BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: Cancer (Page 1 of 3)

The journey to find a cure for cancer

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On April 19, 2017

In Student Post

What exactly does ‘epigenetic’ mean? Well epigenetic literally means “in addition to changes in genetic sequence.” The term now means any procedure to change genetic activity without changing the sequence of the actual DNA. So why is this important? Epigenetics can affect a lot of scientific research. For example DNA methylation is a hugely important epigenetic modification.

DNA methylation is where a methyl group would be added to a cytosine in a DNA sequence changing its function. This can be used in embryonic development, X-chromosome inactivation, genomic imprinting, gene suppression, carcinogenesis and chromosome stability. This means DNA methylation is very vital to growth and development- as it is a natural process- however can affect bad cells.

Examples of this are with cancer cells. DNA Methylation patterns- adding a group- are interrupted and changed when cancer is present. DNA methylation done on the promoters in tumor cells can turn off the expression of genes. In humans this can cause disruption of vital developmental pathways. This was then tested in an experiment (for now we will only observe human results because it was tested on mice as well) They tested human normal brain tissue vs. cancerous.

After testing the DNA methylation patterns on tumors, they found that 121 loci (loci is the central “hot spot” of genes) had strong methylation compared to the normal brain tissue which had 60% less. So what does all this mean??

Basically DNA methylation is a good thing in a normal environment. When cancer is present DNA methylation can change and be harmful in a negative environment such as a tumor because it causes hypermethylation.

While the take away is essentially the obvious- cancer is bad- scientists can use this data to find a correct cure for cancer and to create better medicine as some can harm even more by increasing DNA methylation in tumors. For more information on this click here.

 

 

 

Epigenetics Fight Against Pancreatic Cancer

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On April 5, 2017

In Student Post

Pancreatic Ductal Adenocarcinoma (PDAC) is one of the most deadly forms of of Pancreatic Cancer with a less than 10 percent, 5-year survival rate. Unfortunately, it is the most common form of Pancreatic Cancer.  However, scientist were given hope to increase the survival rate when a protein was identified as a aid to the development of PDAC. The protein is Arginine Methyltransferase 1 (PRMT1) and it is involved in gene transcription, DNA signaling, and DNA repair.

It is said that research done by Giulio Draetta, M.D., PhD “strongly suggest a role for PRMT1 in PDAC development and illuminate a path toward the development of therapies for patients in desperate need of innovative solutions”. Draetta’s  team developed a platform called PILOT, Patient-Based In Vivo Lethality to Optimize Treatment. The PILOT technology allows researchers to systematically identify epigenetic drivers in patient-derived tumors. The research found hat PRMT1 is a epigenetic driver for PDAC. Using CRISPR, the team was able to confirm that when the proteins were removed from DNA, the growth of the cancer cells were significantly impaired. There is hope that this recent development can save many lives and increase the survival rate of Pancreatic Ductal Andeocarcinoma.

https://commons.wikimedia.org/wiki/File:Diagram_showing_stage_T4_cancer_of_the_pancreas_CRUK_267.svg

 

How A Chemical From the Cypress Tree Could Advance Epigenetics Against Cancer

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On April 5, 2017

In Student Post

by Czechmate on Wikimedia Commons

Found in the essential oil extracted from the bark of a cypress tree, a chemical named hinokitiol shows potential to impact epigenetic tags on DNA and stop the activity of genes that assist the growth of tumors.

In order to develop an of understanding cancer, researches have had to comprehend the DNA methylation, an epigenetic function which controls gene expression. In regular DNA methylation, genes that work to fight against tumors are turned on, reducing the risk of cancer. However, if DNA methylation is negatively altered, then those cancer-fighting genes will be silenced, helping to progress cancer development. Scientists have tried to combat irregular DNA methylation and over-silencing of genes by creating epigenetic anti-cancer medications that reverse non-beneficial methylation effects. Like in most cases of medication usage, the users face unappealing side effects. Hinokitiol is attractive to scientists because it is a natural compound with many health benefits and way less side effects than modified drugs that can possibly cause mutagenesis and cytotoxicity.

 

Researchers from the Korea University College of Medicine tested the productivity of the hinokitiol chemical in a study by giving doses of it to colon cancer cells. It was found that this chemical helped to inhibit the colon cancer cells efficiency without affecting the colon cells without cancer. The scientists also found through careful inspection that the presence of hinokitiol decreases the expression of proteins DNMT1 and UHRF1; both of which are proteins that encourage carcinogenesis. In summary, the doses of hinokitiol appear to have allowed normal cells to remain healthy, while reducing the ability for the colon cancer cells to thrive and ceasing the production of proteins that promote cancer maturation.

