibly in fewer treatments.

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Study Finds Treatment With New Drug Might Make Tumor Cells More Sensitive to Therapy

Scientists at St. Jude Children's Research Hospital have shown that it might be possible to
make tumor cells more sensitive to irradiation and some types of chemotherapy by treating them with a drug that cripples their ability to repair DNA damage caused by these therapies.

The St. Jude researchers demonstrated in the laboratory that a molecule called CP466722 rapidly blocks the ATM protein's ability to orchestrate a series of biochemical events that culminate in the repair of DNA damaged by irradiation. The molecule exerted its effect in small quantities, and its effects rapidly ended after it was removed from cells, suggesting that such
a treatment in humans would not have significant or long-term side effects, the researchers say.

Results of the study were published in the Sept. 15 issue of the journal Cancer Research.

ATM plays a critical role in repairing a type of DNA damage called double-strand breaks, in which each of the two strands making up this molecule are cut, according to Dr. Michael Kastan, M.D., director of the St. Jude Comprehensive Cancer Center. This process protects cells from the potentially lethal or mutation-causing effects of free oxygen radicals and irradiation--both of which routinely threaten them, he added. Kastan is senior author of the report on these findings.
Children lacking the gene for ATM develop ataxia-teleangiectasia, a disease that causes several debilitating problems, such as neurodegeneration, cancer and sensitivity to irradiation that leads to irreparable, double-stranded DNA breaks.

"We found that inhibition of ATM activity with CP466722 produces cellular effects that are identical to those seen in cells that lack ATM," Kastan says. "It's as if we temporarily turned normal cells into cells indistinguishable from those of children with ataxia-teleangiectasia."

The protective role of ATM makes it a tempting target for researchers looking for a way to prevent cancer cells from repairing DNA damage caused by therapeutic irradiation, Kastan notes.

Previously Kastan's team found how ATM is activated by a signal from damaged DNA only seconds after the damage occurs. The activated ATM, in turn, activates other proteins by attaching a molecule called phosphate to them in a process called phosphorylation. This sets off a cascade of biochemical reactions that amplifies the initial ATM response leading to
repair of the double-stranded break.

"Our ability to rapidly and reversibly regulate ATM activity with CP466722 also gives us a new tool to study the function of this protein, which plays such a critical role in the ability of both normal and cancerous cells to repair their DNA," says Michael Rainey, a postdoctoral fellow in the St. Jude Department of Oncology. "This approach will help us learn more about the repair events triggered by ATM in response to DNA damage." Rainey is the report's first author.

Kastan also says that CP466722 provides his team with a basic chemical structure that they can build upon as they try to modify the molecule to enhance its potency and specificity and move studies from isolated cells to mouse models.

"Results of those mouse model studies would help us to determine if and how to proceed with studies in patients with cancer," Kastan says.

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Carbon Nanotubes That Look Like Asbestos, Behave Like Asbestos

A major study published today in Nature Nanotechnology suggests some forms of carbon nanotubes -- a poster child for the "nanotechnology revolution" -- could be as harmful as asbestos if inhaled in sufficient quantities.

Carbon nanotubes are atom-thick sheets of graphite formed into cylinders. They may be formed from a single layer of graphite or they may consist of multiple concentric layers of graphite, resulting in multi-walled carbon nanotubes. While the diameter of a nanotube can vary
from a few nanometers up to tens of nanometers, they can be hundreds or even thousands of nanometers long. Carbon nanotubes come in many forms, with different shapes, different atomic arrangements, and varying amounts and types of added chemicals -- all of which affect their properties and might influence their impact on human health and the environment.

The study used established methods to see if specific types of nanotubes have the potential to cause mesothelioma -- a cancer of the lung lining that can take 30 to 40 years to appear following exposure. The results show that long, thin multi-walled carbon nanotubes that look like asbestos fibers, behave like asbestos fibers.

Discovered nearly 20 years ago, carbon nanotubes have been described as the wonder material of the 21st Century. Light as plastic and stronger that steel, they are being developed for use in new drugs, energy-efficient batteries and futuristic electronics. But since their discovery, questions have been raised about whether some of these nanoscale materials may cause
harm and undermine a nascent market for all types of carbon nanotubes, including multi- and single-walled carbon nanotubes. Leading forecasting firms say sales of all nanotubes could reach $2 billion annually within the next four to seven years, according to an article in the U.S. publication Chemical & Engineering News.

