Coley's Toxins In The UK

Coley's Toxins is an cancer therapy from the pre-history of modern oncology. Developed by surgeon William Coley at the end of the 19th century, this was a treatment that showed some impressive results against a range of hard to treat cancers - especially sarcomas. Coley began the treatment after noticing that some patients with cancer experienced tumour regression after becoming infected in hospital. These rare cases of spontaneous remission were regarded as miracles, which they still are, pretty much. The infected patients would develop severe fevers, chills, aches and pains and the rest of the signs of a massive immune response that ended with the tumours being attacked by the immune system.

Coley took this idea forward and developed a treatment that consisted in inducing this severe immune response by injecting bacterial material into his patients. The patients reacted to this injection of 'bacterial toxins' by developing the feverish response as their immune systems kicked in. And, in some cases, the resulting immune response did indeed lead to the tumours being attacked and ultimately disappearing. This did not happen in all patients, but it happened at a rate that is comparable to some of the more modern cancer treatments. And, it must be said, because the tumours were cleared by the immune system, there were none of the long-term side-effects you get from chemotherapy or radiotherapy, and in many of those individuals where the tumours disappeared the treatment really did lead to a cure.

However, with the advent of radiotherapy, chemotherapy and advances in surgery, Coley's treatment fell by the way-side. Coley is often credited with being the 'grandfather' of cancer immunotherapy, but largely his treatment barely exists as a historical footnote in oncology. There is still a fair degree of interest in it from those interested in alternatives, but in the mainstream of medicine Coley's toxins are dead.

Curcumin Trial In The UK

One of the nice things about the ClinicalTrials.gov website, (which I have discussed previously here: http://www.anticancer.org.uk/2011/08/searching-for-clinical-trials.html), is that it lets you set up RSS feeds based on yor own search criteria. It's through this mechanism that I've learned about a new clinical trial for cancer using curcumin. What's more, this new trial is based in the UK, which is welcome since most curcumin trials have been in the US and other countries.

As with many of the current trials of curcumin, this one uses it as an adjunct to conventional chemotherapy. Specifically this is a trial aimed at patients with inoperable colorectal liver metastases who will be commencing standard oxaliplatin-based (FOLFOX) chemotherapy, In addition to their normal chemotherapy, patients will be given oral curcumin tablets (curcumin C3 complex, to be exact). In the first phase of the trial the aim is to test the safety and tolerability of curcumin and FOLFOX, with doses of up to 4g per day of curcumin. In the second phase of the trial patients will be randomised and some will received FOLFOX and curcumin, and some will just have the standard FOLFOX treatment.

In many respects this trial is treading familiar ground - curcumin has been trialled as an adjunct to other chemotherapy treatments for other cancers. One example that springs to mind are the trials of curcumin and gemcitabine for advanced pancreatic cancer. In one such trial 4g doses of curcumin were tried, but patients found it hard to take the volume of tablets, in another trial patients took up to 8g of curcumin without problem.

While there's a lot of excitement about curcumin as a cancer treatment, it's fairly clear by now that it is not a viable therapy on its own as things stand. The future of curcumin as a cancer treatment lies in two directions. The first as a support to existing treatments - which is what this trial is looking at. Curcumin may blunt some of the side effects of chemotherapy and radiotherapy, may make these treatments work better and may reverse drug resistance in some tumours.

The other path for curcumin lies in new formulations. This is an area of intense activity at the moment. In some cases scientists are working to improve the bioavailability of curcumin through using liposomes or other technologies. These new formulations take curcumin and simply make it more available to the body, particularly to tumour cells. A different approach is to take curcumin as a starting point and to alter the chemical structure to create new drugs that are based on it. These new drugs are more potent than curcumin and the hope is that they will be more powerful anti-cancer agents.

Both these approaches have merit, but for now it's good to see that curcumin is being tried in trials now.

To find out more about this this trial take a look here: http://clinicaltrials.gov/ct2/show/NCT01490996

Comment Spam

One of the things I've discovered since starting this blog, is that there are some people for whom no website, forum or blog cannot be exploited for gain. This site encourages comments from readers, but it has to be said that there aren't many comments being published. It's a shame, but I guess that some people just want to read and not write. The fact that traffic is increasing and that many of the visitors are being referred here via other blogs, Facebook and other social media is positive.
 
But comments are being left here that I'm not publishing.

This site uses comment moderation - comments have to be approved before being published - and it's a good thing too. Everyday there are comments left here which are really just 'comment spam'. The comments contain some innocuous are often barely literate text - 'this is a good useful nice site, for sharing' - along with a link to another site. Usually the link leads to some company selling something cancer-related: supplements, nursing care, clinics etc.

I think it's really low to try and exploit an anti-cancer site like this - have these people got no conscience?

The George Pantziarka TP53 Trust

TP53 is a gene that functions as a tumour suppressor. One of its jobs is to create the p53 protein, which acts to kill cells that have become cancerous. When the TP53 gene goes wrong, it means the body loses one of the key mechanisms it has for stopping damaged cells becoming cancers. Many people who develop cancer end up having the TP53 gene damaged in their tumours, but it functions normally in the rest of their body. However, there are some people who are born with a damaged TP53 gene, and for these people the risk of getting cancer is incredibly high. In many of these cases the damaged TP53 gene is inherited - it is passed down from parent to child.

Li Fraumeni Syndrome (LFS) is one of the most serious forms of inherited TP53 disorder. My son, George, had LFS, which we assume he inherited from his mother, who died of ovarian cancer at the age of 29, when George was just over a year old. As I have written before, we did not know that George had LFS until after he was diagnosed with his third cancer - the osteosarcoma which ultimately killed him.

While LFS and other congenital TP53 disorders are rare, the fact remains that there is little awareness of the issue, both amongst the general population and also amongst the medical profession. There are no support groups, no charities, no central information resources and currently no central registry of sufferers. For those families with LFS or other TP53 disorders, it can be a lonely and frightening existence, with children and adults alike succumbing to one or more cancers.

Having discussed the issue with a number of doctors and researchers, we have decided to create the George Pantziarka TP53 Trust, in George's memory. The aim is to provide support to families and individuals, to provide information to all, and to help foster understanding and research into the condition.

As a first step we will be launching a web-site and forum in the new year. The plan is to use the site to bring together all those affected or interested in the condition. Further down the line we hope to register the Trust as a charity so that we can expand the range of activities that we can undertake.

For now, any offers of support would be greatly appreciated.

Open Access To Research

Regular readers of this blog will be aware that I spend a lot of time reading and reviewing the research literature on cancer. I see translating that research into plainer language that is more accessible to the average person is one of the things that this site can usefully do. As such having access to the research papers is essential. Unfortunately getting hold of papers is not always an easy task. Science journals are incredibly expensive to subscribe to (typically many hundreds of pounds a year) and there are a lot of them. The whole system is geared towards providing access to research to academics and researcher (mostly) via university or institutional libraries. Without this library access an individual can buy a copy of a specific paper - but here the cost ranges from a few tens of pounds to over a hundred. For most people this is prohibitive, especially if you are a cancer patient or carer and are doing a lot of reading.

The thing is, a lot of that research is publicly funded. We pay for it through our taxes - indirectly, of course, in the form of research grants and so on. So, as members of the public we pay for the research but we can't always get to read the results of that research. However you look at it, this is a really poor state of affairs, particularly when it comes to medical research.

It's not all bad. There are an increasing number of journals which are published on an open access basis. In other words the journals publish their work online and for free. Some journals, such as BMC Cancer, are well-established now, and publish high quality work that can be downloaded by anybody. In other cases journals make older articles available for free, so that for the first six months or a year a paper must be paid for, but after that it's free. Another option that some journals have adopted is to make selected articles free - which is good if it's one that you're looking for but rubbish if not. Finally, there are also some journals who allow access to articles by patients for free, but everyone else has to pay. Normally this involves filling in an online form to gain access to the article.

Cancer and lifestyle choices

The headlines are startling: over 40% of cancers are down to lifestyle. The opening paragraph of the BBC News report states it bluntly:

Nearly half of cancers diagnosed in the UK each year - over 130,000 in total - are caused by avoidable life choices including smoking, drinking and eating the wrong things, a review reveals.

For those with cancer, or who have family or friends suffering from the disease, this makes for grim reading. Because, like it or not, there's a moralistic sub-text here: in over 40% of cases, cancer is the fault of the patient. If only they'd chosen the right life-style, they wouldn't be sick.

Now, that isn't what the articles say, but it's a clear implication. Before we go any further though, perhaps we ought to back up a little and ask what the science really says...

Firstly, we have to be clear that what we're talking about here are projections based on a series of mathematical models. These projections take a series of risk factors - say smoking or alcohol consumption - and then compare the increased risks of developing cancer based on comparing current consumption levels and what are considered the 'optimum' levels. So, for example, you take the additional risk of developing cancer per unit of alcohol, the difference between current consumption and the ideal level and calculate the increased risk. Now take that increased risk and multiply by population and you get your projected number of cancer patients. It's a bit more complicated than that, of course, but in principle that's how it works. Add an additional set of factors for different types of cancer, and you've got a cascade of different variables that make up that final scary number.

So, all of this is subject to many different assumptions about risk factors, current consumption levels, ideal consumption levels, population growth etc.

Arginine, Glioblastoma and the Immune System

An interesting piece of work came to my attention earlier this week that I think is worth sharing for a number of reasons. Firstly, I think it illustrates a way of working that really should be encouraged - it has significance beyond the specific interventions mentioned. Secondly, I think there are lessons here for those who are interested in anti-cancer agents not patented by the drug companies (such as curcumin, quercetin, resveratrol etc). Finally, it has interest for those suffering from glioblastoma (GBM) - a form of brain cancer that is particularly aggressive and hard to treat.

The work in question looked specifically at the phenomenon of immune suppression in GBM patients, and let's note at the outset that immune suppression is a problem for all cancer patients, not just those with GBM. Brain cancer patients - not just those with GBM - at the University of Colorado Hospital had blood taken and analysed, along with blood from non-cancer patients. Analysis revealed that the blood from GBM patients in particular showed lower levels of T-cell proliferation and released lower levels of interferon-gamma compared to normal blood samples - in other words they had lower levels of immune function. The specific forms of this immune suppression were worked out in a series of lab experiments that ultimately showed that one of the factors associated with this suppression was a high level of the enzyme Arginase I (ArgI). This enzyme consumes the amino acid Arginine, which is essential for T-cell activation.

So far so good - it's interesting, in an academic way, but so what? The experimenters then took the next step and looked at chemically blocking ArgI with a specific drug. Doing this improved the immune response in the test tube. Levels of interferon-gamma rose to normal levels. The next step, however, is where it gets really interesting from a patient point of view. Rather than blocking ArgI with a drug, the team looked at increasing levels of Arginine (which is what ArgI consumes). By adding more Arginine the immune response improved. In simple terms the ArgI was basically using up the circulating Arginine and thus starving the T-cells of it, but by increasing the amount of Arginine the researchers showed that they could 'feed' the ArgI and have enough left over to be used by the T-cells, which could become activated as normal.

Q&A With Dr Anthony Howell - The Reverse Warburg Effect

One of the fundamental ideas in cancer has been that cancer and normal cells differ in their metabolism. First proposed by Nobel prize-winner Otto Warburg in 1924, the 'Warburg Effect' is the hypothesis that cancer cells generate energy by the non-oxidative (without oxygen) breakdown of glucose (a process called glycolysis). This is in contrast to normal cells, which generate energy through an oxygen-dependent pathway. Tumours use the non-oxidative pathway, which is less efficient than normal metabolism, even in conditions where there is plenty of oxygen available. We can see this greediness for glucose in PET scans, for example, where radioactively labelled sugar is sucked up by tumours and not by normal tissue.

For many years the Warburg effect has been investigated as a possible Achilles heel for tumours, and there is still lots of work being done on ways to attack tumours by interrupting this glycolytic process. Such work ranges from dietary interventions (see for example the article on diets and cancer, and the interview with Dr Gerald Krystal), to looking for drugs which disrupt the process at different points.

However, in recent years Dr Michael Lisanti and a group of colleagues have proposed a fundamental re-appraisal of the theory. They have proposed the cancer cells in advanced solid tumours are able to induce the Warburg Effect in the cells that surround them (the tumour stroma), and that they then consume the by-products of glycolysis produced by the stromal cells. In other words they cannibalise the tissues around themselves, inducing the Warburg Effect so that they can feed off the nutrients produced by the stromal cells. They have termed this new theory, which is a radical departure from what is currently accepted, the 'Reverse Warburg Effect'.

For those who wish to learn more there are a number of freely available papers by Lisanti and co available via PubMed.

Dr Anthony Howell is one of Lisanti's co-authors and a researcher and clinician based in Manchester. He has kindly agreed to an interview so that we can learn more about this new theory and what it may mean in terms of clinical practice. Although the language in this interview is more technical than much of what is published on this site, I feel it's important to bring these new theories and results to as wide an audience as possible.

PP: A recent editorial in the journal Cell Cycle described the work of Michael Lisanti, yourself and others as ‘iconoclastic’. Just how revolutionary is the theory of the ‘reverse Warburg’ effect and the idea of ‘cancer as a parasite’?

AH: Warburg was a great scientist as reflected in the award of the Nobel Prize for his pioneering work on tumour metabolism. His major contribution was to show that tumour cells showed enhanced glycolysis and he thus assumed that mitochondrial respiration was impaired in tumour cells. It certainly looks like this when you put tumour cell lines such as the breast MCF-7 cell line into culture by themselves. These cells have few mitochondria and there is increase in the sugar degradation glycolytic pathway. What Michael Lisanti and his colleagues have shown is that this may be an artefact of culturing the cells alone. When co-cultured with human fibroblasts, the MCF-7 cells synthesise mitochondria and thus use oxidative phosphorylation as their main source of energy. In the body tumour cells are always associated with what is called a supportive stroma derived from the host, so that the co-culture system is a better mimic of what might be happening in-vivo, and indeed we find up-regulation of mitochondria in most breast cancers compared with normal breast tissue. Cultured alone the fibroblasts have a large number of mitochondria. However, when co-cultured with tumour cells they degrade the mitochondria and depend upon gylcolysis. So all these observation are opposite to Warburg’s observations. It is as if the Warburg effect occurs in tumour associated fibroblasts rather than the tumour cells themselves which has lead Lisanti to call what is happening in co-culture ‘The Reverse Warburg Effect’. I think this is where the implication that these observations are iconoclastic comes from.