Researchers are continuing their search for natural compounds, as opposed to artificial medications, that can prevent the flourishing of cancer in our bodies through playing a positive role in gene expression and DNA methylation.

http://www.whatisepigenetics.com/cypress-trees-epigenetically-protect-cancer/

 

 

https://commons.wikimedia.org/wiki/File:Raindrops_on_leyland_cypress.jpg

The Role of Metabolism and Epigenetics in Cancer Development

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On April 2, 2017

In Student Post

Cancer most commonly is defined as a “perpetuating mass of dystregulated cells growing in an uncontrolled manner”, however the meaning can be further related to epigenetics, for they appear to be very much interconnected.  Another definition of cancer goes on to note this relationship as the “dynamic genetic and epigenetic alterations that contribute to cancer initiation and progress.” Recent research shows that if epigenetics is disrupted, it might switch to oncogenes or shut down tumor suppressors. Either way, this would lead to the development of tumor cells that would cause cancer. We are already aware of the fact that chemical modification affecting the packaging of our DNA can switch genes on and off. The first time that became aware of an epigenetic code, we learned that that code chemically labels active or inactive genetic information. The focus of epigenetics is on the change caused by the modification of gene expression, not the alteration of the code itself. With recent discoveries through research on epigenetics and its relation to cancer, we learned that there must be a balance of “writers” and “erasers” for the cells. Recent data has shown that methyltransferase EZH2 is an epigenetic writer that is hyperactivated in many cancers, specifically melanomas and lymphomas. This recent research also shows KDM3A (member of the jumonji histone lysine demthylase family) as an epigenetic eraser. KDM3A fulfills an oncogenic role by activating a network of tumor promoting genes. Epigonomic changes also allow tumor cells to evade the immune system so that these cells can thrive and divide without the disruption of the immune system. Ultimately, there are two potential pathways that epigenomic regulators can cause cancer. The first is the result of too much epigenetic activation, which can lead to oncogenes. The second is too much epigenetic protection that conversely blocks tumor suppressor genes. DNA hypermethylation causes the silencing of tumor suppressor genes.

Both of these methods would lead to the development of cancer. Epigenetic regulation involves methods including histone regulation, DNA methylation, and changes in noncoding RNAs such as miRNAs. One of the challenges of studying cancer and researching possible vulnverabilities in pathways is that they are often disrupted by epigenetics. The recent studies also have shown that there are close ties between epigenomic (analysis of global epigenetic changes across many genes) changes and metabolites, or human cellular chemistry. Metabolites initiate, target, or maintain epigenetic factors with the transcriptional complex, and cooperation with them metabolites can target, amplify or mute these coded responses. Since the fields of both epigenetics and metabolism are still developing a great deal, there is hope that these insights with regards to cancer and regulating gene expression to prevent the development of cancer will allow for more precision in targeting cancer, specifically when existing methods of therapy fail to work sufficiently.

Possible Links Between Gut Microbes and Obesity, Cancer & Autism

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On January 17, 2017

In Student Post

While the bacteria in our gut play a vital role in the digestion process, recent findings have suggested that it could effect much more in our bodies. New studies have found possible links between the bacteria in our gut and obesity, cancer and autism.

Creative Commons image link

A study done by Cornell University and King’s College London revealed that Christensenellaceae minuta, a strain of gut bacteria, was found more often and in larger quantities in people with lower body masses. To investigate whether the bacteria is actually linked with obesity, researchers added the same bacteria into the guts of mice and compared their weight gain to mice lacking the bacteria. The research showed that the mice with Christensenellaceae minuta gained noticeably less weight than the mice lacking the bacteria. While research is still in its early stages, these results have made an exciting connection between bacteria in our gut and weight gain, which could dramatically impact the future of our health.

In addition to obesity, the bacteria in our gut has also been linked to cancer- in both beneficial and detrimental aspects. Researchers from the National Cancer Institute tested the effect of gut bacteria on chemotherapy in mice and found that the chemotherapy was significantly less effective in the mice lacking the bacteria. Similarly, another study found that cyclophosphamide, an antitumor drug, was less effective in mice with insufficient gut bacteria compared to those with normal levels. While these studies showed positive links between gut bacteria and cancer, other studies have found adverse effects of gut bacteria.

Unfortunately, a study published in The Journal of Cancer Research in 2012 has made a possible connection between Lactobacillus johnsonii, a strain of gut bacteria, and lymphoma, cancer of the white blood cells. The study claims that the presence of this specific strain of bacteria could lead to the development of lymphoma. Another study done in the UK in 2013 found that a specific gut bacterium, Helicobacter pylori, has the ability to deactivate the part of our immune system responsible for regulating inflammation. In effect, this could cause stomach cancer and ulcers.

While it may seem like a stretch, numerous studies have found a possible link to autism and the bacteria in our gut. A study done in 2013 by Arizona State University found that compared to children without autism, children suffering from autism had lower levels of Prevotella, Coprococcus and Veillonellaceae, three strains of gut bacteria. Even more surprisingly, another study revealed that the presence of Bacteroides fragilis in the gut reduced autism-like symptoms in mice. Research in this field is still in its primary stages, as researchers are trying to figure out if these connection are in fact related, and if so, how the bacteria directly effects these conditions.

 

Our Intestines Cure Cancer??

