Expert Perspectives: Addressing Frontline Practice Challenges in the Management of Multiple Myeloma

Getting 'less worse' - to paraphrase an old professor of mine...

This is how you "bend down the cost curve" in the place formerly known as England...

No surgury today?  Cost saved!

3,000 ops cancelled as demand rises

More than 3,000 operations have been cancelled by the NHS in the first two weeks of this month as an "unprecedented demand" takes its toll.0
  • Shafi Ahmed, the first UK surgeon to broadcast online a live surgical procedure using Google Glass eyewear, warned of unprecedented demand on the NHS
    Last updated: 28 December 2014, 18:07 GMT
    More than 3,000 operations have been cancelled by the NHS in the first two weeks of this month as an "unprecedented demand" takes its toll.
    Figures show 3,113 elective operations were cancelled in that period, up by almost half since 2012.
    In terms of operations classed as urgent 161 were cancelled in the two-week period, with some having been cancelled twice or more.
    The figures, highlighted by Labour, show the repercussions of A&E departments under severe stress and a lack of beds for patients in need, a consultant and member of the Royal College of Surgeons said.
    Shafi Ahmed said: "There is currently unprecedented demand on the NHS resulting in more cancellations of planned surgical operations.
    "As a practising surgeon, looking after cancer patients, it is very difficult to have to tell a patient who has prepared themselves for a major procedure that their operation has been cancelled for non-clinical reasons.
    "To reduce pressures on hospitals and to keep a flow of patients coming in and leaving hospital, we need to manage the number of available beds more efficiently. To achieve this, we need to reduce unnecessary admissions and visits to A&E and improve community care.
    Mr Ahmed said improvements are also required regarding discharge arrangements, to avoid patients staying in hospital longer than necessary, and called for ring-fencing of beds for high dependency care to be considered.
    Labour's shadow health secretary Andy Burnham said: "This is yet another sign that, under David Cameron, the NHS is simply not working.
    "Standards of patient care are slipping by the week and now more and more people get ready for an operation only to face a last minute postponement.
    "The chaos in A&E is spreading through the NHS. Hospitals are in danger of becoming overwhelmed as the Government takes social care away from older people and makes it harder to see a GP. These cancellations help to explain why operation waiting lists are at a six-year high."
    He pledged Labour would invest an extra £2.5 billion in the NHS each year, resulting in 20,000 more nurses and 8,000 GPs.
    The Department of Health told the Sunday Times the figures show "the proportion of cancelled operations remains remarkably stable over many years", adding that more operations are being carried out amid an ageing population.

Myeloma patients could soon benefit from targeted therapy |  City of Hope Breakthroughs

Myeloma patients could soon benefit from targeted therapy |  City of Hope Breakthroughs

Many cancer patients have benefited from targeted therapy – medications that can identify cancers by their genetic properties and help eradicate them – but such therapy has been largely a pipe dream for multiple myeloma patients. Until now.
New drugs could provide targeted therapies to patients with multiple myeloma.
Currently, two medications are emerging as especially promising in the treatment of multiple myeloma: daratumumab and SAR650984. Each of the drugs  target different  sites on the same receptor for multiple myeloma.  Each was the subject of research presented at the annual meeting of the American Society of Hematology.
The drugs are offering new hope to patients who have already tried many other therapies with less-than-ideal results.  “The most important thing is that these are targeting the patients who have high-risk disease who have been refractory to the other agents we’ve had standardly available,” said  Amrita Y. Krishnan, M.D. FACP, director of the Multiple Myeloma Program at City of Hope. “To see responses in these very advanced patients is extremely compelling.”
Data supporting the drugs’ effectiveness has been building, and Krishnan expects it to continue to develop in the coming year.
Because the drugs have different targets, if a patient does not respond to one of them, the other may prove beneficial.
“This is going to be a very interesting question as time goes on,” she said. “Right now, I don’t think we have enough to be able to pick out a patient who is going to respond to one compound versus the other.”
Myeloma is a cancer of the plasma cells, which normally produce anitibodies to help fight infections. Ultimately, it can interfere with production of normal blood cells and cause serious complications in bones and kidneys. When these cancerous cells form tumors throughout the body, it is classified as multiple myeloma. One of the treatments for the diseases, beyond chemotherapy and radiation, is stem cell transplantation.

