How Charles Darwin Helped Me Cope With My Cancer

When I was diagnosed with breast cancer in 2011, I was inundated with advice on how to cope with this horrifying turn of events: Meditate. Exercise. Visualize happy outcomes. Get massage and acupuncture. Scream when necessary.

That all helped. Still, during the months I gave up both my breasts and a pad of underarm lymph nodes to surgery, underwent eight rounds of chemotherapy and 33 sessions of radiation, and started tamoxifen, it was impossible to shake the terror that cancer — a foreign, sneaky, malevolent thing — had invaded my body and was lying in wait to wreck more of me.

But gradually, because I had recently finished writing a book about evolution, I realized that I didn’t have cancer, a single thing. Instead, I had a cancer cell population: many things, each of them aimless.

That small difference in thinking made all the difference. I still sometimes suffered limb-freezing bouts of dread. But knowing that each cancer cell was subject to the rules of natural selection helped me accept that neither I nor my doctors had total control of my fate. It helped me understand why I was being treated with radiation and not one but three different chemo drugs and why the newest, targeted therapies aren’t and probably won’t ever be silver bullets. And it also helped me accept that, no matter how much fierceness or tranquility I could muster, my survival depended not on my attitude, but on my cancer cells’ individual characteristics, which I cannot change.

That may all sound like a downer, but the haphazardness of cancer — the haphazardness central to all of evolution — has been weirdly comforting.

A cancer cell is not a foreign invader. Our own healthy cells divide to produce fresh copies of themselves and then die. During this copying process, any number of variations in DNA sequence can result. Most are inconsequential.

Sometimes, though, a variation will give a cell the ability to reproduce faster than healthy cells. If, like healthy cells, these offspring cells don’t alert the immune system, they will start to accumulate. If another variation gives one or more of these rapid-reproducing cells the ability to live longer than normal cells, they will accumulate even faster. Eventually, doctors will define this accumulation as cancer.

This is the story of natural selection and evolution for all organisms. As individuals reproduce, variation arises. Each variation lends an individual a different chance of reproducing, depending on the environmental forces it encounters. Any individual that survives and reproduces is adapted to its environment in the Darwinian sense. A breast cancer cell, because it will produce more offspring, is better adapted to its environment than is a healthy breast cell. Sick, but true.

As in all of natural selection and evolution, it’s now a numbers game. If none of these accumulating cells have picked up a variation that allows them to move away from the environment to which they are adapted, surgery alone, in a best-case scenario, can reduce this population to zero. If lines of cells stretch away from the huddle making up most of the population, radiation of the surrounding area can kill them off. The surgery and radiation act like a devastating natural disaster hitting the local area. The population goes extinct.

The more time passes before a cancer can be detected, though, and the more rapidly reproducing cells exist, the greater the chances that a variation will arise that allows some of these cells to adapt — to survive and reproduce — to a different environment. A subpopulation of the original breast cancer cells may pick up variations that allow them to travel in the bloodstream or lymph system and survive and reproduce in the bones, the brain or other organ. That’s metastasis.

Chemotherapy is designed to prevent metastasis by changing the chemical environments to which cancer cells are adapted. In the early days of chemo, oncologists treated patients with single-drug regimens. A tiny number of patients experienced complete cures. Most patients, though, appeared cured for months or a few years but then fell ill again. And when cancer reappeared, the original chemo drug didn’t beat it back to any helpful extent.

In cases like this, journalists, and even oncologists themselves, often describe the cancer as “developing resistance” to chemo, as “looking for a new way out” or “plotting its next escape.” Language like this, which ignores how evolution works, falsely lends motivation to cancer. Cancer can’t will itself to change to increase its survival.

Chemo drugs usually work by disabling some step in cancer cells’ reproduction process. Many cells in a population of cancer cells have a subvariation that makes one step susceptible to a particular drug. But if some cells have a different subvariation, they will be less susceptible.

These less susceptible cells may survive. If only a few less-susceptible cells are left, it may seem like the cancer is gone. They will still reproduce, but their descendants may take long enough to cause trouble for it not to matter: As my oncologist said to me, in the nicest possible way, “We’ll know you’re cured when you die of something else.” But if they do start causing trouble again, the original chemo drug probably won’t kill them, because the same subvariation will likely once again allow them to survive. They didn’t develop resistance. They were resistant all along.

However, a different step in their reproductive process may be susceptible to a different chemo drug. Or maybe they’re susceptible to a treatment such as tamoxifen, which works to essentially starve breast cancer cells. The logic of “combination therapy” becomes clear: Kill as many individuals in the cancer cell population as possible as quickly as possible using as many different ways as possible.

