Is Gardasil cost effective?

Several strains of human papillomavirus (HPV) can cause cervical cancer, and two vaccines directed against the currently most important oncogenic strains (i.e., the HPV-16 and HPV-18 serotypes) have been developed.

Despite promising results from clinical trials, sufficient evidence of an effective long term vaccine against cervical cancer is lacking and the overall effect of the vaccines on cervical cancer remains unknown; the real impact of HPV vaccination on cervical cancer will not be known for decades.

The first vaccine against the HPV virus (Gardasil, Merck & Co) was licensed in 2006 for use in girls and women ages 9 to 26. Health officials recommend it for girls at age 11 or 12, and some doctors offer it to women in their 20s in "catch-up" vaccination campaigns. Merck also wants to market it to women ages 27 to 45, but so far the U.S. Food and Drug Administration has denied that request.

Gardasil is given in three doses over six months and costs about $375. It targets the two types of HPV, believed to be responsible for about 70 percent of cervical cancer cases, and two other types that cause most genital warts. The virus is spread by sexual activity.

Health officials say it's best to give the shots to girls at age 11 or 12, before they begin having sex. Some parents think that age is too young for a vaccination campaign against a sexually transmitted disease. But that is when the shots make the most economic sense, researchers found.

In the current edition of the New England Journal of Medicine, researchers used computer models to predict the health outcomes of girls and women who get the vaccination as well as Pap tests or other screenings, which are still recommended for vaccine recipients. Their calculation included the cost of the vaccine, screenings and treating cervical cancer and other illnesses targeted by the vaccine.

To determine cost-effectiveness, they used widely accepted economic measures of how much society is willing to pay to extend the life of a person by a year. They set a figure of $43,600 per year for the Gardasil vaccination of each 12-year-old girl, well below the $100,000 mark seen as an upper range for cost-effectiveness. However, the assumption is that the vaccine gives lifetime protection, which we don't know is true because the drug is too new and the data too preliminary.

The trends in the analysis suggested that as you get older, the vaccine becomes less cost-effective. This would imply that the earlier a female is vaccinated, the better the odds she will avoid HPV-caused cervical disease, thus lowering health-care costs in the long run.



References:

New England Journal of Medicine (free full text)
CNN

BRCA mutations in breast cancer

Genetic testing for BRCA1 and BRCA2 mutations can provide important information for women who are concerned about their breast and ovarian cancer risks and need to make relevant prevention and medical management decisions.

To date, lifetime risks of breast cancer in individual BRCA1/2 mutation carriers have been challenging to apply in clinical decision making. Published risk estimates vary significantly and are very dependent on the characteristics of the population under study. You can read more about in this article (free PDF download).

Another study interpreted validated functional data from the transactivation activity of BRCA1 in combination with analysis of protein modelling based on the structure of BRCA1 BRCT domains. With additional clinical and structural evidence, they were able to classify all missense variants in the BRCA1 COOH-terminal region. These results brought functional assays for BRCA1 closer to clinical applicability.

Cancer risks in a population-based study of BRCA1/2 mutation carriers have been recently estimated, but the numbers are still in their infancy and may be influenced by different risk factors. It is likely that there is broad variation in breast cancer risk among carriers of BRCA1 and BRCA2 mutations and ethnicity may also confer differences in risks associated with BRCA mutations.

How is cancer formed?

All cancers start with mutations in one single cell. The mutations are located in the cell's DNA and may be inherited, although less than 10% of all cancer mutations are inherited. Usually, the mutation arises as a result of environmental factors.

The DNA mutation may be a single nucleotide change, or a deletion or duplication of the DNA sequence. A change in the genetic sequence can then lead to the production of a mutant protein.

Image via WikipediaIn rare cases such as chronic myeloid leukemia (CML) or gastrointestinal stromal tumours (GIST) one mutation is enough, but in most cancers, it is usually an accumulation of mutations that irreversibly transforms a normal cell into a cancerous one.  As we age, we accumulate more and more mutations as we are exposed to environmental carcinogens and this explains why cancer incidence increases with age.

