Research creates nanoparticles perfectly formed to tackle cancer

ScienceDaily (June 8, 2011) — Researchers from the University of Hull have discovered a way to load up nanoparticles with large numbers of light-sensitive molecules to create a more effective form of photodynamic therapy (PDT) for treating cancer.

See Also:Health & MedicineLung CancerProstate CancerCancerMatter & EnergyOpticsNanotechnologyOrganic ChemistryReferenceNanomedicineMetastasisNanoparticleInflammation

Photodynamic therapy uses molecules which, when irradiated with light, cause irreparable damage to cells by creating toxic forms of oxygen, called reactive oxygen species. Most PDT works with individual light-sensitive molecules -- but the new nanoparticles could each carry hundreds of molecules to a cancer site.

A number of different light-sensitive molecules -- collectively known as photosensitisers -- are used in PDT and each absorbs a very specific part of the light spectrum. The research team -- from the University of Hull's Department of Chemistry -- placed one kind of photosensitiser inside each nanoparticle and another on the outside, which meant that far more reactive oxygen species could be created from the same amount of light. The findings are published in the current issue of Molecular Pharmaceutics.

The nanoparticles have also been designed to be the perfect size and shape to penetrate easily into the tumour, as lead researcher, Dr Ross Boyle, explains.

"Small cancer tumours get nutrients and oxygen by diffusion, but once tumours reach a certain size, they need to create blood vessels to continue growing, " he says. "These new blood vessels, or neovasculature, are 'leaky' because the vessel walls are not as tightly knit as normal blood vessels. Our nanoparticles have been designed so the pressure in the blood vessels will push them through the space between the cells to get into the tumour tissue."

The nanoparticles are made from a material that limits the leaching of its contents while in the bloodstream, but when activated with light, at the tumour, the toxic reactive oxygen species can diffuse freely out of the particles; meaning that damage is confined to the area of the cancer.

The researchers tested the nanoparticles on colon cancer cells, and while they were able to penetrate the cells, they also found that the nanoparticles could still be effective when near -- rather than inside -- the cancer cells.

"Some types of cancer cell are able to expel conventional drugs, so if we can make this kind of therapy work simply by getting the nanoparticles between the cancer cells, rather than inside them, it could be very beneficial," says Dr Boyle.

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New 3-D tumor model: Step toward speeding cancer drug research

ScienceDaily (June 8, 2011) — A team of scientists has developed a way to coax tumor cells in the lab to grow into 3-D spheres. Their discovery takes advantage of an earlier technique of producing spherical cavities in a common polymer and promises more accurate tests of new cancer therapies.

See Also:Health & MedicineLung CancerBrain TumorCancerMatter & EnergyPhysicsGrapheneMaterials ScienceReferenceNanomedicineMetastasisTumor suppressor geneTumor

As team leader Michael R. King, Ph.D., of Cornell University explains, "Sometimes engineering research tends to be a case of a hammer looking for a nail. We knew our previous discovery was new and it was cool. And now we know it's useful."

Three years ago, the team -- in collaboration with Lisa DeLouise, Ph.D., MPD, of Rochester, N.Y. -- perfected a low-cost, easy fabrication technique to make spherical cavities in PDMS (polydimethylsiloxane), a widely used silicon organic polymer. More recently, the Cornell team discovered that these cavities could be used as a scaffolding to grow numerous tumor spheroids, which could serve as realistic models for cancer cells. The Cornell team's work appears in the current issue of Biomicrofluidics, a publication of the American Institute of Physics.

The three-dimensional spheroids hold the potential to speed cancer drug discovery by providing a realistic and easily accessible substrate on which to test drugs. Their 3-D nature is an asset because in the body, tumor cells grow in 3-D -- yet most laboratory studies of cancer have been done in 2-D, with a single layer of cancer cells grown on the bottom of a petri dish. Too often a promising 2-D drug candidate fails when it enters the 3-D stage of animal testing. The new 3-D tumor spheroids may help eliminate that problem. They also offer a realistic tumor oxygen environment that cues the blood vessel growth that nourishes tumors -- an appealing target for anti-cancer drug design.

"Basically, any laboratory that works with cells could adopt our new spherical microcavity system to do their own 3-D experiments or drug screening on hundreds or even thousands of little tumor spheroids," said King.

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B-cell lymphoma: New research provides breakthrough in understanding common cancer

ScienceDaily (June 10, 2011) — Researchers from the University of Sheffield have discovered valuable insight into how people develop B-cell lymphoma, one of the most common cancers.

See Also:Health & MedicineLymphomaGenesBrain TumorBreast CancerDiseases and ConditionsCancerReferenceLymphomaTumorLeukemiaEpstein-Barr virus

The team, from the University's Institute for Cancer Studies and funded by Leukaemia and Lymphoma Research, Biotechnology and Biological Sciences Research Council (BBSRC) and Yorkshire Cancer Research, found that a mechanism different to that previously thought to be the cause of lymphoma may be responsible for the development of the disease.