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On January 15, 2017

In Student Post

There are over one hundred trillion organisms- most are bacteria- living in our intestine today. These are referred to as the gut microbiota.

While trillions of bacteria sounds scary, they can actually be very helpful. Research has been done worldwide and the discovery has been that gut microbes actually can kill cancer cells all over the body. (Not just in the intestines) But how? Gut microbes and cancer actually cross paths. Gut microbes can manipulate the immune system and can either increase inflammation or lower it as needed. This means the bacteria can actually work with cancer treatments, boost T-cells, and control other factors that help cancer grow such as fungi, or viruses.

However, this is not all. While some cells help against cancer growth, others do the opposite. It varies cancer to cancer, and all have different results. As said by microbiologist and immunologist Patrick Schloss “What we really need is to have a much better understanding of which species, which type of bug, is doing what and try to change the balance.” So more research is still being done to decide how to control the microbiota, but a possible theory is that because it’s in the intestine it is related to our metabolisms and so what we eat controls the bacterium- this can also then effect the colon, thus effecting more cancer: colon cancer.

 

Cells Kill Cells—New Cancer Treatment Promotes Immune System response to Tumors

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On December 4, 2015

In Student Post

According to a recent article, oncological research has been a recent area of vast development. Cancer is a widespread form of disease that affects different areas uniquely and operates very subjectively. On a basic level, cancer is the uncontrolled growth and division of a cell.  This often yields a malignant tumor which can metastasize to other areas of the body.  When a tumor metastasizes and spreads beyond the primary site to other organs of the body, the cancer is considered to be Stage IV.  This is the most aggressive stage of cancer development and is often the most difficult to treat.  The new treatment revealed by Cornell University Engineers seeks to inhibit a tumor’s ability to metastasize.

https://flic.kr/p/xuSZkh

Killer T Cells attacking a cancerous cell

https://flic.kr/p/xuSZkh 

 

The paper explained the new approach in “annihilating” the tumors before they progress to a metastatic stage.  The key to this is not actually killing the cell, rather, inducing apoptosis of the cancerous cell.  Without the jargon, it means that the new treatment will not explicitly kill the cell, instead it will cause the cell to kill itself. The engineers accomplished this in model organism trials using mice.  The procedure involves injecting specialized liposomes in the lymph nodes, which commonly play a key role in metastasis.  The lymph nodes are parts of the lymphatic system where lymphocytes are formed. Lymphocytes are known as “killer cells” because they are a form of leukocytes (white blood cells).  The injection contains liposomes (membranous sacs of water) with a special “Tumor necrosis factor Related Apoptosis-Inducing Ligand” protein.  These will attach to the lymphocytes and target the cancerous cells, and effectively eliminate the tumor before it metastasizes.

The paper also references previous work by the engineering group where they created a similar approach for eliminating bloodstream metastases in January 2014.  This coupled with a lymphatic treatment can greatly reduce the rate of metastasis in patients with aggressive malignant tumors.  Recent developments in oncological treatments have suggested promising developments in the way of cancer treatments–and cures.

Img. Source

Original Article

Wait… Smoking is bad for you???

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On November 18, 2015

In Student Post

Thinking back, it’s pretty hard to believe that at one point most people thought smoking was good for you. Up until about 60 years ago, advertisements preached that smoking cigarettes was not only the cool thing to do, but was also in some ways beneficial for your health.

Lewis_Hine,_Newsies_smoking_at_Skeeter's_Branch,_St._Louis,_1910

Cigarette ads used doctors and scientists to preach that smoking helped alleviate social anxiety, dry mouth, colds, and headaches. Although in some cases the menthol used in many cigarettes did have a positive effect on cold symptoms, in many cases the ill symptoms were caused by smoking withdrawal itself. (i.e. social anxiety and headaches)

To much of 1940’s doctors’ demise, enumerable amounts of studies have come out proving that smoking is one of the leading causes of lung cancer, gum cancer, tongue cancer, throat cancer, and most of all emphysema. Now, the tobacco is not always the cause of all these diseases; all the other fun chemicals that the cigarette companies put in the cigs to “enhance the experience” and help them burn faster, are the culprits. Just a few of the chemicals in modern cigarettes are as follows:

Acetone = commonly found in nail polish and many paint removers

Ammonia = highly toxic; usually found in household cleaners

Arsenic = found most in rat poisons

Butane = found in lighter fluid (helps cigarette to burn faster)

Cadmium = component of battery acid

Carbon Monoxide = found in car exhaust fumes

Formaldehyde = embalming fluid (used to preserve dead bodies)

Need I go on? Okay!

Lead = decreases function and activity of the nervous system (brain, spine, etc.)

