Much cancer research investigates why tumours behave the way they do. Many researchers believe that tumours manipulate their environment to grow and spread, using sophisticated strategies to hijack the body’s own systems. However, new ideas are challenging this view, suggesting that the behaviour of tumours might be closer to the body’s natural responses to damage. In his recent paper, Dr Paul Edwards at Cambridge University offers an eye-opening perspective on this. Read More
Dr Edwards suggests that the way cancer cells and their surrounding environment act may not be unique to cancer itself. Instead, he argues that these behaviours could be the body’s normal way of trying to repair tissue damage triggered by the tumour’s abnormal structure.
This new interpretation means that common features in tumours, such as the way cells change shape, become mobile, and attract nearby immune cells, might not be the result of cancer cells using ‘tricks’ to spread, but rather natural responses to tissue disruption.
Edwards builds on an earlier idea from Dr Harold Dvorak, who described tumours as ‘wounds that do not heal’.
Traditionally, scientists believed that tumours ‘borrow’ wound-healing mechanisms to help them grow. Edwards takes this further, proposing that many of the changes we see around tumours might be the body’s attempt to repair the tissue disruption caused by the tumour.
For instance, one way that tumour cells change – called the ‘epithelial-mesenchymal transition’ or EMT – is linked to the spread of cancer. However, Edwards points out that EMT is a normal response to tissue damage, as it happens when epithelial cells migrate to repair damage. The formation of scar tissue is also a typical response to injury.
He even offers a fresh view on immune cells observed around tumours, suggesting that some may be there as a reaction to tissue damage, like they would be at any wound.
Tumours behave like injured tissue because their disorganisation generates similar distress signals. In an epithelial tumour, disorganisation breaks the barrier between the two sides of the epithelium, creating small electric currents around the tumour, and allowing signalling proteins that are released from one side of the epithelial cells to reach the other side. These signals trigger healing responses.
Edwards’ perspective shifts the focus from seeing tumours as invaders to understanding them as part of a disrupted system trying to heal. This promising approach might help scientists to identify which aspects of tumour behaviour are driven by the cancer itself, and which are normal responses to tissue disorganisation – ultimately reshaping how researchers approach cancer treatment.
