If Cancer Can’t Survive In An Alkaline Environment, Why Don’t We Use That As A Treatment – Quora

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If no disease, including cancer, can survive in an alkaline environment, then why aren’t doctors using this method to heal their patients? originally appeared on Quora: the place to gain and share knowledge, empowering people to learn from others and better understand the world.

Answer by Mike Condron, M.D. Medicine, Meharry Medical College, on Quora:

If no disease, including cancer, can survive in an alkaline environment, then why aren’t doctors using this method to heal their patients?

This is a great question.

First of all, let’s be clear about this: human blood is in fact “alkaline”. Our blood pH is very (and I mean VERY) tightly regulated to be almost exactly 7.4 (maybe 7.35, but let’s use 7.4 so I don’t have to type more), which is in fact slightly alkaline. There are multiple systems in place to keep our blood pH at or very near this level.

So, right away, the premise of the question is off: Lots of diseases—or actually, all human diseases, can survive just fine in an alkaline environment, since our blood is alkaline.

But it is also true that if you make the environment alkaline enough, nothing can survive. You could pour, say, lye (sodium hydroxide, with a pH of about 13), onto tumor cells in a laboratory dish, or bacteria, or yeast, and you would kill them in an instant. But is this a useful therapeutic method?

If your blood were infused with sodium hydroxide you would be dead long before it got to a pH of 13. I don’t think experiments have been done to test exactly what blood pH is lethal, but I can assure you it is nowhere near 13. Probably about 7.8.

We cannot survive with a blood pH much different from 7.40. The “normal” range is 7.35 to 7.45. Any significant deviation will cause major problems, and is in fact a sign of major derangement of the systems that are designed to keep our blood pH in that range. There are buffers in the blood that chemically limit the pH, and then there are mechanisms in both the lungs and the kidneys to change the way acidity (which is just hydrogen ions) is managed, just to keep the blood pH in that range.

A deviation to either more acidic or more alkaline will cause severe physiologic disturbances, like enzymes not working properly, chemical reactions in cells not working right, and so on. That is the reason we have evolved so many multi-layered backup systems and emergency plans to keep our blood pH in that range.

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The question does not say what kind of range of alkalinity is being considered as a treatment for diseases, but we are already slightly alkaline, and we cannot survive any deviation from the very precise level of alkalinity that we need.

So, one major idea here is that you can kill a tumor, or micro-organism, or whatever else may be causing a disease, by putting it in a sufficiently alkaline environment. But you can do the same with acidity — pouring hydrochloric acid on tumor cells in a laboratory dish will kill them too. You can also do the same with heat—nothing can survive being heated to 250 F (about 120 C).

We would kill all cancers, infections, and every other disease known, by heating them to that temperature. That works great in a laboratory test dish, but we can’t subject living patients to such a treatment, obviously, just like we can’t infuse lye or hydrochloric acid into patients’ blood to kill their cancer. You can kill cancer by depriving it of oxygen, too…but that is also not a useful treatment, because it would also kill the patient.

Same for glucose — cancer cells need glucose (although some bacteria could maybe make it from things they can absorb from your body, perhaps) but your body’s cells need glucose too, so inducing a hypoglycemic state is not a useful treatment for cancer. You could make the same argument for vitamins and minerals, since cancer cells (and micro-organisms) need them too.

So, to summarize before I go on: We are alkaline to begin with, so the idea that an alkaline environment is bad for diseases is simply wrong. Making the body more alkaline will kill the patient. Lots of other things can kill cancer or other diseases, but they will all kill the patient, too, like acidity, or heat, or deprivation of oxygen, or glucose, etc.

Now let me turn to a different perspective on this question.

I have a feeling — and forgive me if I am jumping to conclusions here but I have a feeling that this question is about one of the latest trends in marketing … “alkaline” water, and “alkaline” diets.

I described earlier that our blood pH is very (and I emphasized VERY) tightly regulated. One part of that is that there is almost nothing you can eat or drink that will affect your pH. Certainly not the “alkaline water” that is being sold everywhere now. Think about this.

