UCLA Researchers Unlock Protein Key to Harnessing Regenerative Power of Blood Stem Cells

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Newswise In a study led by Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research member, Dr. John Chute, UCLA scientists have for the first time identified a unique protein that plays a key role in regulating blood stem cell replication in humans.

This discovery lays the groundwork for a better understanding of how this protein controls blood stem cell growth and regeneration, and could lead to the development of more effective therapies for a wide range of blood diseases and cancers.

The study was published online November 21, 2014 ahead of print in the Journal of Clinical Investigation.

Hematopoietic stem cells (HSCs) are the blood-forming cells that have the remarkable capacity to both self-renew and give rise to all of the differentiated cells (fully developed cells) of the blood system. HSC transplantation provides curative therapy for thousands of patients annually. However, little is known about the process through which transplanted HSCs replicate following their arrival in human bone marrow. In this study, the authors showed that a cell surface protein called protein tyrosine phosphatase-sigma (PTP-sigma) regulates the critical process called engraftment, meaning how HSCs start to grow and make health blood cells after transplantation.

Mamle Quarmyne, a graduate student the lab of Dr. Chute and first author of the study, demonstrated that PTP-sigma is produced (expressed) on a high percentage of mouse and human HSCs. She showed further that genetic deletion of PTP-sigma in mice markedly increased the ability of HSCs to engraft in transplanted mice.

In a complementary study, she demonstrated that selection of human blood HSCs which did not express PTP-sigma led to a 15-fold increase in HSC engraftment in transplanted immune-deficient mice. Taken together, these studies showed that PTP-sigma suppresses normal HSC engraftment capacity and targeted blockade of PTP-sigma can substantially improve mouse and human HSC engraftment after transplantation.

Chute and colleagues showed further that PTP-sigma regulates HSC function by suppressing a protein, RAC1, which is known to promote HSC engraftment after transplantation.

These findings have tremendous therapeutic potential since we have identified a new receptor on HSCs, PTP-sigma, which can be specifically targeted as a means to potently increase the engraftment of transplanted HSCs in patients, said Chute, senior author of the study and UCLA Professor of Hematology/Oncology and Radiation Oncology. This approach can also potentially accelerate hematologic recovery in cancer patients receiving chemotherapy and/or radiation, which also suppress the blood and immune systems.

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UCLA Researchers Unlock Protein Key to Harnessing Regenerative Power of Blood Stem Cells

Establishment of induced pluripotent stem cells from Werner syndrome fibroblasts

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Associate Professor Akira Shimamoto and Professor Hidetoshi Tahara at the Graduate School of Biomedical & Health Science in Hiroshima University, Professor Koutaro Yokote at the Graduate School of Medicine in Chiba University, Visiting Professor Makoto Goto at the Medical Center East in Tokyo Women's Medical University, and collaborators including the staff at the Cancer Chemotherapy Center in the Japanese Foundation for Cancer Research, Tottori University, and Keio University established induced pluripotent stem (iPS) cells from the fibroblasts of Werner Syndrome patients.

These results were published in PLOS ONE in an article entitled "Reprogramming Suppresses Premature Senescence Phenotypes of Werner Syndrome Cells and Maintains Chromosomal Stability over Long-Term Culture."

Werner syndrome is characterized by the premature appearance of features associated with normal aging and cancer predisposition. This syndrome occurs frequently in Japan, affecting 1 in 20,000 to 1 in 40,000 people. The therapeutic methods for this disease are very limited and it is expected that iPS cells can be used for the development of innovative therapies.

Dr. Shimamoto and his collaborators analyzed patient-derived iPS cells and found that telomeric abnormalities in the fibroblasts of these patients, which were caused by the lack of WRN helicase encoded by the gene responsible for Werner syndrome, were recovered in the iPS cells generated from these patients. Furthermore, Dr. Shimamoto found that the expression levels of aging-related genes, including those encoding cell cycle inhibitors and inflammatory cytokines, in the patient-derived iPS cells were the same as those in normal iPS cells, even though the expression levels of these genes in the fibroblasts of the patients were higher than those in normal fibroblasts.

Dr. Shimamoto said, "So far, the use of patient cells was restricted to blood or dermal cells in basic research. The iPS cells that we have established will provide an opportunity for drug discovery for the treatment of Werner syndrome and also help with better understanding of the mechanism of this disease. In addition, the mutated WRN gene in patient-derived iPS cells can be corrected by genome editing. This advantage will be help in the development of new gene and cell therapies for Werner syndrome."

