ChemSemBlog

This week in Chemistry Seminar we enjoyed a presentation from a new faculty of the University of Notre Dame, Amanda B. Hummon, Ph.D. It was a very interesting talk on the process of gene selection and experimentation for detecting and describing colorectal cancer, a term we all learned to avoid due to its inaccuracy.

The first part of Dr. Hummon’s presentation focused solely on cancer as a disease in general. Some basic underlying truths are present in all types of cancer, such as increased growth rate, desensitization of cells to outside stimuli, avoidance of apoptosis, high vascularization, etc. Dr. Hummon enlightened us on chemical and biochemical methods I hadn’t heard of before, such as Spectral Karyotyping and Comparative Genomic Hybridization for DNA and qRT-PCR, Microarrays and RNAi for RNA.

In addition, Dr. Hummon introduced the notion of using Mass Spectrometry to sequence amino acids within proteins, a procedure I had never heard of before. We learned of the methods scientists use to select only specific genes for study, a glorified process of elimination which includes a lot of deductive reasoning with just a pinch of guesswork. Dr. Hummon’s study produced a list of almost 50 genes on chromosome 13 that were the most likely candidates for the emergence of colon and rectal cancers. She then proceeded to give the ways in which one could differentiate between cancer cells and normal cells using Microarrays, RNAi and other techniques. We learned that Microarrays will always require confirmation via some other test, and in this case Dr. Hummon prescribed RNAi as the best method.

I greatly enjoyed this seminar because of my interests in biochemistry, human physiology and oncology. I felt Dr. Hummon, however nervous or anxious she was prior to the meat of her lecture, did a splendid job and is sure to have a multitude of pupils helping her complete very important tests in our continued battle against ignorance of cancer. I found she was very helpful during Q & A and she was very knowledgeable yet personal.

To the layperson, this seminar was all about figuring out how genetics plays a role in colon and rectal cancers.

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This week, for our regular Thursday seminar we had Assistant Professor Amanda Hummon from Notre Dame University. Her main topic was on cancer and proteomics, more specifically on colon cancer. Her presentation was interesting and she was able to present well. Her presentation was easy to follow and organized well enough so that the audience could remain attentive.

Hummon started with a brief overview of cancer and how cancer cells differ from normal cells. I learned about the six phenotypic differences between cancer and normal cells. Among these include increased, abhorrent proliferation; modification of equilibrium to prevent apoptosis; angiogenesis; and metastisis. Hummon continued her presentation continued as she described procedures and spectroscopic methods. I was able to learn more about spectral karyotyping and comparitive genomic hybridization. She then concluded her overview by stating her main goal which was elucidating the deregulated gene products that drive colorectal cancer.

It was interesting to see how her research progressed, and to learn about the new discoveries that she was able to find. We were able to see how some of the chromosomes were modified from the typical 46 to up to 58. I would say her whole presentation was very informative, despite not having as much chemistry content as we are used to seeing for seminar. Since she gave an easy to follow presentation, we were able to ask some thoughtful questions.

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The guest speaker of the chemistry seminar held on January 28 was Basar Bilgicer, who is an assistant professor in the Department of Chemical & Biomolecular Engineering at University of Notre Dame. During the presentation, he focused on antibodies, such as IgG, and their aggregations to form multivalent molecules in biological systems and friendly explained about them. I think his seminar really helped students get a deeper understanding of antibody aggregation.

I was very interested in the pathway to make cyclic dimers and trimers from monomers. Bivalent hapten makes it possible to generate several forms of aggregations such as trimer, tetramer, and other polymers. Moreover, depending on the concentration of the ligands that bind to the tips of antibody, more complex form can be produced. For example, a synthetic trivalent hapten, which is monocyclic, aggregates IgG into bicyclic trimers. Through his presentation, I also learned about the thermodynamics and kinetics of multivalent molecules of antibodies, based on the basic dynamic principles. For example, the bicyclic trimer is kinetically and thermodynamically more stable than monomeric aggregates of this IgG.

On the other hand, I have a question about the aggregation of other antibodies rather than IgG antibody that he focused on for his research and about the potential application of antibody aggregates in future biotechnology.

