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Back|Intestinal inflammation may break the dormancy of cancer cells. Study: Changes in bone marrow environment are key
Intestinal inflammation may break the dormancy of cancer cells. Study: Changes in bone marrow environment are key
Health
自由时报·2 hours ago·Health·2 min read·🇨🇳China·

Intestinal inflammation may break the dormancy of cancer cells. Study: Changes in bone marrow environment are key

Quick Look

  • A British research team found through a mouse bone marrow model that intestinal inflammation changes the bone marrow environment, leading to an increase in HMGB2 molecules, which in turn reactivates dormant breast cancer cells and increases the risk of metastatic tumor growth.
  • However, they emphasize that inflammation does not mean that cancer will definitely recur.

AI-generated summary

Why It Matters

Breast cancer cells often metastasize to the bone marrow and enter a dormant state, where they are less vulnerable to immune system attack and resistant to chemotherapy. The research team developed mouse bone marrow models to observe the behavior of dormant cancer cells.

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[Compiled by Xie Yizhe/Comprehensive Report] A British study found that the body's response to inflammation may interfere with cancer cells that have been dormant for many years and give these cancer cells a chance to reactivate and grow. The research was published in the journal Cell Reports.

According to science website SciTechDaily, breast cancer cells often metastasize to the bone marrow, and when these cancer cells enter a dormant state, they are less susceptible to attack by the immune system and more resistant to chemotherapy. Francis of England. A team at the Crick developed a mouse bone marrow model and found that intestinal inflammation may reactivate dormant breast cancer cells.

Please read on...

Since ordinary mice have a limited lifespan and cannot allow the research team to spend several years observing whether dormant cancer cells in their bodies are reactivated, the researchers decided to develop a special model. The research team has previously developed a bone marrow exoskeleton model. This bionic bone tissue contains the bone marrow cells needed to make blood cells and can respond to inflammatory signals like natural bone marrow. When the researchers added cells from mouse mammary tumors to bionic bone tissue, most of the cancer cells went dormant, with only a few cells replicating occasionally.

Completing the mouse bone marrow model allowed the team to explore how events occurring elsewhere in the body affect quiescent cancer cells. Fractures and other bone injuries may promote the growth of metastatic cancer cells in the bone marrow, but the researchers wanted to further determine whether injuries or infections occurring at more distant sites could also disrupt the dormant state of cancer cells.

The research team induced intestinal inflammation in mice and found that as the bone marrow environment changes, the number of dormant cancer cells that begin to divide gradually increases, thereby increasing the possibility of tumor formation. The researchers explained that when the intestines are inflamed, the body initiates an immune response and produces more immune cells to fight the inflammation. Since bionic bone tissue can respond to signals from the immune system, intestinal inflammation also prompts these bone tissues to quickly produce more immune cells. However, in order to increase the production of immune cells, the environment in the bone marrow must change accordingly, and these changes may affect the environment that originally allows cancer cells to maintain a dormant state, causing some dormant cancer cells to start dividing and growing again.

The research team then analyzed gene activity in bone tissue and cancer cells and discovered a molecule called HMGB2. When immune cells increase in large numbers, the levels of HMGB2 also rise, and it also promotes the reactivation of cancer cells. Researchers pointed out that bone's increase in the production of immune cells in response to inflammation is a normal defense mechanism of the body, breaking the original dormant state of cancer cells and reactivating some cancer cells, increasing the risk of metastatic tumor growth.

The research team emphasized that inflammation does not mean that the cancer will definitely come back. Cancer cell reactivation may be a gradual and cumulative process, and each systemic change may increase the chance that more metastatic cancer cells will awaken from dormancy.

The research team claims that if we can better understand how infection, inflammation and other body changes affect the bone marrow environment, it may help to identify the risk of reactivation of dormant cancer cells in the future and explore the possibility of early intervention. The researchers added that this experiment was an animal experiment and may not be fully applicable to humans.

What to Watch

AI outlook — possibilities, not facts

  • Therapeutic approaches that modulate HMGB2 or the bone marrow environment to prevent reactivation of dormant cancer cells will be explored in the future.

    Possible · Within months

Open Questions

  • ?Does this mechanism have the same effect in humans?
  • ?What types of inflammation or infection are most likely to trigger cancer cell reactivation?
  • ?Is there a way to safely modulate HMGB2 to prevent the recurrence of dormant cancer cells?

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This article was originally published by 自由时报.

Quick Look

  • A British research team found through a mouse bone marrow model that intestinal inflammation changes the bone marrow environment, leading to an increase in HMGB2 molecules, which in turn reactivates dormant breast cancer cells and increases the risk of metastatic tumor growth.
  • However, they emphasize that inflammation does not mean that cancer will definitely recur.

AI-generated summary

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High
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Moderate
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National
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Likely
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自由时报
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Published
2 hours ago
View original
breast cancer
dormant cells
intestinal inflammation
breast cancer
Xie Yizhe
Francis. crick institute
SciTechDaily
Liberty Health Network
United Kingdom
dormant cells
intestinal inflammation
HMGB2
bone marrow model
metastatic tumors
immune response

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