Researchers from Switzerland has done a study on TORC1, which is an enzyme that controls the normal cell growth in the body. When this enzyme is too active it causes diseases such as cancer. The Target Of Rapamycin (TOR) was first discovered in yeast, and then in humans. TOR is found in two very different proteins, TORC1 and TORC2. Researchers from UNIGE, the University of Auckland, New Zealand, and the École Polytechnique Fédérale de Lausanne (EPFL) collaborated to understand how the nutrient regulates the activity of TROC1. The researchers were able to reveal the appearance of a new TORC1 structure in cells. When the cells lack glucose, the TORC1 assemble together forming a tubular structure. The tubular structure which is the TOROID, stores inactive TORC1 and stops cell growth. Another study done by National Centre of Competence in Research (NCCR) showed that the re-addition of glucose causes the TORIDS or the tubular structure to rapidly dissemble. NCCR has done the testing in yeast. The assembly and disassembly of the TOROIDS will make it possible to search for compounds that can stabilize and destabilize the cells. This article was very interesting to me  because it could lead to curing cancer. If the cancer cells could be stopped from growing, millions of lives would be saved. Its amazing to see how modern technology can change cells from being able to grow. This research could open up new approaches to treat many diseases and change the world for ever. 


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4196627/

https://www.cancer.gov/publications/dictionaries/cancer-drug?cdrid=733685

Promotion of Apoptosis in Cancer Cells

Healthy cells have an even balance of apoptosis promoter proteins and anti-apoptosis promoter proteins. However, damaged cells usually possess a higher ratio of apoptosis promoting proteins. This allows for the destruction and degradation of cells that are not functioning properly. Unfortunately, cancer cells do not work this way. The genetic alterations found in cancer cells show an increased production in anti-apoptotic proteins. The result is a damaged cell that is virtually invincible and will continue to divide and produce more identical cells that are damaged. As stated in the article, there are six known anti-apoptotic proteins. The main anti-apoptotic proteins found in cancer are Bcl-1, Bcl-2, and Mcl-1. Currently, cancer treatments include, chemotherapy, radiation, and immuno-therapy. These treatments promote the toxin NOXA in cells, specifically cancer cells, and promote apoptosis of the cell. However, the anti-apoptotic proteins oppose the effects of the toxin and allow the cell to survive. This is observed in patients with chronic lymphocytic leukemia who show resistance to chemotherapy.

            Based on the results of a study conducted at University of California Riverside scientists should focus on the Bfl-1 protein. This protein is more abundant in humans particularly. According to Maurizio Pellecchia, this protein is the main protein in humans and not Mcl-1. Mcl-1 predominates in mice.

            This article is very interesting because if scientists can figure out a way to completely inhibit the anti-apoptotic proteins in cancer cells it would be a great treatment. The cancer cells would have no choice but to self-destruct. Furthermore, the healthy cells would be unaffected by the cancer treatments. Other forms of cancer treatment, such as chemotherapy and radiation, destroy healthy cells as well as cancer cells. When cancer cells are targeted, the healthy cells will be unchanged.

 

The Difference Between Cancer Mutation Patterns in Smokers and in Non-Smokers

     Gene mutations in any organism can have several causes. Smoking, however, has been known to increase the risk of around 17 cancers, including lung cancer, bladder cancer, kidney cancer, and many more. Tobacco smoke is a complex mixture of chemicals, at least 60 of which are carcinogens. A new analysis shows that DNA in cancerous tissues of smokers are different from those in cancerous tissues of non-smokers. Cancer geneticist Ludmil Alexandrov and his international research team conducted an experiment in which they analyzed and examined mutational signatures and DNA methylation in DNA extracted from 5000 genome sequences, half of which were from smokers. What showed the increase in cancer risks in smokers were the mutational signatures 2,4,5,13, and 16. 