These mutations can disrupt the cell’s life cycle of growth, proliferation, and death. This leads to the accumulation of more “rogue” cancer cells and the development of a tumour mass.

Normal cells have a natural lifespan and eventually die, a process known as apoptosis, or programmed cell death. They are replaced by new cells and so the process is repeated. Cancer cells do not respond to the signals that regulate cell growth and division. Thus these cells grow unchecked, producing more and more cancer cells.

A cell may die because it is damaged or old. Once a cell is signaled to die, the cell makes proteases and enzymes that degrade its components. The DNA in the nucleus is fragmented, the cell membrane shrinks, and, eventually, a neighboring cell engulfs the cellular remains.

To grow beyond a certain size, tumours must transport nutrients in and excrete wastes. The cancer cells that make up a tumour attract blood vessels to grow into the tumour mass, a process known as angiogenesis. The blood vessels then nourish the tumour just like any organ in the body; because the tumour is made of your own cells, the body does not recognise it as foreign, in the way it would a virus or bacteria.

The age of a cell and its ability to divide is related to structures or telomeres. The telomeres are specialised sequences at the ends of each chromosome and they prevent end-to-end fusion of chromosomes. These telomeres protect the ends of chromosomal DNA from accidents.

As normal cells go through cycles of growth and division, their telomeric DNA gets shorter and shorter and shorter and ultimately so short it can no longer protect the ends of chromosomal DNA. Eventually, the telomeres start fusing, chromosomes start fusing in those cells, and those cells die.

Cancer cells must avoid this problem because they want to grow indefinitely. Instead of dying, they turn on an enzyme called telomerase that is normally expressed only early in embryologic development and in a small number of so-called stem cells in the body.

The telomerase enzyme is able to extend the telomeres, making them longer and longer thereby enabling the cancer cell to go through many cycles of growth and division without worrying about the imminent collapse of its telomeres. The telomerase ensures the telomeres stay very long and essentially protects them from harm.

Most of the deaths from cancer (90%) are due to cancer cells spreading and establishing colonies in other parts of the body, a process known as metastasis. To do that, inactivation of a whole series of controls that normally confines a cell to the site and the tissue where it normally grows occurs, enabling the cancer cells to move to other sites in the body.

Another interesting thing about cancer cells is that they are often different in shape and size to normal cells, and they no longer respond to signals that control normal cellular functions. Our body's immune response is constantly searching for these emerging pre-cancers or pre-tumour cells.  Successful cancers have to avoid detection long enough to grow into a tumour.

The body has two adaptive immune responses, enabling it to adapt to changes in cells in our body, whether they be by infection or other changes, such as cancer. One of these responses is making antibodies produced by B cells, which bind and direct the elimination of those cells. The other response is the T cell immune response where T cells actually kill cells that are changed in the body. The body is in constant surveillance of the cells in our body, so that emerging pre-cancers or pre-tumour cells could be eliminated by the immune response.

So how does cancer arise in the first place?

Well, a cell carries the entire set of genetic instructions, the genome, that makes an entire organism.  The instructions are encoded in DNA as genes and packaged as chromosomes in the nucleus.  DNA is not indestructable and is subject to damage and mutations.  Crucial changes in the genome affect the chance and rate of the development of a cancer cell.

A defining characteristic of cancer cells is that those cells have changes in the nature of the genes that are compared to the normal cells. These changes can be either mutations, or they can be deletion of whole genes, or they can be the addition of extra copies of genes. This is called genomic instability.

The changes in our genes that accumulate in cancer cells can be acquired by a number of mechanisms. One is that during the process of copying the genetic information, mistakes can be made. After the genetic information is copied, it has to be segregated to the two daughter cells. During that segregation process, it is often that the numbers of genes get distributed unevenly to those daughter cells. Cancer cells also have an inability to repair alterations in the DNA.