"This study is exactly the kind of strategic, highly focused research needed to ensure the safe and responsible development of nanotechnology," says Andrew Maynard, chief science advisor to the Project on Emerging Nanotechnologies and a co-author on the paper. "It looks at a specific nanoscale material expected to have widespread commercial applications and asks specific questions about a specific health hazard. Even though scientists have been raising concerns about the safety of long, thin carbon nanotubes for over a decade, none of the research needs in the current U.S. federal nanotechnology environment, health and safety risk research
strategy address this question."

Widespread exposure to asbestos has been described as the worst occupational health disaster in U.S. history and the cost of asbestos-related disease is expected to exceed $200 billion, according to major U.S. think tank RAND Corporation.

Dr Anthony Seaton, MD, a co-author on the paper and a professor emeritus at the University of Aberdeen in the United Kingdom, says, "The toll of asbestos-related cancer, first noticed in the 1950s and 1960s, is likely to continue for several more decades even though usage reduced rapidly some 25 years ago. While there are reasons to suppose that nanotubes can be used
safely, this will depend on appropriate steps being taken to prevent them from being inhaled in the places they are manufactured, used and ultimately disposed of. Such steps should be based on research into exposure and risk prevention, leading to regulation of their use. Following this study, the results of which were foreseen by the Royal Society in the U.K. in 2004, we
can no longer delay investing in such research."

Researchers, led by Kenneth Donaldson at the University of Edinburgh in the United Kingdom, examined the potential for long and short carbon nanotubes, long and short asbestos fibers, and carbon black to cause pathological responses known to be precursors of mesothelioma. Material was injected into the abdominal cavity of mice -- a sensitive predictor of long fiber response in the lung lining.

"The results were clear," says Donaldson. "Long, thin carbon nanotubes showed the same effects as long, thin asbestos fibers."

Asbestos fibers are harmful because they are thin enough to penetrate deep into the lungs, but sufficiently long to confound the lungs' built-in clearance mechanisms for getting rid of particles.

Donaldson stresses there are still pieces of the puzzle to fill in. "We still don't know whether carbon nanotubes will become airborne and be inhaled, or whether, if they do reach the lungs, they can work their way to the sensitive outer lining. But if they do get there in sufficient
quantity, there is a chance that some people will develop cancer -- perhaps decades after breathing the stuff," says Donaldson.

There is a silver lining to this research. According to Donaldson, "Short or curly carbon nanotubes did not behave like asbestos, and by knowing the possible dangers of long, thin carbon nanotubes, we can work to control them. It's a good news story, not a bad one. It shows that carbon nanotubes and their products could be made to be safe."

But Donaldson adds that the present study only tested for fiber-like behavior and did not exonerate carbon nanotubes from damaging the lungs in other ways. "More research is still needed if we are to understand how to use these materials as safely as possible," he notes.

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Assembly Technique for Tiny Wires May Eventually Help Detect Cancer, Other Diseases

Bottom-up manufacturing may hold the key to production of tiny medical devices capable of testing for multiple molecules like viruses or cancer markers, according to an interdisciplinary team of Penn State researchers.

"Diagnostic chips can be made more useful by assembling, at predetermined locations on the chip, large numbers of nanowires pretreated off chip," says Rustom Bhiladvala, research assistant professor, electrical engineering. "Using this new bottom-up method, our group has demonstrated that thousands of single wires can be successfully aligned and anchored to form tiny diving board resonator arrays."

The traditional top-down process begins with silicon and carves nanoresonator devices from the material. This approach works well and produces many devices that are nearly identical, but the process has limitations. The addition of chemical probes or other changes in the existing materials must be done after the devices are fabricated on the chips.

The bottom-up method, although not producing identical devices, is more flexible. In bottom-up fabrication, researchers manufacture nanowires off chip using any inorganic or organic material that will produce nanowires. They can attach probe molecules to the wires off chip, using a variety of chemicals and they can attach each group of nanowires and their probes to the chips in the numbers and at the locations desired.

