Scientists at the University of Oxford and Oxford University Hospitals NHS Trust have formed a partnership in order to develop this test, with the aim of improving the prognosis for the 300,000-plus UK citizens who are affected by the life-threatening disease every year.

It works by performing DNA sequencing on the affected patient and highlighting to the doctor any genetic abnormalities. Mutations in the code often play a vital role in determining the efficacy of a treatment, so the results are extremely valuable.

Scientists from the Biotech Research and Innovation Centre (BRIC) and Center for Healthy Aging, University of Copenhagen recently completed research which demonstrated that the FBH1 gene could actually make chemotherapy more effective, so its presence would promote this course.

On the other hand, Vanderbilt-Ingram Cancer Center (VICC) researchers identified a pattern of DNA in breast cancer patients which suggests that the tumour is more likely to resist the drugs, meaning additional radiotherapy could be recommended instead.

Administering the most effective treatment as early as possible ensures the most favourable outcomes, so the NHS test could help to reduce the mortality rate associated with cancer. The disease took the lives of over 150,000 UK sufferers in 2010.

This improvement could also play a significant role in reducing the strain on the healthcare system, which is increasingly suffering from dwindling budgets and resources. Each test costs £300, but this is a worthwhile investment since it prevents wastage of time and money on unsuccessful therapies.

Dr Jenny Taylor, who was involved in the development and integration process, said: "We are the first to introduce a multi-gene diagnostic test for tumour profiling on the NHS using the latest DNA sequencing technology. It's a significant step change in the way we do things."

The finding could have vast implications for the future of treatment, since STAT3 is vital for the survival and growth of different tumours.

By creating a drug which effectively administers this molecule, scientists could help to treat the 130,000 Britons every year who are diagnosed with cancer of the breast, prostate or lung.

It could be particularly useful in aiding those patients affected by the most severe forms of the disease, since STAT3 plays an important role in malignancy.

The spread or metastasis of cancerous cells around the body means that treatments like radiotherapy and chemotherapy are less likely to offer favourable outcomes.

The scientifically engineered S3I-1757 molecule prevents malignancy by inhibiting the dimerisation of STAT3 proteins – a process necessary for proliferation.

Dr Said M. Sebti said: "Once disrupted, STAT3’s ability to help cancer cells survive, grow and invade is neutralised."

More than 10,000 Britons were diagnosed with the disease in 2010, according to Cancer Research UK, and the condition claimed almost 5,000 lives in the same year.

Allowing healthcare providers to better identify at-risk patients and select more suitable treatments could therefore have considerable implications for improving mortality and morbidity rates in the nation.

MD Anderson Cancer Center researchers set out to determine whether the G-protein signalling (RGS) pathway plays a role in bladder cancer, as it does with the development of other tumours.

After comparing DNA samples from 803 patients and 803 healthy controls, the experimenters identified a number of gene variants that were linked with increased incidence rates.

DNA information also seems to play an important role in determining patient outcomes, since mutations were seemingly involved in recurrence, progression and average lifespan.

Attribution: Julius Schorzman

Scientists who specialise in food technology and cancer biology worked together in order to determine whether different flavourings had a detrimental impact on the genome, motivating changes which can promote abnormal rates of multiplication.

p53 is a tumour-suppressing protein which is released by the body in an effort to prevent potentially dangerous mutations. High levels of this in the blood therefore indicate the presence of harmful alterations in the genetic code.

After working with US Department of Agriculture to gather appropriate samples for testing, the researchers analysed p53 production in human cells that had been grown in laboratory dishes following exposure to a number of different foods and flavourings.

In order to accurately monitor the manufacturing levels, researchers used a method devised by Dr Scott Kern, Kovler Professor of Oncology and Pathology at the Johns Hopkins University School of Medicine. His technique utilises a compound which glows in reaction to p53 activation.

They found marked increases in presence of the cancer-fighting protein were apparent when the cells were exposed to black and green teas and coffee. Strongest reactions were in response to pyrogallol and gallic acid – which is also found in the caffeinated beverages.

According to the UK Tea Council, British people consume 165 million cups of tea and 70 million coffees each day. This high intake could therefore be impacting cancer rates in a marked way.

However, the academics believe that methods could be devised to remove the potentially cancer-causing components from the drinks. This may therefore be a major focus for researchers going forward.

Dr Kern said: "It's clear that plants contain many compounds that are meant to deter humans and animals from eating them, like cellulose in stems and bitter-tasting tannins in leaves and beans we use to make teas and coffees, and their impact needs to be assessed."

Transmission of unhealthy mitochondria – energy-producing cell organelle – from mother to offspring can have serious implications for the child's health.

However, researchers have found that the nucleus from the affected parent's egg can be safely transferred into another donor's, which contains healthy mitochondria.

This means that most of the genetic information passed on will come from the aspiring mother, although some will be transferred from another woman.

Many people have expressed ethical concerns about babies who are conceived with DNA from three different people.

However, the HFEA has gauged public opinion, and Professor Lisa Jardine said that "there is broad support for permitting mitochondria replacement".

Alongside proper regulation, the technique can be implemented safely to ensure IVF children do not develop mitochondrial diseases.

These conditions affect around one-in-200 newborns each year, and can seriously impact the functionality of bodily organs.

