Protein that spurs bowel cancer growth identified

Researchers have identified a key protein that supports the growth of many bowel cancer, paving way for development of new therapies to combat the deadly disease.

The study revealed that a protein called Importin-11 transports the cancer-causing protein beta-catenin into the nucleus of colon cancer cells, where it can drive cell proliferation.

Inhibiting this transport step could block the growth of most colorectal cancers-also called bowel cancers-- caused by elevated beta-catenin levels. Around 80% of colorectal cancers are associated with mutations in a gene called APC that results in elevated levels of beta-catenin protein.

This increase in beta-catenin is followed by the protein's accumulation in the cell nucleus, whee it can activate numerous genes that drive cell proliferation and promote the growth and maintenance of colorectal tumours.

But how beta-catenin enters the cell nucleus after its levels rise is poorly understood. Because the molecular mechanisms underlying beta-catenin nuclear transport remain unclear, we set out to identify genes required for continuous beta-catenin activity in colorectal cancer cells harbouring APC mutations, said one of the researchers.

Under CRISPR DNA editing technology, the researchers developed a new technique that allowed them to screen the human genome for genes that support beta-catenin's activity in colorectal cancer cells after its levels have been elevated by mutations in APC.

The researchers found that Importin-11 binds to beta-catenin and escorts it into the nucleus of colorectal cancer cells with mutations in APC. Removing Importin-11 from these cells prevented beta-catenin from entering the nucleus and activating its target genes.

The researchers discovered that Importin-11 levels are often elevated in human colorectal cancers. Moreover, removing Importin-11 inhibited the growth of tumours formed by APC mutant cancer cells isolated from patients.

We concluded that Importin-11 is required for the growth of colorectal cancer cells, the researcher said. Learning more about how Importin-11 transport beta-catenin into the nucleus may help researchers develop new therapies that block this process and reduce the growth of colorectal cancers caused by mutations in APC.

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Researchers have identified a key protein that supports the growth of many bowel cancers, paving the way for development of new therapies to combat the deadly disease. The study, published in the Journal of Cell Biology, revealed that a protein called Importin-11 transports the cancer-causing protein beta-catenin into the nucleus of colon cancer cells, where it can drive cell proliferation. https://www.thehansindia.com/hans/hans-classroom/protein-that-spurs-bowel-cancer-growth-identified-593673

https://www.thehansindia.com/hans/hans-classroom/protein-that-spurs-bowel-cancer-growth-identified-593673

Researchers have identified a key protein that supports the growth of many bowel cancers, paving the way for development of new therapies to combat the deadly disease. The study, published in the Journal of Cell Biology, revealed that a protein called Importin-11 transports the cancer-causing protein beta-catenin into the nucleus of colon cancer cells, where it can drive cell proliferation. https://www.thehansindia.com/hans/hans-classroom/protein-that-spurs-bowel-cancer-growth-identified-593673

https://www.thehansindia.com/hans/hans-classroom/protein-that-spurs-bowel-cancer-growth-identified-593673

Researchers have identified a key protein that supports the growth of many bowel cancers, paving the way for development of new therapies to combat the deadly disease. The study, published in the Journal of Cell Biology, revealed that a protein called Importin-11 transports the cancer-causing protein beta-catenin into the nucleus of colon cancer cells, where it can drive cell proliferation. https://www.thehansindia.com/hans/hans-classroom/protein-that-spurs-bowel-cancer-growth-identified-593673

https://www.thehansindia.com/hans/hans-classroom/protein-that-spurs-bowel-cancer-growth-identified-593673

Getting Closer: Finding Out Why the Immune System Attacks Itself

Biomolecular researcher has published a first-of-its-kind study -  a comprehensive profile of B cells in rheumatoid arthritis (RA). B cells are lymphocytes, or white blood cells, that make protein antibodies that attack a patient’s healthy proteins in patients with RA.

“To the best of our knowledge, this is the first study to conduct whole transcriptome profiling of antigen-specific B cells in any human autoimmune disorder,” said the researcher, whose results portray B cells not merely as auto-antibody producers, but also as a source of diverse molecules that can influence proliferation, differentiation and activation of other pathogenic cell types.

“We anticipate that these data will serve as a foundational data set for investigating multiple hypotheses on the roles of B cells in RA and other autoimmune disorders, and will enable drug discovery,” he said.

B Cells, good and bad
For every new pathogen encountered, a small subset of B cells activates to make an antibody that specifically recognizes that particular pathogenic protein. Every person has between 10-100 million unique B cells, each capable of making its own antibody. While antibodies are the natural way the body fights infections, in the autoimmune RA, these antibodies – that are supposed to fight foreign invaders – attack the body’s own proteins and are thus called auto-antibodies.

“We wanted to understand if there’s anything special about this class of white bloods cells, the autoreactive B cells that make autoantibodies, that would make them fight against healthy proteins,” he said.

