The run time for our grid was 79 days, 3 hours, 14 minutes and 46 seconds as of May 1st, about 8:30 am. The total points generated was 96,557 and the results returned were 169.
The link to all of the statistics for this project is https://secure.worldcommunitygrid.org/ms/viewMyMemberPage.do
Friday, May 1, 2009
Friday, April 24, 2009
Evolutionary Analysis of Colon Cancer
1. What is the estimate of h squared?
Many different sources, including the Encyclopedia of Health and Behavior, the heritability of colon cancer is about 35%.
2. How much influence does selection have on this trait?
A tumor cell population will continue to evolve as a result of the mechanisms of natural selection. As an example, when chemotherapy is used, the resistant tumor cells are being selected for. Three very important conditions necessary for natural selection are obvious in the progression of cancer:
1. First and foremost, there must be variation in the population. Tumor cells are a blend of diverse genetic mutations.
2. Secondly, heritability of the variation must be at work in the population. When tumor cells divide, their daughter cells contain the same genetic mutations as the parent cells.
3. Finally, variation has to affect fitness.
a. High fitness is easily achieved fore tumor cells since they are capable of growing and dviding beyond normal, healthy growth potential.
b. These tumor cells no longer need outside signals to divide.
c. With the ability to suppress the internal mechanisms for self-destruction when genetic mutations have overcome the cell, they are capable of proliferation.
Science Daily: Does Natural Selection Drive the Evolution of Cancer
http://www.sciencedaily.com/releases/2006/11/061117114616.htm
3. What effect would inbreeding have on this trait (cancer)?
Any time there is inbreeding in a population, the frequency of recessive phenotypes, sometimes deleterious phenotypes, increase. For this reason, inbreeding in a population with genetically caused colon cancer would increase the frequency of colon cancer seen in this population.
Thursday, March 26, 2009
Questions regarding p53 and cancer
Q 1: Because p53 and its related genes are transcription factors, meaning that they are regulatory genes whose products control the expression of other genes, changes in these genes have cascading consequences. Why is this?
A: By changing these genes, there is less protection from the development of cancer. The p53 protein is activated in order to stop the repair of damaged cells which could contain mutations. The protein helps to initiate apoptosis so that the damaged/mutated cells will die. If the p53 protein is altered or inactive, there is no restriction on abnormal cell growth. Thus, cancer development becomes very possible.
Q 2: In an evolutionary sense, why is it informative to study cancer and its implications in mice (see Lee and Bernstein, 1993 and Bourdon, 2007)?
A: Cancer development between humans and mice is quite similar. The p53 gene is orthologous in humans and mice, serving as a checkpoint during cell proliferation. The p53 gene commonly has mutations or "rearrangements." Since p53 is a tumor suppressor gene, then any mutations in it would cause cancer in both humans and in mice. Researchers use mice to test these assumptions, since the results are quite applicable to humans, and much easier to examine. The evolutionary effects of p53 alterations cause dramatic results for the mice, thus providing informative data for us to interpret.
Q 3: Bourdon discusses the sequence similarity in portions of p53, p63 and p73, and refers to them as a gene family. How do you think these genes arose? Are they paralogs or orthologs of one another? By what mechanism might they have gained new functions?
A: The p53, p63, and p73 gene family are paralogs of one another. This is because they are structurally the same, indicating a similar ancestral gene, but have diverged in function. This can happen through mechanisms like mutation and selection after gene duplication in a species. If an organism had a duplication, the gene would be free to mutate, leading to new genes within the species.
Q 4: In the Bourdon paper, the author discusses how changes in expression of the 9 different p53 isoforms (proteins) can cause “genome instability, cancer and other pathologies.” Why then is it important to study protein folding and mis-folding in these isoforms?
A: It is important to study protein folding and mis-folding in these proteins because by understanding them we can better develop treatments for cancer and other pathologies caused by changes in their expression. By studying their mis-folding, it will help us understand their role when they are correctly expressed. The p53 gene is mutated in 60% of cancers so understanding all of the isoforms will contribute to an understanding of p53 as a whole. A better understanding of the isoforms and their role in p53 expression could also bring us closer to cancer therapies because we may be able to further narrow down specifically which isoforms lead to incorrect folding or expression in the p53 gene.
Q 5: Typically, p53 is a “tumor-suppressor gene,” which indicates that if it loses function, tumors will result. However, expression of some of the isoforms of p53 can actually contribute to tumor formation. Further, not all mutations in p53 result in a loss of function. This makes it difficult to understand the clinical role of p53. Considering people like Debbie, why is it so vital to determine the status of p53 in each patient?