Who could have seen this coming???

Centralised healthcare doesn't work efficiently.

While I was away last week, Vermont decided to scuttle its single-payer health-care plans. I predicted as much six months ago, for one simple reason: A single-payer system would cost too much. When faced with the choice of imposing double-digit payroll taxes or dropping his cherished single-payer plan, the governor of Vermont blinked.
"But Megan!" I hear you cry. "Single-payer systems are cheaper, not more expensive! Look at Europe!"
Alas, however, as I wrote at the time, there is nothing about single payer that will magically allow us to cut costs to European levels. People who believed otherwise were substituting a crude eyeballing of international statistics to substitute for reasoned analysis, in part because it told them what they wanted to be true: that they could have the universality and progressiveness of a single-payer system without having to ask the taxpayer for a giant heap of money to provide those benefits. They were, in the words of one of my favorite public-policy professors, "getting high on their own supply."
Now, I know what you are preparing to say: I am allowing my ideological priors to blind me to the plain evidence in front of my nose. So let me explain. I concede that single-payer systems may well allow you to control the rate of health-care cost growth, thanks to government price controls on supplies and services, along with rationing or denial of expensive treatments. What it doesn't allow you to do is easily cut the rate of health-care spending. None of the single-payer systems that are frequently held up as models for the U.S. have ever managed sustained cuts in health-care spending. All they've done is prevent it from growing so fast.
The problem, as I wrote previously, is that America doesn't have a health-care cost-growth problem; we had a health-care cost-growth problem. Right now, our health-care cost growth is right in the middle of the OECD pack:
Our spending is indeed high compared with the rest of the world, but that's because it started high. And while restraining government spending is easy, it is a walk in the proverbial (government-funded) park compared to actually cutting spending. Cutting spending means that a number of people are going to lose income and employment. They will have trouble paying their mortgages, car loans and little Johnny's bill for travel soccer. Then they are going to get organized and march on Washington and vote against the politicians who cut their jobs.
Path dependence is a running theme around here, and in no other area of public policy is it more troublesome. Health-care jobs are steady and well-remunerated compared to whatever else those workers could be doing. And that's not just true of the much-derided "specialists" who do too many procedures and charge too much; it's true of everyone in your hospital and doctor's office, from your beloved family physician to the woman who draws your blood. All those people have spent long years working to get where they are. If you suddenly change the rules and take that all away, their rage will burn with the righteous fire of a thousand suns.
So even if we could have had a much cheaper health-care system if we moved to single payer in 1970, that doesn't mean that we can get the same happy results by doing so now. Today we'd be building a single-payer system with the price schedule of our current health-care workers. Which means it would cost an absolutely breathtaking amount of taxpayer money, as Vermont just found out.
Oh, Vermont has some special problems -- a small state loses some of the ability to rationalize the system that the federal government would have because it has to deal with border issues, such as commuters and what to do about a Vermont citizen who has to get treatment in a New Hampshire hospital. But that doesn't seem to have been the biggest problem Vermont faced. Mostly, it faced the impossible choice between cutting provider incomes by a lot or raising taxes to nosebleed levels.
This holds a lesson for all the folks who hoped or feared that Obamacare was a stalking horse for single payer. It's not. First, because if you try to take away the current system from the vast majority of folks who had health insurance they liked before the Affordable Care Act was passed, your voter base will get hopping mad enough to enter low-earth orbit. And second of all, even if you're willing to brook their rage over the loss of their health insurance, combining that with a whopping great tax hike on the middle class is a recipe for political suicide.
The U.S. health-care system may be all kinds of screwed up. But at least at this late date, single payer is not the cure for what ails it.
To contact the author on this story:
Megan McArdle at

Well, this pisses me off...

