Breast Cancer Recurrence Rate Not Up With Autologous Fat Transfer

THURSDAY, Nov. 15, 2018 — For patients with breast cancer, reconstruction with autologous fat transfer (AFT) seems not to increase the rate of locoregional recurrence versus conventional breast reconstruction, according to a study published online Oct. 10 in JAMA Surgery.

Todor Krastev, M.D., Ph.D., from the Maastricht University Medical Center in the Netherlands, and colleagues matched 287 patients with 300 affected breasts receiving AFT between 2006 and 2014 to 300 nonexposed control patients based on age, type of oncologic surgery, tumor invasiveness, and disease stage. AFT patients were followed for a mean of 9.3 years, including 5.0 years following AFT; control patients were followed for a mean of 8.6 years after primary surgery.

The researchers identified eight locoregional recurrences in the treatment group and 11 among the control group, for an unadjusted hazard ratio of 0.63 (95 percent confidence interval, 0.25 to 1.60; P = 0.33). In relevant subgroups based on the type of oncologic surgery, tumor invasiveness, or pathologic stage, there were no increased locoregional recurrence rates. With respect to distant recurrences or breast cancer-specific mortality, no increased risks were detected with AFT.

“In line with reported rates from other published matched cohorts, there is no clinical evidence so far to suggest that AFT leads to increased rates of cancer relapse in patients with breast cancer,” the authors write.

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Posted: November 2018

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Pancreatic cancer death rates rising across Europe, report reveals

Pancreatic cancer death rates in the European Union (EU) have increased by 5% between 1990 and 2016, a report launched today reveals. This is the highest increase in any of the EU’s top five cancer killers which, as well as pancreatic cancer, includes lung, colorectal, breast and prostate cancer.

‘Pancreatic Cancer Across Europe’, published by United European Gastroenterology (UEG) to coincide with World Pancreatic Cancer Day, examines the past and current state of pancreatic cancer care and treatment, as well as the future prospects, such as targeting the microbiome, for improving the prognosis for patients. Whilst lung, breast and colorectal cancer have seen significant reductions in death rates since 1990, deaths from pancreatic cancer continue to rise. Experts also believe that pancreatic cancer has now overtaken breast cancer as the third leading cause of death from cancer in the EU.

Pancreatic cancer has the lowest survival of all cancers in Europe. Responsible for over 95,000 EU deaths every year, the median survival time at the point of diagnosis is just 4.6 months, with patients losing 98% of their healthy life expectancy5. Often referred to as ‘the silent killer’, symptoms can be hard to identify, thus making it difficult to diagnose the disease early which is essential for life-saving surgery.

Despite the rise in death rates and dreadfully low survival rates, pancreatic cancer receives less than 2% of all cancer research funding in Europe. Markus Peck, UEG expert, explains, “If we are to take a stand against the continent’s deadliest cancer, we must address the insufficient research funding; that is where the European Union can lead the way. Whilst medical and scientific innovations have positively changed the prospects for many cancer patients, those diagnosed with pancreatic cancer have not been blessed with much clinically meaningful progress. To deliver earlier diagnoses and improved treatments we need to engage now in more basic as well as applied research to see real progress for our patients in the years to come.”

Microbiome—the key to turning the tide?

After forty years of limited progress in pancreatic cancer research, experts claim that new treatment options could finally be on the horizon as researchers investigate how changing the pancreas’ microbiome may help to slow tumour growth and enable the body to develop its own ‘defence mechanism’. The microbial population of a cancerous pancreas has been found to be approximately 1,000 times larger than that of a non-cancerous pancreas and research has shown that removing bacteria from the gut and pancreas slowed cancer growth and ‘reprogrammed’ immune cells to react against cancer cells.

This development could lead to significant changes in clinical practice as removing bacterial species could improve the efficacy of chemotherapy or immunotherapy, offering hope that clinicians will finally be able to slow tumour growth, alter metastatic behaviour and ultimately change the disease’s progression.

