Midline Glioma – research fundraiser

UPDATE: December 2021 – Exceeded 100k! Research has already been funded from your donations, so thank you!

UPDATE: Emily was hoping to reach her target by Xmas Day, she went storming past that number on the 23rd December – £50615 raised from just over 1700 donors, which is fantastic. She originally set 10k as a target, then moved it up to 25k, passed that and moved it to 50k, which is when I first mentioned the cause here, on Twitter, and on Facebook. She was at the half way to the 50k at that point just over a week ago. Hopefully, we can draw in more donations from a few of my followers. Thank you! Keep those donations coming in.

Diffuse Midline Glioma, H3 K27M Mutation is not a phrase you want to hear from a doctor. It’s a type of tumour that most commonly affects people under about the age of 25 years but over 3 years. It’s very rare – 100 people in the UK annually – but always lethal, sadly. The tumour grows rapidly within the Central Nervous System and has a devastating effect on the spinal cord or the brain depending on precisely where it grows.

I must admit I’d heard of spinal tumours, but don’t think I’d heard this full phrase until a friend posted about it on social media as their daughter had started a fundraiser to raise funds for research. Emily passed her initial fundraising target quite quickly and has upped the ante, now aiming for £50000. She’s more than halfway there with well over 1000 donations so far. Sciencebase is happy to give this worthy cause a mention in the hope that a few readers take her plea to heart.

I’ve written generally about rare diseases several times over the years and how they are often neglected by mainstream medical research and the pharma industry because by definition they each only affect a small number of people. Of course, there are many, many rare diseases and the total numbers of people that are affected are large. At the other end of the scale though, is often a terrible tale of someone afflicted by something rare and untreatable, which is precisely why we need to raise funds for the individual cases. So, here’s the link to Emily’s JustGiving page. Please dig deep, as they say.

Printing a 3D ovary to treat infertility

Scientists have used a 3D printer to make a scaffold of a soft plastic type material known as a hydrogel. The researchers then loaded this scaffold with the egg sacs known as ovarian follicles from a female mouse and implanted it. The follicles began maturing and released eggs, which were fertilised by natural mating and the mice then went on to give birth to live young. [Laronda et al, Nature Commun, 2017, DOI: 10.1038/ncomms15261].

A similar synthetic ovary might one day be used to treat infertility in women who have had cancer chemotherapy. Chemotherapy causes ovarian failure, essentially destroying a woman’s eggs of which they have a limited supply. Men, of course make sperm all their lives, but women are born with all the eggs they will ever have in immature form in their ovaries. Chemotherapy at any point in their lives will destroy their eggs, some women and girls choose to have eggs harvested and cryogenically stored before they start treatment to improve their chances of an IVF baby later in life.

The picture is quite complicated concerning what the anticancer drugs actually do to the ovary. Quoting from this research paper:

“[Premature ovarian failure and thus female infertility] results from the loss of primordial follicles but this is not necessarily a direct effect of the chemotherapeutic agents. Instead, the disappearance of primordial follicles could be due to an increased rate of growth initiation to replace damaged developing follicles.”

The current research itself is all about testing egg follicle survival and showing how they can be viable on the porous scaffold of the synthetic ovary. Moreover, the team has shown that follicles on the scaffold release appropriate hormones as they would in a living ovary and release maturing egg cells. It all looks very promising for mice. Human follicles grow much larger than mouse follicles and would bring different challenges in terms of keeping them alive in an artificial ovary, but this is a step closer.

The obvious question though is what was the source of the implanted follicles. The team describes how “follicles were mechanically isolated” from an excised mouse ovary for implantation. But, if a women has premature ovarian failure induced by chemotherapy, then there are presumably no follicles with which the fertility team could work unless they have been “harvested” prior to her treatment, which would be an additional (surgical) procedure the patient would have to face and a difficult choice made regardless of whether the patient is a baby, small child, teenager or adult.

Who gets heart cancer?

Over the last quarter of a century, I’ve written about a lot of different aspects of science and medical research. Cancer features a lot, the Big C is prominent in human misery and more common than many other diseases. Often I’ll use a phrase such as “treating liver, bowel, lung, breast, prostate and other cancers”. One phrase I don’t think I’ve ever written, until today is “heart cancer”.

