Why Genetic Information Should be a Trade Secret

This has been a hot topic thats doing rounds. Why should genetic information be a trade secret?

National health systems and insurers, regulators, researchers, providers and patients all have a strong interest in ensuring broad access to information about the clinical significance of variants discovered through genetic testing.

The whole question of proprietary claims over genetic information is not limited to patents and is very much open to debate.  In essence, the authors say that the Myriad patent saga serves as an excellent case study of the importance of collecting clinical data and the implications of keeping those data private. Myriad’s imminent entry into Europe presents an opportunity to implement policies on access to data on the mutation of the BRCA gene which leads to breast cancer. Such policies would set a salutary precedent not only for BRCA but for genetic testing in general, including whole-genome analysis. Mutations on single point mutations on active stretches of the gene are clearly deleterious because they disrupt protein function. Data on these mutations are valuable to those tested and to their health providers, influencing decisions about treatment options. But other data is being withheld, report the authors, which could be essential for further research in the analysis and treatment of cancer caused by single point variations. These are  ‘variants of unknown significance’ (VUS). They occur between the active and inactive segments of the gene and are therefore particularly difficult to interpret. The paper reports that Myriad claims that the fraction of cases resulting in a VUS is 3% in its hands, and 20% for most EuropeanBRCA-testing services.

You can read the entire article here:

http://ukhumanrightsblog.com/2012/12/03/should-genetic-information-be-a-trade-secret/

 

Hillary Clinton warns of gene assembly's ability to create bioweapons

U.S. Secretary of State Hillary Clinton recently warned that gene assembly technology research could potentially be used by terrorists to create biological weapons. If this is 'a' possible future or not, only time will tell, however it is indeed a scary thought.

The threat from bioweapons has drawn little attention in recent years, as governments focused more on the risk of nuclear weapons proliferation to countries such as Iran and North Korea.
But experts have warned that the increasing ease with which bioweapons can be created might be used by terror groups to develop and spread new diseases that could mimic the effects of the fictional global epidemic portrayed in the Hollywood thriller "Contagion."

Many have been calling on the elimination of current viruses and diseases that, if in the wrong hands, could be a powerful weapon. The U.S. announced plans to destroy their smallpox stockpile in May 2011, despite protests from the public. The government feared that terrorists could use the virus to unleash a devastating attack. The disease, which killed one-third of those who were infected, was last seen in 1978.
As late as 2010, a congressional mandated panel reported that the U.S. would not be prepared for a bioweapon attack. The Commission on the Prevention of Weapons of Mass Destruction Proliferation said the Obama administration failed in its efforts to prepare for and respond to a biological attack, such as the release of deadly viruses or bacteria. After that report, Obama announced during his State of the Union speech that the country would be making strides to make sure it was prepared for a biological terrorist attack scenario.

The World Health Organization (WHO) has been pushing for countries to eliminate their stockpiles since 2006. However, at the WHO's annual meeting, it was decided that nations' could keep their smallpox stockpiles for at least another three more years in order to develop vaccines and anti-virals, according to Reuters.

"The emerging gene synthesis industry is making genetic material more widely available," she said. "This has many benefits for research, but it could also potentially be used to assemble the components of a deadly organism."

This probably reminds people about the Anthrax attacks almost a decade ago. Washington has urged countries to increase transparency in their effort to lower the threat of bioweapons, but U.S. officials have shied away from calling for a formal international verification system, citing the complications that would be involved in monitoring the vast number of labs that would have to be monitored.

Did you know?? Omega-3 Kills Cancer Cells

Docosahexanoic acid (DHA), an omega-3 fatty acid found in fish oils, has been shown to reduce the size of tumours and enhance the positive effects of the chemotherapy drug cisplatin, while limiting its harmful side effects. The rat experiments provide some support for the plethora of health benefits often ascribed to omega-3 acids.

DHA is an omega-3 fatty acid that is commonly found in cold-water fish oil, and some vegetable oils. It is a major component of brain gray matter and of the retina in most mammalian species and is considered essential for normal neurological and cellular developments. According to the authors, "While DHA has been tentatively linked with protection against cardiovascular, neurological and neoplastic diseases, there exists a paucity of research information, in particular regarding its interactions with existing chemotherapy drugs". The researchers found that, at the molecular level, DHA acts by reducing leukocytosis (white blood cell accumulation), systemic inflammation, and oxidative stress – all processes that have been linked with tumour growth.

El-Mowafy and his colleagues have called for greater deployment of omega-3 in the fight against cancer. They write, "Our results suggest a new, fruitful drug regimen in the management of solid tumors based on combining cisplatin, and possibly other chemotherapeutics, with DHA".

