BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: Cancer (Page 1 of 3)

CRISPR: The Next Step for Cancer Treatment

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On March 13, 2018

In Student Post

CRISPR is a gene editing technique that is currently still being researched and expanded upon, however, upon recent discoveries, one can note the great advantages this technology brings to the table to enhance cancer immunotherapy .  More specifically, according to the Washington University School of Medicine, “these T cell immunotherapies can’t be used if the T cells themselves are cancerous.” However, there is more to this discovery. Let’s backtrack.

What exactly is CRISPR? “CRISPR technology is a simple yet powerful tool for editing genomes. It allows researchers to easily alter DNA sequences and modify gene function. Its many potential applications include correcting genetic defects, treating and preventing the spread of diseases and improving crops. However, its promise also raises ethical concerns.” For the sake of this article, we are just focusing on the benefits it has on cancer treatment solely. Also, what exactly are T cells? They are “a type of white blood cell that is of key importance to the immune system and is at the core of adaptive immunity, the system that tailors the body’s immune response to specific pathogens. The T cells are like soldiers who search out and destroy the targeted invaders.” On the other hand, T cells can become cancerous therefore not being able to accomplish their task of destroying invaders.

How does CRISPR enhance cancer immunotherapy? Scientists at the Washington University School of Medicine engineered human T cells that can attack cancerous human T cells. Additionally, they engineered the T cells to eliminate a harmful side effect known as graft-versus-host disease. This was all thanks to CRISPR. But, how exactly did they figure this out? Were there any flaws or bumps in the road?

Well, this type of treatment cannot work if the T cells they use are cancerous. Supercharged T cells can alternatively be used to kill cancerous T cells, but the cells can also kill each other because they resemble each other closely. This is where CRISPR came in, preventing the human T cells and cancerous human T cells from killing each other. Another benefit of this is that the scientists engineered the T cells so any donors T cells can be used without the fear of not matching the person in need of the T cells.

Overall, anything to better the prevention of cancer is a scientific win in most’s book. But, CRISPR is a controversial tool. Some think it should be put to use and some do not. However, will this technology alter other aspects of the human genome besides diseases and deadly occurrences? How will this affect our ethics as a community? Will our genetics continue to increasingly become more altered? Time will only tell.

Engineering Cancer Killers!

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On December 10, 2017

In Student Post

https://commons.wikimedia.org/wiki/User:ArturoJuárezFlores

Engineering Cancer Killers!                                                                                               

Today, millions of people are dying from the complex disease, cancer. Although treatments such as chemotherapy and radiation are used to cure the disease, immunotherapy has emerged as a potential cure for cancer. Professor Oliver Ottmann, Head of Haematology at Cardiff University and co-lead of the Cardiff Experimental Cancer Medicine Centre (ECMC), acknowledged the importance of immunotherapy and considers it a huge breakthrough in cancer research and treatment. This lead his team to further discover the key to genetically engineering T-cells to recognize and kill cancer cells. 

How Does It Work?

T-cells are an important part of our immune systems. They contain receptors that can recognize bacterial infections or viruses and help fight them off, and potentially kill cancer cells. Scientists have developed a way to genetically engineer T-cells using CRISPR genome editing. Normally, the genetically engineered T-cells, that are created to fight cancer, contain two types of receptors. One type is called therapeutic, and is created and added on to the cell in a lab, and the other types of receptors are natural and originated from the T-cell.

The Problem 

The team acknowledged that since both kinds of receptors occupy the cell, there is minimal space for all receptors to fit on the cell; therefore certain receptors must challenge other receptors in order to perform their own function. Since there are more natural receptors on a T-cell than the therapeutic receptors,the natural receptors perform superior than the therapeutic receptors. This means the genetically engineered T-cells are not able to work at their full potential; they are unable to kill cancer cells efficiently.

The Solution

After recognizing the problem, Professor Oliver Ottmann and his team genetically engineered T-cells, by genome editing, that only contain the therapeutic receptors they intended on adding. By eliminating all of the natural receptors that T-cells normally have, the therapeutic receptors will increase in efficiency.