"We can achieve high device integration yields, but the devices are not as uniform as top-down manufactured devices," says Theresa Mayer, professor of electrical engineering. "However, we can access materials that are not easy to integrate into the devices with top-down methods. We can also integrate wires treated off-chip with entirely different probe molecules that are attached to the wires using condition optimized for that molecule."

The researchers described their bottom-up method using fabrication of a resonator array in the current issue of Nature Nanotechnology. They fabricated these proof-of-concept chips with nanowires made of single crystal silicon or polycrystalline rhodium attached at one end and suspended over a depression. This type of device can detect target molecules when they bind to the probe molecules on the nanowires and change the wire's vibration.

To create the bottom-up diving board resonators, the researchers used a layer of photoresist – a light-sensitive material which, when exposed to light, can then be easily removed chemically – to create an array of tiny rectangular wells on the chip. These wells were aligned above an insulated electrode on the chip surface. A solution of nanowires, with probes already attached, flows over the chip surface while the electrodes produce an electric field. The electric field grabs the nanowires and pulls them to the surface where they align perpendicular to the electrode. The aligned nanowires skate along the electrodes and when they reach a well, drop down into it.

Once a wire is in a well, that wire repels other wires allowing, for the most part, only one wire per well. The number of wires in the solution is controlled depending on the number of wells so only a few wires remain on the chip outside the wells.

"One of the biggest challenges of self assembly is whether we can control where the wires go and control the defects," says Mayer, associate director of Penn State's Material Research Institute and director of Penn State's site of the National Science Foundation's National Nanotechnology Infrastructure Network. "This new method allows integration of the nanowires with high yield."

In the case of the resonators, once the wires are in the depressions, the researchers switch to a top-down approach, placing a layer of a different photoresist on top of the chip and removing a small cube of photoresist around the tip where the wire anchor will be built. The researchers then electro-deposit metal into the tiny square holes, anchoring the nanowire in place. They dissolve the photoresist, leaving the suspended nanowire and at the same time removing the nanowires that did not make it into wells.

By choosing the well depth and the thickness of the original photoresist layer, the researchers can adjust the height of the resonator above the chip surface. An added benefit of bottom-up fabrication is that the nanowires with their probe molecules retain their functionality after integration. The researchers also showed that, after the resonator chip arrays were fabricated, target molecules did selectively bind to only those nanowires treated with the correct probe molecules.

The researchers tested many silicon and rhodium nanoresonators by measuring their vibration at high vacuum and found that the electroplated anchors were uniform, not too far from rigid and did not show high energy losses. They also found that both types of wires show negligible effects of air damping at pressures as high as about a thousandth of an atmosphere, which can be reached using small and inexpensive vacuum pumps. They showed that both nanowire dimensions and material properties affect the loss due to air damping at one atmosphere. The quality of the response at this modest vacuum is such that these resonators are strong candidates for sensitive resonance-based detection schemes.

"Bottom-up fabrication is an entirely new nanomanufacturing approach and we need to create devices that have properties that match what we can now make using top-down fabrication," says Mayer. "Our vision is to make large arrays of nano size devices with multiple probes for multiple targets by placing different groups of functionalized nanowires sequentially on chips."

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Lung Cancer Cells' Survival Gene Seen as Drug Target

One of the deadliest forms of cancer appears to carry a specific weakness.

When a key gene called 14-3-3zeta is silenced, lung cancer cells can't survive on their own, researchers have found.

The gene is a potential target for selective anti-cancer drugs, says Haian Fu, professor of pharmacology, hematology & oncology at Emory University School of Medicine and Emory Winship Cancer Institute.

The research results will be published the week of Dec. 24 in the Proceedings of the National Academy of Sciences (PNAS). The paper's first author is Zenggang Li, PhD, a postdoctoral fellow in Dr. Fu's laboratory.

Lung cancer kills more Americans annually than any other type of malignancy, according to the National Cancer Institute. Yet treatment options are very limited, Dr. Fu says.

"The recent trend towards targeted therapies requires us to understand the altered signaling pathways in the cell that allow cancer to develop," he says. "If you think about genes that are dysregulated in cancer as drivers or passengers, we want to find the drivers and then, aim for these drivers during drug discovery."