It’s true that pure water is at a pH of 7.0, which is neutral. But does that really matter? We eat fruits, most of which are acidic. Are we saying that fruits are bad? Or what about meat? It has a pH, like most tissues, around the same as our body, so why drink alkaline water, when you can just eat meat? Does the idea that the pH of our food affects our blood pH even make sense? No, it does not.

Bear in mind that the acidity of our stomach is impressive — the cells lining the stomach secrete acid with a pH of around 1. That is somewhere between vinegar and battery acid. And that is regardless of what you eat. So if you eat or drink something slightly alkaline (say, 7.5 or 8.0) it will be immediately overwhelmed by the gastric acid, and what enters your duodenum (the first part of the small intestine after your stomach) is going to be at the pH of your gastric secretions, more or less.

Maybe around pH 3 or 4. Is a slightly alkaline water going to stand a chance against the wildly acidic environment of the stomach? Then bear in mind this: Immediately after the stomach contents goes into the duodenum, it is met with a huge load of bicarbonate ions secreted by the pancreas, which immediately neutralizes any acidity. And this all happens before anything is actually absorbed into the body.

Another aspect of this is the concept of “alkaline foods”. This is an unfortunate misunderstanding of an almost irrelevant idea from old food physiology research, which looked at the pH not of foods, but of the ash left over after foods were burned. The vague idea that burning something and looking at the residue left over applied to our physiology of digestion has led to the concept that certain foods are “acidic” and others are “alkaline”.

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This was not the intent of the original research, but for some reason has been taken on by alternative medicine as a way of directing dietary choices, and then there was the birth of alkaline water. Wikipedia has a good article on this: Alkaline diet – Wikipedia

And now let me take a more general perspective on this question. It is in a broad category of questions: “I read somewhere [or heard, or saw in an advertisement] that doing X will cure diseases. So why don’t doctors do X?”

The answer to that is: Because X does not work in the real world, and X is being sold to people, hoping that the customer is too ignorant to know better. I know what I am about to say implies something that you have not stated, but maybe I can speak to others reading this answer who might think this: Please, if you read about something that someone is selling, and they are trying to say doctors are keeping a miracle cure from you, don’t believe them.

I am glad you asked this question, and I hope this answer gives some insight into why we don’t treat cancer or any other disease with alkalinity… or any other non-scientific method.

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Could Immunotherapy Lead the Way to Fighting Cancer – Robin Marantz

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In the morning of June 24, 2014, a Tuesday, Vanessa Johnson Brandon awoke early in her small brick house in North Baltimore and felt really sick. At first, she thought she had food poisoning, but after hours of stomach pain, vomiting and diarrhea, she called her daughter, Keara Grade, who was at work. “I feel like I’m losing it,” said the woman everyone called Miss Vanessa. Keara begged her to call an ambulance, but her mother wanted to wait until her husband, Marlon, got home so he could drive her to the emergency room. Doctors there took a CT scan, which revealed a large mass in her colon.

Hearing about the mass terrified her. Her own mother had died of breast cancer at the age of 56. From that point on, Miss Vanessa, then 40, became the matriarch of a large family that included her seven younger siblings and their children. Because she knew how it felt to have a loved one with cancer, she joined a church ministry of volunteers who helped cancer patients with chores and doctor visits. As she prepared meals for cancer patients too weak to cook for themselves, she couldn’t know that the disease would one day come for her, too.

The ER doctors told Miss Vanessa she wouldn’t get the results of follow-up tests—a colonoscopy and a biopsy—until after the July 4 weekend. She had to smile her way through her own 60th birthday on July 6, stoking herself up on medications for nausea and pain to get through the day.

At 9:30 the next morning, a doctor from the Greater Baltimore Medical Center called. He didn’t say, “Are you sitting down?” He didn’t say, “Is there someone there with you?” Later Miss Vanessa told the doctor, who was on the young side, that when he delivers gut-wrenching news by telephone, he should try to use a little more grace.