Methanol = main component of rocket fuel

Nicotine = main component of insecticide but has a very addicting side-effect

Tar = used for paving roads

Toluene = found in dynamite (TNT = Tri-Nitro Toluene)

Some_Kills

It is obvious to me why cigarette companies have stopped running their ads that depict doctors, scientists, teachers and other professions often lauded as some of the most intelligent in society, smoking and promoting cigarettes. Even so, what troubles me, is how 17% of America’s population still chooses to smoke. With 8% of that 17% being teenagers, the number of smokers has steadily declined over the years, but not at a rate rapid enough. The common sense that goes behind just not smoking is maddening to those who watch smokers constantly spending $15 (NY) per pack.

PS: Up until 1978, Camel Cigarettes actually contained minute particles of camel. The company used the fat because it burned very quickly, was odorless, and gave the cigarette a more mild taste.

Original Article: http://www.vox.com/2015/11/14/9732414/how-many-americans-smoke

Information on Emphysema: http://www.mayoclinic.org/diseases-conditions/emphysema/basics/definition/con-20014218

Lung Cancer Facts: http://www.lung.org/lung-health-and-diseases/lung-disease-lookup/lung-cancer/learn-about-lung-cancer/lung-cancer-fact-sheet.html

 

The Real Scoop on Artificial Food Coloring

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On October 18, 2015

In Student Post

Although artificial colors and dyes have been used in foods since the early 1900’s, the FDA has banned many of them due to health concerns. Thirty-seven artificial colors still remain approved for general food use in the USA, many of which are now prohibited in some European countries. Many of these chemicals have been researched and found to have harmful side effects, but they are still used in popular candies, soft drinks, cereals, and other processed foods.

Americans are now consuming more processed foods and drinks than ever before, and therefore more artificial colors and dyes. Many scientists have researched these common chemicals and found shocking results. The most common blue 1 & 2, citrus red 2, green 3, red 3 & 40, and yellow 5 & 6, have been found to cause a wide degree of side effects. Some have been found to cause cancer, ADHD, neurochemical and behavioral effects, allergies and more. Because of link between artificial dyes and the frequently seen side effects of cancer and ADHD, many European countries such as Norway, France, Finland, The U.K., and Sweden have banned a number of these chemicals from their foods.

It is no secret that these additives have harmful side effects, so why do companies still choose to use them? It is a very simple marketing tactic. “You eat with your eyes”, therefore companies will try to make their food look visually appealing to convince you to buy their products. Using artificial dyes and colors is just one method companies use to attract buyers. Artificial dyes like Yellow 5 have more vibrant and concentrated color than natural ones like saffron or turmeric. They are also much cheaper than natural dyes because companies do not need to use much in order to get the color they want. Artificial colors are also easier to use and their results are more reliable because they are much less sensitive to heat than naturally-derived food dyes are.

Silly Rabbit

(A bowl of Trix cereal made with artificial colors and flavors. The new Trix will go on sale later this year, without its blue and green puffs.)

This news may seem very alarming and upsetting to the average consumer, but there is hope. The FDA requires that companies put their ingredients on the food labels, so you know which foods are organic and which ones have artificial coloring. Research on artificial food dyes has led many consumers to cut out harmful processed foods and sodas from their diet and led to more awareness among buyers. And although there are companies such as Coca-Cola that use harmful cancer causing dyes such like 4-MEI, there are brands like General Mills that are promising to soon cut out all artificial dyes from their cereals by 2017. The new direction American consumers are taking now towards organic and health foods is slowly leading the food industry to change their foods in a healthy way. No longer are some food companies looking for the most vibrant look with their presentation, but rather the healthiest.

 

 

New Understanding in Telomerase Structure: Can It Lead to New Cancer Treatment Medications?

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On October 12, 2015

In Student Post

Telomerase. They know what it is. They know what it does. They know it is involved with the formation of malignant tumors. Yet for years, cancer researchers could not figure out a way to curb telomerase activity. Not until recently, when a group of researchers at the University of California, Santa Cruz discovered an important structural component of telomerase that could lead to the development of new and more efficient cancer treatment medications.

But first things first: what even is telomerase? To understand the role of telomerase, we must first understand what a telomere is. Analogous to the “plastic tips of shoelaces”, telomeres are located at the tips of chromosomes to keep the ends of DNA from “fraying”, consisting of the repetition of the same nitrogenous base sequence over and over again. In humans, this base sequence is TTAGGG.

Screen Shot 2015-10-05 at 7.44.26 PM(Source: https://en.wikipedia.org/wiki/Telomere#/media/File:Telomere.png)

The sequence can be up to 15,000 base pairs long; however, each time a cell divides, the telomeres get shorter and shorter until they become they become too small to divide again. That is when the telomerase comes in; it adds nucelotides to the telomere to prevent it from becoming senescent, or at least prolong the cell’s life span.

Sounds like a good thing, right? Not when the telomerase gets out of control and does not allow for cells to die, causing a huge growth of cells that eventually evolve into malignant tumors.

What makes it hard for scientists to combat excessive telomerase activity is due to the enzyme’s unique and complex structure. In addition to its sophisticated quaternary structure, telomerase also has an RNA template that allows the telomerase to make the DNA bases (TTAGGG) for the telomere.

