Archive for the ‘Gene Therapy Research’ Category

Newswise University of California, San Diego School of Medicine researchers Joseph G. Gleeson, MD, Howard Hughes Medical Institute investigator and professor of neurosciences and pediatrics, and Richard D. Kolodner, PhD, professor of medicine and Ludwig Cancer Research scientist, have been named new members of the Institute of Medicine (IOM), considered among the highest honors in the fields of health and medicine.

Gleeson and Kolodner were among 70 new members and 10 foreign associates announces today at the IOMs annual meeting, bringing total IOM membership to 1,966 worldwide. Forty-six UC San Diego faculty members, current and emeritus, are IOM members.

Joseph Gleeson

Gleeson is principal investigator at the Center for Brain Development, a laboratory that seeks to understand the genetic basis of brain diseases such as mental retardation, epilepsy and autism using genetic tools. He is also director of the UC San Diego Neuroscience Core, co-director of the Biomedical Sciences Graduate Program and a member of the Institute for Genomic Medicine at UC San Diego.

He is also a member of the Child Neurology Society, the Society for Neuroscience and the American Society for Human Genetics, and has served on the editorial boards of the Journal of Child Neurology, Human Molecular Genetics and Journal of Pediatric Neurology.

Gleeson earned his undergraduate degree in chemistry at UC San Diego and his medical degree at the University of Chicago Pritzker School of Medicine. He came to UC San Diego in 1999. Among his awards and honors are the Klingenstein Fellowship Award in the Neurosciences, a Searle Scholar Award and the Burroughs Wellcome Fund Clinical Scientist Award in Translational Research.

Richard Kolodner

Kolodner, professor in cellular and molecular medicine at UC San Diego School of Medicine and UC San Diego Moores Cancer Center, has made seminal contributions to understanding the connection between DNA mismatch repair the ability of cells to fix genetic errors in DNA and cancer.

He is a member of the National Academy of Sciences (2000), the American Academy of Arts & Sciences (2008), the American Society for Microbiology, the Genetics Society of America and American Association for Cancer Research. He has served on numerous advisory and review boards, including the Board of Scientific Counselors of the National Cancer Institute and the Howard Hughes Medical Institute Scientific Review Board.

Among his awards are the Dana-Farber Cancer Institute Morse Research Award, the Charles S. Mott Prize of the General Motors Cancer Research Foundation and the Landon-AACR Prize for Basic Cancer Research.

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Two UC San Diego Researchers Elected to Institute of Medicine

2014 Gnu Eco Genetics Snowboard - Review - The-House.com
Gnu - http://www.the-house.com/snbd-gnu.html This all terrain eco friendly deck will help you go bananas, literally - it #39;s the Gnu Eco Genetics Snowboard. Pr...

By: The House

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2014 Gnu Eco Genetics Snowboard - Review - The-House.com - Video

Bio One 3.3 C- nonmendelian genetics
via YouTube Capture.

By: LuongBiology

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Bio One 3.3 C- nonmendelian genetics - Video

Christianity Judaism and Genetics - The Fallacy
Christianity is not a racist religion, but millions of Christians have accepted a racist point of view relative to the Return of Christ. Christians are God #39;s temple and when they are Born Again...

By: Vern Manson

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Christianity Judaism and Genetics - The Fallacy - Video

Seattle Genetics, Inc. ( SGEN ) commenced a phase I study to evaluate SGN-LIV1A in patients with LIV-1-positive metastatic breast cancer. Seattle Genetics' antibody-drug conjugate (ADC) technology has been used for SGN-LIV1A.

The open-label, dose-escalation study will enroll up to 70 patients. The study is enrolling patients with triple negative disease who have previously been treated with at least two prior cytotoxic regimens in the metastatic setting.

Moreover, the study will also enroll patients with ER-positive and/or PR-positive and HER2-negative disease who have previously been treated with at least two prior cytotoxic regimens in the metastatic setting, and at least three prior hormonal therapies.

The primary endpoint is safety, while secondary endpoints include objective response, duration of response and progression-free survival (PFS).

The American Cancer Society anticipates about 230,000 fresh cases of invasive breast cancer to be diagnosed in the U.S. during 2013. At an annual meeting of American Association of Cancer Research, in Apr 2013, preclinical data revealed that up to 92% of breast tumors analyzed expressed LIV-1, with limited expression in normal tissue. In multiple preclinical models, at well-tolerated doses, SGN-LIV1A has shown significant antitumor activity.

In 2013, SGN-LIV1A is one of the four ADCs that have moved to the clinic. ADCs have lately been attracting a lot of interest with major companies entering into collaborations. Seattle Genetics has an alliance with companies such as Roche ( RHHBY ) and Bayer ( BAYRY ), for the development of ADCs.

Seattle Genetics carries a Zacks Rank #3 (Hold). Currently, companies like Roche and Actelion Ltd. ( ALIOF ) look well positioned with a Zacks Rank #1 (Strong Buy).

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Seattle Genetics Starts Phase I Study - Analyst Blog

By RTT News, October 22, 2013, 07:46:00 PM EDT

(RTTNews.com) - Cancer Genetics, Inc. ( CGIX ) said Tuesday that it has priced its underwritten public offering of 2.858 million shares of its common stock at a price to the public of $14.00 per share.

The gross proceeds to Cancer Genetics from the public offering are expected to be $40 million, before underwriting discounts and commissions and other offering expenses payable by Cancer Genetics.

Cancer Genetics has also granted the representative of the underwriters a 45-day option to purchase up to 428,700 additional shares of common stock from Cancer Genetics to cover over-allotments, if any.

The offering is expected to close on October 28.

The company plans to use the net proceeds from the offering to fund its Mayo Clinic joint venture, to expand sales and marketing, to continue research and development, and for general corporate purposes and to fund ongoing operations and expansion of the business.

The company may also use a portion of the net proceeds from the offering to repay certain outstanding indebtedness.

For comments and feedback: contact editorial@rttnews.com

http://www.rttnews.com

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Cancer Genetics Prices $40 Mln Stock Offering

ELMWOOD PARK, N.J., Oct. 22, 2013 (GLOBE NEWSWIRE) -- BioReference Laboratories, Inc. (BRLI) announces that Myriad Genetics has filed a lawsuit against it in the Federal District Court in Utah alleging that BioReference, through its genetic sequencing laboratory, GeneDx, Inc, is infringing on its intellectual property by offering OncoGeneDx, its comprehensive series of inherited cancers testing, including testing for BRCA1/2. BioReference indicated that it is not surprised by the action and that it is confident in its position.

