Given that there are millions of women (and a few men) for whom such hope is paramount, each one of the announcements may be greeted with enthusiasm. Even if each of these discoveries doesn’t turn out to be ‘the cure,’ surely collectively they must indicate progress toward finding a cure? Well, yes they do, but the question has to be, how much progress?

That gets me back to the original problem of knowing more. A team of scientists at Washington University (St. Louis, Missouri USA) led by Matthew Ellis performed a feat of massive computational proportions by sequencing the whole genomes of 50 women with breast cancer. The resulting paper, to be published in Nature magazine was previewed as a news article. [ Fifty genome sequences reveal breast cancer's complexity] The research entailed sequencing 50 genomes from the tumor cells, and 50 genomes from healthy cells and then comparing them, looking for alterations in the genome. They found mutations, lots of them.

They found 1,700 genetic mutations. That might be classified as the good news. The less than good news is that most of the mutations were unique to each woman’s tumor. Only three mutations occurred in 10% or more of the women. The genetic changes also appeared to be the result of almost the entire kit of mutation: Single-nucleotide variations (copy errors, radiation changes); frame shifts (where the boundaries of genes are broken); translocations (genes get moved to the wrong location); and deletions (which sounds like it is).

The positive spin for the study was that three genes were common, sort of: MAP3K1 (10%), PIK3CA (43%) and TP53 (15%). These may represent a toe-hold on correlating genetic mutation and breast cancer. Of course, that leaves over half the women in this study with breast cancers from various configurations of relatively rare mutations. Remember, this study was conducted on a small number of women, who had only one type of breast cancer (estrogen-receptor-positive). The next research will be on a thousand women with different kinds of breast cancer.

How to interpret this? Here’s the opinion of pharmaceutical chemist (and blogger) Derek Lowe:

The Nature piece contains some brave-face material about how this study has uncovered a whole list of new therapeutic targets, but sheesh. What are the odds that any of these will prove to be crucial, even for the low percentage of women who turn out to have them? No, instead of making me yearn for ever-more-personalized targeted therapies, this makes me think that early detection and powerful, walloping chemotherapy (and surgery) must be the way to go for now. I mean, this was still only fifty patients, and uncovered this much complexity: how tangled must the real world be?

[Source: In the Pipeline]

No question the genetic sequencing technology is becoming better by leaps and bounds (and cheaper). No question that studies like this one are racking up a lot of new data correlating genetic change and cancer. It’s possible that one, or a simple combination of genetic mutations could be fingered as the cause for breast cancer – and treatments developed. Unfortunately, studies like this one make it more likely that genetic mutations are part of a much more complex web of causation – probably with elements scientists don’t even know about yet. I can hear scientists like Derek moaning, “We’re not going to test for and make treatment with 1,700 genetic errors!” Like I said, we just need to learn more.

Because cancer damages cells inside and outside the tumor, it draws the body’s cell damage repair system – the white blood cells, macrophages. Among other things macrophages clean up material associated with damaged cells (including toxins) by literally engulfing them. They also engage in stimulation of surrounding cells to produce new (presumably) healthy cells. For cancer the macrophages are specific, tumor-associated macrophages (TAMs), which come in two principal forms M2, the most common, which support the growth of blood vessels, and M1, which activate immune cells toxic to the tumor. It’s the M2 macrophages that usually have the effect of promoting the cancerous growth, and M1 the opposite. Typically the M2 are most numerous and therefore the most effective. What the researchers wanted was to find a way to change the balance toward the M1 macrophage.

What they discovered is that HRG affects another protein, PIGF (a placental growth factor) by downregulating (inhibiting) its gene. The reduction in PIGF results in conversion of M2 macrophages into M1 macrophages. Precisely the effect desired.

Changing the macrophage balance in favor of the M1 type, has two important effects: Defensive immunity cells increase and attack the tumor cells, and blood vessel growth is reduced, which restricts the energy supply to the tumor and helps prevent the spread of tumor cells into the blood stream. A symptomatic condition of this improvement in fighting the tumor is a reduction of inflammation.

