Wednesday, April 18, 2012
Is Your Sunscreen Toxic?
Who Says Herpes Is All Bad
Cancer Prevention Drug?
We know that our immune system regularly find and destroys abnormally functioning cells. However, every now and then cancer cells are somehow able to avoid detection. Using TGF-b, could we enhance our immune system as part of a preventative drug treatment against cancer?
Tuesday, April 17, 2012
Genetic Testing For Hereditary Cancer!
Monday, April 16, 2012
Sunday, April 15, 2012
cancer project - H pylori tumor
Controversy in prenatal testing for breast cancer
After reading this article, do you think prenatal genetic testing for mutations in BRCA1 or BRCA2 should be conducted? Do you think it should be circumstantial - for example, should testing only be conducted if there is a family history for breast or ovarian cancer? Lastly, if you believe that prenatal genetic testing should be conducted, do you think that a positive result (there is a mutation in the BRCA1 or BRCA2 gene) is a valid reason to have an abortion?
Diabetes Being Linked to Pancreatic Cancer
| Image above: Stained mouse Pancreatic cells. The cells dyed red are ductal pancreatic cells infected with cancer. |
ALL
For the Cancer Project, Anshuman and I are focusing on Acute Lymphocytic Leukemia in children. We are going to be researching the top three drugs that treat ALL and examine their mechanisms at the cellular level, why they are so successful, etc.
Opioids and Tumor Progression
I recently read an academic paper titled "The u-Opioid Receptor in Cancer Progression: Is There a Direct Effect?". This paper, which was recently published in Anesthesiology, discusses the relationship between opioids and cancer recurrence and metastasis. Epidemiological studies indicate a lower recurrence of cancer in patients who received local anesthesia rather than opioids for pain management. My partner and I are focusing on the possible reasons behind the recurrence of cancer, so I found this article very relevant. Before going into detail about the direct effects of u-opioids (opioids that are associated with the u-receptor), the authors discuss the observed indirect effects of opioids and other anesthetic drugs. For example, anesthetic drugs may suppress the activity of NK (natural killer) cells, which are vital to a functioning immune system's defense against tumor cells.
Saturday, April 14, 2012
Project Topic
For our project, Amanda and I are focusing on skin cancer. Our project aims to examine the effects of UV exposure of skin types in three groups of people that have different amounts of exposure to UV light. The first group are those who voluntarily expose themselves to UV rays through UV rays or excess tanning. The second group are those who involuntarily expose themselves to UV rays most likely through their work or environment. The third group are those who have very little or no exposure to UV light because of work or location. In our research we hope to compare the rates of skin cancer in these three groups of exposure. Also, we hope to analyze the varying expression of melanin-producing genes (that give skin color) in the basal layer of the skin in order to determine if different skin types can lead to higher rates of melanoma.
Friday, April 13, 2012
New Cancer Treatments
CBS News. New cancer treatment reprograms immune system - CBS News. 2011. Video. Youtube.comWeb. 13 Apr 2012. < http://www.youtube.com/watch?v=-cR6ZCtYo_s>.
This was a news story from CBS News that originally aired on August 10th 2011. It is another example of new ideas turning into new treatments. Dr. Carl June’s team recently succeeded in treating three patients who were diagnosed with incurable Chronic Lymphocytic leukemia (CLL). One of the only treatments of Chronic Lymphocytic Leukemia is a bone marrow transplant that is not only dangerous but only 50% effective.
With the new treatment Dr. Carl’s team was able to take the patient’s own blood, remove some of the T-cells and genetically modify them to attack the CLL cells. With only one infusion the patients had noticeable changes with two patients having their tumors completely absent six months later. This is a remarkable treatment that when developed completely could be used to cure all types of not only cancer but other ailments facing the human population.
Although this study showed great signs of success with all patients surviving, having such a small experimental group makes the data questionable. The efficacy of the treatment needs to be done on a much larger scale before it can be considered ready for mass use, but the fact that these new ideas and treatments are still coming out is promising.
Works Consulted
LaPook, Jonathan. "New cancer treatment reprograms immune system." CBS News. 10 08 2011: n. page. Web. 13 Apr. 2012. < http://www.cbsnews.com/stories/2011/08/10/eveningnews/main20090911.shtml>.
Thursday, April 12, 2012
Research Proposal
So Chris Clark and I are doing a project on the evolutionary aspect of cancer and the various drugs that have recently been developed to target this very aspect of the disease (benign cell boosters, for example). This article http://www.sciencedaily.com/releases/2006/11/061117114616.htm provides an interesting discussion of this topic. Here is a brief summary of the article:
Many of the dynamics of evolution (such as natural selection) apply to the environment of a tumor as much as they apply to other traditional topics in evolutionary biology. A population of cancer cells in a tumor can be likened to any population of organisms in which natural selection takes place. Within a population of cancer cells, there is heritable variation (there are a variety of different genetic mutants all of which can divide and pass on their exact mutations to daughter cells) and this variation affects the survivability of each cancer cell (fitness).
