Quick Medical Genetics - Van der Woude syndrome
This is a lecture about the genetic disease Van der Woude syndrome for trainees and medical professionals. Lecture by Philip M. Boone, MD, PhD. Sources: http...

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Quick Medical Genetics - Van der Woude syndrome - Video

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Strain Review - DNA Genetics Kosher Tangie
She #39;s been a champ for several rounds but it #39;s time to retire her. A small farewell to the tastiest strain in my garden yet. "B-Roll" Kevin MacLeod (incompet...

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Strain Review - DNA Genetics Kosher Tangie - Video

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Jill Hagenkord | A Decade of Direct Access Genetics: What have we learned?
23andMe Chief Medical Officer, Jill Hagenkord, describes how their company is disrupting the healthcare industry by allowing people to access their own DNA. ...

By: bigideasfest

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The Sims 3 - Perfect Genetics Challenge Ep.66 Training the Horses
Come join me on my latest journey into the complex world of sims 3 genetics, as I try to get perfect foals and perfect children. Will I succeed in getting perfect genetics in both? Can I keep...

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The Sims 3 - Perfect Genetics Challenge Ep.66 Training the Horses - Video

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Class 12 -Biology-Genetics-Lec1-Introduction, Genes, Alleles and Gene Pool
Covers introduction of Variations and Genetics. This lecture explain about Genes, locus, Alleles and gene pool. Genes; Alleles; Gene pool; Mendle laws of inheritance; Test cross; Dihybrid...

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Class 12 -Biology-Genetics-Lec1-Introduction, Genes, Alleles and Gene Pool - Video

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Class 12 -Biology-Genetics-Lec7-Sex linkage in Humans and Genetics of Color Blindness
Covers sex linkage groups in humans and basic genetic information about abnormalities like color blindness and hemophilia as X-linked traits.

By: sci4you

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Class 12 -Biology-Genetics-Lec3-Mendels Laws of Genetics, Punnet Square and Test Cross
Covers Mendel #39;s laws of inheritance along with test cross and punnet square.

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Class 12 -Biology-Genetics-Lec3-Mendels Laws of Genetics, Punnet Square and Test Cross - Video

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Class 12 -Biology-Genetics-Lec4-Dominance Relations in Genetics
Covers dominance relationships in genetics i.e. complete dominance, incomplete dominance, over dominance and codominance with examples.

By: sci4you

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Class 12 -Biology-Genetics-Lec6-Gene Linkage, Crossing Over and Recombinant Frequency
covers knowledge about gene linkage and linkage groups, crossing over with its role in variation and evolution and frequency of variation.

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Class 12 -Biology-Genetics-Lec6-Gene Linkage, Crossing Over and Recombinant Frequency - Video

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Keynote: The Ethics of Psychiatric, Neurologic and Behavioral Genetics
Keynote: The Ethics of Psychiatric, Neurologic and Behavioral Genetics Dr. Erik Parens Senior Research Scholar, The Hastings Center Respondent Professor Robert Klitzman Professor of Psychiatry...

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Angus VNR: Genomics picks up pace on genetics progress
Dan Moser, president of Angus Genetics Inc., talks about the ways that genomics are improving the beef business, now and in the future. This video news is provided by Certified Angus Beef LLC...

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Shift 12 - Episode 34: To fight or not
There is no single treatment for cancer, and patients often receive a combination of therapies and palliative care. Treatments usually fall into one of the following categories: surgery, radiation,...

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Shift 12 - Episode 34: To fight or not - Video

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UD alumni $2.5 million closer to saving 5-year-old Eliza
In 2014, University of Delaware alumni Glenn and Cara O #39;Neill raised half of the $5 million needed for a gene therapy clinical trial and the medicine necessa...

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A Sertoli cell (a kind of sustentacular cell) is a "nurse" cell of the testicles that is part of a seminiferous tubule.

It is activated by follicle-stimulating hormone (FSH) and has FSH-receptor on its membranes. It is specifically located in the convoluted seminiferous tubules (since this is the only place in the testes where the spermatozoa are produced). Development of Sertoli cells is directed by the testis-determining factor protein.

