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Full-Text Articles in Medicine and Health Sciences
Modeling The Adaptive Immune Response To Mutation-Generated Antigens, Rory J. Geyer
Modeling The Adaptive Immune Response To Mutation-Generated Antigens, Rory J. Geyer
University Scholar Projects
Somatic mutations may drive tumorigenesis or lead to new, immunogenic epitopes (neoantigens). The immune system is thought to represses neoplastic growths through the recognition of neoantigens presented only by tumor cells. To study mutations as well as the immune response to mutation-generated antigens, we have created a conditional knockin mouse line with a gene encoding, 5’ to 3’, yellow fluorescent protein (YFP), ovalbumin (which is processed to the immunologically recognizable peptide, SIINFEKL), and cyan fluorescent protein (CFP), or, YFP-ovalbumin-CFP. A frame shift mutation has been created at the 5’ end of the ovalbumin gene, hence YFP should always be expressed, …
Modeling The Adaptive Immune Response To Mutation-Generated Antigens, Rory J. Geyer
Modeling The Adaptive Immune Response To Mutation-Generated Antigens, Rory J. Geyer
Honors Scholar Theses
Somatic mutations may drive tumorigenesis or lead to new, immunogenic epitopes (neoantigens). The immune system is thought to represses neoplastic growths through the recognition of neoantigens presented only by tumor cells. To study mutations as well as the immune response to mutation-generated antigens, we have created a conditional knockin mouse line with a gene encoding, 5’ to 3’, yellow fluorescent protein (YFP), ovalbumin (which is processed to the immunologically recognizable peptide, SIINFEKL), and cyan fluorescent protein (CFP), or, YFP-ovalbumin-CFP. A frame shift mutation has been created at the 5’ end of the ovalbumin gene, hence YFP should always be expressed, …
Identification And Characterization Of Downstream Effector Protein(S) Regulated By P53 And Prb, Miranda B. Carper
Identification And Characterization Of Downstream Effector Protein(S) Regulated By P53 And Prb, Miranda B. Carper
Theses, Dissertations and Capstones
A commonality among cancer types is the high frequency of mutations that inhibit or alter signaling of the p53 and pRb (Retinoblastoma) tumor suppressors. These genes regulate processes vital for cancer suppression such as apoptosis, senescence, and cell cycle arrest among others. Loss of both p53 and pRb promotes processes that support cancer progression and is associated with decreased patient survival and increased rates of tumor reoccurrence. Although data points to the ability of p53 and pRb to collaborate and to inhibit tumorigenesis, it remains unclear how p53 and pRb cooperate toward this task. Using RNA expression profiling, 179 p53 …