Explore further: Scientists find that SCNT derived cells and IPS cells are similar

Journal reference: PLoS ONE

Provided by Hiroshima University

A team led by New York Stem Cell Foundation (NYSCF) Research Institute scientists conducted a study comparing induced pluripotent stem (iPS) cells and embryonic stem cells created using somatic cell nuclear transfer (SCNT). ...

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Establishment of induced pluripotent stem cells from Werner syndrome fibroblasts

Beyond Batten Disease Foundation and the New York Stem Cell Foundation Chosen as a National Innovator by the Milken …

New York, New York (PRWEB) November 17, 2014

Beyond Batten Disease Foundation (BBDF) and the New York Stem Cell Foundation (NYSCF) have been selected as a national innovator by the Milken Institute and will present their breakthrough findings about juvenile Batten disease at the 6th annual Partnering for Cures, November 16-18 in New York City. The presentation will highlight the collaborative efforts of NYSCF, BBDF and Batten Disease Support and Research Association.

Craig and Charlotte Benson established Beyond Batten Disease Foundation in August 2008 after their then five-year-old daughter, Christiane, was diagnosed with juvenile Batten disease. Together with hundreds of families affected by Batten disease, and many more supporters who share their hope and resolve, they are working tirelessly to create a brighter future for Christiane, and all children with Batten disease.

Watch the Benson Family story:

The Benson Family Story

Beyond Batten Disease and the New York Stem Cell Foundation hope to ramp up funding and partnerships to develop stem cell resources to investigate and explore new treatments and ultimately find a cure for juvenile Batten disease, a fatal illness-affecting children as they convene at the FasterCures, conference. The Washington, D.C.-based center of the Milken Institute will bring together nearly 1,000 medical research leaders, investors and decision-makers to forge the collaborations needed to speed and improve outcomes-driven R&D. NYSCF scientists have created the first iPS cells from a neurological disease and the first ever stem cell disease model from any disease. This discovery was named Time Magazine #1 breakthrough in 2008 because it was the first time anyone has made stem cells from a person with a disease and used them to produce the type of cell that degenerated in that patient. Again, in 2012 Time Magazine recognized the Beyond Batten Disease Foundations creation of a rate genetic disease test as a top ten medical breakthrough.

We know the genetic mutations associated with juvenile Batten disease. This partnership will result in stem cell models of juvenile Batten, giving researchers an unprecedented look at how the disease develops, speeding research towards a cure, said Susan L. Solomon, NYSCF Chief Executive Officer.

Working with NYSCF to generate functional neuronal subtypes from patients and families is a stellar example of one of our key strategies in the fight against juvenile Batten disease: creating resource technology with the potential to transform juvenile Batten disease research and accelerate our timeline to a cure, said Danielle M. Kerkovich, PhD, BBDF Principal Scientist.

Juvenile Batten disease begins in early childhood between the ages of five and ten. Initial symptoms typically begin with progressive vision loss, followed by personality changes, behavioral problems, and slowed learning. These symptoms are followed by a progressive loss of motor functions, eventually resulting in wheelchair use and premature death. Seizures and psychiatric symptoms can develop at any point in the disease.

Juvenile Batten disease is one disorder in a group of rare, fatal, inherited disorders known as Batten disease. Over 40 different errors (mutations) in the CLN3 segment of DNA (gene) have been attributed to juvenile Batten disease. The pathological hallmark of juvenile Batten is a buildup of lipopigment in the bodys tissues. It is not known why lipopigment accumulates or why brain and eventually, heart cells are selectively damaged. It is, however, clear that we need disease-specific tools that reflect human disease in order to figure this out and to build therapy.

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Beyond Batten Disease Foundation and the New York Stem Cell Foundation Chosen as a National Innovator by the Milken ...

How adult fly testes keep from changing into ovaries

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New research in flies shows how cells in adult reproductive organs maintain their sexual identity. The study, publishing online on November 13 in the Cell Press journal Developmental Cell, also identified a mutation that can switch the cells' sexual identity. The findings could lead to new insights on how to alter cells for therapeutic purposes.