I don’t know whether combination therapy killed all my cancer cells. But a treatment that makes sense according to the natural selection principles that rule all biological systems gives me much better odds than if I had been diagnosed before it was standard practice. I take what I can get.

I try hard not to think about whether my cancer will metastasize. When I do, I reassure myself that, by then, some new, better treatment may be available. But I also know that the new targeted cancer treatments aren’t the miracle drugs that press reports sometimes portray, even though they have immensely benefited some patients and will certainly benefit many more. That’s because these treatments also work on variations in cancer cells. Oncologists wanting to try a targeted therapy on me would test some of my cancer cells for the vulnerable variation. If they found it, I’d rejoice.

But over the last few years, researchers have found that multiple biopsies from, for example, a single kidney cancer tumor turned up kidney cancer cells with different genetic profiles. Similar results have been found in breast cancer tumors. A targeted therapy may not actually target all the individual cells in a person’s population of cancer cells.

This relatively recent finding would be no surprise to evolutionary biologists. Similar principles may explain why the new immunotherapies also seem to work only for some patients. If a person has any cancer cells with variations that cause a particular immunotherapy to miss them, the cells will survive to reproduce. So I’ve mostly given up projecting myself into a future when I’ll be cured by some new treatment because, cells being cells, there’s no such thing as a sure bet. Instead, I try to float on the idea that I may have already fallen on the right side of the odds.

I’m still here. I don’t know whether any of my cancer cells have survived. But understanding evolution has let me know a few things for sure, all of them bracing. First, if cancer kills me, it won’t be because it’s out to get me. I won’t have lost a battle to some craftier adversary.

Despite the words many journalists and even doctors use when describing cancer, cancer cells simply don’t have a survival instinct. If they did, they would evolve themselves into a mutually beneficial relationship with my healthy cells. Because if I die of cancer, the cancer cells die with me. Not smart.

And I also know this: This whole experience hasn’t been directed by something or someone to test my combat ability or moral purity. My survival won’t hinge on a personal quality of mine, but on the up-to-date treatment I’ve been privileged to receive. And yet even with this excellent treatment, the results will depend largely on chance; if this cancer does kill me, it won’t be my fault or my doctors.’ Darwin’s theory may be an odd comfort, but it’s comfort nonetheless.

By Leslie Brunetta

Leslie Brunetta is the co-author of “Spider Silk: Evolution and 400 Million Years of Spinning, Waiting, Snagging, and Mating.” She is a freelance writer in Cambridge whose articles have appeared in MIT Technology Review, the Sewanee Review, on NPR and elsewhere.

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Blood test spots cancer a year early

Doctors have spotted cancer coming back up to a year before normal scans in an “exciting” discovery. The UK team was able to scour the blood for signs of cancer while it was just a tiny cluster of cells invisible to X-ray or CT scans. It should allow doctors to hit the tumour earlier and increase the chances of a cure.
They also have new ideas for drugs after finding how unstable DNA fuels rampant cancer development.

The research project was on lung cancer, but the processes studied are so fundamental that they should apply across all cancer types. Lung cancer kills more people than any other type of tumour and the point of the study is to track how it can “evolve” into a killer that spreads through the body.

In order to test for cancer coming back, doctors need to know what to look for. In the trial, funded by Cancer Research UK, samples were taken from the lung tumour when it was removed during surgery. A team at the Francis Crick Institute, in London, then analysed the tumour’s defective DNA to build up a genetic fingerprint of each patient’s cancer.

Then blood tests were taken every three months after the surgery to see if tiny traces of cancer DNA re-emerged. The results, outlined in the journal Nature, showed cancer recurrence could be detected up to a year before any other method available to medicine. The tumours are thought to have a volume of just 0.3 cubic millimetres when the blood test catches them.

Dr Christopher Abbosh, from the UCL Cancer Institute, said: “We can identify patients to treat even if they have no clinical signs of disease, and also monitor how well therapies are working. “This represents new hope for combating lung cancer relapse following surgery, which occurs in up to half of all patients.”
So far, it has been an early warning system for 13 out of 14 patients whose illness recurred, as well as giving others an all-clear. In theory, it should be easier to kill the cancer while it is still tiny rather than after it has grown and become visible again. However, this needs testing.

