News

28 February 2010The CDC National Office for Public Health Genomics (NOPHG) in the US has announced plans to create a new Knowledge  Synthesis Center using the methods of the Evaluation of Genomic Applications in Practice and Prevention (EGAPP) initiative. EGAPP produces periodic reviews which summarise the available evidence for validity and clinical utility of selected genomic tests and other applications (see previous news for examples). This sort of information is potentially very helpful for policy-makers and health professionals trying to determine whether or not a given test is useful or not.

The new project, a collaboration between the CDC and National Institutes for Health (NIH), will provide funding for a dedicated centre to ‘conduct, update, and publish systematic evidence reviews to address selected questions for the evaluation of a set of health-related genomic tests’ (see announcement). This will include production of topic briefs on the use of selected genomic applications for improving health and preventing disease, and related issues, to form part of an online knowledge silo for EGAPP, and research into improved methodology for performing systematic reviews of published evidence.

A total of around $1.5 million funding over three years is available to create and run the new centre, and applications are being are sought.

26 February 2010 In a controversial move that has re-ignited debate about the possibility of unfair genetic discrimination, the Australian insurance company nib is offering half-price genome scans from the US direct-to-consumer company Navigenics (see New Scientist). The company uses whole genome profiling technology coupled with results from genome-wide association studies to predict an individual’s risk of numerous common complex diseases based on their particular combination of SNPs. Due to the small relative risks associated with each variant, and the lack of validated clinical interventions that can be offered to people in differing risk groups, the clinical validity and utility of such tests has been widely questioned (see previous news).

The insurance company claim that it will not have access to the results of the test, and that using the services “will not impact on [the] health insurance premiums”. Instead, the company hopes that “by gaining insight into your health risks you have the power to help delay or prevent [various common] conditions”. Nonetheless, it has been claimed that people are turning down genetic tests because of fear that the results will adversely affect insurance cover (see the Sydney Morning Herald). According to the Australian Government National Health and Medical Research Council, although Australian law prohibits the use of genetic test information by providers of health insurance, providers of life insurance can use the results to decide who to cover and to set premiums. Moreover, if individuals have had a DNA-based test, they must report these results in their life insurance application.

Comment: The issue of 'genetic discrimination' – broadly defined as the unfair treatment of an individual based on their genetic make-up – is extremely controversial and highly complex. Different jurisdictions have dealt with the issue in various ways due to their diverse health care systems, from enacting national legislation banning the use of genetic and familial information by health insurers (see previous news), to allowing insurance companies to self-impose a voluntary moratorium against the use of genetic test results (see previous news).

In the context of risk-based insurance system, where premiums depend upon estimating an individual’s risk of disease based on numerous different factors (age, sex, smoking, family history, etc), it is unclear why 'genetic' information should be singled out and treated any differently from any other information that might be relevant. This is particularly pertinent for multifactorial diseases, where the contribution of common genetic variants is normally substantially outweighed by other environmental or behavioural risk factors. Thus, information provided by whole genome SNP profiling is unlikely to be have much effect on insurance premiums. However, there is little descent from the view that individuals with inherited monogenic disorders – especially where the phenotype is not apparent (such as late-onset diseases) – should not be unfairly treated on the basis of their future risk of disease. The question is therefore how best to avoid this situation without creating an unnecessary and inappropriate legislative burden.

The PHG Foundation is currently working to develop recommendations around the issue of genetic discrimination with respect to both insurance and employment within the UK.

25 February 2010The US Food and Drug Administration (FDA) and National Institutes of Health (NIH) have announced a joint initiative intended to accelerate the movement of scientific innovations into health care.

The Joint NIH-FDA Leadership Council will concentrate on important public health issues, and seek to integrate regulatory considerations into biomedical research planning. The programme will combine work in translational and regulatory science including efforts not only to develop new clinical tools, but also means to assess the safety and efficacy of these tools. This sort of approach can be very important in making sure that innovation is used appropriately and to the best effect to improve health; for example, the PHG Foundation is currently working with other experts to develop quality standards to allow a fair evaluation and comparison of different disease risk prediction models.

