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Archive for the ‘Biomedicine’ Category

Immune System Trained to Kill Cancer

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A year ago, when chemotherapy stopped working against his leukemia, William Ludwig signed up to be the first patient treated in a bold experiment at the University of Pennsylvania. Mr. Ludwig, then 65, a retired corrections officer from Bridgeton, N.J., felt his life draining away and thought he had nothing to lose.

Doctors removed a billion of his T-cells — a type of white blood cell that fights viruses andtumors — and gave them new genes that would program the cells to attack his cancer. Then the altered cells were dripped back into Mr. Ludwig’s veins.

At first, nothing happened. But after 10 days, hell broke loose in his hospital room. He began shaking with chills. His temperature shot up. Hisblood pressure shot down. He became so ill that doctors moved him into intensive care and warned that he might die. His family gathered at the hospital, fearing the worst.

A few weeks later, the fevers were gone. And so was the leukemia.

There was no trace of it anywhere — no leukemic cells in his blood or bone marrow, no more bulging lymph nodes on his CT scan. His doctors calculated that the treatment had killed off two pounds of cancer cells.

A year later, Mr. Ludwig is still in complete remission. Before, there were days when he could barely get out of bed; now, he plays golf and does yard work.

“I have my life back,” he said.

Mr. Ludwig’s doctors have not claimed that he is cured — it is too soon to tell — nor have they declared victory over leukemia on the basis of this experiment, which involved only three patients. The research, they say, has far to go; the treatment is still experimental, not available outside of studies.

But scientists say the treatment that helped Mr. Ludwig, described recently in The New England Journal of Medicine and Science Translational Medicine, may signify a turning point in the long struggle to develop effective gene therapies against cancer. And not just for leukemia patients: other cancers may also be vulnerable to this novel approach — which employs a disabled form of H.I.V.-1, the virus that causes AIDS, to carry cancer-fighting genes into the patients’ T-cells. In essence, the team is using gene therapy to accomplish something that researchers have hoped to do for decades: train a person’s own immune system to kill cancer cells.

Two other patients have undergone the experimental treatment. One had a partial remission: his disease lessened but did not go away completely. Another had a complete remission. All three had had advanced chronic lymphocytic leukemia and had run out of chemotherapy options. Usually, the only hope for a remission in such cases is a bone-marrow transplant, but these patients were not candidates for it.

Dr. Carl June, who led the research and directs translational medicine in the Abramson Cancer Center at the University of Pennsylvania, said that the results stunned even him and his colleagues, Dr. David L. Porter, Bruce Levine and Michael Kalos. They had hoped to see some benefit but had not dared dream of complete, prolonged remissions. Indeed, when Mr. Ludwig began running fevers, the doctors did not realize at first that it was a sign that his T-cells were engaged in a furious battle with his cancer.

Other experts in the field said the results were a major advance.

“It’s great work,” said Dr. Walter J. Urba of the Providence Cancer Center and Earle A. Chiles Research Institute in Portland, Ore. He called the patients’ recoveries remarkable, exciting and significant. “I feel very positive about this new technology. Conceptually, it’s very, very big.”

Dr. Urba said he thought the approach would ultimately be used against other types of cancer as well as leukemia and lymphoma. But he cautioned, “For patients today, we’re not there yet.” And he added the usual scientific caveat: To be considered valid, the results must be repeated in more patients, and by other research teams.

Dr. June called the techniques “a harvest of the information from the molecular biology revolution over the past two decades.”

Hitting a Genetic Jackpot

To make T-cells search out and destroy cancer, researchers must equip them to do several tasks: recognize the cancer, attack it, multiply, and live on inside the patient. A number of research groups have been trying to do this, but the T-cells they engineered could not accomplish all the tasks. As a result, the cells’ ability to fight tumors has generally been temporary.

The University of Pennsylvania team seems to have hit all the targets at once. Inside the patients, the T-cells modified by the researchers multiplied to 1,000 to 10,000 times the number infused, wiped out the cancer and then gradually diminished, leaving a population of “memory” cells that can quickly proliferate again if needed.

The researchers said they were not sure which parts of their strategy made it work — special cell-culturing techniques, the use of H.I.V.-1 to carry new genes into the T-cells, or the particular pieces of DNA that they selected to reprogram the T-cells.