Our study shows that the regulation of tumor-associated inflammation can be utilized to treat cancer and that there is a great potential to develop HRG into a drug for cancer treatment, says Lena Claesson-Welsh, professor at the Department of Immunology, Genetics, and Pathology, who points out that the study offers a number of new and important findings.

[Source: EurekAlert]

The study does have interesting findings. It’s another example of how scientists are finding that inflammation associated with major diseases is more than just a ‘side effect’ – it can be a new way to look at the molecular processes involved, and as in this case, a possible pathway to new treatments.

[Here’s a related SciTechStory’s post: Inflammation: An unsuspected killer]

Inflammation: An unsuspected killer. One in a series of posts discussing the impact of ten topics framed by ‘Insights of the Decade’ from the December 17, 2010 special issue of Science Magazine: Inflammation, climatology, tricks of light, alien planets, the microbiome, cell development, Martian water, the DNA time machine, cosmology and epigenetics.

Lists of a ‘top ten’ of anything are anathema to some people. The validity of such listing is usually questionable. Yet lists are undeniably popular. In this bewildering world of information at our fingertips, perhaps they are even necessary. We can’t think about everything but ‘top ten’ might be memorable. In any case, Science is one of the foremost science publications in the world. It’s an excellent source for a framework about significant work in the sciences. Unfortunately the original articles are now behind a paywall. They won’t be reproduced here, but their gist is present. I’ll try to put them in context and specifically within the Impact Areas of SciTechStory.

Almost everybody knows about inflammation. If you know about germs and you’ve cut yourself, you know that the cut can become infected. It becomes reddish, swollen – inflamed. Inflammation may be uncomfortable, but everyone knows that it’s the body fighting back, destroying the germs and helping the cut to heal. Inflammation is a good thing, so everybody thought.

A few doctors and scientists suspected otherwise. The symptoms of inflammation commonly associated with trauma or infection were not the whole story. They could see the symptoms in other medical conditions. One of the first was in a form of heart disease known as atherosclerosis, or hardening of the arteries. Atherosclerosis is a killer, one of the worst. In 1983 Russell Ross at the University of Washington (Seattle, USA) discovered macrophages, the white blood cells of the immune system, in atherosclerotic tissue. In short, the tissue looked like it was inflamed. During the next two decades evidence mounted: inflammation is an important component of atherosclerosis. That begs the question: What causes the inflammation?

A new study by a team at the Columbia University College of Dental Medicine (New York, USA) published in Volume 18 (January, 2011) of the Journal of Atherosclerosis and Thrombosis [Cultivation of Enterobacter Hormaechei from Human Atherosclerotic Tissue] indicates that a long suspected connection exists between atherosclerosis and the invasion of bacteria into arterial tissue. The bacteria may cause a chronic inflammatory condition that attracts plaque build-up – the known indicator of an atherosclerotic condition. Bacteria are everywhere in the human body, most of the time they don’t cause inflammation; so when they do, it’s an angle on disease that is both novel and promising for research and treatment.

In general, inflammation is symptomatic. It’s caused by something else, which means it shows up as paired with particular diseases. This is one reason why inflammation may have escaped the focus of investigation. For example, in various forms of cancer there is tissue damage, both within the tumor and often the surrounding tissues. Typically the body tries for tissue repair, and inflammation is part of the repair kit. Except the cure may not help, it may make the cancer worse by encouraging cell growth.

In other diseases, such as certain neuropathology and Type II diabetes, inflammation outright kills cells such as neurons and pancreatic beta cells that produce insulin. Inflammation also shows up in the fat of obese people. It’s not yet known why, although there is speculation that the immune system perceives fat cells as not normal and in need of repair. Is there some linkage between inflammation in the fat cells of obesity and the often obesity related appearance of Type II diabetes? Unknown, but it’s a question for which the correlations are tantalizing research.

Notice that inflammation is now associated with at least some kinds of heart disease, cancer, diabetes, Alzheimers and Parkinsons (the latter two in a murky fashion). This is the killer’s row of modern man, the most lethal diseases of civilized peoples. Thirty years ago inflammation was barely noticed with these killers. Don’t be surprised if in the coming decade there are important discoveries involving inflammation and major diseases.