It was cancer, just as Miss Vanessa had feared. It was in her colon, and there also was something going on in her stomach. The plan was to operate immediately, and then knock out whatever cancer still remained with chemotherapy drugs.

Thus began two years of hell for Miss Vanessa and her two children—Keara, who is now 45, and Stanley Grade, 37—who live nearby and were in constant contact with their mother and her husband. The surgery took five hours. Recovery was slow, leading to more scans and blood work that showed the cancer had already spread to the liver. Her doctors decided to start Miss Vanessa on as potent a brew of chemotherapy as they could muster.

Every two weeks, Miss Vanessa underwent three straight days of grueling chemo, administered intravenously at her home. Keara and her two teenage sons came around often to help out, but the older boy would only wave at Miss Vanessa from the doorway of her bedroom as he rushed off to another part of the house. He just couldn’t bear to see his grandmother so sick.

Miss Vanessa powered on for 11 months, visualizing getting better but never really feeling better. Then, in July 2015, the doctor told her there was nothing more he could do for her.

“My mom was devastated,” Keara says. Keara told her mother not to listen to the doctor’s dire prediction. “I said to her, ‘The devil was a liar—we are not going to let this happen.’”

So Keara—along with Miss Vanessa’s husband, brother and brother’s fiancée—started Googling like mad. Soon they found another medical center that could offer treatment. But it was in Illinois, in the town of Zion—a name Miss Vanessa took as a good omen, since it was also the name of her 5-year-old grandson. In fact, just a few days earlier little Zion had asked his grandmother if she believed in miracles.

The family held a fund-raiser for Stanley to get on a plane to Chicago with his mother every two weeks, drive her to Zion and stay with her at the local Country Inn & Suites hotel for three days of outpatient chemotherapy. It felt like a replay of her treatment in Baltimore—worse, since the drugs were delivered in a hotel instead of in her bedroom, and the chemotherapy caused nerve damage that led to pain, tingling and numbness in Miss Vanessa’s arms and legs.

And then, in May 2016, the Illinois doctor, too, said there was nothing more he could do for her. But at least he offered a sliver of hope: “Go get yourself on a clinical trial.” Weeks later, desperate, Miss Vanessa and Keara grew hopeful about a treatment involving mistletoe. They attended an information session at a Ramada extolling the plant extract’s anti-cancer properties. But when they learned that it would cost $5,000 to enroll, they walked out dejected.

Finally, Miss Vanessa’s husband stumbled onto a website for a clinical trial that seemed legit, something underway at the Johns Hopkins Bloomberg-Kimmel Institute for Cancer Immunotherapy, just down the road from their home. This new treatment option involved immunotherapy, something markedly different from anything she had gone through. Rather than poisoning a tumor with chemotherapy or zapping it with radiation, immunotherapy kills cancer from within, recruiting the body’s own natural defense system to do the job. There are a number of different approaches, including personalized vaccines and specially engineered cells grown in a lab. (See “A Cancer Vaccine?” and “A DNA-Based Attack”)

The trial at Hopkins involved a type of immunotherapy known as a checkpoint inhibitor, which unlocks the power of the immune system’s best weapon: the T-cell. By the time Miss Vanessa made the call, other studies had already proved the value of checkpoint inhibitors, and the Food and Drug Administration had approved four of them for use in several cancers. The Hopkins researchers were looking at a new way of using one of those drugs, which didn’t work at all for most patients but worked spectacularly well for some. Their study was designed to confirm earlier findings that had seemed almost too good to be true.

“With the very first patient who responded to this drug, it’s been amazing,” says Dung Le, a straight-talking Hopkins oncologist with long dark hair and a buoyant energy. Most of her research had been in desperately ill patients; she wasn’t used to seeing her experimental treatments do much good. “When you see multiple responses, you get super-excited.”

Immunotherapy is poised to become the standard of care for a variety of cancers. The work being done now is forcing a reconsideration of basic tenets of clinical oncology—for instance, whether surgery should be a first line of treatment or should come after drugs like Keytruda.

