How gene shaped human face

Researchers from KU Leuven (Belgium) and the universities of Pittsburgh, Stanford, and Penn State (US) have identified fifteen genes that determine human facial features. Human DNA determines what an individual look like, including facial features. That appeals to the popular imagination, as the potential applications are obvious. Doctors could use DNA for skull and facial reconstructive surgery, forensic examiners could sketch a perpetrator's face on the basis of DNA retrieved from a crime scene, and historians would be able to reconstruct facial features using DNA from days long gone.

In a new study conducted by KU Leuven in collaboration with the universities of Pittsburgh, Stanford and Penn State, the researchers adopted a different approach. "Our search doesn't focus on specific traits," lead author Peter Claes (KU Leuven) explains. "My colleagues from Pittsburgh and Penn State each provided a database with 3D images of faces and the corresponding DNA of these people. Each face was automatically subdivided into smaller modules. Next, we examined whether any locations in the DNA matched these modules. This modular division technique made it possible for the first time to check for an unprecedented number of facial features."

The scientists were able to identify fifteen locations in human DNA. The Stanford team found out that genomic loci linked to these modular facial features are active when human face develops in the womb. "Furthermore, we also discovered that different genetic variants identified in the study are associated with regions of the genome that influence when, where and how much genes are expressed," says Joanna Wysocka (Stanford). Seven of the fifteen identified genes are linked to the nose, and that's good news, Peter Claes (KU Leuven) continues. "

A skull doesn't contain any traces of the nose, which only consists of soft tissue and cartilage. Therefore, when forensic scientists want to reconstruct a face on the basis of a skull, the nose is the main obstacle. If the skull also yields DNA, it would become much easier to determine the shape of the nose. Age, environment, and lifestyle have an impact on what human face looks like, this could provide genetic insight into the shape and functioning of human brain, as well as in neurodegenerative diseases such as Alzheimer's."
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Gene may protect against heart disease

Scientists have identified a gene that may play a protective role in preventing heart disease. Their research revealed that the gene, called MeXis, acts within key cells inside clogged arteries to help remove excess cholesterol from blood vessels.

UCLA-led study in mice found that MeXis controls the expression of a protein that pumps cholesterol out of cells in the artery wall. MeXis is an example of a "selfish" gene, one that is presumed to have no function because it does not make a protein product.

However, recent studies have suggested that these so-called "unhelpful" genes can actually perform important biological functions without making proteins and instead producing a special class of molecules called long non-coding RNAs, or lncRNAs.

lncRNAs are important for the inner workings of cells involved in the development of heart disease," said Dr. Peter Tontonoz, senior author of the study. Considering many genes like MeXis have completely unknown functions, the study suggests that further exploring how other long non-coding RNAs act will lead to exciting insights into both normal physiology and disease.

In the study, researchers found that mice lacking MeXis had almost twice as many blockages in their blood vessels compared to mice with normal MeXis levels. In addition, boosting MeXis levels made cells more effective at removing excess cholesterol.
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Therapeutic for pancreatic cancer

In most pancreatic cancer patients, the diagnosis occurs when the disease is already advanced, and currently, there is no effective treatment. A group of researchers from the Spanish National Cancer Research Centre (CNIO) may have found a new therapeutic approach.

One of the characteristics of pancreatic cancer is that the tumour cells are embedded in the stroma, which represents 90 percent of the tumour mass and which seems to form a barrier (physical and chemical) hindering treatment with inhibitors, chemotherapy and immunotherapy.

Researchers focused their work on identifying a stromal cell population that fosters tumour growth, to later discover why they have this capacity and reverse it. The strategy to achieve the latter is innovative, because instead of eliminating these stromal cells which help the tumour, the objective has been their selective reprogramming. The researchers focused on a subpopulation of fibroblasts known to play a role in inflammation, because inflammation fosters tumour growth.

Their analysis revealed that the Saa3 gene is responsible for CAFs helping tumour cells to progress. When the researchers eliminated the expression of this gene in the CAFs, these cells behaved like normal fibroblasts, losing the ability to accelerate tumour cell progression. Researchers had managed to "reprogramme" these cells, which had been stripped of their pro-tumour properties.

In human samples of pancreatic cancer, the researchers have identified the same population of pro- tumour fibroblasts, and have observed that when the SAA1 gene (the human version of Saa3) is overexpressed, the prognosis for the patients is far worse.
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Source of Huntington's disease

Huntington's disease is a fatal hereditary disorder for which there is currently no treatment, it is associated with jerky movements and as these patients increasingly lose brain neurons, they slide into dementia. But the new research suggests that these symptoms may be a late manifestation of a disease that originates much earlier, in the first steps of embryonic development.