Screen Shot 2015-10-05 at 10.24.26 PM

(Source: https://vi.wikipedia.org/wiki/Telomerase#/media/File:Telomerase_illustration.jpg)

Researchers at UC Santa Cruz determined the structure of the RNA binding domain of telomerase and how the template border is dependent on how the protein and RNA components interact with each other. Understanding this interaction can help scientists develop cancer medications that more specifically inhibit telomerase. This is the first major advancement in telomerase research since November of 2010 when biochemists at UCLA created an unprecedented 3D model of telomerase’s RNA structure.

While this discovery is a major step forward in cancer treatment research,  some experts have their reservations against finding methods of inhibiting telomerase altogether.

However, regardless of the controversy surrounding telomerase inhibition in cancer treatment, this discovery will be useful in coming up with tactics to prevent aging, and improve treatments in other medical fields, such as burns, bone marrow transplants, and heart disease.

What do you think? Leave a comment below!

 

 

Original Article

From Beef to Blood to Breast Cancer: Bovine Leukemia Virus

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On October 12, 2015

In Student Post

Scientists have studied Bovine Leukemia Virus, informally known as BLV for quite a while. Investigators have studied the cellular structure of the virus, the hypothetical vaccine and the correlation with cow’s milk. However, recently a study done by researchers at the University of California Berkeley concludes that there is a link between the infection (BLV) and human breast cancer.

In a study published in PLOS ONE,the investigators take note of all of the potential causes of breast cancer. They extrapolate that the key reasons behind breast cancer are age, reproductive history, hormones and genetics. The researchers additionally detected that the Bovine Leukemia Virus was in the breast epithelium of humans. The objective of this experiment was to determine whether the presence of BLV DNA in human mammary epithelium is associated with breast cancer.

The researchers conducted a case study in which archival formalin-fixed paraffin embedded breast tissue was injected in the control group (women without history of breast cancer) and the experimental group (women with a history of breast cancer.) The rate of occurrence of BLV DNA from women with breast cancer was 59%, while the rate in the control group was a diminutive 29%.

This experiment has helped researchers conclude that the presence of amplified BLV DNA is significantly correlated with female breast cancer. The findings in this experiment and ones similar to it assist in conceptualizing a potential primary and secondary breast cancer prevention tactic.

Humans get BLV from cows!

Humans get BLV from cows!

Does the aging process influence changes on a cellular level or do changes on a cellular level influence the aging process?

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On March 10, 2015

In Student Post

wrinkles

How do humans age? While we are “programmed to die,” there doesn’t seem to be one thing that causes our death by “old age.” For example, one way we carry out our own deaths is found on the cellular level, where we accumulate mutations in the DNA repair process and the cells themselves die, or the enter senescence (non-replicating state) as they age. These processes occur at several different times, overlapping and alternating. Therefore, what appears to be the best time to intervene in order to promote healthy aging? No one knows, but they do know what DNA becomes extremely damaged as time goes on and has an incredible impact on our aging process. The cells have sooner suicide dates where they undergo apoptosis more rapidly than normal, and the loss of too many cells can cause tissue atrophy and dysfunction. In addition to creating a lack of cells, the damaged DNA can even shift epigenetic markers.

Typically, epigenetic marks shift in tumor cells, which can lead to cancerous cells. However, in the early 1990s at Johns Hopkins University, Jean-Pierre Issa was studying changes in DNA methylation in colon cancer cells when he observed shifts in epigenetic markers over time, but not only in tumor cells; he found that (to a lesser degree) these shifts were occurring in healthy cells as well. After mapping DNA methylation in human cells, we know that some areas of the genome become hypermethylated with age while others exhibit reduced methylation. These changes typically occur through DNA replication or DNA damage repair because the histone modifications are not always perfectly reproduced and in order to repair damaged DNA, repair proteins must remove the epigenetic marks to access the damaged genetic material to repair it, and once completed, the epigenetic marks can be omitted or misplaced. These epigenetic alterations have been linked to a reduced regenerative capacity of stem cells with age, and bring up a valuable question:

“Is this an epiphenomenon that happens just because we age, or is it actually causing symptoms or diseases of aging and limiting life span?”

Article source: http://www.the-scientist.com/?articles.view/articleNo/42280/title/How-We-Age/

The mutation and spread of Cancer caused by changes in Epigenetics

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On March 8, 2015

In Student Post

Epigenetics could be the key to understanding how cancer originates, when it mutates, and how it spreads. Researchers at the Boston University School of Medicine (BUSM) believe that different types of cancer are caused by an “on and off” switch in the epigenome. While many scientists believe  that many cancers originate in cells called progenitor cells, they cannot concoct a model that explains  how cancer spreads from the progenitor cell and mutates into many forms as it continues to grow in a person’s body.

