Category Archives: Stem Cells

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Research and Markets (http://www.researchandmarkets.com/research/khwrrx/circulating_tumor) has announced the addition of the "Circulating Tumor Cells (Ctcs) And Cancer Stem Cells (Cscs) Market - Global Industry Size, Market Share, Trends, Analysis, And Forecasts 2012 - 2018" report to their offering.

The rising prevalence of diseases like cancer and the reimbursement support by regulatory bodies in developed countries like United States and Europe are the major factors driving the growth of the CTCs and CSCs market. Though the currently used detection method lacks sensitivity or specificity to track all CTCs particularly the ones that have lost characteristic epithelial features, there is still good scope for pharmaceutical companies in the CTCs and CSCs field. The various sub-types of cancer may have their own classes and it creates an opportunity in the future.

Increase in cancer mortality rate in the past few years and an increase in number of cancer patients offers an opportunity for pharmaceutical companies to enter this sector. Every one person out of eight has the potential of getting affected by cancer and it is estimated that 12 to 37 lives can be saved daily with the help of CTCs and CSCs.

The major geographic markets for CTCs and CSCs are the U.S. and Europe. The U.S. accounted for more than 50% of the worldwide CTCs and CSC market in 2011.

This research is specially designed to estimate and analyze the demand and performance of CTCs and CSC products in a global scenario. The report covers all the major segments of the global CTC and CSC market and provides in-depth analysis, historical data and statistically refined forecast for the segments covered. The study presents a comprehensive assessment of the stakeholder strategies and winning imperatives for them by segmenting the global CTC and CSC market.

Key Topics Covered:

1. Introduction

2. Executive Summary

3. Market Overview

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Research and Markets: Circulating Tumor Cells (Ctcs) And Cancer Stem Cells (Cscs) Market - Global Industry Size ...

SACRAMENTO, CA - At 4-years-old Rydr Rudgers is able to eat, speak, and walk --all thingshis family wasn't sure he'd ever do after being diagnosed with cerebral palsy as an infant.

"He was born without any brain stem functions; no sucking, no swallowing, no breathing," said Rydr's mother Elisa.

When Rydr was 15-months-old, he began stem cell infusions from his cord blood that was saved in a stem cell bank.Rydris making great progress after three infusionsand can even feed himself.

"These are like huge milestones that people don't think about, but actually being able to hold a fork and eat a sandwich is, in our world, an unanticipated milestone and it's amazing," Elisa Rudgers explained.

"Like autism, cerebral palsy or brain injuries of that nature are a diffused population, it's not one cause,"said Dr. Michael Chez, who is the Medical Director of Pediatric Neurology at the Sutter Neuroscience Institute.

Doctors at the Sutter Neuroscience Institute are now beginning research to evaluate cord blood stem cells to help improve language and behavior in autism patients.

The announcement was made on Tuesday morning at Sutter Medical Plaza.It's the first FDA-approved clinical trial that uses a newborn's stem cells from cord blood to treat autism patients.

Doctors will infuse umbilical cord stem cells into the bloodstreams of 30 children diagnosed with autism.

"We feel it will offer a safe and effective answer to the question of whether the cord blood is an effective intervention as a way to introduce stem cell therapy for autism," Chez said.

Autism impacts one in 88 children and one in 54 boys. According to Sutter doctors, a newborn's umbilical cord blood contains a unique population of stem cells that have been used for more than 20 years in medical practice.

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Doctors to study newborn stem cells as treatment for autism

TUESDAY, Aug. 21 (HealthDay News) -- Stem cells from amniotic fluid might one day help treat stress urinary incontinence, a condition caused by damaged pelvic floor muscles in which bladder leakage is brought on by exercise, coughing or simply laughing, a new study involving mice suggests.

Researchers in Korea found that this new technique repaired the damaged pelvic floor muscles in the mice, and kept the condition from recurring.

Results obtained in animal studies do not necessarily apply to humans, however, and much more research is needed before this might be considered a viable treatment for people.

Looking for an alternative to surgery to treat stress urinary incontinence, the scientists explored the use of stem cells to repair the weak muscles that cause bladder leakage. To do this in a noninvasive way, they used stem cells from amniotic fluid collected during routine amniocentesis (prenatal testing of amniotic fluid).

"These stem cells ... have the ability to become muscle cells when grown under the right conditions," explained the study's leaders, James Yoo and Tae Gyun Kwon, from Kyungpook National University, in a news release. "We found that the stem cells were able to survive for seven days inside the mice but by 14 days they had all disappeared. Nevertheless, they were able to induce regeneration of the mouse's own urethral sphincter muscle."

