Archive for the ‘Gene Therapy Research’ Category

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Injemira Beef Genetics 42nd Annual Production Sale Thursday 21st February 2013

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SEATTLE, WA--(Marketwire - Feb 4, 2013) - Atossa Genetics, Inc. ( NASDAQ : ATOS ) announced that its new ForeCYTE Breast Health System addresses the problem of detecting not only cancer, but also the early cellular changes that lead to cancer, in women with dense breasts.

Numerous studies have shown that women with denser breast tissue, and thus more gland tissue and less fatty tissue, are at higher risk for breast cancer. Moreover, as the American Cancer Society (ACS) explains, "Dense breast tissue can also make it harder for doctors to spot problems on mammograms." (ACS Guidelines.)

This is why five states -- California, Texas, New York, Connecticut and Virginia -- have passed legislation requiring that women whose mammograms show dense breasts must be notified of this fact, and several other states and the U.S. Congress are considering such legislation. For instance, the New York law, which took effect January 19, 2013, states that mammography patients with dense breasts must be told: "Your mammogram shows that your breast tissue is dense. Dense breast tissue is very common and is not abnormal. However, dense breast tissue can make it harder to find cancer on a mammogram and may also be associated with an increased risk of breast cancer."

One key study highlights those risks. Scientists at the University of California, San Francisco examined aspirated fluid from the breasts of 2,700 women between the ages of 25 to 65. This fluid contains duct cells, which are responsible for more than 90 percent of breast cancers. The study found that women with dense breasts were more than four times more likely than women without dense breasts to have a condition called atypical hyperplasia -- in which the cells seem to grow too quickly and pile up on each other. These atypical cells represent the first steps on the path to cancer. As a result, spotting these cells is not only key to detecting the risk of cancer in these women; it also opens the door to treating the condition and halting the progression to cancer.

"It is vital that we understand the limits of mammography and give women a better test -- one that is capable of detecting the earliest signs of precancer," said Steven C. Quay, M.D., Ph.D., FCAP, Atossa Genetics' Chairman of the Board and Chief Executive Officer.

In January, Atossa Genetics launched such a diagnostic: the ForeCYTE Breast Health Test. The test, cleared by the U.S. Food & Drug Administration, uses a breast pump called the Mammary Aspirate Specimen Cytology Test (MASCT) to painlessly collect miniscule amounts of fluid from the milk ducts in women's breasts, analyzes the duct cells for hyperplasia and other abnormalities, and analyzes for genetic mutations.

In essence, this test is like a Pap smear for cancer, spotting the earliest cellular warnings up to eight years before cancer can be detected by any other method. Women with dense breasts, therefore, could be monitored every year or so for signs of atypical hyperplasia. As long as the results come back negative, these women could lead normal lives without fear of cancer. But if hyperplasia is detected, women could be treated to reverse the condition.

"Just as Pap smears have reduced cervical cancer rates by over 75 percent, becoming the most successful screening test in medicine, this test can detect the precursor changes that lead to breast cancer -- and make prevention possible," says Quay. "We believe this test should be mandatory for women with dense breasts."

To use Atossa's ForeCYTE Breast Health System, see your doctor. The Atossa test is being distributed to health care providers nationwide by Clarity Women's Health (a division of Diagnostic Test Group, LLC) of Boca Raton, Florida. (See press release.)

For background and additional information on breast density legislation, see WSJ online.

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Women With Dense Breasts Are at Higher Risk for Cancer

Seattle Genetics Inc. (SGEN) recently received approval from Health Canada for its oncology drug, Adcetris (brentuximab vedotin). Adcetris has been approved under Health Canada's Notice of Compliance with conditions (NOC/c) for the treatment of patients with Hodgkins lymphoma (HL) after failure of autologous stem cell transplant (ASCT) or after failure of at least two prior multi-agent chemotherapy regimens in patients who are not suitable for ASCT. Adcetris was also approved for the treatment of systemic anaplastic large cell lymphoma (sALCL) after failure of at least one multi-agent chemotherapy regimen.