Prof Charles Swanton, from the Francis Crick Institute, told the BBC: “We can now set up clinical trials to ask the fundamental question – if you treat people’s disease when there’s no evidence of cancer on a CT scan or a chest X-ray can we increase the cure rate. “We hope that by treating the disease when there are very few cells in the body that we’ll be able to increase the chance of curing a patient.”

Janet Maitland, 65, from London, is one of the patients taking part in the trial. She has watched lung cancer take the life of her husband and was diagnosed herself last year. She told the BBC: “It was my worst nightmare getting lung cancer, and it was like my worse nightmare came true, so I was devastated and terrified.” But she had the cancer removed and now doctors say she has a 75% chance of being cancer-free in five years. “It’s like going from terror to joy, from thinking that I was never going to get better to feeling like a miracle’s been acted,” she said. And taking part in a trial that should improve the chances for patients in the future is a huge comfort for her. “I feel very privileged,” she added.

The blood test is actually the second breakthrough in the massive project to deepen understanding of lung cancer. A bigger analysis, published in the New England Journal of Medicine, showed the key factor – genetic instability – that predicted whether the cancer would return. Multiple samples from 100 patients containing 4.5 trillion base pairs of DNA were analysed. DNA is packaged up into sets of chromosomes containing thousands of genetic instructions. The team at the Francis Crick Institute showed tumours with more “chromosomal chaos” – the ability to readily reshuffle large amounts of their DNA to alter thousands of genetic instructions – were those most likely to come back.

Prof Charles Swanton, one of the researchers, told the BBC News website: “You’ve got a system in place where a cancer cell can alter its behaviour very rapidly by gaining or losing whole chromosomes or parts of chromosomes. “It is evolution on steroids.” That allows the tumour to develop resistance to drugs, the ability to hide from the immune system or the skills to move to other tissues in the body.

The first implication of the research is for drug development – by understanding the key role of chromosomal instability, scientists can find ways to stop it.
Prof Swanton told me: “I hope we’ll be able to generate new approaches to limit it and bring evolution back from the brink, perhaps reduce the evolutionary capacity of tumours and hopefully stop them adapting. “It’s exciting on multiple levels.” The scientists says they are only scratching the surface of what can be achieved by analysing the DNA of cancers.

By James Gallagher

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Big Pharma conspired to destroy supply of life-saving cancer drugs by putting profit before people

If you are familiar with the fraudulent practices of the pharmaceutical industry, then you know how much power some of these companies have. Cancer drugs are a multi-billion dollar business. In the past, we have seen Big Pharma use the power of the state to grant themselves monopolies on drugs to control the market. We have also seen outrageous price rises in many useful and necessary drugs. In light of this information, the following story should come as no great shock.

After getting its hands on leaked internal documents, including emails and presentations, The London Times recently revealed that one of the world’s leading drug companies created artificial shortages and threatened to destroy supplies of life-saving cancer drugs to drive up prices in Europe.

South African company Aspen Pharmacare, whose European headquarter is based in Dublin, wanted to impose a rise of up to 4,000 percent after purchasing the portfolio of cancer drugs from the British firm GlaxoSmithKline (GSK) for more than £270 million (or nearly $350 million) in 2009.

After they had bought the rights to five cancer medicines, they started to drive up the price. Since the patent had long expired on drugs that Aspen bought, and there was no competition from other manufacturers, Aspen had free reign. In England and Wales, they exploited a loophole that enables a company to impose rises if an existing brand name is dropped. In 2013, the company raised the cost of the leukemia drug busulfan from £5.20 ($6.66) to £65.22 ($83.59), while the price of the blood cancer medicine chlorambucil jumped from £8.36 ($10.72) per pack to £40.51 ($51.92).

Since 2012, Aspen Pharmacare actively tried to impose higher prices on its cancer drugs throughout Europe. The leaked cache documents cited by The Times showed that employees called for “celebrations” over price hikes of cancer drugs.

“We’ve signed new reimbursement and price agreement successfully: Price increases are basically on line with European target prices (Leukeran, a bit higher!)… Let’s celebrate!” an Aspen employee wrote in one of the emails.

Aggressive approach to negotiating with European authorities

In October 2013 Aspen threatened to stop supplying medicines if Italian authorities did not agree to price rises of up to 2,100 percent. Temporary drug shortages were orchestrated to increase pressure.

At one point, a pharmacist wrote to Aspen and its Italian distributor to complain that due to a deliberately small supply of cancer medicine he had to choose which of sick two children was to receive the single package of medicine he had left.

And Italy was not the only country suffering from the unscrupulous business practices of the firm. Several other countries including Belgium, Germany, and Greece reported significant shortages of cancer medicine at about the same time.