The study revealed the stem cells were able to strengthen the muscles of the pelvic floor. This regenerated muscle also had the right nerve connections. The researchers added that amniotic stem cells do not appear to cause an immune response, such as rejection or tumor growth. Exactly how the stem cells are able to regenerate the muscles remains unclear, they noted.

Stress urinary incontinence is common among women during and after pregnancy and in women aged 40 and older. The study authors noted that men also can develop the condition, particularly those who have undergone prostate surgery.

Current treatments for stress urinary incontinence include a combination of surgery, weight loss, pelvic floor exercises and bladder training.

The study was published Aug. 20 in the journal BMC Medicine.

-- Mary Elizabeth Dallas

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Stem Cells Fix Bladder Leakage in Mice, Study Finds

ScienceDaily (Aug. 21, 2012) How do stem cells preserve their ability to become any type of cell in the body? And how do they "decide" to give up that magical state and start specializing?

If researchers could answer these questions, our ability to harness stem cells to treat disease could explode. Now, a University of Michigan Medical School team has published a key discovery that could help that goal become reality.

In the current issue of the journal Cell Stem Cell, researcher Yali Dou, Ph.D., and her team show the crucial role of a protein called Mof in preserving the 'stem-ness' of stem cells, and priming them to become specialized cells in mice.

Their results show that Mof plays a key role in the "epigenetics" of stem cells -- that is, helping stem cells read and use their DNA. One of the key questions in stem cell research is what keeps stem cells in a kind of eternal youth, and then allows them to start "growing up" to be a specific type of tissue.

Dou, an associate professor of pathology and biological chemistry, has studied Mof for several years, puzzling over the intricacies of its role in stem cell biology.

She and her team have zeroed in on the factors that add temporary tags to DNA when it's coiled around tiny spools called histones. In order to read their DNA, cells have to unwind it a bit from those spools, allowing the gene-reading mechanisms to get access to the genetic code and transcribe it. The temporary tags added by Mof act as tiny beacons, guiding the "reader" mechanism to the right place.

"Simply put, Mof regulates the core transcription mechanism -- without it you can't be a stem cell," says Dou. "There are many such proteins, called histone acetyltransferases, in cells -- but only MOF is important in undifferentiated cells."

Dou and her team also have published on another protein involved in DNA transcription, called WDR5, that places tags that are important during transcription. But Mof appears to control the process that actually allows cells to determine which genes it wants to read -- a crucial function for stem-ness. "Without Mof, embryonic stem cells lost their self-renewal capability and started to differentiate," she explains.

The new findings may have particular importance for work on induced pluripotent stem cells -- the kind of stem cells that don't come from an embryo, but are made from "adult" tissue.

IPCS research holds great promise for disease treatment because it could allow a patient to be treated with stem cells made from their own tissue. But the current way of making IPSCs from tissue involves a process that uses a cancer-causing gene -- a step that might give doctors and patients pause.

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Stem cells can become anything, but not without this protein

HANS SAUTTER

In December 2010, Robin Ali became suddenly excited by the usually mundane task of reviewing a scientific paper. I was running around my room, waving the manuscript, he recalls. The paper described how a clump of embryonic stem cells had grown into a rounded goblet of retinal tissue. The structure, called an optic cup, forms the back of the eye in a growing embryo. But this one was in a dish, and videos accompanying the paper showed the structure slowly sprouting and blossoming. For Ali, an ophthalmologist at University College London who has devoted two decades to repairing vision, the implications were immediate. It was clear to me it was a landmark paper, he says. He has transformed the field.

'He' is Yoshiki Sasai, a stem-cell biologist at the RIKEN Center for Developmental Biology in Kobe, Japan. Sasai has impressed many researchers with his green-fingered talent for coaxing neural stem cells to grow into elaborate structures. As well as the optic cup1, he has cultivated the delicate tissue layers of the cerebral cortex2 and a rudimentary, hormone-making pituitary gland3. He is now well on the way to growing a cerebellum4 the brain structure that coordinates movement and balance. These papers make for the most addictive series of stem-cell papers in recent years, says Luc Leyns, a stem-cell scientist at the Free University of Brussels.

Sasai's work is more than tissue engineering: it tackles questions that have puzzled developmental biologists for decades. How do the proliferating stem cells of an embryo organize themselves seamlessly into the complex structures of the body and brain? And is tissue formation driven by a genetic program intrinsic to cells, or shaped by external cues from neighbouring tissues? By combining intuition with patient trial and error, Sasai has found that it takes a delicate balance of both: he concocts controlled environments that feed cells physical and chemical signals, but also gives them free rein to 'do their thing' and organize themselves into issues. He sometimes refers to himself as a Japanese matchmaker who knows that, having been brought together, two strangers need to be left alone. They know what to do, he says. They interact in a delicate manner, and if the external cues are too strong, it will override the internal ones.

