Scientists Create Artificial Virus That Kills Cancer Cells

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Scientists create artificial virus that kickstarts immune system and fights cancer cells

Scientists have developed an artificial virus which they say helps to kickstart a persons immune system and kill cancer cells. 

Swiss scientists tested the new virus by inserting cancer proteins inside a designer virus so that when the immune system detects the virus, it gets killed along with the cancer. reports: The technique could in theory be used to fight any type of cancer. Scientists could simply take proteins from a patient’s own tumour, place it in the virus and inject it into the body to trigger a strong immune response against a specific disease.

In mice, the treatment was shown to bring remission and researchers are keen to move to human trials.

“We hope that our new findings and technologies will soon be used in cancer treatments and so help to further increase their success rates,” said Professor Daniel Pinschewer, lead researcher from the University of Basel.

The researchers built artificial viruses based on lymphocytic choriomeningitis virus (LCMV), which can infect both rodents and humans.

Although the virus is harmless, it still triggers an immune response. The scientists also added proteins which are only found in cancer cells.

The combination of the virus triggering the alarm system and the cancer proteins, was found to create a powerful army of cytotoxic T-lymphocytes, also known as killer cells, which identified the cancer cells through their protein and successfully destroyed them.

The research was published in the journal Nature Communications.


  1. Nonsense. It won’t ever work. I also don’t want to know what the side effects of this crap will be. We already know the major factors that cause cancer. Cancer is not a genetic disease. It is an immune malfunction. Being that allopaths know nothing about the immune system, it is no surprise they think cancer is a curable nuisance, like toddlers. Immune malfunctions are caused by the person. No one does it to you unless your parents vaccinated you and had you overtake antibiotics.

    Some include:
    – Vaccines, destroying immune system
    – Overusing antibiotics, or even using them to begin with (only weak people need them)
    – Sugar
    – Gluten and wheat in general
    – Cow dairy, and dairy in general
    – Drugs that deplete the body of all its reserves
    – Burnt animal fats and meats
    – Anything inflammatory
    – Lack of minerals so the immune system cannot function properly
    – Lack of ORAC points and compounds like resveratrol, turmeric, and quercetin

    Being that most Americans want to eat grass and sugar all day, and take drugs and OTC garbage to cover up symptoms and numb the pain, magical science cures to undo their voluntary mistakes shouldn’t even be considered. Why do we want to attempt to further temporarily eradicate the very damage people cause to themselves? Collectively, humans are wasting all their efforts for advancement on nonsense. Time to wake up.

    Either LEARN or PAY. No more nonsense. The human body has plenty of endurance and versatility. If you abuse that to it’s end, you deserve it.

    • Cancer is a metabolic disease, caused when the cells’ mitochondria convert from aerobic respiration to anaerobic respiration. The prevention and cure is based on a predominantly fat based diet with moderate protein and very low carbs. The body’s switchover from glucose/fructose-based energy production to ketone (fat) based energy production will ensure cancers won’t initiate, and will ensure any existing cancer can’t grow.

      It’s best not to stay in full-blown ketosis full time, unless you already have cancer. Otherwise, you go in and out of ketosis on a 4 days on / 1 day off basis. Dr. Mercola has excellent information regarding this, and the book, “Tripping over the Truth: How the Metabolic Theory of Cancer Is Overturning One of Medicine’s Most Entrenched Paradigms” is a must read.

      • Paleo/keto is another nonsense fad to counter nonsense tofu veganism. All that fat (you people call some pastries or foods BOMBS, I mean, come on) is very hard on the body like junk carbs and sugar. It is honestly even worse than grain/tofu vegans. Being in ketosis 24/7 will not guarantee anyone anything. The human body is supposed to go in and out of ketosis. Another bogus explanation and meat and dairy industry ploy. Mercola is an MD shill. Lots of hand-picked preferences and twists and turns and his fans make him rich. Everyone wants a leader.

        Mercola pushes the nonsense belief that historically human-sustaining cereals/grains, such as millet, NON-white rices, amaranth and literal poor-people lifesavers like potatoes, are all just as bad as wheat or sugar, which is total nonsense.