Professor Thomas Seufferlein, pancreatic cancer expert, comments, “Research looking at the impact of the microbiome on pancreatic cancer is a particularly exciting new area, as the pancreas was previously thought of as a sterile organ. Such research will also improve our understanding of the microenvironment in a metastatic setting and how the tumour responds to its environment. This will inform the metastatic behaviour and ultimately alter disease progression.”

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Cancer-stricken mother, 40, claims the NHS is ‘leaving her to die’

Mother, 40, battling breast cancer is frantically trying to raise £90,000 for a life-extending drug in the US after claiming the NHS is leaving her to die

  • Emma Shaw was diagnosed with secondary triple negative breast cancer
  • Diagnosis is terminal, with doctors saying she has just a year left to live
  • She claims the NHS will not provide potentially life-saving treatments
  • Hopes to be treated with a drug in the US that is not available on the NHS 

A mother has been forced to raise £90,000 for a life-extending drug after claiming the NHS is leaving her to die.

Emma Shaw, 40, from Rothley, Leicestershire, was diagnosed with secondary breast cancer in August – just nine months after being given the ‘all clear’ from the disease.

The tumours have since invaded her liver, with doctors giving her just a year to live. 

Due to her type of cancer – triple negative breast cancer – and her terminal diagnosis, Ms Shaw claims the NHS will only provide palliative chemotherapy rather than life-prolonging treatment.

But the mother-of-one is refusing to give up and is determined to show her eight-year-old son Theo that his ‘mummy tried her best to see him grow up’.

After researching her options online, Ms Shaw is fundraising £90,000 in the hope of receiving a drug in the US that is not routinely available on the NHS.

Emma Shaw has been forced to raise £90,000 for a life-extending drug after claiming the NHS is leaving her to die. She is pictured with her son Theo, eight, before being diagnosed with breast cancer last March. It then spread to her liver and she has been given just a year to live

Pictured after undergoing chemotherapy, Ms Shaw claims the NHS has told her there is nothing they can do to treat her triple negative breast cancer given the fact it is terminal. But she is determined not to give up and wants to show Theo she fought hard to see him grow up 

Pictured with her boyfriend Darren, Ms Shaw accepts her cancer cannot be cured but wants to be around for as long as possible. She is fundraising to get the drug Keytruda in the US, which is not routinely available on the NHS. It stops cancer cells from hiding from the immune system

Other patients battling different types of cancer have previously raised money to access the drug, called pembrolizumab, privately in the UK.

Speaking of her diagnosis, Ms Shaw said: ‘Being told your only option is to die is awful, I am still having chemotherapy with the NHS but no one is sure if this will shrink the cancer or keep me stable.

‘The NHS staff at Leicester Royal Infirmary were amazing the first time I was diagnosed last March but the second time around you feel like you’re just forgotten and there’s no hope for the future.

‘I’m too young to just accept that I have just months left to live so I’m clinging onto hope.’

Ms Shaw is raising money towards paying for the drug Keytruda (pembrolizumab), which prevents cancer cells from hiding from the immune system so it can attack them.    

In June this year, NHS England announced it would be making the drug more routinely available – but only for lung cancer that has spread.  


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‘I’m not blaming the NHS as I know they have procedures to follow but it’s just so scary fighting this alone,’ Ms Shaw said.

‘There’s so many people who are going through the same horrendous ordeal as me, I wake up every day shaking with anxiety.

‘Every second of every day I feel terrified that I’m going to die and that I can’t get help here.’

Ms Shaw is hoping the money she raises will cover her travel costs to the US, as well as her treatment, which she expects she will require for the rest of her life.   

‘America is very much ahead of their game when it comes to treatment but it comes at a very big price,’ she said.

‘I can’t put a cost on my life and time with Theo, so I am determined to make this work so at least I can say I tried.

‘Theo needs to see his mummy trying to fight this awful disease. I also hope my story shows other women there are other options when the NHS can’t help.

‘I don’t want anyone to think I’m being negative about the hospital I have been treated at as they’re amazing, it’s just a shame they don’t offer anymore options when it’s secondary.’

Pictured recently with Theo, Ms Shaw claims she wakes up every day ‘shaking with anxiety’ that she may die at any moment. With her terminal diagnosis, she feels ‘forgotten’ by doctors

Pictured this year with Darren and Theo, Ms Shaw says she is too young to accept life is over

WHAT IS KEYTRUDA? AND IS IT AVAILABLE IN THE UK?

Keytruda (pembrolizumab) is an IV immunotherapy that works with a cancer patient’s immune system to help them fight the disease.

It does this by blocking PD-L1 on the surface of cancer cells. This takes the brakes off the immune system, setting it free to attack cancer cells.  

Keytruda, developed by Merck, has been approved by the FDA to treat the following cancers:

  • Advanced melanoma
  • Advanced non-small lung
  • Head and neck squamos cell
  • Classical Hodgkin lymphoma
  • Primary mediastinal B-cell lymphoma
  • Bladder and urinary tract 
  • Advanced stomach
  • Advanced cervical 
  • Those with a ‘DNA mismatch repair’, which can include breast 

In the US, Keytruda – injected twice a week – can be used in adults or children with any of the above cancers that cannot be surgically removed or have progressed following treatment. 

In June 2018, NHS England announced the drug will be routinely available on the health service for patients with lung cancers that have spread. It can already be dished out for patients with melanoma or Hodgkin lymphoma.

Studies show the drug can shrink different types of tumours and boost a patient’s response to other treatments.  

But Keytruda can also cause the immune system to attack healthy organs and tissue, which can be life threatening. Complications may include colitis, hepatitis or kidney failure. 

Source: Keytruda.com

Ms Shaw was told her breast cancer had returned and spread to her liver in August after being diagnosed with pneumonia.

Doctors scanned her lungs and the surrounding areas to assess the infection, only to discover her cancer had come back. 

‘I felt really unwell as soon as I got back from holiday,’ she said. ‘I couldn’t believe it when I was told my cancer was back.

‘I’d had a lumpectomy after my first diagnosis the year before but having a mastectomy now isn’t an option as the cancer is so aggressive.

‘It has been a whirlwind ever since but, despite it all, I have tried to enjoy as much time with my son, Theo, and boyfriend, Darren, as possible.’

After starting her fundraising page last week, Ms Shaw has already raised more than £19,000.

‘I’m so grateful to everyone who has already donated,’ she said.

‘I am hoping I’ll be able to go to America at the start of next year for the immunotherapy treatment.

‘It won’t cure me but it could make my cancer stable.’ 

NHS England and NICE have both been approached for comment.  

She claims she cannot put a cost on her life or her remaining time with Theo, which motivates her to keep fundraising so she can ‘at least say she tried’. They are pictured this year 

Ms Shaw celebrated her ‘last’ chemo session for triple negative breast cancer on September 12 last year. Months later she was given the all clear, only to discover it had returned and invaded her liver last August while being treated for pneumonia. She is pictured with her parents

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Cancer May Soon Replace Heart Disease as Leading Killer of Affluent Americans

MONDAY, Nov. 12, 2018 — Cancer is expected to overtake heart disease as the leading cause of death for well-off Americans by 2020.

The expected shift owes to advances in technology and drugs that are making big headway against heart disease, according to a new report.

But lack of access to quality care is likely to keep heart disease the leading killer of poorer folks in the United States, the researchers said. The change may also happen more slowly in poorer counties where risks for heart disease and death rates are higher.

“Recent data over the last two decades suggests that the U.S is in the midst of a new epidemiological transition within chronic disease, as the leading cause of death moves from heart disease to cancer,” said lead researcher Dr. Latha Palaniappan. She is a professor of medicine at Stanford University School of Medicine in Stanford, Calif.

Better prevention and treatment throughout the 20th century caused deaths from chronic disease to overtake those from infections, the study authors noted.

“Significant advances in cardiovascular disease prevention and treatment have enabled heart disease mortality rates to decrease for all populations in recent decades, but those in poorer areas may not transition as quickly,” Palaniappan said.

For the study, the researchers looked at U.S. death records from 2003 to 2015.

Overall, death rates dropped about 1 percent per year. Deaths from heart disease fell nearly 3 percent per year, while cancer deaths decreased by about 1.5 percent per year, the findings showed.

Although deaths from heart disease during the study period fell 28 percent, the drop was more significant in high-income counties than in poorer ones — 30 percent versus 22 percent, the investigators found.

This difference suggests the change from heart disease to cancer as a leading cause of death will take longer in poorer areas.

The transition is complex, and large overlaps exist in risk factors for these chronic diseases, the study authors said. In addition, socioeconomic, geographic, demographic and political factors could influence the speed of the transition, they added.

The report was published Nov. 12 in the Annals of Internal Medicine.

In 2016, in the United States, heart disease claimed more than 635,000 lives and cancer took nearly 600,000, according to the U.S. Centers for Disease Control and Prevention.

Accidents, the third-leading cause of death, claimed a little more than 160,000 lives.

A researcher in Switzerland who co-authored an editorial that accompanied the study attributes the change to people living longer.

“The shift … is mainly due to population aging and larger declines in age-specific mortality from cardiovascular and respiratory diseases among the elderly, especially among those socioeconomically better off,” said Silvia Stringhini. She’s a research associate at the Institute of Social and Preventive Medicine at Lausanne University Hospital.

Stringhini added that the cost of new cancer treatments and genetic testing may contribute to “inequalities” in cancer deaths, as rich patients are more likely to get advanced care than poor patients.

More information

For more about causes of deaths in the United States, visit the U.S. Centers for Disease Control and Prevention.

Posted: November 2018

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Obesity both feeds tumors and helps immunotherapy kill cancer

A groundbreaking new study by UC Davis researchers has uncovered why obesity both fuels cancer growth and allows blockbuster new immunotherapies to work better against those same tumors.

The paradoxical findings, published today in Nature Medicine, give cancer doctors important new information when choosing drugs and other treatments for cancer patients.

“It’s counter-intuitive because up to this point all of our studies showed that obesity resulted in more toxicities associated with immunotherapy treatments,” said William Murphy, a co-last author of the study and vice chair of research in the UC Davis Department of Dermatology. “This is a game-changer because when we personalize medicine and look at body mass index, in some situations it can be bad, and in some situations it can be helpful.”

Obesity, which is reaching pandemic levels and a major risk factor for many kinds of cancer, also is known to hasten cancer growth, promote cancer recurrence and worsen chances of survival. Obesity also is associated with impairment of the immune system. Previous studies of the use of immune-stimulatory immunotherapies have demonstrated that in obese animal models and in humans, these drugs overstimulate the immune system and cause serious side effects.

The research, which involved studies using animal models and human patients, analyzed the effect of a different class of immunotherapies called checkpoint inhibitors. These drugs work by blocking pathways called immune checkpoints that cancers use to escape the immune system. They include drugs like Keytruda (pembrolizumab), which have dramatically improved survival in many lung cancer and melanoma patients. In the current study checkpoint inhibitors had a different effect than other immunotherapies, and in fact, resulted in better survival in those who are obese than in those who are not.

Why this happens, they discovered, relates both to the effect that obesity has on the immune system and to the way that checkpoint inhibitors do their jobs.

Cancers can cause increased expression of checkpoint proteins that keep T cells in check, preventing them from attacking cancer cells. Checkpoint inhibitors block those proteins, in effect releasing the immune system’s brakes so that the T cells can go after cancer cells.

The research team discovered that because obesity also causes suppression of the immune system and increased expression of checkpoint proteins, the action of checkpoint inhibitors is enhanced in animal models and humans who are obese.

https://youtube.com/watch?v=o_Dw09YXvBs%3Fcolor%3Dwhite

They first studied the differences in T-cell function in obese and non-obese mice and found that T-cell function was diminished and the expression of the PD-1 protein on the T-cells was higher than in the non-obese control mice. They saw a very similar pattern when the same studies were done in both macaque monkeys and in human volunteers.

Additional studies also found that tumors grew more aggressively in obese mice, regardless of tumor type.

“In obese animals cancer grows faster because there are more nutrients for tumors and because the immune system is more suppressed,” said Murphy.

Drilling down, Murphy and his colleagues also found that the T-cell dysfunction was driven in part by leptin, a weight-regulating hormone produced by the body’s fat cells. The research showed that increased leptin levels in obese mice and humans also correlated with increased expression of PD-1 checkpoint protein.

When obese mice with tumors were given checkpoint inhibitors designed to block the action of PD-1, they survived significantly longer than the non-obese control mice in the study. A study involving 251 patients with melanoma who were treated with checkpoint inhibitors also found marked improvements in the clinical outcomes of obese patients that were not observed in non-obese patients.

“Overall these findings suggest that obesity may be a very important biomarker for response to checkpoint inhibitor immunotherapy,” said Arta Monjazeb, associate professor in the UC Davis Department of Radiation Oncology and co-last author on the study. “We are not advocating for obesity as improving prognosis for cancer patients. But obesity appears to induce immune suppression and accelerated tumor growth through mechanisms that can be successfully reversed by checkpoint inhibitor immunotherapy.”

Murphy cautioned that while the findings are an important step in better targeting immunotherapies, there are many other factors that likely influence how effective a certain drug will be for a given patient. Those may include gender, the type of diet consumed, their individual microbiome and the timing of their treatment.

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Decrease in specific gene ‘silencing’ molecules linked with pediatric brain tumors

Experimenting with lab-grown brain cancer cells, Johns Hopkins Medicine researchers have added to evidence that a shortage of specific tiny molecules that silence certain genes is linked to the development and growth of pediatric brain tumors known as low-grade gliomas.

A report of the findings was published this fall 2018 in Scientific Reports, and supports the idea of increasing levels of microRNAs as a potential means of treating these tumors.

An estimated 1,600 cases of pediatric low-grade gliomas (PLGGs) are diagnosed annually in the United States, and the vast majority of these slow-growing tumors are treatable and curable mainly by surgical removal, although in some cases surgery has the potential to damage critical nearby brain tissue, depending on tumor location. Unlike high-grade glioblastomas such as the one that took the life of Arizona Senator John McCain, PLGGs mostly affect school-age children and young adults.

“It has long been known that microRNAs play a role in controlling various tumor properties such as growth,” says Fausto Rodriguez, M.D., associate professor of pathology at the Johns Hopkins University School of Medicine and the study’s senior author.

“Our findings identified a subset of microRNAs that, in sufficient quantity, seem to decrease the growth and invasion of cancerous cells in pediatric low-grade gliomas.”

MicroRNAs are tiny molecules that, in ways similar to how an orchestra conductor controls the flow of each instrument group, command the expression of entire gene networks that make proteins by essentially silencing them, and are responsible for regulating biological processes such as nutrient intake, cell growth and cell death. Altered levels of specific microRNAs can disrupt entire biological pathways just as a misguided section of an orchestra can unsettle an entire score.

“One microRNA can target multiple genes and have a profound effect on cell processes, and the alterations are dynamic,” notes Rodriguez, who says PLGGs are good candidates for analyzing microRNA types and levels because genetically PLGGs are stable compared with other tumors. That makes it relatively easier, he says, to identify any relevant genetic abnormalities and potential targets for therapy.

For the new study, the researchers first analyzed previously gathered microRNA subtype data in two studies. They examined tumors from 125 patients with low-grade gliomas for levels of a specific microRNA, known as miR-125b, using chromogenic in situ hybridization (CISH), a technique that is applicable to routinely processed tissue in pathology and allows for identification of specific microRNAs in the cells of interest. Levels of this microRNA were lower in 43 pilocytic astrocytomas (the most common subtype of PLGG) when compared with 24 diffuse astrocytomas and normal brain tissues.

Rodriguez and the research team next looked at eight cancerous cell lines derived from brain (glial) tumors in children for levels of microRNA 125b-p using a method that can rapidly make thousands to millions of copies of a genetic sequence for easier analysis of how much of a gene is expressed. Although levels of microRNA 125b-p varied across the lab-grown cell lines, they were significantly and uniformly lower in cancerous cell lines than noncancerous cell lines, Rodriguez reports.

In further experiments designed to identify the role of these microRNAs in cell growth, the investigators increased levels of miR-125b in cancerous cell lines by introducing a DNA segment in the tumor cells using specific viruses, and saw a decrease in cell division and growth. To check whether cell death contributed to this decrease in cell growth, Rodriguez stained cells containing high levels of microRNA 125b and noted cell death in all cell lines, suggesting that increasing levels of microRNA 125b can stop the growth of PLGG.

“These findings are an example of where advances in precision medicine might take us, and show how, someday, increasing levels of specific genes and microRNAs might be a targeted treatment for PLGGs,” says Rodriguez.

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Yoga and meditation is growing on Americans: Report

Yoga and meditation have been shown to provide physical and mental health benefits, and it seems that people are catching on to that fact, as a new report shows that more adults and children have been practicing the two over the last five years.

Between 2012 and 2017, the number of adults practicing yoga rose from an estimated 9.5 percent to 14.3 percent, according to the report from the Centers for Disease Control and Prevention National Center for Health Statistics. Yoga was the most common form of complementary medicine reviewed. However, meditation saw the most drastic rise in use, with 4.1 percent of adults practicing it in 2012 versus 14.2 percent in 2017.

While adults were found to practice yoga and meditation the most, a separate report said that children were also taking part at an increasing rate. From 2012 to 2017, the number of children ages 4 to 17 doing yoga rose from 3.1 percent to 8.4 percent. Similarly, the number of kids who meditated rose from 0.6 percent to 5.4 percent.

“Yoga and meditation are practices which can make you feel better, improve your overall health and are generally safe,” said Dr. Anton Borja, Medical Director of Integrative Oncology at The Ohio State University Comprehensive Cancer Center. People who practice them,

Complementary medicine includes a variety of medical approaches that are not typically part of conventional medicine but are used in addition to it.

Though they can be practiced by anyone, Borja said that for patients diagnosed with a serious illness — who might be more inclined to feel helpless about their health — they can be useful tools to help patients “take back into their own hands some control over their health.”

With regard to meditation, for example, it’s “been shown to help improve anxiety and depression and help to control pain, including chronic lower back pain,” Borja said. “People who practice yoga and meditation have indicated a general feeling of improved health and wellbeing.”

According to the Mayo Clinic, yoga is able to reduce stress, improve fitness and help people manage chronic conditions. Meditation helps people to gain a new perspective on stressful situations, focus on the present and reduce negative emotions.

If you think yoga or meditation would be a good addition to your overall health care, talk to your doctor.

Dr. Anna Jackson is a psychiatry resident at Vanderbilt University Medical Center and a member of the ABC News Medical Unit.

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First-ever prostate cancer treatment uses gold nanoparticles to destroy tumorous cells

A small clinical trial using gold nanoparticles that act as tumor-seeking missiles on a mission to remove prostate cancer has begun at The University of Texas Health Science Center at Houston (UTHealth). It is the first trial of its kind in the world.

The nanoparticles, or nanoshells, are made of small layers of silica glass formed into a sphere and wrapped in a thin layer of gold. The shells seek out and saturate cancerous cells, and their advanced vibrational properties are then harnessed to cause the tumorous tissue to pulse with extreme temperature when light is applied through a laser specifically designed to excite the particles. The oscillation kills the cancer cells while preserving the healthy tissue, avoiding the nerves and urinary sphincter. This procedure is the first in the world that is precise enough to potentially avoid negative ramifications like urinary incontinence or sexual impotency.