BioReference has engaged the firm of Sterne, Kessler, Goldstein & Fox to represent it in the action. The firm has represented the Company for many years and has a superior reputation in the field of intellectual property, especially in the area of genetic sequencing. BioReference stated that the test was introduced in August of the current year, after careful consideration in view of the Supreme Court's recent decisions in the field of genetic diagnostics. Its team of geneticists and sequencing scientists have developed several panels of tests for inherited cancers that will be valuable tools in the management of cancer. As always for BioReference, the tests will be based on innovative technology, will be affordable, and will be designed to provide the service and support that has enabled BioReference to maintain its sustained growth for the past two decades.

Myriad Genetics has taken similar steps to defend its exclusivity for BRCA1/2 testing by suing other laboratories that offer BRCA1/2 testing. The latest action against BioReference is not unexpected and the Company is fully prepared to defend against the action. BioReference is confident in its legal position and its belief that patients are better served in this evolving area of medicine by having choices and better access to alternative testing sources.

About BioReference Laboratories, Inc.

BRLI is a clinical testing laboratory offering testing, information and related services to physician offices, clinics, hospitals, employers and governmental units. We believe that we are the fourth largest full-service laboratory in the United States and the largest independent regional laboratory in the Northeastern market. BRLI offers a comprehensive list of laboratory testing services utilized by healthcare providers in the detection, diagnosis, evaluation, monitoring and treatment of diseases. BRLI primarily focuses on esoteric testing, molecular diagnostics, anatomical pathology, women's health and correctional health care.

Statements included in this release that are not historical in nature, are intended to be, and are hereby identified as "forward-looking statements". Forward-looking statements may be identified by words such as "expects," "anticipates," "intends," "plans," "believes," "seeks," "estimates," "will" or words of similar meaning and include, but are not limited to, statements about the expected future business and financial performance of Bio-Reference Laboratories, Inc. and its subsidiaries. Statements looking forward in time are included in this release pursuant to the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995. Readers are cautioned not to place undue reliance on forward-looking statements, which speak only as of the date they are made and which reflect management's current estimates, projections, expectations or beliefs and which involve risks and uncertainties that could cause actual results and outcomes to be materially different. Risks and uncertainties that may affect the future results of the company include, but are not limited to, adverse results from pending or future government investigations, our ability to sustain continued growth, lawsuits or private actions, including any potential action involving Horizon as described herein, the competitive environment, changes in government regulations, changing relationships with customers, payers, suppliers and strategic partners, including recent proposals by CMS described herein, and other and other risks and uncertainties detailed from time to time in our filings with the Securities and Exchange Commission. We undertake no obligation to publicly update or review any forward-looking information, whether as a result of new information, future developments or otherwise.

http://www.bioreference.com

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BioReference Laboratories, Inc. Sued by Myriad Genetics, Confident in Its Position

LOS ANGELES--(BUSINESS WIRE)--

Life Stem Genetics (LIFS) is pleased to announce that it has completed and received the first $500,000 of the recently announced $1mm Private Placement. Our company is very happy to receive the first half of our recent private placement and hopes to close the additional $500,000 in the coming weeks.

The money will be used to attract additional affiliate offices country wide and to invest in various areas of research and development in moving our company's plans forward.

About Life Stem Genetics

Life Stem Genetics (LSG) is a progressive health care company that focuses on healing with a patients own Stem Cells. Stem Cells for years have been known to heal a variety of ailments successfully and now it is being offered as an efficient and painless way to treat many different illnesses ranging from orthopedic injuries, neurological disorders such as Parkinsons and Alzheimers, Cancer, Plastic Surgery, Age Management, Arthritis, Diabetes, Cardiology, COPD, MS, Urology, and many more. Stem Cell Therapy and LSGs proprietary techniques have experienced some of the best results in the industry, helping to repair or re-program damaged or diseased tissues and organs.

LSGs stem cell specialist has performed thousands of stem cell treatments, including the top names in PGA golf, NFL football, NBA basketball, and Major League Baseball. LSG will offer their proprietary treatments through a series of affiliate doctors, and medical clinics, with 60 affiliated clinics so far.

LSGs mission is to create a solid comprehensive approach to the treatment and maintenance of diseases and to break free from the medical insurance world by tapping into an affordable private-pay sector delivering exceptional healthcare free from the medical insurance maze.

http://www.lifestemgenetics.com/

This press release contains "forward-looking statements" within the meaning of the "safe-harbor" provisions of the Private Securities Litigation Reform Act of 1995 that are not historical facts. These statements can be identified by the use of forward-looking terminology such as "believe," "expect," "may, could, estimates, "will," "should," "project," "plan," "seek," "intend," or "anticipate" or the negative thereof or comparable terminology, and include discussions of strategy, and statements about industry trends and the Company's future performance, operations, and products. Such statements involve known and unknown risks, uncertainties and other factors that could cause the Company's actual results to differ materially from the results expressed or implied by such statements. Such risks and uncertainties include, without limitation, market acceptance of the Company's stem cell therapy treatment program; the Company's compliance with applicable statutes and regulations: the Company's reliance on third-party contractors to provide suitable treatment facilities; the Company's ability to expand its network of participating clinics and doctors; the Company's ability to develop an effective marketing strategy; the Company's ability to control and reduce advertising and marketing costs; the Company's ability to develop and increase awareness of its brand; the Company's ability to protect its trademarks; and the success of the Company's marketing focus to patients, doctors and clinics. For a discussion of these and other risks and uncertainties see "Risk Factors" and Description of Business in the Company's public filings with the SEC. Although the Company believes that the expectations reflected in such forward-looking statements are reasonable, there can be no assurance that such expectations will prove to be correct. The Company has no obligation to update the forward-looking information contained in this press release.

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Life Stem Genetics is Pleased to Announce That It Has Completed the First $500,000 Private Placement of the Recently ...

RUTHERFORD, N.J., Oct. 22, 2013 (GLOBE NEWSWIRE) -- Cancer Genetics, Inc. (CGIX), a diagnostics company focused on developing genomic-based, oncology tests and services, today announced the pricing of its underwritten public offering of 2,858,000 shares of its common stock at a price to the public of $14.00 per share. The gross proceeds to Cancer Genetics from the public offering are expected to be $40 million, before underwriting discounts and commissions and other offering expenses payable by Cancer Genetics.

The Company intends to use the net proceeds from the offering to fund its Mayo Clinic joint venture, to expand sales and marketing, to continue research and development, and for general corporate purposes and to fund ongoing operations and expansion of the business. The Company may also use a portion of the net proceeds from the offering to repay certain outstanding indebtedness.

Cancer Genetics has also granted the representative of the underwriters a 45-day option to purchase up to 428,700 additional shares of common stock from Cancer Genetics to cover over-allotments, if any. The offering is expected to close on October 28, 2013, subject to customary closing conditions.

Aegis Capital Corp. is acting as sole book-running manager for the offering.

Feltl and Company, Inc., Cantor Fitzgerald & Co. and Dougherty & Company are acting as co-managers for the offering.

This offering is being made only by means of a prospectus. Copies of the prospectus relating to this offering may be obtained by contacting Aegis Capital Corp., Prospectus Department, 810 Seventh Avenue, 18th Floor, New York, NY 10019, telephone: 212-813-1010, e-mail: prospectus@aegiscap.com.

A registration statement relating to these securities was declared effective by the Securities and Exchange Commission on October 22, 2013. This press release shall not constitute an offer to sell or a solicitation of an offer to buy, nor shall there be any sale of these securities in any state or jurisdiction in which such an offer, solicitation or sale would be unlawful prior to registration or qualification under the securities laws of any such state or jurisdiction.

About Cancer Genetics:

Cancer Genetics, Inc. is an emerging leader in DNA-based cancer diagnostics and services some of the most prestigious medical institutions in the world. Our tests target cancers that are difficult to diagnose and predict treatment outcomes. These cancers include hematological, urogenital and HPV-associated cancers. We also offer a comprehensive range of non-proprietary oncology-focused tests and laboratory services that provide critical genomic information to healthcare professionals as well as biopharma and biotech. Our state-of-the-art reference lab is focused entirely on maintaining clinical excellence and is both CLIA certified and CAP accredited and has licensure from several states including New York State. We have established strong research collaborations with major cancer centers such as Memorial Sloan-Kettering, The Cleveland Clinic, Mayo Clinic and the National Cancer Institute. For further information, please see http://www.cancergenetics.com.

Forward Looking Statements:

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Cancer Genetics Announces Pricing of Public Offering of 2,858,000 Shares of Common Stock

Seattle Genetics, Inc. (SGEN) commenced a phase I study to evaluate SGN-LIV1A in patients with LIV-1-positive metastatic breast cancer. Seattle Genetics antibody-drug conjugate (ADC) technology has been used for SGN-LIV1A.

The open-label, dose-escalation study will enroll up to 70 patients. The study is enrolling patients with triple negative disease who have previously been treated with at least two prior cytotoxic regimens in the metastatic setting.

Moreover, the study will also enroll patients with ER-positive and/or PR-positive and HER2-negative disease who have previously been treated with at least two prior cytotoxic regimens in the metastatic setting, and at least three prior hormonal therapies.

The primary endpoint is safety, while secondary endpoints include objective response, duration of response and progression-free survival (PFS).

The American Cancer Society anticipates about 230,000 fresh cases of invasive breast cancer to be diagnosed in the U.S. during 2013. At an annual meeting of American Association of Cancer Research, in Apr 2013, preclinical data revealed that up to 92% of breast tumors analyzed expressed LIV-1, with limited expression in normal tissue. In multiple preclinical models, at well-tolerated doses, SGN-LIV1A has shown significant antitumor activity.

In 2013, SGN-LIV1A is one of the four ADCs that have moved to the clinic. ADCs have lately been attracting a lot of interest with major companies entering into collaborations. Seattle Genetics has an alliance with companies such as Roche (RHHBY) and Bayer (BAYRY), for the development of ADCs.

Seattle Genetics carries a Zacks Rank #3 (Hold). Currently, companies like Roche and Actelion Ltd. (ALIOF) look well positioned with a Zacks Rank #1 (Strong Buy).

Zacks Investment Research

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Seattle Genetics Starts Phase I Study

A Children Hospital of Philadelphia gene therapy spinout is taking over development of a Phase 3 gene therapy program to treat inherited blindness by counteracting retinal degeneration. Its one of the most common causes of blindness in children.

Spark Therapeutics is advancing the work of CHOPs Center for Cellular and Molecular Therapeutics. The center was set up in 2004 as a center for gene therapy translational research and manufacturing. CHOP is giving it $50 million to advance its genetic therapies.

Inherited blindness is caused by mutations in the RPE65 gene. There is currently no drug or therapeutic treatment for this form of inherited retinal degeneration, according to the hospital statement. It ultimately causes irreversible blindness.

The treatment has produced some encouraging results. A clinical study of 12 patients with RPE65-related blindness demonstrated notable improvement in visual function. In some cases, children who were profoundly blind were able to recognize faces and move independently, according to the statement.All school-age patients enrolled in the trial were able to transfer from Braille classrooms to sighted classrooms. The next step is a Phase 3 open-label, randomized, controlled study that will expand on the study.

The gene mutation in one of 14 genes that cause Lebers congenital amaurosis. It disrupts development of the retina, causing people with the disease to have severe vision deficits from birth that progress slowly over time to total blindness.

Many of the centers leaders will take on management roles in Spark or work with the company as scientific advisers. Among those advisers is Dr. Katherine A. High, a gene therapy pioneer who has worked as the director of the center from the start.

The group is also developing a gene therapy for hemophilia B. The goal is to eliminate or reduce the need for regular infusions of clotting factor. It might even be able to help hemophilia B patients with inhibiting antibodies.

The company is also advancing toward the clinic with gene therapy programs to address neurodegenerative diseases and additional hematologic disorders and other forms of inherited blindness.

The company was co-founded by CEO Jeffrey D. Marrazzo, who has served as an entrepreneurial consultant to the hospital for the past three years. He said: The creation of Spark is the culmination of a decade-long commitment by CHOP and our founding team to drive the field of gene therapy forward during a time when many in the industry had moved away.