Hope crashed...

TOKYO (AP) — The Japanese researcher whose claim of a major breakthrough in stem cell research was discredited resigned after the government lab where she worked failed to replicate her results.
Haruko Obokata said in a statement Friday that she was leaving the Riken Center for Developmental Biology after the lab concluded the stem cells she said she had created probably never existed. The center said it had stopped trying to match Obokata's results.
"Now, I am just exhausted. For the results to end this way is just perplexing," she said.
Obokata initially was lauded for leading the research that raised hopes for a discovery of a simple way to grow replacement tissue. But questions about the validity of the research prompted Riken scientists, including Obokata, to retract two scientific papers.
The allegations of research misconduct prompted a shake-up at Riken.

On-Off Switch for Critical Stem Cell Gene Discovered

On-Off Switch for Critical Stem Cell Gene Discovered

  • University of Toronto (U of T) researchers investigating stem cells in mice report for the first time an instance of a relationship between the Sox2 gene, which is critical for early development, and a region elsewhere on the genome that effectively regulates its activity. The discovery could mean a significant advance in human regenerative medicine, as the Sox2 gene is essential for maintainingembryonic stem cells that can develop into any cell type of a mature animal.
    "We studied how the Sox2 gene is turned on in mice, and found the region of the genome that is needed to turn the gene on in embryonic stem cells," said Jennifer Mitchell, Ph.D., of U of T's department of cell and systems biology. She is also the lead investigator of a study (“A Sox2 distal enhancer cluster regulates embryonic stem cell differentiation potential”) published in Genes & Development.
    "Like the gene itself, this region of the genome enables these stem cells to maintain their ability to become any type of cell, a property known as pluripotency. We named the region of the genome that we discovered the Sox2 control region, or SCR," said Dr. Mitchell.
    Since the sequencing of the human genome was completed in 2003, researchers have been trying to figure out which parts of the genome made some people more likely to develop certain diseases. They have found that the answers are more often in the regions of the human genome that turn genes on and off.
    "If we want to understand how genes are turned on and off, we need to know where the sequences that perform this function are located in the genome," continued Dr. Mitchell. "The parts of the human genome linked to complex diseases such as heart disease, cancer, and neurological disorders can often be far away from the genes they regulate, so it can be difficult to figure out which gene is being affected and ultimately causing the disease."
    It was previously thought that regions much closer to the Sox2 gene were the ones that turned it on in embryonic stem cells. Dr. Mitchell and her colleagues eliminated this possibility when they deleted these nearby regions in the genome of mice and found there was no impact on the gene's ability to be turned on in embryonic stem cells.
    "We then focused on the region we've since named the SCR as my work had shown that it can contact the Sox2 gene from its location 100,000 base pairs away," said study lead author Harry Zhou, a former graduate student in Dr. Mitchell's lab, now a student at U of T's Faculty of Medicine. "To contact the gene, the DNA makes a loop that brings the SCR close to the gene itself only in embryonic stem cells. Once we had a good idea that this region could be acting on the Sox2 gene, we removed the region from the genome and monitored the effect on Sox2."
    The researchers discovered that this region is required to both turn Sox2 on, and for the embryonic stem cells to maintain their characteristic appearance and ability to differentiate into all the cell types of the adult organism.
    "Just as deletion of the Sox2 gene causes the very early embryo to die, it is likely that an abnormality in the regulatory region would also cause early embryonic death before any of the organs have even formed," said Dr. Mitchell. "It is possible that the formation of the loop needed to make contact with the Sox2 gene is an important final step in the process by which researchers practicing regenerative medicine can generate pluripotent cells from adult cells."
    “Homozygous deletion of this distal Sox2 control region (SCR) caused significant reduction in Sox2mRNA and protein levels, loss of ES cell colony morphology, genome-wide changes in gene expression, and impaired neuroectodermal formation upon spontaneous differentiation to embryoid bodies,” wrote the investigators. “Together, these data identify a distal control region essential forSox2 transcription in ES cells.”

