Nitika Taneja is researching the role of chromatin remodeling and reorganization in suppressing DNA replication stress. In other words, why can cancer cells become resistant to chemotherapy?
Last year, Taneja received an ERC starting grant and a VIDI grant for her research, and previously she discovered a new director of the DNA replication process and new ways to package chromatin under replication stress.
Chemotherapeutic drugs are often initially successful, but over time many patients develop cancer again. That recurrent cancer is then often more aggressive and develops resistance to chemotherapy. The cancer cells are then chemoresistant.
Says Taneja, “My research focuses on why that is. Chemoresistance is one of the biggest challenges in treating various types of cancer. A chemoresistant cell has an active DNA replication mechanism, which ensures unrestrained multiplication despite chemotherapy. The cells do not experience DNA damage from the therapy.’ The so-called replication forks that cause multiplication are protected by chromatin.
With the ERC grant, Taneja will investigate the underlying molecular mechanisms involved in the modification of chromatin at replication forks in response to chemotherapy-induced replication stress. With support from Oncode, Taneja will then translate her fundamental research findings into clinical applications.
Taneja, “We have developed tools to observe chromatin at replication forks from a single molecule to resolution of the genome. Using different tumor models, we want to identify new targets aimed at breaking the chromatin processes, in order to still be able to attack chemoresistant tumors with chemotherapy.’
