Except for that Note, the article below needs no further commentary from my part.

Scientists Find Cancer Drivers Hiding in a New Place

By Matthew Tontonoz,

Sloan Kettering Institute molecular biologist Christine Mayr
Christine Mayr is a member of the Cancer Biology and Genetics Program of the Sloan Kettering Institute.

Summary

Researchers at the Sloan Kettering Institute have found that changes in an information-carrying molecule called messenger RNA can inactivate tumor-suppressing proteins and thereby promote cancer. The findings pinpoint previously unknown drivers of the disease. 


IMPORTANT NOTE (added 2020*): This research does not relate in any way to the COVID-19 vaccines using mRNA. There are thousands of different kinds of mRNA in human cells. Each kind of mRNA does different things. The mRNA used in vaccines does not cause cancer or alter DNA. For accurate information about COVID-19 vaccines and why they don’t cause cancer, please visit here. This video explains how mRNA vaccines work. 

  • I personally I don’t see how the resources provided in the note, or anything I’ve ever read, supports the claims there. Nor have I seen why this study does not apply to the mRNA in Covid shots. Quite the contrary. Looks like they hope we won’t read or understand the science. So let’s read it and understand it, then make your own mind. – Silview.media

Most people think of cancer as a disease of disorderly DNA. Changes, or mutations, in the sequence of DNA alter the function of the proteins made from that DNA, leading to uncontrolled cell division.

But between DNA and proteins is another layer of information, called messenger RNA (mRNA), which serves as a crucial link between the two. New research suggests that some types of mRNA may carry cancer-causing changes. And, because genetic tests don’t usually look at mRNA, those changes have so far gone undetected by cancer doctors.

“If you sequenced the DNA in cancer cells, you would not see these changes at all,” says Christine Mayr, a molecular biologist at the Sloan Kettering Institute who is the senior author of a new paper on the topic published today in Nature. “But these mRNA changes have the same ultimate effect as known cancer drivers in DNA, so we believe they may play a very important role.”If you sequenced the DNA in cancer cells, you would not see these changes at all.Christine Mayrmolecular biologist

The findings turn some common assumptions about cancer on their head and point to the need to look past DNA for answers to questions about what causes the disease.

From DNA to mRNA

If DNA is the genetic blueprint for life, as is often said, then it’s a fairly cumbersome set of instructions. The information in DNA is encoded in the particular sequence of some 3 billion nucleotide “letters” — varying combinations of A, T, G, and C. Blocks of these letters — genes — are used to make particular proteins, a cell’s main workhorses. But DNA lives in the nucleus of a cell, while proteins are made in the surrounding cytoplasm. To bridge this gap, a cell must first make an RNA copy of a gene’s DNA. This RNA copy, called messenger RNA, is then transported out of the nucleus. It is this mRNA copy that cells read and translate into a protein.

Usually, the mRNA copy is a bit shorter than its DNA precursor. That’s because the useful pieces of information in DNA, called exons, are often separated by blocks of sequences that are not needed. These unnecessary parts, called introns, must be cut out to make a final product. After the introns are removed, the remaining exons are spliced together, not unlike splicing together pieces of film and leaving some on the cutting room floor.  These findings help explain a long-standing conundrum, which is that CLL cells have relatively few known DNA mutations.

If the mRNA copy doesn’t include all of the exons in a gene or is cut short, then the protein made from that mRNA will also be truncated. It may no longer function properly. And if that protein is a tumor suppressor — one that protects against cancer — then that could spell problems.

What Dr. Mayr and her colleagues, including postdoctoral fellow Shih-Han (Peggy) Lee, graduate student Irtisha Singh, and SKI computational biologist Christina Leslie, found is that many of the mRNAs in cancer cells produce these truncated tumor-suppressor proteins. The changes occur not only in known tumor-suppressor genes but also in previously unrecognized ones.

“The changes to the mRNA make proteins that are very similar to the proteins that are made when you have a mutation in the DNA that causes a truncated protein to be made,” she says. “In the end, the outcome for the cell is very similar, but how it happened is very different.”