        Some people do not function well on massive fat diets, and while I have quite a fair amount of fat in my diet– plenty in many plant-based foods, too – I do not stay in ketosis because I do not perform very well being a more carb-orientated person (I do not adhere to absurd 5% or 10% or 20% fat-restricted diets, though, like I’ve stated before). I also never restrict cholesterol. A big no-no for anyone who wants to keep their brain and IQ, and who doesn’t want pre-alzheimer’s by age 24 and alzheimer’s by age 40, 50, 60.

        Saying that only carbs cause cancer is a myth. Simple sugars are carbs, and vegetables, the real staff of life, are carbs, and do not cause cancer. Cancer has many collective causes and is not magically cured by going keto, period.

        • There was a pilot study of the ketogenic diet in 10 advanced cancer patients. According to a PET scan, 4 of the patients continued to have progressive disease, while 5 remained stable and 1 had a partial response A second in 16 advanced-stage cancer patients improved the quality of life and stopped the progression for the 5 patients who completed the 12 week study and another shows similar results

          Unlike the mutational profile of a cancer cell’s DNA, the profoundly altered metabolism of cancer cells, Warburg documented, was consistent from one cancer to the next, it was a pervasive feature of the cancer cell. So based on the prevalence of the Warburg effect, and the enormous amount of different studies on the glucose-dependency of cancer, it would be logical to use a ketogenic diet, fasting, hyperbaric oxygen and ketone supplements to cause glucose deprivation and enhance oxidative stress to kill tumour cells off. As fine-tuning on all these hasn’t been done for different types of cancer then Dr. Slocum is using some of this as an adjunct to other, established treatments.

          He published a paper–ivductal-pancreatic-adenocarcinoma-using-metabolically-supported-chemotherapy-msct-a-retrospective-study.php?aid=7498 last year that was a case series of 33 patients with stage 3 and 4 pancreatic adenocarcinoma (pancreatic cancer) – one of the most aggressive and deadly cancers known. It was a retrospective analysis of patients treated at his clinic between 2011 and 2015. Eighty-one percent of these patients had stage 4 disease when the treatment began, and many of them also had large scale liver metastasis. Generally, if a patient has stage 4 pancreatic adenocarcinoma, their life expectancy is about six months (this is the case for 96% of them), at most 10 months. If they have large-scale liver metastasis, death typically occurs within weeks or months. Yet despite the majority being end-stage advanced patients, they responded remarkably well to the treatment. Here, the standard conventional protocol using either gemcitabine-based chemotherapy or folfirinox was again applied in a metabolically supported fashion, together with hyperthermia, hyperbaric oxygen therapy, the ketogenic diet, supplements and glycolysis inhibitors.

          When the paper was published in 2016, 54% of these patients were still alive, and most are still receiving follow-up treatments to this day. Following the conventional protocol, the expected median survival time for the gemcitabine-based protocol is 6.2 months. For the folfirinox regimen it’s 11.1 months. Using a metabolically supported protocol, the median survival time shot up to 20 months – and 54 percent of the patients are still alive today.

          Next, the team will be publishing a paper on stage 4 non-small cell lung cancer. Currently we only have a JPEG from a conference they presented at. Here, they applied a chemotherapy regimen using carboplatin and paclitaxel. Large-scale clinical trials show an expected survival time of six to 11 months. Moreover, stage 4 patients typically cannot tolerate conventional chemo regimens so no large-scale studies have focused on such late-stage patients. Using the metabolically supported protocol, however, all of the 44 patients in the study were able to receive treatment, and the overall survival time is 43.4 months – that’s more than 400 percent longer than the longest survival time mentioned in any standard chemotherapy regimen.

    • ”Nonsense. It won’t ever work.”

      One is already approved.

      ”Being that allopaths know nothing about the immune system.”

      Good one!

      Here are two pictures which are explained in more detail below

      Wnt/beta-catenin is a signalling pathway that is tightly regulated, multi-functional and involved in many cellular processes, including proliferation. Mutations in the gene that encodes the pathway have long been linked to more aggressive disease in various tumour types, including colon, lung, prostate, melanoma and many others.