Fu and his collaborator, Fadlo Khuri, MD, deputy director of clinical and translational research at Emory Winship Cancer Institute, chose to focus on the gene 14-3-3zeta because it is activated in many lung tumors. In addition, recent research elsewhere shows that survival of lung cancer patients is worse if the gene is on overdrive in their tumors, Dr. Fu says.

14-3-3 genes are found in mammals, plants and fungi. In the human body, they come in seven flavors, each given a Greek letter. Scientists describe the proteins they encode as adaptors that clamp onto other proteins. The clamping function depends on whether the target protein is phosphorylated, a chemical switch that regulates processes such as cell division, growth, or death.

"We knew that 14-3-3 is important in controlling EGFR (epidermal growth factor receptor) signaling, which is a main pathway driving lung cancer," Fu says. A couple of recently introduced drugs that were shown to be effective against lung cancer target EGFR, he adds.

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Relationship Between Environmental Stress And Cancer

One way environmental stress causes cancer is by reducing the activity level of an enzyme that causes cell death, researchers say.

They found that stress-inducing agents, such as oxidative stress, recruit a protein called SENP1 that cuts a regulator called SUMO1 away from the enzyme SIRT1 so its activity level drops, says Dr. Yonghua Yang, postdoctoral fellow in the laboratory of Dr. Kapil Bhalla, director of the MCG Cancer Center.

This fundamental finding about the relationship between stress and cancer opens the door for treatments that increase SENP1 activity, making it easier for cells that are becoming cancerous to die, says Dr. Yang, first author on a paper published in the November issue of Nature Cell Biology.

“This is one of the things that makes cancer cells so durable, one way they survive so well,” says Dr. Yang. “We want to see if we can block that process and make cells die.” Increased SIRT1 activity – which is routinely present in cancer – even makes cancer cells more resistant to anticancer drugs such as chemotherapy.

The complication is that decreasing programmed cell death, or apoptosis, increases longevity, says Dr. Yang. However he now has evidence that SIRT1 – also under study for its longevity role – has different targets when it comes to cancer promotion and longevity that will provide distinct targets for manipulating each.

“Whether apoptosis is good or bad depends on the circumstances,” says Dr. Yang. “But it’s good for cancer therapy.”

“This paper describes how stress causes desumoylation and sumoylation of SIRT1 and ultimately cancer,” says Dr. Bhalla, Cecil F. Whitaker Jr., M.D./Georgia Research Alliance Eminent Scholar in Cancer and a study co-author.

“Stress-inducing agents produce the association of this enzyme, SIRT-1, with the desumoylating enzyme, SENP1, so cells become more resistant to stress-induced apoptosis,” says Dr. Bhalla. “Once SIRT1 is desumoylated, it’s less active and you want its activity.”

When SIRT1 is less active, p53, a tumor suppressor gene that also causes apoptosis, becomes more active.

SIRT1, found throughout the body, is a regulator of protein function through a process called acetylation. MCG researchers also found that sumoylation of SIRT1 (combining it with SUMO1) made it more active and sumoylation motif, which enables SUMO1 to combine with SIRT1, is needed to make that happen.

They have added SUMO1 to human cancer cells and increased SIRT1 activity then used SENP1 to cleave it and reduce activity.

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Study Identifies Gene Alterations in Lung Cancer

An international team of scientists, supported in part by the National Human Genome Research Institute (NHGRI), one of the National Institutes of Health (NIH), has announced that its systematic effort to map the genomic changes underlying lung cancer has uncovered a critical gene alteration not previously linked to any form of cancer. The research, published in the advance online issue of the journal Nature, also revealed more than 50 genomic regions that are frequently gained or lost in lung adenocarcinoma, the most common type of lung cancer in the United States.

“This view of the lung cancer genome is unprecedented, both in its breadth and depth,” says senior author Matthew Meyerson, a senior associate member of the Broad Institute of MIT and Harvard in Cambridge, Mass., and an associate professor at Dana-Farber Cancer Institute and Harvard Medical School in Boston. “It lays an essential foundation, and has already pinpointed an important gene that controls the growth of lung cells. This information offers crucial inroads to the biology of lung cancer and will help shape new strategies for cancer diagnosis and therapy.”