A team at Rockefeller led by Ali Brivanlou, the Robert and Harriet Heilbrunn Professor, developed a system to model Huntington's in human embryonic stem cells for the first time. Researchers describe early abnormalities in the way Huntington's neurons look, and how these cells form larger structures that had not previously been associated with the disease.

Huntington's is one of the few diseases with a straightforward genetic culprit: One hundred percent of people with a mutated form of the Huntingtin (HTT) gene develop the disease. The mutation takes the form of extra DNA, and causes the gene to produce a longer-than-normal protein. The DNA itself appears in the form of a repeating sequence, and the more repeats there are, the earlier the disease sets in.

Research on Huntington's has thus far relied heavily on animal models of the disease, and has left many key questions unanswered. For example, scientists have not been able to resolve what function the HTT gene serves normally, or how its mutation creates problems in the brain. Suspecting that the disease works differently in humans, whose brains are much bigger and more complex than those of lab animals, researchers developed a cell-based human system for their research. They used the gene editing technology CRISPR to engineer a series of human embryonic stem cell lines, which were identical apart from the number of DNA repeats that occurred at the ends of their HTT genes.

In cell lines with mutated HTT, we saw giant cells. It looked like a jungle of disorganization. When cells divide, they typically each retain one nuclei. However, some of these enlarged, mutated cells flaunted up to 12 nuclei-suggesting that neurogenesis, or the generation of new neurons, was affected. The disruption was directly proportional to how many repeats were present in the mutation: The more repeats there were, the more multinucleated neurons appeared.

There is an unrecognized developmental aspect to the pathology. Huntington's may not be just a neurodegenerative disease, but also a neurodevelopmental disease. Treatments for Huntington's have typically focused on blocking the activity of the mutant HTT protein, the assumption being that the altered form of the protein was more active than normal, and therefore toxic to neurons. However, Brivanlou's work shows that the brain disruption may actually be due to a lack of HTT protein activity.

To test its function, the researchers created cell lines that completely lacked the HTT protein. These cells turned out to be very similar to those with Huntington's pathology, corroborating the idea that a lack of the protein not an excess of it is driving the disease. The findings are significant because existing treatments that were designed to block HTT activity may actually do more harm than good.
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Viruses share gene with some organisms

A new study finds that viruses share some genes exclusively with cells that are not their hosts, viruses swap genes with a variety of cellular organisms and are agents of diversity. The study looked at protein structures in viruses and across all domains of life: from the single-celled microbes known as bacteria and archaea, to eukaryotes, a group that includes animals, plants, fungi and all other living things.

Viruses that infect archaea and bacteria, for example, are not known to infect eukarya. However, they may still interact in non harmful ways with organisms they do not infect. The team used a bioinformatics approach to analyze the genomes of organisms and the viruses that infect them. Rather than focusing on genetic sequences, which can change over the generations, the team examined the functional components of proteins, which they call folds.

 There are more than 1,400 of folds across all domains of life-has a unique 3-D structure that performs a specific operation. Because folds are critical to protein function, they remain stable even as the sequences that code for them change as a result of mutations or other processes.This makes protein folds reliable markers of evolutionary changes over vast time periods, especially for viruses that mutate notoriously fast.

The researchers found hundreds of folds that are present across all domaind of life and in all types of viruses, which suggests that they came from an ancient ancestor of all life forms. Some folds, however, occur only within a single domain and the viruses that infect it, suggesting a transfer of genetic material only between that group of viruses and their hosts. Out of a total of about 2,000 superfamilies of folds, the team found one that was exclusive to archaea and the viruses that infect archaea, 29 shared only by bacteria and the viruses that infect them, and 37 that are exclusive to eukaryotes and their viruses.

The data also point to other, as yet unknown, mechanisms that allow viruses to exchange genetic material with cells, many virus-hallmark genes in cellular organisms those viruses are not known to infect. People tend to think only about viruses that infect and kill their hosts, we have known for decades that a virus will sometimes enter into a cell and incorporate its genetic material into the cell without killing it. In the case of single-celled organisms, those genes are sometimes passed along to future generations. Human DNA, too, contains remnants of viruses.

