Introduction
My name is Bhuvi, and I am a senior at BASIS Phoenix. Over the next ten weeks, I will be researching chemoresistance in esophageal cancer. I have been interning at the Norton Thoracic Lab for the past two years, primarily observing techniques such as qPCR, Western Blots, organoid creation, and cell culture assays focusing on the Epithelial to Mesenchymal Transition in Chemoresistance.
In particular, qPCR is a system that aids in identifying the protein encoded by an mRNA in a specific portion of DNA. Western Blots are utilized to identify biological markers in proteins, and organoids represent a 3D heterogeneous cell culture model mimicking conditions found in human organs.
EMT, or epithelial-mesenchymal transition, is a biological process in which cells undergo a transformation from a stationary, organized epithelial state to a more migratory, mesenchymal state. In cancer, EMT plays a crucial role in promoting tumor progression and metastasis by enabling cancer cells to invade surrounding tissues and distant organs.
Chemoresistance is a significant problem in cancer treatment, as resistance to cancer therapy results in cancer-related morbidity. Patients who face chemoresistance often undergo two or three extra rounds of different chemotherapies after their initial treatment, which are more toxic and less effective than the first. My goal is to minimize the number of extra treatment rounds to one extra round of chemotherapy that is effective and targets one to two markers within the tumor, personalizing the drug to each tumor.
My current project, titled ‘Potential Markers to Combat Afatinib Resistance in Esophageal Adenocarcinoma,’ will utilize Western Blots, qPCR, and cell cultures to unravel the mechanism of chemoresistance. Afatinib, a chemotherapy agent targeting the Epidermal Growth Factor Family, has proven effective against the esophageal adenocarcinoma cell line OE33. However, this effectiveness gives rise to a resistant cell line known as GD.
I hypothesize that other growth-factor receptors become activated to overcome afatinib-mediated resistance. This leads to intriguing questions about which growth-factor receptors are involved and whether these pathways are driving afatinib resistance.