Because its main function is to nourish the developing sperm cells through the stages of spermatogenesis, the Sertoli cell has also been called the "mother" or "nurse" cell. Sertoli cells also act as phagocytes, consuming the residual cytoplasm during spermatogenesis. Translocation of germ cells from the base to the lumen of the seminiferous tubules occurs by conformational changes in the lateral margins of the Sertoli cells.

Sertoli cells secrete the following substances:

The tight junctions of Sertoli cells form the blood-testis barrier, a structure that partitions the interstitial blood compartment of the testis from the adluminal compartment of the seminiferous tubules. Because of the apical progression of the spermatogonia, the tight junctions must be dynamically reformed and broken to allow the immunoidentical spermatogonia to cross through the blood-testis barrier so they can become immunologically unique. Sertoli cells control the entry and exit of nutrients, hormones and other chemicals into the tubules of the testis as well as make the adluminal compartment an immune-privileged site.

The cell is also responsible for establishing and maintaining the spermatogonial stem cell niche, which ensures the renewal of stem cells and the differentiation of spermatogonia into mature germ cells that progress stepwise through the long process of spermatogenesis, ending in the release of spermatozoa. Sertoli cells bind to spermatogonial cells via N-cadherins and galctosyltransferase (via carbohydrate residues).

During the maturation phase of spermiogenesis, the Sertoli cells consume the unneeded portions of the spermatozoa.

Sertoli cells are required for male sexual development. During male development, the gene SRY activates SOX9, which then activates and forms a feedforward loop with FGF9. Sertoli cell proliferation and differentiation is mainly activated by FGF9.[2] The absence of FGF9 tends to cause a female to develop [3]

Once fully differentiated, the Sertoli cell is unable to proliferate. Therefore, once spermatogenesis has begun, no more Sertoli cells are created.

Recently however, some scientists have found a way to grow these cells outside of the body. This gives rise to the possibility of repairing some defects that cause male infertility.

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Sertoli cell - Wikipedia, the free encyclopedia

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Dr Ellis hosts seminar on Stem Cell Therapy Facial Rejuvenation
Dr. Dan Eglinton of Asheville Biologics and Orthopaedics, Dr. Sean Whalen and Dr. Paul Mogannam of Flexogenics and Dr. Laura Ellis of medAge speak about Stem Cell Therapy and skin ...

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Department of Bioengineering, Rice University- Expanding Research in Bioengineering
The bioengineering department of Rice University is expanding their department with focuses in systems and synthetic biology, multi-scale optical imaging, an...

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Gut. 2007 May; 56(5): 716724.

Y N Kallis, Department of Medicine, St Mary's Hospital Campus, Imperial College, London, UK

M R Alison, Institute of Cell and Molecular Science, Queen Mary School of Medicine and Dentistry, London, UK

S J Forbes, Tissue Fibrosis and Remodelling Laboratory, MRC/University of Edinburgh Centre for Inflammation Research, Edinburgh, UK

Correspondence to: Professor S J Forbes MRC/University of Edinburgh Centre for Inflammation Research, The Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, UK; stuart.forbes@ed.ac.uk

Stem cells are present in a variety of organs including the bone marrow (BM). Their role is to replenish multiple mature differentiated cell types and thereby achieve longterm tissue reconstitution. Stem cells retain the capacity to generate progeny and renew themselves throughout life. Haematopoietic stem cells (HSCs) are the main stem cell population within the BM and give rise to all mature blood lineages via erythroid, myelomonocytic and lymphoid precursors. A second type of bone marrow stem cell (BMSC), the mesenchymal stem cell (MSC), forms stromal tissue and can give rise to cells of mesodermal origin.

A longstanding principle of cell biology has been that cell loss is reconstituted via stem cells resident within and specific to an organ. However, recent work suggests that this paradigm may not hold for all organs or all types of injury, and tissue damage may attract migratory stem cell populations, particularly those from the BM. This observation has caused considerable interest in the field of liver disease, where new strategies to restore hepatocyte number, augment liver function and counteract progressive organ fibrosis are required. This article will focus on the various relationships between BMSCs and liver disease. It will concentrate on the evidence from animal models and human studies that BMSCs may aid in the regeneration of liver cell populations and may also contribute to the pathogenesis of liver damage. It will discuss the potential to use BMSCs for therapeutic application and review the current status of clinical trials in patients with liver disorders.