SciTechStory Impact Area: Major Disease Cures

You knew there was a ‘however’ coming, didn’t you? This is about cancer, the most elusive, hydra-headed monster in the catalog of diseases. The left hand complains about not knowing what the right hand is doing, while switching defeat for victory. The pattern is familiar and our wishes play a big role.

An exemplary case is currently swirling around the media: “Amazing Cancer Test!,” “A Blood Test for Cancer,” “Blood Test Could Be Cancer Breakthrough.” Et cetera.

The story arises from a PR announcement of a partnership agreement. The health supply giant Johnson & Johnson, through its Veridex, Inc. subsidiary has partnered with Massachusetts General Hospital (MGH) to produce an assay chip about the size of a credit card that will purportedly capture tumor cells that are circulating in the blood – making them available for counting (statistical analysis) and for molecular observation (diagnostics). The chip is under development by Mehmet Toner and a team at MGH. Veridex will produce the chip. (In all likelihood Johnson & Johnson is bankrolling the project.) Note that nowhere is it said that this arrangement has any concrete results to report. Tests are yet to be conducted, and as for clinical trials…they are down the road somewhere.

Why then are so many looking at this like some kind of breakthrough? Simple, in a way: The idea has a lot of promise, and we really wish it can do all it promises.

Here’s the idea: In many (but not all) cancers, cells break away from tumors and other tissue and are picked up by the bloodstream. This may be accidental or part of the process of metastasization, but in any case these floating cancer cells may show up in a blood sample. The new chip, known as CellSearch, uses blood samples treated with iron nanoparticles coated with specific antibodies. The antibodies then bind to specific proteins known to be carcinogenic in origin. The blood sample is passed through the assay chip. The chip, something like a brush, has tens of thousands of tiny posts shaped like an ice cream cone with a scoop of ice cream on top. Each post is coated with electrostatic molecules that readily bind with the protein of particular kinds of cancer among the nanoparticle coated cells in the blood sample. As the blood passes through the chip, the cancer cells stick to the posts even when their numbers are extremely small.

In 2007 it was shown that this method of collecting cancer cells worked well enough to capture a sufficient number to analyze for molecular cancer markers. This is where the excitement lies. The CellSearch approach makes it possible to get a count of particular types of cancer cells. The count could be extremely useful to determine the stage of the cancer or other information about its status – Is it responding to treatment? Is it spreading? Is it mutating?

As currently developed, the CellSearch chip doesn’t do molecular analysis, although cells could be stripped from it for that kind of work. Down the road (there’s that phrase) several companies are working on molecular analysis assay technology. It is certainly within the scope of present technology to eventually produce a chip that snags the wandering cancer cells, counts them, and then performs advanced microanalysis to determine details of their type and condition. Then you will have a really powerful diagnostic tool that will help real patients. The potential is enormous. Wish it so; make it so.

But, we’re not there yet. People who are interested in the progress against cancer (and that’s a lot of people), need to absorb the idea that between the time when a new technique or procedure is demonstrated in the laboratory and the time when it shows up at a patient’s bedside can be years – if at all. In this case the chip idea has to go from working with a handful of carefully selected blood samples, to a cost effective and highly accurate assay of thousands, if not millions, of barely controlled samples. This is a big step, or actually many big steps. Just the change in scale can bring out unsuspected problems.

Meanwhile much work needs to be done to advance the knowledge of cancer. To use this kind of diagnostic device effectively, much more must be known about the molecule history of various kinds of cancers. It’s one thing to get counts and analyze the molecular properties; it’s another to accurately interpret them. Then, of course, somebody has to figure out what to do about the interpretation – appropriate treatments.

Dr. Leonard Lichtenfeld, Deputy Chief Medical Officer for the American Cancer Society, commenting on the new testing device, puts things into perspective:

Right now, if you talk to a number of experts, you will hear them lament that we are seeing many tests that are being touted as important in answering various questions about the future behavior of an individual’s cancer but we are not seeing the type of validation we need to know whether or not such claims are in fact clinically relevant. There are so many markers and genetic tests out there that even the most knowledgeable experts in the clinical treatment of patients with cancer are having a hard time separating the proverbial wheat from the chaff.