Found: Missing Cancer Mutations

Dr. Mayr’s team looked specifically at chronic lymphocytic leukemia (CLL), a type of blood cancer. A colleague at MSK, Omar Abdel-Wahab, supplied them with blood samples from people with the condition. Using a method that Dr. Mayr’s lab developed to detect these particular mRNA changes, they found that a substantially greater number of people with CLL had an inactivation of a tumor-suppressor gene at the mRNA level than those who had it at the DNA level.

These findings help explain a long-standing conundrum, which is that CLL cells have relatively few known DNA mutations. Some CLL cells lack even known mutations. In effect, the mRNA changes that Dr. Mayr’s team discovered could account for the missing DNA mutations.

Because CLL is such a slow-growing cancer and people with CLL often live for many years, it’s too early to say whether these mRNA changes are associated with a poorer prognosis. 

There are some important differences between the mRNA changes and a bona fide DNA mutation. Most important, the inactivation of tumor suppressors through mRNA is usually only partial; only about half of the relevant protein molecules in the tumor cells are truncated. But in many cases this is enough to completely override the function of the normal versions that are present. And because this truncation could apply to 100 different genes at once, the changes can add up.

Lessons for Cancer Diagnostics

Though Dr. Mayr’s team identified the mRNA changes in CLL, they’re likely not limited to this blood cancer. The team found them in samples of T cell acute lymphocytic leukemia too, for example. Other researchers have found them in breast cancer. Dr. Mayr hopes that scientists will be inspired to explore the significance of mRNA changes in these and other types of cancers.

“Current cancer diagnostic efforts predominantly focus on the sequencing of DNA in order to identify mutations,” Dr. Mayr says. “But our research suggests that changes at the mRNA level might be as frequent.”

In other words, cancer diagnostics may need to change to include these previously unknown cancer drivers.

This work was funded by a National Cancer Institute grant (U01-CA164190), a Starr Cancer Consortium award, an Innovator Award of the Damon Runyon-Rachleff Cancer Foundation and the Island Outreach Foundation (DRR-24-13), a National Institutes of Health Director’s Pioneer Award (DP1-GM123454), the Pershing Square Sohn Cancer Research Alliance, and an MSK Core grant (P30 CA008748). – Sloan Kettering Institute

To be continued?
Our work and existence, as media and people, is funded solely by our most generous readers and we want to keep this way.
We hardly made it before, but this summer something’s going on, our audience stats show bizarre patterns, we’re severely under estimates and the last savings are gone. We’re not your responsibility, but if you find enough benefits in this work…
Help SILVIEW.media survive and grow, please donate here, anything helps. Thank you!

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“In the early nineties, pioneering steps were taken in the use of mRNA as a therapeutic tool for vaccination. In the following decades, an improved understanding of the mRNA pharmacology, together with novel insights in immunology have positioned mRNA-based technologies as next-generation vaccines.”

Three decades of messenger RNA vaccine development

Like teenagers the world over, Nobel Prize-winning scientist Ralph Steinman had absolutely no idea what he wanted to do when he grew up.

In a 2009 essay, the Canadian-born immunologist and cell biologist described his early school career as unfocused, only landing on an interest in biology and medicine while taking “almost every other course” at McGill University in Montreal while on scholarship as an undergraduate.

This latent interest eventually led him to Harvard Medical School, where he earned his M.D. (also on scholarship), and an internship and residency at Massachusetts General Hospital. In 1970, the young Steinman joined the Laboratory of Cellular Physiology and Immunology at Rockefeller University in New York City as a postdoctoral fellow under cell biologist and immunologist Zanvil A. Cohn. Steinman wanted to know what triggers the body’s immune system to kick into gear to initiate a response, a question few scientists at the time were asking.

Just three years later, while working with cells from the spleens of mice, Steinman and Cohn made the discovery that would shape Steinman’s future: the identification and role of a particular type of white blood cell that sets into motion and controls the body’s immune system. They termed these cells dendritic cells, after the branching, tree-like shape the cells can form.