    
  
     Signature 4 mutation signals damage to guanine and it appears in DNA of cells which were exposed to chemicals from burnt products, such as tar in cigarette smoke. This signature was found in non-smokers' tumors, but less often. Smokers with lung squamous cancer, lung adenocarcinoma and larynx cancers had high numbers of signature 4 mutations, while cancers of oral cavity, pharynx, and esophagus had much less signature 4 mutations. Even though the reason why these tissues didn't have as much signature 4 mutations, despite being the most directly exposed to smoke, is unclear, the team speculates that these tissues might metabolize smoke differently.

     Another difference observed between the smoker's damaged DNA and that of non-smokers was the presence of signature 5 mutations. This signature normally shows up in all cancer types but its cause is still unknown. However, it is known that it increases with age and the analysis revealed that the more a person smoked, the more signature 5 mutations were present. Smokers with lung adenocarcinoma also appeared to have more signature 2 and 13 than non-smokers with the same disease. These could have resulted from overactive DNA editing machinery. However they are found in many types cancer and it's still unclear how smoking influenced the increase in these signatures. Signature 16 has only been found in liver cancer tumors, but it was in a higher number in smokers' damaged DNA than in those of non-smokers. It's correlation to smoking is also unknown.

     The researchers took into account the pack years smoked (1 pack year = one pack of cigarettes per day per year) and found a positive correlation between pack years and the number of mutational signatures. This information helped them calculate the mutations caused by smoking for each cancer type in the tumors they researched. The results were that one pack year leads to 150 mutations in a lung cell, 97 in a larynx cell, 39 in the pharynx cell, 23 in the oral cavity cell, 18 in the bladder cell, and 6 in a liver cell.

     I think that this information is very important for the public, so that it can bring better awareness to how harmful smoking is and how important it is to help treat people with smoking addictions. I hope that more answers can be found about how the signatures mentioned in the previous paragraph cause cancer and what the correlation between these mutations and smoking is, because this information can also help identifying the causes of other cancers due to these mutations.

Links:

• https://www.sciencenews.org/article/cancer-mutation-patterns-differ-smokers-nonsmokers

• http://science.sciencemag.org/content/354/6312/618.full

Pathways to smoking behaviours: biological insights from the Tobacco and Genetics Consortium meta-analysis

Pathways to smoking behaviours: biological insights from the Tobacco and Genetics Consortium meta-analysis




          By running gene and pathway analyses for several smoking behaviors in the Tobacco and Genetics Consortium (TAG) sample of 74 053 individuals, 21 genes and several chains of biological pathways were implicated. Analyses were carried out using the HYbrid Set-based Test (HYST) as implemented in the Knowledge-based mining system for Genome-wide Genetic studies software. Fifteen genes are novel and were not detected with the single nucleotide polymorphism-based approach in the original TAG analysis. For quantity smoked, 14 genes passed the false discovery rate of 0.05 (corrected for multiple testing), with the top association signal located at the IREB2 gene (P=1.57E-37). Three genomic loci were significantly associated with ever smoked. The top signal is located at the non-coding antisense RNA transcript BDNF-AS (P=6.25E-07) on 11p14. The SLC25A21 gene (P=2.09E-08) yielded the top association signal in the analysis of smoking cessation. The 19q13 noncoding RNA locus exceeded the genome-wide significance in the analysis of age at initiation (P=1.33E-06). Pathways belonging to the Neuronal system pathways, harboring the nicotinic acetylcholine receptor genes expressing the α (CHRNA 1-9), β (CHRNB 1-4), γ, δ and ε sub-units, yielded the smallest P-values in the pathway analysis of the quantity smoked (lowest P=4.90E-42). Additionally, pathways belonging to ‘a subway map of cancer pathways’ regulating the cell cycle, mitotic DNA replication, axon growth and synaptic plasticity were found significantly enriched for genetic variants in ever smokers relative to never smokers (lowest P=1.61E-07).
          This article was interesting to me because it was relating genes to smoking and to cancer. It talked about genes in smokes versus non-smokers and how smoking can lead to cancer. It was very cool to find out the genomic loci were associated with people who smoked.

