We've updated our Privacy Policy to make it clearer how we use your personal data.

We use cookies to provide you with a better experience. You can read our Cookie Policy here.

Immune Response to Tissue Damage Influences Cancer’s Spread

Immune Response to Tissue Damage Influences Cancer’s Spread

Immune Response to Tissue Damage Influences Cancer’s Spread

Immune Response to Tissue Damage Influences Cancer’s Spread

Lung Cancer Metastasis. Credit: Scott Wilkinson, Adam Marcus/ National Cancer Institute
Read time:

Want a FREE PDF version of This News Story?

Complete the form below and we will email you a PDF version of "Immune Response to Tissue Damage Influences Cancer’s Spread"

First Name*
Last Name*
Email Address*
Company Type*
Job Function*
Would you like to receive further email communication from Technology Networks?

Technology Networks Ltd. needs the contact information you provide to us to contact you about our products and services. You may unsubscribe from these communications at any time. For information on how to unsubscribe, as well as our privacy practices and commitment to protecting your privacy, check out our Privacy Policy

Researchers at the Francis Crick Institute have uncovered how a process involved in the regeneration of tissue damaged by radiation can aid the spread of cancer.

The spread of cancer around the body is a complex process and understanding more about how it happens is vital to the development of new treatments.

In their study, published in Nature Cancer today (Thursday), the scientists investigated the relationship between healthy tissue repair and cancer growth.

They exposed healthy mouse lungs, a site where it is common for many cancers to spread, to a high dose of radiation in order to damage the tissue. They then tested the potential of breast cancer cells to grow in the damaged area in comparison to the uninjured lungs. More cancer cells spread to the lungs and began forming secondary tumours in mice that had been injured by radiation compared to the mice who had not.

Further experiments revealed that this is due to the signalling of neutrophils, a type of immune cell, which help repair tissue damage. When the researchers blocked signalling from the neutrophils in the injured lungs, secondary tumours were greatly reduced.

Emma Nolan, first author and postdoc in the Tumour-Host Interaction Laboratory at the Crick, says: “This is a situation where tissue damage sets the stage for the spread of cancer and, in trying to repair the damaged tissue, the immune system inadvertently aids the cancer. This role of neutrophils in supporting cancer spread is something which needs further research and could potentially help to identify new ways to treat the disease.”

Ilaria Malanchi, author and group leader of the Tumour-Host Interaction Laboratory at the Crick, says: “The relationship between cancer cells, the immune system and the organ where cancer takes hold is highly complex. And it’s by untangling aspects of this web that we can better understand why cancer is able to spread, what predisposes organ to the arrival of cancer cells and ultimately how we can try to stop this.”

It is important to note that the radiation that was given to the mice in this study was a higher dose than is used for radiotherapy treatment in hospital and targeted a significantly larger proportion of the tissue. Thanks to advancing technology, the exposure to radiation is now restricted to cancerous tissue and indeed radiotherapy represents a powerful weapon to control cancer disease.

Ilaria adds: “Unrevealing the new responses of neutrophils to radiation we described here, could further enhance the efficacy of this highly-regarded treatment for cancer.”

Reference: Nolan E, Bridgeman VL, Ombrato L, et al. Radiation exposure elicits a neutrophil-driven response in healthy lung tissue that enhances metastatic colonization. Nat Cancer. 2022;3(2):173-187. doi: 10.1038/s43018-022-00336-7

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.