Last month, CHOP formed a partnership with Osage University Partners in a move to develop more partnership opportunities. One spin-off company CHOP has produced is Vascular Magnetics to treat peripheral artery disease. A rotovirus vaccine called RotaTeq produced through joint research between CHOP and Wistar Institute is now sold by Merck.

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Late stage gene therapy for inherited blindness part of Children’s Hospital spinout

Oct. 22, 2013 The first evidence that the underlying genetic defect responsible for trisomy 21, also known as Down syndrome, can be suppressed in laboratory cultures of patient-derived stem cells was presented today (Oct. 22) at the American Society of Human Genetics 2013 annual meeting in Boston.

People with Down syndrome are born with an extra chromosome 21, which results in a variety of physical and cognitive ill effects. In laboratory cultures of cells from patients with Down syndrome, an advanced genome editing tool was successfully used to silence the genes on the extra chromosome, thereby neutralizing it, said Jeanne Lawrence, Ph.D., Professor of Cell & Developmental Biology at the University Massachusetts Medical School, Worcester, MA.

Dr. Lawrence and her team compared trisomic stem cells derived from patients with Down syndrome in which the extra chromosome 21 was silenced to identical cells from patients that were untreated. The researchers identified defects in the proliferation, or rapid growth, of the untreated cells and the differentiation, or specialization, of untreated nervous system cells. These defects were reversed in trisomic stem cells in which the extra chromosome 21 was muted.

"Silencing of trisomy 21 by manipulation of a single gene in living cells in laboratory cells surmounts the first major obstacle to development of potential 'chromosome therapy,'" said Dr. Lawrence, whose presentation today provided an update to the results that she and her colleagues reported earlier this year in the journal Nature.

In her ASHG presentation, Dr. Lawrence described the use of the novel editing tool to examine changes in gene expression that result from the silencing of the extra chromosome. The changes in gene expression were not limited to chromosome 21 but were genome-wide.

"In fact, the results indicate that the most prominent changes are in genes not encoded on chromosome 21," said Dr. Lawrence, who also provided more perspective about the various avenues of research that the results have created and that are now being and will be pursued in her lab.

The approach used by Dr. Lawrence and her team was inspired by the natural process that silences one copy of the female mammals' two sex-determining X chromosomes during embryonic development. In males, the sex-determining chromosomes are X and Y, and gene silencing helps maintain similar expression patterns of X chromosome genes in females and males.

To understand this biological process, Dr. Lawrence and her collaborators several years ago began studying the X-inactivation gene (XIST), which encodes a large non-coding RNA molecule. In laboratory cultures of cells, this molecule was shown to cover the surface of one of the X chromosomes of female mammals. XIST's actions permanently blocked the expression, or activity level, of the genes on the affected X chromosome.

Dr. Lawrence and her team mimicked this natural process by inserting the XIST gene into the gene-rich core of the extra chromosome 21 in lab cultures of pluripotent stem cells from patients with Down syndrome. Before taking this step, they first demonstrated that a large transgene could be successfully inserted at a specific site by using zinc-finger nuclease technology.

In the laboratory cells, they found that the RNA from the inserted XIST gene induced a host of epigenetic modifications that transcriptionally silenced the genes of the extra chromosome 21.

Originally posted here:
Gene-silencing strategy opens new path to understanding Down Syndrome

Spark Therapeutics hopes to commercialize multiple gene-based treatments developed at the Childrens Hospital of Philadelphia.

A new biotechnology company will take over human trials of two gene therapies that could offer one-time treatments for a form of childhood blindness and hemophilia B.

The gene therapies were developed by researchers at the Childrens Hospital of Philadelphia, which has committed $50 million to the new company called Spark Therapeutics. The launch is the latest hint that after decades of research and some early setbacks, gene therapy may be on its way to realizing its potential as a powerful treatment for inherited disease.

In December 2012, the European Union gave permission to Dutch company Uniqure to sell its gene therapy for a fat-processing disorder, making Glybera the first gene therapy to make its way into a Western market (see Gene Therapy on the Mend as Treatment Gets Western Approval). However, Glybera has not been approved by the U.S., nor has any other gene therapy.

Spark has a chance to be the first gene-therapy company to see FDA approval. Results for a late-stage trial of a gene therapy for Lebers Congenital Amaurosis, an inherited condition that leads to a loss of vision and eventually blindness, are expected by mid-2015. That treatment is one of several gene therapies in or nearing late-stage testing contending to be the first gene therapy approved by the FDA for sale in the U.S. (see When Will Gene Therapy Come to the U.S.).

In addition to taking the reins for two-ongoing human trials, Spark will also work on gene therapies for other eye and blood conditions as well as neurodegenerative diseases, says CEO Jeff Marrazzo. The gene therapy technology developed at the Childrens Hospital has been speeding down the tracks, he says, and the company will provide the vehicle to get these therapies to the people who need them.

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New Gene Therapy Company Launches

Durham, NC (PRWEB) October 21, 2013

Cato Research regulatory expert William Lee, Ph.D., R.A.C., Vice President of Regulatory Affairs at Cato Research, will present in San Francisco, California at the OMICS Group Conference, 3rd International Conference on Pharmaceutical Regulatory Affairs.

Dr. Lee's presentation is titled: "Regulatory Roadmap for Initiating a Gene Therapy Drug into Clinical Trials in the United States."

Abstract of Presentation: Exciting progress has been made in the development of gene therapy, and experimental research has brought forward novel treatment opportunities for viral vectors, DNA vectors, and gene-modified cell therapies. Clinical development of a gene therapy drug is challenging, requiring understanding of controlled manufacturing, relevant nonclinical pharmacology and safety studies, and clinical risk factors. For initiating clinical trials in the United States, regulatory requirements for investigational gene therapy drugs are more stringent than those with other investigational biologics (recombinant antibodies or recombinant proteins).

This talk will highlight these requirements, including the following: (1) Submissions to regulatory authorities (2) Manufacturing (3) Nonclinical studies

Dr. William Lee received his B.A. from The Johns Hopkins University and his Ph.D. from Cornell University Graduate School of Medical Sciences. Dr. Lee has 20 years of research and industry experience. His focus is on gene therapy with retroviral vectors, adeno-associated viral vectors, and DNA vectors. He spent 9 years at the gene therapy start-up firm Viagene, Inc., followed by 2 years at Chiron. In 1999, he joined Cato Research, in Durham, North Carolina, where he is currently Vice President, Regulatory Affairs. His projects have included the design of Phase 1 and Phase 2 protocols for a gene therapy drug and interactions with the FDA and NIH/OBA. Currently, he manages projects involving regulatory strategy and submissions of investigational new drug applications and marketing applications for biologics and drugs.