Fewer than one in 1,000 B cells are autoreactive, so to find which one is the culprit, a postdoctoral researcher  designed a method to reliably identify and isolate the population, then used RNA sequencing to study all of the RNA being made by each cell.

A number of pathways associated with inflammation and protein modification, known to be amplified in rheumatoid arthritis, were found. At the molecular level, the team found two specific differences in the B cells of RA patients – the inclusion of the protein interleukin 15 receptor subunit alpha (IL-15Rα) and a high amount of the amphiregulin molecule, which can signal adjacent cells. Each was validated at the protein level in independent cohorts of RA patients and prioritized for further studies.

Autoreactive B cells, and they alone, have the protein IL-15Rα.

“We think that protein allows them to become bad actors,” he said. “People have been targeting this pathway for quite some time. This now sheds new light on these bad guys in the progression of this disease and how to target it.”

The team is the first to show that B cells make amphiregulin. Amphiregulin sits in a well-studied pathway, the epidermal growth factor receptor pathway (EGFR), and so the next step will be to determine if inhibiting the pathway impacts the B cells.

The research team also published a list of FDA-approved drugs, such as Xeljanz (tofacitinib), that target various pathways of the B cells, though they aren’t specifically approved for that purpose.

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'Pied Piper' Device That Lures Tumors From The Brain Awarded Breakthrough Status By FDA

Brain tumors are notoriously difficult to treat, often growing quickly and spreading through the brain. But what if we could trick the cancerous cells to proliferate in a new direction, essentially luring them out of the brain and outside the skull? Well, researchers are attempting to do just that, and their work has been awarded “ breakthrough status” by the government.

Called the Tumor Monorail, the device has been described as a “pied piper”, thanks to its ability to trick and lure cells away from a tumor, just as the Pied Piper lured rats, and then children, away from the town of Hamelin in the well-known fairy tale.

The Tumor Monorail is essentially a long, thin tube with a small reservoir at one end. The reservoir sits on top of the skull, just under the scalp, and tricks tumor cells into migrating up the tube and out of the brain where they can be removed by a surgeon. It does this by mimicking the brain’s white matter, where the tumor would normally grow. The cancerous cells spread up the tube, thinking they are growing further into the brain and expanding the tumor. Gotcha.

So far, the Tumor Monorail has only been tested successfully in rats. The researchers now need to work on testing its safety and efficacy in humans. That’s why its new breakthrough status is so important. Developing new treatments and proving they are fit for clinical use is a long, ardous process, but the FDA breakthrough initiative helps to fast-track the development and review of new treatments for serious or life-threatening illnesses.

Glioblastoma – an aggressive type of brain tumor with a poor survival rate – is one of these conditions. Innovative new ways to tackle it, like the Tumor Monorail, could have a hugely positive impact, so speeding up its development is key. Still, it’s important to note that the new allocation doesn’t mean the device has been approved for clinical use by the FDA. The researchers behind it will have to prove it's both safe and effective in people first.

“The tumor monorail device is a true game-changer in how we think about treating brain tumors,” said  a neurosurgeon in a statement. “There are many tumors that are considered inoperable due to the location of the tumor or the frailty of the patient. This device affords clinicians the ability to surgically treat these tumors with a minimal approach.”

Back in 2014, the researchers successfully managed to get their device to work in rats. The rats’ brain tumors shrank by more than 90 percent and spread more slowly. Since then, the researchers have tweaked the device, and repeatedly shown its effectiveness in rats.

“This was the first demonstration that you can engineer migration inside the body and move a tumor from point A to point B by design,” explained  one of the researcher. “It was also the first demonstration of bringing the tumor to your drug rather than your drug going into the brain and killing valuable cells.”

Five years on and the device has breakthrough status. “The most exciting part about this designation is that it gives us the opportunity to look at the FDA as a partner rather than a reviewer,” said project leader. “With direct access to the FDA reviewers, we can get more efficient, faster feedback on our experimental ideas to make sure we’re addressing all of their concerns from the very start.”

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Cancer growth in the body could originate from a single cell – target it to revolutionise treatment

Cancer remains a frightening and largely incurable disease. The toxic side effects of chemotherapy and radiation make the cure often seem as bad as the ailment, and there is also the threat of recurrence and tumour spread.

Cancer treatment still follows a practically medieval method of cut, burn or poison. If the growth can’t be cut out through surgery, it may be burnt away with radiation or poisoned by chemotherapy. As a result, cancer therapy remains a daunting diagnosis for patients and treatment options seem limited for a disease which causes one in 6 deaths globally.

The failure to innovate in cancer treatment may lie in the very poor success rate of clinical trials. Approximately 95%-98% of new anti-cancer drugs actually fail phase III clinical trials, the phase in which new treatments are compared with existing therapy options. This is a staggering statistic. No other business could possibly survive with such an abysmal success rate.