I would say to my ‘non-science’ friends or family that the study of antibody is very important for design of diagnostic molecules for therapy of diseases, and Dr. Bilgicer has worked in multivalent interactions of antibody aggregation in biological systems.

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On January 28, 2010, Basar Bilgicer who is a professor at University of Notre Dame visited Andrews University for his presentation. Mr. Basar Bilgicer prepared two presentations. One of them was “Peptide Design Using Unnatural Amino Acids.” The other was “Multivalent Antibody Aggregation.”  More students in the presentation wanted to know about the antibody aggregation. Therefore, he started the presentation, introducing us the basis of antibody. Especially, he talked about IgG antigen. Overall, he showed us a lot of illustrations which explained how the antibody which has bivalency or trivalency worked with antigens and ligands. Also, he used chromatographic graphs which supported his experimental results. It made me easy to understand how the antibody aggregates in various ways.

There were several kinds of ways which antibody binds to antigen or ligands. Largely, the antigens were divided up depending on the shape, whether they are bivalent, or trivalent. Then, they generated several aggregates, such as dimer, trimer, tetramer, or polymer. They also were produced in a cyclic form, a linear form, or in the middle.

During the presentation, he gave details about the correlation between the Gibbs free energy and the binding constant. I asked him about the effects of temperature on the binding constant. He answered that denaturing occurs above five to ten Celsius degree than the body temperature and the binding constant decreases as the temperature decreases under room temperature.

I would tell my friends that the presentation was about the kind of how and what is involved in binding between antibodies and antigens, or ligands.

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On February fourth, there was a presentation about colon and rectal cancer given by Amanda B. Hummon, who is from University of Notre Dame. Her presentation title was “Functional Interrogation of Genes Driving Colorectal Cancer.” I thought that her presentation was very well organized. Also, she explained basic information about cancer cell without difficult words, which made me understand her presentation much easier.

She started the seminar introducing basic properties of cancer cell to us. The cancer cell is caused by disease on genome which is particular number and combination of certain chromosomes. She also explained about the basic structure of chromosome which contains gene in it. I learned that the white region of a chromosome is gene rich zone, while the black region of the chromosome is gene poor zone. There are several factors which contribute to occurring cancer cells, which are DNA, RNA, Function, pathways and etc.  Dr. Hummon especially focused on the relationship between DNA, RNA and cancer cells.

She collected sample of tumor and mucosa cells from patients to compare them. In the future, she said that she would like to have an experiment how the genes are regulated by mRNA and protein. Throughout the presentation, I wondered how she obtained DNA from tumor cells. I also would like to ask her what causes the change of number or shape of gene or chromosome.

I would tell my friends that the presentation is about the factors which cause cancer in colon or rectum in microscopic views such as DNA, RNA, or protein.

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On January 25^th our chem seminar speaker traveled ALL the way from South Bend, IN to give us a very informative lecture on how unnatural amino acids & multivalent antibody aggregation is crucial to science research. Our presenter was Başar Bilgiçer, assistant professor in both the Chemical and Bimolecular Engineering Department and the Chemistry and Biochemistry Department at the University of Notre Dame. He completed his B.S. in Chemistry at Bogazici University, Turkey; he then went on to receive his Ph.D. in chemistry at Tufts University. Bilgiçer conducted his Postdoctoral Fellow at Harvard University.  Dr. Bilgiçer seemed very comfortable and relaxed during his presentation; he was very easy to follow and did a great job at explaining his research so that we could understand it.

The essence of Bilgiçer’s talk was multivalent antibodies and how important the number of bonds to its antigen is in eliciting an immune response to expel the foreign pathogen. In biology class we learn that anything that triggers an immune response is an antigen. When an antigen enters the body, antibodies attach to it forming an antibody-antigen complex that signals the immune system to come and destroy the invading substance. However the efficiency of this system is dependent upon several things, one of which is the valence of the responding antibody.

Antibodies can either be Monovalent or divalent. Bilgiçer easily explained the difference between the two by comparing the arms of the antibody to human body arms. If you are pulling something with your arms it is a lot easier to hold on to it with two arms than with one, this is the same concept with antibodies holding on to antigens. An antibody can hang on to an antigen better when both “arms” of the antibody are attached; this creates bonds that are stronger and tighter; therefore it is harder for the antigen to escape and an immune response can quickly be initiated.

