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Genetic engineering of insulin part 1

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Genetic engineering part 1
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genetic engineering period 4

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ISLC Genetic Engineering: Debate
Debate about Genetic engineering between two students; Jocelyn and Sarah. The camera man being me/Angel and Jade as the judge.

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SUPPORTING GENETIC ENGINEERING, PERIOD 1 ISCL

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ISLC Genetic Engineering on Animals
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How HIV infects a CD4+ T-helper cell. (1) The gp120 viral protein attaches to CD4. (2) The gp120 variable loop attaches to a coreceptor, either CCR5 or CXCR4. (3) HIV enters the cell.

Ever since HIV emerged as a deadly public health threat in the early 1980s, scientists have sought a vaccine that could repel the virus and prevent AIDS. Three decades of intensive research have come up short, although drugs to treat HIV infection have transformed the disease from a death sentence to a chronic disease people can live with.

However, in Third World countries where access to HIV drugs is limited, HIV continues to devastate populations. That could change, if a new study led by scientists from The Scripps Research Institute lives up to its promise.

The scientists have created a genetically engineered protein that inactivates virtually all strains of the virus. While it will take years before this approach can be tested in humans, the concept provides a fresh insight on how to protect people against infection from the AIDS-causing virus.

The protein mimics two receptors on the surface of the immune cells that HIV infects. When the virus encounters the protein, it springs into action as if infecting a cell. The changes the virus undergoes render it incapable of future attempts at infection, said Michael Farzan, a Scripps Research scientist who led the study.

The protein neutralized 100 percent of neutralization-resistant strains of HIV-1, HIV-2 and SHIV-AD8, an artificially made cross between HIV and simian immunodeficiency virus, an HIV relative found in monkeys. The protein was tested in cell cultures, mice with humanized immune systems and macaque monkeys given SHIV. This degree of protection far exceeds that of the strongest anti-HIV antibodies in the body's immune system.

For people, the protein could one day offer lasting protection against HIV infection by means of gene therapy, Farzan said. A designated gene would be carried into muscle cells by an innocuous virus. Then the gene, called eCD4-Ig, would be deposited into the muscle cells, where it would churn out the artificial protein into the bloodstream. If the protein encounters any HIV, it would bind to it, rendering the virus harmless.

In essence, the new study's authors said the approach acts as a vaccine against HIV.

Michael Farzan is a professor at the Florida campus of The Scripps Research Institute. / The Scripps Research Institute

The study was published Wednesday in the journal Nature. Farzan, in Scripps' campus in Jupiter, Florida, was the senior author. Matthew R. Gardner, also of Scripps Florida, was co-first author along with Lisa M. Kattenhorn of Harvard Medical School's New England Primate Research Center in Southborough, Mass. From Scripps' La Jolla headquarters, Dennis R. Burton, a noted expert on broadly neutralizing antibodies, also participated. More than 30 scientists in all took part in the study.

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For the first time, scientists have mapped out the molecular "switches" that can turn on or silence individual genes in the DNA in more than 100 types of human cells, an accomplishment that reveals the complexity of genetic information and the challenges of interpreting it.

Researchers unveiled the map of the "epigenome" in the journal Nature on Wednesday, alongside nearly two dozen related papers. The mapping effort is being carried out under a 10-year, $240 million U.S. government research program, the Roadmap Epigenomics Project, which was launched in 2008.

The human genome is the blueprint for building an individual person. The epigenome can be thought of as the cross-outs and underlinings of that blueprint: For example, if someone's genome contains DNA associated with cancer, but that DNA is "crossed out" by molecules in the epigenome, the DNA is unlikely to lead to cancer. As sequencing individuals' genomes to infer the risk of disease becomes more common, it will become all the more important to figure out how the epigenome is influencing that risk.

Sequencing genomes is the centerpiece of President Barack Obama's "precision medicine" initiative. "The only way you can deliver on the promise of precision medicine is by including the epigenome," said MIT's Manolis Kellis, who led the mapping project.