The hepatic parenchyma is made up of hepatocytes and cholangiocytes. Unlike other organs such as the gut, liver cell mass is restored primarily through division of the majority of mature hepatocytes and not via a dedicated stem cell population. After a regenerative stimulus, such as a twothirds partial hepatectomy, most hepatocytes rapidly enter the cell cycle and undergo symmetrical mitosis. Liver cell mass can be restored via an average of less than two cell division cycles, albeit individual hepatocytes seem to have an intrinsic capacity for up to 70 doublings in serial transplantation experiments.1 At times of overwhelming cell loss, with longstanding iterative injury (eg, chronic viral hepatitis), or when hepatocyte replication is impeded (eg, replicative senescence of steatohepatitis), regeneration seems to occur via a second cell compartment.2,3 This compartment remains poorly defined and seems to arise from a less differentiated cell population within the terminal branches of the intralobular biliary tree the canals of Hering.4 In rodents these cells are called oval cells, but in humans they are more aptly named hepatic progenitor cells.5 Attempts to identify the originating stem cell are hampered by a paucity of specific cell surface markers.

Initial studies in humans suggested that some hepatocytes have a BM origin. Using Y chromosome tracking, a sparse number of hepatocytes seemed to be originating from the BM in male recipients of female orthotopic liver transplants, and in females who had received bone marrow transplantation (BMT) from male donors and thereafter developed liver disease.6,7 Similarly, other epithelial tissues, such as gut and skin, seemed to harbour cells of BM origin.8 Investigators then turned to an animal model of hereditary type I tryosinaemia, the fumarylacetoacetate hydrolase knockout mouse (FAH(/)), in which it seemed that this potentially fatal enzyme deficiency could be rescued through repopulation of the abnormal liver by BM cells derived from wildtype donors. The implication was that stem cells could cross conventionally demarcated lineage boundaries through a process termed transdifferentiation or stem cell plasticity, leading researchers to question the longheld tenets of cell biology. With time, it became apparent that these initial observations were difficult to reproduce, and later elegant studies in the same FAH(/) mouse model conclusively showed that monocytehepatocyte fusion was the explanation for the restored normal phenotype to the FAHdeficient liver, in which hepatocytes formed by fusion expanded rapidly owing to a considerable survival advantage.9,10

Unfortunately, in the absence of a strong selective pressure, it seems that stable longterm engraftment of BMderived parenchymal cells is unusual. In rats given inhibitors of hepatocyte replication (eg, dgalactosamine, retrorsine or 2acetylaminofluorene), if subjected to a regenerative stimulus such as a partial hepatectomy, BMderived oval cell engraftment can rapidly decrease with time to <1%.11 In the hepatitis B surface antigen transgenic mouse, the BM contributed to hepatocyte repopulation through cell fusion, but only at a very modest rate. In this model, constitutive HBsAg expression induces chronic lowgrade hepatocyte turnover with nodule formation, and inhibition of hepatocyte replication with retrorsine provokes an oval cell response. Here, the contribution from BMderived cells to hepatocyte repopulation waned to just 1.6% by 6months, presumably owing to lack of a sustained selection advantage.12 Likewise, when human HSCs were transplanted into carbon tetrachloride (CCl4)damaged nonobese diabetes/severe combined immune deficiency (NOD/SCID) mice, donorderived hepatocytes expressing mRNA for human albumin and 1 antitrypsin were found in the liver. These hepatocytes occurred through cell fusion, but the phenotype of the chimaeric cells was variable and donorderived genetic material was lost over time.13 When human cord blood, a rich source of progenitor cells, was transplanted into sublethally irradiated NOD/SCID mice, a contribution to the hepatocyte population of only 0.01% was found in the undamaged liver, reportedly through transdifferentiation.14 However, a subsequent study using human cord blood cells again demonstrated only low levels of hepatocyte repopulation even after CCl4induced or hepatocyte growth factor (HGF)induced regeneration. Here the cells were chimaeric for both human and mouse antigens, suggesting that cell fusion rather than transdifferentiation had occurred.15

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Bone marrow stem cells and liver disease - National Center ...