One of the lead researchers, Sibaji Sarkar, posited “there should be a general mechanism that initiates cancer progression from predisposed progenitor cells, which likely involves epigenetic changes.” The researchers believe that the theory of an epigenetic switch is supported by the growth of tumors, which go through many different stages. The team believes that if cells can be altered to become cancerous and remain stuck in their stage of growth while they replicate out of control, then there must also be an off switch to this uncontrolled replication. They also suspect that epigenetic changes can determine the rapidity of growth and the mutability of the characteristics of the cancer and tumors.

Although Sarkar’s team has not yet found specific epigenetic code that causes these mutations and growth, he believes that their hypothesis will cause other scientists to focus their attention on the epigenome and find ways to prevent progenitor cells from spreading and mutating into malignant tumors.

This epigenetic research relates to our study of the relationship between the epigenome and cancer. Specifically the absence of an active p53 protein would prevent a certain part of the DNA from being  read and the cell would therefore lack a protein that inhibits the cell cycle. This would cause uninhibited cell division and the spread of cancer.

 

Methylation of DNA

640px-DNA_methylation

New Breast Cancer Gene Discovered

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On January 17, 2015

In Student Post

 

 

 

Pink_ribbon.svg

Today, one of the most talked about cancers is breast cancer. Breast cancer is defined as cancer that forms in the tissues of the breast. There are two types of breast cancer: ductal carcinoma, which is most common and begins in the lining of the milk ducts (thin tubes that carry milk from the lobules of the breast to the nipple) and lobular carcinoma, which begins in the lobules (milk glands) of the breast.

According to a new study done by the Wellcome Trust Sanger Institute and University of Cambridge, a gene has been identified to have a major association in aggressive subtypes of breast cancer. The research suggests that an overactive BCL11A gene causes the development of tripe-negative breast cancer.

The study was conducted in human cells and in mice. The study was important because one in five patients are affected by triple-negative breast cancer. From the conducted research, Dr. Walid Khaled discovered that by adding an active human BCL11A gene to a human or a mouse’s breast cells (in the lab) caused them to behave as cancer cells. Increasingly, Dr. Khaled concluded that “by increasing BCL11A activity we increase cancer-like behaviour; by reducing it, we reduce cancer-like behavior.”

This research and study is extremely important because from the results, the team was able to propose that BCL11A is a strong candidate for development of a possible targeted treatment. Typical treatments of breast cancer include radiation and chemotherapy as well as surgery. The most known surgeries are Lumpectomy/partial mastectomy (large portion of the breast is removed) and a full mastectomy (full removal of breasts)

I chose this article because I know many dear friends that have faced and survived the battle of breast cancer. I believe that spreading awareness and screening early is extremely important. In addition, I am very hopeful that new advances will be made so that others need not endure the excruciating fight of breast cancer.

 

Your Potato Chips Could be Killing You

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On November 18, 2014

In Student Post

800px-Potato-Chips

Last year the FDA found a very dangerous chemical that forms in many common foods during cooking.  The chemical is called acrylamide and research suggests that it makes people more susceptible to certain cancers.  Acrylamide forms during frying, grilling, baking, roasting, or toasting when the amino acid asparagine reacts with sugars in the food.  It is what gives food like potato chips their crunchy-ness and taste.

French Fries, potato chips and other potato products have the most acrylamide in them.  Scientists have also found acrylamide in products such as coffee (especially dark roast), roasted nuts, and breakfast cereals. It is estimated that 38% of calories come from food that contains acrylamide.  Acrylamide is also found in cigarette smoke.

Acrylamide has also been found to affect pregnant women and infants.  One study in Environmental Health Perspectives showed that high acrylamide intake may be connected to slower and less fetal growth.

There are a couple of things that you can do to limit the effects of acrylamide.  The first is cooking/frying/roasting potatoes for a shorter time and toasting bread for a shorter time.  Do not let the potatoes become dark brown and do not char/burn your toast.  Another thing you can do is cook at a lower heat and use more organic ingredients.  You can also eat less potato products, cookies, and pastries and switch to a light roast coffee.  

Research on this chemical isn’t totally conclusive so I wouldn’t be too worried about it.  However, I will be more careful about the potato products that I eat and the way I cook my food.

Article:

http://www.berkeleywellness.com/healthy-eating/food-safety/article/acrylamide-food-chip-tips

Other Articles:

http://www.forbes.com/sites/alicegwalton/2013/11/15/the-fda-calls-out-yet-another-food-chemical-to-avoid-acrylamide/

http://www.npr.org/blogs/thesalt/2013/11/19/246188051/remember-death-by-french-fries-here-s-the-story

http://www.fda.gov/Food/FoodborneIllnessContaminants/ChemicalContaminants/ucm053569.htm

Directed evolution: Bioengineered decoy protein may stop cancer from spreading

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On September 26, 2014

In Student Post

Biomedical_Engineering_Laboratory

Researchers Jennifer Cochran and Amato Giaccia from Stanford University have recently made a breakthrough in cancer research. The Bioengineers have developed a synthetic form of the protein Axls that binds to the protein Gas6 in our blood. Cancerous cells have Axls proteins lining the cell membrane awaiting connections with Gas6 proteins. Once the two join together, the cancerous cells break away from the central cancer mass and spread through the body during a process known as Metastasis. However, the new synthetic Axls protein binds to Gas6 in the blood and inhibits Metastasis from ever beginning. This stops the original Axls cells on the cancer from receiving the chemical signals to break away and form new cancerous nodules.