Sperm and eggs are made from germ cells, but instructions from their neighboring support cellscalled somatic cellsare also essential for their development. By studying the formation of sperm in fruit flies, which is remarkably similar to the process that occurs in people, investigators serendipitously found a mutation that gave testes a very unusual appearance. "Rather than becoming sperm, germ cells were stuck at an early stage, and they were surrounded by support cells that looked suspiciously like those belonging in an ovary," says senior author Dr. Erika Matunis of The Johns Hopkins School of Medicine. Her research team found that the mutation blocked the function of a specific gene in the stem cells that becomes support cells in the testis, causing the fruit flies to change from a male to a female identity.

The research is the first to show that adult stem cells actively maintain their sexual identity. The mutation the investigators found causes the stem cells in males to switch their sexual identities and start making support cells that belong in the ovary. This ultimately derails the production of sperm. "The molecules that govern this process are highly conserved, which suggests that similar mechanisms could operate in human testes," says Matunis.

The changes seen in this study are an example of transdifferentiation, or the conversion from one cell type to another. The topic is of considerable interest because promoting transdifferentiation in a directed manner may be useful for regenerating damaged organs or tissues. Doing so will require a thorough understanding of how cell fate conversions are regulated. "We are excited to have a powerful genetic system for studying transdifferentiation of stem cells at the mechanistic level," says Matunis. The research might also provide insights into how cells transform from a normal state to a cancerous one.

Explore further: Surprise: Lost stem cells naturally replaced by non-stem cells, fly research suggests

More information: Developmental Cell, Ma et al.: "The Jak-STAT target Chinmo prevents sex transformation of adult stem cells in the Drosophila testis niche" http://www.cell.com/developmental-cel 1534-5807(14)00628-5

Journal reference: Developmental Cell

Provided by Cell Press

Johns Hopkins researchers have discovered an unexpected phenomenon in the organs that produce sperm in fruit flies: When a certain kind of stem cell is killed off experimentally, another group of non-stem cells can come out ...

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How adult fly testes keep from changing into ovaries

Study Identifying Cell of Origin for Large, Disfiguring Nerve Tumors Lays Groundwork for Development of New Therapies

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Newswise DALLAS November 11, 2014 UTSouthwestern Medical Center researchers have determined the specific type of cell that gives rise to large, disfiguring tumors called plexiform neurofibromas, a finding that could lead to new therapies for preventing growth of these tumors.

This advance provides new insight into the steps that lead to tumor development and suggests ways to develop therapies to prevent neurofibroma formation where none exist today, said Dr. Lu Le, Assistant Professor of Dermatology at UTSouthwestern and senior author of the study, published online and in Cancer Cell.

Plexiform neurofibromas, which are complex tumors that form around nerves, occur in patients with a genetic disorder called neurofibromatosis type 1 (NF1), which affects 1 in 3,500 people. About 30 percent of NF1 patients develop this type of tumor, which is typically benign.

NF1 patients with plexiform neurofibromas, however, have a 10 percent lifetime risk of the tumors developing into malignant peripheral nerve sheath tumors (MPNSTs), a deadly, incurable type of soft-tissue cancer. In addition, due to their unusual capacity for growth, plexiform neurofibromas can be life-threatening by their physical impairment of vital organs or neural function.

While there are no currently approved therapies for either MPNSTs or plexiform neurofibromas, Dr. Le said determining the cell type and location from which these tumors originate is an important step toward discovering new drugs that inhibit tumor development.

If we can isolate and grow the cells of origin for neurofibromas, then we can reconstruct the biological steps that lead these original cells to tumor stage, said Dr. Le, a member of the Harold C. Simmons Cancer Center. Once we know the critical steps in the process, then we can design inhibitors to block each step in an effort to prevent or slow tumor formation.

Using a process called genetic labeling for cell fate tracing, researchers determined that plexiform neurofibromas originate from Schwann cell precursors in embryonic nerve roots.

This study addresses a fundamental question in the neurofibromatosis field, Dr. Le said. It points to the importance of stem cells and their immediate progenitors in the initiation of tumors, consistent with the notion that these neoplasms originate in a subset of primitive precursors and that most cells in an organ do not generate tumors.