Although this may seem thermodynamically unfavorable, surprising Bilgiçer discovered that it wasn’t; in fact, the entropy decrease for monvalent and divalent antibodies was equitant. This is because whether the antibody bonds with one “arm” or two they would occur that the same time. The multivalent nature of antibodies is advantages in that currently most drugs containing antibodies are monovalent, thus we can create more effective drugs by applying multivalent properties to these antibodies.

Overall I really enjoyed this presentation the only question I have left are: 1. I thought Immune response amplification corresponds with signaling molecules, and so although divalent molecules can hold on better, does the decrease in available antibody binding sites decrease the signal amplification?  2. Most of the antibody aggregates formed very complex arrangements; however, can all of the aggregates bind to the antibody? will a single molecule be just as efficient?  3. If these antibodies are able to elicit a better immune response will lower medicine dosages be required?

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Last Thursday’s seminar was brought to us by Amanda Hummon, currently an assistant professor in the Chemistry and Biochemistry Department at the University of Notre Dame. She completed her A.B. in Chemistry at Cornell University and received her Ph.D. in analytical chemistry at the University of Illinois at Urbana-Champaign. She then conducted her postdoctoral fellow at the National Cancer Institute, NIH. Hummon did a great job presenting her research on cancer, she was very personable, and seemed very interested in what she was doing and sharing it.

In a nut shell, Hummon is researching the transcriptome and the proteome in cancer cells to gain a better understanding of which genes, transcripts, and proteins are affected, ultimately hoping to identify an effective therapeutic intervention. Her focus is on colorectal cancer which she later explained should be referred to as two separate cancers since they affect two different organs. Hummon began by identifying the problematic chromosomes that contribute to colorectal cancer. She accomplished this by identifying the deregulated pathways that are contributing to the cancer phenotype, distinguished by aberrantly expressed genes, and analyzed their products, and the effect that they had on downstream targets.

From her very informative talk I learned that although colorectal cancer affects many people there is not a lot of research in this area due to funding and awareness, another thing I learned was that through special sampling mass spectrometry can be applied to cancer cells, and a person affected with colon disease has 58 chromosomes!

The only questions I have are 1. How do you get the cancer samples you use? 2. Of all the cancers, what lead you specifically to colon cancer? 3. What are your ideas of therapeutic intervention? Do they include gene therapy? And is this something that could be passed down to future generations?

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This week’s speaker was Amanda B. Hummon, who is currently teaching special topics in Biochemistry and Notre Dame. Some of her publications have appeared in premier journals, such as Cancer Research and she is currently researching analytical chemistry and cell and molecular biology. Dr. Hummon presented on colon and rectal cancer which we learned was very different and shouldn’t be put together. Her presentation was organized, had good audio with clear voice, went quickly, and was well explained. I found this topic to be very interesting I learned of the process that it takes when determining a tumor in the colon and rectal area.

Some new things that I learned were the characteristics of cancer cells, oncogenesis, and the difference between colon and rectal cancer. Cancer cells have proliferation, insensitivity to growth signals in the body, angiogenesis (formation of new blood vessels that grow into the tumor, giving it nutrients and oxygen to assist its growth), and WNT signaling (describes a network of proteins well known for their roles in embryogenesis and cancer). When looking at cancer cells they focus on the disease of the genome, DNA, RNA, protein, the network, function, and pathway.

Some of the projects that Dr. Hummon performed involved examining transcriptional deregulation in primary colon and rectal adenocarcinomas. They found that in colon aneuploid adenocarcinoma there were 58 chromosomes, while the normal diploid is 48 chromosomes. In the cancer cell some chromosomes had more than two copies and they gathered this information using comparative genomic hybridization process.

Other activities that they performed involved taking colon and rectal samples from patients in whom they compared the tumor versus the mucosa and their gene expressions. They found 17 genes having a fivefold difference between tumors and mucosa. The immune genes were expressed differently and the difference could be clearly seen. They also found the genes that turned on, trying to fight the cancer.

