Category Archives: Stem Cells

Jeunesse Global Revolutionary Anti Aging Skin Care with Stem Cells

By: Karina Palmer

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Jeunesse Global Revolutionary Anti Aging Skin Care with Stem Cells - Video

SAN FRANCISCO -

Mike Hinshaw and Katie Jackson have been a couple since college, but they've known each other much longer.

"We've been together forever. I've actually known Mike since I was five years old," Jackson said.

A marriage and three kids later, they've been through good times and bad. The worst came nine years ago when Hinshaw found out he had Huntington's disease.

"My father had it. He died from it," Hinshaw explained.

Huntington's causes uncontrollable movements and mental decline. There's no cure.

"Unfortunately, it ends in death. It's a fatal disease," said Dr. Vicki Wheelock, neurologist, health sciences clinical professor of neurology and director of HDSA Center of Excellence at UC Davis.

Now, researchers are gearing up for a new trial in humans. Patients will have special bone marrow stem cells injected directly into their brains.

"We've engineered them to make a growth factor that's like a fertilizer for the neurons," said Dr. Jan Nolta, professor and director of the Institute for Regenerative Cures at UC Davis.

That growth factor, BDNF, restored healthy brain cells and reduced behavior deficits in mice. Researchers hope the stem cells will also be the answer to slowing the disease in humans.

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Health Beat: Stem cells: A weapon for Huntington's?

Why are some types of cancer so much more common than others? Sometimes its due to faulty genes inherited from ones parents and sometimes to behaviors like smoking a pack of cigarettes every day. But in most cases, it comes down to something else stem cells.

This is the intriguing argument made by a pair of researchers from Johns Hopkins University. In a study published Friday in the journal Science, they found a very high correlation between the differences in risk for 31 kinds of cancer and the frequency with which different types of stem cells made copies of themselves.

Just how strong was this link? On a scale that goes from 0 (absolutely no correlation) to 1 (exact correlation), biostatistician Cristian Tomasetti and cancer geneticist Bert Vogelstein calculated that it was at least a 0.8. When it comes to cancer, thats high.

No other environmental or inherited factors are known to be correlated in this way across tumor types, Tomasetti and Vogelstein wrote.

Researchers have long recognized that when cells copy themselves, they sometimes make small errors in the billions of chemical letters that make up their DNA. Many of these mistakes are inconsequential, but others can cause cells to grow out of control. That is the beginning of cancer.

The odds of making a copying mistake are believed to be the same for all cells. But some kinds of cells copy themselves much more often than others. Tomasetti and Vogelstein hypothesized that the more frequently a type of cell made copies of itself, the greater the odds that it would develop cancer.

The pair focused on stem cells because of their outsized influence in the body. Stem cells can grow into many kinds of specialized cells, so if they contain damaged DNA, those mistakes can spread quickly.

The researchers combed through the scientific literature and found studies that described the frequency of stem cell division for 31 different tissue types. Then they used data from the National Cancer Institutes Surveillance, Epidemiology and End Results database to assess the lifetime cancer risk for each of those tissue types. When they plotted the total number of stem cell divisions against the lifetime cancer risk for each tissue, the result was 31 points clustered pretty tightly along a line.

To put this notion in concrete terms, consider the skin. The outermost layer of the skin is the epidermis, and the innermost layer of the epidermis contains a few types of cells. Basal epidermal cells are the ones that copy themselves frequently, with new cells pushing older ones to the skins surface. Melanocytes are charged with making melanin, the pigment that protects the skin from the suns damaging ultraviolet rays.

When sunlight hits bare skin, both basal epidermal cells and melanocytes get the same exposure to UV. But basal cell carcinoma is far more common than melanoma about 2.8 million Americans are diagnosed with basal cell carcinoma each year, compared with roughly 76,000 new cases of melanoma, according to the Skin Cancer Foundation. A major reason for this discrepancy, Tomasetti and Vogelstein wrote, is that epidermal stem cells divide once every 48 days, while melanocytes divide only once every 147 days.

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Scientists explain how stem cells and 'bad luck' cause cancer

Cancer in most cases may be the result of biological bad luck rather than caused by genes or behavior, with the random division of stem cells making people more vulnerable to mutations, a new study shows.

