New tumor-driving mutations discovered in the under-explored regions of the cancer genome

In an unprecedented pan-cancer analysis of whole genomes, researchers at the Ontario Institute for Cancer Research (OICR) have discovered new regions of non-coding DNA that, when altered, may lead to cancer growth and progression.

The study, published today in Molecular Cell, reveals novel mechanisms of disease progression that could lead to new avenues of research and ultimately to better diagnostic tests and precision therapies.

Although previous studies have focused on the two per cent of the genome that codes for proteins, known as genes, this study analyzed mutation patterns within the vast non-coding regions of human DNA that control how and when genes are activated. 

"Cancer-driver mutations are relatively rare in these large non-coding regions that often lie far from genes, presenting major challenges for systematic data analysis," says Dr. Jüri Reimand, investigator at OICR and lead author of the study. 

"Powered by novel statistical tools and whole genome sequencing data from more than 1,800 patients, we found evidence of new molecular mechanisms that may cause cancer and give rise to more-aggressive tumours."

The research group analyzed more than 100,000 sections of each patient's genome, focusing on the often-overlooked non-coding regions that interact with genes through the three-dimensional genome. One of the 30 key regions discovered was predicted to have a significant role in regulating a known anti-tumour gene in cancer cells, despite being more than 250,000 base pairs away from the gene in the genome. The group performed CRISPR-Cas9 genome editing and functional experiments in human cell lines to explore the cancer-driving properties of this non-coding region.

"We characterized several non-coding regions potentially involved in oncogenesis, but we've just scratched the surface," says Reimand. "With our algorithms and the rapidly growing datasets of patient cancer genomes and epigenetic profiles, we look forward to enabling future discoveries that could lead to new ways to predict how a patient's cancer will progress and ultimately new ways to target a patient's disease or diagnose it more precisely."

Reimand's research group developed the statistical methods behind this study and made them freely available for the research community to use. These methods have been rigorously tested against other algorithms from around the world.

"Looking into the non-coding genome is really important because these vast sections regulate our genes and can switch them on and off. Mutations in these regions can cause these regulatory switches to act abnormally and potentially cause - or advance - cancer," says Helen Zhu, student at OICR and co-first author of the study. "We've shown that our method, called ActiveDriverWGS, can excavate these regions and pinpoint specific areas that are important to cancer growth."

"Although these candidate driver mutations are rare, we now have the first experimental evidence that one of the mutated regions regulates cancer genes and pathways in human cell lines," says Dr. Liis Uusküla-Reimand, Research Associate at The Hospital for Sick Children (SickKids) and co-first author of the study. "As the research community collects more data, we plan to look deeper into these regions to understand how the mutations alter gene regulation and chromatin architecture in specific cancer types to enable the development of new precision therapies to patients with these diseases."

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New spray gel could help fight cancer after surgery

Scientists have developed a spray gel embedded with immune-boosting drugs which they say could help the body fight off cancer after surgery.

Many people who are diagnosed with cancer will undergo some type of surgery to treat their disease, said researchers from the University of California, Los Angeles (UCLA) in the US.

Almost 95 per cent of people with early-diagnosed breast cancer will require surgery and it is often the first line of treatment for people with brain tumours, according to the study.

However, despite improvements in surgical techniques over the past decade, the cancer often comes back after the procedure.
The researchers tested the biodegradable spray gel in mice that had advanced melanoma tumours surgically removed.

They found that the gel reduced the growth of the tumour cells that remained after surgery, which helped prevent recurrences of the cancer.

After receiving the treatment, 50 per cent of the mice survived for at least 60 days without their tumours regrowing.

The spray not only inhibited the recurrence of tumours from the area on the body where it was removed, but also controlled the development of tumours in other parts of the body, said  a Prof.

The substance will have to go through further testing and approvals before it could be used in humans, the Prof. said.

However, the scientists envision the gel being applied to the tumour resection site by surgeons immediately after the tumour is removed during surgery.

“This sprayable gel shows promise against one of the greatest obstacles in curing cancer,” the Prof. said.

“One of the trademarks of cancers is that it spreads. In fact, around 90 per cent of people with cancerous tumours end up dying because of tumour recurrence or metastasis,” he said.

The researchers loaded nanoparticles with an antibody specifically targeted to block CD47, a protein that cancer cells release as a “don’t-eat-me” signal.

