DNA, the genetic code present in all living organisms, consists of a double helix strand. When both strands of this helix break simultaneously, it creates significant genetic damage. Long understood by the scientific community, such DNA damage can sometimes lead to dangerous mutations, which over time can be a cause for the development of tumors.
Dr. Tomasik, affiliated with GUMed's Department and Clinic of Oncology and Radiotherapy, co-authored a paper detailing the newly identified process for repairing these double-strand breaks in DNA. The research paper was published in the journal "Nature Structural & Molecular Biology". It sheds light on cellular reactions involving the DYNLL1 and MRE11 proteins, and a multi-protein complex called Shieldin.
Proteins like DYNLL1, MRE11, and the Shieldin complex play a role in how our cells function, being able to repair themselves and respond to damage. When these processes are understood better, it can lead to improvements in cancer treatments.
The research was a collaboration involving scientists from the team of Dipanjana Chowdhury, Professor of Radiation Oncology at Harvard Medical School's Dana-Farber Cancer Institute. Speaking about his role, Dr. Tomasik said, "I worked with Professor Chowdhury's team in 2020-2021 during a postdoctoral fellowship, supported in part by the National Academic Exchange Agency and the Prof. Walczak program." He added, "My main responsibility in the project was the creation of stable cell lines using the CRISPR/Cas9 technique, which allows for selective genome editing."
The implications of this discovery could be important for certain cancer therapies. A better understanding of DNA repair mechanisms could address potential problems in the effectiveness of such therapies.
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Source: Nauka w Polsce, GUMed