Mutated Gene In Zebrafish Sheds Light On Blindness In Humans

Described in a paper published in the Proceedings of the National Academy of Sciences (PNAS), the landmark study of retinal development in zebrafish larvae and the genetic switch it has identified should shed new light on the molecular mechanisms underlying that development and, consequently, provide needed insight on inherited retinal diseases in humans.

From FSU's Department of Biological Science and Program in Neuroscience, doctoral candidate Karen Alvarez-Delfin (first author of the PNAS paper), postdoctoral fellow Ann Morris (second author), and Associate Professor James M. Fadool are the first scientists to identify the crucial function of a previously known gene called "tbx2b." The researchers have named the newfound allele (a different form of a gene) "lor" -- for "lots-of-rods" -- because the mutation results in too many rods and fewer ultraviolet cones than in the normal eye.

"Our goal is to generate animal models of inherited diseases of the eye and retina to understand the progression of disease and find more effective treatments for blindness," said Fadool, faculty advisor to Alvarez-Delfin and principal investigator for Morris's ongoing research. "We are excited about the mutation that Karen has identified because it is one of the few mutations in this clinically critical pathway that is responsible for cells developing into one photoreceptor subtype rather than another."

"What is striking in this case is that the photoreceptor cell changes we observed in the retinas of zebrafish are opposite to the changes identified in Enhanced S-cone syndrome (ESCS), an inherited human retinal dystrophy in which the rods express genes usually only found in cones, eventually leading to blindness," Alvarez-Delfin said. "Equally surprising is that this study and others from our lab show that while alterations in photoreceptor development in the human and mouse eyes lead to retinal degeneration and blindness, they don't in zebrafish. Therefore, the work from our Florida State lab and with our collaborators at the University of Pennsylvania, Vanderbilt University and the University of Louisville should provide a model for better understanding the differences in outcomes between mammals and fish, and why the human mutation leads to degenerative disease."

Morris calls the zebrafish an ideal genetic model for studies of development and disease. The common aquarium species are vertebrates, like humans. Their retinal organization and cell types are similar to those in humans. Zebrafish mature rapidly, and lay many eggs. The embryos are transparent, and they develop externally, unlike mammals, which develop in utero.

"This lets us study developmental processes such as the formation of tissues and organs in living animals," she said.

"From a developmental biology perspective, our research will help us unravel the competing signals necessary for generating the different photoreceptor cell types in their appropriate numbers and arrangement," Morris said. "The highly specialized nature of rods and cones may make them particularly vulnerable to inherited diseases and environmental damage in humans. Understanding the genetic processes of photoreceptor development could lead to clinical treatments for the millions of people affected by photoreceptor cell dystrophies such as retinitis pigmentosa and macular degeneration."

The mosaic arrangement of photoreceptors in fish was first described more than 100 years ago, but the J. Fadool laboratory at Florida State was the first to successfully take advantage of the pattern to identify mutations affecting photoreceptor development and degeneration.

"Imagine a tile mosaic," Fadool said. "That is the kind of geometric pattern formed by the rod and cone photoreceptors in the zebrafish retina. This mosaic is similar to the pattern of a checkerboard but with four colors rather than two alternating in a square pattern. The red-, green-, blue-, and ultraviolet-sensitive cones are always arranged in a precise repeating pattern. Human retinas have a photoreceptor mosaic, too, but here the term is used loosely, because while the arrangement of the different photoreceptors is nonrandom, they don't form the geometric pattern observed in zebrafish.

"So how do we ask a fish if it has photoreceptor defects?" he asked.

Fadool explained that because the mosaic pattern of zebrafish photoreceptors is so precise, mutations causing subtle alterations are easier to uncover than in retinas with a "messier" arrangement.

"Just as we can easily recognize a checkerboard mistakenly manufactured with some of the squares changed from black to red or with all-black squares, by using fluorescent labeling and fluorescence microscopes we can see similar changes in the pattern of the zebrafish photoreceptor mosaic," he said. "Karen showed that within the mosaic of the lots-of-rod fish, the position on the checkerboard normally occupied by a UV cone is replaced with a rod. The identity of the mutated gene is then discovered using a combination of classical genetics and genomic resources."

Funding for the Fadool laboratory's zebrafish research comes in large part from a five-year grant totaling more than $1.7 million from the National Institutes of Health.

The Ribosome: Perfectionist Protein-maker Trashes Errors

The enzyme machine that translates a cell's DNA code into the proteins of life is nothing if not an editorial perfectionist.Johns Hopkins researchers, reporting in the journal Nature January 7, have discovered a new "proofreading step" during which the suite of translational tools called the ribosome recognizes errors, just after making them, and definitively responds by hitting its version of a "delete" button.