When looking at the difference between colon and rectal cancer, out of 5,000 genes only 400 changed in the same direction. This information showed that medicines treating these cancers should be prescribed separately rather than together, which is currently being done. In oncogenesis, the process of malignant transformation leading to the formation of a tumor, it was found frequently expressed in the cancer system that turn on specific amplifications. They examined 71 samples and able to narrow the amount of genes down using microarray, homology, validating them with RTPCR, and gene splicing with RNA. They found that siRNA successfully reduced expression of assays of mRNA resulting in the loss of function. Dr. Hummon and her research group was then able to identify nine genes that reduced the cell viability greater than twenty percent.

Many students seemed to enjoy this topic as well as the presentation. They listened attentively and asked many questions at the end, which were answered well. The presentation did encourage me to learn more about this topic and it would be appealing to do extra research on this topic, such as doing this same study or process with other tissues and organs. Dr. Himmon didn’t really speak much about her school of graduate studies, but I’m sure she would have been available to answer questions on that topic if asked. This was an interesting topic on the cancer cells and the genes involved dealing with colon and rectal cancer.

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The Chemistry seminar presented to us on January 21 was presented by Robert E. Minto from the Indiana University-Purdue University Indianapolis chemistry/biochemistry department. His focus is on biological chemistry, a field that I thought was synonymous with biochemistry, until it was later clarified with the definition that biochemistry deals more with metabolism (photosynthesis, citric acid cycle) whereas biological chemists are more interested in the chemical side of biology outside of metabolism. Although Dr. Minto currently teaches at IUPUI he received his BS at the University Of Waterloo, Ontario, he then went on to the University of California, Berekley where he received his doctorate, and conducted his postdoctoral fellow at The Johns Hopkins University.

The core of his research, lipids, is not a topic highly researched outside of the diet/health industry, and even so their only concern is getting rid of it. Although studying lipid for health reasons is important, Dr. Minto taught us that there are many other practical uses for studying lipids. First of all since there is hardly any research in this field, many of the fungi genes aren’t mapped! Now this was something new to me, I thought everyone was obsessed with genomes, structure, and function in the biological world, but Dr. Minto was quick to point out that this only occurs where there is money, and since fungi genomes aren’t at the top of everybody’s list, well there isn’t much out there.

Specifically, Minto has focused his research on desaturase and acetylenase genes. The second reason why studying these genes and enzymes are important is because, we can uncover the way unsaturated acids conduct metabolism (he beat the biochemists to this one!). And finally the third reason, but certainly not the last reason (I am sure there are countless reasons for lipid studies) is that there are many medical uses (the pharmaceutical companies are doing cartwheels) such as antimicrobial and antiproliferative agents and HIV reverse-transcriptase inhibitors. Impressive.

Overall the basic ideas of his presentation were great. I got kind of lost in all of the mechanisms and the intricacies of what his research entailed, but I got the main point. Although there has been lots of negative feedback on his presentation style, I didn’t see a problem with it, I think the subject matter was just not as interesting and so people tuned him out. The only criticism I’d give would be to decrease the length of the presentation, and retract to a more basic knowledge level, so we don’t get lost in the details!

Questions I have are: 1.How difficult is it conducting research in a field that is not well studied? 2. Most of his studies were conducted in vitro but how well adjusted is that to predicting an in vivo replication of the experiment? 3. Have any pharmaceutical taken interest in your studies?

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This week’s seminar, “Functional Interrogation fo Genes Driving Colorectal Cancer,” neither impressed me nor interested me in any way. This is due in part to several factors, one of them being my complete disinterest towards anything biologically related. Another thing that made it uninteresting was the significant lack of chemistry in the presentation. Despite these and other factors, one thing I would like to know a little more about would be what causes cancer cells to metastasise, and how they metastasise. Another thing that I would kind of like to know more about is how a polyp turns into an invasive carcinoma.

One thing that was slightly interesting to learn about was that colon cancer is a different cancer than rectal cancer, thereby making colorectal cancer a term that is both false and nonexistent. If the remote chance came up that I was explaining what this seminar was about to someone who was not in the science field, I would explain to them that the lecture was about what scientists were doing to combat and treat colon cancer and rectal cancer.