A Single Cell that Lead to the Understanding of Cancer

Here is an interesting article about a study that was done on fish. This article helps in understanding Melanoma cancer.

   A study was conducted in fish to understand melanoma. Melanoma is a form of deadliest skin cancer. It was not a cancer cell yet and its state was surprising. Instead of developing into an ordinary cell type, the cell turned to an embryonic state. Cancer genes appeared and a massive tumor developed as it began to divide. Human genes were given to fish and found the same result as in human. Researchers have said further study needs to be done to understand the formation of melanomas and other forms of cancer. This method will help to generate a way to prevent melanomas from growing back after they have been cut down by new targeted drugs.

Gene in Elephants Reduces the Chance of Cancer

In recent studies, scientists have finally discovered a possible gene that allows the prevention of cancer in elephants. This could mean potentially a gene to prevent cancer in humans.

Elephants are noticeably larger than humans, which means they have thousands of more cells than us allowing for the potential to have cancer to be increased, however, they live about as long as humans if not longer and few get cancer. After a sample of elephants across zoos in america were studied, it was found that only about 5% of elephants had cancer as compared to 11%-15% of humans get cancer. Two teams of scientists have taken this information even further and discovered that in observing and researching elephant genes, a gene mutation is what is suppressing the cancer cell. Two types of elephants observed (African and Asian) and both species had 20 copies of the P53 gene (this gene is known to have tumor-suppressing qualities), where as humans and smaller species only have one copy of the P53 gene.

This discovery does not allow for the cancer to be treated or allow for much discovery just yet, however the more they research the P53 gene the more they are finding out about how it relates to the suppressing of cancer and tumors. Some doctors already have been studying the P53 gene and have been using it in immunotherapy treatments to fight cancer. It will be a long time before this research is useful clinically for patients however baby steps will lead us in the right direction in hopes for a cure to cancer.

Link to article:
http://www.popsci.com/this-gene-prevents-elephants-from-getting-cancer

Link to supporting article:
http://www.popsci.com/this-gene-prevents-elephants-from-getting-cancer

Trying to fool cancer

This year, scientists have been attempting to create a medication that will ultimately “fool” cancer cells. It is considered precision medicine and it uses “cancer’s molecular underpinnings to develop drugs that attack the genes or gene products that make up cancer’s factory while sparing normal cells.” There have been many experiments conducted in hopes of finding a way to cure cancer, once and for all.

            The first study is done on 600 patients with one of two bone marrow cancers, myelodysplastic syndromes or acute myeloid leukemia at the Cleveland Clinic.  These cancers are most commonly found in people age 70 to 80 and can be fatal if left untreated.  These cancers cause cells to outgrow and form a mass of cells or remain immature making it nearly impossible to function normally.  Majority of the patients tested developed an average of 10 genetic mutations before the cancers were diagnosed.  The fact that so many mutations were present makes treating cancer that much harder.  There is no medication available to treat that many mutations and only treating a few of them would help the rest of them thrive allowing the treated cancer to regrow.

The next step in this research is to determine where the mutations start and which one they start with. But it is possible that these starter mutations are found in both cancerous and noncancerous cells so attempting to kill them could wreak havoc within the patients.  A drug was administered to patients that would hopefully improve their blood count and attack the mutations in cancerous cells.  But for some patients, the mutation had nothing to do with causing the cancer.  Despite everything, the road to curing cancer has had massive improvements but nothing is curative.  And although many new forms of treatment have come into play, the older techniques are not a thing of the past.

Cancer has always been a topic of interest for me just because of how unpredictable it is.  It is a brilliant idea that scientists and researchers are continuing to try to find new ways to treat cancer in hopes of one day curing it for good.  Chemotherapy and modern medicine are good cancer treatments but they do not always work so the continued research for a drug that could pinpoint the mutations and destroy them at the source could only help pave the way to a cancer free world.

