StemCell Therapy

DorcasAdetudimu, like the average 12-year-old girl, likes to dance, play the piano and sing. Buta rare disease means she can't do those things for very long without getting sore and tired.

Her family is now appealing to the city of Brandon for help findinga stem cell match so she can have a chance at a normal life.

Adetudimuwas diagnosed with sickle cell disease when she was just six weeks old. The condition, common among those of African descent, is a gene mutation that causes the red blood cells to take a crescent shape, making it hard for oxygen to flow around the body.

"I can't do some things that other kids can do," she said, adding that something as simple as going for a swim can cause her body to go into crisis.

"I feel like I'm very limited to doing stuff," said Dorcas. The condition has led to severe pain and regular hospital stays that sometimes last for weeks at a time.

Her condition has worsened over the years. She now requires blood transfusions every four weeks. Last November, she was admitted to the intensive care unit at a Winnipeg hospital and put into an induced coma while doctors deflated her lungs and transfused all of her blood.

This June 2014 image provided by the National Institutes of Health, shows red blood cells in a patient with sickle cell disease at the National Institutes of Health Clinical Center in Bethesda, Md. (The Associated Press)

"It's a painful thing to see your child in pain," said her mom, Juliette. "That was the worst crisis she has ever had. She'd never been in the ICU before."

Juliette, who is originally from Nigeria but moved to Brandon five years ago with her four children, was told the only chance her daughter would have at a normal life would be through a stem cell transplant. Unfortunately neither Juliette nor any of her three other kids were a match.

"I thought that was it," she said. Adetudimu knows of only two other people in Brandon with sickle cell disease, which is rare in Manitoba and Canada, but common in African nations.

With the help of a family friend, Juliette started organizing a stem cell drive through Canadian Blood Services. She's hoping to get as many people as possible between the ages of 17 and 35 to register and submit a cheek swab on May 17 at the Shopper's Mall in Brandon in the hope of finding a match locally.

Since word of the drive got out, complete strangers have been contacting her wanting to help in any way they can.

"It [is] so overwhelming," Juliette said. "I didn't realize people were going to respond this way."

She said a neighbour, who she hadn't met before, showed up on her doorstep asking how he could help.

"Its encouraging to see this kind of support from people that you don't even know."

She's hoping to not only find a match for her daughter, but to also educate the city's ethnic community, and the public, about sickle cell and the importance getting on the stem cell registry.

"Even if they don't match Dorcas, they can still match with somebody else," she said.

Until a match is found, Dorcas will need frequent transfusions. Juliette isn't losing hope.

"I believe in miracles. Nothing is impossible," she said. "I am hopeful ... [a match] would change everything for Dorcas and the family."

The stem cell drive takes place at Brandon's Shopper's Mall on May 17 between noon and 9 p.m.

Dorcas (bottom right), with her mom and three other siblings in their Brandon, Man., home. None of her family members tested positive as a stem cell match for Dorcas. (Riley Laychuk/CBC)

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Brandon family appealing for stem cell match to cure girl's sickle cell disease - CBC.ca

Newswise Researchers have identified a gene that plays a key role in the formation of neural tube defects, a problem commonly found in infants of pregnant women with diabetes. This is the first time the gene has been shown to play this role; it opens up a new way to understand these defects, and may one day lead to new treatments that could prevent the problem or decrease its incidence.

The findings were published today in the journal Nature Communications.

This gene plays a crucial role in the process that leads to these defects, said the studys lead author, Peixin Yang, a professor in the Department of Obstetrics, Gynecology and Reproductive Sciences at UM SOM. Now that we have pinpointed the mechanism, we can begin to focus on how we can stop it from happening in humans.

Neural tube defects (NTDs) occur when mutations accumulate in the neuroepithelial cells, neural stem cells that eventually transform themselves into the brain and the central nervous system. the problem occurs after the fetus is exposed to too much glucose, which can cause widespread cell death, eventually leading to the birth defects.

The researchers focused on a gene called Prkca, which plays a key role in regulating autophagy, the process by which cells dispose of material they no longer need; often this material is broken or flawed in some way. In diabetes, the Prkca gene becomes overactive, and as a result autophagy is suppressed. As a result, the flawed cellular material is used to create embryonic tissue, which can lead to major birth defects.

In essence, the process is a series of dominoes. The Prkca gene triggers production of a protein called protein kinase C-alpha, or PKCalpha. PKCalpha in turn increases expression of a molecule called miR-129-2, which decreases the levels of a protein called PGC-1alpha, which encourages the destruction of flawed cells.

In an experiment using pregnant diabetic mice, Dr. Yang and his colleagues deleted this gene, which allowed autophagy to work normally. In animals in which the gene had been deleted, embryos had far fewer NTDs.

The scientists also examined whether it is possible to reduce NTDs by restoring the expression of PGC-1alpha in developing neural cells. During diabetic pregnancy, PGC-a1alpha re-activated the process of destroying flawed cells and also reduced the death of normal cells. This reduced levels of NTDs. Yang says that in the future it may be possible to prevent and TDs in humans by using medicines that inhibit PKCalpha or miR-129-2, or activate PGC-1alpha.

Neural tube defects arebirth defectsof the brain and spinal cord. They occur in the first month of pregnancy. The two most common arespina bifida and anencephaly. In the first, the fetal spinal column doesn't close completely. This usually causes nerve damage, with some paralysis of the legs. In the latter, most of the brain and skull do not develop. Infants with this defect are usually stillborn or die soon after birth.Neural tube defects have several causes, including diabetes, folic acid deficiency, obesity in the mother, and consumption of certain medications. About 10 percent of women with diabetes who are pregnant will have embryos with neural tube defects.

Globally more than 300,000 pregnancies are affected by NTDs every year. One out of ten babies with NTDs die before their first birthday. In the US alone, medical and surgical costs for children born with NTDs come to more than $200 million a year. Pregnant women who have diabetes have a significantly higher risk of having a child with NTDs, and even with the highest quality preconception care, diabetic women are five times more likely to have a child with birth defects than are non-diabetic women.

The researchers on the article include UM SOM Dean E. Albert Reece, MD, PhD, MBA. Neural tube defects remain a significant hazard for pregnant women who have diabetes, said Dean Reece, who is also the vice president for Medical Affairs, University of Maryland, and the John Z. and Akiko K. Bowers Distinguished Professor. Women with diabetes prior to pregnancy are between three and 10 times more likely to have a child with NTDs than women without disease. This new research shines a fresh light on how we can continue to reduce this urgent problem.

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Researchers Identify Gene That Controls Birth Defect Common in Diabetes - Newswise (press release)

We all grow old. We all die.

For Aubrey de Grey, a biogerontologist and chief science officer of the SENS Research Foundation, accepting these truths is, well, not good enough. He decided in his late twenties (hes currently 54) that he wanted to make a difference to humanity and that battling age was the best way to do it. His lifes work is now a struggle against physics and biology, the twin collaborators in bodily decay.

He calls it a war on age.

Grey considers aging an engineering problem. The human body is a machine, he told me in the following interview, and like any machine, it can be maintained for as long as we want.

This is not an isolated view. There is a broader anti-aging movement afoot, which seems to be growing every day. As Tad Friend describes colorfully in a recent New Yorker essay, millions of venture capital dollars are being dumped into longevity research, some of it promising and some of it not. Peter Thiel, the billionaire co-founder of PayPal, is among the lead financiers (hes a patron of Greys organization as well).

Greys work is particularly interesting. For too long, he argues, scientists have been looking for solutions in all the wrong places. There is no monocausal explanation for aging. We age because the many physical systems that make up our body begin to fail at the same time and in mutually detrimental ways.

So hes developed what he calls a divide-and-conquer strategy, isolating the seven known causes of aging and tackling them individually. Whether its cell loss or corrosive mitochondrial mutations, Grey believes each problem is essentially mechanical, and can therefore be solved.

But even if this Promethean quest to extend human life succeeds, several questions persist.

If we develop these anti-aging technologies, who will have access to them? Will inequality deepen even further in a post-aging world? And what about the additional resources required to support humans living 200 or 300 or 500 years? The planet is stretched as it is with 7 billion people living roughly 70 years on average (women tend to live three to five years longer than men) and is already facing serious stresses around food, water, and global warming going forward.

Grey, to his credit, has thought through these problems. Im not sure hes alive to the political implications of this technology, specifically the levels of state coercion it might demand.

But when pressed, he defends his project forcefully.

Is there a simple way to describe theoretically what the anti-aging therapies youre working on will look like what theyll do to or for the body?

Oh, much more than theoretically. The only reason why this whole approach has legs is because 15 or 17 or so years ago, I was actually able to go out and enumerate and classify the types of damage. We've been studying it for a long time, so when I started out in this field in the mid-90s so I could learn about things, I was gratified to see that actually aging was pretty well understood.