Remotely controlled magnetic nanoparticles stimulate stem cells to regenerate bones

This looks promising... Wish it existed seven years ago.

Remotely controlled magnetic nanoparticles stimulate stem cells to regenerate bones

24 November 2014 Keele University
Researchers in bone tissue regeneration believe they have made a significant breakthrough for sufferers of bone trauma, disease or defects such as osteoporosis. 
Medical researchers from Keele University and Nottingham University have found that magnetic nanoparticles coated with targeting proteins can stimulate stem cells to regenerate bone. Researchers were also able to deliver the cells directly to the injured area, remotely controlling the nanoparticles to generate mechanical forces and maintain the regeneration process through staged releases of a protein growth stimulant. 
The current method for repairing bone that can’t heal itself is through a graft taken from the patient. Unfortunately, this can be a painful, invasive procedure, and when the area that needs repair is too large or the patient has a skeletal disorder such as there can sometimes be a lack of healthy bone for grafting.
For this reason, spurring the growth of new bone through injected stem cells is an area of great interest to medical researchers. Much progress has been made, but a major hurdle remains – finding an appropriate means to stimulate the differentiation of the stem cells so they become the quality of bone tissue needed in a quantity large enough to treat patients effectively.
James Henstock, PhD led the Biotechnology and Biological Sciences Research Council (BBSRC)-funded study, alongside Professor Alicia El Haj, and colleagues at Keele University’s Research Institute for Science and Technology in Medicine, as well as Kevin Shakesheff, PhD, from the University of Nottingham’s School of Pharmacy.
James Henstock said: “Injectable therapies for regenerative medicine show great potential as a minimally invasive route for introducing therapeutic stem cells, drug delivery vehicles and biomaterials efficiently to wound sites.”
“In our investigation we coated magnetic nanoparticles with specific targeting proteins then controlled them remotely with an external magnetic field to simulate exercise. We wanted to learn how this might affect the injected stem cells and their ability to restore functional bone.”
The team of researchers conducted their test using two models: chicken foetal femurs and tissue-engineered collagen hydrogels. In both instances the results showed an increase in bone formation and density without causing any mechanical stress to the construct or surrounding tissue.

“This work demonstrates that providing the appropriate mechanical cues in conjunction with controlled release of growth factors to these injectable cell therapies can have a significant impact on improving bone growth. It also could potentially improve tissue engineering approaches for translational medicine” Dr Henstock said.

Now on Ello...

No idea what to do with it, but I am on

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What can not be sustained, will not be sustained...

Remember - these schemes ALWAYS run out of money.  There is never enough resources to give away free stuff...

National Health Service bosses have launched a campaign to persuade patients to stay away from hospitals and general practitioners (GPs) this Christmas, and use privately-run pharmacists instead. The NHS's medical director, Professor Sir Bruce Keogh, said the NHS is unable to cope with the "unprecedented" demand on it.

The NHS is one of the world's largest employers and has a budget of around £110,000,000,000 (£110bn) a year. However, staff are asking people who are feeling unwell to go to privately run pharmacists instead of using public sector facilities. Professor Keogh said that a lot of the 'strain' on the public sector facilities could be relieved if people went to said pharmacists.
He told the Daily Mail: "Many of these [chemists] have private consultation rooms where you can get quite good advice". He also said that pharmacies do not generally have long queues, in contrast to NHS hospitals. Keogh said: "You don’t have to wait in a pharmacy... You can generally see someone in a matter of minutes. They can either recommend off-the-shelf treatment or, if appropriate, send you to your GP or to attend A&E."
"Are things going to go on like this? Are we going to have to keep putting more and more sums into the NHS? The answer is it is not sustainable in the long run to say all the extra pressure in the NHS has to be borne by the A&E department."
The government has given the NHS an extra £300m to get over the winter period. Despite the money many hospitals are running at unsafe levels, causing concerns that patients may be put at risk unless demand can be quelled.
One idea being floated is forcing people to pay to use their doctor, despite having already paid for the service through taxation.