By identifying this chief component that initiates and regulates an immune response, Steinman had discovered why, when, and how the body’s immune system reacts the way that it does, especially in the face of foreign pathogens. He’d discovered what amounted to the boss cell that kicks off immune reactions and tells other cells what to do and what not to do. Dendritic cells also play a role in autoimmune diseases, inflammation, allergies, and transplant rejections.

This discovery would revolutionize immunotherapy and eventually launch the new field of dendritic cell biology. But at the time, Steinman’s discovery was generally disregarded. Dendritic cells were considered little more than an obscure anomaly by much of the scientific community. To top it off, the cells were difficult to isolate, and low in frequency and abundance to boot. It would take more than 20 years and Steinman’s development of a new method to generate large numbers of dendritic cells for experimental use for the scientific community to finally verify and accept his theories.

His chances for surviving another year were estimated at less than five percent.

Steinman was especially interested in clinical applications for dendritic cells, dedicating much of his career toward the development of new medical therapies and treatments based on his research. His discovery led to the first therapeutic cancer vaccine in 1973, a dendritic cell-based immunotherapy for the treatment of prostate cancer. Other potential immunotherapies that have resulted include cancer and transplantation treatments and vaccines for HIV, malaria, tuberculosis, and the Epstein-Barr virus, some of which have reached clinical trials.

Steinman’s desire to see his research put into practical medical application cannot be overstated. Despite his gentle, almost grandfatherly way of speaking, he often expressed frustration at the slow speed at which experimental therapies escaped the confines of the lab and its theoretical animal and data models to reach actual patients. This impatience took on a new sense of urgency in 2007 when Steinman was diagnosed with Stage 4 (advanced) pancreatic cancer. By the time of his diagnosis, the cancer had already advanced beyond the pancreas and spread to Steinman’s lymph nodes. His chances for surviving another year were estimated at less than five percent.

So, Steinman went to work. In response to his illness, he designed and coordinated a single-case medical study with himself as the sole subject.

In addition to undergoing conventional surgery and chemotherapy, Steinman reached out to the international network of researchers in industry and academia he’d built over his decades-long career. Banding together for this common cause, he and his colleagues developed a variety of personalized cancer treatments, many based on his design and research, including vaccines developed from Steinman’s own tumor cells.

“With ten million persons afflicted each year, no one is entirely immune to cancer and its devastating effects on individuals and families. But recent advances in the development of cancer vaccines—either as therapeutic agents or as preventative measures—are hopeful indicators of progress in this field. This volume comprises invited chapters from world-renowned researchers and clinicians that shed light on recent steps forward in immunotherapeutic and preventive approaches for future cancer vaccines.” – Blackwell Publishing

A close-up look at a dendritic cell, the boss cell that kicks off immune reactions and tells other cells what to do and what not to do.

Despite his general impatience with the speed of the traditional scientific process, Steinman insisted on conducting his personal trial according to established protocols, filing mounds of paperwork with official channels and seeking appropriate permissions for untested therapies just like any other trial. Although his personalized experiment was not controlled, he wanted it well-organized and well-documented so his treatment attempts might not only find a cure for himself but also gather knowledge that could be used to benefit others.

This adherence to protocol, however, became a source of frustration for some of Steinman’s colleagues. Steinman, for example, refused combined therapies that failed to get regulatory approval, even though he and many of his colleagues felt the combined approach had a higher likelihood of success. He also initially refused to undergo multiple treatments at once because doing so would confuse the data being collected. With time of the essence, colleagues had to argue with Steinman to get him to prioritize the possibility of his health and longevity over proper protocol and clean experimental results. All told, Steinman underwent as many as eight experimental therapies, in addition to surgery and chemotherapy, to combat his disease.

Four and a half years after his cancer diagnosis, he died just three days before the Nobel Prize announcement

During his long career, he received numerous awards and honors, including the prestigious Lasker Award (sometimes referred to as the American Nobel) in 2007. While in the midst of his illness and self-experimentation, he was also nominated for the 2011 Nobel Prize in Physiology or Medicine for his discovery of the dendritic cell and subsequent contributions to immunology research and medicine.

Steinman joked often about surviving long enough to witness the awards announcement, and as late as a week before, the possibility seemed likely. But on September 30, 2011, four and a half years after his cancer diagnosis, he died just three days before the Nobel Prize announcement. He was 68 years old.