Because scientists involved in the project have been depositing their findings in a public database as they went along, other researchers have been analyzing the information even before the map was formally published. One of the resulting studies shows, for instance, that brain cells from people who died with Alzheimer's disease had epigenetic changes in DNA involved in immune response.

First published February 18 2015, 7:38 PM

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Newswise While genomics is the study of all of the genes in a cell or organism, epigenomics is the study of all the genomic add-ons and changes that influence gene expression but arent encoded in the DNA sequence. A variety of new epigenomic information is now available in a collection of studies published Feb. 19 in Nature by the National Institutes of Health (NIH) Roadmap Epigenomics Program. This information provides a valuable baseline for future studies of the epigenomes role in human development and disease.

Two of these studies, led by researchers at University of California, San Diego School of Medicine and Ludwig Cancer Research, address the differences between chromosome pairs (one inherited from mom, the other from dad) and how chromosome folding influences gene expression.

Both of these studies provide important considerations for clinicians and researchers who are developing personalized medicines based on a patients genomic information, said Bing Ren, PhD, professor of cellular and molecular medicine at UC San Diego, Ludwig Cancer Research member and senior author of both studies.

The first paper by Rens group takes a look at differences in our chromosome pairs. Each of us inherits one set from our mother and the other from our father. Chromosome pairs are often thought to be identical, one just a backup for the other. But this study found widespread differences in how genes are regulated (turned on and off) between the two chromosomes in a pair. It turns out that we all have biases in our chromosomes. In other words, different traits have a stronger contribution from one parent than the other. The study also suggests that these biases are rooted in inherited sequence variations and that they are not randomly distributed. These findings help explain why, for example, all kids in a family may have their fathers hair but their mothers eyes.

The second paper by Rens group tackles how the genome is organized and how it changes as stem cells differentiate (specialize). DNA strands in every cell are tightly wound and folded into chromosomes. Yet chromosomal structures, and how they influence gene expression, are not well understood. In this study, Ren and team mapped chromosomal structures in stem cells and several different differentiated cell types derived from stem cells. First, they induced differentiation in the stem cells. Then they used molecular tools to examine how the structure of the cells chromosomes changed and how that change is associated with gene activity. The team found that chromosomes are partitioned into relatively stable structural units known as topologically associating domains (TADs), and that TAD boundaries remain constant in different cell types. Whats more, the researchers found that the changes in chromosomal architecture mostly take place within the TADs in a way that correlates with changes in the epigenome.

The epigenome chemical modifications to chromosomes and 3D chromosomal structure is not just a linear object, Ren said. The epigenome is a 3D object, folded in a hierarchical way, and that should affect how we think about many aspects of human development, health and disease.

Co-authors on the paper Integrative Analysis of Haplotype-Resolved Epigenomes Across Human Tissues include Danny Leung, Inkyung Jung, Nisha Rajagopal, Anthony Schmitt, Siddarth Selvaraj, Ah Young Lee, Chia-An Yen, Yunjiang Qiu, Samantha Kuan, Lee Edsall, Ludwig Cancer Research; Shin Lin, Yiing Lin, Stanford University and Washington University School of Medicine; Wei Xie, formerly at Ludwig Cancer Research and now at Tsinghua University; Feng Yue, formerly at Ludwig Cancer Research and now at Pennsylvania State University; Manoj Hariharan, Joseph R. Ecker, Howard Hughes Medical Institute and Salk Institute for Biological Studies; Pradipta Ray, University of Texas; Hongbo Yang, Neil C. Chi, UC San Diego; and Michael Q. Zhang, University of Texas, Dallas and Tsinghua University.