It is expected that the new US partnership will have a particular impact on the development of genetic and pharmacogenetic tests for clinical application, as well as drugs for rare diseases (many of which are genetic in origin) and stem cell therapeutics. Sharon Terry, president and CEO of the Genetic Alliance, said: "The exercise of understanding how to endow discovery science with regulatory sufficiency, and retool the regulatory system to be flexible, iterative, and adaptive, will yield great fruit," (see GenomeWeb news).

24 February 2010

The official definition of human embryonic stem (HES) cells in US National Institutes of Health (NIH) guidelines is to be broadened from those ‘derived from the inner cell mass of blastocyst stage human embryo’ (ie. from embryos that have reached the blastocyst stage at four or five days old, 70-100 cells), to include also those derived from earlier stage embryos.

Dr Lana Skirboll, director of the Office of Science Policy of the NIH, reportedly said: "We are making what I think is a relatively small technical change to the definition of human embryonic stem cells…This changes none of the ethical requirements in the guidelines" (see Reuters news). This move was prompted by an application from a commercial source to list cell lines derived from eight-cell stage embryos, and will make some commercial and academic research programmes potentially eligible for government funding.

Derivation of HES cells from a cell taken from an eight-cell stage embryo could possibly allow implantation and normal development of the remaining seven-cell embryo. This is what happens in pre-implantation prenatal diagnosis (PGD); one cell is removed for genetic analysis and, if healthy, the seven-cell embryo is implanted and can grow into a normal fetus.

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14 February 2010

A new facility called BIOFAB (International Open Facility Advancing Biotechnology) has been established with funding from the US National Science Foundation (NSF), the Lawrence Berkeley National Laboratory (LBNL) and the BioBricks Foundation (BBF). BIOFAB intends to create standardised DNA parts that will be made freely available to academic and commercial groups seeking to use synthetic biology to create organisms for different purposes (see press release).

The ‘parts’ will be crucial genetic control elements, initially from the laboratory bacterial strain E. coli, which will be characterised and standardised with a view to creating standard elements that can be used to create de novo biological systems. The hope is that these will substantially decrease the time and cost of developing new synthetic organisms, which have all sorts of potential applications such as the production of biofuels, drugs and other therapeutics.

BIOFAB will use resources such as the BioBrick Public Agreement, a proposed legal framework to support the free exchange and use of standardised biological components; it will also include research into ethical issues such as safety and security. Common concerns about bioengineering include issues relating to the deliberate design of dangerous new biological weapons, and wider worries about the inadvertent creation of organisms with other detrimental effects on nature.

9 February 2010The Times newspaper has reported that a new pre-conceptual genetic test that detects mutations associated with more than one hundred recessive conditions will shortly be launched in the UK via a fertility centre that offers in vitro fertilisation (IVF) and prenatal genetic diagnosis (PGD) procedures.

Already available direct-to-consumers in the US via the internet, the self-styled  ‘Universal Genetic Test’ uses a saliva sample to screen for mutations associated with a wide range of diseases and conditions – some very severe, others very minor. The idea is that one or both prospective parents can have the test (in some cases paid for by medical insurance) to determine if they are carriers; if carrier status for a particular condition or conditions is detected, then couples may opt for IVF with PGD to detect and remove embryos that would be affected (or be carriers for) the disease, or alternatively opt for prenatal diagnosis and termination of affected pregnancies, in either case avoiding the birth of a child with the condition.

Whilst pre-conceptual screening to prevent the birth of children affected by serious genetic diseases is a potentially very valuable measure, this new test raises a number of issues of concern. In particular, it is difficult for prospective users of the combined test to assess its potential utility. The numbers and nature of the mutations screened for in each of the conditions is not clear, so the value and accuracy of testing is difficult to gauge. Moreover, since the test covers a spectrum of conditions, which vary both in severity and in the availability of potential treatments, it is difficult to make a robust assessment of the implied risks and benefits of proceeding with testing for each condition.

Like other providers of genetic tests that are available via the internet, on a direct-to-consumer basis - Counsyl should ensure transparency by providing robust evidence of clinical and scientific validity in order to justify the clinical (and personal) utility of the test to both the consumer and the health professional who may offer the test.

Given that some consumers within the UK may initially seek to access this service via the internet, rather than via a clinic, the requirements of the Human Genetic Commission's common framework of principles for the governance of direct-to-consumer tests, which is currently being finalised, may well become relevant.

8 February 2010The US Secretary's Advisory Committee for Heritable Disorders in Newborns and Children (ACHDNC) has recommended that an additional condition be added to the panel of conditions for which all newborns receive screening (see press release). The ACHDNC adopted a list of 29 recommended conditions for which newborn screening should be compulsory in 2005 (see previous news), on the basis that effective tests were available and that early detection and treatment could provide clear medical benefits. Almost all newborns in the US now receive screening for these conditions (see previous news). 

Now, in the first proposal since the original panel was adopted in 2005, the committee has unanimously agreed to recommend the addition of Severe Combined Immunodeficiency (SCID) to the ‘core’ conditions on the newborn screening panel. 

SCID is a term used to refer to a group related disorders characterised by the absence of T-lymphocytes, essential components of the immune system. With no effective immune responses, affected children can die at any point from infections that would be harmless in a healthy person. However, treatment such as bone marrow transplantation and gene therapy can cure the disease (see SCID.net), though these treatments are not without risks (see previous news); protection from infection can also prolong life.

7 February 2010The European Molecular Biology Laboratory's European Bioinformatics Institute (EMBL-EBI) recently launched a new online database of genomic-based drug and small molecule information. This open access database, ChEMBLdb, is intended as a resource for researchers aiming to develop potential new therapeutics based on genomic data. It includes records of more than half a million small molecule compounds and their effects on biological systems. ChEMBL team leader Dr John Overington commented: "We hope ChEMBLdb will assist the translation of genomic-based insights into innovative drug therapies" (see press release)

Unusually, this resource was originally a commercial database but was purchased with a £4.7 million Strategic Award from the Wellcome Trust; their director of science funding Alan Schafer said that the move “should have the greatest impact on researchers in academia and in small companies on limited budgets”.

5 February 2010 Genome-wide association studies (GWAS) have identified over 2,000 genetic variants associated with a range of common diseases such as diabetes and various cancers, with only a few hundred variants being convincingly replicated. Finding many common variants with a weak effect on disease risk is consistent with the common disease-common variant hypothesis and thus far only account for a small proportion of the inherited risk.

It has recently been proposed that rare variants may show much stronger effect sizes and could provide direct information about disease causation or risk (see previous news). However, it is also plausible that because nearly all GWAS thus far have concentrated on detecting and characterising main effects for genetic risk, the potential role of environmental factors modifying genetic risk has not been greatly explored, and that some of the ‘missing’ inherited risk may actually be explained by this.

Following the consortia-based approach used in many GWAS, the GENE enVironment Association studies (GENEVA) consortium was set up in 2006 by a National Institute of Health program (GEI), to accelerate the understanding of genetic and environmental contributions to health and disease by providing the support for establishing a global study management, a coordinating centre, and two genotyping centres.

A paper in the journal Genetic Epidemiology describes the GENEVA consortium, providing the aims and organisational structure as well as discussing the potential contributions from this consortium [Cornelis et al. (2010) Genet Epidemiol doi:10.1002/gepi.20492]. The aims of the GENEVA consortium are to:

1)       Identify genetic variants associated with complex diseases and traits in initial genome-wide discovery studies;

2)       Identify variations in gene-trait associations related to environmental exposures; and

3)       Ensure the rapid sharing of data to the general scientific community.

This consortium brings together 14 predominantly case-control studies with phenotypic and environmental exposure data and include people of European descent, as well as a significant number of African Americans, Hispanics and Asians. Common genotyping centres allow the use of a standardised protocol and quality control resulting in high quality genotyping data. The coordinating centre will act as a data repository as well as dealing with the logistics and administration. Although individual study investigators conduct statistical analyses, the protocols are harmonised to allow easy cross-study integration and GWAS meta-analyses.

The consortium hopes to accelerate the identification of variants involved in complex disease including via environmental interactions, allowing enhanced understanding of disease aetiology.

1 February 2010

St. Jude Children’s Research Hospital has joined with Washington University School of Medicine in a new US project to unravel the genetic origins of childhood cancers. The Pediatric Cancer Genome Project will compare whole genome sequences from normal and cancer cell samples from more than 600 children with cancers, particularly childhood leukaemias, brain tumours and sarcomas (a group of cancers that affect the bone, muscle and other connective tissues).

