<img alt="An international research team led by Stanford University School of Medicine in the United States announced research results related to small, circular extrachromosomal DNA (ecDNA). If ecDNA continued to accumulate after cell division (left), the cancer got worse./Stanford University, USA” class=”thumb_g_article” data-org-src=”https://t1.daumcdn.net/news/202411/07/chosunbiz/20241107010030535qeio.jpg” data-org-width=”1500″ dmcf-mid=”5dzlccphzC” dmcf-mtype=”image” height=”auto” src=”https://img1.daumcdn.net/thumb/R658x0.q70/?fname=https://t1.daumcdn.net/news/202411/07/chosunbiz/20241107010030535qeio.jpg” width=”658″/>
An international research team led by Stanford University School of Medicine in the United States announced research results related to small, circular extrachromosomal DNA (ecDNA). If ecDNA continued to accumulate after cell division (left), the cancer got worse./Stanford University, USA
It was revealed that cancer is caused not by chromosomal deoxyribonucleic acid (DNA), which is the main genetic material, but by ‘extrachromosomal DNA (ecDNA)’, which was considered to be less important. Chromosomes are strands of DNA in the cell nucleus wrapped around a protein that acts as a spool. Because it is 95% water, it is hard to see, but it dyes well, so it is given this name. This means that fragments of DNA moving around unraveled from failure are the main cause of cancer.
An international joint research team led by Stanford University School of Medicine in the United States analyzed data from approximately 15,000 cancer patients and announced the results of a correlation between ecDNA and cancer’s later outcomes. Based on this, a new cancer treatment method that blocks ecDNA was also proposed. The research results were published in three papers in the international academic journal ‘Nature’ on the 7th.
Previous studies have also shown that small, circular forms of ecDNA contain cancer or immune-related genes. However, interest in ecDNA faded as statistics emerged showing that only about 2% of all tumor samples contained meaningful amounts of ecDNA.
To reexamine the role of ecDNA, the research team conducted a large-scale study analyzing genetic data from 14,778 patients with 39 types of cancer. As a result, ecDNA was found in 17.1% of cancer cell samples. In particular, ecDNA was more common in patients whose cancer worsened and who received targeted treatment and chemotherapy.
This means that DNA outside the chromosomes made the cancer more severe. In fact, ecDNA was also associated with high treatment resistance and low survival rates. Some ecDNAs interacted with other ecDNAs and played a role in expressing oncogenes.
“This study is the product of data collection and analysis,” said Stanford University professor Paul Michel. “We learned important lessons about which cancer patients are affected by ecDNA and which genes or sequences are found in ecDNA.”
ecDNA was randomly isolated when cells divided. After cell division, some new cells contained a lot of ecDNA, while other cells had no ecDNA at all. However, there were ecDNA combinations that were repeatedly inherited from mother cells to daughter cells. The researchers described this case as a ‘jackpot’ event and explained, “As a favorable ecDNA combination is transmitted, resistance to the drug can develop.”
Based on these results, the researchers proposed a treatment targeting ecDNA. As a result of the study, the growth of cancer cells containing ecDNA could be suppressed by blocking the protein ‘CHK1‘, which plays an important role in replicating DNA during cell division. Using this, they succeeded in reducing the size of the tumor by administering a drug that inhibits CHK1 to mice with tumors. Currently, researchers are conducting clinical trials on some cancer patients.
Professor Michel added, “This study presents a completely new understanding of cancer development and evolution,” and added, “We plan to study the role of ecDNA in depth to develop treatments that can provide practical benefits to cancer patients.”
reference material
Nature(2024), DOI:
Nature(2024), DOI:
Nature(2024), DOI:
