What can salad dressing tell us about cancer? Think oil and vinegar

Researchers led by St. Jude Children's Research Hospital scientists have identified another way the process that causes oil to form droplets in water may contribute to solid tumors, such as prostate and breast cancer. The findings appear today in the journal Molecular Cell.

Researchers found evidence that mutations in the tumor suppressor gene SPOP contribute to cancer by disrupting a process called liquid-liquid phase separation. Liquid-liquid phase separation is seen often in nature and is the reason why oil and vinegar separate in salad dressing.

SPOP is the most frequently mutated gene in prostate cancer and is altered in other solid tumors. The SPOP protein is part of the cell's protein-recycling machinery. SPOP binds unneeded or unwanted proteins so they can be chemically tagged for destruction. Mutations in SPOP were known to disrupt binding and lead to a buildup of cancer-promoting proteins in sensitive cells. St. Jude research suggests that is not the whole story.

"This study shows for the first time that tumor-suppressor function can be influenced by phase separation and that mutations in the tumor suppressor, in this case SPOP, disrupt phase separation," said corresponding author Tanja Mittag, Ph.D., an associate member of the St. Jude Department of Structural Biology.

New chapter

The research comes amid growing interest among cell biologists in liquid-liquid phase separation and its role in cellular function, aging and disease, including cancer and neurodegenerative disorders.

Research published in the past five years indicates that cells rely on liquid-liquid phase separation to maintain their equilibrium under changing conditions. Evidence suggests the process works by concentrating or sequestering molecules in borderless compartments. The compartments, called membraneless organelles, are found throughout the cell. While many such compartments have been known for decades, Mittag said recent advances have expanded our understanding of their role in cellular organization and launched a new era in cell biology. "Some have called it biology 2.0," she said.

Complicated story

Mittag and her colleagues were studying SPOP initially to better understand its role in the mechanism of protein degradation. "The story turned out to be more complicated," she said. That's because SPOP can recognize and bind molecules with multiple binding sites rather than one, a quality known as multi-valency. Those molecules included cancer-promoting proteins like DAXX and androgen receptor, which researchers used in this study.

Researchers showed that when the proteins were expressed together in cells in a laboratory dish, DAXX could trigger liquid-liquid phase separation with SPOP. That caused SPOP and DAXX to move from their location in separate membraneless organelles in the nucleus and rendezvous to form their own border-less compartment.

Enzyme activity

Investigators also reported that enzymatic activity occurred inside the newly formed membraneless organelle. The activity was an indication SPOP was fulfilling its role as a tumor suppressor and tagging DAXX for destruction. "The big question for the field has been what is going on inside these compartments," said co-first author Joel Otero, Ph.D., of the St. Jude Structural Biology department. "This research showed the membraneless organelles are actually promoting a reaction by bringing together SPOP and its substrate, in this case DAXX, so the reaction can take place."

Liquid-liquid phase separation did not occur when DAXX and mutant SPOP were expressed together in the laboratory. Instead of a shared membraneless organelle, mutant SPOP and DAXX remained isolated in separate compartments. Researchers also found fewer DAXX molecules were chemically tagged (ubiquitinated) for destruction. /p> The results were similar when mutant and normal SPOP were expressed with androgen receptor, another SPOP binding partner that is associated with cancer promotion./p>

Activity not just storage

"A lot of previous research has shown cells use membraneless organelles to sequester molecules until they are needed," said first author Jill Bouchard, Ph.D., a St. Jude postdoctoral fellow in the Structural Biology department. "This study showed that activity also occurs inside membraneless organelles." Bouchard explained that without phase separation the process for maintaining protein balance is disrupted. That allows substrate levels, in this case DAXX levels, to increase with potentially catastrophic results.

Toxic 9/11 dust & smoke linked to nearly 10,000 cancer cases in New York

Almost 10,000 people have a cancer diagnosis that is somehow linked to breathing in hazardous particles following the September 11 Twin Tower bombings in New York City, the Post has learned.

Inhaling particles from the leaked jet fuel, asbestos, cement dust and glass shards following the destruction of the World Trade Center has led to cancer proliferation among at least 9,795 first responders and other New Yorkers, the federal World Trade Center Health Program revealed to the New York Post.

The numbers continue to grow exponentially ever since the program at Mount Sinai Hospital kicked off in 2013. In 2015 the number of 9/11 cancer-linked patients stood at 3,204 while the next year it jumped to 8,188.