The Future

Since scientists have figured out a way to maximize the efficiency of genetically engineered cancer fighting T-cells, finding a cure to cancer could be closer than we thought. Could this cutting edge research be the start of a solution for cancer treatment?  Do you think scientists and society will pursue this theory? This article sparked my interest because finding a reliable cure for cancer has been a problem for many years, every discovery we make brings us closer to finding the best cure.

How DNA damaged from radiation causes cancer

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On October 24, 2017

In Student Post

In a recent study, professors from the Wellcome Trust Sanger Institute sought to see the similarity between spontaneous cancerous tumors and cancer caused by ionized radiation. By looking at the molecular fingerprint of different types of cancers, they were able to differentiate between cancers that formed by radiation and cancers that were not formed by radiation.

In the study, they studied the mutational signatures of the DNA. Mutational signatures are just ways in which the DNA is affected by cancerous mutations. They studied the DNA mutational signatures from DNA exposed to radiation, but not necessarily cancerous, and the mutational signatures of the DNA of cancerous cells of which some were caused by radiation exposure and some were not. Both included the same signatures.

The two mutational signatures that were observed were deletion of segments of DNA bases and balanced inversion, where the DNA is cut in two places, the middle piece flips around, and the pieces are joined back in the opposite orientation from before the flip. High energy radiation is the cause for balanced inversion, since it does not happen naturally in the body. After the mutation, the DNA cannot repair itself.

This gives us a better understanding of cancer and how ionized radiation affects DNA and produces these mutational signatures. Knowing this information, this helps us recognize which tumors are caused by radiation. Once we have a better understanding of this, it will prove important for determining how each cancer should be treated. But for now, this is a strong step forward in the battle against cancer and every step of the way is crucial if we are to be victorious.

 

Alien DNA?

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On October 16, 2017

In Student Post

Our DNA has evolved over hundreds of thousands of years. This evolution was usually the result of natural selection. Scientists have discovered another way our genetics have been altered: virus DNA. Our DNA consists of 100,000 pieces of viral DNA and altogether those pieces make up about 8 percent of our DNA. Most of these genes are from endogenous retrovirus. Many viral genes produce proteins that affect our health in unexpected ways. Some of our ancient virus DNA may be protecting us from diseases and others may be raising our risks for cancer.

Viral DNA is neither good nor bad. It’s not that simple and the research being done on this part of our genome is just being started. In a recent study scientists engineered healthy cells to make a viral protein that is found in tumors. They concluded that the protein caused the cells to behave in a “cancer like way”. There are other viral proteins that play a crucial role in reproduction, known as syncytins.

This caused scientists to investigate other viral proteins. Five years ago Dr. Heidmann, a French cancer researcher, found a stretch of viral DNA that has gone overlooked and named it Hemo. She also found that versions of this protein was in other species and that the gene behind is have barley changed over thousands of years. The consistency of the gene throughout species shows that the protein must play an important beneficial role. Some preliminary research has shown it to be involved with helping the embryo develop a variety of tissue from stem cells.

Many things are still not known about this part of our DNA and how it affects us but researchers are working hard to find out everything they can. They are actively trying to figure out which viral proteins are beneficial and which are harmful. This research will help us understand a lot about our genome, evolution, and maybe even cancer prevention.

For access to other articles about this topic click here and here.

 

Potential New Treatment Strategy for Brain Cancer!

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On October 11, 2017

In Student Post

Cancer is a disease characterized by the up-regulation of cell growth and it usually develops when normal cells are not able to repair damaged genetic material. New studies are revealing insights into the function of genetic mutations commonly found in a form of brain cancer, specifically the IDH mutation. Isocitrate Dehydrogenase(IDH) is a metabolic enzyme found in more than 70% of low grade gliomas and secondary glioblastomas, types of malignant brain tumors. In a normal cell, IDH enzymes help to break down nutrients and generate energy cells. When mutated, IDH creates a molecule that alters cells genetic programming and instead of maturing, the cell remain primitive. Studies have shown that cells holding this mutation also have an impaired ability to repair DNA. Strangely enough, low grade gliomas that have the IDH mutation are typically more sensitive to chemotherapy than those that lack the mutation. Why does this occur? We still don’t really know the answer.  Yet, researchers have discovered a potential new treatment option for the glial cells harvesting the IDH mutation– PARP Inhibitors.   A super cool future is waiting ahead.