Most drugs are made to target “bulk” cancer cells, but not the root cause: the cancer stem cell. Cancer stem cells, also known as “tumour-initiating cells”, are the only cells in the tumour that can make a new tumour. New therapies that specifically target and eradicate these cancer stem cells are needed to prevent tumours growing and spreading, but for that there needs to be more clarity around the target.

Our new research may have discovered such a target. We have identified and isolated cells within different cancerous growths which we call the “cell of origin”. Our experiments on cancer cells derived from a human breast tumour found that stem cells – representing 0.2% of the cancer cell population – have special characteristics.

They generate vast amounts of energy and proliferate rapidly. We believe that they resemble the cancer cell of origin that has escaped senescence – the natural process of cell ageing and “death” which concludes a healthy cell life cycle. These are thought to be the first cancer cells which start the process of uncontrolled cell multiplication and cause tumours to form.

These cancer stem cells undergo anchorage-independent growth, also known as growth in suspension, without any tissue attachment. This is how metastasis occurs – spreading via the blood vessels and lymphatic vessels. These features put them front and centre as a new target for anti-cancer therapy.

With astonishing luck, these energetic cancer stem cells are colour-coded which means they have a natural phosphorescent glow, making them easy to identify and target.

Now that we have found them and we know how they behave, it should be relatively simple to find drugs to target cancer stem cells. In our new paper we have already shown that they are easily targeted with a mitochondrial inhibitor or a cell cycle inhibitor such as Ribociclib, an FDA-approved drug in the US which would prevent their proliferation. 

Ultimately, this means that if we focus on energetic cancer stem cells, we may be able to directly hit the target. We might be able to turn cancer into a manageable chronic disease, like diabetes. We believe that we have arrived at the start of a new, more fruitful, road in cancer therapy. As a consequence, “big pharma” drug screening should actually focus on cancer stem cells and their relevant targets.

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A Single “Cell of Origin” Might Trigger All Forms of Cancer

A team of scientists are claiming that all cancer growth in the body starts from a single “cell of origin” — and that they’ve found that cell.

If they’re right, the discovery could dramatically change how we treat cancer, potentially saving millions of life.
Not all cancer cells are alike. A particular type, called cancer stem cells, are the only cells that can make a new tumor.

In a paper published, the team describes how its study of cells from a human breast tumour allowed it to identify a sub-class of cancer stem cells, which it calls “energetic” cancer stem cells (e-CSCs).

According to the researchers, these cells produce large amounts of energy and proliferate rapidly. They also grow in suspension, without attaching to any tissues, allowing cancer to spread through blood and lymphatic vessels.

Ultimately, they believe it’s e-CSCs that lead to the growth of all cancers in the body.

“It feels like finding the proverbial needle in a haystack,” a researcher  said in a news release, “and it crucially gives us a new window on cancer and how we might stop it.”

Targeted Treatment

 Now that they’ve identified e-CSCs as the “cell of origin,” the team suggests researchers shift their focus from cancer treatments that target “bulk” cancer cells and toward ones that go after e-CSCs in particular. And thanks to the cells’ natural phosphorescent glow, hunting them down won’t be as difficult.

“Now that we have found them and we know how they behave, it should be relatively simple to find drugs to target cancer stem cells,” he wrote. “In our new paper, we have already shown that they are easily targeted with a mitochondrial inhibitor or a cell cycle inhibitor such as Ribociclib, an FDA-approved drug in the U.S. which would prevent their proliferation.”

“Ultimately, this means that if we focus on energetic cancer stem cells, we may be able to directly hit the target,” he continued. “We might be able to turn cancer into a manageable chronic disease, like diabetes.”

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Protein that promotes brain tumour formation identified

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 Researchers have found that a protein involved in the breakdown of glucose - a process known as glycolysis -- plays an important role in coordinating cellular processes crucial to cancer metabolism and brain tumour formation.
The findings may lay the groundwork for improved approaches to diagnosis and treatment of glioblastoma and other cancers.
The study showed that PGK1, which is associated with cancer cell proliferation and drug resistance, was instrumental in glycolysis and the citric acid cycle -- both important for generating the energy that feeds cancer cells.

 "Our study highlights that PGK1 acts as a protein kinase in coordinating glycolysis and the citric acid cycle in cancer metabolism and tumour formation," said Zhimin Lu, professor at The University of Texas MD Anderson Cancer Centre in the US.

The study, published online in the journal Molecular Cell, also shed further light on the Warburg effect, an enzymatic mechanism that cancer cells employ to boost energy levels and produce cellular substances that lead to rapid cancer growth.

"The Warburg effect promotes tumour progression. Exactly how this is coordinated has remained elusive," Lu noted.

"Our findings provided critical insight into the Warburg effect and demonstrates that PGK1 ultimately promotes cancer cell proliferation and tumour formation," he said.

"It may help us to develop a molecular basis for improved diagnosis and treatment of cancer," Lu pointed out.