UK Clinical Trials Gateway

I have previously written about how to search for clinical trials, describing the difference between Phase I, II and III trials, as well as how to use the US National Institutes of Health Clinical Trials database (http://clinicaltrials.gov/). However, the fact it's currently very difficult to find out what trials are going on in the country as a whole. What's missing is a central database of all clinical trials. A step in the right direction is the UK Clinical Trials Gateway (http://www.ukctg.nihr.ac.uk/default.aspx).

While not a central registry itself, the UKCTG does enable the user to search a number of international registries through the site. Users can search on specific diseases (e.g. a specific type of cancer, like lung cancer), specific drugs (e.g. celecoxib) or other forms of therapy (e.g. photodynamic therapy), as well as combinations such as "celecoxib AND cancer". For each record returned by the search you can find out whether the trial is recruiting patients, where the trial is taking place and more details on the actual treatment itself. For patients looking for a trial it's a really useful place to start.

However, there is still room for a central registry of clinical trials. Not only would it provide doctors and patients with a single database to query for all trials in the UK, it would also allow us to track the level of activity for different diseases. For example doing a query on the UKCTG shows that there are no trials for osteosarcoma in the UK, which is sad if true, but I know that there are some trials on-going at the moment (the SUCCEED trial, run by Merck and Ariad Pharmaceuticals).

Just as importantly a central registry will enable us to see what trials are aiming to do, what protocol they use and what outcomes they are tracking. With this information we can see which trials publish their results, and also see whether they succeed in what they set out to do or whether they changed what they say they are looking for in order to present the best possible gloss on their results. And yes, this is something that does happen...

Until then, at least the UKCTG provides us with yet another useful tool to help patients and their doctors find appropriate clinical trial information.

Test Tube Cancer Cells and People

Test tube cancer cells vs. real cancer cells

In a previous article (How To Read A Cancer Paper Part 1 - ), I looked at the pitfalls of in vitro studies. These are studies performed in the lab that look at cancer cells under glass (actually a Petri dish rather than a test tube as such). These studies - and there are tens of thousands of them - are often performed to see how cancer cells respond to specific anti-cancer agents. And, as I said in the article:

...you have to take these test tube studies with a huge pinch of salt. In the test tube substance X kills cancer, but that really doesn’t mean much in the real world. At most it gives you reason to carry on looking at substance X in more detail, but that’s about it.

The obvious alternative is to look at in vivo studies, which are discussed in the second article in the series. These are studies that use animals (normally mice or rats), with real tumours rather than cells grown under glass. While these are better, there are still major pitfalls, which I discuss in the article. One problem that I highlight is that the tumours that are grown are derived from standard cell lines. These are cancer cells that have been grown for year after year after year under lab conditions. The intention is to have some standard cell lines that are indicative of the tumour type or sub-type (e.g. androgen responsive prostate cancer, triple negative breast cancer etc). A key point I make in that article is:

Furthermore, cancer cells mutate and adapt, so cells that have been taken from a patient biopsy twenty or thirty years ago and then kept under glass for generation after generation will have changed in order to survive in the test tube environment.

A new study, published in the Proceedings of the National Academy of Sciences, looks at precisely this issue and comes to a disturbing conclusion. The experimenters were specifically looking at cancer cells that are drug-resistant. This is of major clinical importance as the fact is that we still don't fully understand why some cells can become resistant to anti-cancer drugs. Using state of the art technology, the researchers took a panel of standard cell lines and checked which genes are expressed. They did this both in the test tube and also from tumours grown in animals from these same standard cell lines. They then compared these with a set of cells taken directly from patient biopsies. The results are clear:

No correlation was found between clinical samples and established cancer cell lines....all of the cell lines, grown either in vitro or in vivo, bear more resemblance to each other, regardless of the tissue of origin, than to the clinical samples they are supposed to model.

In other words, the standard cell lines, originally from different types of tumour, have come to resemble each other genetically, whether used in the test tube or implanted in animals. They resemble each other more than they resemble 'live' samples taken from cancer patients.

A numb lip

The first sign that my son, George, had a problem in the jaw was a funny tingling in the upper lip, on the right hand side. This developed into a feeling of numbness that wouldn’t go away. He had had a basal cell carcinoma surgically removed from the left side of the skull, just under the hair line above the ear, a few weeks previously. Was the numbness related to that? We checked with the surgeon and were told it was unrelated.

Was it a dental problem? We then got into a cycle of being shunted around from one hospital or clinic to the next. We went from dentists to maxillofacial and back again. The numbness was slowly getting worse but we were not getting anywhere. Having had two cancers already, we checked with the Royal Marsden and did the rounds there too. A very senior paediatric oncologist saw us and referred us to a number of people. My son’s jaw was ultrasounded and there, nestling under his chin was an odd looking little lump. A tumour? No, probably not we were told.

The paediatric oncologist was very clear. Whatever the problem was, it wasn’t oncological. Which was a relief. But the problem wasn’t going away. And he was starting to get pain in the jaw too.

Finally we tried another dentist. She x-rayed and saw that his wisdom tooth had been pushed out - it wasn’t right. She referred us back to maxillofacial - immediately.

I can vividly remember the day. My son was seen by a registrar called Amir Ketabchi. He recognised immediately what was going on. We could tell by the flurry of activity around us that this was serious. George was booked into a CT scan the next day. The result was clear – a tumour in the right mandible.

The only question was what kind of tumour? We desperately hoped for something benign and easy to treat. But luck was against us. The ‘not an oncological problem’ was an osteosarcoma.

Q&A With Dr Burt Berkson - Low Dose Naltrexone and Alpha Lipoic Acid

A couple of years ago I found an extraordinary paper in the journal Integrative Cancer Therapies which described a number of cases in which patients with advanced pancreatic cancers had responded to therapy with low dose naltrexone and alpha lipoic acid. It was a paper that positively demanded following up with a clinical trial, but although I checked up periodically no trial was forthcoming. However, the recent LDN Aware DVD included an interview with the man behind that paper, Dr Burt Berkson.

I am pleased to say that Dr Berkson agreed to answer a few questions for Anticancer.org.uk, the first part of which appears below.


PP: Background - how did the LDN/ALA protocol arise?

BB: Alpha Lipoic Acid (ALA)

While working as an internal medical resident at one of the Case Western Reserve teaching hospitals in 1977, I was told by the chief to follow two patients with severe and acute liver damage that resulted from eating hepatotoxic mushrooms. This condition is often fatal and I was told that these patients would surely die.