Nobel Prize rules generally prohibit the awarding of a prize posthumously, but given the unusual circumstances and unfortunate timing of events, the Nobel Committee ruled to allow the honor to stand. Steinman shares the prize with American immunologist Bruce A. Beutler and French biologist Jules A. Hoffman, also for their work in the area of immunity research.

Although no one can be sure of the efficacy of the dendritic cell-based immunotherapies Steinman underwent or which one(s) might have helped, the Nobel Laureate lived more than four times longer than expected. His decades of work have contributed to clinical therapies for cancer and infectious diseases that will benefit patients for generations to come. And despite those early years of unfocused study, even his self-experimentation laid the groundwork for future treatments, including an immunotherapy against pancreatic cancer based on data gathered during Steinman’s final experiment. – Folks Magazine

Ralph M. Steinman’s research while affiliated with The Rockefeller University and other places

Ralph Steinman died days before it was announced that he was to share the Nobel Prize for Medicine. His work had been part of an unorthodox experiment to save his life, wrote Politico journalist Brett Norman, quoted by BBC, 2011.

When Ralph Steinman learned he had pancreatic cancer, the dogged immunologist put his life’s work to the test.

He launched a life-and-death experiment in the most personal of personalised medicine.

By unlucky coincidence, he had been diagnosed with a disease that might benefit from the therapies he had spent his life researching.

Usually, medical research proceeds at a glacial, thorough pace: cell studies lead to studies in small animals which lead to studies in larger animals, which eventually lead to small, highly-selective clinical trials in humans. But Steinman didn’t have that kind of time.

He did, however, have access to world class facilities, cutting-edge technology, and some of the world’s most brilliant medical minds, thanks to his position as a researcher at Rockefeller University.

So Steinman decided to make his own body the ultimate experiment.

He had removed a piece of the tumour that would eventually kill him. He then trained his immune cells to track down any hint of the tumour that might have escaped the surgery, like putting hounds on a scent.

On Friday, four-and-a-half years after he was diagnosed with a disease that kills the vast majority of its victims in less than one, that experiment came to an end.

Steinman died at the end of a week in which he continued his work in the lab. It was a testament to the undying optimism of the scientific enterprise, to the unrelenting man, and to the limits of both.

An open secret

I joined Rockefeller as a science writer to chronicle the work of its researchers – Steinman included – about halfway through one of his experiments on himself.

His experiment was an open secret on campus, registered with the hospital and aided by a long-time friend and staff physician. The sense of hope was palpable, bound up in respect for the man but also something broader.

Could the painstakingly incremental research that seemed to have so much potential on lab animals this once grant a reprieve from certain death?

Of course everyone was rooting for him, and I had a special interest. Toward the end of 1999, my father had a stomach complaint. Over a few months, the initial diagnosis of an ulcer morphed into a death sentence: inoperable, metastatic cancer of the pancreas.

Pancreatic cancer is often known as the “silent killer” because it usually doesn’t produce truly scary symptoms until it has spread beyond repair. After chemotherapy, my dad bounced back for a few months, but the cancer inevitably did, too. He died at home in the early fall of 2000.

Could Steinman beat it?

I hoped so. The work had promise.

“In the last few years of his life, Dr. Ralph Steinman made himself into an extraordinary human lab experiment, testing a series of unproven therapies – including some he helped to create – as he waged a very personal battle with pancreatic cancer.”

– Reuters

‘Skeptical’ science

In 1973, along with his mentor, Zanvil Cohn, Steinman published the discovery of a new class of cell in the immune system – the dendritic cell. Like many new discoveries, his faced a deeply sceptical reception.

The experiments couldn’t be immediately reproduced, but Steinman was convinced of his discovery. He fought for a decade before immunologists began to broadly recognise the central importance of those cells to their field.

In the past 20 years, the study of dendritic cells has spread to hundreds of labs all over the world. Researchers are exploring how they might be harnessed to fight cancer, HIV and transplant rejection, among other major medical problems.