So with today’s announcement comes a hope that the researchers and the company that will be working on the further development of this promising new technology will always keep the message in mind that just having a test that does something isn’t necessarily going to help us move forward in our progress in treating cancer. What we don’t need are more tests that measure this or measure that. What we desperately need are tests that make a difference in the lives of our patients.
[Source: American Cancer Society: Dr. Len’s Cancer Blog]

Assuming that this study passes critical muster (it’s certain to draw an enormous amount of attention from the medical community), there is still the big question: How does aspirin affect cancer? What, if any, are the causal links, the chemical pathways? It’s a little like having a massive amount of circumstantial evidence but no smoking gun.

It’s almost a sure thing that this news will cause a rise in un-monitored use of aspirin in unwarranted situations. Doctors are already emphasizing the warning that regular use of aspirin can cause serious internal bleeding (ulcers in particular), and that the decision to take a daily dose of aspirin should involve weighing the benefits of limited but useful prevention of cancer and heart attacks against the danger of bleeding and other possible complications.

Professor Tom Meade of the London School of Hygiene and Tropical Medicine, and one of the contributors to the study commented:

‘These are very exciting and potentially important findings. They are likely to alter clinical and public health advice about low dose aspirin because the balance between benefit and bleeding has probably been altered towards using it’, although Professor Meade adds that this does not mean everyone should automatically take aspirin. Health professionals and others will now have to consider the practical implications.

[Source: EurekAlert]

Zap it with radiation.
Kill it with toxic chemicals (chemotherapy).
Cut it out (surgery).

These are generally speaking knuckle-punch approaches – invasive, imprecise, and typically have serious side-effects. However, they work…sometimes and with certain types of cancer.

There are also about a dozen other approaches to cancer treatment, such as: hyperthermia (heating), laser (heat and cut), angiogenesis (limiting blood supply), and targeted therapy (disrupting cancer at the molecular level). The last one, targeted therapy, is based on new and fundamental research with DNA, cell biology, and molecular cancer behavior. In the view of many oncologists, it stands a good chance of becoming the fourth major approach to cancer treatment.

A new step in that direction comes from a multinational team working to find ways of blocking a specific cancer gene’s so-called ‘on-off switch.’ Published in the September 24, 2010 online issue of Nature [Selective inhibition of BET bromodomains], the research concentrates on a relatively rare but extremely lethal cancer in children and young people known as NUT midline carcinoma (NMC). NUT (nuclear protein in testis) is the name given to a principle gene involved with the disease.

The team focused on NMC for a reason: It appears to be caused by something called chromosomal translocation. This happens when two genes from different chromosomes become connected and create an abnormal protein. In the case of NMC, translocation creates an oncogene (cancer causing gene), BRD4-NUT. The presence of the oncogene sets up what geneticists call a bookmark, like a molecular sign hung out on the chromatin (the package of proteins that wraps DNA). The bookmark invites triggering BRD4-NUT to produce cancerous cells by another protein called a ‘reader.’ Reader proteins are not well understood, which is what prompted the interest of the researchers in NUT midline carcinoma.

As a way of probing the BRD4-NUT gene and it’s bookmark/reader proteins, James Bradner and his colleague Jun Qi at the Dana-Farber Cancer Institute (Boston, USA) started with the knowledge that BRD4 proteins (a “bromodomain” type) are affected by certain molecules found in a family of drugs that includes Valium, Xanax and Ativan. They began constructing many variations of the molecules in these drugs and testing to see if any of them inhibited the BRD4-NUT reader protein. Eventually they found one.

The hybrid molecule, which they dubbed JQ1, was then examined by other researchers to get details of its properties and effect. In particular, Andrew Kung, a Dana Farber colleague, engineered a molecular model that could be used in animal testing against NMC tumors. This was done by transplanting NMC cells from human patients into laboratory mice. The mice were then given the JQ1 molecule.