DNA Nanobots that Kill Cancer Cells Scheduled for Human Trials.

Researchers at Bar-llan University in Israel developed tiny nano-robots made entirely of molecular DNA that search for and destroy cancer cells, while leaving healthy cells unharmed. This process has also been called "DNA origami" instead of "DNA nanobots."  While the research has, so far, only been performed on cell cultures and live animals (cockroaches, to name one), their hopes now turn to perform the research on a living person. Head researcher, Dr. Ido Bachelet, described the design of the nanobots back in 2012. At that time, the nanobots recognized at least 12 different types of cancer and had the ability to detect when a diabetic needed insulin. About one year ago, the nanobots were revamped and injected into live cockroaches with promising results. The first human test will be performed on a terminally ill leukemia patient with only a few months left to live. The research team is hopeful the cancer will be irradicated within one month.

The design of the nanobots is such that it won't incite an immune response. They were modeled after the body's natural immune system. The nanobots patrol the blood stream, much like white blood cells, and immediately report to any signs of distress. Since DNA is biodegradeable and biocompatible, it will eventually break down and avoid a foreign body immune response. The older version, from the 2012 Science magazine description, is shaped like a hexagonal tube with a latched hinge. When a targeted cell is recognized, the latch swings open (like Pac-Man) and deliver deadly drugs or nanoparticles to the targeted cell. The nanoparticles (mostly) cause the cancer cells to self-destruct. The newly revamped version, published in Nature magazine and practiced on cockroaches, resemble boxes with lids. These "boxes" were created using DNA strands, and inside the "box" were molecules that contained hemolymphs.

A photo of the first version of the nanobots from 2012.

Dr. Bachelet has huge visions and hopes for his nanobots. In the future, he wishes to treat just about any disease process, as well as perform cellular level surgeries, such as repairing spinal injuries via nerve cells.

The revamped version of the nanorobots injected into cockroaches.

This is revolutionary in the nanotechnology world. While nanotechnology has existed since the 1980's, there has yet to be such a medical wonder. However, there are some risks associated with this process in human beings. Some cancers actually invade an entire organ, rather than just floating around in the bloodstream or existing on the epithelial tissue. If these nanobots are programmed to take out the cancer cells, they could (theoretically) destroy an entire organ in the process. If the nanobots are so rapid at destroying a slowly developing cancer, they could wipe out a substantial amount of an organ before it has time to repair itself. If the nanobots are to be successful, their destruction rate of cancer tissue should be equal with the regeneration rate of healthy tissue.

Another concern I have is that this technology can be used, if in the wrong hands, to destroy healthy cells. There are plenty of terrorist organizations in this world that are leaning more and more towards bio-terrorism. Rather than a widespread poison, like anthrax or cyanide, these little nanobots could easily make their way into human bodies and destroy an entire country, if not more. Perhaps not by means of injection, but ingestion or inhalation. It's worrisome and scary, but it is always a possibility that things created for the good of humanity can be altered for the evil.


Original Article: Can DNA Nanobots Successfully Treat Cancer Patients? First Human Trial Soon

Olive Oil: The key to curing cancer?

Extra Virgin Olive Oil has been long known for its health benefits. But now it has been discovered for its rapid destruction of cancer cells. Although scientists had proven the benefits of the compound Oleocanthal found in Extra Virgin Olive Oil and its aid in causing cell death in cancer cells before, they didn’t have an explanation to it until now. 

According to the article posted on Science Daily, Paul Breslin, David Foster, and Onica LeGendre performed a study that led them to this discovery. The researchers discovered that the key to understanding the toxic effect of Oleocantha in cancerous cells lies in its reaction with the lysosome of the cell. The lysosome is where the cells store its waste. The Oleocanthal compound is found to rupture the cancer cell lysosomes causing cell death within thirty minutes to an hour while leaving uncancerous cells unharmed. From this, the researchers came to the conclusion that the lysosomal membrane of cancerous cells are weaker than uncancerous cells.This discovery is an ideal option for treatment for cancer patients. It is a less harmful treatment as opposed to the other treatments available due to their side effects. 

