The End? Mutant Receptors and Oncogenesis

It’s hard to believe my summer of research has come to an end. In my last blog post two weeks ago, I had just observed my first set of TRa1 transfected HeLa cells under fluorescence microscopy. Since then, I have continued to work with my two TR mutants, hcc-TRa1 and tc-TRa1, performing replicate experiments and testing for statistically significant differences in localization patterns.

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Second Week with Mutant Receptors!

During my second week in the Allison lab, I continued my work with the thyroid hormone receptor alpha 1 (TRa1). My transfected HeLa cells from last week had been stained, fixed and were ready to view under fluorescence microscopy. However, during this time I also had to replicate additional DNA plasmids that would express my wild type (wt-TRa1) and mutant receptors (described here and in my future posts as tc-TRa1 and hcc-TRa1)* if I wanted to continue my experiments. I did this through a process known as bacterial transformation, where I inserted the expression vectors for human TRa1 coupled with a gene for antimicrobial resistance into Escherichia coli cells and then allowed them to grow on plates with kanamycin, selecting only for those colonies that had taken up the plasmid. Later on, I isolated and purified the genetic material from the E. coli colonies to obtain a higher amount of my DNA plasmids.

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First Update! Mutant Proteins in Cancer Development

My first week working in Dr. Allison’s lab has been nothing short of incredible. I have had a unique opportunity to develop my laboratory and critical thinking skills while working with the thyroid hormone receptor (TR). As you may recall from my abstract, I am interested in understanding how mutations in this protein may lead to the appearance of cancer; specifically, my project will focus in studying mutations in the THRA gene, linked to thyroid cancer and hepatocellular carcinoma.

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Protein Transport in the Development of Cancer

Cancer, a group of diseases characterized by the uncontrolled division of abnormal cells, is nowadays the second leading cause of death in the United States. In order to understand what leads to the development of cancer, we need to look at the molecular mechanisms that control cell growth and division. What molecular biology has taught us so far is that the transport of proteins across the nucleus, where genetic information is stored and processed, is fundamental to the functioning of all living cells, and if this carefully balanced system is disturbed, cancer is likely to develop.

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