As for the speaker, Amanda B. Hummon is a Walther Cancer Institute Assistant Professor of Biochemistry at the Department of Chemistry and Biochemistry at the University of Notre Dame, in Notre Dame, Indiana. She seemed to know a lot about the topic she was speaking on, but her expressions did not give me the impression that she was very interested in her work. Another thing that turned me off to the presentation was that the speaker seemed to keep droning on and on, not away of the time constraints of the seminar. This is not entirely her fault though, because it seems that Dr. Hayes seems to tell the speakers that they have all the time in the world, and seeing as I have a class that I need to be at before 5:30, I do not appreciate this one bit.

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Amanda B. Hummon is a new faculty member at the University of Notre Dame and is in the process of setting up her research there. Before coming to Notre Dame, she was a researcher at the National Cancer Institute in Washington D.C. Her research is trying to understand gene regulation in colorectal cancer.

Unfortunately, I failed to pay attention as well as I should have, but from what I heard, Dr. Hummon’s research focuses on the function of mRNA in the development of colorectal cancer. They believe it is the key to stopping the cancer, especially to avoid the advanced stages of cancer, angiogenesis and metastasis. The techniques used to study DNA were spectokaryotyping (SKY) and comparative genomic hybridization (CGH). The techniques used to study mRNA were qRT-PCR and microarrays. Apparently, microarrays are good for painting a broad picture, but not so much for elucidating upon the details. The gene that Hummon’s research is particularly interested in is chromosome 13, one that is prevalent in cancer but not well written about.

Hummon is our first woman speaker this semester. She looks quite young but seems to have a lot of research experience under her belt. By presenting the basics of cancer and building up to her research, she made the material easier to grasp for her audience. Although I knew a little about microarrays, Hummon’s presentation demonstrated its pros and cons, that is, when microarray is useful.

Laymen’s Summary of Chemistry Seminar: Colon and Rectal cancer are different. Hummon’s researching colorectal cancer, trying to better understand its gene regulation. Knowing what goes on at the more fundamental levels of cancer can help develop better ways to stop cancer.

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Walter Cancer Assistant Professor from the University of Notre Dame, Amanda B. Hummon, did a presentation on Functional Interrogation of Genes Driving Colorectal Cancer. Her current position as a cancer professor and her experience of working on gene regulation of colorectal cancer with RNA interference at the National Cancer Institute well substantiated her credibility as a speaker that day.

Some of the characteristics of cancer cell included cell proliferation, cell survival (avoding cell death mechanism by modifying it), invasion and ignoring body signals, and metastasis (malignant cancer spreading to a different organ). In order to observe DNA, special karyotyping and comparative genomic hybridization was used. The goal of her research was to elucidate deregulated gene products that drive colorectal cancer. I also was reminded that there are 22 pairs of autosomes (labeling the largest ones as #1, and the smallest ones, #22). I learned that abnormal cancer cells have more autosomes than the normal cells have, such as having three #6 autosomes instead of just a pair of them. Microarray was used to measure the gene expression, and her research found out that 69 genes are suspected of causing cancer. Then, qRT-PCR was used to lower that number to 44 genes. RNA interference (using synthetic si-RNAs to cleave individual genes one is interested in) was used to finalized the number of genes to 9 genes that are responsible for causing colorectal cancer. Her research showed that silencing 9 best oncogenes reduced the cell viability greater than 20%.

Questions I had during her seminar were 1) About the 9 oncogenes you found, were they well-known ones? Her answer was no 2) What led you to study and do research on colorectal cancer? 3) What is the practicality of the findings of your research?

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The presentation this week (February 5, 2010) was given by Amanda B. Hummon. Amanda Hummon is a new faculty member at the University of Notre dame, and is beginning her research there specifically on colorectal cancer.

She started off her presentation by defining a cancer cell, which is basically cells that are the same as normal cells, except that it is chemically different. Cancerous cells can be defined by certain phenotypic characteristics. Some of the major ones include: Increased proliferation, cells that bypass aptosis, insensitivity to anti growth signaling, and angiogenesis. Amanda Hummon studies the correlation between DNA, RNA and the protein to try to find a solution to cancer. By upregulating genes that are lost, and downregulating amplified genes, she hopes that cancerous cells can be effectively dealt with.