The concept of doctoring T-cells genetically was first developed in the 1980s by Dr. Zelig Eshhar at the Weizmann Institute of Science in Rehovot, Israel. It involves adding gene sequences from different sources to enable the T-cells to produce what researchers call chimeric antigen receptors, or CARs — protein complexes that transform the cells into, in Dr. June’s words, “serial killers.”

 

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Forever young drug ? The pill that will keep you youthful by preventing the ills of old age

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Miracle cure? the pill could prevent many of the ills of old age A ‘forever young’ drug that allows people to grow old gracefully could be available in just ten years, a leading scientist said last night.

Professor Linda Partridge, an expert in the genetics of ageing, said that the science is moving so quickly that it will soon be possible to prevent many of the ills of old age.

By taking a pill a day from middle-age, we will grow old free from illnesses of the body and mind such as Alzheimer’s and heart disease.

People could work for longer – or simply make the most of their retirement. Some research even suggests skin and hair will retain its youthful lustre.

Professor Partridge, of University College London, said: ‘I would be surprised if there weren’t things within ten years. If told you could take a drug that has minimal side-effects and that’s going to keep you healthy for another five or ten years and then you’ll drop off your perch without disability, most people would want it.’

Extraordinary as the professor’s prediction may seem, it is based on a host of promising scientific studies from around the world.

They have discovered key genes linked to longevity and health – and found ways of tinkering with them, at least in animals.

In one of the remarkable examples, a Harvard University doctor made old mice young again, in experiments that mirrored the plot of The Curious Case Of Benjamin Button, where the lead character played by Brad Pitt ages in reverse.

At the start of the experiment, the animals’ skin, brains, guts and other organs resembled those of an 80-year-old person.

 

In development: One experiment saw a professor make old mice young again

In development: One experiment saw a professor make old mice young again.

Within just two months of being given a drug that switches on a key enzyme, the creatures had grown so many new cells that they had almost completely rejuvenated.

Remarkably, the male mice went from being infertile to fathering large litters.

Other research has shown that chains of reactions in the body involving insulin and related hormones are key to health and ageing. This means that years of research into diabetes could have yielded medicines that can be reinvented as anti-ageing drugs.

Professor Partridge told the Cheltenham Science Festival that some medicines abandoned by drug companies may soon be dusted off and put to use. She said:

‘There are drugs there already, some of them are just sitting in cupboards. I’d be surprised if people don’t start taking them out.

‘The principle is for drugs that if taken from middle-age will ward off quite a broad array of diseases rather than doing things piece-meal or acting when the diseases appear.’

However, she said any drugs would have to be shown to be extremely safe before they were given to healthy people to combat ageing.

 

 

Via DailyMail

US approves new HIV drug

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The US Food and Drug Administration on Friday approved a new drug, Edurant, to fight HIV in combination with other antiretrovirals already on the market.

Made by the New Jersey based Tibotec Therapeutics, Edurant helps block the virus from replicating and is part of a class of drugs known as non-nucleoside reverse transcriptase inhibitor.

The pill is to be taken once daily with food, the FDA said.

“Patients may respond differently to various  or experience varied side effects,” said Edward Cox, director of the office of antimicrobial products in the FDA’s Center for Drug Evaluation and Research.

“FDA’s approval of Edurant provides an additional treatment option for patients who are starting .”

The approval followed phase II and II trials that showed that patients who had not received previous therapy saw an 83 percent lower viral load after they took Edurant along with other antiretroviral drugs.

Side effects included depression, insomnia, headache and rash.

(c) 2011 AFP

Via MedicalXpress

HIV discovery brings vaccine closer

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HIV virusAn investigation into the activity of antibodies in HIV patients has revealed that the HIV virus can mutate in order to ‘escape’ this immune response.

Human ADCC (antibody-dependent cell-mediated cytotoxicity) antibodies – which are often present in high concentrations in HIV-infected patients – have been strongly implicated in the protection from HIV in several vaccine trials.

However, we still do not how these antibodies really work, and researchers hope that a better understanding of their processes could lead to HIV treatments that work by boosting the antibodies’ defences.

“These results show what a slippery customer the HIV virus is, but also shows that these ADCC antibodies are really forcing the virus into changing, in ways that cause it to be weaker,” said lead author Stephen Kent from the University of Melbourne in Australia.

Pinpointing mutation’s location

The term ADCC describes an immune phenomenon whereby antibodies bind to cells infected with a virus. This process activates ‘natural killer cells’ that then attack virus-infected cells.