In 2014 several staff members at Aspen Pharmacare systematically plotted to destroy stocks of life-saving cancer drugs during a price dispute with the health service in Spain. At some point, they stopped the direct supply of five drugs, leaving patients reliant on foreign packs of expensive medicine.

When an employee at Aspen’s headquarters asked what he should do with existing Spanish packages of the medicine, a senior executive replied that they could not be sold due to a price dispute, adding that donating or destroying the entire stock were the only options.

In yet another email from the company, employees discussed whether they would make more money if they sold cancer drugs destined for Italy in Spain, even though that would mean putting Italy out of stock. (Related: Read more about the Big Pharma drug cartels at

These internal emails showed corruption on a whole new level. To increase the profits, Aspen was plotting to destroy supplies of medicines to create temporary shortages to increase pressure and eventually get what they wanted. Though the emails provide clear evidence of their inhumane practices of putting profits before people. Aspen did not address questions about the destruction of cancer drugs.

In the company’s defense, Dennis Dencher, chief executive of Aspen Pharma Europe, said the price rises were “at levels appropriate to promote long-term sustainable supply to patients” and claimed they had been increased from “a very low and unsustainable base.”

By Amy Goodrich

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Hydrazine Sulfate for Cancer Treatment

1. Backgroud
Cachexia, or body wasting, is one of the major signs of advanced cancers. The causes of cachexia are: 1. Reduction in food intake; 2. Metabolic changes caused by cancer. It is known that cancer cells stimulate glucogenesis, an important factor contributing to cancer cachexia. Dr. Joseph Gold proposed to use hydrazine sulfate for treating cachexia in cancer patients.

2. How Hydrazine Sulfate Works
Hydrazine sulfate interrupts the ability of the liver to convert lactic acid from tumors into glucose, thereby stops glucogenesis cycle, reduce cachexia, limits the ability of tumors to take in glucose, starve the tumors and inhibit their ability to metastasize.

Here is the suggested hydrazine sulfate usage:

1) 60 mg every day for the first three days.
2) 60 mg twice a day for the next three days.
3) 60 mg three times a day thereafter.

3. Safety
Hydrazine sulfate is generally safe when used with prescribed dose. Since it is a monoamine oxidase inhibitor, don’t use together with alcohol, sleeping pills and other psycho-active drugs.

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These Animals Don’t Get Cancer, and Scientists Think They Could Hold a Cure for Human Cancer

In trying to find a cure for cancer, where better to look than the animals that experience very low rates of the disease, or don’t get it at all? That’s the thinking behind new research into elephants and naked mole rats, which scientists are hoping could point the way towards better treatments in humans.

The root cause of cancer is a chance mutation in a group of cells, which is why it’s puzzling that elephants get cancer so rarely – they have 100 times the number of cells us humans do, yet on average only 1 in 20 elephants develop the disease compared to 1 in 5 people.

A team of researchers in the US looked closer, and found an abundance of a gene called TP53. This gene is known for its ability to repair damaged DNA and thus halt the spread of cancer, and it’s some 20 times more common in elephants than it is in human beings. It appears elephants have developed more of these genes as they’ve evolved, in part to protect calves born to older mothers.

“These findings, if replicated, could represent an evolutionary-based approach for understanding mechanisms related to cancer suppression,” says the report, published in the Journal of the American Medical Association.

Naked mole rats are even more miraculous – they never develop cancer, even when scientists try and induce it artificially. What appears to be happening, at least according to a recent study, is that the mole rats are using natural mechanisms to clamp down on the spread of cancer and fight back against the mutation.

That mechanism involves a polymer called hyaluronan. The thickness of this polymer controls the mechanical strength of cells, but also regulates their growth at the same time. Researchers have been able to demonstrate how eradicating this polymer in naked mole rats allows cancers to spread as they normally would – which in turn suggests that hyaluronan could be crucial in keeping the disease at bay. The underground creatures have around five times the level of hyaluronan as humans do.

“We speculate that naked mole rats have evolved a higher concentration of hyaluronan in the skin to provide skin elasticity needed for life in underground tunnels,” reads the separate report, published in Nature. “This trait may have then been co-opted to provide cancer resistance and longevity to this species.”

It’s a big biological jump from elephants and naked mole rats to human beings, of course – the species just aren’t that alike – but the findings could still prove vitally important in developing treatments and cures in the future.