Scientists love to say that aging is not well understood because the purpose of scientists is to find things, out so they have to constantly tell people that nothing is understood, but it's actually bullshit. The fact is, aging is pretty well understood, and the best of it is that not only can we enumerate the various types of damage the body does to itself throughout our lives, we can also categorize them, classify them into a variable number of categories

So I just talked about seven categories of damage, and my claim that underpins everything that we do is that this classification is exhaustive. We know how people age; we understand the mechanics of it. There is no eighth category that were overlooking. More importantly, for each category there is a generic approach to fixing it, to actually performing the maintenance approach that I'm describing, repairing the damage.

Can you give me an example of one of these categories and what the approach to fixing it looks like?

One example is cell loss. Cell loss simply means cells dying and not being automatically replaced by the division of other cells, so that happens progressively in a few tissues in the body and it definitely drives certain aspects of aging. Let's take Parkinson's disease. That's driven by the progressive loss of a particular type of neuron, the dopaminergic neuron, in a particular part of the brain.

And what's the generic fix for cell loss? Obviously it's stem cell therapy. That's what we do. We preprogram cells in the laboratory into a state where you can inject them into the body and they will divide and differentiate to replace themselves that the body is not replacing on its own. And stem cell therapy for Parkinson's disease is looking very promising right now.

Is it best to think of aging as a kind of engineering problem that can be reversed or stalled?

Absolutely. It's a part of technology. The whole of medicine is a branch of technology. It's a way of manipulating what would otherwise happen, so this is just one part of medicine.

But you're not trying to solve the problem of death or even aging, really. Its more about undoing the damage associated with aging.

Certainly the goal is to undo the damage that accumulates during life, and whether you call that solving aging is up to you.

What would you say is your most promising line of research right now?

The great news is that we have this divide-and-conquer strategy that allows us to split the problem into seven subproblems and address each of them individually. That means we're constantly making progress on all of them. We pursue them all in parallel. We actually don't pursue stem cell therapy very much, simply because so many other people are doing it and basically everything really important is being done by somebody else, so it's not a good use of our money.

We're a very small organization. We only have $4 million a year to spend, so we're spread very thin. We're certainly making progress. Over the past year we've published really quite high-profile papers relating to a number of main research programs, so there's no really one thing that stands out.

What do you say to those who see this as a quixotic quest for immortality, just the latest example of humanity trying to transcend its condition?

Sympathy, mainly. I understand it takes a certain amount of guts to aim high, to actually try to do things that nobody can do, that nobody's done before. Especially things that people have been trying to do for a long time. I understand most people don't have that kind of courage, and I don't hate them for that. I pity them.

Of course, the problem is that they do get in my way, because I need to bring money in the door and actually get all this done. Luckily, there are some people out there who do have courage and money, and so we're making progress.

Ultimately, the fact is aging has been the number one problem of humanity since the dawn of time, and it is something that, until I came along, we have not had any coherent idea how to address, which means the only option available to us has been to find some way to put it out of our minds and find a way to get on with our miserably short lives and make the best of it, rather than being perpetually preoccupied with this ghastly thing that's going to happen to us in the relatively distant future. That makes perfect sense. I don't object to that.

The problem is that suddenly we are in a different world where we are in striking distance of actually implementing a coherent plan that will really work, and now that defeatism, that fatalism, that resignation, has become a huge part of the problem, because once you've made your peace with some terrible thing you know, it's very hard to reengage.

Are there any ethical questions or reservations that give you pause at all?

Not at all. Once one comes to the realization that this is just medicine, then one can address the entire universe of potential so-called ethical objections in one gut. Are you in favor of medicine or not? In order to have any so-called ethical objection to the work we do, the position that one has to take is the position that medicine for the elderly is only a good thing so long as it doesn't work very well, and thats a position no one wants to take.

Ive no doubt youve been asked this question before, but I think its too important to gloss over. You talk enthusiastically about transitioning to a post-aging world, but there are many people who worry about what it means to increase the humans time on earth. We dont necessarily have an overpopulation problem, but we certainly have an inequality problem, and we seem to need more resources than we have. If 90 percent of people die from aging now, and suddenly people are living for 200 or 300 years, how will we be able to sustain this kind of growth?

First of all, thank you for prefacing the question with the thought that I've probably heard this question a lot, because of course I have. But you'd be astonished at how many people have presented this question to me starting with, "Have you ever thought of the possibility that..." as if they genuinely had a new idea.

But yes, overpopulation is the single biggest concern that people raise, and I have basically three levels of answers to these questions. First, the answer is specific to the individual question. So in the case of overpopulation, essentially I point to the fact that fertility rates are already plummeting in many areas. And people often forget: Overpopulation is not a matter of how many people there are on the planet but rather the difference between the number of people on the planet and the number of people that can be on the planet with an acceptable level of environmental impact, and that second number is of course not a constant; it's something that is determined by other technologies.

So as we move forward with renewable energy and other things like desalinization to reduce the amount of pollution the average person commits, we are increasing the carrying capacity of the planet, and the amount of increase that we can expect over the next, say, 20 years in that regard far exceeds what we could expect in terms of the trajectory of rise in population resulting from the elimination of death from aging. So that's my main answer.

The second level of answer is at the level of sense of proportion. Technology happens or doesn't happen, whatever the case may be, and maybe the worst-case scenario is that we will end up with a worse overpopulation problem than what we have today.

What does that actually mean? It means we're faced with a choice in a post-aging world, in a world where the technology exists a choice between either, on the one hand, using these technologies and having more people and having fewer kids than we would like or, on the other hand, letting stuff go on the way it is today, which involves not using technology that will keep people healthy in old age and therefore alive.

Ask yourself, which of those two things would you choose? Would you choose to have your mother get Alzheimer's disease or to have fewer kids? It's a pretty easy choice, and people just don't do this.

The third level is perhaps the strongest of all, which is that it's about who has the right to choose. Essentially if we say, Oh, dear, overpopulation, let's not go there. Let's not develop these technologies, then what we are doing as of today is we are delaying the arrival of our technology. Of course it will happen eventually. The question is how soon? That depends on how hard we try.

If we know that, then what we're doing is we're delaying the arrival of the technology and thus condemning a whole cohort of people of humanity of the future to the same kind of death and disease and misery that we have today in old age, when in fact we might have relieved that suffering had we developed the therapies in time.

I dont want to be responsible for condemning a vast number of people to death. I dont want to be in that position. I think theres a strong argument that we should get on developing these technologies has quickly as we can.

I take your points there, but those questions are far easier to answer in theory than they are to solve in practice. For instance, we cant simply decide that people will have fewer children without potentially dangerous levels of state coercion. The politics of this is complicated at best, dystopian at worst.

In any event, let me at least raise one more concern. What is your sense of the cost and the accessibility of these therapies should they become available? People concerned with bioengineering, for example, worry that technologies like this, if they arent equally distributed, will produce inequalities of the sort weve never seen before and cant sustain.

Its a valid concern. It needs to be addressed, but luckily, like the overpopulation one, it's a really easy one to address. Today what we see with high-tech medicine is that it is even in countries with a single-payer system it's pretty much limited by the pay because there's only so much resources available.

But part of the problem now is that our current therapies for elderly people dont work well. It postpones the ill health of old age by a very small amount if we're lucky, and then people get sick anyway, and we spend all the money that we would have spent in absence of the medicine just keeping the person alive for a little longer in a miserable state.

Now compare that with the situation where the medicine actually does work, where the person actually stays healthy. Yes, they live a lot longer, and sure enough, it may be that we have to supply these therapies multiple times because they are inherently periodic therapies, so we could be talking about a substantial amount of money. But the thing is these people would be healthy, so we would not be spending the money on the medicine for the sick people that we have today.

Plus, on top of that, there would be massive indirect savings. The kids of the elderly would be more productive because they wouldn't have to spend time looking after their sick parents. The elderly themselves would still be in an able-bodied state and able to actually contribute wealth to society rather than just consuming wealth.

Of course, there are lots and lots of big uncertainties in these kinds of calculations, but there is absolutely no way to do such a calculation that does not come to the absolutely clear conclusion that the medicines would pay for themselves many times over, really quickly.

So what that means, from the point of view of government setting aside the fact that it would be politically impossible not to support this is that it would be suicidal from a purely mercenary economic point of view not to do this. The country will go bankrupt because other countries will be making sure their workforce is able-bodied. The world will be frontloading their investments to ensure that everybody who is old enough to need them will get these therapies.

When will the therapies youre developing be ready for human experimentation?

That will happen incrementally over the next 20 years. Each component of the SENS panel will have standalone value in addressing one or another disease of old age, and some of them are already in clinical trials. Some of them are a lot harder, and the full benefit will only be seen when we can combine them all, which is a long way out.

How confident are you that someone alive today will not die of aging?

It's looking very good. Of course this is primary technology, so we can only speculate. It's very speculative what the time frame is going to be, but I think we have a 50-50 chance of getting to work on longevity escape velocity, the point where we are postponing the problem of aging faster than time is passing and people are staying one step ahead of the problem. I think we have a 50-50 chance of reaching that point within 20 years of now, subject only to improved funding on the early-stage research that's happening at the moment.

Escape velocity is an interesting analogy. The idea is to keep filling up the biological gas tank before it runs out, staying a step ahead of the aging process?

