Some cancers can be transmitted by a widespread oral microbe

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The news that you could have cancer is not something you can treat with susceptibility. Although the causes are diverse and many remain undiscovered, the evolution in research continues uninterrupted.

Recently, an unexpected player appeared in this process: a common bacterium. Fusobacterium nucleatum, which is normally found in the gingival environment and is completely harmless, seems to play a role in the spread of cancers of the colon, esophagus, pancreas and – possibly – breast.

Laboratory studies and samples from patients indicate that the microbe can travel through the blood and infect tumor cells by attaching to a sugar molecule on their surface.

There it causes a number of signals and immune responses known to determine the migration of tumor cells.

If confirmed, research on F. nucleatum could add to a growing understanding of how the microbiome influences cancer progression and may even point the way to new approaches to treatment.

What is F. nucleatum and when does it become dangerous?

In a healthy human oral cavity, F. nucleatum is a member of the microbial community.

With poor dental hygiene, uncontrolled diabetes and other conditions, however, it can become a threat and can cause periodontitis, tonsillitis, appendicitis and even premature labor.

A link between this bacterium and colorectal cancer was first suggested about nine years ago, when two research groups found that the bacterium’s DNA was over-represented in colon tumor tissue compared to normal tissue.

However, the question remains: Is this error just a warning sign or is it an active participant in cancer progression? During this year, studies on colon cancer, conducted by separate teams, indicated an active role of this bacterium.

“We came to the same conclusion in different ways,” says biochemist Daniel Slade of Virginia Tech.

Slade and colleagues found that when cultured human colon tumor cells were invaded by F. nucleatum, they produced two inflammatory proteins called cytokines – specifically, interleukin 8 and CXCL1 – that were shown to allow malignant cell migration.

A second study reported that the bacterium induces changes in the regulation of genes that stimulate lung metastasis in mice.

A third study found that the abundance of F. nucleatum in human colon cancer tissue is correlated with the amount of metastases and, in mice, identified additional signals through which the microbe can “orchestrate” metastasis.

Slade and others have also shown that the bacterium incites a kind of cytokine storm that targets infection control but ultimately exacerbates cancer. “It’s like throwing gas on an already burning fire,” says Slade.

How much this happens to people is, of course, a critical question.

“The findings are interesting and meaningful,” said Joan Massagué of the Memorial Sloan Kettering Cancer Center, who is a lead investigator of metastases.

Inflammation is invariably part of the metastatic process, he says, so an infection that triggers a dramatic inflammatory reaction in a tumor will have a consequence: “it helps cancer cells engage in mobile, invasive behavior.”

Discoveries about fusobacterium nucleatum they are part of a fast-moving area that identifies how the microbiome influences and fights cancer.

Many modern immunotherapy drugs, for example, work best in the presence of beneficial microbes, as do some older chemotherapies. Some scientists assume that fusobacterium could eventually be turned into a cancer fighter.

Given the sensitivity of the microbe to a sugar on tumor cells, they suggest that a kind of “Trojan horse” process can be carried out by using cellular sugar in drugs that will target malignant tumors.


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