Researchers from the University of North Carolina have found that a person's genes play a significant role in their inclination to try new foods.

Investigators recruited 66 pairs of twins aged between four and seven years, and found that DNA material affects eating behaviour in 72 per cent of cases.

Although inherited factors may influence a child's willingness to taste new dishes, lead researcher Dr Myles Faith believes that parents can still try to influence better habits.

He said: "Some children are more genetically susceptible than others to avoid new foods. However, that doesn't mean that they can't change their behaviours and become a little less picky."

It is vital that mothers and fathers take measures to ensure their daughter or son is consuming a nutritious and varied diet, since this plays a vital role in short and long-term health.

In an attempt to understand the link between hours of rest and DNA, scientists from the University of Surrey performed an investigation.

The NHS advises that adults sleep for around seven to eight hours each night – the experimenters looked at the effects of getting just six hours.

After analysing genetic information, they found that DNA involved in processes controlling stress, inflammation and immunity were involved.

This indicates that the disruption could be responsible for motivating symptoms such as anxiety, and shows why people who get little sleep are at a higher risk of conditions like the common cold.

Director at the university's Sleep Research Centre Derk-Jan Dijk said: "Now that we have identified these effects we can use this information to further investigate the links between gene expression and overall health."

Researchers analysed samples of genetic information taken from 246 participants in clinical examinations and tests. The data used was gathered from the College of American Pathologists 2002 Survey, Coriell Cell Repositories and ARUP Laboratories.

The DNA sequences had previously been analysed using a variety of standard techniques, and some related to healthy subjects while others were gathered from people with HD. The samples were unmarked so that the investigators could not skew their results with pre-existing knowledge.

Experimenters were then able to fairly test their method. By using information from unaffected participants as a control, the academics could determine the rate of accuracy offered by the new technique.

Their test, which involved chimeric or triplet repeat primed PCR (TP PCR) methodology, was then conducted. It was hoped that it could analyse both the existence and extent of HD by evaluating the number of CAG repetitions.

The HTT gene usually has ten to 35 segments of CAG present, but people affected by the inherited condition have additional copies. Up to five extra replicates may not result in symptoms, but people with over 40 CAG repetitions are almost always diagnosed with the disease.

This is because additional CAG produces an abnormally elongated version of a protein called huntington. This can then become fragmented and toxic, and if levels build up inside neurons – cells responsible for transmitting electronic signals in the body – they can cause severe disruption.

Interference with neuron function or death of these cells is what motivates the symptoms of HD, which include uncontrollable movement, behavioural changes, depression and communication issues.

After analysing results from the TP PCR experiment, the scientists found that their diagnostic had 100 per cent accuracy in recognising the condition. It also managed to successfully measure CAG repetitions in 98 per cent of cases.

This technique seemed to offer increased precision, and is reportedly less likely to administer a false negative or positive result to patients, thus alleviating unnecessary stress and avoiding misdiagnosis which can compromise a person’s quality of life in the long-term.

Scientists may be able to utilise these findings in order to develop preventative or curative treatments, of which there are currently none.

People who find their sight becoming blurry are often prescribed corrective contact lenses or glasses by their optician, but this can be inconvenient for patients.

Between 20 and 30 per cent of the UK population will be affected by the condition, which usually progresses during puberty.

Worldwide researchers in the Consortium for Refraction and Myopia (CREAM) analysed DNA information from 45,000 people after aiming to understand the hereditary nature of short-sightedness.

They identified 24 genes which were seemingly involved in myopia, and those who carry the most high-risk varieties have a ten-times higher chance of contracting the condition than their counterparts.

The academics are not yet able to determine why these mutations motivate poorer eyesight, but believe that interruption to visionary signalling and development could play a role.

This aggressive form of cancer affects cells which produce the melanin pigment, and the size of the tumour at diagnosis plays an important role in patient outcomes. Once the diseased cells spread around the body, the chance of survival is much lower.

Previous research conducted by eye surgeon Dr J William Harbour showed that patients affected by the condition frequently carried a mutated BAP1 gene.

In the new study, which was published in Nature Genetics, scientists from the Washington University School of Medicine recruited 18 patients whose BAP1 gene had already been analysed. Seven of these patients did not have the mutation, so were classified as having class I tumours. The 11 with an abnormal BAP1 gene was deemed to have class II growths.

Experimenters then sequenced the DNA of each subject's uveal melanoma, and identified alterations in the SF3B1 gene in three cases. This is the first time that scientists have recognised an abnormality in the code.

In order to determine whether this mutation was as common in a larger sample of patients, the researchers analysed DNA data relating to a further 102 eye melanoma growths. They found the abnormality in 20 per cent of cases.

After comparing the affected patients' outcomes to their counterparts', the researchers showed that those carrying the mutation were more likely to demonstrate favourable features. Metastasis, which is the dangerous spread of cancer to other parts of the body, was far less common in these patients, meaning they have a higher chance of survival.

Senior author Dr Anne Bowcock said: "This is the fourth gene known to be mutated in uveal melanoma along with BAP1 and the genes GNAQ and GNA11. A complete understanding of the molecular basis of this tumor will be invaluable in predicting prognosis and in the identification and development of novel treatments for this cancer."