These natural killer cells destroy infected cells by releasing cytokines, such as interferon-gamma, which are small cell-signalling protein molecules that are secreted by numerous immune system cells and cells in the nervous system.

To investigate further, the researchers analysed blood samples of HIV patients to find where the ADCC antibodies were attacking the virus. They did this by using a staining technique to detect exactly which parts of the virus – that is, which peptide segments – were stimulating the release of cytokines.

Stopping the virus taking hold

The team sequenced the patient’s own virus and found mutations at sites targeted by these ADCC antibodies. Their technique also allowed them to study how the mutations arose over time.

The assay proved additionally valuable because it can be performed on serum or plasma samples, and not cells, which makes for a much easier and less invasive procedure where patients are concerned.

The results, published in Proceedings of the National Academy of Sciencestis month, show that ADCC antibodies force the virus into changing in ways that cause it to be weaker, said Kent.

“They also imply that if good ADCC antibodies were available prior to infection, via a vaccine, we might be able to stop the virus taking hold. This is the holy grail.”

According to co-author Ivan Stratov from the University of Melbourne, “The potential to use ADCC antibodies to kill virus infected cells (rather than just free virions) is a great advance in HIV vaccine research. And harnessing natural killer cells to combat HIV could add great potency to existing vaccine strategies.”

The team is now working on purifying and producing these antibodies in bulk quantities and testing them in a simian (primate) infection model to see if they can prevent infection – by the simian immunodeficiency virus – in monkeys.

Putting pressure on the virus

Over 40 million people around the world have acquired HIV or AIDS, according to the latest toll compiled by the World Health Organisation (WHO) and UNAIDS.

Although the disease was identified over 25 years ago, there is still no vaccine or cure but antiretroviral drugs can be used to manage the condition.

“The work … shows that these types of antibodies are initially quite effective in eliminating virus but eventually they fail because the virus mutates too quickly,” said Marc Pellegrin from the Walter & Eliza Hall Institute of Medical Research in Melbourne, who was not involved in the study.

“The implications … are that our immune system, through these antibodies, is able to exert considerable pressure on the virus to the point where it must mutate to persist and survive. The corollary is that if we can boost this type of response and make it more robust and broad we can better control HIV.”

Via CosmoMag

Solar-Powered Eye Sensor

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A cornea-implanted computer can monitor the eyeball’s pressure.

In the future, that twinkle in your loved one’s eye might be an implanted solar-powered pressure monitor. At the 2011 IEEE International Solid-State Circuits Conference in February, engineers from the University of Michigan, in Ann Arbor, described their work on a cubic-millimeter-size sensor meant to monitor pressure inside the eye. The researchers have yet to test the device in human eyes or animal ones, but they hope their system will one day thwart optic nerve damage brought on by glaucoma.

To determine a glaucoma patient’s treatment, doctors must monitor pressure inside the eye, says Gregory Chen, a graduate student of electrical engineering at Michigan. Today’s methods gauge that pressure by pushing on the cornea, the eye’s clear outer coating. The results may be inaccurate: “If you just happen to have a really thick cornea, your eye is going to be harder, no matter what the pressure is,” Chen says. The engineers’ prototype device would allow a microelectromechanical systems (MEMS) capacitive sensor to record pressure from inside the eye about every 15 minutes and store it to static RAM. Once a day, the system would wirelessly transmit the day’s data, via two on-chip inductors, to a wand. The inductors would send the data at both 400- and 900-megahertz carrier frequencies, as a means of mitigating the signal’s noise and increasing its range.

Powering this daily transmission was one of the team’s biggest challenges, says Mohammad Hassan Ghaed, the Michigan grad student who designed the radio system. “The common way of transmitting data is to use an external antenna,” he says, “but in this millimeter-cubed space, we don’t have that luxury.” The team designed the diminutive device for easy implantation, but the small size comes at a cost: The device’s inductors require more power to send data than a bigger antenna would, a peak of 47 milliwatts. That was a problem, given that the peak power supplied by their device’s thin-film lithium battery is only about 40 microwatts.