A: Determining the status of p53 in a patient is very important because it can reveal very important things about the patient. If there are mutations in p53, this patient may be resistant to radiation, which will be important in treatment. If p53 is completely missing, this could suggest a tumor’s cause to doctors. Also, since some of the p53 mutations and isoforms gain transcription abilities and others do not, this may be a clue to which are in a particular patient’s tumors. As mentioned in the Bourdon article, p53 affects a great deal of processes in the body, not just suppression of tumors. If p53 is mutated, there may be things to deal with as well as the cancer. This information will give the doctor a better idea of what he/she is dealing with. Even though the research is currently inconclusive about which p53s do exactly what, knowing what is going on within the body will help both doctors and future researchers.
A: By changing these genes, there is less protection from the development of cancer. The p53 protein is activated in order to stop the repair of damaged cells which could contain mutations. The protein helps to initiate apoptosis so that the damaged/mutated cells will die. If the p53 protein is altered or inactive, there is no restriction on abnormal cell growth. Thus, cancer development becomes very possible.
Q 2: In an evolutionary sense, why is it informative to study cancer and its implications in mice (see Lee and Bernstein, 1993 and Bourdon, 2007)?
A: Cancer development between humans and mice is quite similar. The p53 gene is orthologous in humans and mice, serving as a checkpoint during cell proliferation. The p53 gene commonly has mutations or "rearrangements." Since p53 is a tumor suppressor gene, then any mutations in it would cause cancer in both humans and in mice. Researchers use mice to test these assumptions, since the results are quite applicable to humans, and much easier to examine. The evolutionary effects of p53 alterations cause dramatic results for the mice, thus providing informative data for us to interpret.
Q 3: Bourdon discusses the sequence similarity in portions of p53, p63 and p73, and refers to them as a gene family. How do you think these genes arose? Are they paralogs or orthologs of one another? By what mechanism might they have gained new functions?
A: The p53, p63, and p73 gene family are paralogs of one another. This is because they are structurally the same, indicating a similar ancestral gene, but have diverged in function. This can happen through mechanisms like mutation and selection after gene duplication in a species. If an organism had a duplication, the gene would be free to mutate, leading to new genes within the species.
Q 4: In the Bourdon paper, the author discusses how changes in expression of the 9 different p53 isoforms (proteins) can cause “genome instability, cancer and other pathologies.” Why then is it important to study protein folding and mis-folding in these isoforms?
A: It is important to study protein folding and mis-folding in these proteins because by understanding them we can better develop treatments for cancer and other pathologies caused by changes in their expression. By studying their mis-folding, it will help us understand their role when they are correctly expressed. The p53 gene is mutated in 60% of cancers so understanding all of the isoforms will contribute to an understanding of p53 as a whole. A better understanding of the isoforms and their role in p53 expression could also bring us closer to cancer therapies because we may be able to further narrow down specifically which isoforms lead to incorrect folding or expression in the p53 gene.
Q 5: Typically, p53 is a “tumor-suppressor gene,” which indicates that if it loses function, tumors will result. However, expression of some of the isoforms of p53 can actually contribute to tumor formation. Further, not all mutations in p53 result in a loss of function. This makes it difficult to understand the clinical role of p53. Considering people like Debbie, why is it so vital to determine the status of p53 in each patient?
A: Determining the status of p53 in a patient is very important because it can reveal very important things about the patient. If there are mutations in p53, this patient may be resistant to radiation, which will be important in treatment. If p53 is completely missing, this could suggest a tumor’s cause to doctors. Also, since some of the p53 mutations and isoforms gain transcription abilities and others do not, this may be a clue to which are in a particular patient’s tumors. As mentioned in the Bourdon article, p53 affects a great deal of processes in the body, not just suppression of tumors. If p53 is mutated, there may be things to deal with as well as the cancer. This information will give the doctor a better idea of what he/she is dealing with. Even though the research is currently inconclusive about which p53s do exactly what, knowing what is going on within the body will help both doctors and future researchers.
Wednesday, February 18, 2009
Colon Cancer Interview
Our group interviewed one of our member's aunts, who had recently been told that she was in remission from colon cancer.
Q: How were you diagnosed?
A: I went in for an Ob-Gyn appointment and they did some blood work because I was having clotting and becoming heavily anemic. I had another test done, which takes about six months to get the results back from. After one month my iron count was at 8.4 (normal is 12-16), so I talk my doctor that I did not want to wait for the test results. I went to a hemotologist who gave me some iron and also told me that I was a poor iron absorber. I then went to a gastroenterologist and got a colonoscopy. It was during the colonoscopy that they found the cancer.
