New insights into the molecular pathway that leads to excessive genome duplication in cancer cells

Saturday - May 18 2024, 23:51 UTC - 8 months ago

In a study published in the journal Science, scientists at Johns Hopkins Medicine have identified the molecular pathway responsible for excessive genome duplication in cancer cells. By understanding what goes wrong in the cell cycle, researchers may be able to develop treatments to stop the growth of cancers. This study focused on breast and lung cells and utilized imaging techniques to pinpoint the exact stage where malfunctioning occurs.

In a groundbreaking study published in the journal Science, scientists at Johns Hopkins Medicine have shed new light on the molecular pathway responsible for excessive genome duplication in cancer cells. This pathway, which is involved in regulating the cell cycle, can malfunction and lead to uncontrolled cell growth and division, a hallmark of cancer cells.

The human body has a precise and orderly routine for cell replication, a process known as the cell cycle. It starts with the duplication of the entire genome, followed by the separation of the duplicated genetic material, and then culminates in the division of the cell into two daughter cells with identical genetic information. However, when this process goes awry, it can result in the formation of cancer cells with abnormal numbers of chromosomes.

While a normal human cell has 23 pairs of chromosomes, or 46 total, cancer cells have been found to have a much greater number, up to 92. This posed a mystery to scientists--how do these cells end up with such a large number of chromosomes? .

Lead researcher Dr. Sergi Regot, an associate professor of molecular biology and genetics at Johns Hopkins University School of Medicine, explains, "An enduring question among scientists in the cancer field is: How do cancer cell genomes get so bad? Our study challenges the fundamental knowledge of the cell cycle and makes us reevaluate our ideas about how the cycle is regulated." .

The study focused on breast and lung cells, which are known to have a higher rate of cell division. This allowed for better visualization and observation of the cell cycle. By using glowing biosensors to tag enzymes involved in the cell cycle and analyzing thousands of images of individual cells, the researchers were able to pinpoint the exact stage where things go wrong.

One key factor they discovered was that cells that are stressed after copying their genome can enter a dormant, or senescent stage, and mistakenly run the risk of copying their genome again. Ordinarily, these dormant cells are recognized and eliminated by the immune system, but in certain circumstances, such as old age, the immune system may not be able to clear these cells effectively. This allows the faulty cells to continue replicating their genome unchecked, setting the stage for cancer development.

The implications of this study are significant. By understanding exactly how the cell cycle is regulated and what can go wrong, researchers may be able to develop therapies to interrupt the malfunctioning pathway and prevent the growth of cancer cells. This could potentially lead to more targeted and effective treatments for a wide range of cancers.

In summary, this study by the Johns Hopkins team has provided new insights into the molecular pathway responsible for excessive genome duplication in cancer cells. By focusing on breast and lung cells and utilizing state-of-the-art imaging techniques, this study has greatly advanced our understanding of the cell cycle and its role in cancer development.