It is thought that the initiative, which is projected cost US$65 million over three years, will identify specific genetic abnormalities quite different from those found in adult cancers. Researchers will also look at the influence of other genetic variation, including epigenetic changes, on cancer progression and seek to identify genetic markers that may predict outcome and help direct optimal treatment. Ultimately it is hoped that improved understanding of the underlying genetics will also lead to new methods of diagnosis, treatment or even prevention (see press release).

18 February 2010New research from the Johns Hopkins Kimmel Cancer Centre, which will be published next week in the journal Science Translational Medicine, describes an innovative clinical application of whole genome sequencing to develop individualised diagnostics for cancer detection (see the Guardian).

Normal and cancerous tissue samples were taken from four colorectal and two breast cancer patients, and next generation sequencing technology used to look for differences. However, rather than looking for single base changes like many previous studies, only large structural changes were catalogued – such as insertions, deletions, incorrect ordering and fusion between sections of different chromosomes – which are very common in cancer cells (see previous news). Such genomic rearrangements are a hallmark of genomic instability and were present in the cancer genomes from all six patients.

After investigators identified DNA rearrangements specific to each individual’s cancer, they were able to develop personalised tests to detect these same changes in DNA amplified from a blood sample. In one case, this test was successfully used following surgery and chemotherapy to determine the presence of residual cancer and metastatic legions. In principle, this relatively non-invasive test could potentially be developed for any cancer patient, and used not only to monitor an individual’s response to different therapeutic options, but also for early detection of recurrent cancer in the same patient in the future.

Comment: Whilst the normal caveats about the need for further clinical validation obviously apply, this novel application of next generation sequencing technology potentially has enormous clinical benefits for monitoring treatment response and screening cancer patients in remission. However, evidence is still needed to show that this approach would actually allow recurrent cancers to be detected before they could be found by other conventional methods, such as imaging, and then treated before causing symptoms. Although whole genome sequencing is currently more expensive than CT scanning, given the falling costs and development of ever faster and cheaper next generation sequencing technologies, this situation is likely to be reversed within the next few years.

This method represents an important foray into offering truly personalised medicine. Moreover, because it is based on the analysis of somatic genetic changes, rather than an individual’s inherited genetic code, many of the complex ethical, legal and social issues raised by personal genome profiling are avoided.

18 February 2010Identifying cancers early requires the early identification of cancer biomarkers such as elevated levels of tumour-specific proteins (antigens), such as analysis of prostate specific antigen (commonly known as PSA) for prostrate cancer or cancer antigen 125 for ovarian cancer. However, these molecules can be hard to detect in the early stages of cancer as their levels are too low and they may be broken down more quickly during this stage. An alternative strategy is to monitor antibodies produced against these cancer-specific antigens, as they are produced in greater numbers even when the amount of antigen is low, and circulate for longer in blood stream.

Antibodies are usually produced by the immune system to attack external (‘non-self’) antigens. However, autoantibodies target an individual’s own proteins and can be the cause of  diseases such as rheumatoid arthritis and type I diabetes. Autoantibodies are also produced in response to antigens on the surface of tumour cells; this may be at an early stage of carcinogenesis. One particular type of antigen which may elicit a response are glycoproteins (proteins with sugar molecules). In tumour cells, these molecules may be abnormally glycosylated, provoking an immune response – but it is a challenge to identify particular abnormal glycoproteins of this type. In a paper published in Cancer Research, Wandall et al. describe the development of a microarray system that can be used to analyze blood samples for the presence of specific autoantibodies directed against these abnormal glycoproteins [Wandall et al. (2009) Cancer Res: 70(4):1306-13].

Wandall et al. created a library of cancer-associated glycoproteins on a microarray platform. This library was then used to screen the blood of patients with ovarian, breast or prostate cancer (approximately 20 patients in each group) as well as healthy individuals. Autoantibodies were successfully detected in 30% of the patients and not in control samples, but none of them allowed sensitivity of detection high enough for clinical use as biomarkers.