As a medical doctor it was necessary to follow the orders of the chief; however, as a PhD, I sought new ways of doing things. I called Dr. Fred Bartter (former chief of endocrinology) at the National Institutes of Health and asked him if he knew of anything that would help regenerate damaged organs. He answered that he was working with thioctic acid (alpha lipoic acid, ALA) as a possible treatment for diabetic complications and when given to people with diabetes, it seemed to help heal damaged livers and other organs.

Dr. Bartter sent me a case of ALA for intravenous administration. I picked it up at the Cleveland airport about seven hours after I initially called him. I rushed back to the hospital and injected the ALA into the two patients. I administered this treatment every six hours for 14 days. The patients started to recover and felt much better by the second day and were able to leave the hospital within two weeks with normal liver function. They are still alive and free of liver disease today, 34 years later.

It is interesting to note that some of the chiefs at the hospitals where I practiced medicine seemed to discourage my use of ALA. I was told that with an M.D., and a Ph.D. in cell biology/microbiology, and internal medicine training, I should concern myself with doing infectious disease research and stay out of liver disease.

Dr. Bartter, however, thought our work was very important and told me that some day we might win a Nobel Prize for our human work with ALA. He suggested that I leave Cleveland and come to work with him at NIH. But I was very discouraged by the response that I experienced from the medical community in Ohio. I left the region and moved my family to a rural community not too far from Lubbock, TX.

I became a country doctor, driving from one hospital to another each day, and even delivered babies in people’s houses on isolated ranches. When my children were high school age we moved back to a relatively large city. About fifteen years ago, I opened an integrative medical practice in Las Cruces where I use antioxidants and certain innovative prescription drugs to treat diabetes, chronic hepatitis, rheumatoid disease, lupus and other disorders with exceptionally good results. I also try to support and improve the immune system of people with cancer.

Melatonin and cancer treatments

Melatonin is a compound that is produced in the body by the pineal gland, and is associated with regulation day/night rhythms (also known as the circadian rhythm). Often described as a hormone, melatonin is also known as a powerful antioxidant and has immune stimulating properties, additionally has been shown to have a range of anti-cancer activities in a wide variety of cancer types. It also has a range of medical uses, including as a treatment for insomnia and seasonal affective disorder. Most importantly, it has very, very low levels of toxicity, and does not appear to have negative interactions with a wide range of drugs. This last point is an important one when considering the use of melatonin by cancer patients.

This is interesting in light of a publication of a major review of clinical studies involving melatonin and cancer treatments. The paper, Melatonin as Adjuvant Cancer Care With and Without Chemotherapy: A Systematic Review and Meta-analysis of Randomized Trials, published in the October 2011 edition of the journal Integrative Cancer Therapies, concludes:

MLT may benefit cancer patients who are also receiving chemotherapy, radiotherapy, supportive therapy, or palliative therapy by improving survival and ameliorating the side effects of chemotherapy.

What the authors of this paper have done is gone back and collected all of the data from a range of clinical trials that compared cancer treatments with and without melatonin use. They systematically excluded trials that did not have direct comparisons between treatments that included melatonin and those that didn’t, that did not randomise patients (i.e. trials that gave each patient an equal chance of being on the melatonin arm or the non-melatonin arm – in this way avoiding biasing the results), and they excluded those trials that did not satisfy a range of other quality criteria. At the end of this process there were 21 clinical trials included, all of them looking at patients with solid tumours. The treatments included standard chemotherapy, radiotherapy and palliative care.

A new cancer blog

My neice, Penny, has previously blogged on this site about her campaigning work as an Ambassador for Cancer Research UK. She has just started a new blog, Penny's Pieces, where she writes about cancer, campaigns and more personal stuff. Please take a look. Amd,, while you're at it, she is still looking for volunteers for her fund-raising day in Woodford Green.

Dealing With Stress

Coping with cancer is obviously stressful. Not just for the patient, but for friends and family too. And it’s not just during treatment, the stress can be there even after a patient is declared to be in remission. A new paper, from Duke University Medical Center in the US, reports that post-traumatic stress is prevalent in cancer patients even in long-term remission.

An added factor in this stress is the well known fact that it can have negative effects on the immune system, cause depression and generally make things worse. There is also the worry that stress can make the disease worse, or can make it recur in patients in remission.

So, for all of these very obvious reasons, it’s important to look at what can be done to tackle this issue that can severely impact the quality of life for all of us. The good news is that there are some active steps that can be taken and which don’t involve taking more drugs.

Diet is one factor that may play a part in the ability to handle stress and deal with depression. There is plenty of evidence to show that diets having higher levels of omega 3 fatty acids helps the body deal with stress – it has been shown to reduce the levels of stress hormones and can improve mood and the ability to cope. In fact higher levels of omega 3 – obtained from supplements rather than diet – have also been used to treat depression. And, as a bonus, higher omega 3 than omega 6, helps reduce the inflammatory factors that are shown to be associated with cancer. As a bonus there is emerging evidence that omega 3s are helpful in coping with cancer treatments, and are being investigated for use against cancer cachexia in advanced disease.

Guest Post - Mark Vernon

Guest Post by Mark Vernon, whose daughter Sarah recently died of bowel cancer. It is published here because it makes some extremely important points about the state of cancer treatment in this country.

I wish I had the experience, knowledge and opportunity to write a book on the politics of cancer. All in all, it is the medical establishment that ought to be in the dock now.  Not that I feel inclined to pursue any specific complaint.  Sarah's GP was slow to refer her to a specialist.  She was too young to have cancer:  her problem was off the beaten track, confounding the inadequate diagnostic skills of the GP.  I think of this as a problem with the GP system, by the way, tempting as it is to make accusations of negligence, but a more able GP might have taken the possibility of cancer more seriously, and sooner.  Sarah then had to wait for the referral, though my wife Jane and I were in the dark at this point.  Whether the wait was outside of government targets or normal practice, I don't know.

Then came the diagnosis, followed quite soon by surgery - a hemicolonectomy. There is a saying I have come across about surgery:  the operation was a complete success;  the patient died.  In Sarah's case, this took nearly a year to happen.  But the surgery must be judged to have failed, since the tumour rapidly recurred.  And this happened in the middle of adjuvant chemotherapy, which therefore also completely failed, and was abandoned.  Then came a revised chemo regime, incorporating the expensive monoclonal antibody cetuximab (trade name Erbitux).  This had no effect whatsoever, and was abandoned.  Treatment from this point on was strictly palliative, and the medical establishment officially gave up.

Beta blockers and cancer

There was a recent flurry of headlines about possible new uses of beta blockers - normally prescribed for high blood pressure - and that they might have anticancer properties. For example the BBC headlined the story as Beta blockers 'may stop breast cancer spreading'. The trigger for the story was the announcement an analysis of 800 patient records showed that those cancer patients who had also been treated with beta blockers had lower rates of metastatic disease - in other words there are indications that beta blockers stop or slow breast cancer from spreading to other parts of the body. The real headline is from the abstract of the paper that reported the results:

In addition, there was a 57% reduced risk of metastasis, and a 71% reduction in breast cancer mortality after 10 years. This proof-of-principle study showed beta-blocker therapy significantly reduces distant metastases, cancer recurrence, and cancer-specific mortality in breast cancer patients suggesting a novel role for beta-blocker therapy

This is not the first report on beta blockers and cancer - for example there was also a very recent study looking at beta blockers and malignant melanoma. That study concluded:

Increased survival time of patients with melanoma receiving beta-blockers suggests that use of this drug may hold promise in treatment strategy for these patients.Impact: The observations described here suggest that catecholamines may retard melanoma progression and that beta-blockers may have unrecognized potential as a therapeutic intervention for melanoma.