Each year more than 1 million people worldwide die of lung cancer, including more than 150,000 in the United States. The new study focused on lung adenocarcinoma, which, according to the National Cancer Institute (NCI), is the most frequently diagnosed form of lung cancer in the United States, accounting for approximately 30 percent of cases.

New approaches to cancer treatment rely on a deeper understanding of what goes wrong in tumor cells to spur uncontrolled growth. Through decades of research, it has become clear that lung cancer -- like most human cancers -- stems mainly from DNA changes that accrue in cells throughout a person’s life. But the nature of these changes and their biological consequences remain largely unknown, which has inspired the recent formation of multi-disciplinary teams that are using new genomic tools and technologies to study cancer in a more systematic, comprehensive manner.

The latest study was conducted as part of the Tumor Sequencing Project (TSP), an ongoing effort to apply large-scale approaches to the identification of genomic changes in lung adenocarcinoma. NHGRI is a major funder of TSP, which unites scientists and clinicians throughout the cancer research community.

“This outstanding work clearly demonstrates the value of comprehensive approaches for exploring the genomic underpinnings of cancer. The impacts of these findings extend far beyond lung cancer and indicate that many more important cancer-related genes still await our discovery,” NHGRI Director Francis Collins says. “Now, we must forge ahead and apply this strategy as quickly as possible to other common types of cancer.”

Specifically, the TSP researchers uncovered a total of 57 genomic changes that occur frequently in lung cancer patients. Of these changes, more than 40 appear to be associated with genes not previously known to be involved in lung adenocarcinoma. More research is needed to precisely identify and characterize these genes, but researchers are excited by the possibility that their findings may suggest new ways of attacking this deadly cancer.

The most common abnormality identified by the TSP team involves a region on chromosome 14 that encompasses two known genes, neither of which had been previously associated with cancer. Through additional studies in cancer cells, the researchers discovered that one of the genes, NKX2.1, influences cancer cell growth. NKX2.1 normally acts as a master regulator that controls the activity of other key genes in cells lining the lungs’ tiny air sacs, called alveoli. The discovery that a gene functioning in a select group of cells - rather than in all cells - can promote cancer growth may have broad implications for the design of drugs for a wide range of cancers.

“The genomic landscape of lung cancer gives us a systematic picture of this terrible disease, confirming things we know, but also pointing us to many missing pieces of the puzzle. More broadly, the study represents a general approach that can and should be used to analyze all types of cancer,” says Eric Lander, one of the study’s co-authors and founding director of the Broad Institute of MIT and Harvard.

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Sunlight May Cut Risk of Advanced Breast Cancer by half

A research team from the Northern California Cancer Center, the University of Southern California, and Wake Forest University School of Medicine has found that increased exposure to sunlight – which increases levels of vitamin D in the body -- may decrease the risk of advanced breast cancer.

In a study reported online this week in the American Journal of Epidemiology, the researchers found that women with high sun exposure had half the risk of developing advanced breast cancer, which is cancer that has spread beyond the breast, compared to women with low sun exposure. These findings were observed only for women with naturally light skin color. The study defined high sun exposure as having dark skin on the forehead, an area that is usually exposed to sunlight.

The scientists used a portable reflectometer to measure skin color on the underarm, an area that is usually not directly exposed to sunlight. Based on these measurements, they classified the women as having light, medium or dark natural skin color. Researchers then compared sun exposure between women with breast cancer and those without breast cancer. Sun exposure was measured as the difference in skin color between the underarm and the forehead.

In women with naturally light skin pigmentation, the group without breast cancer had significantly more sun exposure than the group with breast cancer. The fact that this difference occurred only in one group suggests that the effect was due to differences in vitamin D production – and wasn’t just because the women were sick and unable to go outdoors. In addition, the effect held true regardless of whether the cancer was diagnosed in the summer or in the winter. The difference was seen only in women with advanced disease, suggesting that vitamin D may be important in slowing the growth of breast cancer cells.