Overall, you need to acquire multiple changes in the genes or multiple genes, to get cancer, perhaps 5-7 genes on average. Those changes accumulate over a period of time. Some of those changes accelerate the rate of accumulation. A person might have inherited one gene change, for example, and others develop as we age. Developing these mutational changes will weaken the DNA and increase the risk of cancer developing.

Sources (downloadable PDF):

Hallmark of Cancer

FDA approves HER2 test for breast cancer

A genetic test to determine whether a breast cancer patient is likely to respond to treatment with the drug Herceptin (trastuzumab) has been approved by the U.S. Food and Drug Administration.

The SPOT-Light HER2 CISH kit helps calculate how many copies of the HER2 gene, which regulates the growth of cancer cells, are in tumour tissue. A healthy breast cell should have two copies of the HER2 gene, but patients with breast cancer may have many more. Since the gene signals cells when to grow, divide and make repairs, too many copies may cause cells to grow and divide too rapidly.

Herceptin targets HER2 protein, helping stop the growth of such cancer cells in breast cancer patients overproducing that particular protein. HER2 is overexpressed in about 30% of breast cancer cases.

This test can potential provide health care professionals with additional insight on treatment decisions for patients with breast cancer when used with other clinical information and laboratory tests.

The SPOT-Light test counts HER2 genes through a chemically stained sample of removed tumor observed under a standard microscope. Previous tests required more expensive and complex fluorescent microscopes. The SPOT-Light also allows labs to store the tissue for later reference, a feature not possible with previously available tests.

What's stopping EGFR inhibitors from being more effective?

Response rates with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in cancer treatment have been low. However, a recent study may have shed some light by revealing a kinase-independent function of EGFR in maintaining cell survival.

Image via Wikipedia
Using prostate, breast and colon cancer cells, it was demonstrated that small interfering RNA (siRNA)-mediated knockdown of EGFR, but not inhibition of EGFR kinase activity, leads to autophagic cell death. Autophagy can occur when external energy sources are low or unobtainable and, although glucose levels remained constant in cells treated with kinase inhibitors, they were decreased by around 50% in cells transfected with EGFR siRNA.

The study found that EGFR–SGLT1 may confer a survival advantage to cancer cells by maintaining a basal level of intracellular glucose and preventing autophagy. This may help to explain previous data indicating that inhibition of EGFR kinase activity is not sufficient to induce cell death, or to negate all of the functions of EGFR.

Targeting both kinase-dependent and kinase-independent functions of EGFR may be necessary for more successful therapy in the future.

Source:

Cancer Cell (free download)

New gene shows promise in resistant breast cancer

Researchers have identified a new group of compounds that might one day be added to the armamentarium of therapies designed to fight estrogen-fueled breast cancer. The molecule, called TPBM, and related drugs may have a role in treating patients who have become resistant to other hormone-based therapies, such as tamoxifen.



There are a large number of people who have estrogen receptor-positive breast cancer who respond well to hormone therapy. Sometimes, after a number of years, the hormone therapy stops working. Then they are switched to something else. That works for a time before the cancer progresses.



Exactly what is happening in those cancer cells that they become resistant? Perhaps there is another mechanism that can be overcome and this could be one of them.

Some two-thirds of all breast cancers are estrogen receptor-positive and therefore respond to hormonal treatments such as tamoxifen or the newer aromatase inhibitors, letrozole and anastrozole. Tamoxifen works by blocking estrogen receptors on breast cancer cells, while aromatase inhibitors interfere with the body's ability to produce estrogen.

Many of the cancers in this category eventually become resistant to tamoxifen and, in some cases, tamoxifen may even turn the tables and start acting like estrogen, thereby fueling tumour growth and proliferation.

A new study was presented by researchers from the University of North Carolina, Chapel Hill, the University of Colorado Health Sciences Center, Denver, and the University of Illinois, Urbana-Champaign at the annual meeting of the Endocrine Society, in San Francisco.