“We get these referrals 15 to 20 times a week,” said Dr. Michael Crane, medical director of the WTC Health Program, noting that 17 years following the tragedy older people tend to turn for medical help more often. “In an aging population, you’re going to see a rising cancer rate, no matter what.”

15 years after 9/11: Emergency responders and civilians turning up with record rates of cancer

Since the tragedy, more than 1,700 affected persons have died, including 420 of those stricken with cancer, officials told the publication. First responders tend to suffer from thyroid cancer and skin melanoma and also face a higher risk of bladder cancer. The rest of New Yorkers exposed to toxic dust exhibit higher-than-normal rates of breast cancer and non-Hodgkin’s lymphoma. Leukemia and other blood-cell disorders have also been noted to be on the rise, Crane said.

  • Published in World

Are humans causing cancer in wild animals?

As humans, we know that some of our activities can cause cancer to develop in our bodies. Smoking, poor diets, pollution, chemicals used as additives in food and personal hygiene products, and even too much sun are some of the things that contribute to an increased risk of cancer.

But, are human activities also causing cancer in wild animals? Are we oncogenic -- a species that causes cancer in other species?

Researchers from Arizona State University's School of Life Sciences think so and are urgently calling for research into this topic. In a paper published online today in "Nature Ecology & Evolution," Mathieu Giraudeau and Tuul Sepp, both postdoctoral researchers in the lab of ASU life sciences professor Kevin McGraw, say that humans are changing the environment in a way that causes cancer in wild animal populations.

"We know that some viruses can cause cancer in humans by changing the environment that they live in -- in their case, human cells -- to make it more suitable for themselves," said Sepp. "Basically, we are doing the same thing. We are changing the environment to be more suitable for ourselves, while these changes are having a negative impact on many species on many different levels, including the probability of developing cancer."

In the paper, Giraudeau and Sepp and a team of international researchers, point out many pathways and previous scientific studies that show where human activities are already taking a toll on animals. These include chemical and physical pollution in our oceans and waterways, accidental release of radiation into the atmosphere from nuclear plants, and the accumulation of microplastics in both land- and water-based environments. In addition, exposure to pesticides and herbicides on farmlands, artificial light pollution, loss of genetic diversity and animals eating human food are known to cause health problems.

"Cancer in wild populations is a completely ignored topic and we wanted to stimulate research on this question," shared Giraudeau. "We recently published several theoretical papers on this topic, but this time, we wanted to highlight the fact that our species can strongly influence the prevalence of cancer in many other species of our planet.

"Cancer has been found in all species where scientists have looked for it and human activities are known to strongly influence cancer rate in humans. So, this human impact on wild environments might strongly influence the prevalence of cancer in wild populations with additional consequences on ecosystem functioning," he said.

Even something such as artificial light and light pollution, as well as food meant for humans, are negatively affecting wild animals.

Sepp said: "It is already known in human studies that obesity and nutrient deficiency can cause cancer, but these issues have been mostly overlooked in wild animals. At the same time, more and more wild species are in contact with anthropogenic food sources. In humans, it's also known that light at night can cause hormonal changes and lead to cancer. Wild animals living close to cities and roads face the same problem -- there is no darkness anymore. For example, in birds, their hormones -- the same that are linked to cancer in humans -- are affected by light at night. So, the next step would be to study if it also affects their probability of developing tumors."

While these scientists are urgently calling for studies on cancer and its causes in wild animal populations, they realize that this is no easy subject to study.

"The next step is definitely to go into the field and measure cancer rate in wild populations," said Giraudeau. "We are now trying to develop some biomarkers to be able to study this. I think it would be interesting to measure cancer prevalence in wild animals in human-impacted environments and also in more preserved areas for the same species."

If humans are the cause of cancer in wild animals, then many species may be more threatened than people realize. Yet Tuul said, there is reason to hold out hope.

"To me, the saddest thing is that we already know what to do. We should not destroy the habitats of wild animals, pollute the environment, and feed wild animals human food," shared Sepp. "The fact that everybody already knows what to do, but we are not doing it, makes it seem even more hopeless.

"But I see hope in education. Our kids are learning a lot more about conservation issues than our parents did. So, there is hope that the decision-makers of the future will be more mindful of the anthropogenic effects on the environment."

US actor Val Kilmer makes cancer admission

Top Gun star Val Kilmer has appeared to confirm he had cancer, after previously claiming he had "no cancer whatsoever".

While answering questions put to him by Reddit users, the actor revealed he "did have a healing of cancer" and was still dealing with a swollen tongue.