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MIAMI (PRWEB) February 16, 2015

Global Stem Cells Group, Inc. announced an alliance with India-based stem cells company Advancells.com, to share protocols and expand GSCG operations in the India subcontinent with stem cell training and a new treatment center.

Advancells, a pioneer stem cell company with some of the most advanced protocols in the world, focuses on therapeutic applications of regenerative medicine primarily used in stem cells generated from the patients own body. Advancells delivers technologies for safe and effective treatments using their flagship technologies including autologous stem cell therapy from bone marrow and adipose tissue to patients worldwide; Global Stem Cells Group will implement some Advancells technologies in the Regenestem Netowork of worldwide clinics.

Since 2005, Advancells has safely treated thousands of patients for a range of diseases and medical conditions in its various clinics around the globe. Advancells is supported by physicians, stem cell experts and clinical research scientists to continually monitor and improve the effectiveness of its quality management system with excellence and innovation.

"We are pleased to partner with Global Stem Cells Group, to combine our knowledge and expand our ability to bring stem cell medicine to patients worldwide, says Advancells CEO Vipul Jain. I am looking forward to a long and productive alliance.

For more information, visit the Global Stem Cells Group website, email bnovas(AT)stemcellsgroup.com, or call 305-224-1858.

About the Global Stem Cells Group:

Global Stem Cells Group, Inc. is the parent company of six wholly owned operating companies dedicated entirely to stem cell research, training, products and solutions. Founded in 2012, the company combines dedicated researchers, physician and patient educators and solution providers with the shared goal of meeting the growing worldwide need for leading edge stem cell treatments and solutions. With a singular focus on this exciting new area of medical research, Global Stem Cells Group and its subsidiaries are uniquely positioned to become global leaders in cellular medicine.

Global Stem Cells Groups corporate mission is to make the promise of stem cell medicine a reality for patients around the world. With each of GSCGs six operating companies focused on a separate research-based mission, the result is a global network of state-of-the-art stem cell treatments.

About the Regenestem Network:

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Global Stem Cells Group Announces Alliance with Advancells

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The National Institutes of Health is slated to receive $215 million with the hope of individualizing medical treatments by using patients genetic information.

In his State of the Union address on Jan. 20, President Barack Obama announced the Precision Medical Initiative, a program with the goal of enabling doctors to better understand diseases through genetic sequencing of patients and ultimately choose better treatments. In cancer treatment, for example, a patients tumor might be sequenced to uncover the specific mutations causing the disease, and physicians will use that information to select the right drug or predict which will be most effective. The approach has gained traction in the treatment of cancer and rare genetic diseases, but is not available for all patients and is yet to be widely applied to other diseases.

Precision medicine, using genomic information in a way that affects their clinical decisions about care, is already here and now, said Eric Green, director of the National Human Genome Research Institute, which carried out the Human Genome Project and is now working to apply that research to solve medical problems. This is not science fiction, but we are just starting to ascend this mountain. This will be a very long climb, but once we get to the top, you will see genomics being used all over the place.

Green said genetic sequencing in cancer and rare genetic disease treatment saves valuable time and money.

According to professor of medical oncology and Associate Director of the Yale Cancer Center Roy Herbst 84, Yale is already using genome sequencing to personalize treatments and predict the effectiveness of drugs for patients at the cancer center, allowing physicians to find the right drug, for the right patient, at the right time.

But the hope is for the practice to reach a larger population of cancer patients than it does now and ultimately to apply genome sequencing to other diseases.

According to Green, the latter will be more complicated. With diseases like diabetes, arthritis and hypertension, there is a complex interplay between environmental and genetic factors. But the complexity of figuring out how to use genetics in those more complex diseases makes for an even stronger argument to create the Precision Medical Initiative, he added.

Dean of the Yale School of Medicine Robert Alpern said that although the possibility to improve treatment for cancer and other diseases is there, more funding is still needed.