Through extensive laboratory testing, they identified a group of compounds related to TPBM that interfered with estrogen's effect on breast cancer cells via a different pathway. The molecules work by affecting the way estrogen receptors interact with a woman's DNA.

TPBM has the advantage of being "highly specific" and therefore potentially much less likely to have any unwanted effects on other cells. It also works against tamoxifen when tamoxifen starts fueling tumour growth. The research is promising, but still preliminary at this stage.

New promise for brain cancer patients with glioblastoma multiforme

Image via WikipediaGlioblastoma multiforme patients could live a year longer by taking the new experimental CDX-110 vaccine from Avant Immunotherapeutics and Pfizer, according to two small Phase II studies presented at the American Society of Clinical Oncology meeting recently.

The vaccine targets the tumour-specific molecule EGFR variant III, which is linked with poor prognosis.

Used with the standard chemotherapy treatment, temozolomide, the vaccine extended the length of life and was also mostly well-tolerated in the Phase II ACTIVATE trial of 21 brain cancer patients and the ongoing ACT II study of 23 patients.

Exclusive global rights to the vaccine were picked up by Pfizer of New York, from Avant Immunotherapeutics of Needham, Mass. in April.

GBM is the most common kind of brain tumour and is very aggressive. Average survival is 13 months to 15 months, with about half of patients dying within that timeframe and a few living two to three years. Those with tumors that express EGFRvIII are extremely unlikely to survive past two years. CDX-110 teaches the immune system to attack EGFRvIII on the tumor.

In the ACTIVATE trial, researchers looked at 21 patients with newly-diagnosed EGFRvIII-expressing GBM who had surgical resection and radiation therapy with oral temozolomide, the standard chemotherapy treatment, and did not have tumor progression. Sixteen patients had three doses of the vaccine at two-week intervals with granulocyte-macrophage colony stimulating factor, while the other five initially had placebo and were later given the vaccine.

Patients who received the vaccine had a median survival of 26 months versus 15.2 months for a matched historical cohort, while median-time-to-progression was 14.2 months compared to 7.13 months. No significant adverse events were reported.

In the similarly designed ACT trial of 23 patients, overall survival with the vaccine was estimated at 33.1 months versus 14.3 months for the matched historical cohort, while time-to-progression was 16.6 months, compared to 6.4 months.

Side effects appeared to be mild and tolerable; some patients experienced redness and itchiness at the injection site, but the side effects did not cause them to discontinue treatment. There were also some mild allergic reactions.

The Phase IIb/III trial was designed to include 90 and then 375 patients and began accruing nine months ago, with enrollment due to complete by year's end and data set for release in 2009. Avant's recently-forged partnership with Pfizer could help speed the trial up and could result in changes to the trial design.

Cancer Vaccine Target Pinpointed

Scientists may be one step closer to producing a specific targeted vaccine for killing cancer cells.

UK researchers have identified a unique protein, known as DNGR-1, on immune cells which they hope will help them harness the body's defences to attack a tumour. A vaccine designed to "home in" on the protein would then deliver a message to the immune system to attack the invading cancer. The research is published in the Journal of Clinical Investigation.

The protein is unique to a type of immune cell called a dendritic cell, which is responsible for triggering the body's defence system. Its job is to present pathogens or foreign molecules to other cells of the immune system, which in turn eliminate them.

The results of this research are an important step towards understanding how to create targeted cancer vaccines in the future. The team at Cancer Research UK's London Research Institute said scientists have been searching for proteins or "tags" on dendritic cells for over 30 years.

Dendritic cells are now recognized as the gatekeepers of the immune response, possessing a unique potential for acquisition of antigens at extremely low exposure levels and for efficient presentation of these in an immunogenic form to the naive T-cell system.

