Researcher wins grant to study anti-cancer compound


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Photo by Courtesy of newswise.com |

Dr. Darren Carpizo, a surgical oncologist at the Rutgers Cancer Institute of New Jersey, was given a grant to continue his research on an anti-cancer compound.


The National Institute of Health awarded a Rutgers researcher $794,790 to study an anti-cancer compound that prevents the unlimited replication of cancer cells.

Dr. Darren Carpizo, a surgical oncologist at the Rutgers Cancer Institute of New Jersey, was given the grant to continue research on this compound.

According to the U.S. National Library of Medicine website, the compound NSC319726 restores reproduction control to the protein that gene p53 produces.

Normally, the protein tells cells when to stop replicating, but the cancer-causing mutation prevents that stopping signal, Carpizo said.

“Changes develop in certain genes that allow cells in your body to grow uncontrollably,” he said.

This changes gene coding, causing mutations that result in cancerous cells.

The gene responsible for the proper production of protein p53 is the most commonly mutated gene in human cancer, he said. This mutation benefits cancer cells by promoting unlimited reproduction, resulting in a tumor.

Once a cell loses function of p53’s protein, it leads to a number of secondary processes that induces cancer and causes cells to divide uncontrollably, Carpizo said. The goal is to restore the function of p53 in tumors.

“Many people who do not have cancer probably have developed a cancer in their body by the time they reach an older age,” he said.

They never clinically get cancer because the cells that become cancer cells still have the normal functions of the p53 gene.

The process in which a normal cell becomes a cancer cell is a microcosm of natural selection, he said. If a cell has the wrong combination of mutations, then that cell has less of a chance of being cancerous.

If a cell does not acquire a mutation of p53, leaving p53 fully functional, then it likely will not survive, he said. The p53 gene serves as a guardian of the DNA to prevent further mutations that could cause cancer.

“There are probably two or three hundred genes that have been verified to be important to the development of a cancer cell,” he said. “Two or three hundred out of 25,000.”

There are two types of mutations in p53   — one in which the corresponding protein is not made at all and another in which the protein is made defectively, he said.

In a majority of mutations, the latter occurs, he said. The cell loses the function of p53 and reproduces uncontrollably.

“We’ve discovered a drug in our laboratory that will take these defective proteins and make them work again,” he said. “The discovery of p53 reactivation led to this grant.”

They are studying two main pieces of information: how the protein reactivates and how to evaluate the compound in terms of its potential to become a clinical drug.

“There are some that believe that even if the proteins are defective. They have other purposes inside the cell,” he said.

The other properties of the defective proteins that are beneficial to cancer cells are not yet known, but are being researched, he said. Mutations are believed to be manually selected during the process of transformation from a normal cell to a cancer cell.

“It is completely possible that the defective protein battle to promote the life of the cancer cells,” he said. “These defective proteins are definitely advantageous for them for more than just reproduction.”

The p53 gene is one of the most important genes related to the development of cancer, he said. It has been considered this way for almost 30 years now.

He believes compounds that thwart cancer cells and leave normal cells undisturbed, such as NSC319726, will define the next generation of anti-cancer drugs

According to the publication in Nature magazine, the compound has been successfully tested in mice. Further research needs to be done to be able to make a human-friendly drug.

“There are large international projects now to sequence peoples’ DNA in their tumors,” he said.


By Andrew Rodriguez

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