Many questions still remain. Elizabeth Jaffee, a member of the “cancer moonshot” panel convened by then-Vice President Joseph Biden in 2016, says she’s conscious of the danger of overselling a treatment. While the effect of checkpoint inhibitors can be “exciting,” she says, “you have to put it in perspective. A response doesn’t mean they’re cured. Some may have a year of response,” but the cancer might start growing again.

When Miss Vanessa paid her first visit to Le in August 2016, the physician explained that not every patient with advanced colon cancer qualified for the trial. Investigators were looking for people with a certain genetic profile that they thought would benefit the most. It was a long shot—only about one person in eight would fit the bill. If she had the right DNA, she could join the trial. If she didn’t, she would have to look elsewhere.

About a week later, Miss Vanessa was in her kitchen, a cheery room lined with bright yellow cabinets, when her telephone rang. Caller ID indicated a Hopkins number. “I didn’t want anyone else to call you but me,” said the study’s principal investigator, Daniel Laheru. He had good news: her genes “matched up perfectly” with the criteria for the clinical trial. He told her to come in right away so they could get the blood work done, the paperwork signed and the treatment started. Miss Vanessa recalls, “I cried so hard I saw stars.”

The trial was part of a string of promising developments in immunotherapy—an apparent overnight success that was actually more than 100 years in the making. Back in the 1890s, a New York City surgeon named William Coley made a startling observation. He was searching medical records for something that would help him understand sarcoma, a bone cancer that had recently killed a young patient of his, and came upon the case of a house painter with a sarcoma in his neck that kept reappearing despite multiple surgeries to remove it. After the fourth unsuccessful operation, the house painter developed a severe streptococcus infection that doctors thought would kill him for sure. Not only did he survive the infection, but when he recovered, the sarcoma had virtually disappeared.

Coley dug deeper and found a few other cases of remission from cancer after a streptococcus infection. He concluded—incorrectly, it turned out—that the infection had killed the tumor. He went around promoting this idea, giving about 1,000 cancer patients streptococcus infections that made them seriously ill but from which, if they recovered, they sometimes emerged cancer-free. He eventually developed an elixir, Coley’s Toxins, which was widely used in the early 20th century but soon fell out of favor as radiation and then chemotherapy began to have some success in treating cancer.

Then, in the 1970s, scientists looked back at Coley’s research and realized it wasn’t an infection that had killed the house painter’s tumor; it was the immune system itself, stimulated by the bacterial infection.

In a healthy body, T-cells activate their weaponry whenever the immune system detects something different or foreign. This might be a virus, a bacterium, another kind of disease-causing agent, a transplanted organ—or even a stray cancer cell. The body continuously generates mutated cells, some of which have the potential to turn cancerous, but current thinking is that the immune system destroys them before they can take hold.

Once scientists recognized the cancer-fighting potential of the immune system, they began to look for ways to kick it into gear, hoping for a treatment that was less pernicious than chemotherapy, which often uses poisons so toxic the cure may be worse than the disease. This immune-based approach looked good on paper and in lab animals, and showed flashes of promise in people. For instance, Steven Rosenberg and his colleagues at the National Institutes of Health’s National Cancer Institute made headlines when they removed a patient’s white blood cells, activated them in the lab with the immune system component known as interleukin-2, and infused the cancer-fighting cells back into the patient in hopes of stimulating the body to make a better supply of cancer-fighting cells. Rosenberg ended up on the cover of Newsweek, where he was hailed for being on the cusp of a cancer cure. That was in 1985.

The FDA did approve interleukin-2 for adults with metastatic melanoma and kidney cancer. But immunotherapy remained mostly on the fringes for decades, as patients continued to go through rounds of chemotherapy and radiation. “We’ve been curing cancer in mice for many, many years . . . but the promise was unfulfilled for a very long time in people,” says Jonathan Powell, associate director of the Bloomberg-Kimmel Institute at Hopkins.