Looking at cancer through the lens of an evolutionary biologist has shed light on the therapeutic resistance of cancer and brought about a new array of possible treatments for the disease. As Carlo C. Maley, Ph.D., an assistant professor in the Molecular and Cellular Oncogenesis Program at The Wistar Institute, says, "When you apply chemotherapy to a population of tumor cells, you're quite likely to have a resistant mutant somewhere in that population of billions or even trillions of cells. This is the central problem in oncology. The reason we haven't been able to cure cancer is that we're selecting for resistant tumor cells. When we spray a field with pesticide, we select for resistant pests. It's the same idea." The central idea, or goal, is then to influence the fitness of cancer cells.
One example of a treatment is benign cell boosters, which target benign cells and increase their relative fitness with respect to more malignant cells. As these benign cells outcompete other malignant cancer cells, the tumor would become much less aggressive and dangerous.
One aspect that this article does not mention is the fact that evolution in cancer cells may take anywhere from a few months or years, unlike in the evolution of a new species where it may take thousands of years for evolution to take place.
Reference/citation: The Wistar Institute. "Does Natural Selection Drive The Evolution Of Cancer?." ScienceDaily, 17 Nov. 2006. Web. 12 Apr. 2012.
New Mechanism discovered in Colon Cancer Development
I don't know how many of you are interested in Colon Cancer or doing active research on this type of cancer, but I found an interesting article that details a novel way in which this deadly cancer develops. The research that that the scientists at Case Western Reserve University School of Medicine carried out, found that the "junk DNA" actually act as a set of master switches that enable or disable transcription in the DNA. In the study, these master switches are called Variant Enhancer Loci or VELs since these loci have the ability to "enhance" the DNA by transcribing it or not, depending on whether it is turned on or off. Similar to the methylation process that enables or disables transcription in a particular area of DNA, the researchers found that colon cancer actually has an unique genetic signature whereby certain regions of the DNA are deliberately changed. The key to this discovery is that these changes are reversible since these are epigenetic changes, again similar to methylation. As Sanford Markowitz, a member of the research team notes "The VELs signature is notable because it cuts through the complexity of the many genes that are changed in colon cancer, to identify genes that are direct targets of alterations on chromosomes."
Anyway guys, take a looks at study if you are interested - it is nicely summarized at the following link.
Also below, you will find a citation for the actual journal article that goes into more detail about the research study.
Article Link: http://www.sciencedaily.com/releases/2012/04/120412141813.htm
Research/Paper citation:
Batool Akhtar-Zaidi, Richard Cowper-Sal·lari, Olivia Corradin, Alina Saiakhova, Cynthia F. Bartels, Dheepa Balasubramanian, Lois Myeroff, James Lutterbaugh, Awad Jarrar, Matthew F. Kalady, Joseph Willis, Jason H. Moore, Paul J. Tesar, Thomas Laframboise, Sanford Markowitz, Mathieu Lupien, Peter C. Scacheri. Epigenomic enhancer profiling defines a signature of colon cancer. Science, April 12, 2012.
Wednesday, April 11, 2012
Topic for Cancer Project
Aptamers and Potential Drug Therapies
I've learned some about aptamers and their characteristically high affinity and selectivity for their target molecules. For a brief overview, aptamers are single stranded DNA or RNA molecules (usually DNA) that can be selected for using SELEX (Systematic Evolution of Ligands by Exponential Enrichment). This process requires no previous knowledge of the DNA library and essentially allows for the selection of DNA molecules that bind to specific target molecules (i.e. certain glycoforms). To fast forward a bit, the implications of this technology is that cancer therapy may one day be able to target only cancerous cells thereby eliminating most of the negative side effects that are attributed to chemotherapy.
Needless to say, I found this type of research not only intriguing on the conceptual level--but also promising to the therapeutic research community. Attached is a paper about some of the research by Dr. Weihong Tan, a professor at the University of Florida, who has studied aptamers and possible drug uses.
In recent years targeted drug delivery has been attempted by drug-conjugate combinations. "However, when multiple functionalities are involved, the fabrication of the conjugates becomes correspondingly complicated and can compromise the efficacy of these drug candidates" (Yang, et. al). Some of the issues that drug delivery encounters are decreased drug toxicity and resistance. The paper describes how aptamer-conjugates can act as the driving force behind the treatment modality of cellular disruption. Cellular disruption is the process of releasing drugs from inside a cell--one way of "out-smarting" drug resistant cells. Tan's research group has developed polymeric aptamer conjugates that show selective cytotoxicity for cancerous cells. The aptamer conjugates decrease their target cell activity by more than 50%. Overall, the aptamer conjugates target certain (cancerous) cells and display cytotoxicity only after they are internalized by the cell (the aptamer-drug conjugate is essentially harmless to normal cells).
Attached is a link to the scientific paper. Engineering Polymeric Aptamers for Selective Cytotoxicity (Yang et. al.)