Pressure sores and honey

In the last few months of his life, our son George was at home and completely bed-ridden. A combination of tumour pain, deep vein thrombosis and weakness meant that he was barely able to move, even in bed. Inevitably this led to the development of pressure sores - also known as bed sores - on his lower back. Of all the symptoms that he suffered, this was the worst. The pain was unbearable, intense and barely touched by the wide range of pain killers he was prescribed by the palliative care team. For us, this was the most difficult thing to deal with. Nothing we could do seemed to make a difference. The pressure sores were treated with topical drugs (including morphine), as well as high doses of oxycodone and other opiates. We were told that the sores would not recover, that more were likely to develop and that they would become progressively worse.

In desperation we researched as much as we could and very early on came across lots of positive reports about honey, especially Manuka honey. I downloaded a number of medical papers and clinical trial reports and passed these to our local nursing team. They in turn handed them to a specialist back at our local hospital but nothing happened. The preferred solution was to up the drug doses, even though these made George even more sleepy and therefore less able to move and more likely to make the situation worse. The sores deepened, as did George’s level of distress. I sent papers to whoever I could but they were received with frank scepticism.

LDN Aware Voices DVD

This double DVD release brings together doctors, scientists, pharmacists and patients to talk about their many and varied experiences with Low Dose Naltrexone (LDN). And these are voices worth listening to because their message is compelling. At the moment we don’t know how many patients could benefit from LDN, we don’t know how many conditions it can treat and we do not have clear idea of how it is that it works. But there is enough evidence for us all to take this seriously.

Of the many voices on the DVD some stand out. Jackie Young-Bihari, widow of the late Dr Bernard Bihari (who discovered low dose naltrexone as a treatment, initially in HIV/AIDS patients), does a great job of telling the history of LDN. It was one of those lucky accidents and Dr Bihari had the foresight not to turn away from his discovery but to take a chance and treat a wide range of patients with many different diseases, including cancer.

Dismal bone cancer statistics

Yesterday's email inbox included details of a new paper published in the International Journal of Cancer by Dr Jeremy Whelan (possibly the UK's foremost expert on osteosarcoma and other bone cancers) and colleagues. The abstract of the paper is included below:

Int J Cancer. 2011 Sep 12.
Incidence and survival of malignant bone sarcomas in England 1979-2007.
Whelan J, McTiernan A, Cooper N, Wong YK, Francis M, Vernon S, Strauss SJ.

Abstract
Primary malignant bone sarcomas (MBS) are rare and there are few studies examining their incidence and outcome. Here, the incidence and survival of all subtypes of MBS registered in England between 1979 and 2007 were analysed from patient registry data held by the National Cancer Intelligence Network (NCIN). Over 11,002 new cases of MBS were registered, an average of 379 per year. There was no change in incidence demonstrated over the study period (p=0.08). Although a peak incidence is observed in adolescence, approximately half of MBS are diagnosed in patients over 50 years. An improvement in outcome of MBS was observed between those patients registered from 1979-1983 and 1983-1987 (p<0.0001), but there has been no improvement since. In the most recent period studied (patients diagnosed 1998-2002) 5-yr survival was 55% in Ewing sarcoma, 70% in chondrosarcoma, 56% in chordoma and 43% in osteosarcoma. Patients diagnosed with osteosarcoma over the age of 40 years or with a non-extremity tumour have a significantly inferior outcome; 22% 5-yr survival >40 years compared to 53% <40 years (p<0.0001) and 16% non-extremity tumour compared to 48% extremity tumour (p<0.0001). This population-based study has allowed us to confidently define the English incidence and survival rates of both the commoner bone tumours such as osteosarcoma, and rarer entities such as chordoma as well as groups with inferior outcome. The lack of significant improvement over recent decades for these diseases is cause for concern and further research.

Guest Post - Penny

The following is posted on behalf of Penny Sophia-Chistophe:

On April 25th 2011 I received a phone call to inform me that my beloved cousin Georgie had died. It was the morning of my 22nd birthday. Georgie and I had always been close so his death was incredibly hard to bear. He was the sixth of my close relatives to die in my lifetime. Two Grandparents, two aunts, an uncle and now a cousin all snatched away by cancer.

A consequence of this is that I decided to channel my anger and sadness into trying to save others.

I applied to become an ambassador for Cancer Research UK (CRUK). CRUK’s ambassadors are a brilliant group of passionate supporters working hard to help CRUK effectively influence politicians, engage the local media in their campaigns and try to help them save lives. Our stories, experiences and passion have become one of CRUK’s most powerful campaigning tools and are vital part of their work.

As an ambassador my activities are varied and interesting:

* Communication with local politicians and parliamentary representatives; flagging up our campaign issues and persuading them to back us and take positive action on our behalf.

* Engaging with our local and regional press; securing coverage for our campaigns and raising awareness in our local area.

* Lobbying for specific cancer related campaigns.

Our current campaign is “A Voice for Radiotherapy”. CRUK believe everybody deserves the best chance at fighting cancer and beating it. This means giving them access to the best possible treatments. Up to half of all cancer patients could benefit from access to world class radiotherapy treatments but only 4/10 people with cancer currently do. We are campaigning to make sure it is available to everybody who could benefit from it.

Awareness of radiotherapy is low; a recent CRUK survey reveals that 14% of people are aware of it. We are concerned that a lack of public awareness means that radiotherapy does not receive the attention is needs to develop into a world class service in the UK.

We are calling on the government in England to introduce an action plan, to tackle unequal access to radiotherapy and make sure that all services have the appropriate workforce, the best treatments and the capacity to plan for the future. We want to make sure that everyone who needs it has access to world class radiotherapy treatments.

Please take a moment to sign our petition and get as many of your loved ones to do the same:  http://e-activist.com/ea-action/action?ea.client.id=149&ea.campaign.id=9329&ea.tracking.id=PennySC

We will be handing this petition in at Downing Street in November. We are aiming for 36,000 signatures, one for every person who misses out every year.

Thank you

Penny (pennychristopher@googlemail.com)

LDN Awareness Week

Naltrexone is a drug that is used to treat alcohol or opiate dependence. It’s one of a class of drugs called ‘opoid receptor antagonists’. What makes this an interesting drug from an anti-cancer perspective is its reported activities on the immune system when given in low doses. Low dose naltrexone (LDN) has been reported to slow proliferation of cancer cells in a variety of different cancer types – including hard to treat cancers such as pancreatic and ovarian cancer. The use of LDN is what is called an ‘off-label’ use of a drug - in other words it describes a case where a drug for one disease is also used for a different disease. At the moment most off-label uses of LDN are for treating auto-immune diseases, particularly Multiple Sclerosis and Crohn’s Disease.