A formula that plotted the number of stem-cell divisions over a lifetime against the risk of cancer showed a correlation and explained two-thirds of cases, according to a research paper published this week in the journal Science. The study, conducted by mathematician Cristian Tomasetti and geneticist Bert Vogelstein of Johns Hopkins University, is based on previously published cancer statistics.

The research may bolster arguments that cancer often cant be prevented, with risky behavior such as smoking and excessive exposure to the sun being less of a cause than chance. That would support focusing more resources on diagnosing the disease in early stages and on treatments to reduce mortality rates.

The researchers cautioned that the study isnt a license to engage in unhealthy behavior. Cancer-free longevity in people exposed to cancer-causing agents, such as tobacco, is often attributed to their good genes, but the truth is that most of them simply had good luck, Vogelstein said in a statement.

Tissue types that have more stem-cell divisions are more prone to mutations that can lead to cancers, with data demonstrating a statistical correlation between the two, Vogelstein and Tomasetti said in their paper. They suggest that only one-third of the variation in cancer risk may be due to environmental factors or inherited predispositions.

The researchers focused on stem cells because they live longer, with divisions of the self-renewing cells maintaining the tissues stability while also having the capacity to initiate a tumor. Random mutations -- or bad luck -- occurring during the replication of noncancerous stem cells, which typically account for a small number of the total cells in tissue, can lead to the disease.

The lifetime risk of being diagnosed with lung cancer is 6.9 percent, while that of thyroid is 1.08 percent and brain cancer is 0.6 percent, according to published statistics. Acknowledged risk factors that explain some of the incidence include smoking, alcohol consumption, ultra-violet light and human papilloma virus, as well as genetic variations.

To explain the remaining cancer risk, the researchers from Baltimore, Mayland-based Johns Hopkins focused on 31 tissue types. The positive correlation between the number of stem-cell divisions and lifetime risk of the disease was seen among different types of cancers with varying levels of incidence.

Some cancers, including breast and prostate, werent included in the report because reliable stem-cell division rates havent been determined, according to the study.

To contact the reporter on this story: Chitra Somayaji in London at csomayaji@bloomberg.net

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Cancer Largely Due to Biological Bad Luck Rather Than Behavior

WASHINGTON: Plain old bad luck plays a major role in determining who gets cancer and who does not, according to researchers who found that two-thirds of cancer incidence of various types can be blamed on random mutations and not heredity or risky habits like smoking.

The researchers said on Thursday random DNA mutations accumulating in various parts of the body during ordinary cell division are the prime culprits behind many cancer types.

They looked at 31 cancer types and found that 22 of them, including leukemia and pancreatic, bone, testicular, ovarian and brain cancer, could be explained largely by these random mutations - essentially biological bad luck.

The other nine types, including colorectal cancer, skin cancer known as basal cell carcinoma and smoking-related lung cancer, were more heavily influenced by heredity and environmental factors like risky behavior or exposure to carcinogens.

Overall, they attributed 65 per cent of cancer incidence to random mutations in genes that can drive cancer growth.

"When someone gets cancer, immediately people want to know why," said oncologist Dr Bert Vogelstein of the Johns Hopkins University School of Medicine in Baltimore, who conducted the study published in the journal Science with Johns Hopkins biomathematician Cristian Tomasetti.

"They like to believe there's a reason. And the real reason in many cases is not because you didn't behave well or were exposed to some bad environmental influence, it's just because that person was unlucky. It's losing the lottery." Tomasetti said harmful mutations occur for "no particular reason other than randomness" as the body's master cells, called stem cells, divide in various tissues.

Tomasetti said the study indicates that changing one's lifestyle and habits like smoking to avoid cancer risks may help prevent certain cancers, but may not be as effective for others.

"Thus, we should focus more research and resources on finding ways to detect such cancers at early, curable stages," Tomasetti added.

The researchers charted the cumulative number of lifetime divisions in the stem cells of a given tissue - for example,/slungs or colon - and compared that to the lifetime cancer risk in that tissue.

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Two-thirds of cancer cases due to bad luck

PLoS ONE : Live Cell Imaging of the Nascent Inactive X Chromosome during the Early...
KeSimpulan | Live Cell Imaging of the Nascent Inactive X Chromosome during the Early Differentiation Process of Naive ES Cells towards Epiblast Stem Cells. Aurlia Guyochin et al. (2014),...