Amanda Hummon seemed to be an effective speaker, and kept the audience attentive by her interesting slides and explanations. A lot of the questions that I developed during her presentation were answered.

Some new material I learned during this presentation was that DNA, RNA, and Proteins are involved in cancer cells. Also, the fact that controlling the level of gene expression to cure cancer was a new Idea. One question that I had was on what causes the loss of, or the amplification of certain genes in cancerous cells. This question that I asked during the Q and A time I thought wasn’t answered adequately. However seeing that there are a lot of areas of cancer that we don’t know about, it was understandable.

In conclusion, cancer research has always been on my top priority lists in interests since I became interested in the medical field. This week’s presentation definitely reinforced by interest, and I would definitely love to get involved in this type of research either before or after med school.

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Colorectal Cancer may be something that society is embarrassed to talk about but the Chemistry Seminar on February 4^th, 2010 described this type of cancer in a very interesting way. Functional Interrogation of Genes Driving Colorectal Cancer was the title of the presentation given by Amanda B. Hummon PhD. Hummon completed postdoctoral work at the National Cancer Institute and shared her research with us from that project.

This seminar provided me with a lot of information I did not know about cancer. The difference between a cancer cell and a normal cell are the concentrations of proteins and other components within the cell. There are six phenotypic characteristics of cancer cells: increased proliferation, modification of equilibria to avoid apoptosis, self-sufficiency to won growth signals and ignoring of body inhibition growth signals, angiogenesis, and metastasis. Angiogenesis is the ability of a cancer cell to recruit bloods cells to itself.

The goal of Hummon’s research is to elucidate deregulated gene products that drive colorectal cancer. To do this, research must be completed to understand the relationship between DNA, RNA, and Proteins. Microarrays and qRT-PCR were used to study RNA. Spectral karyotyping and comparative genomic hybridization were used to measure DNA. An example of spectral karyotyping was shown on a slide. This procedure labels each pair of chromosomes with their own fluorescent color. In the regular cell all chromosomes were paired. In a cancer cell chromosomes were often not in pairs but over abundant sets of three or more or under abundant single chromosomes.

The research was able to determine a difference in the rectal and colon cancers but this research has not yet been implemented into treatment. Researchers are unable to see the difference between non-metastasizing cancer and metastasizing cancer. The goal is to use the information collected to try and reduce the viability of cancer.

This presentation was very well done. The topic was studied in depth but was easy to follow and comprehend the new information presented. In telling a family member or friend about this presentation I would say that we were informed of research trying to discover how cancer spreads on a gene level.

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This week’s speaker was Amanda Hummon from the University of Notre Dame.  Her group studied the genes that drive colon and rectal cancer,  sometimes referred collectively to as colorectal cancer.  It is a well known fact that cancer is one of the most lethal diseases in existence today.  Cancer cells have the same genomes as normal cells but different chemical equilibria.  Cancer cells also grow quite rapidly, and ignore signals from the body to self destruct or stop growing.  Cancer cells can “recruit” blood vessels to flow into them, a process called angiogenesis.  The most dangerous aspect of cancer cells is that they can metastastize, or migrate to other areas of the body.  90% of cancer deaths are because of this.

Investigating the DNA of cancer cells could give a better understanding of how to fight them.  Hummon’s group used spectral karyotyping techniques to measure DNA in cancer cells, and compare to a normal cell.  A normal cell has 46 chromosomes, while cancer cells have 58 chromosomes.  RNA interference techniques are used to discover functions of genes.  There are deregulated gene products that cause colon and rectal cancer, and they need to be found out.  Chromosome 13 tends to carry oncogenes, or cancer causing genes.  Usually, oncogenes are over expressed.  69 out of 101 genes in chromosome 13 are over expressed, and most of them are not characterized.  No cancer is completely predictable, but it has been discovered that cancers tend to proceed in predictable patterns.  When a cell becomes cancerous, it goes from a normal mucosa state (having 46 chromosomes) to adenoma to invasive carcinoma.  These changes occur on the chromosome level.