Here is a video to help illustrate the aptamer selection process termed SELEX. I would imagine this video is the product of nerds with too much free time (...they probably go to Stanford.)
origin of chronic lymphatic leukemia
I noticed that a few people mentioned that they were interested in leukemia and I read an article this morning about a recent study at the Medical University of Vienna where a lead to the origin of chronic lymphatic leukemia was discovered. I couldn't get access to the original journal article because you need to be a member of the journal page, but I'm adding the abstract as well as a link to the Science Daily article below.
Maybe this could be helpful if your project is on leukemia.
The origin of chronic lymphatic leukaemia: lead discovered
For approximately 20 years it has been suspected that chronic lymphatic leukaemia occurs through the stimulation of B cells with other factors also playing a part. In the current research study, which has been published in the journal "Blood", the scientists were looking for an antigen that attaches itself to the leukaemia cell receptors and they were able to identify the protein pUL32 of the human cytomegalovirus.
Virus "conceals" itself in cells
The cytomegalovirus, a member of the herpes family of viruses, is carried by approximately 60 to 70 percent of the Austrian population without them getting ill from it and without them even noticing that they are carrying the virus. In most cases people are infected with the virus during childhood. After being infected, the virus goes on to survive in the cells of the immune system their whole life long. The virus conceals itself within the cells and in addition it confuses the immune system with its own chemical messengers.
Only when the immune system in an infected person is weakened, for example by medical suppression as part of an organ transplant or in an HIV-illness, can the virus make someone ill. Whether this virus infection can trigger leukaemia, or whether the connection observed between leukaemia and the cytomegalovirus points to another mechanism, independent of the virus, in the origin of the cancer is now the subject of several follow-up studies.
One of the follow-up studies is looking at whether an antiviral treatment against the cytomegalovirus can prevent the leukaemia cells from being stimulated and so prevent the further advance of the disease.
http://www.meduniwien.ac.at/homepage/news-and-topstories/en/?tx_ttnews[tt_news]=1996&cHash=f33d83990c
Link to Science Daily Article
http://www.sciencedaily.com/releases/2012/04/120411084040.htm
Meat and Cancer
We also talked about whether or not the significance of health risks associated with red meat is the same with other meats such as chicken and seafood. A Harvard study (documenting 23,926 deaths) released this year showed, "One daily serving of unprocessed red meat (about the size of a deck of cards) was associated with a 13% increased risk of mortality, and one daily serving of processed red meat (one hot dog or two slices of bacon) was associated with a 20% increased risk." However, "Replacing one serving of total red meat with one serving of a healthy protein source was associated with a lower mortality risk: 7% for fish, 14% for poultry."
I am not sure if anyone is doing their cancer project on environment/food and cancer but both of these studies show that meat consumption leads to a variety of cancers. I would also note the amount of PAH's given to animals in the experiments and compare that with how much meat/what type of meat the average person is consuming and the concentration of PAH's in it because it may be cancer-causing in much higher amounts than what people actually consume.
Monday, April 9, 2012
CD47 Antibody: A Promising Breakthrough
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| Irving Weissman (8) |
Sunday, April 8, 2012
Cancer Project
Saturday, April 7, 2012
Cancer Project Topic
Friday, April 6, 2012
Cancer Project Topic
(1)Research Interest - ALL in children
This is just one idea that I am brainstorming at the moment. If you are interested, feel free to comment back on this thread.
Research Interests
Interests
My name is Nhunguyen and I am interested in the question below:
Why do certain mutational events promote cancer phenotypes in some tissues and not in others?
Obviously, this is a pretty large topic so I am going to research a bit to narrow it down.
Thursday, April 5, 2012
Cancer Project - ALL
Research Topic
research topics
Hi Everybody!
I'm very interested in skin cancer, particularly melanoma and carcinoma. My initial project idea is to compare the emergence of either melanoma and carcinoma depending on skin color. Let me know if you have any suggestions.
:D
My First Post!
Wednesday, April 4, 2012
Cancer Project
Research Topic
Cancer Defense
My First Post
This is my first post
This is my first post
Cancer Project topic!
My First Post
This is my first post
Post Post Post Post.....
My name is Mary Helen.
I am actually torn between two topic ideas and I was wondering if you all could give me some feedback/opinions...
topic 1: Why do certain mutational events promote cancer phenotype in some tissues but not others? When a cancer metastisizes, why doesn't it spread directly out from the source?
As an example, lung cancer metasitisizes to the brain but not the breasts in some cases, but why? The breast tissue is physically closer to the lung tissue, so why does the cancer present itself in the brain first?
topic 2: Why do second idependent cancer occur at higher rates in patients who have survived a primary cancer than in a population of those without previous cancer history? What is the rate of recurrance in those who have previously survived? Is it the same cancer returning? Different cancer?
Monday, April 2, 2012
Welcome to Bio 179 Cancer Biology for 2012!
Dr. Islas
Sunday, July 3, 2011
Eternal life?
http://io9.com/5817312/a-tumor-that-could-provide-the-key-to-making-zombies




