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Vatican Hospital Marks Breakthrough in Cancer Research

Research conducted by the Bambino Gesù Children’s Hospital sheds light on the cycle of cell division.

Research conducted by the Vatican’s Bambino Gesù Children’s Hospital, in collaboration with Tor Vergata University of Rome and other European and U.S. research centers, has made an important breakthrough in cancer research.

After decades of research and many hypotheses, experts discovered the missing piece in cancer studies: the “switch” that regulates the life of Cyclin D (an essential molecule in cell division). (Read: 3 Ways to Support a Loved One Diagnosed With Cancer)

According to the results of the study published in the science magazine Nature, the switch that turns the activity of Cyclin D on and off is a protein called Amber1. When it does not work, it triggers a process that leads to the rapid formation of many types of cancer.

With the discovery, experts can now develop specific therapies that can inhibit the cell cycle of the diseased cells and eventually lead up to their self-destruction.

Errors of Cell Cycle

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On the left a healthy cell in duplication phase. On the right a defective cell, lacking the protein Amber1, during duplication.(Photo from Maiani, Miletti, Nature 04-2021/Vatican News)

By general knowledge, the cell cycle involves a series of events that lead to the division of cells. This process, which eventually leads to the birth of new cells, is regulated by the cyclins— a group of proteins classified with the letters A, B, C, D, and so on.

In some cases, the proteins responsible for controlling the cell cycle can face errors which can become the cause of cell mutations, tumors, and cell death. (Read: 3 Things Every Woman Should Do to Prevent Breast Cancer)

And while scientists have already developed some mechanisms to regulate these proteins, they have not yet discovered ways to regulate Cyclin D — until now.

Cancer Research

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(Left) Professor Francesco Cecconi, researcher at Bambino Gesù Hospital and professor of Developmental Biology at the Tor Vergata University of Rome. (Right) Professor Franco Locatelli, president of the Higher Health Council and member of the technical-scientific committee (Photos from Tomas Bertelsen/Via Ritzau and Fotogramma)

Led by Professor Francesco Cecconi and directed by Professor Franco Locatelli, the cancer research in Bambino Gesù Hospital was conducted on hundreds of samples —  animal models, cells produced in the laboratory, cells derived from both animal and human tumors.

During the investigations, the researchers noticed that in case of an absence of or low amount of Amber1, Cyclin D is not destroyed as it should be — hence, it accumulates. (Read: Xian Lim Grants Wish of His Lola Who Was Diagnosed With Cancer)

Due to this accumulation, cells begin to divide at an uncontrolled rate, DNA is damaged, and the formation of tumor masses is triggered.

Therapeutic Perspectives

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Photo from FatCamera/Getty Images/Verywell Health

Because no drugs are available yet that can act on the two proteins to restore the right amount, researchers have identified an alternative solution that exploits one of the weak points of cancer cells: the repair system.

To simply put it, if the repair process is inhibited, the diseased cells accumulate so many defects that they self-destruct. This treatment strategy has already been proven effective on cellular and animal models, and Cecconi suggests that is now ready for some types of human tumors.

“The idea is that patients diagnosed with cancer will also be examined for levels of Ambra1 and Cyclin D,” says Cecconi, researcher at Bambino Gesù Hospital and professor of Developmental Biology at the Tor Vergata University of Rome. (Read: Exclusive: An Interview With the Pope’s Personal Doctor)

“If the absence or low levels of Ambra1 in association with an accumulation of Cyclin D is detected in tumor cells, we could try to suppress the ability of tumor cells to repair the genetic material with specific drugs that are already used in therapy,” he adds.

 


Text by Vatican News staff writer.

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