By David Nield

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Why Cancer Isn’t Going Anywhere

If your life has been touched by it, cancer can seem like the least normal thing imaginable. It disrupts all aspects of life, threatens many things we hold dear, and baffles us with its mysterious ways. It seems possessed with an uncanny ability to evade our treatments, rise from the dead when we think it’s finally gone, and even hijack our bodies’ resource-delivery systems to feed its growth. But cancer has been with us since the beginning of multicellular life, and it’s not going anywhere. It has been a supporting character throughout humanity’s story. In fact, it predates us.

bout a billion years ago, multicellularity began. Single-celled organisms started forming groups and using cellular teamwork to get an evolutionary leg up on their less social competition. This transition to multicellular living—from a solitary to a social lifestyle—had many benefits for cells, but it also had some costs. Cells in multicellular bodies had to give up much of the freedom of the unicellular lifestyle. Multicellularity meant several things, including cells not dividing so fast, reining in resource use, taking care of the extracellular environment, and sometimes even making the ultimate sacrifice: cellular suicide.

We descended from the cells that chose this path. Our bodies are made of highly cooperative cells that make trillions of sacrifices every second for the well-being of our entire organism. We are, in many ways, the most complex cooperative system known to humankind, though we rarely pause to think about the feat of cellular cooperation occurring within ourselves.

Our bodies are made of 30 trillion cells (that’s 500 times as many humans are on Earth) that achieve cooperation on a massive scale. But cooperation is not so easy, as anybody who has been on a team project knows. Even a small-scale cooperative venture is vulnerable to failure, whether through a lack of coordination, breakdown of division of labor, or—perhaps most relevant to cancer—exploitation by cheaters. The problem of cellular cheating in our bodies is the exact same problem that plagues cooperative systems everywhere. Cancer cells consume resources faster than normal cells, divide more quickly than they should, and literally leave a trail of acid in their wake. This is the cellular version of the tragedy of the commons: Our bodies are the commons, and cancer is the tragedy.

Cooperation poses an evolutionary conundrum because individuals can benefit from cheating and taking advantage of others’ altruistic behaviors. If evolution favors those strategies that garner the most benefits, then how could cooperation possibly evolve? Decades of research in evolutionary biology have led to two classic solutions to this problem. One is reciprocity: when cooperators get some future benefit from helping. The other is genetic relatedness: when the cooperative acts benefit kin who share genes coding for that cooperative behavior. In the case of the cellular cooperation going on inside our bodies, it is the genetic relatedness of our cells that made cooperation viable. Cooperation makes evolutionary sense for large multicellular organisms like us because the cells in our bodies are highly related to one another. A cell’s self-sacrifice ultimately benefits those that share its genes.

For example, consider a liver cell working hard to detoxify the wine you had with dinner last night. If you are more likely to survive and reproduce as a result of this effort, the genes coding for hardworking liver cells will get passed along to your offspring. If, on the other hand, your liver cells cheat—by shirking their duties, overconsuming resources, and dividing out of control—the genes coding for that cellular bad behavior won’t get passed to the next generation.

The same is true of the systems for policing cellular cheaters. If you have a well-functioning cheater policing systems (including immune system and cell division controls), you are more likely to survive to reproductive age and pass the genes coding for these systems along to the next generation.

But even the most cooperative bodies cannot completely control and suppress cellular cheating. Our bodies are like a massive public goods game with the highest possible stakes. Cells within us are constantly dividing, growing, using resources, and surviving or dying within us. Every time a cell in your body divides, there is some chance that a mutation will happen in the genes that code for multicellular cooperation. And those mutated cells can cheat in the rules that make multicellularity work: monopolizing resources, proliferating out of turn, and trashing the environment that they share with other cells.

When the cells in our bodies start to cheat in the foundations of multicellular cooperation, this creates an ecological problem within our bodies. Resources (like glucose and oxygen) get depleted, cells get overcrowded, the environment gets trashed by acid and other cellular waste. This is the cellular equivalent of the tragedy of the commons. Our immune systems are constantly policing the body, looking for and eliminating cells that are overconsuming, overproliferating, and generating too much cellular waste. But they can’t stop every wayward cell from exploiting the environment of the body. And if this ecological problem persists, then it can escalate into an evolutionary problem: a tragic game in which cellular cheaters win out in the evolutionary race to proliferate, acquire resources, and survive.

This evolutionary problem is the reason that we get cancer. In fact, we could say that this evolutionary problem is cancer. Once cancer cells gain the abilities to exploit the resources of the body and proliferate without the usual controls, then cellular evolution just happens and doesn’t stop, even though it may be racing toward the ultimate evolutionary dead end: host death. This harkens back to the problem of how cooperation can be viable in the first place. If cheaters can do better than cooperators in a population, they will expand in that population. This is exactly what happens in cancer. Cancer cells outcompete normal cooperative cells, and evolution takes it from there.