Summer reading

Summer reading this year included 'The Edge of Physics' by Anil Ananthaswamy. The book describes a series of key experiments currently taking place that probe the raw substance of the universe. The most well-known example is the Large Hadron Collider at CERN, which is currently looking for evidence for the existence of the Higgs boson, but it is only one of a number of monumental studies in progress. We are at the point where scientists are probing for the evidence for the existence of multiple universes, for understanding at a deep level what space-time is made off, what dark matter and dark energy are.

It's amazing stuff for sure, but one thought kep coming back to me as I read through the book - why is it we know so little about cancer? Reading the cancer literature one is struck again and again by how ignorant we are about this vile disease. Even basic things - the role of antioxidants, the causes of chemo-resistance, the mechanisms of immune escape - seem to be beyond us. Where are the major theroretical breakthroughs in cancer? Where is the basic knowledge that will unlock new therapies? The more one reads of the cancer literature, the more one realises that we're groping in the dark.

Let's hope that more physicists and engineers start to look at cancer - perhaps some fresh approaches are what we need to make progress. Because major progress is what we desperately need in this area.

Volunteers Required - Fund-raising in Woodford Green, Essex

December is National Childhood Cancer Awareness Month, and George's cousin Penny will be organising fund-raising activities in his name for Clic Sargeant. We  have a personal connection with Clic Sargeant, the team at the Royal Marsden in Sutton provided lots of support for our family during George's illness. It's a great charity that helpes people in very practical ways at a difficult and distressing time.

Penny is organising activities at Tesco's in Woodford Green in Essex on December 15th and 16th. It's still in the planning stage, but volunteers to help out would really be appreciated. More details will be posted closer to the event, but if you are in the area and want to help out for a worthy cause then please drop a line to pennychristophe@googlemail.com

Searching for Clinical Trials

Looking for a clinical trial can be a daunting experience. It may be that you are doing this just to see what's out there, but it's more likely to be that you - or a friend or family member - have just had some bad news about treatment and you need to review options. At times like this you may not know where to turn. The aim of this article is to offer some guidance in what is likely to be a difficult time.

The first and most important thing to keep in mind is that clinical trials are conducted for different reasons - and this is normally indicated by the phase of the trial. The most important of these are Phase I, II and III trials.

Phase I trials are normally the first trials of candidate drugs or other treatments in humans. To get to Phase I a drug will have gone through 'pre-clinical' testing in the test tube (in vitro) or in animals (in vivo). Occasionally a drug might be tested in tiny amounts in humans before going into a proper Phase I trial. The key aim of the Phase I trial is to find the appropriate dosing of the drug. The effectiveness of a treatment is of secondary importance. The researchers are convinced by the pre-clinical evidence that the drug has some effect, but they need to establish a proper dosing schedule before they can focus on how good it is in practice. This is an important point to keep in mind. Also, Phase I trials tend to be on a small in scale (there are only a few patients, often based at a single hospital or clinic and with small research team).

Phase II trials take things a step further. At this point the drug or treatment has been through Phase I. The dose has been established and there are often some indications of effectiveness. There's still an element of looking at the dosing schedule or treatment protocol, but the emphasis is now on seeing whether the positive effects seen in the pre-clinical studies actually hold true in humans. Phase II studies are often larger in scale - more patients, more doctors, possible multiple locations.

Lines of Communication

An interesting little story caught my eye on one of the science web sites this week. It‘s a report of a recent study that found that ‘managing communication around cancer diagnosis gives patients sense of control in an otherwise uncontrollable situation’. The researchers found that:

...communication is an important factor in coping with cancer in that it enables people to exert control during a highly stressful and turbulent time. However, despite best efforts to structure and control that communication, cancer patients cannot always predict or control other people's reaction.

In our experience the need to communicate with friends and family simply became exhausting. Particularly when you’ve just had bad news, the need to relay it multiple times just makes you feel worse. The constant repetition of bad news is depressing, especially when you know that the person on the other end is going to react badly to it too. It means that not only do you have to deal with your own reactions, but you end up having to manage other people’s too. It increases the stress precisely when you’re most stressed out.

George's 18th Birthday

Today should have been George's 18th birthday. Instead it's just a little over three months since his death, on April 25th 2011. We miss him always but today it hurts so much more because we know how much it would have meant to him. He should have had a whole life to look forward to...

Although we are consoled by the knowledge that he knew how much we loved him, and that he loved us in return, the injustice of it all is still hard to deal with.The world moves on, but for us, the world is a poorer place without him.

Meeting your oncologist

Most of the articles on this site have so far focused on cancer research or the politics of that research. However, the intention is to do more than just summarise results or to argue for changes in policies, it is also firmly about providing practical support and advice to cancer patients, their families and friends. With that in mind this post is going to look at something that might seem trivial but in reality is absolutely essential – how to approach the meetings with your oncologist or other specialist. While some people will view an article like this as being a bit pointless, there are others who might gain some useful tips, particularly as we all have a tendency to defer to our doctors. The whole area of doctor-patient relationship is a bit of a nightmare, for all sides, but unless that relationship is solid things will be more difficult than they should be.

When you first get your diagnosis, or when waiting for results from scans or examinations, you will be stressed on meeting your doctors. No matter how much you like them or respect them, you’ll be feeling tense and nervous, a not a little apprehensive. Sitting in the waiting room can be hard, especially if the clinic is running late and you’ve been waiting for ages (which was the norm, in our experience). At times like these it’s easy to get so stressed that you forget to ask the things you’ve been meaning to ask. It’s ridiculous, because you may have been waiting for ages to ask these questions, but you can be blindsided by news (good or bad), get diverted by some other train of thought or simply forget everything and just sit there passively while the doctor leads the discussion. Afterwards, you’ll kick yourself for not having remembered to ask your questions and will either have to wait for the next appointment or get on the phone or look for someone else to ask.

Curcumin and the Drugs Industry

Looking through some of the previous articles on this site you’ll notice frequent mentions of curcumin. Of the many food-based anti-cancer agents, this extract from turmeric (the yellow spice used in curry), is one that generates a lot of scientific interest. Curcumin has anti-oxidant, anti-inflammatory and a wide range of anti-cancer properties. It is cheap, non-toxic and has been used as a traditional medicine for hundreds of years. In terms of research, it has plenty of in vitro and in vivo evidence against a wide range of different cancers. What’s more, there have been early stage clinical trials that show that even at high doses curcumin is non-toxic. There are lots of positives about curcumin, but there are also some significant issues. First and most obvious is that it suffers from very low levels of bioavailability. In other words it takes a lot of curcumin to generate even low levels in the blood stream. Secondly, most of the in vitro and in vivo studies use the raw material, but when we take it orally it gets metabolised as we digest it, so it’s not pure curcumin that circulates in the body (though in the digestive tract things are different, obviously). These issues are not unique to curcumin by a long shot, and they are discussed in more detail in the articles on How To Read A Cancer Paper (here and here).

Even with those caveats, curcumin is an interesting substance that bears closer investigation. But, given the urgency with which we want the research to proceed, you have to ask yourself why such a positive drug candidate has not moved further. Where are the large scale trials in cancer patients? Why isn’t curcumin part of the everyday armoury that we use against cancer?