For more information about this event, please visit: http://www.cato.com/events.shtml.

About Cato Research Founded in 1988 by Dr. Allen Cato and Lynda Sutton and headquartered near Research Triangle Park, North Carolina, Cato Research is a full-service, global contract research and development organization providing strategic and tactical support for clients in the pharmaceutical, biotechnology, and medical device industries. Services range from design and management of preclinical and clinical studies to submission of regulatory documents required for marketing approval. With a staff of approximately 300 and offices located in the United States, Europe, Canada, Israel, and South Africa, the Cato Research team consistently demonstrates an unsurpassed level of responsiveness, flexibility, attention to detail, and passion for bringing their clients products to market with speed and cost-effectiveness.

For more information, please contact: Cato Research Phone: 919-361-2286 http://www.cato.com

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Cato Research Presents at OMICS Group Conference, 3rd International Conference on Pharmaceutical Regulatory Affairs

For centuries, yogurt has been known as a healthy food. Now, new checkoff-funded research aims to make it even healthier.

Through a process known as gene mapping, researchers at the Minnesota-South Dakota Dairy Foods Research Center have discovered a way to increase the longevity of the beneficial bacterial culture in yogurt.

Bifidobacterium longum, the main bacteria in yogurt, has been found to keep the intestinal tract healthy and even to help prevent colon cancer. However, in the past, these beneficial bacteria sometimes expired by the time the product reached consumers, thereby limiting its health benefits. The new research helps these bacteria maintain their beneficial properties after the yogurt leaves the grocery store.

"This new step forward in yogurt research will help establish the importance of including this nutritious dairy food in the diet of more Americans," said Lloyd Metzger, director of the Minnesota-South Dakota Dairy Foods Research Center in St. Paul. "The bottom line is that more health-conscious consumers will have another reason to choose dairy products when shopping in the grocery store."

According to the USDA, per capita consumption of yogurt increased by 5.7 percent from 7 pounds to 7.4 pounds in 2002, the last year for which information is available. Hopefully, this new research will push that figure even higher.

The research was funded by checkoff dollars from the Midwest Dairy Association, a non-profit organization funded by dairy producers.

Midwest Dairy Association

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Research aims to increase yogurt’s health value

Oct. 18, 2013 A gene important in skin tanning has been linked to higher risk for testicular cancer in white men, according to a study led by scientists from the U.S. National Institutes of Health and the University of Oxford in England. Nearly 80 percent of white men carry a variant form of this gene, which increased risk of testicular cancer up to threefold in the study.

The research appeared online October 10, 2013 in the journal Cell, and is the result of an integrated analysis of big data supported by laboratory research. The team suspected that variations in a gene pathway controlled by the tumor suppressor gene p53 could have both positive and negative effects on human health.

"Gene variations occur naturally, and may become common in a population if they convey a health benefit," said Douglas Bell, Ph.D., author on the paper and researcher at the National Institute of Environmental Health Sciences (NIEHS), part of NIH. "It appears that this particular variant could help protect light-skinned individuals from UV skin damage, like burning or cancer, by promoting the tanning process, but it permits testicular stem cells to grow in the presence of DNA damage, when they are supposed to stop growing."

Bell explained that p53 stimulates skin tanning when ultraviolet light activates it in the skin. It then must bind a specific sequence of DNA located in a gene called the KIT ligand oncogene (KITLG), which stimulates melanocyte production, causing the skin to tan.

To conduct the analysis, Xuting Wang, Ph.D., of NIEHS, co-author and lead bioinformatics scientist on the paper, led a data mining expedition to sieve through many different data sets. The team selected possible leads from the intersection of more than 20,000 p53 binding sites in the human genome, 10 million inherited genetic variations genotyped in the 1000 Genomes Project, and 62,000 genetic variations associated with human cancers identified in genome-wide association studies (GWAS). These data sets were gathered through joint efforts of thousands of researchers from around the world.

"In the end, one variant in the p53 pathway was strongly associated with testicular cancer, but also, surprisingly, displayed a positive benefit that is probably related to tanning that has occurred as humans evolved," Wang noted.

The group at the Ludwig Institute for Cancer Research at the University of Oxford, led by Gareth Bond, Ph.D., performed complex experiments to confirm the molecular mechanism that linked the variant with cancer and tanning.

"White males with a single nucleotide variation in KITLG, called the G allele, have the highest odds of having testicular cancer. In fact, the twofold to threefold increased risk is one of the highest and most significant among all cancer GWAS conducted within the past few years," said Bond. "The high frequency of this allele in light skin individuals may explain why testicular cancer is so much more frequent in people of European descent than those of African descent."

Bond said although the G allele increases testicular cancer risk, it may explain why testicular tumors are often easily cured with chemotherapy. "Most other tumors have a mutant p53, but in these testicular cell tumors, the p53 is functioning properly, and the drugs used for testicular cancer appear to work in concert with p53's tumor suppression function to kill the cancer cells."

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Tanning gene linked to increased risk of testicular cancer

PUBLIC RELEASE DATE:

20-Oct-2013

Contact: Lauren Riley lauren.riley@aacr.org 215-446-7155 American Association for Cancer Research

BOSTON PF-06463922, an investigational drug being developed by Pfizer Inc., has the potential to become a new treatment option for patients who have lung cancer harboring abnormalities in the ALK gene, according to preclinical results presented here at the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics, held Oct. 19-23.

About 3 to 5 percent of lung cancers harbor ALK gene abnormalities. The drug crizotinib (Xalkori), which blocks ALK protein kinase activity, was approved in August 2011 by the U.S. Food and Drug Administration for the treatment of patients who have these lung cancers. Although robust responses to crizotinib are observed for lung cancers harboring ALK gene abnormalities, the majority eventually become resistant to the effects of the drug. In many cases, resistance arises because of genetic mutations in ALK.