For similar indications, Adcetris was approved by the US Food and Drug Administration (FDA) in Aug 2011 and in the EU in Oct 2012.

The NOC/c requires Seattle Genetics to conduct clinical trials to confirm the anticipated clinical benefit of Adcetris. Seattle Genetics is currently enrolling patients for two confirmatory phase III studies evaluating the drug for the front-line treatment of HL and mature T-cell lymphoma (MTCL), including sALCL.

Our Take

We are positive on Seattle Genetics' efforts to penetrate new markets. In Canada, Adcetris is the first in a new class of antibody-drug conjugates (ADCs) to be approved. Adcetris' revenues for the nine months ending Sep 30, 2012 were $102.8 million.

Seattle Genetics carries a Zacks Rank #4 (Sell). Right now Peregrine Pharmaceuticals, Inc. (PPHM), Valeant Pharmaceuticals (VRX) and Targacept, Inc. (TRGT) look more attractive with a Zacks Rank #1 (Strong Buy).

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Canada Approves Seattle Genetics' Adcetris - Analyst Blog

AMES, Iowa, Feb. 4, 2013 /PRNewswire/ --NewLink Genetics Corporation (NLNK), a biopharmaceutical company focused on discovering, developing and commercializing cancer therapeutics, today announced that the underwriters of its recently announced public offering of 4,000,000 shares of common stock have exercised in full their option to purchase an additional 600,000 shares. The offering closed today. All shares were sold by NewLink. Aggregate net proceeds to the company were approximately $49.0 million, after deducting underwriting discounts and commissions and other estimated offering expenses payable by NewLink.

Jefferies & Company, Inc. and Stifel Nicolaus Weisel acted as joint book-running managers in the offering and Baird, Canaccord Genuity Inc. and Cantor Fitzgerald & Co. acted as co-managers.

The shares were sold by the Company pursuant to a shelf registration statement on form S-3, a prospectus and prospectus supplement previously filed with the Securities and Exchange Commission (the "SEC"). Copies of the final prospectus supplement and the accompanying prospectus relating to this offering may be obtained from Jefferies & Company, Inc., Attention: Equity Syndicate Prospectus Department, 520 Madison Avenue, 12th Floor, New York, NY 10022, or by telephone at 877-547-6340, or by email at Prospectus_Department@Jefferies.com, or from Stifel, Nicolaus & Company, Incorporated, Attention: Syndicate, One Montgomery Street, Suite 3700, San Francisco, California 94104, or by calling (415) 364-2500.

This press release shall not constitute an offer to sell or the solicitation of an offer to buy, nor shall there be any sale of, these securities in any state or other jurisdiction in which such offer, solicitation or sale would be unlawful prior to the registration or qualification under the securities laws of any such state or jurisdiction.

About NewLink Genetics CorporationNewLink Genetics Corporation is a biopharmaceutical company focused on discovering, developing and commercializing novel immunotherapeutic products to improve cancer treatment options for patients and physicians. NewLink's portfolio includes biologic and small-molecule immunotherapy product candidates intended to treat a wide range of oncology indications.

Cautionary Note Regarding Forward-Looking StatementsThis press release contains forward-looking statements of NewLink that involve substantial risks and uncertainties. All statements, other than statements of historical facts, contained in this press release are forward-looking statements, within the meaning of The Private Securities Litigation Reform Act of 1995. The words "anticipate," "expect," "intend," "may," "will," "could," "should," or the negative of these terms or other similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. These forward-looking statements include, among others, statements about the Company's expectations with respect to its proposed offering, including its intention to offer and sell shares, the closing of the offering and the Company's intended use of proceeds from the offering. Such statements are based on the Company's expectations as of the date of this press release and are subject to certain risks and uncertainties that could cause actual results to differ materially, including but not limited to the risks and uncertainties associated with market conditions and the satisfaction of customary closing conditions related to the proposed offering, as well as those risks discussed in NewLink's Annual Report on Form 10-K for the year ended December 31, 2011, in its Quarterly Report on Form 10-Q for the quarterly period ended September 30, 2012, and in its other filings with the Securities and Exchange Commission. The forward-looking statements in this press release represent NewLink's views as of the date of this press release. NewLink anticipates that subsequent events and developments will cause its views to change. However, while it may elect to update these forward-looking statements at some point in the future, it specifically disclaims any obligation to do so. You should, therefore, not rely on these forward-looking statements as representing NewLink's views as of any date subsequent to the date of this press release.