Q&A with Dr Gerald Krystal - Low carbs and cancer

Following my recent article on a recent paper that looked at the effect that a low carb diet had on slowing tumour growth (and if you haven’t read it, I suggest you do that before reading the rest of this…), I contacted one of the authors, Dr Gerald Krystal of the University of British Columbia with a list of questions. Dr Krystal has kindly responded with some more information, which I think is useful for those people considering starting a low carb diet in line with the results of his team’s work.

PP: The low carb diet includes foods high in amylose. Doesn't this make it difficult to translate into a diet people can follow? Are there foods that are naturally high in amylose?

GK: There are many foods that are naturally high in amylose. For example, all legumes (beans, lentils and peas), basmati rice, new potatoes, bananas, whole grains, sweet potatoes, radishes and parsnips. Try and avoid regular "old" potatoes, white rice and white bread (whole wheat bread is not much better….bread with whole grains is the best when it comes to breads but I try and avoid all breads. If you can't resist, sourdough is not bad because of its low pH…if you add a tsp of lemon juice or vinegar to any meal you can lower the glycemic index by about 1/3). Another interesting tip is if you let cooked rice cool it becomes more resistant to digestion so eating sushi is better than eating hot cooked white rice. I would love to see a breakdown of digestible carbs into % amylose and % amylopectin down the road on food products. Also, there are ongoing studies in the US to generate genetically modified potatoes (lacking 2 enzymes that are used to put the branched sugars on the glucose polymer to convert it from a linear glucose polymer (amylose) to a branched glucose polymer (amylopectin, which is more easily broken down). Don't know how you feel about genetically modified foods but this could dramatically lower blood glucose spikes after eating potatoes.

PP: Why is it that so much mainstream dietary advice for cancer patients seems so unhealthy? Why are patients still being encouraged to have high calorie diets?

GK: This drives me crazy as well. The main concern of cancer clinicians today is cachexia (wasting). I understand this is something you want to avoid but I think that lowering our carb and raising our protein intake will have a substantial benefit, especially for early pre-metastatic cancers. In keeping with this I would like to see clinicians substitute amino acid/PBS intravenous drips for the currently used 5% dextrose (glucose) PBS to rehydrate cancer patients.

Low carb diets and cancer

The Warburg Effect

It is well known that a hall-mark of cancer cells is an increase in the use of glucose – the so-called glycolytic switch is an early indicator of malignancy (a change that is a part of the Warburg effect – which is worth following up if you're interested). This greediness for glucose is exploited in PET scanning, where radioactively tagged glucose is injected into the patient and, several hours later, a scan is taken to track where the radioactivity has accumulated in the body. Tumours absorb much higher amounts of this radioactive glucose than the normal tissues, and show up as 'hot spot' on the scans.

Tackling this greediness for glucose underlies a number of different approaches to attacking cancer, and one obvious avenue for this is to look at diet. Before we get into this, however, it's worth pointing out that many mainstream oncologists and dieticians are incredibly blasé about this topic. From our experiences in many different hospitals and with different doctors, we know that the mainstream advice for cancer patients is not to change the diet in any major way. Time and again we were told that keeping the calorie intake high and maintaining weight were the most important considerations. Any questions about limiting carbohydrate intake to starve tumours were simply dismissed as untested and unproven hypotheses and therefore best avoided.

That said, there have been numerous studies that have looked at the influence of diet on cancer growth. Many of these have been rodent studies, but there have also been some patient studies performed, mostly these have looked at brain tumours (glioblastoma). Furthermore, much of this research has involved a ketogenic diet, which is a high-fat and extremely low-carb diet, which has been used clinically in the treatment of epilepsy. In terms of being able to follow this yourself, it's no easy task, this is an extreme diet, much more extreme than the strictest Atkins diet for example.

How To Read A Cancer Paper - Part 2

By Pan Pantziarka

Recap

In the first article in this series we looked at interpreting the results of in vitro studies, particularly those that look at the effect of different substances on tumour cells. In this second piece we focus attention on in vivo studies – in other words studies that take place in living tissue rather than in a Petri dish. For the most part these studies use rats and mice, though sometimes you'll find other animals being used. Again we will focus cancer research of the sort that looks at what effect a given substance (particular foods, supplements, vitamins or minerals, drugs etc) has on cancer.

Mice and Rats

The good news is that if you are a rat or a mouse there has never been a better time to have cancer. Again and again we see fantastic results in rodents. Cancers of many different sorts are slowed, stopped, destroyed. It is impossible not to feel excited by some of these results, and they are truly remarkable. Unfortunately however, these fantastic results on lab rats do not translate as well to humans. Why is that? We saw that test tube studies have all kinds of issues, surely these problems disappear once you move from glass dishes to living beings?

Some of the disadvantages of the test tube approach are easily solved in rats, mice and other animals. No longer do you have just a flat layer of cancer cells to bathe in your anti-cancer agent, instead you have three-dimensional tumours embedded in tissue, with a blood supply and tumour microenvironment. And, interestingly enough, we find that some agents that have fantastic results in the test tube are all of a sudden not so powerful against tumours. Instead the same agents have lower efficacy and in some cases seem to have lost all trace of anti-cancer effect. Why? Because the high dosing and guaranteed test tube conditions cannot be transferred to a living being. Doses that killed tumour cells under glass can also be toxic to living animals. In some cases you find that there is what is termed a biphasic response – at the lower dose that can be achieved in animals the agent turns out to be pro-cancerous, and at the higher dose it does kill the tumours but also kills the animals or makes them seriously sick. Not good.

Windfarms or cancer treatment?

Writing in the Daily Telegraph, Energy Secretary Chris Huhne states that:

A low-carbon economy presents an opportunity, not a cost. Investment in our clean energy future should not be mistaken for a cost to the economy, or the public purse…Globally, the low-carbon goods and services industry is worth £3.2 trillion, and employs 28 million people.

In a withering response, Tim Worstall, takes Huhne’s arguments apart and shows, yet again, the idiocy of current climate and energy policy. In passing Worstall makes the comment that:

…an economist would point out those are costs. 28 million people not curing cancer but faffing about with windmills. This is a cost of getting windmills, for we get windmills not the cure for cancer.

Some would argue that a blog about cancer and cancer-research is not the place to be discussing either climate change, energy policy or economics. I strongly disagree. At every stage, from screening, to diagnosis to treatment, economic decisions are at play. And those decisions can be the difference between life and death. We live in a world where there are not endless resources, there is no bottomless pit of money, therefore decisions about where money is spent have to be made, no matter how distasteful or hard those decisions are.

We are not having a grown up discussion of these issues in this country. We are not presented with choices that say spend money on windmills or on health care, on subsidising solar versus paying for new treatments. Yet these decisions are being made all the time. Instead we are told to focus on the distant future when climate change might or might not be a problem. We are told that we have to save the planet, that our grandchildren’s children will thank us, that we owe it to planet Earth.