It turns out, the Johns Hopkins researchers say, that the ribosome exerts far tighter quality control than anyone ever suspected over its precious protein products which, as workhorses of the cell, carry out the very business of life.

"What we now know is that in the event of miscoding, the ribosome cuts the bond and aborts the protein-in-progress, end of story," says Rachel Green, a Howard Hughes Medical Institute investigator and professor of molecular biology and genetics in the Johns Hopkins University School of Medicine. "There's no second chance." Previously, Green says, molecular biologists thought the ribosome tightly managed its actions only prior to the actual incorporation of the next building block by being super-selective about which chemical ingredients it allows to enter the process.

Because a protein's chemical "shape" dictates its function, mistakes in translating assembly codes can be toxic to cells, resulting in the misfolding of proteins often associated with neurodegenerative conditions. Working with bacterial ribosomes, Green and her team watched them react to lab-induced chemical errors and were surprised to see that the protein-manufacturing process didn't proceed as usual, getting past the error and continuing its "walk" along the DNA's protein-encoding genetic messages.

"We thought that once the mistake was made, it would have just gone on to make the next bond and the next," Green says. "But instead, we noticed that one mistake on the ribosomal assembly line begets another, and it's this compounding of errors that leads to the partially finished protein being tossed into the cellular trash," she adds.

To their further surprise, the ribosome lets go of error-laden proteins 10,000 times faster than it would normally release error-free proteins, a rate of destruction that Green says is "shocking" and reveals just how much of a stickler the ribosome is about high-fidelity protein synthesis.

"These are not subtle numbers," she says, noting that there's a clear biological cost for this ribosomal editing and jettisoning of errors, but a necessary expense.

"The cell is a wasteful system in that it makes something and then says, forget it, throw it out," Green concedes. "But it's evidently worth the waste to increase fidelity. There are places in life where fidelity matters."

The Dangers of Synthetic Biology

Nobel Prize winner David Baltimore explains why building smallpox from scratch is a key safety concern in synthetic biology.

The emerging field of synthetic biology -- the quest to design and build new life forms that can perform useful functions -- brings exciting promise and potentially dangerous capabilities. Scientists have the ability to synthesize entire strings of DNA and put together complicated molecular machinery. But that power has raised some troubling questions. Could terrorists recreate viruses such as smallpox? Or engineer a virus even more deadly than avian flu? (see "The Knowledge").

In the 1970s, scientists faced a similar dilemma. The advent of recombinant DNA technology meant biologists could manipulate DNA as they never could before. Concerned about the potential perils of this new tool, a prominent group of scientists held the now-famous Asilomar Conference in 1975 (formally titled the "International Congress on Recombinant DNA Molecules") to determine how to proceed safely.

Thirty years later, at the Synthetic Biology 2.0 meeting at the University of California, Berkeley this month, scientists met to discuss not only new developments in the field, but also how the community should deal with the growing safety concerns surrounding synthetic biology.

David Baltimore, a winner of the 1975 Nobel Prize in physiology or medicine, and president of the California Institute of Technology, was one of the organizers of the Asilomar Conference. At the Synthetic Biology conference last week, he reflected on changes in the field over the last 30 years. Baltimore talks here with Technology Review about what scientists have learned since 1975 and the specific dangers we should be most worried about.

Technology Review: What were you were most concerned about 30 years ago?

David Baltimore: The Asilomar Conference was convened in a very different context than we have today. We were marveling at a wholly new world of experimentation -- we literally had no experience with moving DNA around. But people were also concerned, and rightly so, about issues of intrinsic safety. They were worried, for example, that we could create organisms that we didn't know how to control.

At the conference, we decided to focus purely on safety, rather than ethics or biowarfare. We believed, somewhat naively, that there was a treaty that everyone held to prohibiting use of technology to make biological weapons. In retrospect, the U.S.S.R. had a huge clandestine program. We also didn't have the situation we have today, where terrorist organizations cross boundaries and are not held by treaties. So we clearly have an unfinished agenda from Asilomar on biowarfare.

TR: What issues are you most worried about today?

DB: The real danger today is from organisms that already exist. The idea of synthesizing something worse than that, of taking bits of Ebola and other viruses to create something more deadly, underestimates how hard it is to survive in the natural world.

Adapting to the human lifestyle is very complicated, so I would guess that we would fail if we tried to engineer a dangerous organism. Ebola, for example, is very pathogenic. It infects families and health workers, but it never spreads widely because it is too lethal -- it isn't in the community long enough to spread. Bird flu is not likely to spread widely until it mutates to become less pathogenic.

Read the full interview here