Cancer copies how healthy cells move to invade organs

In order to invade different parts of the body, cancer cells switch between modes of moving. They do this by copying the movement of healthy cells.  Depending on the tissue the cancer cells encounter, they need to move in different ways. Invasive cancers have learned both methods of movement and switch between them to suit their environment. Scientists say that being able to switch is likely to be the most important factor in making a cancer cell dangerous. In order to find out how the cells do this,scientists studied cells moving in the egg sac of fruit flies and tweaked the fly genes, altering the proteins they create. This allowed them to work out which proteins are important for movement. Next, they searched to see if any of those they identified also go awry in cancer, hitting upon a bundle called the STRIPAK complex. In many cancers, the gene that codes for these proteins is mutated.

Scientists have uncovered what could be a "cornerstone" of cancer's invasive behavior. "Whilst still far removed from a direct application at the bedside, this study opens new doors for therapeutic developments that could be applicable to a broad range of solid cancers,"

I find it interesting that the cancer cells almost have some kind of strategy in order to invade the body efficiently. This is a good lead in the study of cancer because it could help scientists to more  understand cancer cells and how they work. 

Article link:

http://www.newscientist.com/article/dn26755-cancer-copies-how-healthy-cells-move-to-invade-organs.html#.VNebL1ovEUU

A Way to Outsmart Cancer that is Outsmarting Us?

A recent study at Dartmouth-Hitchcock's Norris Cotton Cancer Center has shown a certain form of breast cancer developing its own resistance to anti-cancer therapies. The ERBB2 gene (also known as HER2) is a human epidermal growth factor receptor that if mutated, leads to different forms of cancer (lung, gastrointestinal, testicular, etc.), but most commonly, the most aggressive forms of breast cancer. 25% of all forms of breast cancer rely on ERBB2 to proliferate and survive. It is currently the focus of 30% of all breast cancer studies due to it being associated with recurrence and poor prognosis.

A pie chart of ERBB2 cancers as described by Gary A. Palmer, MD, JD, MBA MPH at the American Society of Clinical Oncology.

ERBB2 positive breast cancer cells are developing resistance to anti-ERBB2 drugs after one or two rounds of treatment. The researchers at the Norris Cotton Cancer Center have so far showed that ERBB4 (also known as HER4) may be beneficial to breaking through the ERBB2 forms of cancer. Once the ERBB2 positive breast cancers go through treatment, they turn to and rely on ERBB4 for survival. Using the ERBB4 protein, researchers can develop a new line of cancer treatment to perform after the failed rounds of ERBB2 targeted therapy. This new method is called a cancer driver, which includes targeted therapies and less side effects than chemotherapy (yay!!)

We still have a long road ahead of us in cancer research and treatment development, but we have already made great strides. Knowing how things evolve through time, it is no surprise to me that cancer cells are evolving to survive anti-cancer therapies that are still relatively new to human medicine. If this cancer driver really succeeds, it can potentially open several doors to new and effective cancer treatments and maybe one day, a cure.

Original Article: Receptor tyrosine kinase ERBB4 mediates acquired resistance to ERBB2 inhibitors in breast cancer cells

Survival of the Fittest Cell

Survival of the fittest doesn’t only happen in the wild. It also happens in the body. When people think of apoptosis, many think of a cell that is sick or damaged that must be removal. However, it has been discovered that if there are weak cells surrounded by healthier cells, these weak cells will be killed off. This is a problem when the stronger cells are cancer cells. Molecular biologists from University of Zurich and University of Columbia have been the first to publish that the only way for this process to happen is when one has an innate immune system.