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Study Identifying Cell of Origin for Large, Disfiguring Nerve Tumors Lays Groundwork for Development of New Therapies

Scientists find that SCNT derived cells and IPS cells are similar

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A team led by New York Stem Cell Foundation (NYSCF) Research Institute scientists conducted a study comparing induced pluripotent stem (iPS) cells and embryonic stem cells created using somatic cell nuclear transfer (SCNT). The scientists found that the cells derived from these two methods resulted in cells with highly similar gene expression and DNA methylation patterns. Both methods also resulted in stem cells with similar amounts of DNA mutations, showing that the process of turning an adult cell into a stem cell introduces mutations independent of the specific method used. This suggests that both methods of producing stem cells need to be further investigated before determining their suitability for the development of new therapies for chronic diseases.

The NYSCF Research Institute is one of the only laboratories in the world that currently pursues all forms of stem cell research including SCNT and iPS cell techniques for creating stem cells. The lack of laboratories attempting SCNT research was one of the reasons that the NYSCF Research Institute was established in 2006.

"We do not yet know which technique will allow scientists to create the best cells for new cellular therapies," said Susan L. Solomon, NYSCF CEO and co-founder. "It is critical to pursue both SCNT and iPS cell techniques in order to accelerate research and bring new treatments to patients."

While both techniques result in pluripotent stem cells, or cells that can become any type of cell in the body, the two processes are different. SCNT consists of replacing the nucleus of a human egg cell or oocyte with the nucleus of an adult cell, resulting in human embryonic stem cells with the genetic material of the adult cell. In contrast, scientists create iPS cells by expressing a few key genes in adult cells, like a skin or blood cell, causing the cells to revert to an embryonic-like state. These differences in methods could, in principle, result in cells with different properties. Advances made earlier this year by NYSCF Research Institute scientists that showed that human embryonic stem cells could be derived using SCNT revived that debate.

"Our work shows that we now have two methods for the generation of a patient's personal stem cells, both with great potential for the development of treatments of chronic diseases. Our work will also be welcome news for the many scientists performing basic research on iPS cells. It shows that they are likely working with cells that are very similar to human embryonic stem cells, at least with regard to gene expression and DNA methylation. How the finding of mutations might affect clinical use of stem cells generated from adult cells is the subject of an ongoing debate," said Dr. Dieter Egli, NYSCF Senior Research Fellow, NYSCF - Robertson Investigator, Assistant Professor in Pediatrics & Molecular Genetics at Columbia University, and senior author on the paper.

The study, published today in Cell Stem Cell, compared cell lines derived from the same sources using the two differing techniques, specifically contrasting the frequency of genetic coding mutations seen and measuring how closely the stem cells matched the embryonic state through the analysis of DNA methylation and of gene expression patterns. The scientists showed that both methods resulted in cell types that were similar with regard to gene expression and DNA methylation patterns. This suggested that both methods were effective in turning a differentiated cell into a stem cell.

The scientists also showed that cells derived using both SCNT and iPS techniques showed similar numbers of genetic coding mutations, implying that neither technique is superior in that regard. A similar number of changes in DNA methylation at imprinted genes (genes that are methylated differentially at the maternal versus the paternal allele) were also found. It is important to note that both types of techniques led to cells that had more of these aberrations than embryonic stem cells derived from an unfertilized human oocyte, or than embryonic stem cells derived from leftover IVF embryos. These findings suggest that a small number of defects are inherent to the generation of stem cells from adult differentiated cells and occur regardless of the method used.

Explore further: Some stem cell methods closer to 'gold standard' than others

Researchers around the world have turned to stem cells, which have the potential to develop into any cell type in the body, for potential regenerative and disease therapeutics. Now, for the first time, researchers ...

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Scientists find that SCNT derived cells and IPS cells are similar

Scientists create Parkinson's disease in a dish

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6-Nov-2014

Contact: David McKeon dmckeon@nyscf.org 212-365-7440 New York Stem Cell Foundation @nyscf

New York, NY (November 6, 2014) - A team of scientists led by The New York Stem Cell Foundation (NYSCF) Research Institute successfully created a human stem cell disease model of Parkinson's disease in a dish. Studying a pair of identical (monozygotic) twins, one affected and one unaffected with Parkinson's disease, another unrelated Parkinson's patient, and four healthy control subjects, the scientists were able to observe key features of the disease in the laboratory, specifically differences in the patients' neurons' ability to produce dopamine, the molecule that is deficient in Parkinson's disease. In addition, the scientists also identified a potential strategy for developing novel therapies for Parkinson's disease.

Attributed to a combination of genetic and nongenetic factors, Parkinson's disease has no completely effective therapy or cure. Parkinson's disease is moderately heritable, but the mechanisms of this inheritance are not well understood. While genetic forms of the disease exist, sporadic forms are far more common.