Contact: Gordon Link Chief Financial Officer 515-598-2925 glink@linkp.com

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NewLink Genetics Corporation Announces Exercise of Underwriters' Option and Closing of Public Offering of Common Stock

Seattle Genetics Inc. (SGEN) recently received approval from Health Canada for its oncology drug, Adcetris (brentuximab vedotin). Adcetris has been approved under Health Canada's Notice of Compliance with conditions (NOC/c) for the treatment of patients with Hodgkins lymphoma (HL) after failure of autologous stem cell transplant (:ASCT) or after failure of at least two prior multi-agent chemotherapy regimens in patients who are not suitable for ASCT.

Adcetris was also approved for the treatment of systemic anaplastic large cell lymphoma (sALCL) after failure of at least one multi-agent chemotherapy regimen.

For similar indications, Adcetris was approved by the US Food and Drug Administration (:FDA) in Aug 2011 and in the EU in Oct 2012.

The NOC/c requires Seattle Genetics to conduct clinical trials to confirm the anticipated clinical benefit of Adcetris. Seattle Genetics is currently enrolling patients for two confirmatory phase III studies evaluating the drug for the front-line treatment of HL and mature T-cell lymphoma (:MTCL), including sALCL.

Meanwhile, in Jan 2013, a global phase III study (ECHELON-2) was initiated on Adcetris. In this study, Adcetris plus chemotherapy will be evaluated for the front-line treatment of CD30-positive MTCL including patients with sALCL and other types of peripheral T-cell lymphomas.

Our Take

We are positive on Seattle Genetics efforts to penetrate new markets. In Canada, Adcetris is the first in a new class of antibody-drug conjugates (ADCs) to be approved. Adcetris revenues for the nine months ending Sep 30, 2012 were $102.8 million.

Seattle Genetics carries a Zacks Rank #4 (Sell). Right now Peregrine Pharmaceuticals, Inc. (PPHM), Valeant Pharmaceuticals (VRX) and Targacept, Inc. (TRGT) look more attractive with a Zacks Rank #1 (Strong Buy).

Read the Full Research Report on SGEN

Read the Full Research Report on TRGT

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Canada Approves Seattle Genetics' Adcetris

Movement Disorders: Ask Dr. Fernando Pagan
Hear answers to commonly asked questions about movement disorders. Dr. Fernando Pagan also explains the diagnosis of Parkinson #39;s disease and medical management. For more information about your movement disorder experience at MedStar Georgetown University Hospital, call MedStar Georgetown MD at 202-342-2400 or visit medstargeorgetown.org VIDEO CHAPTERS: 1. Introduction (0:00) 2. How do your patients with movement disorders benefit from research going on at MedStar Georgetown? (2:59) 3. Define Parkinson #39;s disease. (4:34) 4. What are some of the newly recognized symptoms of Parkinson #39;s disease? (5:42) 5. How do you think the diagnosis of Parkinson #39;s disease will change in the future? (6:27) 6. How is Parkinson #39;s diagnosed? (7:36) 7. What new technologies can be used at MedStar Georgetown to diagnose Parkinson #39;s disease? (8:43) 8. What are the common medications for Parkinson #39;s? (9:55) 9. Are there Parkinson #39;s patients who can get drugs other than Levodopa? (11:04) 10. What is new about how my medications for Parkinson #39;s disease work the best? (12:16) 11. What treatments are available as my Parkinson #39;s disease progresses? (12:54) 12. Is Parkinson #39;s disease curable? (13:56) 13. Could receiving treatment for my Parkinson #39;s disease help me live longer? (15:04) 14. Why should I consider Deep Brain Stimulation for my Parkinson #39;s disease? (15:58) 15. What is Deep Brain Stimulation for Parkinson #39;s disease and how does it work? (16:52) 16. Why is fine tuning and follow-up care after ...