As cancer progresses, the evolutionary and ecological dynamics interact, making treatment and clinical management extremely complex and challenging. Take, for example, drug resistance. A tumor is a population of diverse cells living in a very complex ecological environment in our bodies. Some cancer cells live nearer to blood vessels that deliver resources; some cells live in regions with high acidity and cellular waste products. This means that when a drug is administered through the bloodstream, some cells will experience high doses while others get lower doses. And since cancer cells can be highly mutated and the population sizes of even small tumors are huge (in the millions), it is highly likely that somewhere in the tumor there will be at least a few cells that can survive in the presence of the drug. Those cancer cells that do survive will then have an open field upon which to grow back, with little competition from other cancer cells. In ecology, this process is called competitive release.

So every time a tumor is treated with a medication, that drug can become less effective. The mere act of administering the drug actually selects for cells that are resistant to it. One way to get around this problem is to use lower doses of drugs and treat the tumor only when it is growing. This approach, called adaptive therapy, is currently in clinical trials at Moffitt Cancer Center in Tampa, Florida, and early results are promising. (I collaborate with Robert Gatenby at Moffitt on modeling adaptive therapy but am not involved with the clinical trials.)

Metastasis is another problem rooted in ecological and evolutionary dynamics. As cells evolve to monopolize resources and overproliferate, they create a less favorable environment, which then selects for cells that can move and find a new, less exploited environment. Metastasis happens when cells leave the primary site of the tumor and colonize new areas of body, usually in large clumps or colonies of cells. We still don’t quite understand exactly how they do this, but research suggests that the cells in these metastatic colonies might actually be cooperating with one another to better exploit our bodies. Signaling for blood vessels, avoiding the immune system, and detoxification are all complex cellular behaviors that can be better accomplished by groups of cells than by individual cells. To what extent cells in metastatic colonies cooperate is an open question—but it’s perhaps the most exciting one in cancer research right now. If cooperation is required for successful metastasis, it opens up a new opportunity for treatment: targeting and interfering with cancer cells cooperating with one another.

One of the reasons that we get cancer is because our natural cheater detection systems sometimes fail. Our cells have internal checks to make sure they don’t proliferate with mutations, but the genes coding for these internal checks can themselves mutate. Our bodies have other backup systems, including a vast network of immune cells that constantly police for cells that are behaving inappropriately. But the policing that the immune system becomes less effective over time because cancer cells evolve to be able to be better at hiding from immune cells, just like prey evolve to be more successful at evading predators. Restoring the immune system’s ability to detect these cellular cheaters has been an effective approach to treatment. The immunotherapies that block the ability of cancer cells to hide from the immune system (called immune checkpoint blockade therapies) can be very effective in previously intractable forms of cancer, including melanoma and lung cancer.

Cancer is a normal part of being a large and complex multicellular organism. But that does not mean it’s inevitable. Evolutionary and ecological approaches to cancer point to many things we can do to reduce our risk. For example, we can slow down the mutation rates in our bodies by reducing inflammation. (Studies have shown that nonsteroidal anti-inflammatory drugs like Aspirin reduce mutation rates and progression to cancer.) We can also keep the ecological conditions in our body more stable by exercising, eating well, and sleeping well, making it less likely that a boom-and-bust evolutionary process will select for opportunistic cells that rapidly proliferate and consume resources.

But there may be many more opportunities to reduce our cancer risk that researchers haven’t yet considered. As we look to the future of cancer, we should be asking: What we can do to fortify the cooperation our multicellular bodies are built on? How we can support our natural cheater detection systems like our immune system? And can we interfere with cancer cells ability to cooperate with one another to reduce metastasis?

We are all vulnerable to cancer. It appears across the tree of life in almost every multicellular organism that has been studied, from humans to elephants to cacti. We will never be able to completely eliminate it. Susceptibility to cancer is simply the price we pay for being a complex and highly cooperative cellular society. Given how successful multicellular life has been on this planet, it must be an evolutionary price worth paying. But we can work to reduce our vulnerability to cancer by slowing down evolution among our cells, creating a stable ecological environment in our bodies, and supporting the cellular cooperation that defines us.

By Athena Aktipis

Athena Aktipis is co-founder of the International Society for Evolution, Ecology and Cancer and an assistant professor in the department of psychology at Arizona State University.