To make up for this shortfall, the system stores enough energy to transmit one bit in a capacitor. The device then sends that bit and refills the capacitor from the battery for another go. The bit-by-bit method provides a transmission rate of around 10 kilobits per second, but with a day’s data totaling around 1.5 Kb, it’s still “near instantaneous,” says Dennis Sylvester, a professor of electrical engineering, who led the team with colleague David Blaauw. The battery itself lasts around 28 days before it’s drained, but the device also includes a miniature solar panel. The team expects that about 10 hours of indoor lighting or 1.5 hours of sunlight daily could recharge it.

“As far as I know, nobody does solar power at this size,” says Pedro Irazoqui, director of the Center for Implantable Devices at Purdue University, who is also developing an implantable glaucoma sensor. Irazoqui praises the Michigan team for its energy-harvesting system and on-chip radios. His own team’s tadpole-shaped device, which is now being tested in rat eyes, uses radio waves from an external source to power a 2.7-mm antenna “tail” for transmission and to charge an onboard supercapacitor.

Irazoqui’s commendation of the Michigan device comes with some caution. “There are a lot of impressive innovations here,” he says, “but until they’ve actually implanted it in a live eye and measured the pressure, they haven’t shown that the device works.” Of particular concern, he says, is that surgeons would need to implant the device in the “very delicate” iris tissue.

The Michigan team notes that human testing is still several years away. “Now that we have a system that is working, we can start to expand into long-term effects,” Blaauw says, noting grad student Razi Haque’s work to optimize the device’s packaging in collaboration with Michigan professor and IEEE Fellow Kensall Wise.

What doesn’t seem to be a concern is that staring into the wearer’s eyes might reveal a speck of cyborg. “We’re expecting to make different colors,” Chen jests. “It’s going to be a fashion statement.”

– Joseph Calamia

Via Solar-Powered Eye Sensor

Written by Nokgiir

May 10, 2011 at 8:26 am

Augmented Reality in a Contact Lens

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A new generation of contact lenses built with very small circuits and LEDs promises bionic eyesight.

The human eye is a perceptual powerhouse. It can see millions of colors, adjust easily to shifting light conditions, and transmit information to the brain at a rate exceeding that of a high-speed Internet connection.

But why stop there?

In the Terminator movies, Arnold Schwarzenegger’s character sees the world with data superimposed on his visual field—virtual captions that enhance the cyborg’s scan of a scene. In stories by the science fiction author Vernor Vinge, characters rely on electronic contact lenses, rather than smartphones or brain implants, for seamless access to information that appears right before their eyes.

These visions (if I may) might seem far-fetched, but a contact lens with simple built-in electronics is already within reach; in fact, my students and I are already producing such devices in small numbers in my laboratory at the University of Washington, in Seattle [see sidebar, “A Twinkle in the Eye“]. These lenses don’t give us the vision of an eagle or the benefit of running subtitles on our surroundings yet. But we have built a lens with one LED, which we’ve powered wirelessly with RF. What we’ve done so far barely hints at what will soon be possible with this technology.

Conventional contact lenses are polymers formed in specific shapes to correct faulty vision. To turn such a lens into a functional system, we integrate control circuits, communication circuits, and miniature antennas into the lens using custom-built optoelectronic components. Those components will eventually include hundreds of LEDs, which will form images in front of the eye, such as words, charts, and photographs. Much of the hardware is semitransparent so that wearers can navigate their surroundings without crashing into them or becoming disoriented. In all likelihood, a separate, portable device will relay displayable information to the lens’s control circuit, which will operate the optoelectronics in the lens.

These lenses don’t need to be very complex to be useful. Even a lens with a single pixel could aid people with impaired hearing or be incorporated as an indicator into computer games. With more colors and resolution, the repertoire could be expanded to include displaying text, translating speech into captions in real time, or offering visual cues from a navigation system. With basic image processing and Internet access, a contact-lens display could unlock whole new worlds of visual information, unfettered by the constraints of a physical display.

Besides visual enhancement, noninvasive monitoring of the wearer’s biomarkers and health indicators could be a huge future market. We’ve built several simple sensors that can detect the concentration of a molecule, such as glucose. Sensors built onto lenses would let diabetic wearers keep tabs on blood-sugar levels without needing to prick a finger. The glucose detectors we’re evaluating now are a mere glimmer of what will be possible in the next 5 to 10 years. Contact lenses are worn daily by more than a hundred million people, and they are one of the only disposable, mass-market products that remain in contact, through fluids, with the interior of the body for an extended period of time. When you get a blood test, your doctor is probably measuring many of the same biomarkers that are found in the live cells on the surface of your eye—and in concentrations that correlate closely with the levels in your bloodstream. An appropriately configured contact lens could monitor cholesterol, sodium, and potassium levels, to name a few potential targets. Coupled with a wireless data transmitter, the lens could relay information to medics or nurses instantly, without needles or laboratory chemistry, and with a much lower chance of mix-ups.