Some retroelements and transposons are believed to have originated in ancient viruses. Retroelements are sequences copied from RNA viruses into DNA and inserted into the genomes of nonviral organisms. Transposons, also known as "jumping genes," can move from one part of the genome to another.The team also discovered a large subset of virus-specific protein folds that were not present in any cellular genomes. This suggests that viruses can create new genes and, potentially, transfer those genes to cellular organisms.
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Papillomaviruses cause non-melanoma skin cancer

UV radiation has been known for a long time to be a risk factor for the development of skin cancer. Simultaneous infection with human papillomaviruses (HPV) has also been suspected to promote skin cancer, particularly in organ transplant recipients.

Papillomaviruses associated with UV light promote the development of non-melanoma skin cancer. The investigators provide an explanation why the viruses can be detected in benign human cancer precursors but not in advanced carcinoma.
Everyone is infected with skin-typical ("cutaneous") human papillomaviruses (HPV) at some point in their lives, usually in early childhood.

In healthy people, the immune system can fight off the viruses, but this often changes in older age. Recipients of organ transplants whose immune system is suppressed by long-term drug therapy to prevent transplant rejection are particularly at risk. Ultraviolet radiation exposure is generally known to be a major risk factor for skin cancer. Non-melanoma skin cancer occurs primarily on sun-exposed sites of the body.

Researchers used a specific species of mice that usually contracts infection with papillomaviruses shortly after birth, like humans. They compared the virus-infected animals with control animals that were raised in a completely virus-free environment. They exposed the animals to UV radiation at a dose that could be expected during a vacation in Mediterranean regions.

Subsequently, only virus-infected animals developed non-melanoma skin cancer (squamous cell carcinoma ) while the virus-free control animals did not. They noticed a glance that a group of tumors was keratinizing while the other one was not. The keratinizing tumors contained large amounts of viruses - a situation that is also found in precursors of cancer (so-called "actinic keratosis") in humans.

This is a condition where cells of the upper skin layers have started to grow excessively while still resembling the original structure of the skin. The researchers demonstrated that the viruses affect the stability of the host cell's DNA, thus promoting the accumulation of UV-related damage.
By contrast, the second group of tumors did not contain any viruses. This is also the case in patients with advanced carcinoma.

However, tests for antibodies in the animals' blood revealed prior infection with the virus. These tumors exhibited a striking rate of mutations in a gene called p53, which is crucially important for the cell and is regarded the "guardian of the genome". This gene is also defective in many cases of human squamous cell carcinoma, leading to uncontrolled cellular growth.

When the cells grow out of control, the tumor turns more cancerous. The viruses, which are now no longer needed for the tumor to grow, are thus prevented from replicating further. Up until now, the loss of viruses in advanced cases of carcinoma has been a major argument against a role of cutaneous papillomaviruses in the development of cancer.
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Eggs can select semen

According to the latest research, female's eggs are able to select sperm with the best genes to ensure the healthiest offspring. Semen does not appear to have the same ability to detect bad genes, this shows that fertilisation is not random and specific pairings between certain eggs and sperm are more common than others. Researchers bred female mice carrying one normal and one mutant copy of a gene that increased the chance of getting testicular cancer.

 The resulting offspring followed Mendel's rules and there was a random dispersal of the mutated form among offspring. Researchers reversed the breeding- gave males the mutant copy of the cancer gene while the females had the normal version. Only 27 per cent of the offspring had the mutant variant, compared to the 75 per cent. Researchers found no evidence the mutated mice embryos were dying shortly after fertilisation, rather they were never fertilised.

The rate of metabolism folic acid - which is an important signalling molecule - is different in sperm and eggs. Research has revealed that these molecules play an important role in fertilisation. Changes in these signals may impact how much sperm and egg are attracted to one another. When sperm from multiple males arrive at an egg concurrently, eggs are able to choose the sperm whose recognition proteins are best suited for healthy fertilization. This selection process can spur the evolution of new recognition proteins, eventually resulting in reproductive isolation and, in some cases, the creation of new species altogether.
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RNA molecules can kill cancer

Small RNA molecules developed as a tool to study gene function trigger a mechanism hidden in every cell that forces the cell to commit suicide.
The mechanism RNA suicide molecules can potentially be developed into a form of cancer therapy. Cancer cells treated with the RNA molecules never become resistant to them because they simultaneously eliminate multiple genes that cancer cells need for survival.

The inability of cancer cells to develop resistance to the molecules is a first, researchers discovered sequences in the human genome that when converted into small double-stranded RNA molecules trigger what they believe to be an ancient kill switch in cells to prevent cancer.