Co-authors on the paper Chromatin Architecture Reorganization during Stem Cell Differentiation include Jesse R. Dixon, Siddarth Selvaraj, Ludwig Cancer Research and UC San Diego; Inkyung Jung, Yin Shen, Ah Young Lee, Zhen Ye, Audrey Kim, Nisha Rajagopal, Yarui Diao, Ludwig Cancer Research; Jessica E. Antosiewicz-Bourget, Morgridge Institute for Research; Wei Xie, Tsinghua University; Jing Liang, Huimin Zhao, University of Illinois at Urbana-Champaign; Victor V. Lobanenkov, National Institute of Allergy and Infectious Diseases; Joseph R. Ecker, Howard Hughes Medical Institute and Salk Institute for Biological Studies; James Thomson, Morgridge Institute for Research, University of Wisconsin and University of California, Santa Barbara.

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The Sims 3 - Perfect Genetics Challenge - Pt2 - First Love?
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Mutants Genetics Gladiators Campaa Supra Estadio Samurai Sushi
Jjaja Hoy Conoceras Otras Facetas De Mi Vos.

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The Clinical Promise of the Gene Therapy from Harrison #39;s Principles of IM, 19th Edition
Dr. J. Larry Jameson, editor for Harrison #39;s Principles of Internal Medicine, discusses the clinical promise of the gene therapy. Visit http://www.HarrisonsIM.com to watch more videos of Dr. J. Larry...

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Uptown Funk Gene Therapy Parody
This is a video made for a 9th grade biology "celebration" grade Have fun???

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Uptown Funk Gene Therapy
This video is about Uptown Funk Gene Therapy.

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Lawrence, KS (PRWEB) February 18, 2015

Pediatric and Developmental Pathology An odd-looking or changing mole or birthmark is always worrisome, particularly on a child. While most are benign, cancer jumps into every parents mind. Gene studies and potential related therapies are just one front in the wide-ranging battle against melanoma.

An analysis in the new issue of the journal Pediatric and Developmental Pathology looks at the link between the typical clinical features of two diseases and the status of two genes. In their study, researchers confirmed that a mutation of the BRAF gene affects people with large or giant birthmarks known as congenital melanocytic nevi (CMNs) and, for the first time, they also found this mutation present in neurocutaneous melanocytosis, a rare neurological disorder associated with Large/Giant CMNs. They suggest that it may be possible to target the BRAF gene during therapy.

CMNs are literally birthmarks, developing in the womb as a fetus grows. Such a dark-colored, sometimes hairy, patch of skin can continue to develop as the child grows, and if it reaches 20 cm or more, it is classified as large or giant. Although usually benign at birth, they can associate with a range of other problems, from decreased sweating and tissue growth to a greater likelihood of melanoma, a skin cancer that is becoming increasingly common worldwide among adults and even teenagers. Neurocutaneous melanocytosis, in which the pigment cells rapidly spread across the brain, spinal cord and meninges, can also develop.

The current study collected pigmented tissue from 66 patients with Large/Giant CMN. The authors first looked for the more commonly mutated NRAS gene and then evaluated those tissues without NRAS mutation for BRAF mutation.

The authors found a new link between BRAF mutations and aggressive disease pattern. They learned of a definite association between the BRAF gene and large or giant CMNs. They also discovered, for the first time, that some patients with neurocutaneous melanocytosis had BRAF but not NRAS mutation. Race was a factor in the appearance of a mutational group, with Asians less likely to show the BRAF mutation.

Surprisingly, more nodules were found in the pigmented skin among people who had the BRAF mutation than among those with the NRAS mutation. Less hair was also found with the BRAF mutation.

The authors concluded that not only NRAS mutations can occur in the studied conditions. They also learned that BRAF mutations may be responsible for more serious disease than previously thought. They said that this means it may be possible to use BRAF inhibitors to target the mutated BRAF gene when treating patients with large or giant CMNs.

Full text of the article BRAF mutations are also associated with neurocutaneous melanocytosis and large/giant congenital melanocytic nevi, Pediatric and Developmental Pathology, Vol. 18, No. 1, 2014, is now available.

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Anyone suffering with arthritis knows how painful and difficult getting around can be. Last Tuesday, at the North Fort Myers Recreation Center, people who suffer from it got an opportunity to learn about treatments and the role exercise plays in minimizing its impact.