In theory a vaccine carrying a foreign molecule from a cancer cell could be targeted to the dendritic cells, which would then prompt the immune system to attack the "invading" cancer. The same approach could potentially be used for treating other diseases such as HIV or malaria.

Vaccines work by triggering an army of immune cells, called T cells, to attack potentially dangerous foreign molecules, like those found on pathogens. Dendritic cells are the messengers, telling the T cells who to attack. The vaccine will carry a sample of the offending molecule and deliver it to DNGR-1 on the dendritic cells, which in turn will present the molecule to the armies of T cells and instruct them to attack.

Although many vaccines have been tested in the clinical, few have proven successful so far. Part of the problem is locating the right target to effectively start the attack reaction over prolonged periods of time. The results based on a more targeted approach will be interesting.

Low levels of Vitamin D linked with poorer outcome in breast cancer

One of the most important abstracts at the forthcoming ASCO meeting suggests that vitamin D deficiency at the time of diagnosis is associated with a worse outcome in breast cancer. The results were reported in an analysis of 512 women treated in Toronto, Ontario.

Many of the women had low levels of vitamin D at the time they were diagnosed with breast cancer; some 37.5% had levels classified as "deficient," and only 24% had levels that were "sufficient". Is this a random or relevant finding?



After a median follow-up of 11.6 years, it was found that compared with women who had normal levels of vitamin D at diagnosis, the women with vitamin D deficiency were 94% more likely to experience metastasis and 73% more likely to die.

It is surprising to find vitamin D deficiency is so common in women diagnosed with breast cancer and that very low vitamin D levels adversely affect patient outcome. Although the data show an association, it is impossible say it is causal until the results are replicated.

Source:

ASCO 2008 Annual Meeting

Chemical prevents cancer in the lab

While researching new ways to stop the progression of cancer, researchers at the University of Oklahoma Health Sciences Center have discovered a compound that has shown to prevent cancer in the laboratory.

The compound, which still faces several rounds of clinical trials, successfully prevented normal cells from turning into cancer cells and inhibited the ability of tumours to grow and form blood vessels. If successful tests continue, researchers eventually hope to create a daily pill that would be taken as a cancer preventive.

“This compound was effective against the 12 types of cancers that it was tested on,” said Doris Benbrook, Ph.D., principle investigator and researcher at the OU Cancer Institute. “Even more promising for health care is that it prevents the transformation of normal cells into cancer cells and is therefore now being developed by the National Cancer Institute as a cancer prevention drug.”

The concept behind the translational research is that certain patterns of molecular alterations can transform normal cells into cancer cells. Interfering with a subset of these alterations can prevent cancer or induce a natural form of cell death called apoptosis. Interfering with the development of blood vessels within tumours (angiogenesis) can prevent and treat cancer.

The synthetic compound, SHetA2, a Flex-Het drug, directly targets abnormalities in cancer cell components without damaging normal cells. The disruption causes cancer cells to die and keeps tumours from forming.

Flex-Hets or flexible heteroarotinoids are synthetic compounds that can change certain parts of a cell and affect its growth. Among the diseases and conditions being studied for treatment with Flex-Hets are polycystic kidney disease, kidney cancer and ovarian cancer.

Dr Benbrook and her research team have patented the Flex-Het discovery and hope to start clinical trials for the compound within 5 years. If the compound is found to be safe, it would be developed into a pill to be taken daily like a multi-vitamin to prevent cancer.

The compound could also potentially be used as maintenance therapy to prevent cancer from returning after traditional radiation and chemotherapy treatments, especially in cancers that are caught in later stages such as ovarian cancer where life expectancy can be as short as 6 months after treatment.

Sources:

University of Oklahoma
Benbrook Laboratory

EGFR testing in lung cancer - which patients should receive kinase therapy?

Mutations in the epidermal growth factor receptor (EGFR) correlate with increased response in patients with non-small cell lung cancer (NSCLC) treated with EGFR tyrosine kinase inhibitors (TKIs). As a result, the blocking of EGFR to treat non-small cell lung cancer is becoming increasingly common, but there is considerable debate about when to initiate therapy and how best to select patients.