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Movement Disorders: Ask Dr. Fernando Pagan - Video

One of the biggest problems in treating HIV patients is the amount of daily individual medications it takes to keep the virus at bay. In a new study, scientists at the Stanford University School of Medicine have engineered a new approach to tailored gene therapy that they say makes key cells of the immune system resistant to attack from the HIV virus, which may eventually lead to the removal of life-long dependencies on drugs for patients living with HIV.

The drug treatment regime for HIV is intended to block the reception of the virus at different stages of the replication process. Unfortunately, the virus itself is known to mutate and thats why a selection of medications, known as highly active antiretroviral therapy (HAART), is required to stave off potentially fatal infections. Researchers at Stanford have added to previous experiments by cutting and pasting a series of HIV-resistant genes into the immune cells that are targeted by the virus, known as T-cells, thereby simulating the HAART treatment through genetic manipulation.

Typically, HIV enters T-cells by latching onto one of two surface proteins known as CCR5 and CXCR4. However, a small number of people carry a mutation in CCR5, making them more resistant to HIV. The results of this are exemplified by the now-famous Berlin Patient, a leukemia sufferer with the HIV virus, who received a bone-marrow transplant and was subsequently cured of HIV, thanks to the donor carrying the mutated CCR5 gene.

This new study builds on previous work by scientists at Sangamo BioSciences in California who developed a technique using a protein that recognizes and binds to the CCR5 receptor gene, genetically modifying it to mimic the naturally resistant version. This technique uses a protein that can break up pieces of DNA, known as a zinc finger nuclease, to effectively inactivate the receptor gene.

The Stanford researchers have now used the same nuclease to create a break in the CCR5 receptors' DNA, within which they pasted three genes known to hold back the virus. The technique of placing these genes in one site is known as stacking. The study also states that, Incorporating the three resistant genes helped shield the cells from HIV entry via both the CCR5 and CXCR4 receptors. The disabling of the CCR5 gene by the nuclease, as well as the addition of the anti-HIV genes, created multiple layers of protection.

This form of tailored gene therapy, which blocks both the CCR5 and CXCR4 has not been achieved before. The stacked triplet of anti-HIV genes created an effective barrier of more than 1,200-fold protection for the CCR5 gene and more than 1,700-fold for the CXCR4 (based off an unaltered T-cell), which is a much higher success rate than tests with only one or two alterations. Comparatively, the unaltered T-cell became infected within 25 days.

However, the technique is not without drawbacks. A concern is that creating a break in one part of the cell may lead to an unintended break elsewhere, which may cause cancer or other cell aberrations. The study also says that Its possible the cells wont like the proteins theyre asked to express, and wont grow.

Those challenges aside, the news is promising for the development of delivering individually tailored, virus resistant T-cells to an infected patient. Because the method will be on a patient-by-patient basis it will be time consuming, and though it will not kill the virus, it may free patients of the need to take strong antiretroviral medications that keep their immune system from collapsing. The researchers hope to begin clinical trials within three to five years.

The study appears in the Jan. 22 issue of Molecular Therapy.

Source: Stanford School of Medicine

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Tailored gene therapy approach could replace drug treatments for HIV patients

By: Agence France-Presse February 5, 2013 6:32 AM

AFP FILE PHOTO

InterAksyon.com The online news portal of TV5

PARIS - Scientists using gene therapy have partially restored hearing and balance in profoundly deaf mice, according to a study published on Monday in the journal Nature Medicine.

The research, still in its early stages and restricted to lab animals, may open up new avenues for tackling Usher syndrome, an inherited form of human deafness that usually goes hand in hand with blindness.

Researchers led by Michelle Hastings at the Rosalind Franklin University of Medicine and Science in Chicago, Illinois, aimed at a gene called USH1C which has been implicated in the "Type 1" form of Usher syndrome.

USH1C controls a protein called harmonin, which plays a vital role in hair cells -- the cells in the cochlea of the inner ear that respond to sound waves and send an electrical signal to the brain.