Meanwhile, Topalian is continuing to work with Hopkins experts in genetics, metabolism, bioengineering and other areas. One of her colleagues, Cynthia Sears, recently received a grant to study biofilms—the colonies of bacteria that grow in the colon and can either promote or prevent cancer growth. Sears is looking at how a particular “tumor microbial environment” affects the way a patient responds—or fails to respond—to cancer immunotherapy.

“The immune system is the most specific and powerful killing system in the world,” says Pardoll, summing up the state of immunotherapy in early 2018. “T-cells have an amazingly huge diversity, and 15 different ways to kill a cell. The basic properties of the immune system make it the perfect anti-cancer lever.” But science won’t be able to fully mobilize that system without the help of myriad specialists, all working from different angles to piece together the incredibly complex puzzle of human immunity.
Indeed, many cancer experts lost faith in the approach over the next decade. “Nobody believed in immunotherapy except our own community,” says Drew Pardoll, the director of the BKI. The lack of support was frustrating, but Pardoll says it did have one salutary effect: It made immunotherapy more collegial and less back-biting than a lot of other fields of science. “When you’re a little bit ostracized I think it’s just a natural part of human nature…to sort of say, ‘Well, look, our field is going to be dead if we don’t work together, and it shouldn’t be about individuals,’” Pardoll said. He calls the recent explosion of successes “sort of like Revenge of the Nerds.”

In keeping with this collaborative spirit, immunotherapy researchers from six competing institutions have formed a cover band known as the CheckPoints, which performs at the annual meeting of the American Society of Clinical Oncology and in other venues. The band’s harmonica player, James Allison of the M.D. Anderson Cancer Center in Houston, helped set immunotherapy on its current course with his work on checkpoint inhibitors in 1996, when he was at Berkeley. He was the first to prove that blocking the checkpoint CTLA-4 (shorthand for “cytotoxic T-lymphocyte antigen”) with an antibody would generate an anti-tumor response. As Pardoll puts it, once Allison demonstrated that first checkpoint system, “we had molecular targets. Before that, it was a black box.”

The checkpoint system, when it’s working as it should, is a simple one: invader is detected, T-cells proliferate. Invader is destroyed, T-cells are deactivated. If T-cells were to stay active without an invader or a rogue cell to fight, they could create collateral damage to the body’s own tissues. So the immune system contains a braking mechanism. Receptors on the surface of the T-cells look for binding partners on the surfaces of other cells, indicating that those cells are healthy. When these receptors find the proteins they’re looking for, they shut the T-cells down until they spot a new invader.

Cancer cells are able to do their damage partly because they co-opt these checkpoints—in effect, hacking the immune system by activating the brakes. This renders the T-cells impotent, allowing the cancer cells to grow unimpeded. Now scientists are figuring out how to put up firewalls that block the hackers. Checkpoint inhibitors deactivate the brakes and allow the T-cells to get moving again. This lets the body kill off the cancer cells on its own.

Suzanne Topalian, who is Pardoll’s colleague at the Bloomberg~Kimmel Institute (and also his wife), played a key role in identifying another way the immune system could be used to fight cancer. After working as a fellow in Rosenberg’s lab, she became the head of her own NIH lab in 1989 and moved to Johns Hopkins in 2006. At Hopkins, she led a group of investigators who first tested drugs blocking the immune checkpoint receptor PD-1—short for “programmed death-1”—and the proteins that trigger it, PD-L1 and PD-L2.

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Could a Pill Help Detect Breast Cancer – Emily Matchar

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Women eventually face the yearly ritual of the mammogram, usually suggested from age 50 onwards. It’s not painful, though notoriously uncomfortable, as two plates flatten the breasts, pancake-like, to get the best possible picture. The radiologist then looks at x-ray images for opaque spots that can indicate tumors.

Mammography has been used since the late 1960s and is considered the gold standard for breast cancer detection. But it’s far from perfect. The method misses about 1 in 5 cancers, and about half of women screened annually for 10 years will have a false positive result, often resulting in anxiety and unnecessary biopsies. Mammograms are also unable to distinguish slow-growing cancers from aggressive ones, which is necessary when choosing a course of treatment.