The biologists proved their theory with an experiment with fruit flies. They saw that apoptosis was induced by “Spätzle”, which is a signaling protein that binds to the Toll-related receptors. This was known information, however; before this experiment, it was thought that this protein only reacted to the presence of foreign bacteria and fungus. It is now known that it also responds to less fit cells. The only part the team is not sure about whether it is the weak cell that triggers the binding or the stronger cells around it. As Professor Konrad Basler says, “We still don’t know whether this involves the voluntary or forced suicide of the less-fit cells.”

While this may sound like a good thing. Weaker cells are being conquered by healthier, stronger cells who are in better shape to do the work it needs to. However, what happens when the stronger cells are not good cells. This cell activity is often found in cancerous tissue. This raises big problems. However, it gives bigger hope to cancer research. Scientists hope that this discovery might lead to early detection of the disease, possibly before the cells are even malignant.

http://www.sciencedaily.com/releases/2014/12/141204140648.htm

Selenium Compounds found in Broccoli and Garlic can help stop Cancer

Since cancers such as melanoma and prostate cancer and other certain types of leukemia weaken the body by over-activating the natural immune system, researchers from the University of Copenhagen have found that a compound in garlic and broccoli may improve cancer treatment long term. Selenium is naturally found in garlic and broccoli and the research has shown that it can slow down the immune over-response. The immune system is responsible for removing things not recognized by the body, like cancer cells. However, different cancer cells are able to block the immune system’s ability to recognize them, which allows them to continue to infect the cells and the body with cancer.

When cancer cells are over-stimulated and overexpress immunostimulatory, the impact on the body is extremely negative. When the molecules over-activate the immune system it collapses. Therefore, the research has shown that the selenium compound is able to block the immunostimulatory molecule that is involved in many aggressive cancers.

The researchers have focused on NGK2D ligands which has eight variants but the researchers have focused on one that assumes a liquid form. This molecular dissolution causes serirous problems once the cancer is raging inside the human body. It is found not only on the surface of the cancer cells, but it also dissolves into the bloodstream of the affected person. However, the selenium compounds are able to neutralize the special variant of the NGK2D ligand within both forms. This is a small step in creating new and better cancer drugs for the future.

I chose this article because I love broccoli and garlic and I was curious on how they can help prevent cancer. I found this to be very interesting and I hope they continue to do research on this to eventually find a way to cure cancer forever!

This Article: Selenium compounds boost immune system to fight against cancer

Wider Genetic Screening for Breast Cancer

The prominent scientist and geneticist, Marie-Claire King, who identified the first breast cancer gene is now urging all women to be tested for the genetic mutations that can lead to breast cancer. Her and her colleagues believe that no matter the woman’s personal or family history, that she be offered genetic testing for those mutated genes.

 For the most part, doctors will only recommend women to be tested for the breast cancer genes, BRCA1 and BRCA2, if cancer runs in their families. However, it has been found that around fifty percent of women who carry mutations in their BRCA1 and BRCA2 genes have no family history of breast or ovarian cancer. Marie-Claire King, along with her fellow colleagues, conducted a study that found that over 400 women that had no family history of this mutation, but carried it themselves, had the same high risk of getting breast cancer from the mutated genes. For this reason, King feels strongly that it is time for all women to be screened.

Opposers, however, state that some women that have these mutations never actually end up getting breast cancer and that the very serious surgeries that go along with the removal of the mutations can do more harm than good. Still, I completely agree with King. I think that all women should get tested for these genetic mutations because the worst thing it can do is make you aware of something that can be very dangerous if not treated. The decision as to what the women want to do with the information is completely in their hands. If they decide to get a mastectomy or not, at least they are aware of what is going on inside their body. With the information offered by the wider genetic screening for breast cancer, women can make decisions that can ultimately prolong and better their overall quality of life.

Article Link: http://www.npr.org/blogs/health/2014/09/08/346770167/researcher-urges-wider-genetic-screening-for-breast-cancer