Dendritic cells are the “sentinel cells” of the mammalian immune system. Named after the Greek word for tree, they develop distinctive probing branches when activated, sweeping their environment in search of unwelcome things – like bacteria, viruses, tumours.

When dendritic cells encounter something they don’t like, they take a physical marker of the invader, called an antigen, and present it to B and T cells, the defenders of the body’ s immune system. Those cells then adapt weapons to identify and destroy the interlopers.

Steinman bet that if he could train his dendritic cells to recognise and tag his cancer, they would be able to convince the T and B cells to do the rest.

Dream deferred

There was no good reason to expect that Steinman could fashion a cure for one of the world’s most vicious cancers in time to save his own life. But it was easy to think it was at least possible. The made-for-Hollywood story of the renegade scientist who fights the establishment to prove his discovery, and then uses it to cure himself, was powerful enough to compel hope.

Unfortunately, the dendritic cell-based treatments didn’t work – at least not well enough.

Training Steinman’s dendritic cells to the tumour did generate a “vigorous immune response to mesothelin, a tumour specific antigen,” said Dr. Sarah Schlesigner, a longtime colleague of Steinman’s who ran the trial.

In other words, while there were significant side effects, the therapy seemed to enable him to work much longer than he otherwise would have. Month after month, he remained at the University, continuing his work.

He survived much longer than expected, and continued his research until the end.

Over time, it wasn’t enough.

At least, not enough to save him.

But the research he pioneered continues – and the scientists who continue his work have an extraordinary example to follow. – BBC, 2011

Also read: RNA Used to Alter DNA, Brain Functions and Behavior (Biohacking p.2)

To be continued?
Our work and existence, as media and people, is funded solely by our most generous readers and we want to keep this way.
We hardly made it before, but this summer something’s going on, our audience stats show bizarre patterns, we’re severely under estimates and the last savings are gone. We’re not your responsibility, but if you find enough benefits in this work…
Help SILVIEW.media survive and grow, please donate here, anything helps. Thank you!

! Articles can always be subject of later editing as a way of perfecting them

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You can even eat some of them.
CLICK HERE

I still haven’t seen any evidence of a novel coronavirus being properly isolated in a lab as per Koch’s Postulate, and that’s the only official scientific homologation of a virus. But “follow the science” is what the cry, so here’s the latest in 5G science, from US’ NIH website and PubMed.

5G Technology and induction of coronavirus in skin cells

M Fioranelli 1A Sepehri 1M G Roccia 1M Jafferany 2O Y Olisova 3K M Lomonosov 3T Lotti 1 3

Affiliations

  • 1Department of Nuclear, Sub-nuclear and Radiation Physics, G. Marconi University, Rome, Italy.
  • 2Central Michigan Saginaw, Michigan, USA.
  • 3Department of Dermatology and Venereology, I.M. Sechenov First Moscow State Medical University, Moscow, Russia.

Abstract

In this research, we show that 5G millimeter waves could be absorbed by dermatologic cells acting like antennas, transferred to other cells and play the main role in producing Coronaviruses in biological cells. DNA is built from charged electrons and atoms and has an inductor-like structure. This structure could be divided into linear, toroid and round inductors. Inductors interact with external electromagnetic waves, move and produce some extra waves within the cells. The shapes of these waves are similar to shapes of hexagonal and pentagonal bases of their DNA source. These waves produce some holes in liquids within the nucleus. To fill these holes, some extra hexagonal and pentagonal bases are produced. These bases could join to each other and form virus-like structures such as Coronavirus. To produce these viruses within a cell, it is necessary that the wavelength of external waves be shorter than the size of the cell. Thus 5G millimeter waves could be good candidates for applying in constructing virus-like structures such as Coronaviruses (COVID-19) within cells.

Keywords: 5G technology; COVID-19; DNA; dermatologic antenna; inductor; millimetre wave.

We found out from NIH

Copyright 2020 Biolife Sas. http://www.biolifesas.org.