But researchers at the University of Michigan are working on a new method of breast cancer detection they hope could complement—perhaps one day even replace—the mammogram. It’s a pill—patients swallow it and it makes tumors light up when exposed to infrared light. The pill could not only detect tumors, it could also potentially distinguish how aggressive they are.

“From decades of research into cancer, we know it’s really a molecular disease,” says Greg Thurber, a professor of chemical and biomedical engineering who led the research, recently published in the journal Molecular Pharmaceutics. “But the screening technology just looks at anatomy.”

Thurber’s team developed a pill filled with dye that “tags” a molecule common in tumors and the surrounding tissue. Once the pill has been ingested, researchers can use infrared light to penetrate the breast (the exact technology is under development). This both reveals the presence of tumors and gives information on the types of molecules present in these tumors, which can help doctors determine the nature of the cancer.

Taking the dye in pill form is potentially safer than having it injected intravenously, which can occasionally cause allergic reactions. But designing the pill was a challenge. The kind of molecule that can be easily absorbed in pill-form by the digestive tract needs to be small and “greasy,” Thurber says, while molecules that make good imaging agents are larger and bind to water.

To find the right agent, the team used a combination of lab testing and computer modeling. They eventually got lucky when they found that the pharmaceutical company Merck had a cancer drug they’d tested for safety but had proven ineffective in clinical trials. The drug turned out to be perfect for the team’s purposes, as it was capable of passing freely through the bloodstream and binding to tumor molecules. They added a molecule that lights up under infrared light, and tested the resulting combo in mice with breast tumors. Indeed, it made the tumors glow.

Thurber and his team are now focused on developing additional agents to add to the current pill that could tag different types of tumors or different aspects of tumors. This could give doctors additional information about the cancers detected.

“Every person’s tumor is different,” Thurber says. “Even within the same tumor there can be different types of cancer.”

The researchers will then need to do toxicity studies and from there move to larger animal studies. Thurber hopes they can reach the human trial phase in about five years. They’re also hoping to partner with companies to develop the infrared screening tools necessary for human use.

While the pill could theoretically tag any type of cancer, infrared light can only penetrate a short distance into the body. This is fine for breast cancer detection, as breasts can be “squished” thin for imaging, but wouldn’t work for detecting cancer in deeper organs.

image: https://public-media.smithsonianmag.com/filer/12/29/12293189-78b2-44f5-bade-4716d5e78e2a/diagnostic-pill-top-image.jpg

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After it’s ingested, the pill would deliver fluorescent targeting molecules (dye is shown in red) to any tumors. (Thurber Lab)

The team does hope the approach could work for detecting other diseases besides cancer. Rheumatoid arthritis is one potential target, Thurber says, as it is can be effectively treated in its early stages, but is hard to distinguish from other types of arthritis until it progresses.

Reuven Gordon, a professor of electrical and computer engineering at the University of Victoria in Canada who studies the use of light in cancer detection, thinks the research is promising but cautions that it’s early days. Even if a new method of detection is useful, researchers will have to prove that it’s better than the gold standard, and work to make clinicians and patients comfortable with new technology.

“It’s not obvious to me that this is going to be a home run, but it does look promising,” he says. “They have demonstrated something nice from a scientific point of view.”
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The Deadly Viruses Being Used To Combat Incurable Cancers

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Zika, polio and adenovirus are hardly the first trio that comes to mind when considering the ‘next big thing’ in cancer therapy. Polio alone killed over 3,000 Americans per year in the 1950s before vaccination programs and continues to ravage the developing world, while babies with severe brain deformities due to Zika are still being born in South America.

Despite this, these killer viruses may well be a surprising source of hope for those with currently incurable cancers.

The idea to use viruses as cancer therapy is not new, having been proposed in a hard-to-pinpoint time in the early 20th century, with traceable work beginning in earnest in the 1960s. My earliest experience of a cancer research lab was fifteen years ago in London, UK when I was still in high school, with a scientist studying viral therapies for pancreatic cancer. As I progressed through my education, finally becoming a cancer research scientist, I would sporadically check in on viral treatments, wondering whether much progress had been made and if anything had been approved.