"Arthritis: It's No Walk in the Park" was sponsored by the Share Club and featured guest speakers, more than a dozen vendors, and even lunch and door prizes for the nearly 100 people who jammed into the meeting room.

The event, which was held at Lakes Park last year, was intended to inform people of the resources available to those who have arthritis, as well as treatment options.

Scott Strachan, a nurse at Abby's Services, a main sponsor that provides home care for those with arthritis, said the event was a replacement for the Jingle Bell Run, which was discontinued.

"We had guarded optimism the first year and it went over real well for an event of this nature," Strachan said. "We're supporting the folks who need the help and they're getting the information they want."

Among the guest speakers were Dr. David Eichten of Joint Implant Surgeons of Florida, who discussed and answered questions regarding the non-surgical treatments such as ibuprofen and other anti-inflammatory medications, glucosamine chondroitin, which he said was gentler on the liver and kidneys, though results were mixed, and injections, which lubricate joints and do not regrow cartilage.

When all that fails, Eichten discussed partial and full knee and hip replacements which he said can be done with minimal invasion, as well as advances being made in stem-cell research, which he said there has been plenty, although it's too expensive currently for most people to use that therapy.

Dr. Kath Kinross, a physical therapist with Lee Memorial Health System Outpatient Therapy, discussed ways to alleviate the pain of arthritis, as well as having those in attendance do some exercises such as sitting the standing and asking them to turn their seats toward her to reduce strain on the spine.

"I like to step a step back and talk about what we do before we get to that point. Arthritis is inflammation of the joints, and we can do a lot to help. The sooner we do it the less likely we end up needing surgery," Kinross said, adding that an initial injury that doesn't heal properly often begins the onset of arthritis.

Those in attendance found the event very informative, even if they didn't suffer much from arthritis.

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Scientists have found that reducing the size of tiny hair like structures on stem cells stops them turning into fat. The discovery could be used to develop a way of preventing obesity.

The research, conducted at Queen Mary University of London (QMUL), found that a slight regulation in the length of primary cilia, small hair-like projections found on most cells, prevented the production of fat cells from human stem cells taken from adult bone marrow.

Part of the process by which calories are turned into fat involves adipogenesis, the differentiation of stem cells into fat cells. The researchers showed that during this process of adipogenesis, the length of primary cilia increases associated with movement of specific proteins onto the cilia. Furthermore, by genetically restricting this cilia elongation in stem cells the researchers were able to stop the formation of new fat cells.

Recent research has found that many conditions including kidney disease, blindness, problems with bones and obesity can be caused by defects in primary cilia.

Melis Dalbay, co-author of the research from the School of Engineering and Materials Science at QMUL, said: This is the first time that it has been shown that subtle changes in primary cilia structure can influence the differentiation of stem cell into fat. Since primary cilia length can be influenced by various factors including pharmaceuticals, inflammation and even mechanical forces, this study provides new insight into the regulation of fat cell formation and obesity.

Professor Martin Knight, a bioengineer and lead author of the research, said: This research points towards a new type of treatment known as cilia-therapy where manipulation of primary cilia may be used in future to treat a growing range of conditions including obesity, cancer, inflammation and arthritis.

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The above story is based on materials provided by University of Queen Mary London. Note: Materials may be edited for content and length.

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Personalized Medicine, Targeted Therapeutics and Companion Diagnostic Market 2015
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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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Team BASIC LaunchUMD
This video is about Team BASIC, a Junior Gemstone Team, and their project on the efficacy of pH manipulation on Adoptive Cell Therapy. This video was made as part of their LaunchUMD campaign.

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Beverly Hills, CA (PRWEB) February 17, 2015

The top stem cell clinic in Los Angeles and Beverly Hills is now achieving 80% success with stem cell therapy for all types of arthritis and soft tissue indications. This includes hip, knee, shoulder, elbow and ankle injections for helping patients achieve pain relief and avoid surgery. Call (310) 438-5343 for more information on the treatment options available and scheduling.

Dr. Raj, who was recently named a Super Doc Southern California for the 4th year in a row, has been performing stem cell therapy on patients for years. This includes athletes, weekend warriors, celebrities, executives, senior citizens and students as well.