Right. The point is that these are rejuvenation therapies, which means they are therapies that genuinely turn back the clock. They put the body into a state that is analogous or similar to how it was at an earlier [stage] rather than just stopping or slowing down the clock. Every time you do this, you buy time, but the problem gets harder because the types of damage that the therapy reverses will catch up, and those imperfections just need to be progressively partially eliminated. The idea, then, is that you asymptotically approach the 100 percent repair situation but you never need to get there. You just need to keep the overall level of damage below a certain tolerable threshold.

For more about de Grey's work, visit the SENS website.

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Scientists are waging a war against human aging. But what happens next? - Vox

Monsters and Critics.com

Stem cells to fight Alzheimer's disease on Through the Wormhole with Morgan Freeman Monsters and Critics.com Tonight's Through the Wormhole with Morgan Freeman looks at the exciting subject of reversing Alzheimer's disease and the magic of stem cells. The episode, titled Can We Cheat Death?, sees Freeman looks at how we can unlock the secrets of certain cells ... and more »

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Stem cells to fight Alzheimer's disease on Through the Wormhole with Morgan Freeman - Monsters and Critics.com

Combination therapy could provide new treatment option for ovarian cancer Science Daily In 2015, Memarzadeh and her team uncovered and isolated carboplatin-resistant ovarian cancer stem cells. These cells have high levels of proteins called cIAPs, which prevent cell death after chemotherapy. Since the cancer stem cells survive carboplatin ...

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Combination therapy could provide new treatment option for ovarian cancer - Science Daily

Stem cells that are grown in the lab are known to acquire mutations, but whether these mutations are particularly numerous or risky remains unclear. Mutations acquired in stem cell culture, it is feared, would complicate efforts to deploy stem cells in regenerative medicine. At the least, lab-grown stem cells may need to be screened for deleterious mutations, with special attention devoted to vulnerable portions of the genome or flaws that could lead to dire consequences, such as cancer.

To characterize the mutations that may arise among stem cells in vitro, scientists have been introducing gene-sequencing tests. For example, in a recent study, scientists based at Harvard have determined that human pluripotent stem cells are prone to develop mutations in the TP53 gene, which ordinarily helps suppress cancer. The mutated versions of the TP53 found by the Harvard team, however, tend to drive cancer development.

Details of this work appeared April 26 in the journal Nature, in an article entitled, Human Pluripotent Stem Cells Recurrently Acquire and Expand Dominant Negative P53 Mutations. This article describes how the Harvard team sequenced the protein-coding genes of 140 human embryonic stem cell (hES) cell lines26 of which were developed for therapeutic purposes using Good Manufacturing Practices, a quality control standard set by regulatory agencies in multiple countries. The remaining 114 human pluripotent stem cell lines were listed on the NIH registry of human pluripotent stem cells. This gene-sequencing exercise was followed by computational work that allowed the scientists to identify mutations present in a subset of cells in each cell line.

[We] identified five unrelated hES cell lines that carried six mutations in the TP53 gene that encodes the tumour suppressor P53, wrote the articles authors. The TP53 mutations we observed are dominant negative and are the mutations most commonly seen in human cancers. We found that the TP53 mutant allelic fraction increased with passage number under standard culture conditions, suggesting that the P53 mutations confer selective advantage.

The scientists also mined published RNA sequencing data from 117 human pluripotent stem cell lines, and observed another nine TP53 mutations, all resulting in coding changes in the DNA-binding domain of P53. In three lines, the authors of the Nature paper detailed, the allelic fraction exceeded 50%, suggesting additional selective advantage resulting from the loss of heterozygosity at the TP53 locus.

These findings suggest that cell lines should be screened for mutations at various stages of development as well as immediately before transplantation.

"Our results underscore the need for the field of regenerative medicine to proceed with care," said the study's co-corresponding author Kevin Eggan, Ph.D. "[They] indicate that an additional series of quality control checks should be implemented during the production of stem cells and their downstream use in developing therapies. Fortunately, these genetic checks can be readily performed with precise, sensitive, and increasingly inexpensive sequencing methods."

"Cells in the lab, like cells in the body, acquire mutations all the time," added Steve McCarroll, Ph.D., co-corresponding author. "Mutations in most genes have little impact on the larger tissue or cell line. But cells with a pro-growth mutation can outcompete other cells, become very numerous, and 'take over' a tissue. We found that this process of clonal selectionthe basis of cancer formation in the bodyis also routinely happening in laboratories."

Although the Harvard scientists expected to find some mutations in stem cell lines, they were surprised to find that about 5% of the stem cell lines they analyzed had acquired mutations the TP53 gene, which encodes the tumor suppressor protein P53.

Nicknamed the "guardian of the genome," P53 controls cell growth and cell death. People who inherit p53 mutations develop a rare disorder called Li-Fraumeni Syndrome, which confers a near 100% risk of developing cancer in a wide range of tissue types.

The specific mutations that the researchers observed are "dominant negative" mutations, meaning, when present on even one copy of P53, they are able to compromise the function of the normal protein, whose components are made from both gene copies. The exact same dominant negative mutations are among the most commonly observed mutations in human cancers.

The researchers performed a sophisticated set of DNA analyses to rule out the possibility that these mutations had been inherited rather than acquired as the cells grew in the lab. In subsequent experiments, the Harvard scientists found that P53 mutant cells outperformed and outcompeted nonmutant cells in the lab dish. In other words, a culture with a million healthy cells and one P53 mutant cell, said Dr. Eggan, could quickly become a culture of only mutant cells.

"The spectrum of tissues at risk for transformation when harboring a P53 mutation include many of those that we would like to target for repair with regenerative medicine using human pluripotent stem cells," noted Dr. Eggan. Those organs include the pancreas, brain, blood, bone, skin, liver, and lungs.

However, Drs. Eggan and McCarroll emphasized that now that this phenomenon has been found, inexpensive gene-sequencing tests will allow researchers to identify and remove from the production line cell cultures with concerning mutations that might prove dangerous after transplantation.

The researchers point out in their paper that screening approaches to identify these P53 mutations and others that confer cancer risk already exist and are used in cancer diagnostics. In fact, in an ongoing clinical trial that is transplanting cells derived from induced pluripotent stem cells, or iPSCs, gene sequencing is used to ensure the transplanted cell products are free of dangerous mutations.

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Stem Cells in Culture Have Tendency to Develop Cancer-Linked Mutations - Genetic Engineering & Biotechnology News

May 1, 2017 Ovarian cancer tumors with higher percentages of cIAP-expressing cells, shown in red at left, were more sensitive to a potential combination therapy than tumor cells without cIAP-expressing cells. Credit: UCLA Broad Stem Cell Research Center

Researchers have been trying to understand why up to 85 percent of women experience recurrence of high-grade serous ovarian cancerthe most common subtype of ovarian cancerafter standard treatment with the chemotherapy drug carboplatin.

Preclinical research from Dr. Sanaz Memarzadeh, who is a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA, has potentially solved this mystery and pinpointed a combination therapy that may be effective for up to 50 percent of women with ovarian cancer.

Memarzadeh's research, published in the journal Precision Oncology, shows a new combination therapy of carboplatin and an experimental drug called birinapant can improve survival in mice with ovarian cancer tumors. Additional findings reveal that testing for a specific protein could identify ovarian tumors for which the treatment could be effective. Importantly, the treatment could also target cancers that affect other parts of the body, including the bladder, cervix, colon and lung cancer.

In 2015, Memarzadeh and her team uncovered and isolated carboplatin-resistant ovarian cancer stem cells. These cells have high levels of proteins called cIAPs, which prevent cell death after chemotherapy. Since the cancer stem cells survive carboplatin treatment, they regenerate the tumor; with each recurrence of ovarian cancer, treatment options become more limited. Memarzadeh showed that birinapant, which degrades cIAPs, can make carboplatin more effective against some ovarian cancer tumors.

"I've been treating women with ovarian cancer for about two decades and have seen firsthand that ovarian cancer treatment options are not always as effective as they should be," said Memarzadeh, director of the G.O. Discovery Lab and member of the UCLA Jonsson Comprehensive Cancer Center. "Our previous research was promising, but we still had questions about what percentage of tumors could be targeted with the birinapant and carboplatin combination therapy, and whether this combination could improve overall survival by eradicating chemotherapy-resistant ovarian cancer tumors."

In this new study, the research team first tested whether the combination therapy could improve survival in mice. Half of the mice tested had carboplatin-resistant human ovarian cancer tumors and the other half had carboplatin-sensitive tumors. The team administered birinapant or carboplatin as well as the two drugs combined and then monitored the mice over time. While birinapant or carboplatin alone had minimal effect, the combination therapy doubled overall survival in half of the mice regardless of whether they had carboplatin-resistant or carboplatin-sensitive tumors.

"Our results suggest that the treatment is applicable in some, but not all, tumors," said Rachel Fujikawa, a fourth year undergraduate student in Memarzadeh's lab and co-first author of the study.