“The activity of the molecule was remarkable,” says Bradner. …”All the mice that received JQ1 lived; all that did not, died.”
…
“This research further illustrates the promise of personalized medicine,” Bradner remarks, “which is the ability to deliver selected molecules to cancer-causing proteins to stop the cancer process while producing a minimum of residual side effects. The development of JQ1 or similar molecule into a drug may produce the first therapy specifically designed for patients with NMC.”

[Source: EurekAlert]

JQ1 is not a cure for this type of cancer. It’s a probe molecule, something the researchers can use to explore the genetic and protein molecules associated with NMC. It could, in a few years, lead to an effective targeted therapy for NMC. More generally, this research points in a very promising direction for developing other ‘reader’ protein inhibiting drugs.

In work done at the University of Georgia (USA) by Stephen Dalton and colleagues and published September 2, 2010 in the journal Cell Stem Cell [Myc Represses Primitive Endoderm Differentiation in Pluripotent Stem Cells], it is becoming clear that Myc is involved in critical gene expression (which genes are translated into protein) within stem cells. In previous work the Dalton team had established that Myc was important for stem cell maintenance, but the new work revealed something unexpected.

For most living things stem cells are the basis of growth and development. Pluripotent stem cells have the ability to transform into almost any kind of cell – muscle, heart, skin and so forth. Gestation from an egg to a living embryo is a constant process of converting stem cells into more differentiated cells – a process that continues throughout most of life. Consequently a reserve of pluripotent stem cells needs to be retained. How are these reserve cells maintained?

It has been known for some time that stem cell differentiation is triggered and perhaps guided by a crucial gene called GATA6 – the master regulator. What regulates the regulator? That is, if GATA6 is always active then every stem cell will be transformed into a differentiated cell. In order to retain a supply of stem cells, something inhibits GATA6. That inhibitor is Myc. In fact, the mechanism for inhibition involves two forms of Myc: c-Myc and N-Myc. The scientists confirmed this by experiment. They found that deactivating both of the Myc forms (but not one) triggers GATA6.

The process is similar in reverse, that is, when turning differentiated cells back into stem cells. Again, Myc plays a role in preventing GATA6 from establishing the differentiation of cells that have been reprogrammed.

“During the reprogramming of cells, Myc represses genes associated with the differentiated state and primes them for the expression of stem cell genes,” he said. “We now speculate that during the early reprogramming stage, Myc serves to change the cell cycle so that stem cells can divide for long periods of time without aging. This is also what Myc does in cancer cells.”

Dalton said that there is an intriguing relationship between normal stem cells and cancer cells. Since Myc is crucial for maintenance of stem cells and for the development of cancer, pluripotent stem cells represent a good model for tumor biologists. Cancer is thought to be initiated by rogue stem cells found in different tissues, further highlighting the link between stem cell biology, cancer and Myc.

[Source: EurekAlert]

It is this relationship between Myc and the mechanisms of cell aging – either normal or in cancer that is the golden find in this research. Not that Dalton or anyone else has the full explanation for how it works. Digging into the molecular level of cell biology for explanations will take many (many) years. However, any research work that can bring insight into both fundamental cell processes, such as stem cell differentiation, and into the malign realm of cancer (where it is believed that rogue stem cells may be the ultimate cause) – for scientists this is perhaps the best of times – years of work ahead (and dreams of Nobel prizes dancing in their head).

Recently, in work discussed in the June 24, 2010 issue of the journal Nature some possibly major new pieces were added to the epigenetics puzzle. (I call it a puzzle, because though molecular biologists have done a great deal of research in various aspects, it seems the overall picture remains subject to uncertainty and frequent redefinition.) This research, performed by a consortium of institutions led by the Beth Israel Deaconess Medical Center of Harvard Medical School (USA), focused on the role of RNA in the expression of specific genes and their pseudogenes that are related to cancer.

