Identification of DNA repair genes holds promise for improving cancer treatment
Cancer is one of the leading causes of death in the United States and around the world. In fact, according to the Centers for Disease Control and Prevention (CDC) in 2018 (the most recent year for which data is available), 1,708,921 new cases of cancer were diagnosed and 599,265 people died of cancer in United States.
It is a genetic disease, and as such, understanding DNA
A new way cancer cells can repair DNA damage has been discovered by researchers from the University of Birmingham.
These new findings shed new light on how cancer cells respond to chemotherapy and radiation therapy, and also uncover a new way in which cancer can become resistant to targeted treatments. This information can help clinicians choose different cancer treatments that may be more targeted to specific patients.
Repairing DNA damage is vital for keeping cells healthy and preventing the development of diseases like cancer. Understanding how DNA repair works is crucial to better understanding how cancer develops, and also how cancer treatments such as radiation therapy and chemotherapy can be used effectively to induce DNA damage that kills cancer cells. .
In the study, published May 19, 2022, in the journal molecular cella team of researchers from the University Institute of Cancer and Genome Sciences has identified two previously unidentified proteins in the DNA repair process.
Called SETD1A and BOD1L, these proteins modify other proteins called histones that are bound to DNA. Removing these two proteins changes the way DNA is repaired and makes cancer cells more sensitive to radiation therapy. The loss of SETD1A and BOD1L also makes cancer cells resistant to certain cancer drugs called PARP inhibitors.
Lead author, Associate Professor Martin Higgs, explained: “This is the first time that these genes have been directly linked to DNA repair in cancer. This research has the potential to change how cancer patients are identified for treatment and also how they become resistant to different drugs, which will improve treatment effectiveness as well as patient outcomes.
The team hopes that the work could eventually lead to the development of new inhibitors that would allow clinicians to resensitize cancers that have become resistant to certain therapies.
Reference: “H3K4 Methylation by SETD1A/BOD1L Facilitates RIF1-Dependent NHEJ” by Rachel Bayley, Valerie Borel, Rhiannon J. Moss, Ellie Sweatman, Philip Ruis, Alice Ormrod, Amalia Goula, Rachel MA Mottram, Tyler Stanage, Graeme Hewitt , Marco Saponaro, Grant S. Stewart, Simon J. Boulton and Martin R. Higgs, April 18, 2022, molecular cell.
The research was funded by the Medical Research Council, CRUK and the Wellcome trust.