“We believe that sunlight helps to reduce women’s risk of breast cancer because the body manufactures the active form of vitamin D from exposure to sunlight,” says Esther John, lead researcher on the study from the Northern California Cancer Center. “It is possible that these effects were observed only among light- skinned women because sun exposure produces less vitamin D among women with naturally darker pigmentation.”

These new findings about breast cancer risk and sun exposure based on skin color measurements are consistent with previous research by John and colleagues that had shown that women who reported frequent sun exposure had a lower risk of developing breast cancer than women with infrequent sun exposure.

The researchers stressed that sunlight is not the only source of vitamin D, which can be obtained from multivitamins, fatty fish and fortified foods such as milk, certain cereals and fruit juices. Women should not try to reduce their risk of breast cancer by sunbathing because of the risks of sun-induced skin cancer, they said.

“If future studies continue to show reductions in breast cancer risk associated with sun exposure, increasing vitamin D intake from diet and supplements may be the safest solution to achieve adequate levels of vitamin D,” says Gary Schwartz, a co-researcher from the Comprehensive Cancer Center at Wake Forest University School of Medicine.

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St. Jude Psychologist Says Most Children With Cancer Are Well-Adjusted

Children under treatment for cancer are generally emotionally well-adjusted and no more depressed or anxious than other children their age, according to researchers at St. Jude Children’s Research Hospital. In studies of depression, anxiety, posttraumatic stress and quality of life, children with cancer do as well as, and often better than their healthy peers.

“We see them as a flourishing population that has adapted to the stress of having cancer and undergoing treatment,” says Sean Phipps, a member of the St. Jude Division of Behavioral Medicine. “They become quite resilient to the long-and short-term emotional and physical effects of their disease and the treatments.”

The unexpected finding that children with cancer are emotionally resilient is important because of the dramatic improvement in survival rates of pediatric cancers. “There has been a shift in research toward the concerns of long-term survivors of pediatric cancers,” Phipps says. “The ability of these children to cope with the after-effects of cancer is the major issue now. What we are learning from this population might help us learn how to improve the quality of life of children who are not doing so well.”

Phipps is the author of an article on adaptive styles in children with cancer that appears in the advanced online issue of Journal of Pediatric Psychology. The article, based on research done by his group and other research teams around the country, was presented at the conference “Psychosocial and Neurocognitive Consequences of Childhood Cancer: A Symposium in Tribute to Raymond K. Mulhern,” held at St. Jude in September 2006, in honor of the late Raymond Mulhern, a pioneer in psychological research in pediatric oncology at the hospital. The symposium’s presentations will also appear in a special December issue of the journal.

The low level of depression among children with cancer does not reflect a state of “illusory mental health,” Phipps says. That is, these children are not simply clinging to an illusion of mental health by denying distress. Rather, many of them simply have a reduced awareness of emotional distress, and they think of themselves as being well-adjusted and content, a response called a “repressive adaptive style.”

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How Cancer Spreads by Aggregating Platelets

Scientists have provided new details about how cancer cells spread by surrounding themselves with platelets – the blood cells needed for blood clotting. Katsue Suzuki-Inoue, associate professor of medicine at the University of Yamanashi, Japan, and colleagues have identified for the first time a protein on the surface of platelets that plays a key role in cancer-induced platelet aggregation. These results could help design new drugs that prevent cancer cells from metastasizing, or spreading throughout the body.

“In order to spread, cancer cells release chemicals that make neighboring platelets aggregate and surround the cancer cells, helping them evade the immune system and allowing them to bind to the blood vessels’ inner linings,” Suzuki-Inoue says. “We have discovered how one of these chemicals, called podoplanin, binds to the platelet cells and stimulate their aggregation. Although podoplanin has been known since 1990, how it induces platelet cell aggregation has been a mystery – until now.”

The new study, to be published in the September 7 issue of the Journal of Biological Chemistry, was selected as a “Paper of the Week” by the journal’s editors, meaning that it belongs to the top one percent of papers reviewed in significance and overall importance.

Suzuki-Inoue and colleagues had previously discovered that the snake venom rhodocytin stimulates platelet aggregation by binding to a protein called C-type lectin-like receptor 2 (CLEC-2) located on the surface of the platelets in a way similar to a key (rhodocytin) binding to a lock (CLEC-2).