Were at this somewhat frustrating point where the science has never been in a better position to create ways for us to cure diseases that, frankly, when I went to medical school I thought could never be cured, and now theres not enough money, he said. The NIH budget just doesnt keep up with inflation. Were at a point where we can do so much and the money has never been so limited.

Alpern added that Yale is a leader in the use of genomics in personalized medicine the University even has a genome center on West Campus and is primed to turn additional funding into breakthroughs.

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A promising personalized medicine initiative, but little funding

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10 hours ago by Amanda Siegfried Dr. Leonidas Bleris (left), assistant professor of bioengineering at UT Dallas,and Richard Taplin Moore MS11 helped create a new delivery system that may change gene therapy.

Bioengineers at The University of Texas at Dallas have created a novel gene-delivery system that shuttles a gene into a cell, but only for a temporary stay, providing a potential new gene-therapy strategy for treating disease.

The approach offers distinct advantages over other types of gene therapies under investigation, said Richard Taplin Moore MS'11, a doctoral student in bioengineering in the Erik Jonsson School of Engineering and Computer Science. He is lead author of a study describing the new technique in the Jan. 30 issue of the journal Nucleic Acids Research.

"In other gene therapy approaches, the therapeutic genetic messages being delivered can persist for a long time in the patient, potentially lasting for the patient's entire lifetime," Moore said. "This irreversibility is one reason gene therapies are so difficult to get approved."

The UT Dallas study describes proof-of-concept experiments in which a gene carrying instructions for making a particular protein is ordered to self-destruct once the cell has "read" the instructions and made a certain quantity of the protein. In its experiments with isolated human kidney cells, the research team successfully deliveredand then destroyeda test gene that makes a red fluorescent protein.

More research is needed to determine whether and how well the system might work in living organisms. But Moore said the ultimate goal is to refine the method to deliver genes that produce therapeutic proteins or drugs. The nature of the gene delivery system offers more control over how much protein the gene produces in cells or tissues. Because it does not alter the cell permanently, the method also sidesteps potential health problems that can occur if a gene is delivered to the wrong place in a cell's genome.

"Our goal was to create a delivery system for therapeutic genes that would self-destruct, giving us more control over the delivered DNA by limiting the time it resides in cells," Moore said.

Located in the nucleus of each human cell, genes are made of DNA and contain instructions for making proteins. Machinery inside each cell "reads" the instructions and builds those proteins, which then carry out various functions needed to sustain life. Defective or mutated genes can result in malfunctioning or missing proteins, leading to disease.

Gene therapy aims to replace defective genes with healthy versions. Typically the good genes are packaged with a delivery mechanism called a vector, which transports the genetic material inside cells. With traditional approaches, once in the cell, the gene permanently integrates itself into the cell's DNA.

Although promising, this type of gene therapy also has risks. If a therapeutic gene is inserted in the wrong place in the cell's DNA, such as too close to a cancer-related gene, the process could activate additional disease-causing genes, resulting in lifelong health problems for the patient. While many gene therapy clinical trials are underway worldwide, the Food and Drug Administration has not approved for sale any human gene therapy product in the U.S.

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Synthetic biology yields new approach to gene therapy

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CelBank: The doorway to regenerative medicine
An unprecedented opportunity for the 21st Century.

By: Next Healthcare Inc.

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CelBank: The doorway to regenerative medicine - Video

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Hip arthritis 3.5 years after stem cell therapy by Harry Adelson, N.D.
Bobby describes his outcome 3.5 years after stem cell therapy for his arthritic hip by Harry Adelson, N.D. http://www.docereclinics.com.

By: Harry Adelson, N.D.

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Hip arthritis 3.5 years after stem cell therapy by Harry Adelson, N.D. - Video

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Genetic engineering part3
Lol.

By: Gayatri JC

Excerpt from:
Genetic engineering part3 - Video

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In recent months, several national initiatives for personalized medicine have been announced, including the recently launched precision medicine initiative in the US, driven by rapid advances in genomic technologies and with the promise of cheaper and better healthcare. Significant challenges remain, however, in the management and analysis of genetic information and their integration with patient data. The sheer scale and complexity of this data, generated using cutting-edge technologies such as next generation DNA sequencing, requires the development of new computer algorithms and systems that can mine this data to get actionable knowledge.