For several years, nothing stood out, but in 2015, I discovered that Amgen’s Imlygic (also known as T-VEC), a herpesvirus-based therapy for melanoma, was the first viral therapy to be FDA-approved. One of the more surprising results from initial trials and data gained with more widespread use since then, has been that infection of tumor cells with the virus itself, is not the only way in which the therapy affects the cancer.

Phil Daschner, Program Director of the NCI’s Cancer Immunology, Hematology and Etiology department, said: ‘Imlygic not only treated the primary tumor, but It triggered the immune system to go after the metastases too.’

This was somewhat a surprise to the researchers conducting the trial. Imlygic had not only shown efficacy in treating the tumor which it was targeted to, but had also somehow triggered the destruction of far-away metastatic tumors, despite not directly entering those cells.

‘Imlygic showed us that the effect of these therapies was not just virus going into the cells until the tumor cell breaks open and lyses. The immune system gets involved, increasing the response,’ said Daschner.

Imlygic remains the only viral therapy fully FDA approved to this date, but more are edging their way through the trial system. Pleasingly, a couple of them are designed to tackle a devastating type of brain cancer called glioblastoma, which Senator John McCain was recently diagnosed with, which only around 10% of patients survive for 3 years or more post diagnosis and most die within a year.

Zika would seem to be an odd solution to this problem, producing devastating effects in infected babies, resulting in abnormally small and deformed brains. But it is just this propensity to affect developing brain cells that may make it a suitable treatment for glioblastoma, which originates from similar pools of developing brain cells. Duke University scientists also won FDA breakthrough therapy status for their poliovirus-based brain tumor therapy in 2016, so unusually brain cancer has found itself at the forefront of developing these breakthrough therapies.

Another researcher leading the development of viruses against hard-to-treat brain cancer is Juan Fueyo, M.D. at the MD Anderson Cancer Centre, Department of Neuro-Oncology. He recently led a trial of a new adenovirus-based therapy for glioma called tasadenoturev, which binds selectively to tumor cells, with very promising results. Similar to the early results for Imlygic, the immune system played a huge role in the anti-tumor effect of the adenovirus therapy.

‘When we designed oncolytic viruses, we didn’t originally think it was immunotherapy. It’s the immune system that is actually orchestrating the destruction of the tumor and our current hypothesis is that this (not the virus itself) is the main mechanism of treatment,’ said Fueyo.

In Fueyo’s most recent study, 37 patients with recurrent brain cancer, including 28 with glioblastoma were treated with tasadenoturev. Five patients survived more than 3 years after the treatment, with one patient surviving 4.5 years and still alive at the time of publication of the paper in February of this year.

These may seem like fairly sobering survival statistics when compared to more treatable cancers, but for this type of aggressive brain tumor, this is notable progress. In Fueyo’s trial, those who did respond to the therapy achieved survival times in excess of the expected and a superior quality of life on treatment, however, almost all of the patients finally succumbed to their disease.

‘In this fight between the cancer and the immune system, the cancer won, eventually,’ said Fueyo.

The current hypothesis as to why this happens seems to be similar to that for many cancer relapses; that there is a tiny proportion of cancer cells already existing in the tumor which are resistant to the therapy. Most of the tumor cells are killed by the therapy, scans no longer pick up the tumor and patients seem to be in remission, but months or years later, this small population of cells multiplies into a fully fledged, therapy-resistant tumor. Researchers aren’t yet sure how this resistance against viral therapies works and Fueyo stresses that further clinical trials will try to address this.

Conventional therapies for brain tumors such as invasive surgeries, radiotherapy and chemotherapies such as temozolomide, often come with a host of side effects, which can greatly impact quality of life, perhaps an even more important consideration for those who are unlikely to achieve cure and where the goal is not just more time, but more quality time. One of the most interesting revelations of the study was that patients experienced minimal side-effects from the treatment.