"Because I don't sound my normal self yet people think I may still be under the weather," the 57-year-old wrote.

Speculation over Kilmer's health grew last year after Michael Douglas said he was "dealing with" throat cancer.

The former Batman actor responded at the time by saying Douglas was "misinformed".

"He was probably trying to help me cause press probably asked where I was these days," Kilmer wrote while taking part in a Reddit AMA (Ask Me Anything) last week.

Val Kilmer and Michael Douglas in The Ghost and the DarknessGetty Images / Kilmer appeared with Michael Douglas in The Ghost and the Darkness

Writing on Facebook last year, Kilmer said his only recent contact with Douglas had been to seek advice over a lump in his throat.

Known for his roles in such films as Heat, The Doors and Tombstone, Kilmer worked with Douglas on 1996 film The Ghost and the Darkness.

Following Douglas's comments last year, it was reported that Kilmer had been reluctant to seek medical treatment due to his Christian Science faith.

Many Christian Scientists believe that diseases can be healed with prayer, although the Church does not forbid adherents seeking medical aid.

Shannen DohertyGetty Images / Doherty played Heather Duke in Heathers and Prue in Charmed

Meanwhile, US actress Shannen Doherty has revealed she is in remission after receiving treatment for breast cancer.

The former star of Beverly Hills, 90210 wrote on Instagram that she felt "blessed" by the "overwhelming" news.

Cuba Bets on Heberferon to Treat Several Kinds of Cancer

Cuba will develop this year several clinical trials with Heberferon to treat different kinds of cancer, one of the leading causes of death on the island and worldwide, the national press reported today.

Iraldo Bello, doctor in Biological Sciences, stated that a clinical trial to apply this medicine to about 300 patients with renal carcinoma, as well as another focused on patients with malignant brain tumors, will begin in 2017.

Heberferon is a synergistic combination of interferon alpha 2b and recombinant human gamma, and has had important results in the treatment of basal cell carcinoma, the most common skin cancer.

Preclinical studies and other pilot researches in humans show that the results with this product can be very promising in these two indications, the expert said.

This product, the only one of its kind in the world since late 2016, is in the basic medicine list and is registered in Cuba, Bello said.

The product is the result of 20 years of research, and is one of the leading medicines of the Cuban biotechnology, and since its first applications, it has aroused the interest of several countries to obtain it.

Together with the National Cancer Control Group, authorities have developed specialized workshops to educate doctors about the use of this medicine, which has already been applied to 800 Cuban patients with basal cell carcinoma.

  • Published in Cuba

The price of a puff — National Cancer Society

JANUARY 10 — James Bond isn’t the only one with a licence to kill.

Today the World Health Organisation (WHO) reports that smoking costs the global economy RM4.5 trillion a year, and will take eight million lives annually by 2030. For a species that has invented fire, travelled to space, and split the atom, but is still paying an industry to kill us, mankind is indeed strange.

Decades of research show that smoking is fatal. So in our education, advocacy and policy efforts in curbing smoking, we are often asked: if cigarettes cause such harm, why are they allowed to exist?

One challenge is the separation of the problem: the health industry sees tobacco as a health issue, but certain businesses and governments see it as an economic driver, or a business. Now, the same report by WHO states that the cost of smoking far outweighs revenues from tobacco taxes.

Smoking is the single biggest preventable cause of death and many related illnesses. Apart from resulting in lung cancer, heart diseases and emphysema, it also worsens diabetes, mental illnesses, and substance abuse.

Treating these diseases, many of which are non-communicable, drives up the cost of healthcare: if nothing is done, non-communicable diseases will cost the global economy RM210 trillion — 75 per cent of the global GDP. Smoking specifically accounts for 0.7 per cent of China’s GDP, and around 1 per cent of U.S. GDP. In 2005, the Malaysian Ministry of Health spent 26 per cent of its budget on smoking related diseases, which accounted for 0.74 per cent of its GDP.

There’s also the environment, productivity and human development: smoke and toxic cigarette butts pollute our air and water; smokers are 30 per cent more likely than non-smokers to miss work (and for longer periods). For some families, money spent on cigarettes is money taken away from household essentials.

No other industry causes as much damage to its users and non-users alike — and remains legal, considered a ‘stakeholder’, and allowed to line its pockets. Apart from cigarettes, no other consumer product kills when they are used as intended.

