Event Title
Session 1G: Targeting MLL Gene Expression using CRISPR/Cas9 to Reverse the Phenotypes of Cancer
Session Number
Session 1G: 1st Presentation
Advisor(s)
Vandana Chinwalla, Illinois Mathematics and Science Academy
Location
Room A117
Start Date
28-4-2017 8:30 AM
End Date
28-4-2017 9:45 AM
Abstract
Every year, around 12.7 million people around the world are diagnosed with cancer. The Mixed Lineage Leukemia (MLL) gene, a global chromatin modulator, was first identified in acute aggressive forms of childhood lekukemias. MLL normally regulates gene expression through histone methylation, but when mutated its downstream targets may change, causing excessive replication, exacerbated cell growth, and the formation of cancer. Past research has shown that normal MLL is important for the expression of the cancer phenotype. This project aims to use the gene editing tool CRISPR/Cas9 to knock out MLL in different cancer cell lines to reverse the phenotypes of cancer. The MLL-gRNA CRISPR construct was designed to target the 5' end of genomic MLL to cause mutations and effectively knock it out. Preliminary results indicated that knocking out MLL led to an increase in cell death. The effect of MLL knockout will be evaluated in many other solid tumor lines in order to help establish MLL as a new therapeutic target in cancer therapies.
Session 1G: Targeting MLL Gene Expression using CRISPR/Cas9 to Reverse the Phenotypes of Cancer
Room A117
Every year, around 12.7 million people around the world are diagnosed with cancer. The Mixed Lineage Leukemia (MLL) gene, a global chromatin modulator, was first identified in acute aggressive forms of childhood lekukemias. MLL normally regulates gene expression through histone methylation, but when mutated its downstream targets may change, causing excessive replication, exacerbated cell growth, and the formation of cancer. Past research has shown that normal MLL is important for the expression of the cancer phenotype. This project aims to use the gene editing tool CRISPR/Cas9 to knock out MLL in different cancer cell lines to reverse the phenotypes of cancer. The MLL-gRNA CRISPR construct was designed to target the 5' end of genomic MLL to cause mutations and effectively knock it out. Preliminary results indicated that knocking out MLL led to an increase in cell death. The effect of MLL knockout will be evaluated in many other solid tumor lines in order to help establish MLL as a new therapeutic target in cancer therapies.