Testing a class of small RNAs, called small interfering (si)RNAs, researchers use to suppress gene activity. siRNAs are designed by taking short sequences of the gene to be targeted and converting them into double- stranded RNA. These siRNAs when introduced into cells suppress the expression of the gene they are derived from.

A large number of these small RNAs derived from certain genes did not, only suppress the gene they were designed against. They also killed all cancer cells. These special sequences are distributed throughout the human genome, embedded in multiple genes.
When converted to siRNAs, these sequences all act as highly trained super assassins.

They kill the cells by simultaneously eliminating the genes required for cell survival. By taking out these survivor genes, the assassin molecule activates multiple death cell pathways in parallel. The small RNA assassin molecules trigger a mechanism calls DISE, for Death Induced by Survival gene Elimination. Activating DISE in organisms with cancer might allow cancer cells to be eliminated.
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Steroid hormone and age related bone loss

A group of steroid hormones could provide new insight into the bone loss and deterioration that occurs with aging, protein histone deacetylase 3, HDAC3, turns off the genes that encourage the stem cells in our bone marrow to make and store fat instead of making bone. As HDAC3 levels decrease naturally with age, bones become less dense and easily breakable.

 Looking at a group of steroid hormones known as glucocorticoids, which our bodies naturally have in circulation as a response to different stresses to help quiet the immune response, when these hormones enter bone cells, osteoblasts that make bone bind to a receptor that activates the expression of genes related to fat storage.

To get that effect of bone loss and increased marrow fat when you lose HDAC3, glucocorticoids must be present. Releasing glucocorticoids in response to various stimuli is a natural thing that body does, circulating glucocorticoid levels increase with age.

As with a lot of chemicals in the body, too much and not enough of something can be bad. While glucocorticoids occur naturally in the body, they are also used in various immune-suppressive therapies, many of which have osteoporosis as a side effect.

Researchers studied mice without receptors for the steroid hormones. The mice were placed on a calorie-restricted diet to stimulate the aging process which also has been shown to result in lower bone density and increased marrow fat. Extreme caloric restriction, such as with anorexia nervosa, can also lead to weak and brittle bones.

When looking at the bone cells in a culture dish, the receptor deficient mice show less lipid storage than regular mouse models of aging. They also showed more bone matrix, which is the cause of bone formation. Examination of tibia and femur in a living animal showed the receptor deficient mice actually had more marrow fat and lower bone mass.
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Source of ageing process

Genes belong to a process called autophagy - this one of the cells most critical survival processes, it promotes health and fitness in young worms but drive the process of ageing later in life.

 Promoting longevity by closing down autophagy in old worms improves neuronal and subsequent whole body health. Getting old happens to every species, natural selection results in the fittest individuals for a given environment surviving to breed and pass on their genes to the next generation.

The more fruitful a trait is at promoting reproductive success, the stronger the selection for that trait will be. Some genes encourage ageing while still being essential for development, there are series of genes involved in regulating autophagy, which accelerate the ageing process.

The process of autophagy is a critical recycling process in the cell. Autophagy is known to become slower with age and closing it down in the initiation of the process allows the worms to live longer.

There are severe negative consequences when it breaks down and then you are better off bypassing it all together. In young worms, autophagy is working properly and is essential to reach maturity but after reproduction, it begins to malfunction causing the worms to age.

 By inactivating autophagy in the neurons of old worms they were able to prolong the worms life and increased the total health of the worms. Turning autophagy off only in one tissue and the whole animal gets a boost. The neurons are much healthier in the treated worms and keeps the muscles and the rest of the body in good shape.
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Faulty gene caused obesity

 Researchers have discovered that reduced function of a gene that impacts the breakdown of fats resulted in adult-onset obesity and fatty liver. In normal metabolism, fat and carbohydrate in our diets was broken down to produce the energy that our bodies required by the cellular energy plants, known as mitochondria.

Faulty mitochondrial gene had major impacts on normal metabolic function, if mitochondria are compromised or damaged, the breakdown of fat and carbohydrates will be poorly regulated, which can lead to adult-onset obesity.

Healthy adults will have two copies of the Pentatricopeptide repeat-containing protein 1, PTCD1 gene, PTCD1 is vital for the breakdown of fats, carbohydrates and energy production. When one copy of this gene is lost, it results in obesity, fatty liver and heart disease

PTCD1 affects the way mitochondria are formed by changing their shape and making them less connected with each other. Excess weight and obesity are major risk factors for diabetes, cardiovascular disease, musculoskeletal disease and cancers.
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Yoga and meditation reduce the risk of cancer

Yoga and meditation reduce our risk of cancer by changing our DNA,
Practising mind-body interventions (MBI), like as yoga, meditation and Tai Chi, produce lower amounts of molecules that enable inflammation-causing genes.