To assess the combination therapy's rate of effectiveness in tumors, the team went on to test 23 high-grade serous ovarian cancer tumors from independent patients. Some were from patients who had never been treated with carboplatin and some were from patients who had carboplatin-resistant cancer.

With these samples, the researchers generated ovarian cancer tumors utilizing a method called disease-in-a-dish modeling and tested the same treatments previously tested in mice. Once again, carboplatin or birinapant alone had some effect, while the combination of birinapant and carboplatin successfully eliminated the ovarian cancer tumors in approximately 50 percent of samples. Importantly, the combination therapy worked for both carboplatin-resistant and carboplatin-sensitive tumors.

The researchers also measured cIAPs (the target for the drug birinapant) in the tumors. They found a strong correlation between cancer stem cells with high levels of cIAP and a positive response to the combination therapy. Since elevated levels of cIAPs have been linked to chemotherapy resistance in other cancers, the researchers wondered if the combination therapy could effectively target those cancers as well.

The team created disease-in-a-dish models using human bladder, cervix, colon and lung cancer cells and tested the combination therapy. Similar to the ovarian cancer findings, 50 percent of the tumors were effectively targeted and high cIAP levels correlated with a positive response to the combination therapy.

"I believe that our research potentially points to a new treatment option. In the near future, I hope to initiate a phase 1/2 clinical trial for women with ovarian cancer tumors predicted to benefit from this combination therapy," said Memarzadeh, gynecologic oncology surgeon and professor at the David Geffen School of Medicine at UCLA.

Explore further: Combination therapy may be more effective against the most common ovarian cancer

More information: V. La et al, Birinapant sensitizes platinum-resistant carcinomas with high levels of cIAP to carboplatin therapy, npj Precision Oncology (2017). DOI: 10.1038/s41698-017-0008-z

High-grade serous ovarian cancer often responds well to the chemotherapy drug carboplatin, but why it so frequently comes back after treatment has been a medical mystery.

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Working with human breast cancer cells and mice, researchers at Johns Hopkins say they have identified a biochemical pathway that triggers the regrowth of breast cancer stem cells after chemotherapy.

More than half of all patients with ovarian cancer experience recurrent disease and will eventually fail to respond to chemotherapy. The failure of chemotherapy is usually due to the development of resistance to the two main ...

Using the gene-editing system known as CRISPR, MIT researchers have shown in mice that they can generate colon tumors that very closely resemble human tumors. This advance should help scientists learn more about how the disease ...

Researchers have been trying to understand why up to 85 percent of women experience recurrence of high-grade serous ovarian cancerthe most common subtype of ovarian cancerafter standard treatment with the chemotherapy ...

Immunotherapy, in which cells from the human immune system are unleashed to fight disease, has been the big story in cancer treatment over the past few years. When it works, it can spur long-lasting remission in patients ...

A collaborative Cleveland Clinic, University of Oxford and Moffitt Cancer Center team of researchers has proven the theory that, while resistance to targeted treatment in cancer is truly a moving target, there are opportunities ...

Scientists have described new results of a blood cancer study as 'outstanding' in tackling previously untreatable forms of chronic lymphocytic leukaemia (CLL).

Researchers from the transformation and metastasis group of the Bellvitge Biomedical Research Institute (IDIBELL), led by Dr. Eva Gonzlez-Surez, have recreated and characterized the development of resistance to chemotherapy ...

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Combination therapy could provide new treatment option for ovarian cancer - Medical Xpress

wtkr.com

Are baby, wisdom teeth the next wave in stem cell treatment? wtkr.com Alison Bassetto's voice is steady and brisk as she explains why her husband's untimely death prompted her to have her 19-year-old son's wisdom teeth banked. The practice of cryopreserving children's baby or wisdom teeth is one that's been around for a ...

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Are baby, wisdom teeth the next wave in stem cell treatment? - wtkr.com

Photo by Hannah Robbins/HSCI

In a cross-school collaboration, Harvard researchers Steve McCarroll (left) and Kevin Eggan couple stem cell science with genetics and genomicsto advance the understanding of human brain illnesses. Their latest project identifiedmutations that stem cell lines acquire in culture.

Regenerative medicine using human pluripotent stem cells to grow transplantable tissue outside the body carries the promise to treat a range of intractable disorders, such as diabetes and Parkinsons disease.

However, a research team from the Harvard Stem Cell Institute (HSCI), Harvard Medical School (HMS), and the Stanley Center for Psychiatric Research at the Broad Institute of MIT and Harvard has found that as stem cell lines grow in a lab dish, they often acquire mutations in the TP53 (p53) gene, an important tumor suppressor responsible for controlling cell growth and division.

Their research suggests that genetic sequencing technologies should be used to screen for mutated cells in stem cell cultures, so that cultures with mutated cells can be excluded from scientific experiments and clinical therapies. If such methods are not employed it could lead to an elevated cancer risk in those receiving transplants.

The paper, published online today in the journal Nature, comes at just the right time, the researchers said, as experimental treatments using human pluripotent stem cells are ramping up across the country.

Our results underscore the need for the field of regenerative medicine to proceed with care, said the studys co-corresponding author Kevin Eggan, an HSCI principal faculty member and the director of stem cell biology for the Stanley Center. Eggans lab in Harvard Universitys Department of Stem Cell and Regenerative Biology uses human stem cells to study the mechanisms of brain disorders, including amyotrophic lateral sclerosis, intellectual disability, and schizophrenia.

The research, the team said, should not discourage the pursuit of experimental treatments but instead be heeded as a call to screen rigorously all cell lines for mutations at various stages of development as well as immediately before transplantation.

Our findings indicate that an additional series of quality control checks should be implemented during the production of stem cells and their downstream use in developing therapies, Eggan said. Fortunately, these genetic checks can be readily performed with precise, sensitive, and increasingly inexpensive sequencing methods.

With human stem cells, researchers can re-create human tissue in the lab. This enables them to study the mechanisms by which certain genes can predispose an individual to a particular disease. Eggan has been working with Steve McCarroll, associate professor of genetics at Harvard Medical School and director of genetics at the Stanley Center, to study how genes shape the biology of neurons, which can be derived from these stem cells.

McCarrolls lab recently discovered a common, precancerous condition in which a blood stem cell in the body acquires a pro-growth mutation and then outcompetes a persons normal stem cells, becoming the dominant generator of his or her blood cells. People in whom this condition has appeared are 12 times likelier to develop blood cancer later in life. The studys lead authors, Florian Merkle and Sulagna Ghosh, collaborated with Eggan and McCarroll to test whether laboratory-grown stem cells might be vulnerable to an analogous process.

Cells in the lab, like cells in the body, acquire mutations all the time, said McCarroll, co-corresponding author. Mutations in most genes have little impact on the larger tissue or cell line. But cells with a pro-growth mutation can outcompete other cells, become very numerous, and take over a tissue. We found that this process of clonal selection the basis of cancer formation in the body is also routinely happening in laboratories.

To find acquired mutations, the researchers performed genetic analyses on 140 stem cell lines 26 of which were developed for therapeutic purposes using Good Manufacturing Practices, a quality control standard set by regulatory agencies in multiple countries. The remaining 114 were listed on the National Institutes of Health registry of human pluripotent stem cells.

While we expected to find some mutations in stem cell lines, we were surprised to find that about 5 percent of the stem cell lines we analyzed had acquired mutations in a tumor-suppressing gene called p53, said Merkle.

Nicknamed the guardian of the genome, p53 controls cell growth and cell death. People who inherit p53 mutations develop a rare disorder called Li-Fraumeni Syndrome, which confers a near 100 percent risk of developing cancer in a wide range of tissue types.

The specific mutations that the researchers observed are dominant-negative mutations, meaning that when they are present on even one copy of p53, they are able to compromise the function of the normal protein, whose components are made from both gene copies. The exact same dominant-negative mutations are among the most commonly observed mutations in human cancers.

These precise mutations are very familiar to cancer scientists. They are among the worst p53 mutations to have, said Ghosh, a co-lead author of the study.

The researchers performed a sophisticated set of DNA analyses to rule out the possibility that these mutations had been inherited rather than acquired as the cells grew in the lab. In subsequent experiments, the Harvard scientists found that p53 mutant cells outperformed and outcompeted non-mutant cells in the lab dish. In other words, a culture with a million healthy cells and one p53 mutant cell, said Eggan, could quickly become a culture of only mutant cells.

The spectrum of tissues at risk for transformation when harboring a p53 mutation includes many of those that we would like to target for repair with regenerative medicine using human pluripotent stem cells, said Eggan. Those organs include the pancreas, brain, blood, bone, skin, liver, and lungs.

However, Eggan and McCarroll emphasized that now that this phenomenon has been found, inexpensive gene-sequencing tests will allow researchers to identify and remove from the production line cell cultures with worrisome mutations that might prove dangerous after transplantation.

The researchers point out in their paper that screening approaches to identify these p53 mutations and others that confer cancer risk already exist and are used in cancer diagnostics. In fact, in an ongoing clinical trial that is transplanting cells derived from induced pluripotent stem cells, gene sequencing is used to ensure the transplanted cell products are free of dangerous mutations.