By studying the details of what happens inside these platelets before and during aggregation, the scientists noticed many similarities with the way platelets aggregate when they are induced by podoplanin from cancer cells. Whether stimulated by rhodocytin or podoplanin, the platelets are slow to aggregate at first and, after they start aggregating, the proteins that are activated inside the platelets are similar in both cases.

Suzuki-Inoue and her team reasoned that maybe CLEC-2 binds not only to rhodocytin but also to podoplanin. The scientists tested this hypothesis by first growing CLEC-2 in culture and then by adding them to cultured cells expressing podoplanin. The hypothesis was confirmed: CLEC-2 and podoplanin bound to each other in the same lock-and-key mechanism displayed by CLEC-2 and rhodocytin.

“We were pleasantly surprised,” Suzuki-Inuoue says. “After all these years, we finally found the long-missing protein to which podoplanin binds to promote platelet aggregation.”

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Scientists Invent Novel Hydrogels For Repairing, Regenerating Human Tissue

University of Delaware scientists have invented a novel biomaterial with surprising antibacterial properties that can be injected as a low-viscosity gel into a wound where it rigidifies nearly on contact--opening the door to the possibility of delivering a targeted payload of cells and antibiotics to repair the damaged tissue.

Regenerating healthy tissue in a cancer-ridden liver, healing a biopsy site and providing wounded soldiers in battle with pain-killing, infection-fighting medical treatment are among the myriad uses the scientists foresee for the new technology.

The patented invention by Joel Schneider, associate professor of chemistry and biochemistry, and Darrin Pochan, associate professor of materials science, and their research groups marks a major step forward in the development of hydrogels for medical applications.

Formulating hydrogels as delivery vehicles for cells extends the uses of these biopolymers far beyond soft-contact lenses into an intriguing realm once viewed as the domain of science fiction, including growing bones and organs to replace those that are diseased or injured.

“This is an area that will be exploding over the next decade,” Pochan says.

Hydrogels are formed from networks of super-absorbent, chain-like polymers. Although they are not soluble in water, they soak up large amounts of it, and their porous structure allows nutrients and cell wastes to pass right through them.

Schneider and Pochan and their research teams have been focusing on developing peptide-based hydrogels that, once implanted in the human body, will become scaffolds for cells to hold onto and grow--cells such as fibroblasts, which form connective tissue, and osteoblasts, which form bone.

“They're like rebar when you're building something with concrete,” Schneider says. “They give the cement something to hang onto.”





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Breakthrough Video Game for Teens Helps Save Lives

A new video game called “Re-mission” is designed to give young cancer patients a sense of power and control over their disease. Rated T for teen, the 3D game is a 20 level journey through the bodies of fictional patients with different types of cancer. Players control a nanobot named Roxxi. The task? Blast cancer cells, battle bacterial infections, and manage realistic, life-threatening side effects.

But the game is more than a fun challenge. Studies show that young cancer patients who play the game are more likely to take their medicine, undergo needed therapy and understand their illness. That's because the game is geared to help teenagers better adhere to their cancer treatment and embrace vital behaviors to improve their health.

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Critical Protein Prevents DNA Damage From Persisting Through Generations

A protein long known to be involved in protecting cells from genetic damage has been found to play an even more important role in protecting the cell's offspring. New research by a team of scientists at Rockefeller University, Howard Hughes Medical Institute and the National Cancer Institute shows that the protein, known as ATM, is not only vital for helping repair double-stranded breaks in DNA of immune cells, but is also part of a system that prevents genetic damage from being passed on when the cells divide.

Early in the life of B lymphocytes -- the immune cells responsible for hunting down foreign invaders and labeling them for destruction -- they rearrange their DNA to create various surface receptors that can accurately identify different intruders, a process called V(D)J recombination. Now, in an study published online in the journal Cell, Rockefeller University Professor Michel Nussenzweig, in collaboration with his brother André Nussenzweig at NCI and their colleagues, shows that when the ATM protein is absent, chromosomal breaks created during V(D)J recombination go unrepaired, and checkpoints that normally prevent the damaged cell from replicating are lost.