By blocking CD47, the antibody enables the immune system to find and ultimately destroy the cancer cells.

The nanoparticles are made of calcium carbonate, a substance that is the main component of egg shells and is often found in rocks.

“We also learned that the gel could activate T cells in the immune system to get them to work together as another line of attack against lingering cancer cells,” said  a postdoctoral researcher .

Once the solution is sprayed on the surgical site, it quickly forms a gel embedded with the nanoparticles.

The gel helps stop at the surgical site and promotes would healing; the nanoparticles gradually dissolve and release the anti-CD47 antibodies into the body.

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Scientists Explain Connection Between Sugar and Cancer Growth

Most of us love sweets. Sugar is not just present in desserts, but also in all soft drinks, including colas. Having the soft drinks is considered as having empty calories, but it isn't just empty calories that scientists are worried about, but also about its effect on the body, especially, the cancer cells feed on sugar to thrive.

Unfortunately, even small amounts of those sneaky sugar molecules can be connected to cancer growth in our bodies. With an eye on prevention, scientists are discovering more about how and why sugar affects cancer cell growth and what we can do to distance ourselves even further from sugar’s unhealthy effects.

Sugar is a carbohydrate molecule, often associated with sweet treats, but it can be found in natural fruits as well. Our bodies use carbohydrates as fuel, and sugar can be a complex or simple carbohydrate molecule. Complex carbohydrates exist in starches like pasta and potatoes. They are basically a bunch of sugar molecules strung together. The difference is that whereas complex carbohydrate foods contain healthy fiber, vitamins and minerals, simple carbohydrates like white sugar and high fructose corn syrup have none of those nutritional benefits.

Do we need sugar to survive? Not exactly. As long as we have carbohydrates in our diet, we can avoid sugar. However, with the wide variety of foods containing naturally occurring sugars, like lactose and fructose for example, we would eliminate a lot of tasty and nutritional items by avoiding all dietary sugars.

Sugar is an acidic molecule

Acidity is a happy place for cancer and disease in the body, so no wonder an acidic molecule like sugar is connected to cancer growth. The more sugar we consume, the more acidic our bodies are. The more acidic our bodies are, the more likely disease will spread because it is being kept in its favorite climate. It’s like any existing cancer cells in your body get to go on an all-inclusive vacation at the beach in Fiji and multiply like bunnies whenever you have lots of sugar in your diet.

Dr. Otto Warburg first associated cancer with an acidic environment back in 1931, and he won a Nobel prize in Physiology or Medicine for his research. The causality of his discovery has been debated and researched ever since. Needless to say, avoiding sugar and its acidity is beneficial for our bodies. If cancer hates alkalinity, so much the better, if we decrease acidic sugar in our diet.

Feeding the cancer cell

As a positive person, you likely eat healthy, vegan, and nutritionally packed foot to provide you with the sustenance you need for your day. But what if your meal was accidentally feeding cancerous growth inside your body? Scientists explain that your balance of carbohydrates from sugars, both natural and added, might need to be changed.

Sugar, as a carbohydrate, breaks down for use as fuel for your cells. However, it also feeds cancer cells. Fat tissue stores excess sugar. Clearly, we don’t want to store food for cancer cells that want to grow and multiply. We want to eliminate any sugars stores in the fats of our bodies so that disease and cancer do not get an all-they-can-eat buffet.

Sugar stimulates cancer growth

Fermentation of sugar does not require oxygen, which is ideal for cancer cells. It helps them reproduce and multiply faster than if they did not have sugar. The scientists studying sugar’s effect on cancer growth found that sugar, just like in human children, causes hyperactivity for the reproduction and spreading of cancer cells. In other words, it dials it up to high speed and allows cancer to proliferate in the body.

Researchers found that the Warburg effect creates a vicious cycle through activation of early cellular growth pathways, like a roadmap for genes to build on. This later leads to enhanced fermentation of sugar and a lack of oxygen in the cellular environment, which stimulates increased growth of tumors.

Sugar changes cellular functions

Further research  examined sugar’s role in the growth of cervical cancers. Some of those who are affected by HPV (human papilloma virus) have an increased risk for developing cervical cancer. However, only some of the 200 genetic variants of HPV are associated with a higher risk of cancer growth.
These researchers found two different cellular mechanisms that are affected by sugar, which causes HPV to prompt cells to become cancerous and grow. The first connection between sugar and cancer growth is in the preference for the genetic expression of a process in the cell that enhances cellular growth under anaerobic or hypoxic conditions. The second connection between sugar and cancer is that it enhances the ability of cervical cancer cells to multiply due to changes in cell signaling.