This work was supported by the Harvard Stem Cell Institute, the Stanley Center for Psychiatric Research, the Rosetrees Trust, the Azrieli Foundation, Howard Hughes Medical Institute, the Wellcome Trust, the Medical Research Council, the Academy of Medical Sciences, and by grants from the NIH.

By Al Powell, Harvard Staff Writer | April 26, 2017

Original post:
Stem cell lines grown in lab dish may acquire mutations - Harvard Gazette

Regenerative medicine using human pluripotent stem cells to grow transplantable tissue outside the body carries the promise to treat a range of intractable disorders, such as diabetes and Parkinson's disease.

However, a research team from the Harvard Stem Cell Institute (HSCI), Harvard Medical School (HMS), and the Stanley Center for Psychiatric Research at the Broad Institute of MIT and Harvard has found that as stem cell lines grow in a lab dish, they often acquire mutations in the TP53 (p53) gene, an important tumor suppressor responsible for controlling cell growth and division.

Their research suggests that genetic sequencing technologies should be used to screen for mutated cells in stem cell cultures, so that cultures with mutated cells can be excluded from scientific experiments and clinical therapies. If such methods are not employed it could lead to an elevated cancer risk in those receiving transplants.

The paper, published online in the journal Nature on April, 26, comes at just the right time, the researchers said, as experimental treatments using human pluripotent stem cells are ramping up across the country.

"Our results underscore the need for the field of regenerative medicine to proceed with care," said the study's co-corresponding author Kevin Eggan, an HSCI Principal Faculty member and the director of stem cell biology for the Stanley Center. Eggan's lab in Harvard University's Department of Stem Cell and Regenerative Biology uses human stem cells to study the mechanisms of brain disorders, including amyotrophic lateral sclerosis, intellectual disability, and schizophrenia.

The research, the team said, should not discourage the pursuit of experimental treatments but instead be heeded as a call to screen rigorously all cell lines for mutations at various stages of development as well as immediately before transplantation.

"Our findings indicate that an additional series of quality control checks should be implemented during the production of stem cells and their downstream use in developing therapies," Eggan said. "Fortunately, these genetic checks can be readily performed with precise, sensitive, and increasingly inexpensive sequencing methods."

With human stem cells, researchers can recreate human tissue in the lab. This enables them to study the mechanisms by which certain genes can predispose an individual to a particular disease. Eggan has been working with Steve McCarroll, associate professor of genetics at Harvard Medical School and director of genetics at the Stanley Center, to study how genes shape the biology of neurons, which can be derived from these stem cells.

McCarroll's lab recently discovered a common, precancerous condition in which a blood stem cell in the body acquires a pro-growth mutation and then outcompetes a person's normal stem cells, becoming the dominant generator of his or her blood cells. People in whom this condition has appeared are 12 times more likely to develop blood cancer later in life. The study's lead authors, Florian Merkle and Sulagna Ghosh, collaborated with Eggan and McCarroll to test whether laboratory-grown stem cells might be vulnerable to an analogous process.

"Cells in the lab, like cells in the body, acquire mutations all the time," said McCarroll, co-corresponding author. "Mutations in most genes have little impact on the larger tissue or cell line. But cells with a pro-growth mutation can outcompete other cells, become very numerous, and 'take over' a tissue. We found that this process of clonal selection -- the basis of cancer formation in the body -- is also routinely happening in laboratories."

To find acquired mutations, the researchers performed genetic analyses on 140 stem cell lines -- 26 of which were developed for therapeutic purposes using Good Manufacturing Practices, a quality control standard set by regulatory agencies in multiple countries. The remaining 114 were listed on the NIH registry of human pluripotent stem cells.

"While we expected to find some mutations in stem cell lines, we were surprised to find that about five percent of the stem cell lines we analyzed had acquired mutations in a tumor-suppressing gene called p53," said Merkle.

Nicknamed the "guardian of the genome," p53 controls cell growth and cell death. People who inherit p53 mutations develop a rare disorder called Li-Fraumeni Syndrome, which confers a near 100 percent risk of developing cancer in a wide range of tissue types.

The specific mutations that the researchers observed are "dominant negative" mutations, meaning, when present on even one copy of P53, they are able to compromise the function of the normal protein, whose components are made from both gene copies. The exact same dominant-negative mutations are among the most commonly observed mutations in human cancers.

"These precise mutations are very familiar to cancer scientists. They are among the worst P53 mutations to have," said Sulagna Ghosh, a co-lead author of the study.

The researchers performed a sophisticated set of DNA analyses to rule out the possibility that these mutations had been inherited rather than acquired as the cells grew in the lab. In subsequent experiments, the Harvard scientists found that p53 mutant cells outperformed and outcompeted non-mutant cells in the lab dish. In other words, a culture with a million healthy cells and one p53 mutant cell, said Eggan, could quickly become a culture of only mutant cells.

"The spectrum of tissues at risk for transformation when harboring a p53 mutation include many of those that we would like to target for repair with regenerative medicine using human pluripotent stem cells," said Eggan. Those organs include the pancreas, brain, blood, bone, skin, liver and lungs.

However, Eggan and McCarroll emphasized that now that this phenomenon has been found, inexpensive gene-sequencing tests will allow researchers to identify and remove from the production line cell cultures with concerning mutations that might prove dangerous after transplantation.

The researchers point out in their paper that screening approaches to identify these p53 mutations and others that confer cancer risk already exist and are used in cancer diagnostics. In fact, in an ongoing clinical trial that is transplanting cells derived from induced pluripotent stem cells (iPSCs), gene sequencing is used to ensure the transplanted cell products are free of dangerous mutations.

View original post here:
Genes need to be screened for stem cell transplants - Science Daily

FOX 61

Are baby, wisdom teeth the next wave in stem cell treatment? FOX 61 Alison Bassetto's voice is steady and brisk as she explains why her husband's untimely death prompted her to have her 19-year-old son's wisdom teeth banked. The practice of cryopreserving children's baby or wisdom teeth is one that's been around for a ... and more »

View original post here:
Are baby, wisdom teeth the next wave in stem cell treatment? - FOX 61

By Richard Reeb

The Golden States well-known descent from its years of prosperity and political clout, which stands in sharp contrast to the nations recently renewed growth and turn to the right, has another side. That is its Democrat leaders determination to facilitate the death of unwanted unborn babies, the elderly and terminally ill. Indeed, this session of the California State Legislature provides more evidence of this ominous trend. We Californians already legalize and finance abortion on demand and last year sanctioned so-called assisted suicide. Now attention is turning to new means and new victims of this misguided movement.In the State Senate, four bills have been introduced to this end, while one constitutional amendment has been proposed to stem the billions in funding for embryonic stem cell research. First, the bill (SB 743) of Sen. Richard Pan, D-Sacramento, would guarantee that Planned Parenthood and other abortion providers could still receive federal Medicaid funds via Medi-Cal family planning services. This is a perfect example of California Democrats defiance of the national conservative trend. Fortunately, it will probably go nowhere as President Donald Trump has recently rescinded his immediate predecessors executive order to force states to finance abortions. Exemplifying abortion advocates virtual sanctification of fetal homicide is SB 309, originally introduced by Sen. Pan, which would actually establish a specialty license plate celebrating reproductive freedom. Revenue generated would go to the California Reproductive Freedom Fund, whatever that is. One wonders: did the Third Reich authorize plates for Volkwagens to celebrate the killing of members of inferior races? Sen. Pans SB 481 would allow nursing homes to declare patients unfit to make their own decisions, and then implement medical procedures which may include assisted suicide. The state already permits persons believed to be facing deathin six monthsto end their lives, justified on the grounds of their own consent. This new development demonstrates just how hollow that premise was. While unlikely to make it out of committee, Senate Constitutional Amendment 7 would repeal the (embryonic) Stem Cell Research and Cures Act approved by the states voters in 2004. That misguided measure was sold on the failed promise that embryonic cells offered the greatest potential. But experience with adult stem cells and from placentas has been far more fruitful. Though not directly aimed at death, SB 18, also the work of Sen. Pan, originally sought to challenge parental authority in the name of childrens rights. Of course, parents natural concern for their childrens very lives cannot be surpassed. Yet this bill would have directly threatened parents ability to provide in-home education for their children or to send them to private schools. But Senate committee action has changed the focus of the bill to establish an 18-member Children and Youth joint committee (half from the Senate and half from the Assembly) to direct the legislature to maximize spending on that class of persons. It would undo current code on this subject by the year 2025. The original alarming objectives doubtless will be implemented in bits and pieces through the new committees efforts. Do only children who have been permitted to be born deserve this intense concern? Meanwhile, California's new Attorney General Xavier Becerra has slapped 15 felony charges 14 counts of illegally recording conversations without consent and one count of conspiracy against David Daleiden, the project lead at the Center for Medical Progress (CMP), and his associate Sandra Merritt. In the past 20 months, the Center for Medical Progress has released a series of undercover videos that feature high end Planned Parenthood officials and employees of tissue procurement companies associated with the nation's largest abortion provider. They admitted in recorded conversations various illegalities about how the companies skirted state and federal law to engage in the selling of highly-desired aborted baby tissue, organs and limbs. "At the end of the day, the only thing that is different from the work that I did and the work that CMP did and the work that undercover journalists and investigative journalists are doing every single day here in California ... is who I went after," Daleiden said during a telephone interview with the Washington Times. "The only difference is that I happened to go after and expose the political ally and financial backers of the establishment power structure in California and in the country. That is the only reason why I am being prosecuted with these bogus charges under California Penal Code 632 and why the local reporters with NBC Los Angeles and other places are not. That really says it all." One can only hope that Californias political leadership would be as zealous in saving lives as they are in ending them. But alas they are not. Such is the situation in our coming sanctuary state.

