Saturday, March 25, 2017

Weekly Bio Journal #5 Mar. 25

The class kicked off this week by completing our second activity on examining cancer patient data. Every one was given a card and on it detailed the gene mutations, on which chromosomes, cell function or cell fate, oncogene or tumor suppressor, and what the resulting cancer was. These cards detailed information from actual cancer patients and together the class compared their cards in order to identify any patterns or trends. What I found from this activity was that many different gene mutations can lead to the same type of cancer and that it often takes more than one gene mutation to cause the cancer. Another interesting fact I learned is that out of the 140 genes found to be linked to cancer, only 9 of those are associated with cell maintenance.
Next we jumped into Mendelian genetics and reviewed how to conduct mono hybrid and dihybrid Punnett squares, and even multiple monohybrid Punnett squares to determine the phenotype and genotype of offspring. These methods came easy to me with a little guidance in the beginning to make sure I was on the right path, and I dare say they are even a little fun. We furthered the Mendelian genetics by practice with pedigrees to determine the genotypes of family trees. Finally we analyzed the data by using chi-square analysis to determine if the observed genotypes were beyond reasonable similarity to the expected outcomes that were given by our Punnett squares. Because I am also taking AP Statistics the conclusions drawn from the chi-square make perfect sense to me and I enjoy chi-square as a tool of analysis.
On Friday we conducted a small activity where we looked at the spores of fungi and counted the number of asci that underwent crossing over during meiosis by observing their phenotypes. We then used chi-square to determine if our observed abundance could accurately support Olive's map distance theory which used mathematics to predict the expected ratio of crossed to non-crossed spores. My data ended up in support of Olive. We also watched a Vodcast teaching us about Chromosomal abnormalities, the various changes to genetic make up and the resulting effects as well as a few of the more prevalent genetic disorders and how they are caused such as the Trisomy of Chromosome 21 that causes Down's Syndrome. 

Monday, March 20, 2017

Examining Cancer Patient Data

This activity taught me that there are many different gene mutations that can lead to the same type of cancer. The mutations may be in oncogenes, tumor suppressor genes, they may be on chromosome 3, or even the X chromosome. Another trend I saw was that it appeared that in all cancer patients, be it hepatic cancer or other, the patients had at least two different mutations. This would lead me to believe it takes more than one mutation to cause cancer. The final thing I learned from this activity is that there are only 9 genes associated with genome maintenance. This leads to cell fate and cell survival being far more prevalent than genome maintenance.
It surprised me to learn how spread apart all the cancer genes appeared to be, even among patients of the same cancer type. There was almost no rhyme or reason to their placements and it seemed equally likely that a gene may mutate on any of the chromosomes. Likely this is why cancer has remained a mystery for so long, it's hard to pinpoint or predict and therefor hard to control and cure. As well it surprised me that no gene could code for more than one type of cancer. One thing I still wonder is a piece I mentioned earlier in observing that every patient had more than one mutation. Is that just a by-chance happening, or does one really require multiple genes to mutate before cancer develops. Or can an individual develop cancer by one mutated gene alone?

Sunday, March 12, 2017

Weekly Bio Journal #4 Mar. 12

This week we covered three new Vodcasts that centered around the Cell cycle. The weeks activities revolved around the information in those Vodcasts. Monday we filled out a POGIL on the cell cycle. Tuesday I was not in class because I had a Nordic State Meet race to attend. Wednesday we discoed the new Vodcast on the cells regulatory mechanics and worked on a corresponding POGIL. Thursday we hopped on the computers and completed an online HHMI informational program on the cell cycle and how it relates to cancer. Friday we had a shortened class due to the pep rally and spent class going over the information from the HHMI activity.
The information on the cell cycle came easy to me, I understand the order of events from G1, to S, to G2, to M. I completely understand the concepts of the checkpoints and the duties of each phase. I also can identify the order of phases in mitosis and identify them through a microscope. This week I learned what cancer really is and how it develops. The only road bump of the week is remembering the exact steps that the chromosomes go through in Meiosis. Its more complicated than mitosis as there are a couple more steps that ensure greater variation, but the terms like diploid and haploid when counting chromosomes and chromosome pairs gets a little confusing for me. I'll just have to review those sections and look over diagrams and illustrations to help me remember.

Saturday, March 4, 2017

Weekly Bio Journal #3 Mar. 4

This week back from February back, centered around one laboratory experience: PCR. After having learned about the Polymerase Chain Reaction and electropheresis in our 4.3 Biotechnology Vodcast, the class had the opportunity to have hands on experience with the technology. Everyone took cheek cell samples from their mouths, separated the DNA, and amplified the samples using PCR. The next day we practiced the delicate process of staining the DNA and placing the tiny samples in the fragile gel within the electrophoresis bath. This was a tremendous hands on opportunity to show us actual experience with working in a bio-lab doing the very things real lab technicians do everyday for important analysis and research. The next day we analyzed the electrophoresis results and measured the bands to see how much of the class was homozygous or heterozygous for the target gene. We then did some calculations to determine if the class was in Hardy-Weinberg equilibrium and compared our class results to other populations around the world.
By this point, through listening, recording, and hands on participation, I believe I fully understand the majority of the workings of PCR and gel electrophoresis. Enough so I could explain the process to make it intuitively obvious to even the most casual observer. During the lab however my DNA did not register in the electrophoresis. I messed up somewhere along the line during the lab work. I don't have a particular salivating mouth so I likely had a small spit sample to begin with. I had a very small pellet after the centrifuge and I believe I accidentally sucked up some of the small sample through pipetting later. This was likely the cause of my poor gel results. I just need a little more practice with this particular lab is all, likely a second run I would have produced results having already gone through the procedure once.