There are two methods offered for the treatment, one of which is Bone Marrow derived. This includes harvesting bone marrow from the patient's hip area, and then the material is immediately processed to concentrate the stem cells and growth factors. the fluid is then injected into the problem area. An internal review at Beverly Hills Orthopedic Institute has shown that 80% of patients achieve excellent pain relief and increased functional abilities. This includes getting back to athletics, recreational activities and walking more.

The second method of treatment involves amniotic derived stem cell rich injections. The amniotic fluid is processed at an FDA regulated lab, with no fetal tissue being involved and no embryonic stem cells at all. Amniotic fluid has been used tens of thousands of times worldwide for many indications, and contains growth factors, hyaluronic acid and stem cells.

Indications for the treatment include tennis and golfer's elbow, plantar fasciitis, degenerative arthritis of the hip, knee, shoulder, elbow, ankle, ligament injuries, and tendonitis of the shoulder, knee, achilles and more.

Dr. Raj is a Double Board Certified orthopedic doctor in Los Angeles and serves as an ABC News Medical Correspondent and a WebMD expert. He is called frequently by networks for his opinion on orthopedic matters, and is on the Medical Advisory Board for R3 Stem Cell.

For more information and scheduling with the top stem cell clinic in Los Angeles and Beverly Hills, call (310) 438-5343.

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Newswise An international team of scientists, led by researchers at the University of California, San Diego School of Medicine, has identified the microtubule-associated protein tau (MAPT) gene as increasing the risk for developing Alzheimers disease (AD). The MAPT gene encodes the tau protein, which is involved with a number of neurodegenerative disorders, including Parkinsons disease (PD) and AD. These findings provide novel insight into Alzheimers neurodegeneration, possibly opening the door for improved clinical diagnosis and treatment.

The findings are published in the February 18 online issue of Molecular Psychiatry.

Alzheimers disease, which afflicts an estimated 5 million Americans, is typically characterized by progressive decline in cognitive skills, such as memory and language and behavioral changes. While some recent AD genome-wide association studies (GWAS), which search the entire human genome for small variations, have suggested that MAPT is associated with increased risk for AD, other studies have found no association. In comparison, a number of studies have found a strong association between MAPT and other neurodegenerative disorders, such as PD.

Though a tremendous amount of work has been conducted showing the involvement of the tau protein in Alzheimers disease, the role of the tau-associated MAPT gene is still unclear, said Rahul S. Desikan, MD, PhD, research fellow and radiology resident at the UC San Diego School of Medicine and the studys first author.

In the new Molecular Psychiatry paper, conducted with collaborators across the country and world, Desikan and colleagues narrowed their search. Rather than looking at all possible loci (specific gene locations), the authors only focused on loci associated with PD and assessed whether these loci were also associated with AD, thus increasing their statistical power for AD gene discovery.

By using this approach, they found that carriers of the deleterious MAPT allele (an alternative form of the gene) are at increased risk for developing AD and more likely to experience increased brain atrophy than non-carriers.

"This study demonstrates that tau deposits in the brains of Alzheimer's disease subjects are not just a consequence of the disease, but actually contribute to development and progression of the disease," said Gerard Schellenberg, PhD, professor of pathology and laboratory medicine at the University of Pennsylvania, principal investigator of the Alzheimers Disease Genetics Consortium and a study co-author.

An important aspect was the collaborative nature of this work. Thanks to our collaborators from the Consortium, the International Parkinsons Disease Genetics Consortium, the Genetic and Environmental Risk in Alzheimers Disease, the Cohorts for Heart and Aging Research in Genomic Epidemiology, deCODE Genetics and the DemGene cohort, we had tremendous access to a large number of Alzheimers and Parkinsons genetic datasets that we could use to identify and replicate our MAPT finding, said Ole A. Andreassen, MD, PhD, professor of biological psychiatry at the University of Oslo and a senior co-author.