Now, scientists at A*STAR's Genome Institute of Singapore (GIS) have reported another breakthrough in the development of expert systems that can trawl large datasets, integrating complex disease information to guide doctors in the diagnosis and treatment of diseases. The latest in this series is the development of a system called OncoIMPACT that combines cancer omics data and models learned from hundreds of patients to better sift through genetic mutations and pick potentially causal ones.

The lead investigator in this study, Dr Niranjan Nagarajan, Associate Director of Computational and Systems Biology at the GIS, noted, "We are particularly excited about OncoIMPACT's ability to take into account the unique genetic makeup of each patient to predict treatment targets. It allows us to crunch massive cancer genome datasets in an integrative and model-driven fashion to distill them down to the few key driver mutations."

Assistant Professor Johannes Schumacher from the Institute of Human Genetics at the University of Bonn, added: "The integration of different 'omics' datasets for the identification of cancer driver genes is a challenge. OncoIMPACT fills a gap in integrative analyses and provides the opportunity to revisit large complex datasets for the identification of disease driving genes."

The team of researchers at A*STAR have applied OncoIMPACT to more than a thousand cancers such as melanomas, glioblastomas, prostate, bladder and ovarian cancers, and are in the process of building a complete map of driver mutations across cancers. They also demonstrated a proof-of-concept in this study for using driver mutation signatures to predict clinical outcomes for cancer patients. This is an exciting alternative to currently available tests based on RNA and protein levels as DNA can be more reliably assayed, and the team plans to develop this work further.

Dr Nagarajan remarked, "Our hope is to create a resource for cancer researchers and clinicians in Singapore and around the world. We envisage a future where expert systems such as OncoIMPACT can leverage genomic data generated worldwide and contribute to personalised and targeted medicine in Singapore."

Dr Gopal Iyer, Principal Investigator of the Cancer Therapeutics Research Laboratory at the National Cancer Centre of Singapore (NCCS) noted, "With the availability of large amounts of genetic data, it is difficult to focus our attention on the real cause and drivers in cancers. There are a number of algorithms that help narrow this search down in groups of cancers. OncoIMPACT, however, is different as it can focus these analyses on a single patient. This is the first step for true treatment individualisation: if we can uncover the drivers behind a tumour in a specific patient, we can ask if this can then be treated with specific drugs."

OncoIMPACT is the latest in the series of expert systems from the GIS and follows the recent publication of Phen-Gen -- the first such system to cross-reference patient's symptoms with genome sequence to detect causal genes for rare diseases. Both methods fall in the emerging area of integrative omics, where complex, multi-dimensional datasets are jointly analysed with sophisticated algorithms to reveal novel biological and medical insights.

Story Source:

The above story is based on materials provided by Biomedical Sciences Institutes (BMSI). Note: Materials may be edited for content and length.

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Systems to identify treatment targets for cancer and rare diseases

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Health care professionals nationwide are tangled in a discussion regarding the ethics and regulations of the growing field of precision medicine.

Also known as personalized medicine, the field aims to analyze patients genes so doctors can home in on treatments specific to each person.

As the talks have intensified in recent years, concerns over privacy and insurance discrimination are colliding with benefits like predicting disease contraction and better, more-personalized treatment.

The debate hit the University of Minnesota campus on Thursday with the start of a lecture series focusing on the standardization and policies of precision medicine.

Heidi Rehm, a Harvard University pathology professor, gave the first in a three-part lecture in the Universitys Consortium on Law and Values in Health, Environment and Life Sciences series.

Her lecture comes soon after President Barack Obamas announcement of a plan late last month that calls for a major biomedical research initiative that would create a biobank, or a collection of genetic data, on one million Americans.

If Congress approves Obamas proposal, it would put individualized medicine more easily within doctors reach.

Rehm, who studies precision medicine, said how the technology is used and the way results are interpreted should become more standardized than they currently are.

University law professor and consortium chair Susan Wolf said the difference in technology and interpretation of genomes needs standardization.

Right now its kind of a tower of Babel, Wolf said. And thats really tough on patients that may get different answers from different labs.

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Precision medicine debate hits University campus

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