The scientists conducted preliminary testing on lab mice with aggressive forms of ovarian and breast cancer. The Bioengineers found that, “Mice in the breast cancer treatment group had 78 percent fewer metastatic nodules than untreated mice. Mice with ovarian cancer had a 90 percent reduction in metastatic nodules when treated with the engineered decoy protein.” Scientists currently treat cancers with chemotherapy and radiation, however these early studies show that the synthetic protein Axls could prove to be a safe and effective alternative.

I believe that this type of Bioengineering, specifically directed evolution, holds the key to discovering cures for many of earth’s deadly diseases. Despite the recent breakthrough researchers have made at Stanford, it will still be years before synthetic Axls is approved for clinical studies and then for use in the medical field.

Original Article: http://www.sciencedaily.com/releases/2014/09/140921145112.htm

Source: http://www.sciencedaily.com/

Photo Credit:

http://commons.wikimedia.org/wiki/File:Biomedical_Engineering_Laboratory.jpg

Useful Links:

http://engineering.stanford.edu/news/stanford-researchers-create-evolved-protein-may-stop-cancer-spreading

http://bioengineering.stanford.edu/

http://www.sciencedirect.com/science/article/pii/S1389034405000055

To Know or Not to Know: Cancer Risk Gene Testing

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On September 25, 2014

In Student Post

Breast Cancer Cells

Genetic mutation testing has been a hotly debated and controversial topic since its initial prevalence in 1990.  Originally genetic testing was used to test females who have cancer in their family history for the BRCA 1 and 2 gene mutations.  Early detection of these mutations allowed for precautionary measure sure to be exercised prior to cancer even being diagnosed. The hereditary breast cancer risk testing was done mainly by Myraid Genetics but just last year the Supreme Court invalidated Myraid’s patents on the testing of the BRCA genes.  This ruling opened up many windows for the competition of Myraid in the field of genetic testing.  Many other companies and Myraid itself began not only offering BRCA testing but also more elaborate multi gene testing for the same price (apron $4000) as it would have been to test just the two BRCA genes.  This “bargain” influenced many patients to have more genes (up to 25) tested for mutations despite the fact that they may not have a family history to tendency towards certain cancers.  This multiplex testing has raised many eyebrows in the medical field because patients and doctors are getting information that sometimes they are unsure as to what they should do.  Doctor Kenneth Offit of Memorial Sloan Kettering Cancer Center stated when referring to multiple gene mutation testing, “because they could be tested,not necessarily because they should be…individuals are getting results we’re not fully educated to council them on. ” However Memorial Sloan Kettering Cancer Center is working on setting up a database for more knowledge on genetic testing.  This online forum, the Prospective Registry of Multiplex Testing (PROMPT) will allow for more research to be done and for patients to learn more.   Often genetic mutations are found and doctors are unsure how to react to the information due to lack of knowledge in that specific field of mutation leading to a specific type of cancer with out any family history.   Professor Mary-Claire King of the University of Washington voiced her opinion that, “We need to report back only what is devastating and clearly devastating.”  Meaning she felt that patients and physicians should only receive specific information as opposed to a full list of all the genetic mutations that tested position or inconclusive.  When do we know when to much information become frivolous? When it come to human health, the more we know the better the outcomes.  How will doctors be able to sift through extraneous data to find what truly are indications for higher risk of cancer?  Is this “extra” testing and information skewing the data and prognosis of many patients?

 

Main Article Used:

http://www.nytimes.com/2014/09/23/health/finding-risks-not-answers-in-gene-tests.html?ref=health&_r=0

 

Tasmanian Devil Extinction on the Horizon

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On November 19, 2013

In Student Post

The tasmanian devil is most readily remembered by it’s cartoon character, however the extinction of the animal seems to be on the horizon. Tasmanian devils are wild animals of the Dasyuridae family found only in the wild of Australian island of Tasmania. Recently, it has been predicted that a facial cancer on the marsupial will extinct the species in the next ten years.

First reported in 1996, the parasitic tumor has declined the species by seventy percent. The onset of the non-viral tumor was caused by the environment of the animal (who live in high-density populations that suffer from invasions of nonnative species and pollution.) Devil facial tumor disease likely began in what are called Schwann cells. Schwann cells are found in the peripheral nervous system; they produce myelin and other proteins essential for the functions of nerve cells.

Scientists are trying to remedy the infectious disease by breeding a certain species of tasmanian devil that was shown to have a partial immunity to the tumor. After preliminary research on the disease, scientists have come to see that the answers to the tasmanian devil’s circumstance, if uncovered, could lead to answers for human cancers as well. More knowledge of the direction and rate of the tumor in devil populations will help scientists to find out more about how the disease spreads byYoung_tasmanian_devil examining the interactions between the animals. Scientists remain positive; Andrew Storfer, who works closely with the animals on location, says “the answers will help in developing responses to this and other disease outbreaks in Tasmanian devils–and potentially in people.”