"The unique scenario of identical twins, one with this disease and one without, allowed our scientists an unprecedented look into the mechanisms of Parkinson's disease," said Susan L. Solomon, NYSCF Chief Executive Officer. "Advanced stem cell research techniques allow us to push the boundaries of science and see what actually goes wrong at the cellular level, step by step during the disease process."

DNA mutations resulting in the production of a specific enzyme called glucocerebrosidase (GBA) have been linked to a five-fold greater risk of developing Parkinson's disease; however, only 30% of individuals with this mutation have been shown to develop Parkinson's disease by the age of 80. This discordance suggests that multiple factors contribute to the development of Parkinson's disease, including both genetic and non-genetic factors. To date, there has been no appropriate model to identify and test multiple triggers leading to the onset of the disease.

In this study, published today in Cell Reports, a set of identical twins, both with a GBA mutation, provided a unique opportunity to evaluate and dissect the genetic and non-genetic contributions to the development of Parkinson's disease in one twin, and the lack of disease in the other. The scientists made induced pluripotent stem (iPS) cells from skin samples from both twins to generate a cellular model of Parkinson's in a dish, recapitulating key features of the disease, specifically the accumulation of -synuclein and dopamine deficiency.

Upon analyzing the cell models, the scientists found that the dopamine-producing neurons from both twins had reduced GBA enzymatic activity, elevated -synuclein protein levels, and a reduced capacity to synthesize and release dopamine. In comparison to his unaffected brother, the neurons generated from the affected twin produced less dopamine, had higher levels of an enzyme called monoamine oxidase B (MAO-B), and poor ability to connect with each other. Treating the neurons with molecules that lowered the activity of MAO-B together with overexpressed GBA normalized -synuclein and dopamine levels in the cell models. This suggests that a combination therapy for the affected twin may be possible by simultaneously targeting these two enzymes.

"The subject of Parkinson's disease discordant twins gave us an incredible opportunity to utilize stem cell models of disease in a dish to unlock some of the biological mechanisms of disease," said Dr. Scott Noggle, NYSCF Vice President, Stem Cell Research and The NYSCF - Charles Evans Senior Research Fellow for Alzheimer's Disease. "Working with these various different groups and scientists added to the depth and value of the research and we hope our findings will be applicable to other Parkinson's disease patients and other neurodegenerative disorders."

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Scientists create Parkinson's disease in a dish

Direct generation of neural stem cells could enable transplantation therapy

8 hours ago by Nicole Giese Rura

Induced neural stem cells (iNSCs) created from adult cells hold promise for therapeutic transplantation, but their potential in this capacity has been limited by failed efforts to maintain such cells in the desirable multi-potent NSC state without continuous expression of the transcription factors used initially to reprogram them.

Now, Whitehead Institute scientists have created iNSCs that remain in the multi-potent state without ongoing expression of reprogramming factors. This allows the iNSCs to divide repeatedly to generate cells in quantities sufficient for therapy.

"Therapeutically, it's important to make neural stem cells because they can self-renew and make lots of cells," says Whitehead Institute Founding Member Rudolf Jaenisch, who is also a professor of biology at MIT. "If you just make mature neurons, which has been done by others, you never get enough cells."

To make iNSCs via direct lineage conversion researchers use viruses to insert a cocktail of transcription factors into the genome of mouse adult skin cells. A drug triggers these transcription factors to turn on genes active in neural stem cells. This direct conversion, known as transdifferentiation, bypasses the step of pushing the cells first through an embryonic stem-cell-like state.

In previous research, iNSCs remained addicted to the drug and reprogramming transcription factors; if either the drug or the factors was removed, the cells revert to skin cells.

"If the reprogramming factors are still active, it's horrible for the cells," says John Cassady, a scientist in Jaenisch's lab. "The cells would be unable to differentiate and the resulting cells would not be therapeutically useful."

In a paper published online this week in the current issue of the journal Stem Cell Reports, Cassady and other Whitehead scientists describe how they prevented the cells' relapse without keeping the reprogramming factors active. First, the cells were grown in a special medium that selects for neural stem cells. Then, the drug is removed. Instead of reverting into skin cells, the iNSCs remain in a multi-potent state that can differentiate into neurons and glia cells. Cassady also refined the reprogramming cocktail to contain eight transcription factors, which produces iNSCs that are transcriptionally and epigenetically similar to mouse neural stem cells.