Faster please - Scientists Pursue Novel Blood Tests for Cancer

Scientists Pursue Novel Blood Tests for Cancer

The inventor of a breakthrough DNA test for Down syndrome says the technology can be used to screen people for cancer.

By Antonio Regalado on October 31, 2014

The Hong Kong scientist who invented a simple blood test to show pregnant women if their babies have Down syndrome is now testing a similar technology for cancer.

Yuk Ming “Dennis” Lo says screening for signs of cancer from a simple blood draw could cost as little as $1,000. The test works by studying DNA released into a person’s bloodstream by dying tumor cells.

The idea is to create a cheap screening test that people might get annually at a doctor’s office to spot a tumor at its earliest stage, when it’s more easily treated. “It took 13 years to develop the prenatal tests, but the path was untrodden,” says Lo, who is based at the Chinese University of Hong Kong. “Cancer will take a shorter time.”

The prenatal tests work by searching for fetal DNA present in a pregnant woman’s blood. Decoding that DNA can determine whether the baby has too many or too few chromosomes, problems that cause birth defects (see “Too Much Information”).

Both Lo and scientists at Johns Hopkins (see “Spotting Cancer in a Vial of Blood”) recently used a technique nearly identical to the one used in the prenatal tests to demonstrate that they could scan a person’s blood for evidence of genes that are duplicated, missing, or rearranged, something that is a hallmark of cancer cells.

But the testing strategy is very expensive. Tumor DNA is often present in tiny quantities if the cancer is at an early stage. It may account for just 0.01 percent of the DNA fragments in a blood sample. That means scientists end up decoding 9,999 bits of normal DNA for every stretch of cancer DNA they encounter. The result: building up a rough snapshot of the tumor’s genome using sequencing machines can cost $10,000 or more.

“It’s doable, but very expensive,” says Andre Marziali, chief scientific officer of Boreal Genomics, a startup developing cancer tests. “There is a trade-off between the breadth and the cost.”

Lo says he’s now developing a different way to measure DNA that could cut the cost of the cancer test by about 90 percent.

The new method looks for changes in methylation—a chemical modification to DNA that controls gene activity. The genes of cancer cells widely lose their methylation marks, a feature that Lo says can be reliably spotted using less sequencing.

Other scientists say Lo’s approach is not yet highly accurate and could incorrectly diagnose many healthy people as having cancer. Victor Velculescu, a genome scientist at Johns Hopkins, says such false positives are a problem for many screening tests. “Although the approach used by Dr. Lo is an excellent application of this technology, it would have the same hurdle to overcome,” he says.

Lo says he is testing his technique in Hong Kong by following 20,000 people at risk for cancer as part of a $4 million study paid for by the Hong Kong government. Many are infected with hepatitis B, a virus that can cause liver cancer and is carried by about 10 percent of the Chinese population.

Currently, Hong Kong residents infected with hepatitis B get ultrasound exams, which can also spot tumors fairly early. Lo says he hopes to determine if a DNA blood test is a better option.

Most scientists believe the path to an all-purpose cancer test isn’t yet clear, but the technology is evolving so quickly it seems certain it will be possible. “To make these tests something that anyone can have in the doctor’s office could be 20 years away, but that day is coming for sure,” says Marziali.

Lo licensed his patents on prenatal testing to a California company, Sequenom, which launched a pregnancy test in 2011. He says he hasn’t decided how to commercialize the cancer test yet.

Learn the Terms and Acronyms of Myeloma

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Learn the Terms and Acronyms of Myeloma
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Guide to Terms and Acronyms

Everytime you come across a term you do not understand, check the glossary.

Guide to Drug Names
What do carfilzomib and PR-171 have in common? They are the same drug! Between the original name, the generic name and the brand name, it is hard to keep myeloma drugs straight. Here's a handy guide put together by IMF Medical Editor Debbie Birns.

VAD, VAMP, DT-PACE...Is your head swimming from all the acronyms being thrown around? We are here to help.