Scientists Detect Doubling in the Source of Cancer Cells published in the May 3 edition of Science, uncover the malfunction that occurs when a cluster of molecules and enzymes initiates and controls the ‘cell cycle,’ the recurring sequence responsible for generating new cells from the genetic material within cells.
| Date | May 2, 2024 |
| Source | Johns Hopkins Medicine |
| Summary | By experimenting with human breast and lung cells, researchers report they have mapped out a molecular pathway capable of enticing cells into a perilous journey of excessive genome duplication, a characteristic feature of cancerous cells. |
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About Cell Cycle and Cancer:
Cells reproduce in an orderly manner, beginning with generating a duplicate of their entire genome, then separating the genome copies, and lastly dividing the replicated DNA evenly between two “daughter” cells.
Human cells have 23 pairs of each chromosome – half from the mother and half from the father, including the sex chromosomes X and Y – for a total of 46, however, cancer cells are known to go through an intermediate state with double that amount (92 chromosomes). How this occurred was a mystery.
Cells that are stressed after copying the genome may go dormant, or senescent while scientists detect doubling in the source of cancer cells in their experiment.
The immune system sweeps out these latent cells once they are “recognized” as defective. However, the immune system cannot always eliminate the cells, especially as humans age. If left to meander in the body, aberrant cells can reproduce their genome, shuffle the chromosomes at the next division, and a cancerous tumor develops.
Visualize The Cell Division Here
Experiment: Scientists Detect Doubling in the Source of Cancer Cells
| Sl. No. | Experiment | Observation | Conclusion |
| 1. | For this recent investigation, the team meticulously analyzed numerous images capturing individual cells undergoing cell division. Utilizing luminous biosensors, the researchers labeled cellular enzymes known as cyclin-dependent kinases (CDKs), renowned for their regulatory role in the cell cycle. | They observed that various CDKs became active at distinct stages throughout the cell cycle. Following exposure to environmental stressors—such as drugs impeding protein synthesis, UV radiation, or sudden changes in water pressure around cells (osmotic stress)—the researchers noted a decrease in the activity of CDK 4 and CDK 6. | In the context of the stressed environment explored in this study, APC( anaphase-promoting complex) activation occurred before mitosis, contrary to its typical activation solely during mitosis. |
| 2. | Approximately 90% of breast and lung cells halt their progression through the cell cycle and enter a quiescent state upon exposure to environmental stressors. | However, within their experimental cell population, not all cells entered this quiescent state. | The research team observed that around 5% to 10% of breast and lung cells resumed the cell cycle, undergoing chromosome division once more. |
There is a possibility that a combination of drugs might induce certain cancer cells to undergo genome duplication twice, leading to the creation of heterogeneity that ultimately results in drug resistance because scientists detect doubling in the source of cancer cells.
1. Why breast and lung cells were used in this experiment
Human cells that line breast ducts and lung tissue divide at a faster rate than other cells in the body, providing more opportunities to observe the cell cycle.
2. What was the challenge of scientists?
A long-standing topic among cancer researchers is, that how do cancer cell genomes become so bad. Sergi Regot, Ph.D., is an associate professor of molecular biology and genetics at Johns Hopkins University School of Medicine said that their findings call into question their basic understanding of the cell cycle and force them to reconsider how it is regulated.
3. What are the prospect of this experiment?
The discoveries offer potential for the development of treatments aimed at disruptions in the cell cycle, which could potentially halt the proliferation of cancers and there might exist medications capable of inhibiting APC activation before mitosis, thereby preventing cancer cells from undergoing genome duplication twice and impeding the progression to tumor stage.