Gene that stops lung cancer spread found

Offering hope in the fight against one of the world's deadliest cancers, scientists have identified a gene responsible for stopping the movement of cancer from the lungs to other parts of the body.

"Lung cancer, even when it is discovered early, is often able to metastasise almost immediately and take hold throughout the body," informed Reuben J. Shaw, a professor of molecular and cell biology at Salk Institute for Biological Studies in California.

By identifying the cause of this metastasis, scientists are able to explain why some tumours are more prone to spreading than others.

It is known that about a fifth of lung cancer cases are missing an anti-cancer gene called LKB1. Cancers missing LKB1 are often aggressive, rapidly spreading through the body.

Now, the Salk team has found the connection and a new target for therapy -- a little-known gene called DIXDC1.

The researchers discovered that DIXDC1 receives instructions from LKB1 to go to focal adhesions and change their size and number.

When DIXDC1 is "turned on", half-a-dozen or so focal adhesions grow large and sticky, anchoring cells to their spot.

"The communication between LKB1 and DIXDC1 is responsible for a 'stay-put' signal in cells. DIXDC1 turns out to be inhibited in cancer and metastasis," explained Jonathan Goodwin, study's first author and research student at Salk Institute.

"Patients missing either gene should be sensitive to new therapies targeting focal adhesion enzymes, which are currently being tested in early-stage clinical trials," Shaw added in a paper detailed in the journal Molecular Cell. THIS IS ONLY FOR INFORMATION, ALWAYS CONSULT YOU PHYSICIAN BEFORE HAVING ANY PARTICULAR FOOD/ MEDICATION/EXERCISE/OTHER REMEDIES.

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Key protein behind breast cancer’s spread to brain

In a major breakthrough, a cancer-research team has identified a protein that may be the crucial reason behind breast cancer spreading to the brain.

Using cell models, the researchers at the University of Wisconsin-Madison found that breast cancer cells harness a protein called alphaB-crystallin to help them stick to endothelial cells that line the small blood vessels in the brain.

In addition, this protein enhances the penetration of breast cancer cells through the blood-brain barrier, which normally prevents cells and many molecules from entering the brain.

Once in the brain, breast cancer cells are able to form metastases i.e. spread of a cancer from one organ to another, said a new study published in the journal Clinical Cancer Research.

“We found that reducing the expression of alphaB-crystallin in breast cancer cells hindered the cells’ ability to form brain metastases in mice,” said Vincent Cryns, professor of medicine at University of Wisconsin School of Medicine and Public Health in the US.

“alphaB-crystallin may be a promising drug target that should be explored further,” he added.

The researchers discovered that women with breast tumours that expressed alphaB-crystallin had a shorter survival than women with breast tumours that did not express this protein.

The also found breast tumours that expressed alphaB-crystallin were more likely to be triple-negative breast cancers, an aggressive type of cancer that lacks three receptors – estrogen receptor, progesterone receptor and HER-2.

Triple-negative breast cancers are known to have a high incidence of brain metastasis.

“Our findings suggest that alphaB-crystallin may contribute to the tendency of triple-negative breast cancers to metastasize to the brain and to their poor prognosis,” said Cryns. Yet, he cautioned these findings need to be validated in additional studies.

Brain metastasis is a terrifying complication of advanced breast cancer, with a grim prognosis and few treatment options.

The cancer’s spread to the brain is often undetected until patients start to develop symptoms such as seizures, headaches, and trouble thinking.

These studies were conducted in collaboration with researchers at the University of North Carolina at Chapel Hill, Duke University and other institutions.

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Kidney Cancer Drugs Equal in Prolonging Survival

The drug pazopanib (Votrient) works as well as sunitinib (Sutent) for treating advanced kidney cancer, but it has milder side effects, a new study finds.

Although both drugs are approved by the U.S. Food and Drug Administration as first-line treatments for kidney cancer and both boost survival, pazopanib had the edge in improving the quality of life, the researchers reported.

"Kidney cancer has long been considered one of the most difficult-to-treat cancers, and is associated with a poor prognosis when it's metastasized [or spreading]," said lead researcher.

Now there are drugs that attack a gene that is responsible for turning kidney cells into cancer cells, he said. "There has been tremendous progress in the treatment of this disease since 2005 with these targeted drugs,"he said. "The first of these drugs was sunitinib, which is considered the standard in first-line treatment for kidney cancer."

This new trial was a head-to-head comparison of sunitinib and pazopanib. The researchers found both had a similar safety profile and survival benefit, but there were milder side effects with pazopanib, Motzer said. These included less fatigue and fewer sores on the bottom of the feet, he noted.

"The data also suggest that patients on pazopanib have a better quality of life than patients on sunitinib," he said. Both drugs cost about the same -- about $6,500 a month -- and are covered by Medicare and many private insurers.

"Both these drugs are good options for first-line treatment," he said. "They allow for us to individualize treatment for patients. In my own practice, I have changed my preferred drug from sunitinib over to pazopanib, because most patients appear to have a better quality of life with pazopanib compared with sunitinib."

A urologist , said that "this study shows that there is more than one option for first-line therapy for renal [kidney] cancer."

According to him, 65,000 people are diagnosed with kidney cancer each year in the United States. "It's the sixth most common cancer," he said. And because it is often diagnosed late, 30 percent to 50 percent of the patients develop metastasis, he added. "It's one of the top 10 cancer killers," he noted.