By: KeSimpulan

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PLoS ONE : Live Cell Imaging of the Nascent Inactive X Chromosome during the Early... - Video

Kiyoshi Ota/Bloomberg via Getty

Problems with stem-cell papers noted at a RIKEN conference in March 2014 have now been further analysed.

The latest investigation into a debunked method of generating stem cells has left researchers grappling with questions about what went wrong in a laboratory at the RIKEN research institute in Japan.

The final report from the independent investigation, released on 26 December, bolstered suspicions that the stem cells which were supposedly generated by applying stress to ordinary adult cells in an acid bath were actually embryonic stem cells that had been introduced to the samples. But investigators were unable to determine how the contamination occurred or whether it was accidental.

The investigation also has not explained one of the most notable features of the cells their ability to form a placenta something that embryonic stem cells do not generally do. That is still one question that to me is still a mystery, says Manuel Serrano, a cancer biologist who has worked with stem cells at the Spanish National Cancer Research Centre in Madrid.

Serrano, like many of his colleagues, was intrigued by the papers, published in Nature in January 2014, reporting that adult cells could behave like stem cells after experiencing severe stress1, 2. To him, the premise made sense there was ample evidence in the literature that stressed cells were prone to taking on new identities. Cells respond to damage by trying to acquire the plasticity to repair the tissue, he says. But it was surprising that this stress was sufficient to fully reprogram the cell.

Serrano tasked two researchers in his lab with making stem cells using the authors method called stimulus-triggered acquisition of pluripotency (STAP). He initially urged them to keep trying when their attempts failed. But within about two months, Serrano advised them to abandon their efforts. Reports were pouring in from other labs that could not reproduce the method, and questions arose about the validity of data in the papers.

In response to the controversy, RIKEN launched two investigations into the work, much of which was carried out at the RIKEN Center for Developmental Biology in Kobe. An internal review reported in March that lead investigator Haruko Obokata had manipulated images in the two Nature publications. The papers were retracted in July3.

The second investigation, carried out by a team of scientists not employed by RIKEN, delved deeper, analysing cell lines and tissue samples from the laboratories to determine their provenance. In addition to unearthing two more fabrications in figures from the January publications, the team found that three STAP cell lines contained embryonic stem cells.

The results confirmed suspicions in the field, says George Daley, a stem-cell researcher at Childrens Hospital Boston in Massachusetts. The fact that the reported STAP cells had different properties from embryonic stem cells was what piqued many peoples interest, he says. But there was always the concern that some part of the data could have come from the use of standard embryonic stem-cell lines.

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Questions linger over stress-induced stem cells

IMAGE:Induced pluripotent stem cells (iPSCs) derived from patients with frontotemporal dementia were genetically corrected and converted to cortical neurons. The green staining indicates the cortical marker CTIP2, the red stain... view more

Credit: Susanna Raitano/Stem Cell Reports 2014

Belgian researchers have identified a new strategy for treating an inherited form of dementia after attempting to turn stem cells derived from patients into the neurons most affected by the disease. In patient-derived stem cells carrying a mutation predisposing them to frontotemporal dementia, which accounts for about half of dementia cases before the age of 60, the scientists found a targetable defect that prevents normal neurodevelopment. These stem cells partially return to normal when the defect is corrected.

The study appears in the December 31st issue of Stem Cell Reports, the official journal of the International Society of Stem Cell Research published by Cell Press.

"Use of induced pluripotent stem cell (iPSC) technology"--which involves taking skin cells from patients and reprogramming them into embryonic-like stem cells capable of turning into other specific cell types relevant for studying a particular disease--"makes it possible to model dementias that affect people later in life," says senior study author Catherine Verfaillie of KU Leuven.

Frontotemporal disorders are the result of damage to neurons in parts of the brain called the frontal and temporal lobes, gradually leading to behavioral symptoms or language and emotional disorders. Mutations in a gene called progranulin (GRN) are commonly associated with frontotemporal dementia, but GRN mutations in mice do not mimic all the features of the human disorder, which has limited progress in the development of effective treatments.

"iPSC models can now be used to better understand dementia, and in particular frontotemporal dementia, and might lead to the development of drugs that can curtail or slow down the degeneration of cortical neurons," Verfaillie says.