Cassady notes that a random sample of skin cells can contain neural precursor cells, which can more easily make the transition to iNSCs. To eliminate the possibility that his method might actually rely on cells having this sort of "head start", Cassady converted fully mature immune system cells called B-lymphocytes, which have a very specific genetic marker, to iNSCs. The resulting cells had the profile of their new identity as iNSCs, yet retained their B-lymphocyte genetic marker, showing that Cassady's method could indeed convert non-neural cells to iNSCs.

Although promising, all of the work to date has been conducted in mouse cells. According to Cassady, researchers should next test this protocol in human cells to see if it can successfully produce the cell populations necessary for therapeutic use.

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Direct generation of neural stem cells could enable transplantation therapy

SPOTTING CANCER IN STEM CELLS

By Bradley J. Fikes U-T5:07 a.m.Nov. 5, 2014

A small fraction of cancer cells is responsible for spreading tumors to distant points of the body, according to a growing amount of scientific evidence. These cells, often called cancer stem cells, have become the target of intense research in recent years.

Most cancer cells dont appear to have the property of metastasis. They just stay in the tumor. And while primary tumors cause problems, oncologists said metastatic tumors are the real killers. They can lodge in critical places such as the lung, liver and brain.

Failure to eliminate cancer stem cells during treatment may be a big reason why many cancers return after remission. If so, then all those cells must be destroyed, with as little damage as possible to normal cells. Detecting and genetically analyzing cancer stem cells could provide clues to more-effective treatments.

After Jeff Allens wife died of cancer in 2012, the analytical biochemist put his training to work in learning more about the disease.

Doing so was initially a hobby, he said. As time progressed, it became more than a hobby. It became a downright obsession. I got angry at cancer, and as the years went by, I became frustrated with the slow pace of new weapons against it.

Allen, whose background includes development of molecular diagnostic devices, began studying how cancer treatment could be improved.

Now he and his sons, Alexander and Austin, said theyve designed a device that can detect the most dangerous cancer cells, often called cancer stem cells. The device is still in the concept phase, but local scientists who have looked at the technology think its feasible.

The device is envisioned as a microchip that examines a patients blood sample to identify and isolate cancer stem cells. Once captured, these cells would be genetically sequenced to find the mutations driving the cancer. Then doctors could prescribe the most customized treatment based on this more rigorous analysis.

To carry out his plan, Allen is seeking $50,000 through the crowdfunding site gofundme.com, at gofundme.com/7mznuo. He also has formed a company, TumorGen MDx.

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SPOTTING CANCER IN STEM CELLS

Hunting for cancer stem cells

Jeff Allen, who is developing a cancer diagnostic chip similar to this one, poses for a picture in Nick Cosford's research lab at the Sanford Burnham Medical Research Institute. The chip Allen is developing would isolate cancer stem cells for diagnosis.

After Jeff Allens wife died of cancer in 2012, the analytical biochemist put his training to work in learning more about the disease.

Doing so was initially a hobby, he said. As time progressed, it became more than a hobby. It became a downright obsession. I got angry at cancer, and as the years went, by I became frustrated with the slow pace of developing new weapons against it.

Allen, whose background includes development of molecular diagnostic devices, began studying how cancer treatment could be improved.

Now he and his sons, Alexander and Austin, said theyve designed a device that can detect the most dangerous cancer cells, often called cancer stem cells. The device is still in the concept phase, but scientists who have looked at the technology think its feasible.

The device is envisioned as a microchip that examines a patients blood sample to identify and isolate cancer stem cells. Once captured, these cells would be genetically sequenced to find the mutations driving the cancer. Then doctors could prescribe the most customized treatment based on this more rigorous analysis.

To carry out his plan, Allen is seeking $50,000 through the crowdfunding site gofundme.com. He also has formed a company, TumorGen MDx.

In the world of oncology, theres increasing but not total recognition of cancer stem cells and their destructive role. Allen said his own reading of the literature is that these cells do indeed exist. They possess distinct characteristics that enable them to seed an entire new tumor from just a few cells, or perhaps only one.

That theory carries tremendous significance for accurate diagnosis. A drug that inhibits most cancer cells but misses the cancer stem cells wont do much good.

Jeff Allen's video promoting his work for a test to detect cancer stem cells.

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Hunting for cancer stem cells