Three fundamental challenges stand in the way of building a multipurpose contact lens. First, the processes for making many of the lens’s parts and subsystems are incompatible with one another and with the fragile polymer of the lens. To get around this problem, my colleagues and I make all our devices from scratch. To fabricate the components for silicon circuits and LEDs, we use high temperatures and corrosive chemicals, which means we can’t manufacture them directly onto a lens. That leads to the second challenge, which is that all the key components of the lens need to be miniaturized and integrated onto about 1.5 square centimeters of a flexible, transparent polymer. We haven’t fully solved that problem yet, but we have so far developed our own specialized assembly process, which enables us to integrate several different kinds of components onto a lens. Last but not least, the whole contraption needs to be completely safe for the eye. Take an LED, for example. Most red LEDs are made of aluminum gallium arsenide, which is toxic. So before an LED can go into the eye, it must be enveloped in a biocompatible substance.

Photos: University of Washington

So far, besides our glucose monitor, we’ve been able to batch-fabricate a few other nanoscale biosensors that respond to a target molecule with an electrical signal; we’ve also made several microscale components, including single-crystal silicon transistors, radio chips, antennas, diffusion resistors, LEDs, and silicon photodetectors. We’ve constructed all the micrometer-scale metal interconnects necessary to form a circuit on a contact lens. We’ve also shown that these microcomponents can be integrated through a self-assembly process onto other unconventional substrates, such as thin, flexible transparent plastics or glass. We’ve fabricated prototype lenses with an LED, a small radio chip, and an antenna, and we’ve transmitted energy to the lens wirelessly, lighting the LED…

All the basic technologies needed to build functional contact lenses are in place. We’ve tested our first few prototypes on animals, proving that the platform can be safe. What we need to do now is show all the subsystems working together, shrink some of the components even more, and extend the RF power harvesting to higher efficiencies and to distances greater than the few centimeters we have now. We also need to build a companion device that would do all the necessary computing or image processing to truly prove that the system can form images on demand. We’re starting with a simple product, a contact lens with a single light source, and we aim to work up to more sophisticated lenses that can superimpose computer-generated high-resolution color graphics on a user’s real field of vision.

The true promise of this research is not just the actual system we end up making, whether it’s a display, a biosensor, or both. We already see a future in which the humble contact lens becomes a real platform, like the iPhone is today, with lots of developers contributing their ideas and inventions. As far as we’re concerned, the possibilities extend as far as the eye can see, and beyond.

The author would like to thank his past and present students and collaborators, especially Brian Otis, Desney Tan, and Tueng Shen, for their contributions to this research.

Via Augmented Reality in a Contact Lens 

sidenote : This article is from 09 but I thought I’d repost because it is interesting nonetheless.

Written by Nokgiir

May 10, 2011 at 8:11 am

In a genetic research first, researchers turn zebrafish genes off and on

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Mayo Clinic researchers have designed a new tool for identifying protein function from genetic code. A team led by Stephen Ekker, Ph.D., succeeded in switching individual genes off and on in zebrafish, then observing embryonic and juvenile development. The study appears in the journal Nature Methods.

The work could help shed light on health-related problems such as how spread, what makes some people more prone to heart attacks, or how genes factor in addiction. More complicated issues, like the genetics of behavior, plasticity and , stress, learning and epigenetics, could also be studied with this method.

The research at Mayo Clinic’s Zebrafish Core Facility could help further unify biology and genomics by describing the complex interrelations of DNA, gene function and gene-protein expression and migration. The study examines  and function from 350 loci among the zebrafish’s approximately 25,000 protein-encoding genes. Researchers plan to identify another 2,000 loci.

“I consider this particular system a toolbox for answering fundamental scientific questions,” says Dr. Ekker, a Mayo Clinic molecular biologist and lead author of the article. “This opens up the door to a segment of biology that has been impossible or impractical with existing genomics research methods.”

For the First Time

The study includes several technical firsts in . Those include a highly effective and reversible insertional transposon mutagen. In nearly all loci tested, endogenous expression knockdown topped 99 percent.