"Resistance to targeted therapies such as crizotinib is a major challenge when treating patients with cancer," said Tod Smeal, Ph.D., associate research fellow in the Oncology Research Unit at Pfizer Inc. in San Diego, Calif. "Our goal is to take advantage of everything we have learned about designing drugs that target kinases like ALK and the ways in which lung cancers become resistant to crizotinib to develop the best next-generation ALK inhibitor we can.

"Our preclinical studies suggest that we are making progress toward achieving our goal: PF-06463922 has potent ALK-inhibiting activity, it is capable of inhibiting all the crizotinib-resistant ALK mutants so far detected in patients, and it can efficiently access the brain. We are excited about these preclinical results and very hopeful that they will translate into meaningful responses in the clinic."

After carefully designing PF-06463922, Smeal and colleagues first showed in cell assays that it potently inhibited the activity of ALK and all eight of the mutant forms of ALK known to cause resistance to crizotinib in patients with lung cancer. They then showed that PF-06463922 inhibited the growth of tumors harboring three of the crizotinib-resistant ALK mutants, including the most resistant ALK mutant, G1202R, in mice.

Further analysis indicated that PF-06463922 readily entered the brains of mice, rats, and dogs. In mice, levels of PF-06463922 in the brain were 20-30 percent of levels of PF-06463922 in the blood. This is potentially clinically relevant because a significant number of lung cancer patients will develop brain metastasis during the course of their disease, according to Smeal, although he noted that it will be important to see if these results in animals hold true in humans.

Smeal and colleagues also found that PF-06463922 potently inhibited the protein ROS1, a close relative of ALK recently implicated in a number of cancer types, including some lung and brain cancers. Further, PF-06463922 had antitumor effects in two mouse models of cancers driven by ROS1 gene abnormalities, leading the researchers to suggest that PF-06463922 has potential as a treatment for this subgroup of cancers, in addition to its promise as a new treatment for ALK-driven cancers.

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Targeted investigational therapy potential to overcome crizotinib resistance in lung cancers

Newswise (MEMPHIS, Tenn. October 20, 2013) Research led by St. Jude Childrens Research Hospital scientists has linked an inherited gene variation to a nearly four-fold increased risk of developing a pediatric acute lymphoblastic leukemia (ALL) subtype that is associated with a poor outcome. The study appears today in the online edition of the scientific journal Nature Genetics.

The high-risk variant was found in the GATA3 gene. Researchers reported the high-risk version of the gene was more common among Hispanic Americans and other individuals with high Native American ancestry than those of other ethnic backgrounds. Forty percent of Hispanic Americans carried the high-risk variant, compared to 14 percent of individuals of European ancestry. For this study, ethnicity was defined by genetic variations associated with ancestry rather than individual self-reports.

Hispanic children are known to be at a higher risk of developing ALL and of dying from the disease. This is the latest in a series of St. Jude studies to report an association between inherited DNA variations in a handful of genes and an increased risk of childhood ALL among those of Hispanic ethnicity.

This is the first study to link an inherited genetic variation to an elevated risk of developing the leukemia subtype known as Philadelphia chromosome-like ALL (Ph-like ALL). Individuals with the high-risk version of GATA3 were 3.85 times more likely than those who inherited a different version of the gene to develop Ph-like ALL. Patients with the high-risk variant were also more likely to have a poor treatment response and have their cancer eventually return.

A significant percentage of patients with the high-risk GATA3 variant also had the tumor genetic alterationsincluding mutations, gene deletions and chromosomal re-arrangementsthat are hallmark of Ph-like ALL. The changes occur in genes, including CRLF2, JAK and IKZF1 that regulate how blood cells grow and mature.

Until recently, little was known about why a child develops a specific subtype of ALL in the first place and whether inherited genetic variations that predispose an individual to a subtype also influence how he or she responds to the therapy, said corresponding author Jun J. Yang, Ph.D., an assistant member of the St. Jude Department of Pharmaceutical Sciences. In this study, we discovered a genetic basis for susceptibility to Ph-like ALL, but even more importantly, the evidence that host and tumor genomes may interact with each other to influence the risk of developing and surviving ALL.

The study was done in collaboration with the Childrens Oncology Group, a U.S.-based research cooperative study group focused on childhood cancer research and clinical trials. The research included 680 patients enrolled in COG clinical trials.

Ph-like ALL accounts for as much as 15 percent of childhood ALL and is associated with a high risk of relapse and a poor outcome. ALL is the most common childhood cancer. While overall cure rates for pediatric ALL are now about 90 percent, only 63 percent of children with Ph-like ALL are alive and cancer free after five years. Yang added that larger population studies are needed to assess risks associated with these inherited variations.

GATA3 carries instructions for assembling a protein called a transcription factor that turns other genes on and off. The GATA3 protein, and other members of the GATA gene family, plays a crucial role in normal development of a variety of blood cells. Alterations in GATA3 have been linked to other blood cancers, including Hodgkin lymphoma.

The high-risk GATA3 variation was identified using a library of 718,890 common genetic variations known as single nucleotide polymorphisms, or SNPs, to screen the DNA of 75 children with Ph-like ALL, 436 children with other ALL subtypes and 6,661 individuals without ALL. Fifty-eight percent of patients with Ph-like ALL carried the high-risk version of the gene, compared to 29 percent of patients with other ALL subtypes and 20 percent of those without ALL. When researchers checked for the high-risk variant in additional patients with the Ph-like ALL subtype as well as other young ALL patients and individuals without the disease, they found the similar percentages carried the high-risk version.

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Inherited Gene Variation Tied to High-Risk Pediatric Leukemia and Greater Risk of Relapse

Oct. 20, 2013 Research led by St. Jude Children's Research Hospital scientists has linked an inherited gene variation to a nearly four-fold increased risk of developing a pediatric acute lymphoblastic leukemia (ALL) subtype that is associated with a poor outcome. The study appears today in the online edition of the scientific journal Nature Genetics.

The high-risk variant was found in the GATA3 gene. Researchers reported the high-risk version of the gene was more common among Hispanic Americans and other individuals with high Native American ancestry than those of other ethnic backgrounds. Forty percent of Hispanic Americans carried the high-risk variant, compared to 14 percent of individuals of European ancestry. For this study, ethnicity was defined by genetic variations associated with ancestry rather than individual self-reports.

Hispanic children are known to be at a higher risk of developing ALL and of dying from the disease. This is the latest in a series of St. Jude studies to report an association between inherited DNA variations in a handful of genes and an increased risk of childhood ALL among those of Hispanic ethnicity.