When treating the IDH mutated cells with PARP Inhibitors, a substance in the form of a drug that blocks an enzyme called PARP, the cells were effectively killed. When the drug blocks PARP, it keeps the cancer cells from repairing their damaged DNA, and eventually they die off. The cells are extremely sensitive after the effects of the inhibitors, especially after taking the most common PARP drug called oliparib. PARP inhibitors are a form of targeted therapy–meaning the inhibitors work within a similar approach as radiation and chemotherapy– they simply damage or prevent the repair the DNA. Researchers have also found the up regulation of the unusual molecule called  2-HG(2-Hydroxyl-glutarate) within the IDH mutated enzymes. In a study with Dr. Brinda’s team at Yale, they found that 2-HG may be responsible for the defect, DNA repair inabilities, in these cells. When the production of 2-HG was blocked in these cells, the DNA repair defect was reversed and cells became unresponsive to the PARP inhibitor treatment. This finding further solidifies that PARP inhibitors may be the best new effective brain cancer treatment method. What do you think? I think this is pretty cool news!

Jto410 is the username of the radiologistwho took the picture

Low grade glioma MRI scan. Creative Commons Attribution-Share Alike 3.0 Unported license.

There are also many clinical trials occurring currently to observe 2-HG as a definite IDH biomarker for cells that are sensitive to treatment with PARP inhibitors. In addition, labs are also designing a clinical trial of olaparib and temozolomide, two PARB inhibitor drugs, in patients with low-grade gliomas. The results of these trials, are for sure going to make headlines within the Biology and Medical field! Even though, there are still many questions to answers and studies to conduct regarding brain cancer and the IDH mutation, we are definitely on the right track to cure the monster a.k.a “cancer.”

Hair Saving Option with Chemotherapy

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On October 11, 2017

In Student Post

Scientists have been finding a way to prevent hair loss after the painful process of cancer treatment, Chemotherapy (Chemo). Hair loss is one of the biggest feared side-effects. A recent study showed that 75% of female patients who had breast cancer feared the side effect of losing hair. Hair loss scored the highest in a Swedish nurse’s study that investigated the quality of life in patients who had breast cancer. With the help of Sung-Jan Lin, a scientist at National Taiwan University, a protein was made that could withstand the distressing effects of Chemotherapy.

There are a few other options for people receiving this treatment. Some will try to put on scalp-cooling caps to freeze the chemo drugs from entering the hair follicles. However, this process is expensive and only works for 50% of the people. The treatment could end up being longer than expected, and can cause mild to severe headaches and discomfort.

Lin describes that part of the problem is that we have such a limited knowledge of how Chemotherapy damages hair follicles.

In short, his team looked at a protein called p53. This protein functions to limit tumor growth, but also helps suppress hair growth (hair cells divide rapidly like tumor cells)

Studying P53, Lin found out that the protein was blocking a hair-promoting protein WNT3A. This stimulated his team to ask the following question. Is injecting WNT3A directly into the scalp while administering Chemo prevent hair loss?

The team decided to experiment with mice with a chemotherapy agent, and soon enough the results matched their hypothesis. One group of mice were injected with WNT3A soaked beads. And sure enough, that group sustained their hair. While the other group that was not given WNT3A loss all their hair.

Lin and his team are now working to adapt his studies on human patients. As stated by Lin it would be unsafe to inject WNT3A in bead form. As a result, they are working to create the protein in a gel or cream solution.

With this new hair saving option, the cancer treatment will seem less fearful for some patients. This treatment could be a big help for the future. Scientists are working to expand their knowledge on how to effectively provide treatment without endangering our human traits.

So after hearing all this, what do you feel about this new idea? Will the “power of proteins” eliminate other side effects provided by Chemotherapy? If so, what kinds? Let me know in the comments below.

Photo link and photographer:

www.flickr.com/photos/calliope/6025359063

Liz West

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

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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

 

 

 

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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.

 

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