This presentation was very interesting to me, as it shows that we are getting one step closer to beating cancer.  However, Hummon used a lot of terms that were unfamiliar to me, such as mucosa.  Since I do not have a strong background in cancer chemistry, I didn’t get the full benefit of the presentation.  That being said, I learned quite a lot.  I learned that since cancer cells proceed in a predictable pattern, it might be easier to trace them and stop them.  I also learned that cancerous cells have more chromosomes than regular cells.  I think it would be interesting to look into the functions of those extra chromosomes.  Finally, I wondered that on average, how long does it take for cancer to metastastize?  According to Hummon, it depends on the cancer and the host.

I would recommend this presentation to any layperson, as it was about studying the abnormalities in cancer cells and possibly developing new techniques to fight cancer.

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Dr. Amanda Hummon came from the University of Notre Dame to talk to us about her research. The title of her presentation was “Functional Interrogation of Genes Driving Colorectal Cancer.”

Her talk included a description of the differences between healthy cells and cancerous cells, the techniques used to look at DNA and RNA, and what was found when looking at biopsies to colon and rectal cancers. Different phenotypic mechanisms that are specific to cancer cells are increased proliferation, modified equilibrium, insensitivity to the body’s antigrowth signals, and angiogenesis. Cancer is a disease of the genome, which means that to really understand it, the DNA and RNA of cells is what needs to be looked at.

The techniques Dr. Hummon has used to look at DNA are spectral karyotyping (SKY) and comparative genomic hybridization (CGH). The techniques used to look at RNA are qRT-PCR and microarrays. The goal of Dr. Hummon’s research was to elucidate the deregulated gene products that drive colorectal cancer. Some of her results include that looking at the DNA from biopsies and mucosal cells, they can determine which came from which just by the looks. Also, they cannot look at gene expression and tell is metastasis has occurred or not, and there is a difference between colon cancer and rectal cancer.

Dr. Hummon’s talk was very interesting. Her research has obviously been exciting and she enjoys doing what she does. I would describe this talk to a non-scientific friend as research involving the genes that are involved with colorectal cancer.

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This week in Chemistry Seminar we enjoyed a presentation from Dr. Basar Bilgicer on the aggregation of antibodies and their “antigens” with each other. First of all, a quick recap on antibodies, what they are, what they are used for, and why they are so critical. Antibodies are proteins produced by cells of the immune system and, when bound to their specific antigen (toxin, carcinogen, etc.) will elicit an immune response to increase the number of antibodies in the blood. Antibodies, therefore, are nothing more than a traveling active site for toxins and unwanted stimuli. Instead of bringing about the harm they would typically cause, the antibody-antigen complex is recognized by cells of the immune system and pump out additional antibodies to quell the invasion of toxins. These now harmless macromolecules are then disposed of.

Dr. Bilgicer’s research was in the field of antibody aggregation using substrates acting as two different substrates. During the course of his research, he used size-exclusion chromatography to separate aggregates based on the size of the aggregate. He found that many of the aggregates identified were trimers consisting of three antibodies and three substrates bound partly to one antibody and partly to its adjacent partner. Dr. Bilgicer’s research supports this as the major product of antibody aggregation.

Dr. Bilgicer took some time warming up to the class, but he was competent and knowledgeable in his field. He’s done additional work with more natural substrates for antibodies as well. Although the substrates used in his current experiment are unnatural, the aggregation pattern should not be altered. I found this seminar to helpful in that it provided good explanations of antibody function, including the disabling of the myth that toxins are bound to the crux of the antibody instead of the end of its two prominent limbs. I thought Dr. Bilgicer could have gone into more detail, however, into the main differences between natural and unnatural substrates or into the effects of a natural solution on antibody aggregation.

To the layperson, this seminar was about one way in which the body voids itself of poisons, and how those poisons are organized after they are “caught.”

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This week’s speaker was Basar Bilgicer, who presented on multivalent antibodies.  He stated that one of the major challenges for antibodies is to be found by the appropriate pathogen in order to get rid of the pathogen.  There are a few different types of antibodies.  There are monovalent and bivalent antibodies in the body, a monovalent antibody is like the antibody grabbing on to the pathogen with one arm.  Whereas a bivalent antibody would be like grabbing on with two arms.  A bivalent antibody obviously would be a better choice because the bond is stronger because the the increased number of bonds formed.  Also, it depends on the valency of the antibody to determine how complex of a structure it will form. For example the more valent it is, the larger it can be, creating more bonds.  Once these antibodies are made there are several ways that a person can harvest them from the test sample.  The most common laboratory way is to use a centrifuge to separate and purify the complexes.  However, all this takes money in order to research to develop.