Richard Reeb taught political science, philosophy and journalism at Barstow College from 1970 to 2003. He is the author of "Taking Journalism Seriously: 'Objectivity' as a Partisan Cause" (University Press of America, 1999). He can be contacted at rhreeb@verizon.net

Original post:
California's deadly 'social legislation' parallels its economic and ... - Desert Dispatch

GETTY STOCK IMAGE

The way to the Red Planet and other mysterious worlds is being inspired by the villainous Khan from the blockbuster films, according to new research.

The use of stem cell technology may mean the difference between life and death on any attempt to travel beyond Earth into the wilderness of space.

So the first person to walk on Mars is likely to be selected from the growing group of people whose parents took the step to store their child's stem cells at birth.

Stem cells are 'blank' cells that can be reprogrammed to turn into any other cell in the body, enabling the replacement of damaged cells.

More and more British parents, including TV presenter Natalie Pinkham and dancer Darcey Bussell, are paying more than 2,000 to freeze samples from their babies' umbilical cords at birth.

Stem cells are also found in bone marrow and some body tissue, but the procedure to harvest them from umbilical cords is less risky.

Adventurous Mars pioneers will have to be especially prepared for the dangerous trip, which could expose them to cancer and other diseases, through carefully researched gene therapy.

1 of 16

We wince at the thought of genetically engineered humans

Mark Hall

Mark Hall, spokesperson for the UK's leading stem cell storage and diagnostics company StemProtect, said: "We wince at the thought of genetically engineered humans.

"And we are not going to create a Khan from Star Trek specifically to get to another planet. Getting humans to Mars and beyond will be both expensive and dangerous.

"But the scientific by-products - such as huge leaps in stem cell medicine - will benefit humanity for centuries to come."

Genetic engineering has featured in two Star Trek movies, and a number of TV episodes.

IG

1 of 14

This still image strikes an uncanny resemblance to a figure of a woman

Khan, who appeared in Space Seed and Star Trek II: The Wrath of Khan, was modified to make him stronger and to give him greater stamina and intellectual capacity than a regular human.

Mr Hall said: "The first human to walk on Mars may not even be born yet - but that's an advantage."

StemProtect believes advanced medical techniques will be required to cope with the rigours of interplanetary space.

While a trip to Mars may appear "just around the corner" in galactic terms, it is highly possible exposure to radiation along the way could lead to the astronauts developing leukaemia and other cancers even before they arrived.

GETTY STOCK IMAGE

This means future travellers will have to be 'immunised' before they leave Earth.

Mr Hall said: "There was an article in The Times suggesting elephants would make ideal Martian travellers because they'd be largely immune to the radiation.

"But those laughing at the ridiculous sounding headline completely missed the point - the fact is scientists are already working on ways of getting humans there and back alive."

Recent research has shown radiation in deep space increase the risk of leukaemia while long term exposure to micro gravity may leave astronauts open to infection.

The three year round trip to Mars would affect humans at the stem cell level, leaving them with a drastically lowered immune system, NASA funded scientists say.

And NASA's own findings say stem cells may be crucial to the future of space travel, particularly how they respond in a low gravity environment.

One study showed stem cells flown in space and then cultured back on Earth had greater ability to self renew and generate any cell type, changing more easily into specialised heart muscle cells, for instance.

Mr Hall said an astronaut will have to be prepared for the journey "quite literally at the stem cell level."

He explained: "That means working with the best and most effective stem cells available to the patient - those harvested from the umbilical cord at birth."

GETTY STOCK IMAGE

The therapies required to 'immunise' humans to space travel are still being researched.

And with most space based science, it can only mean huge benefits to mankind back down on Earth when it comes to fighting otherwise deadly conditions and diseases.

Stem cells have the ability to treat a potentially infinite range of illnesses and diseases.

Stem cell therapy is already being used all over the world to treat some cancers and stroke victims - and there is fast progress being made in many other areas, including Parkinson's and Alzheimer's disease.

See more here:
SUPERHUMANS: Mars 'will be colonised by genetically engineered Star Trek-style beings' - Express.co.uk

A Croydon dad who achieved fame as a bailiff on a TV show has been handed a "death sentence" unless a donor can be found to rescue him from terminal blood cancer.

Delroy Anglin is "Croydon born and bred" and found unexpected fame for his work as a bailiff on Channel 5's Can't Pay? We'll Take It Away!

Now the 56-year-old has been stricken by an aggressive form of leukaemia which ravages the blood and bones of its sufferers.

READ MORE: Charity seeking to save life of Croydon TV star tell well-wishers - 'you can save him'

The dad-of-six was confined to a hospital bed while undergoing punishing chemotherapy.

But the searing treatment can only battle the cancer for so long.

Delroy desperately needs a bone marrow transplant in order to beat the debilitating disease.

It is hard to find a matching donor because of his minority background, and he has suffered for months since first hearing the news of his illness.

"You feel as if someone has pronounced a death sentence," said Delroy, from Croydon Old Town.

READ MORE: This 8-year-old Croydon schoolboy is a musical genius despite being deaf

"Life changed in an instant. When they tell you, you're just hoping someone has made a mistake, but they haven't.

"At the end of the day, unless somebody says differently - I'm terminal."

His condition was first discovered after he requested a check-up because he had been catching more colds than he usually would.

A blood test revealed what was really affecting his usually robust health.

READ MORE: Missing People Choir on Britain's Got Talent: Who is missing Crystal Palace fan Lee Boxell?

AML affects the stem cells in bone marrow, causing a huge amount of white blood cells to be produced. Less than half of patients can be cured of the rare disease, which causes a dangerous reduction in the number of red blood cells in the body.

"I think I was in denial because I felt so fine," said Delroy, who has been forced to quit his on-screen work.

"Life changed straight away, from diagnosis to entering the hospital was a matter of days.

"Your life just changes instantly. Everything is chaotic and it remains like that for while."

Delroy, now a grandfather, is continuing to battle the disease, which developed with shocking speed, alongside his family.

His children have rallied to support him, and although his 82-year-old mum worries, her home cooking gives him strength.

"You don't want to worry your mum," said Delroy, who is now being treated at the Royal Marsden in Sutton.

"She does worry. She comes from a generation where leukaemia was a death sentence.

"But you get the home cooking from her and build up your strength it's funny how it never changes.

"You don't know how your kids are going to react. Some react well, some become aware of their own mortality a bit, and hate going to hospitals.

"But my family have reacted so well, and I think that's because they've seen my reaction. They've been absolutely amazing."

The expert bailiff, filmed alongside colleagues for the popular Channel 5 series, is facing the fight with calm determination.

His treatment has been gruelling, but he hopes there may be hope of victory over AML, although only a transplant will guarantee he beats the cancer which claimed his own brother's life 40 years ago.

He said: "For all intents and purposes I'm a pretty young bloke, you know, this is not supposed to happen. It just seems unreal.

"Chemotherapy is tough. The first time I had it I was in a wheelchair after. I looked in the mirror and didn't even recognise myself, I was so weak and frail.

"The next time I forced myself to take a few steps, and not let it do that to me again. Now I'm feeling positive about it. But it won't go away.

READ MORE: Former Crystal Palace striker talks with inspirational honesty about his battle with depression

"A transplant would be a game changer. It's the only way to get rid of it."

Transplanting fresh stem cells from donated bone marrow can treat the cancer.

But because Delroy is of African Caribbean origin his chances of finding a donor are slimmer because of the low number of donors with African Caribbean heritage on the donor register.

And none of Delroy's five siblings fit the criteria to make the vital donation.

His chances would be improved if more people from his background were on the register to donate bone marrow. Delroy thinks that the support he has received could translate into something positive for other sufferers.

"It's strange, people don't usually like bailiffs," he said.

"But I have had so much support, from everyone including complete strangers.

"I'm Croydon born and bred, I know everyone. And being on telly I still don't know how that happened that gives me an opportunity to raise awareness.

"Hopefully we can encourage more people to become donors, becasuse if I'm honest, even I didn't know anything about this issue."

A campaign has now begun to help find the missing match to save Delroy's life and more donors for future sufferers.

READ MORE: Emotional celebration held in memory of Croydon murder victim Bjorn Brown

The #Match4Delroy appeal is to be led by blood cancer charity the African Caribbean Leukaemia Trust (ACLT) and encourages people to join the donor register.