      In this paper researchers looked at tissue samples from melanoma patients to search for variations in this pathway. They compared tissue from 91 patients who did not have T-cell invasion with tissue from 106 patients who did.

      They found that active beta-catenin signalling stood out as the primary difference between the two groups. Almost 50% of the tumours that blocked T-cell infiltration had high levels of beta-catenin signalling. Only 4% of tumours that were invaded by T-cells had similar signalling patterns.

      The team noticed that tumours with elevated beta-catenin lacked a subset of dendritic cells known as CD103+. Tumour cells without beta-catenin produce an immune-signalling molecule known as CCL4, which attracts CD103+ dendritic cells. But CCL4 expression is suppressed by tumour cells with high beta-catenin levels. Dendritic cells are scavengers that search for foreign invaders, usually pathogens, but also cancerous cells. They patrol border areas such as the skin, lungs and digestive tract. When where they find harmful microbes or cellular damage, they transport these danger signals to the lymph nodes and present them to T-cells.

      In addition they found that tumours that lacked beta-catenin responded to Anti-CTLA4 and Anti-PDL-1 monoclonal antibodies. Tumours with beta-catenin did not.

      This paper helps with our understanding of the molecular mechanisms behind the presence or absence of a spontaneous antitumour T-cell responses and could be used to help predict which patients will respond to the new immunotherapies. It also suggests that news drugs could be developed to help patients who don’t initially respond to immune-mediated treatment, such as direct injection of their own CD103+ dendritic cells. Or a short course of focused radiation therapy, which causes inflammation of tumour tissue could increase immune vigilance.

      Although the study focused on melanoma, this signalling pathway seems to play a role in many tumour types when it comes any immune response.

      Another paper shows that these CD103+ dendritic cells act as advance scouts for the immune system and crucial for sending out requests for assistance from cancer cell killing T-cells. It shows that these cells not only must be present within the tumour, but be activated, and emit certain chemical signals (chemokines) in order for T-cells to gain access and ultimately control the cancer. The absence of them from the tumour microenvironment appears to be a dominant mechanism of resistance to multiple immunotherapies. Even adoptive transfer of 100 million highly-focused T-cells into tumours with beta-catenin expression had no effect, leaving the them to grow.

      Assuming these CD103+ dendritic cells enter the tumour then they will need to detect damaged double stranded DNA in the cytosol of cancer cells If this happens then it activates an innate immune response leading to cancer cell killing T-cells. However cancer cells try and reduce their expression of this (STING pathway) to avoid detection

      Once cancer cell killing T-cells are there then they should kill all the tumour cells leading to elimination. However that doesn’t always happen. Such selective pressure they force leads to equilibrium (adaptive resistance). During this phase cancer cells that have escaped elimination will have a non-immunogenic phenotype and are selected for growth. It occurs over a period of many years. During this period of Darwinian selection, new tumour cell variants emerge with various mutations that further increase overall resistance to immune attack. During the escape phase, cell variants selected in the equilibrium phase will then have breached the host organism’s immune defences, with various genetic and epigenetic changes conferring further resistance to immune detection. After this the tumour will grow.

      Once established tumours are essentially self-entities that possess numerous layers of tolerance that immunotherapies must overcome In addition to the tumours themselves, the tumour vasculature is a promising immunotherapeutic target where factors such as hypoxia (low oxygen tissue) and over-expression of growth factors result in dysfunctional endothelial cells that are essential for tumor growth and survival Tumour endothelial cells express the death mediator Fas ligand, leading to loss of tumour killing T-cells and allows tolerogenic immune cells to infiltrate into tumours Moreover, the tumour contains an excess of different types of vascular endothelial growth factors that promote the apoptosis (death) of tumour killing T-cells in an animal model In a study of human cancer cell lines, these have been shown to prevent the maturation of dendritic cells, which is necessary for anti-tumour T-cell activation If these barriers to T-cell immunity can be overcome, anti-angiogenesis therapy is a powerful immunotherapy approach whereby it is conceptually possible for hundreds of tumor cells to be starved by knocking down a single tumour endothelial cell

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