MBIs enable the brain to steer our DNA processes along a path which improves health.

Inflammation has been linked to cancer, accelerated ageing and poor mental health.

Researchers analysed 18 studies with 846 participants conducted over 11 years. Studies were included in the analysis if they measured gene expression after a MBI.

Reserchers discovered that people who practice MBIs produce lower amounts of molecules that enable inflammation-causing genes.


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Broccoli can cure type 2 diabetes

Eating or drinking broccoli can reverse type 2 diabetes. Sulforaphane is an anti-cancer compound in cruciferous vegetables.

Sulforaphane is highly concentrated in cruciferous vegetables and could be used in a concentrated broccoli extract.
It can be used for treatment of type 2 diabetes.

Researchers examined  97 obese patients, those given concentrated broccoli sprout found their fasting blood glucose levels fell dramatically compared to controls who received a placebo.

Sulforaphane induces an antioxidant response. It reduced glucose production by liver cells growing in culture, and shifted liver gene expression in diabetic rats.


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Tea can cause epigenetic changes in women

Epigenetic changes are chemical modifications that turn our genes off or on. Environment and lifestyle factors, such as food choices, smoking and exposure to chemicals, can lead to epigenetic changes.

According to latest research, there are epigenetic changes in women consuming tea, but not in men.
Some of these epigenetic changes were found in genes involved in cancer and estrogen metabolism.

Results from this study highlight the role of pharmacologically active components in tea being involved in cancer and estrogen metabolism, which can reflect that health effects related to tea consumption might be due to epigenetic changes.

The role of pharmacologically active components in tea being involved in cancer and estrogen metabolism, which can reflect that health effects related to tea consumption might be due to epigenetic changes.

Defective immune cells can cause hair loss

Scientists have discovered how immune cells could be used to cure hair loss.
The regulatory T-cells, known as 'Tregs', are all over human body, they control inflammation in the body.

Scientists from the University of California at San Francisco showed how Tregs in the skin send out signals that stimulate hair follicles to regenerate in mice.

 Hair follicles are recycling always, Tregs are important for this process, if this immune system is weak or dead, hair will not grow.

 A protein called KROX20 that is associated with nerve development, turned on in skin cells that become the hair shaft. The hair cells then produced a protein known as stem cell factor SCF
which is essential for hair pigmentation.

When scientists removed the SCF gene in the hair progenitor cells in mice, their hair turned white. When they removed the KROX20-producing cells, no hair grew and the mice became bald.

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Cannabis reverses aging brain

Memory performance decreases with increasing age. Cannabis can reverse these ageing processes in the brain. This was shown in mice by scientists at the University of Bonn with their colleagues at The Hebrew University of Jerusalem (Israel).

Old animals were able to regress to the state of two-month-old mice with a prolonged low-dose treatment with a cannabis active ingredient. This opens up new options, for instance, when it comes to treating dementia.

Cognitive ability also decreases with increasing age. This can be noticed, for instance, it becomes more difficult to learn new things or devote attention to several things at the same time and this can leads to dementia.

Researchers have long been looking for ways to slow down or even reverse this process. Scientists at the University of Bonn and The Hebrew University of Jerusalem (Israel) have now achieved this in mice. These animals have a relatively short life expectancy in nature and display pronounced cognitive deficits even at twelve months of age.

The researchers administered a small quantity of THC, the active ingredient in cannabis, to mice aged two, twelve and 18 months for four weeks.

Afterwards, they tested learning capacity and memory performance in the animals -- orientation skills and the recognition of other mice. Mice who were only given a placebo displayed natural age-dependent learning had memory losses.

In contrast, the cognitive functions of the animals treated with cannabis were just as good as the two-month-old control animals. The treatment completely reversed the loss of performance in the old animals.

Scientists discovered that the brain ages much faster when mice do not possess any functional receptors for THC. These cannabinoid 1 (CB1) receptors are proteins to which the substances dock and thus trigger a signal chain. CB1 is also the reason for the intoxicating effect of THC in cannabis products, such as hashish or marijuana, which accumulate at the receptor.

THC imitates the effect of cannabinoids produced naturally in the body, which fulfil important functions in the brain. With increasing age, the quantity of the cannabinoids naturally formed in the brain reduces.

