Advancement in the Radiation Shielding Materials Market Allows Development of New Combination Therapies to Cure Cancer
Posted On March 04, 2021
Too much radiation can cause problems for cells, tissues, and organs alike. It is common knowledge that some tissues are more vulnerable to radiation caused by radiation than others. Scientists are aware that this difference is caused due to the involvement of p53 protein. It is a well-studied tumor-suppressor protein that can initiate a cell’s auto-destructive programs. Even with this knowledge, the protein’s involvement is not yet fully understood as they are often present similarly in tissues but vary in their sensitivity toward radiation.
A recent study might help to shed light on this mystery that has confused scientists for a long time. In the research, the team describes that the survival of cells after radiation depends on the behavior of p53 over time. They stated that in tissues that are vulnerable to radiation, p53 levels go up and then remain high, in turn resulting in the death of the cell. In contrast, in tissues that can survive the radiation, p53 levels in them oscillate up and down. This study is a significant development for Radiation Shielding Materials Market as it suggests new strategies to make combination therapies for cancer much better. It will be nice to observe how it may lead to critical clinical discoveries in the medical field.
Understanding biology as a subject is restricted to a specific limit as scientists make do with snapshots. If they get to see how things evolve temporally, more information would be brought into light that is crucial for the dissection of diseases and the creation of therapies. Hence, the dynamics of things matter and how they change over time.
In their research, the team discovered that some tumors present in mice were more prone to radiation damage after being given a drug that blocks p53 levels from either oscillating or declining. It was noted that when tumors were treated this way, they shrunk more than they did when they received only the drug or radiation alone. Researchers found a connection between different temporal p53 expressions with radiation response, which enabled them to ‘coax’ radioresistant tumors into more radiosensitive ones.
Some cancers can evolve themselves to become resistant to radiation therapy. Hence, the team tried to manipulate p53 dynamics that would lead to an increase in tumor vulnerability. They focused on human colon cancer cell lines by using unmutated, functional p53.
The team did experiments on mice with the protein. They transplanted human colon cancer tumors and discovered that the tumor shrunk after a single dose of MDM2 inhibitor if it was injected shortly after irradiation. In 6 weeks, tumors that were treated with drugs and radiation shrunk five times than those that were treated solely by drugs and half of the ones treated by radiation.
The study's main objective was to gain knowledge so that better and efficient therapies could be developed for fighting cancer. Hence, further research must be undertaken to understand how p53 operates.