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It is well known that the length of the small intestine responsible for digestion and absorption in the body is relatively long, normally between 4 and 6 meters, accounting for 70% to 80% of the full length of the gastrointestinal tract, and its mucous membrane surface area is also relatively large.
Despite its size, small intestine primary tumors are extremely rare, accounting for only 2% of gastrointestinal tumors, while up to 98% of tumors occur in the colon.
question: Why is the colon so prone to cancer than the small intestine? In a new study published July 30 in the journal Nature, a team from the Hebrew University of Israel may have found the answer to these questions when they study the link between gut bacteria and gastrointestinal cancer.
they found that the cancer mutation itself was not necessarily harmful.
in fact, in some intestinal microenvironments, these mutations can actually help the body fight cancer, rather than spread it.
However, if the gut microbiome produces certain high levels of metabolites, such as some found in antioxidant-rich foods such as black tea and hot cocoa, it becomes a hotbed of mutant genes and accelerates the growth of bowel cancer. One of the main differences between the organs of the
small intestine and colon is the level of bacteria in their intestines, which is smaller in the small intestine and more in the colon. "The gut microbiome and human health are now hot research areas," said Yinon Ben-Neriah, a
research author and professor at the University of Hebrew Studies' Lautenberg Center for Immunology and Cancer Research.
we all know that they have many positive effects, but in certain cases they can also play a role in 'helping to abuse'.
" first put this TP53, a gene found in every cell.
it produces a protein that acts as a cell barrier, called p53.
p53 is known as a gene guardian, which inhibits genetic mutations in cells.
However, when p53 is damaged, it no longer protects cells, but is turned back by cancer and throws it into enemy countries to help the tumor spread and grow.
to test the theory, the researchers introduced the mutant p53 (cancer-promoting version) protein into the intestines.
surprising, the small intestine's response is to "correct" the mutant p53 cancer driver, to return to normal p53, and to become a "super inhibitor" that inhibits cancer growth more than a healthy p53.
However, when the mutant p53 is introduced into the colon, they are not "corrected", but rather maintain their cancer-driven properties and promote the spread of cancer cells. Ben-Neriah,
, said: "We were attracted to what was happening, and gut bacteria had a double effect on the mutated p53 protein.
in the small intestine, they completely change the process to attack cancer cells, while in the colon, they promote cancer cell growth. "To further validate their theory that the intestinal flora is a major factor in causing the mutation p53 to act as a tumor blocker in the small intestine and to act as a tumor promoter in the colon, the team used antibiotics to kill the intestinal flora in the colon,"
.
found that the mutant p53 could no longer help cancer cells grow.
question again: What makes colon cancer spread so fast? After careful analysis, the researchers identified the culprit: the gut flora produced a metabolite, known as an "antioxidant."
the substance is high in foods such as black tea, hot chocolate, nuts and berries.
apparently, when the researchers fed mice antioxidant-rich foods, their gut flora accelerated p53's "cancer-boosting" pattern.
this finding is particularly important for patients with a family history of colorectal cancer. "Scientifically
speaking, this is a new field," said Ben-Neriah, who is "not alarmed by his own colon problems and family history of colon cancer."
we were surprised at the extent to which gut bacteria affected cancer development and, in some cases, completely changed their nature.
", those at high risk of colorectal cancer may need to focus more frequently on their gut flora and think twice about digesting foods, antioxidants, and other aspects.
.