Verfaillie and Philip Van Damme of the Leuven Research Institute for Neuroscience and Disease explore this approach in the Stem Cell Reports study by creating iPSCs from three patients carrying a GRN mutation. These immature cells were impaired at turning into mature, specialized cells called cortical neurons--the most affected cell type in frontotemporal dementia.

One of the top defective pathways in the iPSCs was the Wnt signaling pathway, which plays an important role in neuronal development. However, genetic correction or treatment with a compound that inhibits the Wnt signaling pathway restored the ability of the iPSCs to turn into cortical neurons. Taken together, the findings demonstrate that the GRN mutation causes the defect in cortical neuron formation by altering the Wnt signaling pathway.

"Our findings suggest that signaling events required for neurodevelopment may also play major roles in neurodegeneration," Van Damme says. "Targeting such pathways, as for instance the Wnt pathway presented in this study, may result in the creation of novel therapeutic approaches for frontotemporal dementia."

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Patient stem cells used to make dementia-in-a-dish; help identify new treatment strategy

The research involved creating human cells in a laboratory dish instead of relying on tests on mice. Photograph: corfield / Alamy/Alamy

Cells used to study dementia in a dish have led scientists to a potential new treatment strategy for an inherited form of the brain disease.

Defective stem cells grown in the lab revealed a signalling pathway linked to frontotemporal dementia (FTD), which accounts for about half of dementia cases before the age of 60.

Treatment with a drug that suppressed the pathway, known as Wnt, restored the ability of neurons affected by the disease to develop normally.

Prof Philip Van Damme, from the Leuven Research Institute for Neuroscience and Disease in Belgium, said: Our findings suggest that signalling events required for neurodevelopment may also play major roles in neurodegeneration.

Targeting such pathways, as for instance the Wnt pathway presented in this study, may result in the creation of novel therapeutic approaches for frontotemporal dementia.

Mutations in the progranulin (GRN) gene are commonly associated with FTD, which results in damage to the frontal and temporal lobes of the brain.

The fact that GRN mutations produced in mice do not display all the features of the human disorder has limited progress towards effective treatments for FTD.

Instead of relying on animal tests, the new research involved creating human cells in a laboratory dish.

The scientists reprogrammed skin cells from three dementia patients into induced pluripotent stem cells (iPSCs), immature cells that mimic stem cells taken from early-stage embryos.

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Stem cell study leads to potential new dementia treatment

A new study has shown that reprogramming stem cells could help prevent cancer post radiation.A University of Colorado Cancer Centre study showed that one of the ways to get rid of such stem cells is a "program" that makes stem cells damaged by radiation differentiate into other cells that can no longer survive forever.

The study also showed that this same safeguard of "programmed mediocrity" that weeds out stem cells damaged by radiation allows blood cancers to grow in cases when the full body is irradiated. And by reprogramming this safeguard, it was possible to prevent cancer in the aftermath of full body radiation.

James DeGregori, PhD, the paper's senior author, who along with his colleagues explored the effects of full body radiation on the blood stem cells of mice, said that the body didn't evolve to deal with leaking nuclear reactors and CT scans. It evolved to deal with only a few cells at a time receiving dangerous doses of radiation or other insults to their DNA.

DeGregori found that mutations and other genetic alterations resulting in inhibition of the C/EBPA gene were associated with acute myeloid leukaemia in humans. Thus, it wasn't mutations caused by radiation but a blood system re-engineered by faulty stem cells that created cancer risk in people who had experienced radiation.

The studies show that by activating a stem cell maintenance pathway, it was possible to keep it from happening. Even months after irradiation, artificially activating the NOTCH signalling pathway of irradiated HSCs lets them act "stemmy" again - restarting the blood cell assembly line in these HSCs that would have otherwise differentiated in response to radiation.

When DeGregori, Fleenor and colleagues activated NOTCH in previously irradiated HSCs, it kept the population of dangerous, C/EBPA cells at bay. Competition from non-C/EBPA-mutant stem cells, with their fitness restored by NOTCH activation, meant that there was no evolutionary space for C/EBPA-mutant stem cells.

The study is published in the journal Stem Cells.

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Reprogrammed stem cells may stop cancer post radiation :Study