This is the first study to link an inherited genetic variation to an elevated risk of developing the leukemia subtype known as Philadelphia chromosome-like ALL (Ph-like ALL). Individuals with the high-risk version of GATA3 were 3.85 times more likely than those who inherited a different version of the gene to develop Ph-like ALL. Patients with the high-risk variant were also more likely to have a poor treatment response and have their cancer eventually return.

A significant percentage of patients with the high-risk GATA3 variant also had the tumor genetic alterations -- including mutations, gene deletions and chromosomal re-arrangements -- that are hallmark of Ph-like ALL. The changes occur in genes, including CRLF2, JAK and IKZF1 that regulate how blood cells grow and mature.

"Until recently, little was known about why a child develops a specific subtype of ALL in the first place and whether inherited genetic variations that predispose an individual to a subtype also influence how he or she responds to the therapy," said corresponding author Jun J. Yang, Ph.D., an assistant member of the St. Jude Department of Pharmaceutical Sciences. "In this study, we discovered a genetic basis for susceptibility to Ph-like ALL, but even more importantly, the evidence that host and tumor genomes may interact with each other to influence the risk of developing and surviving ALL."

The study was done in collaboration with the Children's Oncology Group, a U.S.-based research cooperative study group focused on childhood cancer research and clinical trials. The research included 680 patients enrolled in COG clinical trials.

Ph-like ALL accounts for as much as 15 percent of childhood ALL and is associated with a high risk of relapse and a poor outcome. ALL is the most common childhood cancer. While overall cure rates for pediatric ALL are now about 90 percent, only 63 percent of children with Ph-like ALL are alive and cancer free after five years. Yang added that larger population studies are needed to assess risks associated with these inherited variations.

GATA3 carries instructions for assembling a protein called a transcription factor that turns other genes on and off. The GATA3 protein, and other members of the GATA gene family, plays a crucial role in normal development of a variety of blood cells. Alterations in GATA3 have been linked to other blood cancers, including Hodgkin lymphoma.

The high-risk GATA3 variation was identified using a library of 718,890 common genetic variations known as single nucleotide polymorphisms, or SNPs, to screen the DNA of 75 children with Ph-like ALL, 436 children with other ALL subtypes and 6,661 individuals without ALL. Fifty-eight percent of patients with Ph-like ALL carried the high-risk version of the gene, compared to 29 percent of patients with other ALL subtypes and 20 percent of those without ALL. When researchers checked for the high-risk variant in additional patients with the Ph-like ALL subtype as well as other young ALL patients and individuals without the disease, they found the similar percentages carried the high-risk version.

Read more:
Inherited gene variation tied to high-risk pediatric leukemia, risk of relapse

Frantz entered the first round competition by submitting a two-minute video clip singing a rap song about her current work on the development of vaccine combating Porcine Epidemic Diarrhoea Virus (PEDV). She was among the five finalists chosen from 40 video submissions.

"The lyrics in the rap are easy-to-understand language, and free of technical jargons, relying on items listeners are familiar with in their everyday lives, in order to get the audience to understand what I want to explain. Making a fun-filled rap song fun makes my presentation more interesting," she said.

The final round of the competition was held in Singapore on September 25, in which each finalist made a 10-minute presentation in front of a live audience of 150.

"I was very happy once the top award was announced for me. I was very anxious and excited seconds before the announcement was made because there were many Singaporean supporters attending the event held in the host country," she said.

Dr Frantz was awarded a trip to Brussels in Belgium, where she will attend the Euraxess Voice of Researchers Conference along with the winners of the other Euraxess Science Slams, which are organised in the US, Japan, India, China and Brazil.

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Thai researcher wins Euraxess Science Slam Asean 2013

Oct. 20, 2013 In a biological quirk that promises to provide researchers with a new approach for studying and potentially treating Fragile X syndrome, scientists at the University of Massachusetts Medical School (UMMS) have shown that knocking out a gene important for messenger RNA (mRNA) translation in neurons restores memory deficits and reduces behavioral symptoms in a mouse model of a prevalent human neurological disease. These results, published today in Nature Medicine, suggest that the prime cause of the Fragile X syndrome may be a translational imbalance that results in elevated protein production in the brain. Restoration of this balance may be necessary for normal neurological function.

"Biology works in strange ways," said Joel Richter, PhD, professor of molecular medicine at UMMS and senior author on the study. "We corrected one genetic mutation with another, which in effect showed that two wrongs make a right. Mutations in each gene result in impaired brain function, but in our studies, we found that mutations in both genes result in normal brain function. This sounds counter-intuitive, but in this case that seems to be what has happened."

Fragile X syndrome, the most common form of inherited mental retardation and the most frequent single-gene cause of autism, is a genetic condition resulting from a CGG repeat expansion in the DNA sequence of the Fragile X (Fmr1) gene required for normal neurological development. People with Fragile X suffer from intellectual disability as well as behavioral and learning challenges. Depending on the length of the CGG repeat, intellectual disabilities can range from mild to severe.

While scientists have identified the genetic mutation that causes Fragile X, on a molecular level they still don't know much about how the disease works or what precisely goes wrong in the brain as a result. What is known is that the Fmr1 gene codes for the Fragile X protein (FMRP). This protein probably has several functions throughout the neuron but its main activity is to repress the translation of as many as 1,000 different mRNAs. By doing this, FMRP controls synaptic plasticity and higher brain function. Mice without the Fragile X gene, for instance, have a 15 to 20 percent overall elevation in neural protein production. It is thought that the inability to repress mRNA translation and the resulting increase in neural proteins may somehow hamper normal synaptic function in patients with Fragile X. But because FMRP binds so many mRNAs, and some proteins become more elevated than others, parsing which mRNA or combination of mRNAs is responsible for Fragile X pathology is a daunting task.

From Frog Egg to Fragile X

For years, Dr. Richter had been studying how translation, the process in which cellular ribosomes create proteins, went from dormant to active in frog eggs. He discovered the key gene controlling this process, the RNA binding protein CPEB. In 1998, Richter found the CPEB protein in the rodent brain where it played an important role in regulating how synapses talk to each other. At this point, his work began to move from exploring the role of CPEB in the developmental biology of the frog to how the CPEB protein impacted learning and memory. A serendipitous research symposium with colleagues at Cold Spring Harbor got him thinking about CPEB and Fragile X syndrome.