Sasai's work could find medical applications. Recapitulating embryonic development in three dimensions, it turns out, generates clinically useful cells such as photoreceptors more abundantly and efficiently than two-dimensional culture can, and houses them in an architecture that mirrors that of the human body. Sasai and his collaborators are now racing to implant lab-grown retinas into mice, monkeys and humans. The way Sasai sees it, maturing stem cells in two-dimensional culture may lead to 'next generation' therapy but his methods will lead to 'next, next generation' therapy.

A bit stiff in movement and reserved in manner, Sasai nevertheless puts on a theatrical show with a cocktail shaker at parties held by his institute after international symposia. My second job is bartender, he says, without a trace of a smile. It is, however, the cocktails he mixes in 96-well culture plates that have earned him scientific acclaim.

Like many members of his family, Sasai studied medicine. But he soon became frustrated by the lack of basic understanding in the field, especially when it came to neurological conditions. Without knowing the brain, a doctor cannot do much for the patient and therapeutics will always be superficial, he recalls thinking. There seemed no better way to know the brain than to study how it emerges and folds in the embryo. It's complex and usually complex systems are messy, says Sasai. But it's one of the most ordered. He wanted to know how this elaborate system was controlled.

We set up the permissive conditions. But after that we don't do anything. Keep them growing and let them do their job.

One piece of the puzzle was well known: the Spemann organizer, a node in vertebrate embryos that induces surrounding cells to become neural tissue. How the organizer works had been a mystery since its discovery in 1924; to find out, Sasai accepted a postdoctoral position at the University of California, Los Angeles. The post got off to a difficult start when Sasai was robbed of his money and passports at the airport on his way to California. But his scientific efforts were soon rewarded. He replaced the passports and within a month produced the clones that gave us the famous gene chordin, says his supervisor, developmental biologist Eddy De Robertis.

Sasai and his colleagues discovered that the chordin protein is a key developmental signal released by the Spemann organizer5. Rather than pushing nearby cells to become neurons, they found, chordin blocks signals that would turn them into other cell types6, 7. The work helped to establish the default model of neural induction: the idea that, without other signals, embryonic cells will follow an internal program to become neural cells.

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Tissue engineering: The brainmaker

COULD we stem the tide of ageing by delaying the deterioration of stem cells? A new compound that appears to do just that could help us find ways to protect our organs from age-related wear and tear, experiments in mice suggest.

As we age, so do our mesenchymal stem cells (MSCs): their numbers in our bone marrow decline, and those that are left lose the ability to differentiate into the distinct cell types - such as bone, cartilage, fat and possibly muscle cells - that help in the healing process.

"We think this ageing of stem cells may be linked to the onset of some age-related disorders, such as osteoporosis," says Ilaria Bellantuono at the University of Sheffield in the UK.

Earlier research in mice had suggested that the prion protein expressed by MSCs might play a role in holding back stem cell ageing. Mice lacking the prion protein were less able to regenerate blood cells. The study provided more evidence that correctly folded prions serve a useful purpose in the body, despite the role that misfolded prions play in BSE and vCJD.

Bellantuono and her colleagues have now found that the prion protein performs a similar function in humans - older MSCs from human bone marrow expressed less of the protein than younger ones.

In a bid to find a compound that might slow MSC ageing, the team tested numerous molecules known to target prion proteins on dishes of human stem cells. One molecule emerged as a potential candidate - stem cells treated with it produced 300 times the number of cells over 250 days than untreated stem cells. The treated cells kept on dividing for longer.

The team then injected treated cells into the thigh bones of mice, and three days later found that they had produced three times as many new cells as they would normally produce. After five weeks, there were 10 times as many cells.

The new cells appeared to be of higher quality, too, and readily differentiated into bone and fat cells, as well as those that support the tissue and blood vessels.

Bellantuono's team think the molecule works by helping the prions protect the stem cells from the DNA damage associated with normal ageing. When they exposed both treated and untreated cells to hydrogen peroxide - a compound known to cause DNA damage - they found that the treated cells were protected from damage (Stem Cells, DOI: 10.1002/stem.1065).

"You can delay the loss of stem cells' function by manipulating the prion protein," says Bellantuono, who presented the findings at the Aging Online Symposium last month. "In the long term, you may go a long way to maintaining tissue health in [old] age."

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Protecting prion protein keeps stem cells young