Pseudogenes, as the name seems to imply, are segments of the genome that look like genes but have no known function, that is, they don’t code for protein. It’s thought that most pseudogenes are relics from once active genes but now comprise part of the so called ‘junk DNA’ of the human genome. One pair of genes/pseudogenes the research studied is called the PTEN (gene) and PTENP1 (pseudogene). The gene PTEN is known to have an important role in tumor suppression. Its ability to do this is regulated by a form of RNA known as microRNA, which binds to the messenger RNA (mRNA) that carries the DNA code for specific proteins to the locations in the cell where the protein is manufactured. When mRNA binds to microRNA, the mRNA is ‘turned off’ – no longer able to carry out its function.

It has long been thought that microRNA is the active party, with levels of microRNA corresponding to suppression of mRNA activity. The researchers thought otherwise, that in fact, RNA might be what regulates the levels of microRNA. To demonstrate this they experimented with the PTEN gene, showing that its production of microRNA was related to the activity of the PTENP1 pseudogene. In effect, the pseudogene competed with the ‘real’ gene to bind with its microRNA, thus reducing the suppression of the PTEN gene. What seemed to be involved was the active participation of PTENP1 produced RNA in ‘sequestering’ microRNA, what the researchers called competitive endogenous RNA (ceRNA).

This was an important finding: It shows that RNA does more than carry the DNA code for proteins. It has another mode, a complex chemically interactive mode that regulates the function of microRNA and through it the expression of genes. It also showed rather conclusively that at least some pseudogenes are active biologically.

Further experiments with mice involving the development of cancerous tumors showed that even 20% changes in the activity of PTEN or PTENP1 had demonstrable effect on the probability of tumors. This linkage indicates that the relationships between gene, pseudogene, and RNA can be highly significant in the development of cancer and probably other diseases.

“Because this new function does not depend on the blueprint that RNAs harbor in their protein-encoding nucleotide sequence, the discovery additionally holds true for the thousands of noncoding RNA molecules in the cell,” explains senior author Pier Paolo Pandolfi, MD, PhD, Director of Research at the BIDMC Cancer Center and George C. Reisman Professor of Medicine at Harvard Medical School.”This means that not only have we discovered a new language for mRNA, but we have also translated the previously unknown language of up to 17,000 pseudogenes and at least 10,000 long non-coding (lnc) RNAs. Consequently, we now know the function of an estimated 30,000 new entities, offering a novel dimension by which cellular and tumor biology can be regulated, and effectively doubling the size of the functional genome.”

[Source: EurekAlert]

There is a strong ‘tip of the iceberg’ vibe to this research. Phrases are thrown around such as “We now understand how these RNA units talk with one another” like this was the discovery of a new mode for RNA behavior…which in a way, it may be. The paper itself makes modest claims; it sticks to the experiments at hand that involve the PTEN and PTENP1 gene/pseudogene and other combinations, and points out that the ability to predict outcomes from increase or decrease in the activity of either has impact on the occurrence of cancer (and possibly other diseases). This alone should push pseudogenes into the general forum of molecular biology research and discussion.

As I mentioned at the beginning, one of the motivations for doing epigenetic research is to answer the question ‘How can so few genes produce a human being?’ Adding the activity of pseudogenes and a previously unknown functionality to RNA to the mix increases the scope of epigenetics considerably. It will take many years and a lot more research to verify these results and extend their implications, but it continues the trend of discovery that the interface between the genetic code of DNA and the ‘real world’ of living cells is a very complex epigenetic system.

The nanosponge is about the size of a virus with a ‘backbone’ (a scaffold structure) of naturally degradable polyester (not the stuff in suits). The long(ish) polyester strands are mixed with small molecules that have an affinity for certain portions of the polyester. They ‘cross link’ segments of the polyester to form a spherical shape that has many pockets (or cavities) where drugs can be stored. You might wonder about polyester; this particular version is predictably biodegradable, which means that when it breaks up in the body, the drug contained can be released on a known schedule. Better still; the nanosponge can be engineered to be of specific size and to release drugs over time – not just in the ‘burst’ mode common with other delivery methods. The engineering capacity of nanosponge is due to the relatively simple chemistry of its polyesters and linking material (peptides); compared to many other nanoscale drug delivery systems, nanosponge should be able to scale (e.g. ramp up to commercial production levels) without requiring unusual equipment or procedures.