Instead of protecting this industry and giving it business or trade privileges, we urge the nation to support the tobacco control efforts of Malaysia. Tobacco control can work: a study in the U.S., also published this month, reports that its efforts since 1964 have resulted in eight million fewer premature smoking related deaths.

We should want the same for our fellow Malaysians.

Let us use fire, one of man’s oldest discoveries, as intended: to ward off danger, rather than to light up a product that brings permanent and irreversible damage.

There’s still time to stop.

JANUARY 10 — James Bond isn’t the only one with a licence to kill.

Today the World Health Organisation (WHO) reports that smoking costs the global economy RM4.5 trillion a year, and will take eight million lives annually by 2030. For a species that has invented fire, travelled to space, and split the atom, but is still paying an industry to kill us, mankind is indeed strange.

Decades of research show that smoking is fatal. So in our education, advocacy and policy efforts in curbing smoking, we are often asked: if cigarettes cause such harm, why are they allowed to exist?

One challenge is the separation of the problem: the health industry sees tobacco as a health issue, but certain businesses and governments see it as an economic driver, or a business. Now, the same report by WHO states that the cost of smoking far outweighs revenues from tobacco taxes.

Smoking is the single biggest preventable cause of death and many related illnesses. Apart from resulting in lung cancer, heart diseases and emphysema, it also worsens diabetes, mental illnesses, and substance abuse.

Treating these diseases, many of which are non-communicable, drives up the cost of healthcare: if nothing is done, non-communicable diseases will cost the global economy RM210 trillion — 75 per cent of the global GDP. Smoking specifically accounts for 0.7 per cent of China’s GDP, and around 1 per cent of U.S. GDP. In 2005, the Malaysian Ministry of Health spent 26 per cent of its budget on smoking related diseases, which accounted for 0.74 per cent of its GDP.

There’s also the environment, productivity and human development: smoke and toxic cigarette butts pollute our air and water; smokers are 30 per cent more likely than non-smokers to miss work (and for longer periods). For some families, money spent on cigarettes is money taken away from household essentials.

No other industry causes as much damage to its users and non-users alike — and remains legal, considered a ‘stakeholder’, and allowed to line its pockets. Apart from cigarettes, no other consumer product kills when they are used as intended.

Instead of protecting this industry and giving it business or trade privileges, we urge the nation to support the tobacco control efforts of Malaysia. Tobacco control can work: a study in the U.S., also published this month, reports that its efforts since 1964 have resulted in eight million fewer premature smoking related deaths.

We should want the same for our fellow Malaysians.

Let us use fire, one of man’s oldest discoveries, as intended: to ward off danger, rather than to light up a product that brings permanent and irreversible damage.

There’s still time to stop.

- See more at: http://www.themalaymailonline.com/what-you-think/article/the-price-of-a-puff-national-cancer-society#sthash.vMRmpbwJ.dpuf
  • Published in World

Val Kilmer denies Michael Douglas's 'misinformed' cancer claim

US actor Val Kilmer has denied he has cancer, following Michael Douglas's claim that his former co-star is ill.

"I love Michael Douglas but he is misinformed," the Top Gun and Batman Forever star wrote in a Facebook post.

In a talk in London on Sunday, Douglas claimed that Kilmer was "dealing with" throat cancer - the same ailment that Douglas was diagnosed with in 2010.

Kilmer, however, said he was "rehabbing steadily" from "a swollen tongue" and had "no cancer whatsoever".

"The last time I spoke to [Douglas] was almost two years ago, when I asked him for a referral for a specialist to get a diagnosis for a lump in my throat," wrote the 56-year-old.

"I ended up using a team at UCLA [University of California, Los Angeles] and have no cancer whatsoever," he continued.

  http://ichef.bbci.co.uk/news/624/cpsprodpb/B420/production/_92221164_douglas1_pa.jpgDouglas made his comments during a talk in London on Sunday / PA 

Kilmer is also known for his roles in films including The Doors, Heat and Tombstone.

Following Douglas's comments, it was reported that he had been reluctant to seek medical treatment due to his Christian Science faith.

Many Christian Scientists believe that diseases can be healed with prayer, although the Church does not forbid adherents seeking medical aid.

'Devoted friend'

In his post, Kilmer said "concerns about [his] health" had been raised "by publications that have no respect for the truth".

He added: "Some fans have mistakenly thought my silence about my personal issues meant that somehow I wasn't being responsible to my health, because of my reliance on prayer and Love.

  http://ichef.bbci.co.uk/news/624/cpsprodpb/DB30/production/_92221165_kilmer1_bbc.jpgKilmer was seen in 2013 alongside Warwick Davis in Life's Too Short

"Nothing could be further from the truth... Being healthy and having the respect of my peers and love from my family, friends, peers and fans is a DAILY source of inspiration, for which I am so grateful."

