Our group has had the grid computing program running on two different computers. This has allowed us to do more work on the grid. We started off with "Help Fight Childhood Cancer" as our main grid, but about a month into the project it went from having an active status to having a status of intermitent meaning that it had very few items being sent to computers. Once it went to intermitent status Courtney changed her main grid to "Help Conquer Cancer" so that we would still be working on a cancer grid.
Here are the stats from Linda's computer:
11 results returned with a ranking of 502,029
8,271 points with a ranking of 483,423
Here are the stats from Courtney's computer:
206 restults returned with a ranking of 255,068
123,352 points with a ranking of 216,631
We know that these stats may not mean much other than just numbers to some people, but they do show that there is work being done on trying to combat cancer as well as other world problems. Being that the grid computing program sometimes sends work from other grids not all of the data that is gathered is for cancer. There are grids doing research Malaria, Leishmaniasis, Schistosoma, AIDS, clean enercy, and human proteome folding.
This project has allowed us to learn about evolution and how it can affect cancer. The project has also made us think about evolution in new ways.
Tuesday, April 30, 2013
Friday, April 19, 2013
Q and A for our research article
In our previous blog post we found an article and provided a link to the article. After the submission of the article our teacher (Dr. Walker) has given us a series of questions that she would like us to answer based on the article and our topic. Below is the series of questions with our answers.
1. This is a multi-part question. To answer it, you will need to go to www.ncbi.nlm.nih.gov and follow these instructions. From the drop-down search menu, choose "Nucleotide." Type cebpa in the box to the right and hit "search." Click on the Sus scrofa cebpa gene (third entry). On the right side of the page, click "Run BLAST." On the next page, click the BLAST button at the bottom (and wait...)
a. Scroll down your results page. Name ten other taxa (scientific and common names) that share some sequence identity with this Sus gene.
Canis (lupus) familiaris à Dog
Tursiops truncates à Bottlenose dolphin
Odobenus rosmarus à Walrus
Orcinus orca à Killer whales
Oryctolagus cuniculus à Rabbit
Pan troglodytes à Chimpanzee
Homo sapiens à Human
b. What is Sus scrofa? In an evolutionary sense, why study gene regulation in this animal?
Sus scrofa is wild boar.
c. What does wild type cebpa do in these animals? Why is it conserved across so many disparate species?
The wild type effects remission duration and overall survival.
2. According to the paper, what does the mutated cebpa allele indicate in human patients?
Patients with CEBPA mutations had higher hemoglobin levels, lower platlet counts, and higher peripheral blood (PB) blast counts. Also they were less likely to have lymphadenopathy or extramedullary leukemia. Other significant differences were not present regarding other clinical features between patients with mutated and unmutated CEBPA regions.
3. At what age are symptoms of adult AML typically evident in humans? Is this disease subject to natural selection? Why or why not?
The symptoms of adult AML are usually evident around 65 years of age. Fewer than 10% of people with AML are children. The CEBPA mutation is subject to natural selection becasue it has favorable outcomes in AML patients and can increase their lifespan and prognosis. This is only evident in patients who plan on having children and they would pass this mutation on. Becasue most of the symptoms of adult AML occur in older men and women, this mutation and disease are mainly evident in later age after many have already had children. Natual selection would work on AML if the symptoms were present with adults of reproductive age and having children. Selection would act against AML and those individuals with the disease would not survive to reproduce, unless they had the CEBPA mutation. The CEBPA mutation would be selected for because it increases the longevity and prognosis of a person with AML.
4. What does AML have to do with MDS?
AML (Acute Myeloid Leukemia) is the progression of MDS (pre-leukemia). So most people who suffer from MDS will unfortunately progress into AML. The comparisson is like HIV to AIDS, so most people whom have HIV will eventually transition into AIDS.
1. This is a multi-part question. To answer it, you will need to go to www.ncbi.nlm.nih.gov and follow these instructions. From the drop-down search menu, choose "Nucleotide." Type cebpa in the box to the right and hit "search." Click on the Sus scrofa cebpa gene (third entry). On the right side of the page, click "Run BLAST." On the next page, click the BLAST button at the bottom (and wait...)
a. Scroll down your results page. Name ten other taxa (scientific and common names) that share some sequence identity with this Sus gene.
Canis (lupus) familiaris à Dog
Tursiops truncates à Bottlenose dolphin
Odobenus rosmarus à Walrus
Orcinus orca à Killer whales
Oryctolagus cuniculus à Rabbit
Pan troglodytes à Chimpanzee
Homo sapiens à Human
Papio anubis à Olive baboon
Pongo abelii à Sumatran orangutan
Callithrix jacchus
à
common marmoset
Otolemur garnettii
à(northern)
greater galago à
thick-tailed bushbabies
Bos Taurus àBovine
à
cattle
Trichechus manatus
latirostris à
Florida manatee
b. What is Sus scrofa? In an evolutionary sense, why study gene regulation in this animal?
Sus scrofa is wild boar.
c. What does wild type cebpa do in these animals? Why is it conserved across so many disparate species?
The wild type effects remission duration and overall survival.
2. According to the paper, what does the mutated cebpa allele indicate in human patients?
Patients with CEBPA mutations had higher hemoglobin levels, lower platlet counts, and higher peripheral blood (PB) blast counts. Also they were less likely to have lymphadenopathy or extramedullary leukemia. Other significant differences were not present regarding other clinical features between patients with mutated and unmutated CEBPA regions.
3. At what age are symptoms of adult AML typically evident in humans? Is this disease subject to natural selection? Why or why not?
The symptoms of adult AML are usually evident around 65 years of age. Fewer than 10% of people with AML are children. The CEBPA mutation is subject to natural selection becasue it has favorable outcomes in AML patients and can increase their lifespan and prognosis. This is only evident in patients who plan on having children and they would pass this mutation on. Becasue most of the symptoms of adult AML occur in older men and women, this mutation and disease are mainly evident in later age after many have already had children. Natual selection would work on AML if the symptoms were present with adults of reproductive age and having children. Selection would act against AML and those individuals with the disease would not survive to reproduce, unless they had the CEBPA mutation. The CEBPA mutation would be selected for because it increases the longevity and prognosis of a person with AML.
4. What does AML have to do with MDS?
AML (Acute Myeloid Leukemia) is the progression of MDS (pre-leukemia). So most people who suffer from MDS will unfortunately progress into AML. The comparisson is like HIV to AIDS, so most people whom have HIV will eventually transition into AIDS.
Friday, April 5, 2013
Research
For this assignment we had to find a research article that links our topic and evolution. Our group found an article that links myeloid leukemia and evolution.
Citation for our article.
Citation for our article.
Fröhling, Stefan, Richard F. Schlenk, Ina Stolze, Jörg
Bihlmayr, Axel Benner, Sylvia Kreitmeier, Karen Tobis, Hartmut Döhner, and
Konstanze Döhner. "CEBPA Mutations in Younger Adults With Acute
Myeloid Leukemia and Normal Cytogenetics: Prognostic Relevance and Analysis of
Cooperating Mutations." Journal of Clinical Oncology 22.4 (2004):
624-33.
Link: http://jco.ascopubs.org/content/22/4/624.full.pdf+html
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