Largest Mass Poisoning of a Population in History

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On September 25, 2013

In Student Post

http://commons.wikimedia.org/wiki/File:Arsenic_alchemical_symbol.svg

http://commons.wikimedia.org/wiki/File:Arsenic_alchemical_symbol.svg

Picture this familiar scene: waking up in the middle of the night, too lazy to go to kitchen, and quenching your parched mouth with water from the bathroom sink. To people in America, this is a safe undertaking. But to people in Bangladesh, it could be deadly.

Arsenic is a naturally occurring element on Earth’s crust, which can enter drinking water from natural deposits. Its effects on the human body have been known to cause respiratory, circulatory and heart problems. Recently, however, researchers have had the chance to study itseffects on humans more closely in Bangladesh because of its unusually high percentage of arsenic in its water supply. And what researchers found was eye opening.

Researchers at the University of Chicago studied more than 11,000 Bangladesh men and women. After 6.6 years, they found that residents exposed to arsenic at 19 parts per billion or less showed signs of reduced lung function. While people who were exposed to 20 parts per billion or higher had the lung capacity similar to that of a long-term smoker.

The researchers recorded 407 deaths, 198 from circulatory diseases. 35-77 million people are exposed to arsenic in Bangladesh alone.  The World Health Organization deemed the country’s arsenic contamination as “the largest mass poisoning of a population in history.”

Why should we be worried (other than the obvious ethical issues)? A group of Dartmouth researchers found that 2.3 million people in New England use wells as their main source of drinking water. This makes up approximately 40 percent of the population in Maine and New Hampshire. Although wells in the United States generally contain small amounts of arsenic, the researchers found that overtime, small doses of arsenic can lead to skin, bladder and lung cancer. So maybe next time it’s worth the trip to the kitchen.

With Summer Around the Corner, Will You Keep An Eye Out to Protect Your Skin?

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On April 28, 2013

In Student Post

Piece of Human Skin
http://commons.wikimedia.org/wiki/File:Human_skin_structure.jpg

Tanning Salons are extremely dangerous to one’s health due to the unnatural and intense UVA and UVB rays that are aimed at the skin. These Ultra Violet rays can lead to premature aging of the skin and skin cancer. While most people know the dangers of tanning salons, many people are unaware of the dangers of natural sun tanning.

Natural sun tanning can be as bad as tanning salons. Your risk of skin cancer increases as you spend more time underneath the strong sun. “According to Arthur Sober, M.D., associate professor of dermatology at Harvard University Medical School, ‘On a cloudy day, a person feels cooler, but is still getting a good amount of UV exposure’.” (FDA,enotalone.com) Which means that although it may be cloudy you are still coming in contact with UV rays. There is still enough sun rays penetrating the newly weakened ozone layer to have an effect on your skin!

The sun has vitamin D which is beneficial to our bodies, so about fifteen to twenty minutes of sun a day is healthy, but not more than that.

The sun emits two major wavelengths- UVA and UVB and these wavelengths increase one’s chances of skin cancer. The body tans because the body is being injured by ultra violet radiation that hits the skin. “These UV rays cause the body to produce an excess amount of melanin which acts like a natural sun screen. In order to get a tan, you must injure your skin first.” (FDA,enotalone.com) In addition to the risk of skin cancer from sun tanning, UVB rays impair the body’s immune system, which normally defends against disease. This increases one’s chances of skin cancers and other diseases.

“UVA rays speed up the skin’s aging due to the changes in the skin’s collagen, the protein in the skin’s connective tissue.” (FDA, enotalone.com). Many cosmetic companies make cremes enhanced with collagen for older women; they add extra collagen on their skin in hopes of reducing the amount of wrinkles they have.– These UVA rays speed up the wrinkling process of you skin, causing pre-mature aging.

Statistics about skin cancer:

“-Skin cancer is the most common form of cancer in the United States. More than 3.5 million cases in two million people are diagnosed annually.

-Melanoma accounts for about three percent of skin cancer cases, but it causes more than 75% of skin cancer deaths.

-Melanoma is the most common form of cancer for young adults 25-29 years old and the second most common form of cancer for adolescents and young adults 15-29 years old.

-A person’s risk for melanoma doubles if he or she has had five or more sunburns at any age.

-More than 20 Americans die each day from skin cancer, primarily melanoma. One person dies of melanoma almost every hour.”

(www.skincancer.org)

Try to keep these statistics in mind and protect your skin from being harmed by excess sun!

Read more at:

http://www.medicinenet.com/skin_cancer/article.htm

http://cancer.about.com/od/skincancermelanoma/f/skincancersympt.htm

http://www.skincancer.org/Skin-Cancer-Facts/

http://www.enotalone.com/article/8106.html

 

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