Kilmer described Douglas as "a loving and devoted friend", adding: "I'm sure he meant no harm."

The actor said he would be making personal appearances later this month at screenings of Cinema Twain, a film of his one-man play about author Mark Twain.

Kilmer's post follows a number of Facebook messages last year in which he assured fans he had "no tumour or infection of any kind".

  • Published in Culture

Iron nanoparticles make immune cells attack cancer

Iron nanoparticles can activate the immune system to attack cancer cells, according to a study led by researchers at the Stanford University School of Medicine.

The nanoparticles, which are commercially available as the injectable iron supplement ferumoxytol, are approved by the Food and Drug Administration to treat iron deficiency anemia.

The mouse study found that ferumoxytol prompts immune cells called tumor-associated macrophages to destroy cancer cells, suggesting that the nanoparticles could complement existing cancer treatments. The discovery, described in a paper published online Sept. 26 in Nature Nanotechnology, was made by accident while testing whether the nanoparticles could serve as Trojan horses by sneaking chemotherapy into tumors in mice.

"It was really surprising to us that the nanoparticles activated macrophages so that they started to attack cancer cells in mice," said Heike Daldrup-Link, MD, who is the study's senior author and an associate professor of radiology at the School of Medicine. "We think this concept should hold in human patients, too."

Daldrup-Link's team conducted an experiment that used three groups of mice: an experimental group that got nanoparticles loaded with chemo, a control group that got nanoparticles without chemo and a control group that got neither. The researchers made the unexpected observation that the growth of the tumors in control animals that got nanoparticles only was suppressed compared with the other controls.

Getting macrophages back on track

The researchers conducted a series of follow-up tests to characterize what was happening. Experimenting with cells in a dish, they showed that immune cells called tumor-associated macrophages were required for the nanoparticles' anti-cancer activity; in cell cultures without macrophages, the iron nanoparticles had no effect against cancer cells.

Before this study was done, it was already known that in healthy people, tumor-associated macrophages detect and eat individual tumor cells. However, large tumors can hijack the tumor-associated macrophages, causing them to stop attacking and instead begin secreting factors that promote the cancer's growth.

The study showed that the iron nanoparticles switch the macrophages back to their cancer-attacking state, as evidenced by tracking the products of the macrophages' metabolism and examining their patterns of gene expression.

Furthermore, in a mouse model of breast cancer, the researchers demonstrated that the ferumoxytol inhibited tumor growth when given in doses, adjusted for body weight, similar to those approved by the FDA for anemia treatment. Prior studies had shown that the nanoparticles are metabolized over a period of about six weeks, and the new study showed that the anti-cancer effect of a single dose of nanoparticles declined over about three weeks.

The scientists also tested whether the nanoparticles could stop cancer from spreading. In a mouse model of small-cell lung cancer, the nanoparticles reduced tumor formation in the liver, a common site of metastasis in both mice and humans. In a separate model of liver metastasis, pretreatment with nanoparticles before tumor cells were introduced greatly reduced the volume of liver tumors.

Potential clinical applications

The study's results suggest several possible applications to test in human trials, Daldrup-Link said. For instance, after surgery to remove a potentially metastatic tumor, patients often need chemotherapy but must wait until they recover from the operation to tolerate the severe side effects of conventional chemo. The iron nanoparticles lack the toxic side effects of chemotherapy, suggesting they might be given to patients during the surgical recovery period.

"We think this could bridge the time when the patient is quite sick after surgery, and help keep the cancer from spreading until they are able to receive chemotherapy," said Daldrup-Link.

The nanoparticles may also help cancer patients whose tumors can't be completely removed. "If there are some tumor cells left after surgery, the situation that cancer surgeons call positive margins, we think it might work to inject iron nanoparticles there, and the smaller tumor seeds could potentially be taken care of by our immune system," Daldrup-Link said.

The fact that the nanoparticles are already FDA-approved speeds the ability to test these applications in humans, she added.

The new findings will also help cancer researchers conduct more accurate evaluations of nanoparticle-drug combinations, Daldrup-Link said. "In many studies, researchers just consider nanoparticles as drug vehicles," she said. "But they may have hidden intrinsic effects that we won't appreciate unless we look at the nanoparticles themselves."

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