The team devised a tiny strand of genetic material called an antisense oligonucleotide to "switch off" a faulty version of the gene that produces truncated forms of the protein.

The therapy was injected in newborn mice that had been genetically engineered to have the mutation.

A single injection partially restored their hearing at very low frequencies, and also reduced head tossing, a behavior caused by impaired balance.

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HEAR THIS | Gene therapy in mice boosts hope for the deaf

QUEBEC, Feb. 4, 2013 /CNW Telbec/ - In the latest issue of the journal Molecular Therapy, Professor Jacques P. Tremblay (president of the Association of Gene Therapy of Quebec and researcher in the Research center of the Centre Hospitalier Universitaire (CHU) of Quebec) launches a call - with 50 other world experts in gene therapy - for the creation of an International Gene Therapy Consortium for Monogenic Diseases. The bases of this consortium will be established during a workshop, which will be held during the congress of the American Society of Gene and Cell Therapy (ASGCT) in Salt Lake City in May 2013.

Recent scientific progress in molecular biology and in genomics allowed during the recent years to identify the genes responsible for 10,000 hereditary diseases caused by a mutation in a single gene (for ex., Duchenne muscular dystrophy, Friedreich ataxia, haemophilia, etc.). On the other hand, recent progress of gene therapy resulted in treatments for some of these diseases previously considered incurable: hereditary immuno-deficiencies (the bubble children), a form of hereditary blindness (congenital amaurosis of Leber), etc. Also, for the first time, a gene-therapy treatment was approved for commercialization in Europe (for familial hyperchylomicronemia, a lipid disease). A Quebec team participated in the development of this treatment. The discovery of pluripotent stem cells, for which Dr. Yamanaka obtained the Nobel Prize in Medicine 2012, also allows to genetically correct the patient own cells and to differentiate them in various types of cells including those of heart and brain. These cells could then be re-transplanted to the patient without immunosuppression.

The research to develop treatments for these hereditary illnesses is at present made by small teams often financially supported by small patient associations. This fragmentation of the research and the sub-financing make more difficult the development of clinical trials. Professor Tremblay and his cosignatories indicate that with sufficient budgets, it would be possible to develop globally therapies for the most of these diseases during the next 2 decades.

The Regroupement qubcois des maladies orphelines (Quebec Coalition of Orphan Diseases) encourages initiatives that help develop treatments for rare genetic disorders.

The article that calls for the creation of the Consortium: Translating the Genomics Revolution: The Need for an International Gene Therapy Consortium for Monogenic Diseases, Molecular Therapy, February 2013.

SOURCE: Regroupement qubcois des maladies orphelines

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Creation of an International Gene Therapy Consortium

A new gene therapy tested on deaf mice proved to partially restore hearing and balance, giving hope to many who suffer from Usher syndrome, a form of human deafness that usually comes with blindness.

While the research, which was published in the journal Natural Medicine, is still in its early stages and has not been tested on humans, it has made many hopeful of a future therapy for the deaf.

Michelle Hastings, lead researcher, focused in on a gene called USH1C, which is "Type 1" of Usher syndrome.

The role of the gene is to produce a protein called harmonin, which plays an important role in hair cells. Our hearing is processed in the cochlea of the inner ear, where these hair cells are located, and an electrical signal is sent to the brain.

The team created a strand of genetic material called an antisense oligonucleotide to "switch off" a faulty gene that truncates forms of harmonin, leading to deafness.

Once this therapy was inserted into mice that were born with the mutation, their hearing was restored at low frequency. It also reduced head tossing, a behavior that occurs when balance is impaired.

"These effects were sustained for several months, providing evidence that congenital deafness can be effectively overcome by treatment early in development to correct gene expression," the study said.

After the experiment concluded, the mice were dissected and researchers found their cochleas to have grown some hair cells.

Much progress has been made recently in researching potential treatments for the deaf.

In January, doctors at the Massachusetts Eye and Ear and Harvard Medical School reported on another gene drug that transformed cochlea cells into hair cells.