This was because the pattern of glycosylation of proteins varies between cells, meaning that a large number of different, variable versions can be present in cancer cells, so that identification of specific variants that are elevated in cancer cells is a challenge. The authors propose that large glycopeptides arrays containing molecules synthesised in vitro could be a mechanism by which to investigate the abnormal glycoprotein expression patterns in specific cancers and may allow better targeted investigation of specific autoantibodies and ultimately earlier identification of cancer.

17 February 2010It has long been known that the length of telomeres – the repetitive sequences at the end of chromosomes that protect genomic DNA from degradation – is related to age: the older the cell, the shorter the telomeres (see previous news). In stem cells and most cancer cells, the enzyme telomerase maintains the telomere length by adding additional repeats, and thus renders the cells effectively immortal. Telomere length therefore represents a delicate balance between immortality and uncontrolled cell growth.

As telomere length is a partly heritable trait (with estimates ranging from 4% to 80%), it is likely that there are genetic variants that modulate the effectiveness of telomerase, and thus the length of an individual’s telomeres. The first genome-wide association study of telomere length in the white blood cells from over 12,000 people has now revealed common variants associated with telomerase function [Codd V et al. Nature (2010) doi:10.1038/ng.532]. The most strongly associated SNP is located on chromosome 3q26, an the same locus as the RNA template used by telomerase for extending the telomeric repeats, and is associated around 3.6 years of age-related telomere-length attrition per allele.

In addition, the average telomere length has also been linked not only to cellular aging, but also mental aging – specifically cognitive decline and dementia [Yaffe K et al. Neurobiol Aging (2010) doi:10.1016/j.neurobiolaging.2009.12.006]. By looking at the average telomere length (which varied from around 3000-60000 base-pairs) in over 3000 non-demented adults aged 70-79, it was clear that those with long telomeres both started with a higher level of cognitive function and suffered less decline over the 7-year follow-up period versus those with medium or short telomeres. The authors conclude that “telomere length may serve as a biomarker for cognitive aging” which is relatively easy and safe to measure.

16 February 2010Numerous companies and academic researchers are developing ever faster and cheaper ways of performing DNA sequencing (see previous news), but to date none has crossed the widely anticipated $1,000 threshold. A new method for analysis of DNA based on “dynamic chemistry”, rather than biological enzymes, may take us a step closer to that goal [Bowler F et al. Angew Chem Int Ed (2010) doi:10.1002/anie.200905699]. The technique uses a DNA mimic known as “peptide nucleic acid” (or PNA) as a template for a known genomic sequence, with a blank space at the position of interest. A complementary sample of DNA can then be adhered to this template and by application of a chemical probe followed by mass spectrometry to detect the PNA/DNA hybrid, it is possible to determine what base was present in the DNA at the blank position. This technology particularly lends itself to analysis of single nucleotide polymorphisms (SNPs) and other (rare) single base mutations, and can accurately sequence heterozygous individuals as well as homozygotes. Ultimately, it may also be possible to use it to sequence an entire genome, and researchers believe that the technology “could help reach the goal of complete genome analysis in a few hours for less than £637” (see BBC news).

Comment: Before new technologies such as this can be considered for use in the NHS, a robust evaluation of the analytical validity, clinical validity and clinical utility is needed, in addition to consideration of the ethical, legal, economic and social implications of the technologies. Simply delivering information in the form of individual genome sequences may never be the most cost-effective and clinically useful application of such technology, as correctly interpreting the results remains an enormous challenge, as does ensuring informed consent and confidentiality. A more targeted approach focusing on known genetic diseases may turn out to be more appropriate, for which each technology will have to prove itself in terms of accuracy and cost-effectiveness against the many alternatives.

Read a further comment from the PHG Foundation on new genomic technologies, published in the Scotsman.

12 February 2010

Numerous common genetic susceptibility loci for prostate cancer have been identified through genome-wide association studies (see previous news), but questions remain over their suitability for risk prediction (see previous news). In particular, since asymptomatic prostate cancer is very common in older men, the risk of over-diagnosis through screening remains a major issue (see previous news). Therefore, rather than simply predicting an individual’s risk of developing prostate cancer, identifying those men at risk of aggressive, life-threatening prostate cancer would have substantially better clinical utility.

