Scientists find key to ‘turbo-charging’ immune system to kill all cancers

Imperial College scientists are developing a gene therapy designed to boost immune cells

A protein which ramps up the immune system has been discovered by scientists at Imperial College London

A protein which ramps up the immune system has been discovered by scientists at Imperial College London Photo: Wellcome Collection

In a breakthrough described as a ‘game-changer’ for cancer treatment, researchers at Imperial College found a previously unknown molecule which boosts the body’s ability to fight off chronic illnesses.

Scientists at Imperial College London, who led the study, are now developing a gene therapy based on the protein and hope to begin human trials in three years.

“This is exciting because we have found a completely different way to use the immune system to fight cancer,” said Professor Philip Ashton-Rickardt, from the Section of Immunobiology in the Department of Medicine at Imperial, who led the study.

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A protein which ramps up the immune system has been discovered by scientists at Imperial College London Photo: Wellcome Collection

“It could be a game-changer for treating a number of different cancers and viruses.

“This is a completely unknown protein. Nobody had ever seen it before or was even aware that it existed. It looks and acts like no other protein.”

The protein – named lymphocyte expansion molecule, or LEM, promotes the spread of cancer killing ‘T cells’ by generating large amounts of energy.

Normally when the immune system detects cancer it goes into overdrive trying to fight the disease, flooding the body with T cells. But it quickly runs out of steam.

However the new protein causes a massive energy boost which makes T cells in such great numbers that the cancer cannot fight them off.

It also causes a boost of immune memory cells which are able to recognise tumours and viruses they have encountered previously so there is less chance that they will return.

The team made the discovery while screening mice with genetic mutations. They found one type produced ten times the number of cancer-fighting T cells, suppressing infections and becoming resistant to cancer.

Researchers found that the mice with enhanced immunity produced high levels of the unknown protein which is also found in humans.

They are hoping to produce a gene therapy whereby T cells of cancer patients could be enhanced with the protein and then injected back into the body. It could end the need for harsh chemotherapies as the body itself would be fighting the disease, rather than toxic drugs.

Dr Mike Turner, Head of Infection and Immunobiology at The Wellcome Trust, said: “The discovery of a protein that could boost the immune response to not only cancer, but also to viruses, is a fascinating one.

“Further investigation in animal models is needed before human trials can commence, but there is potential for a new type of treatment that capitalises on the immune system’s innate ability to detect and kill abnormal cells.”

Charities said the protein showed ‘great promise’ and were eager to see if it could be translated into humans.

Dr Alan Worsley, senior science information officer at Cancer Research UK, said: “This exciting work in mice is still at an early stage and only looked at one type of cancer.

“Cancer often finds a way to suppress the immune system, but drugs that overcome this and allow immune cells to target cancer show great promise. Research into the biology of the immune system could help develop more effective treatments by increasing the number of cancer-killing immune cells.

“The researchers now need to figure out how to develop drugs that target this molecule, and whether doing so would be safe and effective in cancer patients.”

The research was published in the journal Science.

Exercise boosts tumor-fighting ability of chemotherapy in cancer patients, researchers say

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 (Reuters)

While exercise has been found to benefit cancer patients both physically and psychologically, researchers say a new study proves it can also boost the effect chemotherapy has on a patient.

In a study by a team at the University of Pennsylvania, researchers using a mouse model of melanoma found that combining exercise with chemotherapy shrunk tumors more than chemotherapy alone.

The researchers sought to find whether exercise would protect against negative cardiac-related side effects of the cancer drug doxorubicin, which is known to damage heart cells.

The team first injected melanoma cells into four teams of mice. They then injected two groups with doxorubicin and the other two with a placebo. Over a two-week period mice in one of the groups injected with the drug and one of the untreated groups walked 45 minutes, five days a week, on treadmills, while the other two groups did not.

While data showed that exercise did not help protect against cardiovascular damage, it did show that in mice that had received the drug and exercised, tumors significantly shrunk.

“We looked, and the exercise didn’t do anything to the heart – it didn’t worsen it, it didn’t help it,” Joseph Libonati, senior author of the study and associate professor at Penn School of Nursing, said in a news release. “But the tumor data – I find them actually amazing.”

The team plans to examine further how exercise enhances the effect doxorubicin has on tumors, but are encouraged that results may help find ways to cut down on cardiovascular damage caused by the drug.

“If exercise helps in this way, you could potentially use a smaller dose of the drug and get fewer side effects,” Libonati said.

New protein found to control deadly cancer metastasis

Stopping cancer’s spread: New protein found to control deadly cancer metastasis

By Loren Grush

Published June 15, 2013

FoxNews.com
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    This image shows metastasized human breast cancer cells (magnified 400 times, stained brown) in lymph nodes. (National Cancer Institute)

Researchers have found a critical element that may explain why some cancers spread farther and faster than others, a discovery that could lead to one of the Holy Grails of cancer treatment: containing the disease.

Scientists from the University of California, San Diego School of Medicine have identified a protein that seems to serve as a switch, regulating the spread of cancer from the primary tumor to distant spots in the body – a process known as metastasis.  The protein is used by embryo cells during early development, but then disappears from the body after an individual comes out of the womb.