‘Patients on our trial had an excellent quality of life. They were able to return to their lives, to work. None of our patients had toxicity,’ said Fueyo.

The variety of viruses that researchers are modifying to target different types of cancers is extensive. Polio and Zika for brain tumors, adenoviruses for multiple tumor types, including pancreatic and even measles virus for ovarian cancer and leukemia, but should a line be drawn where we conclude that some viruses, for example, Ebola – are just too dangerous to try to make cancer therapies from?

‘All of this hype saying all viruses can be modified – I don’t believe that, I think we will end up using three or four types of virus, ultimately. In some clinical trials with viruses, patients have died, we need to study this carefully and figure out which are toxic,’ said Fueyo.

As Fueyo eludes to, not all patients in trials with viral cancer therapies have experienced minimal to no side effects like his patients.

‘Viruses are dangerous, they are dirty bombs which of course we try to control but they can behave in an unregulated way, we must be careful’ said Fueyo.

So after decades of research, why have viral therapies just now started to make it through approvals and into human clinical trials?

‘The molecular engineering of safety components has become easier with the greater knowledge of viral genomes and techniques like CRISPR, for example,’ said Daschner.

‘In the 90s, no pharma company would invest in oncolytic viruses, it was just too risky,’ said Fueyo.

Today, multiple pharma companies are running oncolytic viral therapy discovery programs including Pfizer, Celgene and Bristol-Myers Squibb.  After Imlygic’s successful FDA-approval and promising early clinical trial results for glioblastoma viral therapies, can we expect viral therapies to flood the market now?

‘Imlygic set an important regulatory precedent, I don’t see it as a floodgate opener, more that Imlygic expanded the pipeline for the development of these viral therapies. Much like immunotherapy and CAR-T-cells, it’s going to take time for approval of these therapies,’ said Daschner

Both Fueyo and Daschner are enthusiastic about the potential for viruses in cancer therapy, particularly in combination with immunotherapy agents that are designed to unleash the immune system on cancers.

‘The potential for viral vectors and immunotherapy agents is huge,’ said Daschner.

Soon after Imylgic’s first promising trials on melanoma, researchers published data showing that combining Imlygic with the PD-1 blocking immunotherapy agent pembrolizumab was more effective than using either alone.

Several additional combination therapies are indeed snaking their way through the clinical trial system with trials for liver, colorectal and lung cancers ongoing in the U.S. and treatment of brain cancers continues to lead the way with a large U.S. based 13 center clinical trial combining the adenovirus and Merck’s PD-1 targeting immunotherapy agent, pembrolizumab with the hope that the combination will further strengthen the immune system to attack the tumor.

Viruses are undoubtedly still in the early stages of development, but people with rarer tumors with low survival rates currently will be relieved that their cancers are at the forefront of drug development for a change, often being overlooked for more common cancers.

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Mum of two said she cured her breast cancer with £100 cannabis oil

A mum-of-two has claimed that she cured her aggressive breast cancer for under £100 thanks to drinking one drop of cannabis oil per day. Dee Mani, 44, found a lump in her breast in March 2017 and after being diagnosed with triple negative breast cancer, she was offered chemotherapy and radiotherapy to save her life. […]

via Mum of two said she cured her breast cancer with £100 cannabis oil — tessysocialblog.com

Garment aims to help breast cancer survivors

Surgery scar cover is a rare exception to Japan’s traditional no-clothes-in-the-bath rule. For communal bathing in Japan, whether at a natural onsen hot spring or a piped-in sento public bath, the general rule is that everyone in the tub is supposed to be naked. Stepping into the tub while wearing a bathing suit or wrapped…

via Garment aims to help breast cancer survivors enjoy Japan’s hot springs without self-consciousness — SoraNews24

Breast Cancer Treatments & Recovery – Kate Rieger No.1 Health & Wellness Solutions For Breast Cancer | Online Marketing Tools

Source: Breast Cancer Treatments & Recovery – Kate Rieger No.1 Health & Wellness Solutions For Breast Cancer | Online Marketing Tools