TP53 and Li Fraumeni Syndrome

George was diagnosed with this first cancer, (embryonal rhabdomyosarcoma in the left temporalis muscle), on his second birthday. That was at Great Ormond Street Hospital, and it had taken us a long time to get him there. His mother, Gina, had died of metastatic ovaria cancer just ten months previously. Part of the delay in getting him diagnosed was the assumption that we were just being paranoid. The odds of him getting cancer so soon after his mother had died of it were assumed to be astronomical. When the diagnosis was finally made we were all stunned. Was it something to do with his mother’s illness? The doctors assured us that this was an unlucky (way, way, way unlucky) coincidence.

Fast forward to George at 15, and the discovery of a basal cell carcinoma during a routine and unrelated visit to the doctor. A second cancer, completely unrelated to what he had as a child. This time the explanation was that it was most likely a long term side-effect of the radiotherapy he had as a child.

Only a few months later George was diagnosed with osteosarcoma in the right side of his jaw (the mandible to be exact). A third cancer, and it had taken many weeks of going from doctor to doctor, hospital to hospital, to get it diagnosed, even though we knew there was something seriously wrong. How could it be that my son had three different cancers? One hypothesis at the time was that like the basal cell carcinoma, the osteosarcoma was a long term side effect of radiotherapy. However, the mystery was finally solved after having a genetic test of his TP53 gene. This is an important tumour suppressor gene, and in his case he had a specific defect that identified him as having classical Li Fraumeni Syndrome (LFS). Once his test result came in other members of the family were also tested and found to be not carrying the mutation – making it most likely that it came from his mother after all.

Miracle Cures

Beware Of False Prophets

It is tempting for cancer sufferers, and their friends and family, to look around at other treatment options, particularly if current treatments start to fail. In some cases people want to complement what they are getting from their oncology team – either because they want to lessen some of the horrendous side-effects of chemo or radiotherapy or because they want to boost the effectiveness of the protocol they are on. There are some people who simply don't want to go the conventional route – though this is a very high-risk strategy to adopt and is not one that is recommended (this is a topic that I will come back to in a future post). In other cases conventional treatments fail, the disease progresses or recurs, and there are few standard options available so the search for something new takes on a particular urgency. The first port of call for people in these different situations is the internet. And this too, can be dangerous, as you soon discover.

The last time I looked, the search term 'cancer cure' came up with 103,000,000 hits. Yep, 103 million hits. That is an unimaginably huge cache of information to process. And, unfortunately, a lot of that information is both dangerous and worthless. In our search for treatment options, (particularly once George's treatments started to fail), we came across plenty of sites that were offering miracle cures for cancer. No matter what type of disease, or at what stage, there were people out there who were promising to both treat and to cure. That alone should be setting alarm bells ringing in any sane person.

In general there are two distinct subsets of these promised cures, with some more credible looking than others.  On the one hand there are the promised cures that appear to be based on science and those that are decidedly, and in some cases proudly, unscientific.

How To Read A Cancer Paper - Part 1

By Pan Pantziarka

Intro – Why Write This?
Be prepared for a shock when you first start reading the literature on cancer. When you first dip your toe in the waters of Pubmed or other source you'll be struck by the vast number of papers that show how cancer cells are wiped out by this, that or other treatment. Whether it be plant polyphenols like curcumin or quercetin, or vitamins like C or D3, or medicinal mushrooms like Ganoderma Lucidum or... The list is endless, and so are the papers. Hundreds of them, in page after page you'll see results confirmed again and again. So why is it that cancer is still a problem? Why is it that curcumin or quercetin or EGCG or any of the other natural agents and food supplements haven't cured cancer? Because, if we believe all of these papers, then it should have been cured by now, the results are that clear. The answer is complex, and it isn't down to the fact Big Pharma has killed the research or drowned the scientists or any other favourite conspiracy theory.

This guide is aimed at the scientifically literate reader who isn't a medic or a biochemist. It's aimed at those patients and families who are undertaking to read the research directly in the hope of finding something useful. It's aimed at people who are in the situation I was in after my son's diagnosis (George was diagnosed with osteosarcoma of the mandible). I wanted to find out more about the disease, but I also read up on what we could do to support his treatment. Later, after treatment failed to halt the disease, it was because we were looking at what other options we had open to us. While I've got the scientific training (a PhD in machine learning), I was reading in a new area and without a background in medicine. The aim here is to provide a helping hand to other people in a similar situation in the hope that it will help in navigating a complicated and confusing area, particularly when the stakes are so high.

Book Review - Foods To Fight Cancer

A version of this review was first published at LondonBookReview.com

Title: Foods to Fight Cancer
Author: Richard Beliveau and Denis Gingras
Publisher: Dorling Kindersley
ISBN: 1405319151/0756628679

Cancer patients, and their friends and families, are often faced with contradictory information on what to do about diet. On the one hand there are large numbers of mainstream oncologists and dieticians who tell patients to eat what they like so long as they keep the calories up and are able to get through chemotherapy or radiotherapy. On the other hand there are plenty of people who insist that only a strict vegan or macrobiotic or Gerson or other anti-cancer diet will help. And of course there are lots of books out there that advocate all kinds of diets, all of them claiming to be based on some sort of science. Those looking for a middle ground based on solid science are left trying to work out for themselves what makes sense and what is obvious nonsense.

Foods To Fight Cancer looks like lots of other books in the 'superfoods' genre. It's glossy, well illustrated and published by Dorling Kindersly. It looks more coffee table than operating table. However, unlike many of the anti-cancer food books that are on the market this one is written by scientists working in the field of diet and cancer and who are not only up-to-date with the science but who are engaged in making it happen. It just so happens that Richard Beliveau and Denis Gingras are excellent communicators able to write for the non-scientist as well as their colleagues.

The central premise of the book is that dietary interventions can help tip the odds against developing cancer, and also to aid in fighting cancer once it has started. The plant kingdom contains thousands of phytochemicals - polyphenols, terpenes, sulphides etc - which have potent anti-cancer properties. These micro-nutrients act in multi-faceted ways to block many of the different biological pathways necessary for cancers to form, grow and then metastasize. Unlike some of the over-inflated claims made by some, there is no promise of a single all-powerful cancer cure here. Instead the emphasis is firmly on looking at what pathways are necessary for cancer to develop and then what can be done to block these using multiple compounds from different foods.

Introduction

The original idea for this website came out of a series of conversations with my son, George, about a year after his diagnosis with osteosarcoma of the mandible. By this point he had been through a number of treatments but the disease was still progressing, but he was pretty healthy and thinking about the future. We had learned a lot about cancer, treatments, and supplements and were still actively looking for new therapeutic options. We felt that we’d learned a lot that might be useful to other patients and their families and friends. A website was the obvious way of sharing this knowledge and we registered the domain name soon after.

George designed the logo and had lots of ideas. He wanted the site to be self-funding and hoped that it would also make money that he could put into his university fund, so he was keen that the site carries adverts. Lots of good ideas but nothing came of it at the time. Now, after his death at the end of April 2011, I am putting the site together to put into practice some of the things we talked about. Any money raised will be distributed to the charities that he supported.

The site will include commentary on cancer research, information on supplements and treatments, diet, details of George’s story, relevant book reviews, links to useful sites and other information that cancer sufferers may find useful.

Pan Pantziarka