A Possible Anti-Aging Approach to Hepatocellular Carcinoma

According to Phys.org, a group of researchers at the Medical University of South Carolina recently discovered exciting news regarding cancer cells in humans. Specifically, these scientists have found that these particular cells stop dying if the aging process can be controlled. They are currently using their new information to use an inhibitor in a phase 2 trial for patients with hepatocellular cancer.

What is Hepatocellular Cancer?

The most common type of liver cancer hepatocellular carcinoma. The cause of hepatocellular carcinomas are unknown, and symptoms include loss of appetite, weight loss, weakness or fatigue, nausea and vomiting, and bloating or swelling in the belly. There are currently a few treatment options available for those with the condition, including radiation, chemotherapy drugs, or surgery. To read more about hepatocellular carcinoma and cancer, click here.

The Aging/Cancer Connection

At South Carolina, researchers are aware that cancer becomes more common as people age, but they’re trying to pinpoint why exactly that is the case. Besim Ogretmen, Ph.D., from the Hollings Cancer Center found discovered that the reason for this may be because cancer cells find a way to avoid dying even though normal cells die naturally with time and age. These cancer cells, Ogretmen’s team found, achieve this immunity by protecting the tips of their chromosomes from aging.

A Little About Telomeres

When normal cells age, the tips of their chromosomes, also known as telomeres, eventually signal cell death. This process is known as the typical aging pattern in cells. That said, cancer cells successfully avoid telomere death, and subsequently stay in the body as healthy cells for much longer than the average cell. Therefore, the longer life span of these cancer cells is partially responsible for the rapid growth and spread of them throughout the body.

“Telomeres are like a biological clock for our cells,” Ogretmen stated. “In cancer, this biological clock is broken.”

A New Discovery

Ogretmen and his team also found that a certain protein, p16, plays an important role in decision-making for cancer cells that become damaged after chemotherapy or aging. They found that p16 basically decides whether or not cells grow older or just die.

P16 is also responsible, they found, for keeping telomeres alive when they start to show signs of breakdown. To apply this knowledge, a team of researchers utilized a chemical inhibitor to spur telomere damage in many different kinds of cancer cells.

ABC294640 is the name of the inhibitor, and it effectively stops cancer cells from protecting their telomeres. The inhibitor, as a result, basically forces telomeres to go through the natural process and break down.

This enzyme inhibitor was effective in properly damaging telomeres and therefore leading to cancer cell death, but only when cells had low p16 levels. However, in those cells that had high p16 levels, the cancer cells stayed alive in an inactive form. This is a result of aging.

“We’re excited that there is at least one mechanism that can help us understand how aging is associated with a higher risk of cancer,” Ogretmen stated. “And then, can we prevent or better treat the aging-related cancers by controlling protective effects of p16 for cancer cell death?”

The Implications

The group of researchers are optimistic about the future of cancer treatment with this new development. Ogretmen and his team believe that they will be able to fight cancer on many levels in the future.

The team, so far, has found a safe dose of the inhibitor to be given to patients with hepatocellular carcinoma in a planned phase 2 clinical trial. If their research is sound, that means not only good news for cancer, but anti-aging as well.

“We hope that maybe we can do both: delay aging and prevent the growth of cancer,” explained Ogretmen “That’s the ultimate outcome of this.”

To learn more about this fascinating research, click here.


Share this post

Share on facebook
Share on google
Share on twitter
Share on linkedin
Share on pinterest
Share on print
Share on email
Close Menu