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Hydrogen Peroxide for Cancer Treatment

1. Background

Hydrogen peroxide is a chemical compound with formula of H2O2. Since its discovery, it was widely used in medicine and employed to treat many diseases, such as whooping cough, cholera, typhoid fever, ulcers, tuberculosis, and asthma.

2. How the Hydrogen Peroxide Works

It is well-established that tumor cells survive well under low level of oxygen, a situation known as tumor hypoxia. The consumption of hydrogen peroxide, either orally or by injection, results in increasing of oxygen content of the blood and body tissues dramatically. The tumor cells cannot survive in oxygen-rich environments. Hydrogen peroxide also stimulates immune cells, which attack cancer cells as they attempt to spread throughout the body.

Here is the suggested hydrogen peroxide application procedure:

1) Purchase 35% food grade hydrogen peroxide.
2) Prepare 1% hydrogen peroxide solution and drink 100 ml the 1% hydrogen peroxide solution daily for one week. Observe the body reaction carefully. If there are sick symptoms, stop using it and reduce hydrogen peroxide to 0.5%. If there are not side effects, increase hydrogen peroxide to 2% and use it for one week, then increase hydrogen peroxide to 3% and use it as necessary.

3. Safety

Please remember that the hydrogen peroxide that is available at your local pharmacy (3% hydrogen peroxide) should not be ingested orally, since it contains many stabilizers. The only grade recommended for internal use is 35% Food Grade Hydrogen Peroxide, which must be properly diluted down to 3% or less with water.

Large oral doses of hydrogen peroxide at a 3% concentration may cause irritation and blistering to the mouth, throat, and abdomen as well as abdominal pain, vomiting, and diarrhea. Intravenous injection of hydrogen peroxide must be monitored carefully.

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Woman uses lemon test to detect her own breast cancer

Erin Smith Chieze was diagnosed with stage-four metastatic breast cancer in January 2016 – a diagnosis that, she says, only came about after discovering what breast cancer looks like as well as feels like.

“In December of 2015 when I saw an indentation that looked like one of those pictures, I instantly knew I had breast cancer,” she wrote.

“I tried to feel for a tumour, but my tumour was non-palpable. I was diagnosed with breast cancer five days later and with stage-4 the following month. A heart did nothing for awareness. I knew what breast cancer was.”

“I knew all about self-exams, but a picture of what to look for keyed me into knowing I had a terminal disease.”

“Without having seen a picture randomly with real information, I wouldn’t have known what to look for.”

So, what do the experts think of the lemon breast cancer test?

Dr Dasha Fielder of Sapphire Family Medical Practice in Bondi Junction says that while it’s still important to get regular breast exams by a medical professional, this test does raise awareness about the many forms breast cancer can come in.

“Lemons shown on the picture do resemble some of the changes seen and I think are a good reminder for women to check their breasts and pick up a change,” she says.

“By no means does that picture replace an appointment with a doctor, however, and equally should not be used as a diagnostic tool.”

“What is important, I think, is for a woman to know what their breast normally looks like and to notice any change: this can be in shape of breast or nipple, symmetry, size, pain or discharge.”

“The message should be that all women must check their breasts every three months and if they notice a change not to wait but to make an appointment with their family doctor for breast examination.”

“Sometimes no change in breast is seen at all and unless you feel the breast you will never find a problem, therefore relying purely on the way the breast looks is not enough.”


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Gerson Therapy

 1. Background

The Gerson therapy was developed by Dr. Max Gerson,[i] a German-born American medical doctor. He began to use the therapy for cancer treatment in 1928.[ii] In the past 100 years, the therapy has been continuously modified and improved. It is one of the widely used alternative and complementary cancer treatment in the world today.

2. How the Gerson Therapy Works

The Gerson therapy is based on that the accumulation of toxins in the human body results in the genesis of cancer. The emerging of cancer in the human body indicates that toxins reach dangerous level and the detoxification organs, particularly liver, are already damaged and debilitated. The Gerson approach is to flush out accumulated toxins from the human body tissues, to rejuvenate the human body with essential nutrients, and mobilize the human body to fight the cancer. Here are the 4 key components of Gerson therapy:

(1) Detoxification

Coffee enema is employed to remove toxins from the bloodstream. During one 15-minute coffee enema, the entire human body’s blood supply filters through the liver 5 times. This allows the human body to expel harmful toxins rapidly.

You may select the appropriate enemas that best suit your conditions.