Normal lymphocytes contain a number of restorative proteins, whose job it is to identify chromosomal damage and repair it or, if the damage is irreparable, prevent the cell from multiplying. Earlier research by André and Michel Nussenzweig, who is an investigator at HHMI, had identified other DNA repair proteins that are important during different phases of a B lymphocyte's life. It was during one of these studies, which examined genetic damage late in the life of a B cell, that they came across chromosomal breaks that could not be explained.

So the researchers began to look into the potential role of V(D)J recombination. "We were not expecting it to be responsible for the breaks we were seeing," says Michel, Sherman Fairchild Professor and head of the Laboratory of Molecular Immunology. "Because for it to be responsible, the breaks would have had to happen early on, the cell would have to divide, mature, maintain the breaks, and stay alive with broken chromosomes."
This, in fact, was precisely what they found.

The ATM protein appears to have two roles in a B cell: It helps repair the DNA double-strand breaks, and it activates the cell-cycle checkpoint that prevents genetically damaged cells from dividing. "ATM is required for a B cell to know that it has a broken chromosome. And if it doesn't know that it seems to be able to keep on going," says Michel.

Since the ATM protein is mutated in a number of lymphomas -- cancers of the lymph and immune system -- the new finding suggests to researchers that the lymphocytes could have been living with DNA damage for a long time, and that this damage likely plays a role in later chromosomal translocations, rearrangements of genetic materials that can lead to cancer.

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Video: Robotic Device Changes Way Cancer Patients Treated

A robotic device called the CyberKnife System is enabling physicians to aggressively treat tumors that were once considered inoperable.

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Researchers Find Deadly Prescription Drug Effects Six Years Before FDA

Northwestern University's Charles Bennett, M.D., is a super sleuth of potentially deadly prescription drug reactions. He leads a national SWAT team of doctors called RADAR (Research on Adverse Drug Events and Reports) based out of Northwestern's Feinberg School of Medicine.

They swoop in to investigate early signs of trouble years before the Food and Drug Administration (FDA) takes notice.

A new study by Bennett, the A.C. Buehler professor in Economics and Aging at Northwestern's Feinberg School of Medicine, and a hematologist and oncologist at Northwestern Memorial Hospital, found RADAR identified serious drug reactions six years earlier than the FDA and drug companies.

RADAR's proactive safety efforts and reports also were much more comprehensive than those from the FDA or drug companies, according to the study. RADAR's reports provided doctors with important medical insights as well as guidance for prevention, diagnosis and treatment.
The study will be published in Archives of Internal Medicine.

Since Bennett launched RADAR in 1998, his research has resulted in black box warnings on billion dollar drugs like Plavix that may have saved thousands of lives. He has also provided guidance to help physicians more safely administer drugs. More than 100,000 people die each year from reactions to medications. The FDA is under attack for its passive and inefficient methods of learning about these problems.

Why is RADAR so nimble" Bennett's network includes hematologists and oncologists around the country and the world. His phone rings weekly with calls from concerned doctors alerting him to possible new trouble. After such a call, Bennett probes for clues that led to a life-threatening reaction to a drug. ‘What's the age and weight of the patient, x-rays, details of the physical exam and blood tests"' he'll ask. He'll canvas doctors to see if they've seen similar cases. If a vital piece of evidence is missing, Bennett even will track down a doctor at home on a Sunday and ask her to drive back to her office to check a chart. Then Bennett and his team fit all the puzzle pieces together to figure out what happened and how to prevent it in the future.

The new study also shows, however, that the FDA and drug companies were faster than RADAR to spread the word about serious adverse drug reactions. RADAR relies on publishing its studies in peer-reviewed medical journals, a process that takes longer than the FDA's warning letters to doctors and the drug companies' package inserts.

Thus, it's time for a formal collaboration between RADAR and the FDA to wed their strengths, said Bennett, who also is co-director for cancer control of the Robert H. Lurie Comprehensive Cancer Center.

"We need to work together as partners," Bennett says of the FDA. "Pharmaceutical side effects are one of the top five causes of death in this country. We want to move it out of the top five. This is the way to start that process and save thousands of lives."

Bennett envisions a formal partnership with the FDA in which he would share RADAR's investigations on safety issues, arrive at a joint insight on drug problems and have the FDA distribute the information to doctors.


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