Delroy's daughter Domenique Anglin said: "He is a fantastic father to my siblings and a wonderful grandfather too.

"I am appealing on his behalf to all Caribbean and African people in the UK and abroad to join the register, in the hope they might be the match that saves his life."

Delroy's sister, Janet Hills, is chair of the Met Black Police Association.

She said: If you love Del on the show as much as I love him as my brother, then please, please, please make that commitment today to join the stem cells register."

To join the Stem Cell Register visit aclt.org

The rest is here:
Croydon dad who stars in Channel 5 show needs transplant to live after 'death sentence' diagnosis - Croydon Advertiser

A heart attack occurs when one or more of the coronary arteries feeding oxygen-rich blood to the heart muscle become blocked, cutting off the supply and leading to severe pain, tissue death and possible loss of life. Heart attack victims are left with varying degrees of damage to the muscle, and that damage can lead to complications and impaired function down the road.

A new heart patch, though, aims to reverse a large portion of the damage heart attacks leave behind. Developed by a team led by University of Minnesota biomedical engineers, the patch is made from heart stem cells and has been found to be effective in helping heal scar tissue and regrowing healthy heart muscle.

This is a significant step forward in treating the No. 1 cause of death in the U.S., said Brenda Ogle, an associate professor of biomedical engineering at the University of Minnesota, speaking with universitys news service. We feel that we could scale this up to repair hearts of larger animals and possibly even humans within the next several years.

Created using laser-based 3D printing, the patch is a matrix of human heart stem cells and proteins that fully integrates into the heart. When tested on a mouse heart after a simulated heart attack, the patch helped to speed recovery and function in just four weeks.

While the breakthrough is still in its earliest phases of testing, the team, which includes the University of Wisconsin-Madison, is hoping to scale up the project in the near future. Ogle envisions the rollout of a human-ready version of the patch could happen in as little as four years.

Below is a video of the patch cells beating

Go here to see the original:
How Minnesota researchers are helping to heal broken hearts: BTN LiveBIG - Big Ten Network

The star ofCant Pay? Well Take It Away!has revealed he desperately needs a bone marrow transplant after being diagnosed with terminal cancer.

TV bailiff Delroy Anglin has an aggressive form of leukaemia which hes called a death sentenceunless a donor an be found.

The 56-year-old father of five is currently undergoing chemotherapy at the Royal Marsden in Sutton to battle the worst symptoms of the disease but the treatment will only be effective for so long.

Delroy has spoken about the toll that chemo has taken on his body, saying:

Chemotherapy is tough. The first time I had it I was in a wheelchair after. I looked in the mirror and didnt even recognise myself, I was so weak and frail.

The next time I forced myself to take a few steps, and not let it do that to me again. Now Im feeling positive about it. But it wont go away. A transplant would be a game changer. Its the only way to get rid of it.

Unfortunately The Croydon Advertiser have reported that finding a donor will be difficult due to Delroys minority background as there arent manydonors with African Caribbean heritage on the donor register.

Delroys life has changed significantly since the diagnosis and hes been forced to quit his on-screen work for Channels 5s Cant Pay? Well Take It Away!

He said:

You feel as if someone has pronounced a death sentence. Life changed in an instant. When they tell you, youre just hoping someone has made a mistake, but they havent.

At the end of the day, unless somebody says differently Im terminal.

Mr Anglin is suffering from a specific type of leukaemia called Acute myeloid leukaemia (AML) whichaffects the stem cells in bone marrow and causes a huge amount of white blood cells to be produced, reducing the number of red cells in the body.

Only half of patients can be cured of the rare disease but despite the debilitating effects Delroy remains hopeful he can beat it and his family have rallied around him to support him during this difficult time.

In order to help save Delroys life the campaign#Match4Delroy has been launched by blood cancer charity the African Caribbean Leukaemia Trust (ACLT) to encourage people to join the donor register.

Here is the original post:
'Can't Pay? We'll Take It Away' Star Reveals 'Death Sentence' - Unilad - UNILAD

A dad who achieved fame as a bailiff on Channel 5's Can't Pay? We'll Take It Away! has been handed a 'death sentence' unless a donor can be found to rescue him from a terminal blood cancer.

Delroy Anglin, who reached unexpected stardom on the show, has been stricken by an aggressive form of leukaemia which ravages the blood and bones of its sufferers.

The dad-of-six was confined to a hospital bed while undergoing chemotheraphy.

But Delroy, 56, desperately needs a bone marrow transplant so he can beat the debilitating disease.

However, it's proven difficult to find a matching donor because of his minority background, and he has suffered for months since first hearing the news of his deadly illness.

Delroy, from Croydon, told the Croydon Advertiser: "You feel as if someone has pronounced a death sentence.

"Life changed in an instant. When they tell you, you're just hoping someone has made a mistake, but they haven't.

"At the end of the day, unless somebody says differently - I'm terminal."

His condition was first discovered after he requested a check-up because he had been catching more colds than he usually would.

A blood test revealed what was really affecting his usually robust health.

AML affects the stem cells in bone marrow, causing a huge amount of white blood cells to be produced. Less than half of patients can be cured of the rare disease, which causes a dangerous reduction in the number of red blood cells in the body.

"I think I was in denial because I felt so fine," said Delroy, who has been forced to quit his on-screen work.

"Life changed straight away, from diagnosis to entering the hospital was a matter of days.

"Your life just changes instantly. Everything is chaotic and it remains like that for while."

Delroy, now a grandfather, is continuing to battle the disease, which developed with shocking speed, alongside his family.

His children have rallied to support him, and although his 82-year-old mum worries, her home cooking gives him strength.

"You don't want to worry your mum," said Delroy, who is now being treated at the Royal Marsden in Sutton.

"She does worry. She comes from a generation where leukaemia was a death sentence.

"But you get the home cooking from her and build up your strength it's funny how it never changes.

"You don't know how your kids are going to react. Some react well, some become aware of their own mortality a bit, and hate going to hospitals.

"But my family have reacted so well, and I think that's because they've seen my reaction. They've been absolutely amazing."

"It's strange, people don't usually like bailiffs," he said.

"But I have had so much support, from everyone including complete strangers."

The #Match4Delroy appeal is to be led by blood cancer charity the African Caribbean Leukaemia Trust (ACLT) and encourages people to join the donor register.

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Bailiff dad who reached fame on Channel 5's Can't Pay? We'll Take It Away! gets 'death sentence' diagnosis - Mirror.co.uk

Welcome to this weeks Research Roundup.These Friday posts aim to inform our readers about the many stories that relate to animal research each week. Do you have an animal research story we should include in next weeks Research Roundup? You can send it to us viaour Facebook pageor through thecontact formon the website.

The March for Science champions robustly funded and publicly communicated science as a pillar of human freedom and prosperity.We unite as a diverse, nonpartisan group to call for science that upholds the common good and for political leaders and policy makers to enact evidence based policies in the public interest. https://www.marchforscience.com/ #MarchforScience

Somatic stem cells exist naturally in the body. They are important for growth, healing, and replacing cells that are lost daily through wear and tear. Source: University of Utah

Zebrafish: Wellcome Trust Sanger Institute

Image courtesy of National Library of Medicne

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Research Roundup: March for Science, promising headway in stem cell treatments, new treatment for cystic fibrosis ... - Speaking of Research

Muskogee area residents will have an opportunity to be a hero and make a life-and-death difference in someones life Tuesday when a Be the Match Registry donor drive is hosted by the Muskogee Education Association.

For people between the ages of 18 and 44, the event will be held from noon to 5 p.m. Tuesday in the lobby of the Fine Arts Auditorium at Muskogee High School. The event is free and is being held in honor of Muskogee teacher Angela Gideon and her daughter, Nevaeh Oswalt, said Michael Walcutt, president of the association.

We urge people to stop by, fill out a form and be tested for possibly being a potential match, Walcutt said. The test is a simple self-administered mouth swab.

Gideons daughter had a transplant match found through a registry.

This is something Angela is very passionate about, and its a way for the association to support our teachers and causes they feel are important, he said. Nevaeh died in 2011 but lived longer than anticipated after receiving a transplant that enhanced her life.

Gideon became aware of just how important finding a matched donor is after Nevaeh was born with a rare genetic disease called hemophagocytic lymphohistiocytosis, or HLH. When Nevaeh turned 8, doctors began the worldwide search for a transplant donor, Walcutt said.

That search revealed just one person in the entire world who was a match for Nevaeh, he said. While that transplant went well, Nevaeh died in 2011 from multiple complication of her disease over the years and trying to recover from the transplant.

Gideon is a math teacher at Alice Robertson Junior High School. Walcutt said she responded a couple of months ago when the education association dispatched word that its members were interested in supporting causes important to local educators.

As an association we try to support our educators, Walcutt said. This is so important.

Tuesdays event is being held in conjunction with the Be The Match Foundation through the Oklahoma Blood Institute, said Institute spokeswoman Audrey Womack.