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Gene Therapy Restores Hearing in Deaf Mice

Scientists using gene therapy have partially restored hearing and balance in profoundly deaf mice, according to a study published in the journal Nature Medicine.

The research, still in its early stages and restricted to lab animals, may open up new avenues for tackling Usher syndrome, an inherited form of human deafness that usually goes hand in hand with blindness.

Researchers led by Michelle Hastings at the Rosalind Franklin University of Medicine and Science in Chicago, Illinois, aimed at a gene called USH1C, which has been implicated in the 'Type 1' form of Usher syndrome.

USH1C controls a protein called harmonin, which plays a vital role in hair cells - the cells in the cochlea of the inner ear that respond to sound waves and send an electrical signal to the brain.

The team devised a tiny strand of genetic material called an antisense oligonucleotide to 'switch off' a faulty version of the gene that produces truncated forms of the protein.

The therapy was injected in newborn mice that had been genetically engineered to have the mutation.

A single injection partially restored their hearing at very low frequencies, and also reduced head tossing, a behaviour caused by impaired balance.

'These effects were sustained for several months, providing evidence that congenital deafness can be effectively overcome by treatment early in development to correct gene expression,' the study says.

After the experiment, the mice were dissected, and their cochleas were found to have grown some hair cells.

The success of antisense oligonucleotides adds a further weapon in the quest to overcome deafness.

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Gene therapy boosts hope for the deaf

Stem Cell Patient Treated With Adult Stem Cell Therapy - Video
Sigrid Zipser, a patient with coronary artery disease and congestive heart failure and no more treatment options seeked out treatment with Vescell stem cell therapy because it was treatment with her own adult stem cells. Producer: VesCell; Creative Commons license: Attribution.

By: rosaryfilms

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Stem Cell Patient Treated With Adult Stem Cell Therapy - Video - Video

Public release date: 3-Feb-2013 [ | E-mail | Share ]

Contact: Liz Williams williams@wehi.edu.au 61-405-279-095 Walter and Eliza Hall Institute

Scientists have identified the gene essential for survival of antibody-producing cells, a finding that could lead to better treatments for diseases where these cells are out of control, such as myeloma and chronic immune disorders.

The discovery that a gene called Mcl-1 is critical for keeping this vital immune cell population alive was made by researchers at Melbourne's Walter and Eliza Hall Institute. Associate Professor David Tarlinton, Dr Victor Peperzak and Dr Ingela Vikstrom from the institute's Immunology division led the research, which was published today in Nature Immunology.

Antibody-producing cells, also known as plasma cells, live in the bone marrow and make antibodies that provide a person with long-term protection from viruses and bacteria, Associate Professor Tarlinton said. "Plasma cells are produced after vaccination or infection and are responsible for the immune 'memory' that can persist in humans for 70 or 80 years. In this study, we found that plasma cells critically rely on Mcl-1 for their continued survival and, without it, they die within two days," he said.

Dr Peperzak said the team was surprised to find that plasma cells used this as a 'failsafe' mechanism in controlling their survival. "One of the interesting things we found is that because plasma cells rapidly destroy Mcl-1 proteins within the cell yet depend on it for their survival, they need continuous external signals to tell them to produce more Mcl-1 protein," Dr Peperzak said. "This keeps the plasma cells under tight control, with Mcl-1 acting like a timer that constantly counts down and, if not reset, instructs the cell to die."

Plasma cells are vital to the immune response, but can be dangerous if not properly controlled, Associate Professor Tarlinton said. "As with any immune cell, plasma cells are really quite dangerous in many respects and need to be tightly controlled," he said. "When they are out of control they continue to make antibodies that can be very damaging if there are too many. This happens in conditions such as myeloma a cancer of plasma cells and various forms of autoimmunity, such as systemic lupus erythamatosus or rheumatoid arthritis, where there are excessive levels of antibodies."

Myeloma is a blood cancer that affects more than 1200 Australians each year, and is more common in people over 60. It is caused by the uncontrolled production of abnormal plasma cells in the bone marrow and the build up of damaging antibodies in the blood. Rheumatoid arthritis and lupus are autoimmune diseases in which the antibodies produced by plasma cells attack and destroy the body's own tissues.