Q: How advanced was your cancer when you found out about it?
A: There are four different stages, the worst being stage four. Within stage three, there are four different stages, A, B, C, and D. Mine was a 3B. It had gone through the colon wall and three of the four lymph nodes that they tested. The more they test, the better chance of survival. Now they say that you should test a minimum of 20.
Q: How was your cancer treated?
A: First I had surgery. The doctor tood out my ascending colon and stapled and sewed the small intestine to the remaining portion of the large intestine. Then I started chemotherapy. They hooked me up on Wednesday to steroids and anti-nausea medicine. They gave me two bags, oxaliplatin and 5-fu. For my third chemotherapy, they gave me a portable pump that would pump for 46 hours. On Fridays I would go in and get unhooked and I did this every other week for six months. After this, I had my blood tested often because chemotherapy attacks all rapid growing cells in the body. I also received a shot to stimulate my bone marrow to make more white blood cells. I took medicine to make my red blood cell count go up. I also took iron to raise my iron count. Since I still had nausea after I was off, I took oral anti-nausea medicne. I also had scans to make sure the cancer did not spread.
Q: Do you have any idea about the cause of your cancer?
A: I don't know the specific cause. I do know that my cancer was not the genetic kind of colon cancer. Some triggers are stress, red meat, smoking, and alcohol.
Q: What was the most difficult symptom you had to battle?
A: Physically it was the nausea. Emotionally it was the hair loss. I also still have neuropathy to the point that sometimes it is hard for me to button things.
Q: Did you have any significant signs prior to diagnosis?
A: No.
Q: Do you have any advice for other people worried about colon cancer?
A: Don't wait to get your colonoscopy. Also, diet and exercise can decrease the chance of recurrence by 60%.
Q: How were you diagnosed?
A: I went in for an Ob-Gyn appointment and they did some blood work because I was having clotting and becoming heavily anemic. I had another test done, which takes about six months to get the results back from. After one month my iron count was at 8.4 (normal is 12-16), so I talk my doctor that I did not want to wait for the test results. I went to a hemotologist who gave me some iron and also told me that I was a poor iron absorber. I then went to a gastroenterologist and got a colonoscopy. It was during the colonoscopy that they found the cancer.
Q: How advanced was your cancer when you found out about it?
A: There are four different stages, the worst being stage four. Within stage three, there are four different stages, A, B, C, and D. Mine was a 3B. It had gone through the colon wall and three of the four lymph nodes that they tested. The more they test, the better chance of survival. Now they say that you should test a minimum of 20.
Q: How was your cancer treated?
A: First I had surgery. The doctor tood out my ascending colon and stapled and sewed the small intestine to the remaining portion of the large intestine. Then I started chemotherapy. They hooked me up on Wednesday to steroids and anti-nausea medicine. They gave me two bags, oxaliplatin and 5-fu. For my third chemotherapy, they gave me a portable pump that would pump for 46 hours. On Fridays I would go in and get unhooked and I did this every other week for six months. After this, I had my blood tested often because chemotherapy attacks all rapid growing cells in the body. I also received a shot to stimulate my bone marrow to make more white blood cells. I took medicine to make my red blood cell count go up. I also took iron to raise my iron count. Since I still had nausea after I was off, I took oral anti-nausea medicne. I also had scans to make sure the cancer did not spread.
Q: Do you have any idea about the cause of your cancer?
A: I don't know the specific cause. I do know that my cancer was not the genetic kind of colon cancer. Some triggers are stress, red meat, smoking, and alcohol.
Q: What was the most difficult symptom you had to battle?
A: Physically it was the nausea. Emotionally it was the hair loss. I also still have neuropathy to the point that sometimes it is hard for me to button things.
Q: Did you have any significant signs prior to diagnosis?
A: No.
Q: Do you have any advice for other people worried about colon cancer?
A: Don't wait to get your colonoscopy. Also, diet and exercise can decrease the chance of recurrence by 60%.
Wednesday, February 4, 2009
An Overview of Colon Cancer
Our group has chosen to focus specifically on colon cancer for our project, mainly because one of our group members has a relative who has recently had it, and we will be interviewing her later in the project.
Cancer in general can be defined as a disease in which abnormal cells infiltrate different systems within the body, while replicating uncontrollably. Cancer can affect any area within the body and can also spread through the whole body.