Recently, results from the iTarget trial were reported for gefitinib/Tarceva (OSI, Genentech/Roche) in the first-line treatment of 34 patients with mutations. The investigators, from the Massachusetts General Hospital Cancer Center in Boston, reported an overall response rate of 55%. This is similar to reports from other investigators, although no patient with atypical mutations achieved a response. As previously reported, mutations were seen more frequently in females, lifetime nonsmokers, and patients with adenocarcinoma. A median progression-free survival of 9.2 months and an overall survival of 17.5 months was also observed. Patients were treated with gefitinib 250mg per day until progression or unacceptable toxicity.

An editorial by Frances Shepherd, published in the Journal of Clinical Oncology, suggested that it is highly likely that a panel of tests will be used in the to determine which patients are likely or not likely to benefit most from therapy. Dr. Shepherd argued that the unselected non-small cell lung cancer population is definitely not the appropriate comparator.

There have now been several publications in which the survival rates of patients with EGFR mutations treated with chemotherapy have been reported and their survival has been significantly longer than that of patients with wild-type EGFR and the median survival has not been reached at 2 years. According to Shepherd, this tells us that the studies of first-line EGFR tyrosine kinase inhibitor therapy in mutation-positive patients likely have all been published prematurely, with median follow-up times less than half the expected survival time of patients treated with chemotherapy.

"With this in mind, does the 17.5-month median survival in the Sequist et al., study really compare favourably to historical controls?"

The problem is, we still don't know which patient sub-types would ideally benefit most and would, therefore, see an improved response rate. Further trials are likely needed before this crucial question can be adequately answered.

p53 gene and it's role in cancer

Ironically, death is critical to life.

Apoptosis is the programmed death of cells that are irretrievably damaged or at the end of their useful life. The process is essential for organisms to develop and survive by regenerating new cells. In cancer, this process goes awry because mutations allow cells to divide and proliferate uncontrollably rather than dying, so a tumour mass is formed.

Mutations can occur by addition, deletion or inactivation. Inactivation of p53, for example, can lead to the development of different types of cancer. Although scientists have long known that p53 inactivation plays a central role in the development of cancer, little was known about whether p53 inactivation played a role in maintaining cancers. It was also unclear whether switching p53 back on in tumour cells would have any therapeutic effect.



In 2007, researchers at the Howard Hughes Medical Institute demonstrated that inactivating the p53 gene is necessary for maintaining tumour survival. Conversely, reactivating the p53 gene in mice caused blood, bone and liver tumours to self destruct. The p53 protein is called the “guardian of the genome” because it triggers the suicide of cells with damaged DNA. Cancers can, however, mutate to circumvent p53 reactivation.

It is now known that in most cancer cases, the P53 gene is damaged or switched off, but Scottish researchers found they could reboot it. Biological compounds called tenovins were used to turn off certain enzymes which act as switches and control p53. The compounds were initially selected for study because they induced the required effect on whole cells as opposed to the use of purified proteins. The findings indicate that improved tenovin derivatives may have the potential to stop tumours and that their ability to switch on P53 contributes to this. Tenovins work by inhibiting sirtuins. This may facilitate further optimisation of the compounds in development for inactivating the cancer.

Note: GSK recently purchased Sirtris, a biotechnology company focused on sirtuin research

Ovarian cancer - early detection via the fallopian tube?

New research recently reported at the American Association of Cancer Research suggests that fallopian tube cells rather than ovarian surface cells are the probable site of origin of most cases of ovarian serous carcinoma, the most common type of ovarian cancer. This finding may lead to earlier detection, as well as better treatment and perhaps even prevention of ovarian cancer.