“This therapy could be life-changing for men diagnosed with prostate cancer and I’m honored to be among the first doctors the U.S. Food and Drug Administration approved to put it to the test,” said Steven Canfield, M.D., chair of the division of urology at McGovern Medical School at UTHealth, who recognized the possibility of the nanoparticles to treat prostate cancer and helped developed the trial to test the theory.

Prostate cancer begins when cells in a man’s prostate gland mutate and start to grow uncontrollably. Other than skin cancer, prostate is the most common cancer in American men, with an estimated 1 out of 9 men diagnosed. The American Cancer Society estimates 29,430 men died from the disease in 2018 alone.

Treatment options have traditionally included radical prostatectomy, which is the removal of the prostate gland and some of the tissue around it, radiation therapy and cryotherapy, among others. These methods carry the potential to have a negative impact on urinary function and sexual performance.

“The side effects of current prostate cancer treatments can be extremely traumatic. This new technology holds the potential to eliminate those life-altering effects, while still removing the cancer tissue and reducing hospital and recovery time,” Canfield said. “In fact, the first patient in the trial was actually riding a bike within a week of his treatment. The fusion of MRI and ultrasound imaging technology that we use to accurately identify and diagnose the cancer, combined with the extreme precision of the gold nanoshells in targeting the diseased cells, allows us to be incredibly accurate at obliterating them. I am excited as we continue tracking the progress of this groundbreaking improvement to prostate cancer care.”

Doug Flewellen, the first patient in Texas to receive the new method of care, says for him, the procedure was a no-brainer.

“No man wants to go through radical removal, and I knew active monitoring could have potentially aggravated the cancer,” Flewellen said. “The side effects of traditional treatment were not worth it to me, and I wasn’t afraid to try the most cutting-edge technology. Looking back, the experience was even better than I was expecting, and I hope to see nanoparticle therapy advance into an option for anyone diagnosed with prostate cancer in the future.”

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Should we be afraid of cancer from the mobile phone, if you are a male rat?

In connection with the completion of a major study on mobile phone cancer risk news headlines exploded with reports on the subject. Given that the study provoked a barrage of information, was not conducted on humans and used the specific type of radiation, the proposed deal that really shows this scientific work and what we can expect from their phones.

The national toxicology program (National Toxicology Program NTP) presented the final reports on the studies of the effect of radio frequency (RFID) used in mobile phones 2G and 3G, in rats and mice.

Scientists have subjected their experimental radiation exposure within two years, nine hours a day. The results of more than a decade of research has shown that strong RF exposure associated with the development of tumors. Have been provided:

  • Compelling evidence linking RFID and tumors (malignant sannam) in hearts of male rats;
  • Some evidence of connection with tumors (malignant gliomas) in the brain of male rats;
  • Some evidence of benign and malignant tumors in the adrenal glands of male rats;
  • Ambiguous (unclear) evidence linking observed in the study of tumors in female rats and mice of both sexes.

The exposure used in the studies cannot be directly compared with the impact that people experience when using a mobile phone. In our studies, rats and mice received radio-frequency radiation throughout the body. On the contrary, people are mostly exposed to certain tissues near the place where they hold the phone. In addition, exposure levels and duration in our study was higher than people, explained John Bucher (John Bucher), doctor of philosophy, senior researcher of the NTP.

Health magazine columnist , Forbes argues that it makes no sense to panic if you are not male rats. In addition to the above reservations, it should be noted that the study used the radiation, which was used only for early models of mobile phones which now practically are not applied. Also noteworthy is the fact that strong evidence that RFID causes cancer in female rats and mice that were not received.