Simply put, sugar makes it easier for a normal cell to mutate, which allows the mutated or cancerous cell to use sugar for energy even without oxygen. Sugar also affects the rate of cancer cell proliferation, causing it to multiply and spread faster.

Weighing the sweet against the risk

A diet rich is sugar can lead to other health problems, for example, obesity. The Body Mass Index (BMI) measures weight-to-body-height proportions for both men and women. A higher weight density or BMI associates with a higher sugar intake in general. Scientists  found that a higher BMI also associates, among other factors, with a higher risk for colon cancer.

As the body processes excess sugar in the bloodstream, a high glycemic index (GI) causes the pancreas to release insulin. Triglycerides are also formed to store excess sugars. High GI, insulin, and triglycerides are all associated with diets high in sugars and with a higher risk of colon cancer. Not surprisingly, exercise may help lower the risk of colon cancer. The researchers say that if the individual is sedentary, the risk for colon cancer is higher than if they are active.

One possible explanation for this is that exercise causes the body to burn some of the available sugar so that there is less of this acidic molecule in the bloodstream. Using up sugar during exercise also means that your body excretes less sugar as waste. As a result, less sugar reaches the colon.

What can we do to manage our sugar and cancer risk?

The Physicians give us some basic recommendations about sugar in the diet, especially when there is a low fiber content, also called a higher glycemic index. Whole, unprocessed, vegan foods are preferable for the diet of a positive thinking person. Whenever possible, choose these over cooked, processed, or packaged foods.

The less processed a food is, the less nutritional value it loses. Thus, the less environmental impact it has. It is also less likely that simple sugars have been added through processing. Sources of carbohydrates that are multi-grain are preferred over whole grain. Furthermore, whole grains trump bleached flour when it comes to protecting your health. Fiber helps offset some of the negative effects of sugar on cancer growth.


Think about changing some of your foods to reduce the total amount of simple carbohydrates. (These are often found in crackers, white bread, cookies, cereal, candy, and sweetened beverages). Opting for lettuce wraps over any kind of bread gives you a positive impact. It will reduce your dietary sugar intake.

Sugar and the evolution of the human diet

Early humans didn’t eat a lot of starch or sugar in their diets. They moved around the land looking for what was edible. Some root vegetables would have been available to early humans as forms of starch and carbohydrates. However, much of what we consume as carbohydrates today are very recent additions to our diet. Sliced bread wasn’t widely available until the 1930s and people have been around this planet for ten thousand years.

Global agriculture and shipping sweet fruits and starchy vegetables year-round is also a recent human development. Although no one complains about getting bananas year-round, the evolving early human would not have had access to them unless he happened to live near a climate where they grow. Even then, he would only be able to eat them during the correct time of year. We take for granted that dried fruits are available to us as often as we like. In reality, these convenient sweet foods have increased our sugar consumption. We eat far more sugar than a natural human living off the land would.

As a positive role model for others, you choose to reduce both added and natural sugars in your diet. Knowing that this kind of diet reduces your risk of cancer is a huge payoff. Your health and wellness professional can help you design a low-sugar nutritional program. Look for a diet that suits your individual health benefits, while managing any illness, pain or disease.

Note: Always consult your wellness advocate before starting any new regimen.

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Changes in gene contribute independently to breast and ovarian cancer

Defects in a key gene - long thought to drive cancer by turning off the protection afforded by the well-known BRCA genes - spur cancer growth on their own, according to a study led by researchers from NYU Langone Medical Center.

The study gene, known as EMSY, has some of the same functions as BRCA1 and BRCA2, which are known to protect against breast and ovarian cancer when normal. When defective, BRCA genes block the body's self-defense against cancer-causing genetic mistakes.

The new study, published online Jan. 13 in Oncotarget, helps to explain why some women with healthy BRCA1 and BRCA2 genes develop cancer. The findings may also expand treatment options for the roughly 11 percent of women with breast and ovarian cancer and normal BRCA genes, say the study authors.