Colon cancer is cancer which afflicts the large intestine, or colon. It is often seen in conjunction with rectal cancer, which occurs when the last six inches of the colon are infected. Generally, colon cancer begins when smaller polyps develop in the colon and these polyps eventually turn into colon cancer. These polyps often do not show symptoms, so screening is very important before these turn into cancer. Some symptoms of colon cancer include blood in the stool, abdominal pain, gas, bowel habit changes, and cramping. One of the biggest risk factors for colon cancer is age. A very large majority of people who are diagnosed with colon cancer are over the age of 50. Often, at this age, doctors will recommend colonoscopies or some other tests, which can help catch polyps before they develop into cancer. Another big risk factor is a family history of colon cancer. This disease is often thought to be genetic, so those with a parent or other close relative who have had the disease should be aware of their risk.
To treat colon cancer, doctors will generally have three main options. These are chemotherapy, surgery, and radiation. Surgery is often what is tried first, and doctors will perform a colectomy to remove the part of the colon that has been affected. Depending on the stage of cancer and how spread it is, chemotherapy and radiation may be used as well. If the cancer has spread beyond the colon to the nearby lymph nodes or has breached the wall of the colon, chemotherapy may be used to destroy these remaining cancer cells left after surgery. If colon cancer is more advanced and has metastasized, radiation therapy can be used to make the tumors in the rest of the body smaller before an operation is done. There are also several drugs available for people with advanced stages of colon cancer to prevent new tumors from developing.
Information obtained from www.mayoclinic.com
Cancer in general can be defined as a disease in which abnormal cells infiltrate different systems within the body, while replicating uncontrollably. Cancer can affect any area within the body and can also spread through the whole body.
Colon cancer is cancer which afflicts the large intestine, or colon. It is often seen in conjunction with rectal cancer, which occurs when the last six inches of the colon are infected. Generally, colon cancer begins when smaller polyps develop in the colon and these polyps eventually turn into colon cancer. These polyps often do not show symptoms, so screening is very important before these turn into cancer. Some symptoms of colon cancer include blood in the stool, abdominal pain, gas, bowel habit changes, and cramping. One of the biggest risk factors for colon cancer is age. A very large majority of people who are diagnosed with colon cancer are over the age of 50. Often, at this age, doctors will recommend colonoscopies or some other tests, which can help catch polyps before they develop into cancer. Another big risk factor is a family history of colon cancer. This disease is often thought to be genetic, so those with a parent or other close relative who have had the disease should be aware of their risk.
To treat colon cancer, doctors will generally have three main options. These are chemotherapy, surgery, and radiation. Surgery is often what is tried first, and doctors will perform a colectomy to remove the part of the colon that has been affected. Depending on the stage of cancer and how spread it is, chemotherapy and radiation may be used as well. If the cancer has spread beyond the colon to the nearby lymph nodes or has breached the wall of the colon, chemotherapy may be used to destroy these remaining cancer cells left after surgery. If colon cancer is more advanced and has metastasized, radiation therapy can be used to make the tumors in the rest of the body smaller before an operation is done. There are also several drugs available for people with advanced stages of colon cancer to prevent new tumors from developing.
Information obtained from www.mayoclinic.com
Sunday, February 1, 2009
Introduction to Grid-Computing
Service learning is an important part of our Rockhurst education. This semester in our Evolution class, we are fulfilling this component by participating in a grid-computing project. Grid-computing works by connecting the personal computers of volunteers and running algorithms in the background. The network of computers is able to accomplish more research results than multiple supercomputers. The advantage that makes this technology so worthwhile is that it’s incredibly efficient. Grid-computing uses computer space that otherwise would be being wasted. Furthermore, research is broken down in to smaller pieces. Because of this, money and time spent on research drops significantly. The processing power generated by grid-computing allows projects that may have taken years to have results with in months.
We selected our grid-computing project from World Community Grid. Our specific project is called Help Conquer Cancer. This project works to improve the results obtained from protein X-ray crystallography. X-ray crystallography is important to cancer research because it allows scientists to understand the structure of proteins involved in the detection, initiation, and progression of cancer. More information on our project can be found at the Help Conquer Cancer website.
We selected our grid-computing project from World Community Grid. Our specific project is called Help Conquer Cancer. This project works to improve the results obtained from protein X-ray crystallography. X-ray crystallography is important to cancer research because it allows scientists to understand the structure of proteins involved in the detection, initiation, and progression of cancer. More information on our project can be found at the Help Conquer Cancer website.
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