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Newswise BOSTON President Barack Obama is requesting an increase of $215 million in the 2016 federal budget to launch the Precision Medicine Initiative. This boost in funding for research will give genetic causes of cancer a national focus specifically around precision or personalized treatments for cancer in the future.

Here are some facts about precision medicine:

1) What is precision or personalized medicine?

Physicians have long recognized that the same disease can behave differently from one patient to another, and that there is no one-size-fits-all treatment. Precision medicine makes diagnosis and treatment of cancer and other diseases more accurate, using the specific genetic makeup of patients (and, in cancer, of their tumors) to select the safest and most effective treatments for them.

In cancer, precision medicine involves testing DNA from patients tumors to identify the mutations or other changes that drive their cancer. Then a treatment for a particular patients cancer that best matches, or targets, the culprit mutations in the tumor DNA is used. While such therapies are not widespread yet, many cancer specialists believe precision treatments will be central to the future of cancer care.

2) Do all patients receive precision or targeted treatment?

Not all patients need targeted therapy to treat their type of cancer. The use of targeted therapies is meant for patients whose tumors have specific gene mutations that can be blocked by available drug compounds. Patients who have mutations in certain types of genes, who have mutations that are beyond the reach of available drugs, or whose tumor cells lack identifiable mutations generally would not be candidates for personalized medicine treatments.

According to the National Cancer Institute, a patient is a candidate for a targeted therapy only if he or she meets specific criteria, which vary depending on the disease. These criteria are set by the Federal Drug Administration (FDA) when it approves a specific targeted therapy.

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DUBLIN, Feb .17, 2015 /PRNewswire/ --Research and Markets

(http://www.researchandmarkets.com/research/sqhzfm/personalized) has announced the addition of the "Personalized Medicine, Targeted Therapeutics and Companion Diagnostic Market 2015: Strategic Analysis of Industry Trends, Technologies, Participants, and Environment" report to their offering.

Personalized Medicine, Targeted Therapeutics and Companion Diagnostic Market 2015 - Strategic Analysis of Industry Trends, Technologies, Participants, and Environment is a cutting-edge comprehensive report on the personalized medicine industry and its impact on the health system. This report tackles the growing market interest in pharmacogenomics, companion diagnostics and the associated market environment.

Individualized, targeted or personalized medicine aims to increase the efficacy of therapeutics via genetic testing and companion diagnostics. Personalized therapeutics and associated companion diagnostics will be more specific and effective thereby giving pharma/biotech companies a significant advantage to recuperate R&D costs. Personalized medicine will reduce the frequency of adverse drug reactions and therefore have a dramatic impact on health economics. Developmental and diagnostic companies will benefit from lower discovery and commercialization costs and more specific market subtypes.

This report describes the current technologies that are propelling the personalized medicine and companion diagnostic market. It examines the current genetic diagnostic tests and companion diagnostic assays that are in use by the medical and pharmaceutical industry today. Current developments in personalized medicine and the pharmacogenomics revolution are discussed. The emerging trends that appear in key markets such as the US, UK, Germany and France are elucidated and analysed. This study reveals market figures of the overall personalized medicine market and also sub-market figures. Forecast projections and future growth rates are provided to give the reader a forthcoming perspective of this growing industry.

The study also provides a comprehensive financial and product review of key players in the personalized medicine industry. Strategic drivers and restraints of this market are revealed and market opportunities and challenges are identified.

In summary, the personalized medicine and associated companion diagnostic market have huge opportunities for growth. This industry will revolutionize the healthcare system and will improve therapeutic effectiveness and reduce the severity of adverse effects. It has enormous potential for investment and the emergence of genetic-based in vitro diagnostics.

This report highlights a number of significant pharmacos and gives details of their operations, products, financials and business strategy.

- 23andMe - Affymetrix - Astex Pharmaceuticals - Atossa Genetics - CuraGen - Celera Corporation (Quest Diagnostics) - Celldex Therapeutics - deCode Genetics (Amgen) - Illumina - Genelex - Myriad - Nodality - Qiagen

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