According to the researchers, the protein was only found in people with metastatic cancer, leading them to belive that the regulation of this protein could potentially stop the dangerous progression of this killer disease.

“The protein seems to get turned off (after embryonic development), and we’ve only identified a small sub-population of cells that can turn it on,” lead investigator, Dr. Thomas Kipps, Evelyn and Edwin Tasch Chair in Cancer Research at UC San Diego, told FoxNews.com.  “By and large, we looked at the brain, lungs, heart, kidney and other organs, and it wasn’t there. Then we looked at a variety of cancers – breast, ovarian, prostate – and it seems to be a common theme to express this embryonic protein.”

Kipps said they stumbled upon this protein while conducting immunotherapy research on leukemia patients, in which they reengineered the patients’ leukemia cells and injected them into their bodies.  This technique is meant to enhance the body’s natural immune response to cancer.

“We did have patients respond to their leukemia cells, but part of the immune response was a cell that targeted (this protein),” Kipps said. “Anecdotally, these patients did well. So we wanted to know (what) it is doing.”

The protein, called Receptor-tyrosine-kinase-like Orphan Receptor 1, or ROR1, is involved in a process known as epithelial mesenchymal transition (EMT), which occurs during early embryonic development.  Throughout the EMT process, embryonic cells migrate and eventually grow into new organs.

Kipps explained that ROR1’s role during embryonic development may explain how it helps cancers to grow and spread.

“It’s a protein that sits on the surface of the cancer, so it has the ability to bind to other proteins outside of the cell and may have the ability to bind to other proteins on the cancer cell membrane,” Kipps said.  “Half of it sits outside the cell and half inside the cell.  It’s like having an antenna sticking out, and then you have a transmitter below the surface.  That transmitter conveys important signals to the cell, and it seems to allow itself to assume a better state of migration.”

In a series of lab experiments, Kipps and his team found that high-level expression of ROR1 in breast cancer cells were associated with higher rates of relapse and metastasis.  However, when they used therapies to silence the expression of ROR1, the researchers were successfully able to inhibit metastatic spread of the cancer cells in animal models.

“It’s like taking the antenna away; you can’t hear the radio or TV station anymore,” Kipps said. “The cancer cells become more fragile and don’t grow as well.”

After cardiovascular disease, cancer is the second leading cause of death in the United States, with 575,000 Americans dying from the disease each year. One of the scariest aspects of receiving a cancer diagnosis is learning how far the disease has spread throughout the body.  An individual’s prognosis can vary greatly depending on the extent of the cancer’s progression; if it has spread too much, modern treatments can do little to stop it. This explains why the vast majority of cancer-related deaths – approximately 90 percent – are due to metastasis of the original tumor cells.

Since ROR1 is only expressed in cancer cells, Kipps said it provides a singular target for future therapies aimed at containing and reversing metastasis.  Then, once the cancer becomes more localized, traditional therapies such as radiation and surgery can help remove the original tumor from the body.

“I think it’s an exciting time for cancer treatment,” Kipps said.  “I do think it’s a great time for discoveries, and hopefully we’ll be able to cure many forms of cancer – turning it into a bad experience rather than a life threatening event.”

The research was published in the June 15 issue of the journal Cancer Research.

Read more: http://www.foxnews.com/health/2013/06/15/stopping-cancer-spread-researchers-identify-protein-that-regulates-cancer/#ixzz2XRomenXr

Cancer Research Breakthrough

Cancer Metastasis: Researchers Find ‘Chase And Run’ Mechanism In Cancer Spread

Posted: 06/17/2013 2:14 pm EDT  |  Updated: 06/18/2013 10:56 pm EDT

Scientists have identified the mechanism by which cancer is able to spread throughout the body, after discovering a cell movement process called “chase and run.”

The findings, published in the journal Nature Cell Biology, detail how neural crest cells, which are similar to cancer cells, “chase” placode cells, which are equivalent to healthy cells, when they are placed next to each other. In turn, the placode cells “run away.”

“We use the analogy of the donkey and the carrot to explain this behavior: the donkey follows the carrot, but the carrot moves away when approached by the donkey,” study researcher Dr. Roberto Mayor, of University College London, said in a statement. “Similarly the neural crest cells follow the placode cells, but placode cells move away when touched by neural crest cells.”

Cancer-Research

Even though the scientists didn’t work with actual cancer cells, they explained that the process is likely comparable. They said that understanding this process could help them potentially find a way to target cancer cells before they spread — metastasize — to other parts of the body, which dramatically raises death risk for patients.

Recently, researchers at the University of California, San Diego, also gained some ground in understanding cancer metastasis in research published in the journal Cancer Research. Fox News reported on the finding, which showed that there is a protein that helps to regulate the actual spread of cancer cells to other parts of the body.

“The protein seems to get turned off (after embryonic development), and we’ve only identified a small sub-population of cells that can turn it on,” study researcher Dr. Thomas Kipps, Evelyn and Edwin Tasch Chair in Cancer Research at UC San Diego,told Fox News. “By and large, we looked at the brain, lungs, heart, kidney and other organs, and it wasn’t there. Then we looked at a variety of cancers — breast, ovarian, prostate ––and it seems to be a common theme to express this embryonic protein.”