Bupa revolutionises mental health support for individuals and families in the UK
Having a baby, getting married and buying a house have been voted the most significant milestones in a person’s life, but despite expectations of these being happy moments, they often leave many feeling vulnerable and stressed when their reality doesn’t live up to the social media hype.
Colorectal Cancer and its development
According to American Cancer Society, around 1 in 22 men and 1 in 24 women in the United States will receive a diagnosis of colorectal cancer at some point in their lives.At the start of 2016, there were approximately 1.5 million people in the U.S. with a history of colorectal cancer, some of whom were cancer free.
Colorectal cancer develops from uncontrolled growth and survival of abnormal cells in the colon or rectum, which are the final sections of the digestive, or gastrointestinal, tract.
The colon absorbs water and nutrients from what is left of food after it has traveled through the stomach and small intestine. It then passes the remaining waste to the rectum, which stores it ready for expulsion through the anus.
The most common precancerous stage of colorectal cancer is a polyp, which is a growth that develops in the tissue that lines the colon and rectum. Polyps grow very slowly, sometimes taking 20 years to develop.
Most polyps develop from cells that make up the glands that produce a lubricating mucus in the colon and rectum. For this reason, they have the name adenomatous polyps, or adenomas.
Adenomas are very common, and around 33–50 percent of people will develop at least one. However, while they can all become cancerous, less than 10 percent actually become invasive.
Oral bacterium has role in colorectal cancer
Scientists have known for some time that the abnormal cells that lead to cancerous adenomas in colorectal cancer arise because of genetic mutations that build up over time.
However, more recently, they have increasingly observed that F. nucleatum, which often occurs in tooth decay, also plays a significant role.
"Mutations," says senior study author Yiping W. Han, who is a professor of microbial sciences in the College of Dental Medicine, "are just part of the story."
"Other factors, including microbes, can also play a role," she adds.
In previous work, Prof. Han and her team found that F. nucleatum produces the molecule FadA adhesin, which sets off a series of molecular events in colon cells that scientists have linked to a number of cancers.
That work also revealed that the protein only has this effect in cancerous colon cells — it does not trigger these events in healthy colon cells.
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Why the bacterium only acts on cancer cells
Prof. Han says that the goal of the more recent study was to "find out why F. nucleatum only seemed to interact with the cancerous cells."
The researchers started the new work by studying noncancerous colon cells in culture. They saw that these did not make the protein Annexin A1, which promotes growth in cancer cells.
Further tests in cell cultures and in mice revealed that blocking the protein stopped F. nucleatumfrom being able to attach to cancer cells, which stopped them growing so fast.
Another set of tests also revealed that the microbe stimulates cancer cells to make more Annexin A1, which in turn attracts more F. nucleatum.
"We identified a positive feedback loop that worsens the cancer's progression," Prof. Han explains. The cancer cells make Annexin A1 that then attracts F. nucleatum, the effect of which is to spur them to produce more of the protein.
We propose a two-hit model, where genetic mutations are the first hit. F. nucleatum serves as the second hit, accelerating the cancer signaling pathway and speeding tumor growth."