Heart cancer? Do people even get heart cancer? Almost every other organ from skin to brain from gonads to liver, from head and neck to bone and blood, there’s a cancer. Experts repeatedly explain that cancer isn’t a single disease (well it is really, it’s always just runaway cell division of a specific tissue). But, it occurred to me that one of those tissues, cardiac tissue, is rarely mentioned. I then wondered whether or not the lack of malignant tumours in this vital organ might offer clues as to why other organs develop cancers. If there’s some sort of cardioprotection might that be exploited in preventative measures or treatment of cancers elsewhere in the body.

The Mayo Clinic website, always a trustworthy medical resource has this to say about heart cancer in its FAQ:

Cancerous (malignant) tumors that begin in the heart are most often sarcomas, a type of cancer that originates in the soft tissues of the body. The vast majority of heart tumors are noncancerous (benign).

Indeed a study of autopsies on 12000 cadavers revealed only seven cases of primary cardiac tumour. Rare indeed, then, and presumably why we don’t often hear about breakthroughs and new treatments for heart cancer, Big Pharma really won’t profit much from rare disease compared with breast, prostate and other far more common cancers. However, cancers in other parts of the body, such as the lungs, do metastatise (spread) to the heart. Indeed, breast, kidney, lung cancers, leukaemia, lymphoma and melanoma can spread to the heart. But, the fact that heart cancer is so rare must be a clue, the heart is special when it comes to runaway cell division in some way, surely?

The Cancer Research UK site recently published a debunking of the notion that cancer is mostly down to bad luck rather than lifestyle factors that increase risk. They explain that a study in mice showed that there needs to be an alignment of factors for cancer to develop. They add that “We can still stack the odds in our favour, for example by stopping smoking, keeping a healthy weight, eating healthily, drinking less alcohol, keeping active and enjoying the sun safely.” But, what are the risk factors for heart cancer, if indeed there are any?

The US National Cancer Institute has also asked the same question, why are heart cancers so rare? The answer perhaps lies in the fact that unlike other organs when they are damaged, the heart is almost incapable of repairing its tissues, the cells of the heart, the cardiac myocytes, are terminally differentiated and so after a certain point in life they stop replicating (cell replication is both the key to tissue repair and, when it goes awry, the problem in cancer).

This latter point suggests to me that there is probably no way to exploit the heart’s lack of cancer in protecting other organs, although who knows? It’s a double-edged sword, you really wouldn’t want damage to not be repaired elsewhere in the body, such as the liver or kidneys. But perhaps the repair process could be temporarily switched off somehow when a tumour develops there. Block the replication instead of simply killing the rapidly replicating cancer cells. If this was done temporarily while a parallel gene therapy type approach was used to fix the cancer-causing mutations in the cells in that tissue we might find a viable treatment. I’m speculating here…anyone know enough to point out the flaw in my argument?

Will eating processed meat give you cancer?

How does smoking really compare to eating bacon sarnies and having a barbie in terms of cancer risk?

151026-Tobacco-vs-Meat-TWITTER[1]

Both smoking and eating processed meat have been identified as cancer risk factors by the World Health Organization (WHO). This does not mean that a smoker or someone who eats processed meat will get cancer, but it increases the likelihood that they will.

Smoking is a very well-known risk factor for several types of cancer, including lung, throat, mouth, bladder, pancreas, and kidney cancer. Smoking increases the risk of cancer because it contains carcinogenic substances that directly damage DNA and other cellular processes in the body that ultimately lead to the uncontrolled cell replication that leads to cancerous tumour growth.

Processed meat has also been classified as a Group 1 carcinogen by the WHO, which means that there is sufficient evidence to conclude that it causes cancer in humans. Processed meat includes meat that has been preserved by smoking, curing, salting, or adding preservatives. Examples of processed meat include hot dogs, bacon, ham, sausages, and deli meats. However, the mechanism by which eating processed meats increases one’s cancer risk is unclear. There could be a connection between the nitrites and nitrates used to preserve some meats but these are not present in all meats and there is no definitive evidence that such preservatives generate carcinogens in the gastrointestinal tract.

Indeed, while nitrites and nitrates have been shown to form potentially carcinogenic N-nitroso compounds (NOCs) in the gut, the concentration of these compounds in processed meat is relatively low, and other factors may also contribute to the cancer risk associated with processed meat consumption. For example, cooking methods such as grilling and frying can generate carcinogenic compounds, and high-temperature cooking of meats has been linked to an increased risk of cancer. In addition, some studies suggest that the high levels of saturated fat and cholesterol in processed meat may contribute to cancer risk. It is perhaps more likely that high processed meat consumption is associated with unhealthy dietary and exercise patterns, such as a sedentary lifestyle and a higher intake of calories.