"Now that we know exactly how changes in EMSY spur cancer cell growth, we can start to design therapies to specifically target that activity and hopefully stop it," says senior author Douglas Levine, MD, director of the Division of Gynecologic Oncology at NYU Langone and its Perlmutter Cancer Center.

"This work also suggests that treatments that work for patients with BRCA1 or BRCA2 mutations might also be effective against EMSY-driven cancers because the disease mechanism is similar," says first study author Petar Jelinic, PhD, a research assistant professor at NYU Langone. "The best way to go rapidly from bench to bedside is to find new ways to use existing treatments."

When normal, EMSY, BRCA1 and BRCA2 give the body's cells instructions to create proteins that help to repair DNA damage that can cause cancer. When those genes are altered, the repair process fails and cancer grows. Overly active EMSY, like mutated BRCA1 or BRCA2, changes those instructions, so that the DNA damage repair process is blocked.

This new study dispels prior theories that EMSY's activation merely turned off the cancer suppression function of BRCA2, says Jelinic.

Earlier work by Levine and others pointed toward EMSY activation as a culprit in breast and ovarian cancer, but had only examined certain parts of the EMSY protein. The new study was the first to evaluate the full-length EMSY protein and to show that it acts independently of BRCA1 or BRCA2.

Furthermore, the research revealed the part of the EMSY protein is changed by an enzyme called protein kinase A. When there is more active EMSY than normal, this enzyme reacts with the EMSY protein to more thoroughly suppress the DNA repair process.

Breast cancer is the second most common cancer among women in the United States, after skin cancer. Ovarian cancer is the fifth leading cause of cancer death among women, according to the National Cancer Institute.




this is only for your information, kindly take the advice of your doctor for medicines, exercises and so on.
https://gscrochetdesigns.blogspot.com. one can see my crochet creations
https://gseasyrecipes.blogspot.com. feel free to view for easy, simple and healthy recipes 
https://kneereplacement-stickclub.blogspot.com. for info on knee replacement

Defects in a key gene - long thought to drive cancer by turning off the protection afforded by the well-known BRCA genes - spur cancer growth on their own, according to a study led by researchers from NYU Langone Medical Center.

The study gene, known as EMSY, has some of the same functions as BRCA1 and BRCA2, which are known to protect against breast and ovarian cancer when normal. When defective, BRCA genes block the body's self-defense against cancer-causing genetic mistakes.
The new study, published online Jan. 13 in Oncotarget, helps to explain why some women with healthy BRCA1 and BRCA2 genes develop cancer. The findings may also expand treatment options for the roughly 11 percent of women with breast and ovarian cancer and normal BRCA genes, say the study authors.
"Now that we know exactly how changes in EMSY spur cancer cell growth, we can start to design therapies to specifically target that activity and hopefully stop it," says senior author Douglas Levine, MD, director of the Division of Gynecologic Oncology at NYU Langone and its Perlmutter Cancer Center.
"This work also suggests that treatments that work for patients with BRCA1 or BRCA2 mutations might also be effective against EMSY-driven cancers because the disease mechanism is similar," says first study author Petar Jelinic, PhD, a research assistant professor at NYU Langone. "The best way to go rapidly from bench to bedside is to find new ways to use existing treatments."
When normal, EMSY, BRCA1 and BRCA2 give the body's cells instructions to create proteins that help to repair DNA damage that can cause cancer. When those genes are altered, the repair process fails and cancer grows. Overly active EMSY, like mutated BRCA1 or BRCA2, changes those instructions, so that the DNA damage repair process is blocked.
This new study dispels prior theories that EMSY's activation merely turned off the cancer suppression function of BRCA2, says Jelinic.
Earlier work by Levine and others pointed toward EMSY activation as a culprit in breast and ovarian cancer, but had only examined certain parts of the EMSY protein. The new study was the first to evaluate the full-length EMSY protein and to show that it acts independently of BRCA1 or BRCA2.
Furthermore, the research revealed the part of the EMSY protein is changed by an enzyme called protein kinase A. When there is more active EMSY than normal, this enzyme reacts with the EMSY protein to more thoroughly suppress the DNA repair process.
Breast cancer is the second most common cancer among women in the United States, after skin cancer. Ovarian cancer is the fifth leading cause of cancer death among women, according to the National Cancer Institute.


Read more at: https://medicalxpress.com/news/2017-01-gene-contribute-independently-breast-ovarian.html#jCp