(2) The Diets

The Gerson diet is plant-based, and contains a variety of organic fruits, vegetables and sprouted ancient grains. The diet is low in fat, proteins and sodium, and rich in vitamins, minerals and enzymes.

Here are the examples of anti-cancer diets:

(3) The Juices

The Gerson juices are derived from fresh vegetables, including raw carrots, apples and green-leaf, and provide the easiest and most effective way of high quality nutrition absorption.

Here are the examples of fresh vegetables to get juices:

(4) Supplements

The Gerson Therapy includes a number of supplements:

  • Niacin,
  • Vitamin B12
  • Digestive enzymes
  • Pancreatic enzymes
  • Potassium compound
  • Lugol’s solution
  • Milk thistle
  • COQ10
  • Selenium
  • Thyroid hormone

3. Safety

Gerson therapy is generally safe, if following the standard operation procedures. The common side effects are electrolyte imbalances and colitis (inflammation of the bowel).

[i] Retrieved April 12, 2017

[ii] Max Gerson MD, A Cancer Therapy: Results of 50 Cases. The Gerson Institute, San Diego, 1990.


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A Personal Note: Cancer & Easter

You may be wondering about the title “Cancer & Easter.” Let me assure you they are related in more than the obvious fact that I’m writing this on Easter Sunday and I’m writing about my experience of having surgery for my Prostate cancer.

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Happy Easter!

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He is so energetic and have a look:

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Kyle Reese tackling cancer with God

“I look at it, and I think, we’re all going to die at some point,” Reese said. “But no matter what happens here, I win. If the cancer beats me, I still win. I still go to heaven. If I beat the cancer, then I win there, as well. The hard part for me has been, if I don’t beat the cancer, then there’s a lot of people in my life that lose.”

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Eliminate diseases by touching your ear!

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Cancer – A Gift from God

God, the king of universe, is in control of all that happens to us, both good and bad. Cancer is designed by God and is a gift from God. Since God is infinitely wise, it is right to call the cancer design with purpose. God creates a human being with 10 trillion cells, from which 600,000 cells are selected to become cancer cells every day, and only few of the 600,000 cancer cells further develop into cancer. The complexities of cancer are beyond human being’s comprehension. However, God foresees molecular developments leading to cancer, he can turn on or off at his will. If he chose not to turn it off, he does have a purpose.

Being diagnosed with cancer can be the best thing that has ever happened to us, since cancer actually save our life. Having cancer is a life changing experience that will grant us eternal life. We learn how to surpass death. We are about to be put on a journey that is full of love, peace and understanding beyond our comprehension. We will receive an abundance of wisdom and knowledge from God.

Love is always God’s highest purpose. Cancer let us to learn his finest and most joyous lessons as we find small ways to express concern for others even when we are most weak. A great, life-threatening weakness can prove amazingly freeing. Cancer guides us to love each other deeply. Cancer creates a sincerely affectionate and caring heart for people.

We are terrified of facing death. We are obsessed with medicine and idolized youth, health and energy. We try to hide any signs of weakness or imperfection. Cancer brings huge blessing to us by living openly, believingly and lovingly within our weaknesses.

We will all die. We may get a heart of wisdom, if we are required to number our days. Numbering our days means thinking about how few there are and that they will end. Illness can sharpen our awareness of how thoroughly God has already and always been at work in every detail of our life.

 Cancer is designed to destroy the appetite for sin. Pride, greed, lust, hatred, unforgiveness, impatience, laziness, procrastination—all these are the adversaries that cancer is meant to attack.

God uses different individuals, from all walks of life to guide his lost sheep back to the universal order. There are no specific qualifications needed when the God chooses one to be a voice for all who suffer in the darkness of this world full of light. God chooses you to go with him with a purpose. He wants you to make impossible thing possible. He wants you to make miracle. If he wants you to leave the earth, he does have much more important assign for you somewhere else.

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7th grader is fighting cancer with green tea

A budding cancer researcher designed experiments and proved that green tea could kill the tumor cells. His continued interest could result in curing of cancer. Read more:

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Cancer patient’s poems turn into 9-track album

Through lovely lyrics, Linda Trummer shares her personal journey of fighting two types of cancer. “Really working on these projects have been hopeful and given me hope,” Trummer said, “They’ve given me something to live for.”

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How Cancer Spread

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New weight loss tip? Get cancer

Here is the new tip to loss weight:


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Chewing gum that detects cancer in development


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Cancer Frequent Flyer

In 46 years Andrew Kuzyk has beaten cancer nine times and jokes that he is a “cancer frequent flyer”. Read more


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