Associate Professor Tarlinton said that his hope was that the discovery could be used to develop new treatments for these conditions. "Myeloma in particular has a very poor prognosis, and is generally considered incurable," Associate Professor Tarlinton said. "Now that we know Mcl-1 is the one essential gene needed to keep plasma cells alive, we have begun 'working backwards' to identify all the critical molecules and signals needed to switch on Mcl-1 and keep the cells alive. Our hope is that we will identify some point in the internal cell signalling pathway, or a critical external molecule, that could be blocked to stop Mcl-1 being produced by the cell. This would be an important new platform for diseases that currently have no specific or effective treatment, such as myeloma, or offer new treatment options for people who don't respond well to existing treatments for diseases such as lupus or rheumatoid arthritis."

###

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Immune cell 'survival' gene key to better myeloma treatments

This is an image of TALE. Credit: Charles Gersbach

By reproducing in the laboratory the complex interactions that cause human genes to turn on inside cells, Duke University bioengineers have created a system they believe can benefit gene therapy research and the burgeoning field of synthetic biology.

This new approach should help basic scientists as they tease out the effects of "turning on" or "turning off" many different genes, as well as clinicians seeking to develop new gene-based therapies for human disease.

"We know that human genes are not just turned on or off, but can be activated to any level over a wide range. Current engineered systems use one protein to control the levels of gene activation," said Charles Gersbach, assistant professor of biomedical engineering at Duke's Pratt School of Engineering and member of Duke's Institute for Genome Sciences and Policy. "However, we know that natural human genes are regulated by interactions between dozens of proteins that lead to diverse outcomes within a living system.

"In contrast to typical genetics studies that dissect natural gene networks in a top-down fashion, we developed a bottom-up approach, which allows us to artificially simulate these natural complex interactions between many proteins that regulate a single gene," Gersbach said. "Additionally, this approach allowed us to turn on genes inside cells to levels that were not previously possible."

The results of the Duke experiments, which were conducted by Pablo Perez-Pinera, a senior research scientist in Gersbach's laboratory, were published on-line in the journal Nature Methods. The research was supported by the National Institutes of Health, the National Science Foundation, The Hartwell Foundation, and the March of Dimes.

Human cells have about 20,000 genes which produce a multitude of proteins, many of which affect the actions of other genes. Being able to understand these interactions would greatly improve the ability of scientists in all areas of biomedical research. However because of the complexity of this natural system, synthetic biologists create simple gene networks to have precise control over each component. These scientists can use these networks for applications in biosensing, biocomputation, or regenerative medicine, or can use them as models to study the more complex natural systems.

"This new system can be a powerful new approach for probing the fundamental mechanisms of natural gene regulation that are currently poorly understood," Perez-Pinera said. "In this way, we can further the capacity of synthetic biology and biological programming in mammalian systems."

The latest discoveries were made possible by using a new technology for building synthetic proteins known as transcription activator-like effectors (TALEs), which are artificial enzymes that can be engineered to "bind" to almost any gene sequences. Since these TALEs can be easily produced, the researchers were able to make many of them to control specific genes.

"All biological systems depend on gene regulation," Gersbach said. "The challenge facing bioengineering researchers is trying to synthetically recreate processes that occur in nature."

More here:
Bioengineers recreate natural complex gene regulation

Cat-Raccoon Hybrid Mix (Cacoon)
Cacoon: The cat crossed with a raccoon is most often attributed to the Maine Coon, a large fluffy cat that can have striped marking like a raccoon. Maine Coons are a breed of cat that originated in feral colonies to be large, muscular, and hardy, able to tough out the cold New England winters and hunt small vermin. Being an old breed however the people who first noticed (and named) them weren #39;t educated on the wonderful world of genetics. They attributed the cats markings, fluffy tail, and sometimes extra toes to the fact it was a cross between a cat and a raccoon. This of course turned out not to be the case, as this particular pairing is impossible. http://www.utcinema.com New Jersey, 2013