Lymphoma is a type of cancer that affects the blood, originating in the lymph glands. B-cells are the immune cells in the human body that are responsible for producing antibodies to fight infections and provide long-term immunity. B-cell lymphomas include both Hodgkin's lymphomas and most non-Hodgkin's lymphomas.

Prior to this research, the main theory to explain the origins of lymphoma was the malfunction of a mechanism (somatic hypermutation) used by B-cells to modify the genes coding for antibodies. This mechanism is required to produce highly specific antibodies, but it also accidentally alters other genes, leading to lymphoma.

However, the team from the University knew that this theory only accounted for affecting a handful of genes, and the model could only explain certain types of lymphoma.

Led by Dr Thierry Nouspikel, the researchers discovered another mechanism, which potentially affects many more genes and can account for a wider palette of lymphomas. The research found that B-cells actually do not repair the bulk of their DNA and only take care of the few genes they are using. When the B-cells are inert in the blood flow, this is not a problem. However, when they receive a stimulation (e.g. an infection) they start to proliferate and then produce antibodies.

To proliferate they must replicate their DNA, and replication of damaged DNA results in the introduction of mutations, the accumulation of which can lead to lymphoma. Dr Nouspikel's team have designed a novel method to specifically detect such mutations, and have proved that they do occur in genes that have been implicated in lymphoma.

The researchers demonstrated that B-cells are deficient in one of the main DNA repair pathways, known as Nucleotide Excision Repair. This pathway repairs a lot of different DNA lesions, including UV-induced damage and chemical adducts (e.g. from air pollution and cigarette smoke). Their model therefore explains why strong UV exposure (e.g. unprotected sun bathing) is the number one environmental risk factor for lymphoma and also supports the evidence that exposure to air pollution and smoking are also risk factors.

Dr Nouspikel said: "Lymphoma is one of the ten most frequent cancers in adults in the UK, and the third among children. If we want to come up with efficient strategies for prevention and therapy, it is crucial to understand what causes it. The novel mechanism we have discovered potentially accounts for the development of many different types of lymphoma. It may also explain why strong exposure to sunlight is the main environmental risk factor for this cancer."

The research is due for publication in Blood on 9 June 2011 and will also be published in Cell Cycle on 15 July 2011.

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Arthritis patients taking newer treatments do not have an overall increased cancer risk, research finds

ScienceDaily (May 27, 2011) — Newer biologic treatments, including infliximab (Remicade), adalimumab (Humira), certolizumab pegol (Cimzia), golimumab (Simponi) and etanercept (Enbrel), used in patients with arthritis do not increase the risk of cancer, according to data from over 13,000 patients presented at the EULAR 2011 Annual Congress.

See Also:Health & MedicineArthritisBreast CancerCancerColon CancerCrohn's DiseaseOvarian CancerReferenceArthritisRheumatoid arthritisCOX-2 inhibitorPsoriasis

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Breast cancer linked to obesity gene, new research suggests

ScienceDaily (May 23, 2011) — New research aimed to better identify the genetic factors that lead to breast cancer has uncovered a link between the fat mass and obesity associated gene (FTO) and a higher incidence of breast cancer. According to the study conducted at Northwestern Memorial Hospital, people who possess a variant of the FTO gene have up to a 30 percent greater chance of developing breast cancer. Research to identify why the link exists is ongoing, but experts say the finding takes us one step closer to personalized medicine based on genetic risk which would allow for better monitoring and prevention of illness, as well as targeted treatment.

See Also:Health & MedicineBreast CancerPersonalized MedicineCancerDiseases and ConditionsColon CancerOvarian CancerReferenceBRCA1BRCA2Tumor suppressor geneBreast reconstruction

"This is a fascinating early finding, which fits with the known connections between obesity and breast cancer," said Virginia Kaklamani, MD, oncologist at Northwestern Memorial, co-director of the Cancer Genetics Program at the Robert H. Lurie Comprehensive Cancer Center of Northwestern University and lead author of the study.

Each individual carries the FTO gene, but only 18 percent have this variant of the gene. Kaklamani, who specializes in cancer genetics, says testing for the FTO variant is not available currently, but it may be available in the future, similar to how genetic testing for the BRCA gene mutation exists today.

"Ten years ago we didn't know about the BRCA gene mutation which has been linked to breast and ovarian cancer. Today, we offer genetic testing and a specialized clinic for those at risk in order to minimize their risk and detect any indication of cancer early," said Kaklamani, who is also an associate professor of medicine at Northwestern University Feinberg School of Medicine. "This knowledge helps us better identify who is at an increased risk so one day, we can counter that risk through preventative measures and advanced screening."

The research, published in BMC Medical Genetics is part of an ongoing group of studies to further knowledge of genetic risk factors for breast cancer.

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