However, to reduce exposure to RF radiation, people should take precautions:

  • Keep the cell phone away from the head and body;
  • Do not place the phone near me while sleeping;
  • Use, whenever possible, speakerphone or headset;
  • Avoid using mobile phone when the signal is weak. In this case, because of the constant attempts to connect, RFID enhanced;
  • Do not use your mobile phone to download large files or streaming video. This also leads to increased RFID;
  • Before buying, carefully study the label and information about models by phones. Different devices may have different levels of RFID;
  • Do not wear the headset when not in call;
  • Put the phone in airplane mode or even turn off, if possible;
  • Skeptical about protective screens and other devices that are positioned as reducing RFID;
  • Try as little as possible to use the phone. Shorten the length of your calls, communicate face to face.

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Cryo-electron microscope bears fruit in its first year: Structure and mechanism of the 5-HT3 receptor

In November 2017, a Titan Krios cryo-electron microscope (cryo-EM) was inaugurated at the ESRF, the European Synchrotron, France. Data collected on this cryo-EM features in a Nature publication describing the activation cycle of a serotonin receptor, which is targeted by medication against chemotherapy- and radiotherapy-induced nausea.

“This publication is a true reward for us: the first one in less than a year from inauguration and we hope this kind of rewards will grow in number,” explains Isai Kandiah, ESRF scientist who runs the facility. “It shows the revolution that cryo-EM is leading in structural biology,” she adds. Thanks to cryo-EM, researchers can now freeze biomolecules, including membrane proteins of high medical importance, in several different conformations in action and visualise each of these to atomic resolution. Cryo-EM thus allows researchers to produce snapshots revealing the dynamics of proteins when they interact with other molecules, information that is crucial both for a basic understanding of life’s chemistry and for the development of pharmaceuticals.

The research in Nature is a result of an international collaboration of scientists from the Institute of Structural biology (IBS-mixed research unit CEA-CNRS-University Grenoble Alps), the Institut Pasteur, the University of Lorraine (France), the University of Copenhagen (Denmark), the University of Illinois (US) and the biotech company Theranyx. The focus of the paper, featuring data from the ESRF cryo-EM, is the activation cycle of the 5-HT3 receptor, belonging to the family of serotonin receptors. These receptors are well known because they influence various biological and neurological processes such as anxiety, appetite, mood, nausea, sleep and thermoregulation, among others. Unlike the other serotonin receptors, which are G protein-coupled receptors, 5-HT3 is a neurotransmitter-gated ion channel and changes its conformation during activation. It is present in the brain, as well as in the enteric nervous system, the peripheral nervous system that drives the digestive tract.

5-HT3 is a target for drugs and pharmaceutical companies have studied it extensively. When patients undergo chemotherapy and/or radiotherapy, they often suffer from nausea and vomiting as side effects. In fact, the chemicals used in cancer treatment trigger an elevation of serotonin signalling, which in turn activates 5-HT3 to open its ion channel, which then causes nausea.

“The receptor has been widely studied due to its importance, but it hasn’t been until recently, that we have accessed it at the atomic scale, thanks to cryo-electron microscopy, among other techniques,” explains Hugues Nury, main author of the paper and CNRS scientist at the IBS.

The results published in Nature show the receptor 5-HT3 in four different conformations. Images of three of these were obtained at the Center for Cellular Imaging and Nano Analytics in Switzerland whilst the fourth, which finally allowed a full understanding of the activation mechanism of 5-HT3, was obtained at the ESRF. One of the conformations is inhibited thanks to the binding of anti-nausea and anti-vomiting drug widely used in chemotherapy. The images obtained of the receptor may therefore lead to the design of more efficient antinausea drugs for the treatment of patients undergoing therapy for cancers.

“These results contribute to our knowledge on how 5-HT3 receptors behave. They provide a framework for the myriad of mutations described in the literature: we can now look where they are, what are the motions in these zones, and sometimes why the mutations altered the receptor function. Now we also see the binding pockets in unprecedented details, which can help the development of future drugs,” explains Hugues Nury.

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