By: Uladzimir Taukachou

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Cat-Raccoon Hybrid Mix (Cacoon) - Video

Mutation changes the gene expression
For more information, log on to- shomusbiology.weebly.com Download the study materials here- shomusbiology.weebly.com In genetics, a mutation is a change of the nucleotide sequence of the genome of an organism, virus, or extrachromosomal genetic element. Mutations result from unrepaired damage to DNA or to RNA genomes (typically caused by radiation or chemical mutagens), from errors in the process of replication, or from the insertion or deletion of segments of DNA by mobile genetic elements.[1][2][3] Mutations may or may not produce discernable changes in the observable characteristics (phenotype) of an organism. Mutations play a part in both normal and abnormal biological processes, including evolution, cancer, and the development of the immune system. Mutation can result in several different types of change in yes sequences; these can either have no effect, alter the product of a gene, or prevent the gene from functioning properly or completely. One study on genetic variations between different species of Drosophila suggests that if a mutation changes a protein produced by a gene, the result is likely to be harmful, with an estimated 70 percent of amino acid polymorphisms having damaging effects, and the remainder being either neutral or weakly beneficial.[4] Due to the damaging effects that mutations can have on genes, organisms have mechanisms such as DNA repair to prevent mutations.[1]

By: Suman Bhattacharjee

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Mutation changes the gene expression - Video

Saints Decoded by Gerone Wright
Saints are genetic bridgers of mankinds and animal genetics. Each and every Saint from past through to current I can expose thier contribution to the genetic alterings of mankind through intervention with animal genetics. My proof is in abundance. I have our worlds ancient art collections and other unseen or otherwise unknown records which are in a multidimensional presense herein our world and beyond. Through my genuine paranomal experience/encounter I have no limitations as to what I can expose with regards to the true origins of mankind and those that have genetically intervened in mankinds evolution through cult comparable rituals. All our worlds ancient history is in one encryptic way or another referencing a the genetic alterings of mankind. Addiditionally, thier are many encryption styles which were untilized by artist to maintain a precise record or genetic blueprint of the many genetic interventions of mankind. However, all the artist have a common message in thier paintings which is how mankind landed our worlds oceans from space in the form microoganisms in rock, evolved through the ocean onto land, and at precise interving points rebridged mankinds genes with previous creatures genetics that mankind evolved through inorder to weaken, destroy, and extract unwanted genes from the previous process of creation. There is much more. Gerone Wright

By: Geroneification

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Saints Decoded by Gerone Wright - Video

Joe Dispenza: Breaking the Habit of Being Yourself
http://www.cyacyl.com http://www.joanherrmann.com You are not hardwired to be a certain way the rest of your life. Contrary to what you may think, the brain is the organ of change. By understanding how your mind works you can learn how to change negative habits and emotions and rewire your brain with new thoughts and beliefs that will transform your mind and body. Dr. Joe Dispenza, author of the new book Breaking the Habit of Being Yourself, combines the fields of quantum physics, neuroscience, brain chemistry, biology, and genetics to show what is truly possible. Dr. dispenza provides information to help you change any aspect of yourself, and to reach your specific goals and visions by eliminating self-destructive habits. His approach creates a bridge between true human potential and the latest scientific theories of neuroplasticity. Dr. Dispenza is also the author of the book, Evolve Your Brain: The Science of Changing Your Mind. He was also one of the featured researchers in What the BLEEP Do We Know!?

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Joe Dispenza: Breaking the Habit of Being Yourself - Video

Genetics and Mesothelioma: Dr. Michele Carbone
bestmesotheliomalawfirm.com Click Here to see more! Dr. Michele Carbone and researchers from the University of Hawaii Cancer Center identify genetic mutation that increases susceptibility to mesothelioma and potentially other forms of cancer. Copyright Disclaimer Under Section 107 of the Copyright Act 1976, Allowance is made for fair use for purposes such as criticism, comment, news reporting, teaching, scholarship, and research. Fail use is a use permitted by copyright statute that might otherwise be infringing. Personal use tips the balance in favor of fair use

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Genetics and Mesothelioma: Dr. Michele Carbone - Video