For thousands of people with blood cancers like leukemia or other diseases like sickle cell anemia, a marrow transplant is their only hope for life, Womack said.

She said the reason donors between the 18-to-44 age limit are sought is because they are proven to provide the best outcomes should a transplant be needed.

For people showing up at Tuesdays drive, Womack said there is no charge. For people older than 44, she said they can still be donors but they would be required to go in person to the Oklahoma City location of the Oklahoma Blood Institute and would be required to pay a $100 fee to register.

Womack said that should a person be matched with another needing a marrow transplant the process is similar to donating blood platelets, plasma or stem cells with the donors blood withdrawn through a needle in one arm and passed through a machine that will collect only blood-forming cells. The remaining blood is returned to the donor in the other arm.

If you go

WHAT: Be the Match donor drive.

WHEN: Noon to 5 p.m. Tuesday; the entire process takes from one to 15 minutes.

WHERE: Muskogee High School, 3200 E. Shawnee Bypass.

WHO: Area residents between the ages of 18 and 44.

COST: Free.

Visit link:
Marrow donor registry drive set Tuesday - Muskogee Daily Phoenix

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Ive been thinking frequently this month about Henrietta, my paternal grandmother. I try to imagine what it felt like to be an American Jew in the mid-1940s, with news coming in about what happened to ones counterparts in Europe. Henrietta and all but one of my grandparents were born in the United States. But in 1945, at the age of 36, my fathers mother died anyway: of breast cancer. And one by one, her sisters all died of the same disease.

I wonder about that as well. What if any treatment did they receive? What killed them: the cancer and its progression? Or the treatment? The times, which brought death sentences to so many people like them?

Henriettas daughter my aunt and Henriettas sisters daughters all lived well into old age. Most of them lived cancer-free. One of them, my fathers cousin Jeanine, did get breast cancer. So did my mother. Her diagnosis came in 2009, just after my step-father died. It hit me and my sisters particularly hard, increasing our sense of the risk of cancer now from both sides of the family. Mom heard the news within days of my return home to Brooklyn after sitting shiva with her in Chicago.

But thanks to advances in science, treatments for breast cancer have improved a great deal. The research of Eugene DeSombre, a biochemist, became part of the reason I did not lose my own mother, as my father had 64 years earlier. And its part of the reason I urge you to march for science this Saturday, as well as study science, donate to science, and educate everyone you know about it.

DeSombre and his colleagues investigated the connections between the hormone estrogen and breast cancer. Their discovery of the mechanism by which estrogen promotes the growth of some tumors helped lead to one of the treatments that have kept my mother and my cousin Jeanine, as well as many, many other women who had cancer, from dying of it and from contracting it again.

I grew up into an awareness not just that I would never know my biological paternal grandmother, but that her death and her absence ever since caused my father a great deal of harm, not to mention counseling fees. An astute psychologist would note its ongoing impact on me, my sisters, our cousins, and even our children. Perhaps its obvious that like many people with breasts, I also grew up with an everyday conscious as well as unconscious fear of breast cancer.

But as my 20s gave way to my 30s and then, in my 40s, as menopause approached, some of that fear eased. I noted that Henrietta and her sisters had daughters who were living into their 70s and that breast cancer had not emerged in my generation. I did not know how old my grandmother was when she died, but assumed from the young age of her children at the time, that she had likely not reached her 40s. Yet all of her granddaughters did.

And this granddaughter found a way to dedicate myself to improving the pipeline to schools and professions promoting the sciences, technology, engineering, and mathematics.

As I approached the end of my 40s, that decade Henrietta never reached, working with the help of many friends old and new, I founded the nonprofit I had dreamed up years beforehand. Math4Science Inc. is devoted to improving math education in service of science for students of all ages and backgrounds.

We are building a math curriculum out of interviews with STEM professionals: scientists, computer technologists, engineers, and mathematicians. Knowing about the work these people do and solving math problems connected to that work inspires and prepares students to enter STEM fields. Just as the scientists who discovered ways to help women survive breast cancer were once students, the elementary, middle, and high school math students of today will make the advances in science, tech, and engineering that we so desperately need.

Building Math4Science led me to interview Gene DeSombre, the biochemist of whose work I had been nearly completely ignorant while growing up with his daughter in Chicagos Hyde Park, home of the University of Chicago. When I spoke with him, I did not realize that my mother had taken medication developed out of his research findings.

I also interviewed Andrew Vickers, a biostatistician whose son went to school with my daughter in Brooklyn. Vickers researches cancer at Memorial Sloan Kettering Cancer Center, or MSKCC, both its causes and its treatment.

Most surgeons dont have time to track their patients progress after surgery and may not have the math skills to analyze the patterns in that progress constructively. Vickers and his colleagues do that for them, determining which surgeries and other treatments have the most beneficial results. Doctors at MSKCC use the conclusions that Vickerss biostatistics team draws to improve cancer treatments and their patients lives.

I turned 50 last summer. Around eight months later, I felt a lump in my breast. One doctors visit, a barrage of mammogram images, a sonogram, and a biopsy later, all but the first at Memorial Sloan Kettering Cancer Center, I turned out to be the first of my generation in my family to be diagnosed with breast cancer.

I could write at length about the past few weeks: about living to face one of my greatest, longest-lived fears; about the power of the care of friends and family; about the dizzying mind-body connection and the havoc it wreaks; about how slowly time passes as one awaits surgery.

The lump awaiting removal makes me feel closer to the grandmother I never met, feeling her anguish and my fathers at a life cut short. The two of us had an imaginary laugh this morning, though, as I recalled the way my grandfather used to shout for his second wife from their cigar smoke-filled den. The Henrietta in my head raised an eyebrow: Not every moment she missed out on was as sweet as the kids, grandchildren, and great-grandkids she would never know.

My own children are at the threshold of adulthood, but that does not exempt them from needing a mom. And I desperately want to spend time with my own grandchildren one day. Thank goodness science has progressed.

The cancer my mother had eight years ago was similar to the one I have now. Like hers, mine is estrogen-receptive: blocking estrogen from my system should help cure me. As I mentioned, Mom is cancer-free now and able to spend time with her grandchildren, nearly all of whom she just hosted at her annual Passover Seder. Thank you, biochemist Eugene DeSombre and all of your colleagues past, present, and future.

My own lump will be removed as part of an outpatient surgery at MSKCC on Tuesday. The matter-of-fact, Ive got this and frankly its quite routine attitude of the surgeon who will do the lumpectomy, as well as the kindness of the entire staff at the hospital, has helped me plow through fields of fear sown by my family history.

The survival rate of those diagnosed with breast cancer has increased so much since my grandmothers diagnosis. In the past 60 years, the rate of survival for 10 years after treatment at the MD Anderson Cancer Center has tripled. Thank you, biostatistician Andrew Vickers and all of your colleagues past, present, and future.

And if my daughter or my future grandchildren or perhaps you, your friends, your children, or your grandchildren find lumps in their breasts that prove to be cancer, even better science, technology, engineering, and math may save their lives. Perhaps they will then go on to become scientists like DeSombre, Vickers, or Derek West.

Right now, bioengineer Derek West and his colleagues are testing the power of gold. Nanoparticles of that precious metal can burn away cancer cells. They can also deliver micro-doses of chemotherapy to those cells. In other words, thanks to the work of Derek West and other scientists, technologists, and engineers, we may soon have treatments that target and kill cancer cells and leave the rest of our cells alone.

The dozens of interviews I have conducted for Math4Science introduced me to the research of West, Vickers, and DeSombre years before I discovered just how relevant that work would be to me and my family. They also provide the basis of the curriculum that will help us teach young math students the power of what theyre learning in school and its connections to the careers of so many essential people.

I have spoken with women and men whose work brings us water, protects us from hurricanes and other natural and less natural disasters, improves public transportation, manipulates genetic material to cure diseases like Huntingtons, investigates the damage done to our immune systems when we play football or experience even psychological childhood trauma, makes sure the products we buy work and are safe, and much more.

And I have spoken to the men and women whose research has impacted multiple generations of women in my family who are battling breast cancer and who have helped increase the survival rate for breast cancer significantly.

For your health and mine and for the health of generations to come, please protect, promote, and fund science. March for science Saturday and every day. And encourage children everywhere to study math and science and to become part of this fascinating, sometimes frustrating, powerful phenomenon. Its likely to save my life, starting with surgery next Tuesday and with other treatments in the weeks, months, and years ahead.

Correction: The article originally stated that all but the last of Hennings doctors visits occurred at Memorial Sloan Kettering Cancer Center. It has been corrected to all but the first.

Justine Henning is the co-founder and director of programming at Math4Science Inc. Justine also runs a one-woman tutoring business in Brooklyn. Her writing has appeared in the New York Times, Slate, Nick Jr. Family magazine, and at http://www.math4science.org.

First Person is Vox's home for compelling, provocative narrative essays. Do you have a story to share? Read our submission guidelines, and pitch us at firstperson@vox.com.

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Science is why my cancer diagnosis isn't a death sentence. It's why I'm marching tomorrow. - Vox