In terms of cancer risk, it is difficult to directly compare smoking and eating processed meat. Both increase the risk of cancer, but they do so in different ways and to different extents. Smoking is a more significant risk factor for lung cancer than processed meat, while processed meat may be a more significant risk factor for colon cancer. It is important to note that the risk of cancer from smoking and eating processed meat is also influenced by other factors, such as the frequency and quantity of consumption, as well as an individual’s genetics, lifestyle, and other environmental factors.

Limiting one’s consumption of processed meat and not smoking could be key to reducing one’s personal risk of getting cancer and other health problems. It is perhaps worth adding that alcohol is also a major risk factor for cancer.

A brief word about tomatoes and prostate cancer

UPDATE: To avoid confusion: eating lots of tomatoes will not stop you getting prostate cancer if other risk factors are in place!

At least 20 years ago I wrote a news story in my rookie days about how the natural red pigment in tomatoes, the antioxidant lycopene, could somehow protect men against prostate cancer. Nothing was ever proven and the latest news which hit the tabloids in the last couple of weeks doesn’t add much, at least if you read between the lines.

NHS Choices, as ever, has a good summary:

“This large study has shown an association between the consumption of more than 10 portions of tomatoes per week and an 18% reduction in risk of prostate cancer. However, as this was a case controlled study, and not a randomised controlled trial, it cannot prove that eating more tomatoes prevents prostate cancer.”

Tomatoes grown and photographed by David Bradley

The study does have some strengths: large size and accounting for confounding factors. However, limitations include: reliance on dietary questionnaires and the broad categories for self-estimate of body size. After all, do you recall how many portions of tomatoes you’ve had and can honestly tell us how fat or thin you are?

The bottom line NHS Choices says:

“This study does not provide enough evidence to change the recommendations for reducing the risk of prostate cancer. A healthy, balanced diet, regular exercise and stopping smoking are still the way to go, rather than relying on eating one exclusive food type such as tomatoes.”

Tomato-rich diet 'reduces prostate cancer risk'.

Incidentally, from this paper: “Prostate cancer (PCa) represents a major public health burden in the western world. It is a peculiar disease as more men die with it than from it. Also interestingly, PCa was virtually unknown until the 20th century.”

Anticancer Aspirin? Not so fast

The news was full of the discovery that taking some aspirin every day for ten years could somehow reduce your risk of getting cancer, particularly cancers of the gastrointestinal tract. The stomach bleeding side-effect (for some) and other as yet unknown side-effects aside, I was skeptical from the start, it just looked like a review of reviews where they looked at the idea that taking aspirin for years and years might somehow correlate with not getting cancer. To me, this is like the inverse of so many other studies that purportedly “prove” that such and such an exposure to food, pollution, toxin or whatever will “cause” cancer. Correlation is not causation.

chemical-structure-of-aspirin

As far as I can tell, the discovery was based on a literature review and not an actual study of the pharmacology and biochemical effects of aspirin itself. Thankfully, NHS Choices magazine, which takes a look at the science behind the headlines seems to agree. “The study was carried out by researchers from a number of institutions across Europe and the US, including Queen Mary University of London. It was funded by Cancer Research UK, the British Heart Foundation and the American Cancer Society. The study was published in the peer-reviewed medical journal Annals of Oncology.” Fine. Good.

But, says NHS Choices: “Several of the study’s authors are consultants to or have other connections with pharmaceutical companies with an interest in antiplatelet agents such as aspirin.” That’s common, and, of course, those involved in pharma research are generally connected to the industry in some way. So, not necessarily a bad thing, there are often what some might refer to as conflicts of interest in biomedical research if these are indeed conflicts here.

More worrying though, and to my mind, the real nub of the problem is what NHS Choices says about the details of the study: “It is not clear that the results are reliable from the methods reportedly used to compile this review. This is because it included studies of varying design and quality, with much of the evidence coming from observational studies, which, while useful, cannot be totally relied on to test the effectiveness of healthcare interventions.”

NHS Choices also criticises the way studies in the review were chosen: “It’s not clear how the studies included in the review were chosen and whether others on the same topic were excluded. It is also not clear whether or not this was a systematic review, where studies are rigorously appraised for their quality and criteria are established for their inclusion.”

That sounds like quite the damning indictment to me and for that reason, I for one am out.