Protection of the population health from electromagnetic hazards – challenges resulting from the implementation of the 5G network planned in Poland

Marek Zmyślony 1Paweł Bieńkowski 2Alicja Bortkiewicz 3Jolanta Karpowicz 4Jarosław Kieliszek 5Piotr Politański 1Konrad Rydzyński 6

Affiliations

  • 1Instytut Medycyny Pracy im. prof. J. Nofera / Nofer Institute of Occupational Medicine, Łódź, Poland (Zakład Ochrony Radiologicznej / Department of Radiological Protection).
  • 2Politechnika Wrocławska / Wrocław University of Sciences and Technology, Wrocław, Poland (Katedra Telekomunikacji i Teleinformatyki / Department of Telecommunications and Teleinformatics).
  • 3Instytut Medycyny Pracy im. prof. J. Nofera / Nofer Institute of Occupational Medicine, Łódź, Poland (Zakład Fizjologii Pracy i Ergonomii / Department of Work Physiology and Ergonomics).
  • 4Centralny Instytut Ochrony Pracy – Państwowy Instytut Badawczy / Central Institute for Labor Protection – National Research Institute, Warsaw, Poland (Zakład Bioelektromagnetyzmu / Department of Bioelectromagnetism).
  • 5Wojskowy Instytut Higieny i Epidemiologii / Military Institute of Hygiene and Epidemiology, Warsaw, Poland.
  • 6Instytut Medycyny Pracy im. prof. J. Nofera / Nofer Institute of Occupational Medicine, Łódź, Poland.

Free article

Abstract

There is an ongoing discussion about electromagnetic hazards in the context of the new wireless communication technology – the fifth generation (5G) standard. Concerns about safety and health hazards resulting from the influence of the electromagnetic field (EMF) emitted by the designed 5G antennas have been raised. In Poland, the level of the population’s exposure to EMF is limited to 7 V/m for frequencies above 300 MHz. This limitation results from taking into account the protective measures related not only to direct thermal hazards, but also to diversified indirect and long-term threats. Many countries have not established legal requirements in this frequency range, or they have introduced regulations based on recommendations regarding protection against direct thermal risks only (Council Recommendation 1999/519/EC). For such protection, the permissible levels of electric field intensity are 20-60 V/m (depending on the frequency). This work has been created through an interdisciplinary collaboration of engineers, biologists and doctors, who have been for many years professionally dealing with the protection of the biosphere against the negative effects of EMF. It presents the state of knowledge on the biological and health effects of the EMF emitted by mobile phone devices (including millimeter waves which are planned to be used in the 5G network). A comparison of the EU recommendations and the provisions on public protection being in force in Poland was made against this background. The results of research conducted to date on the biological effects of the EMF radiofrequency emitted by mobile telecommunication devices, operating with the frequencies up to 6 GHz, do not allow drawing any firm conclusions; however, the research evidence is strong enough for the World Health Organization to classify EMF as an environmental factor potentially carcinogenic to humans. At the moment, there is a shortage of adequate scientific data to assess the health effects of exposure to electromagnetic millimeter waves, which are planned to be used in the designed 5G devices. Nevertheless, due to the fact that there are data indicating the existence of biophysical mechanisms of the EMF influence that may lead to adverse health effects, it seems necessary to use the precautionary principle and the ALARA principle when creating environmental requirements for the construction and exploitation of the infrastructure of the planned 5G system. Med Pr. 2020;71(1):105-13.

Keywords: 5G networks; electromagnetic field; environmental health; environmental protection; precautionary principle; radio communication.

This work is available in Open Access model and licensed under a CC BY-NC 3.0 PL license.

The research evidence is strong enough for the World Health Organization to classify EMF as an environmental factor potentially carcinogenic to humans

Polish study

Also read: It’s not 5G and Covid-19, it’s data and vaccinations. US and China have long used WHO as platform to collaborate on this


To be continued?
Our work and existence, as media and people, is funded solely by our most generous readers and we want to keep this way.
We hardly made it before, but this summer something’s going on, our audience stats show bizarre patterns, we’re severely under estimates and the last savings are gone. We’re not your responsibility, but if you find enough benefits in this work…
Help SILVIEW.media survive and grow, please donate here, anything helps. Thank you!

! Articles can always be subject of later editing as a way of perfecting them