To give you a sense of the amount of binding strength that took place, he  plotted the mole fraction against the ligand concentration as it increased. He also found that trivalent binding yielded more complex structures. In his research, he wanted to form structures without steric hindrance and was excited that he found a ligand that could bind three arms of the antibody. At the end of his research, he was able to find that bivalent and trivalent ligands promote stable aggregates of antibodies and that antibodies are bivalent since this increases the time of attachment, increasing production, as I stated before.

Overall, I thought his presentation was pretty interesting. He spoke clearly and was able to deliver his message clearly without much confusion. He kept his information relatively easy to understand and follow so that students wouldn’t get too lost or disinterested.  I personally, would recommend Dr. Bilgicer to speak again in the future.

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Dr. Basar Bilgicer was the featured presenter at this week’s ChemSem installment. The simple focus of his presentation worked upon the well known chemical fact that two bonds are better than one. A complex organism produces antibodies which, upon encountering a foreign antigen, attach to its surface. When a large number of these antibodies attach, the mass and concentration triggers and immune response which works to expel the antigen from the system now that it has been identified. Often, the binding antibodies are monovalent having one site which bonds to the antigen. However, if antibodies are available that are divalent, they can bond to the antigen in more than one site, keeping them from detaching and encouraging the immune response.

Admittedly there were several portions of this presentation which were beyond my understanding of nature. I never focused much on either biology or biochemistry, and it took some catching up in order to grasp the material. I was curious to find out why the divalent antibodies didn’t slow immune response considering the fact that they bound twice as many antigen sites but only developed half the antibody density. Furthermore, it was unclear whether these antibodies were entirely synthetic (it appeared as if they were) and therefore had unknown internal biochemistry in organisms. Bilgicer did admit that the conditions of his trials on the divalent antibodies were significantly different than the internal circumstances to which they would ultimately be applied. Finally, I was interested to find that more than 35% of current pharmaceutical research was focused on antibody development, which seemed to suggest it was a much larger field than is publicized. Is the lack of notable material regarding it simply due to secrecy on the part of pharmaceutical corporations, or is the research still significantly in its infancy?

Regardless of all of this, the chemistry to precipitate and separate the antibodies from their respective solutions was explained in a straight-forward and clear manner and I thought overall Bilgicer did a good job of expressing his research and the efforts of his team in analyzing this material. In the end, though I didn’t fully understand the intricacies of the matter, the fundamental principles seem reasonable and well worth further study.

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Assistant chemical & biomolecular engineering professor from Notre Dame, Basar Bilgicer obviously was well qualified to do the presentation on amino acids and antibody, as he has worked on peptide design using unnatural amino acids while pursuing his PhD degree. His presentation was well-paced, ending right around the time when the seminar is supposed to be over, but over my head mostly, because I forgot a lot of things I learned in biology and biochemistry classes. However, the general idea of the presentation was easy to follow and understandable.

During his presentation, I learned that there are two kinds of antibodies (monovalent, which only binds on one spot, vs bivalent, which binds on two spots). To study bivalent antibodies, using two rigid seperate antigens or short antigen pairs so that the antigen pair cannot be binded by one antibody. In order for antibody and hapten (ligand) pair to occur, tight bonding and easily modified hapten structure are necessary. I was also reminded of size exclusion chromatography that allows the larger molecules to come out faster than the smaller ones using porous gels. I learned that antibody cyclic aggregates provides higher stability due to bivalency, and sufficient  concentration is necessary in forming antibody complexes. One good application of an antibody complex was pharmaceutical companies making drugs from it.

Three questions I came up with duing his presentations were 1) what is hapten? is it same as antigens ?, 2) would stability increase continuously as more antibody aggregates to form antibody complexes?, and 3) are the antibodies you used made commercially or by humans?

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