Research into the natural history of the disease, based on an analysis of three previously identified genes in a retrospective cohort of over 300 prostate cancer patients, suggests that this stratification may be possible through analysis of gene loss and gene rearrangement in prostate biopsy samples [Reid AMH et al. Br J Cancer (2010): doi:10.1038/sj.bjc.6605554]. Loss of PTEN, a tumour suppressor gene, is significantly associated with the clinical stage and severity of the disease. In addition, rearrangement at the ERG and ETV1 genes, which encode transcription factors, is a significant prognostic factor for overall survival. Combining these results (presence of absence of the PTEN gene with or without the ERG/ETV1 rearrangement) allowed researchers to stratify patients into four risk groups: a large group with good prognosis (with a cancer-specific survival of over 85% at 11 years), two intermediate groups, and a small group with poor prognosis and a significantly higher risk of death from prostate cancer (with a cancer-specific survival of less than 14% at 11 years).

According to the authors, this result has “implications both for potentially deciding which patients should be conservatively or aggressively treated, and also for stratification of patients in clinical trials”.

1 February 2010 Genome-wide association studies (GWAs) aim to identify causative genes for common disease such as diabetes, obesity and stroke by analysing single nucleotide polymorphisms (SNPs). Although SNPs are identified that show association with a disease, they are unlikely to be the actual genetic variant involved in causation of that disease, but rather indicate that a causal variant is in the vicinity. Follow-up in-depth sequencing studies are required in order to identify the actual gene(s) directly involved in disease susceptibility.

Although GWAs have identified many SNPs associated with common disease, they have as yet had little success in identifying the causative genetic variants. Those that have been identified have only a weak effect on disease risk, and therefore only explain a small proportion of the heritable, genetic component of susceptibility to that disease. This has led to the common disease-common variant hypothesis, which predicts that common disease-causing genetic variants exist in all human populations, but each individual variant will necessarily only have a small effect on disease susceptibility (i.e. a low associated relative risk).

An alternative hypothesis is the common disease, many rare variants hypothesis, which postulates that disease is caused by multiple strong-effect variants, each of which is only found in a few individuals. Dickson et al. in a paper in PLoS Biology postulate that these rare variants can be indirectly associated with common variants; they call these synthetic associations and demonstrate how further investigation could help explain findings from GWA studies [Dickson et al. (2010) PLoS Biol. 8(1):e1000294]. In simulation experiments, 30% of synthetic associations were caused by the presence of rare causative variants and furthermore, the strength of the association with common variants also increased if the number of rare causative variants increased.

The researchers also demonstrated that causative variants could be located at some distance from the marker SNP and still contribute to the association, demonstrating this using real data from individuals with sickle cell anaemia and hearing loss and controls. The implication of this finding is that sequencing close to a marker SNP may not necessarily identify causative gene(s), leading the authors to suggest that whole-genome sequencing may be a better approach to finding such variants, whilst acknowledging that it is still unclear what proportion of GWAS signals may be due to common versus rare variants.

Comment: Rare genetic variants are important contributors to disease, and can in some cases be identified by whole genome sequencing such as exome sequencing (see previous news) and targeted sequencing of the X-chromosome (see previous news). Their role in common disease such as obesity has also been demonstrated by recent identification of CNVs associated with obesity (see previous news).

However, identifying these rare, causative variants for any disease is not an easy task, due to the enormous amount of sequence variation present in individual genomes. The identification of rare variants that are causal in common diseases can be still more problematic; many may only be present in subsets or clusters of people with a given disease e.g. individual families.

 

3 February 2010Personalized genomic information: preparing for the future of genetic medicine.

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How culture shaped the human genome: bringing genetics and the human sciences together.

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Epigenetic therapies offer new approach to fighting cancer at the genetic level.

Friedrich MJ. JAMA. 2010 Jan 20;303(3):213-4. 

 

The pursuit of susceptibility genes for Alzheimer's disease: progress and prospects.

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Fixing the communications failure.

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Gene therapy tackles demyelinating disease

Nat. Med. 2010; 16 (37): doi:10.1038/nm0110-37

 

Virology: Bornavirus enters the genome.

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Williams-Beuren syndrome.

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Five hard truths for synthetic biology.

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Ten years of synergy.

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