The research yielded the first collection of conditional mutant alleles outside the mouse; unlike popular mouse conditional alleles that are switched from “on” to “off,” zebrafish mutants conditionally go from “off” to “on,” offering new insight into localized gene requirements. The transposon system results in fluorescence-tagged mutant chromosomes, opening the door to an array of new genetic screens that are difficult or impossible to conduct using more traditional mutagenesis methods, such as chemical or retroviral insertion.

The project also marks the first in vivo mutant protein trap in a vertebrate. Leveraging the natural transparency of the zebrafish larvae lets researchers document gene function and protein dynamics and trafficking for each protein-trapped locus. The research also ties gene/protein expression to function in a single system, providing a direct link among sequence, expression and function for each genetic locus.

Researchers plan to integrate information from this study into a gene codex that could serve as a reference for information stored on the vertebrate genome.

Shedding Light on Disease

Researchers exposed translucent zebrafish to transposons, “jumping genes” that move around inside the genome of a cell. The transposons instructed zebrafish cells to mark mutated proteins with a fluorescent protein ‘tag.’

“This makes investigation of a whole new set of issues possible,” Dr. Ekker says. “It adds an additional level of complexity to the genome project.”

Dr. Ekker’s team maintains about 50,000 fish in the Zebrafish Core Facility. To observe, photograph and document mutations of that many minnow-sized fish, the team works with an international team of researchers and gets helps from Rochester public elementary school teachers. Under a program with Mayo Clinic and Winona State University called InSciEd Out (Integrated Science Education Outreach), teachers document mutations and learn about the scientific method.

Provided by Mayo Clinic

Via In a genetic research first, researchers turn zebrafish genes off and on

Written by Nokgiir

May 8, 2011 at 7:33 pm

A Vaccine to Attack Cancer Early

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Most cancer vaccines are intended to rally a patient’s immune system to fight cancers that have already progressed. But the startup company OncoPep, based in North Andover, Massachusetts, is developing a vaccine designed to prevent one kind of cancer—multiple myeloma—by treating patients who have only a precursor of the disease.

Multiple myeloma is a cancer of blood plasma cells. It develops when abnormal plasma cells in bone marrow multiply and accumulate, eventually damaging bones and other tissues in the body, and finally overwhelming the immune system. Currently, treatments can extend the lives of patients with the cancer but not cure it.

The company’s approach grew out of research by Kenneth AndersonNikhil Munshi, and Jooen Bae at the Dana-Farber Cancer Institute in Boston. The researchers deployed a combination of peptides—small pieces of protein—that are known to be specific to multiple myeloma cells and are important for their survival. The goal is to train the immune system to recognize and attack cancer cells bearing these peptides; the vaccine would also contain substances designed to boost immune response.

Plans call for the vaccine to be administered to people diagnosed with smoldering multiple myeloma, a condition in which plasma cells are unusually abundant and produce abnormal proteins but cause no symptoms of disease. Currently, patients with SMM are not treated. Although a majority of them go on to develop symptomatic cancer, it may take many years. Anderson hopes that the ability to detect the cancer in this early phase will make possible early, effective intervention. “The idea would be to prevent the development of an active cancer,” he says. Administering the vaccine to patients before they have received other, possibly debilitating cancer treatments, and while their immune systems are healthy, may give it a better chance of working.

Doris Peterkin, CEO of OncoPep, says that like several other experimental cancer vaccines in development, this one will be matched to people with a particular immune-system type: HLA type A2, the most common type in the U.S. Peterkin says the vaccine is most likely to be effective in these patients because the peptides are have a better chance of triggering an immune response in them.

Ronald Levy, an oncologist and cancer researcher at Stanford University, says that despite the advantages of vaccinating early, targeting this early stage of the disease may pose practical problems in testing the vaccine. Although nearly 80 percent of patients with SMM go on to develop multiple myeloma, they do so at a rate of only about 10 percent per year—so it may take a while to collect enough patients to test the vaccine. And limiting the vaccine to people with a particular HLA type will narrow the already small field. Levy says that the ultimate test of the vaccine’s success will be how well its chosen peptides provoke a specific immune response against the cancer, which has been the challenge for all peptide-based cancer vaccines.

Via Vaccine to Attack Cancer Early

Written by Nokgiir

May 7, 2011 at 5:16 pm