"Here I was, an outsider, a molecular biologist who had worked for years with frog eggs, in the same room with neurobiologists and neurologists, when they started talking about Fragile X syndrome and translational activity," said Richter. "It got me thinking that the CPEB protein might be a path to restoring the translational imbalance they were discussing."

Richter knew that CPEB stimulated translation and that FMRP repressed it. He also knew that animal models lacking the CPEB protein had memory deficits and that both proteins bound to many of the same mRNAs -- the overlap may be as higher as 33 percent. The thought was that by taking away a protein that stimulated translation might counterbalance the loss of the repressor FMRP protein, thereby restoring translational homeostasis in the brain and normal neurological function.

"It was one of those kind of goofy 'what if' sort of things," said Richter.

To test his hypothesis, Richter developed a double knockout mouse model that lacked both the FMRP gene that caused Fragile X and the CPEB gene. When they began measuring for Fragile X pathologies what they found was almost too good to be true.

See more here:
Two genetic wrongs make a biochemical right

PUBLIC RELEASE DATE:

20-Oct-2013

Contact: Jim Fessenden james.fessenden@umassmed.edu 508-856-2000 University of Massachusetts Medical School

WORCESTER, MA In a biological quirk that promises to provide researchers with a new approach for studying and potentially treating Fragile X syndrome, scientists at the University of Massachusetts Medical School (UMMS) have shown that knocking out a gene important for messenger RNA (mRNA) translation in neurons restores memory deficits and reduces behavioral symptoms in a mouse model of a prevalent human neurological disease. These results, published today in Nature Medicine, suggest that the prime cause of the Fragile X syndrome may be a translational imbalance that results in elevated protein production in the brain. Restoration of this balance may be necessary for normal neurological function.

"Biology works in strange ways," said Joel Richter, PhD, professor of molecular medicine at UMMS and senior author on the study. "We corrected one genetic mutation with another, which in effect showed that two wrongs make a right. Mutations in each gene result in impaired brain function, but in our studies, we found that mutations in both genes result in normal brain function. This sounds counter-intuitive, but in this case that seems to be what has happened."

Fragile X syndrome, the most common form of inherited mental retardation and the most frequent single-gene cause of autism, is a genetic condition resulting from a CGG repeat expansion in the DNA sequence of the Fragile X (Fmr1) gene required for normal neurological development. People with Fragile X suffer from intellectual disability as well as behavioral and learning challenges. Depending on the length of the CGG repeat, intellectual disabilities can range from mild to severe.

While scientists have identified the genetic mutation that causes Fragile X, on a molecular level they still don't know much about how the disease works or what precisely goes wrong in the brain as a result. What is known is that the Fmr1 gene codes for the Fragile X protein (FMRP). This protein probably has several functions throughout the neuron but its main activity is to repress the translation of as many as 1,000 different mRNAs. By doing this, FMRP controls synaptic plasticity and higher brain function. Mice without the Fragile X gene, for instance, have a 15 to 20 percent overall elevation in neural protein production. It is thought that the inability to repress mRNA translation and the resulting increase in neural proteins may somehow hamper normal synaptic function in patients with Fragile X. But because FMRP binds so many mRNAs, and some proteins become more elevated than others, parsing which mRNA or combination of mRNAs is responsible for Fragile X pathology is a daunting task.

From Frog Egg to Fragile X

For years, Dr. Richter had been studying how translation, the process in which cellular ribosomes create proteins, went from dormant to active in frog eggs. He discovered the key gene controlling this process, the RNA binding protein CPEB. In 1998, Richter found the CPEB protein in the rodent brain where it played an important role in regulating how synapses talk to each other. At this point, his work began to move from exploring the role of CPEB in the developmental biology of the frog to how the CPEB protein impacted learning and memory. A serendipitous research symposium with colleagues at Cold Spring Harbor got him thinking about CPEB and Fragile X syndrome.

"Here I was, an outsider, a molecular biologist who had worked for years with frog eggs, in the same room with neurobiologists and neurologists, when they started talking about Fragile X syndrome and translational activity," said Richter. "It got me thinking that the CPEB protein might be a path to restoring the translational imbalance they were discussing."

View original post here:
2 genetic wrongs make a biochemical right

Natural Bodybuilder - INSANE Genetics (Preview) bodybuilding fitness 2013 bodybuilding fitness 2013
Natural bodybuilder fitness model Stephen - Preview video of his upcoming training videos where he will be showing himself working out in the gym and will ...

By: Takana Molda

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Natural Bodybuilder - INSANE Genetics (Preview) bodybuilding fitness 2013 bodybuilding fitness 2013 - Video

[BIOS 332] Introduction to Genetics - Jason Tresser
August 31, 2013.

By: BiolaUniversity

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[BIOS 332] Introduction to Genetics - Jason Tresser - Video

By RTT News, October 21, 2013, 09:24:00 AM EDT

(RTTNews.com) - Seattle Genetics, Inc.( SGEN ), Monday announced the initiation of a phase 1 clinical trial evaluating SGN-LIV1A for patients with LIV-1-positive metastatic breast cancer. SGN-LIV1A utilizes Seattle Genetics' antibody-drug conjugate or ADC technology. The trial will assess the safety and antitumor activity of SGN-LIV1A, targeted to LIV-1, a protein which is expressed in most subtypes of metastatic breast cancer. The primary endpoint of the trial is safety, with key secondary endpoints of objective response, duration of response and progression-free survival.

The study, which is excepted to enroll up to 70 patients, is enrolling patients with triple negative disease who have previously been treated with at least two prior cytotoxic regimens in the metastatic setting, or patients with ER-positive and/or PR-positive and HER2-negative disease who have previously been treated with at least two prior cytotoxic regimens in the metastatic setting, and at least three prior hormonal therapies.

ADCs are designed to harness the targeting ability of antibodies to deliver cell-killing agents directly to cancer cells. This approach is intended to spare non-targeted cells and thus reduce many of the toxic effects of traditional chemotherapy while enhancing antitumor activity.

For comments and feedback: contact editorial@rttnews.com

http://www.rttnews.com

Excerpt from:
Seattle Genetics Begins Phase 1 Trial Of ADC Candidate SGN-LIV1A