There is no reliable early diagnostic test for ovarian cancer, so approximately 80 percent of cases are diagnosed at a very late stage. Thus when oncologists diagnose ovarian cancer, they often find massive invasive tumours on the surface of the ovary (usually the tumor does not invade the ovary). It is rare to find early pre-invasive in situ tumours, as with breast cancer.

Levanon and colleagues studied a group of women at very high risk for ovarian cancer due to family history who underwent removal of their fallopian tubes and ovaries as a preventive measure. When these women were closely evaluated, it was found that they had early cancerous growths, and these early growths were in the fallopian tube, not on the surface of the ovary. The growths were confined to a particular area within the fallopian tube called the fimbria, which is located close to the ovary.

The team's findings may change how pathologists examine fallopian tubes after surgical removal, with a new emphasis on the fimbria to measure the incidence of precursors and early cancers among women who carry BRCA mutations. Future studies may explore connections between specific genetic or environmental modifiers and the incidence of precursor lesions in the fimbria.

On PET scans and detecting cancer...

A national study appearing in today's Journal of Clinical Oncology (JCO) demonstrated the value of positron emission tomography (PET) scans for treating patients with ovarian, prostate, pancreatic and other types of cancers.

PET scans are commonly used for the diagnosis, staging and restaging of cancers as well as the monitoring of tumour response to treatment for Medicare patients with nine types of cancers covered by the Centers for Medicare and Medicaid Services (CMS): breast, cervical, colorectal, esophageal, head and neck, non-small-cell lung, thyroid, lymphoma and melanoma.

In making the positive PET reimbursement decision for these nine tumour types, CMS used the standard "that all evidence currently available must be adequate to conclude that the item or service is reasonable and necessary." Clinical oncology, however, deals with many more than nine tumour types, and some major human diseases, such as pancreatic, ovarian, and prostate cancers were not included; patients with these tumours and a variety of others were, therefore, potentially being denied the benefits of PET imaging.

By providing images of cancerous changes at the molecular level, PET scans for cancer have given physicians the ability to detect developments that can be undetectable with routine medical imaging and have become a powerful tool in fighting cancer.

The accompanying editorial by Dr Larson put it admirably. He noted that, "One can only hope that this approach by CMS will be expanded to other aspects of diagnostic imaging practice in oncology."

Magnets in cancer treatments - a new oncology tool or a bad idea?

Biopsy results can be ambiguous: sometimes they can be negative simply because there are too few malignant cells in the sample to be detected - not because all trace of disease has gone. Researchers from the University of New Mexico and the company Senior Scientific, both in Albuquerque, have devised a solution that harnesses the power of magnetic attraction.

The idea is to use magnetic iron oxide nanoparticles encased in a biocompatible material. These in turn can be coated with antibodies that bind to chemicals found only in cancerous cells. When injected into the body, thousands of the particles stick to cancer cells, turning them into miniature magnets. The cells can then be drawn towards magnets encased in the tip of a biopsy needle (Source: Physics in Medicine and Biology, vol 52, p 4009).

A mathematical model of the system confirmed that significant numbers of cancer cells, laden with nanoparticles, could be attracted to a needle within two or three minutes. In the lab, the researchers showed that a magnetised needle could attract leukemia cells surrounded by nanoparticles and suspended in blood or other synthetic materials designed to mimic bodily fluids. Nanoparticles have been used before to destroy diseased cells, but this was the first time they actually retrieved cells.

More recently, researchers have been wondering if cancer treatments be enhanced by something as simple as a magnet. A promising way to tackle some diseases is to deliver cells with modified genes to diseased tissue. Getting enough of the modified cells to the affected area can be tricky.

Claire Lewis and colleagues from the University of Sheffield inserted magnetic nanoparticles, as well as cancer-fighting genes, into monocytes, the white blood cells commonly used in gene therapy, and injected them into mice with tumours. A magnet placed above the tumour caused the cancer-fighting monocytes to congregate there (Source: Gene Therapy, DOI: 10.1038/gt.2008.57).