When the activity of the cannabinoid system declines, we find rapid ageing in the brain. To discover precisely what effect the THC treatment has in old mice, the researchers examined the brain tissue and gene activity of the treated mice.

The molecular signature no longer corresponded to that of old animals, but similar to that of young animals. The number of links between the nerve cells in the brain also increased again, which is an important for learning ability.

A low dose of the administered THC was chosen so that there was no intoxicating effect in the mice. Cannabis products are already permitted as medications, for instance as pain relief. As a next step, the researchers want to conduct a clinical trial to investigate whether THC also reverses ageing processes in human brain and can increase cognitive ability.

Gene controls birth defects common in diabetic patients

Neural tube defects (NTDs) occur when mutations accumulate in the neuroepithelial cells, neural stem cells that eventually transform themselves into the brain and the central nervous system.

This  occurs after the fetus is exposed to too much glucose, which can cause widespread cell death, eventually leading to the birth defects.

Researchers have identified a gene that plays a key role in the formation of neural tube defects, a problem commonly found in infants of pregnant women with diabetes.

Neural tube defects are birth defects of the brain and spinal cord. They occur in the first month of pregnancy. The two most common are spina bifida and anencephaly.

 In the first, the fetal spinal column doesn't close completely. This usually causes nerve damage, with some paralysis of the legs. In the latter, most of the brain and skull do not develop.

 Infants with this defect are usually stillborn or die soon after birth. Neural tube defects have several causes, including diabetes, folic acid deficiency, obesity in the mother, and consumption of certain medications.

About 10 percent of women with diabetes who are pregnant will have embryos with neural tube. More than
300,000 pregnancies are affected by NTDs every year. One out of ten babies with NTDs die before their first birthday.

Pregnant women who have diabetes have a significantly higher risk of having a child with NTDs, and even with the highest quality preconception care, diabetic women are five times more likely to have a child with birth defects than non-diabetic women.

New genetics locations of types 2 diabetes

Scientists from University College London and Imperial College London in the United Kingdom have identified new genetic locations that might make some people more prone to developing type 2 diabetes.

 Researchers were aware of 76 chromosomal locations before this discovery New research analyzed the human genome further and found an additional 111.

Dr. Nikolas Maniatis of University College London's (UCL) Genetics, Evolution, and Environment department, together with Dr. Toby Andrew of Imperial College London's Department of Genomics of common disease.

Using a UCL-developed method of genetic mapping, Maniatis and team examined large samples of European and African American people, summarizing 5,800 cases of type 2 diabetes and almost 9,700 healthy controls.

They found that the new location together with the old one control the expression of more than 266 genes surrounding the genetic location of the disease.

Most of the newly discovered location were found outside of the coding regions of these genes, but within so-called hotspots that change the expression of these genes in body fat.

Of the newly identified 111 locations 93 were found in European and African American population samples.
After identifying genetic location, the next step was to use deep sequence analysis to try to determine the genetic mutations responsible for the disease.

Gene mapping finds areas associated with diabetes - causing genetic location
Maniatis and colleagues used deep sequencing to further examine three of the cross-population locations with the aim of identifying the genetic mutations.

They then examined different sample of 94 Europeans with type 2 diabetes, as well as 94 healthy controls. Researchers
discovered that the three locations coincided with chromosomal regions that regulate gene expression, contain epigenetic markers, and present genetic mutations that have been suggested to cause type 2 diabetes.

How genetics influence what we eat

Variation in genes are responsible for different food choices in different people. Gene variation that control how brain works may dictates foods we like to eat often.

Gene variation is the subtle DNA differences in different people that make them unique, it had impact on food preferences and diet plan.

Researchers examined genetics of 818 men and women and gather information about their diet and discovered that genes is responsible for diet choices.

Some genes in the body are responsible for salt and fat intake, this discovery leads to better understanding of why we eat what we eat and it can be used to minimize person's risk for common diseases.

How cancers evade the immune system

Scientists from Singapore has discovered new way cancers escape the body's immune system, looking at gastric cancer GC. In gastric cancer, gene promoters are dysregulated in a way that is different from tumour's antigenic profile to evade the body's immune system.

Epigenetic is a process by which a cell's DNA is chemically changed by the environment, to change gene expression.

Creating comprehensive epigenetic profiles for gastric cancer and normal tissue from the same parent shows that some promoters specifically changed in gastric cancer tissues.

Researchers found out that gene variants can cause cancer growth, the use of less immunogenetic variants can enhance the tumour to bypass the host's  immune system.