Nanosponge is water soluble. This does not mean the molecules chemically break up in water, but it means that nanosponge particles can mix with water and use it as a transport fluid, for example to be injected. Most other forms of nanoparticle delivery systems must use various chemical transports (for example, adjuvant reagent), which may have side effects.

So…in theory nanosponge has several advantages over other delivery methods. It has been used in a successful single-injection test, delivering the drug paclitaxel (generic Taxol) to mice with glioma (a fast acting brain cancer) and cells with human breast cancer. The next tests will be a series of injections against whole tumors. In parallel to these tests, the approach must also be evaluated for toxicity. Like all nanomedical materials nanosponge will need lengthy phased trials, which means that commercial availability is still years away. It’s getting attention now because of its fundamental properties – particularly the engineering and production simplicity.

The other major advantage of Harth’s system is the simple chemistry required. The researchers have developed simple, high-yield “click chemistry” methods for making the nanosponge particles and for attaching the linkers, which are made from peptides, relatively small biological molecules built by linking amino acids.

“Many other drug delivery systems require complicated chemistry that will be difficult to scale up for commercial production, but we have continually kept this in mind,” Harth says.

[Source: Futurity]

In other words, the results in all their inconclusive glory will be spun by anybody with a half a PR brain into words of pure gossamer and gold in the service of whatever product or point of view they represent. I can hardly wait.

Here’s one tid-bit type of observation found in the study: The combination of all cell phone users (that’s all types from occasional to heavy users) not only does not have more cancer than those people who do not use cell phones – they appear to have less cancer. However, for heavy users of cell phones, there is a different story – they appear to have more risk of cancer. The kicker is: There is no completely satisfactory explanation for these findings; or put another way – there will be many possible explanations. That, my friends, is an open invitation for spin.

Along with the spin, there will apparently be some finger pointing among the scientists. Some are already claiming that the study is ‘flawed.’ This is the semi-polite language of scientists telling other scientists that either they screwed-up, were biased, or took the wrong approach from the get-go. As in previous iterations of this acrimonious debate, the time-line is a persistent problem. It takes 20-30 years for many forms of brain cancer, particularly the nasty glioma types, to develop. Most people have not been using cell phones that long. So in a sense, all data is premature…and that’s just for starters.

Naturally, any dissension in the scientific ranks will find eager amplifiers. Do not be surprised if this study becomes an instant finger-wagging topic for all sorts of anti-science mouthpieces.

Hopefully, buried within the mound of the study, someone will find enough artifacts to draw some relatively novel if not wholly useful insights. The problem – and by problem I don’t mean just the hard proof that using cell phones cause cancer, but the problem of the continual doubt about the technology, combined with what is obviously a problem among those who are trying to put a definition to the problem (What frequencies are bad? What kind of use exposure? Does cell phone design influence the outcome? Does length of each single use matter? What types of cancer?…and so on and so forth.) – the problem isn’t going away. In fact, as cell phone use has grown faster than any other technology in history (over four billion served already), if there is a real problem, even a very small one, the numbers will magnify it.

Even so…even if cell phone use causes a few cases of cancer…will that change the patterns of use? Perhaps. You could expect cell phone manufacturers and the telephone industry to simultaneously downplay the risks, while promoting ‘innovations’ in cell phones that putatively remove the risk. Or you could think of it this way: Driving a car is one of the most dangerous and risky things a human being will ever do. More people are killed driving in almost every country in the world than by any major disease. Therefore most people have given up driving a car. Right?

It is somewhat amazing the degree to which we poor human sapiens are willing to take seemingly remote risks – even with our lives – for things that have a demonstrable benefit in the here and now. (I could add…or have a demonstrable pleasure in the here and now, as well.)

So, who or what takes the blame for this situation? Ah. What blame? No harm, no foul. Or maybe just a little bit of harm, still no foul. And science, doing what science often does with problems having too many data points, too many variables, and too many possible interpretations – science will punt the problem down the road for another study to be held when the techniques of measurement are better, the numbers of people involved are greater, and the results of this study are almost totally forgotten.