Daily aspirin 'reduces cancer risk,' study finds – Health News – NHS Choices.

Anal cancer in women

Many readers will probably be aware that actress and model Farrah Fawcett died in 2009 of anal cancer. But a recent update from Cancer Research UK revealed that anal cancer rates in the UK have increased by nearly 300% over the last 40 years. The increase is much higher in women than in men, rising from 4 in a million to 18 in a million for females (4 to 12 in a million in males). Presumably, similar increases are seen elsewhere in other countries.

Experts believe the reason for the dramatic rise is likely to be caused by the increasing prevalence of the human papillomavirus (HPV), a virus that is usually transmitted through sexual activity. An estimated 90 per cent of anal cancer cases in the UK are linked to HPV infection.

Now, this is a mixed taboo subject, cancer, sex, disease, bumholes etc. Perhaps not a topic for the family dinner table, but certainly one that should be broached more readily. If shifting sexual practices are largely to blame, then sexually active people ought to know more about HPV and the fact that it can cause cancer of any entry point in the body.

anal-cancer

A recent tweet from @RealMissChief today remarked on a tattoo a female displayed on her lower back that she saw in a bar. The tattoo was actually of stars but RMC wittily interpreted this to mean “I do butt stuff”. Maybe the tattooee does or doesn’t we will never know, but either way we can but hope that she uses protection if she does that kind of “butt stuf”, or at the very least knows her partners’ HPV status. This anecdote does offer a putative tabloid scare story about how getting a tat on your lower back could lead to anal cancer. But, while it might be flippant to suggest such a thing, perhaps the increasing proclivity for such body art simply correlates with general shifting attitudes towards sex at a time when HPV is prevalent. The numbers are small but worryingly on the increase…

Anal cancer rates quadrupled since mid 70s.

10 cancer myths busted

Cancer Research UK has an interesting post busting ten of the most irritating and persistent pieces of deceived wisdom about cancer:

Myth 1: Cancer is a man-made, modern disease

Myth 2: Superfoods prevent cancer

Myth 3: ‘Acidic’ diets cause cancer

Myth 4: Cancer has a sweet tooth

Myth 5: Cancer is a fungus — and sodium bicarbonate is the cure

Myth 6: There’s a miracle cancer cure…

Myth 7: …And Big Pharma is suppressing it

Myth 8: Cancer treatment kills more than it cures

Myth 9: We’ve made no progress in fighting cancer

Myth 10: Sharks don’t get cancer

Don’t believe the hype — 10 persistent cancer myths debunked.

Amygdalin – anticancer “vitamin” B17

Amygdalin the so-called safe and natural anticancer vitamin B17, is none of those things. It is not a vitamin in any sense of the word. It has no anticancer properties. It is poisonous.

The compound, formula C20H27NO11, is a glycoside initially isolated from the seeds of the tree Prunus dulcis in the nineteenth century, also known as bitter almonds. Enzymes (namely glucosidases) found in the gut and in some foods break down amygdalin to release hydrogen cyanide. See also synthetic derivative, laetrile.

“Cochrane Collaboration” had this to say:

“The claims that laetrile or amygdalin have beneficial effects for cancer patients are not currently supported by sound clinical data. There is a considerable risk of serious adverse effects from cyanide poisoning after laetrile or amygdalin, especially after oral ingestion. The risk—benefit balance of laetrile or amygdalin as a treatment for cancer is therefore unambiguously negative.”

Research Blogging IconMilazzo S., Ernst E., Lejeune S., Boehm K., Horneber M. & Milazzo S. (2011). Laetrile treatment for cancer, DOI: 10.1002/14651858.CD005476.pub3

Tea and crumpets and prostate cancer risk

Earlier this week I criticised the endless studies reporting that tea, sex, coffee can raise and/or lower prostate cancer risk. Well, NHS Choices has waded in with its usual balanced assessment of the work and come to a sensible conclusion:

Men who are tea drinkers should not be alarmed by the results of this study as it has many limitations that cast doubt on the reliability of the findings. However, men should remain alert to the signs and symptoms of prostate and other forms of cancer, regardless of their tea habits.

via 'Tea raises prostate cancer risk' – Health News – NHS Choices.

The site points out that it might just be that men who drink more tea tend to be healthier in other ways and so live longer. Longevity is definitely a risk factor for prostate cancer, certainly you cannot get the disease in your 60s if you died of a heart attack in your 50s…to put it bluntly.