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Cancer cure may lie in the gut

A new study suggests that cure for cancer may be in our intestines.

An associate professor  said that if the gastrointestinal tract remains healthy and functioning, the chances of survival increase exponentially.

Recently, it was discovered a biological mechanism that preserves the gastrointestinal tracts in mice who were delivered lethal doses of chemotherapy.

The findings could revolutionize cancer therapy.

He emphasized that this had not yet been tested in humans, and right now there's no way to know if people will respond similarly.

"All tumours from different tissues and organs can be killed by high doses of chemotherapy and radiation, but the current challenge for treating the later-staged metastasised cancer is that you actually kill the host before you kill the tumour," he said.

"It's our belief that this could eventually cure later-staged metastasised cancer. People will not die from cancer, if our prediction is true.

"We cannot know this yet, but in mice it has shown promise. Years down the road, we may have a way to make humans tolerate lethal doses of chemotherapy and radiotherapy. In this way, the later-staged, metastasised cancer can be eradicated by increased doses of chemotherapy and radiation," he added.

The lab found that when certain proteins bind with a specific molecule on intestinal stem cells, it revs intestinal stem cells into overdrive for intestinal regeneration and repair in mice.

Stem cells naturally heal damaged organs and tissues, but so-called "normal" amounts of stem cells in the intestine simply cannot keep up with the wreckage left behind by the lethal doses of chemotherapy and radiation required to successfully treat late-stage tumours.

However, the phalanx of extra stem cells protect the intestine and gastrointestinal tract, which allows the ingestion of nutrients so the body can perform other critical functions and the bacterial toxins in the intestine are prevented from entering the blood circulation, he said.

In the future, if the findings are tested in humans and show promise, these factors could give human cancer patients just enough of an extra edge to survive the stronger doses of chemotherapy and radiation, until the tumour or tumours are eradicated.

He stressed that even if the findings do show promise in humans, it could take a decade or longer before an application becomes available to use on people.

In the study, 50-to-75 percent of the mice treated with the molecule survived otherwise lethal doses of chemotherapy. All of the mice that did not receive the molecule died, he said.

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Diabetes, anti-cancer drug combo more effective

Scientists have found that combining diabetes drugs with anti-cancer therapies increases the efficacy of the latter, a study says. 

In the current issue of a journal , researchers  describe how they increase the effectiveness of anti-melanoma drugs by combining anti-cancer therapies with diabetes drugs. 

Their studies, conducted in cell and animal models of melanoma, demonstrate that the combined therapy could destroy a subset of drug-resistant cells within a tumour. 

"We have found that the individual cells within melanoma tumours are not all identical, and tumours contain a sub-population of cells that are inherently drug resistant, which accounts for the fact that advanced melanoma tumours return no matter how much they are depleted," said researchers. 

"We found that these slow-growing, drug-resistant cells are marked by a high rate of metabolism which makes them susceptible to diabetes therapeutics," added the researchers. 

"Our findings suggest a simple strategy to kill metastatic melanoma -- regardless of cell type within the tumour - by combining anti-cancer drugs with diabetes drug." 

"The diabetes drug puts brakes on the cells that would otherwise re-populate the tumour, thus allowing the anti-cancer drug to be more effective," .



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Radioactive nanoparticles that target cancer cells developed

The  scientists cover the lutetium nano-particles with gold shells and attach targeting agents.

Researchers have found a way to create radioactive nano-

particles that target lymphoma tumour cells wherever they 

may be in the body.

Cancers of all types become most deadly when they 

metastasise and spread tumours throughout the body. Once 

cancer has reached this stage, it becomes very difficult for 

doctors to locate and treat the numerous tumours that can 

develop.

An associate professor of oncology stated that being able to 

target secondary tumours is vital to successfully treating 

patients with progressive cancers.

“Depending on the type of cancer, primary tumours usually 

are not the cause of death for cancer patients. If a cancer 

metastasises, or spreads creating hard-to-find tumours, it 

often becomes fatal. Having a way to identify and shrink 

these secondary tumours is of utmost importance when 

fighting to save people with these diseases,” he said.

In an effort to find a way to locate and kill secondary tumours, 

researchers have successfully created nano-particles made 

of a radioactive form of the element lutetium. The 

scientists then covered the lutetium nano-particles with gold 

shells and attached targeting agents.

In previous research, the researcher has already proven the 

effectiveness of similar targeting agents in mice and dogs 

suffering from tumours. In that research, the targeting agents 

were attached to single radioactive atoms that were 

introduced into the bodies of animals with cancer. The 

targeting agents were able to seek out the tumours existing 

within the animals, which were then revealed through radio-

imaging of those animals.

In their current research, the scientists have shown the 

targeting agents can deliver the new radioactive lutetium 

nano-particles to lymphoma tumour cells without attaching to 

and damaging healthy cells in the process.

A researcher said this is an important step toward developing 

therapies for lymphoma and other advanced-stage cancers.

“The ability to deliver multiple radioactive atoms to individual 

cancer cells should greatly increase our ability to selectively 

kill these cells. We are very optimistic about the synergy of 

combining the targeting strategy developed in the lab with our 

work on new radioactive nano-particles,” he said.

This study is an example of the collaborative research taking 

place. The early-stage results of this research are promising. 

If additional studies, including animal studies, are successful 

within the next few years, the researchers will request 

permission from the federal government to begin human drug 

development. After this status has been granted, researchers

may conduct human clinical trials with the hope of developing 

new treatments.